angiotensin-amide and Cerebral-Hemorrhage

The aim of this study is to describe a case of pathologically proven cerebral amyloid angiopathy-related inflammation (CAA-I) without cerebral microbleeds (CMBs) and its clinical course.. CAA-I is an uncommon variant of cerebral amyloid angiopathy. Keys to diagnosis rely on the physician's awareness of this entity, CMBs on magnetic resonance imaging (MRI), an often favorable response to immunosuppression, and ultimately brain biopsy. CAA-I with no CMBs is rarely reported.. A 76-year-old woman presented with 4 weeks of headaches and was found to have visual neglect on the left part of the visual field. MRI of the brain showed sulcal/gyriform hyperintensity with associated leptomeningeal enhancement in the right occipital lobe on fluid-attenuated inversion recovery (FLAIR) imaging. No CMBs or large parenchymal FLAIR lesions were seen on MRI. Biopsy was consistent with CAA-I. The patient's headaches resolved spontaneously and no immunosuppression was initiated. The patient remained asymptomatic for the 18 months of follow-up.. To the best of our knowledge, there has been only one previous case of pathology-proven CAA-I without CMBs reported and this was associated with a good prognosis. Lack of CMBs and/or large parenchymal FLAIR lesions may be a prognostic factor in this disease.

Topics: Aged; Angiotensin Amide; Cerebral Amyloid Angiopathy; Cerebral Hemorrhage; Diabetes Mellitus; Female; Humans; Inflammation; Magnetic Resonance Imaging

In the late 1970s, high cerebral blood flow was perceived as a cause of intracranial hemorrhage in the preterm infant. Intracranial hemorrhage was diagnosed by computed tomography and ultrasound found to be frequent not only in babies who died. Hemorrhage was soon linked to cerebral palsy in survivors. The analogy was hypertensive hemorrhagic stroke in the adult. Cerebral hemorrhage was perceived as the major (preventable) cause of brain injury in the preterm baby. An immature cerebral autoregulation or a vulnerability of the autoregulation exposed by preceding hypoxia or ischemia therefore became a focus of neonatal brain research in the 1980s. Over the years the focus has changed, first to the pathogenesis of hypoxic-ischemic brain injury, then to the effects of pCO(2), and now 30 years later to a more comprehensive, less clearly hypothesis-driven exploration of the multitude of factors involved in cerebral blood flow and oxygenation. Meanwhile, some basic questions regarding autoregulation remain unanswered, and some concepts from the 1970s still direct clinical practice.

Topics: Angiotensin Amide; Cerebral Hemorrhage; Cerebrovascular Circulation; History, 20th Century; History, 21st Century; Homeostasis; Humans; Hypnotics and Sedatives; Infant; Infant, Newborn; Infant, Premature, Diseases; Neonatology