A case of temporary occlusion of donor artery after secondary generalized seizure in a patient with superficial temporal artery-middle cerebral artery bypass.

Background: To prevent stroke recurrence, a superficial temporal artery-middle cerebral artery (STA-MCA) bypass for atherosclerotic cerebrovascular occlusive disease is performed. Post stroke epilepsy is known as serious sequelae of stroke. Herein, we present a case of a 60-year-old man who underwent STA-MCA bypass for the prevention of stroke recurrence; however, the donor artery was deemed to be temporally occluded secondary to generalized seizure. Case Description: A 60-year-old man was referred to our hospital with a diagnosis of the left cervical internal carotid artery occlusion presenting with mild aphasia and right hemiparesis. He underwent STA-MCA bypass to prevent the recurrence of stroke 1 month after the onset of symptoms. On postoperative day 7, patency of the donor artery was confirmed on magnetic resonance imaging (MRI), and no complications were noted. However, on postoperative day 14, he presented with a secondary generalized seizure. MRI was immediately performed and the donor artery was not patent with no new lesions. Several hours thereafter, the blood flow of the donor artery was confirmed using pulse Doppler; however, during mouth opening, the flow of the donor artery decreased. Computed tomography-angiography confirmed donor artery patency. An encephalogram was conducted and revealed a focal epilepsy which was compatible with stroke on MRI. Conclusion: Post stroke epilepsy caused an unintended and forced mouth opening which led to a temporary occlusion of the donor artery after STA-MCA bypass. Thus, this complication should be recognized, and seizures should be prevented through the administration of prophylactic anti-seizure medication based on risk stratification assessment of post stroke epilepsy.

Walk-In Hospital Admission of Patients with Subarachnoid Hemorrhage: Clinical Presentation and Outcome.

OBJECTIVE: Neurosurgeons occasionally encounter cases of subarachnoid hemorrhage (SAH) in admitted walk-in patients, termed "walk-in SAH." However, their clinical characteristics have not been fully understood. We thus, aimed to investigate several characteristics of patients with walk-in SAH and compare them with those of patients with good grade SAH who arrived at the hospital by ambulance. METHODS: Between January 2011 and January 2018, consecutive patients with World Federation of Neurosurgical Society (WFNS) grade I and II aneurysmal SAH were enrolled. They were dichotomized into walk-in and ambulance groups, and their demographic and disease-related characteristics were compared. Furthermore, predictors associated with unfavorable outcomes were investigated in patients with walk-in SAH. RESULTS: Of 171 patients with World Federation of Neurosurgical Society grade I and II SAH, 68 (39.8%) were categorized as walk-in SAH. The mean time for diagnosis in patients with walk-in SAH was significantly longer than that in patients who arrived by ambulance (P < 0.01). Multivariate analysis demonstrated that a lower rate of hypertension, high grades on the Barrow Neurological Institute scale, and Early Brain Edema Score were significantly associated with walk-in SAH (odds ratio [OR] 0.44, 95% confidence interval [CI] 0.21-0.91, P = 0.03; OR 0.32, 95% CI 0.13-0.76, P = 0.007; OR 0.11, 95% CI 0.02-0.51, P < 0.0001, respectively). Additionally, severe angiographic vasospasm was a significant predictor of unfavorable outcomes in walk-in SAH (OR 37.7, 95% CI 1.10-1290.90, P = 0.04). CONCLUSIONS: Patients with walk-in SAH exhibit radiological characteristics associated with a more favorable outcome among patients with good grade SAH. Therefore, these patients may have a positive prognosis.

[A Case of Cervical Internal Carotid Artery Occlusion Presenting with Subarachnoid Hemorrhage Caused by Rupture of Leptomeningeal Anastomosis].

A 71-year-old man was admitted to our hospital with a diagnosis of subarachnoid hemorrhage (SAH). Angiographies revealed neither aneurysms nor vascular anomalies. However, these images elucidated the occlusion of the left cervical internal carotid artery as well as developed leptomeningeal anastomoses through the ipsilateral posterior cerebral artery, which resulted in blood perfusing the ipsilateral middle and anterior cerebral artery territories. Because the localization of SAH coincided with the developed leptomeningeal anastomosis, we speculated that the rupture of the developed leptomeningeal anastomosis in the basal cistern was the cause of SAH. We performed superficial temporal and middle cerebral artery bypass surgery to prevent rebleeding and ischemic stroke. In patients with occlusion of the internal carotid artery, SAH induced by the rupture of aneurysm formed by hemodynamic stress was recognized. However, rupture of developed leptomeningeal anastomosis should be considered as a possible cause of SAH of unknown origin. (Received March 7, 2016; Accepted August 31, 2016; Published January 1, 2017).

Distribution of internal elastic lamina and external elastic lamina in the internal carotid artery: possible relationship with atherosclerosis.

The intracranial internal carotid artery (ICA) is a muscular artery and lacks external elastic lamina (EEL). Stenosis of the intracranial ICA is relatively uncommon, but the most common site is the cavernous portion. The characteristics of the arterial wall structures were examined using serial 3-mm sections of 32 intracranial ICAs obtained from 50 cadavers to identify where the EEL disappeared. The portions of the ICA where the intima exhibited thickening were also determined. Both the internal elastic lamina (IEL) and EEL were observed in all 32 specimens of the petrous portion of the ICA. Only the IEL was observed in all 32 specimens of the intradural portion of the ICA. The EEL had disappeared in 31 of the 32 specimens of the horizontal segment of the cavernous portion of the ICA. Intimal thickening of the ICA was observed in 23 of 32 ICA specimens, and frequently appeared in the horizontal segment of the cavernous portion of the ICA. The EEL disappeared in the cavernous portion of the ICA, which is the most common site of stenosis of the intracranial ICA. Change in the elasticity of the arterial wall in the cavernous portion may be an important factor in the process of atherosclerosis in the intracranial ICA.

A development of atheromatous plaque is restricted by characteristic arterial wall structure at the carotid bifurcation.

BACKGROUND: It is said atheromatous plaque is located very focally, but there have been few reports regarding this matter. Various aspects of the pathogenesis of the development of atheromatous plaque at the carotid bifurcation have previously been discussed. We have noted the correlation of plaque localization with characteristics of the cervical carotid artery wall. METHODS: Morphological and histopathologic changes in the carotid bifurcation were examined in 72 cadaver cases with or without atheromatous plaque. We determined the level at which the wall structure changed to muscular artery from elastic artery and analyzed its influence on the development of atheromatous plaque. RESULT: Atheromatous plaques at the distal site of the ICA extended within 0 to 37 mm from the carotid bifurcation. The proximal side of the CCA more than 5 mm away from the bifurcation was elastic artery, whereas the distal side of the ICA more than 15 mm from the bifurcation was muscular artery. The area of the carotid bifurcation between elastic artery and muscular artery was a transitional zone. Approximately 80% of them were located within 15 mm, and these areas were coincident with the transitional zone. CONCLUSION: Most atheromatous plaque was located in the transitional zone. The arterial wall structure is related to the development of atheromatous plaque at the cervical carotid bifurcation.