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Korsakoff Syndrome
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Thiamine is a “helper molecule” that allows the brain to function, assisting in the transformation of sugar into other useful molecules (Martin et al., 2003, p. 134). Treating a thiamine deficiency is as simple as adding thiamine back into the person, often with intravenous doses, but the treatment should be completed quickly (Shahani et al., 2015). Korsakoff syndrome is more likely to develop in people who had Wernicke encephalopathy and were not treated quickly or effectively enough for the vitamin deficiency (Arts et al., 2017). Fortunately, fast treatment of WE may prevent the development of KS (Shahani et al., 2015).
Optic Neuritis/Retrobulbar Neuropathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Nutritional Deficiencies of thiamine (B1), riboflavin (B2), folate, B12, and B6 have all been associated with optic neuropathy.3 Patients who follow high protein, ketogenic, and low-carbohydrate diets are at risk for developing thiamine deficiency. Similarly, patients who have undergone gastrointestinal surgery may develop optic neuropathy due to interference with the absorption of vitamin B12.3
Nutritional Deficiencies
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Deepa Bhupali, Fernando D. Testai
Thiamine deficiency: Chronic alcoholism.Malnutrition and malabsorption.Prolonged intravenous feeding.Renal dialysis.Magnesium depletion: magnesium is an essential cofactor in the conversion of thiamine into active metabolites.
Profiling plasma levels of thiamine and histamine in Jordanian children with autism spectrum disorder (ASD): potential biomarkers for evaluation of ASD therapies and diet
Published in Nutritional Neuroscience, 2023
Ayat Hussein B. Rashaid, Mazin Taha Alqhazo, Shreen Deeb Nusair, James B. Adams, Mahmoud Ahmad Bashtawi, O’la Al-Fawares
Neurotransmitters have important effects on brain growth, motor skills, memory, and behavior [9]. Abnormal levels of neurotransmitters could disturb brain development, nerve cell migration, differentiation, and synaptogenesis [10,11]. Thiamine (vitamin B1) is required for all tissues and is concentrated in the liver, heart, kidneys, skeletal muscles and brain [12]. The active form of thiamine is thiamine diphosphate that serves as a cofactor for several enzymes which act primarily in carbohydrate catabolism, and in the biosynthesis of the neurotransmitter acetylcholine [13]. These enzymes are also involved in the antioxidant defense system [12]. Major thiamine uptake occurs by the small intestine via the saturable high transport system [12]. Thiamine deficiency in humans mainly affects the cardiovascular and the nervous system, resulting in a number of pathological conditions such as Wernicke-Korsakoff syndrome, peripheral vasodilation, biventricular myocardial failure, and cerebellar degeneration [12]. Other neuropathology includes bilateral hemorrhagic and necrotic lesions brainstem, diencephalon and cerebellum [12]. Thiamine supplementation can reverse some of these signs but not the severe defects in memory and cognition [12]. In a previous study, thiamine tetrahydrofurfuryl disulfide (TTFD) was found to have a beneficial clinical effect in children with ASD, since 8 out of 10 children involved in the study were clinically improved following TTFD intake [14]. However, thiamine levels were found to be similar in ASD vs. controls in children in the US [15].
Thiamine administration to all patients with alcohol use disorder: why not?
Published in The American Journal of Drug and Alcohol Abuse, 2021
Roberta Agabio, Lorenzo Leggio
There are no scientific or clinical reasons why patients with AUD seen in an ED should not receive thiamine supplementation, yet it appears that this often the exception rather than the norm. For patients with thiamine deficiency, thiamine supplementation is the logical state-of-the-art treatment that these patients should receive. Although there is presently not sufficient evidence to provide recommendations on the optimal route of thiamine administration (15), from a practical standpoint, if the clinical status of the patient does not prevent the safe placement of an intravenous line, the intravenous route may be a pharmacologically better choice while the patient is in the ED or hospitalized. This should be followed by oral thiamine supplementation after discharge. Failure to administer thiamine involves severe and irreversible consequences. It represents the gold-standard treatment for patients with thiamine deficiency, just like insulin is for patients with Type I diabetes mellitus. Thiamine administration has virtually no side effects and is a hydrophilic vitamin, therefore there is no risk of overdosing because it does not accumulate in the body. The only risks are nonspecific to thiamine and related to the site of injection, when given intravenously; these risks are, however, rare (16–18).
Wernicke Encephalopathy in schizophrenia: a systematic review
Published in International Journal of Psychiatry in Clinical Practice, 2021
Erik Oudman, Jan W. Wijnia, Misha J. Oey, Mirjam J. van Dam, Albert Postma
In 80% of the reported cases a full triad of WE was present (Kaineg and Hudgins 2005). This finding could be suggestive for a relatively late recognition of suboptimal thiamine levels leading to WE in schizophrenia. Suboptimal thiamine levels can lead to apathy, a loss of appetite, fatigue, irritability and extrapyramidal symptoms (Sechi and Serra 2007). It is problematic that schizophrenia itself has symptomatology overlapping with the results of thiamine deficiency, leading to possible under recognition of thiamine deficiency. Moreover, it is possible that clinicians are not used to think about WE in non-alcoholic schizophrenic patients. Prompt treatment of the first symptoms suggestive of thiamine deficiency with high doses of parenteral thiamine replacement therapy is necessary to prevent progression of WE (Thomson et al. 2002; Isenberg-Grzeda et al. 2012). According to the European Federation of Neurological Societies and the Royal College of Physicians, parenteral thiamine should be given 500 mg, 3 times daily until symptoms of acute WE resolute (Thomson et al. 2002). Because of the possible increased requirement of thiamine in schizophrenia, it is relevant to check the vitamin status in schizophrenia patients who lose weight, and start prophylactic vitamin therapy.