Kiyoyuki Yanaka

Repair of a tear at the base of a blister-like aneurysm with suturing and an encircling clip : technical note

OBJECTIVE An aneurysm can produce large defects in the parent vessel if the aneurysm tears at the neck of the vessel. The authors present a technique to repair a tear at the base of a blister-like aneurysm encountered during microsurgical clipping of an anterior wall aneurysm of the internal carotid artery. METHODS The repair technique involved suturing and covering the aneurysm with an encircling aneurysm clip. A large tear had destroyed the vessel’s tubular structure, and repair was not sufficient using an encircling clip alone. Two microsuture stitches were placed on the tear, so that a split artery re-formed a tubular structure. The lesion was then covered with Surgicel (Ethicon, Inc., Somerville, NJ) and fibrin glue. When the Surgicel and fibrin glue were applied, the temporary clip on the distal internal carotid artery was removed for a moment, allowing retrograde blood flow to provide the counterforce necessary to maintain the vessel’s tubular structure. An encircling clip was then applied to cover the entire circumference of the lesion. RESULTS This method required only a short occlusion time for arterial repair, thus helping avoid ischemic complications. The patient awoke with transient hemiparesis, but recovery was prompt. CONCLUSION This technique is useful for repairing an aneurysmal tear at its base, especially if the tear is large.

Small unruptured cerebral aneurysms presenting with oculomotor nerve palsy.

OBJECTIVESymptomatic unruptured aneurysms have been considered at relatively high risk for future rupture, and the majority of aneurysms that cause symptoms of mass effect are large. Unruptured aneurysms smaller than 1 cm in diameter sometimes cause neurological symptoms, but their clinical aspects remain obscure. In this article, we review our experience with small unruptured aneurysms presenting with oculomotor nerve palsy. METHODSSixteen patients with unruptured aneurysms smaller than 1 cm presenting with oculomotor nerve palsy were included in this study. The patients’ clinical profiles were reviewed, and factors affecting the recovery of oculomotor function were determined. RESULTSThe mean size of the aneurysms was 5.8 ± 1.4 mm. Eleven patients (68.8%) had preceding retrobulbar pain. Fifteen patients underwent successful microsurgical clipping or intravascular embolization, but one patient died of aneurysm rupture before surgery. Seven patients (43.8%) had a complete recovery of oculomotor function, six (37.5%) had an incomplete recovery, and two (12.5%) remained unchanged after treatment. The mean interval between the onset of oculomotor nerve palsy and treatment was 4.7 ± 3.3 days in patients with complete recovery, 24.2 ± 15.5 days in patients with incomplete recovery, and 41.0 ± 12.7 days in unchanged patients. Early surgery resulted in more complete recovery of neural function (P < 0.01). CONCLUSIONUnruptured aneurysms smaller than 1 cm can cause neurological symptoms of mass effect. We recommend timely surgery, preferably within 5 days, to avoid not only aneurysm rupture but also functional disability even in patients with unruptured aneurysms smaller than 1 cm.

Stable nitroxide Tempol ameliorates brain injury by inhibiting lipid peroxidation in a rat model of transient focal cerebral ischemia.

Oxygen free radicals have been implicated in the pathogenesis of cerebral ischemia and reperfusion injury. 4-Hydroxy-2,2,6,6-tetramethylpiperidene-1-oxyl (Tempol) has been reported as a stable nitroxide and a membrane-permeable free radical scavenger. This study was performed to investigate the mechanism of Tempol in attenuating ischemia-reperfusion injury in a rat model of transient focal cerebral ischemia. We measured the cerebral 2,3-dihydroxybenzoic acid (DHBA) level as the amount of hydroxyl radical production using a microdialysis technique with salicylic acids trapping during ischemia and reperfusion. The concentration of cerebral thiobarbituric acid reactive substances (TBARS), representing the extent of lipid peroxidation by free radicals, and the area of cerebral infarction were also measured. The level of cerebral 2,3-DHBA was increased during ischemia and reperfusion, especially during the early reperfusion stage at the periphery of the infarct area (nearly 500-fold). Intravenous administration of Tempol at the time of reperfusion reduced 2,3-DHBA production (Vehicle group: 472.2+/-196.2, Tempol group: 238.3+/-77.2) and the cerebral TBARS level (Vehicle group: 541.7+/-84.7, Tempol group: 339.0+/-147.2 nmol/g), and decreased the size of the cerebral infarction (Vehicle group: 202.2+/-98.4, Tempol group: 98.5+/-13.7 mm(3)). In contrast, Tempol administered 15 min prior to reperfusion reduced neither the TBARS level nor the size of the infarction. These results indicate that Tempol administration at the time of reperfusion reduced lipid peroxidation by scavenging free radicals, resulting in a reduction of the infarct size.

Awakenings from persistent vegetative state: report of three cases with parkinsonism and brain stem lesions on MRI

Three patients with a persistent vegetative state after severe head injury are reported. They recovered from a prolonged disturbance of consciousness after the administration of levodopa. These patients all had parkinsonian features. On magnetic resonance imaging, the distribution of lesions implied a diffuse axonal injury involving the substantia nigra or ventral tegmental area. The existence of patients whose dopaminergic systems may have been selectively damaged by a severe head injury should be recognised because such individuals may respond to levodopa treatment.

Intracranial dural arteriovenous fistula showing diffuse MR enhancement of the spinal cord: case report and review of the literature.

BACKGROUND Cervical myelopathy resulting from intracranial dural arteriovenous fistula (AVF) is uncommon. Knowledge of the magnetic resonance imaging (MRI) appearance of such lesions is important because many patients with myelopathy are initially examined by MRI, and an incorrect diagnosis could result in delayed or improper treatment. We describe a rare case of myelopathy due to an intracranial dural AVF showing diffuse enhancement of the cervical spinal cord. CASE DESCRIPTION A 64-year-old male presented with progressive myelopathy and respiratory insufficiency. Cerebral angiography disclosed an AVF at the craniocervical junction draining intrathecally into the spinal medullary veins. MRI revealed dilated perimedullary vessels around the craniocervical junction, as well as spinal cord swelling with high signal intensity changes. Diffuse intense enhancement of the cervical spinal cord was also seen on postcontrast images. Embolization via the afferent artery was successfully performed, and the fistula was then microsurgically obliterated via a lateral suboccipital approach. This procedure arrested a rapidly progressive myelopathy. CONCLUSION Intracranial dural AVF showing diffuse enhancement of the spinal cord is extremely rare, and this enhancement effect may indicate pathologic changes of the spinal cord. MRI only is not useful for diagnosis, but also for demonstrating pathologic changes and predicting the outcomes of patients with intracranial dural AVF.

Multiple intracranial arterial stenoses around the circle of Willis in association with Graves' disease: report of two cases.

OBJECTIVE AND IMPORTANCEThe association of Graves’ disease with multiple intracranial arterial stenoses is rare. CLINICAL PRESENTATIONWe report on two Japanese women who experienced the concurrence of Graves’ disease and cerebral ischemia attributable to multiple intracranial arterial stenoses around the circle of Willis. Clinically, these patients demonstrated hyperthyroidism, goiter, ophthalmopathy, and ensuing ischemic strokes. Cerebral angiography demonstrated multiple intracranial arterial stenoses around the circle of Willis in both cases. These cases did not meet the full diagnostic criteria for moyamoya disease, in that there were no abnormal, net-like, collateral vessels, but the other clinical and angiographic findings were consistent with this condition. INTERVENTIONAfter normalization of their hormonal conditions, the patients underwent cerebral revascularization procedures. Both patients achieved excellent recoveries and returned to normal daily life after treatment. CONCLUSIONMultiple intracranial arterial stenoses and Graves’ disease may occur simultaneously. Such cases may offer new insights into the pathogenesis of these two conditions. It is important to study more patients with this dual condition, to obtain more evidence of the relationship between genetic and immunogenic backgrounds.

Symptomatic cerebral vasospasm after intraventricular hemorrhage from ruptured arteriovenous malformation

We present a rare case showing symptomatic vasospasm after intraventricular hemorrhage from a ruptured arteriovenous malformation. No significant subarachnoid hemorrhage in the basal cisterns was observed on computed tomography in the entire course of illness. Although most cases showing vasospasm are associated with the deposition of blood in the basal cisterns, this case suggests the possibility of some other important factor in causing the subsequent development of vasospasm.

Distal anterior choroidal artery aneurysm associated with an arteriovenous malformation. Intraoperative localization and treatment.

BACKGROUND Distal anterior choroidal artery aneurysms are rare. The outcome of patients with distal anterior choroidal artery aneurysms has been poor, and the treatment of such aneurysms is surgically challenging. CASE DESCRIPTION The authors describe the case of an 8-year-old girl with a ruptured distal anterior choroidal artery aneurysm associated with an arteriovenous malformation (AVM). The patient experienced sudden onset of headache and vomiting. Computed tomography revealed an intraventricular haemorrhage, and cerebral angiography demonstrated an aneurysm arising from the distal portion of the right anterior choroidal artery. The patient also had an AVM in the ipsilateral temporal lobe fed by the branches of the middle cerebral artery. A right frontotemporal craniotomy was performed with the aid of intraoperative angiography to eliminate both the AVM and the aneurysm. Intraoperative angiography was helpful in confirming the complete removal of the AVM and in accurate localization of the small and deeply placed distal anterior choroidal artery aneurysm. Both the AVM and the aneurysm were successfully treated and the patient was discharged without any neurological deficits. CONCLUSION This case is the youngest reported patient with a distal anterior choroidal artery aneurysm. This report is also the first to describe an association of such an aneurysm with an AVM. The etiology of the aneurysm formation in this case and surgical strategy for deeply placed vascular lesions are discussed.

Subarachnoid hemorrhage not due to ruptured aneurysm in moyamoya disease.

A patient with moyamoya disease presenting with subarachnoid hemorrhage (SAH) is reported. A 38-year-old Japanese woman developed a sudden onset headache and nausea during hospitalization for a cerebral infarct in the right frontal lobe. CT scan showed SAH in the left frontal sulci. Cerebral angiogram showed stenosis of the distal bilateral internal carotid arteries with moyamoya vessels, and significant transdural anastamoses from the left external carotid artery to cortical arteries on the left frontal cortex. The patient was kept normotensive and underwent a right-sided surgical revascularization procedure, remaining well for three years. SAH not due to ruptured aneurysm in moyamoya disease is rare. The cause of the SAH was thought to be disruption of the transdural anastomotic vessels. Recognition of these fragile vessels in moyamoya disease is essential.

Interhemispheric subdural hematoma caused by a ruptured internal carotid artery aneurysm: case report.

BACKGROUND Interhemispheric subdural hematoma (ISH) usually occurs after head trauma; nontraumatic ISH is extremely rare. CASE DESCRIPTION The authors describe a 62-year-old male presenting with severe headache and ptosis on the left side. Computed tomography (CT) and magnetic resonance imaging disclosed a hematoma in the interhemispheric subdural space without subarachnoid hemorrhage. Cerebral angiography revealed an aneurysm arising from the left internal carotid-posterior communicating artery (IC-PC) junction. The patient underwent emergency clipping of the aneurysm and was discharged without neurological deficit. CONCLUSION Ruptured aneurysms resulting in ISH without subarachnoid hemorrhage have been reported in only a few cases; this is the second case to describe the association of a ruptured IC-PC aneurysm with an ISH. The etiology of ISH formation due to ruptured aneurysms and the diagnosis are discussed.