Repeated Spontaneous Intracranial Epidural Hemorrhage After Hysterical Crying.

BACKGROUND: Spontaneous epidural hemorrhage (EDH) is a rare occurrence that may be caused by vascular anomalies, infections, coagulopathies, or tumors. Spontaneous EDH occurring in patients without specific underlying disease has been reported only as intraspinal lesion but has never been demonstrated in the intracranial area. This study presents a 19-year-old patient with repeated spontaneous intracranial EDH caused twice by hysterical crying. CASE DESCRIPTION: The patient had spontaneous left frontal EDH after hysterical crying. Two years later, she had a similar episode after crying and a new spontaneous right frontal EDH was revealed. There was no obvious risk factor revealed by laboratory and radiologic survey. We postulated that hyperventilation during crying resulted in a sudden decrease in intracranial pressure. The intracranial hypotension induced detachment of the dura from the skull and spontaneous EDH occurred. CONCLUSIONS: Crying or hyperventilation may trigger spontaneous EDH and should be suspected when there are signs of persisting headache and increased intracranial pressure. The prognosis is excellent if early diagnosis and surgical decompression are achieved.

Source localization of the re-build up phenomenon in pediatric moyamoya disease-a dipole distribution analysis using MEG and SPECT.

OBJECTS: The "re-build up" phenomenon is a pathognomonic finding induced after hyperventilation in pediatric moyamoya disease, and is closely related to ischemic attacks. However, its precise mechanism remains unknown. METHODS: In this study, MEG, MRI, and SPECT were used to clarify its mechanism in 4 children with moyamoya disease. Cerebral blood flow before and after acetazolamide administration was measured. Spontaneous magnetic brain activity was measured using a whole-head MEG system. The quantified dipole distribution was shown on 3D-MRI. RESULTS AND CONCLUSION: The original current dipoles of the "re-build up" slow waves were predominantly located in the deep cortical sulci in the area with impaired reactivity to acetazolamide. The results suggested that the re-build up waves derive from the deep cortical sulci due to the reduction in the cerebral perfusion reserve.