Grey matter structural differences in alcohol-dependent individuals with and without comorbid depression/anxiety—an MRI study

Abstract

Although depression and anxiety disorders are common comorbid conditions in alcohol dependence, few structural brain imaging studies have compared alcohol-dependent subjects with and without such comorbidity. In the current study, brain scans of 35 alcohol-dependent with and 40 individuals without diagnosis of a comorbid ICD-10 depressive or anxiety disorder receiving detoxification inpatient treatment were evaluated. Thickness and volumes of automatically segmented neuroanatomical structures were measured in FreeSurfer. Furthermore, associations of brain structure with biological markers and clinical severity markers of alcohol dependence were assessed. Despite comparable addiction severity, the non-comorbid group had evidence of higher cytotoxic effects of alcohol use on hepatic and haematological markers, and showed significantly smaller volumes of total cerebral, and cerebellar grey matter. Similarly, they showed unexpected smaller hippocampal and nucleus accumbens volumes, and thinner frontal, temporal and occipital cortices. Smaller brain volumes correlated with increased markers of hepatic and haematological dysfunction, and with longer duration of alcohol dependence in the non-comorbid group. Evidence of higher biomarkers of alcohol use may be indicative of more severe alcohol dependence or higher vulnerability to ethanol toxicity in this group. Furthermore, psychopathology-related drug treatment, which occurred in 53% of the comorbid group over the recent years, or tissue inflammation may have a moderate effect on the grade of cerebral atrophy in alcohol-dependent patients. Longitudinal studies are needed to investigate this issue more fully.

Imaging beta-amyloid (Aβ) burden in the brains of middle-aged individuals with alcohol-use disorders: a [11C]PIB PET study

“…Our failure to observe significant differences in both global and regional [ 11 C]PiB SUVR values between AUD and HC subjects is consistent with and extends earlier reports showing no elevation in Aβ accumulation in heavy drinkers compared to their abstinent counterparts 8 , as well as with previous post-mortem data that found no significant elevation in aggregation of Aβ in alcohol abusing individuals compared to HCs 6 . The cortical thinning and loss of hippocampal GMV observed in this study are also consistent with previous research in subjects with AUD [40][41][42][43][44] and of a magnitude such that they are likely clinically significant. Specifically, individuals with AD have demonstrated cortical thinning of 3.7% to 6.5% compared to HC 45 and asymptomatic healthy subjects who went on to develop AD have been shown to have a 4.0% lower cortical thickness than their peers who did not develop AD 46 .…”

Neural correlates of visuoperceptive changes in severe alcohol use disorder: A critical review of neuroimaging and electrophysiological findings

“…Changes in EROs do not appear to correlate with alcohol‐related characteristics, as illustrated by the absence of association between the lower spectral power in the alpha frequency measured at occipital regions in individuals with SAUD and alcohol‐related characteristics, including quantity and frequency of drinking (Ehlers & Phillips, 2007). Structural white matter changes and gray matter volumes fluctuations in visuospatial‐related regions such as the occipital or parietal cortex do not appear to vary according to lifetime doses and drinking severity either in most studies (Cardenas et al., 2007; Rando et al., 2011; Sullivan, 2003; Tomasi et al., 2019; Uhlmann et al., 2018; Zhu et al., 2018). There are, however, exceptions, with studies showing a significant relationship between: (i) gray matter shrinkage in parietal (but not occipital) regions and alcohol doses (Fein et al., 2009); (ii) white matter alteration of the superior longitudinal fasciculus and lifetime alcohol consumption (Pfefferbaum et al., 2009).…”

“…Gray matter volume reductions have been reported in parts of the occipital lobe (Durazzo et al., 2015, 2017; Fein et al., 2009; Mackey et al., 2019). Both data‐driven region‐by‐region comparisons (Fortier et al., 2011) and comparisons based on a priori ROI computation (Uhlmann et al., 2018) show that SAUD is associated with decreased occipital cortical thickness. Although occipital changes might not be systematic (Cardenas et al., 2007; Durazzo et al., 2015; Sullivan et al., 2018), volume reductions in other broad cerebral areas involved in visual processing such as the parietal and temporal cortex are also often observed (Durazzo et al., 2015, 2017; Fein et al., 2009; Sullivan et al., 2018).…”

“…V1 damage;Durazzo et al(2015, 2017),Fein et al (2009),Fortier et al (2011),Mackey et al (2019),Rando et al (2011),Uhlmann et al (2018),Wang, Fan, et al (2018), Zhu et al (2018) Potential consequences for visual information filtering, perception of global forms, and high-level visual recognition and categorization; Association with relapse White matter impairment within the occipital cortex and the fronto-occipital fasciculus Reduced intra-visual connections and cortico-cortical top-down connections; Bagga, Sharma, et al (2014), Pandey et al (2018), Rosenbloom et al (2009), Schmahmann and Pandya (2007) Association with behavioral figure copy scores Reduced connectivity in the cuneus, precuneus, lingual, fusiform, mid-occipital and parieto-occipital gyri, and between prefrontal and occipital/parietal regions Alteration of functional hubs of the ventral stream involved in the processing of basic visual properties (e.g., color, shape, size); Chen et al (2019), Karamzadeh et al (2015), Liu et al (2018), Pfefferbaum, Desmond, et al (2001), Wang, Fan, et al (2018), Wang, Zhao, et al (2018), Zehra et al (2019) Lack of communication between multisensory modalities brain areas; Association with relapse As a whole, neuroscience studies promote an explanation of visuoperceptive changes in SAUD that involves the dysregulation of an extensive visual network. Results from this review support the idea that both the ventral and dorsal visual pathways, broadly associated with temporal and parietal regions, as well as their communication channels with distant nodes of the visual system, might be impaired.…”

Treatment of anxiety disorders in alcohol abusers

“…Несмотря на известное сочетание расстройств употребления алкоголя с депрессией и тревогой, нейроморфологические исследования алкоголизма с коморбидными психическими нарушениями немногочисленны. В этой связи большой интерес вызывают данные [6] сканирования мозга 35 пациентов с расстройствами употребления алкоголя и коморбидными психическими нарушениями и 40 пациентов с признаками алкогольной зависимости без сопутствующих психических расстройств (обе группы наблюдались в период алкогольной детоксикации). Нейроанатомические параметры оценивались в соотнесении с биологическими маркерами и клиническими признаками тяжести алкогольных расстройств.…”