From Big Medical Encyclopedia

APALLICHESKY SYNDROME (grech, and - otritsa. + lat. pallium cover, raincoat; annate. — a raincoat of a great brain) — the symptom complex combining the mental and neurologic disorders resulting from switching off of a cerebral cortex — a decortication. It is described in 1940 by E. Kretschmer.

Similar states were described also under other names: «an akinetic mutism» [Keyrns (N. Cairns), 1941], «a posttraumatic catatonia» [Zutter (J. M of Sutter), 1959], «a lyutsidny stupor» [J. Ajuriaguerra, 1954].

Clinical picture. At Ampere-second. the patient is in the awake state, lies with open eyes, but does not fix surrounding objects, on the address, the call, touch and optical irritants does not react; it is impossible to draw attention of the patient, emotional reactions are absent; it is not capable to tell or perform purposeful operations. For Ampere-second. a peculiar dissociation is characteristic — without actually stupefaction, at its relative clarity, entirely there are no mental acts making the maintenance of consciousness. Reflex defense reactions are absent; extremities of the patient can stiffen in the situation which is passively given them. Reactions to pain stimulations happen raised and irradiating, are expressed by twitchings or the chaotic movements. Swallowing is, as a rule, kept.

Ampere-second. often is followed primitive, in particular oral and prehensile, by avtomatizm and reflexes. These motive phenomena — «motor templates» (on Krechmera) — are shown at the beginning of a disease of more difficult exteroceptive avtomatizm (e.g., dehiscence of a mouth, protrusion of language or the prehensile movements at approach of a subject), then, during the deepening of process, reflexes appear more primitive proprioceptive (sucking and prehensile). Depending on character of a basic disease other neurologic frustration are observed: parkinsonism, various, is more often horeoformny, hyperkinesias, sometimes spastic paresis and oculomotor frustration.

Etiology and pathogeny. At the heart of Ampere-second. the progressing atrophic diseases of senile and presenile age at which Ampere-second lie. there can be in a final stage, and various acute diseases of a brain — an injury, hemorrhage, a tumor, inflammatory processes (encephalitis), intoxications (in particular, lighting gas), etc. The main pathogenetic mechanism causing development of Ampere-second., consists in switching off of activity of a cerebral cortex and dominance of trunk mechanisms.

Diagnosis and differential diagnosis. Ampere-second. it is necessary to differentiate with a coma, unlike a cut at Ampere-second. there is no deep stupefaction, and change of a dream and wakefulness can be not broken; with dementia, for a cut full switching off (blockade) of cortical functions is not characteristic, and gradual, first of all quantitative, decrease in level of mental activity or loss of separate mental functions is observed.

Forecast depends on character of the caused Ampere-second. pathological process. Ampere-second. can be manifestation of an end-stage of a disease or is a transitional syndrome (see. Symptomatic psychoses ) with a regreduated current. At atrophic processes the forecast is adverse: Ampere-second. passes into a condition of a cerebrate rigidity, and then into an agonal state. At other etiology of Ampere-second., in particular at the most often observed Ampere-second. after an injury, escaping it in a chronic psychoorganic syndrome is possible gradual (within several months) or is (much more rare) in practical recovery.

Treatment it is directed to the disease which caused Ampere-second. At traumatic Ampere-second. resort to resuscitation.

Bibliography: Ajuriaguerra J., Hecaen H. et Sadoun R. Les troubles mentaux au cours de tumeurs de la rägion mäso-dienc6phalique, Enc£phale, t. 43, p. 406, 1954; Gerstenbrand F. Das traumatische apallische Syndrom, Wien — N. Y., 1967, Bibliogr.; Kretschmer E. Das apallische Syndrom, Z. ges. Neurol. Psychiat., Bd 169, S. 576, 1940; Sutter J. M. e. a. La catatonie post-traumatique, Rev. neurol., t. 101, p. 524, 1959.

E. Ya. Shternberg.