OBJECTIVE Transient neurological symptoms are frequently observed during the early postoperative period after direct bypass surgery for moyamoya disease. Abnormal signal changes in the cerebral cortex can be seen in postoperative MR images. The purpose of this study was to reveal the radiological features of the "cortical hyperintensity belt (CHB) sign" in postoperative FLAIR images and to verify its relationship to transient neurological events (TNEs) and regional cerebral blood flow (rCBF). METHODS A total of 141 hemispheres in 107 consecutive patients with moyamoya disease who had undergone direct bypass surgery were analyzed. In all cases, FLAIR images were obtained during postoperative days (PODs) 1-3 and during the chronic period (3.2 ± 1.13 months after surgery). The CHB sign was defined as an intraparenchymal high-intensity signal within the cortex of the surgically treated hemisphere with no infarction or hemorrhage present. The territory of the middle cerebral artery was divided into anterior and posterior parts, with the extent of the CHB sign in each part scored as 0 for none; 1 for presence in less than half of the part; and 2 for presence in more than half of the part. The sum of these scores provided the CHB score (0-4). TNEs were defined as reversible neurological deficits detected both objectively and subjectively. The rCBF was measured with SPECT using N-isopropyl-p-[I]iodoamphetamine before surgery and during PODs 1-3. The rCBF increase ratio was calculated by comparing the pre- and postoperative count activity. RESULTS Cortical hyperintensity belt signs were detected in 112 cases (79.4%) and all disappeared during the chronic period. Although all bypass grafts were anastomosed to the anterior part of the middle cerebral artery territory, CHB signs were much more pronounced in the posterior part (p < 0.0001). TNEs were observed in 86 cases (61.0%). Patients with TNEs showed significantly higher CHB scores than those without (2.31 ± 0.13 vs 1.24 ± 0.16, p < 0.0001). The CHB score, on the other hand, showed no relationship with the rCBF increase ratio (p = 0.775). In addition, the rCBF increase ratio did not differ between those patients with TNEs and those without (1.15 ± 0.033 vs 1.16 ± 0.037, p = 0.978). CONCLUSIONS The findings strongly suggest that the presence of the CHB sign during PODs 1-3 can be a predictor of TNEs after bypass surgery for moyamoya disease. On the other hand, presence of this sign appears to have no direct relationship with the postoperative local hyperperfusion phenomenon. Vasogenic edema can be hypothesized as the pathophysiology of the CHB sign, because the sign was transient and never accompanied by infarction in the present series.
A 15-year-old boy presented with an anaplastic supratentorial ependymoma causing massive intratumoral calcification, without contributory medical and family history, and manifesting as persistent headache for 2 months. Physical examination found no neurological deficit except for visual defect in the right lower quadrant, with intact visual acuity. Blood examination showed no abnormalities. Cranial computed tomography revealed a huge calcified mass in the left parietooccipital lobe, with extensive perilesional brain edema. Cranial radiography showed diffuse and symmetrical thinning of the calvarial bone. Magnetic resonance imaging confirmed the tumor as an assembly of medullated masses with extraventricular location, 7 × 6.5 × 6.5 cm in diameter, and appearing as heterogeneous intensity on both T 1 -and T 2 -weighted images with inhomogeneous enhancement except for the central cores. The patient underwent tumor resection. Intraoperative findings revealed that the cortical veins overlying the tumor were reddish and moderately engorged. The hypervascular tumor, entirely extraventricular in location, was totally resected without neurological deterioration. Histological examination revealed that the tumor was highly cellular with hyperchromatic nuclei and cell atypia. Necrosis, mitotic figures, and perivascular pseudorosette formations were frequently seen. Immunohistochemical study showed positive staining for glial fibrillary acidic protein, S-100 protein, vimentin, and epithelial membrane antigen, but negative for synaptophysin. The MIB-1 labeling index was 26.5%. The findings were compatible with anaplastic ependymoma (World Health Organization classification grade 3). Ependymoma should be included in the differential diagnosis of a supratentorially located, extraventricular mass with massive intratumoral calcification.
We described pregnancy and delivery management in 9 patients with cerebral arteriovenous malformation (AVM). Six patients presented with intracerebral hemorrhage (ICH) during pregnancy (first hemorrhagic episode); 2 patients presented with headache; and 1 patient with incidental detection of AVM. In the 3 patients with unruptured AVM, the diagnosis was made before pregnancy. In 3 of 6 patients who presented with ICH, AVM removal was performed during pregnancy. One patient required emergency surgery for the mass effect of the hematoma, and 2 patients with Spetzler-Martin grade I and II AVMs underwent elective surgery for the prevention of rebleeding. Radiosurgery for multiple AVMs was performed after delivery in one patient. Surgical resection and radiosurgery were performed after abortion in two patients. Of 3 patients with unruptured AVM, 2 patients became pregnant after radiosurgery and conservative treatment was initiated in 1 patient for Spetzler-Martin grade V AVM. Cesarean section was performed in 5 patients (one with severe uncontrollable pregnancy-induced hypertension) and vaginal delivery in 2 patients (one with grade V AVM). Delivery by obstetrical indication was possible in patients who underwent AVM resection during pregnancy. No rebleeding during pregnancy occurred. The maternal outcome was good except for the 2 patients with consequences of the initial ICH. The fetal outcome was good except for 2 cases of abortion. Pregnancy and delivery management in patients with AVM was successful in our institution. Early surgical intervention for AVM presenting as ICH during pregnancy could prevent rebleeding and improve the maternal and fetal prognosis.
Most of the cases with residual i-AVM lesion and neurological symptoms could deliver vaginally without worsening of symptoms. However, pregnancy with i-AVM can be complicated by rupture of i-AVM. In cases with a residual lesion with indication of treatment and rupture of i-AVM during pregnancy, meticulous care is required during pregnancy and after delivery.
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