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Lecture notes, cheat sheets
Nervous diseases. Cheat sheet: briefly, the most important
Directory / Lecture notes, cheat sheets Table of contents
1. Sensitivity and types of sensitivity disorders Sensitivity - the body's ability to perceive irritations emanating from the environment or from its own tissues and organs. The analyzer consists of three sections: the receptor, the conductive part and the cortical section. Receptors are terminal formations of sensitive nerve fibers that perceive changes in the body or outside it and transmit it in the form of impulses. Receptors are divided into three groups: extero-, proprio- and interoreceptors. Exteroreceptors are represented by tactile, pain and temperature, interoreceptors are located in the internal organs - chemo- and baroreceptors. Proprioreceptors are found in muscles, ligaments, tendons, and joints. Thanks to them, a person has an idea of the position of his body in space. There are several types of sensitivity. Superficial combines pain, temperature and tactile sensitivity. Deep sensitivity includes vibrational, musculoskeletal, pressure and mass sensations, and two-dimensional spatial sensation. There are four variants of sensory impairment: peripheral, segmental, conductive and cortical. The peripheral variant develops as a result of damage to the peripheral nerve and is located in the zone of its innervation. The segmental variant develops as a result of a lesion of the posterior root or spinal ganglion in the case of deep sensitivity, in the case of superficial sensitivity, also with damage to the posterior horn or anterior gray commissure of the spinal cord. The conduction variant of sensory disturbance occurs when the posterior or lateral cords of the brain, brain stem, thalamus, internal capsule, or white subcortical substance are damaged. This violation is characterized by a change in sensitivity below the level of damage to the pathway. The cortical variant occurs when a specific area of the cerebral cortex is damaged. In this case, there is a local loss of sensitivity. Hypesthesia - decreased sensitivity. Hyperesthesia - increased sensitivity. Analgesia - loss of pain sensitivity. A single irritation can be perceived as multiple - polyesthesia. The patient may incorrectly localize the irritation. Usually he points to a symmetrical area from the opposite half of the body - allocheiria. There may be a perversion of perception - dysesthesia. There may be spontaneous sensations of tingling, crawling, tightening - paresthesia. The defeat of the posterior roots of the spinal cord, nerve plexuses and trunks causes the appearance of symptoms of tension. These include the symptoms of Lasegue, Neri, Sikar, Matskevich and Wasserman. The symptom of Lasegue is the occurrence of pain along the sciatic nerve when the leg is bent in the hip joint. Neri's symptom is the occurrence of pain in the lower back when bending the head forward. Symptom Sicard - pain along the sciatic nerve with dorsiflexion of the foot. Symptom Matskevich - pain on the front of the thigh when bending the leg at the knee joint in the supine position. This symptom indicates the pathology of the femoral nerve. Wasserman's symptom - pain on the anterior surface of the thigh when raising the outstretched leg in the supine position. 2. Types of reflections and methods for their determination Reflex - a reaction that occurs in response to irritation of receptors in any reflexogenic zone. Reflexes give an idea of the state of various parts of the human nervous system. The study of reflexes is to determine their nature, uniformity, symmetry. Reflexes may be alive. Hyporeflexia, hyperreflexia (with an extended reflexogenic zone), areflexia (absence of reflexes) may be noted. Reflexes are divided into deep, or proprioceptive (tendon, periosteal, articular), and superficial (skin, mucous membranes). Deep reflexes occur when percussion with a hammer on the tendon or periosteum. As a result, a motor reaction of the corresponding muscle groups is observed. On the upper limbs, the following reflexes are normally determined: a reflex from the tendon of the biceps muscle of the shoulder, from the tendon of the triceps muscle of the shoulder and a carporadial reflex. Skin reflexes occur when a certain skin zone is stroked with a handle of a neurological malleus. Abdominal reflexes are distinguished: upper (occurs when the skin of the abdomen is irritated along the lower edge of the costal arch), middle (occurs when the skin of the abdomen is irritated at the level of the navel) and lower (occurs when the skin is irritated parallel to the inguinal fold). These reflexes consist in the contraction of the abdominal muscles at the appropriate level and the deviation of the navel in the direction of irritation. The following extensor pathological reflexes on the lower extremities are distinguished: Babinski's reflex (extension of the first toe as a result of dashed skin irritation of the outer edge of the sole, up to 2-2,5 years is physiological), Oppenheim reflex (extension of the first toe when running fingers along the ridge tibia downwards to the ankle joint), Gordon's reflex (slow extension of the first toe and fan-shaped divergence of other fingers as a result of compression of the calf muscles), Schaefer's reflex (extension of the first toe as a result of compression of the Achilles tendon). The following pathological flexion reflexes on the lower extremities are distinguished: the Rossolimo reflex (flexion of the toes when the hammer strikes the balls of the fingers quickly), Bekhterev-Mendel reflex (flexion of the toes when the hammer hits its back surface), Zhukovsky's reflex (flexion of the toes when struck with the hammer on its plantar surface under the fingers), Bekhterev's reflex (flexion of the toes when hit with a hammer on the plantar surface of the heel). Flexion pathological reflexes on the upper limbs can be such as the Tremner reflex (flexion of the fingers of the hand with rapid tangential irritations of the palmar surface of the terminal phalanges of the II-IV fingers), the Jacobson-Lask reflex (combined flexion of the forearm and fingers of the hand when struck with a hammer on the styloid process of the radius ), Zhukovsky's reflex (flexion of the fingers of the hand when the hammer strikes the palmar surface), Bekhterev's carpal-finger reflex (flexion of the fingers as a result of percussion with the hammer of the back of the patient's hand). With an increase in tendon reflexes, clonuses appear. They consist in a series of fast rhythmic contractions of a muscle or group of muscles when they are stretched. 3. Formation of voluntary and involuntary movements There are two main types of movements: involuntary and voluntary. Involuntary movements are carried out due to the segmental apparatus of the spinal cord and the brain stem. They proceed according to the type of a simple reflex act. Voluntary movements are acts of human motor behavior (praxia). They are carried out with the participation of the cerebral cortex, the extrapyramidal system and the segmental apparatus of the spinal cord. Voluntary movements are associated with the pyramidal system, which is a department of the nervous system. In its lower part there are neurons that innervate the muscles of the pharynx and larynx. In the middle part - neurons innervating the upper limbs, in the upper part - neurons innervating the lower limbs. The neurons of this part of the cortex control the voluntary movements of the limbs of the opposite half of the body. This is due to the decussation of nerve fibers in the lower part of the medulla oblongata. There are two paths of nerve fibers: cortical-nuclear, which ends at the nuclei of the medulla oblongata, and cortical-spinal. The second pathway contains interneurons in the anterior horns of the spinal cord. Their axons end on large motor neurons located there. Ihaksony passes through the posterior leg of the internal capsule, then 80-85% of the fibers cross in the lower part of the medulla oblongata. Further, the fibers are sent to the intercalary neurons, whose axons, in turn, already approach the large alpha and gamma motor neurons of the anterior horns of the spinal cord. They are peripheral motor neurons of the motor pathway. Their axons are sent to the skeletal muscles, carrying out their innervation. Large alpha motor neurons conduct motor impulses at a speed of 60-100 m/s. This ensures fast movements that are associated with the pyramidal system. The pyramidal path begins in the cerebral cortex, namely from the Betz cells located in the anterior central gyrus. The axons of these cells are sent to the segment of the spinal cord, which they innervate. There they form a synapse with a large motor neuron or with cells of the motor nuclei of cranial nerves. Fibers from the lower third of the anterior central gyrus innervate the muscles of the face, tongue, pharynx, and larynx. These fibers terminate on the cells of the nuclei of the cranial nerves. This pathway is called the cortico-nuclear pathway. The axons of the upper 2/3 of the anterior central gyrus terminate on large alpha motor neurons and innervate the muscles of the trunk and limbs. This pathway is called the corticospinal pathway. After leaving the anterior central gyrus, the fibers pass through the knee and the anterior 2/3 of the posterior pedicle of the internal capsule. They enter the brainstem, pass at the base of the legs of the brain and form pyramids. At the border between the medulla oblongata and the spinal cord, most of the fibers intersect. Then this part is located in the lateral cords of the spinal cord. Uncrossed fibers are located in the anterior funiculi of the spinal cord, forming the Turk's bundle. 4. How the spinal cord works The spinal cord is located in the spinal canal and is a cylindrical cord, its length in an adult is 42-46 cm. In the region of the I cervical vertebra, it passes into the medulla oblongata. At the level of I-II of the lumbar vertebrae, it becomes thinner and turns into a thin thread. The thickness of the spinal cord is 1 cm. It has two thickenings: cervical and lumbar. The spinal cord consists of 31-32 segments, including 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1-2 coccygeal. Segment - a section of the spinal cord containing the anterior and posterior roots. The cervical thickening of the spinal cord is located at the level from the V cervical to the I thoracic segment. It provides innervation to the upper extremities. The lumbar thickening is located from I-II lumbar to I-II sacral segment. It innervates the lower extremities. The anterior roots of the spinal cord include motor fibers, the posterior roots - sensory fibers. In the region of the intervertebral node, these fibers are connected and form a mixed nerve. The spinal cord has an anterior median fissure, a posterior median sulcus, and anterior and posterior lateral sulci, which are arranged symmetrically. There is also an anterior funiculus located between the anterior median fissure and the anterior lateral sulcus; lateral funiculus - between the lateral grooves (anterior and posterior). The posterior funiculus is located between the posterior median and posterior lateral sulci. The anterior roots of the spinal cord emerge from the anterior lateral sulcus. The posterior roots enter the spinal cord at the posterior lateral groove. The central part of the spinal cord is formed by gray matter, the peripheral part is white. Both halves of the spinal cord are connected by spikes of gray and white matter. The anterior gray commissure is located anterior to the central canal, followed by the anterior white commissure. Posterior to the central canal is first the posterior gray and then the posterior white commissures. The primary sensory cells are located in the intervertebral nodes. The posterior horns contain sensory neurons. In the white matter, the fibers of the pathways pass. Thanks to them, the connection of the spinal cord with the brain, as well as its various parts with each other, is carried out. The anterior cord contains fibers of the motor pathways. These pathways include the anterior cortical-spinal (non-crossed pyramidal), vestibular-spinal (vestibulospinal), tectospinal, anterior reticular-spinal. Motor pathways: lateral cortical-spinal-cerebral (crossed pyramidal), red-nuclear-spinal, reticular-spinal, olive-spinal. The lateral cords contain ascending pathways: posterior spinocerebellar, anterior spinocerebellar, lateral spinothalamic. The posterior funiculi contain ascending fibers that form thin and wedge-shaped bundles. 5. Extrapyramidal system and its disorders The extrapyramidal system includes conduction and motor pathways that do not pass through the pyramids of the medulla oblongata. These pathways regulate feedback between the spinal cord, brainstem, cerebellum, and cortex. The extrapyramidal system includes the caudate nucleus, the shell of the lenticular nucleus, the pale ball, the subthalamic nucleus, the substantia nigra and the red nucleus. The center of this system is the spinal cord. Semiotics of extrapyramidal disorders. The main symptoms of disorders of the extrapyramidal system are dystonia (impaired muscle tone) and disorders of involuntary movements, which are manifested by hyperkinesis, hypokinesis and akinesis. Extrapyramidal disorders can be divided into two clinical syndromes: akinetic-rigid and hyperkinetic-hypotonic. The first syndrome in its classical form manifests itself in Parkinson's disease. In this pathology, damage to the structures of the nervous system is degenerative and leads to the loss of neurons of the substantia nigra containing melanin, as well as to the loss of dopaminergic neurons associated with the striatum. Parkinson's disease is usually bilateral. If the pathological process is hereditary, then we are talking about trembling paralysis. If the reason for the loss of neurons is different, then this is Parkinson's disease or parkinsonism. Such causes may be cerebral syphilis, cerebral atherosclerosis, typhoid fever, damage to the midbrain during a tumor or injury, intoxication with various substances, long-term use of reserpine or phenothiosine. Postencephalitic parkinsonism is also distinguished, which is a consequence of lethargic encephalitis. Akinetic-rigid syndrome is characterized by a triad of symptoms (akinesis, rigidity, tremor). Facial expression is characterized by hypo- or amimi-it, which is explained by inhibition of the movement of facial muscles. Speech also suffers as a result of rigidity and tremor of the muscles of the tongue. She becomes dizzy and monotonous. The patient's movements become slow and unfinished. The whole body is in a state of anteflexion. Rigidity is manifested in the extensor muscles. All reflexes become difficult to evoke. The tremor is passive. Hyperkinetic-hypotonic syndrome occurs as a result of damage to the striatum. Hyperkinesis in this syndrome appears when the inhibitory neurons of the neostriatum are damaged. Spasmodic torticollis and torsion dystonia are the most important syndromes of dystonia. This pathology manifests itself in the form of involuntary head movements, such as turns and tilts. Myoclonic twitches result from damage to the red nucleus, the central tegmental tract, or the cerebellum. They are manifested by rapid contractions of different muscle groups. Tics are manifested in the form of rapid muscle contractions of an involuntary nature. 6. Structure and functions of the cerebellum The cerebellum is the center for coordinating movement. It is located in the posterior cranial fossa along with the brain stem. The cerebellum serves as the roof of the posterior cranial fossa. The cerebellum has three pairs of legs. These legs are formed by cerebellar pathways (afferent and efferent). The upper cerebellar peduncles are located at the level of the midbrain, the middle ones are at the level of the pons, and the lower ones are at the level of the medulla oblongata. The cerebellum has three parts: archi-, paleo- and neocerebellum. Archicerebellum includes a nodule and a piece of the cerebellar vermis, which are the most ancient formations. The paleo-cerebellum includes the anterior lobe of the cerebellum as well as the posterior part of the body of the cerebellum. Neocerebellum is the newest formation of the cerebellum and includes all other parts of the vermis and both hemispheres of the cerebellum. The cerebellum consists of two hemispheres and the cerebellar vermis located between them. In each hemisphere there are four pairs of nuclei: spherical, corky, dentate and tent nucleus. The largest nucleus of the cerebellum, located in its central part, is the dentate nucleus. This core has connections with neo- and paleocerebellum. The dentate nucleus receives impulses from Purkinje cells. Efferent fibers from the dentate nucleus pass through the superior cerebellar peduncles, reaching the red nucleus and the ventrolateral nucleus of the thalamus. At the border of the bridge and the midbrain, these fibers intersect. From the thalamus, the fibers go to the motor cortex of the brain. All impulses that enter the cerebellum through afferent fibers end in its cortex or nuclei. These impulses originate in the cerebral cortex, brain stem and spinal cord. The cerebellum receives some impulses from the joints, tendons, and muscles. These impulses travel along the anterior and posterior spinocerebellar tracts. The central processes from the cells of the spinal ganglion enter the spinal cord through its posterior roots, where they split into several collaterals. Another part of the collaterals connects to the cells of the Clarke nucleus located in the dorsal horn of the spinal cord. This nucleus is located from the VIII cervical to the II lumbar segments along the length of the spinal cord. The cells of the thoracic nucleus are the second neurons whose axons form the posterior spinocerebellar tract. The middle cerebellar peduncles are formed by intersecting fibers of the cerebellopontine tract. The superior cerebellar peduncles carry efferent fibers from its nuclei to the red nucleus, thalamus, and reticular formation of the brainstem. The fibers of the anterior spinocerebellar tract pass through these legs. The cerebellum has connections with various motor pathways. The activity of the cerebellum is beyond the control of consciousness, although it has connections with the cerebral cortex. The cerebellum is involved in the regulation of muscle tone, and also provides coordination of movements. Thanks to the cerebellum, there is an idea of the position of the head in space and its movements, which makes it possible to maintain the balance of the body. 7. Types of damage to the cerebellum With the defeat of the archcerebellum, there is an imbalance when standing and walking - cerebellar ataxia. When closing the eyes, cerebellar ataxia does not change. The cause of its occurrence is muscle asynergy. Efferent impulses from the paleocerebellum, by activating the anti-gravitational muscles, form the muscle tone necessary for standing upright and walking upright. The function of paleo- and archicerebellum is aimed at controlling the tone of skeletal muscles. Also, these formations coordinate the function of the muscles of antagonists and agonists, determining normal gait and statics. With the defeat of the paleocerebellum, trunk ataxia develops. Ataxia is a lack of coordination of movements. Ataxia is divided into static, static-locomotor and dynamic. Static ataxia is characterized by imbalance in sitting and standing positions. With static-locomotor ataxia, balance is disturbed when walking and standing. Dynamic ataxia is characterized by an imbalance in the performance of any movements, especially with the help of the upper limbs. Static and static-locomotor ataxia is manifested by a violation of the patient's gait. She becomes staggering, with her legs wide apart. The patient also cannot stand up straight. When walking, the patient deviates in the direction on which the lesion is located. Static and static-locomotor ataxia are also detected using some tests. Romberg's test is that the patient should stand with his eyes closed. At the same time, the arms are extended in front of you, the socks and heels are shifted. There is another version of the Romberg test, in which one leg of the patient is in front of the other. When conducting this test, pay attention to the direction in which the patient's body deviates. Tests for dysmetria and hypermetria are also carried out. Dysmetria is a violation of the measure of the movements performed, which become choppy, quickly performed and are excessive. A test that reveals this pathology consists in the fact that the patient is invited to pick up two objects, different in volume. In this case, the patient cannot place the fingers adequately to the size of the objects. The second test is that the patient stands with his arms extended forward, while the palms are directed upwards. He is invited to rotate his hands palms down. If there is a pathology, then on the side of the lesion, the movements made are made more slowly and with greater rotation. An increase in the volume of movements performed is hypermetry. During Schilder's test, the patient should close his eyes, stretch both arms forward, raise one arm up, and then lower it to the level where the second hand is located, and vice versa. With damage to the cerebellum, the lowering of the raised arm below the level of the outstretched is noted. With damage to the cerebellum, the appearance of scanned speech is noted. The defeat of the cerebellum is accompanied by the appearance of hyperkinesis of various types. There may be a tremor, or intentional trembling. Pathology of the cerebellum is accompanied by a decrease in muscle tone. 8. The structure of the brain The brain consists of two hemispheres, which are separated by a deep groove that reaches the corpus callosum. The corpus callosum is a massive layer of nerve fibers that connect both hemispheres of the brain. Each hemisphere of the brain has five lobes: frontal, parietal, occipital, temporal, and insula. The surface of the brain is covered with a cortex, which has a connection with subcortical structures. This connection is carried out due to the nerve fibers located between the cortex and the very substance of the brain. The cerebral cortex has grooves through which it is divided into convolutions. Furrows are primary, secondary and tertiary. Primary and secondary sulci are permanent, while tertiary sulci are not. In the cerebral cortex, a new, ancient, old and intermediate cortex is distinguished. The neocortex includes a number of areas: occipital, inferior and superior parietal, post- and precentral, temporal, insular, and limbic. The old bark includes the following formations: ammon's horn, dentate fascia, subiculum, taenia tecta The last two types of the cerebral cortex consist of three or one layer of nerve cells. In the structure of the brain, the so-called cortical sections of the analyzers are distinguished, consisting of a nucleus and scattered elements. The nucleus is a compactly located group of neurons of the cerebral cortex, which has a connection with the same department of the nervous system. Scattered elements - cells located at a distance from the nucleus. They perform the same function, but less differentiated. Primary and secondary projection zones are distinguished in the cortex. Primary zones are located in the deep layers of the cortex. Their irritation causes elementary sensations. Secondary projection zones are located in the second and third layers of the cortex. Their irritation leads to the performance of higher brain functions, such as gnosis and praxis. And in the frontal lobe of the cerebral cortex (in the anterior central gyrus and in the paracentral lobule) is the motor center. In the middle frontal gyrus is the center of turning the eyes and head in the opposite direction. In the posterior part of the middle frontal gyrus is the center of written speech. The center for coordination of movements during upright walking, maintaining balance in standing and sitting positions is located in the superior frontal gyrus, its posterior sections. The motor center of speech is located in Broca's gyrus. Anterior to it is the musical motor center, which ensures the tonality of speech, the ability to sing. In the posterior central gyrus of the parietal lobe of the cerebral cortex, there is a projection field of pain, temperature and tactile sensitivity of the opposite half of the body. The center of sterognosis is located in the same gyrus, but posterior to its middle sections. The center for recognizing the scheme of one's own body, its individual parts, is located posterior to the upper sections of the same gyrus. The center of the auditory analyzer is localized in the temporal lobe of the cerebral cortex, namely in the middle part of the superior temporal gyrus. 9. Brain functions and possible violations of these functions The higher brain functions include speech, gnosis and praxis. Speech function is closely related to the functions of writing and reading. Several analyzers take part in their implementation, such as visual, auditory, motor and kinesthetic. For the correct performance of the function of speech, it is necessary to preserve the innervation of the muscles, primarily the tongue, larynx, and soft palate. The safety and condition of the paranasal sinuses and the oral cavity itself also play a significant role, since they perform a resonator function during speech formation. Dysarthria is a violation of the articulation of speech. Occurs with a disorder of the innervation of the speech apparatus. This may be paralysis or paresis of the speech apparatus, damage to the cerebellum or striopallidar system. Dyslalia is the incorrect pronunciation of sounds in speech. Alalia - delayed speech development. Normally, the child begins to speak by 1-1,5 years. Sometimes ala-lia occurs in connection with dementia, in which the child also lags behind in mental development. Speech disorders at the cortical level are agnosias and apraxias. There are two types of speech: sensory and motor. If motor speech is impaired, then speech apraxia occurs. If sensory speech is disturbed, then speech agnosia develops. Gnosis - recognition, thanks to which a person is oriented in space. With the help of gnosis, a person learns the size and shape of objects, their spatial relationship. Gnosis disorders occur when there is a violation of the interpretation of incoming impulses, as well as a violation of the comparison of the received data with the images that are stored in memory. Disorders of gnosis are called agnosia. They are characterized by a loss of a sense of "familiarity" of surrounding objects and the whole world. Agnosia can be total. At the same time, there is a complete disorientation in space. Agnosia can be visual, sensitive, gustatory and olfactory. Visual agnosia develops as a result of damage to the occipital regions of the cerebral cortex, characterized by impaired recognition of objects that the patient sees. Auditory agnosias develop as a result of damage to the cortex in the region of the Heschl gyrus. They are characterized by impaired recognition of sounds that are previously familiar. Sensitive agnosias are characterized by a disorder in the recognition of tactile, pain, temperature and proprioceptive images. Praxis is purposeful action. In the course of his life, a person learns many movements, which are carried out due to the formation of special connections in the cerebral cortex. When these connections are damaged, the ability to perform certain actions is impaired or completely lost, i.e., apraxias are formed, in which there are no paralysis and paresis, muscle tone is also not impaired, elementary motor acts are preserved. Apraxia develops when the pathological focus is localized in the parietal-occipital-temporal region of the dominant hemisphere of the brain, although both halves of the body suffer. 10. Typical symptoms of damage to certain areas of the cerebral cortex Symptoms of damage to individual sections of the cerebral cortex depend on the location of the pathological process. There may be no symptoms of damage, but symptoms of irritation of individual cortical areas. Frontal lobe. Damage to the region of the anterior central gyrus leads to the development of monoplegia, hemiplegia, and insufficiency of the facial and hypoglossal nerves of the central type. If irritation of this area occurs, then motor Jacksonian epilepsy is observed - focal convulsive seizures. With damage to the cortical center of the gaze, which is located in the region of the posterior part of the middle frontal gyrus, paralysis or paresis of the gaze is observed. At the same time, the impossibility of simultaneous rotation of the eyeballs in the direction of the lesion is noted. With irritation of this area, the appearance of adversive convulsive seizures is noted. They begin with a turn of the head, as well as eyeballs in the direction opposite to the lesion. Damage to Broca's center leads to the development of motor aphasia. It can occur in combination with agraphia. With damage to the cortex of the frontal lobe, the appearance of symptoms of oral automatism and grasping reflexes is noted. There are also characteristic changes in the psyche in the form of abulia, apathy, loss of initiative, etc. Parietal lobe. Involvement of the posterior central gyrus results in monoanesthesia, hemianesthesia, and sensitive hemiataxy. With irritation of the same area, the development of Jacksonian seizures occurs, which are characterized by bouts of numbness, tingling, burning and paresthesia in certain places. The defeat of the parietal lobe can lead to astereognosis, anosognosia, apraxia of various types, alexia and acalculia. The temporal share. The defeat of the auditory analyzer area leads to the development of auditory agnosia. If Broca's center (sensory speech center) is affected, then sensory aphasia occurs. Irritation of the cortex of the temporal region can cause memory impairment, twilight disorders of consciousness. Various hallucinations can also be observed: gustatory, olfactory, auditory. Sometimes there are bouts of dizziness, which is associated with damage to the cortical part of the vestibular analyzer. Occipital lobe. Its defeat leads to a variety of visual disorders: homonymous hemianopsia, metamorphopsia, macro- and micropsia, visual hallucinations, photomas. In addition to these disorders, there may be a decrease in visual memory, spatial orientation disorders and contralateral ataxia. 11. The structure of the autonomic and limbic nervous system and their functions The autonomic nervous system regulates all processes occurring in the body (the function of all internal organs, maintaining homeostasis), and it also performs an adaptive-trophic function. Autonomic nerve fibers are present in all cranial and spinal nerves. The autonomic nervous system is divided into central and peripheral divisions. The central section is formed by all cells and fibers in the brain and spinal cord. The peripheral section includes all other formations of the autonomic nervous system. The autonomic nervous system also contains sympathetic and parasympathetic divisions. The central part of the sympathetic nervous system is located in the cortex, nuclei of the hypothalamus, brain stem, reticular formation and lateral horns of the spinal cord. The peripheral part of the sympathetic nervous system starts from the neurons of the lateral horns of the spinal cord, namely from TSS to LII inclusive. The sympathetic trunk is located along the lateral surface of the spine. It has 24 pairs of sympathetic nodes. Of these, 3 cervical, 12 thoracic, 5 lumbar and 4 sacral. From the fibers of the lower - a plexus that innervates the heart. The fibers of the thoracic sympathetic nodes innervate the aorta, lungs, bronchi and abdominal organs. The fibers of the lumbar nodes are sent to the pelvic organs. The parasympathetic nervous system is divided into craniobulbar and sacral divisions. The first section is located in the brain, and the second - in the spinal cord. The segmental apparatuses of the autonomic nervous system are the spinal cord, the autonomic nodes and the sympathetic trunk. The supra-segmental apparatuses are the hypothalamus and the limbic-reticular complex. The hypothalamus is connected to the brain and spinal cord. Thanks to him, neuro-reflex and neurohumoral regulation is provided. The posterior sections of the hypothalamus are associated with the trophotropic system, which is involved in maintaining homeostasis. The hypothalamus is involved in the regulation of wakefulness and sleep, metabolism, endocrine background, genital area, the function of all organs and body systems. The work of the autonomic nervous system proceeds under the control of the limbic-reticular complex. The limbic region includes the para-hippocampal and cingulate gyrus. The limbic system is interconnected cortical and subcortical formations that have common functions and development patterns. The limbic system includes the transparent septum, the vaulted gyrus, the hippocampus, the dentate gyrus, part of the olfactory pathway at the base of the brain, etc. The subcortical structures of the limbic system include the hypothalamus, the caudate nucleus, the nucleus of the frenulum, the putamen, the amygdala, the anterior tubercle of the lamus. The autonomic nervous system is involved in the regulation of vascular tone and cardiac activity, secretory activity of the glands, thermoregulation, regulation of metabolic processes, endocrine function, participates in the innervation of smooth muscles, and performs an adaptive-trophic function. 12. Possible disorders of the autonomic nervous system and methods for their determination Dysregulation of vascular tone is called vegetovascular dystonia. They are characterized by lability of blood pressure, dizziness, sweating, cold extremities, etc. The defeat of the autonomic nervous system is accompanied by a violation of thermoregulation and sweating. In the diencephalic region are the highest centers of thermoregulation. The defeat of this area leads to hyperthermic crises, which are characterized by paroxysmal increases in body temperature. Sweating studies are carried out by using an injection of pilocarpine, warming in a light bath, orally administering aspirin or amidopyrine. Salicylates affect the centers of regulation in the hypothalamus. If the postganglionic fibers of the autonomic nervous system are affected, then the use of these methods does not cause sweating. If the preganglionic fibers or lateral horns of the spinal cord are affected, sweating can only be induced in the affected segments by injections of pilocarpine. If the area of the hypothalamus or its connection with the neurons of the spinal cord is affected, then taking aspirin does not cause sweating. With the help of the autonomic nervous system, the regulation of the function of the pelvic organs is carried out. The innervation of the bladder is carried out by the I-III lumbar segments of the spinal cord. Sympathetic fibers cause a contraction of the sphincter of the bladder and a simultaneous contraction of the detruser. If the tone of the sympathetic nervous system increases, then urinary retention develops. Urination disorders can be manifested by urinary retention or incontinence. With bilateral lesions of the cortical-spinal-cerebral influences, temporary urinary retention occurs. There is an urgent urge to urinate. With the defeat of the spinal centers, true urinary incontinence develops. It is characterized by the constant release of urine in drops as it enters the bladder. The act of defecation is regulated by the autonomic nervous system at the level of II-IV sacral segments of the spinal cord, as well as by the cerebral cortex. Damage to the structures of the autonomic nervous system causes a disorder similar to urination disorders. The parasympathetic division innervates the pupillary sphincter and the ciliary muscle. The remaining muscles of the eye are innervated by the sympathetic division. An increase in the tone of the parasympathetic nervous system leads to miosis, enophthalmos, and slight drooping of the upper eyelid. This triad of symptoms is the Bernard-Horner syndrome. Most often, the syndrome occurs when the spinal cord segments are damaged at the C8-TM level. The defeat of the nodes of the sympathetic trunk leads to hyperpathy, causalgia, impaired sweating, disorders of the skin, subcutaneous fat and bones. The defeat of the ear node causes the appearance of pain that is anterior to the auricle. The defeat of the lateral horns of the spinal cord leads to disorders of the same nature, which are localized in the zone of segmental innervation. Damage to the hypothalamus leads to a variety of syndromes. 13. Paralysis The defeat of any part of the pyramidal tract causes a violation of voluntary movements, which may be complete or partial. The complete loss of voluntary movements is called paralysis, or plegia, partial - paresis. Paralysis can be central or peripheral. Central paralysis develops as a result of damage to the pyramidal tract along the central motor neuron in any area: in the motor cortex, in the internal capsule, in the brain stem or in the spinal cord. Central paralysis has characteristic symptoms, such as muscular hypertension, hyperreflexia, expansion of the reflexogenic zone, clonuses of the feet, kneecaps and hands, pathological reflexes, protective reflexes and pathological synkinesis. Muscular hypertension is characterized by an increase in the tone of the flexors of the arm and extensors of the leg on one side. The Wernicke-Mann pose is formed. It consists in bringing and bending the arm, while the leg is extended. Pathological reflexes can be carpal and foot, which are divided into flexion and extensor. Peripheral paralysis develops as a result of damage to any part of the peripheral motor neuron: large alpha motor neurons, cells of the motor nuclei of the brain stem, anterior root of the spinal cord, nerve plexus, peripheral nerves. Peripheral paralysis is characterized by the following symptoms: areflexia, muscle atony, atrophy, degeneration reaction, fibrillar or fascicular muscle twitching. The symptom complex of movement disorders depends on the level of damage to the pyramidal tract. With damage to the peripheral nerve, atrophy of the muscle group that is innervated by this nerve is noted, reflexes fall out. There are pains, violation of sensitivity and autonomic disorders. The defeat of the anterior roots of the spinal cord causes peripheral paralysis of the muscles that receive innervation from this root, and fascicular twitching. With damage to the anterior horns, peripheral paralysis develops in the zone of innervation of this segment of the spinal cord. Fibrillar muscle twitching, atrophy and degeneration reactions are characteristic. Damage to the lateral funiculus causes central paralysis of the muscles below the level of the lesion. Injuries to the cauda equina lead to peripheral paralysis of the legs, impaired urination, impaired sensitivity in the perineal region, and sharp pains appear. A lesion at the level of the lumbar thickening causes flaccid paralysis and anesthesia of the lower extremities; damage to the thoracic region - spastic paralysis of the legs, impaired sensitivity of all types of conduction type; damage to the cervical thickening - central paralysis of the legs and a violation of the sensitivity of the conductor type. A lesion in the region of the decussation causes paralysis of the lower limb on the opposite side, and the upper limb on the same side. Damage to the brain stem leads to central hemiplegia on the opposite side. Damage to the anterior central gyrus leads to monoparesis. 14. Disorders of cerebral circulation: damage to the internal carotid artery The blood supply to the brain is carried out by the vertebral and internal carotid arteries. The ophthalmic artery departs from the latter in the cranial cavity. The internal carotid artery itself divides into the anterior and middle cerebral arteries. The vertebral arteries join together and form the basilar artery. It, in turn, divides into two posterior cerebral arteries. The vertebral-basilar arterial system is connected to the internal carotid arteries, resulting in the formation of an arterial circle of the cerebrum, which acts as a cerebral anastomosis. Chronic diseases of the aorta and arteries lead to impaired blood flow through the vessels due to obliterating or dilating lesions. The most common causes of obliteration or stenosis of the arteries are: 1) obliterating atherosclerosis; 2) nonspecific aortoarteritis; 3) thromboangiitis obliterans (endarteritis). The internal carotid artery supplies blood to most of the hemispheres - the cortex of the frontal, parietal, temporal regions, subcortical white matter, subcortical nodes, and the internal capsule. The severity of focal changes in the brain and clinical manifestations depend mainly on the state of collateral circulation. With insufficiency of collateral circulation, small foci of cerebral infarction usually occur in areas of adjacent blood supply in the cortical-subcortical regions of the hemisphere, mainly in the basin of the middle cerebral artery. With intracranial thrombosis of the internal carotid artery, extensive foci of infarction develop in the basin of the superficial and deep branches of the middle and anterior cerebral arteries, accompanied by massive neurological symptoms and often leading to death. An occlusive lesion in its initial period proceeds in the form of transient cerebrovascular accidents: patients experience short-term numbness and weakness in the limbs, sometimes aphasic disorders, decreased vision in one eye or other symptoms. Cerebral circulation disorders with persistent focal syndrome proceed differently. The acute form is characterized by a sudden apoplectiform onset. The subacute form develops slowly, over several hours or 1-2 days. The chronic, or pseudotumorous, form is characterized by a very slow (over a number of days or even weeks) increase in symptoms. There is an alternating opto-pyramidal syndrome: blindness or decreased vision, sometimes with atrophy of the optic nerve on the side of the affected artery and pyramidal disorders on the opposite side. The most common symptom is paresis of the opposite limbs, usually of the cortical type with a more severe lesion of the arm, sometimes only monoparesis. With damage to the left carotid artery, aphasia often develops, usually motor. There may also be sensory disturbances, hemianopsia. 15. Damage to the anterior and middle cerebral arteries The superficial anterior cerebral artery branches supply blood to the medial surface of the frontal and parietal lobes, the paracentral lobule, partly the orbital surface of the frontal lobe, the outer surface of the first frontal gyrus, the upper part of the central and superior parietal gyrus, most of the corpus callosum (with the exception of its most posterior parts). The central (deep) branches (the largest of them is the Gubner recurrent artery) supply blood to the anterior thigh of the internal capsule, the anterior sections of the head of the caudate nucleus, the shell of the pale ball, partly the hypothalamic region, the ependyma of the anterior horn of the lateral ventricle. With extensive infarcts in the basin of the anterior cerebral artery, it is characterized by spastic paralysis of the limbs of the opposite side - the proximal arm and distal leg. Often there is a delay (or incontinence) of urine. With bilateral foci, a mental disorder is often noted (aspontaneity, reduced criticism, weakening of memory, etc.). Often there is apraxia of the left hand (with left-sided foci) as a result of damage to the corpus callosum. Sometimes mildly expressed disorders of sensitivity on the paralyzed leg are observed. With a lesion in the supply zone of the paracentral artery, monoparesis of the foot usually develops, simulating peripheral paresis; with damage to the area supplied by the coronosal artery, left-sided apraxia occurs. The following branches of the cerebral artery are distinguished: 1) central (deep) branches that extend from the initial part of the artery trunk and feed a significant part of the subcortical nodes and the internal capsule; 2) cortical branches: the anterior temporal artery, which departs from the initial part of the trunk of the middle cerebral artery and feeds most of the temporal region; ascending branches extending from a common trunk: orbital-frontal, precentral (preroland), central (roland), anterior parietal arteries; posterior parietal, posterior temporal and angular arteries. The basin of the middle cerebral artery is an area in which a heart attack develops especially often. With blockage and narrowing of the artery, it depends on the size of the infarct and its localization, which, in turn, is associated with the level of the occlusive process and the efficiency of collateral circulation. The clinical syndrome in total infarction in the basin of the middle cerebral artery consists of contralateral hemiplegia, hemianesthesia and hemianopsia. With left hemispheric infarcts, at the same time, mixed-type aphasia or total aphasia occurs, with right hemispheric infarctions - anosognosia. If the basin of the posterior cortical branches of the artery does not suffer, then there is no hemianopia, sensory disturbances are less profound, speech is usually impaired by the type of motor aphasia. With a heart attack in the pool of deep branches, spastic hemiplegia is observed, inconsistently - a violation of sensitivity, with foci in the left hemisphere - short-term motor aphasia. With an extensive infarction in the basin of the cortical branches, hemiplegia or hemiparesis is noted with a primary lesion of the function of the hand, violations of all types of sensitivity, hemianopsia, with left hemispheric foci, in addition, aphasia of a mixed type or total, impaired counting, writing, reading, apraxia. 16. Pathologies of the anterior and posterior cerebral arteries The anterior villous artery takes part in the blood supply to the posterior 2/3 of the posterior femur, and sometimes to the retrolenticular part of the internal capsule, caudate nucleus, internal segments of the globus pallidus, the lateral wall of the lower horn, and the lateral ventricle. With occlusion of this artery, the neurological deficit is insignificant, since the area irrigated by it has a richly represented network of anastomoses; more regularly there is a heart attack of the medial part of the pale ball. Its cortical branches supply blood to the cortex and the underlying white matter of the occipital-parietal region, the posterior and medial-basal regions of the temporal region. Central (deep) branches (thalamo-perforating, thalamo-knee, premamillary provide blood to a significant part of the optic tubercle, posterior hypothalamic region, thickening of the corpus callosum, optic crown and hypotuberous nucleus (Lewis) body); branches also branch off from the artery to the midbrain. Homonymous hemianopsia or upper square hemianopsia is observed, morphopsia and visual agnosia occur less frequently. With left hemispheric infarctions, alexia and unsharply pronounced sensory aphasia can be observed. Sometimes they are preceded by transient amnesias. Bilateral infarctions in the occipital cortex may be accompanied by "tubular" vision due to bilateral hemianopia with the preservation of macular vision. If the visual fields and visual acuity in cerebral infarcts in the basin of the posterior cerebral arteries are not grossly disturbed, then certain violations of higher visual functions may be detected. So, with bilateral infarcts at the junction of the parietal and occipital regions, sometimes a syndrome of agnosia on the face (prosopagnosia) occurs, when the patient loses the ability to recognize the faces of relatives and friends while maintaining the ability to recognize surrounding objects. The same syndrome with the same localization may be accompanied by a violation of orientation in space, loss of topographic memory. When the infarction spreads to the medial-basal parts of the temporal region, pronounced memory disorders such as Korsakov's syndrome occur with a predominant impairment of short-term (operational) memory, emotional-affective disorders. When this area is affected, the classic thalamic Dejerine-Roussy syndrome occurs, including hemihypesthesia or hemianesthesia, as well as hyperpathy and dysesthesia, thalamic pain in the half of the body opposite to the focus, transient contralateral hemiparesis; hemianopsia, hyperkinesis of an athetic or choreoathetotic nature, hemiataxia, trophic and vegetative disorders are observed inconsistently. The infarction in the basin of the thalamoperforating artery destroys the posterior part of the hypothalamic region, the dorsomedial nucleus of the optic tubercle, the median nucleus of Lewis, the body of Lewis, and the dentorubrothalamic pathway. The clinical syndrome is characterized by severe ataxia and intentional tremor in the contralateral limbs. 17. Manifestations of damage to the main, vertebral arteries and arteries of the brain stem and midbrain It gives branches to the pons of the brain (pons), the cerebellum and continues with two posterior cerebral arteries. Complete blockage (thrombosis) of the artery is preceded by multiple transient circulatory disorders in the vertebrasil system - dizziness attacks, dysarthria, transient paresis and paralysis of the limbs, cranial nerves and other symptoms. Acute occlusion (thrombosis) of the artery is accompanied by symptoms of a predominant lesion of the brain bridge with a disorder of consciousness up to coma. There are narrow (with a pinhead) pupils, vegetative-visceral crises, hyperthermia, disorder of vital functions. It supplies blood to the medulla oblongata, partly to the cervical spinal cord (anterior spinal artery), and the cerebellum. An occlusive lesion of the extracranial part of the artery is characterized by "spotting" of the lesion of various parts of the basin of the vertebrasil system; often there are vestibular disorders (dizziness, nystagmus), disorders of statics and coordination of movements, visual and oculomotor disorders, dysarthria; less pronounced motor and sensory disturbances. Quite often there are memory disorders, especially for current events, such as Korsakov's syndrome, and transient amnesia. Blockage of the intracranial artery is characterized by a combination of persistent alternating syndromes of lesions of the medulla oblongata with symptoms of transient ischemia of the oral parts of the brain stem, occipital and temporal lobes. As a result, blood flow to the brainstem is limited, and eating symptoms may appear. The blood supply to the brain stem is carried out by branches of the main and vertebral arteries, as well as the posterior cerebral artery. Three groups of branches depart from them: paramedian arteries, feeding mainly the middle parts of the brain stem (at the base); short (enveloping) arteries supplying blood to the lateral sections of the trunk, and long envelope arteries supplying the dorsolateral sections of the trunk and cerebellum. Infarctions in the region of the brain stem are the result of damage to the arteries of the vertebrasil system at various levels. Ischemic lesions of the brain stem are characterized by the well-known "spotting", the dispersion of several, usually small, foci of infarction. Hence the large polymorphism of clinical manifestations in different cases. The paramedian arteries of the midbrain depart from the posterior cerebral and basilar arteries and feed mainly on the middle and medial parts of the legs of the brain. With a heart attack in the pool of these arteries, the so-called lower red nucleus syndrome most often develops - paralysis of the oculomotor nerve on the side of the focus, ataxia and intentional trembling in the contralateral limbs; sometimes there is also choreiform hyperkinesia. With a heart attack that captures the base of the legs of the brain, Weber's syndrome develops. 18. Symptoms of damage to the bridge of the brain The paramedian arteries arise from the basilar artery and supply blood mainly to the base of the pons: the pyramidal tracts, the gray nuclei of the pons, the pons' own fibers, and part of the medial loop. In the region of the tire, the nucleus of the abducens nerve sometimes suffers. Infarction in this area is characterized by contralateral hemiplegia, central paralysis of the facial and hypoglossal nerves (medial pontine infarction). Muscle tone in paralyzed limbs in the initial period after a stroke is usually reduced, protective reflexes are absent or weakly expressed. When the infarction is localized in the lower part of the bridge, paresis of the gaze of the bridge type is noted (the eyes look at the paralyzed limbs) or paralysis of the abducens nerve on the side of the focus. Sometimes peripheral paralysis of the facial nerve on the same side joins this. Bilateral infarction in the basin of the paramedian pontine arteries leads to tetraplegia or tetraparesis, pseudobulbar and cerebellar syndromes. Short envelope branches depart from the main artery and supply blood to the lateral sections of the brain, sometimes the spinothalamic tract, as well as the lateral parts of the medial loop and pyramidal tract. Infarction in the basin of these branches leads to the development of lateral pontine syndrome. Clinically, homolateral cerebellar syndrome is most constantly observed, combined with a violation of sensitivity, and sometimes with pyramidal signs on the opposite side; Horner's syndrome may be noted on the side of the focus. With foci in the middle and lower third of the lateral part of the bridge, a disorder of pain and temperature sensitivity of the skin of the face occurs on the side of the lesion and a disorder of these types of sensitivity on the opposite side of the trunk and extremities, i.e., alternating hemihypesthesia or hemianesthesia may appear. The infarction of the oral sections of the tegmentum of the brain bridge in the area of blood supply to the superior cerebellar artery covers the superior cerebellar peduncle, the spinothalamic bundle, the central pathway of the tegmentum, and partly the posterior longitudinal bundle. Clinically, there is a disorder of pain and temperature sensitivity on the opposite side of the focus, cerebellar disorders on the homolateral side, paresis of the gaze of the bridge type, sometimes nystagmus when looking towards the focus. An infarction in the caudal part of the pontine tegmentum, which is supplied by the anterior inferior cerebellar artery and short circumflex arteries, is accompanied by mild homolateral cerebellar symptoms, dissociated sensory disturbance on the opposite half of the body, and sometimes peripheral facial paralysis on the side of the focus. With bilateral infarcts in the area of the bridge, pseudobulbar syndrome is clearly expressed. The total defeat of the bridge is sometimes accompanied by the so-called locked-in syndrome - deafferentation syndrome, when the patient cannot move his limbs and speak, but he retains consciousness, eye movements and voluntary blinking, which undoubtedly facilitates the patient's contact with others. 19. Damage to the artery of the medulla oblongata and inferior posterior cerebellar artery Paramedian arteries in the oral part of the medulla oblongata depart from the vertebral arteries, in the caudal part - from the anterior spinal artery. They supply blood to the pyramidal tract, medial loop, infranuclear fibers, and nucleus of the hypoglossal nerve. With a heart attack in this area, the so-called medial medulla oblongata syndrome occurs - paralysis of the hypoglossal nerve on the side of the focus The largest branch of the vertebral artery is the long circumflex artery for the medulla oblongata. It nourishes the retrolivar lateral sections of the medulla oblongata (cordial body, region of the vestibular nuclei, descending nucleus and trigeminal nerve root, spinothalamic pathway, nuclei of the glossopharyngeal and vagus nerves) and the cerebellum. A heart attack in this area develops with blockage of the vertebral and inferior posterior cerebellar arteries, clinically it manifests itself as Wallenberg-Zakharchenko syndrome, which is a lateral syndrome of the medulla oblongata. With damage to the lower sections of the brain stem and upper segments of the spinal cord, in the lateral columns of which the reticulospinal path passes, sometimes Undine's syndrome occurs (the name is taken from German mythology) - the loss of the possibility of automatic breathing due to the dissociation of the respiratory center of the medulla oblongata from the spinal motor neurons of the respiratory muscles, while the connections of the latter with the cerebral cortex remain intact. At the same time, breathing in the state of wakefulness is not disturbed, while in a dream, a severe violation of breathing occurs, up to its stop with a fatal outcome. The spinal cord is supplied with blood by the anterior and two posterior spinal arteries. The spinal arteries receive blood from the radicular arteries. The superior system of radicular arteries gives off branches to the cervical and three upper thoracic segments of the spinal cord. The middle system of radicular arteries supplies blood to the thoracic segments IV through VIII. The lower system - Adamkevich's artery - supplies blood to the lower thoracic, as well as all lumbar and sacral segments of the spinal cord. The outflow of blood from the spinal cord is carried out through the radicular veins. Through them, blood flows into the anterior and posterior vertebral plexuses. They are located between the sheets of the dura mater. From the venous plexuses, blood enters the cervical, vertebral, intercostal and lumbar veins. If the venous plexuses expand varicosely, then the spinal cord is compressed in the spinal canal. Neurological symptoms in case of circulatory disorders in the basin of the anterior spinal artery depend on the level of the lesion. If the pathology is higher than the cervical thickening, then spastic tetraplegia develops, superficial sensitivity is disturbed, and central disorders of pelvic functions are observed. If the focus is located in the thoracic region, then spastic paraplegia of the legs is noted. If blood circulation in the basin of the posterior spinal artery is disturbed, then spastic paralysis, disorders of pelvic functions and a violation of deep sensitivity are noted. 20. Meningitis Meningitis is an inflammation of the meninges. There are serous and purulent meningitis. According to the pathogenesis, meningitis is divided into primary and secondary. According to localization, meningitis is divided into generalized and limited, as well as basal and convexital) (on a convex surface). Downstream distinguish fulminant, acute, subacute and chronic meningitis. According to the severity of meningitis is divided into mild, moderate, severe and extremely severe form. According to the etiology, bacterial, viral, fungal and protozoal meningitis are distinguished. There are three mechanisms for the development of meningitis: as a result of an open craniocerebral or vertebral-spinal injury, lymphogenous or perineural spread of the pathogen, hematogenous spread of the pathogen. Meningitis is characterized by three syndromes: common infectious, meningeal, syndrome of inflammatory changes in the cerebrospinal fluid. To clarify the diagnosis, a study of cerebrospinal fluid is performed using bacteriological or other methods. The general infectious syndrome includes fever, chills, leukocytosis, increased ESR, increased heart rate and respiratory rate. Meningeal syndrome includes headache, vomiting, meningeal posture, Kernig's and Brudzinski's symptoms, neck stiffness. The disease begins with the appearance of a headache as a result of irritation of the receptors of the meninges by the inflammatory process and toxins. Vomiting occurs with a headache, is not associated with food intake. Rigidity of the neck muscles is determined when trying to passively bend the head in the supine position and consists in a feeling of resistance that causes pain in the patient. Kernig's symptom is the appearance of pain in the lower back and leg when trying to passively extend it in the knee joint. The leg is bent at the hip joint at a right angle. There is also an increase in sensitivity to loud sounds, various smells. When the eyeballs move, soreness appears. Bekhterev's zygomatic symptom is characteristic - local pain when tapping along the zygomatic arch. A mandatory research method is a lumbar puncture. Meningitis is characterized by an increase in cerebrospinal fluid pressure, a change in the color of the cerebrospinal fluid, pleocytosis, depending on whether serous meningitis or purulent, the number of leukocytes or lymphocytes increases. Epidemic cerebrospinal meningitis is caused by Weikselbaum's meningococcus and is transmitted by droplets and contact. The incubation period is 1-5 days. It is characterized by an acute onset: the temperature rises to 40 ° C, severe headaches appear, vomiting, consciousness is disturbed. Complications of the disease can be cerebral edema and acute adrenal insufficiency. Secondary purulent meningitis can occur with contact, perineural, hematogenous or lymphogenous routes of infection. Characteristic symptoms are weakness, fever up to 40 ° C, headache, vomiting is not constant. A day later, shell symptoms and mental disorders appear. The cranial nerves are often affected. 21. Encephalitis Encephalitis is inflammation of the brain. Classification. I. Primary encephalitis. Viral: 1) arbovirus, seasonal, transmissible (tick spring-summer; Japanese mosquito; Australian; American); 2) viral without a clear seasonality (enteroviral Coxsackie and ECHO; herpetic; influenza; with rabies); 3) caused by an unknown virus (epidemic (Economo)). Microbial and rickettsial (with neurosyphilis, with typhus). II. Encephalitis secondary. Viral: 1) with measles; 2) with chicken pox; 3) with rubella. Post-vaccination (DTP, smallpox vaccine, anti-rabies). Microbial and rickettsial (staphylococcal; streptococcal; malaria; toxoplasma). III. Encephalitis caused by slow infections (demyelinating), subacute sclerosing panencephalitis. According to localization, they are divided into stem, cerebellar, mesencephalic, diencephalic. By the nature of the exudate: purulent, non-purulent. By prevalence: focal, diffuse. The disease can be transmitted in various ways, most often hematogenous. Neurons are destroyed by the virus itself and its toxins. The wall of blood vessels is affected, which leads to edema and vascular disorders of the brain. All encephalitis is characterized by the presence of a prodromal period, general brain symptoms, focal symptoms of damage to the central nervous system. The prodromal period lasts up to several days and is characterized by symptoms of an infectious disease. Common brain symptoms include headache, vomiting, photophobia, disorders of consciousness and psyche. Focal symptoms depend on the localization of the process. Tick-borne encephalitis is caused by a neurotropic virus that enters through the diet or through a tick bite. The incubation period for alimentary infection, with a tick bite is 8-20 days. The disease begins acutely: the temperature rises to 40 ° C, headache, vomiting, aching pains in the lower back and muscles appear. There may be dyspeptic disorders, hyperemia of the skin. The interval between the first and second rise in temperature is 2-5 days. Mental disorders are noted. Tick-borne encephalitis is divided into clinical forms: polio, meningeal, encephalitic, obliterated and polyradiculoneuritis. Vaccine encephalitis develops as a result of an allergic reaction of the brain to the vaccine. Symptoms appear after 1-2 weeks. It is characterized by an acute onset, the temperature rises to 40 ° C, headache, vomiting, and impaired consciousness appear. The appearance of central paralysis is characteristic. In the cerebrospinal fluid, the amount of protein and sugar is increased, lymphocytic cytosis. Measles encephalitis develops 3-5 days after the onset of the rash, characterized by an acute onset. The temperature may not rise, consciousness is disturbed, convulsions may appear. Characterized by meningeal symptoms. Encephalitis with chickenpox develops a week after the onset of the rash. Body temperature rises, consciousness is disturbed, convulsions and meningeal symptoms appear. 22. Neurosyphilis Neurosyphilis is caused by spirochete pallidum. It is divided into early and late. Early neurosyphilis develops in the first 5 years after infection. It is characterized by damage to the meninges and blood vessels. Clinically, it can proceed latently, without meningeal symptoms. Headache, dizziness, tinnitus, pain when moving the eyes, weakness and malaise appear. There are characteristic changes in the cerebrospinal fluid: the amount of protein is 0,5-1,5 g/l, lymphocytic cytosis, and a positive Wasserman reaction. Late neurosyphilis develops no earlier than 8 years after infection. Corresponds to the tertiary period of syphilis. It is characterized by cerebral symptoms, meningeal symptoms, symptoms of cranial nerve damage. Vascular syphilis may develop. It is characterized by changes in the vascular wall. The membranes of the brain are not affected. Neurosyphilis proceeds according to the type of strokes, which can be repeated. Focal symptoms depend on the localization of the process. Vliquore increased the amount of protein to 0,5-1 g/l, monocytosis (20-70 in 1 µl), with special research methods, pale treponemas are determined. Dorsal tabes develops most often 16-25 years after infection. This pathology occurs in approximately 2% of patients and more often affects men. The symptomatology of this form of syphilis is determined by the predominant lesion of the posterior columns and posterior roots of the spinal cord. In the region of the posterior pillars, atrophy is noted, and these zones look like flattened and sunken. Along with the posterior columns, the nerve fibers of the posterior horns also suffer, connecting the latter with the anterior horns of the spinal cord (collateral effect). In most cases, degenerative phenomena are accompanied by inflammatory processes, mainly the pia mater of the dorsal surface of the spinal cord. When dryness affects numerous nerve structures, but most often and deeply degenerative processes affect the system of sensitive peripheral neurons associated with the cells of the intervertebral nodes and their processes, as well as the cells of the nuclei of sensitive cranial nerves and their processes. An early sign is the uneven tendon reflexes of the lower extremities, which first decrease and then disappear (first knee, then Achilles) while maintaining skin reflexes. Disorders of the pelvic organs are very common in dryness. First of all, the function of the bladder suffers in the form of mild urinary retention during urination, in rare cases complete urinary retention occurs. Quite often, weakness of the sphincter of the bladder can develop. Pupillary disturbances are early, frequent and characteristic. They are expressed in the form of miosis, anisocoria, changes in the shape of the pupils, the absence of their reaction to light while maintaining accommodation. There may be primary atrophy of the optic nerve, in connection with this, blindness may occur. Due to damage to the auditory nerve, there is a decrease in hearing in one or both ears. In the spinal tabes, the phenomena of progressive paralysis often join: a sharp weakening of memory, persistent insomnia, dementia, a manic state. There are peripheral and central paralysis of the extremities, but they do not belong to frequent manifestations. The main method of treating patients with all forms of syphilis is specific antisyphilitic therapy, including the use of penicillin, iodine, bismuth. 23. Multiple sclerosis Demyelinating disease, which is characterized by a multifocal lesion of the nervous system and an undulating course. It has an infectious etiology. It is characterized by a long incubation period. The pathogenesis lies in the fact that the infectious agent penetrates the central nervous system, disrupts the synthesis of nucleic acids, and destroys myelin. As a result, antibodies against myelin basic protein are produced, which support demyelination. Inflammatory and proliferative processes in the mesenchymal tissue are also noted. All this leads to the formation of plaques of multiple sclerosis. The hormonal function of the adrenal cortex is disturbed, persistent immunodeficiency develops. The onset of the disease is slow and asymptomatic. The first symptoms are signs of damage to the optic nerve. They consist in a decrease in visual acuity, clarity, the appearance of livestock. There may be cerebellar disorders, sensory disturbances in the extremities. Abdominal reflexes may decrease or disappear. Clinical forms of multiple sclerosis: cerebral, cerebrospinal, spinal, cerebellar, optic, stem. The cerebrospinal form is the most common. It is characterized by multifocality, cerebellar symptoms appear, symptoms of damage to pyramidal formations, visual, oculomotor and other systems. In the spinal form, symptoms of damage to the spinal cord appear. The cerebellar form is characterized by ataxia, dysmetria, handwriting disorders, nystagmus, and slurred speech. The optical form is characterized by a decrease in visual acuity. Examination reveals scotomas, the optic disc is pale, visual fields are narrowed. The stem form is characterized by rapid progression. In the blood, leuko-, lympho-, neutropenia, platelet aggregation is increased, the amount of fibrinogen is increased. In the cerebrospinal fluid, the amount of protein is increased, pleocytosis is 15-20 in 1 μl. The amount of IgG, M, A is increased in serum and cerebrospinal fluid. Computed and magnetic resonance imaging are additional research methods. Chronic progressive disease of the nervous system, which is characterized by damage to the motor neurons of the brain and spinal cord, degeneration of the cortical-spinal and cortical-nuclear fibers. Symptoms of damage to both central and peripheral motor neurons are noted. The onset of the disease is characterized by atrophy of the distal muscles of the arms, fibrillar and fascicular twitches. The lesion is usually symmetrical. The lateral cords of the spinal cord are usually affected, which is manifested by pathological reflexes, expansion of reflexogenic zones, tendon and periosteal reflexes. Muscle tone can be increased or decreased, depending on the type of paresis. The progression of the disease leads to paresis of the legs. Characteristic is the defeat of the nuclei of the IX-XII pairs of cranial nerves, which is manifested by a violation of swallowing, articulation and phonation. The function of the language is broken. The pharyngeal reflex is absent, head movements are limited. 24. Clinical picture of trigeminal neurology Trigeminal neuralgia comes in two forms: primary and secondary (symptomatic). Primary develops independently, without any dependence on the pathological process or condition already existing in the body. Secondary is a complication of an existing disease. Trigeminal neuralgia is possible with diseases of the teeth, paranasal sinuses, general infections and intoxications, narrowing of the mandibular or infraorbital canal, etc. The pathogenesis of the disease is varied. The disease begins with the appearance of a peripheral source of pain impulses. As a result of the spread of pain impulses from a peripheral source, irritation occurs at various levels of the trigeminal nerve, as well as peripheral autonomic formations of the face. Trigeminal neuralgia is characterized by the appearance of intense pain attacks lasting up to several minutes, which are accompanied by reflex contraction of the muscles of the face and autonomic manifestations, such as hypersalivation, lacrimation, flushing of the face. Localization of pain is determined by the zone of innervation of the affected branch of the trigeminal nerve. The interictal period is characterized by the absence of pain. Often trigeminal neuralgia captures the maxillary or mandibular nerves. During a pain attack or immediately after it, pain points are determined, located at the exit points of the branches of the trigeminal nerve. In addition, in places of innervation, in some cases, areas of hyperesthesia are found. There are no organic symptoms in the interictal period. During an attack, pain can be of a different nature: burning, tearing, cutting, shooting, stabbing, as if shocking. Pain attacks may not be single, but follow with a small interval one after another. One of the methods of treatment is alcoholization of the peripheral branches of the trigeminal nerve. In this case, remission occurs quickly. With a short duration of the disease, patients are prescribed anticonvulsants, such as carbamazepine. Applied orally in tablet form, starting with 1 tablet (0,2 g) 1-2 times a day daily. The dose of the drug used is gradually increased, bringing up to 2 tablets (0,4 g) 3-4 times a day. Separately, trigeminal neuralgia of peripheral origin is distinguished, which occurs when a pathological process affects the peripheral part of the nerve. Such pathological processes can be malocclusion, diseases of the paranasal sinuses, teeth and jaws, basal meningitis, etc. The following features are distinguished: the pain focus at the beginning of the disease corresponds to the location of the primary pathological process (injury, inflammation, etc.). A pain attack develops against the background of previous pain sensations in the area innervated by the affected branch of the trigeminal nerve. The duration of the pain attack varies within a few days, the pain weakens gradually. 25. Symptoms of odontogenic trigeminal neuralgia, dental plexalgia and postherpetic neuralgia It occurs with various pathological processes of teeth and jaws, as well as with incorrect methods of their treatment. In addition, various periodontal diseases (gingivitis), osteomyelitis of the upper and lower jaws, the presence of remnants of bone fragments of an extracted tooth in the hole, pulpitis, periodontitis, etc., serve as etiological factors. A combination of any factors with each other is possible. Odontogenic neuralgia usually affects the maxillary and mandibular nerves, which explains the appearance of pain in the areas of innervation of these branches of the trigeminal nerve. The clinic is characterized by a long course, a pronounced severity of symptoms, both painful and vegetative. Treatment is with non-narcotic analgesics. In the acute period, UHF therapy, ultraviolet radiation, ultrasound, diadynamic currents, modulated sinusoidal currents, moderate heat on painful areas are used. During the period of remission, electrophoresis with novocaine or calcium chloride is indicated on the painful zones. To eliminate the focus of inflammation, phonophoresis with hydrocortisone and anti-infective drugs are used. Clinically characterized by intense pain in the upper and lower jaws. Occurs when the upper or lower dental plexus is damaged. For treatment, local anesthetics are used, in particular non-narcotic analgesics (for example, 5-10% lidocaine or anesthesin ointment 3-10 times a day, depending on the intensity of pain). Vitamin preparations are also prescribed. Physiotherapy methods refer to additional methods of treatment. Etiology - herpes zoster virus. There are several forms of the disease: diffuse pain, localized in the face and head (shell symptom complex); acute stage of neuralgia; early and late postherpetic neuralgia. Early postherpetic neuralgia is characterized by a duration of clinical manifestations of up to 6 months, late - from six months to several years. Manifestations are distinguished by a sudden onset. Characteristic is general malaise, fever, headaches. The duration of this period is no more than 3 days. Then the acute stage of the disease begins, characterized by the appearance of intense pains of a burning nature in the areas of innervation of the ophthalmic and maxillary nerves. In more rare cases, the localization of pain covers the zones of innervation of all branches of the trigeminal nerve. Pain is accompanied by swelling and itching of the skin of half of the face on the side of the lesion. After about 5 days, herpetic eruptions appear in the areas of innervation of the damaged branches, the location of which corresponds to the localization of pain. After 1-2 weeks, the herpetic vesicles dry up, crusts appear in their place, which subsequently fall off. An objective examination on the affected half of the face determines hypesthesia, hyperesthesia, hyperpathia. After 3-6 weeks, the manifestations of the disease disappear without a trace. In the treatment, non-narcotic analgesics, interferon, deoxyribonuclease, etc. are used. 26. Neuritis of the facial nerve Most often, neuritis of the facial nerve is caused by a variety of infectious agents against the background of cooling, hypertension, trauma, atherosclerosis of the cerebral vessels, etc. In the case of impaired blood circulation in the vertebral artery, an isolated lesion of the facial nerve is observed. Neuritis can be a complication of such diseases as otitis, parotitis, pathological processes of the base of the brain, in particular, the presence of a focus of inflammation. There is a possibility of sudden development of facial paralysis during anesthesia of the inferior alveolar nerve. Clinic. Usually, neuritis of the facial nerve occurs acutely with the appearance of paralysis or paresis of the facial muscles. More often only one side is affected, only 2% of cases of the disease have bilateral symptoms. Initially, there may be mild pain and paresthesia in the area of the mastoid process and auricle. They precede the development of movement disorders by 1-2 days or occur simultaneously with them. The defeat of the node of the knee of the facial nerve causes the appearance of the most intense pain. Other clinical manifestations of neuritis depend on the level of damage to the facial nerve. Damage to the nucleus provokes the occurrence of isolated paralysis (paresis) of facial muscles. The combination with symptoms of damage to the vestibulocochlear nerve indicates damage to the facial nerve root at the exit from the brain stem. There is a nerve lesion inside the pyramid of the temporal bone to the place where the large stony nerve originates. In this case, xerophthalmia (dry eye), impaired salivation, taste, and hyperacusis join the paralysis of facial muscles. In case of damage to the facial nerve below the place of origin of the large stony nerve, but above the origin of the stapedial nerve, instead of xerophthalmia, lacrimation is observed. The absence of hyperacusis indicates nerve damage after the stapedial nerve has passed. The presence of motor disorders is observed with damage at the exit from the stylomastoid foramen. Treatment. Initially, it is necessary to find out the cause of the disease and eliminate it with the help of a complex of therapeutic measures that affect not only the etiological factor itself, but also all links in the pathogenesis of the disease. It is necessary to prescribe anti-inflammatory drugs, antispasmodics, vasodilators. In case of severe pain syndrome, analgesics are used. To eliminate the inflammatory component, glucocorticoid preparations, such as prednisone, are used. The next goal of the therapy is to accelerate the processes of regeneration of nerve fibers, restore their conductivity. Prevention of atrophy of mimic muscles and development of contractures is carried out. As additional methods of treatment, physiotherapeutic methods are used, such as UHF therapy, ultrasound with hydrocortisone of the affected half of the face and mastoid process. 27. Sciatica The defeat of the roots of the spinal nerves, which is characterized by the appearance of pain, as well as a disorder of the sensitivity of the radicular type, less often - peripheral paresis and paralysis. Peripheral muscle paralysis develops as a result of damage to the anterior roots of the spinal cord. In most cases, the causes that provoke the development of radiculitis are trauma, inflammation, various neoplasms, osteochondrosis of the spinal column, disc herniation, discosis. Clinic. The clinical picture of radiculitis includes symptoms of damage to both the anterior and posterior roots of the spinal cord. Initially, symptoms of damage to the sensitive (posterior) roots appear. The radicular symptom complex includes symptoms of irritation and prolapse. In the early stages of the development of the disease, symptoms of irritation appear. Clinically, the symptoms of irritation are characterized by an increase in periosteal and tendon reflexes, the appearance of pain, paresthesia, and hyperesthesia of superficial types of sensitivity. Symptoms of prolapse include weakening of the tendon and periosteal reflexes up to their complete disappearance, segmental hypesthesia, or anesthesia. Damage to the roots can manifest itself with a variety of symptoms: a symptom of Lasego, Bekhterev, Dejerine, etc. Lesions of the roots cause disturbances in sensitivity, movements and reflexes of the segmental type. Trophic disorders are also possible. The stage of the disease and the localization of the pathological process affect the change in the composition of the cerebrospinal fluid. The initial stage of sciatica is characterized by irritation of the roots, which explains the increase in the number of cellular elements in the cerebrospinal fluid. With the progression of the disease, the pathological process passes to the radicular nerve. Swelling of the nerve develops, the amount of protein increases, there is an increased or normal cytosis. Often the clinical picture of radiculopathy is accompanied by meningeal symptoms. In case of accession of meningeal symptoms, meningora-diculitis is diagnosed. The clinical picture of sciatica is characterized by asymmetry of symptoms. Ganglioradiculitis develops when the pathological process spreads to the spinal ganglion. Clinically, this disease is characterized by the addition of shingles to the symptoms of radiculopathy, which, upon objective examination, is manifested by the presence of a herpetic rash in areas receiving innervation from the fibers of the affected roots. Pain with radiculopathy is called radicular. Strengthening of radicular pain can be caused by coughing, sneezing, lifting weights, straining during the act of defecation, as well as turning the torso and tilting. During the performance of these actions, there is an increase in intraradicular hypertension, which explains the increase in pain. The basis for increased pain are microcirculatory disorders, as well as swelling of the roots and their vaginas. Pain symptoms and pain points are detected with an artificial increase in intraradicular hypertension. The most common symptom of lumbosacral sciatica is the appearance of pain in the lumbar region, as well as the lower limb. Since the sciatic and femoral nerves are formed by fibers of the roots of the lumbar and sacral spinal cord, pain can be localized along these nerves. Usually, pain in the lower limb is localized on the back of the thigh, in the popliteal fossa, foot, fingers, i.e., corresponds to the course of the sciatic nerve. 28. Neuralgia of the external nerve of the thigh With neuralgia of the external cutaneous nerve of the thigh, pain is localized on its outer surface. Neuritis of the femoral nerve is characterized by symptoms of Wassermann's tension and Matskevich. It is necessary to conduct a differential diagnosis with arthrosis-arthritis of the hip joint. A distinctive feature of this disease is the pain that occurs during rotation and abduction of the hip, localized in the region of the hip joint. An additional method of differential diagnosis is an X-ray examination of the hip joint, showing the presence of pathological changes in the acetabulum and femoral head. The characteristic distinguishing features of coxitis are pain during abduction and extension of the hip, limited mobility in the hip joint, changes during x-ray examination. Treatment. During an exacerbation of the disease, rest is shown, as well as the necessary painkillers. The patient is assigned to bed rest until the cessation of acute pain. In this case, the patient should be located on a non-bending bed. It is possible to use local heat in the form of a heating pad, which has a positive therapeutic effect. It is possible to use local procedures, such as banks, mustard plasters, rubbing. Ointments with snake or bee venom included in their composition have a good effect. Produce rubbing these ointments in the localization of pain. Vitamin therapy B1 and B12 is used. In the period of exacerbation of the disease, physiotherapeutic treatment is used: UV irradiation and diadynamic currents on the lumbar region, buttock, core, lower leg. To stop the pain syndrome, hydrocortisone blockades are used, which can be intradermal, subcutaneous, radicular, muscular and epidural. With intradermal novocaine blockade, 0,25-0,5% novocaine is introduced into the lumbar region paravertebral until a lemon peel is formed. At the end of the acute period, traction therapy is used, i.e. traction treatment, with the help of the patient's own body weight or with the help of additional devices. In addition to the above methods, physical therapy, a variety of baths, mud therapy, etc. are used. In the case of prolonged pain syndromes, they resort to the use of sedatives and antidepressants. In the case of a persistent pain syndrome that does not go away after the above measures, pronounced movement disorders, it is possible to use surgical types of treatment. Prolapse of the intervertebral disc, leading to compression of the radicular-spinal artery, pelvic disorders, paralysis and paresis, is an indication for urgent surgical intervention. 29. Cervical radiculopathy and thoracic radiculopathy The clinical picture is dominated by pain syndrome of the type of lumbago. The provoking factor in the occurrence of pain syndrome is physical activity or awkward movement. In this case, the pain occurs suddenly, while the head is set in a forced position. Usually the pain radiates to the forearm and suprascapular region. The appearance of paresthesia in various areas of the upper limb is characteristic. Most often, paresthesias are localized in the fingers. Coughing, sneezing, sudden movements of the head, stress on the cervical spine, abduction or lifting of the affected arm cause an increase in pain. An objective examination in areas receiving innervation from the fibers of the affected root determines hypesthesia or anesthesia (in more rare cases). Perhaps the development of hypotension of the muscles of the affected upper limb. The roots of OVI-OVII are most often affected in the cervical spine. The defeat of these roots leads to a decrease in reflexes, both tendon and periosteal. The most common compression lesion of the cervical roots. With a compression lesion of the roots of OVI and OVII, the clinical picture will be different. Compression radicular syndrome at the level of OVI is manifested by a violation of sensitivity in the area of the skin that receives innervation from its fibers. This area covers the space from the neck and shoulder girdle to the first finger of the affected limb. Sensitive disturbances are shown in the form of pain, paresthesia, then hypesthesia develops. The biceps muscle of the shoulder is also involved in the pathological process, which is manifested by its weakness and hypotrophy, and a decrease in the tendon reflex. Compression lesion of the root of the cervical spinal cord at the level of CV1I is also manifested by a violation of sensitivity in the form of pain and paresthesia in the area receiving innervation from the fibers of this root. In this case, the violation of sensitivity is localized in the area from the neck and shoulder girdle to the II and III fingers of the affected upper limb. The pain syndrome often captures the area of the scapula from the affected side. A distinctive feature of the compression lesion of the CVII root is atrophy and weakness of the triceps muscle of the shoulder, as well as a decrease or complete disappearance of the reflex from its tendon. Simultaneous compression lesion of the cervical roots OVI and OVII is manifested by hypotrophy of the muscles of the forearm and hand. The muscles located in the tenor area are especially affected. The course of the disease can be complicated by the addition of vascular insufficiency of the vertebrobasilar system, as well as spinal disorders. With cervical radiculopathy, the pain syndrome usually lasts 1,5-2 weeks. Therapeutic tactics includes the same principles as in the treatment of lumbosacral sciatica. A feature of the treatment of cervical radiculopathy is traction of the cervical spine. For this purpose, a Glisson loop and a fabric-cotton collar are used. 30. Symptoms of damage to the radial nerve This pathology is more common than other lesions of the nerves of the upper limb. Nerve damage is caused by a number of reasons. The nerve can be affected during sleep if the patient sleeps on a hard surface, while putting his hand under his head or under his torso. Basically, such a lesion occurs during deep sleep, which may be associated with intoxication or fatigue. This is the so-called sleep paralysis. Also, neuropathy of the radial nerve can occur under the influence of prolonged compression by a crutch or tourniquet as a result of fractures of the humerus. In some cases, radial neuropathy can occur due to improper injection technique into the outer surface of the shoulder, which can occur when the nerve is abnormally located. In quite rare cases, factors that provoke damage to the radial nerve can be diseases (such as influenza, pneumonia, typhus, etc.) or intoxication (for example, alcohol or lead poisoning). The function of the radial nerve is mixed. The motor fibers included in its composition innervate the extensor muscles of the forearm, which include triceps, ulnar muscle, hand muscle: radial extensor of the wrist (short and long), extensor of the fingers, extensor of the little finger, long muscle that abducts the thumb, arch support. Innervating the above muscles, the nerve performs the following motor functions: extension in the elbow joint, in the wrist joint, extension of the main phalanges of the fingers, abduction of the thumb, supination of the hand. With damage to the radial nerve at different levels, different clinical manifestations will be noted. The radial nerve can be affected in the armpit, upper third, middle third, and lower third of the shoulder. Damage to the nerve in the armpit and upper third of the shoulder leads to the development of paralysis of the muscles that receive innervation from its fibers. The following clinical picture is characteristic: the hand droops when the hand is raised, the first finger of the hand is brought to the second. The patient cannot straighten the forearm and hand, as the function of the extensor muscles is impaired. It is noted the impossibility of abduction of the first finger of the hand, supination of the forearm. Examination reveals a loss of the ulnar extensor reflex, as well as a decrease in the caroradial reflex. All types of sensitivity on the skin of the I, II and half of the III fingers of the hand are violated. Sensitivity disorders are most often expressed in the form of paresthesias. Damage to the radial nerve in the region of the middle third of the shoulder is clinically characterized by the preservation of the extension of the forearm, as well as the ulnar extensor reflex. Sensitivity on the skin of the shoulder is preserved. The defeat of the ulnar nerve ranks second in frequency among the lesions of all nerves that make up the brachial plexus. In most cases, the cause of neuropathy of the ulnar nerve is its compression in the area of the elbow joint. In addition to compression, ulnar nerve neuropathy can be caused by a fracture of the medial condyle of the shoulder or supracondylar fractures. 31. Symptoms of damage to the axillary and muscular skin The axillary nerve in its function is mixed. The motor fibers of the nerve innervate the deltoid and teres minor muscles. Sensory fibers of the axillary nerve are part of the upper lateral cutaneous nerve of the shoulder and innervate the skin of the outer surface of the shoulder. Damage to the axillary nerve is possible under the influence of a number of reasons. In most cases, axillary neuropathy is caused by an injury, such as a fracture or dislocation of the shoulder, a gunshot wound, prolonged compression of the nerve fiber (for example, with a crutch), incorrect position of the shoulder during sleep or anesthesia, etc. Clinically, the defeat of this nerve is characterized by the fact that the patient cannot take his hand to the horizontal level, which is explained by the development of paralysis and atrophy of the deltoid muscle. There is laxity in the shoulder joint. The sensitivity of the skin of the outer surface of the upper third of the shoulder is also disturbed. In its function, this nerve is mixed. The motor fibers that make up the musculocutaneous nerve innervate the biceps, shoulder and coracobrachial muscles. Sensitive nerve fibers innervate the skin on the outer surface of the forearm. The musculocutaneous nerve includes branches of the lateral nerve of the forearm. With damage to the musculocutaneous nerve, atrophy of the biceps brachii, brachialis, and coracobrachial muscles is noted. There is a loss of the flexion-elbow reflex, as well as a violation of all types of skin sensitivity on the radial surface of the forearm and tenor. 32. Neuropathy of the median nerve Median nerve neuropathy is less common than ulnar nerve injury. Neuropathy can be the result of an injury to the upper limb, nerve damage in the event of a violation of the technique of intravenous injection into the cubital vein, incised wounds of the palmar surface of the forearm above the wrist joint, as well as overexertion of the hand of a professional nature. The function of the median nerve is mixed. The motor fibers of the median nerve innervate the following muscles of the upper limb: the radial flexor of the hand, the long palmar muscle, the flexor of the fingers (superficial and deep), the flexors of the first finger of the hand (long and short), the round and square pronator, the muscle that removes the thumb, and also muscle that opposes the thumb to the hand. Due to the fact that the median nerve innervates the above muscles of the upper limb, when they contract, the following types of movement are carried out: flexion and extension of the II and III fingers in the region of their middle and distal phalanges, flexion of the I finger in the region of its distal phalanx, opposition of I fingers of the hand to the rest of the fingers, pronation of the forearm. Some types of movements are carried out through the innervation of certain muscles by the median nerve together with the ulnar. These types of motor acts include palmar flexion of the hand, flexion of the fingers in the area of their proximal and middle phalanges, with the exception of the thumb. The composition of the median nerve includes sensory fibers that innervate the skin on the radial surface of the hand, the palmar surface from fingers I to IV of the hand, and the back surface of the distal phalanges of these fingers. Damage to the median nerve leads to a violation of pronation, a violation of palmar flexion of the hand, as well as I, II and III fingers. There is a violation of the extension of the II and III fingers in the area of their distal phalanges. The patient loses the ability to bend I, II and III fingers when trying to clench his hand into a fist. The impossibility of opposing the thumb of the hand to the rest is characteristic. Violation of sensitivity is usually localized on the palmar surface of the hand, the same surface of I, II, III and part of the IV fingers, as well as on the back surface of the distal phalanges of the second, third and partially IV fingers of the hand. In most cases, the appearance of pain of a causal nature is characteristic. The atrophy of the muscles of the hand is determined, especially pronounced in the tenor area. As a result of atrophy, the first finger of the hand is installed with the second finger in the same plane. The so-called monkey paw develops. Also, due to atrophy, the impossibility of the thumb to bend when trying to clench the hand into a fist is noted. Vegetovascular disorders are observed, manifested in the form of pallor and cyanosis of the skin, brittle nails, the appearance of erosion and ulcers, impaired sweating, etc. Treatment. Initially, conservative methods of treatment are used, such as B vitamins, anticholinesterase drugs, and physiotherapy. 33. Symptoms of damage to the femoral nerve and parasthesia of the thigh The function of the femoral nerve is mixed. It consists of motor and sensory fibers. The motor fibers of the femoral nerve innervate a number of muscles of the lower limb. These muscles include the iliopsoas, quadriceps femoris, and sartorius. All these muscles, when contracted, perform certain functions that are impaired when the femoral nerve is damaged. The iliopsoas muscle flexes the hip at the hip joint. The quadriceps femoris flexes the thigh and also extends the lower leg. Contraction of the sartorius muscle causes flexion of the lower limb at the knee and hip joints. The sensory fibers of the femoral nerve are part of the anterior cutaneous branches of the femoral nerve and the saphenous nerve. The anterior cutaneous branches innervate the skin on the anterior surface of the two lower thirds of the thigh. The saphenous nerve innervates the anterointernal surface of the lower leg. Damage to the femoral nerve can be localized above the inguinal ligament or below it. With damage to the femoral nerve below the inguinal ligament, a prolapse of the knee reflex, atrophy of the quadriceps femoris muscle, impaired leg extension, and disorders of all types of sensitivity in the area of dermatomes that receive innervation from the saphenous nerve are observed. With damage to the femoral nerve above the inguinal ligament, all of the above symptoms are observed, to which are added manifestations of dysfunction of the iliac psoas muscle. The patient complains of difficulty while walking and running, which is associated with the impossibility of bringing the thigh to the stomach. In addition, there is a violation of all types of sensitivity on the skin of the anterior surface of the thigh. In addition to all these clinical manifestations, there is a symptom of Matskevich and a symptom of Wasserman. Matskevich's symptom is that when the shin of the affected limb is bent, the patient, who is in the prone position, has pain in the anterior surface of the thigh. Wasserman's symptom is manifested by the appearance of pain in the case of raising the outstretched leg up in a patient lying on his stomach. In this case, the pain is localized on the anterior surface of the thigh. With neuralgia of the cutaneous nerve of the thigh or with its neuritis, the appearance of paresthesia in the skin of the thigh is noted. In most cases, this pathology is unilateral. Manifestations of the disease are attacks of paresthesia, manifested by a burning sensation, numbness, tingling with localization in the skin of the outer surface of the thigh. With prolonged standing or walking, paresthesias intensify. Strengthening these sensations requires immediate stop and rest of the affected limb. If you continue walking, paresthesia can turn into burning pain. Attacks of paresthesia occur as a result of pressing the cutaneous nerve of the thigh with a bandage or belt near the anterior superior iliac bone. Most often, hip paresthesia develops in old age. A necessary condition for achieving a positive therapeutic effect is the elimination of the immediate cause that led to the development of hip paresthesia. It is necessary to carry out symptomatic treatment, including the appointment of noshpa, papaverine, massage and thermal procedures are also used. 34. Symptoms of damage to the sciatic and tibial nerves The sciatic nerve in its function is mixed. Of all the peripheral nerves, the sciatic nerve is the largest. The sciatic nerve leaves the pelvic cavity between the ischial tuberosity and the greater trochanter of the femur, where the ischial foramen is located. After that, the sciatic nerve passes along the back of the thigh, heading into the popliteal fossa. Passing along the back of the thigh, the nerve gives off a number of branches that innervate a number of muscles. These muscles are the biceps femoris, the semitendinosus, and the semimembranosus. These muscles flex the lower leg and rotate it inward. In the event that the sciatic nerve is affected high, then the function of the tibial and peroneal nerves is impaired. The loss of their functions is clinically manifested by anesthesia of the skin in the region of the lower leg and foot, peripheral paralysis of the foot and its fingers, as well as the disappearance of the Achilles reflex. In addition, it is noted the impossibility of bending the lower leg of the affected limb. Since the sciatic nerve is mixed, in addition to motor and sensory, it also includes autonomic fibers. This explains the presence of a number of autonomic disorders in lesions of the sciatic nerve. On palpation of the affected limb, a sharp soreness is determined, localized along the sciatic nerve, as well as its branches. The most intense pain sensations are located in places that are poorly covered by soft tissues. On palpation, during the application of irritation, pain sensations radiate up and down along the course of the nerve. According to the function performed, the tibial nerve is mixed. The motor fibers of the nerve innervate a number of muscles of the lower extremity, such as the triceps muscle of the lower leg, the flexors of the foot (long and short), the flexors of the big toe (long and short), the muscle that abducts the big toe, and the posterior tibial muscle. With damage to the tibial nerve, all movements performed during the contraction of the above muscles of the lower limb are violated. Sensory fibers of the tibial nerve are part of the lateral dorsal cutaneous nerve, as well as the lateral and medial plantar nerves. As part of the cutaneous nerve, sensory fibers innervate the skin on the back of the leg. As part of the plantar nerves, sensory fibers innervate the skin of the sole and fingers. The defeat of the tibial nerve is characterized by the following clinical manifestations: the patient cannot produce plantar flexion of the foot and fingers on the affected limb, the impossibility of turning the foot inward is noted, the foot and fingers of the affected limb are in an extended state, this position is called the heel foot. In addition, the patient does not have the ability to rise on the toes of the affected lower limb and steps on the heel when walking. In addition to motor, sensory disorders are also observed. Violated all types of sensitivity on the skin of the back of the leg, sole and finger. In the big toe of the affected limb, there is a loss of muscular-articular feeling. 35. Clinical symptoms of lesions of the tibial, superior gluteal, inferior gluteal and posterior bone nerves This nerve is mixed in its function. The common peroneal nerve divides into two terminal branches, which are the deep and superficial peroneal nerves. Motor fibers are part of both terminal branches of the common peroneal nerve. The superficial peroneal nerve (namely, its motor fibers) innervates the peroneal muscles (long and short). During contraction, these muscles abduct the foot outward and raise its lateral edge. The motor fibers of the deep peroneal nerve innervate the muscles that penetrate the foot. These muscles are the extensors of the foot and the extensors of the fingers. Sensory fibers of the common peroneal nerve innervate the skin on the outer surface of the lower leg and the dorsum of the foot. The defeat of the common peroneal nerve leads to the impossibility of extension of the foot and fingers, and the impossibility of rotating the foot outward is also noted. On examination, a picture of a "horse foot" is observed. It is characterized by pronation and a slight inward turn. In this case, the toes are in a bent position. When walking, the patient is unable to stand on his heel, while he touches the floor with the fingers of the affected foot. To avoid touching the floor with a finger, the patient raises his leg high when walking. When lowering the affected limb, the patient first touches the floor with the toe, the lateral edge of the foot, and then with the entire sole. On the skin of the outer surface of the lower leg and the dorsum of the foot, there is a violation of all types of sensitivity. Since with damage to the common peroneal nerve, the function of the tibial nerve is preserved, there is no violation of the musculo-articular feeling in the toes. The Achilles reflex also remains intact. The superior gluteal nerve is motor in function. Its fibers innervate the middle and small gluteal muscles, as well as the muscle that stretches the fascia lata. With the contraction of the above muscles, the thigh is abducted outward. The defeat of the superior gluteal nerve causes a violation of this movement. In the case of bilateral nerve damage, the patient sways to the sides when walking. This violation is called duck gait. In its function, the lower gluteal nerve is motor. Its fibers innervate the gluteus maximus muscle. The contraction of the fibers of this muscle causes the hip to be abducted posteriorly, as well as the trunk to be straightened from a bent position. Damage to the lower gluteal nerve is manifested by difficulty or inability to perform these movements. According to its function, this nerve is sensitive. Its fibers innervate the skin in the region of the lower buttocks, as well as the back of the thigh. Damage to the posterior cutaneous nerve of the thigh is clinically manifested by a violation or complete loss of all types of sensitivity in the zones of its innervation. 36. Clinical symptoms of lesions of the sciatic and tibial nerves Clinically, this pathology is manifested by the development of paresis or paralysis of the foot and fingers, the flexion of the affected lower limb in the knee joint is disturbed, the Achilles reflex is weakened or completely disappears. In addition to motor disorders, sensory disorders are also noted with sciatic neuritis. On the skin in the area of the posterior surface of the lower leg and the dorsal surface of the foot, there is a violation of superficial types of sensitivity of a peripheral nature. Sharp pain is noted along the sciatic nerve. In addition, the appearance of trophic and vegetative disorders in the affected limb is characteristic. On palpation, a sharp pain along the sciatic nerve is determined. Soreness is located in the points of Balle. These points are located under the gluteal fold (the exit point of the sciatic nerve), on the back of the thigh (popliteal fossa), on the dorsal surface of the foot. For a correct diagnosis, it is necessary to determine the presence of symptoms of tension on the nerve trunks. Neri's symptom is the appearance of pain in the lumbar region that occurs when the patient's head is bent. Symptom Lasego consists of two phases. The first phase is characterized by the appearance of pain in the lumbar region when the patient's outstretched leg is raised. The second phase of the symptom is the disappearance of pain when the patient's leg is bent in the knee joint. Bonnet's symptom: when the lower limb is adducted, pain occurs in the lumbar region or along the sciatic nerve. Symptom Sika-ra is detected when the patient's foot is flexed or unbent and is characterized by the appearance of pain in the popliteal fossa. Vilenkin's symptom occurs with strong percussion in the gluteal region and is manifested by the appearance of pain localized along the sciatic nerve. With this pathology, the drooping of the foot of the affected limb is noted, the impossibility of unbending the foot and fingers. The patient, when walking, cannot stand on his heel and therefore stands on the toes. In addition to motor disorders, there is a violation of sensitivity, localized on the skin in the area of the outer surface of the lower leg, the dorsal surface of the foot, as well as I and II fingers. Usually, neuritis of the common peroneal nerve is caused by trauma, dislocation of the knee joint, as well as various intoxications, such as alcohol, arsenic, and lead. With this pathology, there is difficulty or impossibility of plantar flexion of the foot and fingers on the affected limb. On examination, the foot is elevated. When walking, the patient cannot stand on the toes and therefore leans on the heel. In addition to these disorders, there is hypotension of the calf muscles, as well as their atrophy. There is a loss of the Achilles reflex. On the skin in the area of the posterior surface of the lower leg and the sole of the foot, sensitivity disorders are noted, as well as pain of a burning, unbearable nature. 37. Reasons for the development of a brain abscess A brain abscess is a local accumulation of pus located in the brain tissue. Usually, a brain abscess occurs as a secondary disease, provided there is an infectious focus located outside the central nervous system. Mandatory is the penetration of an infectious agent into the brain. At the same time, not one, but several abscesses can exist. Etiology and pathogenesis. Most often, the causative agents of a brain abscess are the following microorganisms: streptococci, staphylococci, E. coli, fungi, toxoplasma, in more rare cases, an abscess is caused by anaerobic bacteria. According to their pathomorphology, brain abscesses are divided into encapsulated (interstitial) and non-encapsulated (parenchymal). Interstitial abscesses are characterized by the presence of a connective tissue capsule. The capsule separates the area of the abscess from the brain tissue. Usually the capsule is quite well expressed and contains a large number of glial elements. Parenchymal abscesses do not contain a connective tissue capsule. With regard to the prognosis and clinical course, parenchymal abscesses are less favorable, since the accumulation of pus has no boundaries and freely passes into the brain tissue. The pathological appearance of an abscess depends on the reactivity of the affected organism and the virulence of the infectious agent. Interstitial abscesses are formed in case of low virulence of the infectious agent and high resistance of the organism. Parenchymal abscesses occur with low reactivity of the affected organism and high virulence of the infectious agent. There are several mechanisms for the development of brain abscesses: metastatic, contact, traumatic. The metastatic mechanism of occurrence is characterized by the ingress of an infectious agent from an existing purulent focus by the hematogenous route. Purulent foci can be abscesses located on the neck, thigh or foot, osteomyelitis, purulent inflammatory diseases of the lungs and pleura. The contact mechanism of the development of a brain abscess is characterized by the transition of a purulent process from the foci located in the formations of the skull to the brain tissue. These abscesses include otogenic and rhinogenic. Otogenic abscesses are usually a complication of diseases such as mastoiditis, purulent otitis media. Rhinogenic abscesses of the brain are a complication of purulent inflammatory diseases of the paranasal sinuses. In addition, a contact abscess can be a complication of purulent diseases of the orbit, oral cavity and pharynx. The traumatic mechanism of the occurrence of a brain abscess occurs in very rare cases. The cause of a traumatic abscess is a traumatic brain injury, due to which the infectious agent penetrates the crushed brain tissue and causes the development of local purulent inflammation. The occurrence of an abscess in the case of a closed craniocerebral injury is explained by autoinfection. At the same time, its own microflora, which acquires virulent properties, acts as an infectious agent. 38. Clinical picture of brain abscess During the development of an abscess, four stages are distinguished: initial, latent, explicit and terminal. The entire clinical picture of an abscess is characterized by the presence of the following groups of symptoms: general infectious, cerebral, focal. The initial stage (meningoencephalic) is characterized by damage to the meninges in a limited area. There is a gradual spread of the focus from the meninges to the adjacent area of brain tissue. There is a formation of a limited abscess. Clinically, the initial stage is characterized by a progressive deterioration of the patient's condition and symptoms of intoxication (fever, chills). In addition, there are symptoms of irritation of the meninges, which include headache, Kernig's symptom, as well as upper, middle and lower Brudzinski's symptoms. Then the second stage of the abscess develops - latent, which pathomorphologically is characterized by the delimitation of the necrosis zone and the formation of a connective tissue capsule, manifested by the absence of symptoms. The asymptomatic course of the second stage of the abscess is associated with the activation of various adaptive-compensatory mechanisms of the affected organism. In some cases, patients still complain of weakness, fatigue, apathy, decreased ability to work, etc. The latent stage can last up to several months. In the event of decompensation, the development of the third stage of a brain abscess occurs - an explicit stage (neurological). At this stage, there is swelling of the brain and swelling of its substance. In this case, the circulation of cerebrospinal fluid, which was formed as a result of the latent stage, is disturbed. The brain abscess begins to put pressure on the brain structures, which, in turn, leads to an increase in intracranial pressure. These changes contribute to increased headache. In this case, the pain may become permanent. There is an increase in headache in the morning. Localization of pain depends on the location of the abscess. In the case of a breakthrough of pus from the focus of the abscess into the ventricles of the brain, psychomotor agitation of the patient is noted. A distinctive feature of the cerebellar abscess is the presence of the following clinical symptoms: impaired coordination of movements, adiadochokinesis (mainly on the side of the focus), ataxia, nystagmus, hypertension syndrome. The explicit stage of a brain abscess develops in a fairly short period of time (7-8 days). In the absence or incorrect tactics of treatment, a breakthrough of pus into the subarachnoid space or into the ventricles of the brain may occur. In this case, the development of secondary meningitis or purulent ventriculitis occurs. The spread of pus in the medulla leads to damage to the brain stem structures, which is manifested by a dysfunction of the vasomotor and respiratory centers of the medulla oblongata. This determines the onset of the terminal stage of the course of a brain abscess, which in most cases leads to death. 39. Diagnosis and treatment of brain abscess Diagnosis includes a correct and complete history taking, an objective examination and additional methods (instrumental and laboratory). It is necessary to determine the presence in the body of chronic foci of infection, previous craniocerebral injuries, as well as the presence of general infectious, cerebral and local symptoms of a brain abscess. It is necessary to conduct an x-ray examination of the skull, paranasal sinuses. Echoencephalography is essential for making a diagnosis. In this study, in the case of the location of the abscess in the hemisphere, the displacement of the median structures of the brain is determined. Diagnostically valuable is the method of abscessography. In this type of study, air is used, as well as heavy water-soluble contrast agents. The method of abscessography determines the localization of the focus of the abscess, its shape and size. The most informative diagnostic method is computed tomography. With its help, it is possible to carry out differentiation with a tumor formation. Treatment. There are both surgical and conservative methods of treatment of brain abscess. In some cases, despite the fact that surgery is considered the only correct method of treating this pathology, one has to resort to drug therapy. Indications for surgical treatment is the formed abscess capsule, which occurs on the fourth or fifth week after the first signs of pathology are detected, as well as the threat of wedging. The following types of surgical treatment are used: craniotomy, percutaneous abscess drainage. The indication for craniotomy is a large (or multiple) brain abscess. In most cases, an abscess is removed from the brain tissue along with its capsule. The operation is complemented by the introduction of fairly large doses of antibiotics to the patient. Drainage of the focus of the abscess is carried out under the mandatory control of computed tomography. The abscess is drained through a burr hole in the skull. This method of treatment is considered the only correct one if the focus of the abscess is located deep enough in the brain or in its functionally significant area. According to the indications, it is possible to re-drain the affected area. Contraindications to surgical treatment are multiple inoperable brain abscesses, abscesses at the stage of encephalitis, deeply located abscesses. Antibiotic preparations are used as a conservative treatment. The course of antibiotic therapy is usually 6 to 8 weeks. Initially, broad-spectrum antibacterial drugs are prescribed. Then (after receiving the results of a bacteriological study of the cerebrospinal fluid), drugs are prescribed taking into account the sensitivity of the isolated infectious agents. In the case of streptococcal lesions or lesions of the majority of anaerobic microorganisms, benzylpenicillin sodium salt (penicillin G) is prescribed. 40. Extradural abscess Extradural abscess usually has a contact mechanism of occurrence. The source of infection in most cases is osteoperiostitis, a carious process located in the wall of the paranasal sinus, which can occur with their chronic inflammation (frontitis, ethmoiditis, sphenoiditis). The onset of the disease is characterized by the appearance of a limited focus of inflammation in the region of the dura mater, namely its outer layer. Inflammation takes on the character of purulent or necrotic. The pathological process is gradually progressing. Over time, a purulent focus is formed between the skull bone and the dura mater. It is usually delimited from surrounding tissues by granulation tissue and adhesions. Localization of extradural abscess may be different. In the case of frontal sinusitis or ethmoiditis, the purulent focus is located in the anterior cranial fossa. With sphenoiditis, it is located in the middle cranial fossa. The main complaint of extradural abscess is headache. In some cases, it is mistaken for an exacerbation of chronic sinusitis. Often this disease occurs without any symptoms, and its detection is accidental, which occurs during various operations on the paranasal sinuses. The absence of symptoms in this case is due to the fact that the abscess is emptying into the paranasal sinus through a fistula. In some cases, the emptying of the abscess does not occur, and it gradually increases in volume. This increase leads to an increase in intracranial pressure and the appearance of the following symptoms: headache, nausea, vomiting, congestion in the optic nerve head, bradycardia. As a result of an increase in intracranial pressure, compression of the olfactory tract and olfactory bulb can occur, with a violation of the olfactory function. The abducens, facial, trigeminal, glossopharyngeal, and vagus nerves may also be affected. This leads to hypotension of the muscles of the face, impaired eye abduction outward on the affected side, reduction or complete loss of the corneal reflex, paresis of the muscles of the soft palate. The causes of a subdural abscess are varied. It can develop when an extradural abscess passes through the dura mater, can have a hematogenous mechanism of occurrence, and can also be a complication of exacerbated chronic sinusitis. In the subdural space, the abscess is limited to adhesions of the arachnoid, as well as connective tissue and glial elements. If untreated, the pathological process can spread to the entire surface of the meninges, which leads to the development of diffuse leptomeningitis. The occurrence of a subdural abscess leads to an increase in intracranial pressure. The clinical picture is characterized by signs of involvement in the pathological process of the meninges and brain tissue. In blood tests, an increase in ESR and neutrophilic leukocytosis are noted. In the study of cerebrospinal fluid, an increase in protein and cellular elements is determined. Treatment. Use surgical treatment of these abscesses. 41. Epilepsy Epilepsy is a chronic disease that manifests itself with repeated, convulsive or other seizures, loss of consciousness and is accompanied by personality changes. Epilepsy is either primary or secondary. There is also an epileptic syndrome resembling epilepsy. The basis of the disease is increased convulsive readiness. It is due to the peculiarities of metabolic processes in the brain. The development of epilepsy can be provoked by injuries, infections, intoxications and other environmental factors. The clinical picture includes major and minor convulsive seizures, vegetative-visceral and mental seizures, as well as mental disorders. Usually the onset of the disease occurs at the age of 5-15 years. Characterized by a progressive course. The frequency of seizures and their severity gradually increase. The nature of the seizures also changes. A grand mal seizure comes on suddenly. Usually there are no precursors of seizures, although in 1-2 days the state of health may worsen, sleep, appetite may be disturbed, and a headache may appear. In most cases, the seizure is preceded by an aura. Its character depends on the area of the brain that is irritated. The aura lasts for a few seconds. Then the patient loses consciousness and falls. Convulsions appear. Initially, they are tonic and last 15-20 seconds. Then the convulsions become clonic and last 2-3 minutes. Their frequency gradually decreases and general muscle relaxation occurs. This period is characterized by the expansion of the pupils, the absence of their reaction to light, involuntary urination can be observed. For several minutes the consciousness remains soporous, then it gradually clears up. Patients do not remember the seizure itself. After the seizure, the patient's condition is drowsy, lethargic. Small convulsive seizures are characterized by a short-term loss of consciousness. The patient does not fall. During this time, patients can make a variety of movements. Patients do not remember the course of the attack. Symptomatic epilepsy can occur with brain tumors, especially in the frontal and temporal lobes. These epilepsies are characterized by Jacksonian seizures. Status epilepticus is characterized by a series of seizures. The focal aura can be sensory, visual, olfactory, auditory, mental, vegetative, motor, speech and sensitive. The sensory aura is characterized by disturbances of the sense organs. With the visual aura, there is a vision of shiny balls, bright sparks, which is associated with damage to the occipital lobe. Complex visual hallucinations, macro- or micropsia, hemianopsia, amaurosis may appear. The olfactory aura occurs when the temporal lobe is affected. It is characterized by olfactory hallucinations, which are often combined with taste. The psychic aura is manifested by feelings of fear, horror, bliss or joy. The motor aura is manifested by the appearance of motor automatisms. The sensitive aura is characterized by the occurrence of paresthesias in various parts of the body. The treatment of epilepsy is individual, long-term, continuous and complex. After the cessation of seizures, treatment should continue for 2-3 years. The dosage of drugs is gradually reduced. The main thing is the appointment of anticonvulsants. 42. The concept and clinical symptoms of tumors of the nervous system Brain tumors are organic lesions of the central nervous system. Brain tumors are intracranial volumetric processes, which include lesions caused by cystic and granulomatous formations that have an infectious or parasitic etiology. Classification (L. O. Badalyan 1984). I. Neoplasms. 1. Primary: 1) gliomas (astrocytomas, astroblastomas, glioblastomas; oligodendrocytomas, oligodendroblastomas; ependymomas, ependymoblastomas, choroidcarcinomas, choroidpapillomas; medulloblastomas; ganglioneuromas, ganglioastrocytomas, neuroblastomas); 2) meningiomas, arachnoidendotheliomas, hemangiomas, angioreticulomas, angioreticulosarcomas; 3) neuromas, multiple neurofibromas; 4) congenital tumors - craniopharyngiomas, dermoids, teratomas; 5) pituitary tumors - adenomas, fibromas, angiomas, sarcomas, etc.; 6) tumors of the pineal gland - pinealoma, pineal neoblastoma; 7) gliomas of the optic nerve; 2. Metastatic (carcinomas; sarcomas). II. Parasitic cysts and granulomas. 1. Echinococcosis. 2. Cysticercosis. III. Inflammatory lesions of the brain. 1. Tuberculomas. 2. Syphilomas. 3. Cystic arachnoiditis. 4. Abscess of the brain. Brain tumors are manifested by cerebral and focal symptoms. Focal symptoms are the result of increased intracranial pressure, impaired CSF dynamics. Focal symptoms depend on the localization of the tumor, on compression and displacement of the brain tissue. Emotional disturbances, as a rule, are combined with autonomic-visceral dysfunction, which includes vasomotor lability, disorders of the cardiovascular system and the gastrointestinal tract. Headache is the main symptom that always occurs with brain tumors. Headache gradually increases in duration and intensity. In the later stages, it becomes permanent. Headache can be diffuse or localized in a specific area. The localization of the headache sometimes corresponds to the location of the tumor. A characteristic symptom of a brain tumor is vomiting. With volumetric processes of the brain, which are located subtentorially, vomiting is observed constantly. In this case, it can be considered as a focal symptom. Usually vomiting is not accompanied by nausea, often occurs at the height of the headache, and sometimes after vomiting the patient feels relief. With intracranial hypertension, in some cases, epileptiform seizures may appear, which are possible with brain tumors of various localizations. Sometimes they are the first symptom of a tumor. Quite often, pyramidal symptoms appear, and sudden hearing loss, respiratory distress, increased blood pressure, and tachycardia may occur. If the stage of the process goes far enough, then decerebrate rigidity develops. If there is a compression of the roof of the midbrain, then there is a violation of the coordination of the movements of the eyeballs. Upward gaze paralysis is also possible. 43. Methods of diagnosis and treatment of tumors of the nervous system Signs of intracranial hypertension can be determined during additional research methods. When examining the fundus, congestive nipples of the optic nerves are found, which is one of the earliest symptoms in tumors in the posterior cranial fossa. The consequence of stagnation in the fundus is the development of secondary atrophy of the optic nerve, which leads to a decrease in visual acuity. When the tumor is located in the cerebellar vermis, there is a violation of static coordination. Characteristic is a violation of gait: the patient staggers in both directions and often falls. Damage to the cerebellar hemispheres leads to ataxia in the limbs on the side of the lesion. Speech disorder is typical. It becomes scrambled, unevenly modulated. If the tumor compresses the bridge of the brain, then there are symptoms of damage to the V, VI, VII, VIII cranial nerves, which is manifested by a decrease in corneal reflexes, strabismus, diplopia, asymmetry of the nasolabial folds, as well as dizziness and tinnitus. Most brain stem tumors are gliomas. The initial stage of tumor development is characterized by alternating syndromes. Tumors in the midbrain are characterized by the development of oculomotor disorders, ptosis, diplopia, impaired convergence and accommodation, and strabismus. It is also possible to develop alternating syndromes of Weber, Benedict or Claude. When the roof of the midbrain is affected, paresis of the gaze up or down, vertical or convergent nystagmus, hearing loss and ataxia develop. With a tumor of the bridge, paresis of the gaze towards the lesion, alternating Miyar-Gubler and Fauville syndromes, ataxia and vegetative disorders develop. With tumors of the brain stem in the region of the IV ventricle, the clinical picture is characterized by symptoms of liquorodynamic disorders and attacks of occlusion, which are manifested by a sudden headache, vomiting, impaired consciousness, and a violation of the respiratory and cardiovascular systems. With greater accuracy, anamnestic data can indicate the localization of the process. Diagnostics also includes special clinical research methods. Examination of the fundus reveals varicose veins, narrowing of the arteries, and swelling of the optic nerve papilla. When conducting a lumbar puncture, increased pressure of the cerebrospinal fluid is revealed, and when it is examined, protein-cell dissociation is detected. When conducting electroencephalography, distinct changes are noted in the presence of tumors that are localized closer to the surface of the cerebral hemispheres. A radical method of treatment is surgical intervention, which is more effective in early diagnosis of the pathological process and removal of the tumor before the development of severe symptoms of a general and local nature. If the neoplasm, due to its localization or malignancy, is inaccessible for surgical removal, then the method of introducing radioactive isotopes directly into the tumor itself is used, which causes the destruction of the tumor tissue. 44. Signs of a concussion Concussion develops without pronounced morphological changes and is associated with traumatic brain injury. As a result of injury, the CSF wave has a pathological effect on the brainstem and the hypothalamic-pituitary region. Disorder of nervous activity and violation of cortical-subcortical neurodynamics is explained by anatomical and physiological features and increased sensitivity to traumatic damage to the hypothalamic-stem brain. Sudden disturbance of consciousness, lethargy, adynamia, lethargy, drowsiness as a result of traumatic brain injury and other clinical manifestations in the future, as well as their reversibility during the restoration of nerve impulses, is explained by a violation of interneuronal connections of a reversible functional and irreversible organic nature at various levels of the reticular system of the brain stem . A complex pathological process that develops as a result of injury is due to primary reticulocortical-subcortical disorders, which are joined by dyscirculatory phenomena, neurohumoral-endocrine and metabolic disorders that contribute to the development of hypoxia, edema and swelling of the brain. Blood vessels undergo spasm or dilatation, blood flow slows down, stasis develops, the permeability of the vessel wall increases, which leads to plasmorrhagia and diapedesis. Stagnation develops in the venous system with increased pressure. Liquorodynamics is disturbed, which is manifested by a change in the production of cerebrospinal fluid, a violation of its outflow and normal circulation. Clinic. First of all, a concussion is manifested by loss of consciousness, the severity and duration of which depends on the severity of the injury. The acute period is characterized by headache, vomiting, nausea, dizziness, which is aggravated by various movements. Vegetative-vasomotor disorders are often noted: a change in complexion (redness or blanching), a change in pulse, blood pressure, respiratory failure, fever and leukocytosis. At the time of the injury, the pupils were dilated, the reaction to light was sluggish. After injury, nystagmus is often found. It can be persistent and can persist for a long time. When moving the eyeballs, pain is noted. Mild meningeal phenomena are possible. If the injury is severe, then a decrease in muscle tone, asymmetry of facial innervation, tendon and skin reflexes, as well as pathological reflexes are possible. With a mild degree, loss of consciousness is short-lived. There may be no loss of consciousness. In this case, the patients are stunned, orientation in space is disturbed. Patients complain of headache, dizziness, vomiting and general weakness. The average severity of concussion is characterized by a more prolonged disorder of consciousness, retrograde amnesia is characteristic. Drowsiness and lethargy are noted. Patients complain of headache, dizziness, nausea, vomiting and tinnitus. A severe degree of injury is characterized by a prolonged loss of consciousness, disorders of the respiratory and cardiovascular systems. The complexion changes (purple or pale), cold sweat, acrocyanosis appears. It is necessary to provide rest to the patient. Transportation to the hospital is carried out in a supine position. Emergency assistance includes the elimination of disorders from the respiratory and cardiovascular systems, removal from a state of shock. Elimination of disorders of cardiac activity is achieved by the introduction of strophanthin or corglicon. 45. Clinical symptoms of brain contusion, epidural and subdural hematoma It is manifested by cerebral and stem disorders in combination with focal symptoms, which depend on the site of damage to the brain tissue. Symptoms result from bruising of the brain tissue against the inner wall of the vault or base of the skull. A bruise is characterized by a disorder of consciousness in the form of stupor or coma of varying duration and depth. Focal symptoms depend on the localization of the pathological process. Damage to the facial nerve, paresis of the oculomotor muscles, pathological reflexes, movement or sensation disorders, meningeal symptoms, fever, etc. are often determined. First aid and care in the acute period after injury are similar to those for severe concussion. After leaving the acute period, iodine preparations, transcerebral iodine electrophoresis, anticholinesterase drugs, biostimulants are prescribed. In the case of movement disorders, massage and therapeutic exercises are carried out; in case of aphatic disorders, classes with a speech therapist are advisable. Located between the bone and the dura mater. The source of their formation is meningeal arteries, veins of the dura mater, venous sinuses. Epidural hematomas are manifested by cerebral and focal symptoms. Cerebral symptoms are the result of increased intracranial pressure. Focal symptoms depend on the location of the hematoma. With compression of the legs of the brain, divergent strabismus, ptosis, dilation or narrowing of the pupils are noted, the reaction of the pupil to light is absent on the side of compression. With compression of the medulla oblongata, there are violations of the respiratory and cardiovascular systems. The side of the lesion is determined by the site of the oculomotor nerve lesion, which is manifested by pupil dilation on the side of compression, ptosis, impaired pupillary reaction to light, which is dilated on the side of the hematoma. In the study of cerebrospinal fluid, a small admixture of blood is determined. Craniography is used for diagnosis. Develop as a result of damage to the vessels of the dura mater. A characteristic symptom is a bursting, pressing headache. Nausea, vomiting, drowsiness, impaired consciousness are often noted. The pupils become uneven. Subdural hematoma is characterized by the rapid development of stupor or coma on the first day after injury. There are pronounced stem disorders, shell symptoms, reflexes become asymmetric, gradually the reflexes are inhibited. In the cerebrospinal fluid there is an admixture of blood, the study of the fundus reveals congestive optic discs. Subdural hematomas can be chronic, with symptoms progressively worsening over several weeks or years after injury. 46. Skull fractures A fracture of the cranial vault is established during an x-ray of the skull. The fracture is usually related to the severity of the injury. If the skull fracture is closed, then symptoms of both concussion and brain contusion are detected. Linear fractures in the absence of data on the presence of intracranial hematoma or damage to the brain tissue do not require surgical treatment. Operations are performed for depressed fractures of the skull bones. Fracture of the base of the skull is a consequence of a significant intensity of mechanical impact during trauma. Diagnosis of this pathology is based on neurological examination data. Skull fractures are manifested by cerebral symptoms, stem disorders, symptoms of cranial nerve damage, meningeal symptoms, as well as bleeding and liquorrhea from the nose, ears, mouth, and nasopharynx. In most cases, there is bleeding from the external auditory canal, which occurs when the pyramid of the temporal bone is fractured with a rupture of the tympanic membrane. Bleeding from the nose occurs when the ethmoid bone is fractured. With a fracture of the main bone, bleeding from the mouth and nasopharynx is noted. With liquorrhea, damage to the dura mater is noted. In this case, we speak of penetrating damage. The presence of a skull fracture is indicated by prolonged, profuse bleeding from the nose or external auditory canal, in combination with neurological symptoms. If the fracture is localized in the region of the anterior cranial fossa, then a symptom of glasses is noted - bruising in the eyelids and periorbital tissue. With a fracture, this symptom is symmetrical and significantly pronounced. Sometimes there is late exophthalmos. In the case of a fracture in the region of the middle cranial fossa, the formation of a hematoma over the temporal muscle is characteristic. This hematoma is determined by palpation in the form of a tumor of test consistency. A fracture in the region of the posterior cranial fossa is manifested by bruising in the region of the mastoid process. With fractures of the base of the skull, symptoms of damage to the cranial nerves are noted. In most cases, the facial and auditory nerves are affected. In more rare cases, the oculomotor, abducens, trochlear, olfactory, optic, and trigeminal nerves are damaged. In a severe case, a skull base fracture can lead to death immediately after the injury or shortly after it. A complication in violation of the integrity of the dura mater is the development of purulent meningitis. Persistent consequences of a skull fracture are headaches, pyramidal symptoms, and symptoms of cranial nerve damage. Diagnosis of intracranial hemorrhage is based on a lumbar puncture. If there is bleeding and liquorrhea from the external auditory canal, then it is covered with sterile gauze and a bandage is applied. Antibiotics are administered to prevent complications. Drugs that increase blood clotting are used. Surgical treatment is carried out for comminuted and depressed fractures in the parabasal regions and for extensive intracranial hemorrhages. 47. Depression Depression is a mental disorder, the main features of which are: a decrease in mood (hypothymia), a negative, pessimistic assessment of oneself, one's position in the surrounding reality, one's future. Along with this, depression is often accompanied by lethargy, a decrease in incentive motives for activity, dysfunctions in the work of many organs and systems (cardiovascular, respiratory, endocrine, etc.). Depression aggravates the manifestation, aggravates the course of any bodily ailment and complicates its treatment. Significant difficulties are associated with the problem of depression in psychiatry and narcology. The concept of "depression" includes a wide range of psychopathological manifestations that differ in biological structure, severity and duration of disorders. In the previous classification of depressions, they were distinguished within the framework of mental illness (manic-depressive psychosis, schizophrenia, psychogenia, etc.). In accordance with clinical manifestations, the main types of depression were determined: simple (melancholic, anxious, apathetic) and complex (depression with delusions). Among the classic signs of depression, one can distinguish such as feelings of melancholy, feelings of guilt, suicidal manifestations, circadian rhythm disturbances (mood fluctuations during the day with the worst feeling in the morning and slight improvement in the afternoon and evening), anxiety, intellectual and motor inhibition, apathy , dysphoria (sullenness, bitterness, grumpiness, demonstrative behavior and claims to others), anhedonia (loss of a sense of pleasure, inability to experience joy, pleasure, accompanied by a feeling of mental discomfort). According to the modern classification (ICD - 10), the variants of the course of depression are of primary importance: a single depressive episode, recurrent (recurrent) depression, bipolar disorders (change of depressive and manic phases), cyclothymia, dysthymia. According to the severity of depression are divided into mild, moderate and severe. In addition to the above manifestations, depression is accompanied by general somatic symptoms: weakness, arthralgia (joint pain), difficulty breathing, palpitations, weight loss, abdominal pain, insomnia, myalgia (muscle pain), chest pain, loss of appetite, constipation, rapid urination. Depression is one of the constantly present conditions in mental patients. Depression is observed in patients with oncological pathology, coronary artery disease, endocrinological diseases (diabetes mellitus, thyroid lesions), in surgical practice (pre- and postoperative depression). There is also a group of seasonal depressions, depressions of late age, reactive (psychogenic) depressions that occur under the adverse effects of psychosocial stress, mental trauma. 48. Treatment of depression The leading method of treatment of depression at the present stage is psychopharmacotherapy. Along with medicines, methods of physio-, phyto-, and psychotherapy with elements of psycho-correction and other socio-rehabilitation methods are widely used. Conducted in combination with drug treatment, psychotherapy (mainly aimed at correcting depressive distortion of thinking, reducing aggression, hopelessness) is most effective. Since the beginning of the era of psychopharmacology, the main place among the therapeutic effects of depression belongs to antidepressants (thymoanaleptics). In addition to them, drugs of other groups are widely used: Antipsychotics (neuroleptics). They have the following properties: they reduce psychomotor activity, relieve psychomotor agitation, and have an antipsychotic effect. Anxiolytics (tranquilizers). They stop the state of anxiety, emotional tension, fear, sleep disturbance. Nootropics. These are drugs that have a positive effect on the metabolic processes of the brain, increasing the resistance of brain structures to various adverse factors, in particular, to hypoxia and extreme stress. Psychostimulants. They increase mental and physical performance, endurance, reduce the feeling of fatigue. Normotimics. This is a group of drugs that regulate affective manifestations. They are mainly used at the stages of preventive treatment, as a rule, in specialized psychiatric institutions. In the treatment of depression, the use of auxiliary means, such as physiotherapy and herbal medicine, has a good effect. With irritability, sleep disturbance, herbs with a sedative component are used (valerian, motherwort, hawthorn, peony, oregano). Phytoantidepressants are separated into a separate group. These include leuzea, aralia, zamaniha, etc. Among these funds, it is necessary to highlight the extract of St. John's wort. The active substances included in its composition made it possible to create a modern drug gelarium and no-vo-passit. Herbal preparations are well tolerated, have no side effects, can be combined with other drugs and do not show signs of dependence. A special role in the elimination of depressive manifestations belongs to the psychotherapeutic effect. The study of the action of iproniazid showed that it inhibits the enzyme monoamine oxidase (MAO). This enzyme deactivates norepinephrine, dopamine, serotonin (neurotransmitter substances produced by the structures of the nervous system and facilitating the transmission of a nerve impulse). It is these substances that play the most important role in the activity of the central nervous system, and their imbalance causes a number of somatic and psychogenic disorders, one of which is depression. With depression, there is a decrease in the activity of impulse transmission in neurotransmitter systems. 49. Neurosis Neurosis is a disease of the nervous system of a functional nature, resulting from an overstrain of the processes of higher nervous activity. Neuroses account for up to 1/3 of all neurological diseases. Neuroses arise as a result of various duration and severity of mental trauma or chronic overwork. Neurodynamic disorders of higher nervous activity and structures of the hypothalamus play a role in pathogenesis. The state of the autonomic nervous system, past infections and intoxications also play a role. In the clinic of neuroses, emotional-affective and somatovegetative disorders predominate. Patients with neuroses retain a critical attitude towards their condition (in contrast to patients with psychopathy). There are the following types of neurosis: neurasthenia, hysterical neurosis, obsessive-compulsive disorder. Neurasthenia is the most common form of neuroses. It consists of psychogeny and somatogeny. According to clinical manifestations, it is customary to distinguish several forms of neurasthenia. Hypersthenic, which is expressed in increased excitability, incontinence, impaired attention and sleep, increased reaction to minor irritating factors while maintaining working capacity. The form of irritable weakness is characterized by a decrease in working capacity in the evening, weakening of attention, tearfulness, headaches, emotional excitability, and impatience. Patients often pay attention to disturbances in the activity of internal organs, they are suspicious, often fall into a state of anxiety. The hyposthenic form is expressed in adynamia, the presence of asthenic syndrome, apathy, fatigue, insomnia. Vegetative disorders in the form of chilliness, increased sweating, acrocyanosis are characteristic of all forms. The disease usually begins at the age of 20-40 years. In the treatment of patients with neurasthenia, various methods are used: sedatives, antidepressants, physiotherapy (electrosleep, electrophoresis of medicinal substances), psychotherapy. Much attention in the treatment of this disease should be paid to the correction of the somatic sphere. Among the drugs, the use of tranquilizers (Elenium, diazepam, nitrazepam) is effective. From the group of antidepressants, imatriptyline, melipramine, etc. are used in small doses. Grandaxin, sidno-carb are prescribed from psychostimulants. Hysteria is the second most common condition after neurasthenia. The vast majority of patients are women. Its manifestations are varied: seizures, hysterical deafness, dumbness, astasia-abasia, but most patients have disorders of the internal organs, sleep disorders, libido. In the treatment of hysteria, psychotherapy methods, especially hypnosis and physiotherapy techniques (the same as for neurasthenia), give a good effect. 50. Damage to the I and II pair of cranial nerves The olfactory nerve pathway consists of three neurons. The first neuron has two types of processes: dendrites and axons. The endings of the dendrites form olfactory receptors located in the mucous membrane of the nasal cavity. The axons of the first neurons pass into the cranial cavity through the plate of the ethmoid bone, ending in the olfactory bulb on the bodies of the second neurons. The axons of the second neurons make up the olfactory tract, which goes to the primary olfactory centers. The primary olfactory centers include the olfactory triangle, the anterior perforated substance and the transparent septum. The main symptoms include anosmia, hyposmia, hyperosmia, dysosmia, and olfactory hallucinations. The greatest importance is given to anosmia and unilateral hyposmia. This is due to the fact that in most cases bilateral hyposmia and anosmia are caused by acute or chronic rhinitis. Loss or decrease in the sense of smell is the result of damage to the olfactory nerve at a level up to the olfactory triangle. The defeat of the third neuron does not lead to a violation of the olfactory function, since this neuron is located in the cerebral cortex on both sides. Olfactory hallucinations are the result of irritation of the olfactory projection field, which can be with tumor formations in the hippocampus. The first three neurons of the visual pathway are located in the retina. The first neuron is represented by rods and cones. The second neurons are bipolar cells. Ganglion cells are the third neurons of the pathway. Their axons form the optic nerve, which enters the cranial cavity through the optic opening in the orbit. Anterior to the sella turcica, the nerve forms the optic chiasm. Only part of the fibers of the optic nerves crosses. After decussation, the optic fibers are called the optic tract. Due to the decussation of the fibers in each optic tract, there are visual fibers from the same halves of the retina of the right and left eyes. The fibers of the optic tract terminate in the lateral geniculate body, the thalamus cushion, and in the superior colliculi of the quadrigemina. The next neuron is located in the external geniculate body, the axons of which form the Graciole bundle. This bundle ends in the cells of the cerebral cortex located in the region of the spur groove on the inner surface of the occipital lobe. Damage symptoms. Decreased vision (amblyopia) or blindness on the affected side of the optic nerve. The pupil's reaction to light is preserved. With the defeat of part of the neurons of the pathway in the retina or in the optic nerve, a scotoma is formed. It is characterized by the loss of any part of the field of view. It is possible to damage the visual fibers located medially and making a complete intersection, there is a loss of the outer half of the visual field on both sides (the so-called bitemporal hemianopsia), or binosal hemianopsia (loss of half of the visual field on the inside of both eyes with damage to part of the visual fibers located laterally). 51. Damage to the III and IV pairs of cranial nerves The conducting path of the nerve is two-neuron. The central neuron is located in the cells of the cortex of the precentral gyrus of the brain. The axons of the first neurons form a cortical-nuclear path leading to the nuclei of the oculomotor nerve located on both sides. In the brain there are five nuclei of the oculomotor nerve, in which the bodies of the second neurons are located. These nuclei are small- and large-celled. The nuclei are located in the midbrain at the level of the superior colliculi of the quadrigemina in the legs of the brain. From the nuclei of the nerve, the innervation of the external muscles of the eye, the muscle that lifts the upper eyelid, the muscle that narrows the pupil, and the ciliary muscle is carried out. All fibers coming from the nuclei of the oculomotor nerve exit the legs of the brain, pass through the dura mater, cavernous sinus, leave the cranial cavity through the superior orbital fissure and enter the orbit. Damage symptoms. Damage to the nerve trunk leads to paralysis of all oculomotor muscles. When part of the large cell nucleus is damaged, the innervation of the external muscle of the eye is disturbed. Clinically, there is complete paralysis or weakness of this muscle. In case of complete paralysis, the patient cannot open his eyes. With weakness of the muscle that lifts the upper eyelid, the patient opens the eye partially. If the large cell nucleus of the oculomotor nerve is affected, the levator levator muscle of the upper eyelid is the last to be affected, exotropia or external ophthalmoplegia occurs when only the external muscles are damaged. Damage to the oculomotor nucleus is often accompanied by the development of Weber's alternating syndrome, which is associated with simultaneous damage to the fibers of the pyramidal and spinothalamic tracts. Hemiplegia on the side opposite to the lesion joins the clinical manifestations. Damage to the nerve trunk is characterized by external and internal ophthalmoplegia. Internal ophthalmoplegia is accompanied by the appearance of mydriasis, anisocoria, disturbance of accommodation and pupillary reaction to light. Mydriasis occurs as a result of paralysis of the sphincter of the pupil. The conducting path is two-neuron. The central neuron is located in the cortex of the lower part of the precentral gyrus. The axons of the central neurons end in the cells of the nucleus of the trochlear nerve on both sides. The nucleus is located in the brain stem in the region of the inferior colliculi of the quadrigemina. There are located peripheral neurons of the pathway. Nerve fibers, located along the length from the central to the peripheral neuron, make up the cortical-nuclear pathway. The fibers emanating from the nucleus of the trochlear nerve cross in the region of the medullary sail. With the contraction of this muscle, the eyeball turns down and outward. Damage symptoms. An isolated lesion of the IV pair of cranial nerves is extremely rare. Clinically, the defeat of the trochlear nerve is manifested by the limitation of the mobility of the eyeball outwards and downwards. Since the innervation of the superior oblique muscle of the eye is disturbed, the eyeball turns inwards and upwards. With this pathology, double vision (diplopia) will be characteristic, which occurs when looking down and to the sides. 52. Defeat of the V pair of cranial nerves The XNUMXth pair of cranial nerves is mixed. The sensory pathway of a nerve is made up of neurons. The first neuron is located in the semilunar node of the trigeminal nerve, located between the layers of the dura mater on the anterior surface of the pyramid of the temporal bone. The axons of these neurons form a common root of the trigeminal nerve, which enters the bridge of the brain and ends on the cells of the nucleus of the spinal tract, which belongs to the superficial type of sensitivity. Sensory fibers of the trigeminal nerve form three branches: the ophthalmic, maxillary and mandibular nerves. The maxillary nerve has two branches: the zygomatic nerve and the pterygopalatine nerves. The zygomatic nerve innervates the skin of the zygomatic and temporal regions. Sensitive fibers of the maxillary nerve innervate the mucous membrane of the nasal cavity, tonsils, pharynx, soft and hard palate, sphenoid sinus, posterior ethmoid cells. The continuation of this nerve is the infraorbital nerve, which exits through the infraorbital foramen to the face, where it divides into its terminal branches. The infraorbital nerve is involved in the sensitive innervation of the skin of the lower eyelid, the outer wing of the nose, the mucous membrane and skin of the upper lip to the corner of the mouth, the mucous membrane of the vestibule of the nose. The mandibular nerve is mixed. It innervates the masticatory muscles with motor fibers. Sensory fibers innervate the chin, lower lip, floor of the mouth, anterior two-thirds of the tongue, teeth of the mandible, skin of the lower cheek, anterior part of the auricle, tympanic membrane, external auditory canal, and dura mater. Damage symptoms. If the nucleus of the spinal cord is damaged or damaged, a sensitivity disorder of the segmental type develops. In some cases, it is possible to lose pain and temperature sensitivity while maintaining deep types of sensitivity, such as a sense of vibration, pressure, etc. With inflammation of the facial nerve, pain appears in the affected half of the face, which is more often localized in the ear area and behind the mastoid process. Less commonly, it is localized in the region of the upper and lower lips, forehead, and lower jaw. In case of damage to any branch of the trigeminal nerve, the sensitivity of one or more species in the zone of innervation of this branch is disturbed. When the optic nerve is damaged, the superciliary and corneal reflexes disappear. A decrease or complete disappearance of the taste sensitivity of the anterior 2/3 of the tongue on the one hand indicates a lesion of the mandibular nerve on the same side. Also, with damage to the mandibular nerve, the mandibular reflex disappears. Unilateral paresis or paralysis of the masticatory muscles occurs when the motor nucleus of the trigeminal nerve or the motor fibers of the mandibular nerve on the same side are affected. In the case of bilateral damage to the same nerve formations, the lower jaw sags. 53. Damage to the VI pair of cranial nerves Damage to the VI pair of cranial nerves is clinically characterized by the appearance of convergent strabismus. A characteristic complaint of patients is the doubling of the image, located in the horizontal plane. Often the alternating Gubler's syndrome joins with the development of hemiplegia on the side opposite to the lesion. Most often there is a simultaneous defeat of III, IV and VI pairs of cranial nerves, which is associated with the presence of some anatomical features of their location. The fibers of these nerves are closely located with the fibers of other pathways in the brainstem. With damage to the posterior longitudinal bundle, which is an associative system, internuclear ophthalmoplegia develops. Simultaneous lesions of the oculomotor nerves are associated with their close location to each other in the cavernous sinus, as well as to the ophthalmic nerve (the first branch of the trigeminal nerve), the internal carotid artery. In addition, the simultaneous damage to these nerves is associated with their close location at the exit from the cranial cavity. When pathological processes appear on the base of the skull or the basal surface of the brain, in most cases, an isolated lesion of the abducens nerve occurs. This is due to its large extent at the base of the skull. If the motor fibers of the VII pair of cranial nerves are damaged, peripheral paralysis of the muscles of the face on the side of the lesion develops, which is manifested by asymmetry of the face: half of the face on the side of the lesion of the nerve becomes motionless, mask-like, the frontal and nasolabial folds are smoothed out, the eye on the affected side does not close, the palpebral fissure widens, the corner of the mouth is down. Bell's phenomenon is noted - an upward turn of the eyeball when trying to close the eye on the side of the lesion. There is paralytic lacrimation due to the absence of blinking. Isolated paralysis of the mimic muscles of the face is characteristic of damage to the motor nucleus of the facial nerve. In the case of attachment of a lesion to the radicular fibers, the Miyyar-Gubler syndrome (central paralysis of the limbs on the side opposite to the lesion) is added to the clinical symptoms. With damage to the facial nerve in the cerebellopontine angle, in addition to paralysis of the facial muscles, there is a decrease in hearing or deafness, the absence of a corneal reflex, which indicates a simultaneous lesion of the auditory and trigeminal nerves. This pathology occurs with inflammation of the cerebellopontine angle (arachnoiditis), acoustic neuroma. The addition of hyperacusia and a violation of taste indicate damage to the nerve before the large stony nerve leaves it in the facial canal of the temporal bone pyramid. Damage to the nerve above the tympanic string, but below the origin of the stapedial nerve, is characterized by a taste disorder, lacrimation. Paralysis of the mimic muscles in combination with lacrimation occurs in case of damage to the facial nerve below the discharge of the tympanic string. 54. Defeat of the VIII pair of cranial nerves If the fibers of the VIII pair of cranial nerves of the auditory cochlear nuclei are damaged, there is no impairment of hearing function. With damage to the nerve at various levels, auditory hallucinations, symptoms of irritation, hearing loss, deafness may appear. Decrease in hearing acuity or deafness on the one hand occurs when the nerve is damaged at the receptor level, when the cochlear part of the nerve and its anterior or posterior nuclei are damaged. Symptoms of irritation in the form of a sensation of whistling, noise, cod may also join. This is due to irritation of the cortex of the middle part of the superior temporal gyrus by a variety of pathological processes in this area, such as tumors. Front part. In the internal auditory meatus, there is a vestibular node formed by the first neurons of the pathway of the vestibular analyzer. Dendrites of neurons form receptors of the labyrinth of the inner ear, located in the membranous sacs and in the ampullae of the semicircular canals. The axons of the first neurons make up the vestibular part of the VIII pair of cranial nerves, located in the temporal bone and entering through the internal auditory opening into the substance of the brain in the region of the cerebellar pontine angle. The nerve fibers of the vestibular part end on the neurons of the vestibular nuclei, which are the second neurons of the pathway of the vestibular analyzer. The nuclei of the vestibular part are located at the bottom of the IV ventricle, in its lateral part, and are represented by lateral, medial, upper, lower. The neurons of the lateral nucleus of the vestibule give rise to the vestibulo-spinal pathway, which is part of the spinal cord and ends in the neurons of the anterior horns. The axons of the neurons of this nucleus form a medial longitudinal bundle, located in the spinal cord on both sides. The course of the fibers in the bundle has two directions: descending and ascending. Descending nerve fibers are involved in the formation of part of the anterior cord. Ascending fibers are located to the nucleus of the oculomotor nerve. The fibers of the medial longitudinal bundle have a connection with the nuclei of III, IV, VI pairs of cranial nerves, due to which impulses from the semicircular canals are transmitted to the nuclei of the oculomotor nerves, causing the movement of the eyeballs when the body position changes in space. There are also bilateral connections with the cerebellum, the reticular formation, the posterior nucleus of the vagus nerve. Symptoms of the lesion are characterized by a triad of symptoms: dizziness, nystagmus, impaired coordination of movement. There is a vestibular ataxia, manifested by a shaky gait, deviation of the patient in the direction of the lesion. Dizziness is characterized by attacks lasting up to several hours, which may be accompanied by nausea and vomiting. The attack is accompanied by horizontal or horizontal-rotary nystagmus. When a nerve is damaged on one side, nystagmus develops in the direction opposite to the lesion. With irritation of the vestibular part, nystagmus develops in the direction of the lesion. 55. Defeat of IX-X pairs of cranial nerves IX-X pair of cranial nerves mixed. The sensory pathway of the nerve is three-neural. The bodies of the first neuron are located in the nodes of the glossopharyngeal nerve. Their dendrites end with receptors in the posterior third of the tongue, soft palate, pharynx, pharynx, auditory tube, tympanic cavity, and anterior surface of the epiglottis. The axons of the first neurons enter the brain behind the olive, terminate at the cells of the nucleus of the solitary pathway, which are the second neurons. Their axons cross, ending on the cells of the thalamus, where the bodies of the third neurons are located. The axons of the third neurons pass through the posterior leg of the internal capsule and end in the cells of the cortex of the lower part of the postcentral gyrus. The first neuron is located in the lower part of the precentral gyrus. Its axons terminate on the cells of the double nucleus on both sides, where the second neurons are located. Their axons innervate fibers of the stylo-pharyngeal muscle. Parasympathetic fibers originate from the cells of the anterior hypothalamus, ending on the cells of the lower salivary nucleus. Symptoms of damage include taste disturbance in the posterior third of the tongue, loss of sensation in the upper half of the pharynx, and gustatory hallucinations that develop when irritated by cortical projection areas located in the temporal lobe of the brain. Irritation of the nerve itself is manifested by burning pains of varying intensity in the region of the root of the tongue and tonsils lasting 1-2 minutes, radiating to the palatine curtain, throat, ear. The pain provokes talking, eating, laughing, yawning, moving the head. He is mixed. The sensitive pathway is three-neuron. The first neurons form the nodes of the vagus nerve. Their dendrites end with receptors on the dura mater of the posterior cranial fossa, the mucous membrane of the pharynx, larynx, upper trachea, internal organs, the skin of the auricle, and the posterior wall of the external auditory canal. The axons of the first neurons end on the cells of the nucleus of the solitary tract in the medulla oblongata, which are the second neurons. Their axons terminate on thalamic cells, which are the third neurons. The motor pathway begins in the cells of the cortex of the precentral gyrus. Their axons terminate on the cells of the second neurons located in the double nucleus. The axons of the second neurons innervate the soft palate, larynx, epiglottis, upper esophagus, and striated muscles of the pharynx. The autonomic nerve fibers of the vagus nerve are parasympathetic. They start from the nuclei of the anterior hypothalamus, ending in the autonomic dorsal nucleus. Damage symptoms. Paralysis of the muscles of the pharynx and esophagus, violation of swallowing, leading to the ingress of liquid food into the nose. The patient develops a nasal tone of voice, it becomes hoarse, which is explained by paralysis of the vocal cords. In the case of bilateral damage to the vagus nerve, aphonia and suffocation may develop. When the vagus nerve is damaged, the activity of the heart muscle is disrupted, which is manifested by tachycardia or bradycardia when it is irritated. 56. Damage to the XI-XII pair of cranial nerves It consists of two parts: vagus and spinal. The conductive motor pathway is two-neuron. The first neuron is located in the lower part of the precentral gyrus. Its axons enter the brain stem, pons, medulla oblongata, passing through the internal capsule first. The nerve fibers are divided into two parts, ending at different levels of the central nervous system. The second neuron consists of two parts - spinal and vagus. The fibers of the spinal part exit the spinal cord at the CI-CV level, forming a common trunk that enters the cranial cavity through the foramen magnum. After exiting, the nerve fibers are divided into two branches - internal and external. The internal branch passes into the inferior laryngeal nerve. The external branch innervates the trapezius and sternocleidomastoid muscles. Damage symptoms. With unilateral nerve damage, it is difficult to raise the shoulders, turning the head in the direction opposite to the lesion is sharply limited. In this case, the head deviates towards the affected nerve. With bilateral nerve damage, it is impossible to turn the head in both directions, the head is thrown back. When the nerve is irritated, a tonic muscle spasm develops, which is manifested by the appearance of spastic torticollis (the head is turned in the direction of the lesion). With bilateral irritation, clonic convulsions of the sternocleidomastoid muscles develop. For the most part, the nerve is motor, but it also contains a small part of the sensory fibers of the branch of the lingual nerve. The motor pathway is two-neuron. The central neuron is located in the cortex of the lower third of the precentral gyrus. The fibers of the central neurons end on the cells of the nucleus of the hypoglossal nerve on the opposite side. The cells of the nucleus of the XII pair of cranial nerves are peripheral neurons of the pathway. The motor fibers of the XII pair innervate the muscles located in the thickness of the tongue itself, as well as the muscles that move the tongue forward and down, up and back. Damage symptoms. With damage to the hypoglossal nerve at various levels, peripheral or central paralysis (paresis) of the muscles of the tongue may occur. Peripheral paralysis or paresis develops in case of damage to the nucleus of the hypoglossal nerve or nerve fibers emanating from this nucleus. At the same time, clinical manifestations develop in half of the muscles of the tongue from the side corresponding to the lesion. Unilateral damage to the hypoglossal nerve leads to a slight decrease in the function of the tongue, which is associated with the interlacing of the muscle fibers of both of its halves. More severe is bilateral nerve damage, characterized by glossoplegia (paralysis of the tongue). In case of damage to a section of the pathway from the central to the peripheral neuron, central paralysis of the muscles of the tongue develops. In this case, there is a deviation of the tongue in a healthy direction. Authors: Drozdov A.A., Drozdova M.V.
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