Autonomic innervation of the eye (damage to the Yakubovich nuclei - Bernard-Horner syndrome). Parasympathetic innervation of the eye. Innervation of the sphincter of the pupil, ciliary muscle and lacrimal gland Autonomic innervation of the eye Horner's syndrome

The diameter of the pupil is measured with a special pupillometric or millimeter ruler. On average, under conditions of moderate diffuse illumination, it is 3.5-4.5 mm. Anisocoria - a difference in pupil size is possible and normal (almost 30% healthy people), but if it exceeds 0.9 mm, then it should be considered pathological. The smooth muscles of the eyes and their appendages, like other smooth muscles, are innervated by the autonomic nervous system. The size of the pupil depends on the state of the two smooth internal muscles eyes: sphincter pupil and dilator pupil (m. sphincter pupillae et m. dilatator pupillae). The sphincter of the pupil has parasympathetic innervation, and the dilator has sympathetic innervation. If only the parasympathetic innervation is disturbed, the sphincter is paralyzed and the pupil dilates, but it does not react to light; in the case of a disorder of sympathetic innervation, the dilator of the pupil is paralyzed and the pupil is constricted, but it can react to light. Thus, the pupil can be dilated when the sympathetic structures innervating the muscles are excited or when the functions of the parasympathetic structures are suppressed; constriction of the pupil may be a consequence of excitation of parasympathetic structures involved in the innervation of the sphincter of the pupil or suppression of the functions of sympathetic structures. Sympathetic and parasympathetic denervation of the pupil can be differentiated by checking the reaction of the pupil to light and resorting to pharmacological tests (Figs. 30.2 and 30.3), taking into account the hypersensitivity of the neuromuscular receptor that occurs after denervation. Therefore, if, with normal innervation of the pupil, instillation of a solution of adrenaline at a dilution of 1:1000 into the conjunctival sac is not accompanied by pupil dilation, then in the presence of sympathetic denervation, pupil dilation occurs. With parasympathetic denervation, for the same reason, constriction of the pupil occurs when a 2.5% methacholine solution is instilled, whereas normally such a reaction is absent. In patients with complete denervation of smooth muscles that determine pupil width, these tests can reveal both sympathetic and parasympathetic denervation. It should be borne in mind that parasympathetic denervation hypersensitivity develops in 80% of patients with diabetic autonomic neuropathy; it is more often detected in patients with diabetes mellitus for more than 2 years. Constriction of the pupil - miosis - is pathological if its diameter in normal lighting is less than 2 mm. Spastic miosis is caused by excitation of the parasympathetic structures of the oculomotor nerve system (drug-induced spastic miosis can be a consequence of the administration of pilocarpine and other N-cholinomimetics, as well as anticholinesterase drugs that have a similar effect). Paralytic miosis is a consequence of suppression of the sympathetic innervation of the muscle that dilates the pupil, which occurs, in particular, with Horner's syndrome. Moderate bilateral miosis with intact reaction of the pupils to light from - Fig. 30.2. Changes in pupils with right-sided temporotentorial herniation. a — normal state of the pupils; b - irritation of the oculomotor nerve, in connection with this the right pupil is constricted; c — loss of function of the oculomotor nerve, the previously constricted pupil dilates, the reaction of the pupil to light is sluggish, d — on the right the pupil is dilated, does not react to light due to damage to the parasympathetic bundle of the oculomotor nerve, on the left — due to the pupil is constricted by irritation of the oculomotor nerve; d - due to severe bilateral damage to the oculomotor nerves, the pupils on both sides are wide and do not respond to light. Rice. 30.3. Study of pupillary response to light for differential diagnosis damage to the optic and oculomotor nerves. a - damage to the right optic nerve(afferent part of the arc of the pupillary reflex). When the right eye is illuminated, both direct and conjugate reactions of the pupils are absent; when the left eye is illuminated, both reactions are evoked; b — damage to the right oculomotor nerve (the efferent part of the arc of the pupillary reflex). On the right there is no direct reaction of the pupil to light, while the friendly reaction of the pupil of the left eye is preserved. When the left eye is illuminated from the left, a reaction of the pupil to light is caused, while a friendly reaction of the pupil of the right eye is absent. marked during sleep, as well as with bilateral damage to the diencephalic region and with its central transtentorial herniation. Pinpoint pupils that react to light are observed when the pons of the brain is damaged or when intoxicated with narcotic drugs. To identify the reaction of the pupils to light in such cases, you should use a magnifying glass (loupe). Mydriasis is dilation of the pupil. It may be pathological if its diameter under normal lighting is more than 4.5 mm. Paralytic mydriasis is a consequence of dysfunction of the parasympathetic structures of the oculomotor nerve and paralysis of the muscle that constricts the pupil. Thus, unilateral dilatation of the pupil in the absence of its reaction to light in a patient in a coma may be due to compression of the oculomotor nerve or cerebral peduncle due to temporotentorial herniation (Hutchinson’s pupil). Such drug-induced mydriasis can be a consequence of instilling a solution of atropine or other M-anticholinergics into the eye. With paralytic dilatation of the pupil, its direct and friendly reaction to light is disrupted. Spastic mydriasis is a consequence of contraction of the dilator muscle due to irritation of the sympathetic structures innervating it, for example in Petit syndrome. Sympathetic innervation of the smooth muscles of the eye and its appendages is provided by the so-called ciliospinal center, represented by cells of the lateral horns of segments CVI1, - Th(, spinal cord, which have connections with the posterior group of nuclei of the hypothalamic region, passing through the tegmentum of the stem structures and the central gray matter at the cervical level of the spinal cord. Preganglionic fibers extending from the vegetative cells located here, passing through the corresponding anterior spinal roots, spinal nerves and white communicating branches, penetrate the paravertebral sympathetic chain at the level of the stellate ganglion. Having transited the stellate and middle cervical ganglia, they reach the cells of the superior cervical ganglion, where sympathetic impulses switch from preganglionic fibers to the cells of this node and their axons, which are postganglionic fibers. The latter form the sympathetic plexuses of the outer carotid artery and its branches, penetrate the orbit and reach the smooth muscles of the eye: the muscle that dilates the pupil (m. dilatator pupillae), the orbital muscle (m. orbitalis) and the upper muscle of the cartilage of the eyelid (m. tarsalis superior). A disruption of their innervation, which occurs when any part of the path of sympathetic impulses from the ciliospinal center is damaged, leads to paresis or paralysis of these muscles. In this regard, on the side of the pathological process, Horner syndrome (Claude Bernard-Horner syndrome) develops, manifested by constriction of the pupil (paralytic miosis), small (1-2 mm) enophthalmos and so-called pseudoptosis (lowered upper eyelid), causing some narrowing of the palpebral fissure. Due to the preservation of the parasympathetic innervation of the sphincter of the pupil on the side of Horner's syndrome, pupil reactions to light are preserved (for more details, see Chapter 13). Irritation of sympathetic nervous structures can lead to the development of Petit syndrome (“reverse” Horner’s syndrome) - dilation of the pupil and palpebral fissure, slight exophthalmos. The manifestation of the entire triad of symptoms due to irritation of sympathetic structures that conduct impulses from the ciliospinal center is not necessary. More often one encounters only anisocoria due to the dilation of the pupil on the side of irritation of the sympathetic structures. There are many reasons for such anisocoria. One of them may be a tuberculosis focus in the apex of the lung (Roke's symptom). Dilation of the pupil on the left sometimes occurs due to cardiac hypertrophy, aneurysm of the aortic arch. With aortic valve insufficiency, “pulsation” of the pupils is possible: the pupils constrict during systole and dilate during diastole of the heart (Landolfi’s sign). Due to the fact that the ciliospinal center receives impulses from the ergotropic structures of the posterior parts of the hypothalamus, passing through the operculum of the trunk and cervical segments of the spinal cord, damage to these parts of the central nervous system can also cause manifestations of paralytic paresis or paralysis of smooth muscles of the eyes that have sympathetic innervation. Such dysfunctions of the smooth muscles of the eyes, especially the muscle that dilates the pupil, are one of the signs of damage to the tegmentum of the brain stem and can manifest themselves, in particular, in some forms of coma. The nature of the pupillary disorders detected in such cases can help resolve the issue of the cause of pathological manifestations in the trunk, and sometimes the cause of the coma. Narrow pupils that react to light (paralytic miosis) may indicate the metabolic nature of the coma or its condition due to damage to the diencephalic part of the brain. Medium-sized pupils that do not respond to light are usually the result of damage to the roof of the midbrain. A wide pupil that does not respond to light indicates ipsilateral damage to the autonomic parasympathetic nuclei in the midbrain tegmentum, root or trunk of the oculomotor nerve. Very narrow (pinpoint) pupils with intact reaction to light are a sign of damage to the pons of the brain. There are exceptions to these rules. Thus, in metabolic coma caused by poisoning with anticholinergic (cholinolytic) drugs (atropine, scopolamine, etc.), the pupils are sharply dilated and do not respond to light (paralytic mydriasis). Wide pupils that do not respond to light are observed during a large seizure, characteristic of severe hypothermia, may be a sign of brain death. It must be borne in mind that the size of the pupils and their reaction to light can also be influenced by the structures of various parts of the visual analyzer system and the parasympathetic part of the oculomotor nerve system. Thus, a significant decrease in vision and, especially, blindness on one side, caused by damage to the retina or optic nerve, are accompanied by anisocoria due to dilation of the pupil on the side of decreased visual acuity, while there is no direct reaction of the pupil to light, but a friendly - preserved (Hun's symptom). In case of bilateral blindness resulting from damage to the visual system from the retinas to subcortical centers, the pupils are dilated and there is no direct or cooperative reaction of the pupils to light. Pupil dilation may occur with intense headache in patients with hypertensive crisis, during migraine attacks (Rehder's symptom), as well as other severe pain syndromes and pain arising in connection with external influences. The cause of dilated pupils can be stressful psychological traumas and disruptive situations. Anisocoria and deformation of the pupils are often observed in neurosyphilis, then a perverted reaction of the pupils to light is also possible (dilation when the illumination of the retina increases and constriction of the pupils when they darken - Govers' pupillary symptom). Robertson's (Argyll Robertson) syndrome is widely known in neurosyphilis, which is characterized by the absence of a direct and friendly reaction of the pupils to light, while their reaction to convergence and accommodation remains intact, while the pupils are usually narrow and may be uneven and deformed. It must be borne in mind that Robertson's syndrome is nonspecific and sometimes occurs with a tumor or traumatic lesion of the midbrain, diabetes mellitus. It is caused by a violation of the parasympathetic innervation of smooth eye muscles due to irritation of the cells of the parasympathetic nuclei of Edinger-Westphal in the tegmentum of the midbrain. With epidemic encephalitis, a “reverse” Robertson syndrome is possible: the absence of a pupillary reaction to accommodation and convergence while the direct and friendly reaction of the pupils to light is preserved. Hutchinson's pupil is a dilation of the pupil and a disorder of its direct and cooperative reaction to light. This is a sign of a supratentorial, often temporal, tumor or hematoma, which causes the syndrome of herniation of brain tissue into Bichat’s fissure and compression of the oculomotor nerve. Dilation of the pupil on the side of the pathological process can also be a sign of Knapp syndrome, in which, due to compression of the cerebral peduncle in a similar situation, along with homolateral dilation of the pupil on the other side, central hemiparesis occurs. Anisocoria at progressive paralysis known as Baillarger’s sign, named after the French psychiatrist J. Baillarger (1809-1890) who described this sign. Anisocoria due to the dilation of the right pupil may be a sign of appendicitis or cholecystitis (Moskovsky's symptom). The syndrome of the wall of the cavernous sinus (Foy's syndrome), Weber, Benedict, and Claude syndromes are described in Chapter 11. Thus, studying the condition of the eyes and their appendages, gaze, and the condition of the cranial nerves that provide innervation to the external and internal muscles of the eye provides very essential information about the topic and nature of the pathological process, which allows us to develop the most rational medical tactics in each specific case.

Damage to the Yakubovich nuclei or the fibers coming from them leads to paralysis of the sphincter of the pupil, while the pupil dilates due to the predominance of sympathetic influences (mydriasis). Damage to the nucleus of Perlea or the fibers coming from it leads to disruption of accommodation.

Damage to the ciliospinal center or the fibers coming from it leads to constriction of the pupil (miosis) due to the predominance of parasympathetic influences, to retraction of the eyeball (enophthalmos) and slight drooping of the upper eyelid.

This triad of symptoms- miosis, enophthalmos and narrowing of the palpebral fissure - is called Bernard-Horner syndrome. With this syndrome, depigmentation of the iris is sometimes also observed.

Bernard-Horner syndrome is most often caused by damage to the lateral horns of the spinal cord at the level C 8 - D 1 or the upper cervical regions borderline sympathetic trunk, less often - a violation central influences to the ciliospinal center (hypothalamus, brain stem). Irritation of these parts can cause exophthalmos and mydriasis.

To assess the autonomic innervation of the eye, pupillary reactions are determined. The direct and concomitant reactions of the pupils to light, as well as the pupillary reactions to convergence and accommodation, are examined. When identifying exophthalmos or enophthalmos, the state of the endocrine system and family characteristics of the facial structure should be taken into account.

“Children’s neurology”, O. Badalyan

We'll consider autonomous systems to the extent that they take part in the structure of the organ of vision.
While the old remains to a certain extent in force view, according to which two systems in the body - sympathetic and parasympathetic - play opposite roles. The sympathetic system is the alarm system. Under the influence of fear and rage, it is activated and gives the body the ability to cope with emergency situations; in this case, the metabolism is set to increased consumption, to dissimilation. In contrast, the parasympathetic system is set to a state of rest, economical consumption in the metabolic process, assimilation.

To the central neuron transmits excitation further to numerous peripheral neurons. Moreover, stronger stimulation is caused through nn. splanchnici release of adrenaline from the adrenal glands. In both of these ways, so-called mass reactions are carried out. In the parasympathetic system, in contrast, circuits of neurons are used in rows; due to this, responses at the end organs are more limited and precisely timed (for example, the Pupil response).

In addition, both systems differ from each other in their mediators. For the sympathetic system, the neurohumoral transmitter of excitation to the peripheral end organ is adrenaline, for the parasympathetic system it is acetylcholine. This rule, however, still does not remain valid in all cases. So, for example, when the “sympathetic” fibers ending at the pilomotors and sweat glands are excited, acetylcholine is released and the transfer of excitation from the preganglionic to the postganglionic neuron throughout the sympathetic system, as in the parasympathetic system, is also carried out through acetylcholine.

Study of afferent pathways within autonomous systems is just beginning and new fundamental data in this regard will probably be obtained in the coming years. Within the scope of this article, we are dealing primarily with efferent conductors. Of the afferent pathways through which the autonomic system is excited, we will later become acquainted with somatic neurons.

In area eyes The following organs are innervated by the sympathetic system: m. dilatator pupillae, smooth muscle that lifts the eyelid m. tarsalis (Müller - Miiller), t. orbitalis (Landschgrem - Landstrom) - usually a person has a rudimentarily developed muscle stretched over the fissura orbitalis inferior, the lacrimal gland (which also has parasympathetic innervation), blood vessels and sweat glands of the facial skin. It should be mentioned that m. sphincter pupillae, in addition to parasympathetic, also has sympathetic innervation; in response to sympathetic stimulation, he instantly relaxes. The same applies to the ciliary muscle.

Last time exposed I even doubt the presence of a dilator in a rabbit. The dilation of the pupil that occurs in response to sympathetic stimulation is explained by the active contraction of blood vessels in the stroma of the iris and inhibition of sphincter contraction. It would be premature, however, to transfer these views to humans.

All going to the above end organs postganglionic neurites originate in the ganglion cervicale superius. They accompany carotis externa (sweat glands) and carotis interna; from the latter, they enter the cranial cavity for the second time, so that here, too, as sympathetic plexuses, they intertwine various other structures (a. ophthalmica, ramus ophthalmicus n. trigemini, n. oculomotorius).

Ganglion cervicale superius is the last member of a long chain of ganglia, which in the form of a border trunk stretches on both sides from the neck to the sacrum along the spine. The neurites extending from the ganglia of the border trunk to the periphery are called “postganglionic”; they are fleshless (rami communicantes grisei). Preganglionic neurites, which ensure the transmission of excitation from the central nervous system to the border trunk, originate from cells located in the lateral horns of the spinal cord. Collectively, these cells make up the columna intermediolateralis; they extend approximately from the first thoracic to the second lumbar segment of the spinal cord. Accordingly, only from these segments (with the anterior roots) do preganglionic fibers (thoracolumbar autonomic system) depart; These fibers are pulpy (rami communicantes albi).

Preganglionic fibers, supplying the ganglion cervicale leave the spinal cord with roots C8, Th1 and Th2. When the corresponding segments of the spinal cord (upper border of C6, lower border of Th4) are irritated, pupil dilation occurs. In this regard, the upper end of the columna intermediolateralis is called centrum ciliospinale (Bubge).

About the higher located sympathetic " centers“There are only more or less well-founded assumptions. From the nucleus paraventricularis of the hypothalamus, which degenerates after the destruction of the superior cervical sympathetic ganglion (but also after the destruction of the vagal nucleus), impulses seem to go to deeper sympathetic transmission stations. In the midbrain near the nucleus of the oculomotor nerve and in medulla oblongata in the vicinity of the nucleus of the hypoglossal nerve, the presence of sympathetic centers is also suggested. The most true assumption is that sympathetic excitation from the hypothalamus is transmitted through a chain of short neurons in the substantia nigra to the centrum ciliospinale (Budge).

After what has already been said about corticolization of brain stem functions, it seems self-evident that the cerebral cortex also influences the autonomic system (vasomotor, pilomotor, gastrointestinal tract). Electrical stimulation of the second frontal gyrus (area 8, according to Brodmann) causes bilateral dilation of the pupils and palpebral fissures, which suggests the presence of uncrossed and crossed corticofugal fibers. Further down from the hypothalamus in the entire sympathetic system, there seems to be no more exchange of fibers between the right and left halves of the body.

CHAPTER 6. VEGETATIVE (AUTONOMOUS) NERVOUS SYSTEM. LESION SYNDROMES

Autonomic nervous system is a set of centers and pathways that ensure regulation of the internal environment of the body.

The division of the brain into systems is quite arbitrary. The brain works as a whole, and the autonomic system models the activity of its other systems, while at the same time being influenced by the cortex.

6.1. Functions and structure of the ANS

The activity of all organs and systems is constantly influenced by innervation sympathetic And parasympathetic parts of the autonomic nervous system. In cases of functional predominance of one of them, symptoms of increased excitability are observed: sympathicotonia - in the case of predominance of the sympathetic part and vagotonia - in the case of predominance of the parasympathetic part (Table 10).

Table 10.Action of the autonomic nervous system

The basic principle of autonomic regulation is reflex. The afferent link of the reflex begins with a variety of interoceptors located in all organs. From the interoceptors, along specialized autonomic fibers or mixed peripheral nerves, afferent impulses reach the primary segmental centers (spinal or brainstem). From them, efferent fibers are sent to the organs. Unlike the somatic spinal motor neuron, the autonomic segmental efferent pathways are two-neuronal: fibers from the cells of the lateral horns are interrupted in the nodes, and the postganglionic neuron reaches the organ.

There are several types of reflex activity of the autonomic nervous system. Autonomic segmental reflexes (axon reflexes), the arc of which closes outside the spinal cord, within the branches of one nerve, are characteristic of vascular reactions. Viscero-visceral reflexes (for example, cardiopulmonary, viscerocutaneous, which, in particular, cause the appearance of areas of skin hyperesthesia in diseases of internal organs) and cutaneous-visceral reflexes (on the stimulation of which thermal procedures and reflexology are based) are known.

From an anatomical point of view, the autonomic nervous system consists of central and peripheral parts. central part is a collection of cells in the brain and spinal cord.

Peripheral link The autonomic nervous system includes:

Border trunk with paravertebral nodes;

A series of gray (non-pulpy) and white (pulpy) fibers extending from the border trunk;

Nerve plexuses outside and inside organs;

Individual peripheral neurons and their clusters (prevertebral ganglia), united into nerve trunks and plexuses.

Topically, the autonomic nervous system is divided into segmental apparatus(spinal cord, autonomic plexus nodes, sympathetic trunk) and suprasegmental- limbic-reticular complex, hypothalamus.

Segmental apparatus of the autonomic nervous system:

1st section - spinal cord:

Ciliospinal center of the sympathetic nervous system C 8 -Th 1;

Cells in the lateral horns of the spinal cord C 8 -L 2;

2nd section - trunk:

Yakubovich-Westphal-Edinger kernels, Perlia;

Cells involved in thermoregulation and metabolic processes;

Secretory nuclei;

Semi-specific respiratory and vasomotor centers;

3rd section - sympathetic trunk:

20-22 knots;

Pre- and postganglionic fibers;

4th department - fibers in structures peripheral nerves. Suprasegmental apparatus of the autonomic nervous system:

Limbic system (ancient cortex, hippocampus, piriformis gyrus, olfactory brain, periamygdala cortex);

Neocortex (cingulate gyrus, frontoparietal cortex, deep parts of the temporal lobe);

Subcortical formations (amygdala complex, septum, thalamus, hypothalamus, reticular formation).

The central regulatory unit is the hypothalamus. Its nuclei are connected to the cerebral cortex and underlying parts of the brain stem.

Hypothalamus:

Has extensive connections with various parts of the brain and spinal cord;

Based on the information received, it provides complex neuro-reflex and neurohumoral regulation;

Richly vascularized, the vessels are highly permeable to protein molecules;

Close to the cerebrospinal fluid ducts.

The listed features cause increased “vulnerability” of the hypothalamus under the influence of various pathological processes in the central nervous system and explain the ease of its dysfunction.

Each group of hypothalamic nuclei carries out suprasegmental autonomic regulation of functions (Table 11). Thus, the hypothalamic region is involved in the regulation of sleep and wakefulness, all types of metabolism, the ionic environment of the body, endocrine functions, reproductive system, cardiovascular and respiratory systems, activity of the gastrointestinal tract, pelvic organs, trophic functions, body temperature.

IN last years It has been established that a huge role in autonomic regulation belongs to frontal and temporal lobes of the cerebral cortex. They coordinate and control the activity of the vegetative

Rice. 6.1.Limbic system: 1 - corpus callosum; 2 - vault; 3 - belt; 4 - posterior thalamus; 5 - isthmus of the cingulate gyrus; 6 - III ventricle; 7 - mastoid body; 8 - bridge; 9 - lower longitudinal beam; 10 - border; 11 - hippocampal gyrus; 12 - hook; 13 - orbital surface of the frontal pole; 14 - hook-shaped beam; 15 - transverse connection of the amygdala; 16 - anterior commissure; 17 - anterior thalamus; 18 - cingulate gyrus

A special place in the regulation of vegetative functions is occupied by limbic system. The presence of functional connections between limbic structures and the reticular formation allows us to talk about the so-called limbic-reticular axis, which is one of the most important integrative systems of the body.

The limbic system plays a significant role in shaping motivation and behavior. Motivation includes complex instinctive and emotional reactions, such as food and defensive ones. The limbic system, in addition, is involved in the regulation of sleep and wakefulness, memory, attention and other complex processes (Fig. 6.1).

6.2. Regulation of urination and defecation

Muscle base Bladder and the rectum consists predominantly of smooth muscle, and is therefore innervated by autonomic fibers. At the same time, the vesical and anal sphincters include striated muscles, which makes it possible to voluntarily contract and relax them. Voluntary regulation of urination and defecation develops gradually as the child matures. By the age of 2-2.5 years, the child is already quite confident in the skills of neatness, although cases of involuntary urination are still observed during sleep.

Reflex emptying of the bladder is carried out thanks to the segmental centers of sympathetic and parasympathetic innervation (Fig. 6.2). The center of sympathetic innervation is located in the lateral horns of the spinal cord at the level of segments L 1 -L 3. Sympathetic innervation is carried out by the inferior hypogastric plexus and cystic nerves. Sympathetic fibers

Rice. 6.2.Central and peripheral innervation of the bladder: 1 - cerebral cortex; 2 - fibers that provide voluntary control over bladder emptying; 3 - fibers of pain and temperature sensitivity; 4 - cross section of the spinal cord (Th 9 -L 2 for sensory fibers, Th 11 -L 2 for motor fibers); 5 - sympathetic chain (Th 11 -L 2); 6 - sympathetic chain (Th 9 -L 2); 7 - cross section of the spinal cord (segments S 2 -S 4); 8 - sacral (unpaired) node; 9 - genital plexus; 10 - pelvic splanchnic nerves; 11 - hypogastric nerve; 12 - lower hypogastric plexus; 13 - genital nerve; 14 - external sphincter of the bladder; 15 - bladder detrusor; 16 - internal sphincter of the bladder

contract the sphincter and relax the detrusor (smooth muscle). When the tone of the sympathetic nervous system increases, urinary retention(Table 12).

The center of parasympathetic innervation is located in the S 2 -S 4 segments. Parasympathetic innervation is carried out by the pelvic nerve. Parasympathetic fibers cause sphincter relaxation and detrusor contraction. Excitation of the parasympathetic center leads to emptying the bladder.

The striated muscles of the pelvic organs (external sphincter of the bladder) are innervated by the pudendal nerve (S 2 -S 4). Sensitive fibers from the external urethral sphincter are directed to the S 2 -S 4 segments, where the reflex arc closes. Another part of the fibers through the system of lateral and posterior cords goes to the cerebral cortex. Connections between the spinal centers and the cortex (paracentral lobule and upper parts of the anterior central gyrus) are direct and cross. The cerebral cortex provides the voluntary act of urination. Cortical centers not only regulate voluntary urination, but can also inhibit this act.

Regulation of urination is a kind of cyclical process. Filling of the bladder leads to irritation of receptors located in the detrusor, in the mucous membrane of the bladder and the proximal part of the urethra. From the receptors, impulses are transmitted both to the spinal cord and to higher sections - the diencephalic region and the cerebral cortex. Thanks to this, a feeling of urge to urinate is formed. The bladder is emptied as a result of the coordinated action of several centers: excitation of the spinal parasympathetic, some suppression of the sympathetic, voluntary relaxation of the external sphincter and active tension of the abdominal muscles. After completion of the act of urination, the tone of the sympathetic spinal center begins to predominate, promoting contraction of the sphincter, relaxation of the detrusor and filling of the bladder. When the filling is appropriate, the cycle repeats.

Urinary retentionoccurs with sphincter spasm, detrusor weakness, or with bilateral disruption of the connections of the bladder with the cortical centers (due to the initial reactive inhibition of spinal reflexes and the relative predominance of the tone of the sympathetic spinal center). When the bladder overflows, the sphincter may partially open under pressure, and urine is released in drops. This phenomenon is called paradoxical ischuria. Disruption of the sensitive pathways of the urinary reflex leads to loss of the urge to urinate, which can also cause urinary retention, but since the feeling of bladder fullness persists and the efferent apparatus of the reflex is functioning, such retention is usually transient.

Temporary urinary retention, which occurs with bilateral damage to corticospinal influences, is replaced by urinary incontinence due to “disinhibition” of spinal segmental centers. This incontinence is essentially an automatic, involuntary emptying of the bladder as it becomes full and

called intermittent, periodic urinary incontinence. At the same time, due to the preservation of receptors and sensory pathways, the feeling of the urge to urinate takes on an imperative character: the patient must urinate immediately, otherwise involuntary emptying of the bladder will occur; in fact, the urge records the beginning of the involuntary act of urination.

Urinary incontinencewhen the spinal centers are affected, it differs from intermittent in that urine is constantly released drop by drop as it enters the bladder. This disorder is called true urinary incontinence, or paralysis of the bladder. With complete paralysis of the bladder, when there is weakness of both the sphincter and the detrusor, some of the urine accumulates in the bladder, despite its constant release. This often leads to cystitis, an ascending urinary tract infection.

IN childhood Urinary incontinence, predominantly at night, occurs as an independent disease - nocturnal enuresis. This disease is characterized functional disorders urination.

Nervous mechanism defecation is carried out thanks to the activity of the autonomic center of the spinal cord at the level of S 2 -S 4 and the cerebral cortex (most likely, the anterior central gyrus). Damage to corticospinal influences leads first to fecal retention, and then, due to the activation of spinal mechanisms, to automatic emptying of the rectum by analogy with intermittent urinary incontinence. As a result of damage to the spinal defecation centers, feces are constantly released as it enters the rectum.

Fecal incontinence, or encopresis, It is much less common than enuresis, but in some cases it can be combined with it.

Tendency to constipation may be observed with autonomic dysfunction with an increase in the tone of the sympathetic part of the autonomic nervous system, as well as in children who are accustomed to holding stool. Constipation, which can be associated with a wide variety of pathologies of internal organs, should be distinguished from fecal retention caused by damage to the autonomic centers. IN neurological clinic highest value has acute encopresis. Congenital encopresis can be caused by abnormalities of the rectum or spinal cord and often requires surgical treatment.

In clinical practice, disorders caused by impaired autonomic innervation of the eye and impaired tear and salivation are also important.

6.3. Autonomic innervation of the eye

Autonomic innervation of the eye provides dilation or constriction of the pupil (Mm. dilatator et sphincter pupillae), accommodation (ciliary muscle - M. ciliaris), a certain position of the eyeball in the orbit (orbital muscle - M. orbitalis) and partially - raising the upper eyelid ( superior muscle cartilage of the eyelid - M. tarsalis superior).

The sphincter of the pupil and the ciliary muscle, which determines accommodation, are innervated by parasympathetic nerves, the rest by sympathetic ones. Due to the simultaneous action of sympathetic and parasympathetic innervation, the loss of one of the influences leads to the predominance of the other (Fig. 6.3).

The nuclei of parasympathetic innervation are located at the level of the superior colliculi, they are part of the III cranial nerve (Yakubovich-Edinger-Westphal nucleus) - for the sphincter of the pupil and the Perlia nucleus - for the ciliary muscle. The fibers from these nuclei are included in III nerve into the ciliary ganglion, where postganglionic fibers originate to the constrictor pupillary muscle and the ciliary muscle.

The nuclei of sympathetic innervation are located in the lateral horns of the spinal cord at the level of the Q-Th 1 segments. Fibers from these cells are sent to the border trunk, the upper cervical ganglion and then through the plexuses of the internal carotid, vertebral and basilar arteries to the corresponding muscles (Mm. tarsalis, orbitalis et dilatator pupillae).

As a result of damage to the Yakubovich-Edinger-Westphal nuclei or the fibers coming from them, paralysis of the sphincter of the pupil occurs, while the pupil dilates due to the predominance of sympathetic influences (mydriasis). If the nucleus of Perlia or the fibers coming from it are damaged, accommodation is disrupted.

Damage to the ciliospinal center or the fibers coming from it leads to pupil constriction (miosis) due to the predominance of parasympathetic influences, to the retraction of the eyeball (enophthalmos) and easy narrowing of the palpebral fissure due to pseudoptosis of the upper eyelid and mild enophthalmos. This triad of symptoms - miosis, enophthalmos and narrowing of the palpebral fissure - is called Bernard-Horner syndrome,

Rice. 6.3.Autonomic innervation of the head:

1 - posterior central nucleus of the oculomotor nerve; 2 - accessory nucleus of the oculomotor nerve (Yakubovich-Edinger-Westphal nucleus); 3 - oculomotor nerve; 4 - nasociliary branch from the optic nerve; 5 - ciliary node; 6 - short ciliary nerves; 7 - sphincter of the pupil; 8 - pupil dilator; 9 - ciliary muscle; 10 - internal carotid artery; 11 - carotid plexus; 12 - deep petrosal nerve; 13 - upper salivary nucleus; 14 - intermediate nerve; 15 - elbow assembly; 16 - greater petrosal nerve; 17 - pterygopalatine node; 18 - maxillary nerve (II branch of the trigeminal nerve); 19 - zygomatic nerve; 20 - lacrimal gland; 21 - mucous membranes of the nose and palate; 22 - genicular tympanic nerve; 23 - auriculotemporal nerve; 24 - middle meningeal artery; 25 - parotid gland; 26 - ear node; 27 - lesser petrosal nerve; 28 - tympanic plexus; 29 - auditory tube; 30 - single track; 31 - lower salivary nucleus; 32 - drum string; 33 - tympanic nerve; 34 - lingual nerve (from the mandibular nerve - III branch of the trigeminal nerve); 35 - taste fibers to the front / 3 tongues; 36-hyoid gland; 37 - submandibular gland; 38 - submandibular node; 39 - facial artery; 40 - superior cervical sympathetic node; 41 - lateral horn cells TI11-TI12; 42 - lower node of the glossopharyngeal nerve; 43 - sympathetic fibers to the plexuses of the internal carotid and middle meningeal arteries; 44 - innervation of the face and scalp; III, VII, IX - cranial nerves. Parasympathetic fibers are indicated in green, sympathetic in red, and sensory in blue.

also including sweating disorders on the same side of the face. This syndrome is sometimes also observed depigmentation of the iris. Bernard-Horner syndrome is most often caused by damage to the lateral horns of the spinal cord at the level of C 8 -Th 1, the upper cervical parts of the borderline sympathetic trunk or the sympathetic plexus of the carotid artery, less often by a violation of the central influences on the ciliospinal center (hypothalamus, brain stem). Irritation these areas can cause protrusion of the eyeball (exophthalmos) and pupil dilation (mydriasis).

6.4. Tearing and salivation

Lacrimation and salivation are provided by the superior and inferior salivary nuclei, located in the lower part of the brain stem (the border of the medulla oblongata and the pons). From these nuclei, autonomic fibers go as part of the VII cranial nerve to the lacrimal, submandibular and sublingual salivary glands, as part of the IX nerve - to the parotid gland (Fig. 6.3). The function of salivation is influenced by the subcortical nodes and hypothalamus, therefore, when they are damaged, excessive salivation. Excessive salivation can also be detected in severe degrees of dementia. Impaired lacrimation occurs not only when the autonomic apparatus is damaged, but also when various diseases eyes and lacrimal duct, in case of disruption of the innervation of the orbicularis oculi muscle.

At autonomic nervous system research V neurological practice special meaning attached to its following functions: regulation of vascular tone and cardiac activity, regulation of secretory activity of glands, thermoregulation, regulation of metabolic processes, functions of the endocrine system, innervation of smooth muscles, adaptive and trophic influences on the receptor and synaptic apparatus.

In neurological clinics, disorders of vascular regulation, called vegetative-vascular dystonia, which are characterized by dizziness, lability of blood pressure, a sharp vasomotor reaction and coldness of the extremities, sweating and other symptoms.

With lesions of the hypothalamus, sweating on one half of the body is often impaired. In premature babies it is often detected Harlequin's symptom- redness of one half of the body, severe

to the sagittal line, most often observed in the lateral position. When the lateral horns of the spinal cord are damaged, disorders of vegetotrophic functions are observed in the zone of segmental innervation. It should be remembered that the segments of autonomic and somatic innervation do not coincide.

IN clinical practice hyperthermia may occur that is not associated with infectious diseases. In some cases there are hyperthermic crises- paroxysmal increases in temperature, which are caused by damage to the diencephalic region. It also matters temperature asymmetry- difference in temperature between the right and left half of the body.

Also very common hyperhidrosis- increased sweating over the entire surface of the body or on the limbs. In some cases, hyperhidrosis is a family trait. During puberty, it usually intensifies. In neurological practice, acquired hyperhidrosis is of particular importance. In such cases, it is accompanied by other autonomic disorders. To clarify the diagnosis, it is necessary to examine the somatic status of the child.

6.5. Syndromes of damage to the autonomic nervous system

In the topical diagnosis of autonomic disorders, one can distinguish between the levels of autonomic nodes, spinal and brainstem levels, hypothalamic and cortical autonomic disorders.

Symptoms of damage to the nodes of the border trunk (truncite):

Hyperpathia, paresthesia; aching, burning, constant or paroxysmally increasing pain (sometimes causalgia) in the area related to the affected nodes of the sympathetic trunk with a tendency to spread to the same half of the body;

Disorders of sweating, pilomotor, vasomotor reflexes, as a result of which marbling of the skin, skin hypoor hyperthermia, hyperhidrosis or anhidrosis, pastiness or atrophy of the skin appear in the affected area;

Deep reflexes in most cases are inhibited or (less often) disinhibited;

Diffuse atrophic changes in striated muscles develop without an electrical reaction of degeneration; possible atony or hypertension of muscles, sometimes contractures, paresis or rhythmic tremor of the limbs in the area of ​​innervation of the affected part of the sympathetic trunk;

The functions of internal organs associated with the area of ​​damage to the sympathetic trunk are disrupted;

Possible generalization of disorders of autonomic functions over the entire half of the body or the development of autonomic paroxysm of sympathoadrenal or mixed type, often in combination with asthenic or depressive-hypochondriacal syndrome;

Changes occur cellular composition blood (usually neutrophilic leukocytosis), biochemical parameters blood and tissue fluid.

Symptoms of damage to the pterygopalatine node:

Paroxysmal pain in the root of the nose, radiating to eyeball, ear canal, occipital region, neck;

Lacrimation, salivation, hypersecretion and hyperemia of the nasal mucosa;

Hyperemia of the sclera. Symptoms of damage to the ear node:

Pain localized anterior to the auricle;

Salivation disorders;

Sometimes herpetic rashes.

Nerve plexus damage causes autonomic disorders due to damage to the autonomic fibers that make up the nerves. In the zone of innervation of the corresponding nerves, vasomotor, trophic, secretory, and pilomotor disorders are observed.

With damage to the lateral horns of the spinal cord Vasomotor, trophic, secretory, pilomotor disorders occur in the zone of vegetative segmental innervation:

C 8 -Th 3 - sympathetic innervation of the head and neck;

Th 4 -Th 7 - sympathetic innervation of the upper extremities;

Th 8 -Th 9 - sympathetic innervation of the trunk;

Th 10 -L 3 - sympathetic innervation of the lower extremities;

S 3 -S 5 - parasympathetic innervation of the bladder and rectum.

Symptoms of hypothalamic damage:

sleep and wakefulness disorder(paroxysmal hypersomnia, permanent hypersomnia, distortion of the sleep formula, insomnia);

Vegetative-vascular syndrome is characterized by the appearance of paroxysmal vagotonic or sympathoadrenal crises; often they are combined or precede each other;

Neuroendocrine syndrome, which is based on pluriglandular dysfunction with impaired different types metabolism, endocrine and neurotrophic disorders (thinning and dry skin, the presence of ulcers, bedsores, neurodermatitis, interstitial edema, ulcers and bleeding from the gastrointestinal tract), bone changes (osteoporosis, sclerosis, etc.); Neuromuscular disorders in the form of periodic paroxysmal paralysis, muscle weakness and hypotension may also be observed.

Along with pluriglandular disorders, syndromes with clearly defined clinical manifestations are observed when the hypothalamus is damaged. These include: dysfunction of the gonads, diabetes insipidus, etc.

Itsenko-Cushing syndrome. The “bull” type of obesity is characteristic. Fat is predominantly deposited in the neck, upper shoulder girdle, chest, and abdomen. The deposition of fatty tissue on the face gives it a peculiar moon-shaped appearance. The limbs look thin against the background of obesity in the torso area. Trophic disorders are observed: stretch marks on the inner surface of the axillary region, the lateral surface of the chest and abdomen, in the area of ​​the mammary glands, and buttocks. Trophic skin disorders are manifested by dryness, a marbled tint in the area of ​​greatest fat deposition. Along with obesity, such patients experience a persistent increase in blood pressure, in some cases transient arterial hypertension, change in the sugar curve (flattening, double-humped curve), decrease in the level of 17-corticosteroids in the urine.

Adiposogenital dystrophy observed in children with infectious lesions, tumors in the area of ​​the sella turcica, hypothalamus, bottom and lateral walls of the third ventricle. It is characterized by pronounced deposition of fat, more in the abdomen, chest, and thighs. Obesity makes boys look effeminate and girls look mature. Relatively often observed are clinodactyly, changes in the bone skeleton, a lag in bone age from the passport age, and follicular keratitis. In boys, hypogenitalism is expressed in the pubertal and prepubertal periods (underdevelopment of the genital organs, cryptorchidism, hypospadias). In girls, the labia minora are underdeveloped and there are no secondary labia

vy signs. Trophic skin disorders manifest themselves in the form of thinning, appearance acnae vulgaris, depigmentation, marbled tint, increased capillary fragility.

Lawrence-Moon-Biedl syndrome - congenital anomaly development with severe dysfunction of the hypothalamic region. Characterized by obesity, underdevelopment of the genital organs, dementia, growth retardation, pigmentary retinopathy, polydactyly or syndactyly, and progressive loss of vision. The prognosis for life is favorable.

Premature puberty may be caused by tumors in the area of ​​the mamillary bodies or posterior hypothalamus, tumors of the pineal gland. Early puberty is more common in girls and is sometimes combined with accelerated body growth. Along with premature puberty, children exhibit signs of damage to the hypothalamic region - bulimia, polydipsia, polyuria, obesity, sleep and thermoregulation disorders, and mental disorders. Changes in the child's personality are characterized by disorders of the emotional-volitional sphere and behavior. Children often become rude, angry, cruel, with a penchant for theft and vagrancy. Increased sexuality is especially developed in adolescents. In some cases, attacks of excitement periodically occur, followed by drowsiness and bad mood. The neurological status reveals a variety of small-focal symptoms and autonomic-vascular disorders. Obesity and increased secretion of gonadotropic hormone are noted.

Delayed puberty It is detected in adolescence, more often in boys. Characterized by tall stature, disproportionate physique, and female-type obesity. When examined, hypoplasia of the genital organs, cryptorchidism, monorchidism, hypospadias, and gynecomastia are revealed in boys; in girls, a vertical vulva, underdevelopment of the labia majora and glands, lack of secondary hair growth, and delayed menstruation are detected. Puberty of adolescents is delayed until 17-18 years of age.

Cerebral dwarfism - a syndrome characterized by a slowdown or suspension of general development. Occurs when the pituitary gland or hypothalamic region is damaged. Dwarf growth is noted. Bones and joints are short and thin. Epiphyseal-diaphyseal

growth lines remain for a long time open, small head, reduced sella turcica. Internal organs proportionally reduced in size; the external genitalia are hypoplastic.

Diabetes insipidus occurs with neuroinfections, tumors of the hypothalamus. At the core diabetes insipidus there is a reduced production of antidiuretic hormone by neurosecretory cells (supraoptic and paraventricular nuclei). Polydipsia and polyuria are observed; urine has a reduced relative density.

6.6. Symptoms of damage to the limbic system

Damage to the limbic system is characterized by:

Excessive lability of emotions, attacks of anger or fear;

Psychopathic behavior with traits of hysteria and hypochondriacity;

Inappropriate behavior with elements of panache, affectation, theatricality, delving into one’s own painful sensations;

Disinhibition of instinctive forms of behavior (bulimia, hypersexuality, aggressiveness);

Twilight states of consciousness or limited wakefulness;

Hallucinations, illusions, complex psychomotor automatisms with subsequent loss of memory for events;

Violation of memory processes - fixation amnesia;

Epileptic seizures.

Cortical autonomic disorders in isolated form are extremely rare. They are usually combined with other symptoms: paralysis, sensory disturbances, and convulsive attacks.