Kazuyoshi Korosue

Surgical excision of cerebral arteriovenous malformations : late results

A follow-up study of 153 consecutive patients who underwent complete excision of an angiographically visualized intracerebral arteriovenous malformation was conducted. The follow-up period ranged from 0.5 to 10.6 years, with a mean of 3.8 years. The presenting clinical event was hemorrhage in about one-half of the patients and seizure in about one-third. There was a marked tendency for postoperative neurological deficits to improve with time, so that whereas the immediate postoperative rate of serious morbidity was 24.2%, only 7.8% of the patients were found to have serious morbidity at follow-up. An additional 3 patients had died, one of an unrelated carcinoma, making the mortality related to arteriovenous malformation 1.3%. The classification of Spetzler and Martin (43) was used retrospectively; the percentages of Grade I (easiest) through Grade V (most difficult) lesions were 7.8%, 22.9%, 28.8%, 26.8%, and 13.8%, respectively. The early result was well correlated to grade, with good or excellent results in 100%, 94.3%, 88.6%, 61%, and 28.6% of the patients in Grades I through V, respectively. At follow-up, 98.7% of the patients with arteriovenous malformations of Grades I, II, and III were in good or excellent condition. The late morbidity and mortality rates for the patients in Grades IV and V were 12.2% and 38.4%, respectively. Of the patients who did not have seizures before surgery, 8.2% had only one or two seizures during the immediate postoperative period, and 7.1% had late seizures that were well controlled with medication in all. Of the patients who had seizures before surgery, over half were either cured or greatly improved with respect to the seizures.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of cerebral blood flow augmentation by hemodilution in rabbits.

Background and Purpose: Hemodilution is known to increase cerebral blood flow, but it is not known whether the increase in flow is a direct result of a decrease in viscosity or whether it may be due to compensatory vasodilatation in response to the decrease in oxygen carrying capacity that results from hemodilution. This study is designed to investigate this question. Methods: Changes in regional cerebral blood flow were studied in normal and ischemic brains of 15 and 18 rabbits, respectively. In one group of rabbits graded hemodilution was used to reduce arterial oxygen content progressively in stages; in the second group the arterial oxygen content was reduced in similar stages by progressively larger reductions in the concentration of inspired oxygen (hypoxic hypoxia). In the ischemic animals focal ischemia was produced by embolic occlusion of the right middle cerebral artery. Results: In the normal rabbits, hypoxic hypoxia and hemodilution resulted in similar progressive increases in cerebral blood flow as arterial oxygen content fell. In the ischemic animals, there was a significant fall in cerebral blood flow in the ischemic region in all groups after arterial occlusion. Hemodilution resulted in a progressive increase in cerebral blood flow in both ischemic and nonischemic regions. With hypoxic hypoxia, however, cerebral blood flow in the ischemic region showed no increase or a slight decrease. Conclusions: Even though hypoxic hypoxia results in a marked increase in cerebral blood flow in normal brain, it does not significantly change cerebral blood flow in ischemic brain. In contrast, hemodilution resulting in a comparable degree of hypoxemia is capable of significantly increasing cerebral blood flow in ischemic brain. Therefore, the mechanism of blood flow augmentation by hemodilution in ischemic brain is probably related to a direct hemorheologic effect rather than to the resulting hypoxemia. (Stroke 1992;23:1487‐1493)

“Subclinoid” Carotid Aneurysm with Erosion of the Anterior Clinoid Process and Fatal Intraoperative Rupture

We present the case of a patient with an aneurysm of the right internal carotid artery with subarachnoid hemorrhage. The aneurysm had resulted in erosion of the anterior clinoid process, but this was not recognized preoperatively. Intraoperative rupture during drilling of the clinoid necessitated vigorous packing that led to unintended carotid occlusion with subsequent fatal cerebral infarction. Preoperative recognition of the clinoid erosion may have prevented this catastrophe. To call attention to the potential for intraoperative rupture during exposure, we suggest the term subclinoid aneurysm to refer to aneurysms of the internal carotid artery that grow superolaterally and remain confined under the anterior clinoid process.

Acute subdural hematoma associated with nontraumatic middle meningeal artery aneurysm: case report.

A rare case of acute subdural hematoma from rupture of a nontraumatic aneurysm of the middle meningeal artery is described. The subdural hematoma was evacuated and the aneurysm was removed. The literature on nontraumatic aneurysm of the middle meningeal artery is reviewed. The importance of cerebral angiography in the patient with an unexplained subdural hematoma is emphasized.

Evaluation of monoaminergic neurotransmitters in the rat striatum during varied global cerebral ischemia

Neurotransmitter release during cerebral ischemia has been extensively studied and is thought to play a key role in excitotoxic neuronal death. The changes in neurotransmitter release and its metabolism may reflect changes in cellular metabolism during ischemia. The purpose of this study is to assess alterations in extracellular dopamine and serotonin and their metabolites under varied degrees of ischemia in rat striatum to elucidate the pathophysiology of cerebral ischemia. Twenty rats were used to induce varied forebrain ischemia by means of bilateral common carotid artery occlusion along with hemorrhagic hypotension. Cerebral blood flow (CBF) in the striatum was measured every 40 minutes by methods of hydrogen clearance and maintained within certain ranges for 6 hours. Dopamine, serotonin, and their metabolites were measured every 20 minutes by in vivo microdialysis. Varying degrees of ischemia were obtained, ranging from 9.4 to 81.3% of control CBF. The animals were divided into three groups according to CBF levels measured 20 minutes after the induction of ischemia. In the mild ischemia group (n = 5), CBF ranged from 65 to 88% of baseline levels and resulted in only a slight increase of dopamine. In the moderate ischemia group (n = 10), CBF ranged from 21 to 48% of baseline levels and resulted in transient increases of dopamine (24-fold) and serotonin (5-fold). In the severe ischemia group (n = 5), CBF was below 14% of baseline levels and resulted in marked increases in dopamine (462-fold) and serotonin (225-fold). These alterations remained elevated for 3 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of somatosensory evoked potential monitoring to produce a canine model of uniform, moderately severe stroke with permanent arterial occlusion

To develop a reliable canine model of cerebral infarction of moderate size, we compared infarctions caused by permanent occlusion of the following vessels in 42 dogs: 1) the middle cerebral artery (MCA), 2) the MCA and azygous anterior cerebral artery (ACA), 3) the MCA, azygous ACA, and posterior cerebral artery (PCA), and 4) sham-operated controls. The infarction volume was determined at 6 hours in half the animals and at 6 days in the others. Studies of somatosensory evoked potentials (SSEPs) and regional cerebral blood flow (rCBF) were performed before and after arterial occlusion, and good correlation was observed between the decrease in amplitude of the SSEPs and the decrease in rCBF observed after arterial occlusion. Only the groups in which the MCA and azygous ACA were occluded showed moderate infarctions of relatively consistent size. Analysis involving all groups revealed that the animals with SSEP amplitude preserved after vessel occlusion had only small infarctions; thus, preservation of SSEP amplitude after occlusion of the MCA and azygous ACA could in the future be used prospectively as a rejection criterion to improve the uniformity of infarction size. Conversely, animals with loss of SSEP amplitude after vessel occlusion had infarctions of moderate to large size; thus, loss of SSEP amplitude after MCA occlusion alone could in the future be used prospectively as a rejection criterion. When these rejection criteria were retrospectively applied to the groups in which both the MCA and azygous ACA were occluded, the resulting mean infarction volumes +/- 1 SEM) for the acute and chronic subgroups were 20.3 +/- 2.8% and 38.2 +/- 4.5% of the hemisphere, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Hydrocephalus and vasospasm after subarachnoid hemorrhage from ruptured intracranial aneurysms

The relationship of the amount of subarachnoid blood to the incidence of acute hydrocephalus, delayed vasospasm, and chronic hydrocephalus was investigated in 47 patients with subarachnoid hemorrhage from ruptured intracranial aneurysms. Acute hydrocephalus, delayed vasospasm, and chronic hydrocephalus occurred in 29%, 7%, and 14% of Fisher Group 1 & 2 patients respectively, in contrast, 70%, 64%, and 58% of Fisher Group 3 patients (p less than 0.01). Thirty six percents of all patients had both acute hydrocephalus and vasospasm; Thirty two percents had neither. Twenty one percents had acute hydrocephalus, but no spasm; Eleven percents had spasm, but no acute hydrocephalus. Acute hydrocephalus and vasospasm were significantly associated (p less than 0.05). Most of patients with chronic hydrocephalus showed severe subarachnoid hemorrhage on initial CT scan, followed acute hydrocephalus, and highly associated with vasospasm. These sequelae of SAH are closely linked, mainly by the presence of subarachnoid clot, but there may be some direct causal relationship between them.