Article abstract-Pretreatment MRI examinations of 40 immunologically competent patients with primary CNS lym-phoma (PCNSL) were evaluated (24 men, 16 women, median age 63 years). Seventy lesions were found (mean size: 19.9 mm). The number of lesions ranged from one (n 25) to six (n 1). The most frequent locations were the cerebral hemispheres (n 22), the corpus callosum (n 11), and the basal ganglia (n 11). Cerebellar manifestations were found in 10 patients. Ocular (n 2) and medullary cord (n 1) manifestations were rare. Contrast enhancement was encountered in all lesions. Although 39 patients had lesions adjacent to the CSF space, leptomeningeal spread was only present in five patients. Necrosis was seen in two lesions only. Edema was extensive in 24 patients, moderate in 11 patients, and absent in five patients. Contrast-enhancing lesions in contact with the subarachnoid space and without necrosis are characteristic of PCNSL.

BACKGROUND AND PURPOSE: CM-AVM is a recently recognized autosomal dominant disorder associated with mutations in RASA1. Arteriovenous lesions have been reported in the brain, limbs, and the face in 18.5% of patients. We report a novel association between RASA1 mutations and spinal arteriovenous anomalies.

Despite a significantly accelerated reduction in hematoma volume, the development of delayed perifocal edema was intensified by fibrinolytic therapy, which is probably related to the function of tPA as a mediator of edema formation after thrombin release and ischemia. Further experimental and clinical investigations are required to establish the future role of fibrinolysis in the management of SICH.

✓Primary intracerebral hemorrhage (ICH) is associated with a high mortality rate and severe morbidity. The treatment of choice is still controversial, given that data from several clinical trials have not provided convincing evidence to support the efficacy of surgical clot removal. Favoring early clot removal is evidence that the limited release of specific neurotoxins associated with the breakdown products of hemoglobin underlies secondary brain injury. Attention has therefore shifted to perilesional brain injury, especially brain edema, as a potential target for therapeutic intervention in patients with ICH. In this review the authors address current understanding of the causes of edema formation following ICH and the treatment options, which are mostly supportive in nature.