NEUROLOGY AND NEUROSURGERY - YU. V. ALEKSEEENKO - 2014

DISORDERS OF THE PERIPHERAL NERVOUS SYSTEM

In the overall morbidity Structure of populations in many countries, Peripheral Nervous system disorders rank third after common colds and domestic injuries. At the same time, this group of diseases occupies leading positions in terms of temporary disability. A distinctive feature of this group of disorders is an unusually wide spectrum of clinical manifestations of both local and systemic character. On the other hand, peripheral nervous system lesions arise from an extremely diverse range of pathological external and internal influences. In many cases, they represent complications or regular manifestations of internal organ pathologies, Blood disorders, systemic diseases, immune disorders, oncological diseases, metabolic and endocrine disturbances, infectious diseases, poisonings and traumas, and occasionally even iatrogenic conditions. Thus, the recognition and Treatment of peripheral nervous system disorders involve a multidisciplinary team of specialists: neurologists, neurosurgeons, surgeons, traumatologists, rheumatologists, general practitioners, endocrinologists, dentists, nephrologists, otolaryngologists, and several others.

Systematization of Peripheral Nervous System Disorders and Certain Terminology Issues

There is a rather complex Classification of diseases and lesions affecting the peripheral nervous system. From an anatomical perspective, it is convenient to distinguish lesions of the peripheral nerves (isolated or multiple), plexuses, spinal roots, and spinal ganglia.

Taking into account Etiology AND Pathogenesis, all variants of peripheral nervous system lesions are conventionally subdivided into genetically determined, infectious-inflammatory, infectious-allergic, toxic and dysmetabolic, compression-ischemic (tunnel), vertebrogenic, and traumatic. The terms used generally reflect the specific etiological and pathogenetic features of a particular disease variant. The terms “neuritis,” “polyneuritis,“ “plexitis,” “radiculitis,” and “ganglinitis” are appropriately used to describe evident infectious-inflammatory lesions of the peripheral nervous system. The non-infectious Nature of the pathological process (toxic, dysmetabolic, allergic, compression-ischemic lesions) is emphasized by the terms “neuropathy,” “polyneuropathy,” “plexopathy,” and “radiculopathy.” In cases of mechanical damage, it is appropriate to state the traumatic injury of the corresponding nerve, plexus, or ROOT, indicating the degree of its disruption. An isolated lesion of a single nerve is emphasized by the term “mononeuropathy,” whereas multiple involvement is indicated by the term “polyneuropathy” or “polyneuritis.” The predominance of irritation phenomena, particularly excruciating paroxysmal pain, among all other clinical manifestations of peripheral nerve lesions is conventionally designated by the term “neuralgia.”

Pathogenetic Mechanisms and Generalized Characteristics of Clinical Manifestations of Peripheral Nerve Disorders

Pathomorphological changes in diseases and lesions of peripheral nerves may be limited to axonal damage (lesion of the axonal cylinder), represent a demyelinating process with the destruction of the myelin sheath of nerve fibers, or appear as degeneration of nerve fibers distal to the site of injury (Wallerian degeneration). As is well known, peripheral nerves typically contain Three types of fibers: sensory, motor, and autonomic. Their ratio within individual nerve trunks varies, which determines the predominance of specific neurological disorders (sensory, motor, autonomic-trophic) in the clinical picture.

1. Sensory fiber involvement, depending on The Nature of the damage, may be accompanied by both deficit symptoms and signs of irritation. Pain sensations may be detected at the site of injury, along the course of the nerve trunk, and within its innervation zone. Typically, paresthesia, hyperesthesia, or, more frequently, hypoesthesia is observed in the innervation zone of the affected nerves. Disorders of tactile and pain sensitivity are particularly noticeable, although all modalities of sensitivity (superficial and deep) are usually impaired. It must be remembered that in such cases, the area of sensory deficits is always somewhat smaller than the anatomical innervation area of the corresponding nerve due to overlap zones of sensory innervation from neighboring nerves. Multiple peripheral nerve lesions may be accompanied by sensory ataxia.

2. Motor fiber involvement leads to weakness, hypotonia, and Atrophy of the corresponding Muscles, as well as reflex loss (see signs of peripheral paresis or paralysis).

3. Autonomic-trophic disorders may manifest as changes in Skin color and Temperature, skin dryness, impaired Hair and nail growth, trophic ulcers, soft tissue edema, and other disturbances.

The nature of peripheral nerve and Muscle damage can be established using classical electrodiagnostics. The degree and level of peripheral nerve lesions can be determined more precisely using electroneuromyography.

Thus, the universal generalized characteristic of clinical manifestations of a peripheral nerve lesion based on the maximum possible list of signs comprises pain along the course of the affected nerve trunk, as well as pain sensations, paresthesia, hypoesthesia, and hyperesthesia (less commonly) within its innervation zone. There is functional impairment caused by paresis of the involved muscles, accompanied by a decrease in their tone, muscle atrophy, and loss of corresponding Reflexes. A decrease in skin temperature within the innervation zone is detected, sometimes accompanied by Changes in the vascular pattern and skin color, as well as soft tissue edema. However, the specific combination of symptoms depends not only on the type of affected nerve (containing predominantly motor or sensory fibers, or possessing numerous autonomic fibers) but also on the level of the lesion, its etiology, and the specific pathogenesis of the disease.

This spectrum of symptoms characterizes, for example, neuropathies or Traumatic injuries of the NERVES OF THE upper and lower limbs: the radial, ulnar, median, sciatic, femoral, tibial, and peroneal nerves. Sometimes, lesions of these nerves occur against the Background of acute infections. Injection neuropathies may develop (though rarely). However, most frequently, spontaneous mononeuropathies are compression-ischemic in nature (tunnel neuropathies). Examples of such pathology include Carpal tunnel syndrome, meralgia paresthetica (lateral femoral cutaneous neuropathy), femoral nerve neuropathy, piriformis syndrome, and others.

The immediate triggering factors in such pathological conditions are prolonged microtraumatization of the nerve due to stereotyped loads and fixed postures, as well as severe external physical impacts (such as laying parquet flooring, using crutches, etc.). The leading mechanism of damage in this case is the compression of the nerve trunk within a rigid osteofibromuscular canal (due to inflammatory tissue changes and edema) and The Development of ischemia. Important roles are also played by certain predisposing factors: increased vulnerability of peripheral nerves and changes in the neural microvasculature. The development of fibrosis and increased rigidity of anatomical channels are promoted by degenerative-dystrophic joint changes, endocrine disorders, Pregnancy and Lactation, and The Use of oral contraceptives. Comprehensive treatment of tunnel syndromes includes analgesics, vasoactive drugs, NSAIDs, antiepileptic agents (e.g., carbamazepine for persistent neuralgic syndromes), physiotherapy, and therapeutic blocks (local administration of glucocorticoids). Surgical treatment Methods (decompression) are also employed.

Facial Nerve Neuropathy

Facial nerve neuropathy is a specific case of mononeuropathy. The disease can have various etiologies. Essentially, it is a variant of a tunnel lesion of the facial nerve involving inflammation and compression within the bony canal of the Temporal bone (ischemia, edema, and nerve compression). This disorder can be a complication of Inflammatory Diseases of the Inner ear, tumor, vascular, and INFECTIOUS DISEASES OF the Brain, mumps, one of the manifestations of traumatic injuries to the temporal bone pyramid, or multiple peripheral nervous system lesions (acute and chronic inflammatory demyelinating polyneuropathy). In addition, there is an idiopathic variant of facial nerve neuropathy (Bell's palsy), in the pathogenesis of which an autoimmune-inflammatory component can be suspected, although obvious causes are not identified. Provoking factors in this case may include hypothermia, trauma, and cold-related illnesses.

The clinical picture of the disease is characterized by a suddenly developing unilateral paresis of the facial expression muscles. Bell's phenomenon (lagophthalmos) is observed. Pain in the ear and mastoid process regions is possible. The structure of the clinical manifestations of facial nerve neuropathy depends on the level of the lesion and the involvement of the nervus intermedius fibers. Consequently, changes in Hearing (hearing loss, hyperacusis) and taste sensitivity on the anterior 2/3 of the Tongue, dry eye or lacrimation, and impaired salivation may be observed. Diagnosis of facial nerve neuropathy is straightforward. However, it is always necessary to exclude secondary involvement of the facial nerve system. Recovery occurs in 2/3 of patients. Nevertheless, in some cases, facial muscle contracture develops, accompanied by pain in the Muscles of the affected half of the face, increased muscle tone, and pathological synkinesis. Comprehensive therapy includes glucocorticoids, dehydration therapy, vasoactive drugs, NSAIDs, physiotherapy, massage, therapeutic exercise, and reflexotherapy. In the absence of signs of facial muscle contracture, agents that improve neuromuscular transmission (neuromidin) are used. In selected cases, surgical treatment may be indicated.

Trigeminal Neuralgia

Trigeminal neuralgia is one of the most common and excruciating pain syndromes. One of the causes of trigeminal neuralgia is considered to be irritation of the Trigeminal nerve root at the Base of the brain by adjacent small Blood Vessels (a loop of the superior cerebellar artery), which can be confirmed in many cases during surgical treatment. At the same time, trigeminal neuralgia can be secondary due to tumor, inflammatory, or demyelinating diseases, as well as traumatic INJURIES OF THE Skull, brain, Paranasal Sinuses, and the maxillofacial system. The disease typically manifests after the age of 50.

The disorder is characterized by sudden attacks of sharp, piercing, excruciating pain in the facial and gum areas within the innervation zones of individual Branches of the trigeminal nerve. Pain attacks are triggered by talking, chewing, shaving, brushing Teeth, cold wind, etc. Pain attacks usually last for several seconds and are accompanied by autonomic reactions: facial hyperemia, lacrimation, and spasm of facial muscles. The presence of trigger zones is characteristic—these are areas of skin or mucous membranes where irritation or Touch can provoke a pain attack. Neurological examination during the pain-free interval reveals no significant abnormalities. Tenderness may be detected at the exit points of the trigeminal nerve branches. During patient evaluation, all variants of secondary trigeminal neuralgia must be excluded.

Since 1962, carbamazepine (Finlepsin) has been widely used in the treatment of trigeminal neuralgia. The dosage of the drug is selected individually and typically ranges from 400-1200 mg/day. Other antiepileptic drugs may also be used. A positive effect can likewise be achieved with the administration of baclofen. Vasoactive agents are also employed. In the absence of an effect from carbamazepine, blocks of the trigeminal nerve branches using local anesthetics are performed. To eliminate the cause of the disease in some refractory cases, complex neurosurgical stereotactic interventions (vascular decompression of the V nerve root) can be performed.

Herpetic Radiculoganglionitis

The disease is caused by the varicella-zoster virus, most frequently in elderly individuals. Virus reactivation may occur spontaneously or against the background of immunodeficiency states. The pathological process typically involves 1-2 adjacent spinal ganglia (more often in the thoracic region) and posterior roots, or one to two branches of the trigeminal nerve.

In typical cases, 2-3 days after the appearance of general systemic infectious signs, paresthesias and radicular pain develop within the corresponding segmental innervation zones, accompanied by tenderness of regional Lymph Nodes. The pain is usually burning and paroxysmal in character. Subsequently, there is a sequential development of hyperemia, papules, and vesicles filled with serous fluid. After 3-4 days, the vesicles become purulent and transform into crusts. Corneal involvement (keratitis) presents a particular danger. Recovery occurs within 3-6 weeks. Some patients may be troubled for a long time by postherpetic neuralgia after the illness. This condition is characterized by persistent, debilitating pain with episodes of shooting pain in the affected area. During sensitivity testing in the painful area, total anesthesia may be detected. For the treatment of this disease in the acute stage, acyclovir (orally and in ointment form), analgesics, and antihistamines are used. To relieve the pain syndrome, the most effective medications are drugs from the antiepileptic Class that have proven highly successful in treating various chronic pain disorders—gabapentin and pregabalin; tricyclic antidepressants (amitriptyline) are also utilized. Transdermal application forms containing lidocaine and other agents are additionally applied.

Polyneuropathies

Polyneuropathies are characterized by multiple, symmetrical lesions of the peripheral nerves, predominantly in the distal extremities. When the nerve roots of the Spinal Cord are involved in the pathological process, the more precise terms "polyradiculoneuritis" or "polyradiculoneuropathy" are used. Depending on The rate of onset and symptom dynamics, they are classified as acute (less than a week), subacute (up to a month), chronic (more than a month), or recurrent polyneuropathies. Based on pathomorphological features, they are subdivided into axonopathies (damage to nerve fiber axons) and myelinopathies (damage to the myelin sheaths). Similar to focal peripheral nerve lesions, the generalized clinical picture of polyneuropathies includes sensory, motor, and autonomic-trophic disorders. However, these impairments have a more diffuse, "glove-and-stocking" distribution. Electroneuromyography is of paramount importance in diagnosing polyneuropathies, as it helps determine the level and qualitative CHARACTERISTICS OF THE pathological process and differentiates between axonopathies and myelinopathies. In some cases, sural (or superficial peroneal) nerve biopsy can provide significant diagnostic assistance.

Axonal polyneuropathies frequently develop secondary to severe intoxication with arsenic, organophosphates, methyl alcohol, carbon monoxide, avitaminoses, systemic conditions (Collagen Vascular Diseases, blood disorders, Cancer), or medication use (metronidazole, isoniazid, etc.), or they may be of dysmetabolic origin. They are typically characterized by a gradual onset and the primary involvement of the distal nerves of the extremities. Demyelinating polyneuropathies can be autoimmune (Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy), paraneoplastic, toxic, or hereditary. In demyelinating polyneuropathies, both proximal and distal segments of the nerve fibers are affected, manifesting as rapidly progressive changes in both the distal and proximal PARTS OF THE limbs.

Acute Inflammatory Demyelinating Polyradiculoneuropathy (Guillain-Barré Syndrome)

This is an autoimmune disorder characterized by prominent abnormalities in the humoral and cellular immune systems. The primary target of the autoimmune process remains unknown, though it is hypothesized to be directed primarily against lemocytes and myelin, leading to inflammatory changes and segmental demyelination of the spinal and cranial nerve roots. Additionally, axonal damage—specifically axonal degeneration of the peripheral nerves—is observed in some cases. In many patients, respiratory or gastrointestinal infections precede the onset of the disease by a few days or weeks, serving as a triggering factor for the autoimmune cascade. Trauma to the peripheral nervous system, surgical interventions, or vaccination may potentially play a similar role.

The Clinical presentation of acute inflammatory demyelinating polyradiculoneuropathy is dominated by progressive flaccid paresis of the limbs. Weakness typically begins in the musculature of the distal or proximal legs and then spreads upward, involving the muscles of the arms, trunk, neck, and HEAD. Paresis progresses over several days, or more rarely, within a few hours. A picture of peripheral, relatively symmetrical, predominantly distal tetraparesis gradually emerges, which is usually more pronounced in the lower extremities. Involvement of the intercostal muscles and Diaphragm leads to respiratory impairment accompanied by the paradoxical phenomenon of abdominal wall indrawing during inspiration. Deep tendon reflexes are characteristically depressed, and gradual muscle hypotrophy may subsequently develop. Sensory disturbances—such as hypesthesia, parestesthesia, or hyperesthesia in the distal extremities—are less prominent. Patients frequently complain of radicular-type pain in the arms and legs, as well as myalgia. Most patients exhibit positive tension signs. Signs of autonomic dysfunction develop quite frequently, including fluctuations in blood pressure, tachycardia, or bradycardia. Once a certain peak of development is reached, the disease symptoms stabilize. Regression of neurological deficits typically begins after 2 to 4 weeks. Recovery can take anywhere from a few weeks to several months, or occasionally even 1 to 2 years. Relapses occur in 25% of cases.

The diagnosis is established based on the typical clinical picture and progression of neurological deficits (acute flaccid symmetrical tetraparesis with areflexia and mild sensory disturbances), elevated CEREBROSPINAL FLUID (CSF) protein levels with a normal Cell count during the second week of the illness (albuminocytologic dissociation), and characteristic electroneuromyographic findings. Acute inflammatory demyelinating polyneuropathy must be differentiated from various spinal cord lesions that, in the acute stage, present with hypotonic tetra- or paraparesis and areflexia. Furthermore, diphtheria- or porphyria-induced polyneuropathy, as well as polymyositis, must sometimes be ruled out.

Life-threatening complications include respiratory failure resulting from weakness of the respiratory and bulbar muscles, Cardiac Arrhythmias, and other severe autonomic disturbances. Fatal outcomes may also occur due to Pulmonary Embolism or Sepsis. With modern intensive care facilities available, mortality from this disease does not exceed 5%. Significant motor deficits persist in approximately 15–20% of patients. Thus, the majority of patients achieve full recovery of neurological Functions.

Due to the risk of rapid respiratory and cardiac deterioration, acute inflammatory demyelinating polyradiculoneuropathy is considered a medical emergency requiring intensive care and, in some cases, mechanical ventilation. Careful monitoring of respiratory parameters, Cardiac Activity, and bulbar function is essential. Plasmapheresis and intravenous immunoglobulin therapy are most effective during the progressive phase of the disease. Other pathogenetic and symptomatic treatments are also employed (analgesics, NSAIDs, Neurotransmitters, vasoactive agents, Antibiotics, etc.). Measures to prevent contractures and pressure ulcers, management of pelvic organ functions, adequate nutritional support, and Maintenance of the fluid-electrolyte balance are crucial. Early rehabilitation utilizing massage, therapeutic exercise (kinesiotherapy), and physical therapy modalities is of great importance.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)

Unlike the acute variant of demyelinating polyradiculoneuropathy, infections rarely precede this condition. Its development is associated with the presence of certain human leukocyte Antigens (HLA). The autoimmune nature of the disorder is supported by the presence of Antibodies against the cytoskeletal protein β-tubulin in the majority of patients. The initial symptoms include weakness in the distal or proximal legs, ataxia, and paresthesias and numbness in the hands and feet (sensorimotor-type polyneuropathy). Over time, motor deficits progressively involve both proximal and distal limb segments. In some instances, Cranial Nerves are affected (bulbar group, extraocular nerves, facial nerve). Neurological symptoms develop slowly, usually over the course of several months. In approximately one-third of cases, the disease follows a relapsing-remuting course. Cerebrospinal fluid analysis reveals elevated protein levels with a normal cell count. Notably, CIDP develops secondary to systemic conditions (systemic lupus erythematosus, lymphoma, amyloidosis, multiple myeloma, paraneoplastic syndrome, etc.) in roughly 10–20% of cases. This fact determines The Scope of necessary diagnostic workups when establishing a CIDP diagnosis. Occasionally, the initial signs of these underlying conditions manifest several months after the onset of CIDP symptoms.

The treatment of CIDP involves corticosteroids, plasmapheresis, and intravenous IMMUNOGLOBULINS. Immunosuppressive therapy (azathioprine, methotrexate, cyclophosphamide, etc.) is sometimes utilized. Long-term treatment is required, but a favorable outcome can be achieved in the majority of patients.

Diabetic Polyneuropathy

Polyneuropathy is a common complication of Diabetes Mellitus, diagnosed in approximately 15% of patients with the disease. Electrophysiological confirmation is obtained in roughly half of the patients. The exact pathogenesis of diabetic polyneuropathy remains unclear. Proposed mechanisms include ischemic damage to peripheral nerve structures caused by microangiopathy, as well as impaired neuronal METABOLISM. The severity of diabetic polyneuropathy manifestations increases with the degree and duration of hyperglycemia.

The most prevalent form of diabetic polyneuropathy is symmetrical distal sensory polyneuropathy. It predominantly affects the axons of thin unmyelinated or sparsely myelinated sensory and autonomic fibers. In the early stages, the clinical picture in such patients is dominated by sensory disturbances in the feet. Paresthesias (sensations of cold, tingling, burning), hyperesthesia, pain, numbness, or dysesthesias develop, which worsen at night and often subside with walking. Gradually, sensory impairments extend proximally and begin to affect the hands. Examination reveals diminished pain and tactile sensitivity in the distal extremities, along with depressed deep tendon reflexes. Involvement of thick nerve fibers leads to proprioceptive deficits with loss of reflexes and sensory ataxia. Normalizing blood glucose levels may reduce the pain syndrome. Motor deficits are usually limited to mild weakness and atrophy of the FOOT and lower leg muscles. Painless ulcers may appear on the skin of the lower extremities over pressure points, driven not only by autonomic dysfunction but also by microangiopathy, sensory loss, and secondary infection. Arthropathies and foot joint deformities occasionally occur.

Autonomic dysfunction typically accompanies sensorimotor impairments in polyneuropathy, though its manifestations occasionally take center stage (diabetic pandysautonomia). In such cases, symptoms of cardiovascular dysfunction (orthostatic hypotension frequently triggered by Insulin administration and unaccompanied by tachycardia), gastrointestinal involvement (constipation, diarrhea, gastroparesis), and urogenital disturbances (impotence, voiding disorders) dominate the clinical picture. Painless forms of myocardial infarction and sudden cardiac death may occur in this condition.

Symmetrical proximal motor neuropathy develops significantly less frequently in diabetic patients. It has a subacute onset and manifests as weakness and atrophy of the proximal leg muscle groups, and more rarely, the shoulder girdle. Sensory deficits are minimal or even absent, and limb pain is occasionally observed. The neurological deficits in these cases may be driven by autoimmune vasculitis. Elderly diabetic patients may also develop an asymmetrical proximal motor neuropathy characterized by pain in the anterior thigh and lower back, alongside paresis and atrophy of the quadriceps muscles. The prognosis is generally favorable, though recovery can take several months or even years.

Radiculopathy involving the lumbar, sacral, thoracic, or cervical roots occasionally develops in diabetes mellitus. In this state, pain typically does not abate in the supine position and intensifies at night. Furthermore, cranial neuropathy involving the III, IV, and VI cranial nerves may arise in diabetic patients. This condition is observed in elderly individuals and presents with orbital pain and impaired extraocular motility.

Peripheral nervous system involvement may be the initial manifestation of diabetes mellitus. Therefore, blood glucose screening is recommended for all patients presenting with peripheral nerve disorders. However, diabetic neuropathies should only be diagnosed after ruling out other causative conditions and diseases, as the majority of associated neurological symptoms lack sufficient Specificity.

The primary step in treating diabetic neuropathies is the normalization of blood glucose levels. B-complex Vitamins, thioctic acid, actovegin, vasoactive agents (pentoxifylline, etc.), ipidacrine (myoin), and symptomatic therapies (simple analgesics, NSAIDs, gabapentin, pregabalin for pain) are widely used. Physical therapy, massage, and therapeutic exercise are prescribed.

Alcoholic Polyneuropathy

Alcoholic polyneuropathy is one of the most common forms of nervous system damage associated with alcohol abuse. There is reason to believe that the true incidence of the entire spectrum of alcohol-related neurological disorders is likely underestimated. Alcoholic polyneuropathy is a symmetrical sensorimotor polyneuropathy grounded in axonal degeneration. This peripheral nerve lesion may result from the direct Toxic effects of alcohol metabolites (acetaldehyde), thiamine deficiency, and presumably deficiencies in other B-group vitamins (such as Folic acid) stemming from inadequate, poor-quality (predominantly carbohydrate-based) Nutrition. Nevertheless, the precise mechanisms underlying this pathology remain elusive in many specific cases. Alcoholic polyneuropathy in middle-aged and older individuals is frequently misdiagnosed by specialists as dysmetabolic or diabetic, whereas in reality, it most often has a mixed etiology. Histological changes consist of distal axonal degeneration and secondary demyelination, and are non-specific.

Typically, alcoholic polyneuropathy affects the legs more severely than the arms. Patients complain of burning pain, paresthesias, and numbness in the feet and lower legs, accompanied by painful calf muscle cramps. When fibers mediating deep sensation are involved, coordination disturbances—specifically sensory ataxia—may develop. Weakness of the foot and toe extensors appears gradually. Physical examination reveals diminished or absent deep tendon reflexes, tenderness upon Palpation of muscles and soft Tissues overlying major nerve trunks, "stocking-and-glove" hypesthesia, and atrophy of the distal limb muscles. Contact with the skin of the extremities exacerbates the pain. Autonomic disturbances are characteristic, manifesting as hyperhidrosis, edema, skin discoloration in the limbs, and dystrophic nail changes. In many alcohol-dependent patients, polyneuropathy is subclinical and confirmed only via electrophysiological testing. It must be emphasized that patients with alcohol dependence may also suffer from polyneuropathy of other etiologies (diabetes mellitus, vasculitis, Guillain-Barré syndrome, etc.). Alcoholic polyneuropathy must be differentiated from acute alcoholic myopathy, while tabes dorsalis should be ruled out when sensory ataxia is present.

Various drug classes are employed to alleviate pain, including novel antiepileptic agents (gabapentin, pregabalin, carbamazepine) and antidepressants (amitriptyline). Total abstinence from alcohol, a balanced and nutritious diet, courses of thiamine administration (2–3 ml of a 5% solution intramuscularly, followed by 100–200 mg orally per day) combined with other B-complex vitamins, ipidacrine (myoin), therapeutic exercise, and physical therapy halt the progression of polyneuropathy or even promote partial regression of symptoms. However, complete recovery of neurological deficits does not always occur.

Plexopathy

Brachial plexopathy. Lesions of the Brachial Plexus result in total paresis or paralysis of the arm, impairment of all sensory modalities, and severe autonomic-trophic disorders. Patients experience severe and persistent pain in the affected limb. The most common causes of brachial plexus injury include trauma, compression or stretching during a humeral head dislocation, clavicular fractures, penetrating wounds, improper arm positioning during anesthesia, Cervical Ribs, Pancoast tumors and breast cancer, metastatic lesions, etc. Lesions of the upper trunk of the plexus (C5-C6 roots) lead to paralysis of the proximal limb muscles (Erb-Duchenne palsy). Involvement of the lower trunk (C8-Th1 roots) affects the distal parts of the arm (Dejerine-Klumpke palsy). Traction injuries may cause avulsion of the cervical roots from the spinal cord. This condition is characterized by paroxysms of excruciating pain, Horner's syndrome, and signs of spinal cord pathway involvement. Such injuries require early surgical intervention.

Lumbosacral plexopathy. The Lumbosacral plexus can be damaged in pelvic bone fractures, Diseases of the abdominal and pelvic Organs (cervical and prostate cancer, colorectal tumors, retroperitoneal lymphoma, aortic aneurysms, abscesses, etc.), as well as during abdominal, pelvic, and hip surgeries. Trauma may lead to avulsion of nerve roots from the spinal cord. This condition manifests as pain in the lower back, gluteal region, hip joint, and leg, widespread sensory loss, unilateral weakness and atrophy of the Pelvic Girdle and leg muscles, along with absent knee and ankle reflexes. Signs of severe autonomic dysfunction typically occur on the affected side. The localization of motor and sensory deficits depends on the extent of the lesion—specifically, whether the lumbar or sacral Divisions of the plexus are involved.

Treatment largely depends on the underlying cause of the plexopathy. Management includes analgesics, NSAIDs, vasoactive agents, physical therapy, and exercise therapy (physiotherapy). In some cases, reconstructive surgical interventions using microsurgical techniques are performed.

Clinical Cases

Case 1

A 46-year-old man presents with systematic pain, numbness, and decreased strength in his upper and lower extremities, as well as unsteadiness and gait instability. These symptoms appeared approximately three years ago and have been progressively worsening. Physical examination reveals decreased grip strength in the hands and strength in the feet, muscle wasting in the forearms and calves, reduced brachioradialis and knee reflexes, and absent ankle and plantar reflexes bilaterally. In addition, there is a reduction in superficial and deep sensation in the distal parts of the arms and legs, accompanied by cold, clammy, and cyanotic hands and feet. He has a 15-year history of alcohol abuse.

• Identify the main neurological disorders.

• Determine the type of sensory impairment.

• How can the unsteadiness and gait instability be explained?

• Formulate the topographic diagnosis.

• Formulate and justify the clinical diagnosis.

• Outline the directions for Differential diagnosis.

• Name the necessary instrumental neurological examinations.

• Outline the plan for the somatic examination.

• Specify the Morphology/3.html">MAIN DIRECTIONS OF comprehensive therapy.

• Determine the prognosis of the disease.

• Name the most common types of polyneuropathies.

Case 2

A 57-year-old woman complains of sudden, intense, lancinating pain attacks in the upper jaw, left side of the Nose, and cheek, lasting a few seconds. The pain is triggered by chewing, speaking, touching the cheek or gum mucosa, and exposure to cold, recurring 4 to 10 times a day. The pain attacks are accompanied by lacrimation, facial flushing, and spasm of the facial muscles. The pain started about six months ago and was initially attributed to dental disease. Neurological examination reveals no focal neurological deficits. In the interval between

attacks, tenderness persists upon palpation of the soft facial tissues overlying the left infraorbital notch.

• Determine the leading neurological syndrome.

• Formulate the topographic diagnosis.

• Justify and formulate the clinical diagnosis.

• Outline the direction of the differential diagnosis.

• Indicate the schedule of instrumental investigations.

  • WHAT IS A trigger zone?

  • What is the difference between trigeminal neuralgia and trigeminal neuropathy?

  • Name the possible levels of lesion in the trigeminal nerve system.

  • Which medications are most effective in the treatment of trigeminal neuralgia?

  • Name the possible surgical treatment options.

  • Determine the prognosis of the disease.

Case 3

A 22-year-old patient developed mild pain in the left ear and mastoid region following hypothermia. The next morning, he noticed that he could not close his left eye, his Mouth was deviated to the right, and there was a complete loss of movement in the muscles of the left side of his face. Examination revealed that the patient was unable to wrinkle his forehead or close his left eye (the Eyeball deviates upward and outward upon attempting to do so), nor could he puff out his Cheeks. When attempting to show his teeth, the mouth deviates to the right. There are no other abnormalities in the neurological status.

  • List the main neurological disorders.

  • Determine the level of the facial nerve lesion.

  • How does central facial palsy differ from peripheral facial nerve involvement?

  • Name the possible levels of lesion in the facial nerve system.

  • What other symptoms may accompany a facial nerve lesion?

  • Formulate and justify the clinical diagnosis.

  • Outline the main directions for differential diagnosis.

  • Outline the instrumental examination plan.

  • Determine the possible etiopathogenesis of the disease.

  • What should the initial therapy regimen consist of?

  • Outline the management plan for this category of patients.

  • Determine the prognosis of the disease.

Case 4

A 42-year-old man, after prolonged work (laying parquet flooring) in a sitting position with his legs sharply flexed at the knee, hip, and ankle joints, felt numbness along the anterolateral aspect of the right lower leg, as well as the dorsal surface of the right foot and toes. The next day, the numbness was accompanied by pain in the popliteal fossa radiating down the posterolateral aspect of the right lower leg, along with an inability to dorsiflex and evert the right foot. Examination reveals mild Swelling on the dorsum of the foot and hyperhidrosis. The right Achilles reflex is decreased.

  • List the main neurological disorders.

  • Determine the type of sensory disturbances.

  • Determine the type of motor impairments.

   • Formulate the topical diagnosis.

   • Formulate and justify the clinical diagnosis.

   • Determine the possible etiopathogenesis of the disease.

   • Outline the directions for differential diagnosis.

   • State the necessary additional diagnostic examinations.

   • List the core components of treatment.

   • Determine the prognosis of the disease.

Case 5

A 30-year-old man noticed clumsiness and weakness in his hands and forearms in the morning while at work. By evening, weakness in his legs had developed. The next day, he experienced aching pain in the muscles of his arms and legs, and the weakness worsened. Examination revealed a significant decrease in muscle strength and a restricted range of active movements, predominantly in the distal extremities of both upper and lower limbs. Tendon-periosteal reflexes in the arms and legs were depressed. Pathological hand and foot reflexes were absent. A reduction in all modalities of sensation was observed in the distal parts of the arms and legs, along with tenderness upon palpation along the nerve trunks. Nerve stretching signs in the limbs were moderately pronounced. Cerebrospinal fluid analysis showed a protein level of 0,9 g/L and lymphocytes at 12 х 10⁶/L.

   • Identify the leading neurological disorders.

   • Determine the type of motor impairment.

   • Determine the type of sensory disturbances.

   • How can the cerebrospinal fluid test results be interpreted?

   • Name the nerve-stretching signs familiar to you.

   • Formulate the topical diagnosis.

   • Formulate the clinical diagnosis.

   • Indicate possible Variants of the etiology and pathogenesis of the disease.

   • Outline the directions for differential diagnosis.

   • State the necessary additional diagnostic Procedures.

   • List the main elements of the treatment regimen.

   • What constitutes the danger of progressive neurological disorders?

   • Name possible complications.

   • Determine the prognosis of the disease.

Case 6

A 64-year-old man experienced, for no apparent reason, itching followed by severe shooting pain in the right side of his face and the auricular region. He complained of general weakness, dizziness, and tinnitus. A low-grade fever was noted. Two days later, edema, erythema, and vesicular rashes appeared on his cheek and in the area of the auricle. Examination revealed hyperesthesia on the right side of the face. Meningeal signs were absent.

  • List the main neurological disorders.

  • Explain the Water/144.html">Origin of the cutaneous symptoms.

  • Formulate the topical diagnosis.

  • Formulate and justify the provisional clinical diagnosis.

  • Determine the main directions of the differential diagnosis.

  • Outline the plan for instrumental and Laboratory examination.

  • Indicate the Main Components of the therapeutic program.

  • Determine the prognosis of this disease.

  • Name the potential complications and long-term consequences of the disease.