NEUROLOGY AND NEUROSURGERY - Y. V. ALEKSEEΝKO - 2014

VERTEBROGENIC DISORDERS OF THE NERVOUS SYSTEM

It is known that 60% to 90% of people experience at least one episode of lower back pain during their lifetime. Cervical and thoracic pain syndromes are less common. In the United States, low back pain is the fifth most frequent reason for a physician visit (following arterial Hypertension, Pregnancy, routine medical check-ups, and acute upper respiratory infections). Low back pain is the second most common cause of absenteeism in many countries, with vertebrogenic neurological disorders accounting for approximately 25% of all lost workdays. Currently, due to vertebrogenic disorders, about 1% of the population in many economically developed countries has a temporary work disability, and another 1% suffers from chronic disability. A similar situation is observed in various regions around the globe.

The high prevalence of neck or back pain, coupled with a wide spectrum of potential causes, gives this issue a complex, interdisciplinary character. Neurologists, neurosurgeons, general practitioners, urologists, nephrologists, rheumatologists, traumatologists, orthopedists, and surgeons actively participate in the examination and Treatment of such patients. At various stages, assistance is provided by specialists in manual therapy, physical therapy, therapeutic exercise, medical rehabilitation, etc. This clinical problem falls within the purview of primary care providers, general practitioners, and emergency medicine physicians. This is explained not only by the high prevalence of such disorders but also by The Need for broad clinical training to rule out a multitude of systemic pathologies and other pain syndromes caused by trauma, as well as other urgent and life-threatening conditions.

Spinal osteochondrosis (SO) is traditionally regarded as the most frequent cause of neck or back pain. However, only a fraction of individuals with signs of SO develop diverse neurological manifestations of this condition. A major contribution to The Study of neurological complications of SO was made by Belarusian neurologists and neurosurgeons under the leadership of Academician I. P. Antonov — A. F. Smeyanovich, B. V. Drivotinov, G. K. Nedzved, V. Ya. Latysheva, and others.

Etiology AND Pathogenesis of Vertebrogenic Nervous system Disorders

One of the most widespread causes of vertebrogenic nervous system disorders is spinal osteochondrosis (SO). SO is a chronic pathological degenerative-dystrophic process characterized by lesions of the intervertebral discs, as well as reactive Changes in the adjacent vertebrae and the Ligamentous apparatus of the spine. This disease cannot be explained solely by the natural Aging processes of the spine, although the age factor does play a certain role. Neurological manifestations of SO are most commonly detected in middle-aged individuals, i.e., those in their most active years. SO is a multifactorial disease in which the combination of triggering and etiological factors may vary for each patient, yet the mechanisms of its development share a fairly general, stereotypical pattern.

In many cases, The Development of SO can be linked to heavy physical labor, trauma, and excessive physical exertion. Unbalanced physical activity against the Background of a sedentary lifestyle poses a serious threat. Particularly hazardous are heavy lifting, prolonged static loads involving bending and twisting of the torso, and the repeated performance of stereotypical motor tasks. The chronic impact of vibration (working with a jackhammer, driving vehicles) is also of certain significance. The medical history of many patients reveals Structure/19.html">The Importance of repeated macro- and microtraumas of the spine resulting from falls, sudden axial loads, jumping from heights, or occurring during certain sports activities. The absence of bone changes on spondylography in such cases does not rule out damage to the Connective Tissue structures of the spine and paraspinal Muscles, which inevitably leads to altered biomechanics and the overload of individual segments. Also significant are abnormalities in spinal biomechanics caused by Developmental Anomalies and various anthropometric features (Scoliosis, Kyphosis, Spina bifida occulta, transitional vertebrae, limb length discrepancy, etc.). A particularly heavy load falls on the cervical and lumbar spine; therefore, degenerative-dystrophic processes develop most intensely in these regions. It should be noted that many metabolic and hormonal abnormalities contribute to changes in the hydrophilicity, elasticity, and strength of the discs and ligaments, thereby provoking or aggravating the development of SO. A certain role is also played by the fact that by the age of 20, the Blood Vessels supplying the intervertebral discs become obliterated, and thereafter, metabolic processes within them are sustained through the diffusion and osmosis of oxygen and nutrients. Over time, this makes the disc tissue more vulnerable to various pathological influences. In some circumstances, damage to the tissue elements of the disc may be accompanied by the development of autoimmune reactions which, along with constant mechanical stress, maintain inflammatory and degenerative-dystrophic processes.

Thus, under METABOLISM/18.html">The Influence of excessive loads, trauma, and other adverse factors, intervertebral discs may lose their elastic and Shock-absorbing properties. This results in a reduction of disc height, impaired fixation strength of adjacent vertebrae, and increased mobility of the affected spinal segment (instability). Protrusion of the disc walls sideways (disc protrusion) develops, and even disc herniation may occur when tears in the fibrous ring lead to the expulsion of Nucleus pulposus fragments (disc prolapse), including into the lumen of the spinal canal. Sometimes disc herniations penetrate not into the spinal canal, but vertically — through the hyaline Cartilage plate into the vertebral body (Schmorl's nodes). SO is accompanied by The formation of osteophytes — growths at the marginal areas of the vertebral body endplates, with posteriorly directed osteophytes projecting into the spinal canal posing a particular danger. Fixation disorders in the affected spinal segments can be partially compensated by reflex tension in the paraspinal muscles. Over time, excessive mobility of the spinal segments decreases due to the development of widespread fibrosis and the formation of spondylarthritis. However, immobilization of the affected spinal segment usually leads to the overloading of adjacent segments, thereby triggering a gradual spread of similar degenerative-dystrophic changes to them.

Degenerative-dystrophic changes of the spine can be widespread. At the same time, they are frequently an incidental finding during X-ray or MRI examinations of the spine. It must be emphasized that only a subset of patients with signs of SO develop painful neurological complications. The risk of damage to spinal nerve roots, the Spinal Cord, and the blood vessels supplying these structures arises under such circumstances due to the development of posterior and posterolateral osteophytes, disc protrusions, spondylolisthesis, Hypertrophy of the posterior longitudinal or yellow ligaments, etc. Recently, pathological conditions associated with a generalized reduction in the lumen (narrowing) of the spinal canal accompanied by vasoneurological disorders have commonly been referred to as Spinal stenosis.

As a rule, the aforementioned pathological factors cause irritation or compression of the nerve roots and their blood vessels, which is reflected in the terminological definition of this group of neurological disorders: compression radicular syndromes of SO. However, the factor of direct mechanical compression in THE ORIGIN OF vertebrogenic pain syndromes should not be overestimated. In addition to direct compression of roots and vessels by a disc herniation, other Causes and Mechanisms of their involvement in the pathological process may occur: associated aseptic inflammation, edema, venous congestion, and ischemia in the connective and soft tissue formations of the spine in the immediate vicinity of neural structures. The triggering factor in the development of initial clinical manifestations of the disease or an exacerbation may be the stretching or tearing of ligaments, fibrous and cartilaginous disc elements, or local vascular, inflammatory, or allergic disorders. Nevertheless, it should be noted that the likelihood of developing vertebrogenic (especially chronic pain) neurological disorders is also strongly associated with the action of several other nonspecific factors — excess weight, smoking, depression — and increases significantly against the backdrop of Various Forms of psychosocial maladjustment.

In light of modern concepts regarding The Nature of vertebrogenic nervous system disorders, pain may be caused not only by direct or indirect irritation of individual spinal roots and other neural structures, but also by damage to numerous adjacent anatomical structures and the simultaneous engagement of various pain-generation mechanisms. Thus, the causes of pain in the neck or back region may include injuries to the Skin and subcutaneous tissue, joint capsules and articulations, ligaments, periosteum, dura mater and epidural adipose tissue, arterioles and Veins, and paraspinal muscles. Therefore, considering the entire spectrum of potential pathogenetic mechanisms of SO pain manifestations, alongside the typical neuropathic radicular pain syndrome, it is customary to distinguish discogenic, spondylogenic, vasogenic, and myogenic pain syndromes. Differentiating them based on an analysis of Complaints, objective clinical manifestations, and instrument-based examination results remains extremely difficult and is accomplished largely empirically, which largely explains the well-known challenges in selecting individualized effective Pathogenetic Therapy and successful Prevention of vertebrogenic disorders.

Taking into account leading pathogenetic mechanisms and the nature of neurological disorders, it is customary to distinguish reflex, as well as radicular and radiculovascular (compression) neurological manifestations of SO. Neurological disorders can develop at the cervical, thoracic, and lumbosacral levels of the spine. All elements of the spinal Column possess robust sensory innervation; therefore, even in the Cytology/cytology/16.html">Early stages of SO following trauma or hazardous physical exertion, pronounced pain syndromes involving segmental structures of the spinal cord may occur in various Regions of the neck, back, or lower back. Pain may radiate to the arm or leg. It is accompanied by reflex tension of the paraspinal muscles, scoliosis, and signs of Autonomic nervous system irritation. Due to the pain, There is a marked limitation of movement in the spine, shoulder girdle, or Pelvic Girdle. Palpation of soft Tissues at the level of the affected segments typically reveals tenderness at paraspinal points. So-called nerve trunk tension signs (Lasegue, Wasserman, Matzkiewicz, etc.) may be elicited. When reflex pain syndromes of SO develop, signs of spinal cord ROOT damage (Muscle weakness, loss of tendon-periosteal Reflexes) are not detected. At the same time, symptom complexes of root damage, alongside muscular-tonic disorders and tension signs, typically manifest with clear sensory (primarily pain-related), reflex, motor, and autonomic disorders within the corresponding radicular innervation zone. It must be remembered that the appearance of long-tract sensory disturbances, signs of lower paraparesis, or pelvic organ dysfunction indicates spinal cord involvement.

Classification of Vertebrogenic Nervous System Disorders

The following variants of vertebrogenic nervous system disorders are distinguished (I. P. Antonov et al., 1987):

Cervical Level

   Reflex syndromes

   ■ Cervicalgia

   ■ Cervicocranialgia

   ■ Cervicobrachialgia with muscular-tonic, vasoneurological, or neurodystrophic manifestations

   Radicular syndromes

■ Discogenic (vertebrogenic) root lesions

Radiculovascular syndromes

■ Radiculoischemia, myeloradiculoischemia

Thoracic Level

   Reflex syndromes

   ■ Thoratalgia with muscular-tonic, vegetative-vascular, or neurodystrophic manifestations

   Radicular syndromes

■ Discogenic (vertebrogenic) root lesion

Lumbosacral level

   Reflex syndromes

   ■ Lumbago

   ■ Lumbalgia

   ■ Lumboischialgia with muscular-tonic, vegetative-vascular, or neurodystrophic manifestations

   Radicular syndromes

■ Discogenic (vertebrogenic) root lesion

Radicular-vascular syndromes

   ■ Radiculoischemia, myeloradiculoischemia.

The term "vertebrogenic" refers to degenerative-dystrophic changes in the spine (osteochondrosis) as the primary cause of neurological disorders. The term "discogenic" has a narrower meaning, emphasizing that the neurological symptoms are caused by a herniated intervertebral disc.

Vertebrogenic neurological disorders at the cervical level

Reflex syndromes of cervical osteochondrosis manifest primarily as pain. Patients experience aching neck pain, sometimes intense but more often moderate, radiating to the back of the HEAD or the shoulder girdle (cervicalgia, cervicobrachialgia, cervicocranialgia). Movements typically provoke shooting sensations and an intensification of pain. Pain is frequently exacerbated by maintaining a monotonous, prolonged position of the neck and head, by an awkward sleeping position on a pillow, or while sitting at a desk. Discomfort may be discovered in the morning upon waking, or it may arise suddenly after an awkward movement in the neck or shoulder girdle, though it can also develop gradually. There is a restriction of neck mobility in one direction, along with painful tension in the cervical muscles and tenderness upon palpation of the spinous processes of certain cervical vertebrae. Quite often, painful tension is found not only in the Posterior muscle group, but also in the anterior scalene muscle and other muscles.

Some patients may exhibit tenderness in the periarticular Tissues of the shoulder joint with restricted mobility (scapulohumeral periarthrosis). At the same time, shoulder movements in the sagittal plane may remain relatively free, while abduction is significantly limited. In other cases, signs of scapulohumeral periarthrosis are combined with vegetative-trophic changes in the HAND AND WRIST joint (shoulder-hand syndrome).

Radicular syndromes (radiculopathies C_III-C_VIII) caused by cervical osteochondrosis are relatively rare. In such cases, besides neck pain (radiating to the shoulder, forearm, and hand), notable features include clearly defined sensory disturbances in the corresponding dermatomes, Atrophy of the Muscles of the hand, forearm, or arm, and depression of tendon-periosteal reflexes.

Thus, irritation or compression of the C₆ root causes pain in the neck, shoulder, scapular region, and anterior chest wall, spreading along the lateral surface of the arm from the shoulder to the elbow, the posterior surface of the forearm, and to the first digit. Hypesthesia is observed in the thumb and index finger, along with some weakness in the biceps brachii muscle. The biceps tendon reflex is reduced. In C7 radiculopathy, pain has a similar localization in the neck, shoulder, and forearm, extending to the second and third digits of the hand. Hypesthesia in the index and middle fingers, as well as weakness of the triceps brachii muscle, may be detected. The triceps tendon reflex is typically diminished.

Irritation of the vertebral artery sympathetic plexus by osteophytes at the cervical spine level can cause headaches, cochleovestibular disturbances, and visual impairments. This symptom complex is referred to as the posterior cervical sympathetic syndrome. The onset of such disorders is usually facilitated by atherosclerotic lesions of the vertebral Arteries.

Vertebrogenic neurological disorders at the thoracic level

Reflex pain syndromes in the chest (thoratalgia) are most commonly caused by degenerative-dystrophic lesions of the costovertebral and costotransverse joints and their capsules. Spinal radiographs reveal both mild signs of thoracic spine osteochondrosis and symptoms of arthrosis in the corresponding joints, which, nevertheless, is not reliable proof of the vertebrogenic Water/144.html">Origin of the pain syndrome. Thoratalgia primarily presents as pain in various PARTS OF THE thoracic spine that intensifies with movement, sometimes having a shooting and girdle-like character. Upon examination, local tension of the paraspinal muscles and signs of autonomic irritation at the same level can be detected. Palpation of the chest reveals tenderness at paraspinal points and spinous processes, as well as in the intercostal spaces. Restriction of movement in the corresponding spinal segments is observed. Radiculopathies at the thoracic spine level are quite rare. Moreover, reliable identification of thoracic radiculopathies is possible only when multiple adjacent roots are affected.

When examining and treating patients with back pain, a crucial rule must be followed: a Diagnosis of vertebrogenic thoratalgia should only be made after ruling out all other possible causes of chest pain. Such causes may include coronary artery disease and myocardial infarction, Pneumonia, Pleurisy, lung and mediastinal tumors, spinal tumors and metastases, spinal Osteomyelitis, multiple myeloma and other blood disorders, rib and spinal fractures, etc.

Vertebrogenic neurological disorders at the lumbosacral level

Reflex painful muscular-tonic syndromes in the lower back, pelvis, and legs occur due to irritation of the receptors in the annulus fibrosus of the affected disc, the posterior longitudinal, interspinous, and other ligaments, and the joint capsules of the spine, which happens during stretching or tears of these structures, or subluxations in the intervertebral joints.

Lumbago is an acute reflex lumbar pain syndrome characterized by muscle hypertonicity. Severe lower back pain can be triggered by an awkward movement, heavy lifting, a fall, or hypothermia, and typically presents as a sharp shooting pain that forces the patient to freeze in an awkward posture. Less commonly, lower back pain builds up gradually. The pain may be burning, piercing, or bursting, and it intensifies with the slightest movement, attempts to straighten up, standing or sitting, straining, coughing, or sneezing. At the level of the affected segments, there is a sharp restriction of spinal mobility, accompanied by painful spasm of the paravertebral muscles, flattening of the lumbar lordosis, and scoliosis. Palpation reveals tenderness at paravertebral points and the spinous processes of the lumbar vertebrae. Clear sensory or motor deficits of the radicular type are typically absent. Tension signs may be elicited. The pain syndrome is usually accompanied by widespread signs of autonomic dysfunction (such as hyperhidrosis). The pain generally subsides within a few days, less often taking 10-12 days.

Lumbalgia is a chronic reflex pain syndrome with muscle hypertonicity that occurs under circumstances similar to lumbago; however, it develops gradually and is generally less intense. Lower back pain is more often aching or bursting in nature, tends to intensify with movement or when changing posture, and gradually eases in the supine position. Range of motion in the lumbar spine is preserved but somewhat restricted due to pain. Examination reveals characteristic tender points and paravertebral muscle tension.

In lumbosciatica, pain and reflex disturbances are localized not only in the lower back but also in the gluteal region and the posterolateral aspects of the lower limb. As in previous cases, pain may occur suddenly or build up gradually, intensifying with movement, changes in body position, coughing, trunk bending, standing, or sitting. Examination reveals flattening of the lumbar lordosis, paravertebral muscle tension, scoliosis, and restricted lumbar mobility during forward and lateral bending. Tenderness is elicited upon palpation over the spinous processes of the lumbar vertebrae, paravertebral points, along the course of the sciatic nerve, in the popliteal fossa, and over bony prominences (posterior superior iliac spine, inner margin of the greater trochanter of the Femur, and the fibular head). Tension signs (such as Lasègue, Wasserman, and Mackiewicz signs) are present. In lumbosciatica, lower limb muscle strength and tendon reflexes remain intact. However, independent movement by the patient may be significantly limited due to severe pain. Radicular sensory deficits are not observed. At the same time, the pain is frequently accompanied by symptoms of autonomic dysfunction, including altered skin Temperature in the extremities, and hyperhidrosis of the lower back and legs. Most patients experience significant clinical improvement with treatment within 2-3 weeks.

Lumbosacral radiculopathy. Among radicular syndromes associated with spinal osteochondrosis, L₅ and S₁ root involvement symptom complexes are the most common. As with lumbosciatica, the primary manifestation of radiculopathy is typically shooting pain, accompanied by vertebral muscle-tonic syndrome, tension signs, and signs of autonomic dysfunction at the affected levels. In addition, however, there are sensory deficits within the radicular innervation zone, loss of the knee or Achilles reflex, and demonstrable weakness of the corresponding muscles.

Involvement of the L₄ nerve root causes lower back pain radiating to the anterior and inner aspects of the thigh, accompanied by paresthesia and hypesthesia in the same area. Weakness and hypotrophy of the quadriceps femoris muscle, along with a diminished knee reflex, are also detected.

L₅ radiculopathy presents with intense lower back pain radiating to the buttock, the outer thigh, the anterolateral leg, the medial edge of the FOOT, and the big toe. Paresthesia, hypesthesia, and occasionally hyperesthesia are observed within this zone. Findings include reduced strength of the extensor hallucis longus, hypotonia and hypotrophy of the tibialis anterior muscle, and the patient's inability to stand on their heel.

With S₁ radiculopathy, pain is localized in the lower back and radiates to the buttock, the posterolateral thigh, the lateral leg, the lateral edge of the foot, and the fifth toe. Paresthesia, hypesthesia, and less frequently hyperesthesia occur within the root's innervation zone. There is a reduction in the strength of the triceps surae and toe flexors (particularly the flexor digiti minimi), accompanied by hypotonia and hypotrophy of the gastrocnemius muscle. The patient is unable to rise onto their toes on the affected side, and the Achilles reflex is diminished or absent.

Midline disc herniation in the lumbosacral spine can lead to cauda equina syndrome. This condition causes intense lower back and sacral pain radiating to both legs, accompanied by hypesthesia in the gluteal and anogenital regions, as well as pelvic organ dysfunction.

Compression of the radicular-medullary artery (L5, S1) by a disc herniation can lead to radiculoischemia or myeloischemia (spinal stroke or, in subacute cases, so-called myelopathy). This may result in ischemic damage to the anterior horns of the spinal cord in the area of the lumbar enlargement, as well as the conus, epiconus, or lower thoracic spinal cord (a critical watershed zone supplied by adjacent spinal vascular territories). Under such circumstances, Clinical Features typically include foot drop, peripheral and central lower paraparesis, long-tract sensory disturbances below the level of the lesion, and pelvic organ dysfunction.

Clinical features of neurological complications of spinal osteochondrosis

Initial manifestations of neurological complications of spinal osteochondrosis typically appear in young or middle adulthood and are most often associated with trauma or excessive physical strain. In some women, lower back pain first occurs during or after pregnancy. Provoking factors undeniably include hypothermia and psycho-emotional stress. As a rule, reflex and milder forms of neurological disorders—such as lumbago and cervicocranialgia—develop first. The subsequent course of the disease alternates between exacerbations and remissions. Their severity, duration, and proportion are highly individual and vary widely. Subsequent exacerbations generally present with broader symptomatology, and at some stage, reflex neurological disorders may transform into a radicular symptom complex. With a favorable course in the fifth or sixth decade of life, as disc fibrosis and spondylosis develop and other compensatory mechanisms take over, exacerbations become less severe, and the patient's condition generally stabilizes. Under these circumstances, patients only periodically report discomfort and some restriction of lumbar mobility. It should be emphasized that an exacerbation presenting with lower back pain and vertebral muscle-tonic dysfunction in patients with a long history of disease and longstanding signs of radiculopathy (such as a diminished Achilles reflex) can quite often be reasonably interpreted as an episode of lumbosciatica rather than radiculopathy. This is supported by a favorable response to therapy and a relatively rapid recovery. Unfortunately, the progression of spinal osteochondrosis and its neurological complications sometimes leads to severe consequences with significant functional disability.

Determining the correlation between morphological changes in spinal osteochondrosis and neurological deficits is a rather complex issue. The mere presence of degenerative-dystrophic spinal changes (especially "widespread osteochondrosis") is not in itself proof of the vertebrogenic origin of accompanying neurological disorders. Only in recent years have imaging techniques (CT and MRI) helped clarify this matter to some extent. It is evident that spinal nerve root compression in these cases is frequently caused by intervertebral disc herniations. At the same time, a disc herniation can be the source of both reflex neurological disorders and radiculopathy, and in certain situations may cause direct compression or indirect (ischemic) damage to the spinal cord or cauda equina roots. Conversely, disc herniations may remain entirely asymptomatic in some patients and be discovered incidentally during instrumental examinations. Predicting the clinical course when an asymptomatic disc herniation is discovered incidentally is a complex and as of yet unresolved challenge. An evidence-based Conclusion regarding the secondary discogenic or vertebrogenic nature of neurological disorders requires careful analysis and correlation of the localization of degenerative-dystrophic spinal changes with the pattern and level of neurological deficits.

Diagnosis and Differential diagnosis OF neurological complications of spinal osteochondrosis

The diagnosis of reflex and radicular neurological complications of spinal osteochondrosis is based on the presence of a characteristic pain syndrome, vertebral muscle-tonic abnormalities, tension signs, and evidence of corresponding nerve root involvement (motor, reflex, sensory, and autonomic symptoms). In most cases, a fairly characteristic medical history can be elicited.

The neurological syndromes described above are generally non-specific for spinal osteochondrosis and may therefore have a non-vertebrogenic origin. A similar clinical picture of neurological disorders can occur in traumatic and infectious-inflammatory root lesions, neoplastic and metastatic tumors of the spinal cord, its membranes and roots, and epidural abscesses. The differential diagnosis of spinal osteochondrosis includes the following pathological conditions:

✵ osteomyelitis and Tuberculous Spondylitis;

✵ traumatic spinal injuries;

✵ dyshormonal spondylopathy;

✵ multiple myeloma;

✵ spinal tumors and metastatic lesions, etc.

Thus, the standard diagnostic workup for suspected neurological complications of spinal osteochondrosis should include a general medical examination, complete blood count, urinalysis, blood chemistry panel, and plain spinal radiographs in two standard projections. It is important to remember that neither reflex nor radicular vertebrogenic neurological syndromes associated with spinal osteochondrosis are accompanied by fever, inflammatory blood markers, or urinary abnormalities. Instrumental Diagnostic Methods play a significant, albeit non-definitive, role: spinal radiography, CT, and MRI. Spondylography can reveal the following signs of spinal osteochondrosis:

✵ reduced intervertebral disc height;

✵ thickening and deformation of the vertebral body endplates;

✵ marginal osteophytes of the vertebral bodies;

   • altered spinal segment configuration (kyphosis, scoliosis, pseudospondylolisthesis);

As noted earlier, there is no direct and straightforward correlation between the degree of spinal osteochondrosis development and the severity of its neurological complications. CT and, in particular, MRI allow for the detection of structural changes in the vertebrae and intervertebral discs, the identification of disc protrusions and prolapses, hypertrophy of the ligamentum flavum, spinal canal stenosis, and various alterations in the nerve roots, Meninges, and spinal cord. These instrumental diagnostic methods frequently serve not so much to confirm the diagnosis of spinal osteochondrosis as to rule out other pathological processes that may be the cause of neurological disorders. In some cases, to clarify the Nature of the disease—especially in the absence of MRI—CEREBROSPINAL FLUID (CSF) analysis, cerebrospinal fluid hydrodynamic tests, and myelography are performed. Electroneuromyography can be recommended to differentiate lesions of the Nerve Trunks and roots and to confirm the involvement of the anterior horns of the spinal cord.

In the general examination scheme for patients with low back pain syndromes, the primary and most critical task is to differentiate between reflex (nonspecific) pain syndromes, radiculopathy, and specific pathology. Special attention should be paid to the following stages and sections of the examination:

✵ searching for and ruling out red flags;

✵ detailing the pain syndrome;

✵ identifying neurological deficits;

✵ examining the skin and mucous membranes;

✵ examining the Lymph Nodes;

✵ examining the abdomen;

✵ assessing vascular pulsation in the extremities;

✵ rectal examination;

   • identifying psychosocial factors contributing to the decompensation or chronic progression of pain in the absence of improvement.

The presence of so-called "red flags" makes it possible to suspect the development of a specific pathology other than spinal osteochondrosis:

✵ history of trauma;

✵ age <20 or >55 years;

✵ fever;

✵ pain unrelated to physical activity;

✵ history of Cancer;

✵ corticosteroid use;

✵ HIV infection;

✵ unexplained weight loss;

✵ spinal deformity;

✵ changes in general condition;

✵ signs of spinal cord involvement.

As for the specialized neurological examination, it should include the following items:

✵ localization and Description of the nature of the pain syndrome;

✵ assessment of gait and posture;

  • inspection and palpation of the lumbosacral region and paraspinal muscles;

  • evaluation of the range of motion in the lumbosacral spine;

✵ examination of lower limb and anogenital sensation;

✵ evaluation of muscle strength, tone, and condition;

✵ assessment of reflexes;

✵ evaluation of tension signs;

✵ assessment of pelvic organ function.

Currently, it is difficult to single out any single imaging diagnostic method that clearly outperforms others in evaluating patients with vertebrogenic pain syndromes. Overall, CT or MRI scanning can be useful or even necessary under the following circumstances:

  • when the imaging results are likely to influence patient management strategies;

  • in the presence of “red flags” and well-founded suspicion of a specific underlying pathology;

  • in cases of persistent pain syndromes showing no marked improvement after 6–8 weeks of comprehensive conservative therapy;

✵ when considering surgical intervention.

Comprehensive Treatment of Neurological Complications of Spinal Osteochondrosis

Comprehensive therapy for vertebrogenic nervous system disorders, taking into account key pathogenetic mechanisms, should aim to relieve pain and inflammatory responses, normalize microcirculation and venous outflow disorders, reduce muscle spasms, and—once the acute clinical manifestations subside—stimulate compensatory and regenerative processes.

In the hyperacute phase of the disease with severe pain, bed rest with minimal axial load and limited spinal mobility is essential. The patient should be advised to lie on a flat surface in a comfortable position. The duration of bed rest depends on the patient's well-being and, if necessary, may last 2–4 days. It is important to reassure the patient of a favorable outcome and encourage an active lifestyle. Cold or mild dry heat Applications can be used. Temporary immobilization of the affected spinal segment using soft collars, special corsets, or belts may be beneficial. Depending on the patient's condition, activity is gradually increased, though sudden movements, trunk flexion, heavy lifting, and prolonged fixed postures should be avoided for some time.

Quite often, at the very onset of the disease, patients attempt to self-medicate by taking familiar analgesics—metamizole (analgin), acetylsalicylic acid, baralgin, or other readily available combination drugs such as tempalgin, spazgan, pentalgin, etc. Ethyl chloride local sprays, topical analgesics, and counterirritants are also used. However, their effect is usually short-lived and inadequate.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most effective treatments for vertebrogenic pain syndromes: diclofenac, ibuprofen, ketoprofen, aceclofenac, meloxicam, nimesulide, etc. Some of these agents can be administered via intramuscular injection, which is frequently necessary in cases of severe pain. Others are taken orally in tablet or capsule form. Short courses of NSAIDs (5–7 days) are recommended, as prolonged, uncontrolled use of these drugs carries a risk of adverse reactions and complications, primarily concerning the gastrointestinal tract. NSAIDs are also incorporated into topical ointments or gels. NSAID suppositories represent one of the most effective and convenient dosage forms. Table 2.1 lists several NSAIDs frequently prescribed for vertebrogenic pain syndromes.

In certain cases, short-term use of narcotic analgesics may be warranted, though they offer no significant advantages in relieving pain of vertebrogenic origin. It should be noted that aggressive NSAID therapy for vertebrogenic disorders frequently yields only moderate pain relief, quite comparable to the analgesic efficacy of paracetamol or other simple analgesics.

Class="center">Table 2.1. Nonsteroidal Anti-Inflammatory Drugs Frequently Used in Vertebrogenic Pain Syndromes

The aforementioned drugs (diclofenac, etc.) can be administered via compresses with a dimexide solution (concentration must be below 40%). Compresses are applied daily to the painful area of the neck, thoracic spine, or lumbosacral region and left in place for at least 40–60 minutes.

While a wide Selection of NSAIDs is currently available, compelling evidence of significant superiority of certain drug groups over others is still lacking. In many cases, administering even maximum doses of a single NSAID fails to achieve the expected sustained outcome. Under such circumstances, combination therapy may be employed. To potentiate The Effect of NSAIDs, complementary agents can be used, including antispasmodics (papaverine, no-shpa, etc.), desensitizing agents, tranquilizers (diazepam), Vitamins (B12 500–1000 mcg), and antiepileptic drugs (carbamazepine, gabapentin, pregabalin). Centrally acting non-opioid analgesics—selective neuronal potassium channel openers that also exhibit muscle-relaxant and neuroprotective effects—may likewise be utilized. Flupirtine (catadolon), registered in our country, is prescribed at 1–2 capsules 3 times daily (maximum daily dose should not exceed 600 mg) for courses ranging from several days to 3–4 weeks.

To reduce reflex muscle spasms and associated pain, agents with pronounced muscle-relaxant properties are used, such as tolperisone (mydocalm) or tizanidine (sirdalud). These drugs, possessing different Mechanisms of action, can be administered either in combination with NSAIDs or as monotherapy. Tolperisone (mydocalm) features a favorable selective profile, is well tolerated across a wide daily dosage range of 150–450 mg/day, and is safe. It produces no sedation or tolerance, exhibits no interaction with alcohol, and does not impair concentration or motor coordination.

A summarized flowchart of the main diagnostic and therapeutic measures for reflex and radicular vertebrogenic neurological disorders is presented in Table 2.2.

Table 2.2. Generalized management scheme for patients with reflex and radicular vertebrogenic neurological disorders

At the very beginning of the disease, moderate dehydration can be beneficial. For this purpose, furosemide (40 mg) orally or Lasix intramuscularly (2 ml) is prescribed for 3-5 days. In some cases, intravenous administration of mannitol may be recommended. L-lysine aescinate provides a complex anti-edematous, anti-inflammatory, and analgesic effect, which can be prescribed intravenously at 5-10 ml in a 0.9% sodium chloride solution for 2-8 days. A positive effect can be achieved by the short-term administration of prednisolone (60-100 mg orally daily for 3-5 days with a rapid dose reduction) or dexamethasone.

Sometimes an obvious positive result is observed when supplementing the treatment regimen with vasoactive agents—aminophylline, pentoxifylline, troxevasin. The Use of these drugs is justified by the significant role of microcirculatory disorders, vascular spasm, and impaired venous outflow in the mechanisms of vertebrogenic disorders of The Nervous System and, in particular, the causes of pain syndrome development.

In parallel with drug therapy, physiotherapeutic procedures are recommended (sinusoidal modulated currents, diadynamic currents, magnetotherapy, Electrophoresis with novocain, anesthesin, analgin). Some specialists perform radicular blocks with the administration of 2% novocain (lidocaine, hydrocortisone, etc.).

With some easing of pain in the subacute stage of the disease, The Scope of physiotherapeutic procedures is expanded (drug phonophoresis, magnetotherapy, etc.). In addition, therapeutic exercise complexes, massage, various options for traction therapy (dry or underwater), manual therapy, and acupuncture are used. Stimulators of regenerative processes are prescribed. Later, thermal procedures, mud therapy, baths, etc., are carried out. In the remission stage, Therapeutic Exercises are essential, and sanatorium-resort treatment can be useful.

In case of resistant or prolonged vertebrogenic pain syndrome, combination therapy is recommended with more active use of selective cyclooxygenase inhibitors, muscle relaxants (midocalm), flupirtine (catadolon), antidepressants, antiepileptic drugs, and local anesthetics with lidocaine. In the treatment of chronic low back pain, muscle relaxants, flupirtine (catadolon), anticonvulsants, antidepressants, short courses of NSAIDs, chondroprotectors, agents for the treatment and prevention of Osteoporosis, therapeutic exercises, acupuncture, and manual therapy are widely used.

Table 2.2. Generalized management scheme for patients with chronic forms of vertebrogenic pain disorders

Currently, for neurological complications of osteochondrosis, the intake of chondroprotectors is recommended. These are substances that stimulate synthetic processes in cartilage tissue and thereby slow down the development of osteoarthritis, increasing the resistance of cartilage tissue to the action of various damaging factors. This rather heterogeneous group of drugs includes rumalon, struktum, mucosat, alflutop, chondroxide, teraflex, and others. The therapeutic and preventive efficacy of many chondroprotectors requires further study, taking into account their composition, specific mechanisms of action, and available evidence base. When prescribing them, individual CHARACTERISTICS OF THE degenerative-dystrophic process, as well as the form and stage of the disease, must be taken into account.

The question of Surgical treatment arises when comprehensive conservative treatment is ineffective and CT, MRI, or myelography reveals a herniated intervertebral disc that is the cause of pain. Absolute indications for urgent surgical treatment appear when signs of radiculomyelo-ischemia occur, indicating compression of the spinal cord or cauda equina roots by a herniated disc.

Several surgical options have been proposed for removing lumbar intervertebral disc herniations. For a lateral disc herniation, a midline incision of the soft tissues over the spinous processes is performed, along with subperiosteal muscle stripping on the affected side. Resection of fragments of the upper and lower vertebral arches is performed, and the ligamentum flavum is excised in the space between them, exposing the nerve root and the prolapsed disc. The disc and its fragments located in the intervertebral space are removed. To remove midline disc herniations, laminectomy (resection of spinous processes and arches on both sides) is sometimes performed. This allows wide exposure of the dural sac, shifting it aside, and removing the prolapsed disc in a less traumatic manner. During such operations, it is possible to remove osteophytes and eliminate other factors causing root or spinal cord compression. Currently, endoscopic discectomy is widely used, which avoids rough tissue damage during surgery and significantly shortens postoperative recovery time. However, in A number of cases, wide exposure of the affected area is inevitable and even advisable. In cases of spinal instability (spondylolisthesis), various methods of spinal stabilization using special structures are employed.

Prevention of Spinal Osteochondrosis and Its Neurological Complications

The probability of developing severe forms of osteochondrosis and its clinical manifestations can be reduced by limiting inadequate physical loads (activity modification), preventing spinal injuries, developing proper posture, choosing an optimal profession, and observing occupational hygiene standards. Impulse axial loads, deep forward bends, heavy lifting, working with arms extended forward while slightly bending the torso, and prolonged static loads on the shoulder and pelvic girdles are particularly dangerous. Also of great importance are the correction of excess body weight, smoking cessation, a balanced and varied diet, maintaining an active motor regimen, and systematic therapeutic exercises, which help form a natural muscular corset and strengthen the back extensor muscles. Primary and secondary prevention of neurological complications of osteochondrosis primarily involves systematic therapeutic exercises; preventive sessions of manual therapy and massage can also be beneficial. A good effect has been noted from the complex impact of various sanatorium-resort factors. In some cases, the intake of chondroprotectors is necessary (teraflex, alflutop, struktum, mucosat, and others).

Clinical Problems

Option 1

A 48-year-old man has noted stiffness, muscle soreness, and crunching during movements in the neck and shoulder girdle over the past 2-3 years. Pain sensations intensify after physical exertion or hypothermia. About two months ago, without apparent reason, pain developed in the shoulder joint and the right arm, which intensifies when the arm is moved behind the back and is especially troublesome at night, accompanied by a sensation of "pins and needles" and numbness in the hand. This was joined by sensations of constant heaviness and soreness in the back of the head, brief episodes of dizziness, and tinnitus. Examination reveals tension in the paravertebral muscles at the level of the cervical and upper thoracic spine, tenderness upon palpation of the spinous processes of the cervical vertebrae, paravertebral points, and the right shoulder joint, as well as a decrease in skin temperature on the right hand. There is a sharp restriction of Movements of the right shoulder backward and upward. Indistinct zones of hyperesthesia are detected in the region of the right shoulder girdle and on the right arm. Tendon reflexes are symmetrical. Pathological reflexes are not detected.

   • List the main neurological disorders.

   • Explain the origin and nature of the pain sensations and movement restriction in the shoulder joint.

   • How should dizziness and tinnitus be interpreted?

   • Formulate the topographic diagnosis.

   • Formulate and substantiate the preliminary clinical diagnosis.

   • Determine the Morphology/3.html">MAIN DIRECTIONS OF the differential diagnosis.

   • Outline the scheme of instrumental and Laboratory examination.

   • Determine the advisability of performing a CT or MRI scan.

   • Outline the Main Components of the therapeutic management program.

   • Prescribe initial pharmacological treatment.

   • Select the optimal physiotherapy modalities.

   • Determine the prognosis of this condition.

   • Formulate recommendations for the patient.

Option 2

A 40-year-old man complains of pain in the neck and left shoulder girdle, along with pain and a feeling of heaviness in the left arm. The pain radiates along the ulnar aspect of the forearm and hand, accompanied by discomfort in the left hemithorax and generalized weakness. The pain intensifies at night, upon deep inspiration, when tilting the head to the right, and when abducting the arm. Physical examination reveals Swelling of the supraclavicular fossa, tenderness upon palpation of the anterior scalene muscle, reduced grip strength due to pain, and hyperesthesia along the Medial surface of the left arm and forearm. Tendon and periosteal reflexes in the upper extremities are unaffected.

   • List the main neurological deficits.

   • Explain the mechanism underlying the pain syndrome.

   • Explain the origin of sensory disturbances in the arm and chest.

   • Establish the topical diagnosis.

   • Formulate and substantiate a provisional clinical diagnosis.

   • Determine the main directions for differential diagnosis.

   • Outline the instrumental and laboratory diagnostic workup.

   • Assess the appropriateness of performing CT or MRI scans.

   • Outline the main Components of the therapeutic management program.

   • Indicate the optimal physiotherapy prescriptions.

   • Determine the prognosis of this condition.

   • Formulate recommendations for the patient.

Option 3

A 40-year-old man experienced a sudden sharp pain in the lower back and down the posterolateral aspect of the right thigh and lower leg a week ago after bending forward. The pain intensifies with movement, in the upright position, and during coughing; it persists even when lying down at night. Analgesics and local heat application to the lower back provide no relief. He has suffered from recurrent lower back pain for several years, which first appeared after heavy lifting. Following physical exertion and hypothermia, exacerbations occurred three times. During the most recent flare-up, pain in the right leg developed alongside lower back pain, accompanied by scoliosis. Physical examination reveals restricted range of motion in the lumbosacral spine during forward and lateral flexion, flattening of the lumbar lordosis, right-sided scoliosis, and paraspinal muscle spasm, more pronounced on the right. Tenderness is elicited upon palpation of paraspinal points at the L5-S1 level on the right and along the course of the sciatic nerve. There is a moderate positive Lasegue's sign on the right. Hypesthesia is noted along the posterolateral surface of the right thigh and lower leg, and the right Achilles reflex is diminished.

   • Identify the primary neurological disorders.

   • Determine the type of sensory impairment.

   • What does Lasegue's sign consist of?

   • What muscle group's condition and strength should be specifically assessed in this patient?

   • Formulate the topical diagnosis.

   • Formulate and justify the preliminary clinical diagnosis.

   • Outline the directions for differential diagnosis.

   • Present the plan for instrumental and laboratory examination.

   • What is indicated by scoliosis, decreased intervertebral disc heights, and osteophytes detected on spine radiographs?

   • Determine the advisability of performing a CT or MRI scan.

   • List the core components of the therapeutic program.

   • Determine optimal drug prescriptions.

   • Select a set of physiotherapeutic procedures.

   • What measures should be taken if there is no significant positive effect after 3–4 weeks of combination therapy?

   • Indicate the approximate duration of inpatient treatment and temporary disability for this condition.

   • What measures should be recommended to the patient to prevent exacerbations?

Option 4

A 72-year-old patient developed dull lower back pain about six months ago. The pain gradually worsened to unbearable levels and began to radiate to the left thigh. The patient started noticing difficulty walking due to pain and weakness in the leg. Physical examination reveals flattening of the lumbar lordosis, restricted range of motion in the lumbar spine, and paraspinal muscle spasm. Tension signs are more pronounced on the left. Tenderness is elicited upon Percussion of the spinous processes of the L₂-L₃ vertebrae and paraspinal points. Hypesthesia is present along the inner surface of the left thigh. The left knee reflex is diminished. Over the past several years, the patient has experienced frequent and difficult urination.

   • Identify the leading neurological deficits.

   • Name potential causes of gait disturbance.

   • Which muscle group's condition and strength must be specifically assessed in this patient?

   • Determine the type of sensory impairment.

   • Name the most frequent tension signs.

   • Formulate the topical diagnosis.

   • Formulate the preliminary clinical diagnosis.

   • Indicate the main directions for differential diagnosis.

   • Outline a plan and set goals for neurological and somatic examination.

   • What changes might be detected on spinal radiographs in the described case?

   • Determine the advisability of performing a CT or MRI scan.

  • What could be the explanation for the urination disorder?

  • List the main components of the therapeutic program.

  • Select the optimal prescriptions for pain relief.

  • List the necessary physiotherapeutic procedures.

  • Determine the prognosis of the disease.

Case 5

A 54-year-old man has been suffering from recurrent and progressively worsening lumbosacral pain for two years. Two days ago, while lifting a heavy object, he developed severe pain in the lumbosacral region and both legs. Over the next day, he experienced lower extremity weakness, as well as urinary and fecal retention. Examination reveals weakness in the leg muscles, predominantly in the distal parts, and decreased muscle tone. Knee, Achilles, and plantar reflexes are absent. Superficial sensation is decreased along the posterolateral surface of the legs and increased in the perineal region. Lasègue's and Neri's signs are positive. There is tenderness upon palpation of the paravertebral points at the level of the third and fourth lumbar vertebrae. Radiographs of the lumbosacral spine show signs of osteochondrosis.

  • Identify the leading neurological disorders.

  • Indicate the nature of the motor impairments.

  • Name the type of sensory disturbances.

  • Determine the nature of the pelvic function impairment.

  • Formulate the topical diagnosis.

  • Formulate a preliminary clinical diagnosis.

  • Determine the main directions for differential diagnosis.

  • Outline the plan and objectives of instrumental neurological examination.

  • List the main radiological signs of spinal osteochondrosis.

  • Determine the advisability of performing a CT or MRI scan.

  • What cerebrospinal fluid changes are most likely in this condition?

  • How should the arrest of the contrast agent at the level of the 3rd lumbar vertebra during descending myelography be interpreted?

  • Describe the management plan for this patient.

  • Select optimal pharmacotherapeutic prescriptions.

  • State the indications for Surgical Treatment of this condition.

  • Outline the MAIN STAGES OF the surgical intervention.

  • Determine the prognosis of the disease.