[Ruptured C2 Aneurysm of the Internal Carotid Artery with Ipsilateral Unruptured Giant Internal Carotid Artery Aneurysm:A Case Report].

A giant intracranial internal carotid artery(ICA)aneurysm is difficult to treat. We encountered a case with an unruptured giant intracranial ICA aneurysm with a ruptured C2 aneurysm of the ipsilateral ICA. In this case report, we describe how the treatment and review the literature. A 59-year-old man presented with sudden-onset headache and vomiting. He was diagnosed at a local neurosurgical unit as having a subarachnoid hemorrhage and admitted to our hospital. Cerebral angiogram revealed an unruptured giant ICA C3-4 aneurysm with a ruptured aneurysm of the ipsilateral ICA C2. The ruptured aneurysm had a wide neck and was located in the medial wall of the ICA C2;it was difficult to perform neck clipping or coil embolization. We performed a high-flow bypass using a radial artery graft followed by trapping of the left ICA. Postoperative imaging showed no new ischemic damage, and the patency of bypass flow was good. The left ophthalmic artery was perfused from the external carotid artery. Although the patient experienced incomplete left oculomotor nerve palsy and left lower quadrantanopsia, his neurological function had recovered within a year, and he was able to resume his previous work. High-flow bypass with ICA trapping is effective for ICA giant aneurysm. Attention to postoperative ophthalmic function and oculomotor symptoms is important.

[A Case of Ruptured Distal Anterior Choroidal Artery Aneurysm Associated with a Twig-Like Middle Cerebral Artery, Treated with Single-Stage Aneurysm Clipping and STA-MCA Double Anastomoses in the Acute Phase].

We report the case of a patient who has progressed well over 5 years following single-stage aneurysm clipping and superficial temporal artery-middle cerebral artery(STA-MCA)double anastomoses in the acute phase, for a ruptured distal anterior choroidal artery(AChA)aneurysm accompanied by a twig-like MCA. The patient was a 49-year-old female who developed a sudden severe headache and disturbance of consciousness due to subarachnoid hemorrhage and intraventricular hemorrhage(IVH). Cerebral angiography showed a right twig-like MCA associated with an abnormal vascular network and a ruptured aneurysm in the distal AChA. A day after emergency ventricular drainage for acute hydrocephalus, right frontotemporal craniotomy enabled distal AChA aneurysm clipping, together with removal of the IVH via transchoroidal fissure approach, in addition to STA-MCA double anastomoses to prevent recurrence of hemorrhage. The IVH resolved after surgery and no new infarct area was observed. Cerebral angiography revealed the disappearance of the aneurysm, good patency of the double bypass, and reduction of the abnormal vascular network. The patient gradually recovered without any neurological deficits, except for mild memory disturbance. Five years after the surgery, the patient has experienced no recurrence. The single-stage operation of aneurysm clipping and STA-MCA double anastomoses was made possible by devising an approach for a ruptured cerebral aneurysm, even in the acute stage. The successful improvement of cerebral circulation and prevention of cerebral hemorrhage from an early stage could serve as a reference for the treatment of similar hemorrhagic cases.

[A Case of Ruptured Peripheral Cerebral Aneurysm at Abnormal Vessels Associated with Middle Cerebral Artery Stenosis:Similarity to Moyamoya Disease].

We report a case of ruptured peripheral cerebral aneurysm at abnormal vessels associated with severe stenosis at the middle cerebral artery (MCA). A 66-year-old woman was admitted at our hospital with headache on foot. Computed tomography (CT) showed intracerebral hemorrhage in the left fronto-basal area. Three-dimensional-CT and conventional angiogram revealed abnormal vessels, which were similar to those seen in moyamoya disease, with a small enhancement close to the hematoma. On day 11, subsequent cerebral angiogram demonstrated an aneurysm at the peripheral portion of an abnormal vessel arising from the left A2. On day 17, soon after the diagnosis of the ruptured aneurysm was made (while still at the subacute stage), we operated on the aneurysm. Superficial temporal artery (STA)-MCA anastomosis was also performed to preserve cerebral blood flow and reduce hemodynamic stress. Several days after the operation, she had transient aphasia due to hyperperfusion of the MCA territory, but eventually recovered with no neurological deficit at discharge. Follow-up study revealed revascularization from the branches of the external carotid artery as well as the STA. On admission, we initially thought that this patient had abnormal vessels associated with arteriosclerotic MCA stenosis. However, the postoperative clinical course as well as the histopathological specimens of both the abnormal artery with the aneurysm and the STA revealed similar findings to those of moyamoya disease. Although this case did not satisfy the criteria for moyamoya disease, it is conceivable that a single arterial occlusive lesion associated with moyamoya-like vessels might develop in the same mechanism with that of moyamoya disease.

[Ruptured giant fusiform anterior cerebral artery aneurysm treated by proximal clipping with a3-a3 bypass:case report].

Giant fusiform aneurysm of the anterior cerebral artery (ACA) involving the anterior communicating artery (AcomA) is difficult to treat, and its postoperative course is not well known. We treated a patient with subarachnoid hemorrhage (SAH) due to rupture of a giant fusiform aneurysm of the ACA involving the AcomA. Here we describe its treatment and postoperative course, and review the literature regarding ACA involving an AcomA aneurysm that was treated with bypass surgery. A 65-year-old man presented with sudden onset of headache and vomiting. Computed tomography (CT) revealed SAH due to rupture of a giant fusiform ACA involving an AcomA aneurysm. He was admitted to the local neurosurgical unit 5 days after symptom onset. After waiting for vasospasm to resolve, he was transferred to our hospital. Three-dimensional CT demonstrated giant fusiform dilatation (25mm in diameter) of the left ACA (A1-A2), and the AcomA was involved. The perforating branches around the aneurysm were not identified. We performed proximal clipping with A3-A3 bypass for protection of reversal flow to the perforating branches of the left ACA. Postoperative magnetic resonance imaging showed a small infarction in part of the left caudate nucleus and the fornix. Cerebral angiogram revealed complete obliteration of the aneurysm. The patient did not experience palsy or aphasia, but he suffered from transient disturbance of frontal lobe function. A few months later, his cognitive function had recovered, and he was able to resume his normal daily life. Although clinicians should monitor for the development of postoperative neurological symptoms, including cognitive dysfunction proximal clipping with A3-A3 bypass was an effective and reliable treatment for ruptured giant fusiform ACA involving an AcomA aneurysm.

Endovascular treatment of a ruptured blister-like aneurysm at an azygos anterior cerebral artery: A case report and review of the literature.

Background: Endovascular treatment for a ruptured blister-like aneurysm (BLA) has recently become a hopeful approach. BLAs are usually located on the dorsal wall of the internal carotid artery, whereas one located on the azygos anterior cerebral artery (ACA) is so rare, it has never been reported. We report a case of a ruptured BLA arising at the distal bifurcation of an azygos ACA treated by stent-assisted coil embolization. Case Description: A 73-year-old woman presented with a disturbance of consciousness. Computed tomography showed diffuse subarachnoid hemorrhage, which was observed to be particularly dense in the interhemispheric fissure. Three-dimensional rotation angiography showed a tiny and conical bulge on the distal bifurcation of the azygos trunk. Follow-up digital subtraction angiography performed on day 4 showed enlargement of the aneurysm, and a BLA arising at the azygos bifurcation was diagnosed. Stent-assisted coiling (SAC) was performed using a low-profile visualized intraluminal support (LVIS) Jr. stent, which was implanted from the left pericallosal artery to the azygos trunk. Follow-up angiography showed that the aneurysm thrombosed gradually and reached complete occlusion 90 days after onset. Conclusion: SAC for a BLA at the distal bifurcation of an azygos ACA might be an effective treatment option leading to early complete occlusion, but thrombus formation as an intraoperative complication should be noted in the BLA at the bifurcation or the peripheral artery, as in the present case.

[A case of common carotid artery dissection showing remission in short-term].

We report a case of left common carotid artery dissection showing complete remission in the short term. A 48-year-old man presented a 1-week history of weakness in the right arm. Neurological findings revealed mild motor weakness of the right upper extremity. Magnetic resonance imaging (MRI) showed sporadic cerebral infarction and hemorrhagic infarction in the area of the left middle cerebral artery (MCA) and the posterior border zone. Computed tomographic angiography (CTA) revealed irregular stenosis with a smooth surface in the left common carotid artery and ultrasonography indicated an iso-echoic lesion in the same area. ECD-single-photon emission tomography (SPECT) showed low perfusion only in the infarcted territory. Conservative therapy using a free radical scavenger and aspirin was carried out and the patient displayed full neurological recovery. After a 3-week follow-up period, carotid angiography and CTA showed almost complete disappearance of the stenotic lesion.

Hippocampal CA1 neuron survival and cytosolic FKBP12, the 12 kDa FK506-binding protein, after ischemia and tacrolimus treatment in gerbils.

To assess the neuroprotective effect of tacrolimus (FK506) in transient forebrain ischemia models in gerbils, 10.0 mg/kg of FK506 was injected intraperitoneally immediately following reperfusion and at intervals of 1, 3, 6, 9, and 12 h after reperfusion. FK506 produced a significant neuroprotective effect for up to 6 h after 5 min of ischemia. Immunoblot and immunohistochemistry revealed that the amount of FKBP12, the 12-kDa FK506-binding protein, in the cytosol remained unchanged until 12 h after reperfusion. Translocation of FKBP12 from the nucleus to the cytosol was not observed until 24 h after reperfusion. Administration of FK506 did not appear to induce the cytosolic increase in FKBP12. In this study, no correlation was apparent between the post-ischemic therapeutic efficacy of FK506 and the post-ischemic changes in the cytosolic FKBP12.