Treatment with oral thiamine is ineffective because it does not achieve an adequate plasma scientific research concentration [67]. Furthermore, alcohol directly interferes with thiamine uptake [67]. While there is no consensus as to the optimum dose, frequency, route, and duration of thiamine treatment, the EFNS recommends that in cases of suspected WE, thiamine be given in doses of 200 mg three times daily, preferably intravenously. This treatment should be continued until no further improvement in signs and symptoms is evident [19]. Thirdly, assessment of cognitive status should be conducted on an ongoing basis as this will allow any improvement, stabilization, or deterioration to be detected. Acute intoxication and withdrawal may exacerbate cognitive deficits, so assessment following this period (which usually lasts no longer than 2 weeks) may allow a more accurate baseline to be established.

Fourthly, key characteristics associated with alcohol-related cognitive disorders may assist with differentiation from neurodegenerative conditions. These typically involve stabilization or improvement in cognition with abstinence; a cognitive profile involving executive, visuospatial, and memory difficulties with spared language function; and neurological symptoms such as ataxia. Neuroimaging may suggest atrophy in the mammillary bodies, thalamus and cerebellum, and ventricular enlargement, although this may vary from case to case. Patients with ARD and WKS have shown cognitive improvement following treatment with memantine, although these findings require replication [68,69].

Finally, these socially isolated patients are often hospitalized for another health condition and this presents an ideal opportunity for screening, identification, Batimastat and intervention. Conclusions The evidence reflects significant commonality between ARD and WKS. Neuropsychological studies have largely attempted to differentiate these syndromes by limiting individuals with more global cognitive impairment from WKS investigations and by excluding individuals with past symptoms of WKS from ARD studies. However, the validity of this distinction is now being brought into question. While attention has been given to the notion that ARD is likely related to underlying WKS pathology, it appears strange that more credence has not been given to whether WKS may clinically be a form of dementia, given that it typically entails multiple domains of cognitive impairment alongside functional deficits.

While ‘dementia’ in current neurological settings is typically used to describe a progressive disease of the brain, it perhaps more accurately encompasses a deterioration of intellectual or cognitive function that may or may not be progressive in nature [70]. Debate over the utility of the term ARD in selleck chemicals llc the clinical setting ensues [4].