[Spontaneous occlusion of a dissecting aneurysm in the shape of "two dumplings on a skewer" at righ posterior inferior cerebellar artery (PICA): report of a case and neuroradiological findings].

We present a case of a spontaneous dissecting aneurysm at the vertebrobasilar artery including the right PICA in a 44-year-old man, who suffered from headache, hiccup and ataxic gait. The arteriograms showed an irregular narrowing and dilatation in the right PICA and in the vertebrobasilar artery, and showed fusiform dilatations in the bilateral middle cerebral arteries. We observed intramural hematoma and true lumen at the right PICA dissecting aneurysm on T1-weighted images on magnetic resonance imaging (1.5T, MRI), and the intimal flap was enhanced on T1-weighted image after intravenous injection of Gd-DTPA. The shape of the intramural hematoma showed a unique "two dumplings on a skewer" appearance, and the intensity of its hematoma in the false lumen decreased in gradient from adventitia to intimal flap on T1-weighted image on MRI. The dissecting aneurysm of the PICA was occluded spontaneously 1 month later, and it caused cerebellar infarction. However, the patient has been left only with the symptom of slight trunkal ataxia. Various shapes of intramural hematomas on MRI have been reported by Kitanaka in association with intracranial vertebrobasilar dissections. We suggest that "two dumplings on a skewer" shape which corresponds to the flow void of the true lumen, accompanied by intramural hematoma and enhanced intimal flap, on contrast-enhanced T1-weighted image, should be regarded as a true "diagnostic sign" of a dissecting aneurysm.

Unique radiological appearance of a microcystic meningioma.

A 35-year-old female presented with partial complex seizures. Computed tomography (CT) showed a slightly high density mass over the right frontal convexity, with heterogeneous contrast enhancement. T1-weighted magnetic resonance (MR) imaging showed the tumour as a hypo-intense lesion, with faint reticular enhancement after intravenous injection of gadolinium-diethylenetriaminepenta-acetic acid. The tumour was totally removed. The specimen was extremely soft and moist. The histological diagnosis was microcystic meningioma. The tumour cells were composed of typical meningothelial cells and stellate cells. The degenerative character of the tumour may be reflected in the poor enhancement on CT and MR imaging. This faint enhancement effect may be a neuro-imaging characteristic indication of this rare microcystic variant of meningioma.

[Pathophysiologic effects of nitric oxide (NO) and endothelin-1 in global cerebral ischemia in an animal model--an overview]. / Pathophysiologische Effekte von Stickoxid (NO) und Endothelin-1 bei globaler zerebraler Ischämie im Tiermodell--ein Uberblick.

These studies were performed in an attempt to clarify some of the pathophysiologic mechanisms which occur during and after global ischemia. Both nitric oxide and endothelin were demonstrated in gerbils to participate in responses to ischemia. It was shown that endogenous nitric oxide influences early postischemic reperfusion, systemic blood pressure and postischemic dopamine metabolism. Furthermore, the results indicated that nitric oxide played a role in dopamine release and that preischemic intracerebral nitric oxide formation significantly decreased ischemic dopamine release. In addition, ischemic release of endothelin-1 was detected; participation of nitric oxide in this release was observed. Further indication of functional interactions between nitric oxide and endothelin-1 in postischemic reperfusion were indicated by observations that endothelin-1 antagonists inhibited early hypoperfusion caused by Nitro-L-arginin and late hypoperfusion caused by endogenous endothelin-1. Nitric oxide was shown to decrease edema formation during the early postischemic period but contribute to edema formation during the late postischemic period. The findings indicate the importance of nitric oxide in stroke and ischemia.

The effect of nitric oxide inhibition on ischemic brain edema.

The involvement of nitric oxide (NO) in the development of ischemic cytotoxic edema was investigated by inhibiting nitric oxide synthase (NOS) activity with N omega-nitro-L-arginine (NLA). Bilateral carotid artery occlusion (15 min) alone or with release (15 and 60 min) served as a model for edema induction. NLA, N omega-nitro-D-arginine methyl ester (D-NAME) or Ringer's solution were administered 4 hr prior to ischemia or sham operation. Treatment with a stable nitroxide radical, 4-hydroxy-2,2, 6,6-tetramethylpiperidine-L-oxyl (TPL), was used to assess free radical involvement in edema. Accumulation of tissue water was evaluated by measuring specific gravity (SG) of brain cortex and histological examination. There was a greater reduction of cortical SG in early reperfusion (15 min) and a lesser decrease in SG (60 min later) in NLA-than in D-NAME- or Ringer's-treated gerbils. The NLA effect was confirmed by histological examination of the brain tissue. TPL treatment (pre- and postischemic) ameliorated the formation of edema to the same degree as NLA. The findings indicate a biphasic NLA modulation of cytotoxic edema most likely mediated through absence or presence of NO-derived free radicals.

Effects of plasma from hibernating ground squirrels on monocyte-endothelial cell adhesive interactions.

Adhesion and subsequent penetration of leukocytes into central nervous system ischemic tissue proceeds via a coordinated inflammatory mechanism involving adhesion molecules at the blood-endothelium interface. Mammalian hibernation is a state of natural tolerance to severely reduced blood flow-oxygen delivery (i.e., ischemia). Hibernating thirteen-lined ground squirrels were investigated in an attempt to identify factors responsible for regulating this tolerance. Since leukocytopenia is closely associated with entrance into hibernation, the role of leukocyte adhesion to endothelium in this phenomenon was examined. Intercellular adhesion molecule-1 (ICAM-1) is expressed by endothelium and regulates interactions with circulating leukocytes that may result in margination or extravasation. ICAM-1 expression by rat cerebral microvascular endothelial cells (EC) cultured with plasma from hibernating (HP) or nonhibernating (NHP) thirteen-lined ground squirrels was dose dependently increased by HP and, to a lesser extent, by NHP. Treatment of EC with HP coincidentally induced significantly greater increases in monocyte adhesion to EC (37.2%) than were observed with NHP (23.9%). Study of the effects of HP and NHP on monocyte adhesion to EC may identify mechanisms responsible for ischemic tolerance in hibernators and could lead to the development of novel therapeutic approaches to the treatment of stroke.

Cerebral postischemic hypoperfusion is mediated by ETA receptors.

Effect of ETA-receptor antagonist, BQ123, on postischemic hypoperfusion in the presence or absence of nitric oxide synthetase inhibitor, N omega-nitro-L-arginine (NLA), was investigated in Mongolian gerbils. BQ123 given prior to ischemia reversed the early incomplete recovery of cerebral blood flow observed with NLA without affecting the late postischemic hypoperfusion. Additional postischemic administration of BQ123 also reversed (P < 0.01) the late postischemic hypoperfusion seen in NLA-, N omega-nitro-D-arginine methyl ester- or Ringer's-treated animals.

Modulation of striatal dopamine release in cerebral ischemia by L-arginine.

The effect of L-arginine, the precursor of nitric oxide, on ischemic dopamine release from the striatum was investigated in Mongolian gerbils subjected to bilateral carotid artery occlusion (15 min) alone or with reflow (2 h). Dopamine and its metabolites were measured in the striatal extracellular space dialysate after continuous perfusion (2 microliters/min) of artificial extracellular fluid in the presence or absence of 15 mmol/liter L- or D-arginine or 1 mmol/liter nitro-L-arginine. L-Arginine but not D-arginine increased the striatal content of dopamine in pre- and postischemia whereas it lowered the levels of dopamine and 3-methoxytyramine induced by ischemia. In contrast, nitro-L-arginine reduced the preischemic levels of dopamine and 3,4-dihydroxyphenyl-acetic acid, and had no effect on the ischemic release of dopamine. These findings indicate that L-arginine stereospecifically modified the ischemic release and metabolism of dopamine. The data also suggest that the basal level of nitric oxide is not involved in dopamine release during ischemia but may participate in regulating dopamine release under physiological conditions.

Effect of nitro-L-arginine on cerebral blood flow and monoamine metabolism during ischemia/reperfusion in the mongolian gerbil.

Inhibition of nitric oxide synthase with nitro-L-arginine (i.p., 40 mg/kg body weight) in contrast to L-arginine (300 mg/kg body weight) delayed the initial recovery of cerebral blood flow (CBF) and altered dopamine (DA) metabolism in brain ischemia/reperfusion of Mongolian gerbils. Similar changes but more severe were observed with pargyline (monoamine oxidase inhibitor). Data suggest nitric oxide involvement in postischemic CBF recovery and modulation of DA metabolism due to nitro-L-arginine-induced CBF reduction.

[A case of intraventricular cystic meningioma].

We report a case of intraventricular cystic meningioma in the left lateral ventricle. A-44-year-old male patient was admitted with headache on November 25, 1991. Neurological examination revealed acalculia and left homonymous hemianopsia. CT and MRI showed a solid tumor which originated in the body of the left lateral ventricle, and which was associated with a cystic component postero-laterally. Tumor strains fed by the left anterior choroidal artery and the medial and lateral posterior choroidal artery by angiography. The tumor was totally removed via the lateral temporal parietal approach. Histological examination revealed meningotheliomatous meningioma in the solid tumor and only gliosis in the wall of the cyst.