Neurologic Manifestations of Gastrointestinal and Nutritional Disorders.

OBJECTIVE: A tie between nutritional or gastrointestinal and neurologic disease has been recognized for centuries. Many gastrointestinal disorders are associated with neurologic disease through nutritional, immune-mediated, or degenerative pathophysiologies. This article reviews neurologic disorders in patients with gastrointestinal disease and gastrointestinal manifestations in their own neurologic patients. LATEST DEVELOPMENTS: Development of new gastric and bariatric surgical procedures and the widespread use of over-the-counter gastric acid-reducing medications continue to create vitamin and nutritional deficiencies despite modern diet and supplementation. Some supplements, such as vitamin A, vitamin B6, and selenium, themselves are now found to cause disease. Recent work has shown extraintestinal and neurologic manifestations of inflammatory bowel disease. Chronic brain damage in liver disease has been recognized, and the opportunity to intervene may exist in the covert beginning stages. The characterization of gluten-related neurologic symptoms and differentiation from those of celiac disease is an evolving body of work. ESSENTIAL POINTS: Gastrointestinal and neurologic diseases related to common immune-mediated, degenerative, or infectious mechanisms are common and can coexist in the same patient. Furthermore, gastrointestinal disease may cause neurologic complications because of nutritional inadequacies, malabsorption, and hepatic dysfunction. In many cases, the complications are treatable but have subtle or protean presentations. Therefore, the consulting neurologist must be current in knowledge of the growing ties between gastrointestinal and neurologic disease.

Uncertainty of leukoencephalopathies: a case report.

BACKGROUND: Adult-onset leukoencephalopathies are a group of heterogeneous disorders characterized by white matter abnormalities. Leukoencephalopathy is usually encountered in children, but here we report a case with adult-onset leukoencephalopathy. Also, we explore this concept of uncertainty in medicine by discussing the approach to this case that has multiple possible etiologies. CASE PRESENTATION: A 70-year-old Caucasian male presented with a subacute onset of cognitive impairment and mood disturbances associated with behavioral changes. Neuroimaging demonstrated high-intensity lesions involving cerebral white matter. Progressive dementia and cognitive decline followed. Multiple possible etiologies are discussed based on the patient presentation and risk factors. CONCLUSION: Adult-onset leukoencephalopathy can become a diagnostic challenge. Certain approaches need to be developed to explore the uncertainty of such conditions and to improve diagnostic yield.

A Case of Monocytic Pleocytosis in West Nile Virus Encephalitis and Review of the Literature.

West Nile Virus (WNV) encephalitis CSF findings are usually described as polymorphonuclear pleocytosis initially followed by lymphocytic pleocytosis. We report a 68-year-old female with WNV encephalitis monocytic pleocytosis and flaccid quadriparesis with ventral roots enhancement. We suggest the inclusion of neuroinvasive WNV in the differential of encephalopathy with flaccid paralysis despite a monocytic pleocytosis. We also suggest the consideration of neuroinvasive in acute polyneuropathies unresponsive to immunotherapies.

Arc de cercle and dysautonomia from anoxic injury.

Autonomic dysregulation and catatonic posturing are well described following acute cerebral injury. Others have referred to this as diencephalic seizures, sympathetic storms, midbrain dysregulatory syndrome, and, most recently, paroxysmal autonomic instability with dystonia. Some of these syndromes can evolve into malignant catatonia requiring electroconvulsive therapy. Here we report a case of hanging associated anoxic brain injury resulting in severe dysautonomia and an extreme opisthotonus (arc de cercle).