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The "fragility" of the nervous system, especially concerning to its nutrition and metabolism, explains why vitamin deficits are an important cause of neurological pathology. Some deficiency diseases, which can be very severe and irreversible, are still present in our environment; diagnosis, which must be early so as not to delay treatment, can be difficult if we do not have them in mind. In this review we address the most relevant neurological diseases associated with thiamine, folate and cobalamin deficiency, and we focus especially combined subacute degeneration and Wernicke-Korsakoff syndrome.

B vitamin deficiency is a leading cause of neurological impairment and disability throughout the world. Multiple B vitamin deficiencies often coexist, and thus an understanding of the complex relationships between the different biochemical pathways regulated in the brain by these vitamins may facilitate prompter diagnosis and improved treatment. Particular populations at risk for multiple B vitamin deficiencies include the elderly, people with alcoholism, patients with heart failure, patients with recent obesity surgery, and vegetarians/vegans. Recently, new clinical settings that predispose individuals to B vitamin deficiency have been highlighted. Moreover, other data indicate a possible pathogenetic role of subclinical chronic B vitamin deficiency in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. In light of these findings, this review examines the clinical manifestations of B vitamin deficiency and the effect of B vitamin deficiency on the adult nervous system. The interrelationships of multiple B vitamin deficiencies are emphasized, along with the clinical phenotypes related to B vitamin deficiencies. Recent advances in the clinical determinants and diagnostic clues of B vitamin deficiency, as well as the suggested therapies for B vitamin disorders, are described., (© The Author(s) 2016. Published by Oxford University Press on behalf of the International Life Sciences Institute. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Bariatric surgical procedures are increasingly common. In this review, we characterize the neurologic complications of such procedures, including their mechanisms, frequency, and prognosis. Literature review yielded 50 case reports of 96 patients with neurologic symptoms after bariatric procedures. The most common presentations were peripheral neuropathy in 60 (62%) and encephalopathy in 30 (31%). Among the 60 patients with peripheral neuropathy, 40 (67%) had a polyneuropathy and 18 (30%) had mononeuropathies, which included 17 (94%) with meralgia paresthetica and 1 with foot drop. Neurologic emergencies including Wernicke's encephalopathy, rhabdomyolysis, and Guillain-Barré syndrome were also reported. In 18 surgical series reported between 1976 and 2004, 133 of 9996 patients (1.3%) were recognized to have neurologic complications (range: 0.08-16%). The only prospective study reported a neurologic complication rate of 4.6%, and a controlled retrospective study identified 16% of patients with peripheral neuropathy. There is evidence to suggest a role for inflammation or an immunologic mechanism in neuropathy after gastric bypass. Micronutrient deficiencies following gastric bypass were evaluated in 957 patients in 8 reports. A total of 236 (25%) had vitamin B(12) deficiency and 11 (1%) had thiamine deficiency. Routine monitoring of micronutrient levels and prompt recognition of neurological complications can reduce morbidity associated with these procedures.

Metabolic disorders may also be accompanied by neurological symptoms. Diagnosis is ofter difficult because clinical opportunities are rare. But some things can be detected even by simple means. In particular, primary biochemical disturbances are discussed, insofar as they may have an unfavorable effect on the nervous system. Among these are hypoglycemia, hyperglycemia, cerebral nutritional disorders, phenylketonuria. Wilson's disease, folic acid deficiency and acute intermittent porphyria.