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Epidemic lethargic encephalitis Economo

Economic epidemic lethargic encephalitis (synonym: epidemic encephalitis type A, "sleeping" disease) was first recorded in 1915 by the troops near Verdun and described in 1917 by the Austrian neuropathologist K. Economo. The disease in those years proceeded in the form of epidemics that swept many countries of the world. In subsequent years, the disease manifested itself sporadically. Currently, the disease in a typical form is almost not found. The causative agent of epidemic encephalitis is not specified. The disease is slightly contagious.

Clinically and pathomorphologically, epidemic encephalitis can be divided into two stages: acute and chronic. The acute stage is characterized by symptoms and inflammatory phenomena. The chronic stage is characterized by progressively degenerative processes. The acute and chronic stages of epidemic encephalitis are separated by a period of time from several months to 5-10 years.

Pathomorphology. Epidemic encephalitis is characterized by damage to the basal nuclei and brain stem. Mostly cellular elements suffer. Microscopy reveals pronounced inflammatory changes: perivascular infiltration with mononuclear cells and plasma cells in the form of couplings, significant proliferation of microglia, sometimes with the formation of glial nodules. In the chronic stage, the most pronounced changes are localized in the black matter and pale sphere. In these formations, irreversible dystrophic changes in ganglion cells are noted. In place of dead cells, gliotic scars form.

Clinical manifestations. The classical form of epidemic encephalitis in the acute stage begins with a rise in temperature to 38–39 ° С. Mild headache, vomiting, muscle pain, a feeling of general weakness and other symptoms accompanying acute infectious diseases appear. Symptoms of upper respiratory tract damage are possible. The febrile period lasts an average of about 2 weeks. During this period, neurological symptoms appear, which can be very diverse. In the foreground are sleep pathognomonic for this disease, expressed in pathological drowsiness. The patient can be woken up, but he immediately falls asleep again, and in any position and situation not suitable for sleep. Excessive, irresistible sleep can last for 2-3 weeks, and sometimes more. Somewhat less often with epidemic encephalitis, pathological insomnia is observed, when the patient can not fall asleep either day or night. Perhaps a distortion of the normal shift of sleep and wakefulness: the patient sleeps during the day and does not fall asleep at night. Insomnia often replaces the period of pathological drowsiness or precedes it.

The second characteristic sign of the acute stage of epidemic encephalitis is the defeat of large- and small-cell nuclei of the oculomotor, less often abducent nerves. A feature of the disease is that the oculomotor nerve is never involved in the whole process: the function of individual muscles innervated by this nerve is impaired. Patients may have ptosis (single or double-sided), diplopia, anisocoria, paralysis of the gaze (usually vertical), lack of pupil reaction to convergence and accommodation during a live reaction to light (reverse Argyll Robertson syndrome). There are frequent complaints of visual impairment due to paresis of accommodation or diplopia.

Sleep disorders and oculomotor disorders constitute the classic manifestations of epidemic encephalitis described by K.Ekonomo. However, other neurological manifestations may occur in the acute stage of epidemic encephalitis. A little less often than oculomotor disorders, vestibular disorders are observed in the form of dizziness, accompanied by nausea and vomiting. In the neurological status, horizontal and rotatory nystagmus, dizziness, which are the result of damage to the nuclei of the vestibular nerve, are often detected. Often there are vegetative symptoms: hypersalivation, hyperhidrosis, overproduction of the secretion of the sebaceous glands, lability of vasomotor reactions.

Extrapyramidal symptoms characteristic of the chronic stage of epidemic encephalitis are often noted in the acute stage. It can be manifested by hyperkinesis (choreoathetosis, myoclonus, athetosis, blepharospasm. Cramp of the eye), somewhat less often - akinetic-rigid syndrome (akinesis, amimia, muscle rigidity, tendency to catatonia). The occurrence of thalamic, cerebellar and hydrocephalic syndromes, as well as hypothalamic disorders, is described. The acute stage may be accompanied by severe psychosensory disorders (changes in the perception of the shape and color of surrounding objects, visual, olfactory, auditory hallucinations). In severe cases of epidemic encephalitis, disorders of the frequency and rhythm of respiration, cardiovascular activity, respiratory muscle myoclonia, hyperthermia, and impaired consciousness (coma) occur. Possible death due to heart and respiratory failure.

In modern conditions, epidemic encephalitis is atypical, mainly abortive, simulating an acute respiratory infection. Against its background, short-term sleep disorders (drowsiness or insomnia), episodes of diplopia, autonomic dysfunction, hyperkinesis (tics in the muscles of the face and neck), mildly transient oculomotor disturbances can occur.
Allocate as independent vestibular, narcoleptic, epileptiform forms, epidemic hiccups, myoclonic diaphragm muscle cramp episodically occurring over several days).

In the cerebrospinal fluid in the acute stage of epidemic encephalitis, most patients have pleocytosis (mainly lymphocytic) - 40 cells in 1 μl, a slight increase in protein and glucose (glycorachia) - up to 0.5–1 g / l. Leukocytosis with an increase in the number of lymphocytes and eosinophils, an increase in ESR are detected in the blood. On the EEG, generalized changes are detected, slow activity is expressed.

The main clinical manifestation of the chronic stage of epidemic encephalitis is Parkinson's syndrome. Poverty and slowness of movements, amymia, monotonous, slurred, unexpressive speech, pro, latero- and retro-pulsion, a tendency to maintain a given posture, loss of friendly, individualizing motility movements (achherokinesis), paradoxical kinesias are characteristic. There is a loss of interest in the environment, a slowdown in mental processes, importunity. In these motor disorders, a significant role is played by tone disorders, which are usually diffusely increased in plastic type (extrapyramidal rigidity) in both the flexors and extensors, the phenomenon of the “gear wheel” is noted. Oligo– and bradykinesia are combined with characteristic rhythmic hyperkinesis in the form of finely spread tremors in the hands (of the “coin count” type). Hyperkinesis in the chronic stage of epidemic encephalitis can also manifest with blepharospasm, eye cramp (oculogyric crises). Secretory and vasomotor disorders (hypersalivation, skin grease, hyperhidrosis) are typical for parkinsonism.

In the chronic stage of epidemic encephalitis, along with parkinsonism syndrome, endocrine disorders in the form of adiposogenital dystrophy, infantilism, menstrual irregularities, obesity or cachexia, hyperthyroidism, and diabetes insipidus can develop. Usually appear and grow character changes, emotionally volitional sphere. Particularly pronounced changes in the psyche of children (increased eroticism, aggressiveness, antisocial behavior, painful pedantry, evening attacks of psychomotor agitation). Rarely in the chronic stage are epileptiform syndromes, attacks of pathological sleep (narcolepsy).

The course and forecast. The acute stage of epidemic encephalitis can last from 2–4 days to 4 months, sometimes ending with a full recovery. Fatal outcome is observed in 30% of cases. In 35–50% of patients, the acute stage becomes chronic either immediately or at different intervals. Often the symptoms inherent in the chronic stage occur without the previous clearly expressed acute stage. The residual symptoms and syndromes after the acute stage of epidemic encephalitis include headaches, persistent insomnia, distortion of the rhythm of sleep, asthenoneurotic syndrome, depression, lack of convergence, mild ptosis. In children, hypothalamic disorders (endocrine metabolic disorders), changes in the psyche and character, and a decrease in intelligence often remain.

The course of chronic epidemic encephalitis is long, progressive. Symptoms of parkinsonism are gradually increasing, although for some time the condition can stabilize. The prognosis for recovery is poor. Death usually occurs from intercurrent illness or exhaustion.

Diagnostics. The diagnosis of acute epidemic encephalitis is quite difficult and is infrequent. The diagnosis is based on various forms of sleep disturbance in combination with psychosensory disorders and symptoms of a nuclear lesion of the oculomotor nerves. Especially important is the appearance of these symptoms amid a fever and an unclear infectious disease.

The acute stage of epidemic encephalitis should be differentiated from serous meningitis, in which neck muscles are usually stiff, a symptom of Kernig and there is significant pleioitosis in the cerebrospinal fluid.

Diagnosis of the chronic stage of epidemic encephalitis is less difficult. The diagnosis is based on the presence of a characteristic parkinsonism syndrome, endocrine disorders of central genesis, mental changes, the progressive nature of these disorders, especially in combination with some residual acute stages (ptosis, lack of convergence and accommodation). However, Parkinson's syndrome and hypothalamic disorders can develop after an injury and in other processes localized in the subcortical formations (tumor, Parkinson's disease). In these cases, the history data are of great importance for diagnosis: pronounced manifestations of the acute period or erased episodic symptoms of the acute stage against the background of fever and other signs of an unclear infectious disease.
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Epidemic lethargic encephalitis Economo

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