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(From Droege and Bjarngard dorex. Rothmund-Thompson syndrome (defect of a REC-Q like DNA Helicase) is autosomally reces- sively inherited. Iinjected, n ]Cn ©2003 CRC Press LLC Rsoma, j ρi lnrsoma zj 2 2 r π r s o m a z j Autonomic Disorders 187 187 Table 6 The Most Common Clinical and ANS Manifestation in the Wernicke-Korsakoff Syndrome Autonomic signssymptoms Summary of the most common clinical signs and symptoms Pathophysiological mechanism Structure involved Cardiovascular Postural hypotension Arrhythmiasheart blocks ECG changes Alcoholic peripheral neuropathy Malfunctioning sympathetic forex exchange com Hypothalamus, brainstem, postganglionic sudomotor fibers Gastrointestinal Impaired esophageal motility, gastroparesis Extrinsic autonomic nerve control Dysfunction (parasympathetic) Vagal neuropathy Vagus, enteric division of ANS Genitourinary Incontinence Disordered parasympathetic function Bladder autonomic nerve supply Sweating and temperature Hypothermia Hypohidriosis Hypothalamic lesion Early involvement of sympathetic Posterior hypothalamus Sympathetic efferent fibers Pupillary and ocular abnormalities Abnormal pupillary reflexes blurred vision Sympatheticparasympathetic imbalance Brainstem, CNs, peripheral ocular effector organs W-KS is associated with lesions in CNS (hypothalamus, mammillary bodies, cerebellar vermis) and PNS (dying-back peripheral neuropathy; long, distal vagus fibers are affected first, and shorter, proximal forex exchange com fibers get involved later) at central andor peripheral levels exchangr efferent fibers W-KS, Wernicke-Korsakoff syndrome; CNs.
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