Mechtcheriakov S, Brenneis C, Egger K, Koppelstaetter F, Schocke M, Marksteiner J. A widespread distinct pattern of cerebral atrophy in patients with alcohol addiction revealed by voxel-based morphometry. J Neurol Neurosurg Psychiatry 78: 610-614

Department of General Psychiatry, Medical University Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
Journal of neurology, neurosurgery, and psychiatry (Impact Factor: 6.81). 07/2007; 78(6):610-4. DOI: 10.1136/jnnp.2006.095869
Source: PubMed
ABSTRACT
Patients with alcohol addiction show a number of transient or persistent neurological and psychiatric deficits. The complexity of these brain alterations suggests that several brain areas are involved, although the definition of the brain alteration patterns is not yet accomplished.
To determine brain atrophy patterns in patients with alcohol dependence.
Voxel-based morphometry (VBM) of grey matter (GM) and white matter (WM) was performed in 22 patients with alcohol dependence and in 22 healthy controls matched for age and sex.
In patients with alcohol dependence, VBM of GM revealed a significant decrease in density (p<0.001) in the precentral gyrus, middle frontal gyrus, insular cortex, dorsal hippocampus, anterior thalamus and cerebellum compared with controls. Reduced density of WM was found in the periventricular area, pons and cerebellar pedunculi in patients with alcohol addiction.
Our findings provide evidence that alcohol addiction is associated with altered density of GM and WM of specific brain regions. This supports the assumption that alcohol dependence is associated with both local GM dysfunction and altered brain connectivity. Also, VBM is an effective tool for in vivo investigation of cerebral atrophy in patients with alcohol addiction.

Full-text

Available from: Karl Egger
PAPER
A widespread distinct pattern of cerebral atrophy in patients
with alcohol addiction revealed by voxel-based morphometry
Sergei Mechtcheriakov, Christian Brenneis, Karl Egger, Florian Koppelstaetter, Michael Schocke,
Josef Marksteiner
...................................................................................................................................
See end of article for
authors’ affiliations
........................
Correspondence to:
Dr S Mechtcheriakov,
Department of General
Psychiatry, Medical
University Innsbruck,
Anichstrasse 35, A-6020
Innsbruck, Austria;
s.mechtcheriakov@
uibk.ac.at
Received 16 April 2006
Revised 12 October 2006
Accepted 18 October 2006
Published Online First
6 November 2006
........................
J Neurol Neurosurg Psychiatry 2007;78:610–614. doi: 10.1136/jnnp.2006.095869
Background: Patients with alcohol addiction show a number of transient or persistent neurological and
psychiatric deficits. The complexity of these brain alterations suggests that several brain areas are involved,
although the definition of the brain alteration patterns is not yet accomplished.
Aim: To determine brain atrophy patterns in patients with alcohol dependence.
Methods: Voxel-based morphometry (VBM) of grey matter (GM) and white matter (WM) was performed in
22 patients with alcohol dependence and in 22 healthy controls matched for age and sex.
Results: In patients with alcohol dependence, VBM of GM revealed a significant decrease in density
(p,0.001) in the precentral gyrus, middle frontal gyrus, insular cortex, dorsal hippocampus, anterior
thalamus and cerebellum compared with controls. Reduced density of WM was found in the periventricular
area, pons and cerebellar pedunculi in patients with alcohol addiction.
Conclusions: Our findings provide evidence that alcohol addiction is associated with altered density of GM
and WM of specific brain regions. This supports the assumption that alcohol dependence is associated with
both local GM dysfunction and altered brain connectivity. Also, VBM is an effective tool for in vivo
investigation of cerebral atrophy in patients with alcohol addiction.
A
lcoholism can affect the brain and behaviour in a variety
of ways, and multiple factors can influence these effects.
A key goal of brain imaging in the research of alcoholism
is to detect changes in specific brain regions. Previous studies
using different imaging techniques have revealed a general
reduction of brain sizes as well as a consistent association
between heavy alcohol consumption and regional brain
damage. Various cortical regions and parts of the cerebellum
have been suggested to be predominantly involved in alcohol-
associated brain atrophy. Several neuroimaging studies have
recently described global and regional brain atrophy in patients
with alcohol dependence in both cross-sectional and long-
itudinal imaging studies.
1–5
Neuropathological studies con-
ducted on the brains of deceased patients as well as findings
derived from neuroimaging studies of the brains of living
patients, point to increased susceptibility of frontal brain
systems to alcoholism-related damage.
67
Neuropathological
studies have also demonstrated substantial changes in different
brain regions
1
such as parts of cerebral cortex,
8
basal forebrain,
9
thalamus
10
and hypothalamus.
11
Since previous imaging studies applying conventional volu-
metry focused on preselected brain regions,
12 13
the particular
pattern of alcohol-associated brain tissue alterations is not
completely established.
8
Voxel-based morphometry (VBM) is a recently introduced
automated method of indirect volumetry, which allows the
investigation of the entire brain without restriction to a priori
defined regions of interest.
14
In recent years, VBM has been
successfully applied in characterising structural brain differ-
ences in a variety of diseases including schizophrenia,
15
autism,
16
Alzheimer’s disease
17
and dementia with Lewy
bodies.
18
The purpose of this study was to investigate the altered
density of grey matter (GM) and white matter (WM) in the
whole brain of patients with alcohol addiction and to reveal the
atrophy pattern and alteration of different brain regions
induced by chronic alcohol consumption in order to provide
evidence for a preferential vulnerability of some brain regions
with respect to the toxic effects of alcohol.
MATERIALS AND METHODS
Subjects
Patients (n = 22; mean age 53.6 years, range 31–69 years; 14
men and 8 women) with alcohol addiction who were admitted
to the Department of Psychiatry, Innsbruck University Hospital,
Innsbruck, Austria, were included in this study. The following
exclusion criteria were applied: history of illicit drug misuse or
dependency, history of severe benzodiazepine misuse, liver
cirrhosis, major psychiatric disorders (other than alcohol
addiction) as defined by the International classification of diseases,
10th revision, history of severe brain injury, neoplastic brain
processes, history of vascular brain alterations, Wernicke
encephalopathy as defined by clinical operational criteria
19
and general contraindications for magnetic resonance investi-
gation. In all, 22 age- and sex-matched healthy subjects (mean
age 53.7 years, range 31–73 years; 14 men and 8 women)
without a history of alcohol misuse served as controls. Patients
were investigated after alcohol abstinence of at least 10 days.
All patients included in this study had a drinking history of
.10 years. The range of daily alcohol consumption was
between 180 and 310 g/day and the number of smokers was
17 of 22. The level of education was not significantly different
between both groups (patients, mean (SD) 9.7 (2.6) years;
controls, 10.1 (2.3) years).
Alcohol addiction in patients was assessed according to the
International classification of diseases, 10th revision, diagnostic
criteria. Patients underwent neurological and general medical
examination and laboratory testing to exclude other causes of
possible brain alterations. The investigation included chest
radiography, ECG, chemistry profile, complete blood count,
thyroid function tests, vitamin B
12
level, folic acid level and
Abbreviations: CSF, cerebrospinal fluid; GM, grey matter; VBM, voxel-
based morphometry; WM, white matter
610
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Page 1
syphilis serology. Patients were scanned within the framework
of their routine diagnostic investigation and controls gave their
informed consent for this research project. The MRI data
acquisition protocol was approved by the local ethics committee
of the Medical University Hospital Innsbruck, Innsbruck, Austria.
Data acquisition, pre-processing and analysis
All participants were scanned on the same 1.5 T Siemens
Symphony MRI scanner using a T1-weighted fast low-angle
shot three-dimensional sequence with a repetition time of
9.7 ms, an echo time of 4 ms, a matrix size of 2566256 and a
field of view of 230 mm, yielding sagittal slices with a thickness
of 1.5 mm and an in-plane resolution of 0.9860.98 mm. These
raw images were pre-processed using the optimised protocol
described by Good et al
20
and analysed using SPM2 software
(Welcome Department of Neurology, London, UK) implemented
in Matlab V.6.5 (Mathworks, Sherborn, Massachusetts, USA).
Customised template creation
The study group-specific template was created to minimise the
scanner-specific bias by averaging all images from the study-
specific subject group, after being normalised using an affine-
only procedure. Probability maps were obtained by segmenting
the individual normalised images into GM, WM and cerebrosp-
inal fluid (CSF), averaging and smoothing with an isotropic
Gaussian kernel of 8 mm full-width at half-maximum.
Segmentation
The optimised VBM protocol
20
includes two segmentation steps:
(1) segmentation was performed in native space and non-brain
tissue removed automatically by modulation with an individu-
ally derived brain-tissue mask; and (2) segmentation was
performed after applying the normalisation parameters to the
original whole-brain images, including, once again, removing
of non-brain tissue followed by reslicing onto a voxel size of
16161 mm.
Normalisation
The spatial normalisation parameters were estimated by
matching the native spaced individual GM image with the
study-specific GM template.
Modulation
Voxel values of the segmented images were multiplied with the
Jacobian determinants to convert the GM segments into
measures of absolute GM volume, as opposed to relative GM
volume following spatial normalisation.
Smoothing
Finally, all modulated images were smoothed with a 10 mm
full-width at half-maximum Gaussian kernel.
Statistical analyses were performed with SPM2 using the
general linear model-based on the Gaussian field theory. The
global mean voxel values and the total intracranial volumes
(obtained by summing up GM, WM and CSF voxels) were used
as confounding covariates in an analysis of covariance to focus
on the regional differences in GM. The significance level was set
at p,0.05 false discovery rate corrected for multiple compar-
isons across the entire brain volume.
RESULTS
Patients with alcohol addiction demonstrated lower volumes of
GM (patients: mean (SD) 569.4 (63.5) ml; controls: mean (SD)
631.9 (62.75) ml; p = 0.002) and WM (patients: mean (SD)
435.5 (61.2) ml; controls: mean (SD) 470.1 (68.9) ml;
p = 0.085), as well as increased CSF volumes (patients: mean
(SD) 712.7 (137.7) ml; controls: mean (SD) 565.7 (93.2) ml;
p = 0.001). Total intracranial volumes were equal in both
groups (patients: mean (SD) 1717.6 (205.6) ml; controls: mean
(SD) 1667.7 (202.8) ml; p = 0.423).
Table 1 presents GM statistics for different brain regions.
Significantly reduced GM volumes (p,0.001) in patients with
alcohol addiction have been found in the right and left anterior
and dorsal parts of the thalamic region as well as in the left
Table 1 Reduced grey matter volumes in patients with alcohol addiction: anatomical
locations, Brodmann areas, z scores and p values (false discovery rate corrected for multiple
comparisons across the entire volume)
Location BA
Peak coordinates (mm)
Cluster size z Value p Valuexyz
Thalamus
Right 6 213 15 8232 6.27 ,0.001
Left 27 213 15 8232 6.27 ,0.001
Dorsal hippocampus
Right 32 234 25 8232 3.84 0.005
Left 228 245 24 8232 4.74 ,0.001
Precentral gyrus
Right 6 57 27 34 3845 6.21 ,0.001
Left 6 257 211 31 276 5.13 ,0.001
Middle frontal gyrus
Right 9 45 12 32 3845 5.17 ,0.001
Left 9 241 16 28 889 5.31 ,0.001
Left 46 244 27 25 967 4.68 ,0.001
Insula
Right 13 42 219 10 4870 4.74 ,0.001
Left 13 237 20 7 518 3.82 0.005
Cerebellum
Right 40 247 251 2048 4.04 0.003
Left 242 248 251 275 4.02 0.003
BA, Brodmann areas; MNI, Montreal Neurological Institute.
Peak coordinates are given in MNI space (http://www.bic.mni.mcgill.ca).
Patterns of cerebral atrophy in alcohol addiction 611
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Page 2
thalamic nucleus medialis as compared with controls (table 1,
fig 1). Right and left dorsal hippocampus (p = 0.005 and
p,0.001, respectively) and cerebellum (p = 0.003) also showed
significantly reduced GM volumes in patients as compared with
controls (table 1). In patients, precentral gyrus (Brodmann area
6) and middle frontal gyrus (Brodmann area 9) were
significantly (p,0.001) altered in both hemispheres.
Furthermore, area 46 (middle frontal gyrus) showed reduced
volume in the left hemisphere (p,0.001). The insular region
(Brodmann area 13) was found to be altered in the right
hemisphere (p,0.001) as compared with controls.
Table 2 presents the VBM results of WM. Patients with
alcohol addiction showed significant volume loss (p = 0.001) in
the entire periventricular WM (anterior, central and posterior
parts) and reduced volume of the pons (p,0.001) and
cerebellar pedunculi (p,0.001).
An additional analysis focusing on gender differences was
also performed despite the smaller number of female partici-
pants. Age and gender were included as confounding covari-
ates. At a p,0.05 level after correction for multiple
comparisons, no significant regional differences were detected.
DISCUSSION
In this study, we investigated the distribution patterns of brain
atrophy in patients with alcohol addiction using VBM, which
allows the analysis of regional GM and WM partitions without
predefining regions of interest. This method provides the
possibility to analyse complex patterns of brain atrophy also
in those brain regions that are difficult to investigate using
anatomically based methods of volumetry. Previous studies
have shown that VBM is more sensitive in detecting subtle
changes in brain volume than conventional methods of
volumetry.
14 16 20
To minimise methodological bias, we used an
optimised protocol based on the creation of study-specific
templates and the modulation of the segmented GM partitions
to compensate for volume changes in brain normalisation.
20
One of the most intriguing findings of this study is the
pronounced decrease in GM volumes in the thalamus of patients
with alcohol addiction. These data are consistent with several
previous reports on the involvement of thalamic neuronal
circuits in different behavioural changes in patients with alcohol
dependence.
8
On the other hand, our data contradict those of a
previous study demonstrating reduced thalamic volume only in
subjects with Korsakoff’s syndrome but not in subjects with
chronic alcoholism using conventional MRI volumetry.
4
In
contrast with that, George et al
21
have shown that patients with
alcohol addiction, when exposed to alcohol cues, have increased
brain activity in the prefrontal cortex and anterior thalamic
regions, which are associated with regulation of emotions,
attention and appetitive behaviour. The most recent study on
this issue has shown a significant role of the thalamus in
processing cue-related information and in controlling alcohol-
related behaviour.
22
The reduction of GM volumes found in this
study may suggest functional insufficiency of thalamic regions
that are responsible for altered behavioural patterns occurring in
patients with alcohol addiction.
The analysis of our data suggests alcohol-induced alterations
of the posterior hippocampus as well. Although previous
neuropathological studies failed to prove alcohol-associated
neurodegeneration of the hippocampus in human brains,
11
animal models have demonstrated that binge drinking of
ethanol can produce necrotic neurodegeneration in the areas of
the brain most closely associated with the hippocampus.
23
Our
findings support the hypothesis of involvement of the
hippocampus in the brain of patients with alcohol addiction.
There exists ample evidence of possible mechanisms underlying
AB
C
E
D
+10 +12 +14 +27 +30 +33
_
53
_
51
_
45
_
32
_
49
_
45
_
42
_
39
Figure 1 Areas of significant grey and white matter decrease in patients with alcohol addiction relative to healthy controls. Results are illustrated as
statistical parametric map blobs superimposed on the slices of a T1-weighted mean picture in standard stereotactic space from all 44 study participants. The
left side of the figure is the left side of the brain. Threshold was set at p.3.31 (peak). (A) Thalamus, insula; (B) middle frontal gyrus, precentral gyrus; (C)
cerebellum; (D) brainstem; (E) dorsal hippocampus.
612 Mechtcheriakov, Brenneis, Egger, et al
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Page 3
the effect of alcohol on the hippocampus. The hippocampus is
the area with the greatest increase in lipofuscin deposition in
neurons as a result of chronic alcohol consumption.
24
Further,
the fatty acid ethyl esters produced in the brain from ethanol
are known to be particularly damaging to the hippocampus.
25
Our data are further consistent with the previous findings on
involvement of frontal cortical areas in the brain of patients
with alcohol addiction. Numerous neuropsychological studies
demonstrated substantial deficits in frontal executive functions
in patients with alcohol dependence.
62627
Our results suggest
substantial volume reduction in the middle frontal gyrus and
precentral gyrus, although no changes were detected in other
frontal regions. These findings support previous reports on
decreased glucose metabolic rates in middle frontal regions in
patients with alcohol addiction
28
and a reduction of c
aminobutyric acid A/benzodiazepine receptors in superior
medial parts of the frontal lobes.
29
A significant decrease in WM volumes in the pons and
cerebellum in the our study is consistent with the previous results
that have shown the alcohol-associated degeneration of pontine
and cerebellar WM in patients with alcohol addiction,
73031
whereas in healthy subjects these regions have been shown to
remain stable across the entire age span in both men and
women.
32
The significant decrease in periventricular WM found in
our study is also consistent with previous data; however, the
analysis and interpretation of these changes in VBM studies is
difficult because of the possible bias due to partial volume effects.
Even low-to-moderate consumption of alcohol was associated
with brain atrophy in a study of middle-aged men.
5
Ethanol can
increase the release of arachidonic acid from cell membranes and
cause oxidative stress in the brain by increased cyclo-oxygenase
activity. Furthermore, hydroxyethyl free radicals derived directly
from ethanol are nearly as damaging as hydroxyl radicals.
33
There
is also evidence from animal studies that alcohol causes cell
death. Rats fed a liquid diet containing moderate amounts of
ethanol for 6 weeks had a 66.3% decrease in the number of new
neurons and a 227–279% increase in cell death in the dentate
gyrus as compared with rats fed an alcohol-free diet.
34
In general, our data support the previous assumption that the
regional reduction of GM volumes may result from alcohol-
induced neuronal loss, whereas global brain shrinkage might be
caused by loss of WM.
1
Furthermore, our results support
previous findings on alteration of selected regions of the frontal
cortex and cerebellum in patients with alcohol addiction and
suggest the involvement of the anterior thalamus, posterior
hippocampus, insular cortex and periventricular WM in
alcohol-associated brain damage. A causal relationship between
alcohol consumption and regional brain atrophy still demands
further research, whereas VBM seems to represent a tool of
choice for in vivo detection of the brain areas predisposed to
alcohol-induced damage.
Authors’ affiliations
.......................
Sergei Mechtcheriakov, Josef Marksteiner, Department of General
Psychiatry, Medical University Innsbruck, Innsbruck, Austria
Christian Brenneis, Department of Neurology, Medical University
Innsbruck, Innsbruck, Austria
Karl Egger, Michael Schocke, Department of Radiology I, Medical
University Innsbruck, Innsbruck, Austria
Florian Koppelstaetter, Department of Radiology II, Medical University
Innsbruck, Austria
Competing interests: None declared.
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comparisons across the entire volume)
Location BA
Peak coordinates (mm)
z Value p Valuexy z
Pons 2 235 248 5.11 ,0.001
Cerebellum
Pedunculi mediales/inferiores
Right 6 57 27 34 6.21 ,0.001
Left 6 257 211 31 5.13 ,0.001
BA, Brodmann areas; MNI, Montreal Neurological Institute.
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    • "In addition to the changes in the polar regions, there are also changes in the medial temporal cortex, which is one of the structures often reported to be associated with cannabis addiction and where we find a strong bilateral decrease of grey matter volume in the population of regular cannabis users. Such a pattern of atrophy has been also described in other forms of addiction such as alcohol addiction (Mechtcheriakov et al, 2007), but not in heroin users (Denier et al, 2013). However, other patients with severe – non-toxic – behavioral addiction such as pathological gambling (Levine et al, 2005) do not present the same form of atrophy, suggesting that temporal atrophy is indeed associated with cannabis consumption rather than with addictive behavior itself. "
    [Show abstract] [Hide abstract] ABSTRACT: The dose-dependent toxicity of the main psychoactive component of cannabis in brain regions rich with cannabinoid CB1 receptors is well known in animal studies. However, research in humans does not show common findings across studies regarding the brain regions that are affected after long-term exposure to cannabis. In the present study we investigate (using Voxel-based Morphometry) grey matter changes in a group of regular cannabis smokers in comparison to a group of occasional smokers matched by the years of cannabis use. We provide evidence that regular cannabis use is associated with grey matter volume reduction in the medial temporal cortex, temporal pole, parahippocampal gyrus, insula, and orbitofrontal cortex; these regions are rich with cannabinoid CB1 receptors and functionally associated with motivational, emotional, and affective processing. Furthermore, these changes correlate with the frequency of cannabis use in the three months prior to inclusion in the study. The age of onset of drug use also influences the magnitude of these changes. Significant grey matter volume reduction could result either from heavy consumption unrelated to the age of onset or instead from recreational cannabis use initiated at an adolescent age. In contrast, the larger grey matter volume detected in the cerebellum of regular smokers without any correlation with the monthly consumption of cannabis may be related to developmental (ontogenic) processes that occur in adolescence.Neuropsychopharmacology accepted article preview online, 17 March 2014; doi:10.1038/npp.2014.67.
    Full-text · Article · Mar 2014 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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    • "We observed volume loss in the frontal, prefrontal and temporal GM areas as well as WM losses in the cerebellum, brainstem, and around the ventricles, which is consistent with the findings in literature (Chanraud et al., 2007; Pfefferbaum et al., 1992; Pitel et al., 2012; Shear et al., 1996; Sullivan, 2003; Sullivan et al., 2003). Contrary to previously reported findings (Mechtcheriakov et al., 2007), we did not observe a significant reduction in thalamic volume in alcoholics at treatment entry. However, atrophy of the thalamus would have been observed with a less stringent statistical threshold (p < 0.05, FDR). "
    [Show abstract] [Hide abstract] ABSTRACT: Chronic alcohol consumption results in brain damage potentially reversible with abstinence. It is however difficult to gauge the degree of recovery of brain tissues with abstinence since changes are subtle and a significant portion of patients relapse. State-of-the-art morphometric methods are increasingly used in neuroimaging studies to detect subtle brain changes at a voxel level. Our aim was to use the most refined morphometric methods to observe in alcohol dependence the relationship between volumetric changes and interim drinking over a 6-month follow-up. Overall, 19 patients with alcohol dependence received volumetric T1-weighted magnetic resonance imaging (MRI) after detoxification. A 6-month follow-up study was then conducted, during which 11 of them received a second MRI scan. First, correlations were conducted between gray matter (GM) and white matter (WM) volumes of patients at alcohol treatment entry and the amount of alcohol consumed between treatment entry and follow-up. Second, longitudinal analyses were performed from pairs of MRI scans using tensor-based morphometry in the 11 patients, and correlations were computed between the resultant Jacobian maps of GM and WM and interim drinking. Our preliminary results showed that, among others, alcoholics with smaller thalamus at alcohol treatment entry tended to resume with heavy alcohol consumption (p < 0.005 uncorrected [unc.]). Our longitudinal study revealed an overall inverse relationship between recovery of brain structures like the cerebellum, striatum, and cingulate gyrus, and the amount of alcohol consumed over the 6-month follow-up (p < 0.005 unc.). The recovery could be observed not only with strict abstinence but also in cases of moderate resumption of alcohol consumption, when there had been no drastic relapse into alcohol dependence. Those preliminary findings indicate that the volume of the thalamus at treatment entry may have an influence on subsequent interim drinking. There is recovery of certain brain regions even when patients resume with moderate, but not drastic, alcohol consumption.
    Full-text · Article · Jan 2014 · Alcoholism Clinical and Experimental Research
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    • "IFC, STC, ITC, LOC, PCAL, PoCG, MTC.R, IPC.L, LING.R OFC, INS, MFC, ACC, TPC, cerebellum Basal ganglia structures Index Subjects Method Regions significantly different from controls Refs 1 Alcohol 22 users (56.3 years) 22 controls (53.7 years) VBM PreCG, MFG, INS, dHIP, THA, cerebellum Mechtcheriakov et al. (2007) 2 Alcohol 9 users 21 controls VBM THA Reid et al. (2008) 3 Alcohol 69 users (13.4 ± 1.9 years) 58 controls (13.0 ± 2.0 years) SBM Yang et al. (2012) 4 Cocaine 13 users (42 ± 6.3 years) 16 controls (32 ± 6.9 years) VBM AVI, vmOFC, ACC.R, STC Franklin et al. (2002) 5 Cocaine 14 users (36.3 ± 4.7 years) 11 controls (33.8 ± 4.5 years) VBM ACC, mOFC.R, lOFC.R, PFC.R Matochik et al. (2003) 6 Cocaine 19 users (39.5 ± 10.3 years) 17 controls (37.9 ± 12.9 years) VBM PFC, cerebellum.R Brody et al. (2004) 7 Cocaine 22 users (30.8 ± 7.5 years) 23 controls (30.3 ± 7.9 years) "
    [Show abstract] [Hide abstract] ABSTRACT: Accumulating evidence from brain structural imaging studies on heroin dependence has supported links between brain morphological alterations and heroin exposure, particularly in gray matter volume or gray matter density. However, the effects of heroin exposure on cortical thickness and the relationship between cortical thickness and heroin addiction are not yet known. In this study, we acquired 3D high-resolution brain structural magnetic resonance imaging (MRI) data from 18 heroin-dependent individuals (HDIs) and 15 healthy controls (HCs). Using FreeSurfer, we detected abnormalities in cortical thickness in the HDIs. Based on a vertex-wise analysis, the HDIs showed significantly decreased cortical thickness in the bilateral superior frontal, left caudal middle frontal, right superior temporal, and right insular regions compared to the HCs but significantly increased cortical thickness in the left superior parietal, bilateral lingual, left temporal pole, right inferior parietal, right lateral occipital, and right cuneus regions. To supplement these results, a subsequent ROI-wise analysis was performed and showed decreased cortical thickness in the left superior frontal sulcus, left precuneus gyrus, left calcarine sulcus, left anterior transverse collateral sulcus, and the right medial occipital-temporal and lingual sulcus. These regions partially overlapped with the areas identified using the vertex-wise analysis. In addition, we found that the thickness in the right superior frontal and right insular regions was negatively correlated with the duration of heroin use. These results provide compelling evidence for cortical abnormality in HDIs and also suggest that the duration of heroin use may be a critical factor associated with the brain alteration.
    Full-text · Article · Oct 2013 · NeuroImage
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