What are the main components of the lumbar spine. How does the lumbar spine develop during embryogenesis. What are the primary functions of the lumbar spine. How do lumbar vertebrae differ from other vertebrae. What is the role of intervertebral discs in the lumbar spine. How do ligaments contribute to lumbar spine stability.

The Lumbar Spine: An Overview of Its Anatomy and Significance

The lumbar spine, a crucial component of the human skeletal system, plays a vital role in supporting the upper body and facilitating movement. Comprising the lower portion of the spinal column, it extends from the last thoracic vertebra (T12) to the first sacral vertebra (S1). This region consists of five robust and mobile vertebrae, labeled L1 through L5, which work in harmony to disperse axial forces and protect the delicate neural structures within.

Understanding the intricacies of lumbar spine anatomy is essential for healthcare professionals, researchers, and anyone interested in spinal health. This comprehensive exploration delves into the structure, function, and embryological development of the lumbar spine, providing valuable insights into this remarkable anatomical region.

The Three Primary Functions of the Lumbar Spine

The lumbar spine serves three main purposes, each critical for our daily activities and overall well-being:

1. Supporting the upper body
2. Protecting the spinal cord and nerves
3. Enabling diverse truncal motions

Upper Body Support

How does the lumbar spine support the weight of the upper body? The lumbar vertebrae are significantly larger compared to other regions of the vertebral column. This increased size allows them to effectively absorb and distribute axial forces transmitted from the head, neck, and trunk. The unique concave curvature of the lumbar spine, known as lumbar lordosis, plays a crucial role in transferring the upper body mass over the pelvis, facilitating efficient bipedal motion.

Neural Protection

What role does the lumbar spine play in protecting neural structures? The lumbar vertebrae form a protective canal that houses and safeguards the spinal cord and spinal nerves. This arrangement is vital for the unimpeded communication of information between the central nervous system and the lower extremities.

Facilitating Movement

How does the lumbar spine contribute to body movement? The unique structure of the lumbar spine allows for a diverse range of truncal motions, including:

• Flexion
• Extension
• Rotation
• Side bending

This flexibility is essential for performing various daily activities and maintaining overall mobility.

Anatomical Components of Lumbar Vertebrae

Each lumbar vertebra is a complex structure composed of multiple components, each serving specific functions. Understanding these components is crucial for comprehending the overall anatomy and biomechanics of the lumbar spine.

Vertebral Body

What is the primary function of the vertebral body? The vertebral body is the main weight-bearing component of the lumbar vertebra. It is a large, cylindrical structure that provides stability and support to the spine.

Posterior Elements

What structures comprise the posterior elements of a lumbar vertebra? The posterior elements include:

• Pedicles: Two bony projections that connect the vertebral body to the posterior elements
• Laminae: Flat, arched structures that form the posterior wall of the vertebral canal
• Spinous process: A bony projection extending posteriorly from the junction of the laminae
• Transverse processes: Two lateral projections that serve as attachment points for muscles and ligaments
• Articular processes: Four processes (two superior and two inferior) that form the facet joints

Zygapophyseal Joints

What are zygapophyseal joints, and what is their function? Zygapophyseal joints, also known as facet joints, are formed by the articulation of the superior and inferior articular processes of adjacent vertebrae. These joints lie in the sagittal plane and play a crucial role in facilitating flexion and extension of the lumbar spine.

Pars Interarticularis

What is the pars interarticularis, and why is it significant? The pars interarticularis is the portion of the lamina between the superior and inferior articular processes. This region is particularly susceptible to stress fractures (spondylolysis) in the growing spine, making it an area of clinical importance.

The Lumbar Intervertebral Disc: Structure and Function

The lumbar intervertebral disc is a crucial component of the spine, playing a vital role in shock absorption and facilitating movement between vertebrae. Understanding its structure and function is essential for comprehending spinal biomechanics and potential pathologies.

Composition of the Lumbar Disc

What are the main components of a lumbar intervertebral disc? The lumbar disc consists of two primary structures:

1. Nucleus pulposus: A gelatinous inner core
2. Annulus fibrosus: A tough, fibrous outer ring

This unique composition allows the disc to effectively distribute forces and maintain flexibility between vertebrae.

Function of the Lumbar Disc

How does the lumbar disc contribute to spinal function? The primary function of the lumbar disc is shock absorption. It acts as a cushion between vertebrae, dissipating forces and preventing direct bone-on-bone contact. Additionally, the disc’s structure allows for limited movement between vertebrae, contributing to the overall flexibility of the lumbar spine.

Ligaments of the Lumbar Spine: Stability and Support

Ligaments play a crucial role in maintaining the stability and integrity of the lumbar spine. These tough, fibrous structures connect bones and limit excessive movement, protecting the spine from injury.

Longitudinal Ligaments

What are the main longitudinal ligaments of the lumbar spine, and what are their functions?

• Anterior longitudinal ligament (ALL): Runs along the front of the vertebral bodies, resisting lumbar extension, translation, and rotation
• Posterior longitudinal ligament (PLL): Runs along the back of the vertebral bodies, resisting lumbar flexion

Segmental Ligaments

What segmental ligaments are present in the lumbar spine, and what roles do they play?

• Ligamentum flavum: Connects the laminae of adjacent vertebrae, providing elastic support and assisting in maintaining upright posture
• Supraspinous ligament: Runs along the tips of the spinous processes, resisting lumbar flexion
• Interspinous ligament: Connects adjacent spinous processes, also resisting lumbar flexion

These ligaments work in concert to provide stability to the lumbar spine while allowing for controlled movement.

Embryological Development of the Lumbar Spine

The formation of the lumbar spine is a complex process that begins early in embryonic development. Understanding this process provides insights into normal spinal anatomy and potential congenital anomalies.

Initiation of Spinal Development

When does lumbar spine development begin, and what structures are involved? The development of the lumbar spine commences around the third week of gestation. This process is initiated by the notochord, a rod-like structure that secretes growth factors stimulating the ectoderm to transform into the neuroectoderm.

Neurulation and Neural Tube Formation

What is neurulation, and how does it contribute to spinal development? Neurulation is the process by which the neural tube, the precursor to the spinal cord, is formed. This critical step occurs early in embryonic development and is crucial for the proper formation of the central nervous system.

How can errors in neurulation affect spinal development? Disruptions in the neurulation process can lead to various congenital anomalies, ranging from mild conditions like spina bifida to severe malformations such as anencephaly.

Somite Development and Vertebral Formation

How do somites contribute to the formation of the lumbar spine? Around the third week of gestation, pairs of somites develop along either side of the neural tube. These somites differentiate into structures called dermomyotomes and sclerotomes. The sclerotomes then separate into cell clusters that ultimately fuse to form the vertebral bodies and intervertebral discs.

Ossification of Lumbar Vertebrae

What process leads to the formation of bony vertebrae? Each vertebra undergoes a process called endochondral ossification. In this process, mesenchymal cells differentiate into cartilage, which is gradually replaced by bone tissue. This transformation results in the formation of the mature, bony vertebrae of the lumbar spine.

Clinical Significance of Lumbar Spine Anatomy

Understanding the intricate anatomy of the lumbar spine is crucial for healthcare professionals dealing with spinal disorders and injuries. This knowledge forms the foundation for accurate diagnosis, effective treatment, and successful surgical interventions.

Common Lumbar Spine Pathologies

What are some frequent conditions affecting the lumbar spine?

• Herniated discs
• Spinal stenosis
• Spondylolisthesis
• Lumbar radiculopathy
• Degenerative disc disease

Each of these conditions has unique characteristics and management strategies rooted in the understanding of lumbar spine anatomy.

Diagnostic Imaging of the Lumbar Spine

How does knowledge of lumbar anatomy aid in interpreting diagnostic images? A thorough understanding of lumbar spine anatomy is essential for accurately interpreting various imaging modalities, including:

• X-rays
• Computed Tomography (CT) scans
• Magnetic Resonance Imaging (MRI)

This knowledge allows healthcare professionals to identify normal structures, detect abnormalities, and make informed decisions regarding patient care.

Surgical Considerations in Lumbar Spine Procedures

Why is a detailed understanding of lumbar anatomy crucial for spinal surgeons? Lumbar spine surgeries require precise knowledge of the anatomical relationships between vertebrae, nerves, blood vessels, and surrounding soft tissues. This understanding is vital for:

• Planning surgical approaches
• Avoiding iatrogenic injuries
• Achieving optimal surgical outcomes
• Minimizing postoperative complications

From minimally invasive procedures to complex spinal fusions, a comprehensive grasp of lumbar anatomy is indispensable for successful surgical interventions.

Future Directions in Lumbar Spine Research and Treatment

As our understanding of lumbar spine anatomy continues to evolve, new avenues for research and treatment are emerging. These advancements promise to revolutionize the management of lumbar spine disorders and improve patient outcomes.

Regenerative Medicine and Tissue Engineering

How might regenerative medicine impact lumbar spine treatment? Ongoing research in regenerative medicine and tissue engineering holds promise for developing novel treatments for degenerative disc disease and other lumbar spine conditions. Potential applications include:

• Stem cell therapies for disc regeneration
• Bioengineered intervertebral discs
• Growth factor treatments to stimulate tissue repair

Advanced Imaging Techniques

What new imaging technologies are being developed for lumbar spine assessment? Emerging imaging technologies, such as high-resolution MRI and advanced CT techniques, are providing increasingly detailed views of lumbar spine anatomy. These advancements may lead to:

• Earlier detection of spinal pathologies
• More accurate preoperative planning
• Improved monitoring of treatment outcomes

Minimally Invasive Surgical Techniques

How are minimally invasive approaches changing lumbar spine surgery? The development of minimally invasive surgical techniques, guided by detailed anatomical knowledge, is transforming lumbar spine procedures. Benefits of these approaches include:

• Reduced tissue damage
• Shorter recovery times
• Lower risk of complications
• Improved cosmetic outcomes

As these techniques continue to evolve, they promise to make lumbar spine surgeries safer and more effective for patients.

Biomechanical Modeling and Personalized Treatment

How can advanced biomechanical modeling improve lumbar spine care? The integration of detailed anatomical data with sophisticated biomechanical modeling techniques is paving the way for personalized treatment approaches. These models can help:

• Predict the outcomes of various interventions
• Optimize treatment plans for individual patients
• Develop more effective rehabilitation protocols

By combining anatomical knowledge with cutting-edge technology, healthcare professionals can provide increasingly tailored and effective care for patients with lumbar spine disorders.

In conclusion, the lumbar spine is a marvel of anatomical engineering, providing support, protection, and mobility to the human body. Its complex structure, comprising vertebrae, discs, ligaments, and neural elements, works in harmony to facilitate our daily activities. As our understanding of lumbar spine anatomy continues to grow, so too does our ability to diagnose, treat, and prevent spinal disorders. From embryological development to advanced surgical techniques, the study of lumbar spine anatomy remains a critical field in healthcare and biomedical research. By continuing to explore and unravel the intricacies of this remarkable structure, we pave the way for improved patient care and innovative treatments in the future.

Anatomy, Back, Lumbar Spine – StatPearls

Introduction

The lumbar spine comprises the lower end of the spinal column between the last thoracic vertebra (T12) and the first sacral vertebra (S1). The spinal cord in this region has protection from five durable and mobile vertebrae (L1-L5) that allow for the dispersion of axial forces. The spinal cord runs through the center of the vertebral column and terminates in the conus medullaris at the level of the L1-L2 vertebrae. The cauda equina, Latin for horse’s tail, is a bundle of spinal nerve roots that begin at the termination of the spinal cord and descend through the remainder of the canal. The lumbar spine is comprised of bone, cartilage, ligaments, nerves, and muscle. Each of these components plays an integral role in the form and function of the lumbar spine.[1][2]

Structure and Function

There are three main functions of the lumbar spine. First, the lumbar spine assists in supporting the upper body. The lumbar vertebrae (L1-L5) are much larger when compared to other regions of the vertebral column, which allow them to absorb axial forces delivered from the head, neck, and trunk. The lumbar vertebrae form a canal that serves to protect the spinal cord and spinal nerves. This arrangement allows for the communication of information from the central nervous system to the lower extremities and vice versa. The lumbar spine allows for diverse types of truncal motion, including flexion, extension, rotation, and side bending. From a lateral view, the lumbar spine has a concave curvature, referred to as the lumbar lordosis. This curvature is variable in degree and transfers the upper body mass over the pelvis to allow for efficient bipedal motion.[3]

Each lumbar vertebra consists of multiple components. These include the vertebral body and the dorsal structures termed the posterior elements. Immediately dorsal to the vertebral body lie two pedicles that attach to the laminae. The pedicles resist motion and transmit forces from the posterior elements to the vertebral body. From the junction of the two laminae, the spinous process extends posteriorly. At the junction between the pedicles and laminae, four articular processes and two transverse processes reside. The transverse processes extend laterally, serving as attachment points for ligaments and musculature. The superior and inferior articular processes create the zygapophyseal joints (aka facet joints). This joint occurs between the superior articular process of a vertebra and the inferior articular process of the vertebra immediately cephalad. These joints lie in the sagittal plane and participate in flexion and extension of the lumbar spine. The pars interarticularis is the location of the lamina between the superior and inferior articular processes and is prone to the development of stress fractures (spondylolysis) in the growing spine.[1]

The lumbar disc is a fibrocartilaginous structure that is seated between two vertebral body endplates. It is composed of an internal gelatinous nucleus pulposus and an external fibrous annulus fibrosus. The primary function of the lumbar disc is shock absorption. Two longitudinal ligaments lie anterior and posterior to the vertebral body. The anterior longitudinal ligament resists lumbar extension, translation, and rotation. The posterior longitudinal ligament resists lumbar flexion. The segmental ligaments include the ligamentum flavum, which is perforated when performing a lumbar puncture. The remaining segmental ligaments include the supraspinous and interspinous ligaments, which lie between the spinous processes and resist lumbar flexion.[1][4]

Embryology

The development of the lumbar spine begins around the third week of gestation. The notochord initiates this process by secreting growth factors that stimulate the ectoderm to transform into the neuroectoderm. The process of neurulation produces the neural tube, which ultimately develops into the spinal cord. Errors during neurulation may result in numerous congenital anomalies ranging from mild (spina bifida) to severe (anencephaly).[5]

Also occurring around the third week, the paraxial mesoderm develops into pairs of somites along either side of the neural tube. Each somite differentiates into a dermomyotome and sclerotome. The sclerotome separates into cell clusters located caudally and cranially. Neurons from the neural tube penetrate these clusters to innervate individual myotomes and dermatomes. The caudally located cell clusters then fuse with the cranially located clusters of the adjacent sclerotome to create the vertebral body. Between each cell cluster, the interverbal disc develops. Simultaneously, sclerotome cells migrate around the neural tube and fuse dorsally, creating the vertebral arch.[5]

Each vertebra undergoes a process of endochondral ossification, in which the mesenchymal cells differentiate into cartilage and eventually bone. Chondrification centers develop around the sixth week and primary ossification centers in the seventh. These processes are responsible for strengthening the eventual vertebra. Bone remodeling continues throughout the lifespan and is highly dependent on stress and mechanical loads.[5][6]

Blood Supply and Lymphatics

The spinal cord has a rich blood supply stemming from three main longitudinal arteries. A single anterior spinal artery supplies the anterior two-thirds of the cord. On the dorsal side, two posterior spinal arteries supply the posterior one-third of the cord. Several anterior and posterior radicular arteries provide collateral blood supply to the vertebral column. These radicular arteries run along with the ventral and dorsal nerve roots, supplying them with blood. The artery of Adamkiewicz is the largest radiculomedullary artery and provides vascular supply to the lumbar spinal cord. The artery has a variable origin between T8-L2, branching from a posterior intercostal or radicular artery. It typically lies left of the spinal cord and ascends the spinal canal, making a hairpin loop before joining the anterior spinal artery.[7] Specific to the lumbar spine, four pairs of lumbar arteries originate from the abdominal aorta. These paired arteries travel posteriorly along the vertebral bodies to supply each vertebra. These arteries also supply blood to the adjacent musculature, such as the transversus abdominis and internal oblique.

An extensive system of lymphatics in the lumbar region is responsible for draining lymph from the lower limb and pelvis. These lymph nodes are present along the inferior vena cava and aorta. The lumbar lymph nodes receive drainage from the common iliac nodes and deliver this lymph to the thoracic trunk.[7]

Nerves

Five pairs of mixed spinal nerves emerge from either side of the lumbar spinal cord, carrying both motor and sensory nerve fibers—the spinal nerves branch after exiting the neural foramen into ventral and dorsal rami. The dorsal rami supply motor innervation to the erector spinae musculature and sensation to the skin over the back. The ventral rami supply motor and sensory fibers to the remainder of the prevertebral musculature and lower limbs.[8]

The T12 to L4 ventral rami combine to form a network of nerves called the lumbar plexus. The lumbar plexus gives rise to the obturator (L2-L4) and femoral (L2-L4) nerves, respectively. The remaining nerves of the lumbar plexus include the iliohypogastric (T12-L1), ilioinguinal (L1), genitofemoral (L1-L2), and lateral femoral cutaneous nerve of the thigh (L2-L3)—the lumbosacral plexus form from the L4 to S4 ventral rami. The L4 and L5 roots join to form the lumbosacral trunk, which descends into the pelvis to join to sacral plexus. The lumbosacral plexus then gives rise to the sciatic nerve (L4-S3), which branches into the common peroneal and tibial nerves. The sacral plexus also includes the superior gluteal (L4-S1), inferior gluteal (L5-S2), posterior femoral cutaneous of the thigh (S1-S3), and pudendal nerve (S1-S4).[9]

Each lumbar spinal nerve exits below its corresponding vertebra—for example, the L4 nerve exits below the L4 vertebra through the L4-L5 neural foramen. A majority of lumbar disc herniations occur centrally and do not compress the exiting nerve root at the level of the disc. The nerve root most commonly affected exits one level below the herniated disc. For example, an L4-L5 central disc herniation will most commonly compress the L5 nerve root in the lateral recess of the spinal canal. However, in the setting of a far lateral disc herniation, the L4 nerve root is compressed, albeit less commonly. This difference is due to the more central position of the traversing spinal nerves when compared to the more lateral position of the exiting spinal nerves.[8]  

Each spinal nerve supplies an area of skin with afferent sensory fibers. This area of skin is referred to as a dermatome. Each lumbar spinal nerve also innervates a group of muscles with motor fibers, termed a myotome. Dermatomes and myotomes trace back to our embryological development. Dermatomes and myotomes are clinically relevant as they can be used to determine the lumbar spinal nerve(s) involved in the setting of pathology.

This section will focus on the sensory and major muscular innervations of the lumbar spinal nerves. L1 and L2 innervate the iliopsoas muscle and provide sensory innervation to the inguinal crease and medial thigh. L3 partially innervates the adductors, iliopsoas, and quadriceps musculature. L3 provides sensory innervation to the anterior-medial thigh. L4 contributes to the femoral and sciatic nerves, innervating the iliopsoas, adductors, quadriceps, and tibialis anterior. The L4 nerve provides sensory innervation to the anterior thigh and medial lower leg. The L3 and L4 nerves contribute to the patellar reflex arc. L5 innervates the gluteus medius, tensor fascia latae, medial hamstrings, tibialis anterior, extensor hallucis longus, extensor digitorum longus/brevis, peroneus longus, tibialis posterior, and the flexor digitorum longus. L5 provides sensory innervation to the lateral leg and dorsum of the foot. It is clinically important to note that each dermatome overlaps with adjacent dermatomes. Therefore, dense numbness is exceedingly rare in the setting of nerve root compression. Each myotome also overlaps, leading to nearly every muscle of the lower extremity receiving innervation from 2 or 3 lumbar spinal nerves.[8]

Muscles

Many muscles use the lumbar vertebrae as attachment points. These muscles allow for smooth, controlled movement in different functional planes. These muscles also serve a secondary role in stabilization, protection, and proprioception. Three major muscle groups originate or insert on the lumbar spine and aid in movement. First, the extensor group consists of the erector spinae and the multifidi. This group lies posterior to the lumbar spine. In this region, the erector spinae muscles include the longissimus thoracis and iliocostalis lumborum. The contraction of this group results in an extension moment at the lumbar spine. The flexor group lies anterior to the lumbar spine and allows for trunk flexion as well as hip flexion. The psoas major originates from the T12-L4 transverse processes and joins the iliacus in the thigh to become the iliopsoas (composite muscle). The iliopsoas plays a key role in hip flexion and also assists with the arching of the lumbar spine. The abdominal musculature (internal/external oblique, rectus abdominis) plays a more important role in truncal flexion. Finally, a concerted effort involving several muscles is required to create rotation and lateral flexion (side-bending) of the lumbar spine.  The quadratus lumborum, psoas major, abdominal musculature, and multifidi play an important role in creating these motions.[2]

Muscle strains in the lumbar region are typically the result of abnormal tension placed upon a tendon; this can occur from overstretching a muscle, repetitive use, or muscle tearing from excessive force. Most lumbar muscle strains will respond to conservative treatment.

Surgical Considerations

Spinal surgery for the management of low back pain, lumbar radiculopathy, and lumbar spinal stenosis is a consideration after the failure of conservative treatments. Spinal surgery is the first-line treatment in more urgent/emergent conditions such as conus medullaris syndrome, cauda equina syndrome, cancer (primary/metastatic), osteomyelitis/discitis, epidural abscess, and trauma. The surgical technique and instrumentation implemented depend upon patient factors and the diagnosis requiring treatment.

Lumbar decompression is a technique used to relieve pain caused by a compressed nerve root(s). Two of the most common types of nerve root compression are lumbar central canal stenosis and lumbar radiculopathy, reviewed in the next section. Lumbar decompression comes in several forms, including microdiscectomy, foraminotomy, laminotomy, laminectomy, or a combination of these. Laminectomy (surgical removal of the laminae) is considered the standard surgical treatment for the management of lumbar spinal stenosis. If the decompression, as mentioned above, leads to iatrogenic instability, then a fusion is also performed.[10]

Lumbar fusion is a common surgery used to manage discogenic/facetogenic low back pain, radiculopathy, and spinal deformity (scoliosis/spondylolisthesis). Several surgical approaches exist within two main categories, posterior and interbody fusion. The more traditional approach is that of a posterior spinal fusion implementing rods and pedicular screws. Limitations of this approach include the need for thecal sac and nerve root retraction along with iatrogenic injury of the paraspinal musculature. Interbody fusion involves placing an implant such as a cage or bone graft within the intervertebral space following a discectomy (removing the intervertebral disc). Surgical approaches for interbody fusion are multiple (posterior, transforaminal, oblique, lateral, and anterior). Anterior spinal fusion avoids the canal and nerve roots but does introduce complications such as vascular injury and incisional hernia. There is limited comparative data that one approach is superior to another. Following fusion, chronic postoperative complications include pseudoarthrosis (failure of fusion) and adjacent segment degenerative disc disease above/below the fusion level.[11]

Non-surgical treatment can include manipulation therapy and/or physical therapy. The decision regarding whether to use these methods will depend on how acute the injury is, patient compliance, and severity of symptoms.[12]

Clinical Significance

Non-specific low back pain is one of the leading causes of disease burden globally—estimates of indirect costs in the US range from 18. 5 to 28.2 billion dollars. Low back pain can be triggered by physical factors (i.e., poor lifting mechanics) and psychosocial factors. Often a specific trigger is not identified. Low back pain is a symptom of several different disease processes. Triage is necessary to rule out specific disorders that may require urgent/emergent workup and treatment. ‘Red flags’ for the lumbar spine include trauma, age >70, unexplained weight loss, history of cancer, constitutional symptoms, night pain, saddle anesthesia, and impaired bowel or bladder function. Red flags are associated with vertebral fracture, malignancy, infection (osteomyelitis/discitis), and conus medullaris/cauda equina syndrome (reviewed below).[13]

The termination of the spinal cord, termed the conus medullaris, occurs at the L1-L2 vertebrae. This structure is clinically significant for procedures in this area, most notably the lumbar puncture. A lumbar puncture (spinal tap) is performed by inserting a needle between the vertebral lamina to obtain a cerebrospinal fluid sample. This procedure must occur below the level of L2, between L3-L4 or L4-L5 laminae, to avoid the spinal cord. Conus medullaris syndrome results from severe compression or injury of the conus medullaris. The most common etiologies for this condition include trauma, disc herniations, and epidural abscesses. Signs/symptoms of conus medullaris syndrome include severe/sudden onset low back pain, symmetrical weakness of both legs, and sudden loss of bowel and bladder function. Immediate treatment is necessary to prevent permanent damage and to preserve lower extremity neurologic function. Caudal to the conus medullaris in the spinal canal is the cauda equina. The cauda equina is a collection of spinal nerves located from L1-L5 in the spinal canal.  The spinal nerves that make up the cauda equina are the L2-L5, S1-S5, and the coccygeal nerve. Compression of the cauda equina is also a surgical emergency. The most common signs and symptoms include urinary retention, saddle anesthesia (numbness of the perineum/inner thighs), as well as radicular leg pain. [14]

There are several plausible pathoanatomical disorders of the lumbar spine. The surrounding musculature, intervertebral disc, facet joints, and spinal nerves may each serve as potential pain generators. However, most low back pain is ‘non-specific and does not have a pathoanatomical explanation. Diagnostic investigations are typically not indicated in the initial management of low back pain unless a specific disease process would be managed differently due to the investigation. Immediate imaging may be indicated when red flags are present. Plain film radiography followed by MRI of the lumbar spine is the commonly performed sequence as the initial diagnostic workup. In some cases, CT scanning may still play a role.

Lumbar spondylosis (osteoarthritis) results from a degenerative cascade involving the lumbar intervertebral disc and the facet joints. The cascade progresses with age, thought to be initiated by an insult or injury. The cascade is also heavily influenced by genetic factors. The lumbar disc initially develops circumferential annular tears leading to internal disc disruption; this is followed by disc resorption, which leads to loss of disc height and eventual osteophyte (bone spur) development. Degeneration begins with a synovial reaction leading to cartilage disruption within the facet joints, which progresses to the formation of osteophytes, joint capsular laxity, and joint subluxation. The combination of these conditions can lead to segmental spinal instability, referred to as spondylolisthesis (slippage of one vertebra on another). Progressive spondylosis can lead to structural narrowing around the lumbar nerve roots, resulting in radiculopathy and/or spinal stenosis in the lumbar spine. Lumbar spondylosis is a widespread condition that is often asymptomatic, most commonly occurring at the L4-5 segment.[15]  

Compression, injury, or irritation of the lumbar spinal nerve roots can occur from multiple potential sources. Most commonly, this occurs as a consequence of the degenerative cascade or an acute disc herniation. Lumbar radiculopathy (aka sciatica) describes the constellation of symptoms resulting from lumbar nerve compression. Individuals present with variable degrees of radiating pain, paresthesia (numbness/tingling), and weakness in the lower extremities. Lumbar stenosis is a condition in which the narrowing of the spinal canal occurs. This narrowing is usually secondary to degenerative spondylosis and spondylolisthesis. Classically individuals present with low back and/or lower extremity pain/paresthesias, which worsen with lumbar extension, prolonged standing, and ambulation. The pathophysiology appears to be due to mechanical compression of the lumbosacral spinal nerve roots resulting in ischemia.[16][17]

Treatment of low back pain is targeted depending on the diagnosis established. Treatment is initially conservative, incorporating a multidisciplinary approach with a combination of pharmacologic and non-pharmacologic therapies. Non-pharmacological therapies include physical therapy, manual therapy, home exercise, acupuncture, cognitive behavioral therapy, etc. Clinicians can implement interventional treatments such as epidural steroid injections for the management of recalcitrant lumbar radicular pain. Pain emanating from the facet joints can have treatment with medial branch radiofrequency ablation.[13]

Figure

Vertebrae, Lumbar, Ligament, Medial Sagittal Section, Anterior Longitudinal Ligament, Inter vertebral Fibrocartilage, Posterior Longitudinal Ligament, Lamina, Ligamenta Flava, Pedicle, Spinous Process, Interspinal Ligament, Capsular ligament, Supraspinal (more…)

Figure

A Lumbar Vertebra from the side. Contributed by Gray’s Anatomy Plates

Figure

A Lumbar Vertebra from above and behind. Contributed by Gray’s Anatomy Plates

Figure

Lumbar Vertebrae. Contributed by Gray’s Anatomy Plates

Figure

Anatomy of the distal lumbar spine. Image courtesy S Bhimji MD

References

1.

Waxenbaum JA, Reddy V, Williams C, Futterman B. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 10, 2020. Anatomy, Back, Lumbar Vertebrae. [PubMed: 29083618]

2.

Gilchrist RV, Frey ME, Nadler SF. Muscular control of the lumbar spine. Pain Physician. 2003 Jul;6(3):361-8. [PubMed: 16880883]

3.

Boszczyk BM, Boszczyk AA, Putz R. Comparative and functional anatomy of the mammalian lumbar spine. Anat Rec. 2001 Oct 01;264(2):157-68. [PubMed: 11590593]

4.

Devereaux MW. Anatomy and examination of the spine. Neurol Clin. 2007 May;25(2):331-51. [PubMed: 17445732]

5.

Kalamchi L, Valle C. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 8, 2021. Embryology, Vertebral Column Development. [PubMed: 31751107]

6.

O’Rahilly R, Müller F, Meyer DB. The human vertebral column at the end of the embryonic period proper. 3. The thoracicolumbar region. J Anat. 1990 Feb;168:81-93. [PMC free article: PMC1256892] [PubMed: 2323997]

7.

Kaiser JT, Reddy V, Lugo-Pico JG. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 10, 2020. Anatomy, Back, Spinal Cord Arteries. [PubMed: 30725904]

8.

Basit H, Reddy V, Varacallo M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 8, 2021. Anatomy, Back, Spinal Nerve-Muscle Innervation. [PubMed: 30855906]

9.

Singh O, Al Khalili Y. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 10, 2020. Anatomy, Back, Lumbar Plexus. [PubMed: 31424721]

10.

Williams MG, Wafai AM, Podmore MD. Functional outcomes of laminectomy and laminotomy for the surgical management lumbar spine stenosis. J Spine Surg. 2017 Dec;3(4):580-586. [PMC free article: PMC5760430] [PubMed: 29354735]

11.

Mobbs RJ, Phan K, Malham G, Seex K, Rao PJ. Lumbar interbody fusion: techniques, indications and comparison of interbody fusion options including PLIF, TLIF, MI-TLIF, OLIF/ATP, LLIF and ALIF. J Spine Surg. 2015 Dec;1(1):2-18. [PMC free article: PMC5039869] [PubMed: 27683674]

12.

Kuligowski T, Skrzek A, Cieślik B. Manual Therapy in Cervical and Lumbar Radiculopathy: A Systematic Review of the Literature. Int J Environ Res Public Health. 2021 Jun 07;18(11) [PMC free article: PMC8201115] [PubMed: 34200510]

13.

Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet. 2017 Feb 18;389(10070):736-747. [PubMed: 27745712]

14.

Brouwers E, van de Meent H, Curt A, Starremans B, Hosman A, Bartels R. Definitions of traumatic conus medullaris and cauda equina syndrome: a systematic literature review. Spinal Cord. 2017 Oct;55(10):886-890. [PubMed: 28534496]

15.

Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine (Phila Pa 1976). 1978 Dec;3(4):319-28. [PubMed: 741238]

16.

Alexander CE, Varacallo M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 21, 2021. Lumbosacral Radiculopathy. [PubMed: 28613587]

17.

Wu L, Cruz R. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Dec 20, 2020. Lumbar Spinal Stenosis. [PubMed: 30285388]

Where do patients with MRI-confirmed single-level radiculopathy experience pain, and what is the clinical interpretability of these pain patterns? A cross-sectional diagnostic accuracy study | Chiropractic & Manual Therapies

This cross-sectional diagnostic accuracy study used two sources of data: (Part 1 – Pain patterns) a secondary analysis was performed of baseline data collected during a randomized controlled clinical trial (RCT), and (Part 2 – Clinical utility) data were prospectively collected to measure the discriminative ability of the identified pain patterns.

Part 1 – pain patterns

Patient sample

Data from the single-blind RCT had been prospectively collected at the Medical Department of the Spine Centre of Southern Denmark, which is an outpatient secondary care hospital department. Detailed descriptions of the trial procedures have been published elsewhere [14]. Briefly, consecutive patients were included between November 2000 and December 2001 if they were 18–65 years of age and had all of the following: radicular pain to the knee or more distally in one or both legs, leg pain > 3 on a 1–10 point scale at first visit to the clinic, and a duration of radiculopathy between 2 weeks and 1 year. Patients were excluded if they would have been unable to participate in the rehabilitation protocol, had a spinal tumor, previous back surgery, were pregnant, or if their health status was associated with any pending litigation. Informed consent was obtained from all individual participants included in the study.

At baseline, a medical history was obtained and a thorough physical examination of the spine and lower extremities, including assessments of paraesthesia, anaesthesia, straight leg raise, reflexes and muscle testing, were undertaken for all patients by the same examiner who was blinded to treatment allocation. Patients self-completed a questionnaire pack that included anterior and posterior full-body pain drawings. At baseline, almost all (95%, n = 172) patients had between two and four positive neurological signs (hypoalgesia, diminished reflexes, muscle weakness, positive Straight Leg Raise test), with a mean of 2.8 signs.

Immediately following their baseline clinical examination, all participating patients also underwent an MRI examination that was obtained in an open low field 0.2 T, MRI unit using a body spine surface coil. Patients were positioned in supine with extended hips and knees, producing a slight lumbar lordosis.

The imaging protocol consisted of one localizer and four imaging sequences:

• Localizer sequence, 40/10/40 (TR/TE/flip angle), two coronal and three sagittal images in orthogonal planes, one acquisition in 32 s.

• Sagittal T1-weighted spin echo, 621/26 (TR/TE), 144 × 256 matrix, 300 mm FOV, and 11 4 mm slices, distance factor 0. 20, two acquisitions in 6:01 min.

• Sagittal T2-weighted turbo spin echo, 4609/134 (TR/effective TE), 210 × 256 matrix, 300 mm FOV, and 11 4 mm slices, distance factor 0.20, two acquisitions in 8:42 min.

• Axial T1-weighted spin echo, 720/26 (TR/TE), 192 × 256 matrix, 240 mm FOV, and 15 5 mm slices, distance factor 0.25, two acquisitions in 8:49 min.

• Axial T2-weighted turbo spin echo, 6415/134 (TR/effective TE), 180 × 256 matrix, 250 mm FOV, and 15 5 mm slices, distance factor 0.25, one acquisition in 7:49 min.

• Axial images were performed on the three lower lumbar levels. If protrusions were present at higher lumbar levels, relevant supplementing axial series were performed.

The axial sequences (both T1 and T2 weighted), which are central to the diagnosis of herniations and nerve root compromise, were performed at the three lowest levels on all patients (five images each per level). If there were herniations or nerve root compromise at levels in the upper lumbar spine, additional axial sequences were performed at those levels. The slice thickness was 5 mm for axial images to compensate for the low signal-to-noise ratio due to a smaller field of view as compared to the sagittal sequences, for which 4 mm slices were used. Between 16 to 24 slices were obtained, depending on the size of the person.

All MRIs were evaluated by the same consultant radiologist, who was experienced in the use of a standardized research protocol for describing disc lesions [15] and blinded to each patient’s clinical characteristics. Intervertebral discs were classified as: normal, bulging, focal protrusion, broad-based protrusion, extrusion and sequestration, based on the American Society of Radiologists classification at that time [16, 17]. In a previous study, that included the ratings of the same consultant radiologist, the test-retest reproducibility of localization of disc herniation using this protocol was kappa 0.72 (0.55–0.89) [15]. The spinal level of the compressed nerve root was identified by reference to the vertebral location of the axial slice, the sagittal location of the disc lesion and the location of the nerve root relative to others at that vertebral level. Nerve root compromise was classified as; no contact, contact, displacement, compression of nerve root. The test-retest reproducibility of identifying nerve root lesions using this protocol was kappa 0.82 (0.70–0.94) [18].

Pain drawings

Patients were asked to indicate the distribution of their pain by drawing on a pain chart. Their drawing was then discussed with the examiner to ensure comprehension, precision and that numbness and paraesthesia had not been registered as pain. As almost all patients drew with lines and/or zig-zags, prior to electronically scanning the pain chart, the total painful area was delineated by manually filling in the areas while respecting its outside boundaries (Fig. 1).

Fig. 1

An example of one patient’s original pain drawing and after being manually delineated

Each pain drawing was scanned into an electronic image via a standardized process: (i) all drawings were physically the same size, (ii) they were digitised using the same high-quality scanner calibrated with the same settings, (iii) any drawings indicating unilateral left sided pain were mirror-imaged so that all drawings indicated right-sided pain, (iv) all electronic images from patients with same MRI-confirmed disc-level herniation were imported into a single, multi-layered (composite) Adobe Photoshop CS3 file (Adobe Systems Incorporated, San Jose, California, USA). Each disc level-specific composite file was grey-scaled with the overall transparency of each layer calibrated so that the total density of all layers summed to 100%. Therefore, the density (darkness) of the grey scale pain areas on the composite images was representative of the proportion of patients who described pain in that area.

As it eventuated that there were only 5 patients with L4 nerve root irritation in the sample, and as we believed these to be too few to be representative, composite images were created for the L5 nerve root and S1 nerve root only. These composite images were compared with two common dermatomal images, those of Sherrington [19] and of Keegan and Garrett [20], and a subjective judgement made as to their similarity. We adapted the criteria of Murphy et al. [11], who judged a composite pain pattern to be non-dermatomal if the main commonality of the pain distribution was not contained within the area suggested by the dermatome chart to represent the cutaneous distribution of the involved nerve root. Our adaptation was to subjectively judge the proportion of the main commonality that was contained by the dermatome. As Rankine et al. [13] found that psychological distress minimally affected the utility of patients’ pain distribution for classifying the vertebral level of radiculopathy, therefore in our study, the presence of psychological distress was not an exclusion criterion, so that the sample would be more representative of the usual spectrum of patients in clinical practice.

Of the original 181 patients who participated in the RCT, the pain charts from 93 patients were included in this study. The reasons for exclusion were: multilevel disc lesions observed on MRI or L4 nerve root involvement. The pain drawing and MRI scan were obtained on the same day.

In the current study, the reference standard was the empirically-derived unisegmental radiculopathy pain distributions. This study did not seek to determine the association between the reference standard of pre-defined, commonly accepted dermatomal distributions and the presence of clinical or MRI findings, such as undertaken by Beattie et.al (2000) [10]. Instead, we took the empirical approach of ‘letting the pain drawing do the talking’ where all the pain drawings for MRI and clinically-confirmed unisegmental radiculopathy contributed to the collective image that defined pain distribution for that nerve root level. Only then did we look for an association with commonly accepted dermatomes. These two modes of inquiry address different research questions.

Part 2 – clinical utility

In this context, we use the term ‘clinical utility’ to refer to the extent to which a test has the capacity to improve health outcomes [21, 22].

Clinician sample

Participants in this component were 18 clinicians – six physiotherapists, six medical doctors and six chiropractors – purposefully selected from a convenience sample at the Medical Department of the Spine Centre of Southern Denmark, so that two from each profession were in each of three groups. Based on our sample size estimate (see below), individuals in each group were given the task of classifying which of 53 randomly selected individual pain charts came from patients who had an L5 or S1 radiculopathy. Clinicians knew that the pain charts came from patients with either an L5 or S1 radiculopathy but were blind to all other clinical information about individual patients. This was a dichotomous choice for clinicians, as all of the randomly-selected 53 patients (26 with L5 and 27 with S1 radiculopathy) had an MRI and clinically confirmed, single-level radiculopathy involving only one of these nerve roots. A study flow chart is shown in Fig. 2.

Fig. 2

However, the test conditions were different across the groups. Group 1 was not shown the composite pain charts and therefore classified the pain charts based on their previous experience. Group 2 studied the composite pain charts for 2 min and then completed the task using a combination of their previous experience and the memory of the composite drawings. Group 3 could refer to the composite pain charts when classifying each individual pain chart. This design allowed the discriminative ability of the identified pain patterns to be tested, as the groups’ knowledge of the pain patterns ranged from no knowledge through to the pain patterns being visible as they classified each patient as being likely to have either L5 or S1 radiculopathy. Our hypothesis was that exposure to the pain patterns would increase the clinicians’ discriminative ability. The sequence of the pain charts was randomized using Microsoft Excel (Microsoft Corp, Redmond, WA, USA). The nerve root judgements of each clinician were compared to the actual radiculopathy level for each patient and these data were double-entered in the data management system Epidata (Epidata 3.1, The EpiData Association, Odense, Denmark) by two research secretaries.

Sample size calculation

Using Altman’s formula, we powered the study to arbitrarily detect a difference between one group’s 80% correct ratings and a second group’s 70% correct ratings, with a power of 80% [23].

The choice of powering the study to detect a difference of 10% was based on our opinion that smaller between-group differences were unlikely to be clinically important. The resultant sample size required to detect this difference was 294, so we collected 318 ratings within each of the three groups (53 ratings from 6 observers), which was 954 ratings collectively across the three groups.

Comparisons

The proportion of correct ratings for each clinician group was calculated and tested for significant differences across groups using Bonferroni-adjusted inferential confidence intervals [24]. The alpha level for each comparison was determined using the following calculation: ‘alpha/number of comparisons’ = (n x (n-1))/2. As there were 3 pair-wise comparisons, the alpha level for any pair-wise comparison was reset to (0.05/3) = 0.017. Inferential confidence intervals are Bonferroni-adjusted so that if no numerical overlap occurs between compared confidence bands, a difference between proportions can be concluded with 95% confidence, and these were calculated using Microsoft Excel (Microsoft Corp, Redmond, WA, USA).

The proportion of clinicians who correctly classified whether each patient’s radiculopathy was due to an L5 or S1 nerve root irritation was calculated, as were the sensitivity, specificity and likelihood ratios of their judgements. A potential difference in clinicians’ classification accuracy between nerve root levels was examined using a Mann-Whitney-U Test (IBM SPSS v19, Armonk, NY, USA). Every MRI was coded and clinicians were making a dichotomous choice between nerve root levels (L5 or S1). Any cases with missing responses were dropped from the analysis.

Lumbar Radiculopathy (Nerve Root Compression)

Lumbar Radiculopathy (Nerve Root Compression)

Lumbar radiculopathy refers to disease involving the lumbar spinal nerve root. This can manifest as pain, numbness, or weakness of the buttock and leg. Sciatica is the term often used by laypeople. Lumbar radiculopathy is typically caused by a compression of the spinal nerve root. This causes pain in the leg rather than in the lumbar spine, which is called “referred pain.”

Lumbar Radiculopathy Causes

Lumbar radiculopathy may occur when the spinal nerve roots are irritated or compressed by one of many conditions, including lumbar disc herniation, spinal stenosis, osteophyte formation, spondylolithesis, foraminal stenosis, or other degenerative disorders.

Lumbar Radiculopathy Diagnoses

Your spine doctor will consider your medical history and symptoms and give you a physical examination, during which the doctor will look for limitations of movement in the spine, problems with balance, as well as any loss of extremity reflexes, muscle weakness, sensory loss, or abnormal reflexes that may suggest spinal cord involvement.

Plain X-ray and an MRI are the typical imaging tests used to evaluate lumbar radiculopathy. However, a CT myelogram may be used when an MRI is contraindicated due to a pacemaker or spinal cord stimulator, etc.

Lumbar Radiculopathy Symptoms

Lumbar radiculopathy symptoms may include pain, tingling, numbness, weakness, and reflex loss. Lumbar radiculopathy symptoms may present in the leg and foot.

Non-Surgical Treatment of Lumbar Radiculopathy

Interventional treatments for lumbar radiculopathy may include:

• Physical therapy and/or exercises that are designed to stabilize the spine and promote a more open space for spinal nerve roots are recommended.
• Medications, such as non-steroidal anti-inflammatory drugs (NSAIDs) to reduce swelling and pain and analgesics to relieve pain.
• Epidural steroid injections and nerve root injections to help reduce swelling and treat acute pain that radiates to the hips or down the leg

Surgical Treatment of Lumbar Radiculopathy

Surgical treatment can be varied depending on what causes the lumbar radiculopathy. Typically, these treatments involve some way of either decompressing the nerve or stabilizing the spine.

Some of the surgical procedures used to treat lumbar radiculopathy at Emory are:

You’ve Got Some Nerve(s): Exploring the Spinal Nerves

At about 45 cm long, the human spinal cord is an information superhighway that connects the brain to the rest of the body. That may seem tiny compared to even the shortest interstate, but the best thing about the spinal cord is that electrical signals (hopefully) don’t get stuck in traffic! In a fraction of a second, pathways of sensory neurons can transmit information from the tip of your toe all the way to your brain.

Like most big highways, the spinal cord also has “exits” that lead to smaller, local pathways. These exits—the spinal nerves—are what we’re going to be focusing on here. Where are they? What do they connect to? What happens when one of them gets closed down? 

In other words, we’re going on a road trip through the nervous system.

Click here to explore the images from this blog post in 3D using Human Anatomy Atlas 2021 or later!

Introducing the Spine

The first step on our journey along the spine is understanding its components. The spinal cord, encased in connective tissue and supported by the vertebrae, is made up of neural tissue (grey and white matter). The vertebral column, which surrounds the spinal cord, is actually longer than the spinal cord, measuring around 71 cm for men and 61 cm for women. In the average adult human, this column contains 33 vertebrae in five different “sections”:

There are also 23 discs made of gel-like fluid surrounded by cartilage between the vertebrae. They allow for flexibility and shock absorption.

Image from Human Anatomy Atlas.

Your Spinal Nerves and You

Now that we know a little more about the spine, let’s zoom in on the nerves that connect the spinal cord and the rest of the body.

First of all, what is a nerve? A nerve is a group of axons of many neurons, all protected by connective tissue (an axon is the long “tail” of a neuron). Outside the brain, axons can get pretty long. The longest neuron in the body extends from the base of the spine to the big toe—a distance that can measure up to a meter!

Spinal nerves are referred to as mixed nerves because they contain both sensory and motor axons. Sensory neurons and pathways report information about the outside world back to the brain, whereas motor neurons and pathways relay orders from the brain back out to the body. This means that spinal nerves are a vital link between the central nervous system (the brain and the spinal cord) and the peripheral nervous system (neurons everywhere else).

There are 31 pairs of spinal nerves branching off from the spinal cord, named for the parts of the spine where they attach. The spinal nerves on each side of the body are as follows:

• 8 cervical spinal nerves (C01–C08)
• 12 thoracic spinal nerves (T01–T012)
• 5 lumbar spinal nerves (L01–L05)
• 5 sacral spinal nerves (S01–S05)
• 1 coccygeal spinal nerve (coccygeal nerve)

As you can see in the image below, these nerves “peek out” from the spaces between the vertebrae, which are known as neural foramina (sg. foramen). Usually, a spinal nerve will travel through the foramen above the vertebra that shares its number. So, for example, spinal nerve C04 travels through the foramen between vertebrae C03 and C04.

Image from Human Anatomy Atlas.

As is par for the course in the nervous system, spinal nerves branch almost immediately once they exit the foramina. These early branches are called rami (sg. ramus). Posterior rami go on to innervate the skin and muscles of the back, and anterior rami innervate areas such as the trunk and limbs. The anterior rami do this by forming a plexus, clusters of nerves that then split into “named” nerves that innervate more remote areas of the body.

Typically, the anterior rami that form plexuses are those of the cervical, brachial, lumbar, and sacral spinal nerves. The anterior rami of spinal nerves T01–T011 (and S05 and the Coccygeal nerve), on the other hand, don’t form plexuses. Instead, T01–T011’s anterior rami form the intercostal nerves, which wrap around to the front of the body to innervate the intercostal muscles between the ribs as well as a few abdominal muscles.

The next few sections will take a more detailed look at these plexuses and how they connect to other areas of the body.

Head, Shoulders…[Cervical Plexus]

The right and left cervical plexuses are made up of anterior rami from cervical spinal nerves C01–C04 and they innervate anterior neck muscles as well as skin on the neck, head, and shoulder(s). Parts of C05 also contribute to the cervical plexus, but C05 isn’t generally considered to be part of the plexus. 

The phrenic nerve, made up of axons from C03–C05, is also not technically a part of the cervical plexus. However, it is important to note because it innervates the diaphragm. If you’re breathing (which I hope you are!), you can thank the phrenic nerve. In the image below, you can see how C03–C05 connect to the phrenic nerve and how the phrenic nerve extends downwards to the diaphragm.

Image from Human Anatomy Atlas.

Power Cords [Brachial Plexus]

The brachial plexus, composed of the anterior rami of spinal nerves C05–T01, innervate the arms and pectoral girdle. You can use the Latin word for arm, brachium, to remember this!

The brachial plexus is a bit more complex than the cervical plexus because its nerves divide and reunify several times on the way to their destinations. First, the nerves of the brachial plexus form trunks, which each split into anterior and posterior divisions. Then, portions of these divisions unify again to form three cords.

In this image, you can see the spinal nerves exiting the foramina and forming the upper, middle, and lower trunks.

Image from Human Anatomy Atlas.

Here’s a fun fact! Nerves from the anterior division of the brachial plexus generally innervate muscles that flex parts of the arm, and nerves from the posterior division of the brachial plexus usually innervate muscles that extend parts of the arm.

Below, each trunk splits into its two divisions, and the posterior, medial, and lateral cords are formed. You can also see how the nerves dip under the clavicle as the trunks split and reunify into the cords.

Image from Human Anatomy Atlas.

Finally, you can see the main terminal branches of each cord—that is, the “named nerves” that connect back to the spinal nerves of the brachial plexus.

Images from Human Anatomy Atlas.

Portions of C05–T01 form the posterior cord. Its first terminal branch is the axillary nerve, which innervates muscles, such as the deltoids, in the upper arm. Its other terminal branch is the radial nerve, which innervates posterior arm muscles, such as the triceps.

Portions of C08–T01 form the medial cord, which has two(ish) terminal branches. The first of these branches is the median nerve, which also contains portions of the lateral cord. This nerve is responsible for innervating most of the anterior muscles of the upper arm. If you’ve ever whacked your “funny bone” on something, you know what it feels like to hit your ulnar nerve, the other terminal branch of the medial cord.

Lastly, portions of C05–C07 form the lateral cord. Its terminal branches are the median nerve discussed above and the musculocutaneous nerve (try saying that five times fast!), which innervates more anterior arm muscles.

… Knees… [Lumbar Plexus]

Now we’re going to travel down to the lumbar spine and some of the spinal nerves responsible for innervating muscles in the legs and pelvis. The anterior rami of L01–L04 form the lumbar plexus, which innervate the muscles of the thigh and skin of the inside of the leg.

Image from Human Anatomy Atlas.

The nerves of this plexus also divide into anterior and posterior portions. The femoral nerve, which innervates such anterior thigh muscles as the quadriceps femoris (knee extensor) and the hip flexors, is the main branch of the anterior division. The main branch of the posterior division is the obturator nerve, which innervates the thigh adductors (medial thigh muscles).

… and Toes (Indirectly) [Sacral Plexus]

The sacral plexus is composed of the anterior rami of L04–S04 and it has anterior and posterior divisions. Nerves from the anterior division tend to innervate muscles that participate in flexion or plantarflexion in the lower limb, whereas nerves from the posterior division tend to innervate muscles that participate in extension or dorsiflexion. Together, these nerves innervate the pelvis, gluteal region, perineum, and much of the leg.

Image from Human Anatomy Atlas.

When the powers of the anterior and posterior portions of the sacral plexus combine, they form the sciatic nerve. This nerve may not be a superhero (Captain Sciatic Nerve doesn’t have the greatest ring to it), but it is the largest and longest nerve in the body, so it does a lot of work to keep the body running right.

Image from Human Anatomy Atlas.

The anterior portion of the sciatic nerve forms the tibial nerve.

The posterior portion forms the common fibular nerve, which splits into the deep fibular nerve and the superficial fibular nerve. These innervate many anterior and lateral muscles of the leg, respectively.

Images from Human Anatomy Atlas.

Injury to Spinal Nerves — It’s “Radiculous”

You may be asking yourself what happens when something goes wrong with the spinal nerves. For now, we’re going to focus on two examples—one involving a pinching of a spinal nerve, and the other involving a disease that impacts the spinal nerves.

Radiculopathy is the condition that arises when a spinal nerve is pinched. Symptoms often include tingling, pain, loss of feeling, or muscle weakness in the regions of muscle and skin innervated by that nerve.

Let’s consider sciatica (injury to the sciatic nerve, aka lumbar radiculopathy) as an example. Sciatica is frequently caused by a slipped or herniated disc. What does that mean? Sometimes the outside of the disc (fiber) wears down, and the inside of the disc (gel) gets pushed to the side, where it can push on the root of a spinal nerve. When a slipped disc presses too hard on the roots of the sciatic nerve, this often causes pain in the buttock and thigh on one side. Surprise, surprise—these are areas innervated by the sciatic nerve!

Shingles (herpes zoster) is a case in which dermatomes in particular are affected. A dermatome is the region of skin supplied by a spinal nerve. Essentially, shingles happens when the chicken pox virus (varicella-zoster) gets into the posterior root ganglion of one or more spinal nerves and lies dormant in the body, often for many years. When the virus becomes active again, the dermatomes of the affected spinal nerves develop a painful, itchy rash. 

To see how shingles affects dermatomes, take a look at the map of common areas where shingles rashes occur side by side with a dermatome map of the body. The comparison is striking. For example, the patches going around the ribs looks similar to the stripe-like pattern of the dermatomes of the thoracic spinal nerves.

Map of common areas afflicted by shingles:

Images from cdc.gov

Dermatome mapping:

Images from Human Anatomy Atlas.

That’s All, Folks!

Congratulations on completing a whirlwind tour of the spinal nerves, their plexuses, and some of the key nerves they feed into in other areas of the body. You can now navigate the highway of the spinal cord as well as the main roads that branch off from it.

P.S. If you want to learn how to make images like the ones in this article using Human Anatomy Atlas, check out this video! 

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Additional Sources: 

Anatomy of the Spinal Cord (Section 2, Chapter 3) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy

3.1 Introduction

The spinal cord is the most important structure between the body and the brain. The spinal cord extends from the foramen magnum where it is continuous with the medulla to the level of the first or second lumbar vertebrae. It is a vital link between the brain and the body, and from the body to the brain. The spinal cord is 40 to 50 cm long and 1 cm to 1.5 cm in diameter. Two consecutive rows of nerve roots emerge on each of its sides. These nerve roots join distally to form 31 pairs of spinal nerves. The spinal cord is a cylindrical structure of nervous tissue composed of white and gray matter, is uniformly organized and is divided into four regions: cervical (C), thoracic (T), lumbar (L) and sacral (S), (Figure 3.1), each of which is comprised of several segments. The spinal nerve contains motor and sensory nerve fibers to and from all parts of the body. Each spinal cord segment innervates a dermatome (see below and Figure 3.5).

3.2 General Features

1. Similar cross-sectional structures at all spinal cord levels (Figure 3.1).
2. It carries sensory information (sensations) from the body and some from the head to the central nervous system (CNS) via afferent fibers, and it performs the initial processing of this information.
3. Motor neurons in the ventral horn project their axons into the periphery to innervate skeletal and smooth muscles that mediate voluntary and involuntary reflexes.
4. It contains neurons whose descending axons mediate autonomic control for most of the visceral functions.
5. It is of great clinical importance because it is a major site of traumatic injury and the locus for many disease processes.

Although the spinal cord constitutes only about 2% of the central nervous system (CNS), its functions are vital. Knowledge of spinal cord functional anatomy makes it possible to diagnose the nature and location of cord damage and many cord diseases.

3.3 Segmental and Longitudinal Organization

The spinal cord is divided into four different regions: the cervical, thoracic, lumbar and sacral regions (Figure 3.1). The different cord regions can be visually distinguished from one another. Two enlargements of the spinal cord can be visualized: The cervical enlargement, which extends between C3 to T1; and the lumbar enlargements which extends between L1 to S2 (Figure 3.1).

The cord is segmentally organized. There are 31 segments, defined by 31 pairs of nerves exiting the cord. These nerves are divided into 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal nerve (Figure 3.2). Dorsal and ventral roots enter and leave the vertebral column respectively through intervertebral foramen at the vertebral segments corresponding to the spinal segment.

The cord is sheathed in the same three meninges as is the brain: the pia, arachnoid and dura. The dura is the tough outer sheath, the arachnoid lies beneath it, and the pia closely adheres to the surface of the cord (Figure 3.3). The spinal cord is attached to the dura by a series of lateral denticulate ligaments emanating from the pial folds.

During the initial third month of embryonic development, the spinal cord extends the entire length of the vertebral canal and both grow at about the same rate. As development continues, the body and the vertebral column continue to grow at a much greater rate than the spinal cord proper. This results in displacement of the lower parts of the spinal cord with relation to the vertebrae column. The outcome of this uneven growth is that the adult spinal cord extends to the level of the first or second lumbar vertebrae, and the nerves grow to exit through the same intervertebral foramina as they did during embryonic development. This growth of the nerve roots occurring within the vertebral canal, results in the lumbar, sacral, and coccygeal roots extending to their appropriate vertebral levels (Figure 3.2).

All spinal nerves, except the first, exit below their corresponding vertebrae. In the cervical segments, there are 7 cervical vertebrae and 8 cervical nerves (Figure 3.2). C1-C7 nerves exit above their vertebrae whereas the C8 nerve exits below the C7 vertebra. It leaves between the C7 vertebra and the first thoracic vertebra. Therefore, each subsequent nerve leaves the cord below the corresponding vertebra. In the thoracic and upper lumbar regions, the difference between the vertebrae and cord level is three segments. Therefore, the root filaments of spinal cord segments have to travel longer distances to reach the corresponding intervertebral foramen from which the spinal nerves emerge. The lumbosacral roots are known as the cauda equina (Figure 3.2).

Each spinal nerve is composed of nerve fibers that are related to the region of the muscles and skin that develops from one body somite (segment). A spinal segment is defined by dorsal roots entering and ventral roots exiting the cord, (i.e., a spinal cord section that gives rise to one spinal nerve is considered as a segment.) (Figure 3.4).

A dermatome is an area of skin supplied by peripheral nerve fibers originating from a single dorsal root ganglion. If a nerve is cut, one loses sensation from that dermatome. Because each segment of the cord innervates a different region of the body, dermatomes can be precisely mapped on the body surface, and loss of sensation in a dermatome can indicate the exact level of spinal cord damage in clinical assessment of injury (Figure 3.5). It is important to consider that there is some overlap between neighboring dermatomes. Because sensory information from the body is relayed to the CNS through the dorsal roots, the axons originating from dorsal root ganglion cells are classified as primary sensory afferents, and the dorsal root’s neurons are the first order (1°) sensory neuron. Most axons in the ventral roots arise from motor neurons in the ventral horn of the spinal cord and innervate skeletal muscle. Others arise from the lateral horn and synapse on autonomic ganglia that innervate visceral organs. The ventral root axons join with the peripheral processes of the dorsal root ganglion cells to form mixed afferent and efferent spinal nerves, which merge to form peripheral nerves. Knowledge of the segmental innervation of the cutaneous area and the muscles is essential to diagnose the site of an injury.

3.4 Internal Structure of the Spinal Cord

A transverse section of the adult spinal cord shows white matter in the periphery, gray matter inside, and a tiny central canal filled with CSF at its center. Surrounding the canal is a single layer of cells, the ependymal layer. Surrounding the ependymal layer is the gray matter – a region containing cell bodies – shaped like the letter “H” or a “butterfly”. The two “wings” of the butterfly are connected across the midline by the dorsal gray commissure and below the white commissure (Figure 3.6). The shape and size of the gray matter varies according to spinal cord level. At the lower levels, the ratio between gray matter and white matter is greater than in higher levels, mainly because lower levels contain less ascending and descending nerve fibers. (Figure 3.1 and Figure 3.6).

The gray matter mainly contains the cell bodies of neurons and glia and is divided into four main columns: dorsal horn, intermediate column, lateral horn and ventral horn column. (Figure 3.6).

The dorsal horn is found at all spinal cord levels and is comprised of sensory nuclei that receive and process incoming somatosensory information. From there, ascending projections emerge to transmit the sensory information to the midbrain and diencephalon. The intermediate column and the lateral horn comprise autonomic neurons innervating visceral and pelvic organs. The ventral horn comprises motor neurons that innervate skeletal muscle.

At all the levels of the spinal cord, nerve cells in the gray substance are multipolar, varying much in their morphology. Many of them are Golgi type I and Golgi type II nerve cells. The axons of Golgi type I are long and pass out of the gray matter into the ventral spinal roots or the fiber tracts of the white matter. The axons and dendrites of the Golgi type II cells are largely confined to the neighboring neurons in the gray matter.

A more recent classification of neurons within the gray matter is based on function. These cells are located at all levels of the spinal cord and are grouped into three main categories: root cells, column or tract cells and propriospinal cells.

The root cells are situated in the ventral and lateral gray horns and vary greatly in size. The most prominent features of the root cells are large multipolar elements exceeding 25 µm of their somata. The root cells contribute their axons to the ventral roots of the spinal nerves and are grouped into two major divisions: 1) somatic efferent root neurons, which innervate the skeletal musculature; and 2) the visceral efferent root neurons, also called preganglionic autonomic axons, which send their axons to various autonomic ganglia.

The column or tract cells and their processes are located mainly in the dorsal gray horn and are confined entirely within the CNS. The axons of the column cells form longitudinal ascending tracts that ascend in the white columns and terminate upon neurons located rostrally in the brain stem, cerebellum or diencephalon. Some column cells send their axons up and down the cord to terminate in gray matter close to their origin and are known as intersegmental association column cells. Other column cell axons terminate within the segment in which they originate and are called intrasegmental association column cells. Still other column cells send their axons across the midline to terminate in gray matter close to their origin and are called commissure association column cells.

The propriospinal cells are spinal interneurons whose axons do not leave the spinal cord proper. Propriospinal cells account for about 90% of spinal neurons. Some of these fibers also are found around the margin of the gray matter of the cord and are collectively called the fasciculus proprius or the propriospinal or the archispinothalamic tract.

3.5 Spinal Cord Nuclei and Laminae

Spinal neurons are organized into nuclei and laminae.

3.6 Nuclei

The prominent nuclear groups of cell columns within the spinal cord from dorsal to ventral are the marginal zone, substantia gelatinosa, nucleus proprius, dorsal nucleus of Clarke, intermediolateral nucleus and the lower motor neuron nuclei.

Marginal zone nucleus or posterior marginalis, is found at all spinal cord levels as a thin layer of column/tract cells (column cells) that caps the tip of the dorsal horn. The axons of its neurons contribute to the lateral spinothalamic tract which relays pain and temperature information to the diencephalon (Figure 3.7).

Substantia gelatinosa is found at all levels of the spinal cord. Located in the dorsal cap-like portion of the head of the dorsal horn, it relays pain, temperature and mechanical (light touch) information and consists mainly of column cells (intersegmental column cells). These column cells synapse in cell at Rexed layers IV to VII, whose axons contribute to the ventral (anterior) and lateral spinal thalamic tracts. The homologous substantia gelatinosa in the medulla is the spinal trigeminal nucleus.

Nucleus proprius is located below the substantia gelatinosa in the head and neck of the dorsal horn. This cell group, sometimes called the chief sensory nucleus, is associated with mechanical and temperature sensations. It is a poorly defined cell column which extends through all segments of the spinal cord and its neurons contribute to ventral and lateral spinal thalamic tracts, as well as to spinal cerebellar tracts. The axons originating in nucleus proprius project to the thalamus via the spinothalamic tract and to the cerebellum via the ventral spinocerebellar tract (VSCT).

Dorsal nucleus of Clarke is a cell column located in the mid-portion of the base form of the dorsal horn. The axons from these cells pass uncrossed to the lateral funiculus and form the dorsal (posterior) spinocerebellar tract (DSCT), which subserve unconscious proprioception from muscle spindles and Golgi tendon organs to the cerebellum, and some of them innervate spinal interneurons. The dorsal nucleus of Clarke is found only in segments C8 to L3 of the spinal cord and is most prominent in lower thoracic and upper lumbar segments. The homologous dorsal nucleus of Clarke in the medulla is the accessory cuneate nucleus, which is the origin of the cuneocerebellar tract (CCT).

Intermediolateral nucleus is located in the intermediate zone between the dorsal and the ventral horns in the spinal cord levels. Extending from C8 to L3, it receives viscerosensory information and contains preganglionic sympathetic neurons, which form the lateral horn. A large proportion of its cells are root cells which send axons into the ventral spinal roots via the white rami to reach the sympathetic tract as preganglionic fibers. Similarly, cell columns in the intermediolateral nucleus located at the S2 to S4 levels contains preganglionic parasympathetic neurons (Figure 3.7).

Lower motor neuron nuclei are located in the ventral horn of the spinal cord. They contain predominantly motor nuclei consisting of α, β and γ motor neurons and are found at all levels of the spinal cord–they are root cells. The a motor neurons are the final common pathway of the motor system, and they innervate the visceral and skeletal muscles.

3.7 Rexed Laminae

The distribution of cells and fibers within the gray matter of the spinal cord exhibits a pattern of lamination. The cellular pattern of each lamina is composed of various sizes or shapes of neurons (cytoarchitecture) which led Rexed to propose a new classification based on 10 layers (laminae). This classification is useful since it is related more accurately to function than the previous classification scheme which was based on major nuclear groups (Figure 3.7).

Laminae I to IV, in general, are concerned with exteroceptive sensation and comprise the dorsal horn, whereas laminae V and VI are concerned primarily with proprioceptive sensations. Lamina VII is equivalent to the intermediate zone and acts as a relay between muscle spindle to midbrain and cerebellum, and laminae VIII-IX comprise the ventral horn and contain mainly motor neurons. The axons of these neurons innervate mainly skeletal muscle. Lamina X surrounds the central canal and contains neuroglia.

Rexed lamina I – Consists of a thin layer of cells that cap the tip of the dorsal horn with small dendrites and a complex array of nonmyelinated axons. Cells in lamina I respond mainly to noxious and thermal stimuli. Lamina I cell axons join the contralateral spinothalamic tract; this layer corresponds to nucleus posteromarginalis.

Rexed lamina II – Composed of tightly packed interneurons. This layer corresponds to the substantia gelatinosa and responds to noxious stimuli while others respond to non-noxious stimuli. The majority of neurons in Rexed lamina II axons receive information from sensory dorsal root ganglion cells as well as descending dorsolateral fasciculus (DLF) fibers. They send axons to Rexed laminae III and IV (fasciculus proprius). High concentrations of substance P and opiate receptors have been identified in Rexed lamina II. The lamina is believed to be important for the modulation of sensory input, with the effect of determining which pattern of incoming information will produce sensations that will be interpreted by the brain as being painful.

Rexed lamina III – Composed of variable cell size, axons of these neurons bifurcate several times and form a dense plexus. Cells in this layer receive axodendritic synapses from Aβ fibers entering dorsal root fibers. It contains dendrites of cells from laminae IV, V and VI. Most of the neurons in lamina III function as propriospinal/interneuron cells.

Rexed lamina IV – The thickest of the first four laminae. Cells in this layer receive Aß axons which carry predominantly non-noxious information. In addition, dendrites of neurons in lamina IV radiate to lamina II, and respond to stimuli such as light touch. The ill-defined nucleus proprius is located in the head of this layer. Some of the cells project to the thalamus via the contralateral and ipsilateral spinothalamic tract.

Rexed lamina V – Composed neurons with their dendrites in lamina II. The neurons in this lamina receive monosynaptic information from Aß, Ad and C axons which also carry nociceptive information from visceral organs. This lamina covers a broad zone extending across the neck of the dorsal horn and is divided into medial and lateral parts. Many of the Rexed lamina V cells project to the brain stem and the thalamus via the contralateral and ipsilateral spinothalamic tract. Moreover, descending corticospinal and rubrospinal fibers synapse upon its cells.

Rexed lamina VI – Is a broad layer which is best developed in the cervical and lumbar enlargements. Lamina VI divides also into medial and lateral parts. Group Ia afferent axons from muscle spindles terminate in the medial part at the C8 to L3 segmental levels and are the source of the ipsilateral spinocerebellar pathways. Many of the small neurons are interneurons participating in spinal reflexes, while descending brainstem pathways project to the lateral zone of Rexed layer VI.

Rexed lamina VII – This lamina occupies a large heterogeneous region. This region is also known as the zona intermedia (or intermediolateral nucleus). Its shape and boundaries vary along the length of the cord. Lamina VII neurons receive information from Rexed lamina II to VI as well as visceral afferent fibers, and they serve as an intermediary relay in transmission of visceral motor neurons impulses. The dorsal nucleus of Clarke forms a prominent round oval cell column from C8 to L3. The large cells give rise to uncrossed nerve fibers of the dorsal spinocerebellar tract (DSCT). Cells in laminae V to VII, which do not form a discrete nucleus, give rise to uncrossed fibers that form the ventral spinocerebellar tract (VSCT). Cells in the lateral horn of the cord in segments T1 and L3 give rise to preganglionic sympathetic fibers to innervate postganglionic cells located in the sympathetic ganglia outside the cord. Lateral horn neurons at segments S2 to S4 give rise to preganglionic neurons of the sacral parasympathetic fibers to innervate postganglionic cells located in peripheral ganglia.

Rexed lamina VIII – Includes an area at the base of the ventral horn, but its shape differs at various cord levels. In the cord enlargements, the lamina occupies only the medial part of the ventral horn, where descending vestibulospinal and reticulospinal fibers terminate. The neurons of lamina VIII modulate motor activity, most probably via g motor neurons which innervate the intrafusal muscle fibers.

Rexed lamina IX – Composed of several distinct groups of large a motor neurons and small γ and β motor neurons embedded within this layer. Its size and shape differ at various cord levels. In the cord enlargements the number of α motor neurons increase and they form numerous groups. The α motor neurons are large and multipolar cells and give rise to ventral root fibers to supply extrafusal skeletal muscle fibers, while the small γ motor neurons give rise to the intrafusal muscle fibers. The α motor neurons are somatotopically organized.

Rexed lamina X – Neurons in Rexed lamina X surround the central canal and occupy the commissural lateral area of the gray commissure, which also contains decussating axons.

In summary, laminae I-IV are concerned with exteroceptive sensations, whereas laminae V and VI are concerned primarily with proprioceptive sensation and act as a relay between the periphery to the midbrain and the cerebellum. Laminae VIII and IX form the final motor pathway to initiate and modulate motor activity via α, β and γ motor neurons, which innervate striated muscle. All visceral motor neurons are located in lamina VII and innervate neurons in autonomic ganglia.

3.8 White Matter

Surrounding the gray matter is white matter containing myelinated and unmyelinated nerve fibers. These fibers conduct information up (ascending) or down (descending) the cord. The white matter is divided into the dorsal (or posterior) column (or funiculus), lateral column and ventral (or anterior) column (Figure 3.8). The anterior white commissure resides in the center of the spinal cord, and it contains crossing nerve fibers that belong to the spinothalamic tracts, spinocerebellar tracts, and anterior corticospinal tracts. Three general nerve fiber types can be distinguished in the spinal cord white matter: 1) long ascending nerve fibers originally from the column cells, which make synaptic connections to neurons in various brainstem nuclei, cerebellum and dorsal thalamus, 2) long descending nerve fibers originating from the cerebral cortex and various brainstem nuclei to synapse within the different Rexed layers in the spinal cord gray matter, and 3) shorter nerve fibers interconnecting various spinal cord levels such as the fibers responsible for the coordination of flexor reflexes. Ascending tracts are found in all columns whereas descending tracts are found only in the lateral and the anterior columns.

Four different terms are often used to describe bundles of axons such as those found in the white matter: funiculus, fasciculus, tract, and pathway. Funiculus is a morphological term to describe a large group of nerve fibers which are located in a given area (e.g., posterior funiculus). Within a funiculus, groups of fibers from diverse origins, which share common features, are sometimes arranged in smaller bundles of axons called fasciculus, (e.g., fasciculus proprius [Figure 3.8]). Fasciculus is primarily a morphological term whereas tracts and pathways are also terms applied to nerve fiber bundles which have a functional connotation. A tract is a group of nerve fibers which usually has the same origin, destination, and course and also has similar functions. The tract name is derived from their origin and their termination (i.e., corticospinal tract – a tract that originates in the cortex and terminates in the spinal cord; lateral spinothalamic tract – a tract originated in the lateral spinal cord and ends in the thalamus). A pathway usually refers to the entire neuronal circuit responsible for a specific function, and it includes all the nuclei and tracts which are associated with that function. For example, the spinothalamic pathway includes the cell bodies of origin (in the dorsal root ganglia), their axons as they project through the dorsal roots, synapses in the spinal cord, and projections of second and third order neurons across the white commissure, which ascend to the thalamus in the spinothalamic tracts.

3.9 Spinal Cord Tracts

The spinal cord white matter contains ascending and descending tracts.

Ascending tracts (Figure 3.8). The nerve fibers comprise the ascending tract emerge from the first order (1°) neuron located in the dorsal root ganglion (DRG). The ascending tracts transmit sensory information from the sensory receptors to higher levels of the CNS. The ascending gracile and cuneate fasciculi occupying the dorsal column, and sometimes are named the dorsal funiculus. These fibers carry information related to tactile, two point discrimination of simultaneously applied pressure, vibration, position, and movement sense and conscious proprioception. In the lateral column (funiculus), the neospinothalamic tract (or lateral spinothalamic tract) is located more anteriorly and laterally, and carries pain, temperature and crude touch information from somatic and visceral structures. Nearby laterally, the dorsal and ventral spinocerebellar tracts carry unconscious proprioception information from muscles and joints of the lower extremity to the cerebellum. In the ventral column (funiculus) there are four prominent tracts: 1) the paleospinothalamic tract (or anterior spinothalamic tract) is located which carry pain, temperature, and information associated with touch to the brain stem nuclei and to the diencephalon, 2) the spinoolivary tract carries information from Golgi tendon organs to the cerebellum, 3) the spinoreticular tract, and 4) the spinotectal tract. Intersegmental nerve fibers traveling for several segments (2 to 4) and are located as a thin layer around the gray matter is known as fasciculus proprius, spinospinal or archispinothalamic tract. It carries pain information to the brain stem and diencephalon.

Descending tracts (Figure 3.9). The descending tracts originate from different cortical areas and from brain stem nuclei. The descending pathway carry information associated with maintenance of motor activities such as posture, balance, muscle tone, and visceral and somatic reflex activity. These include the lateral corticospinal tract and the rubrospinal tracts located in the lateral column (funiculus). These tracts carry information associated with voluntary movement. Other tracts such as the reticulospinal vestibulospinal and the anterior corticospinal tract mediate balance and postural movements (Figure 3.9). Lissauer’s tract, which is wedged between the dorsal horn and the surface of the spinal cord carry the descending fibers of the dorsolateral funiculus (DFL), which regulate incoming pain sensation at the spinal level, and intersegmental fibers. Additional details about ascending and descending tracts are described in the next few chapters.

3.10 Dorsal Root

Information from the skin, skeletal muscle and joints is relayed to the spinal cord by sensory cells located in the dorsal root ganglia. The dorsal root fibers are the axons originated from the primary sensory dorsal root ganglion cells. Each ascending dorsal root axon, before reaching the spinal cord, bifurcates into ascending and descending branches entering several segments below and above their own segment. The ascending dorsal root fibers and the descending ventral root fibers from and to discrete body areas form a spinal nerve (Figure 3.10). There are 31 paired spinal nerves. The dorsal root fibers segregate into lateral and medial divisions. The lateral division contains most of the unmyelinated and small myelinated axons carrying pain and temperature information to be terminated in the Rexed laminae I, II, and IV of the gray matter. The medial division of dorsal root fibers consists mainly of myelinated axons conducting sensory fibers from skin, muscles and joints; it enters the dorsal/posterior column/funiculus and ascend in the dorsal column to be terminated in the ipsilateral nucleus gracilis or nucleus cuneatus at the medulla oblongata region, i.e., the axons of the first-order (1°) sensory neurons synapse in the medulla oblongata on the second order (2°) neurons (in nucleus gracilis or nucleus cuneatus). In entering the spinal cord, all fibers send collaterals to different Rexed lamina.

Axons entering the cord in the sacral region are found in the dorsal column near the midline and comprise the fasciculus gracilis, whereas axons that enter at higher levels are added in lateral positions and comprise the fasciculus cuneatus (Figure 3.11). This orderly representation is termed “somatotopic representation”.

3.11 Ventral Root

Ventral root fibers are the axons of motor and visceral efferent fibers and emerge from poorly defined ventral lateral sulcus as ventral rootlets. The ventral rootlets from discrete spinal cord section unite and form the ventral root, which contain motor nerve axons from motor and visceral motor neurons. The α motor nerve axons innervate the extrafusal muscle fibers while the small γ motor neuron axons innervate the intrafusal muscle fibers located within the muscle spindles. The visceral neurons send preganglionic fibers to innervate the visceral organs. All these fibers join the dorsal root fibers distal to the dorsal root ganglion to form the spinal nerve (Figure 3.10).

3.12 Spinal Nerve Roots

The spinal nerve roots are formed by the union of dorsal and ventral roots within the intervertebral foramen, resulting in a mixed nerve joined together and forming the spinal nerve (Figure 3.10). Spinal nerve rami include the dorsal primary nerves (ramus), which innervates the skin and muscles of the back, and the ventral primary nerves (ramus), which innervates the ventral lateral muscles and skin of the trunk, extremities and visceral organs. The ventral and dorsal roots also provide the anchorage and fixation of the spinal cord to the vertebral cauda.

3.13 Blood Supply of the Spinal Cord

The arterial blood supply to the spinal cord in the upper cervical regions is derived from two branches of the vertebral arteries, the anterior spinal artery and the posterior spinal arteries (Figure 3.12). At the level of medulla, the paired anterior spinal arteries join to form a single artery that lies in the anterior median fissure of the spinal cord. The posterior spinal arteries are paired and form an anastomotic chain over the posterior aspect of the spinal cord. A plexus of small arteries, the arterial vasocorona, on the surface of the cord constitutes an anastomotic connection between the anterior and posterior spinal arteries. This arrangement provides uninterrupted blood supplies along the entire length of the spinal cord.

At spinal cord regions below upper cervical levels, the anterior and posterior spinal arteries narrow and form an anastomotic network with radicular arteries. The radicular arteries are branches of the cervical, trunk, intercostal & iliac arteries. The radicular arteries supply most of the lower levels of the spinal cord. There are approximately 6 to 8 pairs of radicular arteries supplying the anterior and posterior spinal cord (Figure 3.12).

Test Your Knowledge

Making sense of MRI of the lumbar spine

Xian Zhang Eric Yong

Tom Sutherland

Background

With improved accessibility and increasing use of magnetic resonance imaging (MRI) to evaluate low back pain, general practitioners are exposed to a set of recommended terminology used among the various specialties involved in lumbar spinal conditions.

Objective/s

This article aims to illustrate these descriptive terms, the various lumbar spinal pathology and its clinical implications regarding management.

Discussion

MRI may be useful in specific clinical situations in lumbar back pain, however, the importance of a thorough clinical assessment cannot be overstated. An understanding of the benefits and limitations of MRI in evaluating lumbar back pain and improved communiction between healthcare providers, should allow for optimal management of the patient’s radiologically matched clinical issues.

Lumbar back pain is a common presentation to general practices and hospital emergency departments, with a financial cost alone of $9.17 billion in Australia in 2001.¹ Its management can be complex, requiring a multidisciplinary approach. Identifying an underlying pathological cause with imaging is commonly used when conservative approaches have failed or are insufficient.

Multiple modalities are used with spinal imaging and with increasing access to magnetic resonance imaging and better imaging quality, primary care physicians are being exposed to nomenclature utilised by neuroradiologists and specialists in the field of spinal medicine. This article aims to clarify the terms commonly used and its clinical implications in lumbar spinal imaging.

Clinical presentation

Patients with spinal pathology often present with a range of symptoms. It is useful to differentiate the three most common symptoms – lumbar back pain, sciatica and claudication – as they can assist in determining the source of the patient’s symptoms. While magnetic resonance imaging (MRI) is sensitive in detecting spinal pathology, often it discovers a multitude of conditions that may not have any significant clinical impact.

Lumbar back pain can result from several conditions ranging from facet joint arthropathy to muscular strain. The pain is mainly localised in the back as the term suggests, and tends to arise from locally affected structures.

Sciatica, on the other hand, has a different pattern of pain in terms of distribution and is caused by irritation of a nerve root. This can occur due to the direct compressive effects of an intervertebral disc herniation on a nerve root or an underlying inflammatory process, such as infection causing acute pain in the distribution of a dermatome.

Claudication is traditionally divided into two categories: neurogenic or vasogenic, depending on the underlying cause. It is often described as impaired mobility and dull aching pain in the lower limbs. Central vertebral canal stenosis is a common cause of neurogenic claudication and has a variable pattern, while vascular claudication it is more consistent and reproducible.

The importance of determining symptom chronicity and identifying ‘red flags’ in the history and clinical examination, such as fevers and perineum paraesthesia, are crucial in the formulation of the clinical diagnosis and differentiating benign causes, such as musculoskeletal strain, from more serious conditions such as epidural abscesses or spinal metastases. Certain risk factors such as the patient’s age, medication history (eg. steroid use) and pattern of stiffness may also raise suspicion of ankylosing spondylitis or compression fractures. This would direct further investigation with appropriate serum tests and imaging. Guidelines, such as those developed by the American College of Physicians and Pain Society, can direct diagnostic testing for ‘red flag’ causes of lumbar back pain.²

Magnetic resonance imaging

Magnetic resonance imaging utilises proton resonance technology to obtain soft tissue cross-sectional representations of the spine. The quality of these images allows the diagnostician to make more detailed and accurate assessments of the intervertebral disc and its relation to the neural structures when compared with more traditional methods, such as lumbar and computed tomography (CT) myelograms.

A systematic review of the available literature involving spinal MRI found MRI to be a highly sensitive and but less specific imaging modality for lumbar spinal conditions.³ For example, high sensitivity ranging between 89–100% for disc herniation have been described in previous studies.^4,5 The lower specificity, 43–97% for disc herniation has been highlighted in previous literature and relates to the prevalence of asymptomatic disc degeneration and protrusions resulting in a large number of false positives.⁶ In a group of 57 patients with unilateral lower limb radiculopathy, only 30% of these patients had MRI findings of disc herniation and nerve root compression at the same level as the clinical prediction.⁷ Therefore, when reviewing the imaging, one must exert a degree of care when attributing the patient’s symptoms to the appearance of their lumbar spine.

Lumbar spine anatomy

The lumbar spine consists of five separate vertebrae separated by intervertebral discs and reinforced by multiple ligaments and paravertebral muscles. The thecal sac containing the conus medullaris and nerve roots are located within the central vertebral canal. The nerve roots then exit the spine via the intervertebral foraminal canal obliquely instead of at right angles, which is observed in the cervical spine. Understanding this anatomical relationship allows the clinician to isolate the exact nerve root being irritated by a herniated intervertebral disc (Figure 1).

Figure 1. The relationship of the exiting nerve roots, pedicle (P) and intervertebral disc

The exiting nerve roots traverse the neural foramen and this is divided into sections based on its relationship to the pedicle and zygapophysical joint in the axial and sagittal planes (Figure 2). In the axial plane, the exiting nerve root traverses the subarticular recess from the central zone to the foraminal and extra-foraminal zones. Infra-pedicular, supra-pedicular, pedicular and disc levels are used to separate the areas along the longitudinal axis.

Figure 2. Axial T2-weighted slice of the lumbar spine demonstrating the various zones along the course of the exiting nerve roots from the sub-articular zone (SA) to the foraminal zone (FZ) and the extra-foraminal zone (EF)
P = pedicle; FJ = facet joint TP = transverse process SP = spinous process

Intervertebral discs have a hydrated nucleus pulposus contained within concentric rings of annulus fibrosus. With increasing age, the discs progressively dehydrate resulting in a decrease in T2 signal, which are frequently seen in asymptomatic patients.

Disc pathology

Nomenclature used in reports of spinal imaging has been confusing and inconsistent. Until a consensus review by several working groups in North America developed a recommendation on terminology⁸ used in describing lumbar disc pathology such as disc sequestration and fissures (Table 1).

Annular fissure

Any separation between annulus fibres or avulsion of annulus fibres from the vertebral bodies is defined as an annular fissure. These changes often occur in the setting of asymptomatic disc degeneration. Therefore the term ‘annular tear’ is discouraged as it implies a traumatic trigger. A review of 40 post-discography CT scans found poor correlation between the side of back pain and the side of annular tear in patients with a single level, concordantly painful and fissured discs identified during lumbar discography.⁹

Disc herniation

Disc herniation occurs commonly in two scenarios where the spinal column has sustained trauma in the form of abnormal axial loading or altered dynamics secondary to congenital or acquired spinal deformity. The resulting herniation results in nerve root compression and pain.

Any disc material extending beyond the vertebral bodies is considered a herniated disc. This is described further as ‘disc bulge’, ‘protrusion’, ‘extrusion’ and ‘sequestration’. The fundamental aim of using these terms is mainly a descriptive one and allows effective communication to general practitioners.

The amount of disc extension circum-ferentially on the edges of the vertebral endplate (ring apophyses) is assessed initially; the term ‘bulging disc’ is used to describe extension of the disc around 50–100% of the ring apophyses. Displacement of between 25–50% is described as ‘broad-based herniation’ and <25% as ‘focal herniation’.

A protruded disc is defined as having a wider base when compared with the extent of disc material spreading beyond the vertebral body (Figure 3). Conversely, when the extent of disc spread is greater than the base of the disc extension, it is described as being ‘extruded’. When there is separation between the herniated disc and the parent disc, it is described as being ‘sequestrated’ (Figure 3).

Figure 3. Axial illustration and T2- weighted MRI of the lumbar spine showing disc herniation
A = bulging disc; B = right sided broad based paracentral protrusion; C = sequestration of disc material. Line arrow: separation between the herniated disc (block arrow) and the intervertebral disc space; D = extrusion

In an attempt to correlate clinical findings and radiological evidence, the relation of the herniated disc to the nerve root is carefully examined. Any contact, displacement or inflammatory changes would be reported to allow accurate localisation of the patient’s symptoms to the offending compressive disc lesion.

Central vertebral canal stenosis

Gradual development of central vertebral canal stenosis where there is compression of the nerve roots in the thecal sac (Figure 4) often results in progression of decreasing mobility and neurogenic claudication. In instances where an acute event has occurred, the initial presentation may occur as cauda equina syndrome, urgent surgical decompression is required.

Figure 4. T2-weighted axial slices of the lumbar spine of the same patient at different levels. There is severe central vertebral canal stenosis at the L4–5 level (arrow) with no cerebrospinal fluid and crowded cauda equine nerve roots. At L3–4 the nerve roots can be seen as low signal dots surrounded by bright cerebrospinal fluid

The causes of central vertebral canal stenosis can be divided into congenital and acquired conditions, such as neoplastic and degenerative changes. Degenerative changes include facet osteophytes, ligamentum flavum hypertrophy and disc herniations. While some conditions have a specific/dominant cause, most central vertebral canal stenoses are caused by a combination of conditions.

The severity of central vertebral canal stenosis is visually graded and currently no universal grading scale is being used. Several centres have assessed various grading methods, including measuring the cross-sectional area and morphology of the thecal sac.¹⁰ However, using imaging alone to assess severity is inadequate as there is often a mismatch between the symptomology and MRI findings,¹¹ as well as inter-observer variation between radiologists.

Ankylosing spondylitis

Plain radiography of the affected joints remains the initial imaging method for patients with suspected ankylosing spondylitis. However, clinicians are using MRI more frequently to diagnose this condition and to monitor treatment response. The main features on MRI of the lumbar spine include features demonstrating underlying inflammation and its effects, such as bone marrow oedema, squaring of the vertebral bodies (Romanus lesions), syndesmophyte formation, ankylosis and erosions (Figure 5). The clinical and imaging aspects of this condition are complex and beyond the scope of this article. They are discussed in detail by a group from the United Kingdom.¹²

Figure 5. Sagittal T2-weighted images of the lumbar spine in two separate patients with ankylosing spondylitis. Left: arrows point toward bridging syndesmophytes; right: arrows point toward marrow changes near the endplate, consistent with inflammation

Spondylolisthesis

Spondylolisthesis is defined as a condition where there is malalignment of the lumbar spine in the form of a vertebra slipping out of its normal position relative to the inferior vertebra. This can result in narrowing of the lateral neural foramen and the central spinal canal (Figure 6). Furthermore, pars defects and lumbar spondylosis are commonly associated with spondylolisthesis. The chronic nature of pain experienced by the patient as well as the complex mechanical issues revolving spinal malalignment can often result in failure of conservative treatment and surgical fusion of the affected level maybe required.

Figure 6. Sagittal T2-weighted MRI acquisitions of the lumbar spine. There is anterolisthesis at the L4–5 level, resulting in severe central canal and neural foraminal stenosis with associated nerve impingement

The role of MRI is to determine the severity of any central spinal canal stenosis or neural foramen and to identify a potential cause such as a pars defect. However, due to the static nature of MRI imaging acquired with the patient lying down, stability at the affected level is uncertain. Spinal surgeons have used dynamic lumbar spinal plain X-rays to assess any potential exaggeration of spinal malalignment, which implies further stenosis and nerve impingement. The addition of rigorous dynamic MRI spinal imaging studies in the future may offer a better alternative.

Summary

A better understanding of the benefits and limitations of MRI in evaluating lumbar back pain and the use of a universally accepted terminology by the various specialties involved in patient care, can lead to better treatment outcomes of a patient’s radiologically matched clinical issues.

Conflict of interest: none declared.

References

1. Walker BF, Muller R, Grant WD. Low back pain in Australian adults: the economic burden. Asia Pac J Public Health 2003;15:79–87.
2. Chou R, Qaseem A, Snow V et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med 2007;147:478–91.
3. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586–97.
4. Thornbury JR, Fryback DG, Turski PA, et al. Disk-caused nerve compression in patients with acute low-back pain: diagnosis with MR, CT myelography, and plain CT. Radiology 1993;186:731–8.
5. Janssen ME, Bertrand SL, Joe C, Levine MI. Lumbar herniated disk disease: comparison of MRI, myelography, and post-myelographic CT scan with surgical findings. Orthopedics 1994;17:121–7.
6. Jarvik JG, Hollingworth W, Heagerty PJ, Haynor DR, Boyko EJ, Deyo RA. Three-year incidence of low back pain in an initially asymptomatic cohort: clinical and imaging risk factors. Spine (Phila Pa 1976) 2005;30:1541–8.
7. van Rijn JC, Klemetso N, Reitsma JB, et al. Symptomatic and asymptomatic abnormalities in patients with lumbosacral radicular syndrome: Clinical examination compared with MRI. Clin Neurol Neurosurg 2006;108:553–7.
8. Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93–E113.
9. Slipman CW, Patel RK, Zhang L, et al. Side of symptomatic annular tear and site of low back pain: is there a correlation? Spine (Phila Pa 1976) 2001;26:E165–9.
10. Wiltse LL, Berger PE, McCulloch JA. A system for reporting the size and location of lesions in the spine. Spine (Phila Pa 1976) 1997;22:1534–7.
11. Kovacs FM, Martinez C, Arana E, et al. Uncertainties in the measurement of lumbar spinal stenosis at MR imaging: Are they clinically relevant? Radiology 2012;263:310–1.
12. Tan AL, McGonagle D. Imaging of seronegative spondyloarthritis. Best Pract Res Clin Rheumatol 2008;22:1045–59.

Correspondence [email protected]

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Lumbar Spine Stenosis: A Common Cause of Back and Leg Pain

JAMIE A. ALVAREZ, M.D., and RUSSELL H. HARDY, JR., M.D., University Hospitals of Cleveland/Case Western Reserve University, Cleveland, Ohio

Am Fam Physician. 1998 Apr 15;57(8):1825-1834.

 
Patient information: See related handout on lumbar spinal canal stenosis, written by the authors of this article.

Lumbar spine stenosis most commonly affects the middle-aged and elderly population. Entrapment of the cauda equina roots by hypertrophy of the osseous and soft tissue structures surrounding the lumbar spinal canal is often associated with incapacitating pain in the back and lower extremities, difficulty ambulating, leg paresthesias and weakness and, in severe cases, bowel or bladder disturbances. The characteristic syndrome associated with lumbar stenosis is termed neurogenic intermittent claudication. This condition must be differentiated from true claudication, which is caused by atherosclerosis of the pelvofemoral vessels. Although many conditions may be associated with lumbar canal stenosis, most cases are idiopathic. Imaging of the lumbar spine performed with computed tomography or magnetic resonance imaging often demonstrates narrowing of the lumbar canal with compression of the cauda equina nerve roots by thickened posterior vertebral elements, facet joints, marginal osteophytes or soft tissue structures such as the ligamentum flavum or herniated discs. Treatment for symptomatic lumbar stenosis is usually surgical decompression. Medical treatment alternatives, such as bed rest, pain management and physical therapy, should be reserved for use in debilitated patients or patients whose surgical risk is prohibitive as a result of concomitant medical conditions.

Low back pain resulting from degenerative disease of the lumbosacral spine is a major cause of morbidity, disability and lost productivity. Up to 90 percent of the U.S. population may have significant low back pain at some point.1 In 1984, it was estimated that over 5 million persons were incapacitated as a result of lower back pain.2 The financial impact in terms of health care dollars and lost work hours reaches billions of dollars each year in this country.3 With the increasing longevity of our population and a continually climbing proportion of middle-aged and elderly persons, the problem of lumbosacral pain is a significant health care issue. A ubiquitous and potentially disabling cause of osteoarthritic pain of the lower back and legs is stenosis of the lumbar spinal canal. This treatable condition is often a major cause of inactivity, loss of productivity and, potentially, loss of independence in many persons, particularly older persons.

Because of the slow progression of the disease, the diagnosis may be significantly delayed. Given the potentially devastating effects of this condition, rapid diagnosis and treatment are essential if patients are to be returned to their previous levels of activity.

Normal Anatomy

The lumbar vertebral canal is roughly triangular in shape and is narrowest in its anteroposterior diameter in the axial plane. The average anteroposterior diameter of the lumbar canal in adults, as determined by anatomic and radiographic studies, ranges from 15 to 23 mm.4 The canal is bounded anteriorly by the posterior edge of the vertebral body including the posterior longitudinal ligament, which is closely apposed to the posterior vertebral body surface, laterally by the pedicles, posterolaterally by the facet joints and articular capsules, and posteriorly by the lamina and ligamenta flava (yellow ligaments).

As shown in Figures 1 and 2, entrapment of the cauda equina roots, which pass within the dural sac, can occur as a result of progressive hypertrophy of any of the osseocartilaginous and ligamentous elements surrounding the spinal canal. Moreover, the intervertebral disc, which is composed of a gelatinous, centrally located nucleus pulposus and a peripherally located annulus fibrosus, is prone to rupture or herniate posteriorly or posterolaterally as a result of degenerative changes or trauma, producing neural element compromise.

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FIGURE 1.

Normal anatomic structures of the lumbar spine at the third through the fifth lumbar levels. Note the close association between the nerve roots and the dural tube, and the ligamentum flavum, the facet joints, the pedicles and the lamina. The ligamentum flavum (inter-laminar ligament) attaches laterally to the facet capsules.

FIGURE 1.

Normal anatomic structures of the lumbar spine at the third through the fifth lumbar levels. Note the close association between the nerve roots and the dural tube, and the ligamentum flavum, the facet joints, the pedicles and the lamina. The ligamentum flavum (inter-laminar ligament) attaches laterally to the facet capsules.

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FIGURE 2.

Axial computed tomographic (CT) scan at a single lumbar vertebral level following injection of intrathecal contrast medium. Note the lumbar canal narrowing produced by hypertrophic lamina and pedicles. Posterolateral impingement on the thecal sac gives the classic “cloverleaf” or “trefoil” shape to the canal.

FIGURE 2.

Axial computed tomographic (CT) scan at a single lumbar vertebral level following injection of intrathecal contrast medium. Note the lumbar canal narrowing produced by hypertrophic lamina and pedicles. Posterolateral impingement on the thecal sac gives the classic “cloverleaf” or “trefoil” shape to the canal.

In the lumbar regions, the cone-shaped terminus of the spinal cord (conus medullaris) normally ends at about the L1 or L2 level in adults. Caudal to these levels, the roots of the cauda equina are contained within the subarachnoid space of the dura-enclosed thecal sac (Figure 3). Thus, canal stenosis at lumbar levels results in nerve root dysfunction rather than spinal cord dysfunction.

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FIGURE 3.

Posterior view of the lumbar region of the spinal canal, demonstrating the conus medullaris at the L1 to L2 level and the cauda equina nerve roots inferiorly.

FIGURE 3.

Posterior view of the lumbar region of the spinal canal, demonstrating the conus medullaris at the L1 to L2 level and the cauda equina nerve roots inferiorly.

Pathophysiology

Narrowing of the lumbar canal has many potential causes, and various classification schemes have been devised in order to better describe the pathophysiology of this condition. A classification system proposed by Verbiest5 categorizes the multiple causes of lumbar stenosis into two types: conditions that lead to progressive bony encroachment of the lumbar canal (including developmental, congenital, acquired and idiopathic causes) or stenosis produced by nonosseous structures such as ligaments, intervertebral discs and other soft tissue masses. For practical purposes, however, the etiologies of lumbar stenosis can be divided into congenital or acquired forms.

Few causes of lumbar stenosis are truly congenital. Narrowed or “shallow” lumbar canals may be a result of congenitally short pedicles, thickened lamina and facets, or excessive scoliotic or lordotic curves. These anatomic changes may lead to clinically significant stenosis if additional elements such as herniated intervertebral discs or other space-occupying lesions further narrow the canal and contribute to the compression. Verbiest5,6 noted that lumbar canal diameters from 10 to 12 mm may be associated with claudication if additional elements encroach on the canal, and he referred to this type of stenosis as “relative” canal stenosis.5–7

In most cases, stenosis of the lumbar canal may be attributed to acquired degenerative or arthritic changes of the intervertebral discs, ligaments and facet joints surrounding the lumbar canal. These changes include cartilaginous hypertrophy of the articulations surrounding the canal, intervertebral disc herniations or bulges, hypertrophy of the ligamentum flavum and osteophyte formation.

Some investigators have postulated that the pathologic changes that result in lumbar canal stenosis are the result of so-called micro-instability at the articular surfaces surrounding the canal.7 Micro-instability refers to minute, abnormal repetitive motion of the joints that link adjacent vertebra. These movements are clinically silent yet may result in progressive loss of strength in the joint capsules and lead to reactive bony and cartilaginous hypertrophy, thickening or calcification of the ligamentum flavum, or subluxation of one vertebra on another (spondylolisthesis), all of which may contribute to narrowing of the lumbar canal.

Compression of the microvasculature of the lumbar nerve roots, resulting in ischemia, is believed to be a major contributing factor in the development of neurogenic claudication. Wilson8 classified neurogenic claudication into two major types based on the putative pathophysiologic mechanism: postural or ischemic. Postural neurogenic claudication is induced when the lumbar spine is extended and lordosis is accentuated, whether at rest or during exercise in the erect posture. With extension of the spine, degenerated intervertebral discs and thickened ligamenta flava protrude posteriorly into the lumbar canal, producing transient compression of the cauda equina. In the ischemic form, it is theorized that transient ischemia occurs in compressed lumbosacral roots when increased oxygen demand occurs during walking.

Other acquired conditions that can be associated with lumbar canal stenosis as a result of osseous or fibrocartilaginous hypertrophy include fluorosis, hyperparathyroidism, Paget’s disease, ankylosing spondylitis, Cushing’s disease and acromegaly.1,4

Clinical Presentation

Clinical History

Men are affected with slightly higher frequency than women. Although symptomatic lumbar stenosis is usually a disease of the middle-aged and the elderly, younger patients may also be affected. Typically, the earliest complaint is back pain, which is relatively nonspecific and may result in delayed diagnosis. Patients then often experience leg fatigue, pain, numbness and weakness, sometimes several months to years after the back pain was first noticed. Patients may undergo minor trauma that can exacerbate symptoms, which may lead to a more rapid diagnosis.

Once the leg pain begins, it is most commonly bilateral, involving the buttocks and thighs and spreading distally toward the feet, typically with the onset and progression of leg exercise. In some patients, the pain, paresthesias and/or weakness are limited to the lower legs and feet, remaining present until movement ceases. The lower extremity symptoms are almost always described as burning, cramping, numbness, tingling or dull fatigue in the thighs and legs. Disease onset is usually insidious; early symptoms may be mild and progress to become extremely disabling. Symptom severity does not always correlate with the degree of lumbar canal narrowing.

Classically, the symptoms of lumbar canal stenosis begin or worsen with the onset of ambulation or by standing, and are promptly relieved by sitting or lying down. Thigh or leg pain typically precedes the onset of numbness and motor weakness. Along with numbness and weakness, these symptoms and signs constitute the syndrome of neurogenic intermittent claudication. Patients commonly complain of difficulty walking even short distances and do so with a characteristic stooped or anthropoid posture in more advanced cases. Although standing and walking exacerbate the extreme discomfort, bicycle riding can often be performed without much difficulty because of the theoretic widening of the lumbar canal that occurs with flexion of the back. Some patients actually obtain transient relief of pain by assuming a squatting position, which flexes the trunk. Conversely, lying prone or in any position that extends the lumbar spine exacerbates the symptoms, presumably because of ventral in-folding of the ligamentum flavum in a canal already significantly narrowed by degenerative osseus changes.

Other common symptoms include stiffness of the thighs and legs, back pain (which may be a constant symptom) and, in severe cases, visceral disturbances such as urinary incontinence that may be a result of impingement of sacral roots. Back pain, a symptom in nearly all patients with lumbar stenosis,5 may be present with or without claudication, particularly in the earlier stages of the disorder.

Physical Examination

Physical examination of patients with suspected lumbar stenosis should begin with examination of the back. The curvature of the spine should be noted, and the mobility and flexibility of the spine with any changes in neurologic symptoms during active flexion or extension should be recorded (particularly the presence of leg pain, paresthesias or numbness with extension of the spine). The skin should be inspected for the presence of any cutaneous signs of occult spinal dysraphisms. Occult spinal dysraphisms, or occult spina bifida, are failures in the complete closure of the neural (vertebral) arches, which often have external signs indicating their presence. These signs may include patches of hair, nevi, hemangiomas or dimples on the lower back in the midline. These conditions are rare in the adult population, however.

The straight leg raising test (Lasègue’s sign), which is performed by raising the straight lower extremity and dorsiflexing the foot, is classically associated with reproduction of ipsilateral radicular pain secondary to nerve root compression by a herniated lumbar disc, presumably by stretching the compressed ipsilateral nerve root. Most patients with a true positive straight leg raising sign complain of excruciating sciatica-like pain in the elevated leg at 30 to 40 degrees of elevation. This sign is usually absent in patients with lumbar stenosis.

It should be noted that herniation of disc material and subsequent reparative processes may contribute to the overall picture of stenosis, but acute disc herniations generally produce a clinical picture that differs from the more chronic symptoms of canal stenosis. Patrick’s sign, which reproduces leg pain with lateral rotation of the flexed knee, implies ipsilateral degenerative hip joint disease. This is an important piece of the differential diagnosis in patients with stenosis, some of whom may have both conditions.

Neurologic Examination

The neurologic examination in patients with idiopathic degenerative lumbar stenosis may not reveal significant sensorimotor deficits at rest or in a neutral position. Deep tendon reflexes may be decreased, absent or normal, depending on the chronicity of the caudal root compression. Upper motor neuron signs, such as hyperactive deep tendon reflexes or the presence of pathologic reflexes, such as the Babinski’s sign or Hoffmann’s sign, are typically absent unless there is injury to descending long tracts. With the onset of walking, sensory deficits may appear, and motor weakness or reflex changes may be elicited. Therefore, it is extremely important to perform a thorough neurologic examination before and immediately after symptoms appear following a short period of ambulation. Similarly, changes in the neurologic examination with variations in posture should also be recorded.

Neurogenic vs. Vascular Claudication

The signs and symptoms of neurogenic intermittent claudication should be differentiated from the leg claudication produced by atherosclerotic occlusive disease of the iliofemoral vessels (vascular claudication). Vascular disease is commonly associated with other problems such as impotence in men, dystrophic skin changes (nail atrophy, alopecia), foot pallor or cyanosis, decreased or absent peripheral pulses and arterial bruits. Pain or cramping in the buttocks associated with ambulation is often reported.

Patients with vascular claudication also obtain relief with rest and can very accurately quantitate the distance that they can ambulate before symptoms reappear. However, in contrast to claudication that is due to cauda equina compression, vaso-occlusive leg claudication usually does not occur with changes in posture, and patients typically obtain relief from the leg pain by simply resting the legs even while in the upright position (Table 1).

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TABLE 1

Clinical Differentiation Between Neurogenic and Vascular Claudication

TABLE 1

Clinical Differentiation Between Neurogenic and Vascular Claudication

Examination of the femoral, popliteal and pedal pulses, as well as inspection of the legs and feet for trophic changes, is essential in order to differentiate vascular from neurogenic claudication. Ankle/brachial indexes and bedside Doppler examinations should be performed if any abnormality in the pulses is discovered or if vascular disease is suspected. Significant symptomatic pelvofemoral atherosclerosis and lumbar stenosis occasionally coexist in the same patient, and noninvasive circulation studies or arteriography may be required to rule out vasculopathy.

Imaging/Diagnostic Studies

The diagnosis of lumbar stenosis depends largely on the clinical history and physical examination. Radiographic confirmation of the diagnosis can be accomplished using various imaging modalities. Plain films of the spine by themselves are not diagnostic but may demonstrate degenerative changes in the vertebrae or disc spaces, disclose some forms of occult spina bifida or reveal spondylolisthesis or scoliosis in some patients. The most commonly involved levels are L3 through L5, although clinically significant stenosis can exist at any or all lumbar levels in a given patient. In the past, lumbar myelography was the usual method for establishing a diagnosis, but it is usually not necessary today. Modern neuroimaging techniques such as computed tomographic (CT) scanning and magnetic resonance imaging (MRI) have facilitated the diagnosis in recent years.

Computed Tomography

CT scans with or without intrathecal contrast injection define the bony anatomy in one or two planes, are able to demonstrate the lumbar subarachnoid space well, may demonstrate encroachment of the canal by hypertrophied lamina, osteophytes, facets or pedicles, and can provide excellent visualization of the vertebral canal so that measurements of the canal diameter can be made with improved accuracy and resolution compared with plain myelograms. Three-dimensional reconstructions using CT also demonstrate the anatomy of the vertebral canal.

Hypertrophy of the lamina, pedicles and apophyseal joints, along with a thickened ligamentum flavum, impinge on the posterolateral aspects of the lumbar canal, giving it the classic “cloverleaf” or “trefoil” appearance on axial CT scans (Figure 2). Although the trefoil canal is considered to be virtually pathognomonic for lumbar stenosis, a normal trefoil variant is occasionally encountered in an otherwise completely asymptomatic patient.

Magnetic Resonance Imaging

CT scans with intrathecal contrast injection are able to demonstrate the lumbar subarachnoid space and nerve roots with enhanced sensitivity, but this is an invasive test with potential morbidity. For this reason, MRI scanning, with its multiplanar imaging capability, is currently the preferred modality for establishing a diagnosis and excluding other conditions. MRI depicts soft tissues, including the cauda equina, spinal cord, ligaments, epidural fat, subarachnoid space and intervertebral discs, with exquisite detail in most instances. Loss of epidural fat on T₁-weighted images, loss of cerebrospinal fluid signal around the dural sac on T₂-weighted images and degenerative disc disease are common features of lumbar stenosis on MRI (Figures 4a and 4b).

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FIGURES 4A and 4B.

(Left) Unenhanced T₁-weighted axial magnetic resonance scan at a lumbar level showing severe stenosis. The combination of ligament and facet joint hypertrophy concentrically reduces the diameter of the lumbar canal. The significant reduction in the relative amount of epidural fat and subarachnoid cerebral spinal fluid signal is further evidence of the degree of canal stenosis. (Right) Unenhanced T₁-weighted sagittal magnetic resonance scan of the lumbosacral spine showing severe canal stenosis at the L4-5 level, produced by a combination of disc herniation, spondyloarthritis and posterior element hypertrophy. Compare this stenosis with the moderate degree of stenosis observed at levels above. Mild spondylolisthesis is also evident at L5-S1.

FIGURES 4A and 4B.

(Left) Unenhanced T₁-weighted axial magnetic resonance scan at a lumbar level showing severe stenosis. The combination of ligament and facet joint hypertrophy concentrically reduces the diameter of the lumbar canal. The significant reduction in the relative amount of epidural fat and subarachnoid cerebral spinal fluid signal is further evidence of the degree of canal stenosis. (Right) Unenhanced T₁-weighted sagittal magnetic resonance scan of the lumbosacral spine showing severe canal stenosis at the L4-5 level, produced by a combination of disc herniation, spondyloarthritis and posterior element hypertrophy. Compare this stenosis with the moderate degree of stenosis observed at levels above. Mild spondylolisthesis is also evident at L5-S1.

Electromyelography

Electromyelograms with nerve conduction velocity studies may assist in confirming the multiradicular involvement of cauda equina compression. Electromyelography and nerve conduction velocity may also be helpful in diagnosing demyelinating or inflammatory neuropathies and can be of great benefit in distinguishing vascular from neurogenic claudication in situations where the clinical and radiographic pictures are equivocal. Ultimately, however, imaging studies are essential in the diagnosis of lumbar stenosis and, in most cases, electromyelography and nerve conduction velocity studies will not be required.

Differential Diagnosis

As mentioned previously, compression of the lumbar root may have many causes. However, few conditions produce the typical clinical picture of neurogenic claudication that occurs in lumbar stenosis. Table 2 lists potential causes of cauda equina compression that should be ruled out by appropriate diagnostic studies before a diagnosis of lumbar stenosis is made.

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TABLE 2

Conditions That May Mimic Lumbar Stenosis

TABLE 2

Conditions That May Mimic Lumbar Stenosis

Cauda equina syndromes usually occur as a result of compression of the nerve roots in the lumbosacral spine distal to the conus medullaris. Since the root supply to the lower extremities and genitoperineal regions travels in very close apposition within the thecal sac, external compression such as that occurring with lumbar canal stenosis is manifested by dysfunction in multiple root distributions. For example, pain and other sensory deficits may occur in several lumbar and/or sacral dermatomal territories, as well as weakness in the various muscle groups supplied by these nerve roots.

Cauda equina syndromes also may occur secondary to neoplasms, trauma, and inflammatory or infectious processes. An important reason to obtain MRI scans (as opposed to CT scans) in patients with neurogenic claudication is that MRI aids in the exclusion of more serious conditions, such as tumors of the conus medullaris or cauda equina,9 or infectious processes.

It is rare for patients with tumors of the lumbosacral spine to present exclusively with symptoms suggestive of neurogenic intermittent claudication. In contrast to the back and leg pain associated with degenerative lumbar stenosis, the pain associated with a lumbosacral spinal tumor typically worsens with recumbency, awakens the patient at night and is relieved with walking.8

Lumbar epidural abscesses usually are associated with rapidly evolving neurologic deficits, severe back pain and other clinical manifestations that facilitate the diagnosis. These patients may or may not present with fever but almost always demonstrate back pain and exquisite tenderness to palpation localized to the levels of suppuration.

Pathologic, traumatic or osteoporotic compression fractures of lumbar vertebrae also may present with symptoms of cauda equina impingement. Healing of clinically silent fractures may produce exuberant growth of bone, which may lead to canal stenosis and root impingement. Therefore, a search for a history of treated malignancies, evidence of concurrent malignancies or a history of falls or trauma to the spine may be important to the diagnosis.

Degenerative subluxation of lumbar vertebrae (spondylolisthesis) is another cause of acquired stenosis of the lumbar spinal canal, particularly at the L4 and L5 levels, and may manifest clinically with neurogenic intermittent claudication as well.5 Lumbar stenosis sometimes occurs following posterior lumbar fusions, possibly as a result of reactive bony hypertrophy at or adjacent to the fused segments.

Treatment

Since most patients who develop lumbar stenosis are middle-aged or elderly, it is important to ascertain their relative surgical risks. Although decompressive lumbar laminectomy can be an extensive procedure, most patients, even the elderly, are medically capable of tolerating the procedure. In general, these patients are severely disabled by their symptoms and are usually willing to accept a small degree of risk to obtain relief. Anticoagulation therapy or severe cardiac or respiratory disease may be contraindications to surgery.

Risks and Complications of Decompressive Surgery

The risks of laminectomy depend on the number of levels to be decompressed, concomitant medical problems, difficult anatomy as a result of scarring from previous operations or a markedly stenotic canal that may require extensive bone removal and dissection, as well as the overall risks imposed by general anesthesia. Potential complications of the standard decompressive laminectomy include wound infection, hematoma formation, dural tears with subsequent cerebrospinal fluid leaks and risk of meningitis, nerve root damage and the potential for creating postoperative spinal instability. Surgical blood loss is generally well tolerated, but transfusion may be required. The overall surgical mortality associated with decompressive laminectomy is approximately 1 percent.10

The standard decompressive lumbar laminectomy involves a midline incision over the involved levels, dissection down to the spinous processes and progressive removal or “unroofing” of the posterior elements of the lumbar canal (spinous processes, laminae and pedicles), as well as removal of thickened ligamenta flava.

Typically, multilevel decompressive laminectomies are performed since canal stenosis commonly occurs over several levels. Rarely is excision of herniated intervertebral discs required. Removal of the medial portions of the articular facets is often performed, particularly if there is evidence of osteophyte formation. This maneuver has the potential of creating instability at the levels undergoing surgery if the bone resection is extended too far laterally, particularly if bilateral facetectomies are performed.

An alternative technique7 spares the articular facets on one side and creates a unilateral decompressive hemilaminectomy while undercutting the contralateral lamina, removing the ligamentum flavum and performing unilateral bony fusion as well. Another type of decompressive procedure that has been described with good postoperative success is multilevel laminotomy, whereby “windows” or fenestrations are created by removing the superior aspect of the inferior lamina and the inferior aspect of the superior lamina at involved levels. Proponents of this approach believe that sparing the interspinous ligaments and preserving spinous processes minimizes the risk of postoperative instability.

Recently, increasing attention has been paid to lateral recess stenosis syndrome as a cause of back pain and claudication. The lateral recess is the space within the spinal canal adjacent to the exit zone of the nerve roots.

Some authors believe that, in select circumstances, medial facetectomies, foraminotomies and decompression of the lateral recesses are sufficient to relieve the symptoms of neurogenic claudication.11 Other procedures, such as expansile laminoplasty, which involves the en-bloc removal and loose reattachment of the posterior vertebral arches, have not been studied extensively. Overall, these various procedures have met with mixed results, although some patients will undoubtedly benefit from less extensive decompressive procedures depending on the morphology and anatomic location of their nerve root impingement. Regardless of the surgical approach that is chosen, if decompression is not adequate, relief of symptoms may be incomplete or the problem may recur following a short period of clinical improvement.

Results of Surgical Treatment

Most patients benefit from wide decompression of the lumbar canal. Some reports place the percentage of patients benefiting from surgery at 95 percent, with greater than 90 percent of patients returning to their previous activity levels, regardless of age.12 However, recent reports2,12 dismiss these figures as optimistic, instead claiming long-term neurologic improvement in approximately 65 percent of patients. It is fairly clear, however, that in most patients with clear radiographic and clinical evidence of stenosis, decompressive surgery provides significant relief.

In a recent analysis, comorbid conditions and psychologic factors were found to play a significant role in patients’ individual perceptions of outcome following either laminectomy or laminotomy. Patients with significant comorbid illnesses reported less relief of pain and less functional recovery than expected following decompression.13 In patients with chronic, severe symptoms, decompression of the neural elements may not result in immediate pain resolution, nor are longstanding preoperative motor deficits likely to resolve immediately. Nonetheless, following cauda equina decompression, the relentless progression of neurologic dysfunction may be slowed or halted.

Nonsurgical Treatment for Lumbar Stenosis

Conservative treatment for lumbar stenosis, such as lumbar bracing, bed rest, physical therapy and pain management, has few proven benefits in the long term. Unless debilitating medical conditions prohibit surgery under general anesthesia, medical or nonsurgical management of lumbar stenosis is not a practical option if symptoms are incapacitating. Nonsurgical management of this condition may be attempted initially in patients with mild symptoms of short duration.

Morbidly obese patients with symptoms of neurogenic claudication may improve following institution of a weight loss program. Back strengthening exercises, strict physical therapy regimens and symptomatic management with nonsteroidal analgesics also may benefit some patients initially but, in contrast to patients with herniated intervertebral discs (who often respond favorably to nonsurgical management), patients with lumbar stenosis often show no improvement on long-term follow-up. Their symptoms rapidly return with the resumption of activity. Since many of these persons are severely limited by pain, early surgery is the best way to return them to full activity and independent living.

90,000 Treatment of protrusion of the lumbar spine in Moscow at the Dikul clinic: prices, appointment

Back pain can come from the intervertebral disc, nerves, muscles, bones and facet joints. Disc protrusion is the most common cause of lower back and leg pain in all age groups. Small disc protrusions are often asymptomatic. At the same time, a large protrusion of the disc can protrude both into the foraminal foramen and the spinal canal and lead to an effect on nerve structures with the development of radicular syndrome or stenosis of the spinal canal with the development of such a serious condition as Cauda equine.

Most back pain caused by a slight protrusion of the disc will disappear on its own.

Small protrusions of discs are often poorly visualized on both radiography and MRI examination.

Chronic back pain caused by disc protrusion after injury has a major impact on performance. Treatment of protrusion of the lumbar spine is usually conservative, but in the presence of compression of nerve structures, surgical treatment may be recommended.

Reasons

Aging and wear are usually the main causes of disc protrusion. However, many additional factors can stimulate or accelerate this degenerative condition of the spine, including:

• Sudden injuries, such as those that occur during sports, a car accident, or a severe fall
• Genetic predisposition to degenerative disc disease (osteochondrosis)
• Congenital malformations of the spine
• Obesity or heavy carrying
• Lack of sufficient and regular physical activity
• Malnutrition
• Smoking
• Impact of the position of the person, or repetitive pressure on the discs of the lumbar spine
• As shown in the diagram above, the least pressure on the discs in the lumbar spine occurs in the supine position, while the greatest pressure on the discs occurs in the sitting position, with the torso tilted with a weight, with the center of gravity shifted forward. along the center line.
• It is important to note that while sitting, the impact on the lumbar discs is greater than in the standing position.
• Another cause of disc protrusion in the lumbar spine is excessive force when the vertebrae slip excessively, usually due to excessive stretching or from lifting weights with improper technique.

The muscles of the back try to prevent the spine from bending forward and causing compression, but the applied force vector is significant for them, and therefore the vertebrae slide too much in relation to each other.

Force vectors acting on the lumbar spine while sitting

Symptoms

General symptoms

• Insomnia – secondary to pain
• Weight loss secondary to chronic pain and loss of appetite. Loss of appetite occurs in patients with back pain due to stenosis or cancer of the spine

Back pain

• Discogenic pain.Lumbar discogenic pain is felt in the area of ​​the lumbar dermatome L1-L5.

Lumbar radicular pain

• The nature of the pain is acute and shooting pain.
• Pain is triggered by certain movements (for example, when bending or twisting the trunk, coughing and sneezing).
• Time and intensity of pain – pain at night is more intense
• Pain radiates to the lower limb – along the dermatome of the nerve roots L1, L2, L3, L4, L5 or S1.
• Dermatomal pain due to root compression

L1 root compression – pain spreads to the groin dermatome.

L2 root compression – Pain is felt on the anterior and lateral surfaces of the mid-thigh, mid-thigh, and lateral thigh.

Compression of the L3 root – The pain is felt on the inner and antero-lower part of the thigh.

L4 root compression P- The pain is localized in the lower leg, mainly on the anterior and posterior sides.

Compression L5 P – Pain is felt on the front lateral side of the lower leg and dorsal part of the foot in the region of the middle three toes.

S1 root compression – Pain felt on the lateral side of the feet.

S2 Compression – Pain felt on the back of the thigh and the back of the upper 2/3 of the lower leg.

Tingling spreads along the dermatome of the nerve roots L1-S2

Numbness spreads along the dermatome of nerves L1-S2

Other symptoms of disc protrusion

Paravertebral muscle spasm

• Paravertebral muscle spasm occurs between the L1 and L5 vertebrae.
• Muscle spasms are often persistent and cause severe pain of a secondary nature associated with muscle fatigue and lactic acid build-up in the muscles.

Muscle weakness in the lower limb

• Ischemia of the motor nerve. Strong pressure within the foraminal foramen causes ischemic changes in the motor nerve, resulting in weakness in the leg.
• Movement in the spine. Flexion, extension, abduction, and extension of the lower limb become weak, depending on the level of the root lesion in the lumbar spine.
• Change of position. It is difficult for the patient to get in and out of a sitting or lying position.
• Motor disorders at the level of root damage

L1 – Causes weakness in hip flexion.

L2 – Causes weakness in hip flexion.

L3 – Causes weakness in hip flexion and knee extension.

L4 – Impossibility of extension in the knee and dorsiflexion in the ankle.

L5 – Unable to perform big toe extension, plantar extension, inability to lift the big toe up.

S1 – Causes weakness in knee extension.

Decreased knee and ankle reflexes

• Knee reflex – L2 and L3. The root injury causes an abnormal knee reflex.
• Achilles reflex – reduced or absent in case of damage to the nerve roots L4-5 and S1.

Muscle atrophy

• A decrease in muscle mass is observed on the side of the bulging (protrusion) of the disc
• Muscle wasting or thinning of the leg is associated with leg weakness.

Since the symptoms of protrusion of the lumbar spine are similar to many other more serious conditions, it is very important to carry out a complete diagnosis before starting treatment.

Diagnostics

• MRI – reliable examination for diagnosing small and large disc protrusions.

• Laboratory research
• An increase in ESR may be a sign of an epidural abscess or tumor that is putting pressure on the root
• C-reactive protein – an increase in the level in patients with rheumatological diseases
• Leukocytosis is characteristic of epidural abscess, osteomyelitis, or infections.
• Radiography . Disc protrusion is not visible on x-rays. But this research method allows you to detect the presence of abnormalities, injuries, spondylolisthesis
• KT . CT scan. Small disc protrusions may not show up on CT scans, which can detect medium to large protrusions.
• Myelogram . This research method was often used before in preparation for back surgery, but after the advent of MRI imaging, the need for this diagnostic method has significantly decreased.
• EMG (ENMG). These neurophysiological methods are used to assess nerve damage.
• PET – Bone scanning is only necessary if there is a suspicion of a tumor or infection.
• Bone densitometry . A bone density test can detect a disease such as osteoporosis.

Treatment of protrusion of the lumbar spine

Drug treatment

• OTC Analgesics – Designed for mild to moderate pain.
• Anti-inflammatory drugs – Designed to reduce inflammation of the nerve root caused by irritation and pinching (aspirin, ibuprofen (Motrin, Advil) and naproxen (Aleve).

Prescription Analgesics

• Tramal – prescribed for persistent pain syndrome.
• Opiates – Recommended when other drugs do not relieve pain.
• Opioids are useful in the treatment of chronic, intense pain.

Muscle relaxants

• Mechanism of Action – Stimulates Locus Ceruleus in the brainstem. Muscle relaxants stimulate the ceruleus locus and cause an increase in the release of norepinephrine in the spinal cord. Norepinephrine inhibits the alpha motor neuron and leads to a decrease in skeletal muscle spasm.
• Most commonly used muscle relaxants

  Cyclobenzaprine (Flexeril)

  Soma

  Skelaxin

  Robaxin

Antidepressants

• Effective as an analgesic in the treatment of chronic neuropathic pain.
• Prescribed as an analgesic in cases where the use of other pain relievers (NSAIDs, tramadol or opioids) causes severe side effects.
• For neuropathic pain associated with depression – used as an analgesic and antidepressant.
• Most commonly prescribed antidepressants
• Duloxetine
• Milnacipran
• Tricyclic antidepressants (Elavil)

Sedatives

• Sedatives (such as benzodiazepines) are prescribed to reduce anxiety caused by pain.In addition, they can reduce muscle spasm to some extent and normalize sleep.

Antiepileptic drugs

• The analgesic effect of these drugs is used in the treatment of chronic neuropathic pain.
• Prescribed as an analgesic if the use of NSAIDs, tramadol or opioids is associated with severe side effects.

Most commonly prescribed antiepileptics for pain management:

• Gabapentin (Neurontin).
• Pregabalin (Lyrics).

Interventional Pain Management

• Translaminar epidural corticosteroid injection. An epidural injection of corticosteroids can help reduce disc and nerve root inflammation.
• Caudal corticosteroid injection — Caudal epidural injection is an alternative method of injecting corticosteroids into the epidural space.
• Trans-foraminal epidural injection – targeted injection of cortisone into the area of ​​root compression by disc protrusion.

Manual therapy

This treatment is effective for treating small to medium sized disc protrusions.

Manual therapy often avoids invasive treatments such as interventional pain therapy and surgery.

• Osteopathic Manual Therapy is commonly used in the treatment of lumbar disc protrusion and may be effective within the first month after symptom onset.
• Massage . Using massage therapy helps relieve pain in the superficial and deep layers of muscles and connective tissue. Massage helps to improve blood flow to the muscles as well as reduce muscle spasms.
• LFC
• Stretching and flexibility exercises help restore the mobility of the motor segments of the lumbar spine. Resistance exercise is necessary to strengthen the muscles and strengthen the stability of the spine.
• Physiotherapy (cryotherapy, ultrasound, electrical stimulation, magnetotherapy, TENS (Transcutaneous Electrical Nerve Stimulation) These and other physiotherapy methods are widely used in the treatment of lumbar disc protrusion.
• Acupuncture. The method of treatment is useful when it is necessary to reduce pain and restore conduction along nerve fibers.

Surgical treatment

Surgical decompression of nerves.These operations are performed to relieve pressure on the nerves:

• Microdiscectomy – Microscopic surgery leads to a quick recovery.
• Percutaneous Nucleoplasty . Minimally Invasive Surgical Treatment Provides Fast Recovery
• Discectomy – after skin incision and surgery, the disc is removed.
• Laminectomy – the bone part of the vertebra (lamina) is removed to widen the bone tunnel
• Fusion Surgery – This surgical treatment is used after unsuccessful surgeries to decompress nerves.

What is a dermatome?

A dermatome is an area of ​​skin that is innervated by one spinal nerve. There are 30 pairs of dermatomes in the body, from the skull to the toes, and each of them can be traced back to a specific nerve root. While most dermatome maps show individual areas, there is in fact a significant amount of overlap, understanding how dermatomes work can be important in the treatment and diagnosis of a disease.

Along the body, dermatomes appear as horizontal stripes, each of which corresponds to a specific nerve root.The arms and legs have longitudinal stripes, which explains why the pain sometimes knocks an arm or leg down because it follows the dermatome. The cervical, thoracic, lumbar, and sacral nerves supply nerve fibers with various dermatomes in the body. For example, the back of the leg is covered with a dermatome, which is innervated by the first sacral nerve.

In patients with neurological problems, pain in a specific dermatome can be a very indicative symptom. A doctor can examine the pain to find out which dermatome or dermatome it belongs to, and use that information to look for signs of damage in a specific area.For example, a person with compression of the spine causing a compressed nerve may experience significant pain in the dermatome innervated by that nerve. Likewise, for someone with a shingles outbreak, areas of pain on the body will correspond to specific spinal nerves affected by the virus that causes shingles.

Dermatome pain is a symptom, not a condition, but it can be a very important symptom. Patients who report chronic pain or transient pain in a specific area of ​​their body may reveal important information about a neurological condition or a spinal cord problem, and the doctor can use this information to recommend treatment or refer the patient to a specialist who can address the problem. …

This type of pain can be extremely unpleasant for patients because it has no clear physical cause and may come and go sporadically, depending on the type of injury. The skin may experience itching, burning, or other sensations that don’t actually occur, including a bad cold or severe pain. By tracing pain back to the responsible nerve, the doctor can develop a treatment plan to correct or eliminate the underlying cause so that the patient does not experience unwanted sensations associated with nerve damage or other impaired nerve function.

OTHER LANGUAGES

90,000 Clinical experience with the successful use of a fixed combination of orphenadrine and diclofenac in the treatment of acute spondylogenic pain syndromes

Acute back pain can be accompanied by local, reflected, or radicular pain. Therefore, to understand the therapeutic tactics for pain syndromes, it is important to understand the sources of pain impulses and localization of the morphological substrate of pain.

The SMN (spinal) nerve forms in the intervertebral (foraminal) foramen after the fusion of the posterior and anterior roots of the spinal cord. Three branches depart from it: 1 – anterior (ventral): innervates the muscles of the limbs and trunk; 2 – back (dorsal): to the paravertebral muscles; 3 – recurrent nerve, synuvertebral nerve (r. Meningeus – according to the anatomical nomenclature): upon exiting the MPO, the nerve receives fibers from the sympathetic trunk, then returns to the spinal canal and, branching out, provides efferent, afferent and sympathetic innervation of the articular capsule, the periosteum of the vertebra, the posterior longitudinal ligament, the meningeal membrane, the outer third of the surface of the annulus fibrosus of the disc.

Local pain

Irritation of the nociceptors of the structures innervated by the SVN, as well as the paravertebral muscles innervated by the dorsal branches of the spinal nerves, is the cause of reflex local muscle-tonic pain syndrome (cervicalgia, lumbodynia).

Radicular pain

Radicular pain is mainly associated with areas innervated by the ventral branches of the SMN. It should be noted that of all structures of the peripheral nervous system, this particular nerve is considered the most vulnerable to compression and tension.The pain occurs already when pressing or pulling the meningeal tissue, which contains the preganglionic segment of the posterior root. In this case, irritation of the nociceptors of the nervi nervorum of the spinal nerve also occurs. Radicular pain (cervical and lumbar) with discogenic lesions of the spinal nerve has the following distinctive features: – the spread of pain in the zone of sensitive (dermatome) and motor (myotoma) innervation of the affected SMN; – a feeling of numbness and the passage of an electric current; – concomitant muscle atrophy does not correspond to the innervation zone of a particular peripheral nerve; – lack of vegetative manifestations.There are various clinical patterns in the spread of pain. The pain may initially occur only in the lumbar region or in the thigh, and then radiate throughout the leg to the foot. Another option is the absence of lower back pain with preservation only in the leg (sciatica without lower back pain) [1, 2]. If the root is completely compressed, then the pain can disappear completely, hypoalgesia and hypesthesia develop in the affected dermatome, and a motor defect occurs: for example, sagging of the foot and thumb during compression of the L5 root.A predictively favorable sign is the phenomenon of pain centralization, i.e. when pain is displaced in the proximal direction [3].

Lumboischialgic syndrome

Pain perceived by the patient at a location distant from the structure that is believed to be the pain generator is defined as reflected pain. This broad definition includes pain emanating from visceral and / or somatic structures directly or via reflex pathways.In this case, in the zone of reflected pain, local hyperalgesia, hyperesthesia, muscle tension, and local autonomic reactions may occur. In clinical practice, reflected pain in the form of lumboischialgic syndrome is identified with radicular pain, which leads to incorrect diagnosis and treatment. To designate pain in the lumbar spine irradiating to the leg without signs of radicular pathology, the term pseudoradical syndrome is sometimes used [2, 4]. The most common causes of lumbar ischialgic syndrome are: pathology of the intervertebral joints (spondyloarthrosis), sacroiliac joint syndrome.Irritation of the receptors of the articular capsule of the intervertebral joints in the lumbar spine is considered as the cause of reflex tonic tension and pain syndrome in the paravertebral and ischiocrural muscles of the sciatica type. In a functional and neuroanatomical sense, the sacroiliac joint is considered the lowest pair of facets, and the pattern of its reflected pain resembles that of the lumbar intervertebral joints.

Combined types of pain

Localized back pain may be accompanied by reflected pain and / or radicular pain.The combination of reflected spondylogenic and radicular pain creates certain clinical complications. The nature of the pain can change during the course of the disease. It should be noted that there may be cases of radiculopathy without back pain, and therefore difficulties arise in the differential diagnosis. The pain is often limited to the area above the sacroiliac joint or the area of ​​the foot along the dermatome, and its discogenic nature is often revealed only on the basis of CT and / or MRI data.At first, the most striking manifestations are pain and pathological posture, and later they are replaced by paresthesias and movement disorders. The nature and irradiation of pain in lumbar syndrome are constantly changing: deep pain in the lower back is replaced by unilateral pain in the buttock or sacroiliac region.

Pathogenetic rationale for treatment

The motor reaction to a pathological stimulus is manifested by protective reflexes, accompanied by a change in muscle tone.Muscle overexertion leads to irritation of pain receptors. The pain increases muscle tension. Clinically, this is manifested by forced postures. For example, asymmetric torso flexion with lumbago or lumbar ischialgia. Reflex contraction of some muscle groups and relaxation of others is a defense mechanism for the musculoskeletal system aimed at reducing irritation of pain receptors and minimizing pain. Often, overexcitation of nociceptors and painful muscle spasm form a vicious circle, acquiring not sanogenetic, but pathogenetic significance, which is the rationale for prescribing muscle relaxants.Irritation of the root can also develop without the mechanical effect of disc herniation, and as a result of the ingress of chemical mediators and inflammatory cytokines, formed as a result of microdamage of the degeneratively changed disc and the posterior longitudinal ligament, into the epidural space, which leads to the development of irritative pain syndrome [2]. The goal of analgesic therapy is to interrupt the process of nociception after it is triggered by a pathological stimulus in various parts of the pathways of pain, its perception and response to it [5].It is absolutely proven that the patient should be painfully relieved as soon as possible. The earlier treatment is started and the faster a significant analgesic effect is achieved, the less the likelihood of chronic pain and the better the overall prognosis. The aim of the study was to compare the analgesic efficacy and safety of a fixed combination of diclofenac and orphenadrine (neodolpassse) with the analgesic efficacy and safety of dexketoprofen and tolperisone in patients with acute nonspecific pain in the neck, lower back and in patients with cervical and lumbar radicals.

Research methods

An observational parallel-group clinical study was carried out. We examined and treated 36 patients aged 30-60 years of the 1st (main) and 21 patients of the 2nd group (comparison). There were no significant differences in the groups in occupational composition, gender, age, concomitant pathology, which could affect the outcome of the disease. The duration of the pain history and exacerbation, as well as the indicators of the severity of pain according to the visual analogue scale (VAS) in the study groups were comparable (p> 0.05) All patients gave written informed consent to participate in the study.In the 1st group, patients were injected intravenously with a solution of diclofenac and orphenadrine (neodolpassa) (diclofenac 75 mg and orphenadrine 30 mg) daily for 2 days. In order to optimize the treatment, two subgroups with single and double administration of neodolpass per day were identified. In the 2nd comparison group, 21 patients received intramuscular administration of dexketoprofen and tolperisone daily for 3 days. Inclusion criteria: acute pain in the neck and lumbar region, radicular syndrome, gender – any.Exclusion criteria were myelopathy, clinically significant liver or kidney dysfunction, pregnancy and breastfeeding. The patients were monitored daily, the number of days was recorded during which the pain passed or significantly regressed (by ≥30% according to the VAS). Evaluation of the effectiveness of treatment was carried out on the 2nd and 3rd day of treatment using the VAS. Data processing was carried out using the Primer of Biostatistics, Statistica v. 6 (StatSoft, USA).

Results

According to VAS, the initial level of pain syndrome severity was comparable in the groups.A more pronounced analgesic effect was observed after the second day of treatment in patients who received neodolpassa administration (p <0.05) (Fig. 1). Data were obtained on a more pronounced analgesic effect with a double administration of neodolpass compared with a single administration per day (Fig. 2). No local side effects were observed when administered neodolpassa. Dyspeptic disorders (heartburn, decreased appetite) were identified in two patients (5.5%). In one case, dizziness and tremors appeared after the second injection.After intravenous infusion, the patients most often noted drowsiness — in 4 (11.1%) cases. When monitoring blood pressure, there was a slight increase in systolic pressure immediately after the infusion. No dynamics of diastolic pressure was observed, and it remained stable during the course of therapy (Fig. 4).

Discussion

When studying the efficacy and safety of intravenous administration of a fixed combination of orphenadrine and diclofenac in the treatment of acute spondylogenic pain syndromes, the comparison group consisted of patients receiving intramuscularly non-steroidal anti-inflammatory drug dexketoprofen and muscle relaxant with vasodilating effect tolperisone.The literature contains a sufficient number of studies demonstrating the effectiveness of dexketoprofen in comparison with known analgesics in the treatment of non-specific pain in the neck and lumbar spine [6, 7]. Also, numerous studies have confirmed the effectiveness of tolperisone in the treatment of nonspecific pain in the neck and lumbar spine, and an increase in the analgesic effect has been noted when it is used simultaneously with NSAIDs [5, 8]. The basis for the appointment of muscle relaxants is the protective muscle defense accompanying the development of pain, which is acquiring pathogenetic significance.The centrally acting muscle relaxant orphenadrine is an o-methyl derivative of diphenhydramine, has anticholinergic, antihistamine properties and is used to eliminate pathologically increased skeletal muscle tone [9]. The drug has established itself as an effective treatment for pain accompanied by muscle spasms [10, 11]. A number of studies have shown that the drug has an independent analgesic effect, which is realized not only by reducing muscle spasm, but also indirectly due to the effect on the dopaminergic and histaminergic antinociceptive neurotransmitter systems of the brain [11, 12].In particular, orphenadrine blocks NMDA receptors, h2-histamine receptors, muscarinic receptors, interacts with the norepinephrine reuptake system and, like local anesthetics, inhibits sodium channels, disrupting the conduction of nerve impulses. In the experiment, in terms of the severity and duration of the local anesthetic action, it exceeded lidocaine [9, 11]. In clinical practice, it is important that orphenadrine has a weak sedative effect and reduces the pathologically increased tone of skeletal muscles, without affecting the normal tone and voluntary movements [11].With the combined use of orphenadrine with diclofenac, an additive analgesic effect is observed, which is confirmed by the results of a targeted comparative study of a fixed combination with monotherapy with its ingredients [13].

It should be noted that the fixed combination of diclofenac and orphenadrine is approved by the FDA and is widely used in clinical practice for analgesia in the United States [14]. In this comparative study, we obtained data on a more pronounced, significant difference in pain reduction according to the VAS on day 2 in the group of patients receiving a fixed combination of diclofenac and orphenadrine, compared with the group of patients with intramuscular administration of dexketoprofen and diclofenac.After intravenous infusion, patients most often noted drowsiness — in 4 (11.1%) cases, which from a clinical point of view can be considered a positive effect in dyssomnia caused by pain and muscle spasms. Among 36 treated patients, two patients required further surgical treatment. In one case, the progression of paresis of the foot was the basis for referral to a neurosurgeon. In another case, with radiculopathy C 8 repeated MRI examination of the cervical spine revealed a Pancost tumor.It should be noted that during the period of neodolpassa, the pain syndrome in these patients was significantly reduced.

Conclusion

The use of a fixed combination of orphenadrine and diclofenac is a highly effective and safe treatment for acute spondylogenic pain syndromes. The use of the drug, due to the effect on various pathogenetic mechanisms, is accompanied by a rapid analgesic effect, which can significantly reduce the consumption of analgesic drugs.The issue of continuation and choice of analgesic therapy after a two-day course with neodolpassse requires further study.

Conflict of Interest Statement

This article was supported by Fresenius Kabi LLC. The authors are solely responsible for submitting the final version of the manuscript to print. All authors took part in the development of the concept of the article and writing the manuscript. The final version of the manuscript was approved by all authors.

References / References

1. Defrin R, Brill S, Goor-Arieh I. “Shooting pain” in lumbar radiculopathy and trigeminal neuralgia, and ideas concerning its neural substrates. Pain. 2020; 161 (2): 308-318. 2. Kremer Y. Diseases of the intervertebral discs. Per. from English 2nd edition. Under total. ed. prof. Shirokova V.A. MEDpress-inform; 2015. Krämer J. Intervertebral Disk Diseases. Translated from English. 2nd edition. Prof. Shirokov VA, ed. MEDpress-inform; 2015.(In Russ.). 3. McKenzie RA. The lumbar spine: Mechanical diagnosis and therapy. Waikanae, New Zealand: Spinal Publications; 1981. 4. Mumentaler M, Shter M, Müller-Fall G. Lesion of peripheral nerves and radicular syndromes. M .: MEDpress-inform; 2013. Mumenthaler M, Stöhr M, Müller-Vahl H. Läsionen peripherer Nerven und radikuläre Syndrome. M .: MEDpress-inform; 2013. (In Russ.). 5. Kukushkin M.L., Brylev L.V., Laskov V.B. et al. Results of a randomized, double-blind, parallel study of the efficacy and safety of tolperisone in patients with acute nonspecific lower back pain.Journal of Neurology and Psychiatry. S.S. Korsakov. 2017; 117 (11): 69-78. Kukushkin ML, Brylev LV, Laskov VB, et al. The results of a randomized double-blind parallel study of efficacy and safety of the use tolperisone in patients with acute nonspecific pain in the lower back. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2017; 117 (11): 69-78. (In Russ.). 6. Vorobyova OV Discogenic non-radical back pain: a case study. Medical advice. 2020; 4: 60-65. Vorobieva OV. Discogenic non-radicular low back pain: a clinical case report.Medical Council. 2020; 4: 60-65. (In Russ.). 7. Plotnikova E.Yu., Zolotukhina V.N., Isakov L.K. et al. Efficacy and safety of various non-steroidal anti-inflammatory drugs for acute pain in the neck and back. Neurology, neuropsychiatry, psychosomatics. 2020; 12 (2): 42-47. Plotnikova EYu, Zolotukhina VN, Isakov LK, et al. Efficacy and safety of different nonsteroidal anti-inflammatory drugs for acute neck and back pain. Neurology, Neuropsychiatry, Psychosomatics. 2020; 12 (2): 42-47. (In Russ.). eight.Skorobogatykh K.V., Azimova Yu.E. Comparative efficacy of tolperisone and meloxicam in the treatment of acute nonspecific pain in the cervical spine. Neurology, neuropsychiatry, psychosomatics. 2020; 12 (2): 37-41. Skorobogatykh KV, Azimova YuE. Sravnitel’naya effektivnost ‘tolperizona i meloksikama pri lechenii ostroj nespetsificheskoj boli v shejnom otdele pozvonochnika. Neurology, Neuropsychiatry, Psychosomatics. 2020; 12 (2): 37-41. (In Russ.). 9. Amelin A.V. Fixed combination of orphenadrine and diclofenac as new possibilities for multimodal therapy for pain and muscle spasm.Russian Journal of Pain. 2019; 17 (4): 50-53. Amelin AV. A fixed combination of orphenadrine and diclofenac, as possibilities of multimodal therapy of pain and muscle spasm. Russian Journal of Pain. 2019; 17 (4): 50-53. (In Russ.). 10. Borsodi M, Nagy E, Darvas K. Diclofenac / orphenadrine as a combined analgetic in post-operative relief of pain. Orv Hetil. 2008; 149 (39): 1847-1852. 11. Ushkalova E.A., Zyryanov S.K., Zatolochina KE. Fixed combination of diclofenac and orphenadrine in the treatment of acute pain syndromes.Neurology, neuropsychiatry, psychosomatics. 2020; 12 (1): 100104. Ushkalova EA, Zyryanov SK, Zatolochina KE. The fixed combination of diclofenac and orphenadrine in the treatment of acute pain syndromes. Nevrologiya, neiropsikhiatriya, psikhosomatika. Neurology, Neuropsychiatry, Psychosomatics. 2020; 12 (1): 100-104. (In Russ.). 12. Schaffler K, Reitmeir P, Gschanes A, et al. Comparison of the Analgesic Effects of a Fixed-Dose Combination of Orphenadrine and Diclofenac (Neodolpasse®) with its Single Active Ingredients Diclofenac and Orphenadrine.Drugs in R & D. 2005; 6 (4): 189-199. 13. Malek J, et al. Diclofenac 75mg. and 30 mg. orfenadine (Neodolpasse) versus placebo and piroxicam in postoperative analgesia after arthroscopy. Acta Chir Orthop Traumatol Cech. 2004; 71 (2): 80-83. 14. FDA listing of Orphenadrine citrate registrations. United States Food and Drug Administration. Retrieved February 06, 2016.

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Dermatome What is it, types and clinical significance / Anatomy and physiology | Thpanorama

dermatoma is an area of ​​skin that is innervated by one spinal nerve.In particular, they are controlled by sensory neurons that arise from the spinal nerve ganglion.

There are eight cervical nerves, twelve thoracic nerves, five lumbar nerves, and five sacral nerves. Each of these nerves allows us to feel temperature, touch, pressure, and even pain.

Information travels from a specific area of ​​the skin to the brain. Dermatomes are organized as a stack of discs in a portion of the chest and abdomen, with each disc equipped with a different spinal nerve….

The picture is different in the limbs. Thus, dermatomes run longitudinally along the arms and legs. Thus, each half of each limb has its own dermatome.

Although all people usually have the same overall picture of the organization of dermatomes, specific areas of innervation may differ from person to person, as if they were fingerprints.

The vertebral column has more than 30 different vertebrae, which are divided according to their location, from the neck to the coccyx.They are classified as cervical, thoracic, lumbar, and sacral. Each vertebra contains a specific spinal nerve that will innervate specific areas of the skin.

All nerves, except for the first cervical nerve (C1), are connected to the dermatome. Dermatomes provide a map of the spinal cord, which is very useful for healthcare professionals and researchers. And also for the diagnosis and treatment of pathologies.

There are currently two main charts in the medical profession. The first is Keegan and Garrett’s 1948 map, and the second is Förster’s 1933 map, the latter being the most widely used….

What is a dermatome?

Have you ever wondered why back pain leads to tingling in the legs? Or why do neck cramps make you feel numb in your fingers?

Apparently, this is due to the fact that there is a connection between sensations and disorders on the surface of the skin with specific nerve roots that originate in the spine. Therefore, each region that is innervated by each of these nerve roots is called a dermatome.

Dermatome is subdivided into dermat, which means skin, and oma, which means mass. We have 29 dermatomes in the human body. These nerves are connected to each other, as they arose from the same somite groups during embryonic development. Somites are structures formed on the sides of the neural tube during the fourth week of human development.

For example, nerve fibers on the surface of the skin that cover part of the legs and feet constitute a dermatome that originates from the nerve root of the lower back….

Dermatomes should not be confused with myotomes. On the other hand, myotomes are those that innervate the skeletal muscles of the same group of somites ..

type

Dermatomes, like the spine, are divided into four parts: cervical, thoracic, lumbar and sacral. Each dermatome is classified according to the spinal nerve that innervates it. That is, the seventh cervical nerve innervates the C7 dermatome.

This dermatome gives sensitivity to the skin of the shoulder, parts of the hand, and the index and ring fingers….

Cervical dermatomes

They nourish the skin of the neck, neck, back, arms and hands.

Thoracic dermatomes

These cover the skin of the inner arm, chest, abdomen and mid-back.

Lumbar dermatomes

Invert the skin that lies in the lower back, in the frontal area of ​​the legs, outer thighs and in the upper and lower legs.

Sacral dermatomes

These cover the skin of the genital and anal regions, the back of the legs, the back of the thighs and the calf, in addition to the outer edge of the legs.

However, it is important to note that dermatomes have been discovered in recent years by clinical observation and are only a guideline. Each person can imagine small changes within the dermatomes.

Clinical significance

It is important to know how dermatomes work in a clinical setting to localize nerve or spinal cord lesions.

If certain symptoms are located along the area associated with the dermatome (pain, skin irritation, rash…), it may be related to something related to the nerve root. For example, a herniated disc that compresses the L5 nerve root results in pain and tingling in the lower leg and foot.

Dermatomes are useful for the diagnosis and treatment of various conditions. The main ones are viral diseases, radiculopathy and spinal cord injuries.

Viral diseases

There are certain viral diseases that are found in certain dermatomes, such as shingles.This virus is hidden in the spinal cord, and when it manifests, it travels through the spinal cord, causing a painful skin rash that is associated with this nerve.

Herpes zoster is usually limited to a specific dermatome, such as the chest, leg, or arm. It usually appears years or even decades after recovering from chickenpox.

radiculopathy

This condition consists of pain caused by damage to the root of any nerve. It can also lead to loss or decrease in sensory function.The most common regions of the lesion are L5 and S1, and less often C6 and C7 ..

The pain increases when we put ourselves in a position in which the nerve roots are stretched. It can be cervical or lumbar depending on where the pain is.

Spinal Cord Injuries

When there is a spinal cord injury, the healthcare professional will look for the affected dermatome. To do this, it will start with the part of the skin where the patient has noticed changes. It will travel with a pin or fork on either side of the body until you achieve normal sensation.

You can also check if it records vibration along the vertebrae. Typically, the sensory level is two to three levels below the injury.

References

1. Dermatomes. (N.D.). Retrieved April 16, 2017, from Teach Me Anatomy: teachmeanatomy.info.
2. Dermatome Map – Overview Chart, Anatomy and Clinical Significance. (N.D.). Retrieved April 16, 2017, from Pain care: paincare.org.
3. Dermatomas. (N.D.). Retrieved April 16, 2017.from Queen’s University, Kingston: meds.queensu.ca.
4. Dermatomas. (N.D.). Retrieved on April 16, 2017, from Boundless: boundless.com.
5. Kishner S. (s.f.). Dermatome anatomy. Retrieved on August 12, 2015 from MedScape: emedicine.medscape.com.
6. What is a dermatome? – Definition and distribution. (N.D.). Retrieved on April 16, 2017, from Study: study.com.

FSUE “Nizhny Novgorod prosthetic and orthopedic enterprise”

FSUE “Nizhny Novgorod Prosthetic and Orthopedic Enterprise”

from December 22, 2016 renamed

“NIZHEGORODSKY” BRANCH

Federal State Unitary Enterprise “Moscow Prosthetic and Orthopedic Enterprise”

The company provides prosthetic and orthopedic assistance to the population suffering from diseases and disorders of the musculoskeletal system.

“Nizhny Novgorod” branch of FSUE “Moscow Prosthetic and Orthopedic Enterprise” – one of the leading state enterprises in Russia for the production of prostheses, prosthetic and orthopedic products and orthopedic shoes.

“Nizhny Novgorod” branch of FSUE “Moscow Prosthetic and Orthopedic Enterprise” is the largest manufacturer of prostheses in the Nizhny Novgorod region: hand, forearm, shoulder, after the shoulder, lower leg, thigh, with congenital underdevelopment of the limbs; orthopedic apparatus; tutor; corsets; bandages, etc.technical means of rehabilitation; complex orthopedic shoes, including those with diabetic foot syndrome. The range of products manufactured by the enterprise is extremely diverse: more than 500 different basic standard models, designs, fixtures. At the enterprise you can purchase and order modern technical means of rehabilitation.

The “Nizhny Novgorod” branch of the FSUE “Moscow Prosthetic and Orthopedic Enterprise” operates Medical Rehabilitation Center .

This is one of the best rehabilitation centers in the region for a comprehensive, individual, intensive recovery after:

• injuries of the musculoskeletal system and nervous system,

90,015 surgical interventions (incl.h. about onco-pathology),

90,015 acute and chronic diseases of the joints and spine.

The Center is headed by Doctor of Medical Sciences, Professor of Nizhny Novgorod State Medical Academy Builova Tatyana Valentinovna –

Traumatologist-orthopedist of the highest category, chief specialist in rehabilitation of the Volga Federal District.

The company includes:

Reorganization of FSUE “Nizhegorodskoe PrOP” Ministry of Labor of Russia

90,000 ROLE OF ULTRASONOGRAPHY IN DETERMINING THE MECHANISM OF VERTEBRAL LUMBAR PAIN THE ROLE OF ULTRASONOGRAPHY IN DETERMINING THE MECHANISM OF VERTEBRAL LUMBAR PAIN Kharkiv Medical Academy of Postgraduate Education, Ukraine P.

Y. ABDULLAEV … ROLE OF ULTRASONOGRAPHY IN DETERMINING THE MECHANISM OF THE VERTEBRAL …

chilliness, fever, as a rule, in combination with vegetative symptoms in the innervation zone of the

affected motor segment. The causes of radiculopathy

are posterolateral disc herniation

, ischemia (less often hemorrhage) with subsequent

edema of one root, as well as varicose

expansion of the veins located here as a result of

aseptic inflammation [1, 3, 5].

Degenerative changes lead to gradual dehydration of the intervertebral disc

(IVD) and loss of elasticity. Simultaneously,

but with the dehydration of the nucleus pulposus,

microcracks and ruptures appear in the outer part of the phi-

broz ring. Gradually, the process spreads to the deep sections and through the damaged fibrous ring (FC)

begins to protrude –

degeneratively altered nucleus pulposus.

At a later stage of dehydration, flattening of the disc and bulging of the fibers

FC outside the intervertebral space occur.

Dehydration and fibrotic changes lead

to a decrease in the IVD height.

IVD can be injured in isolation

or be combined with damage to other elements

of the vertebral motor segment: capsule

of the ligamentous apparatus, bone formations.Part

Static rupture (cracking) of the IVD serves

as the starting point for the formation of a hernia of the inter-

vertebral disc (GMPD). With a complete rupture of the

IVD, the so-called

acute traumatic GMPD can immediately form [3–6].

Depending on the relationship of the elements

discs with the surrounding tissues, 4 types are distinguished

HMPD: elastic and sequestered protruding

gap, partial and complete prolapse [2, 3, 6-8].

Elastic protrusion of the IVD – its protrusion

in the direction of the thinned portion of the FC due to a decrease in the IVD volume (due to drying,

fragmentation). Elastic protrusion of the IVD

can cause slight compression of the adjacent spinal nerve

and clinically manifest as

symptoms of root irritation.

The sequestered protrusion of the IVD

is based on the fragmentation of the affected disc, its infringement in the peripheral parts of the coarse fissure

IVD.Such protrusion compresses the adjacent

root of the spinal nerve and is manifested not

only by radicular pain, as well as symptoms

partial conduction disturbance of the compressed root

: a decrease in the corresponding reflex,

hypoesthesia of the root in the innervation zone.

In case of partial prolapse, a part of the ruptured

disc is infringed in the peripheral parts

AF fissures, the other part protrudes beyond the

IVD cases, significantly squeezing the adjacent neurovascular bundle

.Such an intense

compression of the root is clinically manifested by the

syndrome of complete or almost complete impairment of its conduction.

With complete prolapse, the sequesters of the pulpous

nuclei are outside the IVD, are located

under the posterior longitudinal ligament,

can migrate upward or more often downward. With a large mass of

IVD elements dropped out, they roughly squeeze the adjacent

neurovascular bundles, causing a syndrome of com-

cauda equina compression (at the lumbar level)

or myelopathy syndrome.If a small fragment of the nucleus pulposus falls out,

causes slight compression of the spinal nerve.

Traumatic hernias along the IVD diameter

are divided into 4 types: median (median –

), paramedian, posterolateral, lateral or

foraminal.

Posterior-lateral GMPD are observed more often in others. Their localization corresponds to the

thinnest part of the AF, opposite the place of fixation,

of the root in the dural sac.The posterolateral

GMPD compresses one specified root under the

vertebra of the same name.

Paramedian HMPD is observed several times

less often. At the same time, at the lumbar level, not only the root in the place of its exit from the

dural sac, but also the intradural part

of the underlying root are compressed.

Median GMPD at the lumbar level

intradurally compresses two co-

tails of the same name, which are fixed to the posterolateral

walls of the dural sac before their exit to the

underlying level.

Lateral or foraminal GMPD is the most rare localization

, accounting for only 1% of all

hernias. She squeezes the root under the vertebra of the same name

– at the thoracic and lumbar levels.

HMPD along with the root or spinal cord

brain can squeeze the main vessels

of the spinal cord: radiculo-medullary and anterior spinal arteries

. In such cases

diagnostics and decompression should be performed especially urgently, otherwise irreversible postischemic changes

in the spinal cord will have time to occur.Compression of the main

vessels of the spinal cord can be evidenced by

discrepancy of the upper level of neurological

disorders of localization of spinal injury –

nickname, as well as involvement of neurological

disorders in the basin of the squeezed vessel.