Introduction ARBD is characterised by cognitive impairment, a causative link to excessive alcohol ingestion and thiamine deficiency. It is complex; with deficits in anterograde memory, executive function, attention, PS, visuospatial skills and IQ and approximately 25% have ischaemic or traumatic head injury events.1 Oslin’s Alcohol Dementia Criteria 2 recommends assessment after three months for evaluation of long standing cognitive deficits due to abstinence related improvement; not observed in patients with concomitant vascular lesions. Domains studied include verbal fluency (VF), memory, abstraction and perceptual motor skills. There are no treatment guidelines for ARBD cognitive deficits. Various cognitive domains showed some improvement with Donepezil, Rivastigmine and Memantine; but not in PS. Our patient, showed such an improvement with Memantine.
Case summary We present a case of a 68-year-old man with a 30 year history of alcohol dependence of 9 units per day (substantially increased in the 7 years pre-admission), resulting in self-neglect, impulsivity, aggression, hallucinations, and chronic neuropsychiatric sequelae and cognitive impairments. He met the criteria for ARBD1 with prolonged cognitive impairment, causative association with alcohol use requiring thiamine replacement3; CT abdomen showed hepatic atrophy and MRI head demonstrated moderate small vessel disease. Self-neglect, impulsivity, aggression, and hallucinations improved with three month’s alcohol abstinence, however, neuropsychiatric complications persisted. Ten months abstinence- self report mood disorder screening and typical dementia blood screen were unremarkable. A Wechsler Adult Intelligence Scale (WAIS-IV UK) was performed and Memantine commenced (uptitrated to BNF maximum.)
Results The WAIS-IV 3 month follow up showed statistical improvement in Perceptual reasoning, PS and General Ability index.
Discussion Previous ARBD studies indicate abstinence related improvements in delayed recall, VF and general intellectual functioning, but, not in memory and inhibition4. Memantine (non-competitive NMDA antagonist) is associated with improved VF, confrontational naming, word list memory, constructional praxis recall and trail making A; no studies have measured PS using specific neuropsychological tests. PS is associated with the superior longditudinal fasiculus and white matter tracts within parietal and temporal cortices and left middle frontal gyrus5. Functional neuroimaging has shown white matter loss in the prefrontal cortex, superior prefrontal association cortex, cerebellum, hypothalmus and corpus callosum6. Alcohol possibly upregulates NMDA receptors and glutamate excitotoxicity with impaired oligodendrocyte function and white matter lesions7. Memantine, possibly prevents glutamate toxicity and may improve oligodendrocyte function myelination restoration. Therefore, PS improvements may be related to lesion repair secondary to Memantine effect on Oligodendrocyte function.
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