ABSTRACT
BACKGROUND: It is evident from the dsm-iv-tr that alcohol-related impairment is extremely difficult to classify accurately. As a result, cognitive deficits can easily be overlooked. The dsm-5, however, incorporates a new category, namely 'neurocognitive disorders', which may lead to significant improvements in clinical practice. AIM: To compare the classification of alcohol-related cognitive dysfunction in dsm-iv-tr and dsm-5 and to discuss the clinical relevance of the revised classification in the dsm-5. METHOD: We compare the chapters of the dsm-iv-tr and the dsm-5 concerning alcohol-related cognitive impairment and describe the changes that have been made. RESULTS: The dsm-5 puts greater emphasis on alcohol-related neurocognitive impairment. Not only does dsm-5 distinguish between the degree of severity (major or minor neurocognitive disorder), it also distinguishes between the type of impairment (non-amnestic-type versus confabulating-amnestic type). It also makes a distinction between the durations of impairment (behavioural and/or persistent disorders). CONCLUSION: The dsm-5 gives a clearer description of alcohol-related neurocognitive dysfunction than does dsm-iv-tr and it stresses the essential role of neuropsychological assessment in the classification, diagnosis, and treatment of neurocognitive disorders.
Subject(s)
Alcoholism/classification , Cognition Disorders/classification , Diagnostic and Statistical Manual of Mental Disorders , Neurocognitive Disorders/classification , Alcoholism/epidemiology , Cognition Disorders/epidemiology , Comorbidity , Humans , Neurocognitive Disorders/epidemiologyABSTRACT
BACKGROUND: There is a vast amount of scientific evidence for the negative effects of alcohol on the functioning of the whole human body and particularly of the brain. The literature, however, is unclear about whether these functions can fully recover and about how long the abstinence period must be before patients with alcohol use disorder (AUD) can be reliably assessed for cognitive and emotional functioning. AIM: To review current findings on the length of the abstinence period required before a reliable neuropsychological assessment of the cognitive and emotional functioning of AUD patients can be carried out. METHOD: Using PubMed, PsycINFO and Medline, we consulted the literature for the period from 1975 to October 2011 relating to the effects of alcohol abstinence on the brain. RESULTS: The longer the period of abstinence, the greater the improvement in a patient's neuropsychological functioning. In the case of AUD patients, it takes at least six weeks for neuropsychological functioning to return to a fairly stable level. CONCLUSION: An abstinence period of at least six weeks is needed before a reliable neuropsychological assessment can be carried out. This time period minimises the disturbance caused by earlier alcohol abuse. A neuropsychological standard of this kind, involving a six week period of abstinence, is needed for AUD patients if they are to receive an appropriate and individualised neuropsychological assessment.
Subject(s)
Alcoholism/psychology , Cognition Disorders/chemically induced , Cognition/physiology , Cognition Disorders/psychology , Humans , Neuropsychological Tests , Recovery of Function , Time FactorsABSTRACT
The clinical observation that patients with an alcohol amnestic disorder get grey hair at a higher age was investigated by comparing a group of Korsakov patients and patients with alcohol abuse with a reference sample from the literature. Korsakoff patients appeared to be significantly less grey than age-matched alcoholics and controls. Some putative etiological factors including the mechanism of apoptosis are discussed.
ABSTRACT
Deficits in spatial context memory are an important characteristic of Korsakoff's amnesia. In memory for spatial context information, there is evidence for a functional dissociation of three separate processes: (1) binding of object information to locations (i.e. binding complex memories), (2) exact, metric processing of Euclidean co-ordinates, and (3) an integration mechanism. In the present study, these sub-mechanisms were assessed experimentally in a group of Korsakoff patients (N = 20) and compared to healthy controls (N = 20) to see whether selective deficits can be demonstrated. It was found that Korsakoff patients display deficits on all three spatial-memory conditions, which are not the primary result of deficits in visuo-spatial construction and memory for object identity. No evidence for selective impairments could be observed. These impairments can be linked to damage of diencephalic regions and perhaps the parietal cortex.
