Between 50% and 80% of individuals with alcohol use disorders experience mild to severe neurocognitive impairment. There is a strong clinical rationale that neurocognitive impairment is an important source of individual difference affecting many aspects of addiction treatment, but empirical tests of the direct influence of impairment on treatment outcome have yielded weak and inconsistent results. The authors address the schism between applied-theoretical perspectives and research evidence by suggesting alternative conceptual models of the relationship between neurocognitive impairment and addiction treatment outcome. Methods to promote neurocognitive recovery and ways in which addiction treatments may be modified to improve psychosocial adaptation are suggested. Specific suggestions for future research that may help clarify the complex relations between neurocognitive impairment and addiction treatment are outlined.

Most patients with non-lesional temporal lobe epilepsy (NLTLE) will have the findings of hippocampal sclerosis (HS) on a high resolution MRI. However, a significant minority of patients with NLTLE and electroclinically well-lateralized temporal lobe seizures have no evidence of HS on MRI. Many of these patients have concordant hypometabolism on fluorodeoxyglucose-PET ([18F]FDG-PET). The pathophysiological basis of this latter group remains uncertain. We aimed to determine whether NLTLE without HS on MRI represents a variant of or a different clinicopathological syndrome from that of NLTLE with HS on MRI. The clinical, EEG, [18F]FDG-PET, histopathological and surgical outcomes of 30 consecutive NLTLE patients with well-lateralized EEG but without HS on MRI (HS-ve TLE) were compared with 30 consecutive age- and sex-matched NLTLE patients with well-lateralized EEG with HS on MRI (HS+ve TLE). Both the HS+ve TLE group and the HS-ve TLE patients had a high degree of [18F]FDG-PET concordant lateralization (26 out of 30 HS-ve TLE versus 27 out of 27 HS+ve TLE). HS-ve TLE patients had more widespread hypometabolism on [18F]FDG-PET by blinded visual analysis [odds ratio (OR = + infinity (2.51, -), P = 0.001]. The HS-ve TLE group less frequently had a history of febrile convulsions [OR = 0.077 (0.002-0.512), P = 0.002], more commonly had a delta rhythm at ictal onset [OR = 3.67 (0.97-20.47), P = 0.057], and less frequently had histopathological evidence of HS [OR = 0 (0-0.85), P = 0.031]. There was no significant difference in surgical outcome despite half of those without HS having a hippocampal-sparing procedure. Based on the findings outlined, HS-ve PET-positive TLE may be a surgically remediable syndrome distinct from HS+ve TLE, with a pathophysiological basis that primarily involves lateral temporal neocortical rather than mesial temporal structures.

Inasmuch as all subjects except one were still driving and all wished to continue to drive, it is important to note that 63.2% of subjects failed the on-road evaluation. Conversely, 36.8% were judged safe to drive, suggesting that AD diagnosis alone may be insufficient criteria for cessation of driving. A standardized road test may be the only appropriate means of determining driving competence in people diagnosed with AD.

Executive function is an important concept in neuropsychological and cognitive research, and is often viewed as central to effective clinical assessment of cognition. However, the construct validity of executive function tests is controversial. The switching, inhibition, and updating model is the most empirically supported and replicated factor model of executive function (Miyake et al., 2000). To evaluate the relation between executive function constructs and nonexplicitly executive cognitive constructs, we used confirmatory factor reanalysis guided by the comprehensive Cattell-Horn-Carroll (CHC) model of cognitive abilities. Data from 7 of the best studies supporting the executive function model were reanalyzed, contrasting executive function models and CHC models. Where possible, we examined the effect of specifying executive function factors in addition to the CHC factors. The results suggested that little evidence is available to support updating as a separate factor from general memory factors; that inhibition does not separate from general speed; and that switching is supported as a narrow factor under general speed, but with a more restricted definition than some clinicians and researchers have conceptualized. The replicated executive function factor structure was integrated with the larger body of research on individual difference in cognition, as represented by the CHC model.

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The results of the present meta-analysis provide the first clear evidence that children with ECTS display a profile of pervasive cognitive difficulties and thus challenge current conceptions of ECTS as a benign disease or of limited specific or localized cognitive effect.

Thiamine deficiency in the absence of an alcohol-use disorder can cause the full clinical spectrum of WKS, including chronic cognitive impairment and Korsakoff syndrome.

Recent studies that have combined neuropathological data and clinical histories in a retrospective fashion have shown that Wernicke-Korsakoff neuropathology is often unsuspected antemortem and that, in terms of clinical presentation, it is more heterogeneous than previously assumed. Thus, many studies of neurologically normal alcoholics may have been confounded by the inclusion of patients with neurologically asymptomatic Wernicke-Korsakoff neuropathology. Postmortem and in vivo studies have shown that alcoholics, irrespective of neurological diagnosis, have widespread pathology involving many cortical and subcortical sites. In addition, clinical studies have indicated that, like neurologically asymptomatic alcoholics, alcoholic Korsakoff patients may enjoy substantial recovery in cognitive function. Furthermore, the common research strategy of identifying a subset of neurologically diagnosed Wernicke-Korsakoff syndrome as a discrete group of "pure" Korsakoff's amnesia by using a definitional IQ-Wechsler Memory Scale quotient difference may have created a neuropsychological stereotype that is not representative of the broader clinical group. In light of these considerations, the separate treatment of cognitive impairment in groups of alcoholics distinguished by the clinical signs of Wernicke-Korsakoff syndrome may not be justified.