The risk of neurological deterioration after removal of cerebrospinal fluid below the level of a complete spinal subarachnoid block is generally accepted. The actual incidence of deterioration after lumbar puncture in the presence of a complete block remains unknown. The present retrospective case analysis includes a review of 100 patients found to have complete block on myelography: 50 cases with a lumbar puncture and 50 cases with a C1-2 puncture. Each group consisted of a similar age range, neurological status prior to myelography, level of block, and nature of disease. Seven patients (14%) had significant neurological deterioration after lumbar puncture, while no deterioration was seen after a C1-2 puncture. A summary of those cases in which deterioration followed lumbar puncture is presented and the possible pathophysiology is discussed. From this analysis, the estimated risk of downward spinal coning after lumbar puncture below a complete spinal subarachnoid block caused by a mass lesion is at least 14%.

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More than 10 years have elapsed since the introduction of high dose barbiturate administration in the management of patients with severe head injuries. Barbiturate therapy became an accepted method of treatment for increased intracranial pressure when other measures fail. One of the major limiting factors in the use of high dose barbiturate therapy is its significant hypotensive effect on the systemic arterial blood pressure. In seeking ways and means of minimising this hypotensive effect, we designed a study in which the systemic administration of barbiturates is avoided and replaced by selective perfusion of the concerned hemisphere with the drug utilising the intra-carotid route. Twenty-two rats, divided into two groups, were used in the study. Since monitoring of electroencephalographic (EEG) burst suppression serves as a good indicator of the lowest level of cerebral metabolic activity, we used this as the method for determining the desired endpoint of sodium amytal administration in both groups of animals. Group I, the intravenous group, consisted of eleven animals who received sodium amytal intravenously until burst suppression on the EEG was documented. Group II, the intra-carotid group, comprised eleven animals who received intra-carotid sodium amytal until EEG burst suppression was induced. In the intravenous group, a mean dose of 35 mg/kg of sodium amytal was administered before EEG burst suppression was achieved. This dose, however, was accompanied by an almost 50% reduction in systemic blood pressure compared to the pretreatment level. The intra-carotid group required a mean dose of 3.8 mg/kg sodium amytal and this was accompanied by only minor changes in systemic arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

The present study investigates the effects of etoposide-induced blood-brain barrier (BBB) disruption on systemic blood pressure (SBP), intracranial pressure (ICP), and electroencephalographic (EEG) activity. A total of 29 rats were divided into two groups. In Group 1, 8 control animals received intracarotid normal saline; in Group 2, 21 animals received intracarotid etoposide. SBP, ICP, and EEG were monitored continuously under general anesthesia and controlled ventilation after tracheostomy. Intravenous Evans blue dye was used for determination of BBB disruption. Although none of the Group 1 animals showed BBB disruption, 57% of the animals in Group 2 showed marked BBB disruption (3+). A slight but statistically significant increase in ICP was noted in the Group 2 animals with 3+ BBB disruption, although lesser degrees of barrier disruption (1+ or 2+) resulted in no significant alteration in ICP. The amplitude and frequency of the EEG decreased significantly ipsilateral to the side of intracarotid infusion in all animals with 3+ barrier disruption with a tendency to return toward normal within 2 hours. The degree of transient EEG change observed correlates well with the degree of barrier disruption, potentially allowing clinical determination of BBB disruption by this method.