A case of segmental arterial mediolysis with subarachnoid hemorrhage due to anterior cerebral artery dissection followed by internal carotid artery dissection.

BACKGROUND: Segmental arterial mediolysis (SAM) causes subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture and arterial dissection. We encountered a case of SAM-related SAH due to ruptured dissection of the A1 segment of the anterior cerebral artery concomitant with internal carotid artery (ICA) dissection. CASE DESCRIPTION: A 53-year-old man presented with SAH due to a ruptured right A1 dissecting aneurysm. The aneurysm was trapped; however, 7 days after the onset of SAH, he experienced right hemiparesis and aphasia. Angiography showed left ICA dissection; urgent carotid artery stenting was performed, leading to symptom improvement. Abdominal computed tomography angiography showed aneurysms of the celiac and superior mesenteric arteries. He was diagnosed with SAM based on clinical, imaging, and laboratory findings. CONCLUSION: In the acute phase of SAM-related SAH, cerebral ischemia could occur due to both cerebral vasospasm and intracranial or cervical artery dissection.

In-stent hypodense area at two weeks following carotid artery stenting predicts neointimal hyperplasia after two years.

Introduction It has not been reported how long the follow-up study after carotid artery stenting (CAS) should be continued. The purpose of the present study is to clarify the dynamic change of the in-stent neointimal layer and residual arterial lumen by two years following CAS using three-dimensional computed tomography angiography (3D CTA) with volume rendering. Methods Thirty-six stented carotid arteries in 34 consecutive patients were examined by 3D CTA with volume rendering at two weeks and 3, 6, 12, 24 months of follow-up. Results An in-stent hypodense area could be detected in 10 of 36 (27.8%) carotid arteries at two weeks after CAS. In-stent hypodense areas gradually declined thereafter by three months. In the course of longer follow-up, the layer of the in-stent hypodense area (neointimal hyperplasia) continued to grow in size for up to 24 months. Patients with an in-stent hypodense area at two weeks have a thicker layer of neointimal hyperplasia at 24 months than patients without in-stent hypodense area at two weeks' follow-up. The predictive factors for growing neointimal hyperplasia at 24 months in multiple regression analysis are ulcer formation in pretreatment stenosis and the thickness of in-stent hypodense area at two weeks following CAS. Conclusion Our results suggest that follow-up study should be continued for a longer period even if in-stent restenosis could not be detected at one year following CAS. Especially in cases with ulcer formation in pretreatment stenosis and with a subacute in-stent hypodense area after CAS, longer follow-up is strongly recommended.

Vertebral artery dissecting aneurysm with Cushing's syndrome: case report.

A 45-year-old woman presented with subarachnoid hemorrhage of World Federation of Neurosurgical Societies grade IV. Cerebral angiography showed a dissecting aneurysm of the right vertebral artery (VA). Internal trapping of the right VA with coils was performed. The postoperative course was uneventful, but she continued to demonstrate moon facies and experience amenorrhea. Computed tomography demonstrated an adrenal tumor. Laparoscopic adrenalectomy was performed under a diagnosis of Cushing's syndrome caused by an adrenal tumor. Overproduction of cortisol caused by Cushing's syndrome may be related to the development of cerebral aneurysm.

Nestin immunoreactivity in local neurons of the adult rat striatum after remote cortical injury.

Nestin is a marker for the neuronal and glial precursor cells and is expressed in reactive astrocytes after brain injury. Following restricted neocortical injury, we found that cells with neuronal morphology in the adult rat striatum became immunoreactive for both nestin and the neuronal marker, microtubule-associated protein 2 (MAP-2), but not for the astroglial marker, glial fibrillary acidic protein (GFAP). The number of nestin-positive cells transiently increased in the striatum. Continuous administration of 5-bromo-2'-deoxyuridine (BrdU) after cortical injury did not reveal any newly generated neurons in the striatum. Double-labeling fluorescent immunocytochemistry revealed that the nestin-positive striatal cells were also substance-P-positive. These findings suggest that some factors released from the injured cortex may induce nestin immunoreactivity in striatal neurons.