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Levamisole is an imidazole derivative used in the treatment of various cancers, dermatological diseases, and parasitosis. Illegal use of levamisole by mixing it with cocaine in order to increase the psychotropic effects has also increased in recent years. Here we present the clinical, laboratory, imaging findings, treatment, and follow-up information of a year-old girl who presented with seizures due to levamisole, which was prescribed to treat vitiligo. Levamisole-induced leukoencephalopathy should be considered in the differential diagnosis of demyelinating diseases, the neurotoxic effects of the drug should be well understood, and treatment should be initiated as soon as possible. Keywords: cocaine, demyelinating diseases, leukoencephalopathies, levamisole, seizure, vitiligo. Author Guidelines. The Turkish Journal of Pediatrics. Case Report. Turk J Pediatr ; 63 2 : Rare presentation of levamisole-induced leukoencephalopathy in a pediatric patient: seizure. Derya Okur. DOI: How to cite. Turk J Pediatr ; Volume: 63 - Issue: 2 - About the journal. The Turkish Journal of Pediatrics is a peer-reviewed, open access journal. Browse journal. Browse the journal's current, past, and accepted articles. Current issue. Abstracting and indexing. Production and hosting by Akdema Informatics and Publishing.

The Turkish Journal of Pediatrics

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Figure 1. Alcohol-related pictures, their scrambled versions, and affectively neutral pictures of housekeeping items from the International Affective Picture System IAPS , 42 serving as stimuli. The functional response elicited by alcohol-related pictures was compared with the response following neutral IAPS pictures. Figure 2. A priori—defined, literature-based probabilistic regions of interest ROIs. The color-coded ROIs are overlaid on the averaged brain of the whole sample neurological convention. Figure 3. Differences in local gray matter volume computed by voxel-based morphometry. Group differences are overlaid on the averaged brain of the whole sample. Figure 4. Neural responses to alcohol-related cues as measured by blood oxygen level—dependent function magnetic resonance imaging. Figure 5. Brain regions showing an increase in functional connectivity for alcohol-associated cues with the midbrain including the ventral tegmental area \[VTA\] and the subthalamic nucleus \[STN\] the seed region, which is shown in cyan. Effect of brain structure, brain function, and brain connectivity on relapse in alcohol-dependent patients. Arch Gen Psychiatry. Increased brain response elicited by processing of alcohol-associated cues compared to neutral cues in REL compared to CON. Increased brain response elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to CON. Increased brain response elicited by processing of alcohol-associated cues compared to neutral cues in REL compared to ABS. Increased brain response elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to REL. Increased functional connectivity between midbrain seed region elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to CON. Increased functional connectivity between midbrain seed region elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to REL. Whole head regression analysis for subgroup of REL: time until relapse vs. A priori—defined literature based probabilistic ROIs displayed for right and left hemisphere separately. This supplementary material has been provided by the authors to give readers additional information about their work. Context In alcohol-dependent patients, brain atrophy and functional brain activation elicited by alcohol-associated stimuli may predict relapse. However, to date, the interaction between both factors has not been studied. Objective To determine whether results from structural and functional magnetic resonance imaging are associated with relapse in detoxified alcohol-dependent patients. Design A cue-reactivity functional magnetic resonance experiment with alcohol-associated and neutral stimuli. After a follow-up period of 3 months, the group of 46 detoxified alcohol-dependent patients was subdivided into 16 abstainers and 30 relapsers. Participants A total of 46 detoxified alcohol-dependent patients and 46 age- and sex-matched healthy control subjects. Main Outcome Measures Local gray matter volume, local stimulus—related functional magnetic resonance imaging activation, joint analyses of structural and functional data with Biological Parametric Mapping, and connectivity analyses adopting the psychophysiological interaction approach. Results Subsequent relapsers showed pronounced atrophy in the bilateral orbitofrontal cortex and in the right medial prefrontal and anterior cingulate cortex, compared with healthy controls and patients who remained abstinent. The local gray matter volume—corrected brain response elicited by alcohol-associated vs neutral stimuli in the left medial prefrontal cortex was enhanced for subsequent relapsers, whereas abstainers displayed an increased neural response in the midbrain the ventral tegmental area extending into the subthalamic nucleus and ventral striatum. For alcohol-associated vs neutral stimuli in abstainers compared with relapsers, the analyses of the psychophysiological interaction showed a stronger functional connectivity between the midbrain and the left amygdala and between the midbrain and the left orbitofrontal cortex. Conclusions Subsequent relapsers displayed increased brain atrophy in brain areas associated with error monitoring and behavioral control. Correcting for gray matter reductions, we found that, in these patients, alcohol-related cues elicited increased activation in brain areas associated with attentional bias toward these cues and that, in patients who remained abstinent, increased activation and connectivity were observed in brain areas associated with processing of salient or aversive stimuli. To date, only a few neuroimaging studies 1 , 2 assessed factors that predict relapse in alcohol dependence. One major situation often provoking relapse is the confrontation with stimuli that have been regularly associated with alcohol consumption; owing to addiction-related learning processes, these formerly neutral stimuli can become conditioned cues and evoke alcohol craving or relapse even without the presence of alcohol itself. The assumption that alcohol cues can motivate alcohol intake even in the absence of conscious craving is in accordance with the hypothesis of Tiffany and Carter, 9 who suggested that habitual drug intake rather than craving plays a major role in the maintenance of drug addiction. Imaging studies of alcohol-dependent patients identified brain areas activated by alcohol-associated vs neutral cues: the orbitofrontal cortex OFC 11 , 12 ; the medial prefrontal cortex MPFC and the adjacent anterior cingulate cortex ACC 1 , 11 , 13 , 14 ; and the ventral and central striatum, including the nucleus accumbens 12 , 15 - 18 and the basolateral amygdala. Brain function in alcohol-dependent patients may be affected by brain atrophy in cortical and subcortical regions, which has also been associated with the prospective relapse risk 23 for review, see Sullivan Rando et al 25 demonstrated that gray matter volume deficits in medial frontal and posterior parietal-occipital brain regions are predictive of an earlier return to alcohol use in detoxified alcohol-dependent patients. Wrase et al 23 and Benegal et al 26 observed reduced volumes of the cingulate and parahippocampal gyri, as well as the amygdala, in subsequent relapsers and, interestingly, also in young, alcohol-naive subjects at high risk for alcohol dependence due to a positive family history. Furthermore, the latter group showed smaller volumes of the superior frontal gyrus, the thalamus, and the cerebellum than did individuals without a positive family history. In addition, decreases in neuronal integrity as indicated by altered surrogate marker concentration N -acetylaspartate and choline in temporal gray matter and frontal white matter in relapsers compared with abstainers were shown. Bustamante et al 29 observed reduced activation in brain areas related to the attention system the dorsal part of the inferior parietal cortex in cocaine-dependent men compared with healthy subjects during a verbal working memory task while controlling for individual differences in gray matter volume within regions of functional differences. Specifically, we assume decreased gray matter volume in frontocortical and limbic areas in prospective relapsers and an increased brain response toward alcohol-associated cues in the MPFC in the same group. Moreover, we will compare standard functional imaging analyses with a new analytic approach using a local voxelwise correction for gray matter loss as additional information. Chronic alcohol intake may disrupt not only local neuronal functioning but also the connectivity between different brain areas. A study 30 investigating functional connectivity during a backward masking paradigm with smoking-related stimuli in smokers and nonsmokers observed altered connectivity between the anterior cingulate cortex and the amygdala in smokers but not in nonsmokers. A total of 46 abstinent alcohol-dependent patients and 46 healthy control subjects participated in our study. Groups were matched for age and sex Table 1. A standardized clinical assessment using structured clinical interviews 32 , 33 was performed to exclude other Axis I psychiatric disorders in patients and control subjects and to exclude Axis II disorders in the latter group. The severity of alcoholism was assessed using the Alcohol Dependence Scale, 34 and the amount of lifetime alcohol intake was measured by applying the Lifetime Drinking History interview. The socioeconomic status of patients was measured using the Hollingshead Index of Social Position. Patients with neurological or hepatic impairment eg, liver cirrhosis were excluded. Missing data were replaced by the median value for interval-scaled data and by the modal value for ordinal- or nominal-scaled data. All results are listed in Table 1 and Table 2. Alcohol-dependent patients had been detoxified on a ward. All patients were abstinent for at least 1 week mean \[SD\] duration, Current substance or alcohol abuse was checked by random breath and urine testing. After scanning, patients were probed during a 2-week cycle by one of the researchers J. Alcohol consumption was recorded with the Form 90, a standard tool for retrospective assessment of alcohol intake. In accordance with standard clinical trials, 40 , 41 relapse was defined as a consumption of more than 60 g of alcohol in men or more than 40 g of alcohol in women during the assessment period 3 months. The patients were not provided follow-up treatment after detoxification during the period of MRI and relapse assessment. Our study was approved by the ethics committee of the Faculty for Clinical Medicine Mannheim at the University of Heidelberg, Germany, and informed written consent was obtained from all participants. After the follow-up period, the recorded data were analyzed with regard to the subsequent relapse, which divided the group of patients into 16 abstainers and 30 relapsers. Within the abstainers, there was only 1 patient who consumed 10 g of alcohol during the observation period, whereas the other abstainers did not drink any alcohol. In contrast, the smallest amount of alcohol consumed in the group of relapsers during the 3-month follow-up period was g. Relapse occurred after a mean SD In previous studies, 12 , 43 the use of CUE alc elicited a reliable craving in detoxified alcohol-dependent patients. During fMRI scanning, the alcohol-associated and control stimuli were presented in a block design. The paradigm consisted of 5 stimulation blocks per category separated by a fixation condition fixation cross. Three images per stimulation block were randomly presented for 6. The stimulation, as well as fixation periods, had a total duration of After scanning, patients were counseled if they experienced persistent craving for alcohol. The first 3 volumes of each session were discarded to allow for magnetic field stabilization. For anatomical reference and for brain morphometric analysis, a 3-dimensional magnetization-prepared rapid gradient echo image was acquired repetition time, The structural scan of each subject was denoised by applying an optimized blockwise nonlocal means filter algorithm as described by Coupe et al, 47 morphed into the standard space diffeomorphic anatomical registration through exponentiated lie algebra \[DARTEL\] Montreal Neurological Institute \[MNI\] template of healthy control subjects of the IXI \[Information Extraction From Images\] database using the DARTEL normalization as implemented in SPM8, 48 and segmented into tissue classes using the adaptive maximum a posterior 49 and partial volume effect 50 techniques as implemented in the VBM8 toolbox. In a second pass, the procedure was repeated using the group-specific templates. A 1-way analysis of covariance was conducted for the smoothed gray matter segments with the between-subject factor group controls, abstainers, and relapsers and the individual intracranial volume computed with the VBM8 toolbox. Echo-planar imagings were corrected for technical artifacts, such as signal-to-noise decrease in single slices, using the denoising function of the ArtRepair software. The ensuing SPM preprocessing consisted of motion correction, calculation of a mean echo-planar image, stereotactical normalization using the set of transformation parameters obtained from the corresponding structural image which has been coregistered to the mean echo-planar imaging before , resampling to an isotropic voxel size of 3. The resulting voxel time series were high-pass—filtered with a cutoff frequency of seconds. Serial correlations from aliased cardiological and respiratory effects were accounted for using a first-order autoregressive model. Statistical analysis was performed in a 2-stage mixed-effects model. In the first single-subject stage, neural activity was modeled by a boxcar function. The BOLD response was modeled by convolving these boxcar functions with the canonical hemodynamic response function as implemented in SPM. The resulting time courses were down-sampled for each scan to form the explanatory variables of a general linear model. The resulting general linear model comprised 2 regressors for the conditions of interest CUE alc , IAPS neutral , one for the scrambled pictures, one for each of the 6 rigid-body movement parameters estimated during motion correction, and a single constant representing the mean over scans. Weighting parameters for the general linear model were estimated by use of a restricted maximum likelihood fit. For these contrast images, second-level random-effects analyses were conducted with the standard SPM approach and with the BPM toolbox. Taking into account that VBM analysis revealed a massive but locally variable cortical atrophy in the group of alcohol-dependent patients, we used the individual local gray matter volume as a voxel-wise covariate in our BPM analyses. To compare the groups, T contrasts were computed on the resulting parameter estimates. The psychophysiological interaction PPI approach 51 - 53 was used to assess the functional coupling between different brain regions in relation to the experimental context ie, the presentation of alcohol-related stimuli. The PPI is defined as the change in connectivity of one brain area the so-called seed region to another with the experimental or psychological context ie, the alcohol vs the neutral stimuli. To assess the coupling between midbrain and other brain areas, depending on the presentation of the alcohol-related stimuli, the CUE alc block vs the IAPS neutral block were chosen as the psychological factors. To this end, for each subject, the first eigenvariate time series from this position was extracted, adjusted for the effects of interest corrected for variance explained by scrambled pictures and by head movements , and deconvolved with the canonical hemodynamic response function. Finally, the PPI term was reconvolved with the canonical hemodynamic response function. New single-subject general linear models were set up that included the PPI term as the primary regressor of interest, as well as the eigenvariate time series from the midbrain, the psychological variable ie, the weighted linear combination of CUE alc and IAPS neutral , the regressor modeling the scrambled picture presentation, the 6 rigid-body movement parameters, and a constant representing the mean over scans as covariates of no interest. The contrast images of the PPI term for all subjects was subjected to a second-level random-effects analysis. To account for differences in demographic and clinical variables, we included age, sex, number of cigarettes smoked per day, and Hamilton Depression Rating Scale score in all analyses. Compared with the healthy control group, the group of prospective relapsers revealed a pronounced atrophy in cortical midline structures, including almost all the regions of interest the bilateral MPFC, the bilateral ACC, the bilateral OFC, the left amygdala, the bilateral ventral striatum, and the left VTA Table 3 ; Figure 3. Compared with the healthy control group, the group of abstainers showed a similar pattern but showed lower levels of cortical and subcortical atrophy when compared with the group of relapsers Table 3 ; Figure 3. For the comparison between controls and relapsers, no effects toward alcohol vs neutral cues could be found. For the comparison between controls and abstainers and between abstainers and controls, no effects toward alcohol cues could be found within our regions of interest. The present findings suggest that pronounced atrophy in cortical midline structures and an increased brain response in the MPFC during processing of alcohol-related stimuli are associated with the prospective relapse in detoxified alcohol-dependent patients. On the other hand, an increased cue-induced brain response in the midbrain including the VTA and the subthalamic nucleus \[STN\] and an enhanced functional connectivity between the midbrain and the amygdala and between the midbrain and the OFC appear to be protective against relapse. Among prospective relapsers, morphometric analyses revealed pronounced tissue loss in cortical midline structures and in subcortical regions. Abstainers showed similar but less severe patterns of cortical and subcortical volume reductions. These results are in line with several studies 54 - 58 showing distinctive gray matter loss in alcohol-dependent patients. Rando et al 25 observed reduced gray matter volume in the medial frontal and posterior parietal-occipital brain regions in detoxified patients, and this reduction was predictive for early relapse. Moreover, volume reductions in several brain regions, including the superior frontal and cingulate gyri and the amygdala, were found in alcohol-naive high-risk subjects, which suggests that at least part of the volume reductions could be preexisting and predispose to excessive alcohol intake rather than just resulting from neurotoxic effects. On a functional level, the OFC, the ACC, and the MPFC have been shown to be involved in inhibitory control, decision making, reward prediction, salience attribution, and hedonic experience. In human studies, 63 , 64 lesions in the orbitofrontal cortical regions were closely linked to impulsivity, risk-taking behavior, and impaired goal-directed behavior. Our findings could thus help to explain why alcohol-dependent patients with OFC volume reduction may misjudge risky situations or spontaneously consume alcohol despite the conscious decision not to do so. Indeed, several studies 65 , 66 have consistently shown a reduction in frontal metabolism, including the OFC, in alcohol-dependent subjects compared with healthy controls. Interestingly, Tanabe et al 67 observed lower gray matter volume in the bilateral medial OFC of alcohol-dependent subjects, which was correlated with pathological decision making ie, high-risk behavior in a gambling task , although they had been long-term abstainers. Dysfunctional ACC activation by alcohol-associated cues may bias attention toward alcohol-related stimuli and impair error monitoring and extinction of previously rewarding behavior ie, alcohol consumption. The functional BPM analyses which takes individual differences in brain volumes into account in a voxel-by-voxel manner revealed an increased BOLD response during the processing of alcohol cues in the left MPFC in relapsers compared with healthy controls and in relapsers compared with abstainers. This finding is in line with previous research 1 , 21 , 70 showing an enhanced cue-induced brain response in this area, which may mediate an attentional bias toward drug cues. Interestingly, the observed brain response here is more superior than the previous finding from our group 1 ; this might be an effect of sample size or of differences in the covariables used for correction local gray matter volume, as well as age, sex, smoking behavior, and mood effects. Notably, the MPFC is rather large and putatively functionally heterogeneous. Therefore, further studies should explore the specific roles of functional subdivisions within this brain area that are related to cue processing and the risk of relapse. Using fMRI in nonaddicted but heavy drinkers, Kareken et al 71 showed that a family history of alcoholism significantly affects medial frontal responses to the odors of a subject's preferred alcoholic drinks. Subjects with a positive family history for alcoholism displayed a greater response to alcoholic drink odors than did subjects with a negative family history. Compared with the group of relapsers, the group of abstainers showed an increased brain response in the right midbrain. The midbrain region implied in our findings includes the VTA and the STN, brain areas closely linked with dopaminergic regulation of the ventral striatum, a core area of the brain reward system. Evidence for involvement of the STN in the regulation of behavior in conflicting choices comes from human 73 and animal 74 studies. Fleming et al 73 found increased STN activity and strengthened modulation of this activity by the OFC, when default behavior was inhibited in the face of heightened decision difficulty. In the context of addiction, the default behavior usually is associated with drug seeking and intake. In turn, abstinence equals the rejection of the default behavior in alcohol-addicted patients. In this light, STN activity in our abstainers might reflect this ability for a successful inhibition. Moreover, STN activity seems to also depend on addiction history. The latter is in line with a missing STN activation on alcohol cues in our controls. Ventral striatal activation was unexpected and only found when correcting for local gray matter volume. This may be the reason why other studies did not report such a finding. Zink et al 75 and Niznikiewics and Delgado 76 showed that the ventral striatum responds not only to appetitive signals, such as positive reinforcers, but also to negative reinforcers or saliency per se. Therefore, increased ventral striatal activation in prospective abstainers, in conjunction with intact or even increased connectivity between the reported midbrain structures and both the OFC and the amygdala, may indicate an intact value assessment of alcohol cues, including an appreciation of the positive and negative consequences of alcohol. To the best of our knowledge, this is the first study powered to directly compare relapsers and abstainers. Other studies implicating the ventral striatum 16 or the central striatum 1 in alcohol-cue reactivity assessed correlations with alcohol intake rather than group differences 1 and assessed correlations with medication effects, not relapse rates. They suggested that cue-induced activation of the amygdala may primarily be associated with negative affect and the unpleasant effects of previous alcohol intake and may not necessarily be associated with a cue-induced positive motivation to consume alcohol. Wrase et al 23 examined gray matter volume in a group of detoxified alcohol-dependent patients and revealed that a significant decrease of amygdala volume was associated with increased alcohol craving and an increased alcohol intake during a 6-month follow-up period. Makris et al 84 examined cocaine-dependent subjects who were also abusing alcohol and observed that amygdala volume reductions were associated with drug craving. This line of evidence indicates that amygdala function is crucial to evoke aversive affective states toward drug-related cues that may counteract craving and alcohol intake. In turn, preserved integrity of midbrain-amygdala-OFC connectivity could enable detoxified subjects to process aversive aspects of alcohol intake, which may help patients to abstain from further alcohol consumption. In the light of this argument, it is interesting to note that the work by Kareken et al 13 raises the possibility that preexisting genetic mechanisms may alter the mesocorticolimbic circuit's sensitivity including the VTA to reward cues. Possible limitations of the findings of our study are the differences in smoking behavior and negative mood states between the healthy controls and the alcohol-dependent patients, as well as differences between all subgroups in socioeconomic status. However, all statistical analyses remained significant when controlling for these variables. Furthermore, a genotype effect could not be assessed because of the limited sample size. Preserved neural activation and connectivity between the VTA and the amygdala and between the VTA and the OFC, elicited by alcohol-associated stimuli, may help patients to sense the danger of situations in which alcohol is available. Submitted for Publication: May 18, ; final revision received October 1, ; accepted November 28, Additional Contributions: We thank Anthony A. Grace, PhD, for inspiring advice. View Large Download. Table 1. Table 2. Clinical Data of the 2 Patient Groups. Table 3. Detoxification medication eAppendix 2. Increased functional connectivity between midbrain seed region elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to CON eTable 9. Increased functional connectivity between midbrain seed region elicited by processing of alcohol-associated cues compared to neutral cues in ABS compared to REL eTable Manually traced VTA eFigure 2. 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Decreased absolute amygdala volume in cocaine addicts. Ecology and neurobiology of toxin avoidance and the paradox of drug reward. Gene-gene interaction associated with neural reward sensitivity. A susceptibility gene for affective disorders and the response of the human amygdala. An integrated genome research network for studying the genetics of alcohol addiction. See More About Radiology Neurology. Save Preferences. Privacy Policy Terms of Use. This Issue. Views 22, Citations View Metrics. X Facebook More LinkedIn. Original Article. Stimulation protocol. Mri scanning. Data processing and analysis. Voxel-based morphometry. Covariation for potential confounding variables. Statistical thresholds. Sample characterization. Imaging data from vbm. Imaging data from bpm: neural activity during processing of alcohol-related stimuli corrected for local brain atrophy. Imaging data from ppi analyses. Back to top Article Information. Financial Disclosure: None reported. 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