The feasibility of low dose barbiturate administration by intra-carotid infusion to achieve EEG burst suppression--a preliminary report.

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)

Effects of etoposide-induced blood-brain barrier disruption on brain water, intracranial pressure, and cerebral vasomotor tone.

This study investigated the effects of hypertension and water loading on etoposide-induced, reversible blood-brain barrier disruption in a rat model. Twenty-nine animals were divided into four groups: group 1--intracarotid (i.c.) injection of saline followed in 1 h by 5 ml i.c. water; group 2--i.c. etoposide followed by i.c. water; group 3--i.c. saline followed by i.v. metaraminol to increase systemic blood pressure; group 4--i.c. etoposide followed by i.v. metaraminol. Systemic blood pressure and intracranial pressure were monitored continuously. Evans blue staining of the brain was used as a monitor of blood-brain barrier disruption. Animals were killed 1 h after either aramine or water infusion, and the brains removed and inspected for the degree of disruption. After dehydration, brain water was calculated for each hemisphere. Two-thirds of the animals infused with etoposide had evidence of barrier disruption, whereas none of the control animals infused with saline were disrupted. Neither control groups 1 or 3 showed significant change in intracranial pressure after water loading or augmentation of systemic blood pressure, respectively. Group 4 animals failed to demonstrate any significant change in intracranial pressure despite marked barrier disruption and acute hypertension (within the limits of normal autoregulation). A small but statistically significant increase in intracranial pressure was noted in group 2 animals with the greatest degree of barrier disruption. A significant increase in brain water was observed ipsilateral to etoposide infusion in only those animals with the most marked barrier disruption. These results indicate that etoposide-induced blood-brain barrier disruption caused significant increases in brain water without significant alteration of cerebral vasomotor tone or increases in intracranial pressure after water loading except in the most severe disruption. The classic untoward consequences of vasogenic edema were not encountered in the present model.

Physiological and electrophysiological consequences of etoposide-induced blood-brain barrier disruption.

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.

Neurological deterioration after lumbar puncture below complete spinal subarachnoid block.

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%.