Vegetative innervation of the eye symptoms of the lesion. Heading "vegetative innervation of the eyes

CHAPTER 6. VEGETATIVE (AUTONOMOUS) NERVOUS SYSTEM. SYNDROMES OF DEFEAT

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

The division of the brain into systems is rather conditional. 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 under the influence of innervation. sympathetic and parasympathetic parts of the vegetative nervous system. In cases of functional predominance of one of them, symptoms of increased excitability are observed: sympathicotonia - in the case of the predominance of the sympathetic part and vagotonia - in the case of the predominance of the parasympathetic (Table 10).

Table 10The action of the autonomic nervous system

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

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

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 autonomic nervous system includes:

Border trunk with paravertebral nodes;

A number of gray (non-fleshy) and white (fleshy) fibers extending from the boundary trunk;

Nerve plexuses outside and inside organs;

Separate peripheral neurons and their clusters (prevertebral nodes), combined 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 department - 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 department - trunk:

Kernels of Yakubovich-Westphal-Edinger, Perlia;

Cells involved in thermoregulation and metabolic processes;

secretory nuclei;

Semi-specific respiratory and vasomotor centers;

3rd department - 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, olfactory brain, periamygdala cortex);

Neocortex (cingulate gyrus, fronto-parietal cortex, deep parts of the temporal lobe);

Subcortical formations (almond-shaped complex, septum, thalamus, hypothalamus, reticular formation).

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

Hypothalamus:

It 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, vessels highly permeable to protein molecules;

Close to liquor-bearing paths.

These features determine the increased "vulnerability" of the hypothalamus under the influence of various pathological processes in the central nervous system and explain the ease of occurrence of its dysfunction.

Each group of nuclei of the hypothalamus performs suprasegmental vegetative 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, the genital area, cardiovascular and respiratory systems, activity of the gastrointestinal tract, pelvic organs, trophic functions, body temperature.

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

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 - bottom longitudinal beam; 10 - border; 11 - gyrus of the hippocampus; 12 - hook; 13 - orbital surface of the frontal pole; 14 - hook-shaped bundle; 15 - transverse connection of the amygdala; 16 - front spike; 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 speak of 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 the most complex instinctive and emotional reactions, such as food, defensive. The limbic system is also 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 mainly of smooth muscles, therefore it is innervated by autonomic fibers. At the same time, the composition of the bladder and anal sphincters includes striated muscles, which makes it possible to voluntarily contract and relax them. Voluntary regulation of urination and defecation is formed 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 in a dream there are still cases of involuntary urination.

Reflex emptying of the bladder is carried out due 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 the L 1 -L 3 segments. Sympathetic innervation is carried out by the lower hypogastric plexus, cystic nerves. Sympathetic fibers

Rice. 6.2.Central and peripheral innervation of the bladder: 1 - cerebral cortex; 2 - fibers that provide arbitrary control over the emptying of the bladder; 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); 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 muscles). With an increase in the tone of the sympathetic nervous system, there is 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 bladder emptying.

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

The regulation of urination is a kind of cyclic process. Filling the bladder leads to irritation of the 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 the higher departments - the diencephalic region and the cortex of the cerebral hemispheres. Due to this, a feeling of urge to urinate is formed. The bubble is emptied as a result of the coordinated action of several centers: excitation of the spinal parasympathetic, some inhibition of the sympathetic, voluntary relaxation of the external sphincter and active tension of the abdominal muscles. After the completion of the act of urination, the tone of the sympathetic spinal center begins to predominate, which contributes to the contraction of the sphincter, relaxation of the detrusor and filling of the bladder. With appropriate filling, the cycle repeats.

Urinary retentionoccurs with spasm of the sphincter, weakness of the detrusor, or with a bilateral violation of the connections of the bladder with 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 excreted in drops. Such a phenomenon is called paradoxical ischuria. Violation of the sensitive pathways of the urethral reflex leads to the loss of the urge to urinate, which can also cause urinary retention, but since the feeling of overflow of the bladder persists, and the efferent apparatus of the reflex is functioning, such a delay is usually transient.

Temporary urinary retention, which occurs with bilateral lesions of cortico-spinal influences, is replaced by urinary incontinence due to the "disinhibition" of the spinal segmental centers. This incontinence is essentially automatic, involuntary emptying of the bladder as it fills and

called intermittent, intermittent urinary incontinence. At the same time, due to the preservation of receptors and sensory pathways, the sensation of the urge to urinate becomes imperative: the patient must urinate immediately, otherwise involuntary emptying of the bladder will occur; in fact, the urge fixes the beginning of the involuntary act of urination.

Urinary incontinencewith damage to the spinal centers, it differs from intermittent in that urine is constantly excreted 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, part of the urine accumulates in the bladder, despite its constant release. This often leads to cystitis, an ascending urinary tract infection.

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

neural mechanism defecation is carried out due 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). The defeat of cortical-spinal 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 centers of defecation, feces are constantly excreted as they enter the rectum.

fecal incontinence, or encopresis, occurs much less frequently than enuresis, but in some cases can be combined with it.

Tendency to constipation can 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 used to holding stools. 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. AT neurological clinic Acute encopresis is the most important. Congenital encopresis may be due to abnormalities of the rectum or spinal cord and often requires surgical treatment.

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

6.3. Autonomic innervation eyes

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

The sphincter of the pupil and the ciliary muscle, which causes accommodation, are innervated by parasympathetic nerves, the rest are sympathetic. 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, are part of the III cranial nerve (Yakubovich-Edinger-Westphal nucleus) - for the sphincter of the pupil and the nucleus of Perlia - for the ciliary muscle. The fibers from these nuclei go as part of the III nerve to the ciliary ganglion, from where the postganglionic fibers originate to the muscle that narrows the pupil 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. The fibers from these cells are sent to the border trunk, the upper cervical node, and then along the plexuses of the internal carotid, vertebral and basilar arteries they approach the corresponding muscles. (Mm. tarsalis, orbitalis et dilatator pupillae).

As a result of the defeat of the Yakubovich-Edinger-Westphal nuclei or the fibers coming from them, paralysis of the sphincter of the pupil occurs, while the pupil expands due to the predominance of sympathetic influences (mydriasis). With the defeat of the nucleus of Perlia or the fibers coming from it, accommodation is disturbed.

The defeat of the ciliospinal center or the fibers coming from it leads to a narrowing of the pupil (miosis) due to the predominance of parasympathetic influences, to the retraction of the eyeball (enophthalmos) and easy constriction 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.Vegetative innervation of the head:

1 - posterior central nucleus of the oculomotor nerve; 2 - accessory nucleus of the oculomotor nerve (nucleus of Yakubovich-Edinger-Westphal); 3 - oculomotor nerve; 4 - nasociliary branch from the optic nerve; 5 - ciliary knot; 6 - short ciliary nerves; 7 - sphincter of the pupil; 8 - pupil dilator; 9 - ciliary muscle; 10 - internal carotid artery; 11 - carotid plexus; 12 - deep stony nerve; 13 - upper salivary nucleus; 14 - intermediate nerve; 15 - knee assembly; 16 - large stony nerve; 17 - pterygopalatine node; 18 - maxillary nerve (II branch trigeminal nerve); 19 - zygomatic nerve; 20 - lacrimal gland; 21 - mucous membranes of the nose and palate; 22 - knee-tympanic nerve; 23 - ear-temporal nerve; 24 - middle meningeal artery; 25 - parotid gland; 26 - ear knot; 27 - small stony nerve; 28 - tympanic plexus; 29 - auditory tube; 30 - single way; 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 anterior / 3 tongues; 36-sublingual gland; 37 - submandibular gland; 38 - submandibular node; 39 - facial artery; 40 - upper cervical sympathetic node; 41 - cells of the lateral horn TI11-TI12; 42 - the 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. Green color indicates parasympathetic fibers, red - sympathetic, blue - sensitive

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

6.4. Tearing and salivation

Lacrimation and salivation are provided by the upper and lower salivary nuclei located in the lower part of the brain stem (the border of the medulla oblongata and the brain bridge). From these nuclei, vegetative 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 subcortical nodes, the hypothalamus, therefore, when they are damaged, excess salivation. Excessive salivation can also be detected in severe degrees of dementia. Disturbances in tear secretion are noted not only with damage to the autonomic apparatus, but also with various diseases of the eyes and lacrimal duct, with a violation of the innervation of the circular muscle of the eye.

At study of the autonomic nervous system in neurological practice, special importance is attached to the following functions: regulation of vascular tone and cardiac activity, regulation of secretory activity of glands, thermoregulation, regulation of metabolic processes, functions endocrine system, innervation of smooth muscles, adaptive and trophic effects on the receptor and synaptic apparatus.

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

With lesions of the hypothalamus, sweating on one half of the body is often disturbed. Premature babies often have Harlequin symptom- redness of one half of the body, strictly going

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

AT clinical practice hyperthermia may be observed, 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- the difference between the temperature of the right and left half of the body.

Also very common hyperhidrosis- increased sweating all over the body or on the extremities. In some cases, hyperhidrosis runs in families. In puberty, it usually intensifies. Acquired hyperhidrosis is of particular importance in neurological practice. 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 levels of autonomic nodes, spinal and stem levels, hypothalamic and cortical autonomic disorders.

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

Hyperpathy, paresthesia; aching, burning, persistent or paroxysmal pains (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, pastosity or skin atrophy 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 the muscles, sometimes contractures, paresis or rhythmic tremor of the limbs in the zone of innervation of the affected part of the sympathetic trunk;

The functions of the internal organs associated with the affected area of ​​the sympathetic trunk are disturbed;

It is possible to generalize violations of autonomic functions to the entire half of the body or develop an autonomic paroxysm of sympathoadrenal or mixed type, often in combination with asthenic or depressive-hypochondriac syndrome;

There are changes 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 the eyeball, ear canal, occipital region, neck;

Lacrimation, salivation, hypersecretion and hyperemia of the mucous membrane of the nasal cavity;

Hyperemia of the sclera. Ear node symptoms:

Pain, localized anterior to the auricle;

Salivation disorders;

Sometimes herpetic eruptions.

Damage to the nerve plexuses 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, pilomotor disorders are observed.

Damage to the lateral horns of the spinal cord vasomotor, trophic, secretory, pilomotor disorders occur in the zone of autonomic segmental innervation:

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

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

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 damage to the hypothalamus:

sleep and wake disturbance(paroxysmal hypersomnia, permanent hypersomnia, perversion of the sleep formula, insomnia);

The vegetative-vascular syndrome is characterized by the appearance of paroxysmal vagotonic or sympathetic-adrenal crises; often they are combined or precede each other;

Neuroendocrine syndrome, which is based on pluriglandular dysfunction with impaired different types metabolism, endocrine and neuro-trophic disorders (thinning and dryness of the 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 can also be observed.

Along with pluriglandular disorders, lesions of the hypothalamus are accompanied by syndromes with clearly defined clinical manifestations. These include: dysfunction of the gonads, diabetes insipidus, etc.

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

Adiposogenital dystrophy observed in children with infectious lesions, tumors in the area of ​​the Turkish saddle, hypothalamus, bottom and side walls of the third ventricle. It is characterized by a pronounced deposition of fat, more in the abdomen, chest, hips. Obesity makes boys look effeminate, girls look mature. Relatively often, clinodactyly, changes in the bone skeleton, bone age lagging behind the passport age, and follicular keratitis are noted. 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, there are no secondary sexual

you signs. Trophic disorders of the skin are manifested in the form of its thinning, the appearance acne vulgaris, depigmentation, marble shade, increased capillary fragility.

Lawrence-Moon-Beadle Syndrome - congenital anomaly of development with severe dysfunction of the hypothalamic region. It is characterized by obesity, underdevelopment of the genital organs, dementia, growth retardation, retinopathy pigmentosa, polydactyly or syndactyly, progressive visual loss. The prognosis for life is favorable.

premature puberty can be caused by tumors in the area of ​​the mammillary bodies or the posterior hypothalamus, tumors of the pineal gland. Early puberty is more common in girls, sometimes combined with accelerated body growth. Along with premature puberty, children have 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, vicious, cruel, with a penchant for theft, vagrancy. Increased sexuality is especially developed in adolescents. In some cases, periodically there are attacks of excitation, followed by drowsiness, bad mood. AT neurological status various small-focal symptoms, vegetative-vascular disorders are revealed. Obesity, increased secretion of gonadotropic hormone are noted.

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

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

the growth lines remain open for a long time, the head is small, the Turkish saddle is reduced. Internal organs proportionately reduced in size; the external genitalia are hypoplastic.

diabetes insipidus occurs with neuroinfections, tumors of the hypothalamus. At the core diabetes insipidus lies the 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, bouts of anger or fear;

Psychopathic behavior with features of hysteria and hypochondria;

Inadequate behavior with elements of drawing, affectation, theatricality, deepening 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 are extremely rare in isolated form. Usually they are combined with other symptoms: paralysis, sensory disturbances, convulsive attacks.

and in the central nervous system), wherever the fibers of the sympathetic nervous system penetrate. In addition, in these systems, as already noted, there is a different mediation.

Only the segmental apparatus from a functional and morphological position is truly specific vegetative. The presence of dual innervation of organs by sympathetic and parasympathetic fibers is important. The exceptions are the adrenal medulla (reformed sympathetic ganglion) and sweat glands, innervated by sympathetic fibers, at the end of which acetylcholine is released.

The presence of dual innervation of organs is expressed in the opposite effect on the working organ of the parasympathetic and sympathetic divisions of the ANS: vasodilation and constriction, increased and slowed heart rate, changes in the lumen of the bronchi, peristalsis of the gastrointestinal tract, etc. Such an antagonistic effect is a mechanism for adapting the body to changing environmental conditions. At the same time, the strengthening of the functioning of one department under normal physiological conditions leads to compensatory tension in the apparatuses of another department, returning the functional system to homeostatic indicators.

In a state of relative rest, when there is no active work, the segmental vegetative system can provide automated activity for the existence of the organism. In real conditions, adaptation to changing environmental conditions, adaptive behavior, is carried out with the participation of suprasegmental structures that use the segmental ANS as an apparatus for rational adaptation.

Autonomic innervation of the eye

Parasympathetic innervation represented by fibers in the composition of the oculomotor nerve from the nucleus of Yakubovich. Axons are interrupted at the ciliary ganglion, from which postsynaptic fibers approach the muscle that constricts the pupil. As a result of conducting impulses along this efferent path, pupil constriction occurs. This is the efferent part of the pupillary reflex arc to light.

With the defeat of the parasympathetic conductors (nucleus cells, preganglionic fibers, the ciliary node with its postganglionic fibers), the pupil becomes dilated due to contraction of another smooth muscle that dilates the pupil and receives sympathetic innervation.

The nucleus of Perlea of ​​the oculomotor nerve innervates the ciliary muscle. If this innervation is disturbed, accommodation changes.

Sympathetic neurons located in the lateral horns from C7 to Tht segments of the spinal cord. The axons of these cells as part of the anterior roots emerge from spinal canal and in the form of a connecting branch penetrate into the first thoracic and lower cervical nodes of the sympathetic trunk (often these nodes are combined into a stellate node). The fibers, without interruption, pass through it and through the middle cervical node, then end at the cells of the upper cervical sympathetic node. Postganglionic synaptic fibers braid the wall of the internal carotid artery, through which they enter the cranial cavity, and then, with the ophthalmic artery, reach the orbit and end in a smooth muscle, during contraction of which the pupil expands. In addition, sympathetic fibers are in contact with the muscle that expands the palpebral fissure, and with the smooth muscles of the fiber of the orbit, the so-called Müllerian eye muscles. When the impulses traveling through the sympathetic fibers are turned off, at any level from the spinal cord to the eyeball, a triad of symptoms occurs on its side: miosis due to dilator paralysis, constriction of the eye due to damage to the muscle that expands the palpebral fissure, enophthalmos due to paresis of smooth muscle fibers of the retrobulbar fiber. it Claude Ber syndrome nara-horner. It usually occurs when the lateral horn of the spinal cord is damaged (tumor, ischemia, hemorrhage) in the C7-Th zone, segments, stellate or upper cervical sympathetic node (for example, when the node is blocked with novocaine solution), when the tumor is compressed in the apex of the lung, when the wall is damaged internal carotid or ophthalmic artery.

The cells of the lateral horns of the C7-Thj segments of the spinal cord (ciliospinal center) are approached by fibers from the cerebral cortex and hypothalamus. These conductors go in the side

Chapter 8

brainstem and cervical segments of the spinal cord. Therefore, with a focal lesion of one of the halves of the brain stem, in particular, the posterolateral parts of the medulla oblongata, along with other symptoms, the Claude Bernard-Horner triad occurs (for example, with the Wallenberg-Zakharchenko syndrome).

Irritation of sympathetic fibers heading to the eyeball is accompanied by pupil dilation, slight expansion of the palpebral fissure, exophthalmos is possible (Pourfure du Petit syndrome).

Bladder innervation

In neurological practice, dysfunction of the pelvic organs is quite common. Urination is carried out due to the coordinated activity of two muscle groups: the detrusor and the internal sphincter. This happens as a result of the interaction of the somatic and autonomic nervous systems. The muscles of the detrusor and internal sphincter consist of smooth muscle fibers and receive autonomic innervation. While the external sphincter is formed by striated muscle fibers and is innervated by somatic nerves.

The act of urination involves the striated muscles of the anterior abdominal wall and diaphragm of the pelvic floor. Their contraction contributes to a sharp increase in intra-abdominal pressure and thus complements the function of the bladder detrusor.

In general, the segmental apparatus of the spinal cord provides autonomic innervation of smooth muscles and involuntary reflex urination. In an adult, this segmental apparatus is subordinate to the cerebral cortex, which determines the voluntary component of urination.

Automatic emptying of the bladder is provided by two segmental reflex arcs (parasympathetic and somatic). The irritation from stretching its walls along the afferent fibers of the pelvic nerve is transmitted to the parasympathetic cells of the sacral segments of the spinal cord. Impulses along the efferent fibers lead to contraction of the detrusor and relaxation of the internal sphincter. Ras-

Part I. Anatomical and physiological features of the nervous system

closure of the internal sphincter and urine flow into initial departments the urethra puts into operation another reflex arc for the external sphincter, with the relaxation of which the act of urination is carried out. This is how the bladder works in newborns.

In the future, in connection with the maturation of the suprasegmental apparatus, conditioned reflexes are developed, a sensation of the urge to urinate is formed.

The voluntary component of the act of urination is associated with the control of the external urethral sphincter and the accessory muscles of the abdomen and pelvic diaphragm.

Sensory neurons are located in the intervertebral nodes S, s segments of the spinal cord. The dendrites in the pudendal nerve terminate in receptors both in the bladder wall and in the sphincters. Axons, together with the posterior roots, reach the spinal cord, as part of the posterior cords rise to the medulla oblongata. Further, the path follows the vaulted gyrus (sensory area of ​​urination). Along the associative fibers, impulses from this zone follow to the central motor neurons located in the cortex of the paracentral lobe (motor area, urination). The axons of these neurons as part of the pyramidal tract reach the cells of the anterior horns of the S13 segments of the spinal cord. With the anterior roots, the fibers leave the spinal canal and form the pudendal plexus in the pelvic cavity; as part of the pudendal nerve, they approach the external sphincter. With the contraction of this sphincter, it is possible to voluntarily retain urine in the bladder.

The pelvic organs have bilateral cortical innervation. Therefore, in clinical practice, the most serious urinary disorders occur with extensive transverse spinal cord injury or bilateral damage. cortical centers(Table 1). Bilateral damage to the connections of the cortical zones of the bladder with its spinal centers leads to central urination disorders in the form of urinary retention (in acute conditions). In this case, the sphincters are autochthonously and reflexively contracted, and the emptying reflex is absent. Urinary retention subsequently changes to intermittent urinary incontinence due to an increase in ref

We'll consider autonomous systems to the extent that they take part in the structure of the organ of vision.
As long as the old view, according to which two systems in the body - sympathetic and parasympathetic - play an opposite role. The sympathetic system is an alarm system. Under the influence of fear and rage, it is activated and enables the body to cope with emergencies; at the same time, the metabolism is set to an increased consumption, to dissimilation. In contrast, the parasympathetic system is set to a state of rest, economical consumption in the process of metabolism, assimilation.

to the central neuron transmits excitation further to numerous peripheral neurons. A stronger excitation, in addition, causes through nn. splanchnici release of adrenaline from the adrenal glands. Both of these pathways carry out the so-called mass reactions. AT parasympathetic system in contrast, chains of neurons are used in rows; due to this, the responses at the terminal organs are more limited and accurately calculated (for example, the reaction of the Pupil).

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, does not hold true in all cases. So, for example, when “sympathetic” fibers ending at the pilomotor and sweat glands are excited, acetylcholine is released and the transfer of excitation from the preganglionic to the postganglionic neuron in the entire sympathetic system, as well as in the parasympathetic system, is also carried out through acetylcholine.

Exploring afferent pathways within autonomous systems is just beginning and, probably, new fundamental data in this regard will be obtained in the coming years. Within the scope of this article, we deal mainly with efferent conductors. Of the afferent pathways through which the autonomic system is brought into excitation, we will later become acquainted with somatic neurons.

In the area of 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 (Landshgrem - Landstrom) - usually a person has a rudimentary developed muscle stretched over the fissura orbitalis inferior, the lacrimal gland (which also has parasympathetic innervation), blood vessels and sweat glands of the skin of the face. It should be mentioned that m. sphincter pupillae, in addition to parasympathetic, also has sympathetic innervation; in response to sympathetic irritation, he instantly relaxes. The same applies to the ciliary muscle.

Recently exposed even doubt the presence of a dilator in a rabbit. The expansion of the pupil that occurs in response to sympathetic irritation is explained by the active contraction of blood vessels in the stroma of the iris and inhibition of the contraction of the sphincter. It would be premature, however, to transfer these views to man.

All going to the above terminal organs postganglionic neuritis originate in the ganglion cervicale superius. They accompany carotis externa (sweat glands) and carotis interna; with the latter, they enter the cranial cavity for the second time, so that here, as sympathetic plexuses, they braid various other structures (a. ophtalmica, ramus ophtalmicus 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 neuritis extending from the ganglia of the border trunk to the periphery are called "postganglionic"; they are fleshless (rami communicantes grisei). Preganglionic neuritis, which ensures the transmission of excitation from the central nervous system to the borderline trunk, originate from cells located in the lateral horns of the spinal cord. Collectively, these cells make up the columna intermediolateralis; they stretch approximately from the first thoracic to the second lumbar segment of the spinal cord. Accordingly, only these segments (with anterior roots) leave preganglionic fibers (thoracolumbar autonomous system); these fibers are pulpy (rami communicantes albi).

preganglionic fibers, supplying the ganglion cervicale, exit the spinal cord with roots C8, Th1 and Th2. With irritation of the corresponding segments of the spinal cord (upper border of C6, lower border of Th4), pupil dilation occurs. In this regard, the upper end of the columna intermediolateralis is called the centrum ciliospinale (Budzhe-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 nucleus of the vagus), there seem to be impulses to the 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 also suggest the presence of sympathetic centers. The assumption most consistent with reality is that sympathetic excitation from the hypothalamus through a chain of short neurons in the substantia nigra is transmitted to the centrum ciliospinale (Budge).

After what has already been said about corticolization of functions brain stem , it seems self-evident that the cerebral cortex also affects the autonomic system (vasomotor, pilomotor, gastrointestinal tract). Electrical stimulation of the second frontal gyrus (field 8, according to Brodmann) causes a bilateral expansion 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.

Pupil diameter 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 - the difference in the size of the pupils is possible and normal (almost 30% healthy people ), but if it exceeds 0.9 mm, then it should be recognized as 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 of the eye: the sphincter of the pupil and the dilator of the pupil (m. sphincter pupillae et m. dilatator pupillae). The sphincter of the pupil has a parasympathetic innervation, and the dilator has a sympathetic innervation. If only parasympathetic innervation is disturbed, the sphincter is paralyzed and the pupil expands, while it does not react to light; in the case of a disorder of sympathetic innervation, the pupil dilator is paralyzed and the pupil is constricted, but it can react to light. Thus, the pupil can be dilated when the sympathetic structures that innervate it are excited or when the functions of parasympathetic structures are suppressed; constriction of the pupil may be the result 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 (Fig. 30.2 and 30.3), while 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, pupil constriction occurs when a 2.5% solution of methacholine is instilled, while normally there is no such reaction. In patients with complete denervation of the smooth muscles that determine pupil width, these tests can detect both sympathetic and parasympathetic denervation. It should be borne in mind that parasympathetic denervation hypersensitivity develops in 80% of patients with diabetic autonomic neuropathy, more often it is detected in patients with diabetes mellitus for more than 2 years. The narrowing of the pupil - miosis - is pathological if its diameter under normal lighting is less than 2 mm. Spastic miosis is caused by excitation of the parasympathetic structures of the oculomotor nerve system (medicated spastic miosis may be the result 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 the suppression of the sympathetic innervation of the muscle that dilates the pupil, which occurs, in particular, in Horner's syndrome. Moderate bilateral miosis with intact pupillary response to light. 30.2. Pupil changes in right-sided temporo-tentorial herniation. a - the normal state of the pupils; b - irritation of the oculomotor nerve, in connection with this, the right pupil is narrowed; c — prolapse of the 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 respond to light due to damage to the parasympathetic bundle of the oculomotor nerve, on the left — due to irritation of the oculomotor nerve, the pupil is narrowed; e - due to a pronounced bilateral lesion of the oculomotor nerves, the pupils on both sides are wide and do not react to light. Rice. 30.3. Examination of pupillary response to light differential diagnosis damage to the optic and oculomotor nerves. a - defeat of the right optic nerve(afferent part of the pupillary reflex arc). When illuminating the right eye, both direct and friendly reaction of the pupils are absent, when illuminating the left eye, both reactions are evoked; b - damage to the right oculomotor nerve (the efferent part of the pupillary reflex arc). 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, the reaction of the pupil to light is caused, while the friendly reaction of the pupil of the right eye is absent. marked during sleep, as well as with bilateral lesions of the diencephalic region and with its central transtentorial herniation. Pinpoint pupils that react to light are observed with damage to the brain bridge, with intoxication with narcotic drugs. To detect the reaction of pupils to light in such cases, you should use a magnifying glass (magnifying glass). Mydriasis is pupil dilation. It may be pathological if its diameter under normal lighting is greater 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 narrows the pupil. So, unilateral dilation 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 brain stem due to temporotentorial herniation (Hatchinson's pupil). Such drug-induced mydriasis may be the result of instillation of a solution of atropine or other M-anticholinergics into the eye. With paralytic dilation of the pupil, its direct and friendly reaction to light is disrupted. Spastic mydriasis is a consequence of contraction of the muscle that dilates the pupil, with irritation of the sympathetic structures innervating it, for example, in Petit's 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 the CVI1,—Th(, segments of the spinal cord, which have connections with the posterior group of the nuclei of the hypothalamic region, passing through the tegmentum of the stem structures and the central gray matter on the cervical level of the spinal cord.The preganglionic fibers leaving the vegetative cells located here, having passed through the corresponding anterior spinal roots, spinal nerves and white connecting branches penetrate the paravertebral sympathetic chain at the level of the stellate ganglion. Having passed through the stellate and middle cervical nodes, they reach the cells of the upper cervical node, where the sympathetic impulses are switched from the preganglionic fibers to the cells of this node and their axons, which are postganglionic fibers. The latter form sympathetic plexuses of the external 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 superior muscle of the cartilage of the eyelid (m. tarsalis superior ). Violation of their innervation, which occurs when any part of the path of sympathetic impulses from the ciliospinal center to them is damaged, leads to paresis or paralysis of these muscles. In this regard, Horner's syndrome (Claude Bernard-Horner's syndrome) develops on the side of the pathological process, manifested by pupil constriction (paralytic miosis), small (1-2 mm) enophthalmos and the so-called pseudoptosis (drooping of the upper eyelid), causing some narrowing eye gap. In view of the preservation of the parasympathetic innervation of the sphincter of the pupil on the side of Horner's syndrome, the reactions of the pupil to light are preserved (for more details, see Chapter 13). Irritation of sympathetic nerve structures can lead to the development of Petit's syndrome ("reverse" Horner's syndrome) - dilation of the pupil and palpebral fissure, slight exophthalmos. The manifestation of the entire triad of symptoms during irritation of the sympathetic structures that conduct impulses from the ciliospinal center is not necessary. More often one has to meet only anisocoria in connection with the expansion of the pupil on the side of irritation of sympathetic structures. There are many reasons for this anisocoria. One of them may be a tuberculosis focus in the apex of the lung (Roque's symptom). The dilation of the pupil on the left sometimes occurs due to hypertrophy of the heart, aneurysm of the aortic arch. With insufficiency of the aortic valve, "pulsation" of the pupils is possible: the pupils constrict during systole and expand 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 cover of the trunk and the 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 the smooth muscles of the eyes, which have sympathetic innervation. Such disorders of the functions 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 a 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. Small, light-responsive pupils (paralytic miosis) may indicate the metabolic nature of the coma or its diencephalic involvement. Pupils of medium size that do not respond to light are usually the result of damage to the roof of the midbrain. A wide, unresponsive pupil indicates an ipsilateral lesion of the autonomic parasympathetic nuclei in the midbrain tegmentum, root, or oculomotor nerve trunk. Very narrow (pinpoint) pupils with a preserved reaction to light are a sign of damage to the brain bridge. There are also exceptions to these rules. Thus, in metabolic coma caused by poisoning with anticholinergic (anticholinergic) drugs (atropine, scopolamine, etc.), the pupils are sharply dilated and do not respond to light (paralytic mydriasis). Wide, unresponsive pupils are observed during a major seizure, are characteristic of severe hypothermia, and 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. So, a significant decrease in vision, and even more so blindness, on the one hand, due to damage to the retina or optic nerve, are accompanied by anisocoria due to pupil dilation on the side of visual acuity decrease, while there is no direct reaction of the pupil to light, and friendly - preserved (Hun's symptom). With bilateral blindness that has arisen in connection with damage to the visual system from the retinas to the subcortical centers, the pupils are dilated and there is no direct or friendly reaction of the pupils to light. Pupil dilation can occur with intense headache in patients with a hypertensive crisis, with migraine attacks (Reder's symptom), as well as with other severe pain syndromes and pains arising from external influences. The reason for the expansion of the pupils can be stressful psychotrauma and tearing situations. Anisocoria and deformity of the pupils are often observed in neurosyphilis, then a perverted reaction of the pupils to light is also possible (expansion with increased illumination of the retina and narrowing of the pupils with their dimming - the pupillary symptom of Gowers). Robertson's (Argyle Robertson's) syndrome is widely known for 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, 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 the smooth eye muscles due to irritation of the cells of the parasympathetic Edinger-Westphal nuclei in the tegmentum of the midbrain. In epidemic encephalitis, the “reverse” Robertson syndrome is possible: the absence of pupillary reaction to accommodation and convergence with a preserved direct and friendly pupillary reaction to light. Pupil of Hutchinson - dilation of the pupil and disorder of its direct and friendly reaction to light. This is a sign of a supratentorial, more often temporal, tumor or hematoma, which caused the syndrome of wedging of the brain tissue into Bisha's fissure and compression of the oculomotor nerve. Pupil dilation on the side of the pathological process can also be a sign of Knapp's syndrome, in which, due to compression in a similar situation of the brain stem, along with homolateral pupil dilation, central hemiparesis occurs on the other side. Anisocoria in progressive paralysis is known as Bayarzhe's sign, named after the French psychiatrist J. Baillarger (1809-1890), who described this sign. Anisocoria due to the expansion of the right pupil may be a sign of appendicitis or cholecystitis (a symptom of Moscow). Cavernous sinus wall syndrome (Foy syndrome), Weber, Benedict, Claude syndromes are described in Chapter 11. Thus, the study of the condition of the eyes and their appendages, gaze, condition cranial nerves, providing innervation of the external and internal muscles of the eye, provides very significant information about the topic and the nature of the pathological process, which makes it possible to develop the most rational medical tactics in each specific case.

Parasympathetic nerve bundles and fibers pass along with the oculomotor nerve and come from the Yakubovich-Edinger-Westphal nucleus. axons nerve cells from these nuclei, presynaptic fibers are interrupted in the ciliary node located in the orbit. From the ciliary node, the postsynaptic fibers pass to the iris muscle, the constrictor pupil, and the ciliary muscle. Pupil constriction occurs when a nerve impulse occurs under the influence of light irritation of the retinal receptors.
Thus, this group of parasympathetic fibers extending from the anterior part of the nucleus is part of the arc of the pupillary reflex to light.
With various disorders of the parasympathetic innervation of the eye, which can capture different areas of the path, namely: the cell structures of the Yakubovich-Edinger-Westphal nucleus, preganglionic fibers, the ciliary node and its postganglionic fibers. In this case, the passage of a nerve impulse is disrupted or stopped. As a result of such violations, the pupil expands due to paralysis of the sphincter of the pupil and the pupillary reaction to light is disturbed.
The ciliary (ciliary) muscle, consisting of smooth muscle fibers, receives innervation from the back of the Yakubovich-Edinger-Westphal nucleus. In various pathological conditions, there is a violation of the innervation of this muscle, which leads to a weakening or paralysis of accommodation of the eye and a violation or absence of constriction of the pupil during convergence.

Sympathetic innervation

(module direct4)

In the lateral horns of the cervical vertebrae (C vIII) and thoracic vertebrae (T I) there are cells of sympathetic neurons of the spinal cord. As part of the anterior roots, the axons of these nerve cells emerge from the spinal canal, and then nerve fibers penetrate into the lower cervical and first thoracic nodes of the sympathetic trunk in the form of a connecting branch. Often these nodes are combined into a single larger node, which is called "star". Nerve fibers pass through the stellate ganglion without interruption.
Postganglionic sympathetic fibers envelop the wall of the internal carotid artery, together with which they penetrate into the cranial cavity. Then they separate from the carotid artery, reach the orbit and enter it with the first branch of the trigeminal nerve. Sympathetic nerve fibers terminate in smooth muscle fibers of the iris that dilate the pupil. The contraction of this muscle causes the pupil to dilate.
Sympathetic nerve fibers also innervate smooth muscle fibers m. tarsalis (Muller's muscle). With the contraction of this muscle, some expansion of the palpebral fissure occurs. Sympathetic nerve fibers also innervate a layer of bundles of smooth muscle fibers in the zone of the inferior orbital fissure and an accumulation of smooth muscle fibers located around the eyeball.
In various pathological conditions, when impulses are interrupted along the sympathetic fibers at any level - from the spinal cord to the orbit and eyeball, a triad of symptoms occurs on the side of the lesion (right and left), referred to as the Bernard-Horner syndrome (enophthalmos, pupillary constriction and some drooping of the upper eyelid).
To identify pathological conditions eyes associated with autonomic innervation, it is necessary to determine pupillary reactions to light (direct and friendly), check the state of convergence and accommodation, as well as the presence or absence of enophthalmos, and conduct pharmacological tests.