Nobuyoshi Ogata

Moyamoya disease in Europe, past and present status

A questionnaire was distributed in early 1996 to 160 leading European neurological, neuro-pediatric and neurosurgical centers to assess the present status of Moyamoya disease in Europe. The response rate was 43%. Information was obtained on a total of 168 patients, of whom 110 had presented before 1992, and 58 from 1993 onward. 82% of the patients were Caucasian. In all other respects, the clinical findings were similar to those observed in Japan. The present study yields an incidence of 0.3 patients per center per year, which is approximately one-tenth of the incidence in Japan. Alongside these results, the history of the recognition and treatment of this disease in Europe is briefly discussed.

Alterations of a 200 kDa Neurofilament in the Rat Hippocampus after Forebrain Ischemia

Alteration in the concentration of a 200 kDa neurofilament (NF200) in the rat hippocampus after forebrain ischemia and its relationship to hippocampal neuronal death were studied with an anti-200 kDa neurofilament antibody, using immunohistochemical and immunoblotting techniques. In rats subjected to 8 min of transient forebrain ischemia, hematoxylin-eosin staining showed survival of most of the neurons in the hippocampal CA1 region at 1 day and loss of more than 75% of the neurons at 7 days after ischemia. Immunoblotting showed that the concentration of NF200 in the hippocampal homogenate tended to decrease after ischemia, to 69% of that of control at 1 day and to 60% of the control value at 7 days after 8 min of forebrain ischemia. Following 5 min of ischemia as well, the decrease in the concentration of neurofilaments in the hippocampal region preceded histological confirmation of neuronal cell death. These results suggest that degradation of neurofilament triplet proteins occurred even after ischemia of minimal duration and preceded neuronal death. Degradation of cytoskeletal proteins may play an important role in the mechanism of delayed neuronal death after cerebral ischemia.

Paramedian Supracerebellar Approach to the Upper Brain Stem and Peduncular Lesions

OBJECTIVE The infratentorial paramedian supracerebellar approach is useful for lesions involving the upper brain stem or the cerebellar pedunculi. We provide a precise description of this approach and its indications. METHODS Four patients were operated on using this approach. The lesions included a squamous cell carcinoma, a glioblastoma multiforme, a hematoma, and a cavernoma. The lesions involved the quadrigeminal plate, the superior cerebellar peduncle, the middle cerebellar peduncle, and the quadrangular lobule of the cerebellum. RESULTS Postoperatively, there was no apparent aggravation of neurological symptoms. The main advantage of the approach was that the operation can be performed with a wide horizontal view without sacrificing the deep veins. CONCLUSIONS It is concluded that lesions in the superior and inferior colliculus, superior and middle cerebellar peduncles, and quadrangular lobules of the cerebellum can be safely operated on with this approach.

Degradation of Mitochondrial Phospholipids During Experimental Cerebral Ischemia in Rats

Changes in content of brain mitochondrial phospholipids were examined in rats after 30 and 60 min of decapitation ischemia compared with controls, to explore the degradation of the mitochondrial membrane and its relation to dysfunction of mitochondria. Activities of respiratory functions and respiratory enzymes (cytochrome c oxidase; F0F1‐ATPase) decreased significantly during ischemia. Considerable decreases in cardiolipin and phosphatidylinositol content were observed after 60 min, and other phospholipids showed similar but nonsignificant decreases in content. The amount of polyunsaturated fatty acid chains, such as arachidonic and docosahexaenoic acids, was reduced in each phospholipid, in some cases significantly, after 30 and 60 min of ischemia in time‐dependent manners. Degradation of mitochondrial phospholipids during ischemia associated with the deterioration of mitochondrial respiratory functions suggested the significance of such changes in phospholipid content in disintegration of cellular energy metabolism during cerebral ischemia.

Immunohistochemical Assessments of P53 Protein Accumulation and Tumor Growth Fraction During the Progression of Astrocytomas

P53 protein accumulation and growth fraction were assessed immunohistochemically in primary and recurrent astrocytoma with malignant progression. The tumors analyzed were diffusely infiltrating astrocytomas of the cerebral hemispheres and they were graded according to the World Health Organization (WHO) criteria into low grade astrocytoma (grade II), anaplastic astrocytoma (grade III), and glioblastoma (grade IV). The fraction of P53-positive cases, i.e., biopsies containing P53 immunoreactive cells, significantly increased during progression, in group II–III from 65% to 90%, in group II→IV from 68% to 95%, and in group III→IV from 69% to 100%. None of the initially P53-positive cases became P53 negative after progression. During progression, the P53 labeling index (LI)increased significantly in groups II→III (3.5%→9.8%) and II→ IV (3.3%→13%), suggesting that P53 immunoreactive glioma cells may have a growth advantage. The mean proliferating cell index (PI), analyzed by monoclonal antibody MIB-1, increased significantly in groups II→III (2.5%→11%), II→IV (2.9%→19%), and III→IV (8.7%→16%). Gemistocytes showed a significantly lower PI than the average of all tumor cells.

Effect of nerve growth factor on delayed neuronal death and microtubule-associated protein 2 after transient cerebral ischaemia in the rat

The protective action of nerve growth factor (NGF) on delayed neuronal death (DND) after transient cerebral ischaemia and on the associated decrease in microtubule-associated protein 2 (MAP2) has been investigated. Transient forebrain ischaemia was induced for different periods (2 min, 5 min, and 8 min) in male Wistar rats by transient bilateral occlusion of the common carotid arteries and by lowering the systemic blood pressure to 50 mmHg. Histological evaluation of neuronal cell death and immunoblot analysis of MAP2 were made on the first and the seventh days after ischaemia. The mean cell death on the seventh day after ischaemia was 2.0%+/-1.8% in the 2-min group (n=6), 41%+/-19% in the 5-min group (n=6), and 75%+/-20% in the 8-min group (n=6). The concentration of MAP2 in the hippocampal homogenate 24 hours after ischaemia decreased to 82%+/-9% of the control value in the 2-min group (n=6), to 65%+/-8% in the 5-min group (n=6), and to 58%+/-4% in the 8-min group (n=6), and it remained constant at these levels through the seventh day after ischaemia. The protective action of NGF against DND was studied by administering 2 mug of 2.5S NGF (NGF-treated group, n=6) or artificial cerebrospinal fluid (CSF-treated group, n=6) through an osmotic pump implanted in the lateral ventricles 48 hours before the onset of ischaemia. The mean cell death on the seventh day after ischaemia was 42%+/-31% in the CSF-treated group, and 11%+/-15% in the NGF-treated group. The concentration of MAP2 in the hippocampal homogenate on the first day after ischaemia was 75%+/-9% in the CSF-treated group, and 82%+/-6% in the NGF-treated group, and it remained at about the same levels up to the 7th day after ischaemia. These results suggest that, 1: degradation of MAP2 precedes DND, 2: the severity of the preceding decrease of MAP2 correlated well with the severity of the DND, 3: intraventricular NGF has a protective effect against DND, and 4: the effect of NGF brain injury may be mediated by the modulation of MAP2 metabolism.

Regeneration of the Rat Carotid Artery after Clipping Injury. Part II. A Pharmacological Study

This study investigated the natural course of functional recovery of the vascular endothelium and smooth muscle after clipping injury of the rat carotid artery. Vascular injury was induced by clipping the right carotid arteries of Wistar rats. The contractile response to KCl, serotonin (5-hydroxytryptamine), and norepinephrine was decreased immediately after arterial injury. The response to KCl and serotonin recovered within 8 weeks, whereas the response to norepinephrine recovered after 12 weeks. Endothelium-dependent relaxation also disappeared immediately after clipping injury, but the recovery of relaxation in response to acetylcholine and adenosine triphosphate was observed within 1 week. Four weeks after clipping injury, higher doses of acetylcholine induced slight arterial contraction. These findings suggest that the recovery of smooth muscle contractility was slower than the process of endothelial regeneration in the rat carotid artery after clipping injury. Endothelium-dependent relaxation recovered within only a week, although the characteristics of the arterial cholinergic receptors may have changed in the chronic recovery stage.

Intraoperative monitoring during carotid cross-clamping with near-infrared spectroscopy: a preliminary study.

Near infrared spectroscopy (NIRS) is a noninvasive and real-time method for monitoring oxy-[HbO2] and deoxyhemoglobin [Hb] in tissue, and is suitable for intraoperative monitoring. In this study, NIRS monitoring was performed on 10 patients during carotid cross-clamping. The data were analyzed with a theoretical cerebral hemoglobin model developed to identify an ischemic pattern using NIRS parameters. Temporal profiles of changes in [HbO2] and [Hb] were divided into three phases: initial (immediately after clamping), second (during clamping), and last phase (immediately after clamp release). In the initial phase, [HbO2] decreased and [Hb] increased in all the cases. In the second phase, recovery patterns of [HbO2] were classified into three groups: complete (3 patients), incomplete (3 patients), and no recovery (2 patients). In the last phase, the [HbO2] increased and [Hb] decreased. Relative changes in [HbO2] and [Hb] measured by NIRS were correlated with changes in blood flow of the internal carotid artery (ICA) measured by a magnetic flowmeter and stump pressure of the internal carotid arteries. The degree of [HbO2] decrease in the initial phase was significantly correlated with ICA blood flow before clamping (r=0.90, p<0.05). Three of the 4 patients with ICA stump pressure over 50 mmHg showed a complete recovery pattern in the second phase, while all 4 patients with ICA stump pressure under 50 mmHg showed an incomplete recovery or no recovery pattern with NIRS. These results suggest that NIRS is useful in evaluating changes in cerebral blood flow and the extent of hemodynamic reserve during carotid cross-clamping.

Regeneration of the Rat Carotid Artery after Clipping Injury. Part I. A Morphological Study

We investigated the natural course of the morphological regeneration of the endothelium and smooth muscle of the rat carotid artery after clipping injury. Vascular damage was produced by clipping the right carotid arteries of Wistar rats. Endothelial regeneration was confirmed by the injection of Evans blue dye and the detection of factor VIII-related antigen. The volume of the smooth muscle cell layer and the luminal size were measured by computer-assisted morphometric analysis. Immediately after arterial injury, Evans blue dye freely permeated the smooth muscle layer, suggesting that complete endothelial denudation had occurred. Endothelial regrowth started within 24 hours and was fastest on the third and fourth days after injury. The endothelial injury was repaired within 5 days. The area of the smooth muscle layer did not change immediately after clipping injury, but it gradually increased within a month. The luminal area of the injured artery increased during the 3-month recovery period. These findings suggest that endothelial regrowth is completed within a week after clipping injury, whereas smooth muscle cell regrowth is slower. In addition, arteriosclerotic luminal narrowing did not occur during recovery of the rat carotid artery from clipping injury.

Recurrent sleep attacks associated with a craniopharyngioma

Abstract Symptomatic narcolepsy, once regarded as common, is now believed to be very rare. A 32-year-old man had a history of recurrent sleep attacks. A magnetic resonance imaging scan revealed a third ventricle tumor. The tumor was totally removed, and the histology was a craniopharyngioma. The symptoms ceased after the operation. The chronological correlation and the anatomical location of the tumor suggest that the patient had a symptomatic narcolepsy caused by the tumor. This is the first report that documents the cessation of narcolepsy attacks after tumor removal.