Discrepancies among CT, histological, and blood-brain barrier findings in early cerebral ischemia.

The development of ischemic edema and blood-brain barrier (BBB) disruption during the 1st day of experimental cerebral infarction induced by transorbital occlusion of the middle cerebral artery (MCA) in cats was evaluated by computerized tomography (CT) scanning and compared to gravimetric and pathological studies. Regional cerebral blood flow was measured using the hydrogen clearance technique or stable xenon-enhanced CT scanning. Edema was observed gravimetrically and microscopically as early as 1 hour after the onset of ischemia in the cortex and at 3 hours or later in both the cortex and white matter. However, a significant decrease of Hounsfield numbers on the CT scans was not detectable at 1 or 3 hours and was scarcely visible at 9 hours after occlusion. Disruption of the BBB was detected by leakage of Evans blue dye at 3 hours after the occlusion in two of six animals and at 9 hours in five of five animals. However, CT scanning after infusion of contrast material showed no significant increase in Hounsfield number even 24 hours after MCA occlusion. These discrepancies should be emphasized when the dynamics of ischemic edema and BBB disruption are evaluated for clinical therapy by CT scanning.

Observations on cerebral ischaemia in cats at injury threshold levels.

The potential for recovery of brain tissue subjected to ischaemia at a threshold level of injury was evaluated in cats subjected to 20 min middle cerebral artery occlusion. In addition to assessment of regional cerebral blood flow and water content, the permeability of the bloodbrain barrier and morphological changes detected by light microscopy were studied at various time intervals. Our observations revealed that although a similar reduction of blood flow during arterial occlusion was found both in the caudate nucleus and the cerebral cortex, the reactive hyperaemia was consistently higher in the caudate nucleus than in the cortex. After 24 h the caudate nucleus also revealed a significantly higher water content and increased vascular permeability than the cortex. Morphological observations at 24 h in areas affected by ischaemia showed widespread, marked ischaemic neuronal injury, whereas at 3 d there was, in addition, a vigorous proliferative reaction of vascular elements. Cats sacrificed at 14 d revealed a remarkably good preservation of neurons, both in the caudate nucleus and cortex which otherwise showed a few circumscribed, small, infarcts surrounded by normal nerve cells. Our study suggests that neurons injured at threshold level have a considerable capacity for recovery. Otherwise, with a similar degree of ischaemia, the caudate nucleus appears more prone to increased vascular permeability and oedema than the cerebral cortex.

[Arachnoid cyst of the middle cranial fossa with extraocular muscle paresis: case report].

Arachnoid cysts in the middle cranial fossa usually present with skull deformity, intracranial hypertension, epilepsy, focal symptoms and delayed mental development. Some cases, however, have neither symptoms nor signs. We have encountered a patient with an arachnoid cyst of the middle cranial fossa with extraocular muscle paresis and who was treated with cyst wall fenestration with good results. An 11-year-old boy presenting with double vision was diagnosed as having an arachnoid cyst in the middle cranial fossa with extraocular muscle paresis. He had no signs of increased intracranial pressure. This patient underwent a cyst membranectomy. Postoperatively this symptom rapidly subsided. Double vision disappeared two months postoperatively. To our knowledge, if those cases associated with increased intracranial pressure signs are excluded, this is the first case reported so far of a middle cranial fossa arachnoid cyst with extraocular muscle paresis. This report illustrates that extraocular muscle paresis can be caused by an arachnoid cyst in the middle cranial fossa and that knowledge of this could be helpful in its early diagnosis and treatment.

[Hydrocephalus in Paget's disease--a case report].

A case of Paget's disease in an elderly female who had a favourable evolution following ventriculoperitoneal (V-P) shunt is reported. On May 28, 1983, a 52-year-old female was transferred and admitted to us from the Dept. of Neurology because of headache in the occipital region and ataxic gait. On admission, neurological examinations revealed remarkably increased tendon reflexes, ataxic gait, and mild dementia. Headache was also observed, but urinary incontinence was not present. Skull X-ray showed "cotton wool appearance", which was characteristic of Paget's disease. On chemical analysis of blood and urine, serum Al-P and urinary OH-proline level were elevated, which established a diagnosis of Paget's disease. Triventricular dilatation was found on CT scan, and neck tomography showed basilar impression. After admission, the patient was treated with calcitonin, but it was interrupted because of side effects such as nausea and vomiting. Then she gradually took a turn for the worse, particularly dementia became severer. On July 25, 1983, V-P shunt was performed. After operation, "soft landing maneuver" was employed, namely the intraventricular pressure was checked and was gradually lowered with external CSF drainage system for 7 days. Thereafter the patient's head was elevated gradually from supine to sitting position through 7 days. Her hospital course after operation was that of gradual improvement. The purpose of this maneuver was to prevent sudden change of intraventricular pressure that causes aggravation of basilar impression and sudden respiratory arrest.

Retinal blood flow and its autoregulation measured by intraocular hydrogen clearance.

Retinal blood flow (RBF) was measured with polarographic electrodes at the inner retinal surface using the hydrogen clearance technique. This new intraocular technique allowed repeated and reproducible measurements of retinal blood flow. Usually the clearance curves were monoexponential, indicating that hydrogen clearance in only one compartment, the retina, was being measured. In order to quantitatively describe the autoregulation of retinal blood flow with oxygen tension, the retinal blood flow was measured at levels of arterial blood oxygen tension ranging from 20 to 250 mmHg. The retinal blood flow was found to decrease progressively with increased arterial blood oxygen tension. Linear regression analysis showed a statistical fit (P less than 0.01) between retinal blood flow and arterial blood oxygen tension (PaO2): RBF (ml min-1 100 g-1)-1 = 79.2-0.17 x PaO2 (mmHg)-1. The average blood flow in the cat was found to be 56 +/- 10 ml min-1 100 g-1 (mean +/- 1 S.D., n = 11) at an average arterial blood oxygen tension of 128 mmHg.

Effect of aminophylline on postischemic edema and brain damage in cats.

We attempted to ameliorate postischemic edema and brain tissue injury in cats by administering aminophylline to reduce the reactive hyperemia that supposedly aggravates both these sequelae. Forty-one cats were subjected to 1 hour of middle cerebral artery occlusion and were killed after 3 hours, 3 days, or 14 days of recirculation; one half of the cats received 0.916 ml/kg of a 25 mg/ml solution of aminophylline by infusion at a constant rate via the femoral vein starting 10 minutes before release of the occlusion and continuing for 5 minutes after initiation of recirculation; the other half received saline. Regional cerebral blood flow was monitored by the hydrogen clearance method and water content was evaluated by specific gravity measurements after 3 hours of recirculation; the status of the blood-brain barrier was assessed with Evans blue tracer. Morphologic observations were carried out in cats killed after 3 or 14 days of recirculation. Aminophylline-treated cats killed after 3 hours of recirculation showed significantly reduced hyperemia and edema and no leakage of Evans blue, which was present in all untreated cats killed after 3 hours or 3 days of recirculation. Morphologic observations revealed conspicuously more severe ischemic brain tissue damage in the untreated than in the aminophylline-treated cats after 3 and 14 days of recirculation. Our studies indicate the beneficial effect of administration of aminophylline in the amelioration of postischemic edema and brain tissue injury, which is presumably achieved by reduction of reactive hyperemia.