No abstract

A study was designed to investigate hyperperfusion syndrome after the restoration of normal cerebral blood flow in a chronically cerebral ischemic state resulting from high-flow arteriovenous malformations or severe carotid stenosis. A fistula between the left distal common carotid artery and the jugular vein was created and the left vertebral artery was simultaneously occluded in 44 cats to produce a chronic cerebral ischemic state. For control experiments, 10 cats underwent occlusion of the left common carotid and vertebral arteries. Six weeks later, pial arterial behavior, disruption of the blood-brain barrier (BBB), and cerebral histological changes were investigated using three experimental methods. In the first, in which a fistula was occluded under normal conditions, pial arteries contracted to some 80% of the resting state; however, no BBB disruption or histological changes were observed. In the second experiment, in which a 20-minute occlusion of the left middle cerebral artery was performed in the cats with a patent fistula, a 30% to 40% dilated state of the pial arteries continued after recirculation, and BBB disruption-induced cerebral edema and infarction were observed. These findings were more prominent in the cats that underwent occlusion of the fistula. On the other hand, in the control group, the pial arteries returned to resting size within 40 minutes, and no BBB disruption or histological changes were observed. In the third experiment, in which moderate hypertension was induced for 1 hour, the pial arteries dilated much more remarkably; BBB disruption and cerebral edema were revealed to be more extensive in the cases of fistula occlusion than within those with a patent fistula. In the control group, however, the pial arteries contracted 10% during hypertension, while BBB disruption and histological changes were not evident. The results indicate that the perfusion pressure breakthrough threshold in the chronically ischemic brain may not be reduced by the restoration of normal blood flow, but may be decreased by the addition of new ischemic insults or hypertension.

An 83-year-old man presented with gait disturbance, dementia, and urinary incontinence that had progressed over 2 months. Computed tomography (CT) of the brain revealed hydrocephalus due to a well-demarcated, round hyperdense mass in the third ventricle, which was not enhanced by contrast agent. Ten days after the initial evaluation, CT revealed that the cyst in the third ventricle had disappeared. Magnetic resonance imaging revealed spontaneous rupture of the lesion and remnants of cyst wall anchored to the anterior roof of the third ventricle. Thereafter, the symptoms of hydrocephalus subsided. However, 6 months later the patient's condition gradually deteriorated and the ventricles dilated without any evidence of tumor regrowth. Surgical intervention was not performed as the family of the patient withheld consent. The natural history of colloid cysts of the third ventricle remains unclear. Spontaneous rupture of a presumed colloid cyst of the third ventricle should be considered when planning treatment.

BAK-optimized tafluprost is a treatment option to improve the condition of the ocular surface and to maintain IOP control in glaucoma patients with existing SPK who have been previously treated with other BAK-preserved prostaglandin analogs.