The nuclei of the striatum and their functional significance. Basal (subcortical) nuclei of the brain

basal ganglia, called ganglia by histologists of the last century, they are nuclear-type structures that are located in the thickness of the white matter of the forebrain closer to its base. In mammals, the basal ganglia include the highly elongated and curved caudate nucleus and embedded in the thickness of the white matter lenticular nucleus. It is divided into three parts by two white plates: the largest, lying laterally shell, And pale ball, consisting of internal and external sections (Fig. 3.29).

These anatomical formations form the so-called striopallidal system(From Latin striatus - striped and pallidus - pale.) , which, according to phylogenetic and functional criteria, is divided into the ancient part, the paleostriatum, and the new part, the neostriatum. Paleostriatum represented by the globus pallidus, and neostriatum, appearing for the first time in reptiles, consists of the caudate nucleus and putamen, which are collectively called striatum, or striatum. The caudate nucleus and putamen are anatomically related and are characterized by alternating white and gray matter, which justifies the origin of the term striped body.

The striopallidal system is also often referred to as subthalamic nucleus(Lewis body) and black matter midbrain, which form a functional unity with the basal ganglia. The striatum consists mainly of small cells, the axons of which are directed to the globus pallidus and the substantia nigra of the midbrain.

The striatum is a kind of collector of afferent inputs going to the basal ganglia. The main sources of these inputs are the neocortex (mainly sensorimotor), nonspecific nuclei of the thalamus, and dopaminergic pathways from the substantia nigra.

In contrast to the striatum pale ball consists of large neurons and is the concentration of the output, efferent pathways of the striopallidal system. The axons of neurons localized in the globus pallidus approach various nuclei of the diencephalon and mesencephalon, including the red nucleus, where the red nucleus-spinal cord tract of the extrapyramidal motor regulation system begins.

Another important efferent pathway runs from the internal part of the globus pallidus to the anteroventral and ventrolateral nuclei of the thalamus, and from there continues to the motor areas of the cerebral cortex. The presence of this pathway determines a multi-link loop-like connection between the sensorimotor and motor areas of the cortex, which occurs through the striatum and globus pallidus to the thalamus. It is noteworthy that, as part of this striopallidothalamocortical pathway, the basal ganglia act as an afferent link in relation to the motor areas of the cerebral cortex. Numerous connections of the striopallidal system with various parts of the brain indicate its participation in integration processes, however, to date, much remains unclear in the knowledge about the functions of the basal ganglia.

The basal ganglia play an important role in regulation of movements And sensorimotor coordination. It is known that when the striatum is damaged, athetosis - slow worm-like movements of the hands and fingers.

Degeneration of cells of this structure also causes another disease - chorea, expressed in convulsive twitching of the facial muscles and muscles of the limbs, which are observed at rest and when performing voluntary movements. However, attempts to elucidate the etiology of these phenomena in animal experiments did not yield results. Destruction of the caudate nucleus in dogs and cats did not lead to hyperkinesis, characteristic of the diseases described above.

Local electrical stimulation of certain areas of the striatum causes so-called circulatory motor reactions, characterized by turning the head and torso in the direction opposite to the irritation. Stimulation of other areas of the striatum, on the contrary, leads to inhibition of motor reactions caused by various sensory stimuli.

The presence of certain discrepancies between experimental and clinical data apparently indicates the occurrence of systemic disturbances in the mechanisms of movement regulation during pathological processes in the basal ganglia. Obviously, these disorders are associated with changes in the function of not only the striatum, but also other structures.

As an example, we can consider the possible pathophysiological mechanism of the occurrence of parkinsonism. This syndrome is associated with damage to the basal ganglia and is characterized by a complex of symptoms such as hypokinesia - low mobility and difficulty transitioning from rest to movement; waxy rigidity, or hypertonicity, independent of the position of the joints and the phase of movement; static tremor(trembling), most pronounced in the distal limbs.

All these symptoms are caused by hyperactivity of the basal ganglia, which occurs when the dopaminergic (most likely inhibitory) pathway that runs from the substantia nigra to the striatum is damaged. Thus, the etiology of parkinsonism is due to dysfunction of the striatum and midbrain structures, which are functionally combined into the striopallidal system.

To clarify the role of the basal ganglia in the implementation of movements, data from microelectrode studies are successfully used. Experiments on monkeys have shown a correlation between the discharges of neurons in the striatum and slow, side-to-side worm-like movements of the paw. As a rule, the neuron discharge precedes the onset of slow movement, and during fast “ballistic” movements it is absent. These facts allow us to conclude that striatal neurons are involved in the generation of slow movements that are subject to correction by sensory feedback. The basal ganglia represent one of the levels of a movement regulation system built on a hierarchical principle.

Receiving information from the associative zones of the cortex, the basal ganglia are involved in creating a program of targeted movements, taking into account the dominant motivation. Next, the relevant information from the basal ganglia enters the anterior thalamus, where it is integrated with information coming from the cerebellum. From the thalamic nuclei, impulses reach the motor cortex, which is responsible for implementing the program of purposeful movement through the underlying brainstem and spinal motor centers. So, in general terms, we can imagine the place of the basal ganglia in the entire system of motor centers of the brain.

Date of publication: 2014-12-30; Read: 124 | Page copyright infringement

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Lenticular nucleus(nucl.

Basal ganglia and their functions

lentiformis) is located lateral and anterior to the thalamus. It is wedge-shaped with the apex facing the midline. Between the posterior facet of the lenticular nucleus and the thalamus is located posterior limb of internal capsule(crus posterius capsulae internae). The anterior face of the lentiform nucleus below and in front is fused with the head of the caudate nucleus.

Two stripes of white matter divide the lenticular nucleus into three segments: the lateral segment - shell(putamen), which has a dark color, is located on the outside, and the two ancient parts globus pallidus(globus pallidus) conical in shape facing the middle.

Caudate nucleus

Caudate nucleus(nucl. caudatus) has a club-shaped shape and is curved backwards.

Its anterior part is expanded, called the head (caput) and is located above the lenticular nucleus, and its posterior part - the tail (cauda) passes above and lateral to the thalamus, separated from it by the medullary stripes (stria medullaris). The head of the caudate nucleus participates in the formation of the lateral wall of the anterior horn of the lateral ventricle (cornu anterius ventriculi lateralis). The caudate nucleus consists of small and large pyramidal cells. Between the lentiform and caudate nuclei there is an internal capsule (capsula interna).

Inner capsule(capsula interna) is located between the thalamus, lentiform and caudate nuclei and is a layer of white matter formed by projection fibers on the way to the cortex and from the cortex to the underlying parts of the central nervous system.

On a horizontal section of the cerebral hemisphere at the level of the middle of the thalamus, the internal capsule is white and resembles the shape of an angle open outward. The internal capsule is divided into three sections: front leg(crus anterius capsulae internae), knee(genu capsulae internae) and hind leg(crus posterius capsulae internae).

Above the inner capsule, the fibers form radiant crown(corona radiata). The short anterior leg of the capsule is formed by axons that arise from the cells of the frontal lobe cortex and go to the thalamus (tr.

frontothalamicus), into the red nucleus (tr. frontorubralis), to the cells of the bridge nuclei (tr. frontopontinus). In the knee of the internal capsule there is a corticonuclear tract (tr. corticonuclearis), connecting the cells of the motor cortex with the nuclei of the motor cranial nerves (III, IV, V, VII, IX, X, XI, XII). The posterior limb of the internal capsule is slightly longer than the anterior one and borders the thalamus and the lentiform nucleus. In its anterior part there are fibers emanating from the cells of the posterior sections of the frontal (motor) cortex and heading to the nuclei of the anterior columns of the spinal cord.

Somewhat posterior to the corticospinal tract are fibers running from the lateral nuclei of the thalamus to the posterior central gyrus, as well as from cortical cells to the nuclei of the thalamus. The posterior leg contains fibers passing from the cortex of the occipital and temporal lobes to the pontine nuclei. In the posterior section, auditory and visual fibers pass, starting from the internal and external geniculate bodies and ending in the temporal and occipital lobes.

Along the entire length of the internal capsule there are transverse fibers that connect the lentiform body with the caudate nucleus and the thalamus. Fan-shaped diverging fibers of all pathways forming the internal capsule form the corona radiata in the space between it and the cerebral cortex. Minor damage to small areas of the internal capsule due to the compact arrangement of the fibers causes severe disorders of motor functions and loss of general sensitivity, hearing and vision on the side opposite to the injury.

Striatum

Striatum receives afferent impulses mainly from the thalamus, partly from the cortex; sends efferent impulses to the globus pallidus.

The striatum is considered as an effector nucleus that does not have independent motor functions, but controls the functions of a phylogenetically older motor center - pallidum a (globus pallidus).

The striatum regulates and partially inhibits the unconditioned reflex activity of the globus pallidus, i.e.

That is, it acts on it in the same way as the globus pallidus acts on the red nucleus. The striatum is considered the highest subcortical regulatory and coordination center of the motor apparatus.

In the striatum, according to experimental data, there are also higher vegetative coordination centers that regulate metabolism, heat generation and heat removal, and vascular reactions.

Apparently, in the striatum there are centers that integrate and unite unconditioned reflex motor and autonomic reactions into a single holistic act of behavior.

The striatum influences organs innervated by the autonomic nervous system through its connections with the hypothalamus. With lesions of the striatum, a person experiences athetosis - stereotypical movements of the limbs, as well as chorea - strong abnormal movements that occur without any order or sequence and involve almost all the muscles (“St. Vitus’s dance”).

Both athetosis and chorea are considered to be the result of a loss of the inhibitory influence that the striatum has on the pallidum.

Pale ball

Pale ball(globus pallidus), pale nucleus, is a paired formation that is part of the lenticular nucleus, which is located in the cerebral hemispheres and is separated by an internal capsule. The pallidum is the motor nucleus. When it is irritated, you can get a contraction of the neck muscles, limbs and the entire torso, mainly on the opposite side.

The pallid nucleus receives impulses via afferent fibers coming from the thalamus and closing the thalamo-pallidal reflex arc. The pallid nucleus, being effector-connected with the centers of the midbrain and hindbrain, regulates and coordinates their work.

One of the functions of the pallidum is considered to be inhibition of the underlying nuclei, mainly the red nucleus of the midbrain, and therefore, when the globus pallidus is damaged, a strong increase in the tone of the skeletal muscles is observed - hypertonicity, i.e.

because the red nucleus is freed from the inhibitory influence of the globus pallidus. The thalamo-hypothalamo-pallidal system takes part in higher animals and humans in the implementation of complex unconditioned reflexes - defensive, orientation, food, sexual.

In humans, when stimulating the globus pallidus, the phenomenon of almost doubling the volume of short-term memory was obtained.

Investigating the spatiotemporal relationships between speech elements (vowel phonemes) and recorded impulse activity, a correlation was identified indicating the involvement of a particular structure in the process of auditory memory. In a number of cases, such relationships were obtained by studying the globus pallidus and the dorsomedial thalamic nucleus.

Amygdala nucleus

Amygdala nucleus(corpus amygdaloideum), or amygdaloid complex, is a group of nuclei and is localized inside the anterior pole of the temporal lobe, lateral to the septum of the perforated substance.

Amygdaloid complex is a structure included in the limbic system of the brain, which is characterized by a very low threshold of excitation, which can contribute to the development of epileptiform activity.

The complex contains both larger (pyramidal, pear-shaped) and medium-sized (multipolar, bipolar, candelabra-shaped) and small cells.

The amygdaloid complex is divided into a phylogenetically older - corticomedial - and a newer basal-lateral part. The group of corticomedial nuclei is characterized by low acetylcholinesterase (AChE) activity and is largely associated with olfactory function, forming projections to the paleocortex. The connection with sexual function is confirmed by the fact that stimulation of these nuclei facilitates the secretion of luliberin and folliberin.

Neurons of the basal lateral nuclei are characterized by higher AChE activity, give a projection to the neocortex and striatum, and also facilitate the secretion of ACTH and growth hormone. When the amygdaloid complex is stimulated, convulsions, emotionally charged reactions, fear, aggression, etc. occur.

Fence

Fence(claustrum) - a thin layer of gray matter, separated by the outer capsule of white matter from the lenticular nucleus. The fence below is in contact with the cores of the front perforated substance(substantia perforata anterior).

They assume participation in the implementation of oculomotor reactions of tracking an object.

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Functions of the basal ganglia

rice. 66) . nucleus caudatus), shell ( putamen) and globus pallidus ( globulus pallidusclaustrum). All these four nuclei are called the striatum ( corpus striatum).

There is also striatum (s triatumnukleus lentioris

66. A - Location of the basal ganglia in the volume of the brain. The basal ganglia are shaded red, the thalamus is shaded gray, and the rest of the brain is blank. 1 – Globus pallidus, 2 – Thalamus, 3 – Putamen, 4 – Caudate nucleus, 5 – Amygdala (Astapova, 2004).

In the basal ganglia .

.

Excitatory pathways

Braking paths from the striatum go to black matter and after switching - to the nuclei of the thalamus (Fig.

Rice. 68. Nerve pathways secreting various types of neurotransmitters in the basal ganglia. Ax – acetylcholine; GABA – gamma-aminobutyric acid (Guyton, 2008)

In general, the basal ganglia, having bilateral connections with the cerebral cortex, thalamus, and brainstem nuclei, are involved in the creation of programs of targeted movements, taking into account the dominant motivation. In this case, the neurons of the striatum have an inhibitory effect (transmitter - GABA) on the neurons of the substantia nigra. In turn, neurons of the substantia nigra (transmitter - dopamine) have a modulating effect (inhibitory and excitatory) on the background activity of striatal neurons.

Functions of the striatum.

Defeat

Functions of the globus pallidus.

Brain nuclei and their functions

Destruction of the globus pallidus adynamia makes it difficult to implement available conditioned reflexes and worsens development of new

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Functions of the basal ganglia

The basal ganglia are the massive subcortical nuclei of the telencephalon. They are located deep in the white matter of the hemispheres. These include

• caudate nucleus (consists of head, body and tail),

lenticular nucleus (consists of the putamen and the globus pallidus – globus pallidus – paired formation),

· fence,

· amygdala.

These nuclei are separated from each other by layers of white matter, forming the inner, outer and outer capsules.

The caudate and lentiform nuclei together form an anatomical formation - the striatum (corpus striatum).

Caudate nucleus and putamen

The caudate nucleus and putamen have a similar histological structure.

Their neurons belong to type II Golgi cells, i.e. they have short dendrites and a thin axon; their size is up to 20 microns. These neurons are 20 times more numerous than type I Golgi neurons, which have an extensive network of dendrites and are about 50 microns in size.

The functions of any brain formation are determined primarily by their connections, of which the basal ganglia have quite a lot.

Basal ganglia

These connections have a clear focus and functional outline.

The caudate nucleus and putamen receive descending connections primarily from the extrapyramidal cortex through the subcallosal fasciculus. Other areas of the cerebral cortex also send large numbers of axons to the caudate nucleus and putamen.

The main part of the axons of the caudate nucleus and putamen goes to the globus pallidus, from here to the thalamus, and only from it to the sensory fields.

Consequently, there is a vicious circle of connections between these formations. The caudate nucleus and putamen also have functional connections with structures lying outside this circle: with the substantia nigra, red nucleus, Lewis body, vestibular nuclei, cerebellum, γ-cells of the spinal cord.

The abundance and nature of the connections between the caudate nucleus and the putamen indicate their participation in integrative processes, the organization and regulation of movements, and the regulation of the work of vegetative organs.

Irritation of field 8 of the cerebral cortex causes excitation of neurons in the caudate nucleus, and field 6 causes excitation of neurons in the caudate nucleus and putamen.

A single stimulation of the sensorimotor area of ​​the cerebral cortex can cause excitation or inhibition of the activity of neurons in the caudate nucleus. These reactions occur within 10-20 ms, which indicates direct and indirect connections between the cerebral cortex and the caudate nucleus.

The medial nuclei of the thalamus have direct connections with the caudate nucleus, as evidenced by the reaction of its neurons, which occurs 2-4 ms after stimulation of the thalamus.

The reaction of neurons in the caudate nucleus is caused by skin irritations, light and sound stimuli.

In the interactions between the caudate nucleus and the globus pallidus, inhibitory influences prevail.

If the caudate nucleus is irritated, most of the neurons of the globus pallidus are inhibited, and a smaller part is excited. If the caudate nucleus is damaged, the animal develops motor hyperactivity.

The interaction of the substantia nigra and the caudate nucleus is based on direct and feedback connections between them. It has been established that stimulation of the caudate nucleus increases the activity of neurons in the substantia nigra. Stimulation of the substantia nigra leads to an increase, and destruction leads to a decrease in the amount of dopamine in the caudate nucleus.

It has been established that dopamine is synthesized in the cells of the substantia nigra and then transported at a speed of 0.8 mm/h to the synapses of neurons in the caudate nucleus. In the caudate nucleus, up to 10 mcg of dopamine accumulates in 1 g of nervous tissue, which is 6 times more than in other parts of the forebrain, the globus pallidus, and 19 times more than in the cerebellum. Thanks to dopamine, a disinhibitory mechanism of interaction between the caudate nucleus and the globus pallidus appears.

The caudate nucleus and globus pallidus take part in such integrative processes as conditioned reflex activity and motor activity.

This is detected by stimulation of the caudate nucleus, putamen and globus pallidus, destruction and by recording electrical activity.

Stimulation of the caudate nucleus can completely prevent the perception of painful, visual, auditory and other types of stimulation. Irritation of the ventral region of the caudate nucleus reduces, and the dorsal region increases salivation.

When the caudate nucleus is stimulated, the latent periods of reflexes lengthen and the alteration of conditioned reflexes is disrupted.

The development of conditioned reflexes against the background of stimulation of the caudate nucleus becomes impossible. Apparently, this is explained by the fact that stimulation of the caudate nucleus causes inhibition of the activity of the cerebral cortex.

At the same time, when the caudate nucleus is irritated, some types of isolated movements may appear.

Apparently, the caudate nucleus has, along with inhibitory and excitatory structures.

From the point of view of functional anatomy, the caudate and lentiform nuclei are combined with the concept striopallidal system. The striatal system includes the caudate nucleus and putamen, and the pallidal system includes the globus pallidus.

The striatum is considered the main receptive field of the striopallidal system. Fibers from 4 main sources end here

cerebral cortex,

visual thalamus,

· substantia nigra,

· amygdala.

Cortical neurons have an excitatory effect on striatal neurons.

Neurons of the substantia nigra have an inhibitory effect on them.

The axons of the striatal system neurons end on the pallidum neurons and have an inhibitory effect on them.

The pallidum is the output structure of the striopallidal system.

The bulk of efferent fibers converge to it.

Neurons of the globus pallidus have an excitatory effect on motor neurons of the spinal cord.

The striopallidal system is the center of the extrapyramidal system. Its main function is the regulation of voluntary motor reactions. With her participation, the following are created:

· optimal posture for the intended action;

· optimal balance of tone between antagonist and synergist muscles;

· smoothness and proportionality of movements in time and space.

When the striopallidal system is damaged, dyskinesia develops - a violation of motor acts.

Hypokinesia – pallor and inexpressiveness of movements. Strengthening the inhibitory influence of the striatal system on the pallidal system.

Hyperkinesia (trochea) - strong abnormal movements performed without any order or sequence, which involve the entire musculature - “St. Vitus’s dance.” Reason: loss of inhibitory influence of the striatal system on the pallidal system.

The amygdala is part of the limbic system.

The basal ganglia provide regulation of motor and autonomic functions and participate in the implementation of integrative processes of higher nervous activity.

Disturbances in the basal ganglia lead to motor dysfunctions, such as slowness of movement, changes in muscle tone, involuntary movements, and tremors.

These disorders are recorded in Parkinson's disease and Huntington's disease.

Pale ball

The globus pallidus (globus pallidus s. pallidum) has predominantly large type I Golgi neurons. Connections between the globus pallidus and the thalamus, putamen, caudate nucleus, midbrain, hypothalamus, somatosensory system, etc. indicate its participation in the organization of simple and complex forms of behavior.

Stimulation of the globus pallidus using implanted electrodes causes contraction of the muscles of the limbs, activation or inhibition of γ-motoneurons of the spinal cord.

In patients with hyperkinesis, irritation of different parts of the globus pallidus (depending on the location and frequency of irritation) increased or decreased hyperkinesis.

Stimulation of the globus pallidus, unlike stimulation of the caudate nucleus, does not cause inhibition, but provokes an orienting reaction, movements of the limbs, feeding behavior (sniffing, chewing, swallowing, etc.).

Damage to the globus pallidus causes in people hypomimia, mask-like appearance of the face, tremor of the head and limbs (and this tremor disappears at rest, during sleep and intensifies with movements), and monotony of speech.

When the globus pallidus is damaged, myoclonus is observed - rapid twitching of the muscles of individual groups or individual muscles of the arms, back, and face.

In the first hours after damage to the globus pallidus in an acute experiment on animals, motor activity sharply decreased, movements were characterized by incoordination, the presence of incomplete movements was noted, and a drooping posture occurred when sitting.

Having started moving, the animal could not stop for a long time. In a person with dysfunction of the globus pallidus, the onset of movements is difficult, auxiliary and reactive movements disappear when standing up, friendly movements of the arms when walking are disrupted, and a symptom of propulsion appears: long-term preparation for movement, then rapid movement and stopping. Such cycles are repeated many times in patients.

Fence

The claustrum contains polymorphic neurons of different types.

It forms connections primarily with the cerebral cortex.

The deep localization and small size of the fence present certain difficulties for its physiological study. This nucleus is shaped like a narrow strip of gray matter located beneath the cerebral cortex deep in the white matter.

Stimulation of the fence causes an indicative reaction, turning the head in the direction of irritation, chewing, swallowing, and sometimes vomiting movements.

Irritation from the fence inhibits the conditioned reflex to light and has little effect on the conditioned reflex to sound. Stimulation of the fence during eating inhibits the process of eating food.

It is known that the thickness of the fence of the left hemisphere in humans is somewhat greater than that of the right; When the right hemisphere fence is damaged, speech disorders are observed.

Thus, the basal ganglia of the brain are integrative centers for the organization of motor skills, emotions, and higher nervous activity, and each of these functions can be enhanced or inhibited by the activation of individual formations of the basal ganglia.

Functions of the basal ganglia

The main structures of the basal ganglia ( rice. 66) . The basal ganglia are the caudate nucleus ( nucleus caudatus), shell ( putamen) and globus pallidus ( globulus pallidus); some authors attribute the fence to the basal ganglia ( claustrum).

All these four nuclei are called the striatum ( corpus striatum). There is also striatum (s triatum) - this is the caudate nucleus and putamen. The globus pallidus and shell form a lentiform nucleus ( nukleus lentioris). The striatum and globus pallidus form the striopallidal system.

66. A - Location of the basal ganglia in the volume of the brain. The basal ganglia are shaded red, the thalamus is shaded gray, and the rest of the brain is blank.

1 – Globus pallidus, 2 – Thalamus, 3 – Putamen, 4 – Caudate nucleus, 5 – Amygdala (Astapova, 2004).

Caudate nucleus Lenticular nucleus

B – Three-dimensional image of the location of the basal ganglia in the volume of the brain (Guyton, 2008)

Functional connections of the basal ganglia. In the basal ganglia there is no input from the spinal cord, but there is direct input from the cerebral cortex.

The basal ganglia are involved in motor functions, emotional and cognitive functions.

Excitatory pathways They go mainly to the striatum: from all areas of the cerebral cortex (directly and through the thalamus), from the nonspecific nuclei of the thalamus, from the substantia nigra (midbrain)) (Fig.

Rice. 67. Connection of the basal ganglia circuit with the corticospinocerebellar system for the regulation of motor activity (Guyton, 2008)

The striatum itself has a mainly inhibitory and, partially, excitatory effect on the globus pallidus.

From the globus pallidus the most important path goes to the ventral motor nuclei of the thalamus, from them the excitatory path goes to the motor cortex of the cerebrum. Some fibers from the striatum go to the cerebellum and to the centers of the brain stem (RF, red nucleus and then to the spinal cord.

Braking paths from the striatum go to black matter and after switching - to the nuclei of the thalamus (Fig. 68).

68. Nerve pathways secreting various types of neurotransmitters in the basal ganglia. Ax – acetylcholine; GABA – gamma-aminobutyric acid (Guyton, 2008)

Motor functions of the basal ganglia. In general, the basal ganglia, having bilateral connections with the cerebral cortex, thalamus, and brainstem nuclei, are involved in the creation of programs of targeted movements, taking into account the dominant motivation.

In this case, the neurons of the striatum have an inhibitory effect (transmitter - GABA) on the neurons of the substantia nigra. In turn, neurons of the substantia nigra (transmitter - dopamine) have a modulating effect (inhibitory and excitatory) on the background activity of striatal neurons.

When dopaminergic influences on the basal ganglia are disrupted, movement disorders such as parkinsonism are observed, in which the concentration of dopamine in both nuclei of the striatum drops sharply. The most important functions of the basal ganglia are performed by the striatum and the globus pallidus.

Functions of the striatum.

Participates in turning the head and body and walking in a circle, which are part of the structure of indicative behavior. Defeat the caudate nucleus in diseases and when destroyed in experiments leads to violent, excessive movements (hyperkinesis: chorea and athetosis).

Functions of the globus pallidus.

Has a modulating effect to the motor cortex, cerebellum, RF, red nucleus. When stimulating the globus pallidus in animals, elementary motor reactions predominate in the form of contraction of the muscles of the limbs, neck and face, and activation of eating behavior.

Destruction of the globus pallidus accompanied by a decrease in motor activity - occurs adynamia(pallor of motor reactions), and also it (destruction) is accompanied by the development of drowsiness, “emotional dullness”, which makes it difficult to implement available conditioned reflexes and worsens development of new(impairs short-term memory).

Subcortical nuclei (nucll. subcorticales) are located deep in the white matter of the hemispheres. These include the caudate, lenticular, amygdaloid nuclei and fence (Fig. 476). These nuclei are separated from each other by layers of white matter, forming the inner, outer and outer capsules. A horizontal section of the brain shows alternation of white and gray matter of the subcortical nuclei.

Topographically and functionally, the caudate and lenticular nuclei are combined into the striatum (corpus striatum).

The caudate nucleus (nucl. caudatus) () is club-shaped and curved backwards. Its anterior part is expanded, called the head (caput) and is located above the lenticular nucleus, and its posterior part - the tail (cauda) passes above and lateral to the thalamus, separated from it by the medullary stripes (stria medullaris). The head of the caudate nucleus participates in the formation of the lateral wall of the anterior horn of the lateral ventricle (cornu anterius ventriculi lateralis). The caudate nucleus consists of small and large pyramidal cells. Between the lentiform and caudate nuclei there is an internal capsule (capsula interna).

The lentiform nucleus (nucl. lentiformis) is located lateral and anterior to the thalamus. It is wedge-shaped with the apex facing the midline. Between the posterior edge of the lenticular nucleus and the thalamus is the posterior leg of the internal capsule (crus posterius capsulae internae) (Fig. 476). The anterior face of the lentiform nucleus below and in front is fused with the head of the caudate nucleus. Two stripes of white matter separate the nucl. lentiformis into three segments: the lateral segment - the shell (putamen), which has a darker color, is located on the outside, and two ancient parts of the pale ball (globus pallidus) of a conical shape are facing the middle.

476. Horizontal section of the large brain.
1 - genu corporis callosi; 2 - caput n. caudati; 3 - crus anterius capsulae internae; 4 - capsule externa; 5 - claustrum; 6 - capsula extrema; 7 - insula; 8 - putamen; 9 - globus pallidus; 10 - crus posterius; 11 - thalamus; 12 - plexus chorioideus; 13 - cornu posterius ventriculi lateralis; 14 - sulcus calcarinus; 15 - vermis cerebelli; 16 - splenium corporis callosi; 17 - tr. n. cochlearis et optici; 18 - tr. occipitopontinus et temporopontinus; 19 - tr. thalamocorticalis; 20 - tr. corticospinalis; 21 - tr. corticonuclearis; 22 - tr. frontopontinus.

The claustrum is a thin layer of gray matter separated by an outer capsule of white matter from the lenticular nucleus. The fence below is in contact with the nuclei of the anterior perforated substance (substantia perforata anterior).

The amygdala nucleus (corpus amygdaloideum) is a group of nuclei and is localized inside the anterior pole of the temporal lobe, lateral to the septum perforatum. This nucleus can only be seen in a frontal section of the brain.

These structures (ganglia) are located directly under the cortical part of the telencephalon. They significantly affect the motor functionality of the human body. Their violation mainly affects muscle tone.

The subcortical ganglia of the brain are dense anatomical structures localized in the white matter of the cerebral hemispheres.

The ganglion structures are connected to:

• Lenticular and caudate nuclei of the brain
• Fence
• Amygdala

The subcortical nuclei of the ganglion have membranes, which include white matter. The caudate nucleus, together with the lentiform nucleus, is anatomically represented by the striatum.

Ganglion structures are responsible for a number of significant functions that specifically control well-being and support the normal functioning of the central nervous system.

Three large subcortical nuclei form the extrapyramidal system, which is involved in controlling movements and maintaining muscle tone.

Functions

The main function of the ganglia is to slow down or accelerate the transmission of impulses from the thalamus to the cortical areas that are responsible for motor functions.

The caudate nucleus, the terminal ganglion, makes up the striopalidal system and is responsible for muscle contraction.

Basically, the telencephalon ensures normal communication between the nuclei and the cortical part of the brain, controls the intensity of the motor abilities of the limbs, as well as their strength indicators.

The basal caudate nucleus is located in the white matter of the frontal lobule. Moderate nuclear dysfunction contributes to the occurrence of impaired motor functionality, especially symptoms observed during any physical activity of the patient, including normal walking.

The purpose of the basal ganglia is closely related to the activity of the hypothalamus and pituitary gland. Most often, a number of disorders in the structure and functions of the ganglia are accompanied by a decrease in the functions of the pituitary gland.

Additional structures

The fence appears to be a thin layer of gray matter, which is localized between the shell and the insula. The entire fence is literally enveloped by a white substance that forms two capsules:

• External, which is localized between the fence and the shell
• The outermost one, located next to the island

The ganglia of the terminal section are represented by the amygdala, which is characterized by an accumulation of gray matter, and are located in the temporal part, under the shell. The amygdala is also thought to communicate with the olfactory center and limbic system. Neuronal fibers end their journey in this body.

The limbic system, or visceral brain, stands out for its structural complexity. The functions of the limbic system are multifaceted, as is the specificity of its structure.

Limbics are responsible for:

• Autonomic reactions
• Active activities aimed at acquiring and developing skills
• Psychological and emotional processes

Pathological conditions of the ganglia

If the subcortical caudate nucleus of the brain is damaged, the symptoms appear gradually. First of all, this is manifested by a deterioration in a person’s general well-being, a constant feeling of weakness throughout the body arises, confidence in one’s abilities is lost, and subsequently a depressive state and apathy towards the environment develop.

Experts have found that characteristic pathological changes lead to the occurrence of a number of other diseases:

1. Functional deficiency of the basal ganglia

As a rule, it occurs at an early age. Today, statistics show that the number of children with this type of disease has increased sharply. The pathology is mainly formed due to genetic characteristics and in most cases is inherited. This pathology also occurs in older patients, in whom it leads to Parkinson’s disease.

1. Cysts and neoplasms

A pathological neoplasm in the brain occurs as a result of abnormal metabolism, atrophy or damage to soft tissue, as well as infectious processes. The most unfavorable complication caused by the pathology of the basal ganglia is hemorrhage. If in this case the patient is not provided with timely medical care, then a possible rupture of the cavity will result in death.

A benign neoplasm or cyst that does not increase in size causes virtually no inconvenience to the patient. If the doctor notes the progression of the evolution of the ganglia, the patient is assigned a disability.

Signs of defeat

Symptoms of ganglion damage are distinguished by characteristic pathological manifestations. The severity of the symptoms depends on the degree of damage and the nature of the disease.

The following symptoms are identified:

• Characteristic twitching of the limbs, reminiscent of tremor
• Uncontrolled voluntary movements of the limbs
• Weakened muscle tone, which manifests itself in the form of characteristic weakness and aches of the whole body
• Involuntary movements characterized by constant repetition of a certain motor activity
• Impaired memory functions and lack of understanding of what is happening around

Symptoms appear gradually. It can manifest itself in a sharp form and also, on the contrary, very slowly. In any case, even a single manifestation of a symptom is not recommended to be ignored.

Diagnosis and prognosis of pathology

The primary diagnosis of the pathological condition of the basal ganglia is a standard examination by a neurologist, based on the results of which a number of laboratory tests and diagnostic methods are then prescribed.

The predominant method for diagnosing the ganglion site is magnetic resonance imaging, which allows you to most accurately determine the pronounced lesion. Additionally, research methods such as:

• Various tests
• CT scan

The final prognosis of the disease is made depending on the nature of the lesion and the reasons that caused the pathology of the basal ganglia. If the patient's condition gradually worsens, then he is prescribed a certain series of drugs that will be used throughout his life. Only a highly qualified neurologist can give an accurate assessment of the severity of the lesion and prescribe competent treatment.

The basal ganglia provide motor functions that are different from those controlled by the pyramidal (corticospinal) tract. The term extrapyramidal emphasizes this distinction and refers to a number of diseases in which the basal ganglia are affected. Familial diseases include Parkinson's disease, Huntington's chorea and Wilson's disease. This paragraph discusses the issue of the basal ganglia and describes objective and subjective signs of disturbances in their activity.

Anatomical connections and neurotransmitters of the basal ganglia. The basal ganglia are paired subcortical accumulations of gray matter, forming separate groups of nuclei. The main ones are the caudate nucleus and putamen (together forming the striatum), the medial and lateral plates of the globus pallidus, the subthalamic nucleus and the substantia nigra (Fig. 15.2). The striatum receives afferent input from many sources, including the cerebral cortex, thalamus nuclei, brainstem raphe nuclei, and substantia nigra. Cortical neurons associated with the striatum release glutamic acid, which has an excitatory effect. Neurons of the raphe nuclei associated with the striatum synthesize and release serotonin. (5-GT). Neurons of the substantia nigra pars compacta synthesize and release dopamine, which acts on striatal neurons as an inhibitory transmitter. The transmitters released by the thalamic conductors have not been defined. The striatum contains 2 types of cells: local bypass neurons, the axons of which do not extend beyond the nuclei, and the remaining neurons, the axons of which go to the globus pallidus and the substantia nigra. Local bypass neurons synthesize and release acetylcholine, gamma-aminobutyric acid (GABA), and neuropeptides such as somatostatin and vasoactive intestinal polypeptide. Neurons of the striatum that have an inhibitory effect on the substantia nigra pars reticularis release GABA, while those that excite the substantia nigra release substance P (Fig. 15.3). Striatal projections to the globus pallidus secrete GABA, enkephalins and substance P.

Rice. 15.2. Simplified schematic diagram of the main neuronal connections between the basal ganglia, thalamus optic and cerebral cortex.

Projections from the medial segment of the pallidum form the main efferent pathway from the basal ganglia. CC - compact part, RF - reticular part, YSL - midline nuclei, PV - anteroventral, VL - ventrolateral.

Rice. 15.3. Schematic diagram of the stimulating and inhibitory effects of neuroregulators secreted by neurons of the basal ganglia pathways. The striatal region (outlined by the dashed line) indicates neurons with efferent projection systems. Other striatal transmitters are found in intrinsic neurons. The + sign means excitatory nossynaptic influence. The -- sign means inhibitory influence. YSL - midline nuclei. GABA-?-amnobutyric acid; TSH is a thyroid-stimulating hormone. PV/VL - non-medioventral and ventrolateral.

Axons emerging from the medial segment of the globus pallidus form the main efferent projection of the basal ganglia. There are a significant number of projections passing through or adjacent to the internal capsule (the lemniscus and lenticular fasciculus passing through Forel's areas) to the anterior and lateral ventral nuclei of the thalamus, as well as to the intralamellar nuclei of the thalamus, including the paracentral nucleus. The mediators of this pathway are unknown. Other efferent projections of the basal ganglia include direct dopaminergic connections between the substantia nigra and the limbic region and the frontal cortex of the cerebral hemispheres; the reticular part of the substantia nigra also sends projections to the nuclei of the thalamus and to the superior colliculus.

Modern morphological studies have revealed the distribution of ascending fibers from the thalamus in the cerebral cortex. Ventral thalamic neurons project to the premotor and motor cortex; The medial nuclei of the thalamus project primarily to the prefrontal cortex. The supplementary motor cortex receives many projections from the basal ganglia, including the dopaminergic projection from the substantia nigra, while the primary motor cortex and premotor area receive many projections from the cerebellum. Thus, there is a series of parallel loops connecting specific formations of the basal ganglia with the cerebral cortex. Although the precise mechanism by which various signals are translated into coordinated goal-directed action remains unknown, it is clear that the significant influence of the basal ganglia and cerebellum on the motor cortex is largely due to the influence of the thalamus nuclei. The main projections of the cerebellum, passing through the superior cerebellar peduncle, end together with fibers coming from the globus pallidus in the ventral anterior and ventrolateral nuclei of the thalamus opticum. In this part of the thalamus, a wide loop is formed, consisting of ascending fibers from the basal ganglia and cerebellum to the motor cortex. Despite the obvious significance of these formations, stereotactic destruction of the ventral parts of the thalamus can lead to the disappearance of manifestations of familial essential tremor, as well as rigidity and tremor in Parkinson's disease, without causing functional disorders. Ascending thalamocortical fibers pass through the internal capsule and white matter, so that when lesions occur in this area, both the pyramidal and extrapyramidal systems can be simultaneously involved in the pathological process.

The axons of some cortical neurons form an internal capsule (corticospinal and corticobulbar tracts); they also project into the striatum. A complete loop is formed - from the cerebral cortex to the striatum, then to the globus pallidus, to the thalamus and again to the cerebral cortex. Axons emerging from the paracentral nucleus of the thalamus give projections back to the striatum, thus completing the loop of subcortical nuclei - from the striatum to the globus pallidus, then to the paracentral nucleus and again to the striatum. There is another loop of basal ganglia between the striatum and the substantia nigra. Dopaminergic neurons of the substantia nigra pars compacta project to the striatum, and individual striatal neurons secreting GABA and substance P send projections to the substantia nigra pars reticularis. There is a reciprocal connection between the reticular and compact parts of the substantia nigra; the reticular part sends projections to the ventral part of the thalamus optica, the superior colliculus, and also to the reticular formation of the brainstem. The subthalamic nucleus receives projections from the formations of the neocortex and from the lateral segment of the globus pallidus; neurons within the subthalamic nucleus form reciprocal connections with the lateral segment of the globus pallidus and also send axons to the medial segment of the globus pallidus and the reticular part of the substantia nigra. The neurochemical agents involved in these processes remain unknown, although the involvement of GABA has been identified.

Physiology of the basal ganglia. Recordings of the activity of neurons in the globus pallidus and substantia nigra in a state of wakefulness, performed in primates, confirmed that the main function of the basal ganglia is to support motor activity. These cells are involved at the very beginning of the movement process, as their activity increases before movement becomes visible and detectable by EMG. Increased activity of the basal ganglia was associated primarily with movement of the contralateral limb. Most neurons increase their activity during slow (smooth) movements, while others increase in activity during fast (ballistic) movements. In the medial segment of the globus pallidus and the reticular part of the substantia nigra there is a somatotopic distribution for the upper and lower limbs and face. These observations made it possible to explain the existence of limited dyskinesias. Focal dystonia and tardive dyskinesia can occur with local disturbances of biochemical processes in the globus pallidus and substantia nigra, affecting only those areas in which the hand or face is represented.

Although the basal ganglia are motor in function, it is impossible to establish a special type of movement mediated by the activity of these nuclei. Hypotheses about the functions of the basal ganglia in humans are based on the obtained correlations between clinical manifestations and the localization of lesions in patients with disorders of the extrapyramidal system. The basal ganglia are a cluster of nuclei around the globus pallidus, through which impulses are sent to the thalamus optic and further to the cerebral cortex (see Fig. 15.2). The neurons of each accessory nucleus produce excitatory and inhibitory impulses, and the sum of these influences on the main pathway from the basal ganglia to the thalamus optic and the cerebral cortex, with a certain influence from the cerebellum, determines the smoothness of movements expressed through the corticospinal and other descending cortical pathways. If one or more accessory nuclei is damaged, the amount of impulses entering the globus pallidus changes and movement disorders may occur. The most striking of them is hemiballismus; a lesion of the subthalamic nucleus apparently removes the inhibitory effect of the substantia nigra and globus pallidus, which leads to the appearance of violent involuntary sharp rotational movements of the arm and leg on the side opposite to the lesion. Thus, damage to the caudate nucleus often leads to chorea, and the opposite phenomenon, akinesia, in typical cases develops with the degeneration of cells of the substantia nigra that produce dopamine, freeing the intact caudate nucleus from inhibitory influences. Lesions of the globus pallidus often lead to the development of torsion dystonia and impaired postural reflexes.

Basic principles of neuropharmacology of the basal ganglia. In mammals, the transfer of information from one nerve cell to another usually involves one or more chemical agents released by the first neuron into a special receptor site of the second neuron, thus changing its biochemical and physical properties. These chemical agents are called neuroregulators. There are 3 classes of neuroregulators: neurotransmitters, neuromodulators and neurohormonal substances. Neurotransmitters such as catecholamines, GABA, and acetylcholine are the best known and clinically significant class of neuroregulators. They produce short-latency transient postsynaptic effects (eg, depolarization) close to their site of release. Neuromodulators, such as endorphins, somatostatin and substance P, also act in the excretory zone, but do not usually cause depolarization. Neuromodulators appear to be able to enhance or weaken the effects of classical neurotransmitters. Many neurons containing classical neurotransmitters also accumulate neuromodulatory peptides. For example, substance P is found in brainstem raphe neurons that synthesize 5-HT, and vasoactive intestinal peptide, together with acetylcholine, is found in many cortical cholinergic neurons. Neurohormonal substances, such as vasopressin and angiotensin II, differ from other neuroregulators in that they are released into the bloodstream and transported to distant receptors. Their effects initially develop more slowly and have a longer duration of action. The differences between different classes of neuroregulators are not absolute. Dopamine, for example, acts as a neurotransmitter in the caudate nucleus, but its mechanism of action in the hypothalamus is a neurohormone.

The neurotransmitters of the basal ganglia are the most well studied. They are also more susceptible to the effects of medications. Neurotransmitters are synthesized in the presynaptic terminals of neurons, and some, such as catecholamines and acetylcholine, accumulate in vesicles. When an electrical impulse arrives, neurotransmitters are released from the presynaptic ending into the synaptic cleft, spread in it and connect with special areas of the receptors of the postsynaptic cell, initiating a number of biochemical and biophysical changes; the sum of all postsynaptic excitatory and inhibitory influences determines the probability that a discharge will occur. Biogenic amines dopamine, norepinephrine and 5-HT are inactivated by reuptake by presynaptic terminals. Acetylcholine is inactivated by intrasynaptic hydrolysis. In addition, the presynaptic terminals contain receptor sites called autoreceptors, irritation of which usually leads to a decrease in the synthesis and release of the transmitter. The affinity of the autoreceptor for its neurotransmitter is often much higher than that of the postsynaptic receptor. Drugs that excite dopamine autoreceptors should reduce dopaminergic transmission and may be effective in treating hyperkinesias such as Huntington's chorea and tardive dyskinesia. According to the nature of the response to the effects of various pharmacological agents. receptors are divided into groups. There are at least two populations of dopamine receptors. For example, stimulation of the D1 region activates adenylate cyclase, while stimulation of the D2 region does not have such an effect. The ergot alkaloid bromocriptine, used in the treatment of Parkinson's disease, activates D2 receptors and blocks D1 receptors. Most antipsychotics block D2 receptors.

Clinical manifestations of damage to the basal ganglia. Akinesia. If we divide extrapyramidal diseases into primary dysfunctions (a negative sign due to damage to connections) and secondary effects associated with the release of neuroregulators (a positive sign due to increased activity), then akinesia is a pronounced negative sign or deficiency syndrome. Akinesia is the inability of the patient to actively initiate movement and perform normal voluntary movements easily and quickly. The manifestation of a lesser degree of severity is defined by the terms bradykinesia and hypokinesia. Unlike paralysis, which is a negative sign due to damage to the corticospinal tract, in the case of akinesia, muscle strength is preserved, although there is a delay in achieving maximum strength. Akinesia should also be distinguished from apraxia, in which the demand to perform a certain action never reaches the motor centers that control the desired movement. Akinesia causes the greatest inconvenience to people suffering from Parkinson's disease. They experience severe immobility and a sharp decrease in activity; they can sit for quite a long time practically without moving, without changing their body position, and spend twice as much time compared to healthy people on everyday activities such as eating, dressing and washing. Restricted movement is manifested by the loss of automatic cooperative movements, such as blinking and freely swinging the arms when walking. As a result of akinesia, the well-known symptoms of Parkinson's disease, such as hypomimia, hypophonia, micrographia, and difficulty rising from a chair and walking, appear to develop. Although the pathophysiological details remain unknown, the clinical manifestations of akinesia support the hypothesis that the basal ganglia significantly influence the initial stages of movement and the automatic execution of acquired motor skills.

Neuropharmacological data suggest that akinesia itself is the result of dopamine deficiency.

Rigidity. Muscle tone is the level of muscle resistance during passive movement of a relaxed limb. Rigidity is characterized by a prolonged stay of the muscles in a contracted state, as well as constant resistance to passive movements. In extrapyramidal diseases, rigidity at first glance may resemble spasticity that occurs with lesions of the corticospinal tract, since in both cases there is an increase in muscle tone. Differential diagnosis can be made based on some clinical features of these conditions already during examination of the patient. One of the differences between rigidity and spasticity is the distribution pattern of increased muscle tone. Although stiffness develops in both flexor and extensor muscles, it is more pronounced in those muscles that help flex the torso. Stiffness in large muscle groups is easy to identify, but it also occurs in small muscles of the face, tongue, and throat. In contrast to rigidity, spasticity usually results in increased tone in the extensor muscles of the lower extremities and in the flexor muscles of the upper extremities. In the differential diagnosis of these conditions, a qualitative study of hypertonicity is also used. With rigidity, resistance to passive movements remains constant, which gives reason to call it “plastic” or “lead tube” type. In cases of spasticity, a free gap may be observed, after which a “jackknife” phenomenon occurs; muscles do not contract until they are stretched to a significant extent, and later, when stretched, muscle tone decreases rapidly. Deep tendon reflexes do not change with rigidity and become more active with spasticity. Increased activity of the muscle stretch reflex arc leads to spasticity due to central changes, without increasing the sensitivity of the muscle spindle. Spasticity disappears when the dorsal roots of the spinal cord are cut. Rigidity is less associated with increased activity of the arc of segmental reflexes and more dependent on increased frequency of alpha motor neuron discharges. A special form of rigidity is the cogwheel sign, which is especially characteristic of Parkinson's disease. When a muscle with increased tone is passively stretched, its resistance may be expressed in a rhythmic twitching, as if it were controlled by a ratchet.

Chorea. Chorea, a disease whose name is derived from the Greek word meaning dance, refers to common arrhythmic hyperkinesis of a fast, impetuous, restless type. Choreic movements are characterized by extreme disorder and variety. As a rule, they are long-lasting, can be simple or complex, and involve any part of the body. In complexity, they can resemble voluntary movements, but they are never combined into a coordinated action until the patient includes them in a purposeful movement in order to make them less noticeable. The absence of paralysis makes normal purposeful movements possible, but they are often too fast, unstable and deformed under the influence of choreic hyperkinesis. Chorea may be generalized or limited to one half of the body. Generalized chorea is the leading symptom of Huntington's disease and rheumatic chorea (Sydenham's disease), causing hyperkinesis of the muscles of the face, trunk and limbs. In addition, chorea often occurs in patients with parkinsonism in case of overdose of levodopa. Another well-known choreiform disease, tardive dyskinesia, develops against the background of long-term use of antipsychotics. The muscles of the cheeks, tongue and jaws are usually affected by choreic movements in this disease, although in severe cases the muscles of the trunk and limbs may be involved. Sydenham's chorea is treated with sedatives such as phenobarbital and benzodiazepines. Antipsychotics are commonly used to suppress chorea in Huntington's disease. Drugs that enhance cholinergic conduction, such as phosphatidylcholine and physostigmine, are used in approximately 30% of patients with tardive dyskinesia.

A special form of paroxysmal chorea, sometimes accompanied by athetosis and dystonic manifestations, occurs in sporadic cases or is inherited in an autosomal dominant manner. It first appears in childhood or adolescence and continues throughout life. Patients experience paroxysms that last for several minutes or hours. One of the varieties of chorea is kinesogenic, that is, it occurs during sudden, purposeful movements. Factors that provoke chorea, especially in those individuals who were diagnosed with Sydenham's disease in childhood, may be hypernatremia, alcohol consumption and diphenin intake. In some cases, seizures can be prevented with anticonvulsant medications, including phenobarbital and clonazepam, and sometimes levodopa.

Athetosis. The name comes from a Greek word meaning unstable or changeable. Athetosis is characterized by the inability to hold the muscles of the fingers, toes, tongue, and other muscle groups in one position. Long-lasting, smooth involuntary movements occur, most pronounced in the fingers and forearms. These movements consist of extension, pronation, flexion and supination of the hand with alternating flexion and extension of the fingers. Athetotic movements are slower than choreiform ones, but there are conditions called choreoathetosis in which it can be difficult to distinguish between these two types of hyperkinesis. Generalized athetosis can be seen in children with static encephalopathy (cerebral palsy). In addition, it can develop in the case of Wilson's disease, torsion dystonia and cerebral hypoxia. Unilateral posthemiplegic athetosis is observed more often in children who have had a stroke. In patients with athetosis that developed against the background of cerebral palsy or cerebral hypoxia, other movement disorders are noted that arise as a result of concomitant damage to the corticospinal tract. Patients are often unable to perform individual independent movements with the tongue, lips and hands; attempts to make these movements lead to contraction of all the muscles of the limb or some other part of the body. All types of athetosis cause rigidity of varying degrees of severity, which, apparently, causes the slowness of movements in athetosis, in contrast to chorea. Treatment of athetosis is usually unsuccessful, although some patients experience improvement when taking drugs used to treat choreic and dystonic hyperkinesis.

Dystonia. Dystonia is an increase in muscle tone, leading to the formation of fixed pathological postures. In some patients with dystonia, postures and gestures may change, becoming awkward and pretentious, due to uneven strong contractions of the muscles of the trunk and limbs. Spasms that occur with dystonia resemble athetosis, but are slower and more often affect the muscles of the trunk than the limbs. The phenomena of dystonia intensify with purposeful movements, excitement and emotional overstrain; they decrease with relaxation and, like most extrapyramidal hyperkinesis, completely disappear during sleep. Primary torsion dystonia, previously called deforming muscular dystonia, is often inherited in an autosomal recessive manner in Ashkenazi Jews and in an autosomal dominant manner in individuals of other nationalities. Sporadic cases have also been described. Signs of dystonia usually appear in the first two decades of life, although later onsets of the disease have also been described. Generalized torsion spasms can occur in children suffering from bilirubin encephalopathy or as a result of cerebral hypoxia.

The term dystonia is also used in another meaning - to describe any fixed posture that occurs as a result of damage to the motor system. For example, dystonic phenomena that occur with a stroke (bent arm and extended leg) are often called hemiplegic dystonia, and in parkinsonism - flexor dystonia. In contrast to such persistent dystonic phenomena, some drugs, such as antipsychotics and levodopa, can provoke the development of temporary dystonic spasms that disappear after stopping the drug.

Secondary, or local, dystonia is more common than torsion dystonia; these include diseases such as spasmodic torticollis, writer's cramp, blepharospasm, spastic dystonia and Meige's syndrome. In general, with local dystonia, the symptoms usually remain limited, stable and do not spread to other parts of the body. Local dystonias often develop in middle-aged and older people, usually spontaneously, without a hereditary predisposition factor or previous diseases provoking them. The most famous type of local dystonia is spastic torticollis. With this disease, constant or prolonged tension occurs in the sternocleidomastoid, trapezius and other muscles of the neck, usually more pronounced on one side, leading to a forced turn or tilt of the head. The patient cannot overcome this violent posture, which distinguishes the disease from a habitual spasm or tic. Dystonic phenomena are most pronounced when sitting, standing and walking; Touching the chin or jaw can often help relieve muscle tension. Women aged 40 years get sick 2 times more often than men.

Torsion dystonia is classified as an extrapyramidal disease even in the absence of pathological changes in the basal ganglia or other parts of the brain. Difficulties in selecting medications are aggravated by insufficient knowledge about changes in neurotransmitters in the case of this disease. Treatment of secondary dystonic syndromes also does not bring noticeable improvement. In some cases, sedatives such as benzodiazepines, as well as large doses of cholinergic drugs, have a positive effect. Sometimes a positive effect occurs with the help of levodopa. Improvement is sometimes noted with treatment using bioelectrical control; psychiatric treatment is not beneficial. In severe spastic torticollis, most patients benefit from surgical denervation of the affected muscles (from C1 to C3 on both sides, C4 on one side). Blepharospasm is treated with botulinum toxin injections into the muscles surrounding the eyeball. The toxin causes a temporary blockade of neuromuscular transmission. Treatment must be repeated every 3 months.

Myoclonus. This term is used to describe short-term violent random muscle contractions. Myoclonus can develop spontaneously at rest, in response to stimulation, or during targeted movements. Myoclonus may occur in a single motor unit and resemble fasciculations, or simultaneously involve groups of muscles, resulting in changes in the position of the limb or deformation of targeted movements. Myoclonus results from a variety of generalized metabolic and neurological disorders collectively called myoclonus. Posthypoxic intentional myoclonus is a special myoclonic syndrome that develops as a complication of temporary anoxia of the brain, for example, during short-term cardiac arrest. Mental activity is usually not affected; Cerebellar symptoms occur due to myoclonus, involving the muscles of the limbs and face, and voluntary movements and voice are distorted. Action myoclonus distorts all movements and greatly impairs the ability to eat, talk, write, and even walk. These phenomena can occur with lipid storage disease, encephalitis, Creutzfeldt-Jakob disease, or metabolic encephalopathies arising from respiratory, chronic renal, hepatic failure or electrolyte imbalance. For the treatment of postanoxic intentional and idiopathic myoclonus, 5-hydroxytryptophan, a precursor of 5-HT, is used (Fig. 15.4); Baclofen, clonazepam and valproic acid are used as alternative treatments.

Asterixis. Asterixis (“fluttering” tremor) is called rapid irregular movements that occur as a result of short-term interruptions of background tonic muscle contractions. To some extent, asterixis can be considered negative myoclonus. Asterixis can be observed in any striated muscle during its contraction, but it is usually clinically presented as a short-term drop in postural tone with recovery upon voluntary extension of the limb with backward flexion at the wrist or ankle joint. Asterixis is characterized by periods of silence from 50 to 200 ms during continuous study of the activity of all muscle groups of one limb using EMG (Fig. 15.5). This causes the wrist or shin to drop down before muscle activity resumes and the limb returns to its original position. Bilateral asterixis is often observed in metabolic encephalopathies, and in the case of liver failure it has the original name “liver clap.” Asterixis can be caused by certain medications, including all anticonvulsants and the radiographic contrast agent Metrizamide. Unilateral asterixis can develop after brain lesions in the area of ​​​​the blood supply of the anterior and posterior cerebral arteries, as well as due to small focal lesions of the brain, covering formations that are destroyed during stereotactic cryotomy of the ventrolateral nucleus of the thalamus.

Rice. 15.4. Electromyograms of the muscles of the left arm in a patient with posthypoxic nonintentional myoclonus before (a) and during (b) treatment with 5-hydroxytryptophan.

In both cases the hand was in a horizontal position. The first four curves show the EMG signal from the wrist extensor, wrist flexor, biceps and triceps muscles. The lower two curves are recordings from two accelerometers located at right angles to each other on the arm. Horizontal calibration is 1 s, and - prolonged high-amplitude jerky twitches during voluntary movements on the EMG are represented by arrhythmic discharges of bioelectrical activity, interspersed with irregular periods of silence. The initial positive and subsequent negative changes occurred synchronously in the antagonist muscles; b - only mild irregular tremor is observed, the EMG has become more uniform (from J. N. Crowdon et al., Neurology, 1976, 26, 1135).

Hemiballism. Hemiballism is called hyperkinesis, characterized by violent throwing movements in the upper limb on the side opposite to the lesion (usually of vascular origin) in the region of the subthalamic nucleus. A rotational component may occur during movements of the shoulder and hip, flexion or extension movements in the hand or foot. Hyperkinesis persists during wakefulness, but usually disappears during sleep. Muscle strength and tone may be slightly reduced on the affected side, precise movements are difficult, but there are no signs of paralysis. Experimental data and clinical observations indicate that the subthalamic nucleus appears to have a controlling influence on the globus pallidus. When the subthalamic nucleus is damaged, this restraining influence is eliminated, leading to hemiballismus. The biochemical consequences of these disturbances remain unclear, but indirect evidence suggests that increased dopaminergic tone occurs in other structures of the basal ganglia. The use of antipsychotics to block dopamine receptors, as a rule, leads to a decrease in the manifestations of hemiballismus. If there is no effect from conservative treatment, surgical treatment is possible. Stereotactic destruction of the homolateral globus pallidus, thalamic fasciculus, or ventrolateral nucleus of the thalamus can lead to the disappearance of hemiballismus and normalization of motor activity. Although recovery may be complete, some patients experience varying degrees of hemichorea involving the muscles of the hand and foot.

Rice. 15.5. Asterixis recorded from the outstretched left arm of a patient with encephalopathy caused by taking metrizamide.

The top four curves were obtained from the same muscles as in Fig. 15.4. The last curve was obtained from an accelerometer located on the dorsum of the hand. Calibration 1 s. The recording of a continuous voluntary EMG waveform was interrupted in the region of the arrow by a short involuntary period of silence in all four muscles. After a period of silence, a change in posture followed with a convulsive return, which was recorded by the accelerometer.

Tremor. This is a fairly common symptom, characterized by rhythmic vibrations of a certain part of the body relative to a fixed point. As a rule, tremor occurs in the muscles of the distal limbs, head, tongue or jaw, and in rare cases - the trunk. There are several types of tremor, and each has its own clinical and pathophysiological characteristics and methods of treatment. Often, several types of tremor can be observed simultaneously in the same patient, and each requires individual treatment. In a general medical institution, most patients with suspected tremor are actually dealing with asterixis that has arisen against the background of some kind of metabolic encephalopathy. Different types of tremor can be divided into separate clinical variants according to their location, amplitude and influence on goal-directed movements.

Tremor at rest is a large-scale trembling with an average frequency of 4-5 muscle contractions per second. Typically, tremor occurs in one or both upper extremities, sometimes in the jaw and tongue; is a common symptom of Parkinson's disease. This type of tremor is characterized by the fact that it occurs during postural (tonic) contraction of the muscles of the trunk, pelvic and shoulder girdle at rest; volitional movements temporarily weaken it (Fig. 15.6). With complete relaxation of the proximal muscles, the tremor usually disappears, but since patients rarely achieve this state, the tremor persists constantly. Sometimes it changes over time and can spread from one muscle group to another as the disease progresses. Some people with Parkinson's disease do not have tremor, in others it is very weak and limited to the muscles of the distal parts; in some patients with Parkinson's disease and in people with Wilson's disease (hepatolenticular degeneration), more pronounced disorders are often observed that also involve the muscles of the proximal parts. In many cases, plastic type rigidity of varying degrees of severity occurs. Although this type of tremor brings certain inconvenience, it does not significantly interfere with the performance of purposeful movements: often a patient with tremor can easily bring a glass of water to his mouth and drink it without spilling a drop. Handwriting becomes small and illegible (micrographia), the gait is mincing. Parkinson's syndrome is characterized by resting tremors, slowness of movement, rigidity, flexion postures without true paralysis, and unsteadiness. Parkinson's disease is often combined with tremor that occurs during severe anxiety caused by a large crowd of people (one of the types of enhanced physiological tremor - see below), or with hereditary essential tremor. Both concomitant conditions are aggravated by an increase in the level of catecholamines in the blood and are reduced by taking drugs that block beta-adrenergic receptors, such as anaprilin.

Rice. 15.6. Tremor at rest in a patient with parkinsonism. The upper two EMG curves were taken from the extensors and flexors of the left hand, the lower curve was taken with an accelerometer located on the left hand. Horizontal calibration 1 s. Resting tremor occurs as a result of alternating contractions of antagonist muscles with a frequency of approximately 5 Hz. The arrow indicates the change in EMG after the patient bent the hand back and the tremor at rest disappeared.

The exact pathological and morphological picture of changes in resting tremor is not known. Parkinson's disease causes visible lesions primarily in the substantia nigra. Wilson's disease, in which tremor is combined with cerebellar ataxia, causes diffuse lesions. In older people, tremors at rest may not be accompanied by rigidity, slowness of movements, hunched posture and immobility of facial muscles. Unlike patients with parkinsonism, people with similar manifestations have preserved mobility; there is no effect from taking antiparkinsonian drugs. It is impossible to accurately predict in any given case whether tremor is the initial manifestation of Parkinson's disease. Patients with unsteadiness when walking and tremors at rest in the proximal limbs (rubal tremor) as a symptom of cerebellar disorders can be distinguished from patients with parkinsonism by the presence of ataxia and dysmetria.

Intention tremor develops with active movement of the limbs or when holding them in a certain position, for example, in an extended position. The amplitude of the tremor may increase slightly with more subtle movements, but never reaches the level observed in the case of cerebellar ataxia/dysmetria. Intention tremor easily disappears when the limbs are relaxed. In some cases, Intention tremor is a sharp increase in normal physiological tremor that can occur in some situations in healthy people. Similar tremor can also occur in patients with essential tremor and Parkinson's disease. This process involves the arm in an extended position, the head, lips and tongue. In general, this tremor is a consequence of a hyperadrenergic state, and sometimes has an iatrogenic origin (Table 15.2).

When α2-adrenergic receptors are activated in muscles, their mechanical properties are disrupted, which leads to the occurrence of intention tremor. These disorders manifest themselves in damage to the afferent formations of the muscle spindle, which leads to disruption of the muscle stretch reflex arc and contributes to an increase in the amplitude of physiological tremor. These types of tremor do not occur in patients with a violation of the functional integrity of the muscle stretch reflex arc. Drugs that block α2-adrenergic receptors reduce increased physiological tremor. Intention tremor occurs in many medical, neurological and psychiatric diseases, so it is more difficult to interpret than resting tremor.

Table 15.2. Conditions in which physiological tremor increases

Conditions accompanied by increased adrenergic activity:

Anxiety

Taking bronchodilators and other beta mimetics

Excited state

Hypoglycemia

Hyperthyroidism

Pheochromocytoma

Peripheral intermediates of levodopa metabolism.

Excitement before performing in public

Conditions that may be accompanied by increased adrenergic activity:

Taking amphetamines

Taking antidepressants

Withdrawal syndrome (alcohol, drugs)

Xanthines in tea and coffee

Conditions of unknown etiology:

Treatment with corticosteroids

Increased fatigue

Treatment with lithium drugs

There is also another type of intention tremor, slower, usually as a monosymptom, occurring either in sporadic cases or in several members of the same family. It is called essential hereditary tremor (Fig. 15.7) and can appear in early childhood, but more often develops later in life and is observed throughout life. Tremor brings certain inconvenience, as it seems that the patient is in an excited state. A peculiar feature of this tremor is that it disappears after taking two or three sips of an alcoholic drink, but after the cessation of the effect of alcohol it becomes more pronounced. Essential tremor is reduced when taking hexamidine and β-blockers that affect the activity of the central nervous system, such as anaprilin.

Rice. 15.7. Action tremor in a patient with essential tremor. The recording was made from the muscles of the right arm during backward bending of the hand; Otherwise, the records are similar to those in Fig. 15.4. Calibration 500 ms. It should be noted that during action tremor, discharges of bioelectrical activity on the EMG with a frequency of approximately 8 Hz occurred synchronously in the antagonist muscles.

The term intention tremor is somewhat inaccurate: pathological movements are certainly not intentional, intentional, and the changes would be more correctly called tremor ataxia. With true tremors, as a rule, the muscles of the distal parts of the limbs suffer; the trembling is more rhythmic, usually in one plane. Cerebellar ataxia, which causes a minute-by-minute change in the direction of pathological movements, manifests itself with precise, targeted movements. Ataxia does not manifest itself in stationary limbs even during the first stage of voluntary movement, however, as movements continue and greater precision is needed (for example, when touching an object, a patient’s nose, or a doctor’s finger), jerky, rhythmic twitching occurs, making it difficult to move the limb forward, with fluctuations in sides. They continue until the action is completed. Such dysmetria can create significant interference for the patient in performing differentiated actions. Sometimes the head is involved (in the case of a staggering gait). This movement disorder undoubtedly indicates damage to the cerebellar system and its connections. If the lesion is significant, every movement, even raising a limb, leads to such changes that the patient loses his balance. A similar condition is sometimes noted in multiple sclerosis, Wilson's disease, as well as vascular, traumatic and other lesions of the midbrain tegmentum and subthalamic region, but not the cerebellum.

Habitual spasms and tics. Many people have habitual hyperkinesis throughout their lives. Well-known examples include sniffing, coughing, protruding the chin, and the habit of fiddling with the collar. They are called habitual spasms. People who perform these actions recognize that the movements are purposeful, but they are forced to do them to overcome feelings of tension. Habitual spasms may decrease over time or with the patient’s willpower, but when attention is distracted, they resume again. In some cases, they become so ingrained that a person does not notice and cannot control them. Habitual spasms are especially common in children aged 5 to 10 years.

Tics are characterized by stereotypical, unintentional, irregular movements. The best known and most severe form is Gilles de la Tourette syndrome, a neuropsychiatric disease with movement and behavior disorders. As a rule, the first symptoms of this disease appear in the first twenty years of life; men get sick 4 times more often than women. Movement disorders include multiple short-term muscle spasms, known as tics, in the face, neck and shoulders. Vocal tics often occur, and the patient makes grunting and barking sounds. Changes in behavior manifest themselves in the form of coprolalia (swearing and repetition of other obscene expressions) and repetition of words and phrases heard from others (echolalia). The origin of Gilles de la Tourette syndrome is unknown. The pathophysiological mechanisms also remain unclear. Treatment with antipsychotics reduces the severity and frequency of tics in 75-90% of patients, depending on the severity of the disease. Clonidine, a drug from the group of adrenergic agonists, is also used to treat Gilles de la Tourette syndrome.

Examination and differential diagnosis for extrapyramidal syndromes. In a broad sense, all extrapyramidal disorders must be considered from the point of view of primary deficiency (negative symptoms) and emerging new manifestations (changes in body position and hyperkinesis). Positive symptoms arise due to the release of the immobile formations of the nervous system responsible for movements from the inhibitory effect, and the resulting disturbance in their balance. The doctor must accurately describe the observed movement disorders; one should not limit oneself to the name of the symptom and fit it into a ready-made category. If the doctor knows the typical manifestations of the disease, he will easily identify the full symptoms of extrapyramidal diseases. It must be remembered that Parkinson's disease is characterized by slowness of movements, weak facial expressions, tremors at rest and rigidity. It is also easy to identify typical changes in posture in the generalized form of dystonia or spasmodic torticollis. In the case of athetosis, as a rule, instability of postures, continuous movements of the fingers and hands, tension are observed, with chorea with characteristic rapid complex hyperkinesis, with myoclonus with impulsive jerking movements leading to a change in the position of the limb or torso. With extrapyramidal syndromes, purposeful movements are most often impaired.

Particular diagnostic difficulties arise, as in the case of many other diseases, in early or latent forms of the disease. Parkinson's disease often goes undetected until tremors appear. Unbalance and the appearance of a shuffling gait (walking in small steps) in older people are often mistakenly attributed to loss of confidence and fear of falling. Patients may complain of nervousness and restlessness and describe difficulty moving and soreness in various parts of the body. If there are no symptoms of paralysis and reflexes are not changed, these complaints can be regarded as rheumatic or even psychogenic in nature. Parkinson's disease may begin with hemiplegic manifestations, and for this reason vascular thrombosis or a brain tumor may be misdiagnosed. In this case, diagnosis can be facilitated by identifying hypomimia, moderate rigidity, insufficient amplitude of arm swing when walking, or disturbances in other combined actions. Wilson's disease should be excluded in every case of atypical extrapyramidal disorders. Moderate or early chorea is often confused with increased excitability. Examination of the patient at rest and during active movements is crucial. However, in some cases it is impossible to distinguish a simple restless state from the early manifestations of chorea, especially in children, and there are no laboratory tests to make an accurate diagnosis. Noting the initial changes in postures during dystonia, the doctor may mistakenly assume that the patient has hysteria, and only later, when the changes in postures become stable, can a correct diagnosis be made.

Movement disorders often occur in combination with other disorders. Extrapyramidal syndromes usually accompany lesions of the corticospinal tract and cerebellar systems. For example, with progressive supranuclear palsy, olivopontocerebellar degeneration and Shy-Drager syndrome, many signs of Parkinson's disease are observed, as well as impaired voluntary movements of the eyeballs, ataxia, apraxia, postural hypotension or spasticity with a bilateral Babinski sign. Wilson's disease is characterized by resting tremor, rigidity, slowness of movement, and flexion dystonia in the trunk muscles, while athetosis, dystonia, and intention tremor occur rarely. Mental and emotional disturbances may also occur. Gellervorden-Spatz disease can cause generalized rigidity and flexion dystonia, and in rare cases choreoathetosis can occur. In some forms of Huntington's disease, especially if the disease began in adolescence, rigidity gives way to choreoathetosis. With spastic bilateral paralysis, children may develop a combination of pyramidal and extrapyramidal disorders. Some of the degenerative diseases that cause damage to both the corticospinal tract and the nuclei are described in Chapter. 350.

Morphological studies of the basal ganglia, as well as data from studies of the content of neurotransmitters, make it possible to evaluate lesions of the basal ganglia and monitor the treatment of such diseases. This is best illustrated by Huntington's and Parkinson's diseases. In Parkinson's disease, the content of defamine in the striatum is reduced due to the death of neurons in the substantia nigra and degeneration of their axonal projections to the striatum. As a result of a decrease in dopamine levels, striatal neurons that synthesize acetylcholine are freed from inhibitory influence. This results in a predominance of cholinergic nerve transmission over dopaminergic transmission, which explains most of the symptoms of Parkinson's disease. Identification of such an imbalance serves as the basis for rational drug treatment. Drugs that enhance dopaminergic transmission, such as levodopa and bromocriptine, are likely to restore balance between the cholinergic and dopaminergic systems. These drugs, prescribed in combination with anticholinergic drugs, are currently the mainstay of treatment for Parkinson's disease. The use of excessive doses of levodopa and bromocriptine leads to the occurrence of various hyperkinesis due to overstimulation of dopamine receptors in the striatum. The most common of these is craniofacial choreoathetosis; generalized choreoathetosis, tics in the face and neck, dystonic changes in posture, and myoclonic jerks may also develop. On the other hand, the prescription of drugs that block dopamine receptors (for example, neurolentics) or cause depletion of accumulated dopamine [Tetrabenazine or reserpine] can lead to the occurrence of parkinsonism syndrome in apparently healthy people,

Huntington's chorea is in many respects the clinical and pharmacological opposite of Parkinson's disease. In Huntington's disease, characterized by personality changes and dementia, gait disturbance and chorea, neurons in the caudate nucleus and putamen die, leading to depletion of GABA and acetylcholine while dopamine remains unchanged. Chorea is thought to result from a relative excess of dopamine compared to other neurotransmitters in the striatum; Drugs that block dopamine receptors, such as antipsychotics, generally have a beneficial effect on chorea, while levodopa increases it. Likewise, physostigmine, which enhances cholinergic transmission, may reduce symptoms of chorea, whereas anticholinergic drugs increase them.

These examples from clinical pharmacology also demonstrate the delicate balance between stimulatory and inhibitory processes in the basal ganglia. In all patients, the various clinical manifestations noted during treatment are due to changes in the neurochemical environment, while morphological damage remains unchanged. These examples illustrate the possibilities of drug treatment of lesions of the basal ganglia and give reason to be optimistic about the prospects for treating patients with extrapyramidal movement disorders.

Bibliography

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Handbook of Physiology/Ed. V. B. Brooks, sect. I.: The Nervous System, vol. II: Motor Control, part 2. Bethesda: Amer. Physiol. Society, 1981, 1017-1062.

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One of the most inexplicable things in the universe is the brain. Almost nothing is known about it with regard to its operating principles. From a physiological point of view, this organ has been well studied, but most people have more than a superficial understanding of its structure.

The majority of educated people know that the brain is two hemispheres, covered with a cortex and convolutions; it consists of several sections and somewhere there is gray and white matter. We will talk about all this in special topics, and today we will look at what the basal ganglia of the brain are, which few have heard of and know about.

Structure and location

The basal ganglia of the brain is a collection of gray matter in the white matter, located at the base of the brain and part of its anterior lobe. As we can see, the gray matter not only forms the hemispheres, but is also located in the form of separate clusters called ganglia. They have a close connection with the white matter and cortex of both hemispheres.

The structure of this region is based on a slice of the brain. It includes:

• amygdala;
• striatum (composed of the caudate nucleus, globus pallidus, putamen);
• fence;
• lenticular nucleus.

Between the lenticular nucleus and the thalamus there is a white substance called the internal capsule, and between the insula and the fence is the external capsule. Recently, a slightly different structure of the subcortical nuclei of the brain has been proposed:

• striatum;
• several nuclei of the midbrain and diencephalon (subthalamic, pedunculopontine and substantia nigra).

Together they are responsible for motor activity, motor coordination and motivation in human behavior. This is all that can be said for sure about the function of the subcortical nuclei. Otherwise, they, like the brain as a whole, are poorly understood. Absolutely nothing is known about the purpose of the fence.

Physiology

All subcortical nuclei are again conventionally combined into two systems. The first is called the striopallid system, which includes:

• pale globe;
• caudate nucleus of the brain;
• shell.

The last two structures consist of many layers, which is why they are grouped under the name striatum. Ballus pallidus is a brighter, lighter color and is not laminated.

The lenticular nucleus is formed by the globus pallidus (located inside) and the shell, which forms its outer layer. The amygdala and the amygdala are components of the limbic system of the brain.

Let's take a closer look at what these brain nuclei are.

Caudate nucleus

Paired component of the brain related to the striatum. The location is in front of the thalamus. They are separated by a strip of white matter called the internal capsule. Its anterior part has a more massive thickened structure, the head of the structure is adjacent to the lenticular core.

Structurally, it consists of Golgi neurons and has the following characteristics:

• their axon is very thin, and dendrites (processes) are short;
• nerve cells have reduced physical dimensions compared to normal ones.

The caudate nucleus has close connections with many other distinct brain structures and forms a very wide network of neurons. Through them, the globus pallidus and thalamus interact with sensory areas, creating pathways with closed circuits. The ganglion also interacts with other parts of the brain, and not all of them lie in its vicinity.

Experts do not have a consensus on what the function of the caudate nucleus is. This once again confirms the scientifically unfounded theory that the brain is a single structure, any of its functions can be easily performed by any part. And this has been repeatedly proven in studies of people injured due to accidents, other emergencies and diseases.

It is certainly known that it takes part in autonomic functions and plays an important role in the development of cognitive abilities, coordination and stimulation of motor activity.

The striatal nucleus consists of layers of white and gray matter alternating in a vertical plane.

Black substance

The component of the system that is most involved in the coordination of movements and motor skills, maintaining muscle tone and controlling postures. Participates in many autonomic functions, such as breathing, cardiac activity, and maintaining vascular tone.

Physically, the substance is a continuous strip, as was believed for decades, but anatomical sections have shown that it consists of two parts. One of them is a receiver that sends dopamine to the striatum, the second - a transmitter - serves as a transport artery for transmitting signals from the basal ganglia to other parts of the brain, of which there are more than a dozen.

Lenticular body

Its location is between the caudate nucleus and the thalamus, which, as stated, are separated by the external capsule. In front of the structure, it merges with the head of the caudate nucleus, which is why its frontal section has a wedge-shaped shape.

This nucleus consists of sections separated by a thin film of white matter:

• shell – darker outer part;
• pale ball.

The latter is very different in structure from the shell and consists of type I Golgi cells, which predominate in the human nervous system, and are larger in size than their type II. According to neurophysiologists, it is a more archaic brain structure than other components of the brain nucleus.

Other nodes

The fence is the thinnest layer of gray matter between the shell and the island, around which there is a white substance.

The basal ganglia are also represented by the amygdala, located under the shell in the temporal region of the head. It is believed, but not known for sure, that this part belongs to the olfactory system. It is also where the nerve fibers coming from the olfactory lobe end.

Consequences of physiological disorders

Deviations in the structure or functioning of the brain nuclei immediately lead to the following symptoms:

• movements become slow and awkward;
• their coordination is disrupted;
• the appearance of voluntary muscle contractions and relaxations;
• tremor;
• involuntary pronunciation of words;
• repetition of monotonous simple movements.

In fact, these symptoms make it clear about the purpose of the nuclei, which is clearly not enough to learn about their true functions. Memory problems are also observed periodically. If you have these symptoms, you should consult a doctor. He will also prescribe procedures for more accurate diagnosis in the form of:

• ultrasound examination of the brain;
• computed tomography;
• taking tests;
• passing special tests.

All these measures will help determine the extent of the lesion, if any, and also prescribe a course of treatment with special drugs. In some situations, treatment can be lifelong.

Such violations include:

• deficiency of ganglia (functional). It appears in children due to genetic incompatibility of their parents (the so-called mixing of blood of different races and peoples) and is often inherited. In the last decade, there have been more and more people with such disabilities. It also occurs in adults and progresses to Parkinson’s or Huntington’s disease, as well as subcortical paralysis;
• a basal ganglia cyst is the result of improper metabolism, nutrition, atrophy of brain tissue and inflammatory processes in it. The most severe symptom is cerebral hemorrhage, followed shortly by death. The tumor is clearly visible on MRI, has no tendency to increase, and does not cause inconvenience to the patient.