Clinical Presentations of Lumbar Disc Degeneration and Lumbosacral Nerve Lesions

Int J Rheumatol. 2020; 2020: 2919625.

Worku Abie Liyew

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Corresponding author.

Academic Editor: Bruce M. Rothschild

Received 2020 Apr 25; Revised 2020 Jun 26; Accepted 2020 Jul 13.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lumbar disc degeneration is defined as the wear and tear of lumbar intervertebral disc, and it is mainly occurring at L3-L4 and L4-S1 vertebrae. Lumbar disc degeneration may lead to disc bulging, osteophytes, loss of disc space, and compression and irritation of the adjacent nerve root. Clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous. Discogenic pain is usually felt in the lumbar region, or sometimes, it may feel in the buttocks, down to the upper thighs, and it is typically presented with sudden forced flexion and/or rotational moment. Radical pain, muscular weakness, and sensory defects associated with lumbosacral nerve lesions are distributed on lower extremities, the buttock, lower abdomen, and groin region. A lumbosacral plexus lesion presents different symptoms in the territories of the lumbar and sacral nerves. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg, while sacral plexus lesion presents clinical symptoms at nerve fibers destined for the sciatic nerve, common peroneal nerve, and pudendal nerve. Weakness of ankle inversion, plantar flexion, and foot drop are the main clinical manifestations of the sacral plexus lesion area. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot. On examination, foot eversion is usually stronger than foot dorsiflexion. The patients may also present with pain and difficulty of bowel movements, sexual dysfunction assessments, and loss of cutaneous sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum.

1. Background of the Study

Lumbar disc degeneration is defined as the wear and tear of lumbar disc that act as a cushion for the spine. Lumbar disc degeneration can occur at any level, but mainly, it occurs on L3-L4 and L4-S1 vertebrae [1, 2]. It begins with small tears in the annulus of the disc to a decrease in the water content of the nucleus pulposus of the discs. The degenerative disc leads to disc bulging, osteophytes, disc space loss, and compression and irritation of the adjacent nerves [3]. With advanced degeneration, it loses water content and disc height (), and it leads to segmental instability and causes degenerative spondylosis and scoliosis. The advanced degenerative changes affect disc facet joints and surrounding soft tissue and can result in canal narrowing also known as degenerative stenosis [3]. Because each lumbar disc is in direct contact with two or three pairs of dorsal roots, disc degeneration may compress the adjacent nerve root [4, 5]. This can cause the pain syndrome but, more characteristically, causes neuropathic pain and neurological symptoms and, in severe cases, dysfunction of the nerve [6, 7].

(a) Normal intervertebral disc and spinal nerve root. (b) Degenerated intervertebral disc and pinched spinal nerve root [63].

Risk factors causing lumbar disc degeneration disease and associated lumbosacral nerve compression includes advancing age, socioeconomic status [8], torsional stress [9], smoking, obesity [10–12], heavy lifting, vibration [10], trauma, immobilization [13], psychosocial factors, gender, height, hereditary, genetic factors [8, 11], and occupations like machine drivers, carpenters, and office workers [14–16]. Genetic inheritance plays a significant role in the rate of degradation. Approximately 50–70% disc degeneration is caused by an individual’s genetic inheritance [17, 18]. Disc degeneration becomes prevalent and common in the individual’s 40s and usually in the lower lumbar spine. Some individuals, however, can become inflicted by this disease much earlier than the norm, depending on both the severity of their genetic deficiencies and lifestyles.

Lumbar disc degeneration and associated nerve lesion account for a large amount of lost productivity in the workforce. It is the most common cause of lower back pain throughout the world [3]. Lower back pain is the single most common cause of disability at the age of 45 years and the second most common reason for primary care physician visits [2, 8]. Intervertebral degeneration and associated low back pain have a huge socioeconomic impact and place a burden on health services worldwide. People throughout the world spend more than 100 billion US dollars/year for the treatment of low back pain [2].

In lumbar disc degeneration, accurate diagnosis is difficult, treatment is controversial, and failures are common. MRI is considered to be the cornerstone and special investigation to confirm the diagnosis of LDD and associated nerve lesions. However, between 38% and 52% of asymptomatic individuals demonstrated significant lumbar disc bulging on MRI [19, 20]. Some physicians may diagnosis lumbar disc degeneration on MRI with ought to detail clinical presentations, and others may use back pain alone as a symptom of lumbar disc degeneration [21, 22]. For example, a significant imaging finding of a right disc bulge at L5/S1 in a patient with symptoms of left L4/L5 nerve root distribution is a discordant finding [23]. As a result, imaging findings may not correlate with a patient’s disc problem and it results in the distrust of physicians on the part of patients and vice versa [22, 24, 25]. A basic understanding of the clinical presentations and pain distribution is important in the case of lumbar disc degeneration, and associated lumbosacral nerve lesion is important to diagnosis and disease conditions of a patient with the suspected lumbar disc degeneration. Therefore, the goal of this review is to assess all possible peripheral clinical presentations for lumbar disc degeneration and associated lumbosacral nerve lesions. The discussion of this review is limited to the peripheral clinical presentations and symptoms of lumbar disc degeneration and lumbosacral nerve lesions in the lower back region.

2. Anatomy of Healthy Lumbar Intervertebral Discs and Lumbosacral Nerves

In the lumbar region of the spine, there are five fibrocartilaginous lumbar intervertebral discs [26] which are named based on the vertebrae above and below them, for example, the L4-L5 disc found between L4 and L5 vertebrae. Lumbar intervertebral discs are important to transfer body weight and muscle activity arising from the upper body region to the lower body region. They also provide flexibility, extension, flexion, and torsion and provide protection to the spinal nerves, spinal cord, and the vertebrae themselves [27].

Compared to the discs of the thoracic and cervical spine, the lumbar discs are taller and wider measuring approximately 7–10 mm in thickness and 4 cm in diameter (anterior-posterior plane) [28]. The lumbar discs become shorter during the day due to the weight of the upper body, and sleeping for a minimum of 5 hours helps the discs regain their original shape [27]. The lumbar discs tend to be of greater height anteriorly than posteriorly, and this tendency is especially the greatest being the L5/S1 disc, causing the lumbar spine’s natural convex curvature similar to the cervical spine [29, 30]. Morphologically, the discs are cylindrical with its shape being determined by the integrity of the annulus fibrosus [31]. Because of the mobility of the lumbar spine and the high loads applied to it, discs have a significantly higher chance of becoming damaged from bending and torsion, making it the most common spinal part for disc injury [32]. 90% of lumbar disc degeneration occurs at the L4-L5 or the L5-S1 disc space [27].

Posterior to the lumbar intervertebral disc, there are five paired anterior and posterior lumbar nerve roots (L1-L5) that exit below the corresponding lumbar vertebra through the respective foramen () [5]. Upon exiting the spinal column, the posterior and anterior spinal nerve roots combine around the intervertebral foramen and form five paired mixed lumbar spinal nerves. The mixed spinal nerves contain both motor and sensory nerve fibers. Mixed spinal nerves immediately divide into posterior ramus and anterior ramus. The posterior and anterior rami contain both sensory and motor nerve fibers [33]. Since most disc herniations occur posterolaterally, the root that exits the foramen below the herniated disc gets compressed. So, a disc bulge at L4/L5 will compress the L5 root, and a protrusion at L5/S1 will compress the S1 root.

Lumbar discs and adjacent lumbar nerve roots [38, 64].

The ventral rami of the lumbar and sacral nerves (L1- S4) form the lumbosacral plexus of the body (). Because some fibers from the lumbar plexus contribute to the sacral plexus via the lumbosacral trunk, the two plexuses are often considered together as the lumbosacral plexus. The lumbar plexus is formed by roots from L1 to L4, and the sacral plexus is by L4–S4 roots. The lumbosacral plexus gives branches that innervate structures of the lower abdomen, some pelvic genitalia, and lower limbs.

Anatomy of the lumbosacral plexus [26].

The lumbar plexus is located on the anterior surface of the posterior abdominal wall. The important nerves emerging from lumbar plexuses are the femoral nerve (the posterior division of the anterior primary rami of L2-L4), the obturator nerve (the anterior division of the anterior primary rami of L2-l4), lateral femoral cutaneous nerve (posterior division of the anterior rami of L2-L3), and iliohypogastric, ilioinguinal, and genitofemoral nerves, which originate mainly from L1 (). Lumbar nerves are responsible for thigh flexion and adduction and leg extension and provide sensory innervation of the anterior and lateral thigh and medial regions of the leg [34]. The iliohypogastric, ilioinguinal, and genitofemoral nerves are important to innervate transverse and the oblique abdominal muscles [34, 35].

Anatomy of the lumbar plexus [38].

The femoral nerve is the largest terminal branch of the lumbar plexus. It provides motor innervation to the anterior thigh muscles (quadriceps) and sensory innervation to the skin of the anterior thigh and the anteromedial aspect of the leg (). The femoral nerve arises from the posterior cords of the lumbar plexus (L2-L4) and passes deep to the inguinal ligament. It descends vertically to the anterior thigh through the center of the femoral triangle, just lateral to the femoral artery and vein. Once it passes the inguinal ligament, it divides into deep motor branches and superficial cutaneous branches. The superficial branch divides into the medial cutaneous and anterior cutaneous nerve of the thigh. The femoral nerve terminates as the sensory saphenous nerve of the leg. The deep branch mainly supplies muscles of the anterior compartment of the thigh, leg extensor muscles. The first motor branch innervates the iliacus. This muscle, in conjunction with the psoas major, causes medial rotation of the hip. The deep branch of the femoral nerve then descends to supply the Sartorius (the tailor’s muscle). Once it passes through the femoral canal, it supplies the pectineus, a small muscle in the medial compartment of the thigh. Finally, the nerve supplies the four heads of the quadriceps femoris (vastus medialis, vastus lateralis, vastus intermedius, and rectus femoris), prime movers for leg extension at the knee joint and thigh flexion and critical for standing and stepping function. The medial and anterior cutaneous nerves of the thigh innervate the skin of the anterior thigh and the medial surface of the thigh, and saphenous nerve supplies the medial surface of the leg from the knee to the foot. The lateral femoral cutaneous nerve is a separate sensory nerve arising from L2 and L3 and supplies sensation over the lateral thigh [34, 36–38].

Anatomy of femoral and obturator nerves and their innervation [38].

The obturator nerve (L2–L4) () passes through the large obturator foramen of the pelvis and enters the medial compartment of the thigh by passing through the obturator foramen accompanied by the obturator artery. The obturator nerve innervates the adductor muscles of the thigh, medial compartment muscles. As it goes through the foramen, it divides into anterior and posterior branches. The anterior division of the obturator nerve, lying deep to the adductor longus on the surface of the adductor brevis, gives branches to the adductor longus, the adductor brevis, and the gracilis and the skin of the medial part of the thigh. The posterior division of the obturator nerve emerges through the obturator externus after supplying it to lie on the adductor magnus. It supplies the adductor magnus and gives a branch which accompanies the femoral artery into the popliteal fossa to supply the capsule of the knee joint. The obturator nerve controls the adduction and rotation of the thigh. A small cutaneous zone on the internal thigh is supplied by a sensory fiber [34, 38].

The sacral plexus arises from the ventral rami of L4–S4 (). The sacral plexus is situated on the posterior pelvic wall, anterior to the piriformis muscle. The ventral rami of the sacral nerves come together on the lower part of the greater sciatic foramen and unite to form a broad triangular band of nerves that innervates the lower limbs. The apex of the band is continued through the greater sciatic foramen into the gluteal region to form the sciatic nerve (L4, L5, and S1-3), the largest and longest nerve, in the body. Other branches of the sacral plexus are the superior gluteal (L4-S1), inferior gluteal (L5-S2), pudendal (S2-S4), and posterior femoral cutaneous (S2-S3) nerves. The sacral plexus also gives muscular branches to the quadratus femoris and inferior gemellus (L4-S1), obturator internus and superior gemellus (L5-S2), piriformis (S1-S2), and levator ani, coccygeus, and sphincter ani externus (S4) muscles and also contributes branches to pelvic splanchnic nerves (S2-S4) [38].

The sciatic nerve and its branch innervate all regions of the lower limb except the anterior and medial regions of the thigh [38]. The sciatic nerve leaves the pelvis by passing through the greater sciatic notch, then courses deep to the broad gluteus maximus muscle and enters to the thigh just medial to the hip joint. From there, it descends through the posterior thigh deep to the hamstrings, which it innervates. Superior to the knee joint, it branches into the tibial nerve (L4-S3), medial division, and the common fibular nerve (L4-S2), lateral division. The tibial nerve then continues posteriorly in the timeline to the calf, innervating the posterior compartment muscles of the leg (plantar flexor muscles), intrinsic foot muscles, and sensation in the sole of the foot. The common fibular nerve travels laterally and around the fibular head, dividing into the deep fibular and superficial fibular branches, which supply the muscles of the anterior (dorsiflexors) and lateral compartments (foot evertors) of the leg, respectively. The superficial fibular nerve also forms a sensory branch that supplies sensation to the anterolateral lower leg and dorsum of the foot while the deep fibular nerve supplies sensation to the web space between the first and second toes [38].

The pudendal nerve is a mixed sacral nerve (motor 20%, sensory 50%, and autonomic 30%) [39] that provides cutaneous and muscular innervation to the majority of the perineum (), anal canal, anus, and external male and female genetalia (scrotum, penis, mons pubis, labia majora, labia minora, clitoris, external vaginal orifice, and urethra). The pudendal nerve originates from the ventral rami of the sacral nerves (S2-S4) and then passes through the greater sciatic foramen, below the level of the piriformis (). It passes the back of the ischial spine, between the sacrospinous and the sacrotuberous ligaments, and it enters the perineum via the lesser sciatic foramen [40–42]. The main trunk of the pudendal nerve takes an extrapelvic course superficial to the coccygeus muscle. In the upper half of the pudendal canal or within it, the pudendal nerve gives rise to the inferior rectal nerve, and at the end of the canal, it gives rise to the perineal nerve and dorsal nerves of the penis and clitoris. The inferior rectal nerve exits the pudendal canal medially and extends motor and sensory branches. Motor branches innervate the levator ani, external anal sphincter, and the cutaneous branches to perianal skin and the scrotum or labia. Perineal nerve supplies the perineum, vagina, urethra, male scrotum, labia, transverse perineal muscle, and urethral sphincter, and the dorsal nerve of the clitoris or penis supplies skin of the clitoris/penis, bulbocavernosus, and ischiocavernosus muscles [43, 44].

Anatomy of the sacral plexus [38].

Anatomy of the pudendal nerve. (a) Origin and course of destination. (b) Pudendal nerve in the male perineum. (c) Pudendal nerve in the female perineum [1, 2].

3. Clinical Presentation of Lumbar Disc Degeneration and Lumbosacral Nerve Lesion

A patient’s clinical presentations and symptoms are important diagnostic tools to identify lumbar disc degeneration and lumbosacral nerve lesion. For this, the physician must conduct a physical examination and should ask many questions related to the problems [45]. Straight leg raising is the most commonly used method to diagnose lumbar disc degeneration and associated lumbosacral nerve lesions. The patient lies in the supine position, and the leg is elevated from the ankle, with the knee remaining straight. Normal patients can elevate the leg 60 to 90 degrees without pain. Patients with disc problems can only elevate the leg from 30 to 40 degrees due to produce pain. Ipsilateral straight leg rising is more sensitive, but less specific than contralateral straight leg rising. That is, nearly all patients with disc problem have pain on the straight leg raising on the affected side, but straight leg raising causes pain in many other conditions (e.g., severe hip arthritis). However, contralateral straight leg raising does not produce pain on the affected side unless the pain is due to root disease [46].

Symptoms and clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous innervation defect. Discogenic pain is caused by a damaged intrinsic intervertebral disc in the lumbar region [47]. As the disc begins to degenerate, the disc itself becomes painful and movements that place stress on the disc may result in discogenic pain that comes from the disc. This is similar to any other body part injury, such as a broken bone or a cut in the skin. Discogenic pain is usually felt in the lumbar region. The pain may also feel like it is coming from the buttocks, lower thoracic, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes [48]. Patients with discogenic pain associated with lumbar disc degeneration may present with suddenly forced flexion and/or rotational moment, and some patients may have a spontaneous onset of symptoms. Classic discogenic pain is aggravated by activities that load the disc, such as sitting, standing, walking, flexion, rotation/twisting, lifting, vibration (e.g., riding in a car), coughing, sneezing, laughing, and the Valsalva maneuver [48].

Lesion of the lumbosacral plexus by lumbar disc degeneration leads to a lumbosacral radicular syndrome. This syndrome is characterized by a radiating pain in one or more lumbar or sacral nerve dermatomes and decreased motor function. Sometimes, it may be regarded as sciatica, ischias, or nerve root pain [49]. Radicular pain and radiculopathy are sometimes used interchangeably, although they certainly are not synonyms. In the case of radicular pain, only radiating pain is present from an inflamed or compressed nerve root. As an example, an inflamed nerve root in the lower back may radiate pain into the leg, while in the case of radiculopathy, motor loss may occurs when a compressed or inflamed nerve root results in neurological deficits, such as problems with reflexes, numbness, and/or weakness. Both syndromes frequently occur together, and radiculopathy can be a continuum of radicular pain.

Lower extremity radicular pain and radiculopathy problems due to lumbar disc degeneration are caused by compression of neural structures in the lumbosacral region [47]. Lumbar disc degeneration may compress neural structures in the lumbosacral, and this results in lumbosacral nerve roots and lumbosacral plexus lesions. Lesion of these structures results in radicular pain, weakness, numbness, or difficulty controlling specific muscles of the lower extremities, buttock, lower abdomen, and groin region. Radicular pain may be confined to a single nerve root or may involve groups of nerve roots. Pain may be of sudden or insidious onset. Radicular pain is often worsened with axial loading, sitting, standing, and bending, lifting, or twisting, and the pain feels better while walking, changing position, lying down, or even running. Numbness, tingling, weakness in the extremities, and strong pain that tends to come and go are also the features of nerve compression in the lumbosacral region [47].

Lesion of the lumbosacral plexus by lumbar disc degeneration is divided clinically into those affecting the lumbar plexus and the sacral plexus. A lumbar plexus lesion may cause symptoms in the territories of the iliohypogastric, genitofemoral, ilioinguinal, femoral, and obturator nerves [50, 51]. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg. In lumbar plexus lesion, decrease or absence of knee jerk is common [51, 52].

Similar to lumbar plexus lesion, the sacral plexus lesion also presents with muscular weakness, loss of cutaneous sensation, and pain in the distribution areas of sacral plexus branches and gluteal nerve, sciatic nerve, tibial nerve, peroneal nerves, and pudendal nerve. In sacral plexus lesions, the muscular weakness of the lower extremities is significant. These include weakness in hip extension (gluteus maximus), hip abductors and internal rotators (gluteus medius and tensor fascia latae), knee flexion (hamstring muscles), and all muscles of the leg and foot supplied by the peroneal and tibial nerves. The diminished sensation may involve the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot. The ankle jerk may be diminished or absent [34, 51].

Lesions of the sacral plexus result in weakness of the posterior thigh and muscles of the leg and feet. During sacral nerve plexus lesion, nerve fibers destined for the sciatic nerve, and the common peroneal nerve is often affected. Sciatica is defined as “pain in the distribution of the sciatic nerve due to pathology of the nerve itself.” The term “sciatica” may be confused with radicular pain as it has been used to describe any pain, including referred pain felt in the leg along the distribution of the sciatic nerve. Nevertheless, the term “sciatica” remains in common usage both in clinical practice and in publications [53, 54]. The use of the term sciatica should only be in the context of the above definitions and, as such, be distinguished from any or all other forms of pain felt in the leg, particularly referred pain [55].

Sciatica is the most common neuropathies of the lower extremities, second to common fibular neuropathy. One of the most common presentations of sciatic neuropathy is foot drop, because ankle dorsiflexion weakness, with or without lower extremity sensory impairment, may also be associated with several other clinical syndromes. Patients often experience abrupt pain radiating down the posterolateral limb, with weakness and numbness evolving more gradually [56]. In sciatic neuropathy, the clinical findings are often more consistent with injury to the common fibular division rather than tibial division, sometimes mimicking a common fibular neuropathy at the knee. This finding is particularly true of more distal lesions, as they may not affect the flexors of the knee, or of less severe sciatic nerve injury. Because the common fibular division has fewer and larger fascicles and less supportive tissue compared with the tibial division, it is thought to be more vulnerable to compression. Also, the common fibular division is tauter, and secured at the sciatic notch and fibular neck, resulting in greater potential for stretch injury [54].

Common peroneal nerve lesion is clinical characterized by weakness of foot inversion, plantar flexion, foot drop or dorsiflexor, and depressed ankle jerk [54]. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot [57]. Foot drop is the main feature of fibular neuropathy, and it is due to paralysis of the dorsiflexor muscles of the foot. The difficulty of eversion may be present due to peroneal muscle involvement. On examination, foot eversion is usually stronger than foot dorsiflexion. Other muscles of the posterior compartment are normal [58]. In a large study of common peroneal neuropathy, physicians clinically misdiagnosed 43% of patients as a sciatic neuropathy. This was usually because of the difficulty in assessing ankle inversion and eversion in the presence of foot drop. In sciatic neuropathy, gluteal, hamstring muscles and tibialis posterior muscles are involved [58].

Patients with pudendal nerve injury due to a sacral nerve plexus lesion typically present motor weakness of perineal muscles [59], pain, and burning sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sometimes, the pain may refer to the groin, medial thigh, buttock, and abdomen. These patients may also suffer from constipation, pain, and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction (uncomfortable arousal, decreased sensation, impotence, and ejaculatory dysfunction) [60, 61]. Pain due to pudendal nerve lesion is aggravated by sitting, other flexion activities of the hip (sitting, squatting, bicycling, and exercising) whereas standing or lying down relieves the discomfort [60–62].

4. Conclusion

During the diagnosis of patients with lumbar disc degeneration and lumbosacral nerve lesions, physicians should not use the MRI solely. It is important to assess and understand clinical presentations and pain distribution of lumbar disc degeneration and lumbosacral nerve lesions. They have to assess the patient’s discogenic pain in the lumbar region, weakness of hip flexion, knee extension, and flexion, thigh adduction, ankle inversion, plantar flexion, and foot drop, perineal muscles. The patient’s pain and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction assessments are also critical. Besides, it is important to evaluate the loss of cutaneous sensation in the lower abdomen, inguinal region, over the medial, lateral, and anterior aspect of the thigh, the medial lower leg and in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sensory loss may also present along the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot during the sacral plexus.

Acknowledgments

The author would like to thank Binalfew Tsehaye and Biksegn Wubie for their comments and input on this review.

Conflicts of Interest

The author declares that he has no competing interests.

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Clinical Presentations of Lumbar Disc Degeneration and Lumbosacral Nerve Lesions

Int J Rheumatol. 2020; 2020: 2919625.

Worku Abie Liyew

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Corresponding author.

Academic Editor: Bruce M. Rothschild

Received 2020 Apr 25; Revised 2020 Jun 26; Accepted 2020 Jul 13.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lumbar disc degeneration is defined as the wear and tear of lumbar intervertebral disc, and it is mainly occurring at L3-L4 and L4-S1 vertebrae. Lumbar disc degeneration may lead to disc bulging, osteophytes, loss of disc space, and compression and irritation of the adjacent nerve root. Clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous. Discogenic pain is usually felt in the lumbar region, or sometimes, it may feel in the buttocks, down to the upper thighs, and it is typically presented with sudden forced flexion and/or rotational moment. Radical pain, muscular weakness, and sensory defects associated with lumbosacral nerve lesions are distributed on lower extremities, the buttock, lower abdomen, and groin region. A lumbosacral plexus lesion presents different symptoms in the territories of the lumbar and sacral nerves. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg, while sacral plexus lesion presents clinical symptoms at nerve fibers destined for the sciatic nerve, common peroneal nerve, and pudendal nerve. Weakness of ankle inversion, plantar flexion, and foot drop are the main clinical manifestations of the sacral plexus lesion area. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot. On examination, foot eversion is usually stronger than foot dorsiflexion. The patients may also present with pain and difficulty of bowel movements, sexual dysfunction assessments, and loss of cutaneous sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum.

1. Background of the Study

Lumbar disc degeneration is defined as the wear and tear of lumbar disc that act as a cushion for the spine. Lumbar disc degeneration can occur at any level, but mainly, it occurs on L3-L4 and L4-S1 vertebrae [1, 2]. It begins with small tears in the annulus of the disc to a decrease in the water content of the nucleus pulposus of the discs. The degenerative disc leads to disc bulging, osteophytes, disc space loss, and compression and irritation of the adjacent nerves [3]. With advanced degeneration, it loses water content and disc height (), and it leads to segmental instability and causes degenerative spondylosis and scoliosis. The advanced degenerative changes affect disc facet joints and surrounding soft tissue and can result in canal narrowing also known as degenerative stenosis [3]. Because each lumbar disc is in direct contact with two or three pairs of dorsal roots, disc degeneration may compress the adjacent nerve root [4, 5]. This can cause the pain syndrome but, more characteristically, causes neuropathic pain and neurological symptoms and, in severe cases, dysfunction of the nerve [6, 7].

(a) Normal intervertebral disc and spinal nerve root. (b) Degenerated intervertebral disc and pinched spinal nerve root [63].

Risk factors causing lumbar disc degeneration disease and associated lumbosacral nerve compression includes advancing age, socioeconomic status [8], torsional stress [9], smoking, obesity [10–12], heavy lifting, vibration [10], trauma, immobilization [13], psychosocial factors, gender, height, hereditary, genetic factors [8, 11], and occupations like machine drivers, carpenters, and office workers [14–16]. Genetic inheritance plays a significant role in the rate of degradation. Approximately 50–70% disc degeneration is caused by an individual’s genetic inheritance [17, 18]. Disc degeneration becomes prevalent and common in the individual’s 40s and usually in the lower lumbar spine. Some individuals, however, can become inflicted by this disease much earlier than the norm, depending on both the severity of their genetic deficiencies and lifestyles.

Lumbar disc degeneration and associated nerve lesion account for a large amount of lost productivity in the workforce. It is the most common cause of lower back pain throughout the world [3]. Lower back pain is the single most common cause of disability at the age of 45 years and the second most common reason for primary care physician visits [2, 8]. Intervertebral degeneration and associated low back pain have a huge socioeconomic impact and place a burden on health services worldwide. People throughout the world spend more than 100 billion US dollars/year for the treatment of low back pain [2].

In lumbar disc degeneration, accurate diagnosis is difficult, treatment is controversial, and failures are common. MRI is considered to be the cornerstone and special investigation to confirm the diagnosis of LDD and associated nerve lesions. However, between 38% and 52% of asymptomatic individuals demonstrated significant lumbar disc bulging on MRI [19, 20]. Some physicians may diagnosis lumbar disc degeneration on MRI with ought to detail clinical presentations, and others may use back pain alone as a symptom of lumbar disc degeneration [21, 22]. For example, a significant imaging finding of a right disc bulge at L5/S1 in a patient with symptoms of left L4/L5 nerve root distribution is a discordant finding [23]. As a result, imaging findings may not correlate with a patient’s disc problem and it results in the distrust of physicians on the part of patients and vice versa [22, 24, 25]. A basic understanding of the clinical presentations and pain distribution is important in the case of lumbar disc degeneration, and associated lumbosacral nerve lesion is important to diagnosis and disease conditions of a patient with the suspected lumbar disc degeneration. Therefore, the goal of this review is to assess all possible peripheral clinical presentations for lumbar disc degeneration and associated lumbosacral nerve lesions. The discussion of this review is limited to the peripheral clinical presentations and symptoms of lumbar disc degeneration and lumbosacral nerve lesions in the lower back region.

2. Anatomy of Healthy Lumbar Intervertebral Discs and Lumbosacral Nerves

In the lumbar region of the spine, there are five fibrocartilaginous lumbar intervertebral discs [26] which are named based on the vertebrae above and below them, for example, the L4-L5 disc found between L4 and L5 vertebrae. Lumbar intervertebral discs are important to transfer body weight and muscle activity arising from the upper body region to the lower body region. They also provide flexibility, extension, flexion, and torsion and provide protection to the spinal nerves, spinal cord, and the vertebrae themselves [27].

Compared to the discs of the thoracic and cervical spine, the lumbar discs are taller and wider measuring approximately 7–10 mm in thickness and 4 cm in diameter (anterior-posterior plane) [28]. The lumbar discs become shorter during the day due to the weight of the upper body, and sleeping for a minimum of 5 hours helps the discs regain their original shape [27]. The lumbar discs tend to be of greater height anteriorly than posteriorly, and this tendency is especially the greatest being the L5/S1 disc, causing the lumbar spine’s natural convex curvature similar to the cervical spine [29, 30]. Morphologically, the discs are cylindrical with its shape being determined by the integrity of the annulus fibrosus [31]. Because of the mobility of the lumbar spine and the high loads applied to it, discs have a significantly higher chance of becoming damaged from bending and torsion, making it the most common spinal part for disc injury [32]. 90% of lumbar disc degeneration occurs at the L4-L5 or the L5-S1 disc space [27].

Posterior to the lumbar intervertebral disc, there are five paired anterior and posterior lumbar nerve roots (L1-L5) that exit below the corresponding lumbar vertebra through the respective foramen () [5]. Upon exiting the spinal column, the posterior and anterior spinal nerve roots combine around the intervertebral foramen and form five paired mixed lumbar spinal nerves. The mixed spinal nerves contain both motor and sensory nerve fibers. Mixed spinal nerves immediately divide into posterior ramus and anterior ramus. The posterior and anterior rami contain both sensory and motor nerve fibers [33]. Since most disc herniations occur posterolaterally, the root that exits the foramen below the herniated disc gets compressed. So, a disc bulge at L4/L5 will compress the L5 root, and a protrusion at L5/S1 will compress the S1 root.

Lumbar discs and adjacent lumbar nerve roots [38, 64].

The ventral rami of the lumbar and sacral nerves (L1- S4) form the lumbosacral plexus of the body (). Because some fibers from the lumbar plexus contribute to the sacral plexus via the lumbosacral trunk, the two plexuses are often considered together as the lumbosacral plexus. The lumbar plexus is formed by roots from L1 to L4, and the sacral plexus is by L4–S4 roots. The lumbosacral plexus gives branches that innervate structures of the lower abdomen, some pelvic genitalia, and lower limbs.

Anatomy of the lumbosacral plexus [26].

The lumbar plexus is located on the anterior surface of the posterior abdominal wall. The important nerves emerging from lumbar plexuses are the femoral nerve (the posterior division of the anterior primary rami of L2-L4), the obturator nerve (the anterior division of the anterior primary rami of L2-l4), lateral femoral cutaneous nerve (posterior division of the anterior rami of L2-L3), and iliohypogastric, ilioinguinal, and genitofemoral nerves, which originate mainly from L1 (). Lumbar nerves are responsible for thigh flexion and adduction and leg extension and provide sensory innervation of the anterior and lateral thigh and medial regions of the leg [34]. The iliohypogastric, ilioinguinal, and genitofemoral nerves are important to innervate transverse and the oblique abdominal muscles [34, 35].

Anatomy of the lumbar plexus [38].

The femoral nerve is the largest terminal branch of the lumbar plexus. It provides motor innervation to the anterior thigh muscles (quadriceps) and sensory innervation to the skin of the anterior thigh and the anteromedial aspect of the leg (). The femoral nerve arises from the posterior cords of the lumbar plexus (L2-L4) and passes deep to the inguinal ligament. It descends vertically to the anterior thigh through the center of the femoral triangle, just lateral to the femoral artery and vein. Once it passes the inguinal ligament, it divides into deep motor branches and superficial cutaneous branches. The superficial branch divides into the medial cutaneous and anterior cutaneous nerve of the thigh. The femoral nerve terminates as the sensory saphenous nerve of the leg. The deep branch mainly supplies muscles of the anterior compartment of the thigh, leg extensor muscles. The first motor branch innervates the iliacus. This muscle, in conjunction with the psoas major, causes medial rotation of the hip. The deep branch of the femoral nerve then descends to supply the Sartorius (the tailor’s muscle). Once it passes through the femoral canal, it supplies the pectineus, a small muscle in the medial compartment of the thigh. Finally, the nerve supplies the four heads of the quadriceps femoris (vastus medialis, vastus lateralis, vastus intermedius, and rectus femoris), prime movers for leg extension at the knee joint and thigh flexion and critical for standing and stepping function. The medial and anterior cutaneous nerves of the thigh innervate the skin of the anterior thigh and the medial surface of the thigh, and saphenous nerve supplies the medial surface of the leg from the knee to the foot. The lateral femoral cutaneous nerve is a separate sensory nerve arising from L2 and L3 and supplies sensation over the lateral thigh [34, 36–38].

Anatomy of femoral and obturator nerves and their innervation [38].

The obturator nerve (L2–L4) () passes through the large obturator foramen of the pelvis and enters the medial compartment of the thigh by passing through the obturator foramen accompanied by the obturator artery. The obturator nerve innervates the adductor muscles of the thigh, medial compartment muscles. As it goes through the foramen, it divides into anterior and posterior branches. The anterior division of the obturator nerve, lying deep to the adductor longus on the surface of the adductor brevis, gives branches to the adductor longus, the adductor brevis, and the gracilis and the skin of the medial part of the thigh. The posterior division of the obturator nerve emerges through the obturator externus after supplying it to lie on the adductor magnus. It supplies the adductor magnus and gives a branch which accompanies the femoral artery into the popliteal fossa to supply the capsule of the knee joint. The obturator nerve controls the adduction and rotation of the thigh. A small cutaneous zone on the internal thigh is supplied by a sensory fiber [34, 38].

The sacral plexus arises from the ventral rami of L4–S4 (). The sacral plexus is situated on the posterior pelvic wall, anterior to the piriformis muscle. The ventral rami of the sacral nerves come together on the lower part of the greater sciatic foramen and unite to form a broad triangular band of nerves that innervates the lower limbs. The apex of the band is continued through the greater sciatic foramen into the gluteal region to form the sciatic nerve (L4, L5, and S1-3), the largest and longest nerve, in the body. Other branches of the sacral plexus are the superior gluteal (L4-S1), inferior gluteal (L5-S2), pudendal (S2-S4), and posterior femoral cutaneous (S2-S3) nerves. The sacral plexus also gives muscular branches to the quadratus femoris and inferior gemellus (L4-S1), obturator internus and superior gemellus (L5-S2), piriformis (S1-S2), and levator ani, coccygeus, and sphincter ani externus (S4) muscles and also contributes branches to pelvic splanchnic nerves (S2-S4) [38].

The sciatic nerve and its branch innervate all regions of the lower limb except the anterior and medial regions of the thigh [38]. The sciatic nerve leaves the pelvis by passing through the greater sciatic notch, then courses deep to the broad gluteus maximus muscle and enters to the thigh just medial to the hip joint. From there, it descends through the posterior thigh deep to the hamstrings, which it innervates. Superior to the knee joint, it branches into the tibial nerve (L4-S3), medial division, and the common fibular nerve (L4-S2), lateral division. The tibial nerve then continues posteriorly in the timeline to the calf, innervating the posterior compartment muscles of the leg (plantar flexor muscles), intrinsic foot muscles, and sensation in the sole of the foot. The common fibular nerve travels laterally and around the fibular head, dividing into the deep fibular and superficial fibular branches, which supply the muscles of the anterior (dorsiflexors) and lateral compartments (foot evertors) of the leg, respectively. The superficial fibular nerve also forms a sensory branch that supplies sensation to the anterolateral lower leg and dorsum of the foot while the deep fibular nerve supplies sensation to the web space between the first and second toes [38].

The pudendal nerve is a mixed sacral nerve (motor 20%, sensory 50%, and autonomic 30%) [39] that provides cutaneous and muscular innervation to the majority of the perineum (), anal canal, anus, and external male and female genetalia (scrotum, penis, mons pubis, labia majora, labia minora, clitoris, external vaginal orifice, and urethra). The pudendal nerve originates from the ventral rami of the sacral nerves (S2-S4) and then passes through the greater sciatic foramen, below the level of the piriformis (). It passes the back of the ischial spine, between the sacrospinous and the sacrotuberous ligaments, and it enters the perineum via the lesser sciatic foramen [40–42]. The main trunk of the pudendal nerve takes an extrapelvic course superficial to the coccygeus muscle. In the upper half of the pudendal canal or within it, the pudendal nerve gives rise to the inferior rectal nerve, and at the end of the canal, it gives rise to the perineal nerve and dorsal nerves of the penis and clitoris. The inferior rectal nerve exits the pudendal canal medially and extends motor and sensory branches. Motor branches innervate the levator ani, external anal sphincter, and the cutaneous branches to perianal skin and the scrotum or labia. Perineal nerve supplies the perineum, vagina, urethra, male scrotum, labia, transverse perineal muscle, and urethral sphincter, and the dorsal nerve of the clitoris or penis supplies skin of the clitoris/penis, bulbocavernosus, and ischiocavernosus muscles [43, 44].

Anatomy of the sacral plexus [38].

Anatomy of the pudendal nerve. (a) Origin and course of destination. (b) Pudendal nerve in the male perineum. (c) Pudendal nerve in the female perineum [1, 2].

3. Clinical Presentation of Lumbar Disc Degeneration and Lumbosacral Nerve Lesion

A patient’s clinical presentations and symptoms are important diagnostic tools to identify lumbar disc degeneration and lumbosacral nerve lesion. For this, the physician must conduct a physical examination and should ask many questions related to the problems [45]. Straight leg raising is the most commonly used method to diagnose lumbar disc degeneration and associated lumbosacral nerve lesions. The patient lies in the supine position, and the leg is elevated from the ankle, with the knee remaining straight. Normal patients can elevate the leg 60 to 90 degrees without pain. Patients with disc problems can only elevate the leg from 30 to 40 degrees due to produce pain. Ipsilateral straight leg rising is more sensitive, but less specific than contralateral straight leg rising. That is, nearly all patients with disc problem have pain on the straight leg raising on the affected side, but straight leg raising causes pain in many other conditions (e.g., severe hip arthritis). However, contralateral straight leg raising does not produce pain on the affected side unless the pain is due to root disease [46].

Symptoms and clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous innervation defect. Discogenic pain is caused by a damaged intrinsic intervertebral disc in the lumbar region [47]. As the disc begins to degenerate, the disc itself becomes painful and movements that place stress on the disc may result in discogenic pain that comes from the disc. This is similar to any other body part injury, such as a broken bone or a cut in the skin. Discogenic pain is usually felt in the lumbar region. The pain may also feel like it is coming from the buttocks, lower thoracic, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes [48]. Patients with discogenic pain associated with lumbar disc degeneration may present with suddenly forced flexion and/or rotational moment, and some patients may have a spontaneous onset of symptoms. Classic discogenic pain is aggravated by activities that load the disc, such as sitting, standing, walking, flexion, rotation/twisting, lifting, vibration (e.g., riding in a car), coughing, sneezing, laughing, and the Valsalva maneuver [48].

Lesion of the lumbosacral plexus by lumbar disc degeneration leads to a lumbosacral radicular syndrome. This syndrome is characterized by a radiating pain in one or more lumbar or sacral nerve dermatomes and decreased motor function. Sometimes, it may be regarded as sciatica, ischias, or nerve root pain [49]. Radicular pain and radiculopathy are sometimes used interchangeably, although they certainly are not synonyms. In the case of radicular pain, only radiating pain is present from an inflamed or compressed nerve root. As an example, an inflamed nerve root in the lower back may radiate pain into the leg, while in the case of radiculopathy, motor loss may occurs when a compressed or inflamed nerve root results in neurological deficits, such as problems with reflexes, numbness, and/or weakness. Both syndromes frequently occur together, and radiculopathy can be a continuum of radicular pain.

Lower extremity radicular pain and radiculopathy problems due to lumbar disc degeneration are caused by compression of neural structures in the lumbosacral region [47]. Lumbar disc degeneration may compress neural structures in the lumbosacral, and this results in lumbosacral nerve roots and lumbosacral plexus lesions. Lesion of these structures results in radicular pain, weakness, numbness, or difficulty controlling specific muscles of the lower extremities, buttock, lower abdomen, and groin region. Radicular pain may be confined to a single nerve root or may involve groups of nerve roots. Pain may be of sudden or insidious onset. Radicular pain is often worsened with axial loading, sitting, standing, and bending, lifting, or twisting, and the pain feels better while walking, changing position, lying down, or even running. Numbness, tingling, weakness in the extremities, and strong pain that tends to come and go are also the features of nerve compression in the lumbosacral region [47].

Lesion of the lumbosacral plexus by lumbar disc degeneration is divided clinically into those affecting the lumbar plexus and the sacral plexus. A lumbar plexus lesion may cause symptoms in the territories of the iliohypogastric, genitofemoral, ilioinguinal, femoral, and obturator nerves [50, 51]. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg. In lumbar plexus lesion, decrease or absence of knee jerk is common [51, 52].

Similar to lumbar plexus lesion, the sacral plexus lesion also presents with muscular weakness, loss of cutaneous sensation, and pain in the distribution areas of sacral plexus branches and gluteal nerve, sciatic nerve, tibial nerve, peroneal nerves, and pudendal nerve. In sacral plexus lesions, the muscular weakness of the lower extremities is significant. These include weakness in hip extension (gluteus maximus), hip abductors and internal rotators (gluteus medius and tensor fascia latae), knee flexion (hamstring muscles), and all muscles of the leg and foot supplied by the peroneal and tibial nerves. The diminished sensation may involve the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot. The ankle jerk may be diminished or absent [34, 51].

Lesions of the sacral plexus result in weakness of the posterior thigh and muscles of the leg and feet. During sacral nerve plexus lesion, nerve fibers destined for the sciatic nerve, and the common peroneal nerve is often affected. Sciatica is defined as “pain in the distribution of the sciatic nerve due to pathology of the nerve itself.” The term “sciatica” may be confused with radicular pain as it has been used to describe any pain, including referred pain felt in the leg along the distribution of the sciatic nerve. Nevertheless, the term “sciatica” remains in common usage both in clinical practice and in publications [53, 54]. The use of the term sciatica should only be in the context of the above definitions and, as such, be distinguished from any or all other forms of pain felt in the leg, particularly referred pain [55].

Sciatica is the most common neuropathies of the lower extremities, second to common fibular neuropathy. One of the most common presentations of sciatic neuropathy is foot drop, because ankle dorsiflexion weakness, with or without lower extremity sensory impairment, may also be associated with several other clinical syndromes. Patients often experience abrupt pain radiating down the posterolateral limb, with weakness and numbness evolving more gradually [56]. In sciatic neuropathy, the clinical findings are often more consistent with injury to the common fibular division rather than tibial division, sometimes mimicking a common fibular neuropathy at the knee. This finding is particularly true of more distal lesions, as they may not affect the flexors of the knee, or of less severe sciatic nerve injury. Because the common fibular division has fewer and larger fascicles and less supportive tissue compared with the tibial division, it is thought to be more vulnerable to compression. Also, the common fibular division is tauter, and secured at the sciatic notch and fibular neck, resulting in greater potential for stretch injury [54].

Common peroneal nerve lesion is clinical characterized by weakness of foot inversion, plantar flexion, foot drop or dorsiflexor, and depressed ankle jerk [54]. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot [57]. Foot drop is the main feature of fibular neuropathy, and it is due to paralysis of the dorsiflexor muscles of the foot. The difficulty of eversion may be present due to peroneal muscle involvement. On examination, foot eversion is usually stronger than foot dorsiflexion. Other muscles of the posterior compartment are normal [58]. In a large study of common peroneal neuropathy, physicians clinically misdiagnosed 43% of patients as a sciatic neuropathy. This was usually because of the difficulty in assessing ankle inversion and eversion in the presence of foot drop. In sciatic neuropathy, gluteal, hamstring muscles and tibialis posterior muscles are involved [58].

Patients with pudendal nerve injury due to a sacral nerve plexus lesion typically present motor weakness of perineal muscles [59], pain, and burning sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sometimes, the pain may refer to the groin, medial thigh, buttock, and abdomen. These patients may also suffer from constipation, pain, and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction (uncomfortable arousal, decreased sensation, impotence, and ejaculatory dysfunction) [60, 61]. Pain due to pudendal nerve lesion is aggravated by sitting, other flexion activities of the hip (sitting, squatting, bicycling, and exercising) whereas standing or lying down relieves the discomfort [60–62].

4. Conclusion

During the diagnosis of patients with lumbar disc degeneration and lumbosacral nerve lesions, physicians should not use the MRI solely. It is important to assess and understand clinical presentations and pain distribution of lumbar disc degeneration and lumbosacral nerve lesions. They have to assess the patient’s discogenic pain in the lumbar region, weakness of hip flexion, knee extension, and flexion, thigh adduction, ankle inversion, plantar flexion, and foot drop, perineal muscles. The patient’s pain and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction assessments are also critical. Besides, it is important to evaluate the loss of cutaneous sensation in the lower abdomen, inguinal region, over the medial, lateral, and anterior aspect of the thigh, the medial lower leg and in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sensory loss may also present along the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot during the sacral plexus.

Acknowledgments

The author would like to thank Binalfew Tsehaye and Biksegn Wubie for their comments and input on this review.

Conflicts of Interest

The author declares that he has no competing interests.

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Clinical Presentations of Lumbar Disc Degeneration and Lumbosacral Nerve Lesions

Int J Rheumatol. 2020; 2020: 2919625.

Worku Abie Liyew

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Corresponding author.

Academic Editor: Bruce M. Rothschild

Received 2020 Apr 25; Revised 2020 Jun 26; Accepted 2020 Jul 13.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lumbar disc degeneration is defined as the wear and tear of lumbar intervertebral disc, and it is mainly occurring at L3-L4 and L4-S1 vertebrae. Lumbar disc degeneration may lead to disc bulging, osteophytes, loss of disc space, and compression and irritation of the adjacent nerve root. Clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous. Discogenic pain is usually felt in the lumbar region, or sometimes, it may feel in the buttocks, down to the upper thighs, and it is typically presented with sudden forced flexion and/or rotational moment. Radical pain, muscular weakness, and sensory defects associated with lumbosacral nerve lesions are distributed on lower extremities, the buttock, lower abdomen, and groin region. A lumbosacral plexus lesion presents different symptoms in the territories of the lumbar and sacral nerves. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg, while sacral plexus lesion presents clinical symptoms at nerve fibers destined for the sciatic nerve, common peroneal nerve, and pudendal nerve. Weakness of ankle inversion, plantar flexion, and foot drop are the main clinical manifestations of the sacral plexus lesion area. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot. On examination, foot eversion is usually stronger than foot dorsiflexion. The patients may also present with pain and difficulty of bowel movements, sexual dysfunction assessments, and loss of cutaneous sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum.

1. Background of the Study

Lumbar disc degeneration is defined as the wear and tear of lumbar disc that act as a cushion for the spine. Lumbar disc degeneration can occur at any level, but mainly, it occurs on L3-L4 and L4-S1 vertebrae [1, 2]. It begins with small tears in the annulus of the disc to a decrease in the water content of the nucleus pulposus of the discs. The degenerative disc leads to disc bulging, osteophytes, disc space loss, and compression and irritation of the adjacent nerves [3]. With advanced degeneration, it loses water content and disc height (), and it leads to segmental instability and causes degenerative spondylosis and scoliosis. The advanced degenerative changes affect disc facet joints and surrounding soft tissue and can result in canal narrowing also known as degenerative stenosis [3]. Because each lumbar disc is in direct contact with two or three pairs of dorsal roots, disc degeneration may compress the adjacent nerve root [4, 5]. This can cause the pain syndrome but, more characteristically, causes neuropathic pain and neurological symptoms and, in severe cases, dysfunction of the nerve [6, 7].

(a) Normal intervertebral disc and spinal nerve root. (b) Degenerated intervertebral disc and pinched spinal nerve root [63].

Risk factors causing lumbar disc degeneration disease and associated lumbosacral nerve compression includes advancing age, socioeconomic status [8], torsional stress [9], smoking, obesity [10–12], heavy lifting, vibration [10], trauma, immobilization [13], psychosocial factors, gender, height, hereditary, genetic factors [8, 11], and occupations like machine drivers, carpenters, and office workers [14–16]. Genetic inheritance plays a significant role in the rate of degradation. Approximately 50–70% disc degeneration is caused by an individual’s genetic inheritance [17, 18]. Disc degeneration becomes prevalent and common in the individual’s 40s and usually in the lower lumbar spine. Some individuals, however, can become inflicted by this disease much earlier than the norm, depending on both the severity of their genetic deficiencies and lifestyles.

Lumbar disc degeneration and associated nerve lesion account for a large amount of lost productivity in the workforce. It is the most common cause of lower back pain throughout the world [3]. Lower back pain is the single most common cause of disability at the age of 45 years and the second most common reason for primary care physician visits [2, 8]. Intervertebral degeneration and associated low back pain have a huge socioeconomic impact and place a burden on health services worldwide. People throughout the world spend more than 100 billion US dollars/year for the treatment of low back pain [2].

In lumbar disc degeneration, accurate diagnosis is difficult, treatment is controversial, and failures are common. MRI is considered to be the cornerstone and special investigation to confirm the diagnosis of LDD and associated nerve lesions. However, between 38% and 52% of asymptomatic individuals demonstrated significant lumbar disc bulging on MRI [19, 20]. Some physicians may diagnosis lumbar disc degeneration on MRI with ought to detail clinical presentations, and others may use back pain alone as a symptom of lumbar disc degeneration [21, 22]. For example, a significant imaging finding of a right disc bulge at L5/S1 in a patient with symptoms of left L4/L5 nerve root distribution is a discordant finding [23]. As a result, imaging findings may not correlate with a patient’s disc problem and it results in the distrust of physicians on the part of patients and vice versa [22, 24, 25]. A basic understanding of the clinical presentations and pain distribution is important in the case of lumbar disc degeneration, and associated lumbosacral nerve lesion is important to diagnosis and disease conditions of a patient with the suspected lumbar disc degeneration. Therefore, the goal of this review is to assess all possible peripheral clinical presentations for lumbar disc degeneration and associated lumbosacral nerve lesions. The discussion of this review is limited to the peripheral clinical presentations and symptoms of lumbar disc degeneration and lumbosacral nerve lesions in the lower back region.

2. Anatomy of Healthy Lumbar Intervertebral Discs and Lumbosacral Nerves

In the lumbar region of the spine, there are five fibrocartilaginous lumbar intervertebral discs [26] which are named based on the vertebrae above and below them, for example, the L4-L5 disc found between L4 and L5 vertebrae. Lumbar intervertebral discs are important to transfer body weight and muscle activity arising from the upper body region to the lower body region. They also provide flexibility, extension, flexion, and torsion and provide protection to the spinal nerves, spinal cord, and the vertebrae themselves [27].

Compared to the discs of the thoracic and cervical spine, the lumbar discs are taller and wider measuring approximately 7–10 mm in thickness and 4 cm in diameter (anterior-posterior plane) [28]. The lumbar discs become shorter during the day due to the weight of the upper body, and sleeping for a minimum of 5 hours helps the discs regain their original shape [27]. The lumbar discs tend to be of greater height anteriorly than posteriorly, and this tendency is especially the greatest being the L5/S1 disc, causing the lumbar spine’s natural convex curvature similar to the cervical spine [29, 30]. Morphologically, the discs are cylindrical with its shape being determined by the integrity of the annulus fibrosus [31]. Because of the mobility of the lumbar spine and the high loads applied to it, discs have a significantly higher chance of becoming damaged from bending and torsion, making it the most common spinal part for disc injury [32]. 90% of lumbar disc degeneration occurs at the L4-L5 or the L5-S1 disc space [27].

Posterior to the lumbar intervertebral disc, there are five paired anterior and posterior lumbar nerve roots (L1-L5) that exit below the corresponding lumbar vertebra through the respective foramen () [5]. Upon exiting the spinal column, the posterior and anterior spinal nerve roots combine around the intervertebral foramen and form five paired mixed lumbar spinal nerves. The mixed spinal nerves contain both motor and sensory nerve fibers. Mixed spinal nerves immediately divide into posterior ramus and anterior ramus. The posterior and anterior rami contain both sensory and motor nerve fibers [33]. Since most disc herniations occur posterolaterally, the root that exits the foramen below the herniated disc gets compressed. So, a disc bulge at L4/L5 will compress the L5 root, and a protrusion at L5/S1 will compress the S1 root.

Lumbar discs and adjacent lumbar nerve roots [38, 64].

The ventral rami of the lumbar and sacral nerves (L1- S4) form the lumbosacral plexus of the body (). Because some fibers from the lumbar plexus contribute to the sacral plexus via the lumbosacral trunk, the two plexuses are often considered together as the lumbosacral plexus. The lumbar plexus is formed by roots from L1 to L4, and the sacral plexus is by L4–S4 roots. The lumbosacral plexus gives branches that innervate structures of the lower abdomen, some pelvic genitalia, and lower limbs.

Anatomy of the lumbosacral plexus [26].

The lumbar plexus is located on the anterior surface of the posterior abdominal wall. The important nerves emerging from lumbar plexuses are the femoral nerve (the posterior division of the anterior primary rami of L2-L4), the obturator nerve (the anterior division of the anterior primary rami of L2-l4), lateral femoral cutaneous nerve (posterior division of the anterior rami of L2-L3), and iliohypogastric, ilioinguinal, and genitofemoral nerves, which originate mainly from L1 (). Lumbar nerves are responsible for thigh flexion and adduction and leg extension and provide sensory innervation of the anterior and lateral thigh and medial regions of the leg [34]. The iliohypogastric, ilioinguinal, and genitofemoral nerves are important to innervate transverse and the oblique abdominal muscles [34, 35].

Anatomy of the lumbar plexus [38].

The femoral nerve is the largest terminal branch of the lumbar plexus. It provides motor innervation to the anterior thigh muscles (quadriceps) and sensory innervation to the skin of the anterior thigh and the anteromedial aspect of the leg (). The femoral nerve arises from the posterior cords of the lumbar plexus (L2-L4) and passes deep to the inguinal ligament. It descends vertically to the anterior thigh through the center of the femoral triangle, just lateral to the femoral artery and vein. Once it passes the inguinal ligament, it divides into deep motor branches and superficial cutaneous branches. The superficial branch divides into the medial cutaneous and anterior cutaneous nerve of the thigh. The femoral nerve terminates as the sensory saphenous nerve of the leg. The deep branch mainly supplies muscles of the anterior compartment of the thigh, leg extensor muscles. The first motor branch innervates the iliacus. This muscle, in conjunction with the psoas major, causes medial rotation of the hip. The deep branch of the femoral nerve then descends to supply the Sartorius (the tailor’s muscle). Once it passes through the femoral canal, it supplies the pectineus, a small muscle in the medial compartment of the thigh. Finally, the nerve supplies the four heads of the quadriceps femoris (vastus medialis, vastus lateralis, vastus intermedius, and rectus femoris), prime movers for leg extension at the knee joint and thigh flexion and critical for standing and stepping function. The medial and anterior cutaneous nerves of the thigh innervate the skin of the anterior thigh and the medial surface of the thigh, and saphenous nerve supplies the medial surface of the leg from the knee to the foot. The lateral femoral cutaneous nerve is a separate sensory nerve arising from L2 and L3 and supplies sensation over the lateral thigh [34, 36–38].

Anatomy of femoral and obturator nerves and their innervation [38].

The obturator nerve (L2–L4) () passes through the large obturator foramen of the pelvis and enters the medial compartment of the thigh by passing through the obturator foramen accompanied by the obturator artery. The obturator nerve innervates the adductor muscles of the thigh, medial compartment muscles. As it goes through the foramen, it divides into anterior and posterior branches. The anterior division of the obturator nerve, lying deep to the adductor longus on the surface of the adductor brevis, gives branches to the adductor longus, the adductor brevis, and the gracilis and the skin of the medial part of the thigh. The posterior division of the obturator nerve emerges through the obturator externus after supplying it to lie on the adductor magnus. It supplies the adductor magnus and gives a branch which accompanies the femoral artery into the popliteal fossa to supply the capsule of the knee joint. The obturator nerve controls the adduction and rotation of the thigh. A small cutaneous zone on the internal thigh is supplied by a sensory fiber [34, 38].

The sacral plexus arises from the ventral rami of L4–S4 (). The sacral plexus is situated on the posterior pelvic wall, anterior to the piriformis muscle. The ventral rami of the sacral nerves come together on the lower part of the greater sciatic foramen and unite to form a broad triangular band of nerves that innervates the lower limbs. The apex of the band is continued through the greater sciatic foramen into the gluteal region to form the sciatic nerve (L4, L5, and S1-3), the largest and longest nerve, in the body. Other branches of the sacral plexus are the superior gluteal (L4-S1), inferior gluteal (L5-S2), pudendal (S2-S4), and posterior femoral cutaneous (S2-S3) nerves. The sacral plexus also gives muscular branches to the quadratus femoris and inferior gemellus (L4-S1), obturator internus and superior gemellus (L5-S2), piriformis (S1-S2), and levator ani, coccygeus, and sphincter ani externus (S4) muscles and also contributes branches to pelvic splanchnic nerves (S2-S4) [38].

The sciatic nerve and its branch innervate all regions of the lower limb except the anterior and medial regions of the thigh [38]. The sciatic nerve leaves the pelvis by passing through the greater sciatic notch, then courses deep to the broad gluteus maximus muscle and enters to the thigh just medial to the hip joint. From there, it descends through the posterior thigh deep to the hamstrings, which it innervates. Superior to the knee joint, it branches into the tibial nerve (L4-S3), medial division, and the common fibular nerve (L4-S2), lateral division. The tibial nerve then continues posteriorly in the timeline to the calf, innervating the posterior compartment muscles of the leg (plantar flexor muscles), intrinsic foot muscles, and sensation in the sole of the foot. The common fibular nerve travels laterally and around the fibular head, dividing into the deep fibular and superficial fibular branches, which supply the muscles of the anterior (dorsiflexors) and lateral compartments (foot evertors) of the leg, respectively. The superficial fibular nerve also forms a sensory branch that supplies sensation to the anterolateral lower leg and dorsum of the foot while the deep fibular nerve supplies sensation to the web space between the first and second toes [38].

The pudendal nerve is a mixed sacral nerve (motor 20%, sensory 50%, and autonomic 30%) [39] that provides cutaneous and muscular innervation to the majority of the perineum (), anal canal, anus, and external male and female genetalia (scrotum, penis, mons pubis, labia majora, labia minora, clitoris, external vaginal orifice, and urethra). The pudendal nerve originates from the ventral rami of the sacral nerves (S2-S4) and then passes through the greater sciatic foramen, below the level of the piriformis (). It passes the back of the ischial spine, between the sacrospinous and the sacrotuberous ligaments, and it enters the perineum via the lesser sciatic foramen [40–42]. The main trunk of the pudendal nerve takes an extrapelvic course superficial to the coccygeus muscle. In the upper half of the pudendal canal or within it, the pudendal nerve gives rise to the inferior rectal nerve, and at the end of the canal, it gives rise to the perineal nerve and dorsal nerves of the penis and clitoris. The inferior rectal nerve exits the pudendal canal medially and extends motor and sensory branches. Motor branches innervate the levator ani, external anal sphincter, and the cutaneous branches to perianal skin and the scrotum or labia. Perineal nerve supplies the perineum, vagina, urethra, male scrotum, labia, transverse perineal muscle, and urethral sphincter, and the dorsal nerve of the clitoris or penis supplies skin of the clitoris/penis, bulbocavernosus, and ischiocavernosus muscles [43, 44].

Anatomy of the sacral plexus [38].

Anatomy of the pudendal nerve. (a) Origin and course of destination. (b) Pudendal nerve in the male perineum. (c) Pudendal nerve in the female perineum [1, 2].

3. Clinical Presentation of Lumbar Disc Degeneration and Lumbosacral Nerve Lesion

A patient’s clinical presentations and symptoms are important diagnostic tools to identify lumbar disc degeneration and lumbosacral nerve lesion. For this, the physician must conduct a physical examination and should ask many questions related to the problems [45]. Straight leg raising is the most commonly used method to diagnose lumbar disc degeneration and associated lumbosacral nerve lesions. The patient lies in the supine position, and the leg is elevated from the ankle, with the knee remaining straight. Normal patients can elevate the leg 60 to 90 degrees without pain. Patients with disc problems can only elevate the leg from 30 to 40 degrees due to produce pain. Ipsilateral straight leg rising is more sensitive, but less specific than contralateral straight leg rising. That is, nearly all patients with disc problem have pain on the straight leg raising on the affected side, but straight leg raising causes pain in many other conditions (e.g., severe hip arthritis). However, contralateral straight leg raising does not produce pain on the affected side unless the pain is due to root disease [46].

Symptoms and clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous innervation defect. Discogenic pain is caused by a damaged intrinsic intervertebral disc in the lumbar region [47]. As the disc begins to degenerate, the disc itself becomes painful and movements that place stress on the disc may result in discogenic pain that comes from the disc. This is similar to any other body part injury, such as a broken bone or a cut in the skin. Discogenic pain is usually felt in the lumbar region. The pain may also feel like it is coming from the buttocks, lower thoracic, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes [48]. Patients with discogenic pain associated with lumbar disc degeneration may present with suddenly forced flexion and/or rotational moment, and some patients may have a spontaneous onset of symptoms. Classic discogenic pain is aggravated by activities that load the disc, such as sitting, standing, walking, flexion, rotation/twisting, lifting, vibration (e.g., riding in a car), coughing, sneezing, laughing, and the Valsalva maneuver [48].

Lesion of the lumbosacral plexus by lumbar disc degeneration leads to a lumbosacral radicular syndrome. This syndrome is characterized by a radiating pain in one or more lumbar or sacral nerve dermatomes and decreased motor function. Sometimes, it may be regarded as sciatica, ischias, or nerve root pain [49]. Radicular pain and radiculopathy are sometimes used interchangeably, although they certainly are not synonyms. In the case of radicular pain, only radiating pain is present from an inflamed or compressed nerve root. As an example, an inflamed nerve root in the lower back may radiate pain into the leg, while in the case of radiculopathy, motor loss may occurs when a compressed or inflamed nerve root results in neurological deficits, such as problems with reflexes, numbness, and/or weakness. Both syndromes frequently occur together, and radiculopathy can be a continuum of radicular pain.

Lower extremity radicular pain and radiculopathy problems due to lumbar disc degeneration are caused by compression of neural structures in the lumbosacral region [47]. Lumbar disc degeneration may compress neural structures in the lumbosacral, and this results in lumbosacral nerve roots and lumbosacral plexus lesions. Lesion of these structures results in radicular pain, weakness, numbness, or difficulty controlling specific muscles of the lower extremities, buttock, lower abdomen, and groin region. Radicular pain may be confined to a single nerve root or may involve groups of nerve roots. Pain may be of sudden or insidious onset. Radicular pain is often worsened with axial loading, sitting, standing, and bending, lifting, or twisting, and the pain feels better while walking, changing position, lying down, or even running. Numbness, tingling, weakness in the extremities, and strong pain that tends to come and go are also the features of nerve compression in the lumbosacral region [47].

Lesion of the lumbosacral plexus by lumbar disc degeneration is divided clinically into those affecting the lumbar plexus and the sacral plexus. A lumbar plexus lesion may cause symptoms in the territories of the iliohypogastric, genitofemoral, ilioinguinal, femoral, and obturator nerves [50, 51]. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg. In lumbar plexus lesion, decrease or absence of knee jerk is common [51, 52].

Similar to lumbar plexus lesion, the sacral plexus lesion also presents with muscular weakness, loss of cutaneous sensation, and pain in the distribution areas of sacral plexus branches and gluteal nerve, sciatic nerve, tibial nerve, peroneal nerves, and pudendal nerve. In sacral plexus lesions, the muscular weakness of the lower extremities is significant. These include weakness in hip extension (gluteus maximus), hip abductors and internal rotators (gluteus medius and tensor fascia latae), knee flexion (hamstring muscles), and all muscles of the leg and foot supplied by the peroneal and tibial nerves. The diminished sensation may involve the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot. The ankle jerk may be diminished or absent [34, 51].

Lesions of the sacral plexus result in weakness of the posterior thigh and muscles of the leg and feet. During sacral nerve plexus lesion, nerve fibers destined for the sciatic nerve, and the common peroneal nerve is often affected. Sciatica is defined as “pain in the distribution of the sciatic nerve due to pathology of the nerve itself.” The term “sciatica” may be confused with radicular pain as it has been used to describe any pain, including referred pain felt in the leg along the distribution of the sciatic nerve. Nevertheless, the term “sciatica” remains in common usage both in clinical practice and in publications [53, 54]. The use of the term sciatica should only be in the context of the above definitions and, as such, be distinguished from any or all other forms of pain felt in the leg, particularly referred pain [55].

Sciatica is the most common neuropathies of the lower extremities, second to common fibular neuropathy. One of the most common presentations of sciatic neuropathy is foot drop, because ankle dorsiflexion weakness, with or without lower extremity sensory impairment, may also be associated with several other clinical syndromes. Patients often experience abrupt pain radiating down the posterolateral limb, with weakness and numbness evolving more gradually [56]. In sciatic neuropathy, the clinical findings are often more consistent with injury to the common fibular division rather than tibial division, sometimes mimicking a common fibular neuropathy at the knee. This finding is particularly true of more distal lesions, as they may not affect the flexors of the knee, or of less severe sciatic nerve injury. Because the common fibular division has fewer and larger fascicles and less supportive tissue compared with the tibial division, it is thought to be more vulnerable to compression. Also, the common fibular division is tauter, and secured at the sciatic notch and fibular neck, resulting in greater potential for stretch injury [54].

Common peroneal nerve lesion is clinical characterized by weakness of foot inversion, plantar flexion, foot drop or dorsiflexor, and depressed ankle jerk [54]. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot [57]. Foot drop is the main feature of fibular neuropathy, and it is due to paralysis of the dorsiflexor muscles of the foot. The difficulty of eversion may be present due to peroneal muscle involvement. On examination, foot eversion is usually stronger than foot dorsiflexion. Other muscles of the posterior compartment are normal [58]. In a large study of common peroneal neuropathy, physicians clinically misdiagnosed 43% of patients as a sciatic neuropathy. This was usually because of the difficulty in assessing ankle inversion and eversion in the presence of foot drop. In sciatic neuropathy, gluteal, hamstring muscles and tibialis posterior muscles are involved [58].

Patients with pudendal nerve injury due to a sacral nerve plexus lesion typically present motor weakness of perineal muscles [59], pain, and burning sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sometimes, the pain may refer to the groin, medial thigh, buttock, and abdomen. These patients may also suffer from constipation, pain, and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction (uncomfortable arousal, decreased sensation, impotence, and ejaculatory dysfunction) [60, 61]. Pain due to pudendal nerve lesion is aggravated by sitting, other flexion activities of the hip (sitting, squatting, bicycling, and exercising) whereas standing or lying down relieves the discomfort [60–62].

4. Conclusion

During the diagnosis of patients with lumbar disc degeneration and lumbosacral nerve lesions, physicians should not use the MRI solely. It is important to assess and understand clinical presentations and pain distribution of lumbar disc degeneration and lumbosacral nerve lesions. They have to assess the patient’s discogenic pain in the lumbar region, weakness of hip flexion, knee extension, and flexion, thigh adduction, ankle inversion, plantar flexion, and foot drop, perineal muscles. The patient’s pain and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction assessments are also critical. Besides, it is important to evaluate the loss of cutaneous sensation in the lower abdomen, inguinal region, over the medial, lateral, and anterior aspect of the thigh, the medial lower leg and in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sensory loss may also present along the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot during the sacral plexus.

Acknowledgments

The author would like to thank Binalfew Tsehaye and Biksegn Wubie for their comments and input on this review.

Conflicts of Interest

The author declares that he has no competing interests.

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Clinical Presentations of Lumbar Disc Degeneration and Lumbosacral Nerve Lesions

Int J Rheumatol. 2020; 2020: 2919625.

Worku Abie Liyew

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Biomedical Science Department, School of Medicine, Debre Markos University, Debre Markos, Ethiopia

Corresponding author.

Academic Editor: Bruce M. Rothschild

Received 2020 Apr 25; Revised 2020 Jun 26; Accepted 2020 Jul 13.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lumbar disc degeneration is defined as the wear and tear of lumbar intervertebral disc, and it is mainly occurring at L3-L4 and L4-S1 vertebrae. Lumbar disc degeneration may lead to disc bulging, osteophytes, loss of disc space, and compression and irritation of the adjacent nerve root. Clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous. Discogenic pain is usually felt in the lumbar region, or sometimes, it may feel in the buttocks, down to the upper thighs, and it is typically presented with sudden forced flexion and/or rotational moment. Radical pain, muscular weakness, and sensory defects associated with lumbosacral nerve lesions are distributed on lower extremities, the buttock, lower abdomen, and groin region. A lumbosacral plexus lesion presents different symptoms in the territories of the lumbar and sacral nerves. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg, while sacral plexus lesion presents clinical symptoms at nerve fibers destined for the sciatic nerve, common peroneal nerve, and pudendal nerve. Weakness of ankle inversion, plantar flexion, and foot drop are the main clinical manifestations of the sacral plexus lesion area. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot. On examination, foot eversion is usually stronger than foot dorsiflexion. The patients may also present with pain and difficulty of bowel movements, sexual dysfunction assessments, and loss of cutaneous sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum.

1. Background of the Study

Lumbar disc degeneration is defined as the wear and tear of lumbar disc that act as a cushion for the spine. Lumbar disc degeneration can occur at any level, but mainly, it occurs on L3-L4 and L4-S1 vertebrae [1, 2]. It begins with small tears in the annulus of the disc to a decrease in the water content of the nucleus pulposus of the discs. The degenerative disc leads to disc bulging, osteophytes, disc space loss, and compression and irritation of the adjacent nerves [3]. With advanced degeneration, it loses water content and disc height (), and it leads to segmental instability and causes degenerative spondylosis and scoliosis. The advanced degenerative changes affect disc facet joints and surrounding soft tissue and can result in canal narrowing also known as degenerative stenosis [3]. Because each lumbar disc is in direct contact with two or three pairs of dorsal roots, disc degeneration may compress the adjacent nerve root [4, 5]. This can cause the pain syndrome but, more characteristically, causes neuropathic pain and neurological symptoms and, in severe cases, dysfunction of the nerve [6, 7].

(a) Normal intervertebral disc and spinal nerve root. (b) Degenerated intervertebral disc and pinched spinal nerve root [63].

Risk factors causing lumbar disc degeneration disease and associated lumbosacral nerve compression includes advancing age, socioeconomic status [8], torsional stress [9], smoking, obesity [10–12], heavy lifting, vibration [10], trauma, immobilization [13], psychosocial factors, gender, height, hereditary, genetic factors [8, 11], and occupations like machine drivers, carpenters, and office workers [14–16]. Genetic inheritance plays a significant role in the rate of degradation. Approximately 50–70% disc degeneration is caused by an individual’s genetic inheritance [17, 18]. Disc degeneration becomes prevalent and common in the individual’s 40s and usually in the lower lumbar spine. Some individuals, however, can become inflicted by this disease much earlier than the norm, depending on both the severity of their genetic deficiencies and lifestyles.

Lumbar disc degeneration and associated nerve lesion account for a large amount of lost productivity in the workforce. It is the most common cause of lower back pain throughout the world [3]. Lower back pain is the single most common cause of disability at the age of 45 years and the second most common reason for primary care physician visits [2, 8]. Intervertebral degeneration and associated low back pain have a huge socioeconomic impact and place a burden on health services worldwide. People throughout the world spend more than 100 billion US dollars/year for the treatment of low back pain [2].

In lumbar disc degeneration, accurate diagnosis is difficult, treatment is controversial, and failures are common. MRI is considered to be the cornerstone and special investigation to confirm the diagnosis of LDD and associated nerve lesions. However, between 38% and 52% of asymptomatic individuals demonstrated significant lumbar disc bulging on MRI [19, 20]. Some physicians may diagnosis lumbar disc degeneration on MRI with ought to detail clinical presentations, and others may use back pain alone as a symptom of lumbar disc degeneration [21, 22]. For example, a significant imaging finding of a right disc bulge at L5/S1 in a patient with symptoms of left L4/L5 nerve root distribution is a discordant finding [23]. As a result, imaging findings may not correlate with a patient’s disc problem and it results in the distrust of physicians on the part of patients and vice versa [22, 24, 25]. A basic understanding of the clinical presentations and pain distribution is important in the case of lumbar disc degeneration, and associated lumbosacral nerve lesion is important to diagnosis and disease conditions of a patient with the suspected lumbar disc degeneration. Therefore, the goal of this review is to assess all possible peripheral clinical presentations for lumbar disc degeneration and associated lumbosacral nerve lesions. The discussion of this review is limited to the peripheral clinical presentations and symptoms of lumbar disc degeneration and lumbosacral nerve lesions in the lower back region.

2. Anatomy of Healthy Lumbar Intervertebral Discs and Lumbosacral Nerves

In the lumbar region of the spine, there are five fibrocartilaginous lumbar intervertebral discs [26] which are named based on the vertebrae above and below them, for example, the L4-L5 disc found between L4 and L5 vertebrae. Lumbar intervertebral discs are important to transfer body weight and muscle activity arising from the upper body region to the lower body region. They also provide flexibility, extension, flexion, and torsion and provide protection to the spinal nerves, spinal cord, and the vertebrae themselves [27].

Compared to the discs of the thoracic and cervical spine, the lumbar discs are taller and wider measuring approximately 7–10 mm in thickness and 4 cm in diameter (anterior-posterior plane) [28]. The lumbar discs become shorter during the day due to the weight of the upper body, and sleeping for a minimum of 5 hours helps the discs regain their original shape [27]. The lumbar discs tend to be of greater height anteriorly than posteriorly, and this tendency is especially the greatest being the L5/S1 disc, causing the lumbar spine’s natural convex curvature similar to the cervical spine [29, 30]. Morphologically, the discs are cylindrical with its shape being determined by the integrity of the annulus fibrosus [31]. Because of the mobility of the lumbar spine and the high loads applied to it, discs have a significantly higher chance of becoming damaged from bending and torsion, making it the most common spinal part for disc injury [32]. 90% of lumbar disc degeneration occurs at the L4-L5 or the L5-S1 disc space [27].

Posterior to the lumbar intervertebral disc, there are five paired anterior and posterior lumbar nerve roots (L1-L5) that exit below the corresponding lumbar vertebra through the respective foramen () [5]. Upon exiting the spinal column, the posterior and anterior spinal nerve roots combine around the intervertebral foramen and form five paired mixed lumbar spinal nerves. The mixed spinal nerves contain both motor and sensory nerve fibers. Mixed spinal nerves immediately divide into posterior ramus and anterior ramus. The posterior and anterior rami contain both sensory and motor nerve fibers [33]. Since most disc herniations occur posterolaterally, the root that exits the foramen below the herniated disc gets compressed. So, a disc bulge at L4/L5 will compress the L5 root, and a protrusion at L5/S1 will compress the S1 root.

Lumbar discs and adjacent lumbar nerve roots [38, 64].

The ventral rami of the lumbar and sacral nerves (L1- S4) form the lumbosacral plexus of the body (). Because some fibers from the lumbar plexus contribute to the sacral plexus via the lumbosacral trunk, the two plexuses are often considered together as the lumbosacral plexus. The lumbar plexus is formed by roots from L1 to L4, and the sacral plexus is by L4–S4 roots. The lumbosacral plexus gives branches that innervate structures of the lower abdomen, some pelvic genitalia, and lower limbs.

Anatomy of the lumbosacral plexus [26].

The lumbar plexus is located on the anterior surface of the posterior abdominal wall. The important nerves emerging from lumbar plexuses are the femoral nerve (the posterior division of the anterior primary rami of L2-L4), the obturator nerve (the anterior division of the anterior primary rami of L2-l4), lateral femoral cutaneous nerve (posterior division of the anterior rami of L2-L3), and iliohypogastric, ilioinguinal, and genitofemoral nerves, which originate mainly from L1 (). Lumbar nerves are responsible for thigh flexion and adduction and leg extension and provide sensory innervation of the anterior and lateral thigh and medial regions of the leg [34]. The iliohypogastric, ilioinguinal, and genitofemoral nerves are important to innervate transverse and the oblique abdominal muscles [34, 35].

Anatomy of the lumbar plexus [38].

The femoral nerve is the largest terminal branch of the lumbar plexus. It provides motor innervation to the anterior thigh muscles (quadriceps) and sensory innervation to the skin of the anterior thigh and the anteromedial aspect of the leg (). The femoral nerve arises from the posterior cords of the lumbar plexus (L2-L4) and passes deep to the inguinal ligament. It descends vertically to the anterior thigh through the center of the femoral triangle, just lateral to the femoral artery and vein. Once it passes the inguinal ligament, it divides into deep motor branches and superficial cutaneous branches. The superficial branch divides into the medial cutaneous and anterior cutaneous nerve of the thigh. The femoral nerve terminates as the sensory saphenous nerve of the leg. The deep branch mainly supplies muscles of the anterior compartment of the thigh, leg extensor muscles. The first motor branch innervates the iliacus. This muscle, in conjunction with the psoas major, causes medial rotation of the hip. The deep branch of the femoral nerve then descends to supply the Sartorius (the tailor’s muscle). Once it passes through the femoral canal, it supplies the pectineus, a small muscle in the medial compartment of the thigh. Finally, the nerve supplies the four heads of the quadriceps femoris (vastus medialis, vastus lateralis, vastus intermedius, and rectus femoris), prime movers for leg extension at the knee joint and thigh flexion and critical for standing and stepping function. The medial and anterior cutaneous nerves of the thigh innervate the skin of the anterior thigh and the medial surface of the thigh, and saphenous nerve supplies the medial surface of the leg from the knee to the foot. The lateral femoral cutaneous nerve is a separate sensory nerve arising from L2 and L3 and supplies sensation over the lateral thigh [34, 36–38].

Anatomy of femoral and obturator nerves and their innervation [38].

The obturator nerve (L2–L4) () passes through the large obturator foramen of the pelvis and enters the medial compartment of the thigh by passing through the obturator foramen accompanied by the obturator artery. The obturator nerve innervates the adductor muscles of the thigh, medial compartment muscles. As it goes through the foramen, it divides into anterior and posterior branches. The anterior division of the obturator nerve, lying deep to the adductor longus on the surface of the adductor brevis, gives branches to the adductor longus, the adductor brevis, and the gracilis and the skin of the medial part of the thigh. The posterior division of the obturator nerve emerges through the obturator externus after supplying it to lie on the adductor magnus. It supplies the adductor magnus and gives a branch which accompanies the femoral artery into the popliteal fossa to supply the capsule of the knee joint. The obturator nerve controls the adduction and rotation of the thigh. A small cutaneous zone on the internal thigh is supplied by a sensory fiber [34, 38].

The sacral plexus arises from the ventral rami of L4–S4 (). The sacral plexus is situated on the posterior pelvic wall, anterior to the piriformis muscle. The ventral rami of the sacral nerves come together on the lower part of the greater sciatic foramen and unite to form a broad triangular band of nerves that innervates the lower limbs. The apex of the band is continued through the greater sciatic foramen into the gluteal region to form the sciatic nerve (L4, L5, and S1-3), the largest and longest nerve, in the body. Other branches of the sacral plexus are the superior gluteal (L4-S1), inferior gluteal (L5-S2), pudendal (S2-S4), and posterior femoral cutaneous (S2-S3) nerves. The sacral plexus also gives muscular branches to the quadratus femoris and inferior gemellus (L4-S1), obturator internus and superior gemellus (L5-S2), piriformis (S1-S2), and levator ani, coccygeus, and sphincter ani externus (S4) muscles and also contributes branches to pelvic splanchnic nerves (S2-S4) [38].

The sciatic nerve and its branch innervate all regions of the lower limb except the anterior and medial regions of the thigh [38]. The sciatic nerve leaves the pelvis by passing through the greater sciatic notch, then courses deep to the broad gluteus maximus muscle and enters to the thigh just medial to the hip joint. From there, it descends through the posterior thigh deep to the hamstrings, which it innervates. Superior to the knee joint, it branches into the tibial nerve (L4-S3), medial division, and the common fibular nerve (L4-S2), lateral division. The tibial nerve then continues posteriorly in the timeline to the calf, innervating the posterior compartment muscles of the leg (plantar flexor muscles), intrinsic foot muscles, and sensation in the sole of the foot. The common fibular nerve travels laterally and around the fibular head, dividing into the deep fibular and superficial fibular branches, which supply the muscles of the anterior (dorsiflexors) and lateral compartments (foot evertors) of the leg, respectively. The superficial fibular nerve also forms a sensory branch that supplies sensation to the anterolateral lower leg and dorsum of the foot while the deep fibular nerve supplies sensation to the web space between the first and second toes [38].

The pudendal nerve is a mixed sacral nerve (motor 20%, sensory 50%, and autonomic 30%) [39] that provides cutaneous and muscular innervation to the majority of the perineum (), anal canal, anus, and external male and female genetalia (scrotum, penis, mons pubis, labia majora, labia minora, clitoris, external vaginal orifice, and urethra). The pudendal nerve originates from the ventral rami of the sacral nerves (S2-S4) and then passes through the greater sciatic foramen, below the level of the piriformis (). It passes the back of the ischial spine, between the sacrospinous and the sacrotuberous ligaments, and it enters the perineum via the lesser sciatic foramen [40–42]. The main trunk of the pudendal nerve takes an extrapelvic course superficial to the coccygeus muscle. In the upper half of the pudendal canal or within it, the pudendal nerve gives rise to the inferior rectal nerve, and at the end of the canal, it gives rise to the perineal nerve and dorsal nerves of the penis and clitoris. The inferior rectal nerve exits the pudendal canal medially and extends motor and sensory branches. Motor branches innervate the levator ani, external anal sphincter, and the cutaneous branches to perianal skin and the scrotum or labia. Perineal nerve supplies the perineum, vagina, urethra, male scrotum, labia, transverse perineal muscle, and urethral sphincter, and the dorsal nerve of the clitoris or penis supplies skin of the clitoris/penis, bulbocavernosus, and ischiocavernosus muscles [43, 44].

Anatomy of the sacral plexus [38].

Anatomy of the pudendal nerve. (a) Origin and course of destination. (b) Pudendal nerve in the male perineum. (c) Pudendal nerve in the female perineum [1, 2].

3. Clinical Presentation of Lumbar Disc Degeneration and Lumbosacral Nerve Lesion

A patient’s clinical presentations and symptoms are important diagnostic tools to identify lumbar disc degeneration and lumbosacral nerve lesion. For this, the physician must conduct a physical examination and should ask many questions related to the problems [45]. Straight leg raising is the most commonly used method to diagnose lumbar disc degeneration and associated lumbosacral nerve lesions. The patient lies in the supine position, and the leg is elevated from the ankle, with the knee remaining straight. Normal patients can elevate the leg 60 to 90 degrees without pain. Patients with disc problems can only elevate the leg from 30 to 40 degrees due to produce pain. Ipsilateral straight leg rising is more sensitive, but less specific than contralateral straight leg rising. That is, nearly all patients with disc problem have pain on the straight leg raising on the affected side, but straight leg raising causes pain in many other conditions (e.g., severe hip arthritis). However, contralateral straight leg raising does not produce pain on the affected side unless the pain is due to root disease [46].

Symptoms and clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous innervation defect. Discogenic pain is caused by a damaged intrinsic intervertebral disc in the lumbar region [47]. As the disc begins to degenerate, the disc itself becomes painful and movements that place stress on the disc may result in discogenic pain that comes from the disc. This is similar to any other body part injury, such as a broken bone or a cut in the skin. Discogenic pain is usually felt in the lumbar region. The pain may also feel like it is coming from the buttocks, lower thoracic, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes [48]. Patients with discogenic pain associated with lumbar disc degeneration may present with suddenly forced flexion and/or rotational moment, and some patients may have a spontaneous onset of symptoms. Classic discogenic pain is aggravated by activities that load the disc, such as sitting, standing, walking, flexion, rotation/twisting, lifting, vibration (e.g., riding in a car), coughing, sneezing, laughing, and the Valsalva maneuver [48].

Lesion of the lumbosacral plexus by lumbar disc degeneration leads to a lumbosacral radicular syndrome. This syndrome is characterized by a radiating pain in one or more lumbar or sacral nerve dermatomes and decreased motor function. Sometimes, it may be regarded as sciatica, ischias, or nerve root pain [49]. Radicular pain and radiculopathy are sometimes used interchangeably, although they certainly are not synonyms. In the case of radicular pain, only radiating pain is present from an inflamed or compressed nerve root. As an example, an inflamed nerve root in the lower back may radiate pain into the leg, while in the case of radiculopathy, motor loss may occurs when a compressed or inflamed nerve root results in neurological deficits, such as problems with reflexes, numbness, and/or weakness. Both syndromes frequently occur together, and radiculopathy can be a continuum of radicular pain.

Lower extremity radicular pain and radiculopathy problems due to lumbar disc degeneration are caused by compression of neural structures in the lumbosacral region [47]. Lumbar disc degeneration may compress neural structures in the lumbosacral, and this results in lumbosacral nerve roots and lumbosacral plexus lesions. Lesion of these structures results in radicular pain, weakness, numbness, or difficulty controlling specific muscles of the lower extremities, buttock, lower abdomen, and groin region. Radicular pain may be confined to a single nerve root or may involve groups of nerve roots. Pain may be of sudden or insidious onset. Radicular pain is often worsened with axial loading, sitting, standing, and bending, lifting, or twisting, and the pain feels better while walking, changing position, lying down, or even running. Numbness, tingling, weakness in the extremities, and strong pain that tends to come and go are also the features of nerve compression in the lumbosacral region [47].

Lesion of the lumbosacral plexus by lumbar disc degeneration is divided clinically into those affecting the lumbar plexus and the sacral plexus. A lumbar plexus lesion may cause symptoms in the territories of the iliohypogastric, genitofemoral, ilioinguinal, femoral, and obturator nerves [50, 51]. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg. In lumbar plexus lesion, decrease or absence of knee jerk is common [51, 52].

Similar to lumbar plexus lesion, the sacral plexus lesion also presents with muscular weakness, loss of cutaneous sensation, and pain in the distribution areas of sacral plexus branches and gluteal nerve, sciatic nerve, tibial nerve, peroneal nerves, and pudendal nerve. In sacral plexus lesions, the muscular weakness of the lower extremities is significant. These include weakness in hip extension (gluteus maximus), hip abductors and internal rotators (gluteus medius and tensor fascia latae), knee flexion (hamstring muscles), and all muscles of the leg and foot supplied by the peroneal and tibial nerves. The diminished sensation may involve the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot. The ankle jerk may be diminished or absent [34, 51].

Lesions of the sacral plexus result in weakness of the posterior thigh and muscles of the leg and feet. During sacral nerve plexus lesion, nerve fibers destined for the sciatic nerve, and the common peroneal nerve is often affected. Sciatica is defined as “pain in the distribution of the sciatic nerve due to pathology of the nerve itself.” The term “sciatica” may be confused with radicular pain as it has been used to describe any pain, including referred pain felt in the leg along the distribution of the sciatic nerve. Nevertheless, the term “sciatica” remains in common usage both in clinical practice and in publications [53, 54]. The use of the term sciatica should only be in the context of the above definitions and, as such, be distinguished from any or all other forms of pain felt in the leg, particularly referred pain [55].

Sciatica is the most common neuropathies of the lower extremities, second to common fibular neuropathy. One of the most common presentations of sciatic neuropathy is foot drop, because ankle dorsiflexion weakness, with or without lower extremity sensory impairment, may also be associated with several other clinical syndromes. Patients often experience abrupt pain radiating down the posterolateral limb, with weakness and numbness evolving more gradually [56]. In sciatic neuropathy, the clinical findings are often more consistent with injury to the common fibular division rather than tibial division, sometimes mimicking a common fibular neuropathy at the knee. This finding is particularly true of more distal lesions, as they may not affect the flexors of the knee, or of less severe sciatic nerve injury. Because the common fibular division has fewer and larger fascicles and less supportive tissue compared with the tibial division, it is thought to be more vulnerable to compression. Also, the common fibular division is tauter, and secured at the sciatic notch and fibular neck, resulting in greater potential for stretch injury [54].

Common peroneal nerve lesion is clinical characterized by weakness of foot inversion, plantar flexion, foot drop or dorsiflexor, and depressed ankle jerk [54]. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot [57]. Foot drop is the main feature of fibular neuropathy, and it is due to paralysis of the dorsiflexor muscles of the foot. The difficulty of eversion may be present due to peroneal muscle involvement. On examination, foot eversion is usually stronger than foot dorsiflexion. Other muscles of the posterior compartment are normal [58]. In a large study of common peroneal neuropathy, physicians clinically misdiagnosed 43% of patients as a sciatic neuropathy. This was usually because of the difficulty in assessing ankle inversion and eversion in the presence of foot drop. In sciatic neuropathy, gluteal, hamstring muscles and tibialis posterior muscles are involved [58].

Patients with pudendal nerve injury due to a sacral nerve plexus lesion typically present motor weakness of perineal muscles [59], pain, and burning sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sometimes, the pain may refer to the groin, medial thigh, buttock, and abdomen. These patients may also suffer from constipation, pain, and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction (uncomfortable arousal, decreased sensation, impotence, and ejaculatory dysfunction) [60, 61]. Pain due to pudendal nerve lesion is aggravated by sitting, other flexion activities of the hip (sitting, squatting, bicycling, and exercising) whereas standing or lying down relieves the discomfort [60–62].

4. Conclusion

During the diagnosis of patients with lumbar disc degeneration and lumbosacral nerve lesions, physicians should not use the MRI solely. It is important to assess and understand clinical presentations and pain distribution of lumbar disc degeneration and lumbosacral nerve lesions. They have to assess the patient’s discogenic pain in the lumbar region, weakness of hip flexion, knee extension, and flexion, thigh adduction, ankle inversion, plantar flexion, and foot drop, perineal muscles. The patient’s pain and difficulty of bowel movements, burning during urination, painful intercourse, and sexual dysfunction assessments are also critical. Besides, it is important to evaluate the loss of cutaneous sensation in the lower abdomen, inguinal region, over the medial, lateral, and anterior aspect of the thigh, the medial lower leg and in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum. Sensory loss may also present along the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee, and almost the entire foot during the sacral plexus.

Acknowledgments

The author would like to thank Binalfew Tsehaye and Biksegn Wubie for their comments and input on this review.

Conflicts of Interest

The author declares that he has no competing interests.

References

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Degenerative Disc Disease | Michigan Medicine

When you come to the University of Michigan Health Comprehensive Spine Program for degenerative disc disease, you’ll be evaluated by our multidisciplinary team of specialists who will work with you to determine a personalized treatment plan. Our goal is to offer the most advanced and least invasive treatment to help improve your quality of life.

What is Degenerative Disc Disease?

Degenerative disc disease refers to changes in the discs in the spine, most often due to the aging process or to a spinal injury. Spinal discs are soft, compressible discs that separate the spine’s interlocking bones, or vertebrae. These discs serve as shock absorbers that enable the spine to bend and twist.

While degenerative disc disease can happen anywhere in the spine, it typically affects the lumbar (lower back) region or the cervical (neck) region. Degenerative disc disease can also affect the thoracic (middle) region of the spine.

Changes in the discs can cause back or neck pain as well as other issues, including: 

• Osteoarthritis, a type of arthritis associated with aging in which cartilage that protects and cushions joints breaks down. 
• Spinal stenosis, the narrowing of the spinal canal, the open space in the spine that holds the spinal cord.

Symptoms

For many individuals, degenerative disc disease may not cause any symptoms. Others, however, may experience back or neck pain and stiffness. The location of your pain depends on the affected disc: 

• A degenerative disc in the neck area may result in neck or arm pain or numbness. 
• A degenerative disc in the lower back may result in pain or numbness in the back, buttock or leg, difficulty walking and lack of balance or coordination. 
• Occasionally, bowel and bladder control problems may occur with spinal cord stenosis or significant nerve compression.

Diagnosis

Our collaborative team begins by conducting a complete medical history and physical exam as well as a review of any symptoms, injuries or illnesses, previous treatment, or habits and activities that could be responsible for your pain.

Testing is done using the most advanced technologies and may include: Imaging such as X-rays, CT scans or MRI of the affected area. An EMG to assess the electrical activity of the nerves and muscles. A discogram to evaluate back pain and help determine whether the degenerated disc is the cause of pain.

 After your diagnostic tests are completed, our specialists will talk with you about your treatment options.

Treatment

Non-surgical Treatment

Most cases of degenerative disc disease can be managed without surgery through our comprehensive pain program focused on interventional therapies. Non-surgical treatment is based on symptoms and is aimed at reducing pain and improving function. Treatment may include: 

• Physical therapy and exercises to help strengthen specific muscles to help the back heal and reduce the frequency of painful flare-ups. 
• Pain management, including anti-inflammatory and pain medications, muscle relaxers, manual manipulation, steroid injections, electrical stimulation, radiofrequency ablation and heat/ice therapy. 
• Traditional medicine combined with holistic therapies such as yoga, healing touch and acupuncture. 

Surgical Treatment

When symptoms related to disc degeneration don’t improve with conservative treatment or if there is a progression of neurologic symptoms, surgery may be recommended. The goal of surgery is to relieve pressure on the nerves and stabilize the degenerated disc(s). Our spine specialists are skilled in the use of minimally invasive techniques that incorporate advanced navigation and robotics procedures, leading to faster recovery, less discomfort and shorter hospitalizations.

Treatment options include: 

• Laminectomy: Removal of fragments of bone and soft tissue if spinal stenosis or significant nerve compression are involved. Depending on certain factors, this may be performed as a minimally invasive procedure or an open procedure. For more severe cases in which there is significant nerve compression, a laminectomy may be combined with a spinal fusion. 
• Spinal Fusion: A procedure that reduces the movement in the damaged spine segment by permanently connecting two or more vertebrae using screws and rods to stabilize the spine. A bone graft is also typically performed using additional bone to fill in gaps between the vertebrae and stimulate the healing process. 
• L5-S1 Anterior Lumbar Interbody Fusion: A procedure performed in the lower spine (typically L4-L5 or L5-S1) in which the disc is removed and a cage/interbody fusion is placed between the discs to help restore disc height and indirectly decompress the affected nerve(s). This procedure is performed through the abdomen versus the back, resulting in a smaller incision and quicker healing.

Contact Us

You’re about to make an important decision, and we want to help you make a good one. Our staff will be glad to talk with you about your options and how we can help. Please visit our Make an Appointment page for more information.

Degenerative Disc Disease: Causes, Symptoms & Treatment

Overview

What is degenerative disc disease?

Degenerative disc disease is when your spinal disks wear down. Spinal disks are rubbery cushions between your vertebrae (bones in your spinal column). They act as shock absorbers and help you move, bend and twist comfortably. Everyone’s spinal discs degenerate over time and is a normal part of aging.

When the cushions wear away, the bones can start to rub together. This contact can cause pain and other problems, such as:

How common is intervertebral disc degeneration?

Almost everyone has some disc degeneration after age 40, even if they don’t develop symptoms. It can lead to back pain in about 5% of adults.

Who might get degenerative disc disease?

Degenerative disc disease is most common in older adults. Some factors increase your risk of developing degenerative disc disease, including:

• Acute injuries, such as falling.
• Obesity.
• Biological sex, with women being more likely to experience symptoms.
• Smoking.
• Working a physically demanding job.

Symptoms and Causes

What are the symptoms of degenerative disc disease?

The most common symptoms of degenerative disc disease are neck pain and back pain. You may experience pain that:

• Comes and goes, lasting for weeks or months at a time.
• Leads to numbness or tingling in your arms or legs.
• Radiates down your buttocks and lower back.
• Worsens with sitting, bending or lifting.

What causes degenerative disc disease?

Spinal disks wear down as a normal part of aging. Especially after age 40, most people experience some disc degeneration. However, not everyone experiences pain.

You might have pain if your spinal disks:

• Dry out: Your disks have a soft core that mostly contains water. As you get older, that core naturally loses some water. As a result, disks get thinner and don’t provide as much shock absorption as they used to.
• Tear or crack: Minor injuries can lead to small cracks in your spinal disks. These tears are often near nerves. Tears can be painful, even when they are minor. If the outer wall of your spinal disk cracks open, your disk may bulge out of place, known as a herniated disk, which may compress a spinal nerve.

What does degenerative disc pain feel like?

Degenerative disc pain:

• Can happen in the neck or lower back.
• May extend into the arms and hands or into the butt and legs.
• Can be mild, moderate or severe.
• May start and stop.
• Can get worse after certain activities such as bending, twisting or lifting.
• Can get worse over time.

Diagnosis and Tests

How is degenerative disc disease diagnosed?

To diagnose degenerative disc disease, your healthcare provider may start by asking you about your symptoms. Questions may include:

• When does the pain start?
• Where do you feel pain?
• What activities cause the most pain?
• What activities decrease the pain?
• Did you have an injury or accident that led to pain?
• Do you have other symptoms, such as tingling or numbness?
• How far can you walk?

Your healthcare provider may use imaging scans such as X-ray, CT or MRI. These tests can show your healthcare provider the state and alignment of your disks. Your provider may also conduct a physical exam to check your:

• Nerve function: Your provider may use a reflex hammer to check your reactions. Poor or no reaction could mean you have damaged or compressed nerves.
• Pain levels: Your provider may touch or press on specific areas of your back to measure your pain levels.
• Strength: Muscle weakness or shrinking (atrophy) could mean you have nerve damage or degenerated disks.

Management and Treatment

How is degenerative disc disease treated?

Usually, your healthcare provider will recommend noninvasive treatment options first. Your treatment may include:

• Physical therapy: Participating in strengthening and stretching exercises with a trained healthcare provider.
• Medications: Taking nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxers or steroids.
• Steroid injections: Injecting medicine near your spinal nerves, disk or joints to reduce inflammation and pain.
• Radiofrequency neurotomy: Using electric currents to burn sensory nerves and prevent pain signals from reaching your brain.

Can I treat degenerative disc disease at home?

Some people find pain relief through at-home remedies. At-home treatments may decrease pain for a short time. But they are not a long-term treatment for severely degenerated discs. You may try:

• Exercise: Low-impact activity such as walking or swimming can strengthen back muscles and relieve some pain.
• Hot and cold therapy: Alternating ice packs and heating pads every 10 to 15 minutes up to three to four times per day may reduce soreness and inflammation.
• Stretching: Gentle yoga and stretching throughout the day may improve posture and relieve tension.

Do I need surgery for degenerative disc disease?

Many patients do not need surgery for degenerative disc disease. But if you have tried multiple nonsurgical treatments and have persistent pain and/or weakness, surgery may be a good option.

Or your surgeon may use one of a few types of spinal decompression surgery:

• Diskectomy: Removing part of a spinal disc to relieve pressure on your nerves.
• Foraminotomy: Expanding the opening for your nerve roots by removing tissue and bone.
• Laminectomy: Taking out a small portion of bone from your lower spine (lamina).
• Osteophyte removal: Removing bone spurs (osteophytes).
• Spinal fusion: During this procedure, your surgeon connects two or more vertebrae to improve stability.

Prevention

How can I prevent degenerative disc disease?

You can prevent or slow the progression of spinal degeneration through lifestyle changes. Some of these include:

Outlook / Prognosis

What is the outlook for people with degenerative disc disease?

Many people use nonsurgical and at-home treatments to manage pain long-term. If you have mild to moderate back pain, you will need to continue treatment to keep the pain at bay.

Most people who have surgery for degenerative disc disease experience long-term pain relief. Even after surgery, you need to continue exercising and stretching to keep your back strong and healthy.

Does degenerative disc disease increase my risk for other conditions?

Degenerated discs can increase your risk of developing other spinal conditions. Common spine problems include:

Living With

What else should I ask my doctor?

You may want to ask your healthcare provider:

• What is the most likely cause of degenerative disc disease?
• How can I slow the progression of the disease?
• What nonsurgical treatments are most likely to relieve pain?
• What will happen if I choose not to have surgery?
• How can I prevent pain from returning after surgery?

A note from Cleveland Clinic

Degenerative disc disease occurs when your spinal disks break down. When these disks wear out, people typically experience back pain and stiffness. You may find pain relief with nonsurgical treatments such as physical therapy and spinal injection. For some people, home remedies like hot and cold therapy can decrease pain. When pain is severe, you may benefit from spinal injections or spine surgery. A spine specialist can help you determine which treatment is best for you.

Degenerative Disc Disease: Causes, Symptoms & Treatment

Overview

What is degenerative disc disease?

Degenerative disc disease is when your spinal disks wear down. Spinal disks are rubbery cushions between your vertebrae (bones in your spinal column). They act as shock absorbers and help you move, bend and twist comfortably. Everyone’s spinal discs degenerate over time and is a normal part of aging.

When the cushions wear away, the bones can start to rub together. This contact can cause pain and other problems, such as:

How common is intervertebral disc degeneration?

Almost everyone has some disc degeneration after age 40, even if they don’t develop symptoms. It can lead to back pain in about 5% of adults.

Who might get degenerative disc disease?

Degenerative disc disease is most common in older adults. Some factors increase your risk of developing degenerative disc disease, including:

• Acute injuries, such as falling.
• Obesity.
• Biological sex, with women being more likely to experience symptoms.
• Smoking.
• Working a physically demanding job.

Symptoms and Causes

What are the symptoms of degenerative disc disease?

The most common symptoms of degenerative disc disease are neck pain and back pain. You may experience pain that:

• Comes and goes, lasting for weeks or months at a time.
• Leads to numbness or tingling in your arms or legs.
• Radiates down your buttocks and lower back.
• Worsens with sitting, bending or lifting.

What causes degenerative disc disease?

Spinal disks wear down as a normal part of aging. Especially after age 40, most people experience some disc degeneration. However, not everyone experiences pain.

You might have pain if your spinal disks:

• Dry out: Your disks have a soft core that mostly contains water. As you get older, that core naturally loses some water. As a result, disks get thinner and don’t provide as much shock absorption as they used to.
• Tear or crack: Minor injuries can lead to small cracks in your spinal disks. These tears are often near nerves. Tears can be painful, even when they are minor. If the outer wall of your spinal disk cracks open, your disk may bulge out of place, known as a herniated disk, which may compress a spinal nerve.

What does degenerative disc pain feel like?

Degenerative disc pain:

• Can happen in the neck or lower back.
• May extend into the arms and hands or into the butt and legs.
• Can be mild, moderate or severe.
• May start and stop.
• Can get worse after certain activities such as bending, twisting or lifting.
• Can get worse over time.

Diagnosis and Tests

How is degenerative disc disease diagnosed?

To diagnose degenerative disc disease, your healthcare provider may start by asking you about your symptoms. Questions may include:

• When does the pain start?
• Where do you feel pain?
• What activities cause the most pain?
• What activities decrease the pain?
• Did you have an injury or accident that led to pain?
• Do you have other symptoms, such as tingling or numbness?
• How far can you walk?

Your healthcare provider may use imaging scans such as X-ray, CT or MRI. These tests can show your healthcare provider the state and alignment of your disks. Your provider may also conduct a physical exam to check your:

• Nerve function: Your provider may use a reflex hammer to check your reactions. Poor or no reaction could mean you have damaged or compressed nerves.
• Pain levels: Your provider may touch or press on specific areas of your back to measure your pain levels.
• Strength: Muscle weakness or shrinking (atrophy) could mean you have nerve damage or degenerated disks.

Management and Treatment

How is degenerative disc disease treated?

Usually, your healthcare provider will recommend noninvasive treatment options first. Your treatment may include:

• Physical therapy: Participating in strengthening and stretching exercises with a trained healthcare provider.
• Medications: Taking nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxers or steroids.
• Steroid injections: Injecting medicine near your spinal nerves, disk or joints to reduce inflammation and pain.
• Radiofrequency neurotomy: Using electric currents to burn sensory nerves and prevent pain signals from reaching your brain.

Can I treat degenerative disc disease at home?

Some people find pain relief through at-home remedies. At-home treatments may decrease pain for a short time. But they are not a long-term treatment for severely degenerated discs. You may try:

• Exercise: Low-impact activity such as walking or swimming can strengthen back muscles and relieve some pain.
• Hot and cold therapy: Alternating ice packs and heating pads every 10 to 15 minutes up to three to four times per day may reduce soreness and inflammation.
• Stretching: Gentle yoga and stretching throughout the day may improve posture and relieve tension.

Do I need surgery for degenerative disc disease?

Many patients do not need surgery for degenerative disc disease. But if you have tried multiple nonsurgical treatments and have persistent pain and/or weakness, surgery may be a good option.

Or your surgeon may use one of a few types of spinal decompression surgery:

• Diskectomy: Removing part of a spinal disc to relieve pressure on your nerves.
• Foraminotomy: Expanding the opening for your nerve roots by removing tissue and bone.
• Laminectomy: Taking out a small portion of bone from your lower spine (lamina).
• Osteophyte removal: Removing bone spurs (osteophytes).
• Spinal fusion: During this procedure, your surgeon connects two or more vertebrae to improve stability.

Prevention

How can I prevent degenerative disc disease?

You can prevent or slow the progression of spinal degeneration through lifestyle changes. Some of these include:

Outlook / Prognosis

What is the outlook for people with degenerative disc disease?

Many people use nonsurgical and at-home treatments to manage pain long-term. If you have mild to moderate back pain, you will need to continue treatment to keep the pain at bay.

Most people who have surgery for degenerative disc disease experience long-term pain relief. Even after surgery, you need to continue exercising and stretching to keep your back strong and healthy.

Does degenerative disc disease increase my risk for other conditions?

Degenerated discs can increase your risk of developing other spinal conditions. Common spine problems include:

Living With

What else should I ask my doctor?

You may want to ask your healthcare provider:

• What is the most likely cause of degenerative disc disease?
• How can I slow the progression of the disease?
• What nonsurgical treatments are most likely to relieve pain?
• What will happen if I choose not to have surgery?
• How can I prevent pain from returning after surgery?

A note from Cleveland Clinic

Degenerative disc disease occurs when your spinal disks break down. When these disks wear out, people typically experience back pain and stiffness. You may find pain relief with nonsurgical treatments such as physical therapy and spinal injection. For some people, home remedies like hot and cold therapy can decrease pain. When pain is severe, you may benefit from spinal injections or spine surgery. A spine specialist can help you determine which treatment is best for you.

90,000 What are degenerative changes in the intervertebral disc?

Closer to the age of 20-25, when the human body reaches biological maturity, natural age-related changes begin to occur in the intervertebral discs. Discs begin to gradually coarse, lose moisture and elasticity. The seals on the discs cause their height to decrease over time. As a result, the spine as a whole decreases axial elasticity, and a decrease in the gap between the vertebrae causes compression of the lateral nerve roots.The loss of height of the intervertebral disc can also trigger the formation of bony growths (ostephytes and bone spurs), which can put pressure on the spinal cord and nerve roots, causing them to compress.

These changes could have gone unnoticed, if not for the formation of hernial protrusions of the discs – one of the most dangerous and complex diseases of the spine. Frequent injuries of the spine due to excessive loads when lifting weights, sharp turns of the body and head, sharp flexion-extension lead to rupture of discs and formations of hernial protrusions, which put pressure on the spinal cord and its roots, cause pain and other symptoms, such as weakness muscles of the neck, back, limbs, or tingling in them.Long-term neglect of the symptoms of root and spinal cord compression can lead to disability.

The main signs of degenerative-dystrophic lesions of the spine:

• Radicular pain syndrome (radiculopathy) caused by a hernial protrusion of the intervertebral disc, against the background of a pronounced decrease in the patient’s activity and ability to work.
• Radiculopathy caused by the invasion of osteophytes into the lumen of the spinal canal.
• Dysfunction of the spinal cord and spinal roots in the form of paralysis and loss of organ function due to hernial disc protrusion (myelopathy).
• A noticeable, reliable decrease in the height of the gap between the vertebral bodies, revealed on the roentgenogram.

As a rule, in such cases, conservative therapy against these manifestations is ineffective, and patients with pain in the lumbar spine, not receiving relief from conservative therapy, are forced to turn to surgeons with their chronic and recurrent forms of the disease. In addition to severe pain, the indication for urgent surgical treatment in these cases is considered to be, in addition to severe pain, gross neurological disorders: switching off the sensitivity of the limbs, a sharp drop in the muscle strength of the arms and legs, loss of some organs of their functions (for example, urinary incontinence).

Symptoms of spinal stenosis

Symptoms of spinal stenosis manifest themselves in different ways, depending on the location and severity of the stenosis. In 95% of cases, they are represented by severe pain, in 71% of cases – impaired sensitivity, in 33% of cases, paralysis of the limbs is possible.

One of the characteristics of stenosis of the spinal canal of the lumbar region in 90% of cases is the shortening of a possible long walk on foot due to the sharp manifestation of the above symptoms.Often of this kind, the gross discomfort that occurs during walking spreads to the gluteal region and thighs and forces the patient to stop moving. In this case, the patient is no longer able to take even a few steps.

The indicated range of symptoms noticeably decreases when the trunk is tilted forward, when sitting on a chair or in the supine position, since in this case the spinal canal is released. When bending forward, the pressure on the posterior edge of the intervertebral disc decreases, the size of the protrusive protrusion decreases, and as a result, the pressure on the nerve structures decreases.So, for example, cycling in the case of spinal stenosis does not have any particular problems. However, if you straighten your back, lean back, you will create pressure on the posterior edge of the intervertebral disc, the protrusion (hernial) protrusion of the disc will increase, additional narrowing of the spinal canal will occur, and the pain sensations, accordingly, will intensify.

Treatment

Decompression surgery is widely used to relieve irritated nerve bundles and compressed spinal cord.The degree of intervention in this case depends on the characteristics that are inherent in different patients. However, in order to prevent re-narrowing of the spinal canal, it is precisely decompression in the damaged part of the vertebra and effective stabilization of the state to maintain mobility is required.

Surgical approaches for different cases are as follows:

• Decompression. During the decompression procedure, the vertebral arch, bone spurs, thickened ligaments and joints, bulging or sagging intervertebral discs that put pressure on nerve structures can be removed by a surgeon on one or more vertebral segments.
• Decompression with rigid stabilization / fixation. The surgical decompression procedure can subsequently cause instability of the vertebrae at the site of intervention. To prevent it, the technique of combining the vertebrae with a submerged screw structure can be used. This technique is called transpedicular fixation / stabilization (TPF) surgery. The operation of installing TPF systems requires a lot of operating time, complex equipment in the operating room and a lot of workload on the staff and the patient.The union of the vertebrae with a metal structure firmly and rigidly limits their mobility.
• Decompression with interspinous stabilization using the Coflex® implant. Installation of the Coflex® (Coflex) implant ensures the stability of the spine at the decompression site without rigid union of the vertebrae. Moreover, the Coflex® implant (Coflex), in addition to ensuring the stability of the spine, allows you to maintain movement in the operated area, as well as the normal height of the lumen between the vertebrae.

Protrusion and herniated disc of the lumbar spine – Kozyavkin’s method

The human spine consists of vertebrae, between which are intervertebral discs. They allow the spine to move and provide cushioning, softening the load. The disc consists of a hard outer annulus fibrosus and a soft inner nucleus pulposus.

In the presence of certain conditions, the structure of the annulus fibrosus first changes (disc degeneration), then protrusion of the intervertebral disc appears without rupture of the annulus fibrosus (protrusion).When a herniated disc occurs, the annulus fibrosus ruptures and a small part of the nucleus pulposus is pushed out.

When placed posteriorly, it can compress the membrane covering the spinal cord (dural sac) and cause back pain. When a hernia is placed postero-laterally, it can compress the nerve root that is next to it. So there are pains in the groin, buttock, leg, changes in urination, bowel movements, and the like. Not all hernias require treatment, since they often do not compress the dural sac and nerve root, and if they do, it is not always so as to cause serious complaints.

Despite their strength, the intervertebral discs have some weak points. There are no blood vessels in the intervertebral discs. The disc is nourished by diffusion (impregnation) from the surrounding tissues. In this case, nutrients are more actively supplied to the disc only at the moment of spinal movements.

The modern lifestyle of a person does not provide the necessary physical activity (for example, office work), which leads to a deterioration in the nutrition of the intervertebral discs and, as a consequence, a decrease in their strength and rupture.Hard physical labor also creates a no less destructive effect on the intervertebral disc, especially associated with lifting weights and working in an uncomfortable position (for example, working in the field in a bent position).

Rupture of the annulus fibrosus and the formation of a herniated disc can occur even if the disc is injured during excessive single physical exertion (for example, when lifting a heavy object, especially forward).

In recent years, more and more attention has been paid to the genetic weakness of the spine.In particular, after numerous studies conducted with the participation of twins who lead completely different lifestyles, it has been proven that 60-70% of degenerative changes in the spine depend on genetics. This is especially true in cases where we observe herniated intervertebral discs in adolescents and young people.

Other risk factors for a herniated disc include:

• • Smoking. Tobacco smoking increases the risk of herniated discs because oxygen levels in the blood decrease, which leads to a lack of vital nutrients in the tissues of the body.
• • Weight. Being overweight puts additional stress on the discs in the lower back. Sometimes it is impossible to get rid of back pain without bringing the weight back to normal.
• • Growth. Tall people are at increased risk of a herniated disc. Men taller than 180 cm and women taller than 170 cm are considered tall.

If leg and lower back pain occurs, you may sometimes need several days of bed rest to relieve it.However, you should not stay in bed for more than 2-3 days, as this can lead to weakening of the muscles in the spine and increased pain.

In the first weeks after the onset of pain, it is not recommended to perform any special exercises, do fitness, aerobics, jogging, shaping, etc. To maintain physical fitness at this time, you can recommend swimming, moderate walking.

If you feel an increase in pain during any physical activity, stop it immediately.Among the drugs, non-steroidal anti-inflammatory drugs, such as diclofenac, ibuprofen, meloxicam, celebrex, naproxen, acetaminophen, etc., can temporarily improve the condition. However, taking them, you cannot exceed the recommended daily dose and the total duration of administration (10-15 days).

You should also take these drugs with caution for people with diseases of the stomach and intestines (gastritis, ulcer).

Decisive in the diagnosis of spinal diseases are such examination methods as:

• • Magnetic resonance imaging (MRI). A magnetic field is used to create images of your body. This study is used to confirm the localization of a herniated disc and to identify the affected nerves and other structures. MRI is the gold standard for diagnosing herniated intervertebral discs.
• • Computed tomography (CT). Better than MRI shows the state of the bones, but poorly shows the state of soft tissues.

It should be remembered that in some cases, a herniated disc can be a serious problem and, if not treated promptly, can cause irreversible damage to nerve structures, which in turn can lead to weakness in the limbs, disruption of the pelvic organs, or even paralysis.

Symptoms indicating the severity of the nerve root injury:

• • Leg pain, especially when it spreads below the knee, is a characteristic symptom of a herniated disc. It is often accompanied by a feeling of “goose bumps” and numbness in the legs.
• • Low back pain (often onset weeks or months before leg pain appears), pain worse when sitting, coughing, sneezing, trying to bend forward, and turning to your side while sleeping.

If you have any of the following symptoms, contact your neurosurgeon immediately:

• • you lose control of urination;
• • You lose control of your bowel movements;
• • you feel numbness in the perineum;
• • you have weakness of movement in your leg (foot, knee)
• • you have symptoms of paralysis

delaying time can lead to the irreversibility of lost functions (control over the pelvic organs, the ability to walk).

One of the complex and effective methods of treating protrusions and disc herniation is the Intensive Neurophysiological Rehabilitation System (Professor Kozyavkin’s Method).

To assess the possibility of undergoing treatment using our system, you need to:

1. send neurological status data and examinations (MRI, CT).
2. make an appointment with a clinic doctor (requires MRI, CT)

Intervertebral disc replacement is a minimally invasive surgical method to restore painless patient mobility

Information: Intervertebral disc replacement

• Duration of hospital stay: 2 days after cervical disc replacement and 10 days in lumbar region
• Inpatient rehabilitation: 14 days after cervical disc replacement and 21 days in lumbar region
• Earliest flight home: 7 days after cervical disc replacement and 21 days after lumbar replacement
• Recommended time to fly home: 14 days post-cervical disc replacement and 21 days lumbar prosthesis
• Showering is possible: 7 days after cervical disc replacement and 10 days after lumbar replacement
• Duration of incapacity for work: 4 weeks after both operations
• Suture removal: No sutures after cervical disc prosthetics, 14 days after lumbar disc prosthetics
• Driving is possible: 7 days after cervical disc prosthetics and 28 days lumbar disc prosthetics
• Cost of surgery: 12.000 EUR regardless of department

When is an intervertebral disc replacement necessary? © Spinal Kinetics

When is a complete spinal disc replacement necessary?

Complete disc replacement is necessary for patients suffering from a pinched nerve in the lumbar spine due to degenerative disc disease.

For more than ten years, intervertebral disc prostheses have been in constant development. After numerous processes of their modernization, artificial discs have become a significant and reliable alternative for the treatment of degenerative changes in the intervertebral discs.

The modern M6 intervertebral disc prostheses are an excellent alternative to the previously known and successful vertebral fusion surgery.

Why is spinal disc replacement preferable to fusion?

Advantages of intervertebral disc prosthetics in relation to spinal fusion:

• Maintain mobility of the spine
• Fast recovery and recovery after surgery
• Long-term improvement of body biomechanics (flexibility and mobility)
• Ability to return to professional activities and sports in a short time
• No wear on adjacent segments of the spine
• Implantation of the M6 ​​disc prosthesis restores the natural mobility of the human spine

For several years, fusion has been the only treatment for pain in the lumbar spine.

This method was also used for fixation in various deformations. With every decade, the methods of achieving bone block by spinal fusion have improved. Despite this, with spinal fusion there is a risk of degenerative changes in the vertebrae, as well as wear of the intervertebral discs (discopathy) in the adjacent segments of the spine.

Spinal fusion is a safe and effective method, but it has a negative impact on the dynamics and biomechanics of the human spine, which can limit the patient’s mobility.

Over the years, intervertebral disc prostheses have been improved to the point that today they are a successful and reliable alternative for the treatment of intervertebral disc degeneration.

Modern M6 intervertebral disc prostheses are an excellent alternative to the already proven method of fusion.

What predictions are given after implantation of an artificial intervertebral disc?

Artificial intervertebral discs help improve mobility in the damaged segment of the spine.

A new generation of intervertebral disc prostheses – dynamic endoprostheses of intervertebral discs M6

Natural properties of the intervertebral disc:

• The natural membrane (annulus fibrosus) of the intervertebral disc consists of an annular layer of connective tissue
• Elastic shell allows movement in any direction
• The soft elastic core of the intervertebral disc has a shock-absorbing effect
• The shell of the intervertebral disc prosthesis is also elastic.This improves mobility and at the same time provides stability.

Implantation of an intervertebral disc prosthesis does not adversely affect your mobility

Rice. 3: The artificial intervertebral disc can move in six dimensions of the natural mobility of the spine © Spinal Kinetics

Natural intervertebral disc supports the mobility of the spine from any angle and acts as a shock absorber.In order to avoid the loss of natural mobility of the spine, the prosthesis must have the same property.

It should be noted that only with the help of modern technologies for replacing the intervertebral disc (prosthesis of the intervertebral disc M6) it became possible to preserve the natural dynamics of the human spine.

Lumbar disc prosthesis M6-L is designed to restore the anatomy and physiology of the intervertebral disc. In addition, it supports the natural biomechanics of the spine, providing a reliable and long-term solution to the problem.

Artificial intervertebral disc?

Rice. 4 The prosthesis consists of two hinges, each of which structurally consists of a plate with an insert of a friction unit. The surface of the plates follows the anatomical shape of the vertebral bodies, which reduces damage at the time of implantation and reliably stabilizes the endoprosthesis. © Spinal Kinetics

Modern endoprostheses of the intervertebral disc contain a moving nucleus that allows movement in all directions, similar to a natural biological disc.

This invention provides a stable and reliable fixation of the vertebrae, which, in turn, prevents displacement in any direction. In addition, a more complete restoration of the anatomical structure of the spine and its functionality is achieved.

Advantages of the artificial intervertebral disc

The lumbar disc prosthesis M6-L fully corresponds to the structure of the intervertebral disc. A similar result could be achieved using an ultra-modern design, which performs the functions of the annulus fibrosus, as well as the nucleus pulposus.Experience with this type of endoprostheses shows only positive results.

Many patients have already been convinced of the quality of this method offered in famous German blades: it is a reliable and safe intervention that relieves patients with degeneration of the lumbar spine discs from pain and gives longer-term results than the established method of fusion.

For information on whether this method can help you or your family member, click on the link below.

Replacement of the intervertebral disc of the lumbar spine (lumbar disc prosthesis M6-L)

Highly qualified surgeons of the Gelenk Klinik perform total endoprosthetics of the lumbar disc by making a small incision in the abdominal cavity. This minimally invasive method guarantees minimal scarring and speeds up the recovery process.

Who Needs Lumbar Disc Replacement Surgery?

Indications for an operation to replace the intervertebral disc with an artificial one

• MRI shows degeneration of the intervertebral disc
• The cause of the pain was determined by the neurosurgeon
• Unsuccessful conservative treatment
• Complete elimination of other causes of chronic pain
• Chronic pain for more than six months

This surgery is often recommended for patients with back pain for more than six months.Based on MRI, our specialists can easily determine that these pains may be the first signs of intervertebral disc degeneration. However, our highly trained neurosurgeons will be rather wary of claiming that the cause of these pains is actually intervertebral disc degeneration.

Many patients with this problem sometimes do not even feel pain. And only in the case of prolonged pain, the cause of which is the degeneration of the intervertebral disc, the patient is referred for surgery.For this reason, in order to perform an operation to replace an intervertebral disc, it is necessary to have complete information about the patient’s medical history.

In order for the operation to be successful, it is necessary to establish the exact cause of the pain.

Lumbar spine surgery is performed only if the pain cannot be eliminated using methods such as physiotherapy or manual therapy.

Contraindications for implantation of a lumbar spine prosthesis

Implantation of a disc of the lumbar spine should not be performed in the following cases:

• Severe osteoporosis
• Vertebral body destruction
• Osteoarthritis of the facet joints
• Tumors of the spine

Inflammatory diseases

• Injuries to the spinal ligaments
• Severe form of spinal stenosis

Access to the intervertebral disc and adjacent vertebral bodies is performed from the anterior lumbar approach.Then the end surface of the vertebral bodies is cleaned in order to prepare them for the implantation of an artificial prosthesis.

The damaged disc is removed (discectomy) and a disc of the lumbar spine M6-L is inserted into the interbody space using special high-precision instruments. After successful insertion of the M6-L disc, the incision is sutured.

In the M6-L there are two external titanium plates with keels for fixing the disc in the bone tissue of the vertebral body, which are coated with plasma titanium sputtering, which stimulates the growth of bone into metal plates, which in turn ensures long-term fixation and stability of the disc in the bone.

After the operation, the surgeon carefully checks the position of the endoprosthesis. In addition, X-rays are taken to determine the condition of the endoprosthesis.

This animated film shows the principles of artificial lumbar disc implantation. Today, the Gelenk-Klinik Orthopedic Clinic uses more modern M6-L lumbar disc prostheses than those shown in this video. However, the course of the operation remains the same.

Rehabilitation after implantation of an artificial disc of the lumbar spine

This surgery usually does not provide any special restrictions on physical activity.Independent movement on the day of surgery is possible and even encouraged. The time spent in the clinic after the operation is 2-5 days.

After the wound has healed, the patient is discharged home. A special corset must be worn for six weeks. After that, the patient can return to work and usual hobbies.

Training of muscles weakened due to the operation

After surgery, immobility during the healing process negatively affects both the lumbar and cervical spine artificial limbs.Therefore, for muscle recovery, we recommend that patients undergo a special rehabilitation program.

In the event of a lumbar spine disc replacement, a three-week stay in a rehabilitation clinic is recommended after the operation.

90,000 Treatment of degenerative-dystrophic diseases of the spine in the clinic SOYUZ

Treatment of osteochondrosis of the cervical spine

Cervical osteochondrosis is characterized by a variety of symptoms, in addition to compression and reflex manifestations, with this disease cerebral symptoms are not uncommon: occipital migraines, fainting, tinnitus, hearing loss, swallowing disorders, visual impairment.They are associated with the anatomical features of the blood supply to the brain, as well as with the connection of the sympathetic ganglia of the neck with the vessels of the brain.

Treatment of osteochondrosis of the cervical spine is primarily aimed at eliminating the pain syndrome and dysfunctions of the nerve roots. Therapy is most often conservative, it is selected taking into account the phase of the destructive process and the severity of the patient’s condition. In order to release the squeezed nerve structures and restore the physiological shape of the spinal column, orthopedic methods are used – special collars, as well as traction traction of the spinal column.To relieve pain and relieve muscle tension, blockades are prescribed, including intraosseous ones.

In treatment for cervical osteochondrosis various drugs are used:

· Non-steroidal anti-inflammatory drugs;

Chondroprotectors;

Muscle relaxants;

· Blood flow improving agents;

· Vitamin and mineral complexes;

Analgesics.

Physiotherapy is also effective to relieve pain and improve tissue trophism: UV irradiation, pulse currents, electroneurostimulation, electrophoresis, ultrasound, phonophoresis.Massage and physiotherapy exercises are required, reflexology is widely used. Treatment of osteochondrosis of the cervical spine of the second and third degree with severe radiculitis and significant neurological disorders is carried out in a hospital setting. If the condition worsens, a neurosurgeon’s consultation is necessary.

Treatment of lumbar osteochondrosis

Lumbar osteochondrosis is manifested by pain in the affected area, sometimes lumbago develops – a severe acute pain syndrome due to which the patient cannot move.Reflex symptoms cause pain and neurotrophic changes in the lower extremities. Possibly impaired function of the large intestine or urinary system. Treatment of lumbar osteochondrosis in the early stages consists in providing motor rest (wearing a special corset and bandage) and drug therapy. Shown novocaine blockade to relieve pain. At later stages, bed rest is needed, in the absence of contraindications, a course of treatment with corticosteroids is carried out.Physiotherapy is mandatory, according to indications, a stretching of the spinal column is prescribed. In severe cases, surgery is necessary.

Treatment of osteochondrosis of the lumbosacral region

Lumbosacral osteochondrosis is manifested by pain, hypotension and hypotrophy of the muscles of the lower extremities, dysfunctions of the cauda equina of the spinal cord. Treatment of osteochondrosis of the lumbosacral region consists in ensuring motor rest or adherence to bed rest, prescribing drugs (analgesics, muscle relaxants, drugs that increase blood flow, and others).With a strong pain syndrome, blockades with local anesthetics are shown. Physiotherapy and traction therapy are widely used.

If any back pain occurs, it is necessary to consult a doctor to clarify the diagnosis and select an adequate therapy.

90,000 Degenerative-dystrophic diseases of the spine – Clinics of Belarus

Degenerative-dystrophic diseases of the spine is a set of chronic diseases characterized by the development of degenerative changes in various tissues of the spine, which leads to damage to the structures of the spine and manifests itself in the development of pain syndrome and neurological deficits.

Among degenerative-dystrophic diseases of the spine are distinguished: osteochondrosis, spondyloarthrosis, spondylosis, herniated intervertebral discs, degenerative spondylolisthesis. The listed diseases often develop together against the background of a general degenerative-dystrophic lesion of the spine.

As degenerative changes increase, stenosis (narrowing) of the spinal and radicular canals occurs, which leads to compression (compression) of the neural structures located in these anatomical formations of the spine.

Clinical manifestations of this pathology are very diverse: from a feeling of mild discomfort, numbness, feeling of “creeping” to severe pain syndrome, loss of sensitivity, muscle weakness and dysfunction of the pelvic organs. As the disease progresses and symptoms increase, a person is deprived of the ability to move freely and to take care of himself.

In the Republic of Belarus , patients with degenerative-dystrophic diseases are examined in accordance with international standards and using the latest equipment.Digital radiography of the spine, including functional (if indicated) is performed, for optimal visualization of the affected segments of the spine, X-ray computed tomography (RCT), magnetic resonance imaging (MRI) with intravenous contrast enhancement are performed. Thanks to the use of electroneuromyography, it is possible not only to clarify the level of damage, but also to assess the degree of pathological changes in the neural structures of the spine.

Conservative treatment of degenerative-dystrophic diseases of the spine is carried out under the supervision of a neurologist.In cases of deterioration of the condition, lack of effect from the therapy, examination is carried out by a vertebrologist, who determines the indications for surgical treatment.

At present, the following surgical methods of treatment of degenerative-dystrophic diseases of the spine are used in the Republic of Belarus:

• Removal of herniated intervertebral discs by inter- (hemi) laminectomy;

• Laser vaporization of herniated intervertebral discs;

• Medial facetectomy, foraminotomy;

• Posterior-lateral decompression, anterior decompression, including endoscopic;

• Stabilizing operations using titanium implants, transpedicular fixators, interspinous stabilizers;

• Transplantation of auto-, allograft bone.

One operation can include several surgical methods, for example, posterolateral decompression is most often complemented by the installation of a transpedicular fixator, anterior decompression – fusion with bone auto- and allografts and the installation of an interbody titanium implant. The operation to remove a herniated disc along with inter- (hemi) laminectomy with concomitant spondyloarthrosis may include medial facetectomy and foraminotomy.

In the Republic of Belarus, methods of minimally invasive spinal surgery have become widespread, which include various techniques of endoscopy with video assistance, puncture laser vaporization of herniated intervertebral discs, percutaneous installation of stabilizing metal structures under the control of surgical computer navigation.

The choice of a method of surgical treatment of degenerative-dystrophic diseases of the spine depends on the type of pathology, the general condition of the patient and many other factors. Each of these methods has its own list of indications and contraindications, depending on which the surgeon chooses the optimal method of surgical treatment for a particular patient.

Approximate cost of the service

Surgical treatment of disc diseases of the lumbar spine

What is the lumbar spine?

The lumbar spine is a complex system of bones, muscles, cartilage and nerves designed to support the weight of the upper body and allow movement in many directions.The lower back formally begins with the lumbar spine, located just below the cervical and thoracic spine and just above the sacrum. The lumbar spine consists of five vertebrae, which are designated L1 through L5.

Intervertebral disc of the lumbar spine

There are discs between all vertebrae – shock-absorbing cushions that ensure proper separation, stability and mobility of the lumbar vertebrae.Each disc has an outer fibrous membrane that resembles a car tire (called an “annulus fibrosus”), in the center of which is a gel-like substance (called a “nucleus pulposus”). The nucleus and ring function as one unit and absorb shock, help stabilize the spine, and provide limited mobility between all vertebrae.

Intervertebral disc of the lumbar spine

Degeneration of discs of the lumbar spine (LSP)

As we age, the discs of the lumbar spine begin to flatten and wear out.Flattening the disc causes the vertebrae to converge closer, which can increase stress not only on the disc itself, but also on the surrounding joints, muscles, and nerves. This process is called lumbar disc degeneration and can lead to several painful conditions.

Treatment of disc degeneration of the lumbar spine

Modern treatments

For most patients, non-surgical, or conservative, treatments will be effective in treating the symptoms of lumbar disc degeneration.Such treatment may include a combination of rest, physical therapy, pain relievers, or anti-inflammatories. If pain persists despite treatment, surgery is considered. Your doctor will explain the different types of treatment available to you, giving you all the information you need to make a decision.

Spinal fusion

The most common surgical treatment for lumbar disc degeneration is fusion, which involves removing the damaged and painful disc and replacing it with a bone graft.Over time, the bone graft connects to the vertebrae above and below the interbody space, resulting in two vertebrae fused into a single bone. The goal of fusion is to eliminate pain by blocking movement between two vertebrae and restoring the proper distance between them. Thus, spinal fusion can reduce or eliminate chronic lower back pain. However, in this case, movement and damping are also blocked in this segment, as a result of which the adjacent segments are further subjected to increased stress, which can accelerate degeneration (this condition is called “degeneration of discs at the level of adjacent vertebrae”).

Replacement of the disc of the lumbar spine with an artificial one

An artificial disc replacement has been developed as an alternative to fusion. The damaged disc is removed and replaced with an artificial disc. The purpose of the artificial disc is to restore the proper distance between the vertebrae and at the same time to maintain the mobility inherent in a healthy disc. This mobility can prevent disc degeneration at the level of adjacent vertebrae.

Mobility can prevent disc degeneration at the level of adjacent vertebrae

The M6-L artificial lumbar disc is an innovation in artificial disc replacement thanks to its unique design based on the properties of the natural disc.The M6-L is the only artificial disc with an artificial core (made of polycarbonate-urethane) and a fibrous ring (made of polyethylene). The design of the artificial nucleus and ring M6-L provides the same mobility characteristics as a natural disc. Large-scale biomechanical testing of an artificial disc of the lumbar spine M6-L demonstrated the quality of mobility equivalent to that of a healthy disc. Together, the artificial core and ring M6-L are compressive and provide a controlled amplitude of “natural” movement.This “natural” mobility is designed to give you the freedom to naturally move your back while minimizing stress on adjacent discs and other important spinal joints, and preventing or slowing disc degeneration at the level of adjacent vertebrae. The M6-L has two outer titanium plates with keels to reinforce the disc in the bone of the vertebral body. These outer plates are coated with plasma titanium sputtering, which stimulates bone growth into metal plates, which ensures long-term fixation and stability of the disc in the bone.

Artificial disc of the lumbar spine M6-L

What will happen during the operation?

Surgical treatment for disc replacement in the Zdorovye 365 clinic is carried out by Dubskikh A.O. neurosurgeon, the highest category.

The course of the operation to replace the disc of the anterior surface of the neck consists of several stages: First, the patient is made a small incision 3-4 cm long to access the cervical spine. The damaged disc will be removed (discectomy), releasing the pinched nerve (decompression).Then a special “artificial disc” implant is placed in the space occupied by the disc using special high-precision instruments. The purpose of the artificial disc is to restore the proper distance between the vertebrae and at the same time to maintain the mobility inherent in a healthy disc. After a special “artificial disc” implant is installed, the incision is sutured.

Disk deleted

Determining the size of the disk M6-L

Installation of artificial disc of the lumbar spine M6-L

Artificial disc of the lumbar spine M6-L installed

What can I expect after surgery?

After the operation, you will be in the clinic for 3 days.