Autonomic innervation of the eye. Sympathetic influences on the organ of vision

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

Innervated organ	Action of sympathetic nerves	Action of parasympathetic nerves
Heart	Strengthen and speed up heart contractions	Relaxes and slows down heart contractions
Arteries	Cause arterial narrowing and increase blood pressure	Causes dilation of arteries and lowers blood pressure
Digestive tract	Slow down peristalsis, reduce activity	Accelerate peristalsis, increase activity
Bladder	Causes bladder relaxation	Causes bladder contraction
Bronchial muscles	Dilates the bronchi, makes breathing easier	Causes contraction of the bronchi
Muscle fibers of the iris	Midriaz	Miosis
Muscles that lift the hair	Cause hair to rise	Cause hair to stick
Sweat glands	Increase secretion	Reduce secretion

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 section - fibers in the structures of 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, the reproductive system, the cardiovascular and respiratory systems, the activity of the gastrointestinal tract, pelvic organs, trophic functions, body temperature .

In recent 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

Indicator	Division of the hypothalamus
Indicator	*front middle rear*
Cores	Paraventricular, suprachiasmatic, lateral and medial parts of the supraoptic nuclei	Posterior parts of the supraoptic nuclei, central gray matter of the ventricle, mamilloinfundibular (anterior part), pallidoinfundibular, interfornical	Mamilloinfundibular (posterior), Lewis body, papillary body
Regulation of functions	They participate in the integration of the functions of the trophotropic system, which carries out anabolic processes that maintain homeostasis. Participates in carbohydrate metabolism	Participates in fat metabolism.	Participate in the integration of the functions of the predominantly ergotropic system, which adapts to changing environmental conditions. Participates in carbohydrate metabolism.
Irritation	Increased tone of the parasympathetic part of the autonomic system: miosis, bradycardia, decreased blood pressure, increased secretory activity of the stomach, accelerated gastrointestinal peristalsis, vomiting, defecation, urination	Hemorrhages, trophic disorders	Increased tone of the sympathetic part of the autonomic system: mydriasis, tachycardia, increased blood pressure
Defeat	Diabetes insipidus, polyuria, hyperglycemia	Obesity, sexual infantilism	Lethargy, decreased body temperature

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

The muscular base of the bladder and 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 is directed through the system of lateral and posterior cords 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.

Type of violation	Lesion in the nervous system	Clinical manifestations
Central	Damage to the corticospinal tracts	Urgency, urinary retention, intermittent urinary incontinence
Peripheral	Damage to the parasympathetic spinal center	Paradoxical ischuria
	Damage to the sympathetic spinal center	True urinary incontinence with preserved detrusor tone
	Damage to the sympathetic and parasympathetic spinal centers	True urinary incontinence with detrusor atony
Functional disorders	Dysfunction of the limbic-hypothalamic regions of the brain	Nocturnal urinary incontinence, daytime partial urinary leakage

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 functions, 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 acquires 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 occurs mainly at night as an independent disease - nocturnal enuresis. This disease is characterized by functional disorders of 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 can be observed with autonomic dysfunction with increased 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 a neurological clinic, acute encopresis is of greatest importance. 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 (the upper muscle of the 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 nerves. 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. Fibers from these nuclei go as part of the III nerve to the ciliary ganglion, from where postganglionic fibers originate to the muscle that constricts 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. 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 border sympathetic trunk or the sympathetic plexus of the carotid artery, and 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 lacrimal secretion is observed not only in cases of damage to the autonomic apparatus, but also in various diseases of the eyes and tear duct, and in cases of impaired innervation of the orbicularis oculi muscle.

At autonomic nervous system research 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 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 not associated with infectious diseases may be observed. 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 extremities. 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 the 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;

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

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

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 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 body;

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; they often combine or precede each other;

Neuroendocrine syndrome, which is based on pluriglandular dysfunction with disruption of various types of 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, changes in the sugar curve (flattening, double-humped curve), and 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 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 developmental anomaly with severe dysfunction of the hypothalamic region. It is 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.

Precocious puberty can be caused by tumors in the area of the mamillary bodies or the 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 overall development. Occurs when the pituitary gland or hypothalamic region is damaged. Dwarf growth is noted. Bones and joints are short and thin. Epiphyseal-diaphyseal

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

Diabetes insipidus occurs with neuroinfections, tumors of the hypothalamus. Diabetes insipidus is based on 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 hypochondriasis;

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.

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 C 8 - D 1 level or the upper cervical parts of the border sympathetic trunk, less often by a violation of the central influences on the cilio-spinal 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

Parasympathetic nerve bundles and fibers pass along with the oculomotor nerve and come from the Yakubovich-Edinger-Westphal nucleus. The axons of nerve cells from these nuclei, presynaptic fibers, are interrupted in the ciliary ganglion located in the orbit. From the ciliary ganglion, postsynaptic fibers pass to the iris muscle, the constrictor pupil and the ciliary muscle. Constriction of the pupil occurs when a nerve impulse occurs under the influence of light stimulation of the retinal receptors.
Thus, this group of parasympathetic fibers coming from the anterior part of the nucleus is part of the arc of the pupillary reflex to light.
For various disorders of the parasympathetic innervation of the eye, which can involve various zones of the pathway, namely: the cellular structures of the Yakubovich-Edinger-Westphal nucleus, preganglionic fibers, the ciliary ganglion and its postganglionic fibers. In this case, the passage of the nerve impulse is disrupted or stopped. As a result of such disorders, the pupil dilates due to paralysis of the sphincter of the pupil and the pupillary reaction to light is impaired.
The ciliary (ciliary) muscle, consisting of smooth muscle fibers, receives innervation from the posterior part of the Yakubovich-Edinger-Westphal nucleus. In various pathological conditions, the innervation of this muscle is disrupted, which leads to weakened or paralyzed accommodation of the eye and impaired or absent pupillary constriction 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 the 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-shaped”. Nerve fibers pass through the stellate ganglion without interruption.
Postganglionic sympathetic fibers envelop the wall of the internal carotid artery, with which they penetrate into the cranial cavity. Then they are separated from the carotid artery, reach the orbit and enter it with the first branch of the trigeminal nerve. Sympathetic nerve fibers end in the smooth muscle fibers of the iris, which dilate the pupil. Contraction of this muscle causes the pupil to dilate.
Sympathetic nerve fibers also innervate smooth muscle fibers m. tarsalis (Müller muscle). When this muscle contracts, a slight widening of the palpebral fissure occurs. Sympathetic nerve fibers also innervate the layer of smooth muscle fiber bundles in the area of the inferior orbital fissure and the accumulation of smooth muscle fibers located around the eyeball.
In various pathological conditions, when impulses traveling along sympathetic fibers at any level are interrupted - from the spinal cord to the orbit and eyeball, on the affected side (right and left) a triad of symptoms occurs, referred to as Bernard-Horner syndrome (enophthalmos, constriction of the pupil and some drooping of the upper eyelid).
To identify pathological conditions of the eye 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.

Parasympathetic system Innervates the sphincter of the pupil, the ciliary muscle and the lacrimal gland in the eye area.

A) Pupil sphincter And ciliary muscle The peripheral “postganglionic” fibers (gray, soft) going to both these smooth muscles arise from the ganglion ciliare. The origin of pregangliopairic (white, soft) fibers is limited vegetative nuclei in the midbrain in the immediate vicinity of the magnocellular nuclei of the oculomotor nerve.

These are " small cell» lateral nucleus of Edinger-Westphal for the homolateral pupil and medial nucleus of Perlia for accommodation (and concomitant pupillary constriction in both eyes?). These fibers leave the brain stem along with the oculomotor nerve (III), go further in its trunk and in a branch to m. obliquus interior to the ciliary ganglion. After removal of the ciliary ganglion, the reaction of the pupil to convergence, and in isolated cases also the reaction to light, may remain.
Thus, some parasympathetic fibers as if bypassing the ciliary ganglion. After removal of the ciliary ganglion, atrophy of the iris has also been described.

b) Lacrimal gland. Postganglionic fibers arise from the ganglion spbenopalatinum. Through n. zygomaticus they reach ramus lacrimalis n.trigemini and together with it go to the gland. Preganglionic fibers originate from the nucleus salivatorius superior in the medulla oblongata; Preganglionic fibers for the sublingual and submandibular salivary glands originate from the same nucleus. They initially go together in the n. intermedins, then the fibers for the lacrimal gland branch off and form n. petrosus superficial major go to the ganglion.

From the above it is clear that, unlike sympathetic ones, they are located close to the peripheral end organs and sometimes even inside the latter. These in the head area also include ganglion submaxillarc (for the sublingual and submandibular lacrimal gland) and ganglion oticum (for the parotid gland). It should also be noted that preganglionic parasympathetic fibers arise only from the brain stem (craniobulbar autonomic system) and the sacral spinal cord, while sympathetic fibers arise from the sternolumbar segments.

Our knowledge about suprasegmental parasympathetic centers even more imperfect than about the sympathetic centers. It is believed that this is the nucleus supraopticus in the hypothalamus, which has connections with the pituitary funnel. The cerebral cortex also controls parasympathetic functions (heart, gastrointestinal tract, bladder, etc.). With irritation of the frontal lobe, along with constriction of the pupil, lacrimation was also noted. Irritation of the area peristriata (area 19, according to Brodmann) caused constriction of the pupil.

In general, the organization of an autonomous system seems even more complex than organization of the somatic system. Only both terminal links are clearly outlined in the efferent circuits of neurons: preganglionic and postganglionic fibers. In the end organs, parasympathetic and sympathetic fibers are so closely mixed that they are histologically indistinguishable from each other.

We will 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.

Damage in area A would cause ptosis, in area B - ptosis and miosis, in area C - enophthalmos and in area D - all components of Herner's syndrome (according to Walsh)

In the 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 in order to entwine various other structures here as sympathetic plexuses (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 the 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, throughout the entire sympathetic system, there seems to be no more exchange of fibers between the right and left halves of the body.