Symptom complexes of damage to the cortical-muscular tract at different levels. Spinal cord lesions: symptoms and syndromes

Spinal cord diseases have always been a fairly common problem. Even minor areas of damage to this most important structure of the central nervous system can lead to very sad consequences.
Spinal cord

This is the main part, along with the brain, of the human central nervous system. It is an oblong cord 41-45 cm long in adults. It performs two very important functions:

1. conductive - information is transmitted in a two-way direction from the brain to the limbs, precisely along numerous tracts of the spinal cord;
2. reflex - the spinal cord coordinates the movements of the limbs.

Spinal cord diseases, or myelopathy, are a very large group of pathological changes, different in symptoms, etiology and pathogenesis.

They have only one thing in common - damage to various structures of the spinal cord. At the moment, there is no unified international classification of myelopathies.

Based on etiological characteristics, spinal cord diseases are divided into:

• vascular;
• compression, including those associated with intervertebral hernias and spinal column injuries;
• degenerative;
• infectious;
• carcinomatous;
• inflammatory.

The symptoms of spinal cord diseases are very diverse, since it has a segmental structure.

Common symptoms of spinal cord damage include pain in the back, aggravated by physical activity, general weakness, and dizziness.

The remaining symptoms are very individual and depend on the damaged area of ​​the spinal cord.

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Symptoms of spinal cord damage at different levels

When the I and II cervical segment of the spinal cord is damaged, it leads to the destruction of the respiratory and cardiac centers in the medulla oblongata. Their destruction leads in 99% of cases to the death of the patient due to cardiac and respiratory arrest.

Tetraparesis is always noted - complete shutdown of all limbs, as well as most of the internal organs.
Damage to the spinal cord at the level of the III-V cervical segments is also extremely life-threatening.

Innervation of the diaphragm ceases, and is possible only due to the respiratory muscles of the intercostal muscles. If the damage does not spread over the entire cross-sectional area of ​​the segment, individual tracts may be affected, thereby causing only paraplegia - disabling the upper or lower extremities.

Damage to the cervical segments of the spinal cord in most cases is caused by injuries: a blow to the head during diving, as well as during an accident.

If the V-VI cervical segments are damaged, the respiratory center remains intact, and weakness of the muscles of the upper shoulder girdle is noted.

The lower extremities are still left without movement and sensitivity when the segments are completely affected. The level of damage to the thoracic segments of the spinal cord is easy to determine. Each segment has its own dermatome.

The T-I segment is responsible for innervation of the skin and muscles of the upper chest and armpit area; segment T-IV - pectoral muscles and skin in the nipple area; thoracic segments from T-V to T-IX innervate the entire chest area, and from T-X to T-XII the anterior abdominal wall.

Consequently, damage to any of the segments in the thoracic region will lead to loss of sensitivity and limitation of movement at the level of the lesion and below. There is weakness in the muscles of the lower extremities and absence of reflexes of the anterior abdominal wall. Severe pain is noted at the site of injury.

As for damage to the lumbar regions, this leads to loss of movement and sensitivity of the lower extremities.

If the lesion is located in the upper segments of the lumbar region, paresis of the thigh muscles occurs and the knee reflex disappears.

If the lower lumbar segments are affected, then the muscles of the foot and lower leg suffer.

Lesions of various etiologies of the conus medullaris and cauda equina lead to dysfunction of the pelvic organs: urinary and fecal incontinence, erection problems in men, lack of sensitivity in the genital area and perineum.

Vascular diseases of the spinal cord

This group of diseases includes spinal cord strokes, which can be either ischemic or hemorrhagic.

Vascular diseases of the brain and spinal cord have a common etiology - atherosclerosis.

The main difference between the consequences of these diseases is the disruption of higher nervous activity in vascular diseases of the brain, loss of various types of sensitivity and muscle paresis.

Spinal cord hemorrhagic stroke, or spinal cord infarction, is more common in young people as a result of ruptured blood vessels. Predisposing factors are increased tortuosity, fragility and incompetence of blood vessels.

It most often occurs as a result of genetic diseases or disorders during embryonic development that cause abnormalities in the development of the spinal cord.

Rupture of a blood vessel can occur in any part of the spinal cord, and symptoms can be given only according to the affected segment.

In the future, as a result of the movement of a blood clot with cerebrospinal fluid through the subarachnoid spaces, the lesions may spread to adjacent segments.

Ischemic stroke of the spinal cord occurs in elderly people as a result of atherosclerotic changes in blood vessels. A spinal cord infarction can cause not only damage to the vessels of the spinal cord, but also to the aorta and its branches.

As in the brain, in the spinal cord, transient ischemic attacks may occur, which are accompanied by temporary symptoms in the corresponding segment.

In neurology, such transient ischemic attacks are called intermittent myelogenous claudication. Unterharnscheidt syndrome is also distinguished as a separate pathology.

MRI diagnostics of vessels of the extremities

Intermittent myelogenous claudication occurs during prolonged walking or other physical activity. Manifests itself in sudden numbness and weakness of the lower extremities. After a short rest the complaints disappear.

The cause of this disease is atherosclerotic changes in blood vessels in the lower lumbar segments, resulting in ischemia of the spinal cord.

The disease should be differentiated from damage to the arteries of the lower extremities, for which MRI diagnostics of the vessels of the extremities and the aorta is performed with a contrast agent.

Unterharnscheidt syndrome. This disease first appears mainly at a young age.

Caused by vasculitis and malformation of blood vessels in the vertebrobasilar region.

Syndromes of spinal cord damage in this disease: tetraparesis and loss of consciousness suddenly occur, which disappear after a few minutes.

A diagnosis of hysterical personality disorder and epileptic seizure should be carried out.

Compression lesions of the spinal cord

Compression, or infringement of the spinal cord occurs for several reasons:

1. Vertebral hernia- the resulting hernial sac compresses the segment. Most often, it is not complete compression of the entire segment, but of its horns: anterior, lateral or posterior. If the anterior horns of the spinal cord are damaged, a decrease in muscle tone and sensitivity occurs in the corresponding segment or dermatome, since the anterior horns have sensory and motor fibers. When the lateral horns are compressed, disturbances of the autonomic nervous system occur in the corresponding segment. The manifestations of this disease are varied: pupils dilate for no reason, sweating, mood swings, tachycardia, constipation occur, blood glucose levels and blood pressure increase. Often, when contacting therapists with such complaints, symptomatic treatment is prescribed, and a diagnostic search is aimed at the affected organ. Only when back pain occurs is a correct diagnosis made after an MRI. Compression of the posterior horns leads to partial, or less often, complete loss of sensitivity, also in a certain segment. Diagnosis in such cases does not cause any particular difficulties. Treatment of all intervertebral hernias is surgical. All non-traditional and traditional conservative treatment methods only temporarily relieve the symptoms of the disease.
2. Tumor process in the spinal cord or vertebrae Vertebral compression fracture
3. Vertebral compression fractures. These types of fractures most often occur when falling from a height on the legs, and less often on the back. Vertebral fragments can compress or cut the spinal cord. In the first case, the symptoms are the same as with hernias. In the second case, the forecasts are much worse. If the spinal cord is cut, the conduction system will be completely disrupted in the underlying sections. Unfortunately, the consequences of such injuries remain throughout life.
   Most often, incomplete dissection of the spinal cord occurs, that is, only some spinal tracts are damaged, which again leads to a variety of symptoms. Nowadays, computer or magnetic resonance imaging allows one to determine the location of the lesion with an accuracy of 0.1 mm.
4. Degenerative processes of the spine are the most common causes of spinal cord damage. Cervical spondylosis and lumbar (lumbar) osteoarthritis of the spine is the destruction of the bone tissue of the vertebrae, with the formation of connective tissue, as well as osteophytes. As a result of tissue proliferation, compression of the cervical spinal cord occurs. The symptoms of this disease are similar to hernial compression, but more often it has a concentric lesion, which contributes to damage to all the horns and roots of the spinal cord.
5. Infectious diseases of the spinal cord- a group of diseases of various etiologies. According to the duration of the course, acute, subacute and chronic myelitis are distinguished; according to the degree of prevalence: transverse, multifocal, limited.

Due to their occurrence, the following forms of myelitis are distinguished:

• Viral myelitis. The most common pathogens are polio, herpes, rubella, measles, influenza viruses, and less commonly, hepatitis and mumps. Neurological symptoms are varied and depend on the affected segments and the spread of infection. Common symptoms for all infectious lesions are increased body temperature, severe headaches and back pain, impaired consciousness, and increased muscle tone in the extremities. The greatest danger is the involvement of the cervical spinal cord in the infectious process. In the cerebrospinal fluid, during a lumbar puncture, a high content of protein and neutrophils is found.
• Bacterial myelitis. Occurs in acute meningococcal meningitis, as a result of the movement of cerebrospinal fluid along with bacteria, and also as a consequence of syphilis. Meningococcal meningitis of the spinal cord is very severe, with total inflammation of the membranes of the brain and spinal cord. Even with modern treatment, mortality remains quite high. Currently, long-term consequences and complications of syphilis are quite rare, but still relevant. One such complication is tabes spinal cord. Tabes spinalis is a tertiary neurosyphilis that affects the spinal roots and posterior columns, leading to loss of sensation in certain segments. Tuberculosis of the spinal cord
• Spinal cord tuberculosis stands apart among bacterial lesions. Tuberculosis enters the spinal cord in three ways: hematogenously - with the primary tuberculosis complex and disseminated tuberculosis, lymphogenously - with tuberculosis affecting the lymph nodes, contact - with a nearby infection, for example in the spine. By destroying bone tissue, mycobacterium creates cavernous lesions that create a compressive effect on segments of the spinal cord. In this case, the back pain in the affected area is pronounced, which undoubtedly facilitates the diagnostic task.
• Oncological diseases Spinal cord lesions are divided into malignant and benign. The former include spinal cord ependymoma and sarcoma. Ependymoma grows from cells lining the central canal of the spinal cord. With significant growth, compression of the spinal tracts occurs, which leads primarily to visceral disorders and loss of segmental sensitivity, followed by paraplegia. Sarcoma grows from poorly differentiated connective tissue cells, i.e. from muscles, bones, dura mater. The greatest danger is represented by clear cell sarcoma, which competes with melanoma in terms of malignancy and metastasis, but is much less common. Benign tumors of the spinal cord include lipoma, hemangioma and dermoid cyst of the spinal cord. Since these tumors are ectramedullary, treatment is surgical. Rapid and significant growth (a dermoid cyst of the spinal cord reaches 15 cm in length), early manifestation of pain and radicular syndromes of the spinal cord, forces a laminectomy of the spine, with removal of the tumor, in order to produce decompression and prevent persistent paralysis. Spinal cord meningioma develops from cells of the arachnoid membrane. Meningioma, like a cyst and lipoma, can reach impressive sizes, causing compression of the spinal cord roots. But a distinctive feature of meningioma is the frequent development of massive bleeding, which is quite difficult to stop. Treatment of meningioma is also surgical. Often, meningiomas are present from birth, but due to slow growth they appear in adulthood. Inflammation of the spinal cord
• Inflammatory diseases spinal cord include most of the above. Inflammation of the spinal cord and meninges occurs in infectious diseases, carcinomatosis, and degenerative changes. The reaction, occurring both in the brain itself and in the membranes and spine, leads to inflammatory edema and compression of the roots, and sometimes the horns of the spinal cord.

Source: http://lechuspinu.ru/drugie_bolezni/zabolevaniya-spinnogo-mozga.html

Spinal cord diseases

Knowledge of the anatomical structure of the spinal cord (segmental principle) and the spinal nerves extending from it allows neuropathologists and neurosurgeons in practice to accurately determine the symptoms and syndromes of damage.

During a neurological examination of the patient, going from top to bottom, the upper limit of the onset of sensitivity and motor activity of the muscles is found. It should be remembered that the vertebral bodies do not correspond to the spinal cord segments located underneath them.

The neurological picture of spinal cord damage depends on the damaged segment.

As a person grows, the length of the spinal cord lags behind the length of the surrounding spine.

During its formation and development, the spinal cord grows more slowly than the spine.

In adults, the spinal cord ends at the level of the body of the first lumbar L1 vertebra.

The nerve roots extending from it will go further down to innervate the limbs or pelvic organs.

The clinical rule used to determine the level of damage to the spinal cord and its nerve roots is:

1. cervical roots (except the root C8) leave the spinal canal through the foramina above their corresponding vertebral bodies,
2. The thoracic and lumbar roots leave the spinal canal under the vertebrae of the same name,
3. the upper cervical segments of the spinal cord lie behind the vertebral bodies with the same numbers,
4. the lower cervical segments of the spinal cord lie one segment above the corresponding vertebra,
5. the upper thoracic segments of the spinal cord lie two segments higher,
6. the lower thoracic segments of the spinal cord lie three segments higher,
7. lumbar and sacral segments of the spinal cord (the latter form the conus medullaris) are localized behind the vertebrae Th9–L1.

To clarify the distribution of various pathological processes around the spinal cord, especially with spondylosis, it is important to carefully measure the sagittal diameters (lumen) of the spinal canal. The normal diameters (lumen) of the spinal canal in an adult are:

• at the cervical level of the spine - 16-22 mm,
• at the thoracic level of the spine -16-22 mm,
• L1–L3- about 15-23 mm,
• at the level of the lumbar vertebrae L3–L5 and below - 16-27 mm.

Neurological syndromes of spinal cord diseases

If the spinal cord is damaged at one level or another, the following neurological syndromes will be detected:

1. loss of sensation below the level of his spinal cord lesion (level of sensitivity disorders)
2. weakness in the limbs innervated by descending nerve fibers of the corticospinal tract from the level of the spinal cord lesion

Sensory disturbances (hypoesthesia, paresthesia, anesthesia) may appear in one or both feet. The sensory disorder may spread upward, mimicking peripheral polyneuropathy.

In the event of a complete or partial interruption of the corticospinal and bulbospinal tracts at the same level of the spinal cord, the patient experiences paralysis of the muscles of the upper and/or lower extremities (paraplegia or tetraplegia).

In this case, symptoms of central paralysis are revealed:

• increased muscle tone
• deep tendon reflexes are increased
• pathological Babinski's symptom is detected

During examination of a patient with spinal cord injury, segmental disorders are usually detected:

1. a band of sensitivity changes near the upper level of conductive sensory disorders (hyperalgesia or hyperpathia)
2. hypotension and muscle atrophy
3. isolated loss of deep tendon reflexes

The level of sensory disturbances according to the conduction type and segmental neurological symptoms roughly indicate the localization of the transverse lesion of the spinal cord in the patient.

An accurate localizing sign is pain felt along the midline of the back, especially at the thoracic level. Pain in the interscapular region may be the first symptom of spinal cord compression in a patient.

Radicular pain indicates the primary localization of the spinal cord lesion in the region of its outer masses. When the cone of the spinal cord is affected, pain is often noted in the lower back.

In the early stages of a transverse spinal cord injury, the limbs may show decreased muscle tone (hypotension) rather than spasticity due to the patient's spinal shock. Spinal shock may last for several weeks.

It is sometimes mistaken for an extensive segmental lesion. Later tendon and periosteal reflexes in the patient become elevated.

In transverse lesions, especially those caused by infarction, paralysis is often preceded by short clonic or myoclonic convulsions in the limbs.

Another important symptom of transverse spinal cord lesion is dysfunction of the pelvic organs, manifested in the form of urinary and fecal retention in the patient.

Compression within (intramedullary) or around the spinal cord (extramedullary) can present clinically in a similar way.

Therefore, one neurological examination of the patient is not enough to determine the location of the spinal cord lesion.

Neurological signs that indicate the localization of pathological processes around the spinal cord (extramedullary) include:

• radicular pain,
• Brown-Séquard hemi-spinal syndrome,
• symptoms of peripheral motor neuron damage within one or two segments, often asymmetrical,
• early signs of corticospinal tract involvement,
• significant decrease in sensitivity in the sacral segments,
• early and pronounced changes in the cerebrospinal fluid (CSF).

Neurological signs that indicate the localization of pathological processes inside the spinal cord (intramedullary) include:

1. hard-to-localize burning pain,
2. dissociated loss of pain sensitivity while maintaining muscle-joint sensitivity,
3. preservation of sensitivity in the perineal area and sacral segments,
4. late-onset and less pronounced pyramidal symptoms,
5. normal or slightly altered composition of the cerebrospinal fluid (CSF).

A lesion within the spinal cord (intramedullary) that involves the innermost fibers of the spinothalamic pathways but does not involve the outermost fibers that provide sensation to the sacral dermatomes will present with no signs of injury. The perception of pain and temperature stimuli in the sacral dermatomes (nerve roots S3–S5).

Brown-Séquard syndrome is a complex of symptoms of a half lesion of the diameter of the spinal cord. Brown-Séquard syndrome is clinically manifested by:

• on the side of the spinal cord injury - paralysis of the muscles of the arm and / or leg (monoplegia, hemiplegia) with loss of muscle-articular and vibrational (deep) sensitivity,
• on the opposite side - loss of pain and temperature (superficial) sensitivity.

The upper limit of pain and temperature sensitivity disorders in Brown-Séquard syndrome is often determined 1-2 segments below the site of spinal cord injury, since the fibers of the spinothalamic tract, after forming a synapse in the posterior horn of the spinal cord, pass into the opposite lateral cord, rising upward. If there are segmental disorders in the form of radicular pain, muscle atrophy, extinction of tendon reflexes, then they are usually one-sided.

The spinal cord is supplied by one anterior spinal artery and two posterior spinal arteries.

If the lesion of the spinal cord is limited to the central part or affects it, then it will predominantly damage the neurons of the gray matter and segmental conductors that produce their decussation at this level. This is observed with contusion during spinal cord injury, syringomyelia, tumor and vascular lesions in the anterior spinal artery.

With central damage to the cervical spinal cord, the following occurs:

1. weakness of the arm, which is more pronounced compared to weakness of the leg,
2. dissociated sensitivity disorder (analgesia, i.e. loss of pain sensitivity with distribution in the form of a “cape on the shoulders” and the lower part of the neck, without anesthesia, i.e. loss of tactile sensations, and with preservation of vibration sensitivity).

Lesions of the conus spinal cord, localized in the L1 vertebral body or below, compress the spinal nerves that make up the cauda equina. This causes peripheral (flaccid) asymmetric paraparesis with areflexia.

This level of damage to the spinal cord and its nerve roots is accompanied by dysfunction of the pelvic organs (dysfunction of the bladder and intestines).

The distribution of sensory disorders on the patient's skin resembles the outline of the saddle, reaches the level of L2 and corresponds to the zones of innervation of the roots included in the cauda equina.

Achilles and knee reflexes in such patients are reduced or absent. Patients often report pain radiating to the perineum or thighs.

With pathological processes in the area of ​​the conus of the spinal cord, pain is less pronounced than with lesions of the cauda equina, and disorders of the bowel and bladder functions occur earlier. Achilles reflexes fade away.

Compression processes can simultaneously involve both the cauda equina and the conus spinal cord, which causes a combined syndrome of peripheral motor neuron damage with increased reflexes and the appearance of a pathological Babinski sign.

When the spinal cord is damaged at the level of the foramen magnum, patients experience weakness in the muscles of the shoulder girdle and arm, followed by weakness in the leg and arm on the opposite side on the affected side. Volumetric processes of this localization sometimes cause pain in the neck and back of the head, spreading to the head and shoulders. Another evidence of a high cervical level (up to the segment Th1) lesions is Horner's syndrome.

Some spinal diseases can cause sudden myelopathy without previous symptoms (like a spinal stroke).

These include epidural hemorrhage, hematomyelia, spinal cord infarction, prolapse (prolapse, extrusion) of the nucleus pulposus of the intervertebral disc, and vertebral subluxation.

Chronic myelopathies occur with the following diseases of the spine or spinal cord:

Source: http://www.minclinic.ru/vertebral/bolezni_spinnogo_mozga.html

Major diseases of the spinal cord

The spinal cord belongs to the central nervous system. It is connected to the brain, nourishes it and the membrane, and transmits information. The function of the spinal cord is to correctly transmit incoming impulses to other internal organs.

It consists of various nerve fibers through which all signals and impulses are transmitted. Its basis is in white and gray substances: white consists of nerve processes, gray contains nerve cells.

Gray matter is located at the core of the spinal canal, while white matter completely surrounds it and protects the entire spinal cord.

Spinal cord diseases are all characterized by a great risk not only for health, but also for human life. Even minor temporary deviations sometimes cause irreversible consequences.

Thus, incorrect posture can doom the brain to starvation and trigger a number of pathological processes. It is impossible not to notice the symptoms of disorders in the spinal cord.

Almost all symptoms that can be caused by spinal cord diseases can be classified as severe manifestations.

Symptoms of spinal cord disease

The mildest symptoms of spinal cord disease are dizziness, nausea, and periodic pain in muscle tissue.

The intensity of the disease can be moderate and variable, but more often the signs of spinal cord damage are more dangerous.

In many ways, they depend on which particular department has undergone the development of pathology and what kind of disease is developing.

Common symptoms of spinal cord disease:

• loss of sensation in limbs or body parts;
• aggressive back pain in the spinal region;
• uncontrolled bowel or bladder emptying;
• pronounced psychosomatics;
• loss or limitation of movement;
• severe pain in joints and muscles;
• paralysis of limbs;
• amyotrophy.

Symptoms may vary and be supplemented depending on which substance is affected. In any case, it is impossible not to see signs of spinal cord damage.

Spinal cord compression

The concept of compression means a process in which compression or compression of the spinal cord occurs.

This condition is accompanied by multiple neurological symptoms that can cause certain diseases. Any displacement or deformation of the spinal cord always disrupts its functioning.

Often, diseases that people consider harmless cause severe damage not only to the spinal cord, but also to the brain.

So, otitis media or sinusitis can cause an epidural abscess. In diseases of the ENT organs, the infection can quickly enter the spinal cord and provoke infection of the entire spinal column.

Quite quickly, the infection reaches the cerebral cortex and then the consequences of the disease can be catastrophic. In severe cases of otitis, sinusitis or a prolonged phase of the disease, meningitis and encephalitis occur.

Treatment of such diseases is complex, and the consequences are not always reversible.

Read also: Spinal cord cauda equina syndrome and its treatment

Hemorrhages in the spinal cord area are accompanied by severe pain throughout the entire spine.

This happens more often from injuries, bruises, or in case of serious thinning of the walls of the vessels surrounding the spinal cord.

The location can be absolutely any; the cervical spine most often suffers as it is the weakest and most unprotected from damage.

The progression of a disease such as osteochondrosis or arthritis can also cause compression. As osteophytes grow, they put pressure on the spinal cord, and intervertebral hernias develop. As a result of such diseases, the spinal cord suffers and loses its normal functioning.

Tumors

Like any organ of the body, tumors can appear in the spinal cord. It is not even malignancy that is of main importance, since all tumors are dangerous for the spinal cord. The location of the tumor is important. They are divided into three types:

1. extradural;
2. intradural;
3. intramedullary.

Extradural ones are the most dangerous and malignant, and have a tendency to rapidly progress. They occur in the hard tissue of the brain membrane or in the vertebral body. An operative solution is rarely successful and involves a risk to life. This category includes tumors of the prostate and mammary glands.

Intradurals are formed under the hard tissue of the brain membrane. These are tumors such as neurofibromas and meningiomas.

Intramedullary tumors are localized directly in the brain itself, in its main substance. Malignancy is critical.

For diagnosis, MRI is more often used as a study that gives a complete picture of spinal cord carcinoma. This disease can only be treated surgically. All tumors have one thing in common: conventional therapy is ineffective and does not stop metastases.

Therapy is appropriate only after successful surgery.

Intervertebral hernia

Intervertebral hernias occupy a leading position in a number of spinal cord diseases. Initially, protrusions form, only over time it becomes a hernia.

With this disease, deformation and rupture of the fibrous ring occurs, which serves as a fixation for the disc core. Once the ring is destroyed, the contents begin to leak out and often end up in the spinal canal.

If an intervertebral hernia affects the spinal cord, myelopathy is born. The disease myelopathy means dysfunction of the spinal cord.

Sometimes the hernia does not manifest itself and the person feels normal. But more often the spinal cord is involved in the process and this causes a number of neurological symptoms:

• pain in the affected area;
• change in sensitivity;
• depending on the locality, loss of control over the limbs;
• numbness, weakness;
• violations in the functions of internal organs, more often the pelvis;
• the pain spreads from the waist to the knee, capturing the thigh.

Such signs usually manifest themselves provided that the hernia has reached an impressive size.

Treatment is often therapeutic, with medications and physiotherapy.

The only exception is in cases where there are signs of failure of internal organs or serious damage.

Myelopathy

Non-compressive myelopathies are complex diseases of the spinal cord. There are several varieties, but it is difficult to distinguish them from each other.

Even MRI does not always allow an accurate determination of the clinical picture.

The CT results always show the same picture: severe tissue swelling without any signs of external compression of the spinal cord.

Necrotizing myelopathy involves several segments of the spine. This form is a kind of echo of significant carcinomas, distant in location. Over time, it provokes the birth of paresis and problems with the pelvic organs in patients.

Carcinomatous meningitis is found in most cases when there is a progressive cancerous tumor in the body. Most often, primary carcinoma is located either in the lungs or in the mammary glands.

Prognosis without treatment: no more than 2 months. If treatment is successful and on time, life expectancy is up to 2 years. Most deaths are associated with advanced processes in the central nervous system. These processes are irreversible and brain function cannot be restored.

Inflammatory myelopathies

Arachnoiditis is most often diagnosed as a type of inflammatory process in the brain or spinal cord. It must be said that such a diagnosis is not always correct and clinically confirmed.

A detailed and high-quality examination is necessary. It occurs against the background of previous otitis, sinusitis, or against the background of severe intoxication of the whole body.

Arachnoiditis develops in the arachnoid membrane, which is one of the three membranes of the brain and spinal cord.

A viral infection provokes a disease such as acute myelitis, whose symptoms are similar to those of other inflammatory diseases of the spinal cord.

Diseases such as acute myelitis require immediate intervention and identification of the source of infection.

The disease is accompanied by ascending paresis, severe and growing weakness in the limbs.

Infectious myelopathy is expressed more specifically. The patient cannot always understand and correctly assess his condition. The most common cause of infection is herpes zoster, a complex disease that requires long-term therapy.

Spinal cord infarction

For many, even such an unfamiliar concept as spinal cord infarction.

But due to severe circulatory disorders, the spinal cord begins to starve, its functions are so disrupted that this leads to necrotic processes.

Blood clots appear and the aorta begins to dissect. Almost always several departments are affected at once. A wide area is covered, and a general ischemic infarction develops.

Also Read: Symptoms of Inflammation of the Spinal Cord

Even a minor bruise or injury to the spinal column can be the cause. If there is already an intervertebral hernia, then it can collapse if injured.

Then its particles enter the spinal cord. This phenomenon is unstudied and poorly understood; there is no clarity in the very principle of penetration of these particles.

There is only the fact of detection of particles of destroyed tissue of the nucleus pulposus of the disc.

The development of such a heart attack can be determined by the patient’s condition:

1. sudden weakness to the point of failure of the legs;
2. nausea;
3. temperature drop;
4. Strong headache;
5. fainting.

Diagnosis is only using MRI, treatment is therapeutic. A disease such as a heart attack is important to stop in time and stop further damage. The prognosis is often positive, but the patient’s quality of life may deteriorate.

Chronic myelopathy

Osteochondrosis is recognized as a killer of the spinal column; its diseases and complications can rarely be reversed to a tolerable state.

This is explained by the fact that 95% of patients never carry out preventive measures and do not visit a specialist at the onset of the disease. They seek help only when pain prevents them from living.

But at such stages, osteochondrosis already triggers processes such as spondylosis.

Spondylosis is the end result of dystrophic changes in the structure of the spinal cord tissue. The disturbances cause bone growths (osteophytes), which ultimately compress the spinal canal.

The compression can be severe and cause central canal stenosis. Stenosis is the most dangerous condition; for this reason, a chain of processes can start that involve the brain and central nervous system in the pathology.

Treatment of spondylosis is often symptomatic and aimed at alleviating the patient’s condition. The best result can be accepted if it is ultimately possible to achieve stable remission and delay further progression of spondylosis. It is impossible to reverse spondylosis.

Lumbar stenosis

The concept of stenosis always means compression and narrowing of some organ, channel, vessel. And almost always stenosis poses a threat to human health and life.

Lumbar stenosis is a critical narrowing of the spinal canal and all its nerve endings. The disease can be either a congenital pathology or an acquired one.

Stenosis can be caused by many processes:

• osteophytes;
• vertebral displacement;
• hernias;
• protrusion.

Sometimes a congenital anomaly is worsened by an acquired one.

Stenosis can occur in any part and can affect part of the spinal column or the entire spine. The condition is dangerous, the solution is often surgical.

I. Damage to the peripheral nerve - flaccid paralysis of the muscles innervated by this nerve. Occurs when peripheral and cranial nerves are damaged (neuritis, neuropathy). This type of distribution of paralysis is called neural.

II. Multiple lesions of the nerve trunks - signs of peripheral paralysis are observed in the distal parts of the limbs. This pattern is called polyneuritic distribution of paralysis. Such paralysis (paresis) is associated with pathology of the distal parts of several peripheral or cranial nerves (polyneuritis, polyneuropathy).

III. Damage to the plexuses (cervical, brachial, lumbar, sacral) is characterized by the occurrence of flaccid paralysis in the muscles innervated by this plexus.

IV. Damage to the anterior horns of the spinal cord, anterior roots of the spinal cord, nuclei of the cranial nerves characterized by the occurrence of peripheral paralysis in the area of ​​the affected segment. Lesions of the anterior horns, in contrast to lesions of the anterior roots, have clinical features:

Presence of fasciculations and fibrillations

- “mosaic” lesion within one muscle

Early and rapidly progressing atrophy with degeneration reaction.

V. Damage to the lateral columns of the spinal cord is characterized by the occurrence of central paralysis below the level of the lesion on the side of the lesion and loss of pain and temperature sensitivity on the opposite side.

Caused by pathology of the lateral corticospinal tract. In this case, central paralysis is determined on the side of the lesion in the muscles receiving innervation from segments from the level of the lesion and below.

VI. Transverse spinal cord lesion(bilateral damage to the pyramidal fasciculi and gray matter).

· In case of damage to the upper cervical segments of the spinal cord (C1-C4) the pyramidal tracts for the upper and lower extremities will be damaged - central paralysis of the upper and lower extremities will occur (spastic tetraplegia).

· With damage to the cervical enlargement of the spinal cord the pyramidal tracts for the lower extremities will be damaged, as well as the motor neurons of the anterior horns innervating the upper extremities - peripheral paralysis will occur for the upper extremities and central paralysis for the lower extremities (superior flaccid paraplegia, lower spastic paraplegia).

· With lesions at the level of the thoracic segments the pyramidal tracts for the lower extremities are interrupted, the upper extremities will remain unaffected ( lower spastic paraplegia).

· With damage at the level of the lumbar enlargement motor neurons of the anterior horns innervating the lower limbs are destroyed (lower flaccid paraplegia).

VII. Damage to the pyramidal fasciculus in the brain stem observed with lesions in one half of the trunk. It is characterized by the occurrence of central hemiplegia on the side opposite to the lesion and paralysis of any cranial nerve on the side of the lesion. This syndrome is called alternating.

VIII. Damage to the internal capsule characterized by the occurrence of contralateral “three hemi-syndrome”: hemiplegia, hemianesthesia, hemianopsia.

IX. Lesion of the anterior central gyrus x characterized by the occurrence of central monoparesis depending on the location of the lesion. For example, brachiofacial palsy with damage to the lower part of the contralateral precentral gyrus.

Irritation of the anterior central gyrus causes epileptic seizures; seizures can be local or generalized. During local convulsions, the patient’s consciousness is preserved (such paroxysms are called cortical or Jacksonian epilepsy).

Clinical symptoms and diagnosis of movement disorders.

Diagnosis of movement disorders includes the study of a number of indicators of the state of the motor sphere. These indicators are:

1) motor function

2) visible muscle changes

3) muscle tone

4) reflexes

5) electrical excitability of nerves and muscles

Motor function

It is tested by examining active (voluntary) movements in the striated muscles.

By severity Disorders of voluntary movements are divided into paralysis (plegia) and paresis. Paralysis– this is a complete loss of voluntary movements in certain muscle groups; paresis– incomplete loss of voluntary movements, manifested by a decrease in muscle strength in the affected muscles.

By prevalence paralysis and paresis, the following options are distinguished:

- monoplegia or monoparesis– disorder of voluntary movements in one limb;

- hemiplegia or hemiparesis– disorder of voluntary movements in the limbs of one half of the body;

- paraplegia or paraparesis– disorder of voluntary movements in symmetrical limbs (in the hands – top paraplegia or paraparesis, in the legs - lower paraplegia or paraparesis);

- triplegia or triparesis– movement disorders in three limbs;

- tetraplegia or tetraparesis – disorders of voluntary movements in all four limbs.

Paralysis or paresis caused by damage to the central motor neuron is designated as central; paralysis or paresis caused by damage to a peripheral motor neuron is called peripheral.

Methodology for identifying paralysis and paresis includes:

1) external inspection

2) study of the volume of active movements

3) study of muscle strength

4) carrying out special tests or tests to identify mild paresis

1) External inspection allows you to detect or suspect a particular defect in the state of motor function by the patient’s facial expressions, his posture, the transition from a lying position to a sitting position, and getting up from a chair. A paretic arm or leg often assumes a forced position until contractures develop. Thus, a patient with central hemiparesis can be “recognized” by the Wernicke-Mann position – flexion contracture in the arm and extension contracture in the leg (“the hand asks, the leg squints”).

Particular attention is paid to the patient's gait. For example, a “cock” gait and stepping for paresis of the peroneal muscle group.

2) Volume of active movements is defined as follows. According to the doctor’s instructions, the patient himself makes active movements, and the doctor visually assesses their possibility, volume and symmetry (left and right). Typically, a number of fundamental movements are examined in order from top to bottom (head, cervical spine, trunk muscles, upper and lower extremities).

3) Muscle strength is studied in parallel with active movements. When studying muscle strength, the following method is used: the patient is asked to perform an active movement, then the patient holds the limb in this position with maximum strength, and the doctor tries to perform the movement in the opposite direction. At the same time, he evaluates and compares on the left and right the degree of effort that is required for this. The study is assessed by five-point system: full muscle strength - 5 points; slight decrease in strength (yielding) – 4 points; moderate decrease in strength (full range of active movements under the influence of gravity on the limb) – 3 points; the possibility of full movement only after the removal of gravity (the limb is placed on a support) – 2 points; preservation of movement (with barely noticeable muscle contraction) – 1 point. In the absence of active movement, if the weight of the limb is not taken into account, the strength of the muscle group under study is assumed to be zero. With muscle strength of 4 points they speak of mild paresis, 3 points – about moderate, in 2-1 – about deep.

4) Special samples and tests must be carried out in the absence of paralysis and clearly perceptible paresis. With the help of tests, it is possible to identify muscle weakness, which the patient does not subjectively feel, i.e. so-called “hidden” paresis.

Table No. 3. Tests for identifying hidden paresis

Spinal cord(medulla spinalis) - part of the central nervous system located in the spinal canal. The spinal cord has the appearance of a white cord, somewhat flattened from front to back in the area of ​​thickenings and almost round in other parts.

In the spinal canal it extends from the level of the lower edge of the foramen magnum to the intervertebral disc between the I and II lumbar vertebrae. At the top, the spinal cord passes into the brain stem, and at the bottom, gradually decreasing in diameter, it ends with the conus medullaris.

In adults, the spinal cord is much shorter than the spinal canal, its length varies from 40 to 45 cm. The cervical thickening of the spinal cord is located at the level of the third cervical and first thoracic vertebra; The lumbosacral thickening is located at the level of the X-XII thoracic vertebra.

The anterior median (15) and posterior median sulcus (3) divide the spinal cord into symmetrical halves. On the surface of the spinal cord, at the exit sites of the ventral (anterior) (13) and dorsal (posterior) (2) roots, two shallower grooves are revealed: anterior lateral and posterior lateral.

A segment of the spinal cord corresponding to two pairs of roots (two anterior and two posterior) is called a segment. The anterior and posterior roots emerging from the segments of the spinal cord unite into 31 pairs of spinal nerves. The anterior root is formed by processes of motor neurons of the nuclei of the anterior horns of the gray matter (12). The anterior roots of the VIII cervical, XII thoracic, and two upper lumbar segments, along with the axons of somatic motor neurons, include neurites of the cells of the sympathetic nuclei of the lateral horns, and the anterior roots of the II-IV sacral segments include the processes of neurons of the parasympathetic nuclei of the lateral intermediate substance of the spinal cord. The dorsal root is represented by the central processes of false unipolar (sensitive) cells located in the spinal ganglion. The central canal passes through the gray matter of the spinal cord along its entire length, which, expanding cranially, passes into the fourth ventricle of the brain, and in the caudal part of the conus medullaris forms the terminal ventricle.

The gray matter of the spinal cord, consisting mainly of nerve cell bodies, is located in the center. In cross sections, it resembles the shape of the letter H or has the appearance of a “butterfly”, the anterior, posterior and lateral sections of which form the horns of gray matter. The anterior horn is somewhat thickened and located ventrally. The dorsal horn is represented by a narrow dorsal part of the gray matter, extending almost to the outer surface of the spinal cord. The lateral intermediate gray matter forms the lateral horn.
Longitudinal collections of gray matter in the spinal cord are called columns. The anterior and posterior columns are present throughout the entire length of the spinal cord. The lateral column is somewhat shorter, it begins at the level of the VIII cervical segment and extends to the I-II lumbar segments. In the columns of gray matter, nerve cells are united into more or less distinct groups-nuclei. Around the central canal there is a central gelatinous substance.
White matter occupies the peripheral parts of the spinal cord and consists of processes of nerve cells. The grooves located on the outer surface of the spinal cord divide the white matter into anterior, posterior and lateral cords. Nerve fibers, uniform in origin and function, within the white matter are combined into bundles or tracts that have clear boundaries and occupy a specific position in the cords.

There are three systems of pathways functioning in the spinal cord: associative (short), afferent (sensitive) and efferent (motor). Short association fascicles connect segments of the spinal cord. Sensory (ascending) tracts are directed to the centers of the brain. The descending (motor) tracts provide communication between the brain and the motor centers of the spinal cord.

Along the spinal cord there are arteries supplying it with blood: the unpaired anterior spinal artery and the paired posterior spinal artery, which are formed by large radiculomedullary arteries. The superficial arteries of the spinal cord are interconnected by numerous anastomoses. Venous blood from the spinal cord flows through the superficial longitudinal veins and anastomoses between them along the radicular veins into the internal vertebral venous plexus.

The spinal cord is covered with a dense cover of the dura mater, the processes of which, extending from each intervertebral foramen, cover the root and the spinal ganglion.

The space between the dura mater and the vertebrae (epidural space) is filled with venous plexus and fatty tissue. In addition to the dura mater, the spinal cord is also covered by the arachnoid and pia mater.

Between the pia mater and the spinal cord is the subarachnoid space of the spinal cord, filled with cerebrospinal fluid.

There are two main functions of the spinal cord: its own segmental reflex and conductor, which provides communication between the brain, torso, limbs, internal organs, etc. Sensitive signals (centripetal, afferent) are transmitted along the dorsal roots of the spinal cord, and motor signals are transmitted along the anterior roots ( centrifugal, efferent) signals.

The spinal cord's own segmental apparatus consists of neurons for various functional purposes: sensory, motor (alpha, gamma motor neurons), autonomic, interneurons (segmental and intersegmental interneurons). All of them have direct or indirect synaptic connections with the conduction systems of the spinal cord. Neurons of the spinal cord provide muscle stretch reflexes - myotatic reflexes. They are the only spinal cord reflexes in which there is direct (without the participation of interneurons) control of motor neurons using signals transmitted along afferent fibers from muscle spindles.

RESEARCH METHODS

Myotatic reflexes are manifested by shortening of the muscle in response to its stretching when the tendon is struck with a neurological hammer. They differ in locality, and according to their condition, the topic of spinal cord damage is determined.

The study of superficial and deep sensitivity is important. When the segmental apparatus of the spinal cord is damaged, sensitivity in the corresponding dermatomes is impaired (dissociated or total anesthesia, hypoesthesia, paresthesia), and vegetative spinal reflexes change (viscero-motor, vegetative-vascular, urinary, etc.).

Based on the state of motor function of the extremities (upper and lower), as well as muscle tone, the severity of deep reflexes, and the presence of pathological hand and foot signs, one can assess the safety of the functions of the efferent conductors of the lateral and anterior cords of the spinal cord. Determining the zone of disturbance of pain, temperature, tactile, joint-muscular and vibration sensitivity allows us to assume the level of damage to the lateral and posterior cords of the spinal cord. This is facilitated by the study of dermographism, sweating, and vegetative-trophic functions.

To clarify the topic of the pathological focus and its relationship with surrounding tissues, as well as to determine the nature of the pathological process (inflammatory, vascular, tumor, etc.), additional studies are carried out to resolve issues of therapeutic tactics. During a spinal puncture, the initial cerebrospinal fluid pressure and patency of the subarachnoid space are assessed (liquid dynamic tests); cerebrospinal fluid is subjected to laboratory testing.

Important information about the state of motor and sensory neurons of the spinal cord is obtained through electromyography and electroneuromyography, which make it possible to determine the speed of impulses along sensory and motor nerve fibers and to record evoked potentials of the spinal cord.

Using X-ray examination, damage to the spine and the contents of the spinal canal (the membranes of the spinal cord, blood vessels, etc.) are detected.

In addition to survey spondylography, if necessary, tomography is performed, which makes it possible to detail the structures of the vertebrae, the size of the spinal canal, detect calcification of the meninges, etc. Highly informative methods of X-ray examination are pneumomyelography, myelography with radiocontrast agents, as well as selective spinal angiography, venospondylography.

The anatomical contours of the spine and the structures of the spinal canal of the spinal cord are well visualized using computed tomography and magnetic resonance imaging.

The level of block of the subarachnoid space can be determined using radioisotope (radionuclide) myelography. Thermography is used in the diagnosis of various spinal cord lesions.

Topical diagnostics

Lesions of the spinal cord are manifested by symptoms of irritation or loss of function of motor, sensory and autonomic-trophic neurons. Clinical syndromes depend on the localization of the pathological focus along the diameter and length of the spinal cord; the topical diagnosis is based on a set of symptoms of dysfunction of both the segmental apparatus and the conductors of the spinal cord. When the anterior horn or anterior root of the spinal cord is damaged, flaccid paresis or paralysis of the corresponding myotome develops with atrophy and atony of the innervated muscles, myotatic reflexes fade, fibrillation or “bioelectric silence” is detected on the electromyogram.

With a pathological process in the area of ​​the dorsal horn or dorsal root, sensitivity in the corresponding dermatome is disrupted, deep (myotatic) reflexes, the arc of which passes through the affected root and segment of the spinal cord, decrease or disappear. When the dorsal root is damaged, radicular shooting pains first appear in the area of ​​the corresponding dermatome, then all types of sensitivity are reduced or lost. When the posterior horn is destroyed, as a rule, sensitivity disorders are of a dissociated nature (pain and temperature sensitivity is lost, tactile and articular-muscular sensitivity is preserved).

Bilateral symmetrical dissociated sensitivity disorder develops with damage to the anterior gray commissure of the spinal cord.

When the neurons of the lateral horns are damaged, autonomic-vascular, trophic disorders and disturbances in sweating and pilomotor reactions occur (see Autonomic nervous system).

Damage to the conduction systems leads to more common neurological disorders. For example, when pyramidal conductors in the lateral cord of the spinal cord are destroyed, spastic paralysis (paresis) develops of all muscles innervated by neurons located in the underlying segments. Deep reflexes increase, pathological hand or foot signs appear.

If sensory conductors in the lateral cord are damaged, anesthesia occurs downward from the level of the pathological focus and on the side opposite to the lesion. The law of eccentric arrangement of long conductors (Auerbach - Flatau) allows us to differentiate the development of intramedullary and extramedullary pathological processes in the direction of spread of sensitivity disorders: the ascending type of sensitivity disorders indicates an extramedullary process, the descending type indicates an intramedullary process. The axons of the second sensory neurons (dorsal horn cells) pass into the lateral cord of the opposite side through two overlying segments of the spinal cord, therefore, when identifying the upper limit of conduction anesthesia, it should be assumed that the pathological focus is located two segments of the spinal cord above the upper limit of sensitivity disorders.

When the posterior cord is destroyed, joint-muscular vibration and tactile sensitivity on the side of the lesion is disrupted, and sensitive ataxia appears.

When half the diameter of the spinal cord is affected, central paralysis occurs on the side of the pathological focus, and on the opposite side - conduction pain and temperature anesthesia (Brown-Séquard syndrome).

Symptom complexes of spinal cord lesions at its various levels

There are several main symptom complexes of damage at different levels. Damage to the entire diameter of the spinal cord in upper cervical region (I-IV cervical segments of the spinal cord) is manifested by flaccid paralysis of the neck muscles, paralysis of the diaphragm, spastic tetraplegia, anesthesia from the level of the neck and downwards, dysfunction of the pelvic organs of the central type (urinary and fecal retention); Possible radicular pain in the neck and back of the head.

A lesion at the level of the cervical thickening (segments CV-ThI) leads to flaccid paralysis of the upper extremities with muscle atrophy, disappearance of deep reflexes in the arms, spastic paralysis of the lower extremities, general anesthesia below the level of the lesion, dysfunction of the pelvic organs of the central type.

Destruction of lateral horn cells at the CVIII-ThI level causes Bernard-Horner syndrome.

Damage to the thoracic segments is characterized by lower spastic paraplegia, conduction paraanesthesia, the upper limit of which corresponds to the level of the location of the pathological focus, urinary and fecal retention.

When the upper and middle thoracic segments are affected, breathing becomes difficult due to paralysis of the intercostal muscles; damage to the TX-XII segments is accompanied by paralysis of the abdominal muscles. Atrophy and weakness of the back muscles are detected. Radicular pain is girdling in nature.

Damage to the lumbosacral thickening (segments LI-SII) causes flaccid paralysis and anesthesia of the lower extremities, urinary and fecal retention, impaired sweating and pilomotor reaction of the skin of the lower extremities.

Damage to the segments of the epiconus (Minor's epiconus syndrome) is manifested by flaccid paralysis of the muscles of the LV-SII myotomes with the disappearance of Achilles reflexes (with preservation of the knee reflexes), anesthesia in the area of ​​the same dermatomes, urinary and fecal retention, and impotence.

Damage to the conus segments (segments (SIII - SV)) is characterized by the absence of paralysis, peripheral dysfunction of the pelvic organs with true urinary and fecal incontinence, absence of the urge to urinate and defecate, anesthesia in the anogenital zone (saddle anesthesia), impotence.

Horse's tail (cauda equina) - damage to it gives a symptom complex very similar to damage to the lumbar enlargement and conus medullaris. Peripheral paralysis of the lower extremities occurs with urinary disorders such as retention or true incontinence. Anesthesia on the lower extremities and perineum. Severe radicular pain in the legs is characteristic and for initial and incomplete lesions - asymmetry of symptoms.

When a pathological process destroys not all, but only part of the diameter of the spinal cord, the clinical picture consists of various combinations of disturbances in movement, coordination, superficial and deep sensitivity, disorders of the function of the pelvic organs and trophism (bedsores, etc.) in the denervated area.

The most common types of incomplete damage to the diameter of the spinal cord are:

1) damage to the anterior (ventral) half of the diameter of the spinal cord, characterized by peripheral paralysis of the corresponding myotomes, central paralysis and conduction pain and temperature anesthesia below the level of the pathological focus, dysfunction of the pelvic organs (Preobrazhensky syndrome);

2) damage to one half of the diameter of the spinal cord (right or left), clinically manifested by Brown-Séquard syndrome;

3) damage to the posterior third of the diameter of the spinal cord, characterized by impaired deep, tactile and vibration sensitivity, sensory ataxia, conduction parasthesias (Williamson syndrome);

4) damage to the anterior horns of the spinal cord, causing peripheral paralysis of the corresponding myotomes (poliomyelitis syndrome);

5) damage to the centromedullary zone or posterior horn of the spinal cord, manifested by dissociated segmental anesthesia in the corresponding dermatomes (syringomyelic syndrome).

In the topical diagnosis of spinal cord lesions, it is important to remember the discrepancy between the level of location of the spinal cord segments and the vertebral bodies. It should be taken into account that in case of acute damage to the cervical or thoracic segments (trauma, hematomyelia, myeloischemia, etc.), developing paralysis of the lower extremities is accompanied by muscle atony, absence of knee and Achilles reflexes (Bastian's law). The slow development of the process of such localization (for example, with a tumor) is characterized by symptoms of spinal automatism with protective reflexes.

With some lesions of the posterior cords at the level of the cervical segments of the spinal cord (tumor, multiple sclerosis plaque, spondylogenic myeloischemia, arachnoiditis), when the head is tilted forward, a sudden pain piercing the entire body occurs, similar to an electric shock (Lhermitte's symptom). For topical diagnosis, the sequence of symptoms of dysfunction of the spinal cord structures is important.

Determining the level of spinal cord damage

To determine the level of damage to the spinal cord, in particular its upper border, radicular pain, if any, is of great importance. When analyzing sensory disorders, it should be taken into account that each dermatome, as noted above, is innervated by at least 3 segments of the spinal cord (in addition to its own, another upper and one lower neighboring segments). Therefore, when determining the upper limit of anesthesia, it is necessary to consider the affected level of the spinal cord, located 1 - 2 segments higher.

Changes in reflexes, the spread of segmental movement disorders and the upper limit of conduction are equally used to determine the level of damage. Sometimes it can also be useful to study sympathetic reflexes. For example, in areas of the skin corresponding to the affected segments, there may be an absence of reflex dermographism, piloarrector reflex, etc.

The so-called “mustard plaster” test can also be useful here: narrow strips of dry mustard plaster paper are cut, moistened and applied to the skin (you can fix them with transversely glued strips of adhesive plaster), one below the other, along the length, in a continuous strip. Differences in vascular reactions above the level of the lesion, at the level of segmental disorders and below them, in the territory of conduction disorders, can help clarify the topic of spinal cord damage.

For spinal cord tumors, the following techniques can be used to determine their level of location:

Herniation symptom. During a lumbar puncture, if there is a blockage of the subarachnoid space, as the cerebrospinal fluid flows out, a difference in pressure is created and it decreases in the lower part of the subarachnoid space, below the block. As a result, a “movement” downwards, “wedging” of the tumor is possible, which determines increased radicular pain, worsening conduction disorders, etc. These phenomena can be short-term, but sometimes they are persistent, determining deterioration in the course of the disease. The symptom is more typical for subdural extramedullary tumors, for example, for neurinomas, which originate more often from the posterior roots and are usually somewhat mobile (Elsberg, I.Ya. Razdolsky).

Close to described cerebrospinal fluid rush symptom(I.Ya. Razdolsky). Again, in the presence of a block, and more often also with subdural extramedullary tumors, there is an increase in radicular pain and worsening of conduction disorders when the head is tilted to the chest or when the jugular veins are pressed on both sides of the neck (as when taking Quekenstedt). The mechanism of occurrence of the symptom is almost the same; only here it is not the decrease in fluid pressure in the subarachnoid space below the block that affects, but its increase above it due to venous stasis inside the skull.

Spinous process symptom(I.Ya. Razdolsky). Pain when tapping on the spinous process of the vertebra, at the level of which the tumor is located. The symptom is more typical for extramedullary and extradural tumors. It is best caused by shaking not with a hammer, but with the hand of the examiner (“pulp of a fist”). Sometimes, in this case, not only radicular pains appear (aggravate), but also peculiar paresthesias arise: “feeling of an electric discharge” (Cassirer, Lermitte,) - a feeling of electric current passing (or “goosebumps”) down the spine, sometimes in the lower limbs.

May also have a known significance radicular positional pain(Dandy - Razdolsky). In a certain position, which causes, for example, tension in the posterior root from which the neuroma arises, radicular pain of the corresponding level arises or intensifies.

Finally worthy of attention Elsberg-Dyck sign(x-ray) - abnormal increase in the distance between the roots of the arches from 2 to 4 mm at the level of tumor localization (usually extradural).

When projecting the affected segments of the spinal cord onto the vertebrae, it is necessary to take into account the discrepancy in the length of the spinal cord and spine and carry out the calculation according to the instructions given above. For orientation in the spinous processes of the vertebrae, the following data can be used:

- the highest vertebra visible under the skin is the VII cervical, i.e. the lowest cervical vertebra;

- the line connecting the lower corners of the shoulder blades passes above the VII thoracic vertebra;

- the line connecting the tops of the iliac crests (cristae lliacae) runs in the space between the III and IV lumbar vertebrae.

In processes leading to filling of the cavity of the intravertebral canal (for example, with tumors) or causing adhesions in the subarachnoid space (with arachnoiditis), valuable data for localizing the process can sometimes be obtained by myelography, i.e., radiography when contrast solutions are introduced into the subarachnoid space. It is preferable to administer “heavy” or descending solutions (oil) by suboccipital puncture; the contrast agent, descending downwards in the cerebrospinal fluid, in case of obstruction in the subarachnoid space, stops or is temporarily delayed at the level of the block and is detected on radiography in the form of a shadow (“stop” contrast).

Less contrast images are obtained with pneumomyelography, i.e., when air is injected through a lumbar puncture in a sitting patient; the air, rising upward through the subarachnoid space, stops under the “block” and determines the lower border of the existing obstruction.

To determine the level of the “block” (for tumors, arachnoiditis, etc.), a “staircase” lumbar puncture is sometimes used, usually only in the spaces between the LIV - LIII - LII vertebrae (puncture of higher sections can be dangerous due to possible injury from the needle to the spinal brain). Below the blockade of the subarachnoid space, protein-cell dissociation is observed, above - the normal composition of the cerebrospinal fluid; Below the blockade there are symptoms of Queckenstedt and Stuckey, above - their absence (the norm).

Cylindrical. cord located in the spinal canal. Two thickenings - cervical (C5-Th1 - innerv. lower end) and lumbar (L1-2-S lower end). 31-31 segments: 8 cervical (C1-C8), 12 thoracic (Th1-Th12), 5 lumbar (L1-L5), 5 sacral (S1-S5), and 1-2 coccygeal (Co1-Co2). The image is also sharpened below. the conus medullaris, which is connected by the filum terminale, has reached. coccygeal vertebrae. At the level of each segment, 2 pairs of anterior and posterior roots depart. On each side they merge into the medullary cord. The gray thing has hind horns, sod. feelings. cells; anterior horns, sod. engine class, and side horns in the cat. location veget. cute. and parasymp. neurons. The white matter consists of nerve fibers and is divided into 3 cords: posterior, lateral and anterior. Upper cervical region (C1-C4)- paralysis or irritation. diaphragm, spastic terminal paralysis, loss of all types of sensations, urinary dispersion. Cervical thickening (C5-D2) – transfer upper paralysis. horse, spastic lower; loss of sensation, urinary disorders, Horner's sim. Thoracic region (D3- DVII) - spastic lower paraplegia final, loss of urine, loss of sensation in the lower half of the body. Lumbar thickening (L1- S2)- reph. paralysis and anesthesia of the lower parts, urination patterns. Conus medullaris (S3- S5)- loss of feeling in the region. perineum, urine dispersion. Ponytail - perf. lower paralysis. con-th, raster. urine, anesthesia on the lower. con-x and perineum.

18. Sensory and motor systems in case of damage to the anterior and posterior roots, plexuses, peripheral nerves.

Peripheral trunk damage. nerve- disturbance of all types of senses in the area of ​​cutaneous innervation of this nerve, paresis, muscle atony, areflexia, hyporeflexia, atrophy. Damage to the plexus trunks- anesthesia, hypoesthesia of all types of senses, pain, paresis, muscle atony, areflexia, hyporeflexia, atrophy. Cervical: n.occipitalis minor (CI-CIII) - lesser occipital nerve, severe pain (cervical neuralgia); n. auricularis magnus (CIII) – large auricular nerve, senses, pain; n. supraclavicularis (CIII-CIV) – supraclavicular nerves, senses, pain; n. phrenicus (CIII-CIV) – nerve of the diaphragm, paralysis of the diaphragm, hiccups, shortness of breath, pain. Damage shoulders. plexuses - flaccid atrophic. paralysis and anesthesia top. con-th with loss of elbow extension. and flexor muscles. reflexes. Damage to the posterior sensory root- paresthesia, pain, loss of all types of sensation, segmental character: circular on the trunk, strip-longitudinal on the limbs, muscle atony, areflexia, hyporeflexia, atrophy. Damage to the anterior roots– segmental distribution of paralysis.

19. Clinical manifestations of damage to half the diameter of the spinal cord. Brown-Sicard syndrome. Clinical examples.

Lesion on the side of the lesion: loss of deep sensitivity, impairment of articular-muscular sense in the presence of central paralysis downward from the level of the lesion, on the contrary. side – conduction pain and temperature anesthesia, violation. superficial sensitivity. As a clinical forms of spinal circulation disorders. According to the hemorrhagic type, hematomyelia is distinguished (Brown-Sicart syndrome). Signs of spinal cord damage occur suddenly, after physical activity or injury. I observed a strong pain radicular syndrome with irradiation in all directions, dagger-like girdling pains along the spine, headache, nausea, vomiting, slight stupor, lethargy are not uncommon. Def. Kernig's symptom, in combination with Lasegue's pain symptom, stiffness of the neck muscles. May occur with myelitis, spinal cord tumors.

20. Ipair. olfactory nerve and olfactory system. Symptoms and syndromes of damage.n. olfactorii. The fibers begin from the olfactory bipolar cells, in the mucous membrane of the superior turbinate, the axons enter the cranial cavity through the ethmoid bone → 1st neuron ends in the olfactory bulb located in the anterior cranial fossa → 2nd neuron reach the olfactory triangle, the anterior perforated plate and the septum pellucidum → 3rd neuron parahippocampal gyrus, piriformis gyrus, hippocampus. Loss: ↓ - hyposmia ; heightened sense of smell - hyperosmi I; perversion of smell - dysosmia, sense of smell. hallucinations – with psychosis and epilepsy. seizures . Research: allow you to smell various odorous substances.

21. IIpair. Optic nerve and visual system. Signs of damage at various levels.n. opticus. 1st neuron retinal ganglion cells enter the cranial cavity through the foramen opticum → at the base of the brain and anterior to the sella turcica they intersect, forming a chiasma (internal fibers intersect, external or temporal ones do not intersect) → optic tracts → cerebral peduncles → afferent part of the arc of the pupillary reflex, visual centers - superior colliculi 2nd neuron→ into the external geniculate bodies and the cushion of the visual thalamus "thalamic neuron". → external genicular body → internal capsule → as part of the Graziole bundle → cortical region. Research: 1. visual acuity: ↓ - amblyopia ; total loss - amaurosis .2. color vision: complete flower blindness – achromatopsia; impaired perception of individual colors - dyschromatopsia; color blindness – inability to distinguish between green and red colors.3. field of view: N – outward 90˚, inward 60˚, downward 70˚, upward 60˚.- concentric – narrowing of the field of view on both sides; scotoma – loss of individual areas; - hemianopsia – loss of half of vision. Homonymous hemianapsia – loss of the right and left visual fields of each eye. Heteronymous – loss of both internal and external fields of vision: bitemporal – loss of temporal visual fields; binasal – loss of internal half When damaged retina or vision nerve blindness occurs, ↓ visual acuity, with damage. chiasmata - heteronymous hemianopsia, with lesions. sees paths after the cross - homonymous lunge. vision, with a lesion in the visual field. tract - homonymous hemianopsia, with lesions. sees cortex – square hemianopsia.

22. III, IV, VI pairs. Oculomotor, trochlear and abducens nerves and oculomotor system. Innervation of gaze. Gaze paresis (cortical and stem). IIIpair -oculomotorius. Nuclei in the midbrain, along the bottom of the cerebral aqueduct, at the level of the superior colliculus → emerge at the base of the brain → leaves the skull and is divided into branches: superior inn-t superior rectus muscle, inferior inn-t three external muscles of the eye: inferior rectus, oblique, internal . Laterally, large cell nuclei, inn-t transverse stripes. muscles (oculomotor, levator upper eyelid). Paramedial small cell nuclei of Yakubovich – Edinger – Westphal, Inn-I muscle of the constrictor pupil. Damage: 1) divergent strabismus and the inability to move the affected eyeball inward and upward; 2) exophthalmos – protrusion of the eye from the orbit; 3) ptosis – drooping upper eyelid; 4) mydriasis – dilation of the pupil due to paralysis of the muscles that constrict the pupil and the absence of a direct and friendly reaction of the pupil to light; 5) paralysis of accommodation – deterioration of vision at close distances. IVpair -n. trochlearis. The nucleus is at the bottom of the aqueduct at the level of the lower colliculi → the fibers go upward, cross in the anterior medullary velum → going around the cerebral peduncles, exit it and pass along the base of the skull into the orbit (through the superior orbital fissure). Inn the muscle rotates the eyeball outward and downward. Damage: convergent strabismus, diplopia. VIpair -n. abducens. The nucleus lies at the bottom of the IV ventricle → bends around the fibers of the facial nerve and goes to the base → exits at the border of the pons and medulla oblongata in the region of the cerebellopontine angle → enters the orbital cavity through the superior orbital fissure. Inn-t lateral rectus muscle of the eye. Damage: convergent strabismus, diplopia. If all nerves are affected, complete ophthalmoplegia occurs. Innervation of eyeball movements is realized. cortical center of gaze, located in the posterior part of the middle frontal gyrus → internal. capsule and cerebral peduncles, decussation, through neurons of the reticular formation and honey prot. the bundle transmits impulses to the nuclei of the III, IV, VI nerves.

23. Vsteam. Trinity nerve. Sensory and motor parts. Symptoms of lesions.n. trigeminus. Nuclei in the brainstem → sensory fibers arise from the gasserian ganglion ( 1st neuron)→ enter the cerebrum: fibers of pain and tactile sensitivity end in n. tractus spinalis, and tactile and joint-muscular sensitivity end in the nucleus n. terminalis ( 2nd neuron) → nuclear fibers form a loop entering the opposite medial lemniscus → thalamus opticum ( 3rd neuron) → internal capsule → end in the posterior central gyrus. The dendrites of the Gasserian ganglion make up a sensitive root: the orbital nerve leaves the skull through the superior orbital fissure, the maxillary nerve through the foramen rotundum, the mandibular nerve through the foramen ovale. The motor root, together with the maxillary nerve, goes to the masticatory muscle. when the engine is damaged. fibers, the lower jaw, when opening the mouth, deviates towards the lesion. muscles. When paralyzed, they chew everyone. muscles, the lower jaw droops, when damaged. Department. the branches of the raster have developed. in the innervir zone. given nerve, the response fades away. reflexes. Damage eye socket nerve leads to loss of the corneal and supraorbital reflex. When damaged gasserian node or root, the feeling falls in the innerviral zones. all branches of the 5th pair, pain, illness. when pressed at the exit points on the face. when the nuclei on the face are damaged, they are dissociated. raster of feelings (loss of pain and temperature).

Movement - a universal manifestation of life activity, providing the possibility of active interaction of both the component parts of the body and the whole organism with the environment by moving in space. There are two types of movements:

1) involuntary- simple automated movements, which are carried out due to the segmental apparatus of the spinal cord, brain stem, like a simple reflex motor act;

2) arbitrary (targeted)- arising as a result of the implementation of programs formed in the motor functional segments of the central nervous system.

In humans, the existence of voluntary movements is associated with the pyramidal system. Complex acts of human motor behavior are controlled by the cerebral cortex (middle sections of the frontal lobes), the commands of which are transmitted through the pyramidal tract system to the cells of the anterior horns of the spinal cord, and from them through the peripheral motor neuron system to the executive organs.

The movement program is formed on the basis of sensory perception and postural reactions from the subcortical ganglia. Correction of movements occurs through a feedback system with the participation of a gamma loop, starting from the spindle-shaped receptors of intramuscular fibers and closing on the gamma motor neurons of the anterior horns, which, in turn, are under the control of the overlying structures of the cerebellum, subcortical ganglia and cortex. The motor sphere of a person is so completely developed that a person is able to carry out creative activities.

3.1. Neurons and pathways

Motor tracts of the pyramidal system (Fig. 3.1) consist of two neurons:

1st central neuron - cell of the cerebral cortex;

2nd peripheral neuron - motor cell of the anterior horn of the spinal cord or motor nucleus of the cranial nerve.

1st central neuron located in layers III and V of the cerebral cortex (Betz cells, medium and small pyramidal

Rice. 3.1.Pyramid system (diagram):

A)pyramidal tract: 1 - cerebral cortex; 2 - internal capsule;

3 - cerebral peduncle; 4 - bridge; 5 - intersection of pyramids; 6 - lateral corticospinal (pyramidal) tract; 7 - spinal cord; 8 - anterior corticospinal tract; 9 - peripheral nerve; III, VI, VII, IX, X, XI, XII - cranial nerves; b) convexital surface of the cerebral cortex (fields

4 and 6); topographic projection of motor functions: 1 - leg; 2 - torso; 3 - hand; 4 - brush; 5 - face; V) horizontal section through the internal capsule, location of the main pathways: 6 - visual and auditory radiation; 7 - temporopontine fibers and parieto-occipital-pontine fascicle; 8 - thalamic fibers; 9 - corticospinal fibers to the lower limb; 10 - corticospinal fibers to the muscles of the trunk; 11 - corticospinal fibers to the upper limb; 12 - cortical-nuclear pathway; 13 - frontal-pontine tract; 14 - corticothalamic tract; 15 - anterior leg of the internal capsule; 16 - elbow of the internal capsule; 17 - posterior leg of the internal capsule; G) anterior surface of the brain stem: 18 - decussation of pyramids

cells) in the area anterior central gyrus, posterior parts of the superior and middle frontal gyri and paracentral lobule(4, 6, 8 cytoarchitectonic fields according to Brodmann).

The motor sphere has a somatotopic localization in the anterior central gyrus of the cerebral hemisphere cortex: the centers of movement of the lower extremities are located in the upper and medial sections; the upper limb - in its middle section; head, face, tongue, pharynx, larynx - in the lower middle. The projection of body movements is presented in the posterior section of the superior frontal gyrus, the rotation of the head and eyes is represented in the posterior section of the middle frontal gyrus (see Fig. 3.1 a). The distribution of motor centers in the anterior central gyrus is uneven. In accordance with the principle of “functional significance”, the greatest representation in the cortex are those of the body that perform the most complex, differentiated movements (centers that provide movement of the hand, fingers, and face).

The axons of the first neuron, going down, converge like a fan, forming the corona radiata, then pass through the internal capsule in a compact bundle. From the lower third of the anterior central gyrus, the fibers involved in the innervation of the muscles of the face, pharynx, larynx, tongue, pass through the knee of the internal capsule, in the trunk they approach the motor nuclei of the cranial nerves, and therefore this path is called corticonuclear. The fibers that form the corticonuclear tract are directed to the motor nuclei of the cranial nerves (III, IV, V, VI, VII, IX, X, XI) of both their own and the opposite side. The exception is the corticonuclear fibers that go to the lower part of the nucleus of the VII and to the nucleus of the XII cranial nerves and carry out unilateral voluntary innervation of the lower third of the facial muscles and half of the tongue on the opposite side.

Fibers from the upper 2/3 of the anterior central gyrus, involved in the innervation of the muscles of the trunk and limbs, pass into anterior 2/3 posterior limbs of the internal capsule and in the brain stem (corticospinal or actually pyramid path) (see Fig. 3.1 c), and the fibers are located outside to the muscles of the legs, and inside - to the muscles of the arms and face. At the border of the medulla oblongata and the spinal cord, most of the fibers of the pyramidal tract form a cross and then pass as part of the lateral cords of the spinal cord, forming lateral (lateral) pyramidal tract. The smaller, uncrossed part of the fibers forms the anterior funiculi of the spinal cord (anterior pyramidal

path). The crossover is carried out in such a way that the fibers externally located in the crossover zone, innervating the leg muscles, are located inside after the crossover, and, conversely, the fibers to the arm muscles, located medially before the crossover, become lateral after moving to the other side (see Fig. 3.1 d ).

In the spinal cord, the pyramidal tract (anterior and lateral) gives off segmental fibers to alpha major neurons of the anterior horn (second neuron), directly communicating with the working striated muscle. Due to the fact that the segmental zone of the upper extremities is the cervical enlargement, and the segmental zone of the lower extremities is the lumbar enlargement, fibers from the middle third of the anterior central gyrus end predominantly in the cervical enlargement, and from the upper third - in the lumbar enlargement.

Motor cells of the anterior horn (2nd, peripheral neuron) located in groups responsible for contraction of the muscles of the trunk or limbs. In the upper cervical and thoracic sections of the spinal cord, three groups of cells are distinguished: anterior and posterior medial, which provide contraction of the muscles of the body (flexion and extension), and central, innervating the muscles of the diaphragm and shoulder girdle. In the area of ​​the cervical and lumbar thickenings, these groups are joined by the anterior and posterior lateral, innervating the flexor and extensor muscles of the limbs. Thus, in the anterior horns at the level of the cervical and lumbar thickenings there are 5 groups of motor neurons (Fig. 3.2).

In each of the groups of cells in the anterior horn of the spinal cord and in each motor nucleus of the cranial nerves, there are three types of neurons that perform different functions.

1. Alpha large cells conducting motor impulses at high speed (60-100 m/s), providing the possibility of rapid movements, are associated primarily with the pyramidal system.

2. Alpha small neurons receive impulses from the extrapyramidal system and exert postural influences, providing postural (tonic) contraction of muscle fibers, and perform a tonic function.

3. Gamma neurons receive impulses from the reticular formation and their axons are directed not to the muscle itself, but to the proprioceptor contained in it - the neuromuscular spindle, affecting its excitability.

Rice. 3.2.Topography of motor nuclei in the anterior horns of the spinal cord at the level of the cervical segment (diagram). On the left is the general distribution of anterior horn cells; on the right - nuclei: 1 - posteromedial; 2 - anteromedial; 3 - front; 4 - central; 5 - anterolateral; 6 - posterolateral; 7 - posterolateral; I - gamma efferent fibers from small cells of the anterior horns to the neuromuscular spindles; II - somatic efferent fibers giving collaterals to medially located Renshaw cells; III - gelatinous substance

Rice. 3.3.Cross section of the spine and spinal cord (diagram):

1 - spinous process of the vertebra;

2 - synapse; 3 - skin receptor; 4 - afferent (sensitive) fibers; 5 - muscle; 6 - efferent (motor) fibers; 7 - vertebral body; 8 - node of the sympathetic trunk; 9 - spinal (sensitive) node; 10 - gray matter of the spinal cord; 11 - white matter of the spinal cord

The neurons of the anterior horns are multipolar: their dendrites have multiple connections with various afferent and efferent systems.

The axon of a peripheral motor neuron leaves the spinal cord as part of anterior root goes into plexuses and peripheral nerves, transmitting a nerve impulse to the muscle fiber (Fig. 3.3).

3.2. Movement disorder syndromes (paresis and paralysis)

The complete absence of voluntary movements and a decrease in muscle strength to 0 points, caused by damage to the cortico-muscular pathway, is called paralysis (plegia); limitation of range of motion and decrease in muscle strength to 1-4 points - paresis. Depending on the distribution of paresis or paralysis, they are distinguished.

1. Tetraplegia/tetraparesis (paralysis/paresis of all four limbs).

2. Monoplegia/monoparesis (paralysis/paresis of one limb).

3. Triplegia/triparesis (paralysis/paresis of three limbs).

4. Hemiplegia/hemiparesis (unilateral paralysis/paresis of the arms and legs).

5. Upper paraplegia/paraparesis (paralysis/paresis of the arms).

6. Lower paraplegia/paraparesis (paralysis/paresis of the legs).

7. Cross hemiplegia/hemiparesis (paralysis/paresis of the arm on one side and the leg on the opposite).

There are 2 types of paralysis - central and peripheral.

3.3. Central paralysis. Topography of central motor neuron lesion Central paralysis occurs when the central motor neuron is damaged, i.e. with damage to Betz cells (layers III and V) in the motor zone of the cortex or pyramidal tract all the way from the cortex to the anterior horns of the spinal cord or the motor nuclei of the cranial nerves in the brain stem. The following symptoms are characteristic:

1. Muscular spastic hypertension, upon palpation, the muscles are tense, compacted, "jackknife" symptom contractures.

2. Hyperreflexia and expansion of the reflexogenic zone.

3. Clonus of the feet, kneecaps, lower jaw, hands.

4. Pathological reflexes.

5. Defensive reflexes(reflexes of spinal automatism).

6. Decreased skin (abdominal) reflexes on the side of paralysis.

7. Pathological synkinesis.

Synkinesias are involuntary movements that occur during active movements. They are divided into physiological(for example, swinging your arms while walking) and pathological. Pathological synkinesias occur in a paralyzed limb when the pyramidal tracts are damaged and are caused by the loss of inhibitory influences from the cerebral cortex on intraspinal automatisms. Global synkinesis- contraction of the muscles of paralyzed limbs, which occurs when muscle groups on the healthy side are tense. For example, when a patient tries to rise from a lying position or stand up from a sitting position on the paretic side, the arm is bent at the elbow and brought to the body, and the leg is extended. Coordinating synkinesis- when trying to make any movement with a paretic limb involuntarily

another movement appears, for example, when trying to flex the lower leg, dorsiflexion of the foot and big toe occurs (tibial synkinesis or tibial Strumpel phenomenon). Imitative synkinesis- involuntary repetition by a paretic limb of those movements that are performed by a healthy limb. Topography of central motor neuron lesions at different levels

Anterior central gyrus irritation syndrome - clonic convulsions, motor Jacksonian seizures.

Syndrome of damage to the cortex, corona radiata - hemi/monoparesis or hemi/monoplegia on the opposite side.

Knee internal capsule syndrome (damage to the corticonuclear pathways from the lower third of the anterior central gyrus to the nuclei of the VII and XII nerves) - weakness of the lower third of the facial muscles and half of the tongue.

Syndrome of damage to the anterior 2/3 of the posterior thigh of the internal capsule - uniform hemiplegia on the opposite side, Wernicke-Mann position with a predominance of spastic tone in the arm flexors and leg extensors (“the hand asks, the leg squints”) [Fig. 3.4].

Rice. 3.4.Wernicke-Mann pose: A- on right; b- left

Brain stem pyramidal tract syndrome - damage to the cranial nerves on the side of the lesion, on the opposite side hemiparesis or hemiplegia (alternating syndromes).

Pyramidal tract lesion syndrome in the decussation area at the border of the medulla oblongata and spinal cord - cross hemiplegia or hemiparesis (affecting the arm on the side of the lesion, the leg on the contralateral side).

Pyramidal tract lesion syndrome in the lateral cord of the spinal cord - central paralysis below the level of the lesion homolaterally.

3.4. Peripheral paralysis. Topography of peripheral motor neuron lesions

Peripheral (flaccid) paralysis develops when a peripheral motor neuron is damaged (cells of the anterior horns or motor nuclei of the brain stem, roots, motor fibers in the plexuses and peripheral nerves, neuromuscular synapse and muscle). It manifests itself with the following main symptoms.

1. Muscle atony or hypotension.

2. Areflexia or hyporeflexia.

3. Muscular atrophy (hypotrophy), which develops as a result of damage to the segmental reflex apparatus after some time (at least a month).

4. Electromyographic signs of damage to peripheral motor neurons, roots, plexuses, peripheral nerves.

5. Fascicular muscle twitching, resulting from pathological impulses of a nerve fiber that has lost control. Fascicular twitching usually accompanies atrophic paresis and paralysis during a progressive process in the cells of the anterior horn of the spinal cord or the motor nuclei of the cranial nerves, or in the anterior roots of the spinal cord. Much less often, fasciculations are observed with generalized damage to peripheral nerves (chronic demyelinating polyneuropathy, multifocal motor neuropathy).

Topography of peripheral motor neuron lesions

Anterior horn syndrome characterized by atony and muscle atrophy, areflexia, electromyographic signs of damage to the peripheral motor neuron (at the level of the horns)

ENMG data. Asymmetry and patchiness of the lesion (due to possible isolated damage to individual groups of cells), early onset of atrophy, and fibrillar twitching in the muscles are typical. According to stimulation electroneurography (ENG): the appearance of giant and repeated late responses, a decrease in the amplitude of the M-response with a normal or slightly slower rate of propagation of excitation, no disruption of conduction along sensory nerve fibers. According to needle electromyography (EMG): denervation activity in the form of fibrillation potentials, positive sharp waves, fasciculation potentials, “neuronal” type motor unit potentials in the muscles innervated by the affected segment of the spinal cord or brain stem.

Anterior root syndrome characterized by atony and muscle atrophy mainly in the proximal parts, areflexia, electromyographic signs of damage to the peripheral motor neuron (at the level of the roots) according to ENMG. Typically combined damage to the anterior and posterior roots (radiculopathy). Signs of radicular syndrome: according to stimulation ENG (impaired late responses, in the case of secondary damage to the axons of nerve fibers - a decrease in the amplitude of the M-response) and needle EMG (denervation activity in the form of fibrillation potentials and positive sharp waves in the muscles innervated by the affected root, Fasciculation potentials are rarely recorded).

Peripheral nerve syndrome includes a triad of symptoms - motor, sensory and autonomic disorders (depending on the type of peripheral nerve affected).

1. Motor disorders characterized by atony and muscle atrophy (usually in the distal parts of the limbs, after some time), areflexia, signs of peripheral nerve damage according to ENMG.

2. Sensory disorders in the area of ​​nerve innervation.

3. Autonomic (vegetative-vascular and vegetative-trophic) disorders.

Signs of impairment of the conductive function of motor and/or sensory nerve fibers, according to stimulation ENG data, appear in the form of a slowdown in the speed of propagation of excitation, the appearance of chronodispersion of the M-response, and conduction blocks

excitement. In the case of axonal damage to the motor nerve, denervation activity is recorded in the form of fibrillation potentials and positive sharp waves. Fasciculation potentials are rarely recorded.

Symptom complexes of lesions of various nerves and plexuses

Radial nerve: paralysis or paresis of the extensors of the forearm, hand and fingers, and with high damage - the abductor pollicis longus muscle, the “dangling hand” pose, loss of sensitivity on the dorsal surface of the shoulder, forearm, part of the hand and fingers (dorsal surface of I, II and half of III ); loss of the reflex from the triceps tendon, inhibition of the carporadial reflex (Fig. 3.5, 3.8).

Ulnar nerve: a typical “clawed paw” is the impossibility of clenching the hand into a fist, limitation of palmar flexion of the hand, adduction and extension of the fingers, extension contracture in the main phalanges and flexion contracture in the terminal phalanges, especially the fourth and fifth fingers. Atrophy of the interosseous muscles of the hand, lumbrical muscles going to the 4th and 5th fingers, hypothenar muscles, partial atrophy of the forearm muscles. Impaired sensitivity in the innervation zone, on the palmar surface of the fifth finger, the dorsum of the fifth and fourth fingers, the ulnar part of the hand and the third finger. Sometimes trophic disorders and pain radiating to the little finger are observed (Fig. 3.6, 3.8).

Median nerve: violation of palmar flexion of the hand, I, II, III fingers, difficulty in opposition of the thumb, extension of the middle and terminal phalanges of the II and III fingers, pronation, atrophy of the muscles of the forearm and thenar (“monkey hand” - the hand is flattened, all fingers are extended, the thumb is close brought to the index). Loss of sensitivity on the hand, palmar surface of the 1st, 2nd, 3rd fingers, radial surface of the 4th finger. Vegetative-trophic disorders in the innervation zone. In case of injuries to the median nerve - causalgia syndrome (Fig. 3.7, 3.8).

Femoral nerve: with a high lesion in the pelvic cavity - impaired flexion of the hip and extension of the leg, atrophy of the muscles of the anterior surface of the thigh, inability to walk up stairs, run, jump. Sensitivity disorder on the lower 2/3 of the anterior surface of the thigh and the anterior inner surface of the leg (Fig. 3.9). Loss of the knee reflex, positive symptoms of Wasserman, Matskevich. At low level

Rice. 3.5.Symptom of “dangling hand” with damage to the radial nerve (a, b)

Rice. 3.6.Symptom of “clawed paw” with damage to the ulnar nerve (a-c)

Rice. 3.7.Symptoms of the “monkey hand” with damage to the median nerve (“obstetrician’s hand”) [a, b]

Rice. 3.8.Innervation of cutaneous sensitivity of the upper limb (peripheral type)

Rice. 3.9.

lesions - isolated lesion of the quadriceps femoris muscle.

Obturator nerve: violation of hip adduction, leg crossing, hip outward rotation, atrophy of the hip adductors. Sensitivity disorder on the inner surface of the thigh (Fig. 3.9).

External cutaneous nerve of the thigh: sensitivity disorder on the outer surface of the thigh, paresthesia, sometimes severe neuralgic paroxysmal pain.

Sciatic nerve: with a high complete lesion - loss of function of its main branches, the entire group of leg flexor muscles, inability to flex the leg, paralysis of the foot and fingers, foot drop, difficulty in

walking, atrophy of the muscles of the back of the thigh, all muscles of the lower leg and foot. Sensitivity disorder on the anterior, outer and posterior surfaces of the leg, dorsal and plantar surfaces of the foot, fingers, decreased or loss of the Achilles reflex, severe pain along the sciatic nerve, soreness of Vallee's points, positive symptoms of tension, antalgic scoliosis, vasomotor-trophic disorders, in case of injury sciatic nerve - causalgia syndrome.

Gluteal nerves: violation of hip extension and pelvic fixation, “duck walk”, atrophy of the gluteal muscles.

Posterior cutaneous nerve of the thigh: sensitivity disorder on the back of the thigh and lower buttocks.

Tibial nerve: impaired plantar flexion of the foot and toes, outward rotation of the foot, inability to stand on toes, atrophy of the calf muscles, atrophy of the foot muscles,

Rice. 3.10.Innervation of cutaneous sensitivity of the lower limb (peripheral type)

Rice. 3.11.Symptom of “equine foot” with damage to the peroneal nerve

retraction of the interosseous spaces, a peculiar type of foot - “heel foot” (Fig. 3.10), sensitivity disorder on the back surface of the leg, on the sole, plantar surface of the fingers, decrease or loss of the Achilles reflex, vegetative-trophic disorders in the innervation zone, causalgia.

Peroneal nerve: limitation of dorsiflexion of the foot and toes, inability to stand on the heels, drooping of the foot downward and rotation inward (“horse foot”), a kind of “cock’s gait” (when walking, the patient raises his leg high so as not to touch the floor with his foot); atrophy of the muscles of the anterior outer surface of the leg, sensitivity disorder along the outer surface of the leg and dorsum of the foot; the pain is not pronounced (Fig. 3.11).

When the plexuses are damaged motor, sensory and autonomic disorders occur in the area of ​​innervation of this plexus.

Brachial plexus(C 5 -Th 1): persistent pain radiating throughout the arm, aggravated by movements, atrophic paralysis of the muscles of the entire arm, loss of tendon and periosteal reflexes. Impairment of all types of sensitivity in the area of ​​innervation of the plexus.

- Superior brachial plexus(C 5 -C 6) - Duchenne-Erb palsy: predominant damage to the muscles of the proximal arm,

sensitivity disorder along the outer edge of the entire arm, loss of the reflex from the biceps brachii muscle. - Inferior brachial plexus(From 7 - Th 1)- Dejerine-Klumpke palsy: disorder of movements in the forearm, hand and fingers while maintaining the function of the muscles of the shoulder girdle, impaired sensitivity on the inner surface of the hand, forearm and shoulder, vasomotor and trophic disorders in the distal parts of the hand, loss of the carporadial reflex, Bernard-Horner syndrome.

Lumbar plexus (Th 12 -L 4): the clinical picture is due to high damage to three nerves arising from the lumbar plexus: the femoral, obturator and external cutaneous nerve of the thigh.

Sacral plexus (L 4 -S 4): loss of function of the peripheral nerves of the plexus: the sciatic with its main branches - the tibial and peroneal nerves, the superior and inferior gluteal nerves and the posterior cutaneous nerve of the thigh.

The differential diagnosis of central and peripheral paralysis is presented in table. 1.

Table 1.Symptoms of central and peripheral paralysis

In practice, we encounter diseases (for example, amyotrophic lateral sclerosis) in which symptoms characteristic of both central and peripheral paralysis are revealed: a combination of atrophy and grossly expressed hyperreflexia, clonus, and pathological reflexes. This is explained by the fact that a progressive degenerative or acute inflammatory process mosaically, selectively affects the pyramidal tract and cells of the anterior horn of the spinal cord, as a result of which both the central motor neuron is affected (central paralysis develops) and the peripheral motor neuron (peripheral paralysis develops). With further progression of the process, the motor neurons of the anterior horn are increasingly affected. With the death of more than 50% of the anterior horn cells, hyperreflexia and pathological reflexes gradually disappear, giving way to symptoms of peripheral paralysis (despite the ongoing destruction of the pyramidal fibers).

3.5. Half-spinal cord lesion (Brown-Séquard syndrome)

The clinical picture of Brown-Séquard syndrome is presented in Table. 2.

Table 2.Clinical symptoms of Brown-Séquard syndrome

Complete transverse spinal cord lesion characterized by development