SummaryIt has been our observation that in the presence of concave deformity of the skin flap following large decompressive craniectomy, unexpected neurological deterioation would occur independently of the primary disease or natural improvement would be unduly impaired, and that such unfavorable phenomena were reversed by cranioplasty. In order to know the true incidence and the nature of this phenomenon, 33 consecutive cases were analyzed. Nine of 30 patients (30%) with flat or sinking skin flap showed prompt improvement following cranioplasty. The best 'candidates' for maximum benefit of cranioplasty were those with moderate grade neurological deficits in addition to the presence of concave deformity of skin flap (successful rate of 88%; 7 among 8 patients).Other factors influencing the results were primary disease (favorable to meningioma), time elapse from the decompressive craniectomy, presence of shunt system, CSF pressure and EEG changes before and after cranioplasty. EEG changes had well coincided with clinical course.The characteristic phenomenon would be described as "the syndrome of the sinking skin flap," considering that neurological deterioration may be due solely to effect of concave deformity of the skin flap upon the underlying brain tissue.
Autologous brain tumor specific CTLs were induced from the patient's PBL by a mixed lymphocyte-tumor culture, and were maintained for more than 2 months in a medium containing exogenous IL-2. The autologous T cell line containing specific CTL was administered into the tumor-bed for the treatment of malignant glioma. In 2 cases out of 5, tumors regressed more than 50% in diameter. One of these patients is still alive now with full of his social activities, and it is 104 weeks after the initiation of the immunotherapy. Autologous T cell lines were safely administered in all cases without any complications nor toxicities.
SUMMARY Three Japanese families with moya-moya disease in six patients are presented. These six patients were among 49 cases of confirmed moya-moya disease in our experience, and the familial incidence was more than 12%. A relatively high familial incidence (7%) was found in the total Japanese scries emphasising the important hereditary components in the pathogenesis of the disease. (Fig. 2) and WISC were essentially the same as in the previous studies.Case 1.2 This 11 year old girl was the younger sister of case 1
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