Seit 30 Jahren werden Neuroimaging-Befunde in zunehmendem Maße als Beweismittel im Strafverfahren eingesetzt. Unzweifelhaft hat die moderne Bildgebungsforschung wichtige Erkenntnisse auch über die neuronalen Grundlagen von kriminologisch relevantem Verhalten geliefert. Dennoch ergeben sich speziell hinsichtlich der Anwendung von Neuroimaging im Rahmen der forensischen Einzelfallbeurteilung von Tätern zahlreiche Besonderheiten und Limitationen. Der Beitrag gibt eine kasuistisch illustrierte Übersicht über den bisherigen praktischen Umgang mit Neuroimaging-Befunden im Gerichtssaal und die zugrunde liegende neurowissenschaftliche Evidenz.

BACKGROUND:Accumulating evidence from postmortem and magnetic resonance imaging (MRI) studies suggests that abnormalities of medial temporal lobe structures are critically involved in the pathogenesis of schizophrenia. It is still unclear, however, whether certain abnormalities are already present in individuals at ultra high-risk (UHR) for transition into psychosis. Recent studies involving patients at UHR showed contradictory results for hippocampal volume, and only 1 study reported that amygdalar volume was unchanged between healthy patients and those at UHR. Furthermore, no subregions of the hippocampus have been investigated in people at UHR. METHODS:We recruited 29 UHR patients, 23 first-episode patients and 29 age- and sex-matched healthy controls. We measured hippocampal and amygdalar volumes from MRI scans by use of BRAINS2 to manually trace the regions of interest. The hippocampi were divided in 2 regions: head and corpus/tail. RESULTS:Patients at UHR had significantly smaller volumes of the hippocampus corpus and tail bilaterally, but not of the head, compared with healthy controls. Group differences for the right hippocampus corpus and tail volume remained significant after we controlled for whole brain volume and other covariates. We found that UHR patients who later developed psychosis had smaller right hippocampus corpus and tail volumes than did those who did not develop psychosis. First-episode patients had significantly smaller left amygdalar volumes than did healthy individuals or those at UHR. LIMITATIONS:Our study had a small sample size, and we were unable to control for the effects of medication. CONCLUSION:Our findings suggest that parts of the hippocampal-amygdalar complex are involved in the pathogenesis of schizophrenia. Reduction of hippocampus corpus and tail volumes may be indicative of the prodromal phase of schizophrenia and represent risk factors for transition into psychosis. Further investigations are needed to determine whether structural changes of the left amygdala play a role during transition from the prodromal phase to the first manifest episode of schizophrenia.

This evaluation study of social therapeutic tandem groups deals with the early as well as the long term psychosocial support with coping with illness and everyday life that is offered to patients suffering from Alzheimer's disease and their relatives. Central to this is the analysis of inhibiting or supporting factors to the effectiveness of the parallely run social therapeutic support groups for patients and family members. The aims, for patients and their relatives (mostly spouses/partners) alike, are social support, activation, knowledge acquisition, a shame- and taboo-free way of dealing with the illness and the accompanying hardships as well as preventing insufficient or inappropriate health care services. The results of this primarily qualitative pilot study will be summarized in a manual for the nation wide implementation of psychosocial early intervention programs promoting a higher quality of life.

Reward processing depends critically on dopaminergic neurotransmission in the ventral striatum. The common polymorphism val(158)met of catechol-O-methyltransferase (COMT) accounts for significant interindividual variations in dopamine (DA) degradation, although the direct effect of COMT on striatal DA might be limited. Using fMRI we assessed the influence of COMT val(158)met genotype on brain activations elicited by the anticipation of monetary gains and losses in forty-four healthy volunteers. We found that the met(158) allele, which is presumably linked to higher synaptic DA levels, was associated with higher responses in ventral striatum to loss incentives. There was a linear relationship between the number of met(158) alleles and ventral striatal activity. Furthermore, we observed a similar gene-dose effect in the anterior temporal cortex, a region that has been linked to the coupling of sensory information with emotional contents. Temporal cortex also showed enhanced connectivity to the ventral striatum during the processing of incentive stimuli. Increased ventral striatal reactivity to loss incentives related to the met(158) allele might contribute to the observed association of the met(158) allele to higher loss aversion behaviour. Current evidence and our results are compatible with an interpretation that construes this effect of COMT genotype on striatal reactivity as a result of a cortico-striatal interaction.

The neurodevelopmental hypothesis of schizophrenia, which was established 30 years ago and discussed controversially for a long time, postulates that pre- and perinatally acting cerebral noxae cause disturbances of corticogenesis in the developing neuronal fibre systems which are essential for later onset of the disease. During recent years the cerebral alterations of schizophrenic patients could be further characterized as area-, layer-, and cell type-specific changes in temporolimbic and frontal regions leading to specific abnormalities of intrinsic and extrinsic connectivity. Animal models allowed for realistic imitations of these structural lesions and for elucidating their functional consequences concerning transmitter systems and behaviour. With modern neuroimaging techniques microstructural changes and alterations in cerebral activation can be exactly demonstrated and related to the specific psychopathologic features of schizophrenia.

Die vor 30 Jahren formulierte und zunächst umstrittene Entwicklungsstörungshypothese zur Pathogenese schizophrener Störungen besagt, dass prä-/perinatal auf das Gehirn einwirkende Noxen zu pathologischen Veränderungen der Kortikogenese und der sich entwickelnden neuronalen Bahnsysteme führen, welche für den späteren Ausbruch der Erkrankung von wesentlicher ätiologischer Bedeutung sind. In den letzten Jahren konnten die zerebralen Veränderungen schizophrener Patienten mit Hilfe neuer neuropathologischer Methoden genauer als areal-, schicht- und zelltypspezifische Alterationen charakterisiert werden, durch die es zu spezifischen Abnormitäten im Bereich der intrinsischen Verschaltungen und der transregionalen Vernetzungen vor allem temporolimbischer und frontaler Hirnregionen kommt. Tiermodelle ermöglichen eine realistische Imitation dieser Strukturläsionen und damit die Aufklärung ihrer funktionellen Implikationen auf der Transmitter- und der Verhaltensebene. Mit den modernen bildgebenden Techniken können zunehmend sowohl die mikrostrukturellen Alterationen als auch zerebrale Aktivierungsänderungen exakt dargestellt und zu spezifischen psychopathologischen Merkmalen schizophrener Störungen in Beziehung gesetzt werden.

Die Evaluationsstudie sozialtherapeutischer «Tandemgruppen» widmet sich der frühzeitigen wie langfristigen psychosozialen Unterstützung bei der Krankheits- und Alltagsbewältigung präsenil erkrankter Demenzpatienten und ihrer Angehörigen. Zentral ist hierbei die Analyse hemmender und fördernder Faktoren für die Wirksamkeit der parallel angebotenen psychosozialen Patienten- und Angehörigengruppen. Zielsetzungen, gleichermaßen für die Erkrankten wie für ihre Angehörigen, meist Ehe- und Lebenspartner, sind sozialen Rückhalt, Aktivierung, Wissenserwerb, einen schamfreien, enttabuisierenden Umgang mit der Erkrankung und den damit einhergehenden Belastungen zu fördern sowie einer Unter- und Fehlversorgung vorzubeugen. Die Ergebnisse dieser primär qualitativ angelegten Pilotstudie sollen zur flächendeckenden Implementierung psychosozialer Frühinterventionen, hier präsenil erkrankter Demenzpatienten, zur Förderung von mehr Lebensqualität in einem Handbuch zusammengefasst werden.

Introduction: Recently, a novel N-methyl-D-aspartate (NMDA) receptor subunit, NR3A, has been discovered in the brain. This subunit decreases NMDA receptor activity by modulating the calcium permeability of the receptor channel and current density in cortical cells. Because the NR3A is expressed in the human prefrontal cortex, we hypothesized that genetic variations of the NR3A subunit modulate prefrontal activation. Methods: Electromagnetic activity during selective attention (auditory oddball task with target processing) was measured in 281 healthy subjects. Genotyping of a missense variation (rs10989591, Val362Met) of the NR3A gene was performed. Results: Individuals carrying Val/Val genotype showed significantly reduced frontal P300 amplitudes compared with Met/Met subjects. Subsequent low-resolution electromagnetic source analysis revealed that this group difference is likely caused by reduced activation in the inferior frontal gyrus. Conclusions: It was shown for the first time that the genetic constitution of the subunit composition of NMDA receptor regulation might be relevant for prefrontal information processing in humans. The results underline the pivotal role of glutamate in frontal lobe function and indicate that the NR3A subunit could be a plausible candidate gene for diseases with prefrontal dysfunctions.

OBJECTIVE:In animals, nicotine, the primary psychoactive constituent of tobacco smoke, reduces neurogenesis and increases cell loss in both hippocampus and cortex. Accordingly, tobacco smoking has been linked to reduced performance on cognitive paradigms requiring attention and working memory in humans. However, few prior studies have tested for evidence of structural brain alterations in human tobacco smokers. In this study, proton magnetic resonance spectroscopy was used to assess the effects of chronic smoking on neuronal integrity of the hippocampus and anterior cingulate cortex (ACC).METHODS:Absolute concentrations of N-acetylaspartate, total choline (tCho), and total creatine were measured in the left hippocampus and ACC in 13 chronic tobacco smokers and 13 nonsmokers matched for age, sex, and education.RESULTS:The N-acetylaspartate concentration was significantly reduced in smokers relative to nonsmokers in the left hippocampus but not in the ACC. There were no group differences in the tCho and total creatine concentrations in either voxel. However, ACC tCho concentration was positively correlated with magnitude of lifetime exposure to tobacco smoke (pack-years).CONCLUSION:The results are consistent with prior observations of hippocampal neuronal damage in rodents receiving nicotine and working memory deficits in human tobacco smokers. The positive relationship between tCho and lifetime tobacco exposure suggests that a component of tobacco smoke, presumably nicotine, may increase cortical membrane turnover or modify cell density. Together, these results add to growing evidence that nicotine exerts neurotoxic effects in human brain, although an a priori nature of the findings cannot be ruled out.

Growing evidence from animal studies indicates brain-damaging properties of nicotine exposure. Investigations in humans found a wide range of functional cerebral effects of nicotine and cigarette smoking, but studies focusing on brain damage are sparse. In 22 smokers and 23 never-smokers possible differences of the cerebral structures were investigated using magnetic resonance imaging and voxel-based morphometry. Significantly smaller grey matter volume and lower grey matter density (P = 0.05, corrected) were observed in the frontal regions (anterior cingulate, prefrontal and orbitofrontal cortex), the occipital lobe and the temporal lobe including parahippocampal gyrus, in smokers than in never-smokers. Group differences of either grey matter volume or grey matter density were also found in the thalamus, cerebellum and substantia nigra, among other regions. Smokers did not show greater volumes than never-smokers in any cerebral region. Magnitude of lifetime exposure to tobacco smoke (pack-years) was inversely correlated with volume of frontal and temporal lobes and cerebellum (P = 0.001, uncorrected). The data indicate structural deficits of several cortical and subcortical regions in smokers relative to never-smokers. The topographic profile of the group differences show some similarities to brain networks known to mediate drug reinforcement, attention and working memory processing. The present findings may explain in part the frequently reported cognitive dysfunctions in chronic cigarette consumers.

OBJECTIVE:Chronic smoking and nicotine exposure are accompanied by impaired cognitive task performance, modulated cerebral activity in brain imaging studies, and neuritic damage in experimental animals. The profile of the described dysfunctions matches frontal lobe circuits which also play a role in reward processing and reinforcement behavior. However, it is largely unknown if cerebral dysfunctions are reversible or persist during long term abstinence.MATERIALS AND METHODS:Cortical activation during auditory target processing (oddball task, P300 component) was recorded with 32-channel EEG in 247 healthy subjects consisting of 84 smokers, 53 former smokers (mean time of abstinence 11.9 years), and 110 never smokers.RESULTS:Both current smokers and former smokers exhibited significantly diminished P300 amplitudes (Cz, Pz) relative to never smokers. Neuroelectric source analysis (low resolution brain electromagnetic tomography) revealed a hypoactivation of the anterior cingulate, orbitofrontal, and prefrontal cortex in smokers compared to never smokers. A similar profile of hypoactivation was observed in former smokers.CONCLUSION:For the first time, evidence is provided that dysfunctional activation of frontal lobe networks in smokers is also present in long term abstainers.

Melatonin has been postulated to have diverse properties, acting as an antioxidant, a neuroprotector, or a stabilizer within the circadian timing system, and is thus thought to be involved in the aging process and Alzheimer's disease (AD). We used computed tomography to determine the degree of pineal calcification (DOC), an intra-individual melatonin deficit marker, as well as the size of uncalcified pineal tissue, in 279 consecutive memory clinic outpatients (AD: 155; other dementia: 25; mild cognitive impairment: 33; depression: 66) and 37 age-matched controls. The size of uncalcified pineal tissue in patients with AD (mean 0.15 cm(2) [S.D. 0.24]) was significantly smaller than in patients with other types of dementia (0.26 [0.34]; P=0.038), with depression (0.28 [0.34]; P=0.005), or in controls (0.25 [0.31]; P=0.027). Additionally, the DOC in patients with AD (mean 76.2% [S.D. 26.6]) was significantly higher than in patients with other types of dementia (63.7 [34.7]; P=0.042), with depression (60.5 [33.8]; P=0.001), or in controls (64.5 [30.6]; P=0.021). These two findings may reflect two different aspects of melatonin in AD. On the one hand, the absolute amount of melatonin excretion capability, as indicated by uncalcified pineal volume, refers to the antioxidant properties of melatonin. On the other hand, the relative reduction in melatonin production capability in the individual, as indicated by DOC, refers to the circadian properties of melatonin.

BACKGROUND Cigarette smoking has been associated with mood enhancing properties and modulating effects on serotonin activity. The loudness dependence (LD) of the auditory-evoked N1/P2-component has been related to serotonergic neurotransmission, i. e. the allelic variants in the promoter of the 5-hydroxytryptamine-transporter (5-HTT) gene (SCL6A4). Moreover, smoking behavior has been associated to the 5-HTT-genotype. It was hypothesized that cigarette smoking modulates the LD and this effect was expected to interact with the 5-HTT-genotype. METHODS 5-HTT-genotype and LD were determined in 63 healthy smokers and 114 nonsmokers. RESULTS LD was significantly affected by smoking status (p = 0.008) and 5-HTT-genotype (p = 0.045) but not by smoking*genotype-interaction or daily cigarette consumption. Current smokers exhibited a significantly weaker LD compared to nonsmokers. 5-HTT-genotype showed no significant effect on smoking behavior. DISCUSSION The results indicate a higher serotonergic activity in smokers as compared to nonsmokers independent of 5-HTT-genotype. Since former smokers and never smokers showed similar LDs, the serotonin enhancing effect of smoking seems to be a characteristic state, which may contribute to the maintenance of smoking behavior.