Non-aneurysmal subarachnoid hemorrhage in aplastic or twig-like middle cerebral artery: A case report and literature review.

BACKGROUND: Aplastic or twig-like middle cerebral artery (Ap/T-MCA) is a rare vascular anomaly that can cause hemorrhagic and ischemic stroke. Ap/T-MCA can induce aneurysms due to the fragility of the vessel wall, consequently leading to subarachnoid hemorrhage. Herein, we report a case of Ap/T-MCA with subarachnoid hemorrhage without an aneurysm. CASE PRESENTATION: A 67-year-old man presented to our hospital with a sudden onset of headache. Computed tomography of the head revealed subarachnoid hemorrhage (SAH) in the left Sylvian fissure; however, no aneurysm was observed on digital subtraction angiography. Following conservative treatment, follow-up imaging showed no aneurysm or no recurrent stroke. CONCLUSION: Non-aneurysmal SAH is a possible indication of vessel wall fragility in Ap/T-MCA; however, a standardized treatment strategy for this condition remains to be established.

A Case of Tracheo-innominate Artery Fistula after Tracheostomy Successfully Treated with a Covered Stent.

A 78-year-old man underwent a tracheostomy after embolization for a dural arteriovenous fistula. Seventy days after tracheostomy, arterial bleeding appeared through the tracheal stoma. The bleeding stopped spontaneously. However, two days later, arterial bleeding reappeared, and he was diagnosed with a tracheo-innominate artery fistula (TIF). He then underwent urgent endovascular covered stent placement. After the procedure, there was no bleeding. TIF can be a fatal complication after tracheostomy and it is generally treated with open chest surgery. However, a successful endovascular treatment for TIF has recently been reported and may yield better results.

A case of simple stenting for ruptured basilar perforator aneurysm.

Ruptured aneurysms in perforating arteries are uncommon. We report a case of a basilar perforator artery aneurysm that was treated successfully using simple stenting to induce a rectifying effect without using a coil. In this case, coiling for the aneurysm was attempted initially, but it failed because of anatomical and practical problems. After placement of two stents in the basilar artery, the aneurysm was occluded completely without any neurological deficits at 100 days after the procedure. Although superselective coil embolization is ideal even in a small perforator aneurysm, simple stenting for a parent artery is a preferable treatment, especially in challenging cases for coil embolization of the aneurysmal dome.

A Case of Brainstem Infarction That Was Found to Be Vertebral Artery Dissection in a Short Period after the Diagnosis of Atherothrombotic Infarction.

Objective: We report a case of vertebral artery dissecting aneurysm that caused right lateral medullary infarction, which was treated by endovascular therapy. Case Presentations: A 57-year-old man developed right-side headache and dysarthria on the day before presentation, and exhibited mouth dropping and dysphagia the following day. Initial MRI demonstrated right lateral medullary infarction with atherothrombotic change with no vessel lesion, and we started infusion and medication administration. Later MRI revealed bilateral vertebral artery dissection, and we treated the growing right vertebral artery dissecting aneurysm by stenting and coils. Conclusion: The possibility of dissecting lesions should be considered in cases of medullary infarction. Stenting and coil treatment is a useful option for bilateral dissecting vertebral aneurysms.

Metal artifact reduction algorithm for image quality improvement of cone-beam CT images of medium or large cerebral aneurysms treated with stent-assisted coil embolization.

PURPOSE: The aim of the present study was to assess image quality improvement using a metal artifact reduction (MAR) algorithm in cases of medium or large cerebral aneurysms treated with stent-assisted coil embolization (SAC), and to analyze factors associated with the usefulness of the MAR algorithm. METHODS: We retrospectively evaluated the cone-beam computed tomography (CBCT) data sets of 18 patients with cerebral aneurysms treated with SAC. For subjective analysis, images of all cases with and without MAR processing were evaluated by five neurosurgeons based on four criteria using a five-point scale. For objective analysis, the CT values of all cases with and without MAR processing were calculated. In addition, we assessed factors associated with the usefulness of the MAR by analyzing the nine cases in which the median score for criterion 1 improved by more than two points. RESULTS: MAR processing improved the median scores for all four criteria in 17/18 cases (94.4%). Mean CT values of the region of interest at the site influenced by metal artifacts were significantly reduced after MAR processing. The maximum diameter of the coil mass (< 17 mm; odds ratio [OR], 4.0; 95% confidence interval [CI], 1.2-13.9; p = 0.02) and vessel length covered by metal artifacts (< 24 mm; OR, 2.3; 95% CI, 1.1-4.7; p = 0.03) was significantly associated with the usefulness of the MAR. CONCLUSIONS: This study suggests the feasibility of a MAR algorithm to improve the image quality of CBCT images in patients who have undergone SAC for medium or large aneurysms.

NADH fluorescence imaging and the histological impact of cortical spreading depolarization during the acute phase of subarachnoid hemorrhage in rats.

OBJECTIVE Although cortical spreading depolarization (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH) in clinical settings, the pathogenicity of CSD is unclear. The aim of this study is to elucidate the effects of loss of membrane potential on neuronal damage during the acute phase of SAH. METHODS Twenty-four rats were subjected to SAH by the perforation method. The propagation of depolarization in the brain cortex was examined by using electrodes to monitor 2 direct-current (DC) potentials and obtaining NADH (reduced nicotinamide adenine dinucleotide) fluorescence images while exposing the parietal-temporal cortex to ultraviolet light. Cerebral blood flow (CBF) was monitored in the vicinity of the lateral electrode. Twenty-four hours after onset of SAH, histological damage was evaluated at the DC potential recording sites. RESULTS Changes in DC potentials (n = 48 in total) were sorted into 3 types according to the appearance of ischemic depolarization in the entire hemisphere following induction of SAH. In Type 1 changes (n = 21), ischemic depolarization was not observed during a 1-hour observation period. In Type 2 changes (n = 13), the DC potential demonstrated ischemic depolarization on initiation of SAH and recovered 80% from the maximal DC deflection during a 1-hour observation period (33.3 ± 15.8 minutes). In Type 3 changes (n = 14), the DC potential displayed ischemic depolarization and did not recover during a 1-hour observation period. Histological evaluations at DC potential recording sites showed intact tissue at all sites in the Type 1 group, whereas in the Type 2 and Type 3 groups neuronal damage of varying severity was observed depending on the duration of ischemic depolarization. The duration of depolarization that causes injury to 50% of neurons (P50) was estimated to be 22.4 minutes (95% confidence intervals 17.0-30.3 minutes). CSD was observed in 3 rats at 6 sites in the Type 1 group 5.1 ± 2.2 minutes after initiation of SAH. On NADH fluorescence images CSD was initially observed in the anterior cortex; it propagated through the entire hemisphere in the direction of the occipital cortex at a rate of 3 mm/minute, with repolarization in 2.3 ± 1.2 minutes. DC potential recording sites that had undergone CSD were found to have intact tissue 24 hours later. Compared with depolarization that caused 50% neuronal damage, the duration of CSD was too short to cause histological damage. CONCLUSIONS CSD was successfully visualized using NADH fluorescence. It propagated from the anterior to the posterior cortex along with an increase in CBF. The duration of depolarization in CSD (2.3 ± 1.2 minutes) was far shorter than that causing 50% neuronal damage (22.4 minutes) and was not associated with histological damage in the current experimental setting.

Combined gene therapy with vascular endothelial growth factor plus apelin in a chronic cerebral hypoperfusion model in rats.

OBJECTIVE The aim of this study was to evaluate whether combined gene therapy with vascular endothelial growth factor (VEGF) plus apelin during indirect vasoreconstructive surgery enhances brain angiogenesis in a chronic cerebral hypoperfusion model in rats. METHODS A chronic cerebral hypoperfusion model induced by the permanent ligation of bilateral common carotid arteries (CCAs; a procedure herein referred to as "CCA occlusion" [CCAO]) in rats was employed in this study. Seven days after the CCAO procedure, the authors performed encephalo-myo-synangiosis (EMS) and injected plasmid(s) into each rat's temporal muscle. Rats were divided into 4 groups based on which plasmid was received (i.e., LacZ group, VEGF group, apelin group, and VEGF+apelin group). Protein levels in the cortex and attached muscle were assessed with enzyme-linked immunosorbent assay (ELISA) on Day 7 after EMS, while immunofluorescent analysis of cortical vessels was performed on Day 14 after EMS. RESULTS The total number of blood vessels in the cortex on Day 14 after EMS was significantly larger in the VEGF group and the VEGF+apelin group than in the LacZ group (p < 0.05, respectively). Larger vessels appeared in the VEGF+apelin group than in the other groups (p < 0.05, respectively). Apelin protein on Day 7 after EMS was not detected in the cortex for any of the groups. In the attached muscle, apelin protein was detected only in the apelin group and the VEGF+apelin group. Immunofluorescent analysis revealed that apelin and its receptor, APJ, were expressed on endothelial cells (ECs) 7 days after the CCAO. CONCLUSIONS Combined gene therapy (VEGF plus apelin) during EMS in a chronic cerebral hypoperfusion model can enhance angiogenesis in rats. This treatment has the potential to be a feasible option in a clinical setting for patients with moyamoya disease.

[A Case of Traumatic Vertebral Arteriovenous Fistula Treated by Internal Trapping of the Vertebral Artery].

BACKGROUND: Traumatic vertebral arteriovenous fistula (TVAVF) is an uncommon disease that occurs after traumatic injury. Here we report a case of TVAVF presenting with cervical bruit successfully treated by internal trapping using coils. CASE PRESENTATION: A 66-year-old man was transferred to our hospital after falling into a ditch. Initial CT revealed a C2 fracture into the right transverse foramen, and the patient had been treated with conservative management. A vascular abnormality was suspected because the patient exhibited cervical bruit on admission. CT angiography revealed right TVAVF at the V2 segment of the right vertebral artery (VA) near the C2 fracture. Digital subtraction angiography also revealed right TVAVF between the V2 segment of the right VA and the vertebral venous plexus, draining into the right internal jugular vein and the deep cervical vein as well as the intracranial venous system. The fistula was also opacified by retrograde flow from the contralateral VA through the union, while the flow in the basilar artery was antegrade. The patient was diagnosed with TVAVF with large transection of the right VA, and underwent endovascular treatment with internal trapping of the right VA using coils starting distal to the transection and proceeding in a proximal direction. After treatment, the right VAVF and right VA were completely occluded. The patient achieved clinical symptom resolution with no neurological deficits. CONCLUSION: Endovascular treatment with internal trapping of the VA using coils is safe and effective against TVAVF.

Pituitary apoplexy caused by hemorrhage from pituitary metastatic melanoma: case report.

Melanoma metastases to the pituitary gland are extremely rare, with only a few reported cases. We report an unusual case of pituitary metastatic melanoma in which the patient presented with pituitary apoplexy. A 68-year-old man presented general fatigue and anorexia following sudden headache. Neurological examination disclosed bitemporal hemianopsia. Computed tomography (CT) scans revealed a suprasellar mass including intratumoral hematoma. Magnetic resonance (MR) images demonstrated a circumscribed mass lesion in the intra- and suprasellar regions, compressing the optic chiasm. Surgical exploration was performed through a transsphenoidal approach, and a mixture of tumor and necrotic tissue with old hematoma was obtained. The histological examination of the specimen revealed a partly necrotic, malignant tumor with focal melanotic pigmentation. Histopathologically, the diagnosis was consistent with pituitary apoplexy caused by hemorrhage from pituitary metastatic melanoma.