The effects of dihydroergotamine in patients with head injury and raised intracranial pressure

Abstract

In the first study 6 patients with raised intracranial pressure due to brain oedema following head injury were given dihydroergotamine because of low perfusion pressure. The intracranial pressure fell simultaneously with the increase in arterial pressure. The intracranial pressure fell from 24±2 mmHg by a maximum of 12±1 mmHg after a single intravenous injection of 0.25 mg of dihydroergotamine and remained at a low level for 35–70 min before stabilizing at a new level 5±1 mmHg below the baseline. The initial rapid and marked decrease in intracranial pressure may be the result of a reduced intracranial blood volume, due predominantly to constriction of the more voluminous venous capacitance vessels (by analogy with the corresponding vascular effect of dihydroergotamine on skeletal muscle and skin.) In the second study, experiments using sympathectomized cat skeletal muscle, showed that dihydroergotamine also reduced the hydrostatic capillary pressure, inducing absorption of fluid from the interstitial tissue to blood. It is suggested that a similar transcapillary absorption effect in the damaged brain may be an explanation for the observation that the intracranial pressure stabilized at a level below the initial one following dihydroergotamine.