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Pain dermatome. Understanding Radicular Pain and Dermatomes: Debunking Common Misconceptions

How do dermatomes relate to radicular pain. What are the limitations of using dermatome maps for diagnosis. Why is evidence-based practice crucial in treating radicular pain. How can practitioners better assess and treat patients with sciatica symptoms.

The Complexity of Back Pain and Radiculopathy

Back pain is a multifaceted condition with numerous potential causes and manifestations. One crucial distinction in diagnosing and treating back pain is the presence or absence of radiculopathy, commonly known as sciatica. Radiculopathy involves neurological symptoms that extend beyond the back, often affecting the legs and feet.

Radiculopathy symptoms can include:

  • Numbness
  • Tingling sensations
  • Pins and needles
  • Muscle weakness
  • Dull or sharp pain

The presence of radiculopathy often indicates a more complex condition, potentially involving nerve root compression or irritation. This can lead to a less favorable prognosis compared to uncomplicated lower back pain.

Dermatomes: Understanding Their Role in Diagnosis

In an attempt to localize and diagnose the source of radicular pain, practitioners often turn to dermatome maps. A dermatome refers to an area of skin innervated by a specific spinal nerve. These maps have been a staple in medical textbooks for decades, purportedly allowing clinicians to pinpoint the affected spinal level based on the distribution of a patient’s symptoms.

However, recent research has called into question the reliability of traditional dermatome charts. A 2019 study involving 93 patients with confirmed L5 and/or S1 nerve root irritation found that even experienced practitioners (including physiotherapists, medical doctors, and chiropractors) were only able to correctly identify the affected dermatome 50% of the time.

Limitations of Dermatome Maps

This study highlights several important limitations of relying too heavily on dermatome maps:

  1. Individual variability: Dermatomes can vary considerably between individuals.
  2. Overlap: There is significant overlap between adjacent dermatomes.
  3. Non-specific patterns: Radicular pain may not always follow the expected dermatomal pattern.

The Importance of Evidence-Based Practice in Treating Radicular Pain

Given the limitations of traditional diagnostic tools like dermatome maps, it’s crucial for practitioners to adopt an evidence-based approach to treating radicular pain. This involves staying up-to-date with the latest research and adjusting clinical practices accordingly.

Evidence-based practice in the context of radicular pain involves:

  • Recognizing the limitations of dermatomal patterns in diagnosis
  • Utilizing a comprehensive assessment approach
  • Considering multiple factors that may contribute to a patient’s symptoms
  • Adapting treatment plans based on individual patient presentations

Alternative Approaches to Diagnosing and Treating Radicular Pain

While dermatome maps may not be as reliable as once thought, they can still provide valuable information when used in conjunction with other diagnostic tools. Practitioners should consider a multifaceted approach to assessing and treating patients with suspected radiculopathy.

Comprehensive Physical Examination

A thorough physical examination should include:

  • Range of motion testing
  • Muscle strength assessment
  • Reflex testing
  • Sensory examination
  • Special tests specific to suspected pathologies

Advanced Imaging Techniques

In cases where clinical findings warrant further investigation, advanced imaging techniques may be employed:

  • Magnetic Resonance Imaging (MRI)
  • Computed Tomography (CT) scans
  • Electromyography (EMG)

These tools can provide more detailed information about the underlying causes of radicular pain, such as herniated discs or spinal stenosis.

Patient-Centered Care: Beyond Dermatomes

While understanding the anatomical basis of radicular pain is important, practitioners should prioritize a patient-centered approach to care. This involves considering the individual’s unique presentation, lifestyle factors, and treatment goals.

Key Components of Patient-Centered Care

  • Active listening to the patient’s description of symptoms
  • Educating patients about their condition and treatment options
  • Collaborating with patients to develop personalized treatment plans
  • Regularly reassessing and adjusting treatment as needed

Multimodal Treatment Approaches for Radicular Pain

Effective management of radicular pain often requires a combination of treatment modalities. These may include:

  • Physical therapy and targeted exercises
  • Manual therapy techniques
  • Pain management strategies (e.g., medication, nerve blocks)
  • Lifestyle modifications
  • Ergonomic adjustments
  • Psychological support for pain coping strategies

By employing a diverse range of evidence-based treatments, practitioners can address the multifaceted nature of radicular pain and improve patient outcomes.

The Future of Radicular Pain Diagnosis and Treatment

As our understanding of radicular pain continues to evolve, so too must our diagnostic and treatment approaches. Ongoing research is likely to yield new insights into the complex relationship between spinal pathology, nerve root compression, and symptom presentation.

Emerging Areas of Research

  • Advanced neuroimaging techniques for more precise diagnosis
  • Genetic factors influencing susceptibility to radicular pain
  • Novel pharmacological interventions targeting specific pain pathways
  • Regenerative medicine approaches for nerve repair and regeneration

As these areas of research progress, practitioners must remain committed to lifelong learning and continuous improvement in their clinical skills.

Empowering Patients in Their Recovery Journey

While the complexities of radicular pain can be challenging for both patients and practitioners, an informed and collaborative approach can lead to better outcomes. By educating patients about the nature of their condition and involving them in the treatment process, practitioners can foster a sense of empowerment and improve adherence to treatment plans.

Key Points for Patient Education

  • The variable nature of radicular pain and its symptoms
  • The limitations of traditional diagnostic tools like dermatome maps
  • The importance of a comprehensive, individualized treatment approach
  • The role of self-management strategies in long-term recovery

By providing patients with this knowledge, practitioners can help them become active participants in their own recovery process.

Conclusion: Embracing Complexity in Radicular Pain Management

The evolving understanding of radicular pain and its relationship to dermatomes underscores the need for a nuanced, evidence-based approach to diagnosis and treatment. While traditional tools like dermatome maps may have limitations, they can still provide valuable insights when used as part of a comprehensive assessment strategy.

Practitioners must remain adaptable, continuously updating their knowledge and skills to provide the best possible care for patients with radicular pain. By embracing the complexity of this condition and adopting a patient-centered, multimodal approach to treatment, healthcare providers can improve outcomes and enhance the quality of life for those suffering from radicular pain.

As research in this field continues to advance, it is crucial for both practitioners and patients to stay informed about new developments and emerging treatment options. By working together and leveraging the latest evidence-based practices, we can strive for more effective management of radicular pain and better overall spinal health.

Sciatic Pain and Dermatomes – Burlington Sports Therapy

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There are many different causes and types of back pain and there are many different structures in the spine that can become irritated and generate pain.

Radiculopathy (Sciatica)

One important distinction that might impact the course of recovery is whether there are any leg symptoms of a neurological nature.  The medical term we use to describe these symptoms is radiculopathy, but the more commonly-known term is “sciatica”.  Radiculopathy is normally characterized by symptoms of numbness, tingling, pins and needles, weakness and pain (dull or sharp).  As you can see, the symptoms can be quite variable!  Lower back pain without any signs or symptoms of radiculopathy typically has a more favourable course.  Lower back pain with an associated radiculopathy usually has a poorer prognosis.  For many people, the symptoms of radiculopathy are more uncomfortable than the lower back pain that is occurring.

Dermatomes and Dermatome Maps

When a patient presents with symptoms that extend from the lower back and down the leg, many practitioners become curious as to where in the leg or foot the symptoms are occurring.  This can give clues as to what nerve is involved and then we can determine what level of the spine may be at fault. Perhaps then the treatment can be more specific to the area of the spine that is causing the problem.

A dermatome is a medical term that we use for localizing these symptoms.  A dermatome refers to the area of the skin that the person is experiencing symptoms in a pattern that has been established as characteristic for a certain spinal level.  For decades medical and rehabilitation textbooks have dermatome diagrams that can help practitioners figure out what level of the spine is involved when a patient points to a certain distribution of symptoms.  Can these dermatome charts be trusted though?

An interesting 2019 study looked at 93 patients with radiculopathy. These patients had nerve root irritation affecting the L5 and/or S1 nerve roots (which is very common).  18 practitioners (6 physio, 6 MD and 6 chiropractors) examined the dermatome patterns in these patients and in the end, they were only correct 50% of the time!

Dermatomes can be used as an approximate at best.  Perhaps best to use it as a general idea for whether a patient has nerve root irritation or not.  It would not be supported by the evidence to use clinical symptom patterns in order to determine which spinal level is involved.  We can use dermatomes to help assist us in knowing whether a person has radiculopathy, but we can’t confidently tell a patient at what specific level of their spine may be the cause since there is a lot of variability.  The good news is that under most circumstances it shouldn’t impact a practitioner’s ability to provide evidence-based care and assist the patient in overcoming their pain.

Evidence-informed Practice

At Burlington Sports Therapy we pride ourselves on being evidence-informed practitioners. Through an effort to keep abreast of the best available literature, we strive to provide better treatment and give better recommendations to our patients.  Perhaps contrary to what we were taught in school, newer research has shed light on the reliability of the traditional dermatome charts. They are not useless, but perhaps we can say that there’s a lot of overlap in dermatomes. Dermatomes vary considerably among different people and radicular pain may not follow these dermatomal patterns.

If you’re experiencing lower back pain, please give us a call, we can help!

By Dr. Kevin McIntyre B.Kin., DC

 

References

Albert HB, Hansen JK, Sogaard H & Kent P. Where do patients with MRI-confirmed single-level radiculopathy experience pain, and what is the clinical interpretability of these pain patterns? A cross-sectional diagnostic accuracy study. Chiropractic & Manual Therapies 2019; 27: 50.

Murphy DR, Hurwitz EL, Gerrard JK, Clary R. Pain patterns and descriptions in patients with radicular pain: does the pain necessarily follow a specific dermatome? Chiro Osteopath 2009; 17:9.

Taylor CS, Coxon AJ, Watson PC, Greenough CG. Do L5 and S1 nerve root compressions produce radicular pain in a dermatomal pattern? Spine 2013; 38(12): 995–8.

 

 

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3 Truths University didn’t tell you about Radicular Syndrome

May 9, 2020
  |  6 min read

I’m sure a lot of students and therapists out there have learned that radicular pain and radiculopathy follow a dermatomal distribution. But is that really true and exactly like we have learned it from textbooks?
First of all, let’s distinguish between radicular pain and radiculopathy. Even though “radicular pain” and “radiculopathy” are synonymously used in the literature, they are not the same. Radicular pain is defined as “pain evoked by ectopic discharges originating from a dorsal root or its ganglion”. It’s the neuropathic, electric pain that patients feel shooting down the leg.

Radicular syndrome is the umbrella term for radicular pain (pain originating from the radix) and radiculopathy (conduction block along a spinal nerve or root)

Radiculopathy is yet another, distinct entity. It is a neurological state in which conduction is blocked along a spinal nerve or its roots (Bogduk et al. 2009). This leads to objective signs of loss of neurologic function such as sensory loss called hypoesthesia or anesthesia in the severe form, motor loss called paresis or atrophy in the severe form, or impaired reflexes called hyporeflexia or areflexia if they are completely absent. If radicular pain or radiculopathy or both are present, we are talking about radicular syndrome, which is an umbrella term.

Does radicular pain follow a dermatomal pattern?

Okay, so now let’s see if radicular pain follows a dermatomal pattern. A study by Murphy et al. (2009) observed pain patterns in patients with radicular pain and found the following:

Radicular pain in the cervical spine followed a dermatomal distribution in only 30% of cases, while in the lumbar spine, it was slightly better with 36%. Now let’s look at specific dermatomes separately.

For the cervical levels, only C4 seems to be more or less reliable with 60% – although we have to be careful with the interpretation here as there were only 2 patients with an affected nerve root at C4. All other levels do not seem to be reliable.

It doesn’t get much better for the lumbar spine:

It seems that only level S1 might be more or less reliable with 65% of patients with an S1 nerve root compression reporting pain in the dermatomal distribution of S1. All other levels did not follow a dermatomal distribution regularly. It has to be said though that Murphy and colleagues included patients with multi-level disease, which probably decreased the reliability a bit. Another, more recent study by McAnany et al. (2019) observed pain patterns in cervical radiculopathy. They found that only 54% fit the regular dermatome pattern described in the Netter anatomy book. In the non-standard distribution, dermatomal levels differed by 1.68 levels either cranially or caudally from the standard.

Radicular pain only seems to reliably follow a dermatomal distribution in nerve roots C4 (60%) and S1 (65%)

How reliable are dermatomes, myotomes, and reflexes?

Okay, so if radicular pain is not reliable and mostly reported as a shooting, electric pain along the whole distribution of the arm or the leg – how reliable are our dermatomes, myotomes, and reflexes?

A study by Rainville et al. (2017) compared sensory changes and weakness in patients with C6 and C7 radiculopathy. They concluded that these symptoms have limited value to differentiate between the two levels. Al Nezari et al. (2013) performed a meta-analysis to see if a peripheral neurological examination is able to diagnose the level of lumbar disc herniation. They state that sensory, motor, and reflex testing all had a low sensitivity, moderate specificity, and limited diagnostic accuracy to determine the level of disc herniation. So while a neurological examination may help to confirm the presence of radicular syndrome and to assess hypofunction to establish a baseline and to monitor treatment progress, it cannot determine the affected level of nerve root compression.

Now, what is the reason that our dermatome maps are so unreliable? The literature mentions several possibilities. First, there is huge variability in the brachial and lumbosacral plexus. If we look at cadaver studies for the brachial plexus, a typical textbook anatomy of the brachial plexus was only found in 37-77% of cases. Two major variations are described in the brachial plexus:

Figure from Sakellariou et al. (2014)

We are talking of “prefixation” when nerve root C4 contributes considerably to the plexus and T1 does not or only minimally. This variation has a prevalence of between 26-48%. The second variation is called “postfixation”. This is the case if there is only little or no contribution from C5 and considerable innervation from T2. This variation is present in 4% of the population. A prefixation or postfixation can shift the observed pattern of cervical radiculopathy cranial or caudal depending on the anatomic variant present.

A second reason is that intradural connections of rootlets in more than 50% of cadavers are found by C5 and C6 and C6 and C7. Such a connection between rootlets of different nerve roots is called anastomosis.

Third, textbooks commonly used in medical health programs contain multiple, conflicting dermatome maps. On top of that, the seminal basis that formed dermatomal maps is flawed in various ways. For example, the map created by Garrett and Keegan in 1948 has never been confirmed by follow-up studies up to this day, yet this map is mostly used in textbooks. Lee et al.(2008) evaluated the literature and created a composite dermatome map based on published data from 5 papers they considered to be the most experimentally reliable. Their map looks like this, which might be a bit different from what you and we have learned at school:

Okay, let’s summarize: So neither radicular pain nor radiculopathy seem to follow a strict dermatomal pattern of maps we have learned in school. So with our clinical examination, we’re probably not able to determine which nerve root is affected. At the same time, this information is probably way more important for surgeons than for us as physiotherapists. If someone is suffering from radicular symptoms coming from L5 or S1 won’t probably change our management strategy in any important way. You may want to continue doing your neurological assessment to confirm radiculopathy and to evaluate the degree of hypofunction. At the same time keep in mind the high degree of anatomical variation and that predicting the affected level is impossible.

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Alright, we hope this answered the question thoroughly. Comment down below if you were surprised about the actual evidence and if you have any further questions. A lot of this information and much more can be found in our online course on the spine.

Thanks a lot for reading!

Kai

Physiotutors started as a passionate student project and I’m proud to say it has evolved into one of the most respected continuing education providers for physiotherapists around the globe. Our main goal will always remain the same: to help physiotherapists make the most out of their studies and careers, enabling them to provide the best evidence-based care for their patients.

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Pathophysiological basis of pain syndrome in childbirth

Pain as an integrative function of the body mobilizes a wide variety of functional systems to protect the body from the effects of harmful factors and includes emotional, motor-vegetative and humoral manifestations, in general, identical stress responses to adverse effects [1, 2 ]. Disclosure of physiological links that provide a variety of signs of pain is carried out through the study of the central and peripheral structures of the nervous system involved in the perception, transmission and analysis of pain stimuli, as well as by studying the mechanisms that regulate the flow of pain impulses to the brain [3].

The neurophysiology of labor pain is represented by a complex multi-neuron reflex arc, the main links of which, like any other type of pain, can be represented by the following triad: impulsation resulting from irritation of peripheral nociceptors; the reaction of the central structures of the brain to receive the appropriate impulses; efferent response, which is a combination of emotional, vegetative and motor reactions. Thus, the nervous system, reacting to a damaging effect, is essentially a transport highway through which afferent information flows from the focus of damage to the centers of pain sensitivity of the spinal cord and brain, and each of its levels is characterized by a certain component of the pain reaction [4]. In the phenomenon of labor pain, two components of pain sensitivity are conventionally distinguished: visceral and somatic.

Visceral component of pain response

Visceral pain occurs early in the first and second stages of labour. The contractile activity of the uterus and the opening of the cervical canal play a leading role in the occurrence of visceral pain. There is evidence from J. Bonica and H. Chadwick [5] that manual palpation of the body of the uterus during caesarean section under local infiltration anesthesia was not accompanied by labor-like pain [5]. At the same time, manual impact on the cervix in women during caesarean section reproduced labor pain. It is possible that sensitization of cervical afferent fibers before and during childbirth can cause pain in the first stage of labor, in contrast to Bregston-Hicks contractions (false, rehearsal), which appear towards the end of pregnancy and are not accompanied by them [6, 7]. However, prior sensitization of these nociceptors appears to be necessary to make them sensitive to uterine contractions [8] and to increase signaling to the dorsal horn of the spinal cord [9]. An indicator of sensitization during childbirth is hyperalgesia, which occurs in response to mechanical stimulation of the skin of the lower abdomen, resulting in a total convergence of impulses coming from the ends of afferent fibers of both the skin of the lower abdomen and the cervix [10].

With each contraction of the uterus, pressure is transferred to the lower uterine segment and cervix, causing them to stretch and dilate, simultaneously activating baro- and mechanoreceptors [11]. Active labor activity is characterized by activation of baro- and mechanoreceptors with a high threshold of excitability. The increase in perceived pain intensity commonly seen with the progression of contractions may in part be due to the lowering of the nociceptor response threshold caused by repeated stimulation as a result of uterine contractions. In addition, a number of substances released during rupture of myometrial cells during repeated uterine contractions lead to stimulation of chemoreceptors. These released substances include bradykinin, histamine, serotonin, acetylcholine, potassium ions, and substance P [12]. Myometrial ischemia due to contraction of uterine arteries is another mechanism in these cellular responses [13, 14].

The resulting afferent impulse is transmitted through thin unmyelinated C-fibers, which, as part of sympathetic fibers, pass through the paracervical zone, upper, middle, and lower hypogastric nerve plexuses, getting into the lower thoracic and lumbar sympathetic trunk [15, 16]. Pain fibers from the sympathetic trunk, passing through the white connecting branch associated with the spinal nerves from Th x to L I , as part of the posterior roots, are sent to the posterior horns of the spinal cord, ending in a synapse on the cells of the second neurons. Repeated afferent impulses cause increased sensitivity of the second neurons in the dorsal horn, central sensitization, which leads to an increase in signal transmission in the ascending pathways [17]. It is believed that the parasympathetic innervation of the uterus is of little importance in the transmission of uterocervical pain [11].

Irradiation of pain along C-fibers is ensured by the presence of a wide synaptic connection between the C-fibers themselves and the possibility of direct transmission of excitation to neighboring axons due to the crossing of some of the fibers at the level of the posterior horn. Such a wide diffusion during the conduction of a pain impulse is typical when it comes from the visceral organs (P. K. Anokhin, 1962). This phenomenon explains the fact that women in labor describe this pain as dull and poorly localized (diffuse feeling of pain) and not always sensitive to opioids.

At the beginning of the first stage of labor, pain correlates with dermatomes * Th XI and Th XII . By the end of the first period, the pain spreads to the dermatomes Th x to L I . Thus, pain sensations are localized in the lower abdomen, sacrum and back.

Somatic component of pain response

Somatic pain occurs in addition to visceral pain at the end of the first stage of labor, reaching a maximum in the second period. It is associated with irritation of the endings of the afferent nerves that innervate the vaginal part of the cervix, perineum and vagina, as a result of tension and stretching of the uterine ligaments and peritoneum, pressure on bone structures, ligaments of the pelvis, stretching, ischemia and trauma to the pelvic floor, perineum and vagina. In addition, contraction of the ganglia adjacent to the cervix and lower part of the uterus is believed to cause additional nociceptive input during the end of the first and beginning of the second stages of labor [18]. The somatic component manifests itself during the “lowering” of the presenting part of the fetus to the pelvic floor against the background of increasing regularity and intensity of contractions.

Somatic pain is transmitted by myelin Aδ fibers, which provide a high speed of nerve impulse conduction. Transmission of impulses occurs through the pudendal nerve and perineal branches of the posterior cutaneous nerve of the thigh to the spinal cord at the level of segments S II -S IV . Somatic fibers from the skin branches of the ilioinguinal and femoral-genital nerves also carry afferent impulses to segments L I and L II .

In the second stage of labor, in addition to the areas already captured, the pain extends to the upper part of the lower extremities and is felt as pressure on the lower back and perineum. At the end of the second stage of labor, somatic pain is acute and clearly localized in the vagina, rectum, and perineum. It radiates to adjacent dermatomes Th x and L I and is more resistant to opioids compared to visceral pain.

One of the main substrates of intracentral interaction in the posterior horns of the spinal cord is the gelatinous substance (lamina II), which lies in the path of the afferent canals and receives collaterals from most afferent fibers (visceral and somatic). It is assumed that the neurons of the gelatinous substance control the interaction of visceral and skin afferent flows, which is directly related to the mechanism of referred pain [19].].

After initial processing in the gelatinous substance, the stimuli are transmitted by the interneurons of the spinothalamic tract to the thalamus, where all ascending nociceptive pathways form synapses as they move to the brain. In the thalamus, information is redistributed to the somatosensory cortex, which performs spatiotemporal and sensory-descriptive analysis of pain, taking into account its location, intensity, and duration [20]. An important role is played by the relationship of the thalamus with the limbic system involved in the implementation of the affective-emotional aspect of pain, and the prefrontal cortex of the brain, which is considered the most important area for the cognitive-rational assessment of pain (decision making, differentiation of conflicting thoughts and motives, differentiation and integration of objects and concepts , concentration of attention on the necessary objects) [21, 22]. Both the prefrontal and limbic regions are involved in the regulation of mood and anxiety symptoms, and activation of these regions may enhance the perception of pain [23]. The transmission of impulses through the spinoreticular tract to the reticular formation of the brain contributes to the activation of motor, autonomic and sensory functions, causing excitation and the emotional component of pain.

The basis of the stated concept of pain are theories of specificity and intensity regimen. Nevertheless, pain remains a complex phenomenon, the definition and mechanisms of which have undergone various changes in medicine over the years [24].

Theories of pain

Thus, R. Melzack and P. Wall [25] put forward the theory of the “entrance gate”, according to which an important role in the entry of pain impulses into the CNS through fibers of various types belongs to feedback mechanisms localized in the gelatinous substance of the dorsal horns of the spinal cord. Excitation of thick sensory fibers (Aα and Aß) during stimulation closes the “gates of pain”, while exposure to thin fibers (Aδ and C) opens the “gates” [25].

Subsequently, R. Melzack [26, 27] transformed the concept of the “entrance gate” into the neuromatrix theory. Viewing the brain as the ultimate mechanism for evaluating certain characteristics of pain, it takes into account the confluence of multiple factors, including past experience, cultural background, emotional state, cognitive information, stress management, and the immune system, in addition to the most negative sensory input.

Numerous components of the neuromatrix that determine the perception of pain are produced by three parallel networks: sensory-descriptive (somatosensory components), affective-motivational (components of the limbic system) and evaluative-cognitive (thalamocortical components) [26]. The model also takes into account the additional influence of the neuroendocrine, autonomic nervous system and the modulation of the immune system. Synaptic inputs to these networks can be either phasic (short bursts such as cutaneous sensory input or attention span) or tonic (longer modulating signals such as cultural baggage and past experience). The summation of the three parallel processes forms a personal perception of pain and a “program of action”, including conscious and unconscious strategies for dealing with pain, used by a woman in childbirth.

It should be noted that the contradictions in the mechanisms of pain have become the subject of research in several directions, not only by pathophysiologists, but also by clinicians who are constantly faced with the problem of pain in their daily work. Among the main directions, one can distinguish the development of neurochemical studies of the neurotransmitter mechanisms of pain, the study of the role of opioid receptors and endogenous morphines, as well as the central structures in the implementation of the pain response.

Pain control mechanisms

At present, there is no doubt about the polyneurochemistry of the nociceptive and antinociceptive systems of the brain, which can be considered as one of the leading factors that ensure the reliability of integral pain integration. An important role is played by neurotransmitters (acetylcholine, norepinephrine, serotonin), as well as calcitonin-gene-related peptide and substance P, each of which is associated with the provision of certain components of the psychophysiological phenomenon of pain [28, 29].

Another important structure of pain modulation is the central periaqueductal gray matter of the brainstem (CPGR). Most of the opioid-induced antinociceptors originate from this structure, and the same site is the main one for descending inhibitory pathways [30]. Receiving nociceptive impulses from the posterior horns of the spinal cord, the CSVM is bilaterally connected to the hypothalamus, frontal cortex, and amygdala, areas responsible for the control of emotions, in particular, anxiety and fear, which may explain the effect of emotions on the modulation of pain perception [31].

Stimulation of the periwire gray matter activates enkephalin-releasing neurons located in the raphe nuclei of the brainstem. Serotonin released from the raphe nuclei, reaching the posterior horn of the spinal cord, forms synapses with “inhibitory interneurons” located in the II plate (gelatinous substance). When activated, these interneurons release endogenous opioid neurotransmitters that bind to μ-opioid receptors on the axons of C- and Aδ-fibers that carry pain signals from peripherally activated nociceptors. Activation of μ-opioid receptors inhibits the release of substance P from first-order neurons and, in turn, inhibits the activation of second-order neurons, which are responsible for the transmission of pain signals along the spinothalamic tract to the ventral posterolateral nucleus of the thalamus. Thus, the nociceptive signal is suppressed before it can reach the cortical areas that interpret the signals as “pain” [32].

It is also necessary to note the significant role of opioid receptors and endogenous morphines in the regulation of pain sensitivity as neurotransmitters and neuromodulators of the nociceptive and antinociceptive systems of the brain. According to studies [33], receptive fields in posterior horn neurons are dynamic and can change the frequency of pain impulse transmission to the brain in response to changes in stimuli, neurotransmitters, and neuromodulators.

The analgesic properties of β-endorphins in the relief of labor pain were evaluated by T. Oyama et al. [34]. The study included 14 women in labor (7 primiparous and 7 multiparous), who, when the cervix was dilated by 3.5—5 cm, subdurally at the level of L III —L IV 1 mg of synthetic β-endorphin was administered. The authors demonstrated a fast (onset of action after 3.5±0.5 min) and long-term (mean duration 18.8±1.6 h) analgesic effect of the synthetic analog. At the same time, its administration did not affect labor activity and the intrauterine state of the fetus.

The results of studies have shown a progressive increase in the concentration of ß-lipotrophin, ß-endorphin and γ-lipotrophin in the mother’s blood to a maximum by the 32nd week of pregnancy [35]. An increase in the concentration of endogenous peptides during pregnancy may be one of the factors responsible for the decrease in the sensitivity of pregnant women to local and general anesthetics. The minimum alveolar concentrations of halothane and isoflurane decrease in pregnant women by 25% and 40%, respectively [35]. Thus, an increase in the concentration of peptides should be considered as an endogenous protective mechanism that is activated against the background of progressing pregnancy and has a regulatory effect on pain during childbirth.

Currently, the ability of oxytocin to modulate pain and induce analgesia is of increasing scientific interest, which is confirmed by a number of clinical studies [36-38]. S. Gutierrez et al. [39] demonstrated that pain and hypersensitivity caused by peripheral nerve injury regress faster in rats if it occurs shortly before delivery, and subarachnoid administration of oxytocin (into the cerebrospinal fluid) induces antihypersensitization, which can be counteracted by an oxytocin receptor antagonist. The considered protective mechanism reflects the delay in oxytocin signaling at the level of the spinal cord in the postpartum period [39].

Acting on the central and peripheral nervous system, oxytocin directly reduces the activity of spinal neurons that receive sensory information [40], excites interneurons in the spinal cord that inhibit gamma-aminobutyric acid (GABA-interneurons) [41, 42], reduces Aδ/C -afferent ascending nociceptive impulsation [42]. Additional mechanisms include the involvement of endogenous opioid [43] and cannabinoid [44] systems modulating pain perception. Subarachnoid injection of oxytocin in rats with symptoms of inflammation caused an antinociceptive effect by activating oxytocin receptors, as well as μ- and κ-opioid receptors involved in oxytocin-induced somatic analgesia at the spinal level [45]. In addition to somatic analgesia, subarachnoid administration of oxytocin can also be an effective pharmacological treatment for visceral pain by inhibiting nociceptive responses to acute bladder irritation [46].

In addition, Z. Tan et al. [47] revealed a biphasic effect of oxytocin: low doses of oxytocin increase GABA-activated fluxes leading to suppression of primary sensory transmission, while its higher doses decrease presynaptic inhibition of GABA interneurons. These results are consistent with a recent study by P. Juif and P. Poisbeau [48], which showed that intravenous injections of low doses of oxytocin induced oxytocin-mediated antinociception, while its higher doses induced vasopressin-V1A-mediated nociception in male rats.

The presented new data on the ability of oxytocin to modulate the pain response and induce oxytocin-induced analgesia seem to be a promising scientific direction that requires further study of specific mechanisms for the realization of these effects both at the spinal and supraspinal levels, which may open up new possibilities for the use of low doses of oxytocin as an anesthetic.

Thus, the modern understanding of the neurophysiological mechanisms of pain is based on the existence of specific pain afferent systems in the brain, consisting of certain types of fibers and specialized groups of nerve cells in the spinal cord and brain stem. The brainstem contains neuronal systems (serotonin-, endorphin-, dopamine- and noradrenergic) that regulate the sensitivity of various levels of pain afferent systems in a synaptic and neurohumoral way. Therefore, understanding the pathogenesis of labor pain as a multidimensional process provides the basis for a differentiated patient-oriented approach to its management, which includes a wide range of pharmacological and non-pharmacological methods.

The authors declare no conflict of interest.

* dermatome — area of ​​skin innervated by nerve fibers of one dorsal nerve root.

Shoulder pain and its causes

Shoulder pain is a very common condition. The complex structure of the shoulder with its complex muscle control system, complex structure of nerve endings and close proximity to the cervical spine – all of these factors can somehow be associated with the appearance of pain in the shoulder.

It is not always easy for even a very experienced expert to determine which structure is responsible for pain symptoms. Patients presenting for care with very similar symptoms have very different disease patterns. So, for example, one patient may have a herniated disc in the lower cervical region, while another may suffer from calcification of the tendons of the shoulder. The third patient, who was diagnosed with arthrosis of the shoulder joint, may experience the same pain symptoms as the first two. It takes a great deal of experience, ideally combined with the ability to use X-ray and ultrasound images, to make a correct diagnosis.

Pain at the side of the shoulder

Many patients who come to us complain of pain outside the shoulder, often slightly below the actual location of the shoulder joint. These patients suggest that they have a problem with the muscles in the upper arm, rather than a disease of the shoulder. Many are surprised that the root cause of the pain is precisely the violations in the shoulder area, and the pain in the arm is already an “echo” of these violations. Using simple methods, such as simple palpation of the shoulder and forearm, one can find confirmation of the assumption that this area is still the cause of pain. On palpation of the shoulder, we usually find pain points in the area of ​​the head of the humerus and the acromial process of the clavicle, and not where the pain is usually localized, i.e. well below the shoulder.
Pain in the side is often caused by a disease of the tendons and periarticular sac, as, for example, occurs with calcification and impingement syndrome.

Schm Pain in the upper part of the shoulder

Pain in the upper part of the shoulder with a possible “echo” in the back of the head is often associated with the acromioclavicular joint. And here, with the help of simple palpation, preliminary conclusions can be drawn about whether the guess regarding the diagnosis is correct. Diseases of the acromioclavicular joint often cause the joint to swell and enlarge. Since the acromioclavicular joint is not covered with muscles, this can be very well felt when probing. The presence of swelling or enlargement is a direct indication of the cause of the pain. Soreness on palpation over the joint also indicates a disease of the acromioclavicular joint.

Pain in the front of the shoulder indicates a disease of the anterior joint capsule and long tendons of the biceps muscle. Pain symptoms associated with wear and tear of the main shoulder joint (glenohumeral joint) often appear in this area as well.

Pain in the cervical spine or degeneration of the intervertebral discs /strong>
As already mentioned, diseases of the cervical spine and, in particular, degeneration of the intervertebral discs in the cervical spine can also cause pain. Due to the pressure of the disk on the nerve passing into the arm, pain spreads. The figure on the left shows the dermatomes of the cervical spine in the area of ​​the shoulder.