Umeo Ito

Regional cerebral blood flow and stroke index after left carotid artery ligation in the conscious gerbil

We measured the regional cerebral blood flow in both hemispheres of Mongolian gerbils subjected to permanent left carotid artery ligation, using [3H]nicotine as the tracer. At 1, 3 and 6 h post-ligation, neurological signs were recorded and a stroke index score was tallied for each animal. In conscious control gerbils, mean cerebral blood flow on the left side was 1.10 +/- 0.08 (S.E.M.) ml X g-1 X min-1 at the cerebral cortex, 0.58 +/- 0.02 at the hippocampus and 0.69 +/- 0.04 at the diencephalon. Animals with a stroke index score exceeding 10 were considered symptomatic. We noted a close relationship between regional cerebral blood flow and the stroke index score. In symptomatic animals, regional cerebral blood flow in the ischemic hemisphere at 1, 3 and 6 h post-ligation was less than 0.21 ml X g-1 X min-1 at the cortex and diencephalon, and less than 0.09 ml X g-1 X min-1 at the hippocampus. We suggest that unilaterally ligated gerbils manifesting a stroke index score greater than 10 represent a good experimental model for the study of ischemia.

High Colloid Oncotic Therapy for Contusional Brain Edema

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patients initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

Chronological Changes in Brain Edema Induced by Experimental Intracerebral Hematoma in Cats

To investigate the temporary profile of changing perifocal brain edema around an intracerebral hematoma (ICH), we developed an experimental ICH model using cats. The developing perifocal edema in the white matter around the hematoma was measured by means of a gravimetric technique. Edema was more severe near the ICH, and declined with increasing distance. Edema was mild 2 hours after the onset of the ICH, and was most severe in all the regions examined 3 days later. Edema decreased but still existed in all regions 7 days after the onset of the ICH. The results suggest that the mechanism of the development of edema associated with ICH seems to differ from that associated with a cold injury. This experimental ICH model proved to be useful for the study of formation, expansion, and resolution of edema associated with ICH.

Cerebral Changes during Recirculation Following Temporary Ischemia in Mongolian Gerbils

Studies on cerebral changes during recirculation after temporary ischemic insult were carried out in the Mongolian Gerbil which frequently shows anomaly of the circle of Willis. In this animal, occlusion of one side of the common carotid artery resulted in a large focal ischemia of the ipsilateral hemisphere in about 30%. Animals susceptive to ischemia could be selected by neurological symptoms observed soon after the carotid occlusion. Following temporary ischemia of 15, 30 mins., 1 hr., 3, 6 and 9 hrs., the cerebral circulation was resumed by releasing the carotid occlusion for different time lengths. A multidisciplinary and comparative approach which included a) histopathological study, b) morphological assessment on Blood-Brain Barrier (BBB) damage by Evans Blue for protein leakage and on edema, c) morphological evaluation of “no-reflow phenomenon” by injection of carbon black, d) contact autoradiographic assays on regional cerebral blood flow (rCBF) with 14C-antipyrine was made. 1. The histopathological change is related to the duration of ischemia and recirculation. The ischemic lesion appears to progress (or mature) after re-establishment of the circulation. The rate of “maturation” is related to the intensity of the ischemic insult, i.e. the shorter the occlusion time, the later the onset of tissue damage. Neuronal recovery was suggested by time course histological study. 2. The incidence and time of appearance of the BBB lesions following recirculation is related directly to the duration of the ischemic insult. When the duration of ischemia was 30 mins., BBB damage was demonstrated in 50% of animals only at 20 hours after re-establishment of the circulation. On the other hand, BBB damage was always seen in all animals at one hour after recirculation, when the duration of ischemia was 6 hours. 3. Although the duration of “no-reflow phenomenon” relates to the length of ischemia, the phenomenon is transient and lasts about 10 minutes in animals suffering from temporary ischemia up to 6 hours. 4. Following cerebral ischemia for one hour, bi-phasic, reactive hyperemia which includes oligemic phase in between was observed. Later hyperemia associates una voce with the appearance of severe tissue damage, which progressed continuously following release of carotid occlusion. The breakdown of BBB accompanied both severe tissue damage and local increase of rCBF. The histopathological changes as well as BBB damage for protein tracer appears and progresses concurrently after recirculation. Increased rCBF (luxury perfusion) was always noted when the tissue damage was severe.

Osteochondroma of the posterior clinoid process report of a case with special reference to its histogenesis

SummaryThere have been some controversial opinions as to the nature and origin of cartilaginous tumors arising from the base of the skull. An autopsy case of a giant osteochondroma arising from the posterior clinoid process is presented. The tumor connected to the posterior clinoid process in an exostotic fashion resulted, clinically, in left abducens paralysis. The tumor was encpsulated by thin fibrous tissue which was connected to the inner layer of the dura mater adjacent to the posterior clinoid process. Histologically, the tumor consited of multiple osteocartilaginous nodules which were connected by osteo-fibrous connective tissue of high vascularity. Each nodule represented a pattern similar to enchodral ossification. Precise gross and histological examinations of the tumor confirmed that it was not enchondromatous but was osteochondromatous in nature.

CT Enhancement After Three Hours of Continuous Contrast — Infusion in Acute Stage of Cerebral Infarction

There is general agreement that in stroke victims, enhancement of the infarcted tissue on the computed tomography (CT) image occurs 2–4 weeks after the stroke episode1,8,11,13,15,16. On the other hand, a hypodense mass effect due to brain edema develops within a week of the episode7,10,11, 13,16. Therefore, the question arises whether in human cerebral infarction the blood-brain barrier (BBB) change is an earlier event than is usually accepted3. To obtain a high blood concentration of the contrast medium for a prolonged period of time, we employed long-term continuous infusion of contrast medium rather than the conventional bolus injection, to study CT enhancement during the acute phase of cerebral infarction.

Malfunction of V-P Shunt System Equipped with Antisiphon Device in Normal-pressure Hydrocephalus

Three patients with normal-pressure hydrocephalus, who were treated by installation of a low-pressure ventriculo-peritoneal (V-P) shunt system equipped with anti-siphon device, did not show improvement of clinical signs and ventricular size on CT. While, the lumbar infusion manometric test in horizontal patient position showed good functioning of the shunting system in all 3 patients. However, the clinical signs and ventricular size on CT were remarkably improved by replacing the shunt system to the low pressure V-P shunt system which was not equipped with anti-siphon device. The shunt malfunction seemed to be caused by the anti-siphon function itself of the previous shunt system which was equipped with anti-siphon device, especially when the patients were kept sitting and/or standing during the daily activity.

Brain Edema and Eeg During Ischemia and After Restoration of Blood Flow

The present study is aimed towards the following; 1) to elucidate the mechanisms underlying brain edema which develops during ischemia and following the restoration of cerebral blood flow, 2) to analyze the relationship between the degree of brain edema and the duration of temporary ischemia prior to cerebral blood flow restoration, and 3) to correlate the functional recovery of the brain assessed by computer analyzed EEG to the duration of ischemia and to the degree of brain edema.