Tensor-based morphometry of cannabis use on brain structure in individuals at elevated genetic risk of schizophrenia

Moorhead, T. William J.; McIntosh, Andrew M.; Owens, David C.; Johnstone, Eve C.; Lawrie, Stephen M.

doi:10.1017/s0033291712002668

Cited by 13 publications

(10 citation statements)

References 59 publications

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“…The finding that CHR cannabis users showed reduction in hippocampal volumes compared to CHR non-users after being matched on alcohol use patterns is consistent with the results of one study that used automated tensor-based morphometry analysis to detect gray matter loss in right anterior hippocampus in individuals at genetic risk of schizophrenia who endorsed using cannabis over a 2-year period (Welch et al, 2013). Individuals with heavy cannabis use and otherwise minimal psychiatric comorbidities show morphologic reductions in the hippocampus (Lorenzetti et al, 2015), and dose-related reductions in hippocampal volume have been seen in otherwise healthy chronic cannabis users (Yucel et al, 2008).…”

Section: Discussionsupporting

confidence: 82%

“…A second study used manual tracing technique and showed that people at familial risk of schizophrenia who consumed cannabis over a 2-year period showed bilateral volume loss in the thalamus, but not in the hippocampus or amygdala, compared to a non-exposed group (Welch et al, 2011b). A third study used an automated tensor-based morphometry analysis to detect gray matter loss in right anterior hippocampus (Welch et al, 2013). Together these finding suggest that people at familial risk of schizophrenia are particularly sensitive to the risk-modifying effects of cannabis on thalamic and perhaps hippocampal structure, but not on amygdala volumes.…”

Section: Introductionmentioning

confidence: 99%

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Relation between cannabis use and subcortical volumes in people at clinical high risk of psychosis

Buchy

Mathalon²,

Cannon

et al. 2016

Psychiatry Research: Neuroimaging

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Among people at genetic risk of schizophrenia, those who use cannabis show smaller thalamic and hippocampal volumes. We evaluated this relationship in people at clinical high risk (CHR) of psychosis. The Alcohol and Drug Use Scale was used to identify 132 CHR cannabis users, the majority of whom were non-dependent cannabis users, 387 CHR non-users, and 204 healthy control non-users, and all participants completed magnetic resonance imaging scans. Volumes of the thalamus, hippocampus and amygdala were extracted with FreeSurfer, and compared across groups. Comparing all CHR participants with healthy control participants revealed no significant differences in volumes of any ROI. However, when comparing CHR users to CHR non-users, a significant ROI × Cannabis group effect emerged: CHR users showed significantly smaller amygdala compared to CHR non-users. However, when limiting analysis to CHR subjects who reported using alcohol at a ‘use without impairment’ severity level, the amygdala effect was non-significant; rather, smaller hippocampal volumes were seen in CHR cannabis users compared to non-users. Controlling statistically for effects of alcohol and tobacco use rendered all results non-significant. These results highlight the importance of controlling for residual confounding effects of other substance use when examining the relationship between cannabis use and neural structure.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Relation between cannabis use and subcortical volumes in people at clinical high risk of psychosis

Buchy

Mathalon²,

Cannon

et al. 2016

Psychiatry Research: Neuroimaging

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“…Current cannabis use in people with an at-risk mental state has also been linked to decreased volumes of posterior as well as anterior cingulate cortices [ 40 ]. Interestingly, two longitudinal studies of genetic high risk samples have reported decreases in thalamic, superior frontal and hippocampal volumes following exposure to cannabis over a 2-year follow-up period [ 17 , 41 ]. Longitudinal data in first-episode schizophrenia has indicated cortical thinning in several regions known to share topographic connections with the thalamus including lateral PFC and anterior cingulate cortex [ 42 ], in addition to accelerated gray matter volume loss and ventricular enlargement [ 43 ], following exposure to cannabis during a 5-year follow-up period.…”

Section: Discussionmentioning

confidence: 99%

Evaluating the impact of cannabis use on thalamic connectivity in youth at clinical high risk of psychosis

et al. 2015

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BackgroundDisruptions in thalamic functional connectivity have been observed in people with schizophrenia and in youth at clinical high risk (CHR) of psychosis. However, the impact of environmental risk factors for psychosis on thalamic dysconnectivity is poorly understood. We tested whether thalamic dysconnectivity is related to patterns of cannabis use in a CHR sample.Methods162 CHR and 105 control participants were assessed on cannabis use severity, frequency, and age at onset of first use as part of the North American Prodrome Longitudinal Study and completed resting-state fMRI scans. Whole-brain thalamic functional connectivity maps were generated using individual subjects’ anatomically defined thalamic seeds.ResultsThalamic connectivity did not significantly correlate with current cannabis use severity or frequency in either CHR or controls. In CHR cannabis users, a significant correlation emerged between attenuated thalamic connectivity with left sensory/motor cortex and a younger age at onset of cannabis use. CHR who used cannabis before age 15 did not differ on thalamic connectivity as compared to CHR who used after age 15 or CHR who were cannabis naïve. No group differences in thalamic connectivity emerged when comparing CHR separated by moderate/high use frequency, low-frequency or cannabis naïve.ConclusionsAlthough a younger age at onset of cannabis use may be associated with disrupted thalamo-cortical coupling, cannabis use does not appear to be an identifying characteristic for thalamic connectivity in CHR with moderate/high use frequency compared to low-frequency users or CHR who are cannabis naïve.Electronic supplementary materialThe online version of this article (doi:10.1186/s12888-015-0656-x) contains supplementary material, which is available to authorized users.

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“…Other studies found increased grey matter density within the left dorsolateral prefrontal cortex and have suggested this alteration may in part explain the observation between cannabis use and cognitive function in those with schizophrenia (Schnell et al, 2012). Some of these conflicting findings of the effects in psychosis may in part stem from the observation that structural brain changes in schizophrenia may in fact represent a core feature of the illness, with volume loss within the thalami, hippocampus and prefrontal regions being already present in individuals who are at increased risk of developing schizophrenia, and that cannabis use is associated with further volume reductions and the potential transition from ultra-high risk to disease state in genetically disposed individuals (Welch et al, 2013). …”

Section: Cannabis and The Endocannabinoid Systemmentioning

confidence: 99%

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

Davis

Eyre

Jacka

et al. 2016

Neuroscience & Biobehavioral Reviews

279

209

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Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype—the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.

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Tensor-based morphometry of cannabis use on brain structure in individuals at elevated genetic risk of schizophrenia

Cited by 13 publications

References 59 publications

Relation between cannabis use and subcortical volumes in people at clinical high risk of psychosis

Relation between cannabis use and subcortical volumes in people at clinical high risk of psychosis

Evaluating the impact of cannabis use on thalamic connectivity in youth at clinical high risk of psychosis

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

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