Hideki Tanabe

Significance of ST segment elevation in electrocardiograms in patients with ruptured cerebral aneurysms

SummaryTwenty-three patients with aneurysmal subarachnoid haemorrhage (SAH), who showed an ST segment elevation in their electrocardiograms (ECG), were examined.There were 12 males and 11 females, with a mean age of 61 years. The clinical condition on admission was Hunt and Kosnik grade II in four, III in seven, IV in one, and V in 11 patients. Computerized tomography (CT) also revealed many cases of diffuse, thick SAH or intracerebral or intraventricular haematoma. Laboratory examinations including serum electrolyte, pH, and PaO2 revealed no abnormalities that might have influenced the ECG. Elevation in the levels of myocardial enzymes in serum was observed in two of the nine patients examined, although the elevation was only slight in one of them. Echocardiography, which was performed on several occasions on all patients, and cardiac catheterization, which was performed on eight patients, revealed a reduction in the motion of the left ventricular apex that was synchronous with ST segment elevation. This is the first report about these phenomena. No abnormalities were observed in the coronary artery. The elevated ST segment was normalized within one week in all patients, accompanied by normalization of the apical wall motion recorded on echocardiograms. In four patients, however, T wave inversion accompanied the improvement of the ST segment and was normalized within three months after the onset.These results suggest that ST segment elevation in the acute stage of SAH reflects transient cardiac dysfunction rather than myocardial injury. In some patients, however, the elevated serum levels of myocardial enzymes or T wave inversion suggested the presence of myocardial injury. Close follow-up seems to be necessary in such cases

What should be done, what should not be done in microvascular decompression surgery

Abstract The purpose of microvascular decompression surgery (MVD) was to obtain a perfect and permanent cure for hyperactive dysfunction of cranial nerves without causing complications and recurrences. From the experiences of long-term follow-up of a large series of patients with MVD for trigeminal neuralgia (TGN), hemifacial spasm (HFS) and glossopharyngeal neuralgia (GPN), the tactics for satisfactory treatment were described as follows: (1) correct diagnosis of symptoms, (2) correct identification of the offending vessel(s), (3) appropriate reposition of offending vessels (prosthesis should not be inserted between the nerve and the artery; the tough, arteriosclerotic offending vessel could be replaced by fixing its loop to the dura), (4) axis of the 5th cranial nerve should be straightened after decompression, (5) flocculus should be retracted in a perpendicular fashion to the axis of the 8th cranial nerve, together with an Auditory Brainstem Response (ABR) monitoring to preserve the 8th cranial nerve function. The delay of latency of the 5th wave of ABR should not exceed 1.0 ms and the reduction of amplitude should be less than 40% (critical limit), and (6) mastoid air cells should be carefully packed with bone wax and eye ointment wrapped in Surgicel (Ethicon, Somerville, NJ).