Background and Purpose-Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia. Methods-Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and Ͼ14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2. Results-The 11 patients with hyponatremia (serum sodium concentration of Ͻ135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (PϽ0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (PϽ0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (PϽ0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients. Key Words: hyponatremia Ⅲ natriuretic peptide, brain Ⅲ subarachnoid hemorrhage H yponatremia after SAH has been reported to have an incidence of 30% to 40%. Recent studies have demonstrated that this phenomenon is frequently associated with hypovolemia, which is caused not by the syndrome of inappropriate secretion of ADH but by CSW. Conclusions-We1,2,3 However, the cause of CSW is still controversial. Some authors have reported that ANP 4,5 and digoxinlike peptides 6 may cause the hyponatremia, while others have suggested that these agents are not involved. 7,8 BNP, which was isolated from porcine brain in 1988, 9 causes natriuresis and diuresis. It has recently become possible to measure BNP accurately by immunoradiometric assay. We investigated whether BNP was related to hyponatremia after SAH by measuring plasma BNP concentrations with use of an immunoradiometric assay in patients with acute SAH. Subjects and Methods Patients and ManagementEighteen patients (4 men and 14 women without cardiac, renal, or endocrine diseases; meanϮSD age, 62.3Ϯ10.8 years) with SAH verified by CT scan were investigated from January 1995 through December 1996. All patients underwent cerebral angiography and aneurysm clipping within 48 hours of the onset, except for 1 patient in whom angiography failed to identify the source of hemorrhage. Each patient received intravenous fluid at approximately 2500 to 3000 mL/d to maintain a central venous pressure of 4 to 12 cm H 2 O. Sodium administration ranged from 280 to 320 mEq/d in patients without hyponatremia, while sodium loss was replaced according to urinary excretion when hyponatremia occurred. When symptomatic vasospasm occurred, ozagrel sodium (Xanbon, Kissei Pharmaceutical Co Ltd) was intravenously administered at 80 mg/d in pa...

Schwannoma is a benign peripheral nerve sheath tumor originating from Schwann cells. Most intracranial schwannomas arise from vestibular nerve and schwannoma in the suprasellar region is extremely rare. A 64-year-old man presented with walking disturbance and blurred vision for three months. Lateral hemianopsia in the left eye and brachybasia were observed. Magnetic resonance imaging revealed a suprasellar tumor with strong contrast enhancement associated with communicating hydrocephalus. The cerebrospinal fluid tap test improved gait disturbance. Hypothalamic stimulation test revealed hypo-reaction of GH, FSH and LH. After ventriculo-peritoneal shunting, the tumor was totally removed via a bilateral front-basal approach with a clinical diagnosis of craniopharyngioma. No adhesion was observed between the tumor and surrounding structures such as meninges and brain. The histopathological diagnosis was schwannoma. Here we report a case of suprasellar schwannoma associated with communicating hydrocephalus that has not ever been previously reported, with special reference to its pathogenesis.

We conclude that diffuse enhancement indicates extravasation from broken vessels that continue to bleed and that diffusely enhancing hematomas will be rapidly enlarged. We think that postcontrast MRI can be very useful for predicting the progression of acute EDHs and SDHs.

The authors present the case of a 37-year-old man with definite moyamoya disease in whom angiographic findings drastically changed. The patient presented with left hemiparesis due to lacunar infarction. Angiography initially disclosed a narrow right carotid artery (CA) siphon and severe stenosis of the horizontal segment of the left middle cerebral artery. Four years later, the patient experienced right-central facial paresis, which developed because of a small putaminal hematoma. Angiography results demonstrated occlusion of the internal CA siphons bilaterally, with moyamoya vessels. It therefore appears that in some adults, moyamoya disease is accompanied by very progressive vascular changes.

A 62-year-old male presented with glioblastoma multiforme in the left frontal lobe manifesting as motor aphasia, subsequent to a malignant lymphoma in the right orbit. He underwent subtotal removal of the right orbital mass presenting as right exophthalmos which was shown by histological examination to be non-Hodgkin's lymphoma. He received 30 Gy Lineac irradiation to the right orbit. His post-operative course was satisfactory. Magnetic resonance (MR) imaging with gadolinium-diethylenetriaminepenta-acetic acid (Gd-DTPA) 7 months later demonstrated a small spotty enhanced lesion in the left frontal lobe. He developed motor aphasia 1 year after irradiation. MR imaging disclosed an enhanced mass in the left frontal lobe, which was totally removed. Histological examination revealed glioblastoma multiforme. Patients with malignant lymphoma may develop a subsequent second malignant tumor. MR imaging with Gd-DTPA is quite useful for early detection of a second brain tumor.