M. Gotoh

Experimental study of venous circulatory disturbance by dural sinus occlusion

SummaryUsing a newly devised model of dural sinus occlusion, we investigated the pathophysiology of venous haemorrhage as well as venous circulatory disturbance. The superior sagittal sinus (SSS) and diploic veins (DV) were occluded in 16 cats. Intracranial pressure (ICP), cerebral blood volume (CBV) and regional cerebral blood flow (rCBF) were measured for 12 hours after the occlusion. At the end of the experiment, cerebral water content was estimated. In another 8 cats additional occlusions of cortical veins were carried out. In both groups, the blood-brain barrier permeability was evaluated with Evans blue or horseradish peroxidase.The SSS and DV occlusion produced a significant increase in ICP and CBV concomitant with a significant decrease in rCBF. Cerebral water content also increased significantly. However, there was no transition of Evans blue and horseradish peroxidase through the cerebral vessels, and no haemorrhages could be observed. In contrast, the additional occlusion of cortical veins produced haemorrhagic infarctions with Evans blue extravasation in 6 out of the 8 cats.These data suggest that dural sinus occlusion may lead to an increase in CBV and cerebral water content resulting in intracranial hypertension and decreased rCBF. The brain oedema in this model seemed to be mainly hydrostatic oedema, and might also be contributed by cytotoxic oedema. The additional occlusion of cortical veins might be essential in the development of haemorrhage in this model, and the blood-brain barrier was also disrupted in these areas.

The relationship between brain surface elastance and brain re-expansion after evacuation of chronic subdural hematoma

BACKGROUND Brain stiffness has been thought to be a factor affecting brain re-expansion after the evacuation of chronic subdural hematoma. METHODS As an index of brain stiffness, the pressure for compressing the brain using an ophthalmodynamometer was defined as brain-surface elastance. This elastance in 14 patients was measured and analyzed in relation to brain re-expansion. RESULTS Patients with an enlarged subdural space on computed tomography 1 month after the operation had higher elastance. There was a correlation between high elastance and high age. CONCLUSIONS Measuring the elastance after evacuation of the hematoma may help predict the persistence of a subdural space.

Sequential changes in MR images of the brain in acute carbon monoxide poisoning.

Two cases of acute carbon monoxide poisoning are presented in this paper. Sequential magnetic resonance (MR) images of the brain showed abnormal lesions in the bilateral globus pallidus and/or in the subcortical white matter. The MR images disclosed that the severity of the white matter lesions correlated with the prognosis in acute carbon monoxide poisoning. However, they did not always correspond to the neurological condition in the acute and subacute stages.

Magnetic resonance imaging of patients with intention tremor

We evaluated the magnetic resonance images of the patients with intention tremor. Five patients out of seven had some atrophic structures or changes in signal intensity in the cerebello-rubral thalamic tract. Moreover, the T2-weighted images of the patients group detected the dentate and red nuclei more poorly than those of our control group. From these results, the etiological significance of the tract was confirmed and the mechanism of the intention tremor onset was discussed.

Superoxide scavenging activity in the extracellular space of the brain in forming edema.

We carried out a time course study of cerebral superoxide scavenging activity using a modified microdialysis technique. Twelve cats were divided into two groups; six were the reperfusion injury models, and six were cold injury models. In the reperfusion injury model, dialysates were collected during 60 minutes of middle cerebral artery occlusion and at 300 minutes during reperfusion. In the cold injury model, dialysates were collected 240 minutes after the injury. Regional cerebral blood flow on the injured side decreased during occlusion in the reperfusion injury model and 60 minutes after injury in the cold injury model. In the reperfusion model, superoxide scavenging activity, as determined with electron spin resonance, increased in the first 30 minutes and decreased 300 and 330 minutes after occlusion. In the dialysate, albumin increased 180 minutes after cold injury, which may show the progress of vasogenic edema. An increase in water content was observed on the injured side of both models, and a correlation between water content and superoxide scavenging activity was found in the reperfusion injury model. By this technique, a method of detecting the alteration of superoxide scavenging activity in the extracellular space of the brain was established.

Endogenous Superoxide Dismutase Activity in Reperfusion Injuries

To elucidate the relationship between reperfusion injuries and free radicals, we monitored the endogenous superoxide dismutase (SOD) activity by intracerebral microdialysis. Six cats underwent a transient occlusion of the middle cerebral artery for 60 minutes after microdialysis probes were implanted bilaterally into the white matter under the ectosylvian gyrus. Dialysates were collected at 30 minute intervals over the course of 5 hours after reperfusion. The SOD activity of the dialysates was measured with electron spin resonance spectrometry. Regional cerebral blood flow was measured simultaneously and the water content of the white matter was assayed at the end of the experiment. After reperfusion, SOD activity increased significantly in the first 30 minutes compared with the preoperative value, and decreased over 4-4.5 hours and 4.5-5 hours in the occluded side. The water content in the occluded side was significantly higher than that in the contralateral side. The highest SOD activity during reperfusion and the water content in the occluded side seemed to correlate, although not significantly. A leakage of intracellular SOD or a reactive increase of SOD activity in response to the reperfusion injury are possible mechanisms of increase in extracellular SOD.

Superoxide scavenging activity in vitro and in the cerebral extracellular space measured by microdialysis.

Using the electron spin resonance (ESR) spin-trapping method and a high molecular cut-off membrane, we measured the superoxide scavenging activity in dialysates obtained from microdialysis. The activity in the dialysates of the Cu,Zn-superoxide dismutase (SOD) solution and feline serum were measured in vitro, and the recovery rate was calculated to be 12.88 +/- 0.9% in Cu,Zn-SOD solution and 21.52 +/- 4.38 in feline serum, which was significantly different. This difference was believed to originate from the higher osmotic pressure due to proteins in the serum and substances other than Cu,Zn-SOD that acted as antioxidants in the serum. In an in vivo study, microdialysis probes were implanted into the cerebral hemispheres in 6 cats. The sequential changes of superoxide scavenging activity were measured for 16 h and during induced cardiac arrest. No significant difference was observed and the microdialysis technique itself did not seem to cause the significant alteration of the activity in the extracellular space, although at cardiac arrest, the activity varied widely. This method can be used to study the reaction against superoxide injury in further experiments involving brain insult.

Effect of External Decompression on Cerebral Venous System Occlusion

Decompressive craniectomy (external decompression) is available for patients with uncontrollable intracranial hypertension. However, some authors have reported that external decompression has no beneficial effects due to edema enhancement [1]. We have developed a new experimental model of cerebral venous system occlusion [8]. The venous occlusion in this model led to intracranial hypertension. In this study, we investigated the effect of decompressive craniectomy on the cerebral circulation and cerebral edema in this model.

Experimental Study on Cerebral Venous Circulatory Disturbance

It is well known that the disturbance of cerebral venous circulation, such as resulting from dural sinus thrombosis or occlusion of large cerebral veins or dural sinus during surgery, often leads to brain swelling which causes neurological deficits. However, the pathophysiology of venous circulatory disturbance is poorly understood because of difficulties in making standardized experimental models. In this study, the authors have developed a new experimental model and studied the pathophysiology of cerebral venous circulatory disturbance using this model.

Experimental Study in Cerebral Venous Circulatory Disturbance: With Special Reference to Venous Hemorrhage

Using a new devised model of dural sinus occlusion, we investigated the pathophysiology including venous hemorrhage. Sixteen cats received, the occlusion of superior sagittal sinus(SSS) and diploic veins(DV). Intracranial pressure(ICP), cerebral blood volume(CB V) and regional cerebral blood flow(rCBF) were measured for 12 hours. At sacrifice, cerebral water content was determined. Other 8 cats received the additional occlusion of cortical veins(CV). In both groups, the blood-brain barrier(BBB) permeability was evaluated with Evans blue. The SSS and DV occlusion produced a significant increase in ICP and CBV and a significant decrease in rCBF. Cerebral water content also increased significantly. However, neither extravasated Evans blue nor venous hemorrhage could be observed, when thrombus was defined within SSS. Contrarily, the additional CV occlusion produced hemorrhagic infarctions in 6 cats, where Evans blue dye extravasated. These data suggest that durai sinus occlusion led to an increase in CBV and cerebral water content resulting in intracranial hypertension, and decreased rCBF. The brain edema in this model seemed to be hydrostatic edema. The obstruction of CV might be essential in the development of hemorrhage in this model, and the BBB was disrupted in these areas.