Tsementzis S A
Ann Clin Res. 1984;16 Suppl 42:1-91.
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.
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.
去大脑强直患者常出现颅内高压。在猫和头部受伤患者中探讨了导致这种效应的因素及其相互关系。
分别和联合研究的因素包括中心静脉压、胸内压、腹内压和全身动脉压的升高。由此建立的基线用于研究这些因素对因局灶性立体定向中脑损伤而致去大脑状态的猫颅内压（ICP）的影响。当出现以下情况时，ICP几乎没有变化或没有变化：强直主要为单侧。双侧肢体强直极为严重。当出现以下情况时，ICP持续升高：躯干强直导致胸内压和腹内压同时升高。在脑血管自身调节功能受损的情况下出现全身动脉压升高。
在脑弹性改变情况下表现出明显双侧强直的头部受伤患者中，研究了去大脑强直所带来的复杂临床问题的动态变化及处理方法。通过测量印刷电路电机诱发的手腕共振频率来量化强直程度。在整个研究过程中测量脑弹性、ICP、胸内压和血压。研究了药物性肌肉麻痹对ICP和强直的影响。似乎明显的去大脑强直会使ICP升高。这种关系是直接的；强直或脑弹性越大，则ICP升高幅度越大，反之亦然。主要负责的两个因素是肌肉张力亢进和脑弹性。ICP升高是由强直引起的，虽然可能并非总能降低异常升高的弹性，但强直肯定可以消除。只要脑血管自身调节机制完好，强直的自发减弱或通过肌肉松弛剂消除强直可使ICP恢复到先前的静息水平。泮库溴铵产生的松弛比地西泮或氯丙嗪更深、更持久。在机械通气期间，ICP的变化对损伤的预后有预测价值。
