Peripheral neuropathy. Causes, symptoms, diagnosis and treatment.

The collective concept of neuropathy of the lower extremities combines pathologies of the peripheral nervous system in the legs. They manifest themselves with a variety of symptoms, including sensory, motor and vegetative-trophic disorders.

Diagnosis of this vertebrogenic disease is not difficult, and treatment started at an early stage allows for recovery in almost 100% of cases. It is a lesion of the peripheral system, one or more nerves, and, as a rule, is associated with impaired nutrition of nerve fibers and the development of degenerative processes in their membranes.

Causes of neuropathy of the lower extremities

The development of the disease may be associated with the following factors:

• long-term exposure to toxic substances (drugs, alcohol, arsenic, lead, mercury, etc.);
• metabolic disorders (diabetes mellitus, thyroid dysfunction, chronic renal failure);
• long-term hypovitaminosis;
• injuries;
• taking certain medications;
• infections (chickenpox, diphtheria, mumps, HIV infection);
• autoimmune diseases (for example, Guillain-Baré syndrome);
• burdened by heredity (genetically determined pathologies, for example, Charcot-Marie-Tooth amyotrophy).

Definition

Radiculopathy is a symptom, not an independent disease, a symptom of a disease of the peripheral nervous system, the cause of which in most cases is protrusion or herniation of the intervertebral disc and arthrosis of the vertebral joints. And before continuing, I would like to start with the anatomy of the spine and the structure of the nervous system.

According to the classification of vertebrae, free vertebrae are distinguished:

• cervical vertebrae – 7 pcs.
• thoracic vertebrae – 12 pcs.
• lumbar vertebrae – 5 pcs.

and fused:

• sacral vertebrae – 5 pcs.
• coccygeal vertebrae – 3-5 pcs.

A distinctive feature of the cervical vertebrae is the presence of an opening in the transverse process - the vertebral arteries pass through it. Another distinctive feature is the atlas and axial vertebrae (1st and 2nd vertebrae), they are atypical, they lack a body, spinous and articular processes. 3 - 7 cervical vertebrae - typical.

In any typical vertebra, the body, arch and process are distinguished, and their connections are distinguished according to the parts of the vertebra.

The vertebral bodies are connected to each other through intervertebral discs, anterior and posterior longitudinal ligaments.

The arches are connected by the ligamentum flavum.

Among the processes, spinous, transverse and articular (upper and lower) are distinguished. The spinous processes are connected by the interspinous ligament, the transverse ones by the intertransverse ligament, and the articular processes by the intervertebral joints.

All vertebrae form the spinal column among themselves, and when the vertebrae connect, intervertebral foramina are formed (right and left), through which spinal nerves and vessels pass.

The spinal column does not occupy a strictly vertical position; it has physiological curves. The curve facing backward is called kyphosis, and the curve facing forward is called lordosis.

The spinal cord located inside the spinal canal begins from the foramen magnum and ends to the first lumbar vertebra (LI) in men, 2 lumbar vertebra (LII) in women.

There are 124 roots extending along the spinal cord. 62 posterior and 62 anterior, from which 31 pairs of spinal nerves are formed.

Having understood the anatomy of the spine and the formation of nerve roots, you can move on to the disease.

All back pain can be divided into specific, nonspecific and radicular.

So, radiculopathy is a disease caused by compression (damage) of a nerve root, causing radicular pain in the back. Compression occurs due to the fact that the intervertebral disc, which performs a shock-absorbing function in the spine, begins to protrude under external loads and a non-functioning muscle corset. Thus forming a protrusion, and subsequently a herniation of the intervertebral disc.

For understanding, here are statistics on the prevalence of back pain:

• specific – 85% (due to muscles, ligaments, tendons, small joints),
• nonspecific – 10% (vertebral fracture, tuberculosis, osteomyelitis, abscess, spinal stenosis, neoplasm, ankylosing spondylitis, etc.)
• radicular up to 4%.

In other words, the prevalence of radiculopathy is 4% of all back pain syndromes.

Classification of lower extremity neuropathy

The following types and forms of the disease are distinguished:

• inflammatory (develops due to inflammation of nerve tissue);
• toxic (occurs as a result of poisoning of the body with toxins);
• allergic (caused by individual hypersensitivity to environmental factors);
• traumatic (develops as a result of injuries to the lower extremities);
• axonal (accompanied by destruction of the axial cylinder of the nerve fiber);
• demyelinating (occurs in multiple sclerosis, encephalomyelitis).

According to the duration of its course, it can be acute and chronic, and according to the affected area - distal (affects distant parts of the legs) and proximal (affects the upper parts of the legs).

Diagnosis of neuropathy and angiopathy

The diagnosis of diabetic neuropathy is based on symptoms, history, and clinical examination. During the exam, your doctor may check your muscle strength and tone, tendon reflexes, and sensitivity to touch, temperature, and vibration.

Additional diagnostic tests:

• Nerve conduction studies. This test checks how well the nerves in the arms and legs conduct electrical signals.
• Electromyography (EMG). Often performed in conjunction with nerve conduction studies, electromyography measures the electrical discharges produced in your muscles.
• Quantitative sensory testing. This non-invasive test is used to evaluate how responsive nerves are to vibration and temperature changes.
• Vegetative testing. The reaction of blood pressure in different body positions and the ability to sweat are assessed.

Lower extremity neuropathy clinic

Nerve fibers in the human body are divided into three types: motor, sensory, and autonomic. Manifestations of neuropathy depend on which types of fibers are involved in the pathological process:

1. Motor neuropathy is manifested by weakness of individual muscle groups, causing difficulty in movement, and is accompanied by cramps and spasms. The pathological process spreads from bottom to top, and in severe forms can deprive a person of the ability to move independently.
2. Sensory neuropathy is accompanied by pain and individual sensitivity to external factors (for example, ordinary touching the skin on the legs causes intense pain).
3. Autonomic neuropathy is characterized by increased sweating, imbalance in the urinary process, etc.

Clinical manifestations of lower extremity neuropathy include:

• stabbing, burning, bursting pain in the legs;
• feeling of “pins and needles”, a foreign body under the skin;
• impaired recognition of hot and cold, increased or decreased pain threshold, problems with feeling the surface under your feet when moving;
• decreased tendon reflexes (usually Achilles and knee);
• muscle spasms and cramps;
• progressive muscle weakness;
• muscle atrophy;
• dryness and thinning of the skin on the legs, hair loss, age spots;
• swelling, trophic ulcers.

Causes of the disease

Patients do not always seek help in a timely manner. The reason for this is the numerous misconceptions associated with this disease. So, many are sure that causeless pain will go away on its own. But this is not true; over time, the pathology progresses and treatment becomes more difficult.

The cause of nerve dysfunction is several factors at the same time. In diabetes, damage occurs due to impaired blood supply and metabolism in the nerve tissue, the formation of edema and compression, and the synthesis of antibodies to the membrane of the nerve trunks. As a result, they atrophy and lead to the appearance of pathology.

Toxic and infectious lesions are also associated with the destruction of the outer sheath of nerve fibers. With alcoholism, vitamin B12 deficiency, excess B6 and nutritional disorders, small peripheral nerve processes - axons - are primarily destroyed, which causes loss of sensitivity in the hands or feet.

Vascular atherosclerosis, thrombosis of small capillaries, together with metabolic disorders, also cause neuropathy. This type of damage affects the optic nerve. In pregnant women, polyneuropathy is associated with the production of antibodies, disruption of nerve nutrition and toxic damage from their own metabolic products.

Hereditary neuropathies are characterized by genetic disorders that lead to changes in metabolism and the accumulation of toxic substances in tissues. They damage the myelin sheath of the nerve. In some cases, a hereditary disease leads to gradual atrophy of groups of nerves and severe motor and sensory disorders that cannot be treated.

Features of treatment of neuropathy of the lower extremities

Identification of the provoking factor (endocrine disorders, infections, injuries, etc.) is the basis for the development of therapy. The latter is aimed at eliminating the negative impact of the detected disease on the nerve fibers.

How to treat lower extremity neuropathy itself? Treatment of this disease is complex and includes:

• drug therapy aimed at improving the conduction of impulses along nerve fibers, muscle relaxation, pain relief, replenishing vitamin deficiencies, getting rid of toxins, etc.;
• physical therapy (to maintain muscle tone);
• physiotherapy (manual therapy, laser therapy, electrical stimulation, vacuum therapy).

More information about the treatment of the disease can be found on the website of the CDC "IntegraMed" (formerly "NDC").

Treatment

The goal of treatment for polyneuropathy is to treat the underlying disease and minimize symptoms. If laboratory tests and other examinations indicate that there is no underlying disease, the doctor may recommend watchful waiting to see if the symptoms of neuropathy improve on their own. If there is exposure to toxins or alcohol, your doctor will recommend avoiding these substances.

Drug treatment

Medicines used to relieve pain from polyneuropathy include:

• Painkillers such as paracetamol or NSAIDs reduce pain
• Medicines containing opioids, such as tramadol (Conzip, Ultram ER and others) or oxycodone (Oxycontin, Roxicodone and others), can lead to dependence and addiction, so these drugs are generally prescribed only when other treatments have no effect.
• Anticonvulsants. Medications such as gabapentin (Gralise, Neurontin) and pregabalin (Lyrica), developed to treat epilepsy, can significantly reduce the pain of neuropathy. Side effects of these drugs may include drowsiness and dizziness.
• Capsaicin. A cream containing this substance (found naturally in hot peppers) can be used to provide some relief from the symptoms of neuropathy. But given the irritating effect of capsaicin on the skin, not all patients can tolerate the effects of capsaicin creams.
• Antidepressants. Some tricyclic antidepressants, such as amitriptyline, doxepin, and nortriptyline (Pamelor), can be used to reduce neuropathy pain through their actions on the central nervous system.
• The serotonin and norepinephrine reuptake inhibitor duloxetine (Cymbalta) and the antidepressant venlafaxine (Effexor XR) may also relieve pain from peripheral neuropathy caused by diabetes. Side effects may include dry mouth, nausea, drowsiness, dizziness, decreased appetite, and constipation.
• Intravenous immunoglobulin is the mainstay of treatment for chronic inflammatory demyelinating polyneuropathy and other inflammatory neuropathies.
• Alpha lipoic acid. Used to treat peripheral neuropathy in Europe for many years. This antioxidant helps reduce symptoms. You should discuss taking alpha lipoic acid with your doctor because it may affect your blood sugar levels. Other side effects may include stomach upset and skin rash.
• Herbs. Some herbs, such as evening primrose oils, may help reduce neuropathic pain in patients with diabetes.
• Amino acids. Amino acids such as acetyl-L-carnitine may help improve symptoms of peripheral neuropathy in patients undergoing chemotherapy and in patients with diabetes. Side effects may include nausea and vomiting.

In addition to drug treatment, other treatment methods may be used.

• Myostimulation allows, to a certain extent, to restore the conduction of nerve impulses through the muscles.
• Plasmapheresis and intravenous administration of immunoglobulin.
• Exercise therapy. If you have muscle weakness, physical activity can improve muscle strength and tone. Regular exercise, such as walking three times a week, can reduce neuropathy pain, improve muscle strength, and help control blood sugar levels. Exercises such as yoga and tai chi can also be quite effective.
• Acupuncture. Impact on biologically active points improves the sensitivity of nerve receptors and reduces pain.

Recommendations for patients with polyneuropathy

• It is necessary to take care of your feet, especially if you have diabetes. You should check your feet daily for blisters, cuts, or calluses. Soft, loose cotton socks and soft boots should be worn.
• You need to quit smoking. Smoking can affect circulation in the extremities, increasing the risk of foot problems and other neuropathy complications.
• Eat healthy. A healthy diet is especially important to ensure that the patient receives the necessary vitamins and minerals.
• We must avoid drinking alcohol. Alcohol can worsen the symptoms of polyneuropathy.
• Monitoring blood glucose levels in the presence of diabetes will help keep blood glucose levels under control and may help improve neuropathy.

Prevention

The patient must take preventive measures that will help avoid relapse or the occurrence of a dangerous disease. They include enriching the diet with vitamins, regular monitoring of blood sugar levels, and complete cessation of smoking, drugs and alcoholic beverages.

To prevent the disease, it is recommended:

• wear comfortable shoes that do not pinch the foot, impairing blood flow;
• regularly inspect your shoes to avoid the formation of fungus;
• avoid walking long distances;
• do not stand in one place for a long time;
• wash your feet with cool water or do contrast baths, which helps improve blood circulation in the body.

Victims in remission are strictly prohibited from taking medications without the consent of the attending physician. It is important to promptly treat inflammatory diseases, take precautions when working with toxic substances that have a detrimental effect on the body, and regularly perform therapeutic physical exercises.

Pathogenesis

The onset of the development of the disease is two factors that are related to each other: mechanical irritation of the root and/or spinal ganglion and inflammatory changes in the perineural tissue that occur as a result of penetration of the disc into the epidural space.

In this case, factors of root compression can be both disc herniations and bone growths (uncovertebral, spondyloarthritic). Compression can also be caused by hypertrophied ligaments and periarticular tissues, vascular structures (epi- and subdural hematomas, arteriovenous malformations, epidural hemangiomas).

Until now, “blank spots” remain in the pathophysiological concept of radicular pain. It is assumed that the basis of radicular pain is axonal dysfunction caused by various etiological factors, including neural compression, ischemia, damage by inflammatory and other biologically active substances. Spinal roots (unlike peripheral nerves) have a weak blood-neural barrier, making the axon more susceptible to compression injury.

Increased vascular permeability due to mechanical compression of the root leads to endoneurial edema. As a result, a precedent arises that prevents full capillary blood supply and the formation of interneural fibrosis. The spinal root receives up to 58% of its nutrition from the surrounding cerebrospinal fluid (CSF). Perineural fibrosis prevents the complete supply of axonal tissue with nutrients due to diffusion from the CSF, which also contributes to increased sensitivity of the fiber to pressure.

Studies using experimental root compression have shown that even at minimal pressure (5–10 mm Hg) venous blood flow ceases.

The occlusion pressure of the radicular arterioles is significantly higher (approximately corresponds to mean blood pressure), but depends on the potential for venous stasis. Ischemia of nerve fibers or venous congestion leads to biochemical changes that can maintain pain sensations.

Work with experimental root compression demonstrates that compensatory diffusion of nutrients from the CSF is impaired in the setting of epidural inflammation or in the presence of fibrosis.

Recent studies have shown that degenerative changes in the nucleus pulposus and annulus fibrosus can lead to local neural changes and the synthesis of algogenic agents such as metalloproteinases, tumor necrosis factor (TNF), interleukin (IL)-6 and prostaglandin E2. Pathogenetically, the pain syndrome in radiculopathy is of a mixed nature, including nociceptive and neuropathic components.

Diseases of the peripheral nervous system

Diseases of the peripheral nervous system (neuritis, polyneuritis, neuropathy).

Among the most frequently diagnosed diseases of the human peripheral nervous system, there are several forms of neuritis, cries, neuralgia, as well as all sorts of these pathologies, which have different topography and most often manifest as sharp and sometimes mild pain of a permanent nature. By the way, such a common radiculitis is also a peripheral lesion.

Diseases of the peripheral nervous system are the most common in neurological clinics and account for up to 50% of outpatients. Not presenting, as a rule, a threat to the lives of patients, they are the main cause of disability.

The causes of damage to the peripheral nervous system can be acute and chronic infections, trauma, intoxication, hypovitaminosis, ischemia, hypothermia, compression, and degenerative changes in the spine.

Pathomorphologically, when a peripheral nerve is damaged, swelling and disintegration of the myelin sheath, proliferation of Schwann cells are observed first, and then structural changes occur in the nerve fibers themselves. In this case, vasodilation, exudation, perivascular edema, and hemorrhages are noted in the connective tissue sheaths of the nerve.

If inflammatory phenomena predominate in etiopathogenesis, then peripheral pathology is designated with the ending “it”, if metabolic - then “ia”. If the cause of the disease is degenerative changes in the spine, then the diagnosis is supplemented with the words “vertebrogenic”, “spondylogenic”.

Pathologies of the peripheral nervous system by location

Depending on the location and pathogenesis, the following diseases of the peripheral nervous system are distinguished.

Neuritis (neuropathy)

- a disease in which pathomorphological changes in the nerve are accompanied by disturbances in motor, sensory and autonomic functions. Neuralgia is characterized by attacks of pain along the nerve without signs of organic damage.

This pathology of the peripheral nervous system is caused mainly by metabolic, degenerative processes in the nerve fiber, with minor inflammatory changes in it.

• Polyneuritis
  (polyneuropathy) is damage to many nerves.
• Plexitis
  is a lesion of the nerve plexus.
• Ganglionitis
  is a lesion of the intervertebral nodes.
• Radiculitis
  is a lesion of the spinal cord roots.
• Radiculoneuritis
  is a simultaneous lesion of the spinal cord roots and nerve trunks.
• Myeloradiculoneuritis
  - damage to the spinal cord, roots and nerve trunks.

The most common forms of disorders of the peripheral nervous system are vertebrogenic pathology (osteochondrosis), neuritis (neuropathy) and neuralgia. Moreover, the most often affected are those nerves whose trunks pass through narrow bone canals - facial, trigeminal, sciatic.

Peripheral nervous system disorders: facial neuritis

Neuritis of the oculomotor nerve.

The disease is predominantly of vascular, inflammatory, diabetic origin. Observed in intracranial tumors.

Such peripheral neuritis is manifested by drooping of the upper eyelid (ptosis), dilation of the pupil (mydriasis), divergent strabismus and double vision (diplopia).

Treatment

according to the etiology of the disease, vitamin therapy, biostimulants.

Neuropathy (neuritis) of the facial nerve.

Lesions of other cranial nerves are more common.

The cause of the disease can be hypothermia, infection, trauma, inflammation of the ear or meninges, tumors of the base of the skull. Since the trunk of the facial nerve passes through a narrow bone canal and its terminal branches are located superficially, the nerve is easily injured, and during inflammatory processes tissue swelling develops, which leads to compression of the nerve and the vessels that supply it.

This peripheral nerve neuritis develops acutely or subacutely. There are peripheral and central facial palsy.

Peripheral paralysis is characterized by facial asymmetry - the face is skewed towards the healthy side. On the affected side, the skin folds are smoothed, the eye does not close (lagophthalmos), when trying to close the eye, the eyeball turns up (Bell's sign), food gets stuck behind the cheek, teeth are grinned more in the healthy direction. Dry eyes or watery eyes, disturbances in hearing, taste and salivation may occur.

With central paralysis, only smoothness of the nasolabial fold and drooping of the corner of the mouth are observed.

A complication of this disease of the peripheral nerves can be persistent contracture of the affected muscles and tonic muscle spasm - facial hemispasm.

Diagnostics

is based on clinical data and to clarify the diagnosis, an LOP examination, skull radiography, and computed tomography are sometimes performed.

Treatment

This disease of the peripheral nervous system must begin early and correspond to the cause of the lesion. For infectious-inflammatory origin, salicylates, methenamine, indomethacin, acyclovir, and prednisolone are prescribed.

In parallel with the etiological treatment, vasodilators are prescribed: dibazol, aminophylline, trental, nicotinic acid, decongestants (Lasix, furosemide, hypothiazide), vitamins

From 5-7 days of illness, thermal procedures (UHF, paraffin, ozokerite) are prescribed.
In the recovery period, prozerin, aloe, FiBS, ultrasound with hydrocortisone are used on the mastoid process and the affected half of the face, electrical stimulation of the facial muscles, exercise therapy, acupuncture massage, and acupuncture.
If there is no effect within 12 months, they resort to neurosurgical intervention.

Care consists of instilling moisturizing eye drops and wearing glasses during the day. At night, apply eye ointment and cover your eyes with a bandage.

Prevention:

avoid hypothermia, anti-epidemic measures.

Neuritis of the peripheral nerves of the extremities: symptoms and treatment of neuropathies

Neuropathies of the peripheral nerves of the extremities are most often caused by external trauma or compression of the nerve trunk. It is possible that the nerve in the bone canal may be pinched, compressed in deep sleep, when throwing back the arm, during prolonged anesthesia, or when applying a tourniquet. Also, the cause of neuritis can be infections, ischemia, and intoxication.

Radial nerve neuropathy.

It manifests itself as a symptom of a “dangling hand,” while the patient cannot straighten the arm at the wrist and elbow joints, cannot abduct the thumb and supinate the palm, the carporadial reflex decreases, and sensitivity on the dorsal surface of the 1st, 2nd, and 3rd fingers is impaired.

Ulnar nerve neuropathy is characterized by a “bird’s foot” deformity of the hand as a result of paralysis and atrophy of the small muscles of the hand; violation of adduction and abduction of fingers; pain and decreased sensitivity on the 5th and 4th fingers.

Median nerve neuropathy.

It manifests itself as a violation of flexion of the hand and fingers in the interphalangeal joints, opposition of the thumb; impaired sensitivity on the lateral surface of the palm and 1-4 fingers. Also symptoms of such peripheral neuropathy are atrophy of the muscles of the forearm and flattening of the palm like a “monkey’s paw”. The patient cannot clench his fingers into a fist. Characterized by severe pain with a causal tinge and pronounced vegetative-vascular and trophic disorders (hyperhidrosis, hyperkeratosis, brittle nails, atrophy and cyanosis of the skin).

Neuropathy of the external cutaneous nerve of the thigh (Roth disease)

. Occurs as a result of infection, intoxication (alcohol, nicotine, diabetes), atherosclerosis, and long-term nerve injury. This peripheral nerve neuropathy manifests as paresthesia and pain along the outer thigh. The pain is worse at night and especially in an upright position and when walking. Hyper- or hypoesthesia is determined along the outer surface of the thigh.

Neuropathy (neuritis) of the peroneal nerve.

It is characterized by drooping of the foot and the inability to straighten it and the toes. The patient cannot stand on his heel. The muscles of the anterior surface of the lower leg atrophy. Sensitivity on the outer surface of the lower leg and the dorsum of the foot is impaired. The gait becomes step-like, “cock-like.”

Neuropathy (neuritis) of the tibial nerve.

Leads to impaired flexion of the foot and fingers. The patient cannot stand on his toes. The muscles of the back of the lower leg atrophy, and the Achilles reflex fades. Sensitivity disturbances are noted along the back surface of the lower leg and sole; severe pain and vegetative-trophic disorders.

Treatment

peripheral neuropathy of the extremities includes the use of vitamins B, C, nicotinic acid, aloe extract, proserin, and, if necessary, analgesics.

Physiotherapy is widely used:

• UHF
• Ural Federal District
• Electrophoresis
• Ultrasound
• Laser and magnetic therapy
• Massage
• Exercise therapy

Care consists of preventing persistent paresis and contractures (suspension, bandages, splints for fixing the limb, orthopedic shoes), teaching the patient the elements of therapeutic exercises. If there is no recovery within two months, surgery is indicated.

Lesions of peripheral nerves: neuralgia

Trigeminal neuralgia.

A disease of peripheral nerves with severe pain and a relapsing course.

The cause may be infections, intoxications, atherosclerosis, hypothermia, pathological processes at the base of the skull, in the paranasal sinuses, teeth, orbits, and narrowing of the bone openings.

The main symptom of this disease of the peripheral system

- attacks of sharp shooting pain in the zone of innervation of one or more branches of the nerve. The pain lasts a few seconds, less often - minutes. Pain is provoked by excitement, chewing, talking, touching the tongue to sensitive points (triggers) of the mucous membrane of the mouth and gums. Therefore, patients may develop obsessive fear, and in order not to provoke an attack, they freeze, hold their breath, and are afraid to make the slightest movement. Attacks may be accompanied by redness of half the face, cramps of facial muscles, lacrimation, and copious nasal discharge. During the interictal period, one can detect hyperesthesia in the area of ​​the affected branch and pain at the point of its exit.

When the trigeminal nerve ganglion is damaged, constant burning pain and herpetic rashes are observed. Herpetic keratitis is especially dangerous when the first branch of the nerve is affected.

Treatment

primarily aimed at eliminating the cause of the disease.

Next, analgesic and anti-inflammatory drugs are prescribed (analgin, sedalgin, reopirin, indomethacin, pentalgin):

To suppress neuralgic paroxysms, carbamazepine (finlepsin), trimethin, convulex clonazepam, neurontin, lamictal are used:

They also stimulate metabolic processes (retabolil, solcoseryl, actovegin, B vitamins): Baclofen is also used: For herpetic rashes, acyclovir, herpesin are prescribed:

Physiotherapy includes UHF, ultraviolet irradiation, diadynamic currents, SMT, novocaine electrophoresis, laser therapy..

Care

consists in creating a protective regime, preventing the patient from hypothermia and feeding him non-hot, well-purified food.

Neuralgia of the pterygopalatine ganglion (Slader syndrome).

The disease is caused by the same reasons as trigeminal neuralgia. Symptoms of this disease of the peripheral nervous system are attacks of pain in the eye, root of the nose, jaw, teeth spreading to the tongue, soft palate, ear, and cervicohumeral area. Sometimes the pain covers half of the head, noise, dizziness, and ringing in the ear appear. At the same time, half of the face turns red, tearing and salivation intensify. The attack lasts up to one hour.

Treatment and care

are carried out according to the same scheme as for trigeminal neuralgia. As a local therapy, the middle nasal passage is lubricated with novocaine.

Neuralgia of the glossopharyngeal nerve.

Occurs more often in older people. Causes: atherosclerosis, tumors, scars, osteophytes. This disorder of the peripheral system is characterized by attacks of severe pain in the root of the tongue, tonsils, radiating to the ear, eye, and neck. In this case, the patient experiences dry mouth, cough, and excessive salivation.

Treatment

carried out as with trigeminal neuralgia; locally - lubricating the root of the tongue with cocaine.

Neuralgia of the occipital nerve.

Caused by hypothermia, infections, degenerative processes in the spine, arachnoiditis and tumors of the posterior cranial fossa. The disease is characterized by attacks of pain in one half of the back of the head, radiating to the ear, neck, shoulder girdle, and shoulder blade. The pain intensifies with movement, coughing, sneezing. Possible forced head position. With this disorder of a peripheral nature, pain in the nerve exit points and sensitivity disorders in the occipital area are noted.

Treatment

underlying disease, pain medications, vasodilators, vitamins, locally - UV irradiation, UHF.

Intercostal neuralgia.

It can be primary and secondary, i.e. arising against the background of other diseases, especially with pathology of the spine (osteochondrosis, tumors, tuberculosis) and internal organs (lungs, pleura, liver).

The disease is characterized by girdling, shooting pains spreading from the spine along the intercostal spaces around the chest. The pain intensifies with movements and deep breaths. There are sensitivity disorders in the area of ​​innervation of the intercostal nerves, pain in the paravertebral and intercostal points. Loss of abdominal reflexes and paresis of the abdominal muscles are possible. When the intervertebral ganglion is involved in the process, symptoms of herpes zoster appear. To clarify the diagnosis, a thorough examination of the patient is necessary in order to exclude the secondary nature of neuralgia.

Treatment includes eliminating the cause of the disease, painkillers (analgin, baralgin, diclofenac, indomethacin):

Anticonvulsants (finlepsin, 0.2 g 1-2 times a day):

Vitamins, physiotherapy (UHF, DDT),

Care

provides for the creation of a gentle regime, the choice of a comfortable position, and the prevention of hypothermia.

Shingles (ganglionitis, herpetic intercostal neuralgia).

The disease is caused by the neurotropic herpes zoster virus and is provoked by hypothermia. In the spinal nodes and their cranial analogues, an inflammatory process develops, spreading to the nerves and roots.

The disease begins with general malaise, fever and pain in the area of ​​innervation of the affected ganglion (most often in the thoracic region). After 2-3 days, redness and rashes of very painful blisters filled with serous fluid appear at the site of pain. The vesicles often fester, forming pustules that become covered with a crust that falls off after a few days.

When the gasserian node is damaged, rashes appear on the skin of the forehead, upper eyelid, bridge of the nose and on the membranes of the eye, which can result in keratitis and blindness.

Some patients who have had herpes zoster experience pain for a long time (postherpetic neuralgia) and relapses are possible.

Treatment includes antiviral drugs (acyclovir 0.8 x 3, retrovir 0.25 x 5, valacyclovir), detoxification (hemodez), dehydration (furosemide), chimes, analgesics (azafen 0.025 x 6, pyrazidol 0.05 x 3, mexiletine , finlepsin, amitriptyline, herpesin):

Tebrofen ointment, gassipol, and ultraviolet radiation are used topically.

Polyneuritis and polyneuropathy of peripheral nerves

Polyneuritis

- multiple lesions of peripheral nerves of infectious origin.

Polyneuropathy

- toxic damage to the nerves as a result of intoxication of the body, metabolic disorders, allergic reactions, circulatory disorders. If, along with the nerves, their radicular part is affected, then polyradiculoneuritis is determined.

Anatomically, with polyradiculoneuritis, inflammatory changes (edema, hyperemia, infiltration) of the roots are determined, and signs of myelin decay and degeneration of the axial cylinders are visible in the peripheral nerves. Moreover, if the pathological process is limited to mesenchial formations of the membranes and vessels, then this is interstitial neuritis. If it is accompanied by damage to nerve fibers (demyelination, disintegration of axial cylinders), then it is interstitial-parenchymal neuritis. With polyneuropathies, degenerative changes in nerves occur with a predominance of decay of their myelin sheaths or nerve fibers.

Polyneuritis and polyneuropathy are manifested by pain and paresthesia in the distal parts of the extremities, peripheral paralysis, sensitivity disorders of the “glove” and “sock” type and vegetative-trophic disorders (dryness, thinning of the skin or its hyperkeratosis, cyanosis, trophic ulcers).

Infectious polyneuritis of viral etiology is characterized by an acute onset with general malaise, fever, pain and paresthesia in the extremities.

Subsequently, weakness, atrophy, paralysis of the muscles of the arms and legs, and sensory disturbances develop. The nerve trunks are sharply painful on palpation. Reversal of symptoms is slow.

Treatment includes antiviral drugs, antibiotics, analgesics, corticosteroids, vitamins, and biostimulants.

Acute infectious polyradiculoneuritis usually occurs in the cold season and begins acutely with a rise in temperature, catarrhal symptoms, pain and paresthesia in the distal extremities. Sensitivity disorders of the peripheral type, pain in the nerve trunks, tension symptoms, distal paralysis and vegetative-vascular disorders are determined.

One of the most common forms of multiple lesions of the nervous system is acute infectious Guillain-Barré polyradiculoneuritis. The disease begins acutely with a rise in temperature and catarrhal symptoms, usually in the cold season. Patients develop rapidly increasing weakness in the legs, difficulty walking, and pain along the nerve trunks.

Characterized by symmetrical flaccid paralysis, starting from the lower extremities and covering the muscles of the trunk, upper extremities, neck, lesions of the cranial nerves, sensitivity disorders and sharp protein cell dissociation in the cerebrospinal fluid. The course of this form of the disease is benign.

Another type of polyradiculoneuritis is ascending Landry's palsy.

, in which the anterior roots are predominantly affected. Characterized by an acute onset and rapid course of the disease. The disease begins with paresthesia, pain, weakness, and paralysis of the legs, which quickly, within 2-3 days, spread to the upper limbs and cranial nerves, primarily the bulbar ones. In this case, speech and swallowing are impaired, breathing and cardiac problems occur. Death is common.

Treatment consists of suppressing the autoimmune inflammatory reaction (prednisolone, or its analogues, intravenous bolus up to 1.5-2.1 g per day for the first 3 days, followed by a dose reduction and switching to tablet drugs), administration of antibiotics (benzylpenicillin up to 20 million units per day, gentamicin, rifampicin) and hexamethylenetetramine: Reducing pain (analgin, voltaren): Detoxification (hemodez, glucose): Improving neuromuscular transmission (prozerin intramuscularly 1-2 ml twice a day, galantamine, ATP, B vitamins) :Immunoglobulin and plasmapheresis are also used:

If swallowing is impaired, glucose, albumin, and hydrolysine are administered intravenously; If breathing is impaired, resuscitation measures are carried out. After the acute phenomena subside, ultraviolet irradiation, UHF sessions, light massage, passive movements are carried out, biostimulants and vitamins are administered. 2-3 months after the process has subsided, hydrogen sulfide and radon baths, mud applications, and exercise therapy can be prescribed. Diphtheria polyneuritis occurs two to three weeks after diphtheria. It mainly affects the cranial nerves - the vagus, facial and abducens. The appearance of bulbar disorders is especially dangerous. After recovery, the voice may remain deaf for many years. Treatment is carried out by urgent administration of anti-diphtheria serum (5-10 thousand units). To prevent an anaphylactic reaction, 0.5-1.0 ml of serum is first injected under the skin, and after 12-24 hours the entire dose is injected.

Allergic (anti-rabies) polyneuritis

is a consequence of an allergic reaction to the vaccine. After the start of vaccinations, the patient develops dizziness, weakness, dyspepsia, and diffuse pain. Then the temperature rises; vomiting, uncontrollable, severe headache appear, flaccid paralysis of the limbs and pelvic disorders develop. Reversal of symptoms is rapid.

Diabetic polyneuropathy develops against the background of hyperglycemia.

It is characterized by paresthesia, itching and pain in the legs, sensitivity disorders in the distal extremities, and extinction of the Achilles and knee reflexes. Possible damage to the oculomotor nerves and autonomic ganglia.

Treatment includes correction of hyperglycemia (diabetes, insulin), vitamins, trental, coplamine, nootropics, analgesics, biostimulants, anabolic steroids, lipostabils, thioctacid:

Alcoholic polyneuropathy

develops subacutely with chronic alcohol intoxication. The disease begins with paresthesia, burning pain in the feet against the background of pronounced autonomic disorders (cyanosis, coldness, sweating) of the extremities.

In the distal sections, paresis develops, superficial and deep sensitivity is impaired (sensitive ataxia), and muscle atrophy appears. Korsakov's syndrome is very characteristic - loss of memory for recent and current events, confabulation, temporal and spatial disorganization.

Treatment consists of eliminating alcohol, prescribing large doses of B vitamins, benfogamma, mil-gamma, vasodilators (spasvin) and other drugs used for polyneuropathies.

Polyneuropathy in pregnant women is associated with impaired vitamin metabolism and liver failure. Characterized by paresis, peripheral sensitivity disorders, extinction of reflexes, disorders of autonomic innervation in the form of hyperhidrosis, coldness of the extremities. Possible Landry syndrome.

Lesions of the peripheral nervous system: plexitis

Cervical plexitis

Caused by infections, tumors, tuberculosis and injuries to the cervical spine. It manifests itself as pain and sensory disturbances in the back of the head, ear, neck, upper scapula and shoulder. Disturbances in the function of the phrenic nerve are characteristic (breathing problems, hiccups, complete or partial immobility of the diaphragm).

Brachial plexitis

occurs after shoulder injuries, collarbone fractures, infections, pathologies of the spine and lungs. Depending on the location of the lesion, upper, lower and total brachial plexitis are distinguished.

Upper (Duchenne-Erb palsy)

manifested by pain in the upper third of the shoulder, decreased reflex with the biceps, difficulty in shoulder abduction, supination, flexion of the arm at the elbow joint, as well as impaired sensitivity on the outer surface of the shoulder and forearm.

Lower (Dejerine-Klumpke palsy)

characterized by pain and sensitivity disorders on the inner surface of the shoulder and forearm, paresis and atrophy of the muscles of the hand and forearm, and a decrease in the carporadial reflex. Possible Horner-Bernard syndrome.

Total plexitis

is rare, characterized by pain in the supra- and subclavian region, radiating to the arm, loss of reflex

c, paresis and sensory impairment in the entire arm, severe vegetative-vascular disorders.

Lumbosacral plexitis

occurs as a result of infections, intoxications, diseases of the pelvic and abdominal organs, during pregnancy, during pathological childbirth and injuries to the spine and pelvic bones. Clinically, plexitis is manifested by pain and loss of sensitivity in the buttock, thigh and lower leg, loss of the knee and Achilles reflexes, paresis of the foot and atrophy of the muscles of the buttocks and thighs.

Treatment is similar to that of polyneuropathy.

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