What substances play a major role in the extrapyramidal. Extrapyramidal system
Exam questions:
1.17. Cerebellum: anatomy, physiology, symptoms of damage.
1.21. Striopallidar system: anatomy, physiology, symptoms of the lesion.
2.19. Parkinson's disease: etiology, pathogenesis, clinic, treatment, disability examination.
Practical skills:
1. Collection of anamnesis in patients with diseases nervous system.
2. Examination of muscle tone and assessment of motor disorders in a patient
6. Study of stato-locomotor functions
Anatomical and physiological features of the cerebellum
Cerebellum located on the dorsal surface of the brain stem, connected to it by 3 pairs of legs, acts together with the cortex hemispheres, extrapyramidal system when interacting with afferent and efferent pathways and provides body balance, stabilization of the center of gravity, consistency of muscle activity, accuracy of purposeful movements.
1. The principal structure of the cerebellum and its connections:
Each hemisphere of the cerebellum receives information from the homolateral half of the body,
The cerebral cortex is contralaterally connected to the cerebellar cortex and spinal cord,
The main flow of afferent information passes through the lower and middle legs (the exception is the Govers path), efferent information passes through the upper legs (the exception is the cerebellar-bulbar path),
All afferent information first enters the cells of the cerebellar cortex (3 layers - molecular, Purkinje cells, granular), and then to the own nuclei of the cerebellum.
2. Components:
- Archicerebellum(vestibulocerebellum, flocconodular lobe) - vestibular pathway :
1) vestibular nucleus of ankylosing spondylitis(body of neuron II) - lower legs of the cerebellum -
2) bark archcerebellum(body of III neuron) -
3) nucleus fastigii(body of IV neuron) of its side -
4) lower cerebellar peduncles - cerebellar-bulbar tract to the nuclei of its side + Russell's arcuate bundle to the nuclei of the other side (surrounds the contralateral upper peduncle) -
5) vestibular nuclei of Deiters(body of V neuron) - vestibulospinal tract.
- paleocerebellum(spinocerebellum, anterior lobe) - pathways of cerebellar proprioception:
1) proprioceptor - spinal cord (body)Ineuron)- posterior roots of the spinal cord -
- Flexig's path(posterior) - base of the posterior horns of the spinal cord [ clark core] (body II of the neuron, tractus spinocerebellaris dorsalis) - lateral cords of the spinal cord homolaterally - lower cerebellar peduncles ->
- gowers way(anterior) - the region of the intermedial cells of the posterior horns of the spinal cord (the body of the II neuron, tractus spinocerebellaris ventralis) - first cross- lateral cords of the spinal cord contralaterally - second cross in the cerebral sail - the upper legs of the cerebellum -\u003e
2) paleocerebellum bark(body of III neuron) -
3) nucl. globosusetemboliformis(spherical and cork-shaped nuclei, the body of the IV neuron) - the upper legs of the cerebellum - the Wernecking cross -
4) contralateral red nucleus(body of V neuron) - Trout cross - rubrospinal path his side.
- neocerebellum(pontocerebellum, posterior lobe) - paths from the cerebral cortex:
1) cerebral cortex -
- fronto-bridge-cerebellar pathway- anterior sections of the superior and middle frontal gyrus (body of neuron I) - centrum semiovale - anterior leg of the internal capsule - internal departments bases of the legs of the brain ->
- occipital-temporal-bridge-cerebellar pathway- posterior-lower sections of the parietal and temporal lobes (body of neuron I) - posterior sections of the posterior leg of the internal capsule - outer section of the base of the legs of the brain ->
2) bridge core of its side (body of the II neuron) - decussation - middle cerebellar peduncles -
3) neocerebellum bark(body of III neuron) -
4) nucl.dentatus(body of IV neuron, dentate nucleus) -
5a) dentorubrospinal path - superior cerebellar peduncles - Wernecking's decussation for fibers of the frontal bundle (!) - contralateral red nucleus(body of the V neuron) - Trout decussation for the fibers of the frontal bundle (!) - rubrospinal path his side.
5 B) dentothalamic pathway - superior cerebellar peduncles - decussation in the anterior medullary velum - posterior ventral oral nucleus of the thalamus(body of V neuron)
3. Cerebellar peduncles:
- Upper:
afferent - 1) anterior spinal tract (Govers),
efferent - 2) dentorubral path, 3) dentothalamic path, 4) to the RF.
- Average:
afferent - 1) pontocerebellar tracts.
- Lower:
afferent - 1) vestibulocerebellar, 2) olivocerebellar (from the contralateral inferior olive), 3) posterior spinocerebellar path (Flexiga), 4) from the Russian Federation,
efferent - 5) cerebellar-bulbar path (from the core of the tent to the vestibular nuclei).
4. Research methods
- Static coordination(pathology - static ataxia) :
1) Romberg test(the patient stands with legs shifted and arms extended forward) with complication options: eye closure(increased instability in sensitive ataxia), tilting and tilting of the head(Sarbo test - increased instability in vestibular ataxia), "rope walker pose"(feet on the same line - detection of mild disorders).
2) grahe reception- the subject is seated with closed eyes, legs closed on the edge of a chair with his head thrown back and offered to stand up
- Dynamic coordination- tests are carried out with open and closed eyes (pathology - dynamic ataxia) :
1) Finger-nose test(tip hit index finger patient to the tip of the patient's nose) - in pathology: hypermetry, intentional tremor (trembling when performing an action);
2) Index test(getting the tip of the index finger into the hammer) - in pathology Key words: hypermetry, intentional tremor ;
3) Schilder's test(the patient stretches his arms horizontally forward and closes his eyes, the examiner raises the patient's hand up and asks him to return it back to the horizontal level) - in pathology: hypermetry;
4) Heel test(lying on his back, the patient raises his leg up, then puts the heel of this leg on the opposite knee and slides it down the lower leg) - in pathology: hypermetry, intentional tremor;
5) Pronator test- test for diadochokinesis (rapid alternation of pronation and supination of the hands) - in pathology: adiadochokinesis (asymmetric performance of an action)
6) Stuart-Holmes symptom- "reverse push" (the patient's arm is bent at the elbow so that the fist is located at chest level at a distance of about 7-10 cm from it, the patient is asked to actively resist the doctor pulling his hand towards himself, while the doctor suddenly releases his hand - the fist is normal must not hit the patient in the chest)
- Tests for asynergy:
1) cerebellar s-m Babinsky(cannot sit up from a supine position without the help of hands);
- Handwriting assessment(pathology - megalography - a sharp increase in handwriting),
- Speech assessment(pathology - chanted speech [jerky pronunciation of sounds]).
Cerebellar syndromes
1. Flocconodular syndrome:
- astasia-abasia: static ataxia prevails over atactic gait(with legs wide apart)
- central nystagmus,
2. Paleocerebellum Syndrome:
- astasia-abasia: atactic gait(with legs wide apart) prevails over static ataxia(moderate)
3. Neocerebellum lesion syndrome:
- dynamic ataxia(hypermetry, intentional tremor, adiadochokinesis),
- asynergy, megalography, scrambled speech.
- atactic gait with a deviation to the side of the defeat,
diffuse muscular hypotension
Anatomical and physiological features of the regulation of movement and muscle tone
1. Levels of organization of the traffic regulation system according to N.A. Bernshtein (1947):
- Stem-spinal- axial muscle tone, maintaining balance and general tone.
- Talamo-pallidar- stereotypes, movements of large muscle groups that require temporary organization and continuous proprioceptive correction.
- Pyramidal striatal- performing movements in space that require orientation in the "spatial field", that is, the environment.
- Parieto-premotor- purposeful, semantic movements and manipulations with objects that require knowledge about the properties of the object.
- superior cortical- writing and speaking.
2. Stem-spinal systems of regulation of muscle tone
- Medial (ventromedial) system
1) Structural components:
- Reticulospinal (pontine, medial)- from the nuclei of the RF bridge (increased tone of the axial muscles and extensors)
- Vestibulospinal (lateral)- from the lateral vestibular nucleus (decreased tone of the flexors and increased extensors)
- Lateral reticulospinal (medullary) - from the giant cell nucleus of the medulla oblongata (decreased extensor tone)
- Medial vestibulospinal- from the medial vestibular nucleus (regulation of head position, labyrinth reflexes)
- Interstisiospinal- from the interstitial nucleus of Cajal - continuation of the medial longitudinal bundle (body torsion)
- Serotonergic- from the pontomedullary nucleus of the suture - and noradrenergic- from the blue nucleus (suppression of flexor activity)
2) Path data function consists in maintaining the tone of the axial muscles and proximal muscles (mainly anti-gravity muscles - extensor muscles) and act both ipsi and contralateral.
3) When they are defeated gross functions suffer - trunk-limb synergies (standing up, walking, etc.). With bilateral damage at the level of the upper trunk, the medial system predominates due to its lower location in the trunk with the formation decerebrate rigidity.
- Lateral (dorsolateral) system
1) Structural components:
- Rubrospinal- from the red core - Trout cross (increased flexor tone)
- Corticospinal (pyramidal)- 30-40% are fibers from the premotor cortex (decrease in extensor tone, increase in flexor tone) - implementation of the action of the striopallidar system.
- Tectospinal- from the superior tubercles of the quadrigemina - Meinert's fountain-like cross (coordination of the position of the neck, head, eyes in response to the startle reaction)
2) Path data function consists in maintaining the tone of the distal muscles (mainly flexors - fine motor skills of the limbs) and act only contralateral.
3) When they are defeated impaired fine motor skills of the limbs.
Anatomical and physiological features of the basal ganglia
Basal ganglia are heterogeneous accumulations of gray matter in terms of their function and are located in the thickness white matter hemispheres near the lateral ventricles of the brain:
- striatum- caudate nucleus (nucl.caudatus) and shell (putamen),
- Pallidum- internal and external pale ball (globus pallidum), [functionally associated with the formations of the trunk: 1) black substance, 2) red nuclei, 3) subthalamic nucleus (Lewis body)],
- Fence(claustrum),
- Almond nucleus(amygdala) - participates in the regulation of polo-social behavior.
Striopallidar (extrapyramidal) system
Striopallidary system provides consistent, consistent in strength and duration, the inclusion of individual neurons and fibers of the pyramidal pathway for the implementation of diffuse, massive movements of the body, the work of all muscles in the process of movement (Fig. dotted arrows - GABA, solid - glutamate).
1. The principle of operation of the striopallidary system:
- Action acceptor(application point) of the striopallidary system is frontal cortex.
- Direct pathway for frontal cortex regulation: 1) striatum(shell) inhibits 2) complex (Pi/SNr), low activity of which leads to activation 3) thalamus(anterior ventral and anterior ventral oral nucleus), which leads to to activate and prepare the movement .
- Indirect pathway of frontal cortex regulation: 1) striatum slows down 2) outer ball(Re), the low activity of which in turn increases the activity of the 3) complex internal ball and reticular part of the substantia nigra(Pi/SNr), which leads to the deceleration of the nuclei 4) thalamus and inhibition of excessive movements .
- Black substance (compact part) regulates the level of activity of the shell, releasing dopamine (gray arrows) and acting on dopamine receptors (D1 - activates, D2 - inhibits), damage to it leads to activation of direct way, hyperactivity - direct.
- Subthalamic nucleus of Lewis (STh) - enhances the action of the indirect path
2. Evaluation of the function of the striopallidar system
- Muscle Tone Assessment:
1) techniques for detecting hypertonicity(“plastic”, “gear wheel”), Noyka-Ganeva’s technique - when lifting the leg, the tone in the arm increases.
2) posture fixation tests (postural reflexes): 1) extension in the wrist joint, 2) dorsal extension of the foot (Westphal test), 3) "air cushion" test (in a lying patient, the head is raised by the occipital region, and then the palm is sharply transferred to the neck - normally - falling on the pillow)
3) methods for detecting hypotension: Orshansky's test
- Assessment of physiological synkinesis:
1) pendulum swing test of the upper and lower limbs- checking the physiological synkinesis of the hands when walking and swinging the legs while sitting on a chair.
- Techniques for detecting hidden hyperkinesis:
1) writing with eyes closed(sample of Kherson),
2) test "sheet of paper"(a sheet of paper placed on the brush increases the tremor).
3) picking up small items(Jager-King test)
- Handwriting assessment(micrography in hypokinesia/megalography in hyperkinesia).
- Evaluation of the walking function.
Syndromes of lesions of the extrapyramidal system
The defeat of the extrapyramidal system is characterized by a change in muscle tone, motor and autonomic functions, and emotional disorders.
1. Classification by etiology:
- primary(idiopathic) - Huntington's chorea, Parkinson's disease,
- secondary(symptomatic) - rheumatic chorea, vascular parkinsonism
- multisystem degenerative diseases of the CNS(hepatolenticular degeneration)
2. Classification by the nature of movements: hypokinetic (parkinsonism) and hyperkinetic (athetosis, chorea, ballism, tics, myoclonus, tremor):
- Akinetic-rigid syndrome - is formed with the development of a functional deficiency of the influence of pallidum or substantia nigra on the reticular formation (pallidar syndrome, hypertensive-hypokinetic syndrome, amyostatic syndrome, parkinsonian syndrome):
1) Akinesia (hypokinesia) includes :
- bradykinesia- slowness of movement bradilalia- monotonous speech bradypsychia, hypomia;
- oligokinesia- difficulty initiating movement, poverty and inexpressiveness of movements, micrography, catalepsy, parkinsonian gait(with difficulty, small and frequent steps), acheirokinesis(when walking, the hands of people with akinetic-rigid syndrome are motionless);
2) Rigidity- hypertonicity ("gear wheel", "wax doll"), postural reflexes
3) Tremorrest- in the distal parts of the limbs, asymmetrical, frequency 3-6 Hz, observed at rest and disappears when performing voluntary movements (the phenomenon of "counting coins", "rolling pills");
+ postural instability(propulsion, retropulsion, lateropulsion).
- Hypotonic-hyperkinetic syndrome- formed when there is a functional deficiency of the inhibitory effect of the striatum on the underlying motor centers (striatal syndrome). Hyperkinesis- excessive motor acts involving separate parts body and limbs, disappearing in a dream and intensifying when performing voluntary movements.
1) Characteroccurrence:
- spontaneous(chorea, ballism, some myoclonus),
- promotional(kinetic tremor, torsion dystonia, writing spasm),
- reflex(reflex myoclonus),
- semi-arbitrary(restless legs syndrome).
2) Motor pattern:
- rhythmic(tremor),
- tonic(torsion dystonia, athetosis),
- clonic(myoclonus, chorea, tics).
3) Duration: persistent and paroxysmal
4) Distribution: focal, segmental, multifocal and generalized
3. Classification according to the substrate of the lesion:
- Striatum Syndrome (Striatum) - a decrease in the activity of the striatum leads to inhibition of the indirect pathway and disinhibition of the direct pathway - hyperkinesis (chorea or less often athetosis) and muscle atony.
- Subthalamic nucleus syndrome (Matzdorf-Lhermitte)- a decrease in the activity of the subthalamic nucleus leads to disinhibition of the direct path - contralateral hemiballismus (sweeping throwing movements, mainly in the proximal limbs) with mild hypotension
- substantia nigra syndrome- a decrease in the activity of the substantia nigra leads to the activation of the indirect pathway and inhibition of the direct one - parkinsonism (akinesia + rigidity + rest tremor)
- Pale ball syndrome - extrapyramidal rigidity, brady-oligokinesia, gait disturbance (acheirokinesis, pro-retro-lateropulses), general stiffness, fine rest tremor, motor stiffness, gear wheel, petitioner's posture (medial part of the pale ball).
Parkinson's disease and secondary parkinsonism
parkinsonism- a neurological syndrome characterized by oligobradykinesia, muscle rigidity, rest tremor and impaired postural reflexes.
1. Parkinson's disease (G20) - an idiopathic, slowly progressive degenerative disease of the central nervous system, caused by degeneration of pigmented dopaminergic neurons in the dense part of the substantia nigra and other dopamine-containing nuclei of the brainstem and manifested by motor, autonomic, mental disorders. The prevalence in the general population is 13 per 100,000, over 60 years old - 1%. The peak incidence is 55-65 years, men suffer 1.5 times more often. There are also juvenile PD with a debut before the age of 20 and PD with an early onset - from 21 to 40 years.
- Etiology and pathogenesis: not known (genetic factors, external environment) -> acceleration of neuronal degeneration in the substantia nigra (oxidative stress and apoptosis of neurons) -> accumulation of Lewy bodies -> impaired dopamine metabolism -> predominance of the indirect pathway over the direct
- Clinic and diagnostics:
1) Criteria for the diagnosis of PD:
Presence of 2 out of 3 symptoms,
Asymmetry or unilateral onset,
Good response to levodopa drugs.
2) Against the diagnosis:
Acute onset and gradual progression
Indications for transplanted stem encephalitis,
Paresis of vertical gaze
The presence of pyramidal and cerebellar signs, amyotrophy,
Early appearance of vegetative and cognitive disorders.
- Differential diagnosis:
1) Secondary parkinsonism: vascular, medicinal (neuroleptic), posttraumatic, postencephalitic (neuroborreliosis, neurosyphilis, etc.), toxic (manganese, carbon monoxide, drugs)
2) Parkinsonism-plus: progressive supranuclear palsy, multiple system atrophy, diffuse Lewy body disease, corticobasal degeneration, Wilson-Konovalov disease, Machado-Jozef disease, etc.
3) Essential tremor- kinetic and postural tremor with a frequency above 8 Hz, bilateral, with predominant involvement of the hands and head, no hypertonicity and hypokinesia.
- Treatment:
1) Goals:
In the early stages - restoration of impaired motor functions with minimal doses of the drug ("not excellent, but decent")
In the later stages - symptomatic treatment and prevention of complications of therapy.
2) Indications for hospitalization:
Difficult diagnostic cases
Selection of therapy
3) Non-drug treatment:
Protein-restricted diet (protein reduces absorption of levodopa)
Adequate motor activity
4) Drug treatment:
L-DOPA preparations (levodopa); L-DOPA + DOPA-decarboxylase inhibitor (sinemet, nakom, duellin, madopar);
Dopamine receptor agonists (bromkriptin-parlodel, pronoran, mirapex);
MAO-B inhibitors (selegiline-umex);
COMT inhibitors (tolcapone);
Cholinolytics (trihexyphenidyl-cyclodol);
Glutamate receptor agonists (amantadine-PK-Merz).
- Workability examination: terms of VN - 20-30 days, with persistent disability - at the ITU.
Clinical forms of hyperkinesis
1. Athetosis- slow worm-like, artsy movements in the distal limbs and on the face with the formation of transient contractures.
2. Chorea- fast, non-rhythmic, uncoordinated contractions in large groups muscles: gettington - etiology: AD, trinucleotide expansion on chromosome 4, onset age 50-60 years, morphology: death of neurons in the caudate nucleus (death of D2 neurons - the indirect pathway is hyperactive - hyperkinesis, then the death of D1 neurons - activation of the direct pathway - akinesia), clinic- beginning with the face or distal extremities - generalization (dancing, tense gait) - the appearance of signs of parkinsonism), treatment: clonazepam, baclofen, neuroleptics.
3. Tremor- stereotypical rhythmic clonic hyperkinesis: large-scale (rubral) tremor, intentional tremor (occurring when performing purposeful movements), static tremor (rest tremor, decreasing when performing voluntary movements).
4. Myoclonus- short, lightning-fast clonic twitches of muscles and groups of muscle fibers (more often in the proximal parts of the limbs, without causing movement of the limb).
5. Tiki- fast clonic twitches of a limited muscle group of a stereotypical nature, imitating voluntary movements.
6. Ballism (hemiballism)- large-scale, violent, "throwing" movements of the limbs, produced with great force .
7. Torsion dystonia- convulsive corkscrew hyperextension of the spine in the lumbar and cervical region with the formation of fanciful postures, manifested during voluntary movements, scoliosis, hyperlordosis. In the initial stage, the manifestation of torsion dystonia can be spastic torticollis- convulsive contractions of the neck muscles with turning the head to the side, to the shoulder, tilting the head back and shrugging the shoulders
Conscious muscle contraction is provided by the pyramidal system. However, when performing one or another voluntary movement, a person does not think about which muscles need to be reduced at the moment. Ordinary movements, carried out due to the coordinated action of many muscles, are performed automatically, imperceptibly to attention, and the change in some muscle contractions by others is involuntary. The most advanced are automated movements. They are energetically stingy, optimal in terms of volume, time, energy costs. The sequence, the duration of muscle contractions, the perfection of movements are provided by the extrapyramidal system, which, in comparison with the pyramidal system, is a phylogenetically older motor-tonic apparatus. The extrapyramidal system creates the prerequisites for the performance of motor reactions, the background against which fast, precise, differentiated movements are carried out, prepares the muscles for action, and provides an appropriate distribution of tone between different muscle groups. The extrapyramidal system is directly involved in the formation of a certain posture of a person, motor manifestations of emotions, creates an individual expression of human movements. It ensures the performance of automated, memorized motor stereotyped acts, as well as unconditioned reflex protective movements.
1 - bark big brain; 2 - caudate nucleus; 3 - shell; 4 - pale ball; 5 - thalamus; 6 - lateral vestibular nucleus; 7 - reticular formation; 8 - roof of the midbrain; 9 - the core of Darkshevich (medial longitudinal bundle); 10 - black substance; 11 - red core; 12 - subthalamic nucleus (Luysi); 13 - descending stem-spinal tract.
The extrapyramidal system includes numerous cellular structures located in the head and spinal cord, as well as their afferent and efferent pathways.
There are four levels in the extrapyramidal system:
- cortical formations - premotor zones of the cerebral hemispheres;
- subcortical (basal) nuclei: caudate nucleus and lenticular nucleus, consisting of a shell, medial and lateral pale ball;
- main stem structures: substantia nigra, red nuclei, reticular formation, subthalamic nucleus, nucleus of the medial longitudinal fasciculus (Darkshevich), vestibular nuclei, midbrain roof;
- the spinal level is represented by descending pathways ending near the cells of the anterior horns of the spinal cord. Further, extrapyramidal influences are sent to the muscles through the system of alpha and gamma motor neurons.
In evolutionary terms, according to morphological and functional features, the extrapyramidal system is divided into two parts - neostriatal and paleostriatal (or pallidonigral). The neostriatal system (neostriatum) includes cortical structures, the caudate nucleus and the shell. The palleostriatal system consists of the lateral and medial globus pallidus, substantia nigra, the subthalamic nucleus, the nucleus of the medial longitudinal fasciculus, the vestibular nuclei, the roof of the midbrain, and some other structures. The neostriatal and paleostriatal systems, functioning in concert and balancing each other, are conditionally combined into a striopallidary system. The neostriatal system is younger than the paleostriatic one, both phylogenetically and ontogenetically. It is considered the highest subcortical regulatory and coordination center for the organization of movements, a powerful inhibitory regulator of the motor system. It inhibits the paleostriatal system, which activates the motor function.
The basal nuclei are the main structures of the extrapyramidal system. They have a large number of connections with other parts of the nervous system, which ensure the inclusion of extrapyramidal apparatus in the system of voluntary movements. Afferent fibers carry information from the thalamus, cerebellum, and mesh formation. The neostriatal system receives afferent connections from many parts of the cerebral cortex, especially from the motor areas of the frontal lobe. Descending impulses from the extrapyramidal system through the structures of the middle and medulla oblongata (red nuclei, vestibular nuclei, mesh formation, quadrigemina plate, motor nuclei of cranial nerves) enter the segmental apparatus, coordinating the tone and motor activity of the muscles.
The functions of the extrapyramidal system are carried out due to the presence of neurotransmitters in its structures. The substantia nigra contains neurons that produce dopamine, which is formed into granules here. Dopamine enters the caudate nucleus via the dopaminergic nigrostriatal pathway, where it is released in the synaptic apparatus. Dopamine inhibits the function of the caudate nucleus by blocking the production of the excitatory mediator acetylcholine by striatal cholinergic neurons. Thus, dopamine reduces the inhibitory effect of the caudate nucleus on motility. Dopamine also enters the limbic structures, the hypothalamus, and the frontal lobe of the brain, providing control over mood, behavior, and the onset of motor acts. A decrease in its content in these structures leads to an increase in the inhibitory effects of the caudate nucleus on motor activity with the onset of hypo- or akinesia, emotional disorders. In addition, the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is produced in the caudate nucleus, which is transferred to the substantia nigra via the gamkergic strionigral pathway and controls the synthesis of dopamine. In the structures of the extrapyramidal system, there are other neurotransmitters - norepinephrine, serotonin, glutamic acid, neuropeptides. The function of all mediator systems is normally balanced, there is a balance between them. When it is violated, various pathological clinical syndromes occur.
Damage to the substantia nigra and degeneration of the nigrostriatal pathway leads to a decrease in the synthesis and amount of dopamine, which is clinically manifested by the picture of hypertensive-hypokinetic syndrome, or parkinsonism. The syndrome is named after English doctor James Parkinson (J. Parkinson, 1755-1824), who in 1817 described a hereditary disease with muscle rigidity, akinesia and tremor, later called Parkinson's disease. Similar symptoms also occur after a traumatic brain injury, carbon monoxide poisoning, manganese, after lethargic encephalitis and for other reasons. In such cases, it is called parkinsonism, indicating the etiology (toxic, post-encephalitic, post-traumatic, etc.). With the development of parkinsonism, the effect of dopamine on the caudate nucleus decreases, which, as a result of an increase in cholinergic activity, is disinhibited and enhances its inhibitory effect on motor activity. Hypokinesia, muscle rigidity, and static trembling (tremor) occur. Hypokinesia or akinesia (poverty of movements) is manifested by a combination of symptoms - hypomimia, rare blinking, monotony of speech (bradilalia), micrography, the disappearance of friendly movements, especially in the hands while walking (acheirokinesis), a decrease in general motor activity, initiative of movement, a violation of the process of inclusion in traffic. In such cases, patients seem to freeze during movements, cannot immediately start walking, and mark time. When walking, they cannot stop immediately. The gait is slow, with small steps, shuffling, with a tendency to accelerate. While walking forward, the patient cannot suddenly stop, the trunk seems to be ahead of the lower limbs, balance is disturbed and the patient may fall. This phenomenon is called propulsion. Also, the patient cannot suddenly stop while walking backward (retropulsion) or to the side (lateropulsion).
Muscle rigidity that occurs with parkinsonism is characterized by an increase in muscle tone evenly in all muscle groups, in the form of waxy or plastic rigidity. When carrying out passive movements in the limbs, a kind of discontinuity, stepwise stretching of the muscles, called the symptom of "gear wheel", is sometimes observed. General stiffness, increased muscle tone determine the characteristic posture of the patient: the head is tilted forward, the torso is bent, the arms are bent at the elbow joints (the petitioner's position).
Trembling has a small rhythmic character, with a frequency of 4-5 oscillations per 1 s, occurs at rest, increases with excitement, decreases or disappears during sleep and voluntary movements. First, trembling appears in the hand of one hand (such as "counting coins" or "rolling pills", "flexion-extension" of the fingers). With the progression of the disease, it spreads by hemitype, covers the head (like "yes-yes") or becomes generalized. Often there are autonomic disorders in the form of increased salivation, greasiness of the skin, excessive sweating, delayed bowel movements. Most patients with parkinsonism have a mental disorder of the type of lack of initiative, lethargy, a characteristic peculiar viscosity, importunity, a tendency to repeat the same questions, depression, and dementia (dementia) may occur in the later stages of the disease.
Sometimes patients with parkinsonism have paradoxical kinesias, when they temporarily, due to a short decrease in muscle tone, can quickly perform voluntary movements (dance, skate, etc.). Such a phenomenon, which has not yet found a final explanation, can be observed after waking up, during stressful situations. Patients with parkinsonism are characterized by the appearance of the so-called fixation rigidity, which leads to an increase in tonic postural reflexes (position reflexes). Their essence lies in the fact that the return to the initial position of the body part after the movement is violated. So, as a result of an increase in plastic tone in the muscles of the neck and proximal parts of the upper limbs, the head of the patient, who is lying on his back, raised by the doctor, seems to freeze in this position, and then slowly lowers (symptom of "air cushion"). The patient's leg, passively bent at the knee joint, lying on his stomach, remains in this position even after the cessation of irritation, and slowly lowers. After a sharp passive dorsiflexion of the foot, it retains this position for some time.
To detect latent extrapyramidal muscular hypertension, the Neuk-Ganev test is used. When checking muscle tone in the upper limb by passive movements in the elbow joint, the patient is asked to raise his leg. Simultaneous raising of the lower limb leads to an increase in tone in the muscles of the arm.
Correction of mediator shifts in parkinsonism is carried out using anticholinergic drugs (cyclodol, parkopan, amizil) and agents that stimulate dopaminergic transmission (L-Dopa, sinemet, nakom, madopar, parlodel, umex, midantan, simetrel, etc.).
The symptom complex of damage to the neostriatal system and its connections leads to excessive "facilitation" of movements, resulting in a hyperkinetic-hypotonic syndrome. The main manifestations of this syndrome are extrapyramidal hyperkinesis - a variety of involuntary, violent movements, diffuse or in a certain area of the body, which are combined with hypotension or muscle atony.
Varieties of extrapyramidal hyperkinesis are chorea, athetosis, torsion dystonia, hemiballism, myoclonus, tick. Chorea is characterized by polymorphic, rapid, non-rhythmic, erratic violent movements in various muscle groups, which are aggravated by excitement and disappear during sleep. Twitching of the muscles of the face leads to the appearance of grimaces, limbs to gesticulation. There is a violation of gait (the patient seems to be dancing), speech, writing. The patient cannot hold his protruding tongue due to hyperkinesis of the tongue, sometimes bites it, especially when the eyes are tightly closed at the same time. With significant muscle hypotension (chorea mollis), reflexes are not caused, pseudoparesis occurs. If muscle tone in the limbs is slightly reduced, tendon reflexes are preserved. Can be observed Gordon's symptom-2. When a knee jerk is induced, due to the tonic tension of the quadriceps femoris, the unbent lower leg seems to freeze for a moment in an unbent position, and can also perform several pendulum-like, gradually fading movements (a symptom of the pendulum). Choreic hyperkinesias are observed in Huntington's chorea, chorea minor (Sydenham's chorea), chorea of pregnant women.
Athetosis occurs as a result of tonic spasm in the muscles and is characterized by violent slow, worm-like movements in the distal limbs with a tendency to overextension, as well as in the muscles of the face and tongue. Typical athetosis of the fingers, when each finger performs slow artsy movements independently, independently of the others. Athetosis in the muscles of the face leads to the appearance of various grimaces, in the tongue - to unintelligible speech. Athetosis occurs as a result of a neuroinfection transferred in the prenatal period, with fetal asphyxia or a discrepancy between the Rh factor of the mother and fetus.
Torsion dystopia is a tonic spasm of various muscle groups, mainly of the trunk, which manifests itself while walking. Hyperkinesis artsy, often rotational around the longitudinal axis of the body (corkscrew). In such patients, due to uneven muscle tension, a curvature of the spine occurs. The onset of torsion dystonia can manifest itself as torticollis, since the cervical muscles are the first to be affected.
Hemiballismus is, as a rule, non-rhythmic, unilateral, rough, large-scale movements of the limbs, more often the upper one. Reminds me of the flapping of a bird's wing. Occurs more often with vascular pathology in the subthalamic nucleus (Lewis body).
Myoclonus - short lightning-fast clonic twitches of individual muscles or their groups, so fast that there may not be movement of the limbs in space. Sometimes patients with myoclonus have generalized convulsive seizures, accompanied by dementia (myoclonus epilepsy). Myoclonus occurs in the pathology of the cerebellar-red nuclear connections of the lower olive, neostriatum. If myoclonus is constant, stereotypical, has a clear localization, it is called myorhythmia. It often occurs in the muscles of the face, tongue, pharynx, soft palate, and diaphragm.
Tic - a rapid contraction of individual muscle groups, creating various, as a rule, stereotyped movements. The muscles of the neck and face suffer. The patient twitches his neck, as if adjusting his collar; throws back his head, as if straightening his hair, raises his shoulder, performs blinking movements, wrinkles his forehead, raises and lowers his eyebrows. In contrast to the neurotic, functional non-permanent tic, the extrapyramidal tic is characterized by constancy and stereotype.
Most hyperkinesias caused by damage to the extrapyramidal system disappear during sleep, and increase with excitement and voluntary movements.
According to the clinic, hyperkinetic-hypotonic syndrome seems to be the opposite of Parkinson's syndrome. This antagonism is the result of the emergence of opposite mediator shifts. So, in a hereditary disease - Huntington's chorea - in the neostriatal system, a decrease in the amount of acetylcholine and GABA K, as well as the enzymes responsible for their synthesis, was revealed. The amount of dopamine is increased. Therefore, for the treatment of patients with Huntington's chorea, drugs that suppress dopaminergic transmission are used - reserpine, chlorpromazine, haloperidol, lithium preparations.
When examining the functions of the extrapyramidal system, the movements and posture of the patient, facial expressions, expressiveness of speech are evaluated, muscle tone is checked, hyperkinesias, psycho-emotional disorders and autonomic disorders are detected.
The conscious contraction of a particular muscle is provided by the pyramidal system. But, performing this or that voluntary movement, a person does not think about which muscles need to be reduced at the right time. Habitual movements that require the coordinated action of many muscles are performed automatically, imperceptibly to attention, and the change of one muscle contraction by another is involuntary. The most advanced are automated movements. They are energetically stingy, optimal in terms of volume, time, energy costs. The sequence, the duration of muscle contractions, the perfection of movements is provided by the extrapyramidal system, which, in comparison with the pyramidal, is the oldest motor-tonic apparatus in phylogenetic terms. The extrapyramidal system creates the prerequisites for the performance of motor reactions, the background on which fast, precise, differentiated movements are made, prepares the muscles for action, provides an appropriate distribution of tone between different muscle groups, which is necessary to perform movements of any complexity. The extrapyramidal system is directly involved in creating a certain posture of a person, motor manifestations of emotions, creates an individual expression of human movements. It ensures the performance of automated, memorized motor stereotyped acts, as well as unconditional reflex protective movements (Fig. 3).
Rice. 3. Scheme of the extrapyramidal system: 1 - cerebral cortex, 2 - caudate nucleus, 3 - shell; 4 - pale ball; 5 - thalamus, 6 - lateral nucleus; 7 - reticular formation; 8 - tire of the midbrain; 9 - the core of Darkshevich (medial longitudinal bundle); 10 - black substance; 11 - red core; 12 - subthalamic nucleus; 13 - descending stem-spinal tract
The extrapyramidal system includes numerous cellular structures located in the brain and spinal cord, as well as their afferent and efferent pathways.
In the extrapyramidal system, four levels can be distinguished (Fig. 3):
cortical formations - premotor zones of the cerebral hemispheres;
subcortical (basal) nuclei: caudate and lenticular nuclei, consisting of a shell, lateral and medial pale ball;
main stem formations: substantia nigra, red nuclei, reticular formation, subthalamic nucleus, nuclei of the medial longitudinal bundle (Darkshevich), vestibular nuclei, midbrain tegmentum;
the spinal level is represented by closely connected descending pathways that end at the cells of the anterior horns of the spinal cord. Further, extrapyramidal influences go to the muscles through the system of alpha and gamma motor neurons.
In evolutionary terms, according to morphological and functional features, the extrapyramidal system is divided into two parts: neostriatal and paleostriatal (or palydonigral). The neostriatal system (neostriatum) includes: cortical structures, caudate nucleus and putamen. The paleostriatal system includes: lateral and medial globus pallidus, substantia nigra, subthalamic nucleus, nucleus of the medial longitudinal bundle, vestibular nuclei, tegmentum medulla and some other structures. The neostriatal and paleostriatal systems, which function in concert, balance each other, are conditionally united by the concept of the striopallidary system. The neostriatal system is younger than the paleostriatic one, both in phylogenetic and ontogenetic respects, it is considered the highest subcortical regulatory and coordinating center for the organization of movements, a powerful inhibitory regulator of the motor system. It inhibits the paleostriatal system, which activates the motor function.
The subcortical nuclei are the leading structures of the extrapyramidal system. They have a large number of connections with other parts of the nervous system, which ensure the inclusion of extrapyramidal apparatus in the system of voluntary movements. Afferent fibers carry information from the thalamus, cerebellum, and reticular formation. The neostriatal system receives afferent connections from many parts of the cerebral cortex, especially from the motor areas of the frontal lobe. Descending impulses from the extrapyramidal system through the structures of the middle and medulla oblongata (red, vestibular nuclei, reticular formation, motor nuclei of the cranial nerves) enter the segmental apparatus, coordinating the tone and motor activity of the muscles. The functions of the extrapyramidal system are carried out due to the presence and its structures of neurotransmitters. The substantia nigra contains neurons that produce dopamine, which is formed here into granules. The latter, via the dopaminergic nigrostriatal pathway, enters the caudate nucleus, where it is released in synoptic apparatuses. Dopamine inhibits the function of the caudate nucleus by blocking the production of the excitatory mediator acetylcholine by striatal cholinergic neurons. Thus, dopamine reduces the inhibitory effect of the caudate nucleus on motility. Dopamine also enters the limbic structures, the hypothalamus and the frontal lobe of the brain, providing control over mood, behavior, and the onset of motor acts. A decrease in its content in these structures leads to an increase in the inhibitory effects of the caudate nucleus on motor activity with the onset of hypo- or akinesia, emotional disorders.
In addition, the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is produced in the caudate nucleus, which is transferred to the substantia nigra via the gamkergic strionigral pathway and controls the synthesis of dopamine. In the structures of the extrapyramidal system, there are other neurotransmitters - norepinephrine, serotonin, glutamic acid, neuropeptides. The function of all mediator systems is normally balanced, there is a balance between them. In case of its violation, various pathological clinical syndromes arise. Damage to the substantia nigra and degeneration of the nigrostriatal pathway leads to a decrease in the synthesis and amount of dopamine, which is clinically manifested by a picture of hypertensive-hypokinetic syndrome, or parkinsonism.
This name of the syndrome comes from the name of the English physician James Parkinson, who in 1817 described a hereditary disease with muscle rigidity, akinesia and tremor, which later became known as Parkinson's disease. Similar symptoms also occur due to traumatic brain injury, carbon monoxide poisoning, manganese, after lethargic encephalitis and for other reasons. In this case, it is called parkinsonism, adding etiology (toxic, post-traumatic, etc.).
In the presence of parkinsonism, the effect of dopamine on the caudate nucleus decreases, which, due to an increase in cholinergic activity, is disinhibited and enhances its inhibitory effect on motor activity. Hypokinesia, muscle rigidity and static tremor occur. Hypokinesia or akinesia (poverty of movements) is manifested by a combination of symptoms - hypomimia, rare blinking, monotony of speech (bradilalia), micrography, the disappearance of friendly movements, especially in the upper limbs when walking (acheirokinesis), a decrease in general motor activity, initiative of movement, a violation of the process of inclusion in traffic. When moving, the patients seem to freeze, they cannot immediately start the procession, they mark time. The gait is slow, with small steps, shuffling, with a tendency to accelerate. While moving forward, the patient cannot suddenly stop. In this case, the torso is allegedly ahead of the lower limbs, balance is disturbed, and the patient may fall. This phenomenon is called propulsion. Also, the patient cannot suddenly stop while walking backward (retropulsion) or sideways (lateropulse).
Muscle stiffness, which occurs in the case of parkinsonism, is characterized by an increase in muscle tone evenly in all muscle groups, in the form of waxy or plastic rigidity. With passive movements in the limbs, there is sometimes a kind of discontinuity, a stepwise stretching of the muscles, which is called a symptom. "gear wheel". General stiffness, increased muscle tone determine the patient's characteristic posture: the head is tilted forward, the torso is hunched, the arms are bent at the elbow joints (the petitioner's position).
jitter has a fine-rhythmic character with a frequency of 4-5 oscillations per 1 s, occurs at rest, increases in case of excitement, decreases or disappears during sleep and voluntary movements. First, trembling occurs in the hand of one hand (such as "counting coins" or "rolling pills", "flexion-extension" of the fingers). As the disease progresses, it spreads by hemitype, covers the head (like "yes-yes") or becomes generalized. Autonomic disorders often occur in the form of increased salivation, greasiness of the skin, excessive sweating, and delayed bowel movements. Most patients have mental disorders such as lack of initiative, lethargy, a peculiar viscosity, importunity, a tendency to repeat the same questions, depression, and dementia (dementia) may occur in the later stages of the disease.
Sometimes patients with parkinsonism show paradoxical kinesias when they temporarily, due to a short decrease in muscle tone, can quickly perform voluntary movements (dance, skate, etc.). Such a phenomenon, which has not yet found a definitive explanation, can be observed after waking up, during stressful situations. Patients with parkinsonism are characterized by the appearance of the so-called fixation rigidity, which leads to an increase in tonic postural reflexes (position reflexes). Their essence lies in the fact that the return to the initial position of the body part after the movement is violated. So, due to an increase in plastic tone in the muscles of the neck and proximal parts of the upper limbs, the head of the patient, who is lying on his back, raised by the doctor, seems to freeze in this position, then slowly lowers (a symptom of an air cushion). Passively bent at the knee joint, the lower limb of the patient, lying on his stomach, remains in this position even after the cessation of irritation, and slowly lowers. After a sharp passive dorsiflexion of the foot, it maintains this position for some time.
To detect latent extrapyramidal muscular hypertension, the Neuk-Ganev test is used. When checking muscle tone in the upper limb by passive movements in the elbow joint, the patient is asked to raise his leg. Simultaneous raising of the lower limb causes an increase in tone in the muscles of the upper limb.
Correction of mediator shifts in the presence of parkinsonism is carried out using anticholinergic drugs (cyclodol, parkopan, amizil) and agents that stimulate dopaminergic transmission (levodopa, sinemet, nakom, madopar, parlodel, yumex, midantan, simetrel, etc.).
Extrapyramidal system - this is a system of cortical, subcortical and stem nuclei of the brain and pathways connecting them to each other, as well as to the motor nuclei of the cranial nerves of the brain stem and anterior columns of the spinal cord, which performs involuntary automatic regulation and coordination of complex motor acts, regulation of muscle tone, maintenance postures, organization of motor manifestations of emotions.
The composition of the extrapyramidal system:
The cerebral cortex;
Basal nuclei of the telencephalon: caudate and lenticular;
Subthalamic nucleus and nuclei of the thalamus of the diencephalon;
Red nucleus and substantia nigra, nuclei of the roof of the midbrain;
vestibular nuclei;
Kernels of the lower olive;
Cerebellum;
Kernels of the reticular formation;
Conducting paths.
Functions of the extrapyramidal system:
Providing complex automated movements (crawling, swimming, running, walking, spitting, chewing, and others);
Maintaining muscle tone and its redistribution during movement;
Participation in the articulation of speech and mimic expressive movements;
Maintaining the segmental apparatus in readiness for action.
25. Limbic system.
limbic system- a non-specific brain system associated with the olfactory analyzer, the main function of which is the organization of holistic behavior and the integration of physiological activity processes.
Functions of the limbic system:
Emotional-motivational behavior and adaptation to the conditions of the external and internal environment;
Complex forms of behavior: instincts, food, sexual, defensive, change of phases of sleep and wakefulness;
Regulatory influence on the cortex and subcortical formations to establish the necessary correspondence of activity levels.
Composition of the limbic system:
Cortical structures: limbic lobe (cingulate, parahippo-campal, dentate and ribbon gyrus) and hippocampus;
Subcortical formations: the basal part of the telencephalon, structures of the diencephalon (papillary bodies, nuclei of the leash), sections of the midbrain (interpeduncular nucleus, central gray matter) and pathways that provide a connection between these structures.
Features of the limbic system– formation between the nuclei of bilateral bonds and a multitude of closed circles of different diameters and lengths (large and small).
Large limbic circle:
Compound: hippocampus - vault - mastoid bodies of the hypothalamus - mastoid-thalamic bundle of Vic d'Azira - anterior nuclei of the thalamus - thalamic radiance - cingulate gyrus - parahippocampal gyrus - hippocampus.
Function: providing memory and learning processes.
Lesser limbic circle:
Compound: amygdala - hypothalamus - reticular formation of the midbrain - amygdala.
Function: regulation of aggressive-defensive, food and sexual forms of behavior.
26. Patterns in the structure of motor pathways .
Descending, Efferent, Motor, Conscious (Tr. Cortico ...), Reflex (from subcortical formations).
Among the tracts are Chief PyramidPath, which consists of 3 paths. The first one runs from neurons of the precentral gyrus to motor neurons concentrated in the nuclei of the brainstem - this is corticonuclearpath. Two other paths: corticospinal front and side go from the precentral gyrus to the nuclei of the anterior horns of the spinal cord. The fibers of each tract have decussations in different parts of the brain.
Cortico-nuclear path of conscious movement crosses over the nuclei of cranial nerves in the brain stem. It includes two neural reflex arcs.
Lateral and anterior corticospinal tracts also conduct conscious impulses. The lateral pathway crosses at the border of the medulla oblongata and spinal cord, forming pyramidal cross. The anterior pathway is crossed in the spinal cord.
Cortical-bridge-cerebellar the path crosses in the bridge at the level of the middle cerebellar peduncles. The first motor neurons are located in the cortex of the frontal, temporal, parietal and occipital lobes. They pass their axons through the internal capsule (knee). The second neurons lie in the motor nuclei of the bridge and the cortex of the cerebellar hemispheres. Axons from the cerebellum exit through the middle peduncle to the motor nuclei of the pons, where they switch.
Descending extrapyramidal tracts of unconscious movements belong to the ancient ways, and they always begin in the subcortical structures of the brain. Their reflex arcs have two neural composition and crossovers at different levels of the brain. Some of them pass only on one side, without forming crosses.
Red nuclear-spinal the way of regulation and coordination of muscle tone and automatic muscle contractions crosses in the midbrain.
Vestibulo-spinal way of balance and coordination of movements.
Covering-spinal tract visual-auditory unconditioned reflexes.
Olivo-spinal automatic way muscle tone a.
Posterior longitudinal beam- the way of coordinating the movements of the eyeballs, head and neck.
Bundle fibers connect the motor nuclei III, IV, VI pairs of cranial nerves and nuclei of the anterior horns of the spinal cord of the cervical and thoracic regions.
Characteristics of the pyramidal pathways.
pyramidal – Tractuspyramidalis(volitional, conscious) conduct impulses from the cortex to the motor nuclei and further to the muscles. They are divided into: fibrae corticospinales and fibrae corticonucleares
Fibrae (tractus) corticospinalis
1 neuron - giant pyramidal cell (Betz) - neuron of the fifth layer of the cortex of the precentral gyrus
The paths pass through the internal capsule in its posterior leg just behind the knee.
In the midbrain, the path fibers are located in the legs of the brain, in their middle part.
In the area of the bridge - the fibers run in the ventral part of the bridge
In the medulla oblongata - in the pyramids.
At the border with the spinal cord, 85% of the paths cross (decussatio pyramidum), the remaining 15% go to the spinal cord without crossing and pass to the opposite side in the corresponding segment of the spinal cord.
2 neuron - cell of the motor nucleus of the anterior horn of the spinal cord.
The axon of the second neuron passes as part of the anterior root, funiculus and branches of the spinal nerve to the skeletal muscle.
Fibrae (tractus) corticonuclearis (corticobulbaris)
1 neuron - giant pyramidal cell (Betz) of the fifth layer of the cortex in the precentral gyrus
The path passes in the knee of the internal capsule
2 neuron - cells of somatic motor nuclei of cranial nerves
The axon of the second neuron passes as part of the cranial nerve to the muscle
The path gives branches to its own and opposite side, with the exception of the nuclei of X11 and V11 pairs of cranial nerves
Characteristics of motor extrapyramidal pathways.
Extrapyramidal The paths conduct impulses to the muscles from the subcortical centers: the basal nuclei of the hemispheres, the dorsal (visual) tubercle, the red nucleus, the substantia nigra, the olive nuclei, the nuclei of the vestibular nerve, the reticular formation. The extrapyramidal system automatically maintains the tone of the skeletal muscles and ensures the work of the muscles of the antagonists. Extrapyramidal pathways include: tractus rubrospinalis, tractus tectospinalis, tractus reticulospinalis, tractus olivospinalis, tractus vestibulispinalis. The tracts begin in the corresponding subcortical nuclei (1 neuron). The axons of the first neurons, having previously made the transition to the opposite side, switch to the motor cells of the anterior horns of the spinal cord, the processes of which end in the skeletal muscles. The extrapyramidal system also includes the paths of cortical-cerebellar correlation (tractus cortico-ponto - cerebello - dentato - rubro - spinalis.
Fundamental morphological differences between central and peripheral paralysis.
PARALYSIS - complete loss of motor functions with a lack of muscle strength.
Paresis- weakening of motor functions with a decrease in muscle strength.
Paralysis and paresis develop as a result of various pathological processes (trauma, hemorrhage, etc.) in the central or peripheral part of the nervous system.
Central paralysis
1. Muscle groups are diffusely affected, there are no lesions of individual muscles Moderate atrophy
2. Spasticity with increased tendon reflexes
3.Extensor plantar reflex, Babinsky's symptom
4. There are no fascicular twitches
peripheral paralysis
1. Individual muscles may be affected
2. Severe atrophy, 70-80% of the total mass
3. Lethargy and hypotonia of the affected muscles with loss of tendon reflexes Plantar reflex, if called, then of a normal, flexion type
4. There may be fasciculations; electromyography reveals a decrease in the number of motor units and fibrillation
Regularities in the structure of sensitive pathways.
Ascending, Centripetal, Afferent, Sensitive (...), Conscious (to the cortex), reflex.
Characteristics of conscious afferent pathways.
Proprioceptive pathways of the cortical direction
Fasciculus gracilis (Goll) and Fasciculus cuneatus (Burdach).
1 neuron
The axon as part of the posterior root goes to the spinal cord, without entering the gray matter of the posterior horn, lies in the posterior cords and goes to the medulla oblongata (tractus gangliobulbaris)
2 neuron - nucleus gracilis et nucleus cuneati lies in the tubercles of the same name in the medulla oblongata
The axons of the second neurons, bending ventrally and moving to the opposite side, give rise to the formation of a medial loop
(Lemniscus medialis - tractus bulbothalamicus)
3 neuron - cells of the lateral nucleus of the dorsal (visual) tubercle
The processes of the third neurons (tractus thalamocorticalis) pass through the posterior leg of the internal capsule and reach the precentral and postcentral gyri (cells of the fourth layer of the cortex).
Characteristics of reflex afferent pathways.
proprioceptivewaycerebellardirections
Tractus spinocerebellaris anterior (Gowers) et spinocerebellaris posterior (Flechsig)
1 neuron - pseudounipolar cell of the spinal ganglion
The dendrite of the first neuron ends with a receptor in muscles, tendons, ligaments, joints
The axon as part of the posterior root enters the gray matter of the spinal cord and switches to the body of the second neuron
2 neuron: for Gowersa - nucleus intermediomedialis
for Flechsiga - nucleus thoracicus
The axons of the second neuron of the Gowersa pathway through the anterior white commissure go to the lateral funiculus of the opposite side, rise to the medulla oblongata, the pons and in the superior medullary velum pass to the opposite side and reach the cortex of the vermis through the superior cerebellar peduncle. The axons of the second neuron of the Flechsiga pathway go to the lateral funiculus of the same side, rise to the medulla oblongata and reach the cortex of the worm through the inferior cerebellar peduncle.
medial loop.
A bundle of white matter fibers formed by the axons of the thin and wedge-shaped nuclei conducts conscious proprioceptive pathways and pathways of general sensitivity, because. spinothalamic pathways join it.
Commissural nerve fibers of the brain, their structure.
Commissural nerve fibers connect similar areas of the two hemispheres. The nerve fibers of the brain are divided into associative, commissural and projection - they all form pathways for nerve impulses. Associative fibers connect cells within one hemisphere, and in the spinal cord - at the level of one half. Commissural fibers connect the right and left hemispheres, the right and left halves of the spinal cord. Projection fibers connect the higher and lower structures of the brain: the cells of the cortex with the cells of the nuclei and organs. They are divided into ascending (sensory) and descending (motor) pathways or tracts.
Commissural fibers, which are part of the so-called cerebral commissures, or adhesions, connect the symmetrical parts of both hemispheres. The largest cerebral commissure is the corpus callosum, corpus callosum , connects the parts of both hemispheres related to neoncephalon .
Two brain spikes comissura anterior and comissura inferior , which are much smaller in size, are rhinencephalon and connect: comissura anterior - olfactory lobes and both parahippocampal gyri, comissura fornicis - hippocampus.
Under the corpus callosum is the so-called vault, fornix , representing two arched white strands, which, in their middle part, corporis fornicis , are interconnected, and diverge in front and behind, forming pillars of the vault in front, columnae fornicis , behind - the legs of the arch, crura fornicis . crura fornicis , heading back, descend into the lower horns of the lateral ventricles and pass there into fimbria hippocampi . Between crura fornicis under splenium corporis callosi stretched transverse bundles of nerve fibers, forming commissionura fornicis . The front ends of the arch, columnae fornicis , continue down to the base of the brain, where they end in corpora mamillaria passing through the gray matter hypothalamus . Columnae fornicis limit the interventricular openings lying behind them, connecting the III ventricle with the lateral ventricles. Ahead of the pillars of the vault is the anterior commissure, commissionura anterior , having the appearance of a white transverse crossbar, consisting of nerve fibers. Between the front of the vault and Genu corporis callosi a thin vertical plate of brain tissue is stretched - a transparent septum, septum pellucidum , in the thickness of which there is a small slit-like cavity, cavum septi pellucidi .
Morphological bases of the alternating syndrome.
Alternating syndromes- syndromes that combine damage to the craniocerebral nerves on the side of the focus with conduction disorders of motor and sensory functions on the opposite side.
They occur when the anatomical components of the brain stem are affected: the legs of the brain - pedincular cross syndromes, the bridge - pontine, the medulla oblongata - bulbar. They also include cross hemiplegia - damage to the pyramidal pathway that crosses at different levels of the brain. Therefore, for example, paralysis or paresis of the right arm and left leg occurs with lesions below the brain stem. With the opposite hemianesthesia, the ascending pathways are damaged: spinothalamic and bulbothalamic cycles, fibers of the medial loop.
Neurology and neurosurgery Evgeny Ivanovich Gusev
3.2. Extrapyramidal system
3.2. Extrapyramidal system
The term "extrapyramidal system" refers to subcortical and stem extrapyramidal formations and motor pathways that do not pass through the pyramids of the medulla oblongata. Part of this system are also those bundles that connect the cerebral cortex with extrapyramidal gray structures: the striatum, the red nucleus, the substantia nigra, the cerebellum, reticular formation and barrel tire cores. In these structures, impulses are transmitted to the intercalary nerve cells and then descend as tegmental, red nuclear-spinal, reticular and vestibulo-spinal and other pathways to the motor neurons of the anterior horns of the spinal cord. Through these pathways, the extrapyramidal system influences spinal motor activity. The extrapyramidal system, consisting of projection efferent nerve pathways starting in the cerebral cortex, including the nuclei of the striatum, some nuclei of the brain stem and the cerebellum, regulates movements and muscle tone. It complements the cortical system of voluntary movements, voluntary movement becomes prepared, finely "tuned" for execution.
The pyramidal pathway (through the interneurons) and fibers of the extrapyramidal system ultimately occur on the anterior horn motor neurons, alpha and gamma cells, and affect them by both activation and inhibition.
The extrapyramidal system is phylogenetically older (especially its pallidar part) than the pyramidal system. With the development of the pyramidal system, the extrapyramidal system moves into a subordinate position.
The extrapyramidal system consists of the following main structures: the caudate nucleus, the shell of the lenticular nucleus, the pale ball, the subthalamic nucleus, the substantia nigra and the red nucleus. The level of the lower order of this system is the reticular formation of the tegmentum of the brainstem and the spinal cord. FROM further development of the animal world, the paleostriatum (pale ball) began to dominate these structures. Then, in higher mammals, the neostriatum (caudate nucleus and shell) acquires a leading role. As a rule, phylogenetically later centers dominate over earlier ones. This means that in lower animals the supply of innervation of movements belongs to the extrapyramidal system. Fish are a classic example of "pallidar" creatures. In birds, a fairly developed neostriatum appears. In higher animals, the role of the extrapyramidal system remains very important, despite the fact that as the cerebral cortex develops, phylogenetically older motor centers (paleostriatum and neostriatum) are increasingly controlled by a new motor system, the pyramidal system.
striatum- the leading center among the structures that make up the extrapyramidal system. It receives impulses from various areas of the cerebral cortex, especially from the frontal motor area of the cortex, which includes fields 4 and 6. These afferent fibers are organized in a somatotopic projection, go ipsilaterally and are inhibitory (braking) in their action. Reaches the striatum and another system of afferent fibers coming from the thalamus. From the caudate nucleus and the shell of the lenticular nucleus, the main afferent fibers are sent to the lateral and medial segments of the globus pallidus, which are separated from each other by the internal medullary plate. There are connections from the ipsilateral cerebral cortex to the substantia nigra, the red nucleus, the subthalamic nucleus, and the reticular formation.
Caudate nucleus and shell of the lenticular nucleus have two "channels" of connections with black matter. On the one hand, afferent nigrostriatal fibers are described as dopaminergic and reduce the inhibitory function of the striatum. On the other hand, the strionigral pathway is GABAergic and has an inhibitory effect on dopaminergic nigrostriatal neurons. These are closed feedback loops. GABAergic neurons, through gamma neurons in the spinal cord, control muscle tone.
All other efferent fibers of the striatum pass through the medial segment pale ball. They form rather thick bundles of fibers. One of these bundles is called the lenticular loop. Its fibers originate in the ventral part of the medial segment of the pale nucleus and run ventromedially around the posterior crus of the internal capsule to the thalamus and hypothalamus, as well as reciprocally to the subthalamic nucleus. After crossing, they connect with the reticular formation of the midbrain, from which a chain of neurons forms the reticular-spinal path (descending reticular system), ending in the cells of the anterior horns of the spinal cord.
The main part of the efferent fibers of the pale ball goes to the thalamus. This is the pallidothalamic bundle, or Trout field H1. Most of its fibers end in the anterior thalamic nuclei, which project to cortical area 6. The fibers that start in the dentate nucleus of the cerebellum end in the posterior thalamic nucleus, which projects to cortical area 4. All these thalamocortical connections transmit impulses in both directions. In the cortex, thalamocortical pathways synapse with corticostriatal neurons and form feedback loops. Reciprocal (coupled) thalamocortical junctions facilitate or inhibit the activity of cortical motor fields.
The fibers of the basal nuclei that descend to the spinal cord are relatively few and reach the spinal cord only through a chain of neurons. This nature of the connections suggests that the main function of the basal ganglia is to control and regulate the activity of the motor and premotor cortical fields, so voluntary movements can be performed smoothly, continuously.
The pyramidal path begins in the sensorimotor region of the cerebral cortex (fields 4, 1,2, 3). It is at the same time the fields in which the extrapyramidal motor pathways begin, which include corticostriatal, corticorubral, corticonigral and corticoreticular fibers going to the motor nuclei of the cranial nerves and to the spinal motor nerve cells through the descending chains of neurons.
Most of these cortical connections pass through the internal capsule. Consequently, damage to the internal capsule interrupts not only the fibers of the pyramidal pathway, but also the extrapyramidal fibers. This break is the cause of muscle spasticity.
Semiotics of extrapyramidal disorders. The main signs of extrapyramidal disorders are disorders of muscle tone (dystonia) and involuntary movements (hyperkinesis, hypokinesis, akinesis), which are absent during sleep. Two clinical syndromes can be distinguished. One of them is characterized by a combination of hyperkinesis (automatic violent movements due to involuntary muscle contractions) and muscle hypotension and is caused by damage to the neostriatum. The other is a combination of hypokinesis and muscle hypertension or rigidity, and is seen with involvement of the medial globus pallidus and substantia nigra.
Akinetic-rigid syndrome(syn.: amyostatic, hypokinetic-hypertonic, pallidonigral). This syndrome in its classical form is found in tremor paralysis, or Parkinson's disease. The pathological process in this disease is degenerative, leading to the loss of melanin-containing neurons of the substantia nigra. The lesion in Parkinson's disease is usually bilateral. With unilateral cell loss, clinical signs are observed on the opposite side of the body. In Parkinson's disease, the degenerative process is hereditary. This loss of substantia nigra neurons may be due to other causes. In such cases, trembling paralysis is referred to as Parkinson's syndrome or parkinsonism. If it is a consequence of lethargic encephalitis, it is called postencephalitic parkinsonism. Other conditions (cerebral atherosclerosis, typhoid, cerebral syphilis, primary or secondary involvement of the midbrain in a tumor or injury, intoxication with carbon monoxide, manganese and other substances, long-term use of phenothiazine or reserpine) can also cause parkinsonism.
The clinical manifestations of the akinetic-rigid syndrome are characterized by three main features: hypokinesia (akinesis), rigidity and tremor. At hypokinesia the patient's mobility slowly decreases. All mimic and expressive movements gradually drop out or slow down sharply. Starting a movement, such as walking, is very difficult. The patient first takes a few short steps. Having started the movement, he cannot suddenly stop and takes a few extra steps. This continued activity is called propulsion. Facial expression becomes mask-like (hypomimia, amimia). Speech becomes monotonous and dysarthric, partly caused by rigidity and tremor of the tongue. The body is in a fixed flexion position of anteflexion, all movements are exceptionally slow and unfinished. Hands do not participate in the act of walking (acheirokinesis). All mimic and friendly expressive movements characteristic of the individual are absent.
In contrast to the spastic increase in muscle tone rigidity can be felt in the extensors as a "wax" resistance to all passive movements. Muscles cannot be relaxed. With passive movements, you can feel that the tone of the antagonist muscles decreases stepwise, inconsistently (a symptom of a cogwheel). The raised head of a lying patient does not fall when suddenly released, but gradually falls back onto the pillow (head drop test). In contrast to the spastic state, proprioceptive reflexes are not elevated, and pathological reflexes and paresis are absent. It is difficult to evoke reflexes and it is impossible to increase the knee jerk with the Jendraszyk maneuver.
Most patients present with passive tremor having a low frequency (4-8 movements per second). Passive tremor is rhythmic and is the result of the interaction of agonists and antagonists (antagonistic tremor). In contrast to intentional tremor, antagonistic tremor stops during purposeful movements. Rolling pills or counting coins are signs of Parkinson's tremor.
The mechanism that causes the appearance of the three listed signs has not been fully elucidated. Akinesis is possibly related to the loss of dopaminergic transmission of impulses to the striatum. Akinesis can be explained as follows: damage to the neurons of the substantia nigra causes the loss of the influence of inhibitory descending nigroreticulospinal impulses on Renshaw cells. Renshaw cells, which have a connection with large ?-motor neurons, reduce the activity of the latter by their inhibitory effect, which makes the initiation of voluntary movement more difficult.
Rigidity can also be explained by the loss of substantia nigra neurons. Normally, these neurons have an inhibitory effect on striatal impulses, which in turn inhibit the globus pallidus. Their loss means that efferent pallidar impulses are not inhibited. The descending path of the pale ball forms synapses with reticulospinal neurons; which facilitate the action of intercalary neurons in the circuit of the tonic stretch reflex. In addition, impulses emanating from the medial part of the globus pallidus reach area 6a through the thalamic nuclei and, through the corticospinal fibers, also have a facilitating effect on the intercalary neurons in the tonic stretch reflex circuit. There is a violation of muscle tone, called rigidity.
If the efferent cells and fibers of the globus pallidus are destroyed by stereotaxic surgery in its medial part or in the region of the lenticular loop, or the thalamic nucleus, rigidity decreases.
Stereotactic operations of coagulation of the medial part of the pale ball, pallidothalamic fibers or dentatothalamic fibers and their terminal thalamic nucleus are shown in some patients.
Hyperkinetic-hypotonic syndrome. Develops with damage to the striatum. Hyperkinesias are caused by damage to the inhibitory neurons of the neostriatum, the fibers of which lead to the globus pallidus and substantia nigra. In other words, there is a violation of neuronal systems higher order, which leads to excessive excitation of the neurons of the underlying systems. As a result, hyperkinesis of various types occurs: athetosis, chorea, spastic torticollis, torsion dystonia, ballism, etc.
Athetosis usually caused by perinatal damage to the striatum. It is characterized by involuntary slow and worm-like movements with a tendency to hyperextension of the distal parts of the limbs. In addition, there is an irregular, spastic increase in muscle tension in agonists and antagonists. As a result, postures and movements are rather eccentric. Voluntary movements are significantly impaired due to the spontaneous onset of hyperkinetic movements, which can involve the face, tongue and thus cause grimaces with abnormal tongue movements. Spasmodic bursts of laughter or crying are possible. Athetosis can be combined with contralateral paresis. It can also be bilateral.
Facial paraspasm- tonic symmetrical contractions of the facial muscles of the mouth, cheeks, neck, tongue, eyes. Sometimes blepharospasm is observed - an isolated contraction of the circular muscles of the eyes, which can be combined with clonic convulsions of the muscles of the tongue and mouth. Paraspasm occurs sometimes during a conversation, eating, smiling. Increases with excitement, bright lighting. Disappears in a dream.
Choreic hyperkinesis characterized by short, rapid, involuntary twitches that develop randomly in the muscles and cause various kinds of movements, sometimes resembling arbitrary ones. First, the distal parts of the limbs are involved, then the proximal ones. Involuntary twitches of the facial muscles cause grimaces. In addition to hyperkinesis, a decrease in muscle tone is characteristic. Choreic movements with slow development can be a pathognomonic sign in Huntington's chorea and chorea minor, secondary to other brain diseases (encephalitis, carbon monoxide poisoning, vascular diseases). The striatum is affected.
Spasmodic torticollis and torsion dystonia- the most important syndromes of dystonia. In both diseases, the putamen and centromedial nucleus of the thalamus are usually affected, as well as other extrapyramidal nuclei (globus pallidus, substantia nigra, etc.). Spasmodic torticollis is a tonic disorder that is expressed in spastic contractions of the muscles of the cervical region, leading to slow, involuntary turns and tilts of the head. Patients often use compensatory techniques to reduce hyperkinesis, in particular, they support their heads with their hands. In addition to other muscles of the neck, the sternocleidomastoid and trapezius muscles are especially often involved in the process.
Spasmodic torticollis may be an abortive form of torsion dystonia or an early symptom of another extrapyramidal disease (encephalitis, Huntington's chorea, hepatocerebral dystrophy).
Torsion dystonia is characterized by passive rotational movements of the trunk and proximal limb segments. They can be so pronounced that without support the patient can neither stand nor walk. The disease can be symptomatic or idiopathic. In the first case, birth trauma, jaundice, encephalitis, early Huntington's chorea, Hallervorden-Spatz disease, hepatocerebral dystrophy (Wilson-Westphal-Strumpel disease) are possible.
ballistic syndrome usually occurs in the form of hemiballismus. It is manifested by rapid contractions of the proximal muscles of the limbs of a rotating nature. With hemiballismus, the movement is very powerful, strong (“throwing”, sweeping), since very large muscles contract. Arises as a result of damage to the subthalamic nucleus of Lewis and its connections with the lateral segment of the pale ball. Hemiballismus develops on the side contralateral to the lesion.
Myoclonic jerks usually indicate a lesion in the region of the triangle of Guillen - Mollare: the red nucleus, the inferior olive, the dentate nucleus of the cerebellum. These are fast, usually erratic contractions of various muscle groups.
Tiki- rapid involuntary muscle contractions (most often the circular muscle of the eye and other muscles of the face).
Hyperkinesias presumably develop as a result of the loss of the inhibitory effect of the striatum on the underlying neuronal systems (pale ball, substantia nigra).
Pathological impulses go to the thalamus, to the motor cortex, and then along the efferent cortical neurons.
In elderly patients with cerebral atherosclerosis, one can often find signs of parkinson-like disorders or hyperkinesis, especially tremor, a tendency to repeat words and phrases, final syllables of words (logoclonia) and movements (polykinesia). There may be a tendency to pseudo-spontaneous movements, but true choreiform or athetoid movements are relatively rare. In most cases, the symptoms are due to miliary and somewhat large necrotic lesions of the striatum and globus pallidus, which are found in the form of scars and very small cysts. This condition is known as lacunar status. The tendency to recurrence and logoclonia is considered to be due to similar lesions of the caudate nucleus, and the tremor is due to the putamen.
Automated Actions- complex motor acts and other sequential actions that occur without consciousness control. Arise with hemispheric foci that destroy the connections of the cortex with the basal nuclei while maintaining their connection with the brain stem; appear in the limbs of the same name with the focus.
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