[Disorders of consciousness as a manifestation of neurologic disease]

Seventy-nine patients admitted in the neurological Intensive care unit because of severe disturbances of consciousness has been evaluated. Protocol based on previous experiences in evaluation of unconsciousness patients was used. Forty-four patients died and thirty-five survived. In 46 patients cause of illness was intracerebral hemorrhage. In 44 of them the cause of hemorrhage was arterial hypertension and in two of them rupture of a-v malformation. The majority of patients actually 41 of them showed hemispheral localization of intracerebral hematoma and five subtentorial. Pontien hemorrhages was found in three and cerebellar in two patients. In majority of 24 patients with hemispheral localization of intracerebral hematoma who showed progressive deterioration of consciousness the signs of descendent transtentorial herniation were found. The symptoms of uncal herniation were rare. In three patients with subtentorial localization of intracerebral hematoma who died signs of upward transtentorial herniation were observed. In 16 patients with ischemic cerebrovascular accident who showed disturbances of the consciousness at the admittance or soon after, nine patients died and seven survived. The cause of their condition were great hemispheral, smaller brain stem ischemic lesion, or deterioration of consciousness was related to the somatic illness. Patients with great ischemic lesions showed similar course of consciousness deterioration as it was observed in patients with hemispherical intracerebral hematomas with difference that biphasic course of illness characterized with temporary stagnation or even slight improvement of patients condition and than secondary progression of deterioration was seen only in patients with intracerebral hematoma, probably because of secondary ischemic complications. Ten patients were admitted because of subarachnoidal and two of them because of intraventricular hemorrhage. Six of them died and four survived. These patients has rupture of great sacular aneurysm with fast development of high intracranial pressure. In two of them the cause of death was rerupture of aneurysm. Stuporous patient with hemispheral neoplasm showed development of descendent transtentorial herniation which was stopped by anti oedematous and corticosteroid therapy. Comatose patient with brisk response on oculocephalic stimulation and normal papillary light reflexes was suspected on intoxication rather than structural brain lesion. He recovered by diuretics and forced rehydratation. After becoming conscious barbiturate intoxication was confirmed. Three patients were admitted in coma because of poisoning with CO, two patients died. Two patients admitted in epileptic status showed late diencephalic state of coma and they survived after anti epileptics and antioedematous treatment.