[Subarachnoid hemorrhage caused by a dissecting aneurysm of the internal carotid artery: case report and review of the literature].

A case of subarachnoid hemorrhage (SAH) resulting from a ruptured intracranial dissecting aneurysm of the internal carotid artery (ICA) is reported. A 58-year-old woman presented with headache and vomiting. A CT showed diffuse SAH. A cerebral angiography demonstrated a dissecting aneurysm at the C2 segment of the right ICA. In the present case, trapping with STA-MCA anastomosis was performed and the postoperative course was uneventful. Postoperative follow-up cerebral angiogram detected no aneurysm. SAH caused by the rupture of a dissecting aneurysm of the ICA has been considered rare. To our knowledge, there have been only 29 cases. We discuss the clinical characteristics with a review of the literature.

[The posterior inferior cerebellar artery arising from the internal carotid artery directly: a variant of the persistent primitive hypoglossal artery].

We reported a rare case of the posterior inferior cerebellar artery arising from the internal carotid artery directly. A 33-year-old male was admitted to our hospital with the complaint of throbbing type headache. CT showed no abnormal findings. A saccular aneurysm at the bifurcation of the left middle cerebral artery was revealed by MR angiography and the left internal carotid angiography. The right internal carotid angiography demonstrated an anomalous branch originating at the level of the C1/2 in the cervical portion of the internal carotid artery. This branch terminated as the posterior inferior cerebellar artery without an interposed segment of the vertebro-basilar artery. The ipsilateral vertebral artery was aplasia. T2-weighted MR image showed a flow-void penetrating the right hypoglossal canal. This vessel was confirmed an artery passing through the hypoglossal canal with the source images of the three-dimensional time-of-flight MR angiography. We diagnosed it as a kind of variant of the persistent primitive hypoglossal artery. The persistent primitive hypoglossal artery is composed of the proximal segment derived from the primitive hypoglossal artery, and the distal segment consisting of portions of the lateral anastomotic channels (primitive lateral basillo-vertebral anastomosis) which give rise to the posterior inferior cerebellar artery. We speculated that this variant resulted from the persistence of the proximal segment, which communicated with the stem of the posterior inferior cerebellar artery via the distal segment, and next, the disconnection of the posterior inferior cerebellar artery origin with the vertebral artery due to the aplasia of right vertebral artery and the involution of the distal segment connected to the basilar artery.

Intravenous administration of thioredoxin decreases brain damage following transient focal cerebral ischemia in mice.

Thioredoxin (TRX) is induced by a variety of oxidative stimuli and shows cytoprotective roles against oxidative stress. To clarify the possibility of clinical application, we examined the effects of intravenously administered TRX in a model of transient focal cerebral ischemia in this study. Mature male C57BL/6j mice received either continuous intravenous infusion of recombinant human TRX (rhTRX) over a range of 1-10 mg/kg, bovine serum albumin, or vehicle alone for 2 h after 90-min transient middle cerebral artery occlusion (MCAO). Twenty-four hours after the transient MCAO, the animals were evaluated neurologically and the infarct volumes were assessed. Infarct volume, neurological deficit, and protein carbonyl contents, a marker of protein oxidation, in the brain were significantly ameliorated in rhTRX-treated mice at the dose of 3 and 10 mg/kg versus these parameters in control animals. Moreover, activation of p38 mitogen-activated protein kinase, whose pathway is involved in ischemic neuronal death, was suppressed in the rhTRX-treated mice. Further, rhTRX was detected in the ischemic hemisphere by western blot analysis, suggesting that rhTRX was able to permeate the blood-brain barrier in the ischemic hemisphere. These data indicate that exogenous TRX exerts distinct cytoprotective effects on cerebral ischemia/reperfusion injury in mice by means of its redox-regulating activity.

Activation of p38 kinase in the gerbil hippocampus showing ischemic tolerance.

Ischemic tolerance is a phenomenon in which brief episodes of ischemia protect against the lethal effects of subsequent periods of prolonged ischemia. The authors investigated the activation of p38 mitogen-activated protein kinase (p38) in the gerbil hippocampus by Western blotting and immunohistochemistry to clarify the role of p38 kinase in ischemic tolerance. After the 2-minute global ischemia, immunoreactivity indicating active p38 was enhanced at 6 hours of reperfusion and continuously demonstrated 72 hours after ischemia in CA1 and CA3 neurons. Pretreatment with SB203580, an inhibitor of active p38 (0-30 micromol/l), 30 minutes before the 2-minute ischemia reduced the ischemic tolerance effect in a dose-dependent manner. Immunoblot analysis indicated that alteration of the phosphorylation pattern of p38 kinase in the hippocampus after subsequent lethal ischemia was induced by the preconditioning. These findings suggest that lasting activation of p38 may contribute to ischemic tolerance in CA1 neurons of the hippocampus and that components of the p38 cascade can be target molecules to modify neuronal survival after ischemia.

[A ruptured mycotic aneurysm, simultaneously associated with acute subdural hematoma and intracerebral hemorrhage: case report and review of the literature].

A case is reported of a patient with simultaneous subdural hematoma and intracerebral hemorrhage associated with a ruptured intracranial mycotic aneurysm. A 65-year-old woman, with a history of low grade fever for over a month, presented with disturbance of consciousness. A CT showed bilateral acute subdural hematomas and parenchymal hematomas in the occipital lobes. Cerebral angiography demonstrated a distal middle cerebral aneurysm. Cardiac ultrasonography showed a verruca at the mitral valve. The incidence of ruptured mycotic aneurysm presenting with acute subdural hematoma is extremely rare. To our knowledge, there have been only seven cases. The present case is discussed with reference to a review of the literature.