Resting brain perfusion in alcohol-induced psychotic disorder: A comparison in patients with alcohol dependence, schizophrenia and healthy controls

Gp, Jordaan; Jm, Warwick; Rh, Hewlett; Ra, Emsley

doi:10.1016/j.pnpbp.2010.01.018

Cited by 10 publications

(6 citation statements)

References 39 publications

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“…The AIPD group generally performed poorer on all tasks, but a statistically significant poorer performance was only recorded for tasks assessing immediate verbal memory, delayed verbal recall and abstract verbal reasoning abilities. These findings support the notion that several brain regions [15, 50] and possibly several neurotransmitter systems [6] are involved in the pathogenesis of AIPD. Of particular interest is the the perisylvian language network.…”

Section: Resultssupporting

confidence: 88%

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Cognitive changes in alcohol-induced psychotic disorder

et al. 2017

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AimsThis study aimed to explore the neuro-cognitive deficits of alcohol-induced psychotic disorder as compared to the cognitive deficits of uncomplicated alcohol dependence.MethodsParticipants were recruited from the acute psychiatric admission wards of the Department of Psychiatry, University of Stellenbosch and Stikland and Tygerberg Academic Hospitals in the Western-Cape, South Africa. Participants who met DSM IV TR criteria (American Psychiatric Association. Diagnostic and statistical manual of mental disorders. American Psychiatric Association, Washington, DC, 2000) for Alcohol Dependence and for alcohol-induced psychotic disorder, respectively, were included. Participants who met criteria for another current DSM IV TR Axis I disorder were excluded. A structured interview was done prior to neuropsychological assessment to ascertain current mental state and to obtain relevant demographic detail and history. Neuropsychological assessments were performed and supervised by clinical psychologists at either Tygerberg or Stikland Hospital.ResultsThe groups were matched demographically with similar period of abstinence prior to assessment. The alcohol-induced psychotic disorder group experienced first psychotic symptoms at age 35. The results reflected statistically significant differences on tasks measuring immediate memory; recall upon delay; exaggeration of memory difficulty and abstract thinking.ConclusionThis study concurs with earlier literature that some cognitive deficits are greater in alcohol-induced psychotic disorder compared to uncomplicated alcohol dependence.

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Section: Resultssupporting

confidence: 88%

“…This may partially explain the occurrence of psychotic symptoms and supports frontal and temporal lobe involvement in AIPD [15, 50]. In addition, both groups scored within the average range for word initiation even though the AIPD group’s performance was slightly poorer than that of the AD group.…”

Section: Discussionmentioning

confidence: 66%

Cognitive changes in alcohol-induced psychotic disorder

et al. 2017

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“…For example, in healthy subjects cannabis use and alcohol abuse are associated with the incidence of psychotic experiences [32][33][34][35]. Alcohol abuse can also induce psychotic disorders [36]. Moreover, empirical evidence has demonstrated that alcohol use is correlated with subsequent brain abnormalities and increased risk of psychosis in subjects at high genetic risk for schizophrenia [37].…”

Section: Figurementioning

confidence: 99%

Linking substance use with symptoms of subclinical psychosis in a community cohort over 30 years

et al. 2012

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Linking substance use with symptoms of sub-clinical psychosis in a community cohort over 30 yearsRössler, W; Hengartner, M P; Angst, J; Ajdacic-Gross, V Abstract: Aims The aim of the study was to examine the temporal associations between substance use and subclinical psychosis symptoms. Design Data from a prospective community study sampled within a single cohort over 30 years were analysed with discrete-time hazard models. Setting General population-based sample. Participants At initial sampling in 1978 males (n = 292) were 19 and females (n = 299) were 20 years old. Measurements Two psychosis syndromes representing 'schizotypal signs' and 'schizophrenia nuclear symptoms' and various substance use variables including cannabis, alcohol, tobacco and multiple-drug use (i.e. cannabis combined with other drugs). Findings In bivariate analyses, schizotypal signs were predominantly associated with regular cannabis use in adolescence (OR = 2.29, 95% CI 1.32-3.97). Schizophrenia nuclear symptoms were mainly related to alcohol (OR = 1.84, 95% CI 1.00-3.38) and multiple-drug use (OR = 2.35, 95% CI 1.38-4.02) during adolescence. Multivariate analyses showed that, in particular, regular cannabis use during adolescence was associated with the occurrence of subsequent schizotypal symptoms over a 30-year period (OR = 2.60, 95% CI; 1.59-4.23), whereas multiple-drug use in adolescence was associated predominantly with schizophrenia nuclear symptoms (OR = 1.75, 95% CI 1.01-3.03). Alcohol misuse was only slightly associated with the onset of such symptoms. Conclusions A significant portion of the occurrence of subclinical psychosis symptoms in adulthood can be attributed to excessive cannabis and multiple-drug use during adolescence. This is in line with the hypothesis that long-term sensitization of dopaminergic brain receptors plays a role in developing psychotic symptoms. Multivariate analyses showed that in particular regular cannabis use during adolescence was associated with the occurrence of subsequent schizotypal symptoms over a 30-year period (OR=2.60, 95%-CI=1.59-4.23), whereas multiple-drug use in adolescence was predominantly associated with schizophrenia nuclear symptoms (OR=1.75, 95%-CI=1.01-3.03). Alcohol misuse was only slightly associated with the onset of such symptoms.Conclusions: A significant portion of the occurrence of subclinical psychosis symptoms in adulthood can be attributed to excessive cannabis and multiple-drug use during adolescence. This is in line with the hypothesis that long-term sensitization of dopaminergic brain receptors plays a role in developing psychotic symptoms.

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“…During alcohol withdrawal, regional cerebral blood flow (rCBF) relative to controls was abnormally low throughout the cortex, but particularly in frontal (1–4), temporal (3, 5–7), and cerebellar (8–10) regions, even without evidence of structural abnormalities (11). Recovery can accompany prolonged sobriety (1, 3).…”

Section: Introductionmentioning

confidence: 99%

A Selective Insular Perfusion Deficit Contributes to Compromised Salience Network Connectivity in Recovering Alcoholic Men

Sullivan

Müller‐Oehring

Pitel

et al. 2013

Biological Psychiatry

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Background Alcoholism can disrupt neural synchrony between nodes of intrinsic functional networks that are maximally active when resting relative to engaging in a task, the default mode network (DMN) pattern. Untested, however, are whether the DMN in alcoholics can rebound normally from the relatively depressed task-state to the active resting-state and whether local perfusion deficits could disrupt network synchrony when switching from conditions of rest to task to rest, thereby indicating a physiological mechanism of neural network adaptation capability. Methods Whole-brain, 3D pulsed-continuous arterial spin labeling (PCASL) provided measurements of regional cerebral blood flow (rCBF) in 12 alcoholics and 12 controls under three conditions: pre-task rest, spatial working-memory task, post-task rest. Results With practice, alcoholics and controls achieved similar task accuracy and reaction times. Both groups exhibited a high-low-high pattern of perfusion levels in DMN regions during the rest-task-rest runs and the opposite pattern in posterior and cerebellar regions known to be associated with spatial working memory. Alcoholics showed selective differences from controls in the rest-task-rest CBF pattern in the anterior precuneus and CBF level in the insula, a hub of the salience network. Connectivity analysis identified activation synchrony from an insula seed to salience nodes (parietal, medial frontal, anterior cingulate cortices) in controls only. Conclusions We propose that attenuated insular CBF is a mechanism underlying compromised connectivity among salience network nodes. This local perfusion deficit in alcoholics has the potential to impair ability to switch from cognitive states of interoceptive cravings to cognitive control for curbing internal urges.

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Resting brain perfusion in alcohol-induced psychotic disorder: A comparison in patients with alcohol dependence, schizophrenia and healthy controls

Cited by 10 publications

References 39 publications

Cognitive changes in alcohol-induced psychotic disorder

Cognitive changes in alcohol-induced psychotic disorder

Linking substance use with symptoms of subclinical psychosis in a community cohort over 30 years

A Selective Insular Perfusion Deficit Contributes to Compromised Salience Network Connectivity in Recovering Alcoholic Men

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