Disorders of movement and sensitivity become. Hypersensitivity, HSP: what is it? Causes of numbness of the skin of the legs

Pathomechanism and causes

Sensitivity disturbances can be manifested by symptoms of decrease (weakening or absence of one or more types of sensitivity) and / or symptoms of increase (pathological sensations in the form of paresthesia, such as tingling or numbness, or hypersensitivity to sensory stimuli - pain, hyperesthesia).

Causes: pathological processes that damage peripheral receptors located in various tissues and organs, sensory fibers peripheral nerves, afferent pathways of the spinal cord and brain stem, thalamus and cortical centers in the parietal lobe.

Causes various kinds sensory disturbances, depending on the level of damage nervous system→ . Short-term and transient paresthesias do not indicate damage to the nervous system. Causes of paresthesia, depending on the level of the lesion → .

Diagnostics

1. History and physical examination: the type, severity, circumstances of occurrence and localization of sensory disturbances should be assessed. Tactile sensitivity examine by touching the body with a piece of thin paper or cotton on a stick, pain sensitivity- needle, sensation of temperature- using two test tubes with warm and cold water (from the tap). Investigating sensitivity, it is compared on symmetrical parts of the body, the limits of sensitivity disorders are determined as accurately as possible and compared with the areas of innervation of individual peripheral nerves and individual dermatomes → .

2. Ancillary research: neuroimaging (CT, MRI) of the brain and / or spinal cord, electrophysiological studies (sensory conduction; sensory evoked potentials) depending on the estimated level of damage.

Clinical manifestations of sensory disturbances can be divided into three main groups - symptoms of irritation, symptoms of loss, symptoms of perversion (Fig. 3).

table 2

Investigation of different types of sensitivity

Rice. 3. Types of sensory disorders

Paresthesia- unpleasant, unusual, spontaneous and mostly short-term sensations that occur without causing irritation from the outside (crawling, tingling, burning, etc.). Their occurrence is often associated with compression-ischemic effects (prolonged squatting, cross-legged position, etc.) and can be triggered by certain tests.

Pain is the most common symptom of irritation—it is an unpleasant sensory and emotional experience associated with or described in terms of existing or potential tissue damage (definition by the International Association for the Study of Pain).

Local pain got its name for the reason that the localization of the felt pain coincides with the place of painful irritation (pathological process).

projection pain (from lat. . pro- forward, jaceo- I throw) do not coincide with the place of primary sensory irritation, but are projected onto the periphery. Thus, compression of the posterior root causes pain in the limb, contusion of the ulnar nerve in the area of ​​the elbow joint is associated with the appearance of pain in the IV–V fingers of the hand.

irradiating pain (from lat. irradio- I emit rays) are associated with the spread of irritation from one branch involved in the pathological process to others, free from the direct impact of the pathological process. In this way, in particular, pains can spread along all branches trigeminal nerve with the defeat of only one of them, for example, with pathology of the teeth.

The variant of irradiation of pain are reflected pain. With pathology internal organs pain can spread to areas of certain dermatomes (viscerosensory phenomenon), which are called Zakharyin-Ged zones.

jet pain occurs when the nerve (root) is compressed or stretched. So, pressure on the nerve trunks, where they are located superficially or adjacent to the bone (Valle's points, trigeminal points, etc.), causes pain. IN clinical practice tension symptoms are widely used. Symptom Lasegue (lying on the back: the first phase - when bending in hip joint pain appears in rear surface thighs and lower legs, the second phase - when bending in knee joint pain disappears) indicates a lesion sciatic nerve and (or) lower lumbar roots, upper sacral roots (L 4 -L 5 , S 1 -S 2). Wasserman's symptom (lying on the stomach: when the hip joint is extended, pain appears in the groin and along the front surface of the thigh) and Matskevich's symptom (lying on the stomach: when the knee joint is bent, pain appears in the groin and along the front surface of the thigh) indicate a lesion femoral nerve and (or) upper lumbar roots (L 1 -L 3). To a large extent, the symptoms of Neri (forced tilt of the head and tension of the roots cause pain in the area of ​​​​innervation of suffering roots), Dejerine (coughing, sneezing, straining cause pain in the area of ​​​​innervation of suffering roots) are largely similar. Tension symptoms may also be positive in spondylogenic syndromes such as lumbalgia.

Phantom pain occurs in people who have undergone amputation of a limb or part of it: irritation of the nerves containing the continuation of fibers from the amputated fragment of the limb in the stump (neuroma, etc.) causes a sensation of pain in the missing parts of the limbs.

Pain in the area of ​​anesthesia (pain anesthesia) - the presence of pain in the area with lost sensitivity (complete anatomical nerve break). The mechanism of pain of this nature is similar to the mechanism of the appearance of phantom pain.

Depending on the predominant involvement in the pathological process of somatic or vegetative fibers, somatalgia and sympathalgia are distinguished. The latter are usually diffuse in nature, difficult to describe and localize, often accompanied by vegetative-vascular and trophic disorders.

Causalgia (Pirogov-Mitchell's disease, erythromelalgia) - sympathetic pain, characterized by paroxysmal intense and excruciating burning pains. It is characteristic of partial damage to large nerves containing a large number of vegetative fibers (median, ischial, tibial), in conditions of pronounced psycho-emotional stress (in war, etc.).

There are two stages of causalgia:

1) the stage of local pain, when bouts of burning pain are provoked by irritation in the area of ​​the damaged nerve;

2) repercussive stage, when attacks of burning pain go beyond the border of the innervation of the affected nerve (radiating neuralgia); an attack can be caused by irritation of any part of the skin or any sense organ (synesthesialgia), unpleasant emotions or memories of them (synpsychalgia).

Hyperesthesia- increased sensitivity - also usually indicates irritation and overexcitation of sensitive conductors.

Anesthesia- complete loss of all or certain types of sensitivity, hypoesthesia - Decreased sensitivity. Rarely, congenital absence of pain sensitivity is an unfavorable factor of ontogeny, which significantly complicates adaptation to the environment.

Dissociation(splitting of sensitivity) - a violation of some types of sensitivity while maintaining others.

Astereognosis- loss of the ability to recognize familiar objects by palpation with closed eyes, which occurs when the parietal lobes are damaged and stereognosis is lost. Pseudoastereognosis is similar to true astereognosis, however, it occurs with the loss of simple sensitivity (it also makes it impossible to describe the properties of an object).

Qualitative disturbances of sensitivity characterized by a perverted perception of information. Possible options are:

Dysesthesia - perverted perception of irritation: heat - like cold, touch - like pain (allodynia), etc.

Polyesthesia - a single stimulus is perceived as multiple. Synesthesia is a feeling of irritation not only in the place of its application, but also in another area, more often in the segment of the same name opposite side.

allocheiria - the patient localizes the place of irritation in a symmetrical area of ​​the opposite side.

Bifurcation of pain - when applying painful irritation, first there is a feeling of touch, after a certain interval - pain.

Hyperpathy- a peculiar form of sensory disturbance, with sufficient grounds, can be attributed both to the symptoms of irritation and to the symptoms of loss. Hyperpathy is characterized by:

- primary violation of complex types of sensitivity and fine differentiation of weak stimuli;

- increasing the threshold of perception;

– intense nature of sensations;

- the presence of a significant latent period from the application of irritation to its perception;

- long aftereffect (preservation of sensations after the cessation of irritation);

- an unpleasant emotional coloring.

The results of the study of various types of sensitivity (the prevalence and nature of violations) should preferably be indicated and recorded graphically on special forms.

Considering the various options for pain, one cannot but briefly touch on their mechanisms, more precisely, the theory of “pain control gates” by Melzak and Wall. It has already been mentioned earlier that a gelatinous substance is isolated in the composition of the posterior horn ( substantia gelatinosa) like a crescent adjacent to the posterior end of the posterior horn. In the animal kingdom, the gelatinous substance is a phylogenetically late acquisition. In humans, it is most powerfully developed in the region of the nuclei of the trigeminal nerve and the upper cervical region, directly adjoining the spinal nucleus of the trigeminal nerve ( nucl. spinalis n. trigemini). This substance stretches from top to bottom along the entire length of the posterior horns of the spinal cord. Its quantity decreases according to the levels of discharge of the roots and nerve endings.

The fibers of pain and temperature sensitivity of the posterior roots in the posterior horns end not only at the own nuclei of the posterior horns, but also in the gelatinous substance. The latter inhibits the transmission of impulses of all modalities coming from the peripheral nerves ("closes the gate"). Afferent non-painful (for example, tactile) impulses coming through thick myelin fibers activate the gelatinous substance, “closing the gate”. Pain impulses coming through thin unmyelinated fibers inhibit the gelatinous substance, increasing the transmission of impulses ("open the gate"). Suprasegmental descending influences can also contribute to "closing the gate".

The “gate control of pain” theory explains many aspects of pain syndrome formation. For example, dysfunction of myelin fibers when a peripheral nerve is damaged can lead to impaired activation substantia gelatinosa, "opening the gate" and the development of causalgia.

The human body is able to perceive and analyze various stimuli, for example, a person distinguishes between heat and cold, humidity and dryness, feels touch, pain, vibration. In the absence of sensitivity of certain parts of the body, for example, with numbness, discomfort, weakening pain or with pain in the lost limb, sensation is impaired. The following sensitivity disorders are distinguished: quantitative, qualitative and dissociated.

Quantitative Violations

Quantitative disturbances of sensitivity are different, for example, the absence, weakening or strengthening of sensations. A characteristic disorder of quantitative disturbance is complete absence pain (analgesia). Since pain is one of the most early symptoms certain diseases, its absence poses a serious danger to human health.

Loss of sensation occurs as a result of impaired conduction of the sensory nerves of the central and peripheral nervous systems. With damage to the nerves, a weakening of perception is possible, for example, hypesthesia - a condition in which superficial sensitivity to touch decreases, hypalgesia - an abnormally low perception of pain. The susceptibility of irritants can painfully increase. This usually occurs with inflammation of the nerve pathways or with mechanical irritation. Very low resistance to low temperatures- cold hypersthesia, abnormally high sensitivity of the body to painful stimuli - hyperalgesia, increased susceptibility - hyperesthesia.

Qualitative violations

Qualitative disorders are diagnosed when a sensation occurs that is inadequate to the stimulus (touch is perceived as pain, heat or cold, etc.). Such disorders occur when the thalamus of the diencephalon is damaged. Qualitative perceptual disturbances include other disorders, such as paresthesias. All these sensations cannot be objectively confirmed.

Dissociated disorders

In the presence of this type of violation, the patient feels pressure and touch, but he does not have pain and temperature sensations. This occurs when the spinal-thalamic tract is damaged, along which impulses are transmitted caused by the following stimuli: pressure, touch, pain and temperature.

Possible reasons

In all cases of sensory disturbances, as a rule, the nerves are affected or irritated. Short-term disturbances of sensation, manifested by numbness, "crawling crawling", can occur when the nerve is compressed, for example, when staying in an uncomfortable position for a long time. In this case, blood circulation in a certain part of the body is temporarily disturbed or a nerve is irritated. A common cause of sensory impairment is damage intervertebral discs cervical spine and inflammation of the vertebrae. In this case, compression of the spinal nerve or peripheral nerves occurs. In places innervated by the affected nerves, paresthesias occur. The cause of sensitivity disorders can be injuries, rheumatic, diseases, inflammations.

Each nerve innervates a specific part of the human body. Therefore, a violation of the perception of sensations occurs in that part of the body in which the nerve is affected or irritated, for example, nerves that innervate a certain part of the skin depart from the nerve roots of the peripheral nervous system. When the nerve root is damaged, the sensitivity of the entire corresponding dermatome is disturbed. With the defeat of only one nerve, the sensitivity of only a small area of ​​​​the body is disturbed. The localization of sensory disturbances and their nature depend on the location of the lesion and on how much the central nervous system is affected - the spinal cord and brain.

Damage to the nerves is accompanied by a decrease in sensitivity, which over time can lead to the death of nerve fibers. Therefore, with a long-term disorder of a certain sensation in the same part of the body, you should urgently consult a doctor.

Anesthesia

Anesthesia - elimination of susceptibility by the introduction of anesthetic substances by injection, orally, inhalation, as well as the introduction of drugs into the spinal canal. During anesthesia, there is a loss of pain, temperature and tactile perception of surrounding objects.

Sensory Disorders- disturbances in the body's ability to perceive various types of sensitive stimuli, which is one of the main functions of the nervous system. Sensory disturbances can manifest as burning, tingling, numbness, etc.

sensory symptoms are the result of dysfunction of receptors - nerve endings that perceive mechanical, thermal or chemical irritation. There are four types of sensations:

• tactile sensitivity - perceived by receptors located on the skin, for example, the sensation of pain, temperature, taste.
• sensory sensitivity - perceived by the senses, such as sight and hearing.
• deep sensitivity - perceived by receptors located in the muscles, tendons and labyrinth inner ear(for example, a sense of balance.)
• visceral sensitivity - perceived by receptors found in the internal organs and walls of blood vessels.

Causes of sensory disturbance

Causes of abnormal sensations very varied. They can occur as a result of developmental defects (genetic factors), pathological consequences of pregnancy, as well as:

• anomalies in the development of the spinal cord
• sciatica
• tumors, cysts
• multiple sclerosis
• Vitamin B12 deficiency
• brain diseases such as stroke
• disc protrusion

Some types of sensory impairment

analgesia- loss of pain sensitivity. It is characteristic of many diseases and traumatic lesions of the nervous system.

Thermal anesthesia- loss of temperature sensitivity

hypoesthesia- decreased sensitivity

Hyperesthesia- increased sensitivity. At the same time, the place and nature of the impact (cold, touch, etc.) is felt correctly.

hyperalgesia- excessive pain sensitivity.

Polyesthesia- a single stimulus is perceived as multiple. A possible sign of damage to the parietal lobe of the brain.

allocheiria- the patient localizes irritation not in the place of its application, but in symmetrical areas on the opposite side.

Dysesthesia- perverted perception of receptor affiliation (for example, cold can be perceived as tingling, painful irritation as heat).

Paresthesia- spontaneously arising sensations of numbness, tingling, "crawling", tightening, burning. Usually short term.

Hyperpathy- the appearance of a sharp feeling of unpleasant when applying irritation. It is characterized by an increase in the threshold of perception of stimuli (hypesthesia), the lack of precise localization of irritation ( unpleasant feeling captures the whole area), a long latent period and a long period of aftereffect (perception lags behind the irritation in time, an unpleasant sensation persists for a long time after the stimulus has ceased).

Sensitivity disorders: diagnosis

A patient with dysesthesia should come to a neurologist. Diagnosis is based mainly on questioning the patient and a very detailed physical examination. Sometimes you may need to analyze the cerebrospinal fluid. important role in the diagnosis sensory disturbances play neurological tests (eg electromyography).

Sensory Disorder: Treatment

There are many therapies used depending on the etiology, including pharmacology, physical-chemical methods, physical rehabilitation. Sometimes the intervention of a surgeon is necessary.

If you notice a violation of sensitivity in yourself, then the first thing you need to do is contact a neurologist, who will prescribe special procedures for you to identify the causes of this violation. The thing is that a violation of sensitivity can be a symptom of a serious disease, so it is important to accurately diagnose the disease.
You may be prescribed X-rays of the spine, MRI, lumbar puncture, electromyography, etc. And based on the data obtained, the doctor will be able to prescribe a comprehensive, effective treatment.

1. Neural type of sensory disorders. Occurs when sensory or mixed nerves (its main trunk or sensory branches) are damaged. Sensory disorders in neuritis ( inflammatory processes) and neuropathies - non-inflammatory lesions (compression-ischemic, traumatic, toxic, etc. - see Chapter 11) do not fundamentally differ in the topical localization of sensory disorders and are characterized by the following main features:

- sensitivity disorders can have the character of symptoms of irritation (pain, paresthesia, hyperpathy, soreness of the nerve trunk on palpation, positive symptoms of tension, soreness of nerve exit points) and (or) symptoms of prolapse (anesthesia, hypoesthesia, etc.);

- symptoms of prolapse and irritation are most pronounced in the zone of autonomic innervation. Irritation symptoms predominate more often. It should be taken into account that for some pain syndromes(for example, at the repercussion stage of causalgia), pain can also occur outside the zone of innervation of the affected nerve;

- for pain during irritation of the nerve, a special character is typical: shooting, burning, “tearing”, caused or aggravated by palpation or nerve tension, they are accompanied by pronounced vegetative-trophic disorders. Such pains in combination with other symptoms of irritation without symptoms of prolapse determine the clinical picture of neuralgia, and the presence of symptoms of prolapse (in combination with symptoms of irritation or without them) already allows us to speak of neuritis (neuropathy).

- a pathological process leading to a neural type of sensory disorders may be limited to one or several nerves (mono-, multi-, multiple neuritis or neuropathy - see subsection 2.16).

The main causes of neuralgia are irritation of the nerve due to its partial compression, which is most often due to tunnel syndrome - compression of the affected nerve in the bone or fibrous canal (trigeminal neuralgia, etc.), as well as other local pathological processes (tumors, metastases, hematomas, adhesive process and etc.).

The development of neuropathies with predominantly sensitive disorders is observed with concussion of the nerve (neuropraxia), as well as with some tunnel neuropathies and reflex-dystrophic syndromes (causalgia). In other forms of the above pathology of mixed nerves, sensory disorders are also noted, but they are usually combined with the neural type of movement disorders or are significantly inferior to the latter in severity.

2. Polyneuritic type of sensitivity disorders. Occurs as a result of inflammatory (polyneuritis) or non-inflammatory (polyneuropathy) lesions predominantly of the distal parts of the peripheral nerves. Sensitivity disorders are characterized by the following features:

- localization mainly in the distal parts of the extremities according to the type of "gloves" and (or) "socks", symmetry, lack of a clear boundary of sensitive disorders;

- among the sensitive disorders, symptoms of irritation can be observed - pain, paresthesia, hyperesthesia, hyperpathy, soreness of the nerve trunks on palpation and tension, and (or) symptoms of prolapse - hypesthesia, anesthesia;

- symptoms of loss and (or) irritation affect, as a rule, all types of sensitivity, although their severity may vary depending on the nature of the pathological process and the stage of the disease;

- often specific symptoms are detected that occur as a result of disorders of deep sensitivity: in the legs - sensitive ataxia, in the hands - pseudoathetosis and (or) false astereognosis;

- the above sensitivity disorders are often combined with vegetative-trophic disorders of predominantly distal localization.

The presence and nature of sensory disorders, as well as their severity, are determined primarily by the etiological factors of polyneuritis or polyneuropathy. Polyneuritis with a purely sensory variant of the polyneuritic syndrome is significantly more common only in tuberculosis, early neurosyphilis, and typhus. Polyneuropathies with predominantly sensitive disorders include: alcoholic, diabetic, as well as polyneuropathies with deficiency folic acid, endocrine diseases (hypothyroidism, pathology of the pituitary gland), drug intoxication (isoniazid, PASK, etc.), tumors of internal organs. Acute inflammatory demyelinating polyradiculoneuropathy of Guillain-Barré can begin with polyneuritic sensory disorders, although motor polyneuritic disorders further develop and predominate.

3. Radicular type of sensitivity disorders. This type of peripheral variant is characterized by a violation of all types of sensitivity and radicular pain in the form of bands that are transverse on the trunk, and longitudinal on the limbs (Fig. 1.4).

They can occur with the pathology of the posterior root, the Babinski-Najotte radicular nerve (part of the root from the dura mater to the spinal ganglion), the spinal ganglion, spinal cord of Sicard(formed as a result of the fusion of the motor and sensory roots). Etiological factors their lesions are diverse: infectious-toxic, infectious-allergic, compression-ischemic, traumatic, toxic, dysmetabolic, hereditary (see subsection 11.4).

Among them, the dominant frequency is the pathology of the spinal cord of a non-inflammatory nature (funiculopathy), which in the domestic literature is traditionally referred to as sciatica. Clinical picture radicular syndrome is characterized by the following symptoms:

- radicular sensitivity disorders, radicular pain and paresthesia in the area of ​​the corresponding dermatome;

- symptoms of root tension in combination with reactive pain;

- muscular-tonic syndromes;

- local pain in the area where the roots exit from the intervertebral foramina (Valle's points);

- a combination of radicular sensory and radicular movement disorders varying degrees expressiveness;

- when involved in the pathological process of the spinal ganglion (herpetic ganglionitis), the above clinical symptoms, characteristic of the radicular type of sensitivity disorders, are complemented by herpetic eruptions.

When establishing the nosology of the radicular type of sensitive disorders, it should be borne in mind that in most cases various vertebrogenic pathologies can lead to its development:

- vertebrogenic pathology of a predominantly degenerative-dystrophic nature (the main ones are pathology of the intervertebral discs, deforming spondylosis, spondylarthrosis, ossifying ligamentosis, narrow spinal canal syndrome);

- inflammatory lesions of the vertebral bodies (spondylitis purulent, tuberculous, brucellosis, fungal, etc.);

– tumors of the vertebral bodies (primary benign and malignant, metastatic tumors, multiple myeloma);

- anomalies in the development of the spine ( spina bifida, additional cervical vertebra, anomalies of the craniovertebral junction, etc.);

- spinal dysplasia (fibrous dysplasia, Scheuermann-Mau disease, Paget's disease, achondroplasia, spondylo-epiphyseal dysplasia);

- endocrine-metabolic osteodystrophy (more often with hyperparathyroidism, hypothyroidism, diabetes);

– traumatic lesions of the spine (soft tissue contusion, sprain, ligament rupture, fractures of bodies, arches, processes, traumatic hernias).

Unlike radicular syndromes of the lumbosacral and cervical regions, radicular syndromes of the thoracic level are extremely rarely the result of degenerative-dystrophic processes in thoracic region spine. The development of radicular thoracalgia is usually associated with inflammatory (spondylitis), systemic (Bekhterev's disease) and metastatic lesions. It should also be taken into account that radicular pains of the cervical and thoracic levels may have a reflected character due to the pathology of the organs of the chest or abdominal cavity.

1.10. Spinal variant of sensory disorders

The spinal variant of sensitivity disorders may be due to damage to the posterior horn and sensory pathways in the spinal cord (segmental and conductive types, respectively).

1. Segmental spinal type. Occurs when the posterior horn of the spinal cord and the anterior white commissure are damaged. When the posterior horn is affected, it manifests itself as disorders of only pain and temperature sensitivity in the zone of the corresponding dermatomes, which are similar in localization to the incoming root (radicular-segmental zones of sensitive disorders) while maintaining deep and largely tactile sensitivity - a dissociated disorder of superficial sensitivity in the corresponding segments. Paresthesia is not typical. There are no motor disturbances. The segmental type of sensitivity disorders has, as a rule, upper and lower levels (boundaries). Dull and aching posterior horn pains predominate. A segmental variant of sensory disorders due to lesions of the posterior horn is observed in syringomyelia and syringomyelitic syndrome of other etiologies (see subsection 3.6). In cases of damage to the anterior white commissure, sensitivity disorders are dissociated in nature, they are symmetrical (“butterfly”).

2. Conductive spinal type with damage to the lateral and posterior cords . It is caused by damage to the lateral spinothalamic pathway in the lateral cords, a thin bundle (Gaulle) and a wedge-shaped bundle (Burdach) in the posterior cords. With a transverse lesion of the spinal cord, the conductor type is characterized by a violation of deep sensitivity from the level of the lesion on its side, a violation of superficial sensitivity two segments below the lesion on the side contralateral to the lesion. It occurs in spinal strokes, injuries and tumors of the spinal cord, demyelinating diseases, isolated lesions of the posterior cords (neurosyphilis, funicular myelosis, Friedreich's ataxia, Roussy-Lewy disease, atypical forms neural amyotrophies with predominant disorders of deep sensitivity, etc.).

3. Conduction spinal type with damage to the anterior white commissure . Clinically differs from the segmental type by the symmetry (on both sides) of dissociated sensory disorders.

Sensory disorders are the most important component of spinal cord injury syndromes: Brown-Sequard syndrome, complete transverse spinal cord injury syndrome, etc. (see Chapter 3).

1.11. Cerebral variant of sensory disorders

It can occur with damage to the sensory nuclei of the cranial nerves (nuclear type), cerebral structures, pathways of general sensitivity to various levels (medulla, pons varolii, midbrain, visual tubercle, internal capsule, radiant crown) and the cerebral cortex - respectively conductive cerebral and cortical types. common feature conduction cerebral disorders of sensitivity is that they are localized on the side of the body opposite to the lesion (hemianesthesia, sometimes alternating).

1. Damage to the pathways of general sensitivity in the brain stem below the thalamus. It is characterized primarily by the occurrence of alternating syndromes: on the side of the lesion, a defect in a certain cranial nerve (s) is detected, and on the opposite side, isolated disorders of all types of sensitivity according to the conduction type (hemianesthesia or hemihypoesthesia) or in combination with other hemidisorders: pyramidal, cerebellar, etc. .

2. The defeat of the visual tubercle. At the same time, conductive sensory disorders are usually included in the “three hemi” syndrome: hemianesthesia, hemiataxia, hemianopsia. Often, when the visual tubercle is affected, peculiar thalamic pains occur in the opposite half of the body - hemialgia. They are perceived as a painful feeling of cold or burning, are difficult to describe to the patient and are poorly localized.

3. Damage to the internal capsule. Sensory disorders arise due to damage to the fibers of the third sensory neurons in the posterior third of the posterior thigh of the internal capsule. They are characterized by hemianesthesia or deep hemihypoesthesia of all types of sensitivity on the side of the body contralateral to the lesion without a convincing difference in their severity in the arm and leg. Sensory disorders are usually included in the "three hemi" syndrome: hemianesthesia, hemiplegia, hemianopsia.

4. The defeat of the radiant crown. It is characterized by more limited in extent sensory disorders, which capture mainly the upper (brachiofacial localization) or lower limb. With extensive damage to the radiant crown, sensory disorders can be combined with hemiparesis and are characterized, in contrast to capsular, by uneven distribution in the arm or leg, up to monoparesis and monohypoesthesia of the limb.

5. Cortical damage. Cortical sensory disorders can be caused by lesions of the posterior central gyrus and parietopostcentral sections, as well as the superior parietal lobule.

The defeat of the posterior central gyrus and parieto-postcentral divisions may be manifested by symptoms of prolapse and (or) irritation.

Symptoms of prolapse. The localization of sensory disorders corresponds to the somatotopic localization of the pathological focus (half of the face, arm, leg), and their severity is greatest in the distal parts of the arm or leg - pseudopolyneuritic type in the form of one "glove" or "sock". predominantly deep and complex types sensitivity. A number of specific symptoms are possible: afferent paresis, afferent (kinesthetic) apraxia, oral apraxia, afferent motor aphasia, false astereognosis.

Irritation symptoms usually manifest as paresthesias, localized or spreading along half of the body (respectively, without a "march" and with a "march" - a sensitive variant of Jacksonian epilepsy).

The defeat of the upper parietal lobule. With symptoms of prolapse, sensitivity is upset on the entire half of the body without asymmetry in the arm or leg, true astereognosis in one or both hands is characteristic, and afferent paresis is often noted. Symptoms of irritation in the form of paresthesias occur simultaneously on the entire half of the body (hemiparesthesias), and may also manifest as adversive seizures due to damage to the posterior adversive field.

1.12. Functional variant of sensory disorders

The distribution of sensory disorders does not correspond to any of the organic types and is determined by the patient's personal ideas about the nature of sensory disorders. signs functional disorders sensitivity:

– the boundaries of sensory disorders vary from study to study;

- usually patients, presenting hemianesthesia, indicate its boundaries strictly along the midline. At organic lesion this cannot be on the trunk, since the boundary of sensitive disorders in this case is always shifted towards the latter;

- if you conduct a sensitivity study in the initial state, and then shift the fold of the skin of the abdomen to the side, i.e. artificially make a new midline, then the patient in both cases will complain of sensitivity disorders along the midline (with an organic lesion, the boundary of the disorders will shift along with the skin);

- sensitivity disorders are often distributed according to the anatomical principle (up to the elbow or axillary fold, etc.).

A functional variant of sensitive disorders can occur in people with neurosis, psychopathy, endogenous mental illness.

DISORDERS OF INvoluntary AND VOLUNTARY MOVEMENTS

2.1. Types of movements

Movements are divided into involuntary and voluntary.

Involuntary movements- these are movements that occur regardless of the desire of a person in response to the influence of various stimuli. Such reflex movements are inherent in every biological species, are formed by the time of birth, and are inherited. Their anatomical and physiological substrate is a reflex arc or a reflex ring that closes at the level of the spinal cord or brain stem.

Arbitrary movements are movements of varying degrees of complexity, divided into three groups:

1. Elementary conscious-volitional movements. They are differentiated motor acts that are voluntary and at the same time have a relatively simple character - raising an arm or leg, bending them at the joints, etc. These movements are “launched” on the basis of an efferent impulse formed in the primary cortical field of the motor analyzer (mainly the precentral gyrus).

2. Motor praxis. These are more complex motor acts that are developed in the course of a person's life on the basis of experience, skill, practice and are fixed by a stereotype. The programming of such movements (combing, making the bed, writing, etc.) is carried out in special cortical zones (secondary, or associative), and their implementation is also carried out through the primary cortical field of the motor analyzer and its efferent connections.

3. Automated movements - running, walking, crawling, swimming, etc. - relatively arbitrary, since their implementation has a memorized character and is carried out as a single motor act. Such movements are predominantly the prerogative of the extrapyramidal system and the cerebellum, and the motor fields of the cerebral cortex have a mainly regulating effect on them.

2.2. Central and peripheral motor neurons
cortical-muscular pathway

For the implementation of voluntary movement, it is necessary that the motor impulse that arose in the corresponding areas of the cerebral cortex be conducted to the skeletal (striated) muscles. It provides a cortico-muscular pathway (tractus cortico-muscularis), consisting of two parts: the first part is represented by the central motor neuron; the second is a peripheral motor neuron.

Central motor neuron. According to classical concepts, the bodies of neurons, from which the cortical-muscular path originates, are located in the anterior central gyrus - the primary cortical field of the motor analyzer. For a long time it was believed that the central motor neuron starts only from the bodies of the internal large pyramidal neurons (Betz cells) located in the fifth layer of the anterior central gyrus, which predetermined its name - the pyramidal path. According to the data recent years, only 27-40% of the axons of the cortical-muscular tract begin from the anterior central gyrus, and only 3-4% directly from Betz cells, about 20% of the fibers of the cortical-muscular tract originate from the somatosensory cortical zone (postcentral gyrus), and the rest - from the premotor zone, paracentral and other areas of the brain. The axons of these neurons end on the motor neurons of the anterior horns of the spinal cord (cortical-spinal tract - tractus corticospinalis) and on the motor nuclei of the cranial nerves (cortical-nuclear pathway - tractus corticonuclearis).

peripheral motor neuron formed by motoneurons of the anterior horns of the spinal cord and motor nuclei of the cranial nerves, as well as their axons, which reach, as part of a number of formations of the nervous system (anterior roots, spinal nerves, plexuses, peripheral or cranial nerves), the performing muscles.

2.3. Anatomy of the corticospinal and corticonuclear pathways

Cortico-spinal tract starts mainly from the upper 2/3 of the anterior central gyrus and paracentral lobule; some of the axons originate in the adjacent premotor region, in the posterior central gyrus and in the superior parietal lobule (Fig. 2.1).

In the cortex of the anterior central gyrus, pyramidal neurons are localized according to the rule of "motor homunculus" (Penfield scheme). This means that in the uppermost sections of the anterior central gyrus there are neurons that begin the efferent pathways for the leg muscles: in the paracentral lobule there are neurons that provide movement of the muscles of the foot, and in the upper sections of the anterior central gyrus there is a sequential somatotopic projection for the muscles of the lower leg and thigh. Further, neurons are sequentially arranged, giving rise to efferent nerve pathways to the muscles of the body. The middle third of the anterior central gyrus is occupied by neurons that provide innervation to the muscles of the hand. The area of ​​somatotopic projection zones in the anterior central cortex is proportional to the complexity of the movements performed by a certain group of muscles, with the largest area occupied by the somatotopic projection of the muscles of the hand (especially thenar muscles).

Axons from the above areas of the anterior central gyrus pass through the radiant crown, the anterior 2/3 of the posterior femur of the internal capsule and then follow the ventral surface of the brainstem. At the border between the medulla oblongata and the spinal cord, 80% of the fibers of the cortical-spinal tract pass to the opposite side, forming a pyramidal decussation with similar fibers of the opposite side. (decussatio pyramidum). Crossed fibers are sent to the lateral funiculus of the spinal cord, occupying its posteromedial section in the form of a lateral cortical-spinal tract (tractus corticospinalis lateralis). This path provides voluntary movements of both the muscles of the trunk and the limbs. About 20% of the fibers remain uncrossed, forming the anterior corticospinal tract (tractus corticospinalis anterior). This pathway provides voluntary movements mainly in the muscles of the trunk and neck. The fibers of the lateral cortical-spinal tract are located in the spinal cord in accordance with the Auerbach-Flatau law and, at the same time, switch segmentally to the motor neurons of the anterior horns of the spinal cord.

Cortico-nuclear pathway begins mainly from the lower third of the anterior central gyrus and the adjacent premotor region. Here, a clear somatotopic projection of the muscles innervated by the cranial nerves is also determined, and in the lowest part of the precentral gyrus there are neurons for the muscles of the pharynx, larynx, soft palate, tongue, chewing and mimic muscles. The axons of the corticonuclear pathway pass through the radiant crown, the genu of the internal capsule, and the brainstem. Here, its fibers make a partial supranuclear decussation, ending on the motor nuclei of the cranial nerves of their own and opposite sides. The exception is part of the cortical-nuclear pathway, ending at the nucleus XII and the lower part of the nucleus VII of the nerve - these fibers make a complete supranuclear decussation and therefore end on the corresponding motor nuclei (XII, lower half of VII) only on the opposite side.

2.4. Plegia and paresis

Plegia or paralysis- complete loss of voluntary movements in a particular muscle group.

Paresis- partial loss of voluntary movements in a particular muscle group, characterized by a decrease in the strength and volume of active movements in the affected muscles.

Depending on the prevalence, the following variants of paralysis and paresis are distinguished:

- monoplegia, or monoparesis, - plegia or paresis is determined only in the muscles of one arm or leg;

- hemiplegia, or hemiparesis, - plegia or paresis captures the muscles of both the arms and legs on one or opposite (alternating hemiplegia or hemiparesis) sides of the body;

- paraplegia, or paraparesis, - plegia or paresis are determined only in the muscles of only both arms or legs (respectively, upper or lower paraplegia or paraparesis);

- triplegia, or triparesis, - plegia or paresis captures three limbs;

- tetraplegia, or tetraparesis, - plegia or paresis captures both arms and legs.

2.5. General Clinical signs movement disorders

Plegia (paresis) can be detected during a clinical examination based on the following signs:

1) decrease in the volume of active movements and (or) muscle strength;

2) change in muscle tone;

3) atrophy or hypotrophy of paretic muscles;

4) fasciculations and fibrillations of the affected muscles;

5) increase or decrease (up to the absence) of physiological reflexes, closing on the paretic muscles;

6) the presence of pathological reflexes;

7) the presence of protective reflexes and pathological synkinesis. Depending on the type of plegia or paresis - peripheral or central - the various symptoms listed above form the clinical core of peripheral or central paralysis.

2.6. Methodology for studying the strength of muscles of various muscle groups

Muscle strength is examined in parallel with active movements, since their volume does not decrease with mild paresis. The strength of the muscles of the hands is determined by a dynamometer. When studying the strength of other muscles, the manual method is used in two modifications.

During the first modification, the doctor interferes with the active movement, determines and compares the resistance force in the corresponding muscles on the left and right. So, for example, the doctor suggests the patient to bend the arm in the elbow joint on the left and actively prevents this bending. Then the strength of the biceps muscle of the shoulder is also determined right hand, and the strength of the active movement on the left and right is compared.

More often, another modification is used: the patient is asked to perform an active movement without any resistance. Next, the patient holds the arm or leg in this position with maximum force, and the doctor tries to move 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. For example, the strength of the biceps muscle of the shoulder is determined by trying to straighten the arm already bent at the elbow joint, first on the left, then on the right. (video 1, "Tests for the detection of latent paresis")

2.7. Muscle functions and their innervation

Muscle functions and their innervation are presented below (Table 2.1).

Table 2.1

Function and innervation of muscles

2.8. General symptomatology of peripheral paralysis (paresis)

Peripheral paralysis or paresis is a disorder of voluntary movements that occurs when a peripheral motor neuron is damaged - the motor neurons themselves or their axons. Peripheral paralysis is characterized by the following features:

1) hypotrophy (atrophy) of paretic muscles;

2) decrease in muscle tone in the paretic muscles - muscle hypotension (atony);

3) loss or decrease (areflexia or hyporeflexia) of physiological myotatic and superficial reflexes, which are closed through the affected part of the peripheral motor neuron;

4) reaction of degeneration in paretic muscles;

5) fasciculations or fibrillations in paretic muscles.

2.9. Muscular hypotension in peripheral paralysis (paresis)

Under muscle tone(Fig. 2.2) understand the tension in which the muscles are outside of active movement.

Maintenance and redistribution of muscle tone is provided by the γ-loop. The first link of the γ-loop is the γ-motoneurons of the anterior horns of the spinal cord. From γ-motoneurons go thin γ-fibers to intrafusal muscle fibers that are part of the muscle spindles - muscle proprioceptors. The spindles are considered to be tension receptors responsible for maintaining a constant length of the muscle. Impulses conducted by γ-fibers cause contraction of intrafusal muscle fibers in the regions of both poles of the spindle, thereby leading to tension in its equatorial part. This change is immediately registered by the anulospiral endings braiding the nuclear bags in the spindle (each spindle has two fibers with a nuclear bag and four with a nuclear chain). Their action potential increases the tone of the working muscle.

The nerve impulse arising from irritation of the anulospiral receptors goes from the spindle receptors along the peripheral and central process of the spinal ganglion cell and enters the spinal cord through the posterior root. As a result, the impulse returns predominantly to the same segment from which the given γ-loop started. Here, the impulse "switches" to α-large and α-small motor neurons of the anterior horn, as well as to Renshaw cells. α-Large motor neurons provide impulses that cause rapid (phasic) contraction and maintain muscle trophism. α-Small motor neurons transmit excitation to slow-twitch tonic motor units. The α-large motor neuron gives off a collateral to the Renshaw cell, and this cell, in turn, reconnects with the anterior horn motor neuron, exerting an inhibitory effect on it. Thus, the main functions of Renshaw cells are the function of recurrent inhibition of the α-large motor neuron when it is too strongly excited and the function of reciprocal innervation due to the fact that the impulse from the Renshaw cell reaches the α-motor neurons of one segment from both sides. As a result, along the axons of α-large and α-small motor neurons, the impulse reaches the extrafusal muscle fibers, causing their phasic or tonic contraction.