Temporal Association Cortex Research Articles

Longitudinal pattern of regional brain volume change differentiates normal aging from MCI

Neuroimaging measures have potential as surrogate markers of disease through identification of consistent features that occur prior to clinical symptoms. Despite numerous investigations, especially in relation to the transition to clinical impairment, the regional pattern of brain changes in clinically normal older adults has not been established. We predict that the regions that show early pathologic changes in association with Alzheimer disease will show accelerated volume loss in mild cognitive impairment (MCI) compared to normal aging. Through the Baltimore Longitudinal Study of Aging, we prospectively evaluated 138 nondemented individuals (age 64-86 years) annually for up to 10 consecutive years. Eighteen participants were diagnosed with MCI over the course of the study. Mixed-effects regression was used to compare regional brain volume trajectories of clinically normal individuals to those with MCI based on a total of 1,017 observations. All investigated volumes declined with normal aging (p < 0.05). Accelerated change with age was observed for ventricular CSF (vCSF), frontal gray matter, superior, middle, and medial frontal, and superior parietal regions (p < or = 0.04). The MCI group showed accelerated changes compared to normal controls in whole brain volume, vCSF, temporal gray matter, and orbitofrontal and temporal association cortices, including the hippocampus (p < or = 0.04). Although age-related regional volume loss is apparent and widespread in nondemented individuals, mild cognitive impairment is associated with a unique pattern of structural vulnerability reflected in differential volume loss in specific regions. Early identification of patterns of abnormality is of fundamental importance for detecting disease onset and tracking progression.

Impaired small-world efficiency in structural cortical networks in multiple sclerosis associated with white matter lesion load

White matter tracts, which play a crucial role in the coordination of information flow between different regions of grey matter, are particularly vulnerable to multiple sclerosis. Many studies have shown that the white matter lesions in multiple sclerosis are associated with focal abnormalities of grey matter, but little is known about the alterations in the coordinated patterns of cortical morphology among regions in the disease. Here, we used cortical thickness measurements from structural magnetic resonance imaging to investigate the relationship between the white matter lesion load and the topological efficiency of structural cortical networks in multiple sclerosis. Network efficiency was defined using a 'small-world' network model that quantifies the effectiveness of information transfer within brain networks. In this study, we first classified patients (n = 330) into six subgroups according to their total white matter lesion loads, and identified structural brain networks for each multiple sclerosis group by thresholding the corresponding inter-regional cortical thickness correlation matrix, followed by a network efficiency analysis with graph theoretical approaches. The structural cortical networks in multiple sclerosis demonstrated efficient small-world architecture regardless of the lesion load, an organization that maximizes the information processing at a relatively low wiring cost. However, we found that the overall small-world network efficiency in multiple sclerosis was significantly disrupted in a manner proportional to the extent of total white matter lesions. Moreover, regional efficiency was also significantly decreased in specific brain regions, including the insula and precentral gyrus as well as regions of prefrontal and temporal association cortices. Finally, we showed that the lesions also altered many cortical thickness correlations in the frontal, temporal and parietal lobes. Our results suggest that the white matter lesions in multiple sclerosis might be associated with aberrant neuronal connectivity among widely distributed brain regions, and provide structural (morphological) evidence for the notion of multiple sclerosis as a disconnection syndrome.

Effects of demographic factors on cortical thickness in Alzheimer's disease

The aim of this study was to investigate the effect of demographic factors (age of onset, sex and years of education) on the distribution of cortical thickness in a large sample of patients with Alzheimer's disease (AD). The study participants consisted of 193 AD patients and 142 controls with no cognitive impairment (NCI) that were measured with cortical thickness across the entire brain. The effects of demographic factors on cortical thickness were analyzed by applying linear regression after controlling confounding factors. Older individuals in NCI group showed more cortical thinning in frontal, temporal association cortices and insula than younger participants. Early onset AD was associated with cortical thinning in the parietal lobe, whereas late onset AD was associated with cortical thinning in the medial temporal region. The NCI group demonstrated sex-related differences in cortical thickness, although those differences were not present in the AD group. While the education effect was absent in NCI individuals, high levels of education in the AD group correlated with cortical thinning in the frontal and temporoparietal association cortices. Our results show that AD with earlier onset and higher education had suffered more pronounced cortical atrophy in specific parts of the brain than their counterparts, which may be related to cognitive reserve theory.

Retrieval from Episodic Memory: Neural Mechanisms of Interference Resolution

Selectively retrieving a target memory among related memories requires some degree of inhibitory control over interfering and competing memories, a process assumed to be supported by inhibitory mechanisms. Evidence from behavioral studies suggests that such inhibitory control can lead to subsequent forgetting of the interfering information, a finding called retrieval-induced forgetting [Anderson, M. C., Bjork, R. A., & Bjork, E. L. Remembering can cause forgetting: Retrieval dynamics in long-term memory. Journal of Experimental Psychology: Learning, Memory & Cognition, 20, 1063-1087, 1994]. In the present functional magnetic resonance imaging study, we investigated the neural processes underlying retrieval-induced forgetting and, in particular, examined the extent to which these processes are retrieval (i.e., selection) specific. Participants actively retrieved a subset of previously studied material (selection condition), or were re-exposed to the same material for relearning (nonselection condition). Replicating prior behavioral work, selective retrieval caused significant forgetting of the nonretrieved items on a delayed recall test, relative to the re-exposure condition. Selective retrieval was associated with increased BOLD responses in the posterior temporal and parietal association cortices, in the bilateral hippocampus, and in the dorsolateral prefrontal cortex. Medial and lateral prefrontal areas showed a strong negative linear relationship between selection-related neural activity and subsequent forgetting of competitors. These findings suggest reduced demands on inhibitory control processes when interference is successfully resolved during early selective retrieval from episodic memory.

Dissociable neural effects of stimulus valence and preceding context during the inhibition of responses to emotional faces

Socially appropriate behavior requires the concurrent inhibition of actions that are inappropriate in the context. This self-regulatory function requires an interaction of inhibitory and emotional processes that recruits brain regions beyond those engaged by either processes alone. In this study, we isolated brain activity associated with response inhibition and emotional processing in 24 healthy adults using event-related functional magnetic resonance imaging (fMRI) and a go/no-go task that independently manipulated the context preceding no-go trials (ie, number of go trials) and the valence (ie, happy, sad, and neutral) of the face stimuli used as trial cues. Parallel quadratic trends were seen in correct inhibitions on no-go trials preceded by increasing numbers of go trials and associated activation for correct no-go trials in inferior frontal gyrus pars opercularis, pars triangularis, and pars orbitalis, temporoparietal junction, superior parietal lobule, and temporal sensory association cortices. Conversely, the comparison of happy versus neutral faces and sad versus neutral faces revealed valence-dependent activation in the amygdala, anterior insula cortex, and posterior midcingulate cortex. Further, an interaction between inhibition and emotion was seen in valence-dependent variations in the quadratic trend in no-go activation in the right inferior frontal gyrus and left posterior insula cortex. These results suggest that the inhibition of response to emotional cues involves the interaction of partly dissociable limbic and frontoparietal networks that encode emotional cues and use these cues to exert inhibitory control over the motor, attention, and sensory functions needed to perform the task, respectively.

The rat temporal association cortical area 2 (Te2) comprises two subdivisions that are visually responsive and develop independently

In this study, we have used the expression of non-phosphorylated neurofilament (NNF), a protein that exhibits differential areal and laminar neuronal patterning, to assess the chemoarchitectural organization of the rat temporal association cortex (Te). Since expression of NNF is associated with the latter stages of neuronal development, this enabled us to profile the hierarchical development of this region of the cortex. We also examined the expression of the protein Fos, the product of the immediate-early gene cFos, as a neuronal activity marker to determine which areas within this region are visually responsive. Our findings reveal the existence of two previously undescribed subdivisions within the dorsal and ventral domains of the rat temporal association cortical area 2 (Te2) which we have termed Te2d and Te2v, respectively. We also demonstrated the early maturation of the caudal region of Te2d while preceding the primary visual cortex. Within this region of the cortex, the Fos protein indicates that both subdivisions are visually responsive.

Corpus callosal area differences and gender dimorphism in neuroleptic-naïve, recent-onset schizophrenia and healthy control subjects

The study of corpus callosal morphometry is important to unravel the underlying connectivity disturbance in schizophrenia. We studied the corpus callosal area in schizophrenia subjects compared to healthy subjects, while controlling for several confounders that could affect morphometric measures of the corpus callosum (CC). Areas of the whole CC and its sub-regions obtained by two geometric partitioning schemes were studied in 23 right-handed neuroleptic-naïve, recent-onset, schizophrenia patients and compared with 23 right-handed age-, sex- and education-matched healthy subjects. The patients did not differ from controls in whole CC area. On tripartite division of the CC, the area of the anterior sub-region was significantly higher in patients compared to controls. On radial division into 5 sub-regions, the anterior truncus area was significantly higher in patients compared to controls. There was a significant effect of gender (F>M) on the area measures; however there was no significant diagnosis⁎gender effect. Age, age of onset, duration of illness and psychopathology ratings did not show any significant correlations with whole CC area and area of CC sub-regions. The finding of increased area of the anterior truncus that possibly comprises white fibres connecting the temporal association cortices could be indicative of an “abnormal functional hyperconnection” involving these regions in positive symptom schizophrenia. Additionally, the finding of females having larger areas of the whole CC and of the anterior and middle sub-regions could reflect a “normal hyperconnection” underlying increased ambilaterality in females.

Cellular localization and distribution of dopamine D 4 receptors in the rat cerebral cortex and their relationship with the cortical dopaminergic and noradrenergic nerve terminal networks

The role of the dopamine D 4 receptor in cognitive processes and its association with several neuropsychiatric disorders have been related to its preferential localization in the cerebral cortex. In the present work we have studied in detail the regional and cellular localization of the dopamine D 4 receptor immunoreactivity (IR) in the rat cerebral cortex and its relationship to the dopaminergic and noradrenergic nerve terminal networks, since both dopamine and noradrenaline have a high affinity for this receptor. High levels of D 4 IR were found in motor, somatosensory, visual, auditory, temporal association, cingulate, retrosplenial and granular insular cortices, whereas agranular insular, piriform, perirhinal and entorhinal cortices showed low levels. D 4 IR was present in both pyramidal and non-pyramidal like neurons, with the receptor being mainly concentrated to layers II/III. Layer I was observed to be exclusively enriched in D 4 IR branches of apical dendrites. Finally, mismatches were observed between D 4 IR and tyrosine hydroxylase and dopamine β-hydroxylase IR nerve terminal plexuses, indicating that these receptors may be activated at least in part by dopamine and noradrenaline operating as volume transmission signals. The present findings support a major role of the dopamine D 4 receptor in mediating the transmission of cortical dopamine and noradrenaline nerve terminal plexuses.

The influence of sex chromosome aneuploidy on brain asymmetry

The cognitive deficits present in individuals with sex chromosome aneuploidies suggest that hemispheric differentiation of function is determined by an X-Y homologous gene [Crow (1993); Lancet 342:594-598]. In particular, females with Turner's syndrome (TS) who have only one X-chromosome exhibit deficits of spatial ability whereas males with Klinefelter's syndrome (KS) who possess a supernumerary X-chromosome are delayed in acquiring words. Since spatial and verbal abilities are generally associated with right and left hemispheric function, such deficits may relate to anomalies of cerebral asymmetry. We therefore applied a novel image analysis technique to investigate the relationship between sex chromosome dosage and structural brain asymmetry. Specifically, we tested Crow's prediction that the magnitude of the brain torque (i.e., a combination of rightward frontal and leftward occipital asymmetry) would, as a function of sex chromosome dosage, be respectively decreased in TS women and increased in KS men, relative to genotypically normal controls. We found that brain torque was not significantly different in TS women and KS men, in comparison to controls. However, TS women exhibited significantly increased leftward brain asymmetry, restricted to the posterior of the brain and focused on the superior temporal and parietal-occipital association cortex, while KS men showed a trend for decreased brain asymmetry throughout the frontal lobes. The findings suggest that the number of sex chromosomes influences the development of brain asymmetry not simply to modify the torque but in a complex pattern along the antero-posterior axis.

Virtual needle pain stimuli activates cortical representation of emotions in normal volunteers

Psychological factors are known to play an extremely important role in the maintenance and development of chronic pain conditions. However, it is unclear how such factors relate to the central neural processing of nociceptive transmission in healthy individuals. To investigate this issue, the activation of the brain was studied in 30 healthy volunteers responding to virtual pain stimuli by fMRI. In the first series of the study (non-preconditioned study), 15 participants were shown a digital video demonstrating an injection needle puncturing the right palm. In the second series of the study (pre-conditioned study), same-task paradigms were used for another 15 participants. Prior to the fMRI session, real needle punctuate stimuli were applied to the right palm of participants for pre-conditioning. fMRI analysis revealed that bilateral activations in anterior insula (BA45), parietal operculum (S2: BA40), premotor area, medial globus pallidus, inferior occipital gyrus (BA18), left temporal association cortex, right fusiform gyrus, right parietal association cortex and cerebellum occurred due to the task in the preconditioned group. On the other hand, right parietal operculum (S2: BA40), premotor area, parietal association cortex, left inferior frontal gyrus and bilateral temporal association cortex were activated in the non-preconditioned group. In addition, activation of anterior insula, inferior frontal gyrus, precentral gyrus and cerebellum significantly increased in the preconditioned group compared with the non-preconditioned group. These results suggest that the virtual needle puncture task caused memory retrieval of unpleasant experiences which is possibly related to empathy for pain, resulting in the activation of specific brain areas.

Structural Insights into Aberrant Topological Patterns of Large-Scale Cortical Networks in Alzheimer's Disease

Recent research on Alzheimer's disease (AD) has shown that cognitive and memory decline in this disease is accompanied by disrupted changes in the coordination of large-scale brain functional networks. However, alterations in coordinated patterns of structural brain networks in AD are still poorly understood. Here, we used cortical thickness measurement from magnetic resonance imaging to investigate large-scale structural brain networks in 92 AD patients and 97 normal controls. Brain networks were constructed by thresholding cortical thickness correlation matrices of 54 regions and analyzed using graph theoretical approaches. Compared with controls, AD patients showed decreased cortical thickness intercorrelations between the bilateral parietal regions and increased intercorrelations in several selective regions involving the lateral temporal and parietal cortex as well as the cingulate and medial frontal cortex regions. Specially, AD patients showed abnormal small-world architecture in the structural cortical networks (increased clustering and shortest paths linking individual regions), implying a less optimal topological organization in AD. Moreover, AD patients were associated with reduced nodal centrality predominantly in the temporal and parietal heteromodal association cortex regions and increased nodal centrality in the occipital cortex regions. Finally, the brain networks of AD were about equally as robust to random failures as those of controls, but more vulnerable against targeted attacks, presumably because of the effects of pathological topological organization. Our findings suggest that the coordinated patterns of cortical morphology are widely altered in AD patients, thus providing structural evidence for disrupted integrity in large-scale brain networks that underlie cognition. This work has implications for our understanding of how functional deficits in patients are associated with their underlying structural (morphological) basis.

In vivo PET study of 5HT 2A serotonin and D 2 dopamine dysfunction in drug-naive obsessive-compulsive disorder

There are several lines of evidence, the majority indirect, suggesting that changes in serotonergic or dopaminergic neurotransmission may contribute to the pathogenesis of obsessive-compulsive disorder (OCD). We evaluated the co-occurrence of serotonergic and dopaminergic dysfunctions in OCD subjects, all drug-naive, with no co-morbidity and homogeneous for symptoms. Each subject underwent two positron emission tomography (PET) scans to measure in vivo both serotonin (5-HT 2A) and dopamine (D 2) receptor distribution. For this, we used [ 11C]MDL and [ 11C]Raclopride, highly selective antagonists of 5-HT 2A and D 2 receptors, respectively. The comparison with a control group was carried out using both voxel-wise (SPM2) and regions of interest (ROI) approaches. There was a significant reduction of 5-HT 2A receptor availability in frontal polar, dorsolateral, and medial frontal cortex, as well as in parietal and temporal associative cortex of OCD patients. We also found a significant correlation between 5-HT 2A receptor availability in orbitofrontal and dorsolateral frontal cortex and clinical severity, suggesting a specific role for serotonin in determining the OCD symptoms. There was also a significant reduction of [ 11C]Raclopride uptake in the whole striatum, particularly in the ventral portion, possibly reflecting endogenous dopaminergic hyperactivity. The co-existence of serotonergic and dopaminergic dysfunction in the same homogeneous group of drug-naive OCD patients provides in vivo evidence for the complex molecular mechanisms of OCD, and represents the basis for further studies on the effect of therapeutic agents with specific modulatory effects on these neurotransmission systems.

Influence of mild hyperglycemia on cerebral FDG distribution patterns calculated by statistical parametric mapping

In clinical cerebral 2-[(18)F]fluoro-2-deoxy-D: -glucose positron emission tomography (FDG-PET) studies, we sometimes encounter hyperglycemic patients with diabetes mellitus or patients who have not adhered to the fasting requirement. The objective of this study was to investigate the influence of mild hyperglycemia (plasma glucose range 110-160 mg/dl) on the cerebral FDG distribution patterns calculated by statistical parametric mapping (SPM). We studied 19 healthy subjects (mean age 66.2 years). First, all the subjects underwent FDG-PET scans in the fasting condition. Then, 9 of the 19 subjects (mean age 64.3 years) underwent the second FDG-PET scans in the mild hyperglycemic condition. The alterations in the FDG-PET scans were investigated using SPM-and region of interest (ROI)-based analyses. We used three reference regions: (1) SPM global brain (SPMgb) used for SPM global mean calculation, (2) the gray and white matter region computed from magnetic resonance image (MRIgw), and (3) the cerebellar cortex (Cbll). The FDG uptake calculated as the standardized uptake value (average) in SPMgb, MRIgw, and Cbll regions in the mild hyperglycemic condition was 42.7%, 41.3%, and 40.0%, respectively, of that observed in the fasting condition. In SPM analysis, the mild hyperglycemia was found to affect the cerebral distribution patterns of FDG. The FDG uptake was relatively decreased in the gray matter, mainly in the frontal, temporal, and parietal association cortices, posterior cingulate, and precuneus in both SPMgb-and MRIgw-reference-based analyses. When Cbll was adopted as the reference region, those decrease patterns disappeared. The FDG uptake was relatively increased in the white matter, mainly in the centrum semiovale in all the reference-based analyses. It is noteworthy that the FDG distribution patterns were altered under mild hyperglycemia in SPM analysis. The decreased uptake patterns in SPMgb-(SPM default) and MRIgw-reference-based analyses resembled those observed in Alzheimer's disease. Under mild hyperglycemia, we can recommend Cbll as the reference region to detect decreased uptake patterns. We should pay special attention to controlling the diet condition, monitoring hyperglycemia, and optimizing the reference region in SPM analysis, particularly in the diagnosis of early Alzheimer's disease in clinical FDG-PET.

Fluoro-2-Deoxy-D-Glucose (FDG)-PET in APOEε4 Carriers in the Australian Population

Apolipoprotein E-epsilon4 (APOEepsilon4) has been associated with increased risk of developing Alzheimer's disease (AD) and regional cerebral glucose hypometabolism, as measured by fluoro-2-deoxy-D-glucose-positron emission tomography (FDG-PET). We report here preliminary data from studies that aim to determine whether cerebral glucose hypometabolism is observed in APOEepsilon4 positive, cognitively intact individuals between the ages of 50 and 80, and whether there is an additional impact of subjective memory complainer (SMC) status on glucose metabolism determined by NeuroStat analysis. FDG-PET was conducted in 30 community dwelling, APOE-epsilon4 carriers without clinical evidence of dementia and objective cognitive impairment as assessed using a neuropsychological battery. Neurological soft-signs (NSS) were also assessed. Glucose hypometabolism was demonstrated in the anterior and posterior cingulate cortex and in the temporal association cortices in APOEepsilon4 carriers compared to the normative NeuroStat database. This pattern was particularly evident in APOEepsilon4 heterozygous individuals. SMC showed hypometabolism in the aforementioned brain regions, whereas non-SMC showed no significant pattern of glucose hypometabolism. FDG-PET with NeuroStat analysis showed that APOEepsilon4 carriers have mild glucose hypometabolism in areas associated with AD. SMC may be associated with AD-related differences in regional cerebral glucose metabolism. These findings are currently being investigated in a larger group of APOEepsilon4 carriers.

Crossed Cerebellar Diaschisis in Acute Ischemic Stroke: A Study with Serial SPECT and MRI

This study evaluated the relationship between crossed cerebellar diaschisis (CCD) and (1) lesion volume and location in the acute phase and 1 week after stroke onset and (2) clinical outcome. Twenty-two patients with cerebral ischemic stroke underwent single-photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI) within 48 h and on day 8 from onset. Interhemispheric asymmetric indices (AI) on SPECT were calculated for medial, intermediate, and lateral zones of the cerebellum. Lesion volumes and locations were obtained from diffusion-weighted MRI. Neurological status and 3-month clinical outcome were evaluated. Within 48 h, lesion locations in the temporal association cortex and pyramidal tract of the corona radiata were independent determinants for the AI of the medial zone (R(2)=0.439). Lesion locations in the primary, premotor, and supplementary motor cortices, primary somatosensory cortex, and anterior part of the posterior limb of the internal capsule were determinants for the AI of the intermediate zone (R(2)=0.785). Lesions in the primary motor cortex, premotor, and supplementary motor cortices and in the genu of the internal capsule were determinants for the AI of the lateral zone (R(2)=0.746). On day 8, the associations were decreased. The AIs of the intermediate and lateral zones and lesion location in the parietal association cortex were independently associated with the 3-month clinical outcome (R(2)>0.555). Acute CCD is a result of functional deafference, while in the subacute phase, transneuronal degeneration might contribute to CCD. CCD in the intermediate and later zones is a better indicator than that in the medial zone.

Different cerebral cortical areas influence the effect of subthalamic nucleus stimulation on parkinsonian motor deficits and freezing of gait

Inconsistent response in freezing of gait (FOG) with levodopa treatment or STN DBS makes the pathogenesis difficult to understand. We studied brain areas associated with the expression of STN DBS effect on parkinsonian motor deficits and FOG. Ten Parkinson's disease patients with typical FOG were included. One month before STN DBS, we performed [(18)F]-deoxyglucose PET scans and measured the UPDRS motor and modified FOG (mFOG) scores during levodopa off and on periods. At two months after STN DBS, same rating scores were measured. The percentage improvement of mFOG and UPDRS motor scores by STN DBS during levodopa off period was calculated. We searched for brain areas in which glucose metabolism correlated with the improvement of mFOG and UPDRS motor scores by DBS. During levodopa off period, STN DBS improved the UPDRS motor scores by 32.3% and the mFOG scores by 56.6%. There was no correlation between the improvements of both scores. The improvement of UPDRS motor score by DBS correlated with the metabolic activities of rostral supplementary motor area (Brodmann's area 8; BA8), anterior cingulate cortex (BA32), and prefrontal cortex (BA9). On the other hand, there was a positive correlation between the improvement of mFOG score by DBS and the metabolic activity of the parietal, occipital, and temporal sensory association cortices. In conclusion, dysfunction of different cerebral cortical areas limits the beneficial effects of DBS on parkinsonian motor deficits and FOG.

Changes in the Regional Cerebral Perfusion After Eye Movement Desensitization and Reprocessing: A SPECT Study of Two Cases

Eye movement desensitization and reprocessing (EMDR) has emerged as a promising new treatment for trauma and other anxiety-based disorders. However, the neurobiological mechanism of EMDR has not been well understood. This study reports changes in the resting regional cerebral blood flow after successful EMDR treatment in two patients with posttraumatic stress disorder (PTSD). Brain 99mTc-ECD-SPECT (Technetium 99m–ethyl cysteinate dimmer–single photon emission computerized tomography) was performed before and after EMDR, and, in addition, a pre- and posttreatment comparison was made with 10 non-PTSD participants as a control group. After EMDR, cerebral perfusion increased in bilateral dorsolateral prefrontal cortex and decreased in the temporal association cortex. The differences between participants and normal controls also decreased. Changes appeared mainly in the limbic area and the prefrontal cortex. These results are in line with current understanding of neurobiology of PTSD. EMDR treatment appears to reverse the functional imbalance between the limbic area and the prefrontal cortex.

Reduced planum temporale volume and delusional behaviour in patients with schizophrenia

The structural abnormality of planum temporale (PT), a part of the superior temporal heteromodal association cortex involved in auditory and language processing, has been implicated in the pathophysiology of schizophrenia. However, its relationship to clinical manifestations remains unclear. Magnetic resonance images were obtained from 17 right-handed Japanese men with schizophrenia and from 22 age-, handedness-, and parental socioeconomic-status-matched healthy Japanese men in order to manually evaluate grey matter volumes of Heschl's gyrus (HG) and PT. Psychiatric symptoms were assessed using positive and negative syndrome scale among the patients. Compared with healthy participants, patients with schizophrenia were associated with a statistically significant PT grey matter volume reduction without left or right lateralization, whereas HG volume was preserved. Smaller right PT volume was significantly correlated with more severe delusional behaviour in the patients. Previous investigations have focused on smaller-than-normal left PT in the pathophysiology of schizophrenia; however, the present results suggest a possible role of the right PT, which is involved in social cognition such as understanding the intentions of others, in the production of psychotic experiences in patients with schizophrenia.

Cortical thickness in single- versus multiple-domain amnestic mild cognitive impairment

Amnestic mild cognitive impairment (aMCI) can be classified into single domain (S-aMCI) and multiple domain (M-aMCI) subtypes. However, there have been no studies that specifically investigate the structural differences that support this classification. In an attempt to compare regional cortical thickness in two subtypes of aMCI, we aimed to map the distribution of cortical thinning using a surface based cortical analysis of magnetic resonance imaging. The cortical thickness across the entire brain was measured in 9 patients with S-aMCI, 22 patients with M-aMCI, and 61 normal healthy subjects. Differences in the patterns of cortical thinning between S-aMCI and M-aMCI were assessed using ANCOVA on a vertex-by-vertex basis, and statistical maps of differences in cortical thickness between the groups were constructed using a surface model. Relative to controls, S-aMCI patients showed cortical thinning in the left medial temporal lobe, and M-aMCI patients showed cortical thinning in the left medial temporal lobe, precuneus, and anterior and inferior basal temporal, insular, and temporal association cortices. When the two MCI groups were directly compared, M-aMCI patients showed cortical thinning in left precuneus. Our studies suggest that M-aMCI is a transitional state between S-aMCI and Alzheimer's disease, and that the cortical thinning is evidence that the precuneus is responsible for the multiple cognitive impairments in M-aMCI.

Impairment of odor recognition in Parkinson's disease caused by weak activations of the orbitofrontal cortex

Olfactory dysfunction and abnormalities of olfactory brain structures are found in patients with Parkinson's disease (PD), and a number of studies have reported that olfactory dysfunction is caused by abnormalities of the central olfactory systems. We previously analyzed electroencephalograms (EEGs) and respiration simultaneously in normal subjects while testing for detection and recognition of odors. We identified changes in respiration pattern in response to odor stimuli and found inspiratory phase-locked alpha oscillations (I-α). The genesis of I-α were identified in olfactory-related areas including the entorhinal cortex, hippocampus, amygdale and orbitofrontal cortex with an EEG dipole tracing method. In the present study, we used the same protocol in PD patients and compared results of PD with those of age-matched controls. All PD patients detected odor, but 5 out of 10 showed impaired odor recognition. Changes in breathing pattern associated with emotional changes during exposure to odor stimuli were not observed in PD patients. I-α waveforms were not observed; however, positive waves followed by negative waves were identified approximately 100 ms after inspiration onset. Dipoles of this component were localized in the entorhinal cortex for odor detection in all patients and in the entorhinal cortex and middle temporal gyrus for PD patients who could discriminate odors. Odor recognition in PD could be subserved by a different neural circuit from that of normal subjects, done through the temporal association cortex as a subsystem for recognizing the odor; however, the system may not be associated with the odor-induced emotions.