The Effect of THIOPENTAL and MANNITOL of Acute Intracranial Hypertension in Severe Head Injury and the Other Comatous Patients

Laboratory and clinical evidence indicates a potentially important role for barbiturates in the management of brain injury and intracranial hypertension. The present report describes our experience with the thiopental and mannitol therapy in 30 consecutive patients who were over 20mmHg of intracranial pressure(ICP) in severe head injuries and the other comatous conditions. The anothers have analyzed the effects of thiopental on outcome in comatous 30 patients by continuous monitoring of ICP. High dose barbiturate therapy was induced with an intravenous bolus of thiopental, 40mg/kg and the infusion of barbiturates intermittently continued until control of the ICP(below 20mmHg) was obtained. In those patients responding to thiopental, the daily mannitol requirement was reduced from 3.5 to 0.5mg/kg/day. Our overall results are presented; 1) In patients with intracranial mass lesions only very high ICP(>40mmHg) on barbiturate management was significantly associated with a poor neurological deficit and outcome from injury, while the patients with any increased in ICP above 20 to 29mmHg was associated with a moderate neurological disability and better outcome with thiopental and mannitol treatment. 2) In patients with surgical mass lesion ICP between 20 to 29mmHg was significantly associated good neurological picture and outcome, but the patients in ICP above 40mmHg, had a 75% motality. 3) Decreases in ICP over 20mmHg were seen in 75%of the patient who had managed with thiopental and mannitol. 4) Thiopental responders have returned to a good recovered and minimal deficit, but thiopental nonresponsiveness was associated with a completely unfavorable outcome:5 deaths, 1 vegetative survior.

Two Cases of Infantile Hydranencephaly

The term hydranencephaly designates the condition in which large protions of the cerebral hemispheres have been reduced to membranous sacs within a cranium of relatively normal size. Only basal ganglia and remnants of the mesencephalon are found at the base of the skull. We have experienced the 2 cases of infantile hydranencephaly. In surveying the pathogenesis of the hydranencephaly, it becomes apparent that the distribution of most of the lesions falls into certain distinct patterns, which is characterized by almost completely absent of both cerebral hemispheres and by relative gross preservation of the basal ganglia, a portion of lower temporal and occipital and contents of the posterior fossa in our experienced 2 cases. In our cases, the condition may present a defect in vascular ontogenesis or the outcome of vascular occlusion of both internal carotid arteries and their main branches on carotid angiogram and CT scan. This paper presents the essential features for the clinical diagnosis, suggesting pathogenesis in 2 cases of infantile hydranencephaly.

A Case of Diencephalic Syndrome

Diencephalic syndrome of infancy which is characterized by progressive and profound emaciation often with normal or accelerated skeletal growth, hyperkinesias, hypotension, and hypoglycemia. The profound emaciation so characteristic this syndrome has yet to be explained. The diencephalic syndrome is caused by low grade astrocytoma, ependymoma in the third ventricle including the hypothalamus. Authers report a case of diencephalic syndrome which was confirmed in this patient with ependymoma in the region of anterior hypothalamus by transcallosal approach.

Response of Hypothalamic Hypophyseal Hormones to Stimulation and Lesion in the Thalamus and Hypothalamus

Plasma levels of growth hormone(GH), luteinizing hormone(LH) and cortisol were determined by radioimmunoassay following radiofrequency(RF) stimulation or coagulation of various nuclei in thalamus and hypothalamus. RF stimulation or coagulation of many nuclei in thalamus and hypothalamus consisted of pulvinar and dorsomedial nucleus in thalamus and anterior and posterior hypothalamic nuclei in hypothalamus. Anterior thalamic stimulation resulted in highly significant increase of plasma LH, GH, cortisol and TH levels. However thalamic stimulation resulted no change in the level of various plasma hormones. Hypothalamic lesion produced significantly decreased plasma LH, GH and cortisol levels. Plasma cortisol and LH levels were highest 2 hours after stimulation while GH levels did not increased until 6 hours and TH until 72 hours respectively after stimulation. The significant difference in latency for beginning of hormone secretion suggests that GH, cortisol and LH may be controlled by several separate neuronal networks. Plasma GH and cortisol levels were lowest 72 hrs after coagulation of the anterior hypothalamic area, while GH, cortisol and LH levels did not change following stimulation or coagulation of posterior hypothalamic nucleus and thalamic nucldi. It was also noted that the anterior hypothalamic stimulation or coagulation caused increased or decreased in GH, cortisol, and LH than that observed from stimulation or coagulation of other hypothalamic and thalamic nuclei respectively.