Dimethyl sulfoxide (DMSO) has shown promise as a drug for the treatment of intracranial hypertension. In this report, we describe our experience in six patients, two who received a bolus administration of 10% DMSO and four who received a 20% solution titrated against the intracranial pressure (ICP). Five of the patients in this series suffered from severe head injury, and one had a cortical venous thrombosis associated with pregnancy. The first two patients were treated with a rapid infusion of a 10% solution of DMSO. Initially, the ICP was satisfactorily controlled using this method. Over time, however, fluid overload, severe electrolyte disturbances, and an ultimate loss of ICP control occurred. In subsequent patients, a 20% solution titrated against the ICP was used. Although ICP control was better achieved using this method of administration, problems with fluid management and electrolytes occurred again despite a high level of vigilance. In addition, because of the solvent properties of DMSO and its propensity over time to dissolve most standard intravenous infusion systems, mechanical difficulties in its administration were encountered in all six patients. The mechanism of action of DMSO is not well understood. It differs from the barbiturates, but acts too rapidly to function solely as a diuretic. The drug is extremely complex to use, and difficulties with its administration may make its risks ultimately greater than its potential benefits. Until more laboratory data are available concerning its use and better delivery systems are developed, neurosurgeons are cautioned against treating intracranial hypertension with DMSO.
A simple technique is described for a venous graft between the common carotid artery and the extracranial vertebral artery. In the case described, the vertebral artery was shown angiographically to be occluded and reconstituted by collateral vessels. This patient had symptoms of vertebrobasilar insufficiency which resolved postoperatively.
Albino rabbits with experimental brain edema produced by a cryogenic lesion or by a cryogenic lesion combined with a metabolic blocker, 6-aminonicotinamide, were given 1 g of a 10% solution of dimethyl sulfoxide (DMSO) per kg by intravenous bolus. Simultaneous recording of intracranial pressure (ICP), systemic arterial pressure (SAP), and central venous pressure and electroencephalography were performed while the animals were mechanically ventilated at a constant PaCO2 (PaCO2, 38 to 42 torr). One hour after the administration of DMSO, the rabbits were killed by air embolus, and the brain was removed promptly for the determination of wet and dry weights and electrolyte content. The ICP at 15, 30, and 60 minutes after DMSO was lower in both groups; ICP was significantly lower at 30 minutes (p less than 0.5) in the cold lesion group and at 15 minutes in the combined group (p less than 0.05). These was no significant change in SAP after DMSO in either group. There was s significant reduction of brain water content after DMSO in the combined lesion group (p less than 0.005 for the left hemisphere and p less than 0.025 for the right); there was no significant reduction of water content in the group with a cold lesion only.
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