Motor disorders (impaired motor function): types, causes, treatment, symptoms, signs. Movement disorders in mental disorders

Each disease of the National Assembly is characterized by certain symptoms and syndromes, the identification of which allows you to determine the location of the lesion of the National Assembly (to establish a topical diagnosis). A symptom is understood as a sign of a disease, a syndrome in neurology is a set of persistent symptoms characterized by a certain pathological condition of the nervous system and united by their common passage. In case of damage or diseases of the nervous system, a person experiences disturbances in the form of motor, sensory, coordination, mental, vegetative, and other disorders.

Motion - a manifestation of vital activity that provides the possibility of active interaction of both the constituent parts and the whole organism with the environment. Movement can be involuntary (reflex, unconscious) and voluntary (conscious). The main formation that provides the regulation of voluntary movements is the pyramidal system, which connects the motor centers of the cerebral cortex with the motor nuclei of the cranial nerves and the motor (motor neurons) of the anterior horns of the spinal cord into the cortico-muscular path.

involuntary motor responses are unconditional and occur in response to pain, sound, light, and other irritations and muscle strains. Voluntary motor responses arise as a result of the implementation of certain motor programs and are carried out with muscle contraction.

Motor disorders are manifested by damage in the connection between the motor area of ​​the cerebral cortex (anterior central gyrus) and muscles, as well as damage to the cortical-muscular pathway. At the same time, regardless of the level at which the connection is broken, the muscle loses its ability to contract and paralysis develops. Paralysis- complete absence of voluntary movements. The nature of paralysis depends on which motor neuron is damaged - central or peripheral.

When the central (first) motor neuron is damaged, a central or spastic paralysis. More often, central paralysis occurs when there is a violation of cerebral circulation and is characterized by:

1) increased muscle tone (muscle hypertension or spasticity),

2) high tendon and periosteal reflexes hyperreflexia,

3) pathological extensor and flexion reflexes,

4) clonuses - rhythmic, repeated, not long
damped contractions of any muscle group during
certain methods of calling,

5) protective reflexes - involuntary movements, expressed in flexion or extension of a paralyzed limb when it is irritated (prick, cooling, etc.),

6) involuntary friendly movements in response to
purposeful or involuntary movement - synkinesis,

7) a lesion in the region of the brain stem leads to the development
alternating syndromes: a combination of FMN pathology on the side of the pathological focus and spastic hemiplegia on the opposite side.

If the peripheral (second; motor - neuron) is damaged, peripheral or flaccid paralysis, which is characterized by:

1) decrease or loss of muscle tone - hypotension or muscle atony,

2) malnutrition of muscles - atrophy of paralyzed muscles,

3) hyporeflexia - a decrease or areflexia by the absence of tendon reflexes,

4) violation of electrical excitability - the reaction of rebirth.

With flaccid paralysis, there are not only voluntary, but also reflex movements. If there are no sensory disorders in flaccid paralysis, then the cells of the anterior horn of the spinal cord are affected, which is characterized by fibrillar twitching of the mouse of the reaction of degeneration and the early appearance of muscle atrophy. Damage to the anterior spinal roots is characterized by fascicular muscle twitching, areflexia and muscle atony in the area of ​​innervation. If a sensory disturbance is added to the movement disorders, this means that the entire peripheral nerve is damaged.

Damage to the peripheral nerve m.b. incomplete, then the patient develops muscle weakness. This phenomenon of partial movement disorders - a decrease in muscle volume and strength is called paresis. Paresis of the muscles of one limb is called monoparesis, two limbs - paraparesis, three - triparesis, four - tetraparesis. With a half lesion of the body (right arm and right leg), hemiparesis develops. Localization of the lesion causes pathological changes at various levels: if the spinal cord is affected in its diameter above the cervical thickening (inflammation, trauma, tumor), then the patient develops spastic tetraplegia,

The term plegia correlates with the concept of paralysis and denotes the complete absence of contractions of the corresponding muscles. With mildly disturbed muscle tone, the phenomena of apraxia are noted, the impossibility due to the inability to perform purposeful practical actions for self-service.

Movement disorders may be expressed and impaired coordination - ataxias, which is of two types: static and dynamic. Static ataxia- imbalance when standing (in statics), checked by stability in the Romberg test, dynamic ataxia- imbalance in the disproportion of the motor act (shaky, uncertain gait with arms wide apart). Ataxia occurs with pathology of the cerebellum and vestibular apparatus. Other cerebellar disorders: nystagmus- rhythmic twitching of the eyeballs, more often when looking to the side; scanned speech- jerky speech with accents at certain intervals; misses- overshooting when performing a purposeful movement, and diadochokinesis- uncoordinated movements of the hands during their rotation in an extended position (the hand lags behind on the side of the lesion); dysmetria- violation of the amplitude of movements; dizziness; intentional trembling- trembling (tremor) when performing precise movements. Movement disorders are sometimes accompanied by hyperkinesias, involuntary movements devoid of physiological significance. Various types of hyperkinesis occur in the pathology of the extrapyramidal system.

Hyperkinesias include:

- convulsions- involuntary contractions clonic- rapidly alternating muscle contractions and tonic- long-term muscle contractions, convulsions - the result of irritation of the cortex or brain stem;

- athetosis- slow artsy (worm-like) contractions of the muscles of the limbs (usually fingers and toes), appear in the pathology of the cortex;

- jitter- involuntary rhythmic oscillatory movements of the limbs or head with damage to the cerebellum and subcortical formations;

- chorea - fast erratic movements, similar to deliberate antics, dancing;

- tick - short-term monotonous clonic twitches of individual muscle groups (often the face);

- facial hemispasm - attacks of convulsive twitching of the muscles of one half of the face;

- myoclonus - fast, lightning-fast contractions of individual muscle groups.

Lesions of the spinal cord at its various levels, along with motor disorders, are also manifested by sensory disorders.

Sensitivity - the ability of the organism to perceive irritations from the environment or from its own tissues or organs. Sensory receptors are classified into exteroreceptors(pain, temperature, tactile receptors); proprioreceptors(located in muscles, tendons, ligaments, joints), providing information about the position of the limbs and torso in space, the degree of muscle contraction; interoreceptors(located in internal organs).

Interoceptive sensitivity they call sensations arising from irritation of internal organs, vessel walls, etc. It is connected with the sphere of autonomic innervation. Allocate also special sensitivity, arising in response to irritation from the outside of the senses: sight, hearing, smell, taste.

The most common sign of sensory irritation is pain. Pain- this is a real subjective sensation due to the applied irritation or pathology in tissues or organs. With the defeat of the nerve fibers that carry out somatic innervation, there are somatalgia. Such pains are permanent or periodic, not accompanied by vegetative manifestations. When involved in the process of fibers of autonomic sensory innervation, develop sympathy. These pains are deep, pressing, permanent or intermittent, accompanied by vegetative reactions - goosebumps, sweating, trophic disorders. Pain of girdle nature or going along the limb received; title radicular pain. Causalgia- burning pain. Pain can wear local, projection, irradiating, reflected phantom, reactive character.

local pain occurs in the area of ​​​​existing painful irritation. Projection pain - the localization of pain does not coincide with the site of the existing irritation (with a bruise of the elbow joint, pain in 4-5 fingers of the hand). irradiating pain that spreads from one branch of the irritated nerve to another. Reflected pain is a manifestation of painful irritation in diseases of the internal organs. Phantom pain occurs in people who have undergone amputation, in the stump of cut nerves. Reactive pain - pain in response to compression or tension of a nerve or root.

Other types of sensory impairment: anesthesia- complete lack of sensitivity; hypoesthesia- reduced sensitivity; hyperesthesia- Hypersensitivity, which in most cases is accompanied by pain in the zone of innervation (neuralgia). paresthesia- a feeling of tingling, "crawling", numbness. Dysesthesia- perverted perception of stimuli, when tactile is perceived as painful, etc. Polyesthesia- a type of perversion of pain sensitivity, in which a single irritation is perceived as multiple. Hemianesthesia- loss of sensation in one half of the body, one limb - monoanesthesia, in the legs and lower body - paraanesthesia. hypoesthesia- lowering the perception of both the entire sensitivity and its individual types. Hyperpathy- a condition in which even the slightest irritation exceeds the threshold of excitability and is accompanied by pain and a long aftereffect. Senestopathy- a variety of painful, long-term disturbing sensations of burning, pressure, constriction, etc., which do not have obvious organic causes for the occurrence. Violation of some types of sensitivity while maintaining others, is called dissociated disorders.

Disorders of sensitivity of the peripheral type may be. neural- violation of all types of sensitivity in the area supplied by the affected nerve; polyneuritic symmetrical disorders in the distal extremities; radicular- violation of all types of sensitivity in the zone of the corresponding dermatomes.

Neuro-psychic activity. It includes speech, thinking, memory, complex motor skills (praxis), comprehension of various objects of the external world (gnosia), etc.

Speech is the ability to pronounce and understand words and phrases, to comprehend them, connecting them with certain concepts.

Aphasia- violation of speech due to damage to the cortical centers of analysis and synthesis of words within one hemisphere of the left in right-handers and right - in left-handers. Aphasia m.b. sensory, motor, amnestic, total.

Sensory aphasia consists in a violation of the understanding of oral speech due to the defeat of the feeding center of the sound images of words, but the speech is preserved. This center is located in the temporal region of the brain. His defeat also leads to such a violation of speech functions as reading.

motor aphasia- violation of oral speech due to damage to the cortical center of motor speech automatisms, the patient understands the speech addressed to him. The center is located in the left frontal lobe (in right-handers). In such patients, the function of writing is also upset.

Amnestic aphasia- violation of the ability to name familiar objects, with knowledge of their purpose. The speech of such patients is poor in nouns, they forget the names of surrounding things, objects, etc. The syndrome is often combined with sensory aphasia, auditory memory is impaired. The cortical center is located at the junction of the temporal, occipital and parietal lobes of the left hemisphere (in right-handers).

Total aphasia- violation of writing, all types of speech and its understanding (occurs with extensive lesions).

Alexia- violation of reading and reading comprehension due to the defeat of the center for storing written images of speech. The lesion is in the parietal region, combined with sensory aphasia.

dysarthria- occurs with paralysis or paresis of the articulatory apparatus (usually the tongue), speech becomes illegible, incomprehensible.

Agraphia- writing disorder due to damage to the cortical center of motor automatisms (in the frontal region). It is combined with motor aphasia, difficulty in understanding what is written by the patient himself.

Apraxia- violation of purposeful motor skills due to damage to the cortical center of complex actions. Patients cannot fasten buttons, comb their hair, eat with a spoon, etc. Often the sequence of actions is disturbed, superfluous, unnecessary movements appear (parapraxia), or the patient gets stuck on some kind of movement (perseveration). Apraxia occurs when the cortex is damaged in the parietal-temporal-occipital region.

Allocate motor, ideational and constructive apraxia. At motor apraxia goal-directed movements by oral order and by imitation are upset. At ideational apraxia- disorder of movements according to the oral order and safety of actions on imitation. Constructive Apraxia- this is a special type of movement disorder when the patient is not able to construct a whole from parts, arrange letters, numbers, there are no spatial relationships, etc.

agnosia- violation of recognition processes with preservation or slight change in the perceiving function of the sense organs.

Gnosis closely related to memory. There are the following types of agnosia:

- visual ("mental blindness")- impaired recognition of objects and things, with the preservation of vision, the lesion in the occipital region;

- auditory ("mental deafness")- disorder of recognition, the outside world by characteristic sounds (clock ticking while maintaining hearing, the lesion in the temporal region, combined with sensory aphasia;

- odor agnosia- violation of the recognition of odorous substances by a characteristic odor with the preservation of the olfactory function. The focus is localized in the deep parts of the temporal lobe;

- agnosia of taste- loss of the ability to recognize familiar substances with the preservation of taste sensations, the focus is in the central gyrus;

- astereognosis- not recognizing objects by touch with sufficient preservation of deep and superficial sensitivity, focus in the parietal lobe;

- agnosia of parts of one's own body- violation of the body scheme, confuses the left and right sides of his body, feels the presence of three legs, four arms, etc., the focus is in the interparietal sulcus.

Disorders of consciousness.

Consciousness is the highest form of reflection of reality, which is a set of human mental processes.

Types of impaired consciousness are conditionally divided into syndromes of turning off consciousness and syndromes of clouding of consciousness.

Syndromes of turning off consciousness: stupor("load") - increasing the threshold of perception. Speech contact with the patient is filled with difficulty due to lethargy, lethargy, disorientation, impaired attention, etc. The condition is characteristic of a brain tumor.

Sopor- a condition in which patients do not respond to verbal appeals, are motionless, although with loud repeated appeals they open their eyes, try to pronounce the words, but soon melt away to respond to any stimuli. Unconditioned and deep reflexes are preserved. The condition is characteristic of a tumor, TBI, and other conditions.

Coma - the deepest inclusion of consciousness with the absence of unconditioned and conditioned reflexes (with the exception of vital ones. The state of coma is typical for head injury, cerebral stroke, severe intoxication, infectious diseases.

Confusion Syndromes: Delirious Syndrome- violation of orientation in one's own personality. Visual, auditory, tactile hallucinations are characteristic. The syndrome manifests itself in mental illness (schizophrenia), alcohol intoxication ("delirious tremens").

Twilight clouding of consciousness- a sharp "narrowing of the field of consciousness", a twilight state in the form of hallucinatory manifestations of anxiety. fear, anger, etc. or automatic nocturnal reactions like sleepwalking.

Trance- a short-term condition in which the patient performs impulsive purposeful actions, which he does not remember in the future. Twilight state and trance are characteristic of epilepsy, TBI.

Various types of disorders of higher nervous activity are observed in patients with cerebrovascular accidents (strokes), tumors, abscesses, intoxications, inflammation of the meninges, etc.


Similar information.


These include tremor, dystonia, athetosis tics and ballism, dyskinesias and myoclonus.

Classification of causes, symptoms, signs of movement disorders

Movement disorder Classification, causes, symptoms, signs
Tremor = rhythmic oscillatory movements of a body part

Classification: rest tremor, intentional tremor, essential tremor (usually postural and action), orthostatic tremor Parkinsonism is characterized by rest tremor. Essential tremor has often been present for many years before seeking medical attention and is usually bilateral; in addition, a positive family history is often noted. Intentional and action tremors are often combined with damage to the cerebellum or efferent cerebellar pathways. Orthostatic tremor is expressed mainly by instability in the standing position and high-frequency trembling of the muscles of the legs.

Causes of increased physiological tremor (according to the standard of the German Society of Neurology): hyperthyroidism, hyperparathyroidism, kidney failure, vitamin B2 deficiency, emotions, stress, exhaustion, cold, drug/alcohol withdrawal syndrome

Drug tremor: neuroleptics, tetrabenazine, metoclopramide, antidepressants (mainly tricyclics), lithium preparations, sympathomimetics, theophylline, steroids, antiarrhythmic drugs, valproic acid, thyroid hormones, cytostatics, immunosuppressive drugs, alcohol

Dystonia = long-lasting (or slow), stereotyped and involuntary muscle contraction, often with repeated twisting movements, unnatural postures and abnormal positions Classification: Adult idiopathic dystonias are usually focal dystonias (eg, blepharospasm, torticollis, dystonic writing spasm, laryngeal dystonia), segmental, multifocal, generalized dystonias, and hemidystonias. Rarely, primary dystonias (autosomal dominant dystonias, eg, dopa-responsive dystonia) or dystonias within an underlying degenerative disease (eg, Hallerforden-Spatz syndrome) occur. Secondary dystonias have also been described, for example, in Wilson's disease and in syphilitic encephalitis. Rare: dystonic status with respiratory failure, muscle weakness, hyperthermia and myoglobinuria.

Tics = involuntary, sudden, brief and often repetitive or stereotyped movements. Tics can often be suppressed for a period of time. Often there is an obsessive desire to perform a movement with subsequent relief.
Classification: motor tics (clonic, dystonic, tonic, eg, blinking, grimacing, head nodding, complex movements, eg, grasping objects, adjusting clothing, copropraxia) and phonic (vocal) tics (eg, coughing, coughing, or compound tics → coprolalia, echolalia). Juvenile (primary) tics often develop in association with Tourette's syndrome. Causes of secondary tics: encephalitis, trauma, Wilson's disease, Huntington's disease, drugs (SSRIs, lamotrigine, carbamazepine)

Choreiform movement disorders = involuntary, non-directional, sudden and brief, sometimes complex movements Athetosis = slow choreiform movement, accentuated distally (sometimes worm-like, writhing)

Ballismus/hemiballismus = severe form with throwing motion, usually unilateral, affecting the proximal limbs

Huntington's chorea is an autosomal dominant neurodegenerative disease that is typically accompanied by hyperkinetic and often choreiform movements (the lesion is located in the striatum). Non-genetic causes of chorea: lupus erythematosus, chorea minor (Sydenham), chorea of ​​pregnancy, hyperthyroidism, vasculitis, drugs (eg, levodopa overdose), metabolic disorders (eg, Wilson's disease). Causes of hemiballismus/ballisma are typical lesions of the contralateral subthalamic nucleus, but other subcortical lesions should also be considered. Most often we are talking about ischemic foci. Rarer causes are metastases, arteriovenous malformations, abscesses, lupus erythematosus, and drugs.
Dyskinesias = involuntary, prolonged, repetitive, purposeless, often ritualized movements

Classification: simple dyskinesias (eg, tongue sticking out, chewing) and complex dyskinesias (eg, stroking, repetitive leg crossing, marching movements).

The term akathisia describes motor restlessness with complex stereotyped movements (“the inability to sit still”), its cause is usually antipsychotic therapy. Tardive dyskinesia (usually in the form of dyskinesia of the mouth, cheeks and tongue) occurs due to the use of antidopaminergic drugs (neuroleptics, antiemetics, such as metoclopramide).

Myoclonus = sudden, involuntary, brief muscle twitches with visible motor effects of varying degrees (from barely perceptible muscle twitches to severe myoclonus affecting the muscles of the body and limbs)

Classification: Myoclonus can occur at the cortical, subcortical, reticular and spinal levels.

They may be focal segmental, multifocal, or generalized.

  • Association with epilepsy (juvenile epilepsy in West syndrome, Lennox-Gastaut syndrome; progressive myoclonic epilepsy in Unferricht-Lundborg syndrome, Lafort body disease, MERRF syndrome)
  • Essential causes (sporadic, hereditary myoclonus usually with early onset) Metabolic disorders: hepatic encephalopathy, renal failure (dialysis encephalopathy due to chronic aluminum intoxication), diabetic ketoacidosis, hypoglycemia, electrolyte imbalance, pH crisis
  • Intoxications: cocaine, LSD, marijuana, bismuth, organophosphates, heavy metals, drug overdose
  • Drugs: penicillin, cephalosporin, levodopa, MAO-B inhibitors, opiates, lithium, tricyclic antidepressants, etomidate
  • Storage diseases: lipofuscinosis, salidoses
  • Trauma/hypoxia: Lance-Adams syndrome (post-hypoxic myoclonic syndrome) after cardiac arrest, respiratory failure, traumatic brain injury
  • Paraneoplasia
  • Infections: encephalitis (typically in subacute sclerosing panencephalitis after measles infection), meningitis, myelitis, Creutzfeldt-Jakob disease
  • Neurodegenerative diseases: Huntington's chorea, Alzheimer's dementia, hereditary ataxias, parkinsonism

Diagnosis of movement disorders

Hyperkinetic movement disorder is initially diagnosed based on the clinical presentation:

  • Rhythmic, such as tremor
  • Stereotypic (same repetitive movement), e.g. dystonia, tic
  • Irhythmic and non-stereotypical, such as chorea, myoclonus.

Attention: drugs that were taken several months ago can also be responsible for the movement disorder!

In addition, brain MRI should be performed to differentiate between primary (eg, Huntington's disease, Wilson's disease) and secondary (eg, drug) causes.

Routine laboratory tests should primarily include electrolyte levels, liver and kidney function, and thyroid hormones.

It seems appropriate, in addition, the study of cerebrospinal fluid to exclude a (chronic) inflammatory process in the central nervous system.

In myoclonus, EEG, EMG and somatosensory evoked potentials help to determine the topographic and etiological characteristics of the lesion.

Differential diagnosis of movement disorders

  • Psychogenic hyperkinesias: In principle, psychogenic movement disorders can mimic the full range of organic movement disorders listed in the table. Clinically, they appear as abnormal, involuntary, and non-directional movements associated with walking and speech disturbances. Movement disorders usually begin acutely and progress rapidly. Movements, however, are most often heterogeneous and variable in severity or intensity (unlike organic movement disorders). It is not uncommon for several movement disorders to be present as well. Often, patients can be distracted and thereby interrupt movement. Psychogenic movement disorders may increase if they are observed ("spectators"). Often, movement disorders are accompanied by "inorganic" paralysis, diffuse or difficult to classify anatomically sensitization disorders, as well as speech and walking disorders.
  • Myoclonias can also occur "physiologically" (=without underlying disease), such as sleep myoclonus, post-syncopal myoclonus, hiccups, or post-exercise myoclonus.

Treatment of movement disorders

The basis of therapy is the elimination of provoking factors, such as stress in essential tremor or drugs (dyskinesia). The following options are considered as options for specific therapy for various movement disorders:

  • For tremor (essential): beta-receptor blockers (propranolol), primidone, topiramate, gabapentin, benzodiazepine, botulinum toxin with insufficient action of oral drugs; in treatment-resistant cases with severe disability - according to indications, deep brain stimulation.

Tremor in Parkinson's disease: Initial treatment of torpor and akinesis with dopaminergics, with persistent tremor, anticholinergics (note: side effects, especially in elderly patients), propranolol, clozapine; with therapy-resistant tremor - according to indications, deep brain stimulation

  • With dystonia, in principle, physiotherapy is also always carried out, and sometimes orthoses are used.
    • for focal dystonia: trial therapy with botulinum toxin (serotype A), anticholinergics
    • with generalized or segmental dystonia, first of all, drug therapy: anticholinergics (trihexphenidyl, piperiden; attention: visual impairment, dry mouth, constipation, urinary retention, cognitive impairment, psychosyndrome), muscle relaxants: benzodiazepine, tizanidine, baclofen (in severe cases, sometimes intrathecal), tetrabenazine; in severe cases resistant to therapy, according to indications - deep brain stimulation (globus pallidus internus) or stereotaxic surgery (thalamotomy, pallidotomy)
    • children often have dopa-responsive dystonia (often also responds to dopamine agonists and anticholinergics)
    • dystonic status: observation and treatment in the intensive care unit (sedation, anesthesia and mechanical ventilation if indicated, sometimes intrathecal baclofen)
  • With tics: explanation to the patient and relatives; drug therapy with risperidone, sulpiride, tiapiride, haloperidol (second choice due to unwanted side effects), aripiprazole, tetrabenazine, or botulinum toxin for dystonic tics
  • For chorea: tetrabenazine, tiapride, clonazepam, atypical antipsychotics (olanzapine, clozapine) fluphenazine
  • For dyskinesias: cancel provocative drugs, trial therapy with tetramenazine, for dystonia - botulinum toxin
  • For myoclonus (usually difficult to treat): clonazepam (4-10 mg/day), levetiracetam (up to 3000 mg/day), piracetam (8-24 mg/day), valproic acid (up to 2400 mg/day)

Psychomotor is a set of motor acts of a person, which is directly related to mental activity and reflects the peculiarities of the constitution inherent in this person. The term "psychomotor", in contrast to simple motor reactions that are associated with the reflex activity of the central nervous system, denotes more complex movements that are associated with mental activity.

The impact of mental disorders.

With various kinds of mental illness, there may be violations of complex motor behavior - the so-called psychomotor motor disorders. Rough focal brain damage (for example, cerebral atherosclerosis) usually leads to paresis or paralysis. Generalized organic processes, such as brain atrophy (reduction of the brain in volume) are accompanied in most cases by lethargy of gestures and facial expressions, slowness and poverty of movements; speech becomes monotonous, gait changes, general stiffness of movements is observed.

Psychiatric disorders also affect psychomotor. Thus, manic-depressive psychosis in the manic phase is characterized by general motor excitation.

Some psychogenic disorders in mental illness lead to sharply painful changes in psychomotor. For example, hysteria is often accompanied by complete or partial paralysis of the limbs, reduced strength of movements, and frustrated coordination. A hysterical fit usually makes it possible to observe various expressive and protective mimic movements.

Catatonia (a neuropsychiatric disorder that manifests itself in a violation of voluntary movements and muscle spasms) is characterized by both minor changes in motor skills (weak facial expressions, deliberate pretentiousness of posture, gestures, gait, mannerisms), and vivid manifestations of catatonic stupor and catalepsy. The latter term refers to numbness or stiffness, accompanied by a loss of the ability to voluntary movements. Catalepsy can be observed, for example, in hysteria.

All movement disorders in mental illness can be divided into three types.

Types of movement disorders.

  1. hypokinesia(disorders that are accompanied by a decrease in motor volume);
  2. hyperkinesia(disorders that are accompanied by an increase in motor volume);
  3. dyskinesia(disorders in which involuntary movements occur as part of normally smooth and well-controlled movements of the limbs and face).

The category of hypokinesia includes various forms of stupor. Stupor is a mental disorder characterized by inhibition of any mental activity (movements, speech, thinking).

Types of stupor in hypokinesia.

1. Depressive stupor (also called melancholic stupor) manifests itself in immobility, a depressed state of mind, but the ability to respond to external stimuli (addresses) is preserved;

2. Hallucinatory stupor occurs with hallucinations provoked by poisoning, organic psychosis, schizophrenia; with such a stupor, general immobility is combined with facial movements - reactions to the content of hallucinations;

3. Asthenic stupor manifests itself in indifference to everything and lethargy, in unwillingness to answer simple and understandable questions;

4. Hysterical stupor is typical for people with a hysterical temperament (it is important for them to be the center of attention, they are overly emotional and demonstrative in expressing feelings), in a state of hysterical stupor, the patient lies motionless for a very long time and does not respond to calls;

5. Psychogenic stupor occurs as a reaction of the body to severe mental trauma; such a stupor is usually accompanied by increased heart rate, increased sweating, fluctuations in blood pressure and other disorders of the autonomic nervous system;

6. Cataleptic stupor (also called wax flexibility) is characterized by the ability of patients to stay in the position given to them for a long time.

Mutism (absolute silence) is also referred to as hypokinesia.

Hyperkinesia.

Types of excitations in hyperkinesia.

1. Manic excitement caused by an abnormally elevated mood. In patients with mild forms of the disease, behavior remains purposeful, although accompanied by exaggerated loud and rapid speech, movements remain well coordinated. In severe forms of movement and the patient's speech are not connected in any way, motor behavior becomes illogical.

2. Hysterical excitement, which is most often a reaction to the surrounding reality, this excitement is extremely demonstrative and intensifies if the patient notices attention to himself.

3. Hebephrenic excitation, which is a ridiculous, cheerful, meaningless behavior, accompanied by pretentiousness of facial expressions, is typical for schizophrenia.

4. Hallucinatory excitation - a live reaction of the patient to the content of his own hallucinations.

The study of psychomotor is extremely important for psychiatry and neurology. The patient's movements, his postures, gestures, manners are regarded as very significant signs for a correct diagnosis.


GRODNO STATE MEDICAL INSTITUTE

DEPARTMENT OF NEUROLOGY

LECTURE

Topic: SYNDROMES OF MOTOR DISORDERS.

PERIPHERAL AND CENTRAL PARALLY.


learning goal . Consider the issues of organization of movements in the process of evolution of the nervous system, anatomy, physiology and topical diagnosis of movement disorders.

1
Lecture content (2). 1. Evolution of the nervous system, definition and types of movement disorders. 2. Peripheral movement disorders. 3. Syndromes of central movement disorders. 4. Differential diagnosis of paralysis.

Grodno, 1997

Motion- one of the main manifestations of life, both in the most primitive creature and in a highly organized organism, which is a person. To understand the complex motor functions of a person, it is necessary to briefly recall those stages of development that the nervous system went through in the process of evolution from the simplest forms to the most differentiated form in humans.

A primitive being lacks differentiation into a receptor apparatus that perceives irritation and an effector apparatus that reacts. With the advent of the ganglion cell, it becomes possible to transmit information from the receptor organ to the muscle cell. At the initial stage of development of the central nervous system, the independence of the nervous apparatuses in its separate segments continues to exist, each of which, basically, refers to a certain metamer of the body. The ventrally located motor cell, which subsequently develops into the cell of the anterior horn, is initially connected only with the peripheral centripetal, receptor, and effector terminal apparatus of the same one segment.

The next stage of development is the emergence of intersegmental connections of the motor cell of the anterior horn with the receptor apparatus of not only adjacent, but also distant segments of the spinal cord, which in turn leads to a complication of the motor function. As the brain develops further, pathways are added that serve to regulate the function of the motor cells of the anterior horn from the higher parts of the nervous system. Thus, the organ of vision exerts a regulatory influence on the motor cell of the anterior horn through the tractus tecto-spinalis, the organ of balance through the tractus vestibulo-spinalis, the cerebellum through the tractus rubro-spinalis and subcortical formations through the tractus reticulo-spinalis. Thus, the cell of the anterior horn is influenced by a number of systems important for movements and muscle tone, connected, on the one hand, with the entire musculature, and, on the other hand, through the thalamus and reticular substance with all receptor apparatuses.

In the course of further phylogenetic development, the most important path arises - tractus cortico-spinalis pyramidal, which originates mainly in the anterior central gyrus of the cerebral cortex and, in contrast to the paths listed above, which contribute to the implementation of large mass movements, conducts impulses to the cells of the anterior horns for the most differentiated, voluntary movements.

Consequently, the cell of the anterior horn is, as it were, a pool into which many irritations flow, but from which only one stream of impulses flows to the muscle - this is the final motor path. The cells of the anterior horns of the spinal cord in the brainstem correspond to the cells of the nuclei of the motor cranial nerves.

It becomes obvious that these motor disorders are fundamentally different depending on whether the final motor pathway or any of the pathways that regulate it is affected.

Movement disorders can be divided into the following types:


  • paralysis due to damage to the bulbar or spinal motor neurons;

  • paralysis due to damage to the cortico-spinal, cortico-bulbar or stem descending (subcortico-spinal) neurons;

  • coordination disorders (ataxia) as a result of lesions of the afferent and efferent fibers of the cerebellar system;

  • violations of movements and body position due to damage to the extrapyramidal system;

  • apraxia or non-paralytic disorders of purposeful movements due to damage to certain areas of the brain.
This lecture discusses objective and subjective symptoms that develop as a result of damage to peripheral motor neurons, cortico-spinal and other conduction systems of the brain and spinal cord.

Definitions of movement disorders.
In everyday medical practice, the following terminology is used to characterize movement disorders:


  • paralysis (plegia) - the complete absence of active movements, due to the interruption of one or more motor pathways from the brain to the muscle fiber;

  • paresis - limitation of active movements due to a decrease in muscle strength.
In addition to weakness, an important functional disadvantage is loss of fluidity of movement.

Peripheral movement disorders.
Peripheral motor neuron palsy is caused by physiological blockade or destruction of anterior horn cells or their axons in the anterior roots and nerves. The main clinical signs of damage to the peripheral motor neuron are:


  • hypo - areflexia - loss of tendon reflexes;

  • hypo - atony - lethargy and a drop in the tone of the affected muscles;

  • degenerative atrophy, muscular (qualitative-quantitative), 70-80% of the total muscle mass;

  • both muscle groups and individual muscles are affected;

  • plantar reflex, if called, then normal, flexion type;

  • fasciculations, with electromyography, a decrease in the number of motor units, fibrillation.
Objective and subjective symptoms of damage to the peripheral motor neuron vary depending on the localization of the pathological process. . The topical diagnosis is formed on the basis of knowledge of the symptoms characteristic of the defeat of various parts of the peripheral motor neuron (anterior horns of the spinal cord - motor roots - nerves).

Syndromes of lesions of the anterior horns. Characterized by the presence of movement disorders of the peripheral type without sensory disturbances. There are paralysis of the muscles innervated by different nerves. Particularly typical is the asymmetrical distribution of paralysis. With an unfinished pathological process, fibrillations are possible with corresponding changes in the EMG. The defeat of the anterior horn cells rarely captures the entire length of the spinal cord. Usually the process is limited to one area or another, often characteristic of individual forms of the disease.

The syndrome of damage to the cells of the anterior horns of the spinal cord is the leading one in the clinic poliomyelitis, one of the severe and already common diseases of childhood. This is an acute viral infection, the causative agent of which has a significant affinity for the cells of the anterior horns of the spinal cord and the motor nuclei of the trunk. After a relatively short acute general infectious period, peripheral paralysis develops, which at first are more widespread, and then concentrate in limited segments, where destructive changes in the cells of the anterior horns are especially strong.

Dispersed localization of the process at different levels is characteristic. Often it is limited to one side and touches some of the muscles belonging to the same spinal segment. The distal ends of the limbs are affected less frequently. Much more often, paralysis is localized in the proximal sections: on the arms - in the deltoid muscle, in the muscles of the shoulder, on the legs - in the quadriceps, in the muscles of the pelvic girdle. With poliomyelitis, not only the muscles atrophy, but also the growth of the bones of the corresponding affected limb is disturbed. Persistent areflexia is characteristic, corresponding to the affected segments.

Damage to the cells of the anterior horns of the spinal cord with localization in the cervical region is characteristic of another neuroviral infection - spring-summer tick-borne encephalitis. The disease occurs in the spring and summer months and develops acutely 10-15 days after the tick bite. Against the background of general infectious symptoms of the disease, already in the first days one can note the appearance of paralysis, initially common, involving the arms and shoulder girdle, later usually limited to the muscles of the neck, shoulder girdle and proximal parts of the arms. Atrophies develop early, often with fibrillar twitches. Paralysis of the muscles of the legs and trunk are rare.

Anterior horn syndrome is the main clinical sign spinal amyotrophy of Werdnig-Hoffmann . The disease belongs to the group of hereditary. The first symptoms appear in the second half of life. Flaccid paresis is initially localized in the legs, then quickly spread to the muscles of the trunk and arms. Muscle tone and tendon reflexes fade. Typical fasciculations, fibrillation of the tongue with the development of bulbar palsy. Lethal outcome by 14-15 years.

The syndrome of damage to the anterior horns is included in the picture of the disease, which is not limited to the peripheral neuron, but also extends to the central motor neuron - to the pyramidal pathway. A clinical picture emerges amyotrophic lateral sclerosis , characterized by amyotrophy and pyramidal symptoms, followed by the development of bulbar palsy.

In some cases, anterior horn syndrome is part of the clinical picture of diseases such as syringomyelia, intramedullary tumor of the spinal cord.

Syndromes of damage to the anterior roots. Diseases of the anterior roots are characterized by atrophic paralysis, which is difficult to distinguish from paralysis in the defeat of the cells of the anterior horns of the spinal cord. It should be especially noted that these purely radicular atrophies are never accompanied by fibrillar twitches. In this case, coarser fascicular twitching of the muscles can be observed. Since the anterior roots are usually affected as a result of disease of the membranes of the spinal cord or vertebrae, along with the syndrome of the anterior roots, symptoms from the posterior roots, spine and spinal cord are almost always present.

Plexus syndromes. The anterior and posterior roots of the spinal cord, having joined in the intervertebral foramen, form the spinal nerve, which, upon exiting the spine, divides into the anterior and posterior branches. The posterior branches of the spinal nerves are sent to the skin and muscles of the neck and back. The anterior branches, anastomosing with each other, form plexuses in the cervical and lumbosacral regions.

Cervical plexus syndrome (C1-C4) is characterized by paralysis of the deep cervical muscles in combination with paralysis or symptoms of irritation of the phrenic nerve. It occurs with tumors, enlarged lymph nodes, purulent and other processes in the upper cervical vertebrae, lung cancer, aortic and subclavian artery aneurysms. Brachial plexus syndromes are manifested in a combination of paralysis of individual muscles related to different nerves. When the entire brachial plexus is affected due to a dislocation of the shoulder or a fracture of the clavicle, a gunshot wound or a birth injury, all the muscles of both the shoulder girdle and the upper limb are affected.

According to the topographic division of the plexus into two parts, two main forms of brachial plexus paralysis are clinically distinguished upper (Erba-Duchene) And lower (Dejerine-Klumpke ). The upper type of plexus paralysis develops when a certain area above the collarbone is damaged to the finger outward from the sternocleidomastoid muscle (Erb's point), where the 5th and 6th cervical nerves connect to form a plexus. At the same time, raising and abducting the arm, bending at the elbow is impossible. With lower paralysis, which is much less common than the upper one, the small muscles of the hand, individual muscles of the palmar surface of the forearm suffer.

The syndrome of the lumbosacral plexus is manifested by symptoms of damage from the femoral and sciatic nerves. Etiological factors are tumors and fractures of the pelvis, abscesses, enlarged retroperitoneal nodes.

Syndromes of central movement disorders.
Central paralysis occurs as a result of damage to the cortico-spinal, cortico-bulbar and subcortico-spinal neurons. The corticospinal tract originates from the giant and small Betz cells of the anterior central gyrus, the premotor zone of the superior frontal and postcentral gyri and is the only direct connection between the brain and the spinal cord. Fibers to cranial nerve nuclei separate at the level of the midbrain, where they cross the midline and travel contralaterally to the corresponding nuclei in the brainstem. The intersection of the cortico-spinal tract is carried out at the border of the medulla oblongata and spinal cord. Two-thirds of the pyramidal path intersect. Subsequently, the fibers are directed to the motor cells of the anterior horns of the spinal cord. Central paralysis occurs when the cerebral cortex, subcortical white matter, internal capsule, brainstem, or spinal cord is affected and is characterized by the following common clinical features:


  • increased muscle tone by the type of spasticity (the "jackknife" phenomenon);

  • hyperreflexia of deep and areflexia of superficial reflexes;

  • moderate muscle atrophy of a quantitative type (from inactivity);

  • pathological symptoms of extensor (s-m Babinsky) and flexion (s-m Rossolimo) type;

  • increased protective reflexes;

  • the presence of pathological synkinesis (friendly movements);
If the cortico-spinal tracts are damaged in humans, the distribution of paralysis will be different depending on the location of the focus and the nature of the pathological process (acute, chronic). So for the defeat of the anterior central gyrus, focal epileptic seizures and central paresis or paralysis of one limb on the opposite side are characteristic; for the subcortical process - contralateral hemiparesis with a predominance in the arm or leg; for the internal capsule - hemiplegia with subsequent outcome in the Wernicke-Mann position; for the brain stem - hemiplegia with damage to the nuclei of the cranial nerves (alternating syndromes) and for the spinal cord - hemi-monoparesis - plegia (depending on the level of the lesion). The severity of movement disorders in each case varies widely and depends on many reasons.

Bilateral prolapse of the cortico-bulbar function. paths (from the cortex to the nuclei of the cranial nerves) gives a picture of _pseudobulbar paralysis with a disorder of chewing, swallowing, with dysarthria (speech impairment due to paralysis of the muscles involved in articulation). At the same time, the face is ammimic, the mouth is half open, saliva flows from it. Unlike bulbar palsy, chewing muscles and muscles of the tongue are not atrophic, there are no fibrillar twitches. All tendon reflexes of the face are increased. Characterized by violent laughter and crying. Pseudobulbar paralysis is caused by bilateral hemispheric lesions, often developing at different times. The combination of pseudobulbar palsy with tetraplegia can occur when the base of the pons is damaged.

Damage to the central neuron of the motor pathway occurs in many diseases of the brain and spinal cord, in particular, in various types of vascular pathology (strokes), multiple sclerosis, amyotrophic lateral sclerosis, trauma, tumors, abscesses, encephalitis.

Differential diagnosis of paralysis.

When diagnosing paralysis, the localization and distribution of muscle weakness should be taken into account. A diagnostic sign may have the presence or absence of atrophy of the muscles of the paretic limb.

Monoplegia. It must be remembered that this prolonged immobility of the limb can lead to its atrophy. However, in this case, atrophy usually does not reach such a degree of severity, as it happens with diseases that lead to muscle denervation. Tendon reflexes do not change. Electrical excitability and EMG deviate little from the norm.

The most common cause of monoplegia without a decrease in muscle mass is damage to the cerebral cortex. With damage to the cortico-spinal tract at the level of the capsule, trunk and spinal cord, monoplegia syndrome rarely occurs, since the fibers leading to the upper and lower limbs are compactly located in these sections. The most common cause of monoplegia is damage to the vessels of the cerebral cortex. In addition, some injuries, tumors, abscesses can cause similar symptoms. Weakness in one limb, especially in the lower one, can develop with multiple sclerosis and spinal tumors, especially in the early stages of the disease.

Paralysis, accompanied by muscle atrophy, is characteristic of a pathological process in the spinal cord, roots or peripheral nerves. The level of damage can be determined by the nature of the distribution of weakness in the muscles, as well as using additional paraclinical diagnostic methods (CT, NMR, and others). Shoulder atrophic monoplegia can occur with brachial plexus injury, poliomyelitis, syringomyelia, amyotrophic lateral sclerosis. Femoral monoplegia is more common and may be due to damage to the thoracic and lumbar spinal cord in trauma, tumors, myelitis, multiple sclerosis. Unilateral paralysis of the lower limb may be the result of compression of the lumbosacral plexus by a retroperitoneal tumor.

Hemiplegia. Most often, paralysis in humans is expressed in the appearance of unilateral weakness in the upper and lower limbs and half of the face. Localization of the lesion, as a rule, is established by the corresponding neurological manifestations. Among the causes of hemiplegia, lesions of the vessels of the brain and brain stem (strokes) predominate. Less significant causes include trauma (brain contusion, epidural and subdural hematomas, brain tumor, abscess, encephalitis, demyelinating diseases, complications after meningitis).

Paraplegia. Paralysis of both lower extremities can develop due to lesions of the spinal cord, spinal roots and peripheral nerves. As a rule, with acute injuries of the spinal cord, paralysis of all muscles below this level occurs. In the case of extensive damage to the white matter, sensitive disorders often occur below the level of the lesion, the function of the sphincters of the bladder and intestines is disturbed. Intermittent spinal block (dynamic block, protein elevation, or cytosis) often occurs. With an acute onset of the disease, difficulties sometimes arise in differential diagnosis from neural paralysis, since in any acute process, spinal shock can lead to complete areflexia.

The most common causes of acute paraplegia (or tetraplegia) are spontaneous hematomyelia in vascular malformations of the spinal cord, thrombosis of the anterior spinal artery with infarction, dissecting aortic aneurysm, occlusion of the spinal arteries with subsequent infarction (myelomalacia), spinal cord injury, and tumor metastases.

Subacute (rarely acute) development of paraplegia is observed in post-vaccination and post-infectious myelitis, acute demyelinating myelitis (Devic's disease), necrotizing myelitis, and epidural abscess with spinal cord compression.

Chronic paraplegia can develop with multiple sclerosis, spinal cord tumors, herniated disc of the cervical spine, chronic epidural infectious processes, familial spastic paraplegia, syringomyelia. A parasagittal meningioma can serve as a source of chronic asymmetric paraplegia.

Tetraplegia. Possible causes of tetraplegia are similar to those of paraplegia, except that this spinal cord lesion is most often located at the level of the cervical spinal cord.

Isolated paralysis. Paralysis of an isolated muscle group indicates damage to one or more peripheral nerves. Diagnosis of damage to a single peripheral nerve is based on the presence of weakness or paralysis of a muscle or muscle group and deterioration or loss of sensation in the area of ​​​​innervation of the nerve of interest. An EMG study is of great diagnostic value.

Violations and their causes in alphabetical order:

movement disorder

Movement disorders can occur both with central and peripheral damage to the nervous system. Movement disorders can occur both with central and peripheral damage to the nervous system.

Terminology
- Paralysis - a violation of the motor function that occurs due to the pathology of the innervation of the corresponding muscles and is characterized by the complete absence of voluntary movements.
- Paresis - a violation of the motor function that occurs due to the pathology of the innervation of the corresponding muscles and is characterized by a decrease in the strength and / or amplitude of voluntary movements.
- Monoplegia and monoparesis - paralysis or paresis of the muscles of one limb.
- Hemiplegia or hemiparesis - paralysis and paresis of both limbs, sometimes the face on one side of the body.
- Paraplegia (paraparesis) - paralysis (paresis) of both limbs (either upper or lower).
- Quadriplegia or quadriparesis (also tetraplegia, tetraparesis) - paralysis or paresis of all four limbs.
- Hypertonicity - increased muscle tone. There are 2 types:
- Muscle spasticity, or classic pyramidal paralysis, is an increase in muscle tone (mainly arm flexors and leg extensors), characterized by uneven resistance in various phases of passive movement; occurs when the pyramidal system is damaged
- Extrapyramidal rigidity - a diffuse uniform wax-like increase in muscle tone, equally pronounced in all phases of active and passive movements (muscle agonists and antagonists are affected), due to damage to the extrapyramidal system.
- Hypotension (muscle lethargy) - a decrease in muscle tone, characterized by their excessive compliance during passive movements; usually associated with damage to the peripheral motor neuron.
- Paratonia - the inability of some patients to completely relax the muscles, despite the instructions of the doctor. In milder cases, stiffness is observed with rapid passive movement of the limb and normal tone with slow movement.
- Areflexia - the absence of one or more reflexes, due to a violation of the integrity of the reflex arc or the inhibitory effect of the higher parts of the nervous system.
- Hyperreflexia - an increase in segmental reflexes due to a weakening of the inhibitory effects of the cerebral cortex on the segmental reflex apparatus; arises, for example, at defeat of pyramidal ways.
- Pathological reflexes - the general name of the reflexes found in an adult with damage to the pyramidal tracts (in young children, such reflexes are considered normal).
- Clonus - an extreme degree of increased tendon reflexes, manifested by a series of rapid rhythmic contractions of a muscle or muscle group, for example, in response to a single stretch.

The most common form of movement disorders are paralysis and paresis - loss or weakening of movements due to impaired motor function of the nervous system. Paralysis of the muscles of one half of the body is called hemiplegia, both upper or lower limbs - paraplegia, all limbs - tetraplegia. Depending on the pathogenesis of paralysis, the tone of the affected muscles can either be lost (flaccid paralysis) or increased (spastic paralysis). In addition, peripheral paralysis (if it is associated with damage to the peripheral motor neuron) and central (as a result of damage to the central motor neurons) are distinguished.

What diseases cause movement disorders:

Causes of movement disorders
- Spasticity - damage to the central motor neuron throughout its entire length (cerebral cortex, subcortical formations, stem part of the brain, spinal cord), for example, in a stroke involving the motor zone of the cerebral cortex or the corticospinal tract
- Rigidity - indicates dysfunction of the extrapyramidal system and is caused by damage to the basal ganglia: the medial part of the pale ball and black substance (for example, with parkinsonism)
- Hypotension occurs in primary muscle diseases, cerebellar lesions and some extrapyramidal disorders (Huntington's disease), as well as in the acute stage of pyramidal syndrome
- The phenomenon of paratonia is characteristic of lesions of the frontal lobe or diffuse cortical lesions
- Coordination of motor activity may be impaired due to muscle weakness, sensory disorders or damage to the cerebellum
- Reflexes decrease with damage to the lower motor neuron (cells of the anterior horns, spinal roots, motor nerves) and increase with damage to the upper motor neuron (at any level above the anterior horns, with the exception of the basal ganglia).

Which doctors should I contact if there is a movement disorder:

Have you noticed a movement disorder? Do you want to know more detailed information or do you need an inspection? You can book an appointment with a doctor– clinic Eurolaboratory always at your service! The best doctors will examine you, study the external signs and help identify the disease by symptoms, advise you and provide the necessary assistance. you also can call a doctor at home. Clinic Eurolaboratory open for you around the clock.

How to contact the clinic:
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(+38 044) 206-20-00


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