[Myonecrosis following cerebral arterial spasm in meningitis. Case report].
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Biomedical subjects
Publications and source records attributed to K Kashihara.
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Fenestration or duplication of the internal carotid artery is extremely rare. A review of the literature revealed only two such cases by angiography. We present two further cases of internal carotid artery fenestration, incidentally disclosed by angiography. The embryological basis and the clinical significance of this anomalous condition were discussed. Case 1. A 47-year-old woman was admitted to hospital on May 13, 1982, after the first attack of subarachnoid hemorrhage. Four-vessel angiography showed a saccular aneurysm arising at the trifurcation of the right middle cerebral artery. In addition, a fenestration of the right internal carotid artery was demonstrated at the level of the atlas: the cervical portion of the vessel distal to the level of C-2 was markedly elongated and dilated in caliber. Moreover, the right external carotid artery occupied a dorso-lateral position relative to the internal carotid artery. Case 2. A 51-year-old man was admitted to hospital on April 20, 1983, for evaluation of grand mal seizures. CT scans and four-vessel angiograms showed a malignant glioma of the right temporal lobe. Additionally, a fenestration of the right internal carotid artery was identified at the level of the atlantoaxial joint, and the vessel was dilated in caliber at the level of C-1 to C-2.
A systematic radiological and pathological study of the cerebral arteries was made in an autopsy case of meningitis associated with three phases of cerebral arteriopathy. The latter consisted of vasospasm, vasodilatation, and organic stenosis. A marked change in the caliber of the cerebral arteries was demonstrated 3 times. Vasospasm, the stimulus phenomenon, was produced by the surrounding purulent material. Vasodilatation, the paralytic phenomenon, was presumably due to decreased contractile energy in association with myonecrosis. Organic stenosis, the repair process, was due to the organization of subendothelial edema with resultant intimal thickening. Evidence of increased endothelial permeability, subendothelial proliferation of smooth muscle cells, and necrosis of the latter in the media is presented in both light and electron micrographs.
Rats received once daily injections of methamphetamine (MAP; 4 mg/kg/day) intraperitoneally, at most 100 times. Enhanced ambulatory activity by MAP reduced during the long-term administration of MAP. The mean rating score of MAP-induced abnormal behavior, including locomotion, stereotyped behavior, motor inhibition and the response to acoustic stimulation, increased until 56th injection of MAP. But after that, the score tended to decrease mainly because the injected MAP failed to keep the movement of rats reduced under acoustic stimulation. Neither the time course of these rating score nor the decrease in [3H] spiperone binding sites, examined after the injection of MAP 100 times, seemed to develop along with the repeated MAP administration. Thus, the changes in both behavior and [3H] spiperone binding sites produced by repeated MAP would not necessarily indicate the symptoms of MAP-induced psychosis in man, because the susceptibility to psychosis in man increases along with the time of MAP injection. It is presumed that the animal model of psychosis produced by administration of MAP is important not as a model of psychotic symptoms, but as a model of increased susceptibility to psychosis induced by MAP.
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The presence of high and low affinity 3H-spiperone binding sites was demonstrated in both the rat striatum and mesolimbic area. Dopaminergic receptor component was displaced by 10 microM 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (ADTN), and serotonergic receptor component by 0.2 microM mianserin. Dopaminergic receptor component was saturated at less than the range of ligand concentrations labeling the high-affinity binding sites. Treatment with 4 mg/kg of methamphetamine (MAP) for 14 days, followed by a 7-day drug-free period, resulted in significant changes in the maximal number of binding sites (Bmax) at the high-affinity sites (an increase in the mesolimbic area and a decrease in the striatum), but no significant changes in Bmax at the low affinity sites. The long-lasting increase in mesolimbic Bmax at the high-affinity 3H-spiperone binding site may be an underlying basis for MAP-induced behavioral hypersensitivity (reverse tolerance).
In this report, the relationship of acoustic neuromas to the adjacent cranial nerves is discussed. On T1-weighted images, the trigeminal nerve was detected in all 13 cases. Mild to marked compression of these nerves by the tumors was observed in eight cases. The extent of compression did not always correspond to the clinical symptoms. In four cases with a maximum tumor diameter of 2 cm or less, the 7th and 8th cranial nerves were identified. There was no facial palsy in these patients. Two patients with a tumor diameter of more than 2 cm also had no facial palsy. All patients, including those with small tumors, complained of hearing loss and/or tinnitus. While MR imaging has some limitations, it is an effective imaging modality for showing the relationship between tumors and nerves.