مقاله انگلیسی رایگان در مورد اختلالات متابولیکی سیستمیک و تغذیه ای – الزویر 2018

Vitamin deficiencies

Metabolic encephalopathies

Calcium metabolic disorders

References

Abstract

Vitamin deficiency disorders display a wide variety of neurologic signs and symptoms, the pathogenesis of which is not clearly understood. Metabolic encephalopathies (hepatic, hypoglycemic, and uremic) have to be considered in the differential diagnosis of patients with cognitive impairment, motor disturbances, psychiatric symptoms, seizures, and neuropathies. Calcifications (vascular wall and parenchymal) occur in the normal aging brain and in neurodegeneration; some associated genes are already described.

Thiamine (vitamin B1) Wernicke encephalopathy

Wernicke–Korsakoff syndrome is one of the most frequently seen neurologic disorders associated with long-term and heavy alcohol abuse (Victor et al., 1971). Clinical signs of Wernicke encephalopathy may present with acute or subacute onset. Ocular alterations consist of retinal hemorrhage, pupillary changes, extraocular muscle palsy, gaze palsy, and nystagmus. The site of pathology is the tegmentum of the brainstem. Autonomic changes include hypo- or hypertension, hypo- or hyperthermia, cardiac arrhythmias, and respiratory failure. The site of pathology is the hypothalamus and the dorsal nucleus of the vagus. Depression of consciousness, reduced alertness from obtundation to coma may exist. The site of pathology is the periaqueductal gray. Ataxia (vestibular and/or cerebellar dysfunction) is found, whereby the site of pathology is the vestibular region of the medulla and cerebellum. Korsakoff amnestic syndrome is characterized by impairment of recent memory, including verbal and nonverbal material. It occurs after recovery from Wernicke encephalopathy. The sites of pathologic changes are the dorsomedial nuclei of the thalamus, mammillary bodies, and relay stations of the limbic lobe. Brain regions involved in Wernicke encephalopathy include the walls of the third ventricle, the mammillary bodies (atrophy in chronic cases), the dorsomedial nuclei of the thalami, the periaqueductal gray matter, and the floor of the fourth ventricle. Both conditions appear to have an identical neuropathology characterized by hemorrhages and other lesions around the ventricular system (Halliday et al., 1994). Acute Wernicke encephalopathy is macroscopically characterized by soft consistency and yellow to brown discoloration of the tissue and petechial hemorrhages around the third and fourth ventricles, medial hypothalamus, thalamus, and periaqueductal gray matter. Microscopic changes consist of edema, hypertrophy of endothelial cells, extravasation of erythrocytes, and reactive astrogliosis. No apparent changes in neurons are seen.