OBJECTIVE: To report the occurrence of neurogenic stunned myocardium in the context of a hydrocephalus due to a third ventricle colloid cyst. DESIGN: Case report. SETTING: Neurocritical care unit of a university hospital. PATIENT: The case of a 33-year-old woman with an intraventricular cerebral colloid cyst who developed hydrocephalus, cardiac arrest and survived is presented. Workup was consistent with neurogenic stunned myocardium in the context of acute hydrocephalus due to an intraventricular colloid cyst. RESULTS: The patient had decreased left ventricular ejection fraction, apex-sparing areas of hypokinesis and akinesis, wall motion abnormalities not matching a particular vascular territories, the peak troponin T level of 0.09 ng/ml and had normal coronary arteries at angiography. Seven days after the initial event the cardiac function recovered. Tumor resection was successfully performed. At 10 months after discharge, the only complaint was mild memory disturbance, she was completely functional with no evidence of seizures or of cardiac dysfunction. CONCLUSION: The sudden elevation of intracranial pressure, with the subsequent decreased cerebral perfusion pressure induces a vigorous cerebro-protective neuroendocrine system activation that can lead to the neurogenic stunned myocardium. Sudden death in patients with colloid cysts may be related to acute neurogenic cardiac dysfunction, and not necessarily cerebral herniation(s), as previously thought.
OBJECTIVE: To report the occurrence of neurogenic stunned myocardium in the context of a hydrocephalus due to a third ventricle colloid cyst. DESIGN: Case report. SETTING: Neurocritical care unit of a university hospital. PATIENT: The case of a 33-year-old woman with an intraventricular cerebral colloid cyst who developed hydrocephalus, cardiac arrest and survived is presented. Workup was consistent with neurogenic stunned myocardium in the context of acute hydrocephalus due to an intraventricular colloid cyst. RESULTS: The patient had decreased left ventricular ejection fraction, apex-sparing areas of hypokinesis and akinesis, wall motion abnormalities not matching a particular vascular territories, the peak troponin T level of 0.09 ng/ml and had normal coronary arteries at angiography. Seven days after the initial event the cardiac function recovered. Tumor resection was successfully performed. At 10 months after discharge, the only complaint was mild memory disturbance, she was completely functional with no evidence of seizures or of cardiac dysfunction. CONCLUSION: The sudden elevation of intracranial pressure, with the subsequent decreased cerebral perfusion pressure induces a vigorous cerebro-protective neuroendocrine system activation that can lead to the neurogenic stunned myocardium. Sudden death in patients with colloid cysts may be related to acute neurogenic cardiac dysfunction, and not necessarily cerebral herniation(s), as previously thought.