Diencephalon. White matter of the cerebral hemispheres

Exam questions:

1.19. Visual thalamus: anatomy, physiology, symptoms of damage.

1.20. Hypothalamus: anatomy, physiology, symptoms of damage.

1.22. Internal capsule: anatomy, physiology, symptoms of damage.

1.23. White matter of the cerebral hemispheres, corpus callosum, commissural and associative fibers: anatomy, physiology, symptoms of damage.

1.26. Olfactory and taste analyzers: structure, research methods, symptoms of damage.

1.27. Visual analyzer: structure, research methods, symptoms of damage.

2.16. Hypothalamic syndrome: etiology, clinical picture, treatment.

Practical skills:

1. Taking anamnesis in patients with diseases of the nervous system.

Anatomical and physiological features and syndromes of diencephalon lesions

Diencephalon located paramedian around the third ventricle, includes the thalamus, hypothalamus, epithalamus and metathalamus.

1. Thalamus (visual thalamus) - located on both sides of the third ventricle and divided into nuclei (more than 150 nuclei) by layers of white matter, it contains the anterior tubercle (anterior part of the thalamus) and the cushion (posterior part of the thalamus) and is externally delimited by the internal capsule.

- Anatomical division of the thalamic nuclei:

1) front,

2) ventrolateral,

3) medial,

4) rear,

5) intralamellar (intralaminar).

- Functional division of the thalamic nuclei:

1) Specific nuclei of the thalamus:

- somatosensory nuclei: medial lemniscus, spinothalamic tract, trigeminothalamic tract a lateral posteroventral complex [

1) ventrocaudal parvocellular nucleus (V.c.pc) - pain and temperature sensitivity (internal part - face, external part - body and limbs),

2) ventrocaudal internal nucleus (V.c.i.,VPM) and ventrocaudal outer nucleus (V.c.e, VPL) - touch and deep sensitivity of the face (VPM) and body (VPL),

3) ventral intermediate nucleus (V.i.m) - from muscle spindles

] à somatosensory cortex fields(3a, 3b, 1, 2);

- taste kernels: single coreà tract of the solitary nucleus à medial section ventrocaudal internal nucleus(V.c.i.,VPM) à cortex islet;

- visual nuclei: retinaà optic nerve à chiasm à optic tract à lateral geniculate body(retinotopic order) à field 17,

- auditory nuclei: kernelsVIII nerveà lateral lemniscus+trapezoid body à medial geniculate body(tonotopic order) à field 41,

- nuclei of the extrapyramidal system:

1) dentate nucleus (nucl.dentatus) + red core a dentothalamic pathway a posterior ventral oral nucleus(V.o.p) à motor field (4),

2) pale ball à anterior ventral oral nucleus(V.o.a) + anterior ventral nucleus(VA) à premotor cortex (6a).

2) Secondary and nonspecific nuclei of the thalamus:

Mastoid bodies à fornix (mastoid-thalamic tract of Vic D’Azira) à anterior nucleus(A) à limbic system (field 24),

Pale ball a dorsal nucleus(D.sf) à limbic system (field 23),

- dorsal lateral nucleus[oral dorsal (D.o) à prefrontal cortex; intermediate dorsal (D.i.m) à parietal lobe],

- medial nucleus(M) ßà prefrontal cortex (destruction - frontal syndrome),

- posterior core (cushion)à associative fields of the parietal and occipital lobes,

- intralaminar nuclei- part of the nonspecific brain system.

- Thalamic lesion syndrome - thalamus syndrome(retrolenticular, Dezherina-Roussi):

1) contralateral hemihypesthesia(superficial and deep sensitivity) - somatosensory nuclei (loss),

2) spontaneous burning pain in the contralateral half of the body, not relieved by analgesics - somatosensory nuclei (irritation),

3) contralateral homonymous hemianopsia- lateral geniculate body,

4) homolateral hemiataxia, choreoathetosis- ventral oral (extrapyramidal nuclei),

5) paresis of facial muscles when expressing emotions(Vincent's symptom) - anterior nucleus and connections with the limbic system,

6) transient hemiparesis without contractures- swelling of the posterior thigh of the internal capsule.

2. Hypothalamus (subthalamus) - located downward from the optic thalamus, includes 32 pairs of highly differentiated nuclei.

- The main nuclei of the hypothalamus ( Le Gros-Clark, with modifications ):

I.Medial hypothalamus:

1. Anterior (supraoptic) group(integration of the parasympathetic nervous system, hypothermic center - vasodilation, antipyretic substances)

- anterior hypothalamic field,

- preoptic region(medial and lateral), including the ventrolateral nucleus - hypnogenic center (?),

- supraoptic core- production of vasopressin (antidiuretic hormone) - to the posterior pituitary gland - increased reabsorption of water and sodium in the distal tubules of the kidneys;

- paraventricular nucleus- production of oxytocin - to the posterior pituitary gland - stimulation of smooth muscle activity (for example, the pregnant uterus), plays a role in the mechanisms of orgasm;

- suprachiasmatic nucleus- regulation of circadian rhythms (sleep-wakefulness) - has a direct connection with the retina (along with the superior colliculus, lateral geniculate body and pretectal region).

2. Middle (tuberal, periventricular) group(regulation of the activity of the endocrine glands and metabolism):

- ventromedial nucleus- satiety center (activation when weight decreases below the “normal weight point”, with bilateral damage - bulimia), sexual arousal center (women)

- dorsomedial nucleus,

- arcuate (periventricular, infundibular) nucleus- synthesis of releasing hormones.

- posterior hypothalamic field

3. Posterior (mammillary) group(integration of the sympathetic nervous system):

- posterior nucleus- hyperthermic center - vasoconstriction, endopyretics,

- kernels mamillary body(lateral and medial) - part of the limbic system (memory, learning) - afferent - from the amygdala and hippocampus through the fornix, efferent - mamillothalamic (Vic d'Azira) fascicle - to the anterior nucleus of the thalamus, and mamillosegmental - to the tegmentum of the midbrain (defeat - Korsakov's syndrome).

II. Lateral hypothalamus(diffuse arrangement of neurons around the medial fasciculus) :

1. lateral nucleus- center of hunger and thirst (activation when the weight exceeds the “normal weight point”, if damaged - anorexia),

2. lateral hypothalamic field

3. tuberolateral nucleus

4. tubero-mamillary nucleus

5. perifornical nucleus(mediator - hypocretin-orexin) - a system for switching states of wakefulness and sleep (damage - narcolepsy), has projections to the blue nucleus and the ventral tegmental field.

III. Subthalamic region:

1. subthalamic nucleus(Lewis body) - part of the extrapyramidal system,

2. Trout fieldsI andII,

3. uncertain zone.

- Hypothalamic lesion syndrome - hypothalamic syndrome- a set of autonomic, endocrine, metabolic and trophic disorders caused by damage to the hypothalamus.

1) Etiology:

Traumatic brain injury

Neuroinfection;

Tumor

Chronic stress

2) Clinic- a complex of signs of damage to the hypothalamus with the obligatory presence of neuroendocrine disorders.

- Vegetative-vascular (permanent and crisis) - fluctuations in blood pressure and pulse, cardialgia, marbling of the skin, hyperhidrosis, hypothermia, weather lability, etc.

1) Sympathoadrenal crises- palpitations, tachycardia, headache, heart pain, chills, pallor, numbness and coldness of the extremities, increased blood pressure, fear of death.

2) Vagoinsular crises- heat in the head, suffocation, heaviness of breathing, increased peristalsis and the urge to defecate, nausea, bradycardia, decreased blood pressure.

- Thermoregulatory disorders (permanent low-grade fever and crisis hyperthermia) - more in the morning, lower In the evening, does not respond to NSAIDs (Hollo test), depends on emotional stress,

- Motivational disturbances (bulimia, thirst, changes in libido) and sleep and wakefulness disorders(insomnia, hypersomnia),

- Neuroendocrine disorders :

1) Plurigladnular dysfunction(general endocrine dysfunction without specific symptoms) - dry skin, neurodermatitis, trophic ulcers, swelling, osteoporosis, etc.,

2) Adiposogenital dystrophy - obesity(on the back of the head, shoulders, stomach, chest and hips) + absence of secondary sexual characteristics and impotence (decreased libido),

3) Acromegaly- excessive growth of the nose, ears, lower jaw, hands and feet, some internal organs,

4) Hypothalamic-pituitary cachexia of Simmonds(cachexia, trophic disorders, hair loss, tendency to constipation, genital hypotrophy, arterial hypotension) or Sheehan's syndrome(without cachexia),

5) Delayed or premature puberty,

6) Itsenko-Cushing syndrome- cushingoid + cutaneous striae + osteoporosis + hypertension + hirsutism in women/lack of beard growth in men + amenorrhea/impotence.

3) Treatment(mainly pathogenetic)

Drugs that selectively affect the state of sympathetic or parasympathetic tone (pyrroxan, grandaxin, eglonil, bellataminal)

Dehydration agents

Anti-inflammatory drugs (for sluggish processes and during exacerbation)

3. Epithalamus (suprathalamus)- located above the roof of the midbrain, limits the posterior sections of the 3rd ventricle, participates in the regulation of circadian rhythms by changing the concentration of serotonin (wakefulness) and melatonin (sleep), regulation of autonomic function and inhibition of sexual behavior. René Descartes considered this area to be the “seat of the soul,” traditionally associated with the sixth chakra and the “third eye.”

- Anatomical division:

1) Pineal body (epiphysis), connected to the brain by two plates of white matter (the upper plate goes into the leash, the lower plate goes down to the posterior commissure of the brain).

2) Leashes (habenula), connected to each other by soldering, and leash cores.

- Epithalamic lesion syndromes- since the pineal gland is closely related to the quadrigeminal, the most common lesion syndrome is tegmentum syndrome (Parinaud)

4. Metathalamus (foreign countries)- medial and lateral geniculate body.

Anatomical and physiological features and syndromes of damage to the visual analyzer

II pair - N.Opticus

1. Anatomy of the visual analyzer:

- Path of visual information:

1) visual impulse receptor - retina: transducer element - sticks(twilight vision) and cones(color vision) a

2) bipolar cells (bodyI) à

3) ganglion cells (bodyII)à optic nerve (n.opticus) à optic chiasm (chiasma opticum, only the medial parts of the optic nerves cross) à optic tract (tractus opticus) à

4) cortical path:

- nuclei of the lateral geniculate body(corpus geniculatum laterale) (bodyIII)à central optic tract (regio optica) à posterior 1/3 of the posterior femur of the internal capsule à Graziole radiance (Meyer's loop - inferior outer quadrants - superomedial visual field)

- occipital lobe bark cerebral hemispheres along the edges of the calcarine sulcus (bodyIV)(sulcus calcarinus, field 17) - wedge (upper lip)- lower visual fields (upper parts of the retina) + lingual gyrus (lower lip)- upper visual fields (lower parts of the retina);

5) subcortical path:

- superior colliculus nucleus quadrigeminal plates (nucleus colliculi superior) (bodyIII):

a) tractus tectospinalis(protective reflex motor tract of responses to a strong light impulse);

b) medial longitudinal fasciculus(friendly movement of the eyeballs, reaction to light and accommodation).

- thalamic cushion(pulvinar thalami) (bodyIII)

- Stereometric matching of the visual path:

1) upper half of the retina ( lower visual fields) à upper part of the path à wedge,

2) the lower half of the retina ( upper visual fields) à lower part of the path à lingual gyrus,

3) medial part of the retina ( lateral visual fields) à in the nerve - medially, in the chiasm - decussation, in the tract - supero-medially à further from the pole of the occipital lobe,

4) lateral part of the retina ( medial visual fields) à in the nerve - laterally, in the chiasm - do not cross, in the tract - inferolaterally à further from the pole of the occipital lobe,

5) macular zone (central field of view) à in the nerve - centrally, in the chiasm - centrally, in the tract - centrally à at the pole of the occipital lobe on both sides.

2. Arc of the pupillary reflex

- Lightà Rods and cones à

- bipolar cells(body of the first afferent neuron) a

- ganglion cells(body of the II afferent neuron) à optic nerve (n.opticus) à optic chiasma (chiasma opticum) à optic tract (tractus opticus) à

- nuclei of the lateral geniculate body(corpus geniculatum laterale) (body of III afferent neuron) à

- pretectal nuclei(body of interneuron) AT BOTH SIDESà

- Yakubovich-Edinger-Westphal kernel(body of the first efferent neuron) a

- ciliary ganglion(gang.ciliare) (body of the II efferent neuron) à constriction of the pupil.

3. Optic pathway syndromes

- Retinal and optic nerve syndrome:

- amaurosis- complete loss of vision in one eye,

- amblyopia- decreased visual acuity in one eye,

- change in visual fields- tubular narrowing, scotomas (visual field defect that does not merge with its peripheral boundaries);

2) changes in the fundus:

- primary atrophy- nerve damage - and secondary- due to swelling of the nipple nerve,

- congestive optic disc,

- degenerative-dystrophic changes in the retina;

3) reduction or loss of direct reaction to light (rupture of the afferent link) while maintaining the friendly one (preservation of the efferent part)

- Optic chiasm syndrome:

1) reduction or loss of sensitivity: scotomas of the temporal or nasal fields

- bitemporal hemianopsia(medial sections) or scotomas of the temporal fields,

- binasal hemianopsia(lateral sections) or scotomas of the nasal fields,

- amblyopia;

2) changes in the fundus:

- primary atrophy DZN;

3) reduction or loss of direct reaction to light while maintaining a friendly one (in “blind” fields)

- Optic Tract Syndrome:

1) decrease or loss of sensitivity:

- homonymous hemianopsia contralateral,

- lack of macular vision contralateral;

2) changes in the fundus:

- primary atrophy DZN;

3) reduction or loss of direct and friendly reaction to light on the part of hemianopsia;

- Graziole bundle syndrome:

1) irritation option:

- visual hallucinations homonymous contralateral,

2) dropout option:

- homonymous hemianopsia contralateral (macular vision preserved),

- preservation of the pupillary reflex.

- Visual cortex syndrome:

1) irritation option:

- visual hallucinations(including macropsia, micropsia, metamorphopsia),

- preservation of the pupillary reflex,

2) dropout option:

- quadrant homonymous hemianopsia,

- preservation of the pupillary reflex,

- visual agnosia (failure to recognize objects).

4. Research methods:

- complaints: 1) decreased visual acuity, loss of visual fields or parts thereof, 2) visual hallucinations,

- status: 1) checking visual acuity (Sivtsev tables), 2 ) checking color perception (Rabkin or Ishihara tables), 3) checking visual fields (perimetry), 4) fundus examination (assessment of the condition of the optic nerve head)

Anatomical and physiological features and syndromes of damage to the olfactory analyzer

I pair - N. Olfactorius

1. Anatomy of the olfactory analyzer:

- Pathway for olfactory information:

1) odorant receptor - the mucous membrane of the superior turbinate,

2) olfactory bipolar cells (bodyI)(~10 million), peripheral processes end in club-shaped thickenings with olfactory hairs à filae olfactoriae (unmyelinated, through lamina cribrosa) à

3) mitral cellsbulbusolfactoria (bodyII)à tractus olfactorius à substantia perforata anterior rostralis à

Stria olfactoria medialis (medial bundle) à areasubcallosa (bodyIII) and bulbus olfactorius;

Stria olfactoria intermedia (intermediate bundle)à trigonumolfactorium (bodyIII)

Stria olfactoria lateralis (lateral fasciculus) à circle of Peipetz [arched gyrus (cingulum) à hook of the parahypocampal gyrus (uncus)à Ammon's horn à hippocampus à fornix (fornix) à corpus mamillare] à

Amygdala;

Transparent septum (diagonal Broca's bundle - to the tonsil);

Tr.mamillotegmentalis à superior colliculi

Bundle of Vic d'Azir à anterior nucleus of the thalamus à posterior thigh of the internal capsule à ventral surface of the frontal lobe

- Cortical olfactory center located in the medio-basal regions of the temporal lobe and the hippocampus. The primary olfactory centers have bilateral cortical connections. The centers and connections of the olfactory analyzer are part of the limbic-reticular system.

- Vomeronasal organ (vomeronasal organ, Jacobson organ) - the peripheral part of the additional olfactory system of some vertebrates, the receptor surface - directly behind the region of the olfactory epithelium in the projection of the vomer. A connection between the vomeronasal system and the functions of the genital organs, sex-role behavior and the emotional sphere has been discovered. Reacts to volatile pheromones and other volatile aromatic substances (VAS), most of which are not perceived as odor or are poorly perceived by smell; in some mammals there is a characteristic movement of the lips (phlehmen) associated with the capture of VAS in the area of the Jacobson's organ:

1) pheromone releasers- inducing an individual to take some immediate action and is used to attract mating partners, signals about danger and inducing other immediate actions.

2) pheromone primers- the formation of some specific behavior and influence on the development of individuals: for example, a pheromone secreted by a queen bee prevents the sexual development of other female bees.

2. Theories of smell- the olfactory epithelium is covered with a fluid produced in special glands; molecules of odorous substances dissolve in this liquid, and then reach the olfactory receptors and irritate the endings of the olfactory nerve.

- Adsorption of odorants when breathing;

- Enzyme theory- 4 groups of enzymes that form electrical potential;

- Wave theory- high frequency waves

- Electronic theory- electrochemical energy

- Stereochemical theory- the shape of the odorant molecule - 7 primary odors = 7 cell types (according to Eimur), complex odors are made up of primary ones: 1) camphor (eucalyptus), 2) acrid (vinegar), 3) ethereal (pears), 4) floral (roses) ), 5) mint (menthol), 6) musky (musk deer glands), 7) putrefactive (rotten eggs).

3. Olfactory pathway syndromes:

- Symptoms of loss:

1) hypo(an)osmia- decrease (absence) of smell (rhinogenic lesions, damage to the olfactory nerves and bulbs, damage to the olfactory triangle, bulb, tract of the anterior perforated substance).

2) olfactory agnosia- failure to recognize familiar smells (damage to the limbic system and temporal lobe). A. Kitzer (1978) believes that when the olfactory pathways are damaged, anosmia to olfactory substances develops; when the cortical centers are damaged, the recognition of odors to olfactory, trigeminal, and glossopharyngeal substances is impaired.

- Symptoms of irritation:

1) hyperosmia- increased sensitivity to odors,

2) parosmia- qualitative change in odors, distortion of odors, inadequate perception of odors (cacosmia)

3) olfactory hallucinations- feeling of a non-existent smell.

4. Olfaction research methods

It must be remembered that some strong odors can be perceived by other sensory nerves (trigeminal, glossopharyngeal).

- Olfactory set(W. Bornstein) consists of 8 substances: 1) washing soap, 2) rose water, 3) bitter almond water, 4) tar, 5) turpentine, 6) ammonia (V), 7) acetic acid (V), 8 ) chloroform (IX).

- Zwaardemaker olfactometer.

Anatomical and physiological features and syndromes of damage to the taste analyzer

1. Anatomy of a taste analyzer:

- Path of taste information:

1) receptor - mucous membrane of the tongue,

- receptor on the anterior 2/3 of the tongue - facial nerve (VII) - gang.inf.nn.glossopharingei (bodyI) ->

- receptor on the back 1/3 of the tongue - glossopharyngeal (IX) - gang.inf.nn.vagi (bodyI) ->

- receptor on the epiglottis- wandering (X) - gang.geniculi (bodyI) ->

2) nucl.solitarius (bodyII) => tractus solitarius =>

3) ventrolateral nucleus of the thalamus (bodyIII)=> posterior 1/3 of the posterior limb of the internal capsule =>

4) insula and base of the postcentral gyrus (bodyIV).

2. Types of taste sensitivity:

- salty- lateral surfaces of the tongue (concentration of sodium ions, less often potassium),

- sour- lateral surfaces of the tongue (concentration of hydrogen ions),

- sweet- tip of the tongue (specific receptor),

- bitter- root of the tongue (specific receptor),

- "umami"- root of the tongue (specific receptor for glutamate),

- "Chile"- root and back of the tongue (pain receptor).

3. Syndromes of damage to the taste analyzer

- Symptoms of loss:

1) hypo(a)geusia- decrease (absence) of taste.

- Symptoms of irritation:

1) hypergeusia- increased sensitivity to smells and tastes,

2) taste hallucinations- feeling of a non-existent smell or taste.

4. Methods for studying taste sensitivity

- drip method(applying standard solutions with a volume of 10 ml (temperature 25 0 C) to different parts of the tongue with pipettes, with rinsing the mouth for 3-5 seconds, at intervals for bitter irritants for 3 minutes, and for other irritants for 2 minutes):

1) 20% sugar solution - sweet,

2) 10% solution of table salt - salty,

3) 0.2% hydrochloric acid solution is acidic,

4) 0.1% solution of quinine sulfate is bitter.

Anatomical and physiological features and syndromes of damage to the white matter of the cerebral hemispheres

White matter of the brain consists of nerve conductors and is divided into three types of fibers, depending on the level of information exchange:

1. Projectionfibers- connect the cerebral hemispheres with the underlying parts of the brain (stem and spinal cord), the most significant location of the projection fibers is internal capsule - a dense layer of projection fibers that looks like an obtuse angle, open outward and located between the caudate nucleus and the optic thalamus on one side and the internal globus pallidus on the other

- Structure of the internal capsule:

1) Front leg- contains efferent fibers from the frontal cortex to the thalamus ( frontothalamic tract) and cerebellum ( frontopontocerebellar tract).

2) Knee- descending fibers corticonuclear pathways providing motor innervation to cranial nerves.

3) Rear leg - front 2/3- descending fibers of the pyramidal ( corticospinal) paths to the anterior horns of the spinal cord and back 1/3- ascending fibers of the pathways of deep and superficial sensitivity ( thalamocortical pathway), ascending pathways of the visual and dry analyzer (to the occipital and temporal lobes) and descending fibers occipitotemporal ponsocerebellar tract

- Syndromes of damage to the internal capsule:

1) front thigh:

- frontal ataxia, astasia-abasia(frontopontine tract),

- cortical gaze paresis(from the anterior adversive field to the posterior longitudinal fasciculus).

2) knee of the internal capsule:

- paresis of the lower facial muscles and deviation of the tongue from the focus (corticonuclear pathway).

3) back thigh:

- contralateral hemi anopsia(fibers to 17,18,19),

- contralateral central hemi plegia(corticospinal tract),

- contralateral hemi anesthesia(thalamo-cortical fibers).

2. Commissural fibers- connect topographically identical areas of the right and left hemispheres:

- Main commissural fibers:

1) corpus callosum- cortex of the frontal, parietal, occipital lobes,

2) anterior commissure- olfactory areas (part of the frontal and medial parts of the temporal lobes),

3) commissure of the arch- temporal lobe cortex, hippocampus, peduncles of the fornix,

4) posterior medullary commissure and frenulal commissure- structures of the diencephalon.

- Syndromes separation of the hemispheres:

1) Complete corpus callosum crossing syndrome:

- sensory phenomena: anomia- ignoring, inability to name objects perceived by the subdominant hemisphere (left visual field, left hand);

- motor phenomena: dyspopia-dysgraphia- division of the functions of writing and drawing between the dominant and subdominant hemispheres, respectively; reciprocal coordination disorder;

- speech phenomena: the impossibility of correctly reading and writing words placed in the left visual field while the same is preserved for the right.

2) Partial syndromes of intersection of the corpus callosum:

- anterior sections:

1) violation of reciprocal coordination,

2) violation of orientation in space and time.

- middle sections:

1) auditory anomia,

2) tactile anomia,

- posterior sections:

1) dyspopia-dysgraphia,

2) left-sided apraxia,

3) visual anomia (sometimes homonymous hemianopia on the left).

3.Associative fibers- unite different parts of the cortex within one hemisphere (see Cortex)

- long(distant areas of the cortex),

- short(neighboring convolutions).

Thalamic infarctions are rare (approximately 11% of all vertebrobasilar infarctions) but can present with a variety of symptoms and be rapidly fatal if not diagnosed promptly and treated appropriately. If the lesion in the thalamus is small, this leads to the development of a stroke with isolated hemihypesthesia or hemihypesthesia and hemiparesis (i.e., lacunar syndrome). Cerebellar ataxia (if the dentato-thalamic tract is affected) may also be observed in the affected limbs. However, thalamic lesions involving thalamo-cortical projections can also lead to the development of aphasia and impairment of verbal memory (with damage to projections in the dominant hemisphere), impairment of visuospatial perception (with damage to projections to the subdominant hemisphere) and visual hallucinations. Large thalamic lesions compressing the midbrain can lead to the development of various additional symptoms, such as vertical gaze paresis, constriction of the pupils (miosis), apathy, depression of consciousness, saltiness (and apathy). Moreover, bilateral paramedian thalamic infarction may present with severe retrograde and anterograde amnesia as a result of occlusion of a single small branch of the proximal posterior cerebral artery (artery of Percheron). Thus, thalamic infarctions can present with a variety of symptoms, sometimes only drowsiness, confusion and amnesia, but the key point is the acute onset.

The arterial blood supply to the thalamus is carried out by 5 arteries, of which 3 main ones (thalamoperforating, thalamogenicular and posterior villous) are branches of the posterior cerebral artery (PCA). The other two, the anterior villous artery (a branch of the internal carotid artery (ICA) and the polar or tuberothalamic arteries (branches of the posterior communicating artery, PCA), belong to the territory of the carotid system).

The optic thalamus is vascularized predominantly by vessels from the PCA and the P1 and P2 segments of the PCA. Despite the various options and anomalies, there are 4 main vascular zones of the thalamus: anterior, paramedian, inferolateral and posterior. The polar (or tuberothalamic arteries) from the PCA supply the anterior region of the thalamus, the paramedian (or thalamoperforating) arteries from the P1 segment of the PCA supply blood to the parmedian zone, the thalamogenic arteries - to the inferolateral zone, and the posterior choroidal artery from the P2 segment of the PCA - to the posterior part of the optic region. mound. In 1/3 of cases, polar arteries are absent, vascularization occurs from the paramedian arteries.

Research conducted by S.M. Vinichuk et al. (2012), indicate that thalamic infarction is more often localized in the paramedian and inferolateral regions, less often in the border vascular zones - lateral (side) and central; The incidence of bilateral thalamic lesions is only 4.6% of all isolated thalamic infarcts. Acute ischemia of the paramedian territory accounts for about 22–35% of all thalamic infarctions. This area of the optic thalamus is vascularized by arteries (thalamo-subthalamic, or thalamo-perforating), arising directly from the P1 segment of the PCA on both sides, but in 1/3 of cases - from one leg, known as the artery of Percheron (hereinafter - AP). AP, that is, the posterior thalamo-subthalamo-paramedian artery, is the only artery that arises to the right or left of the median precommunal (mesencephalic) segment of the PCA. At the level of the subthalamus, it divides and supplies blood on both sides to the lower middle and anterior parts of the thalamus and subthalamus. The paramedian arteries of the PCA are highly variable; they can supply blood to the anterior territory of the thalamus and participate in the blood supply to the midbrain and rostral part of the brainstem in cases where the polar arteries are absent.

It is believed that posteromedial infarctions of the thalamus are caused mainly by atherosclerotic lesions of cerebral vessels and cardioembolism, and ventrolateral ones by microangiopathy. The localization of atheromatous lesions in the PCA or in one of its branches, as well as the degree of narrowing, determine the onset, severity and nature of the clinical syndrome. Other factors play a less important role: collateral blood flow through the PCA and blood viscosity. Even in the presence of an atherosclerotic plaque, the main mechanism for the development of stroke is usually embolism of the PCA or its branches. Changes in the PMA cause the appearance of syndromes, which are divided into 2 groups:

1st– cortical lesion syndromes caused by changes in the post-communal segment of the PCA;

2nd– syndromes of damage to the midbrain, subthalamus and thalamus associated with atherosclerotic narrowing, atherosclerotic or embolic occlusion of the proximal precommunal segment of the PCA.

With occlusion of the PCA trunk, an infarction develops with unilateral or bilateral involvement of the subthalamus and medial thalamus, as well as a lesion on the same side of the cerebral peduncle and midbrain with corresponding clinical symptoms.

The anatomical features of the blood supply to the visual thalamus contribute to the emergence of various clinical syndromes, which often complicate the diagnosis of stroke in determining the carotid or vertebrobasilar region.

Infarctions in the area of blood supply to the polar arteries are manifested by neuropsychological disorders, among which acute amnesia with the inability to remember new events (fixation anterograde amnesia) is the main symptom. Patients with bilateral infarctions in this area develop abulia and severe amnestic disturbances, which do not tend to decrease over time. Mild transient hemiparesis or hemisensory disturbances on the contralateral side may occasionally be noted. Unilateral infarction in the paramedian vascular region is accompanied by the development of posteromedial thalamic syndrome with acute impairment of consciousness, vertical paresis of upward gaze and cognitive disorders; Speech disorders and apraxia are also possible. Ischemia in this vascular zone occurs due to atheromatous or cardioembolic (40% of cases) occlusion of the thalamo-subthalamic AA, damage to which can cause an isolated bilateral thalamic infarction or a combined thalamic infarction involving other brain structures.

Bilateral paramedian thalamic infarcts are characterized by a classic triad of symptoms: acute disturbance of consciousness, neuropsychological symptoms and disturbance of vertical gaze (associated with damage to the interstitial nucleus of the medial longitudinal fasciculus, located between the diencephalon and midbrain). Depression of the level of consciousness of varying degrees of severity, up to coma, is observed in all patients (it is believed that depression of consciousness is a consequence of damage to the posterior parts of the dorsolateral and interlaminar nuclei, as well as a disruption of their connection with the ascending reticular formation and the anterior, orbitofrontal and medial prefrontal cortex). Lethargic sleep may occur, when the patient is difficult to awaken, or hypersomnia—patients are arousable, but may fall into deep sleep soon after stimulation ceases. Violation of the function of vertical gaze is manifested by paresis of upward gaze or a combination of paresis of upward and downward gaze. In its pure form, paresis of downward gaze is found only in cases of bilateral paramedian infarctions. Horizontal dysfunction is less common. Sometimes convergent strabismus is observed. Neuropsychological disorders begin to appear as disturbances of consciousness decrease. Patients remain disoriented, anxious and apathetic. Characteristic symptoms are amnesia and abulia, akinetic mutism, thalamic dementia (the latter occurs when the medial dorsal nucleus of the thalamus is damaged along with the mammillary bodies). CT and MRI with occlusion of the AP can detect bilateral lesions in the subthalamus and middle-lower parts of the thalamus, resembling a butterfly in outline.

With an infarction of two areas of the thalamus, paramedian and polar, amnesia is more profound and persistent than when only one paramedian is involved. It is believed that this is due to ischemia of the mammilothalamicus tractus zone, the anterior and dorsolateral nuclei of the thalamus.

Lesion of the AP can cause bilateral infarction of the paramedian thalamus involving the midbrain. In contrast to an isolated lesion of the thalamus opticus, the clinical features of thalamic-subthalamic paramedian infarcts are: the presence of paresis of the third pair of cranial nerves with contralateral hemiparesis or hemiataxia, bilateral complete ptosis (blepharoptosis), paresis or paralysis of upward gaze or paresis (paralysis) of upward and downward gaze, pseudoparesis of the VI pair of cranial nerves with convergent strabismus.

The anterior mesencephalic arteries can sometimes form common connections with the thalamic-subthalamic arteries. Blockage of the arteries can lead to infarction in an area that includes: the bilateral mesencephalic gray matter around the aqueduct of Sylvius, the nuclei of the third pair and their branches, the intralaminar and parafascicular nuclei, parts of the median and central nuclei, the anterior cerebellar peduncle and its chiasm, the medial third of the cerebral peduncle. Mesencephalothalamic syndrome develops, which includes neuro-ophthalmological, behavioral and motor disturbances as a result of an unusual combination of clinical signs.

Differential diagnosis of paired lesions of the thalamus includes metabolic (Wilson's disease, Fahr's disease) and toxic processes (Wernicke encephalopathy, central pontine myelinolysis), infections (viral encephalitis, Creutzfeldt-Jakob disease), vascular lesions (ischemia in the AP basin, occlusion of the vein of Galen, aneurysm basilar artery) and brain tumors (gliomas, astrocytomas).

Differentiation between bilateral arterial and venous infarctions of the thalamus is carried out taking into account the size of the infarction, the presence or absence of edema, and ischemia in other areas of the brain. Venous infarctions are usually larger in size and accompanied by swelling. Involvement of the deep veins (internal cerebral vein, vein of Galen, straight sinus), which drain venous blood from the thalamus, can lead to various manifestations of venous hypertension: acute headache with nausea, vomiting, seizures and changes in mental status. Venous thrombosis can manifest itself with various symptoms, among which cerebral disorders, epileptic seizures, involvement of cranial nerves and neuropsychiatric disorders dominate the clinical picture. Venous infarcts do not have a specific vascular region like isolated arterial thalamic lesions, but involve multiple regions. Neuroimaging usually reveals bilateral ischemia of the thalamus and basal ganglia; hemorrhagic transformation of venous infarction is considered common.

Differential diagnosis is also carried out with the superior basilar syndrome (“top of the basilar syndrome”), which is caused by occlusion of the rostral parts of the basilar artery (aneurysm, vasculitis) and leads to infarctions of the midbrain, thalamus, partially temporal and occipital lobes. The clinical manifestations of this syndrome are very diverse and include oculomotor (paresis of vertical gaze, III – VI pairs of cranial nerves), visual (hemianopsia, cortical blindness, “optical ataxia”) and pupillary disorders, disturbances of consciousness and behavior (coma, somnolence, delirium, peduncular hallucinosis, memory impairment), motor and sensory symptoms.

Literature:

article “Ischemic thalamic infarctions” by V.A. Yavorskaya, O.B. Bondar, E. L. Ibragimova, V.M. Krivchun, Kharkov Medical Academy of Postgraduate Education, City Clinical Hospital No. 7, Kharkov (International Medical Journal, No. 1, 2009) [read];

article “Isolated thalamic infarction: clinical syndromes, diagnosis, treatment and outcome” by S.M. Vinichuk, M.M. Prokopiv, L.N. Trembling; Alexandrovskaya Clinical Hospital, Kyiv; National Medical University named after. A.A. Bogomolets, Kyiv (magazine “Ukrainian Medical Book of Hours” No. 2, 2012) [read];

article “Clinical manifestations of stenoses and occlusions of intracranial arteries of the vertebrobasilar region (literature review)” E.L. Ibragimova, City Clinical Hospital No. 7, Kharkov (magazine “Ukrainian Newsletter of Psycho-Neurology” No. 2, 2010) [read];

article “Thalamic infarctions in the Percheron artery basin: clinical picture and diagnosis” Fursova L.A., Belarusian Academy of Postgraduate Education; Naumenko D.V., State Institution “5th Clinical Hospital”, Minsk, Belarus (International Neurological Journal, No. 1, 2013) [read];

article “Bilateral paramedian infarcts of the thalamus” by L.A. Fursova, D.V. Naumenko; Belarusian Medical Academy of Postgraduate Education, 5th City Clinical Hospital of Minsk (Healthcare magazine No. 12, 2012) [read];

article “Unusual manifestation of unilateral infarction in the paramedian region of the thalamus in the basin of the thalamo-perforating artery as a result of embolic occlusion of the artery of Percheron against the background of an existing patent foramen ovale: case report and review of the literature on the topic” Hirad Yarmohamma (Department of Internal Medicine, Cleveland Clinic Foundation, Cleveland , Ohio, USA), Andrei Carasca (Department of Neurology, Lenox Hill Hospital, New York, New York, USA), Hooman Yarmohammadi (Department of Diagnostic Radiology, University Hospitals Case Medical Center, Cleveland, Ohio, USA), Daniel P. Hsu (Division of Neuroradiology, Department of Diagnostic Radiology, University Hospitals Case Medical Center, Cleveland, Ohio, USA); International Neurological Journal, No. 1, 2013 [read] or [read];

presentation “Stroke in the Percheron artery basin: anatomical background, clinical picture, diagnosis, treatment” V.A. Sorokoumov, M.D. Selkin, M.K. Barbuhatti [read];

article “Bilateral thalamic stroke in a patient with a patent foramen ovale and hereditary thrombophilia” M.Yu. Brovko, L.A. Akulkina, V.I. Sholomova, A.Sh. Yanakaeva, L.A. Strizhakov, M.V. Lebedeva, V.V. Zakharov, A.V. Volkov, A.V. Lazareva, M.A. Kinkulkina, N.N. Ivanets, V.V. Fomin; Clinic named after EAT. Tareev University Clinical Hospital No. 3, First Moscow State Medical University named after. THEM. Sechenov; Clinic of Nervous Diseases named after. AND I. Kozhevnikov University Clinical Hospital No. 3, First Moscow State Medical University named after. THEM. Sechenov; Clinic of Psychiatry and Narcology named after. S.S. Korsakov University Clinical Hospital No. 3, First Moscow State Medical University named after. THEM. Sechenova, Moscow (Therapeutic Archive magazine No. 11, 2018) [read]

thalamic dementia:

article “Thalamic dementia” by M.M. Odinak, A.Yu. Emelin, V.Yu. Lobzin, A.V. Kashin; Military Medical Academy named after. CM. Kirova, St. Petersburg (Journal of Neurology and Psychiatry, No. 6, 2011) [read];

article “Acute dementia due to bilateral infarction of the visual thalamus. Clinical observation" Kuzmina S.V., Federal State Budgetary Educational Institution of Higher Education "First St. Petersburg State Medical University named after. Academician I.P. Pavlova" Ministry of Health of the Russian Federation, St. Petersburg (Neurological journal, No. 2, 2017) [read];

article “Thalamic dementia” in bilateral stroke of the visual thalamus: dynamics of cognitive disorders” Federal State Budgetary Educational Institution of Higher Education “Nizhny Novgorod State Medical Academy” Ministry of Health of the Russian Federation, Nizhny Novgorod (Neurological Journal, No. 2, 2017) [read]

Topical diagnosis: ischemic lesion of the thalamus (site)

March 22nd, 2016 , 05:54 am

Coma is a state of complete absence of consciousness resulting from a violation of the function/structure of vital systems/organs. In turn, consciousness is a background state of the brain that allows one to experience a subjective experience of any type as a whole and provide a report (answer) adequate to these experiences (verbal, motor, emotional, etc.).

Any voluntary (subjective, conscious) human action corresponds to a certain pattern of neural activity in various areas of the brain. First, the normal level of consciousness (wakefulness) depends on the activating influence on the cerebral hemispheres from groups of neurons located in the reticular activating system (RAS) of the brain stem. Secondly, to ensure a normal level of consciousness, the integrity of the cerebral hemispheres, the RAS and their connections is necessary.

Therefore, the main causes of coma are:

■ lesions of the brain stem, damaging or suppressing the RAS (it should be remembered that damage to the brain stem, causing damage to the RAS and, as a result, the development of a coma, may primarily be caused by extensive damage to one or both hemispheres, which have a compressive effect on the brain stem).

When we talk about “damage,” we mean either mechanical destruction of vital areas of the brain stem or cerebral cortex (organic coma), or a global disruption of metabolic processes in the brain (metabolic coma). Coma of metabolic origin can occur due to cessation of the delivery of energy substances (hypoxia, ischemia, hypoglycemia) or damage to the neurophysiological reactions of neuronal membranes (drug or alcohol intoxication, epilepsy or acute traumatic brain injury).

Consciousness has quantitative (waking) and qualitative (filling consciousness) components. The first (quantitative) reflects the very fact of the brain’s readiness to accept and respond to external and internal stimuli and clinically corresponds to formal wakefulness (not sleep, eyes open). However, in a healthy person, wakefulness should not only be in itself, but also qualitatively filled with behavior adequate to the circumstances (emotions, motivations, knowledge of oneself and the world around us). In the phylogenetic aspect, wakefulness appeared earlier than the filling of consciousness and was “localized” in various structures of the brain. Thus, the preservation of the RAAS (ascending reticular activating system), located in the table of the brain, is primarily responsible for wakefulness. While the cerebral cortex is mainly responsible for filling consciousness.

This phylogenetic and spatial separation of the two components of consciousness causes a number of clinical phenomena. Firstly, there can be wakefulness without filling consciousness, but there can be no filling of consciousness without wakefulness. Secondly, a small-scale lesion of the brain stem can cause a pronounced depression of consciousness and, on the contrary, even with extensive lesions of the cerebral cortex, consciousness can be quantitatively reduced slightly. Thirdly, the restoration of consciousness follows the path of restoring first the quantitative component, and then the qualitative, but not vice versa. Fourthly, there are isolated violations of only the qualitative component of consciousness.

In neuroreanimatology, more attention is paid to the quantitative assessment of acute disorders of consciousness. The most widely used instrument in the world to quantify consciousness is the Glasgow scale. It has high reproducibility, that is, the test results are the same for most doctors who examined a particular patient. The most effective use of the scale is when exchanging information between paramedics (ambulance employees) in the starting mode. In patients with signs of dislocation syndrome against the background of structural brain damage, the Pittsburgh Brain Stem Score (PBSS) is useful for assessing brain stem damage in comatose patients. Recently, the new Mayo Clinic com scale (FOUR Scale) has been gaining popularity. It combines the properties of the previous two and is maximally adapted to the conditions of the intensive care unit, as it has a breathing section.

source: Methodological materials for residents of the department of anesthesiology and resuscitation “Acute cerebral insufficiency” Belkin A.A., Davydova N.S., Levit A.L., Leiderman I.N., Ural State Medical University; Ekaterinburg, 2014

According to the concept of Plum and Posner (1966), the main pathomorphological mechanisms of coma are either bilateral diffuse damage to the cerebral cortex (anatomical and/or metabolic), or damage to the brain stem, or a combined disorder at these levels.

Switching between the RAS brainstem and thalamic (and then cortical) areas is carried out using neurotransmitters. It has been established that acetylcholine and norepinephrine have the greatest effect on awakening. Cholinergic fibers connect the midbrain with other parts of the upper brainstem, the thalamus optic, and the cerebral cortex. These pathways are thought to mediate the relationship between clinical awakening and the corresponding EEG pattern observed after administration of certain cholinergic drugs such as physostigmine. It is known that noradrenergic neurons of the locus coeruleus and serotonergic cells of the raphe pons nuclei send diffuse projections to the cerebral cortex. Serotonin and norepinephrine provide important functions in regulating the sleep-wake cycle. Their role in arousal and coma is not entirely clear, although the excitatory effects of amphetamines are probably due to the release of catecholamines.

The thalamus and cortex send signals to each other, back and forth, in complex patterns. Sometimes these connections are local: certain areas of the cortex or thalamus are connected to certain areas of each other. Sometimes they are diffuse and global, so that one area of the thalamus can establish extensive and complex connections with different areas throughout the cortex. The areas of the cerebral cortex that appear most important for consciousness and that interact with the thalamus at the time of return of consciousness are located in the posterior cortex (in the association area at the intersection of the lateral temporal, occipital and parietal [parietal] cortices) and in the central parietal cortex. High-frequency neuroelectric activity in areas linking these cortical areas with the thalamus appears to be essential for the state of consciousness, perhaps because they integrate separate contents of consciousness into a coherent whole.

read also article “Neurotransmitter foundations of consciousness and unconscious states” E.V. Alexandrova, O.S. Zaitsev, A.A. Potapov Research Institute of Neurosurgery named after. acad. N.N. Burdenko RAMS, Moscow (magazine “Issues of Neuro-Surgery” No. 1, 2014) [read]

December 6th, 2015 , 06:56 am

Definition. A medial minor stroke hematoma (MIH) of the brain is a hematoma with a volume of less than 40 cm3, which is located medial to the internal capsule - in the thalamus () with possible spread to the midbrain (thalamo-mesencephalic hematoma).

Pathogenesis. The study of the pathogenesis of hemorrhagic stroke (HI) allowed us to draw the conclusion that if in large hematomas the severity of the disease is determined by the rapidly occurring compression of the brain substance with occlusive hydrocephalus and herniation, then in MIS the prevalence of perifocal and secondary ischemia of the brain substance, triggered by activated platelets, worsening microcirculation and cerebral perfusion. The development of the ischemic-hypoxic cascade is associated with a violation of oxidative phosphorylation and the active release of cytokines, leading to damage to lysosome membranes and the release of autolytic enzymes into the intercellular space of brain tissue, which causes the progression of secondary ischemia and secondary vascular spasm.

Clinic. Medial MIH manifests itself (suddenly and reaches a maximum within a few seconds) with contralateral hemianopsia, contralateral hemiparesis, hemianesthesia and “thalamic hand” - flexion at the wrist and metacarpophalangeal joints with simultaneous extension at the interphalangeal joints. Sometimes choreo-athetoid hyperkinesis occurs on the affected side. Some time after hemorrhage, thalamic pain often occurs (as part of the Dejerine-Roussy syndrome). Also, hemorrhages in the optic thalamus are often accompanied by a breakthrough of blood into the third ventricle (usually with the breakthrough of massive hematomas of this localization).

Diagnostics. Immediately after hospitalization, a [spiral] CT (MRI) of the brain is indicated to determine the nature of the stroke and clarify the anatomical features of the hemorrhage (standard). When performing a CT (MRI) it is necessary to determine: the presence and topical location of the pathological focus (foci); volume of each type of lesion (hypo-, hyperdense part) in cm3; position of the midline structures of the brain and the degree of their displacement in mm; state of the cerebrospinal fluid-containing system of the brain (size, shape, position, deformation of the ventricles) with determination of ventriculocranial coefficients; condition of the brain cisterns; the condition of the grooves and fissures of the brain.

The volume of hemorrhage is determined either using the program supplied by the tomograph manufacturer, or using the ABC/2 formula, where A is the largest diameter, B is the perpendicular diameter to A, C is the number of slices x slice thickness. Patients who plan to use neuronavigation during surgery are also scanned in the mode that is necessary for subsequent image transfer to a specific navigation station.

Cerebral angiography (CT or MR angiography) is performed if the presence of a vascular malformation or arterial aneurysm is suspected in the absence of a history of hypertension, the patient’s young age (less than 45 years) and the location of the hematoma, atypical for hypertensive hemorrhage, but characteristic of rupture of an arteriovenous malformation or aneurysm (recommendation).

Treatment. Advances in neuronavigation have made it possible to access very small hemorrhages (hematomas), including thalamic ones. Navigation units combined with a computed tomograph make it possible to correlate CT data with landmarks on the patient’s head in real time and perform hematoma puncture (stereotactic method) from any convenient and safest access for the surgeon (in such cases, brain scanning is performed with a special localizer attached to the head , and a personal computer is used to calculate coordinates; target selection is carried out on a computer monitor).

In case of medial (thalamic and thalamocapsular) MIG, it is advisable to perform surgical intervention when the volume of the hematoma [thalamus] is more than 10 cm3 (with the volume of the thalamo-mesencephalic hematoma more than 5 cm3), accompanied by severe neurological deficit (with the volume of the hematoma less than 10 cm3, the advantage of surgical treatment over the conservative method not proven).

To reduce brain trauma during surgery for medial MIG, a special surgical approach has been developed and clinically tested, allowing one to approach the thalamic region without affecting the most functionally important pathways and basal ganglia of the brain (K.E. Makhkamov, Zh.M. Kuzibaev, 2009 [Republican Scientific Center for Emergency Medical Care, Tashkent, Uzbekistan]). This technique consists of neuroendoscopic puncture removal and drainage of the medial hematoma through the anterior or posterior horn of the lateral ventricle. The technique is performed in two ways, depending on the breakthrough of the MIG into the ventricles of the brain.

The first method is used when blood breaks into the ventricles of the brain by introducing a neuroendoscope on a trocar with directed aspiration and washing out intraventricular hemorrhage (IVH) through the working channel of the neuroendoscope. To do this, a burr hole is placed on the side of the hemisphere with MIG at the projection points of the anterior or posterior horn of the lateral ventricle and a trocar with an endoscope is inserted. After removal of the IVH, the stroke-hematoma is punctured. After puncture, the liquid part of the hematoma is aspirated with a drainage tube inserted through the working channel of the trocar. At the final stage of the operation, a drainage tube is left in the hematoma bed in order to carry out local fibrinolysis (LF) of residual blood in the postoperative period. For LF, the first generation thrombolytic drug streptokinase is used. The drug is administered through drainage at intervals of 6 hours at a dose of 15,000 IU, diluted in physiological sodium chloride solution. After administration of the drug, the drainage tube is closed for 2 hours for exposure.

The second method of neuroendoscopic puncture removal of MIG is used in the absence of blood breakthrough into the ventricles of the brain, i.e. when there is no need for neuroendoscopic removal of IVH. In this case, a channelless thin neuroendoscope with a thin-walled drainage tube attached to it is inserted through a burr hole placed at the projection points of the anterior or posterior horn of the lateral ventricle. The hematoma is punctured through the anterior or posterior horn of the lateral ventricle under endovideo surveillance, followed by removal of the endoscope and aspiration of blood through the drainage tube. The installed drainage tube is used to perform LF of residual blood in the postoperative period.

You can read more about local fibrinolysis in the article “Local fibrinolysis of non-traumatic intracerebral and intraventricular hemorrhages” by Yu.V. Pilipenko, Sh.Sh. Eliava, O.D. Shekhtman, A.S. Kheireddin; FSBI "Research Institute of Neurosurgery named after. N.N. Burdenko" RAMS, Moscow (magazine "Questions of Neurosurgery" No. 6, 2012) [

Thalamus is an ovoid-shaped formation (in the diagram - a “red” structure), consisting of several groups of gray matter nuclei.

The right and left thalamus are strategically located at the top of the brain stem and serve to switch information going to and from the cerebral cortex. Due to its anatomical structure and vascularization, the thalamus allows for a wide variety of symptoms of ischemic thalamic strokes. These differences are characterized by the prototypical clinical findings and detection of lesions by neuroimaging.

Knowledge of the vascular anatomy and blood supply areas of the thalamus allows us to determine the vasotopic nature of the lesion. The thalamus is supplied by four arteries (which arise from the bifurcation of the artery basilaris, the posterior communicating artery and the proximal portion of the posterior cerebral artery - see circle of Willis):
1. polar;
2. thalamic-subthalamic;
3. thalamo-geniculate;
4. posterior choroidal medial and lateral.

1 . Polar arteries(known as the tuberothalamic, anterior internal optic arteries, or premammillary branch) usually arise from the posterior communicating artery. They supply blood to the anteromedial and anterolateral parts of the thalamus, including the reticular nuclei, mamillothalamic tract, part of the ventral lateral nuclei, dorsomedial nuclei and the lateral part of the anterior pole of the thalamus.

2 . Thalamico-subthalamic arteries(known as paramedian thalamic, deep intrapeduncular arteries, posterior internal optic artery, thalamoperforative branch) arise from the proximal P1 peduncular segment of the posterior cerebral artery. They supply the posteromedial thalamus, including the rostral (coracoid) interstitial nuclei of the medial longitudinal fasciculus, the posterior inferior portion of the dorsomedial nuclei, the parafascicular nuclei, the intralaminar nucleus, and sometimes the mamillothalamic tract.

3 . Thalamo-geniculate(thalamogeniculate) arteries arise in the form of 6-10 arteries from the P2 segment of the posterior cerebral artery surrounding the cistern. They supply the ventrolateral thalamus, including the ventral posterior lateral and ventral posterior medial nuclei, the lateral portion of the centromedian nuclei, and the coracolateral (rostrolateral) part of the cushion.

4 . Posterior choroidal arteries(medial and lateral) originate from the P2 segment of the posterior cerebral artery surrounding the cistern, immediately after the origin of the thalamogenicular arteries. They supply blood to the cushion and posterior part of the thalamus, geniculate bodies, and anterior nucleus.

Summarizing Having said the above, the blood supply territories of the thalamus can be divided into the following four large zones:
1 . , supplied by the polar arteries.
2 . , supplied by thalamic-subthalamic arteries.
3 . , supplied by thalamogenic arteries.
4 . , supplied by the posterior choroidal arteries (the thalamus may be variably supplied by the anterior choroidal artery, but this has no clinical significance).

Thalamic infarcts are divided into four groups, corresponding to the four main arterial zones of blood supply.

. Infarctions in the area of blood supply of the polar arteries manifested by neuropsychological disorders. Patients are abullic, apathetic and sloppy; A similar clinic is observed in cases of acute damage to the frontal lobe. In left-sided infarctions, dissomnia predominates with minimal aphasic disorders. In patients with left- or right-sided infarcts, the underlying neuropsychological dysfunction may be acute amnesia with an inability to remember new events. Impaired verbal response is more common in left-sided infarcts, whereas visual memory deficits predominate in right-sided infarcts. In patients with bilateral infarctions in the area of the blood supply of the polar arteries, abulia and severe amnestic disorders are observed, which do not tend to decrease over time. Mild transient hemiparesis or hemisensory disturbances on the contralateral side may occasionally be noted (

The brainstem ends in the very anterior parts with a cluster of gray matter, already divided in half by the third ventricle of the brain into the rudiments of the left and right hemispheres.

In the lower stages of phylogeny, before the appearance of the real brain, these large basal ganglia were the terminal station for all sensory impulses; They also contain mechanisms for the implementation of motor reactions of the body. The focus of the sensitive subcortical centers is the thalamus (Fig. 19, 20). The thalamus develops from the lateral wall of the diencephalon ( diencephalon) in the area of protrusion of the optic vesicles and therefore was previously called the optic thalamus ( thalamus opticus).

Rice. 19. A sagittal section at the level of the diencephalon and brainstem demonstrates the junction of the diencephalon and midbrain, as well as the structures surrounding the third ventricle (according to P. Duus):

1 – pineal gland; 2 – posterior commissure; 3 – leash core; 4 – medullary stripes of the thalamus; 5 6 – pedicle of the arch; 7 – transparent partition; 8 – interventricular foramen (Monroe); 9 – anterior commissure; 10 – interthalamic fusion; 11 – hypothalamic sulcus; 12 – end plate; 13 – visual deepening; 14 – optic chiasm (chiasma); 15 – deepening of the funnel; 16 – pituitary gland; 17 – neurohypophysis; 18 – gray tubercle; 19 – mastoid body; 20 – quadrigeminal plate; 21 – midbrain aqueduct; 22 – IV ventricle

Rice. 20. Section of the diencephalon in the frontal plane (according to P. Duus):

1 – vascular basis of the third ventricle; 2 – hypothalamus; 3 – nucleus of the mastoid body; 4 – subthalamic nucleus; 5 – corpus callosum; 6 – choroid plexus of the third ventricle; 7 – vault; 8 – choroid plexus of the lateral ventricle; 9 – body of the caudate nucleus; 10 – zonal layer; 11 – reticular nucleus of the thalamus; 12 – internal and external medullary plates of the thalamus; 13 – thalamus, lateral group of nuclei; 14 – thalamus, centromedian nucleus; 15 – thalamus, medial group of nuclei; 16 – III ventricle, interthalamic fusion; 17 – pale ball; 18 – internal capsule; 19 – visual tract; 20 – undefined zone; 21 – mastoid-thalamic tract; 22 - cerebral peduncle

Gray matter, which is part of the thalamus, forms several groups of thalamic nuclei: anterior (anterodorsal, anterioventral, anteromedial); median (anterior and posterior paraventricular nuclei, rhomboid nucleus and connecting nucleus); medial (dorsal medial nucleus); ventral (dorsal nucleus, anterior ventral nucleus, ventrolateral nucleus, posterolateral ventral nucleus, posteromedial ventral nucleus, centromedian nucleus, posterolateral nucleus); posterior group (nucleus of the lateral geniculate body, nucleus of the medial geniculate body, cushion nuclei) (Fig. 20, 21). There are a total of 150 thalamic nuclei.

Functionally, three main groups of nuclei can be distinguished:

1. A complex of specific, or relay, thalamic nuclei through which afferent impulses of a certain modality are conducted (tactile, pain, visual, auditory impulses, etc.); These are mainly the anterior parts of the thalamus, the lateral and medial geniculate bodies, and the leash.

2. Nonspecific thalamic nuclei, through which afferent impulses of uncertain modality pass with their diffuse projection in the cerebral cortex (visceral sensitivity, proprio- and enteroreception with switching to vasomotor reactions, intrasecretory and other processes), mainly the medial parts of the tubercle, periplastular parts ( partes paralaminares) and reticular nucleus ( nucl. reticularis thalami), as well as the subthalamic nucleus.

Rice. 21. Nuclei of the thalamus (according to P. Duus):

1 – anterior nuclei of the thalamus; 2 – anteroventral nucleus; 3 – anterior ventrolateral nucleus; 4 – ventral intermedial nucleus; 5 – posterior ventrolateral nucleus; 6 – posteromedial ventral nucleus; 7 – dorsal lateral nucleus; 8 – posterior lateral nucleus; 9 – intralamellar (intralaminar) nuclei; 10 – dorsal medial nucleus; 11 – centromedian nucleus; 12 – thalamic cushion; 13 – medial geniculate body; 14 – lateral geniculate body

3. Associative nuclei of the thalamus, through which impulses pass from other nuclei of the thalamus to the associative (secondary and tertiary) fields of the cerebral cortex; These are mainly the lateral parts of the thalamus, the pillow ( pulvinar thalami).

The morphofunctional study of the thalamus is far from complete, so there are different options for combining subcortical formations. Yes, leash ( habenula) belongs to the epithalamus (together with the pineal gland and posterior commissure); geniculate bodies - to the metathalamus; subthalamic nucleus - to the hypothalamus. Currently, cortical-subcortical relationships involving the thalamus are represented as a vicious circle: thalamus - frontal lobes - caudate nucleus - pallidum - thalamus, etc.

Clinical manifestations of thalamic lesions are characterized by the following triad of signs: hemianesthesia, hemiataxia, hemianopsia.

Total contralateral hemianesthesia (or hemihypesthesia) of thalamic origin is often combined with hemialgia: painful sensations of either burning or coldness. A drop of cold water can cause extremely excruciating pain. Simply touching the skin is extremely painful. Any perceptions (visual, auditory, olfactory) can cause hyperalgesia due to a decrease in the threshold of irritation. Negative emotions worsen the patient’s condition, positive emotions improve it, with the formation of an addiction to pleasant affects.

Hemiataxia thalamic origin is of a mixed sensitive-cerebellar nature.

Homonymous contralateral hemianopsia – loss of the visual fields of the same name (right or left) opposite to the lesion, is a consequence of damage to the lateral geniculate bodies and the pillow.

Other symptoms of damage to the thalamus include the phenomenon of “emotional facialis,” i.e. paresis of the facial muscles (especially weak mobility of the corner of the mouth) on the side opposite to the affected thalamus in a patient with emotional facial expressions (smile) while maintaining the performance of facial movements on task. Also, lesions of the thalamus are characterized by peculiar contractures or postures, for example, “obstetrician’s hand”: the hand is bent at the wrist joint and brought to the ulnar side, straight fingers are brought to the center “in a duck”, the forearm can be bent and pronated. When trying to straighten the arm and stretch it forward, severe ataxia and choreic athetosis (thalamostriatal connections) appear; the rigidity characteristic of capsular contractures is absent.

Other syndromes involving the thalamus

Dejerine–Roussy syndrome: hemianesthesia, hemiataxia, hemihyperpathy with paroxysmal pain, mild transient hemiplegia without contractures, choreiform and athetotic movements, forced laughter, crying.

Foix–Chiari–Nicolescu syndrome, or superior red nucleus syndrome: hemitremor of an intentional nature, mild sensory disorders, unstable choreoathetosis, sometimes in combination with a thalamic arm (unfixed Gilman contracture).

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Description:

Thalamic syndrome - observed when the visual thalamus is damaged. Clinical symptoms are varied and depend on the functional role of the damaged structures.

Symptoms:

When turning off a. thalamo-geniculata on the side opposite to the lesion in the thalamus, the following symptoms develop:

   1. hemihypesthesia or hemianesthesia with a pronounced disturbance of deep sensitivity, sometimes without disturbances of sensitivity on the face,
   2. hyperpathia or dysesthesia, paroxysmal or constant severe pain, spreading to the entire half of the body (thalamic),
   3. loss of vibration sensitivity,
   4. transient hemiparesis without pronounced muscle spasticity and pathological Babinski reflex,
   5. muscles of the affected half of the body,
   6. trochaic and athetoid movements in the fingers, pseudo-athetotic movements when stretching the arm forward and with other tensions, a peculiar position of the hand (“thalamic hand”) - the hand is slightly bent, the fingers are extended in the distal phalanges and half-bent in the main ones, the forearm is slightly bent and pronated
   7. hemiataxia,
   8. sometimes homonymous,
   9. Nothnagel facial paresis,
   10. attention gap.

Causes:

The most common cause of the classic thalamic syndrome, described in 1906 by J. Dejerine and G. Roussy, is vascular disorders in the system of deep branches of the posterior cerebral artery that supplies the visual thalamus - a.thalamo-geniculata.

Treatment:

Treatment of the underlying disease. Thalamic pain is reduced when taking antipsychotics in combination with antidepressants. For particularly severe and persistent pain, surgical intervention is indicated - stereotactic destruction of the posterior ventrolateral nucleus of the thalamus.

Source: article (review) “Ischemic thalamic infarctions” by prof. V.A. Yavorskaya, O.B. Bondar, E.L. Ibragimova, V.M. Krivchun (Kharkiv Medical Academy of Postgraduate Education, City Clinical Hospital No. 7, Kharkov); The article was published in the journal “International Medical Journal” No. 1’2009. The review presents: features of the blood supply to the thalamus, zones of damage to the thalamus depending on the territory of its blood supply, identification of clinical symptoms characteristic of each zone when a focus of ischemia develops in it.

Thalamus is an ovoid-shaped formation (in the diagram - a “red” structure), consisting of several groups of gray matter nuclei.

Thalamic infarcts are divided into four groups, corresponding to the four main arterial zones of blood supply.

. Infarctions in the area of blood supply of the polar arteries manifested by neuropsychological disorders. Patients are abullic, apathetic and sloppy; A similar clinic is observed in cases of acute damage to the frontal lobe. In left-sided infarctions, dissomnia predominates with minimal aphasic disorders. In patients with left- or right-sided infarcts, the underlying neuropsychological dysfunction may be acute amnesia with an inability to remember new events. Impaired verbal response is more common in left-sided infarcts, whereas visual memory deficits are more prevalent in right-sided infarcts. In patients with bilateral infarctions in the area of the blood supply of the polar arteries, abulia and severe amnestic disorders are observed, which do not tend to decrease over time. Sometimes mild transient hemiparesis or hemisensory disturbances on the contralateral side may be observed (to the list of territories).

. Infarctions in the area of blood supply to the paramedian thalamic-subthalamic arteries are characterized by a classic triad of symptoms: acute depression of consciousness, neuropsychological disorders, disturbances of vertical (and horizontal) vision.

Acute depression of consciousness. Lethargic sleep is noted and patients are difficult to awaken. There may be hypersomnia - patients are awakenable, but may fall into deep sleep soon after cessation of stimulation, and may be in a coma resembling hypoxic or metabolic. Impaired consciousness may be associated with the involvement of the intralaminar nuclei and reticular formation of the midbrain in the process. Sometimes there is an absence of such disturbances of consciousness at the onset of the disease with paramedian thalamic-subthalamic infarctions.

Impaired vertical vision function: with paresis/paralysis of upward gaze or a combination of paresis/paralysis of upward and downward gaze. Strabismus is also characteristic. In its pure form, paresis/paralysis of downward gaze is found only in cases of bilateral paramedian infarctions. Horizontal dysfunction is less typical and consists of hypometric contralateral impulses and a decrease in the degree of ipsilateral tracking - “intrainstalled impulses.” Sometimes a disconjugated disorder such as acute esotropia - convergent strabismus - is noted.

Neuropsychological disorders in the form of anxiety occur as the impairment of consciousness decreases. After some time, neuropsychological disorders become more obvious: patients are disoriented, carefree and apathetic. Amnesia with difficulty remembering and confabulation come first. Patients with a right-sided lesion may experience temporary neglect. Some patients have mild hemiparesis or hemisensory impairment on the contralateral side. Movement disturbances such as asterixis, tremor, or dystonia may occur in the contralateral limbs, usually within a few weeks. Blepharospasm may also occur. In patients with bilateral paramedian thalamic-subthalamic infarcts, neuropsychological impairments are more significant and lasting than in patients with homolateral infarcts. The most significant symptoms are amnesia and abulia with spontaneous decrease and increase in lethargy. Some patients have an insatiable desire to sleep; Some may change their mood with uncontrolled use of objects that do not make sense in a given situation, which can also be observed in patients with damage to the frontal lobe (to the list of territories).

. Lateral thalamic infarcts are located in the territory supplied by the thalamic arteries and are characterized by three common clinical syndromes (! It should be noted that cognitive abilities and behavior are preserved in patients with lateral thalamic infarcts).

Purely sensory stroke. The onset of the disease is usually marked by paresthesia or numbness of one side of the body, soon followed by the development of isolated hemisensory deficits. Sensory disturbances are usually mild and involve only part of the body (face and arm, face only, trunk, and upper and lower extremities). This can be explained by the fact that many fibers of the spinothalamic tract do not reach the somatosensory nuclei of the thalamus. Some of the fibers in the trunk leave the spinothalamic tract and are directed to the ascending reticular formation. All types of sensitivity can be affected, dissociation is lost with preservation of pain and temperature sensitivity. Sensory dysfunction may be transient or permanent. Over weeks and months, delayed onset pain sometimes develops on the affected side.

Sensorimotor stroke. The sensory disorders described above are accompanied by motor disorders on the same side in the form of hemiparesis, increased tendon reflexes and Babinski's symptom. This syndrome results from an extension of the infarcted area to the posterior portion of the internal capsule adjacent to the ventrolateral nuclei. With an extensive infarction of the ventrolateral, medial or thalamoparietal parts of the thalamus, a gross disturbance of superficial and deep sensitivity develops.

Infarcts in the lateral parts of the thalamus (the basin of the branches of a. thalamogeniculata) are manifested by motor disorders (clumsiness and ataxia), which are part of the structure of the thalamic Dejerine-Roussy syndrome and have a clinical feature that is associated with a violation of movement patterns as a result of damage to extrapyramidal fibers coming from: 1. from the basal ganglia through the ansa lenticularis; 2. from the superior cerebellar peduncles and the red nucleus, which form synapses in the ventrolateral nuclei of the thalamus; 3. from the posterior femur of the internal capsule, which is adjacent to the ventrolateral part of the thalamus.

Even with disorders of the muscular-articular sense, patients may experience characteristic features of the cerebellar type of hemiataxia, hypermetry, oscillations (twitching) and dysdiadochokinesis. Some patients lose the ability to stand and walk, which becomes the predominant symptom and is called “thalamic astasia.” Movement disturbances such as hemidystonia and hand twitching may take several weeks to develop, especially in patients with sensory disturbances and ataxia. A characteristic feature is the peculiar position of the hand with outstretched arms - the “thalamic hand.” Cognitive abilities and behavior are preserved in patients with lateral thalamic infarcts (