An infantile case of surgically resected brain stem cavernous angioma is presented. This 21-month-old boy was admitted to our department after repeated severe pontine hemorrhage. A deeplying lesion with hematoma was successfully removed via the IV ventricle approach. Few infantile cases of this lesion have been presented previously, and the approaches to brain stem cavernous angiomas in infants are discussed.

Brain Neoplasms↗

PubMedDate not supplied

Effects of carbonic anhydrase inhibitor on the otolithic organs of developing chick embryos.

Carbonic anhydrase appears to be involved in the process of otoconial formation. The purpose of this investigation was to observe the morphologic change in the surface structure of the otolithic organ in developing chick embryos after injection of the carbonic anhydrase inhibitor, acetazolamide. Acetazolamide (1.5, 3, or 6 mg/0.06 mL/egg) was injected into the yolk sac of the embryo of the fifth day of incubation. Embryo specimens were collected on the 11th, 13th, and 18th days of incubation. The chicks were killed on the third day posthatching, and the surfaces of the otolithic organs were observed under a scanning electron microscope. A marked disturbance in otoconial formation was noted in both utricle and saccule, marked by a decrease or absence of otoconia. A widely exposed meshwork structure of otolithic membrane was observed, with sensory cilia penetrating the meshwork small holes in many instances. There were also several otoconial abnormalities, such as the appearance of only a single giant otoconium, or from several to dozens of giant otoconia, and rough, spongy-surfaced global substances entirely covering the maculae. Clearly, carbonic anhydrase inhibitor (acetazolamide) injected into the yolk sac of developing chick embryos alters and inhibits normal otoconial morphogenesis.

Acetazolamide↗

PubMedDate not supplied

Calcium entry blocker ameliorates ischemic neuronal damage in monkey hippocampus.

Effects of treatment with (+/-)-1-(3,4-dimethoxyphenyl)-2-(4- diphenylmethylpiperazinyl)ethanol dihydrochloride (NC-1100), a calcium entry blocker, on ischemic neuronal damage were investigated. Monkeys were subjected to temporary occlusion of eight (bilateral common carotid, internal and external carotid, and vertebral arteries) major arteries. Blood flow was restored after 5, 10, 13, and 15 min occlusion, and NC-1100 (1 mg/kg) was then immediately infused intravenously. Monkeys were killed by perfusion fixation 5 days after occlusion. All brain regions were then histologically investigated for ischemic neuronal changes. Physiological data of NC-1100-treated subjects were not significantly different than those of untreated subjects. Heart rate tended to decrease after ischemia in treated subjects. Occlusion of 8 arteries for 10 to 15 min produced ischemic neuronal damage confined exclusively to the CA1 subfield of the hippocampus. Treatment with NC-1100 markedly reduced ischemic neuronal damage in the CA1 subfield of the hippocampus. It is suggested that postischemic treatment with the calcium entry blocker, NC-1100, might protect the brain from the ischemic damage produced in patients suffering from transient ischemia.

Animals↗