The Clinical Dilemma of Anticoagulation Use in Patients with Cerebral Amyloid Angiopathy and Atrial Fibrillation.

PURPOSE OF REVIEW: This review highlights current management of patients with concomitant cerebral amyloid angiopathy (CAA) and atrial fibrillation (AF). We review quantifying risk of ischemic and hemorrhagic stroke as well as treatments to minimize future risk. RECENT FINDINGS: Ischemic stroke risk in AF can be quantified by CHA2DS2-VASc and assessing left atrial echocardiographic characteristics. Patients deemed not low risk by CHA2DS2-VASC should be anticoagulated. CAA increases intracranial hemorrhage risk. CAA biomarkers include cortical microbleeds (CMBs), cortical superficial siderosis (cSS), convexal subarachnoid hemorrhage (cSAH), and lobar intracerebral hemorrhage (ICH). CAA with prior lobar ICH has an annual recurrence rate of 8.9%. CAA with cSAH carries an even higher annual lobar ICH risk of 19%. CMBs are associated with a dose-dependent risk of ICH, which rises with OACs. In patients with AF, antithrombotics should be avoided in CAA with predominant ICH, cSS, or cSAH features. Those with ≥ 2 CMB require in-depth risk-benefit analysis using a multidisciplinary approach.

CNS small vessel disease: A clinical review.

CNS small vessel disease (CSVD) causes 25% of strokes and contributes to 45% of dementia cases. Prevalence increases with age, affecting about 5% of people aged 50 years to almost 100% of people older than 90 years. Known causes and risk factors include age, hypertension, branch atheromatous disease, cerebral amyloid angiopathy, radiation exposure, immune-mediated vasculitides, certain infections, and several genetic diseases. CSVD can be asymptomatic; however, depending on location, lesions can cause mild cognitive dysfunction, dementia, mood disorders, motor and gait dysfunction, and urinary incontinence. CSVD is diagnosed on the basis of brain imaging biomarkers, including recent small subcortical infarcts, white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces, and cerebral atrophy. Advanced imaging modalities can detect signs of disease even earlier than current standard imaging techniques. Diffusion tensor imaging can identify altered white matter connectivity, and blood oxygenation level-dependent imaging can identify decreased vascular reactivity. Pathogenesis is thought to begin with an etiologically specific insult, with or without genetic predisposition, which results in dysfunction of the neurovascular unit. Uncertainties regarding pathogenesis have delayed development of effective treatment. The most widely accepted approach to treatment is to intensively control well-established vascular risk factors, of which hypertension is the most important. With better understanding of pathogenesis, specific therapies may emerge. Early identification of pathologic characteristics with advanced imaging provides an opportunity to forestall progression before emergence of symptoms.

Adult Intestinal Botulism: A Rare Presentation in an Immunocompromised Patient With Short Bowel Syndrome.

The cholinergic heat-labile neurotoxin produced by Clostridium species is primarily responsible for the clinical manifestations of botulism. The classic phenotypic presentation of botulism consists of subacute descending flaccid paralysis with intact sensory function. Traditionally, it is classified into 3 main forms (foodborne, wound-related, and infantile) on the basis of primary site of toxin entry into the human nervous system. Toxemia is the common pathophysiology in all forms of botulism. Adult intestinal toxemia botulism is an extremely rare form of the disease with pathogenesis similar to that of infant-type botulism. Symptomatic adults usually have an anatomic abnormality in the gastrointestinal tract leading to changes in normal gut flora. The current case is an addition to the growing literature on this unusual clinical variant of botulism.