Attacks of immobility or "congealing". Causes and Symptoms
Last reviewed: 26.11.2021
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The states of permanent or periodic immobility, "congealing", akinesia, aspontaneity, areactivity of different origin refer to the so-called negative neurological symptoms. Their pathogenesis, etiology and clinical classification have not yet been fully systematized. They can have subcortical (extrapyramidal), frontal (motivational), stem (akinetic), cortical (epileptic), neuromuscular (synaptic) origin. Finally, the condition of immobility can be a manifestation of psychotic disorders or conversion disorders. All these diseases, as a rule, are manifested by other characteristic clinical symptoms and paraclinic abnormalities in EEG, MRI, electrolyte metabolism, glucose metabolism, neuropsychological tests, and (in the first place) in the corresponding changes in the neurological and mental status. Analysis of clinical manifestations has priority in most of these cases.
The main clinical forms of immobility or "hardening":
A. Frizing episodes (freezing, motor block, solidification).
- Parkinson's disease.
- Multiple system atrophy.
- Normotensive hydrocephalus.
- Dyscirculatory (chronic ischemic) encephalopathy.
- Primary progressive frisiting-dysbasia.
B. Epilepsy.
C. Cataplexy.
D. Catalepsy (in the picture of mental illness)
E. Psychogenic areactivity.
F. Attacks of immobility in hypoglycemia (diabetes mellitus).
G. Paroxysmal myoplegia.
- Hereditary periodic paralysis.
- Symptomatic periodic paralysis (thyrotoxicosis, hyperaldosteronism, gastrointestinal tract diseases leading to hypokalemia, hypercorticism, hereditary hyperplasia of the adrenal glands, excessive secretion of the antidiuretic hormone, kidney diseases, iatrogenic forms of mineralocorticoids, glucocorticoids, diuretics, antibiotics, thyroid hormones, salicylates, laxatives) .
A. Frizing episodes (freezing, motor blocks, congealing)
Parkinson's disease belongs to the most common diseases, in the clinical manifestations of which often occurs frisiting episodes. Episodes of solidification often develop during the "offw-period, that is, the period of" shutdown "(but can also be observed in the" on "-period). Most clearly they are manifested in walking. Patients begin to experience difficulties when trying to start moving ("a symptom sticking to the floor of the legs"). It is difficult for the patient to take the first step; he as though can not choose a leg with which it is necessary to begin movement. A characteristic marking on the spot develops. In this case, the center of gravity of the body begins to move forward in the direction of movement, and the legs continue to often trample in place, which can cause the patient to fall even before the movement begins. Another situation, in which frisbings are often found, are associated with turns, the torso during walking. Turning the torso during walking is a typical risk factor for the fall of the patient. A narrow space, such as a door on the path of a patient, can provoke congestion. Sometimes frisiting comes spontaneously without external provoking moments. The appearance of freezing episodes increases the risk of falls in the patient. The presence of motor blocks is usually accompanied by deterioration of postural reflexes, aggravation of dysbasia. Physiological synergies are lost, instability develops in walking and standing, it is difficult for patients to prevent falls. Friction can affect any motor function, including a variety of movements during self-service (the patient literally freezes during any action), as well as walking (sudden stops), speech (there is a long incubation period between the doctor's question and the patient's response) and a letter. The presence of concomitant clinical manifestations of parkinsonism (hypokinesia, tremor, postural disorders) complement the typical picture of the external appearance of the patient with Parkinsonism.
The diagnosis is made clinically. The frequency of frizzing episodes correlates with the duration of the disease and the duration of treatment with prefacial preparations.
Multiple systemic atrophy (MCA) can also manifest itself, among other typical syndromes (cerebellar ataxia, progressive vegetative failure, Parkinsonism syndrome), and frizzing episodes, the pathogenesis of which appears to be also associated with progressive Parkinson syndrome within the ISA framework.
Normotensive hydrocephalus, in addition to dementia and urinary incontinence, also manifests a disruption to the gait (Hakim-Adams triad). The latter were called apraksii walk. The inconsistency of steps is revealed, discoordination between the movements of legs and trunk, disruptive, unstable, uneven and unbalanced walking. The patient walks insecurely, with noticeable caution and slower compared to a healthy person. Perhaps the emergence of frisiting episodes. A patient with a normotensive hydrocephalus may externally resemble a patient with Parkinson's syndrome, which often serves as a reason for a diagnostic error. But it is useful to remember that there are rare cases of the development of true parkinsonism in the syndrome of normotensive hydrocephalus, in which, the more fris- ing episodes can be observed.
Etiology of normotensive hydrocephalus: idiopathic; consequences of subarachnoid hemorrhage, meningitis, craniocerebral trauma with subarachnoid hemorrhage, operation on the brain with bleeding.
Differential diagnosis of normotensive hydrocephalus is carried out with Alzheimer's disease, Parkinson's disease, Huntington's chorea, and multi-infarct dementia.
To confirm the diagnosis of normotensive hydrocephalus resort to CT, less often - to ventriculography. A test is proposed with an assessment of cognitive functions and dysbasia before and after the extraction of the cerebrospinal fluid. This test also allows patients to be selected for a bypass operation.
Dyscirculatory encephalopathy, especially in the form of a multi-infarction state, is manifested by diverse motor disorders in the form of bilateral pyramidal (and extrapyramidal) signs, reflexes of oral automatism and other neurological and psychopathological disorders. In the lacunar state, there may also be a gait like "marche a petits pas" (small short irregular shuffling steps) against the background of pseudobulbar paralysis with swallowing disorders, verbal disorders and parkinsonian-like motility. There may also be episodes of congealing during walking. These neurologic manifestations are supported by an appropriate picture of CT or MRI, reflecting a multifocal or diffuse lesion of the brain tissue of vascular origin.
The primary progressive frisbling-dysbasia is described as an isolated single symptom in the elderly (60-80 years and older). The degree of violations by the type of friction gait varies from individual motor blocks with external obstacles to severe disabilities with a complete inability to begin walking and requiring significant outside support. Neurological status usually does not show abnormalities, except for the often revealed postural instability of one degree or another. There are no symptoms of hypokinesia, tremor and rigidity. Analyzes of blood and cerebrospinal fluid show no abnormalities. CT or MRI is normal or exhibits mild cortical atrophy. Therapy with levodopa or dopamine agonists does not bring relief to patients. Gait disorders progress without affiliation with any other neurologic symptoms.
B. Epilepsy
Epilepsy with fits of "hardening" is typical for small seizures (absences). Isolated absences are observed exclusively in children. Similar seizures in adults should always be differentiated with pseudoabsances in temporal epilepsy. A simple typical absense is clinically expressed in a sudden onset of a very brief (a few seconds) deenergia. The child interrupts the started speech, reading the verse, writing, moving, communicating. The eyes "stop", the expression is frozen. General motor skills "freezes". With simple absences on the EEG, symmetrical peak-wave complexes with a frequency of 3 per second are detected. All other forms of absences with other clinical "additives" or other EEG-support are referred to atypical ab-sans. The end of the seizure occurs instantly, leaving no indisposition or stunning. Children often continue the action begun before seizure (reading, writing, playing, etc.).
C. Cataplexy
Cataplexy in narcolepsy is manifested by attacks of sudden loss of muscle tone, which is provoked by emotions (laughter, joy, less often - surprise, fear, resentment, etc.), less often - intense physical exertion. Partial attacks of cataplexy are more common, when loss of tonus and weakness are observed only in some muscles: the head descends forward, the lower jaw is lowered, speech is upset, knees are bent, objects fall out of hands. At the generalized attacks there comes full immobility, the patient quite often falls. There is a decrease in muscle tone and the disappearance of tendon reflexes.
D. Catalepsy
For catalepsy (in the picture of mental illness with catatonic syndrome), the phenomenon of "waxy flexibility", given unusual "frozen postures", "strange motor skills" is characteristic of coarse mental disorders in the picture of schizophrenia (DSM-IV). Catatonia is a syndrome that rarely has a neurological origin: it is described in the case of non-convulsive forms of epileptic status (ictal catatonia), and also with some gross organic lesions of the brain (brain tumor, diabetic ketoacidosis, hepatic encephalopathy), which, however, refinement. Much more often catatonic stupor develops in the picture of schizophrenia.
E. Psychogenic Areactivity
Psychogenic areaktivnost in the form of seizures can sometimes be observed in the picture of pseudo-fits simulating an epileptic attack or fainting (pseudo-syncope) or proceeding entirely in the form of immobility and mutism (conversion hysteria). Here, the principles of clinical diagnosis that are used to diagnose psychogenic paralysis, seizures and hyperkinesis.
F. Attacks of immobility in hypoglycemia (diabetes mellitus)
Can be observed as an option for reversible hypoglycemic coma.
G. Paroxysmal myoplegia
Depressive stupor in the picture of severe psychotic depression usually does not have the nature of an attack, but proceeds more or less permanently.
Conditions that resemble short "congestion" or "fading" can sometimes be observed in the syndrome of hyperexplexia (see section "Starter syndrome").
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