The effect of decerebrate rigidity on intracranial pressure in man and animals.
Patients with decerebrate rigidity frequently show intracranial hypertension. The factors responsible for this effect and their inter-relationships were explored in cats and in patients with head injuries.


METHODS
The factors examined, separately and in combination, were elevation of central venous, intrathoracic, intra-abdominal and systemic arterial pressures. The baselines thus established were used for the investigation of the effects of these factors on the intracranial pressure (ICP) in cats which had been rendered decerebrate by focal stereotactic mesencephalic lesions. Little or no change occurred in the ICP when: Rigidity was mainly unilateral. Bilateral limb rigidity was extreme. Persistent elevation of ICP occurred when: Truncal rigidity resulted in the simultaneous elevation of the intrathoracic and intra-abdominal pressures. Elevation of the systemic arterial pressure occurred in the presence of defective cerebrovascular homeostasis. Human: The dynamics and management of the complex clinical problem posed by decerebrate rigidity were investigated in patients with head injuries who exhibited well-developed bilateral rigidity under conditions of altered cerebral elastance. Rigidity was quantified by measuring the resonant frequency of the wrist induced by a printed-circuit motor. The brain elastance, ICP, intrathoracic and blood pressures were measured throughout the study. The effect of pharmacological muscle paralysis on the ICP and rigidity was examined. It appeared that well-developed decerebrate rigidity increased the ICP. The relationship was direct; the greater the rigidity or cerebral elastance, the greater the rise in ICP and vice versa. The two factors mainly responsible were muscle hypertonicity and cerebral elastance. The rises in ICP were caused by the rigidity and although it may not always be possible to reduce the abnormally increased elastance, the rigidity can certainly be abolished. As long as the cerebral vascular homeostatic mechanisms were intact, spontaneous waning of the rigidity or its abolition by muscle relaxants returned the ICP to its previous resting level. Pancuronium produced much deeper and more lasting relaxation than either diazepam or chlorpromazine. During the period of mechanical ventilation, alterations in ICP were of prognostic value as regards the outcome of the injuries.
D000293:Adolescent; D000328:Adult; D000818:Animals; D001930:Brain Injuries / Q000503:physiopathology / Q000628:therapy; D002415:Cats; D002648:Child; D003655:Decerebrate State / Q000209:etiology / Q000503:physiopathology*; D006168:Guinea Pigs; D006439:Hemodynamics; D006801:Humans; D007427:Intracranial Pressure; D008297:Male; D009127:Muscle Rigidity / Q000503:physiopathology*; D009129:Muscle Tonus; D012121:Respiration, Artificial