Cases reported "Decerebrate State"

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1/4. MR findings of decerebrate rigidity with preservation of consciousness.

    We describe a case of decerebrate rigidity, with preservation of consciousness, caused by a discrete pontine tegmentum lesion identified on MR imaging. Lesions within a certain brain stem region are responsible for decerebrate rigidity in animal studies, but there has been a lack of MR imaging evidence in humans. This report also implies that a discrete lesion was responsible for the decerebrate rigidity, while consciousness was preserved.
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2/4. Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration.

    Certain decerebrate lesions of brain stem or hypothalamus induce pharmacologically reversible hypertension and hyperthermia in animals. We observed three young patients with episodic decerebration, hyperthermia, hypertension, and hyperventilation during recovery from comas of different etiologies. The shared pathology on neurologic examinations and computed tomographic scans was hypothalamic-mesencephalic dysfunction, suggesting a diencephalic-brain-stem disconnection syndrome or brain-stem release mechanism. propranolol was the most effective drug tested, but only two patients responded, one dramatically. This novel clinical syndrome may have localizing and therapeutic significance in pediatric coma that needs to be further defined in future studies.
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3/4. Successful resuscitation of an elderly patient following cardiac arrest: possible role of reduction of reactive oxygen.

    The presence of hyperoxia during reperfusion following brain ischemia has been shown in experimental animals to result in increased mortality and increased lipid peroxidation. Although no human studies have been reported, prolonged hyperoxia after resuscitation from cardiac arrest probably would result in increased cerebral injury. We report the case of an 88-year-old man who had a 5- to 6-minute cardiac arrest and then had decerebrate posturing during the post-resuscitation period, indicating that he had suffered a significant ischemic/anoxic insult. Early attention was paid to normalizing the arterial Po2 following resuscitation, which, according to experimental evidence, contributed to his eventual complete recovery of neurologic function, including mental state.
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4/4. 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. animals: 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.
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