Spatial patterns of intrinsic brain activity in mild cognitive impairment and Alzheimer's disease: a resting-state functional MRI study

We used resting-state functional MRI to investigate spatial patterns of spontaneous brain activity in 22 healthy elderly subjects, as well as 16 mild cognitive impairment (MCI) and 16 Alzheimer's disease (AD) patients. The pattern of intrinsic brain activity was measured by examining the amplitude of low-frequency fluctuations (ALFF) of blood oxygen level dependent signal during rest. There were widespread ALFF differences among the three groups throughout the frontal, temporal, and parietal cortices. Both AD and MCI patients showed decreased activity mainly in the medial parietal lobe region and lentiform nucleus, while there was increased activity in the lateral temporal regions and superior frontal and parietal regions as compared with controls. Compared with MCI, the AD patients showed decreased activity in the medial prefrontal cortex and increased activity in the superior frontal gyrus and inferior and superior temporal gyri. Specifically, the most significant ALFF differences among the groups appeared in the posterior cingulate cortex, with a reduced pattern of activity when comparing healthy controls, MCI, and AD patients. Additionally, we also showed that the regions with ALFF changes had significant correlations with the cognitive performance of patients as measured by mini-mental state examination scores. Finally, while taking gray matter volume as covariates, the ALFF results were approximately consistent with those without gray matter correction, implying that the functional analysis could not be explained by regional atrophy. Together, our results demonstrate that there is a specific pattern of ALFF in AD and MCI, thus providing insights into biological mechanisms of the diseases.     

Cinguloparietal atrophy distinguishes Alzheimer disease from semantic dementia

BACKGROUND: Progressive brain atrophy is associated with Alzheimer disease (AD) and other dementias. Regional differences in brain atrophy may reflect clinical features of disease. OBJECTIVE: To identify regions of cerebral atrophy that are associated with AD vs other dementias. SETTING: University hospital dementia clinic. PARTICIPANTS: Eleven patients with AD and 11 with semantic dementia (SD), matched for age, sex, education, and degree of overall cognitive impairment and 15 normal controls. METHODS: Voxel-based morphometry was used to compare patterns of gray matter loss, measured on T1-weighted magnetic resonance images, between patients with AD or SD, a subtype of frontotemporal lobar degeneration, and controls. Statistically significant differences in regional gray matter concentration, after multiple-comparisons correction, between groups of subjects were identified. RESULTS: Patients with AD were more impaired than those with SD on tests of visuospatial function and on simple calculations. Consistent with these neuropsychological deficits, the most significant area of atrophy in the AD group was the left parietal cortex vs controls (z = 5.0; P =.04). Compared with SD, AD was associated with more atrophy in the left parietal lobe (z = 5.6; P =.04) and bilaterally in the posterior cingulate/precuneus (z = 5.1; P =.04). A discriminant function analysis demonstrated that the degree of atrophy of right posterior cingulate, left parietal lobe, right amygdala, and right anterior temporal lobe structures correctly classified 96% of the patients. CONCLUSION: Alzheimer disease is associated with a specific pattern of cortical atrophy compared with SD.     

Patterns of brain atrophy in frontotemporal dementia and semantic dementia.

OBJECTIVE: To identify and compare the patterns of cerebral atrophy associated with two clinical variants of frontotemporal lobar degeneration (FTLD): frontotemporal dementia (FTD) and semantic dementia (SemD). METHODS: Twenty patients with FTLD were classified as having FTD (N = 8) or SemD (N = 12) based on current clinical criteria. Both groups showed a similar spectrum of behavioral abnormalities, as indicated by the neuropsychiatric inventory. T1-weighted MRI was obtained for each patient and 20 control subjects. The regions of focal gray matter tissue loss associated with both FTD and SemD, as well as those differing between the two groups were examined using voxel-based morphometry. RESULTS: Regions of significant atrophy seen in both groups were located in the ventromedial frontal cortex, the posterior orbital frontal regions bilaterally, the insula bilaterally, and the left anterior cingulate cortex. The FTD, but not the SemD, group showed atrophy in the right dorsolateral frontal cortex and the left premotor cortex. The SemD, but not the FTD, group showed tissue loss in the anterior temporal cortex and the amygdala/anterior hippocampal region bilaterally. CONCLUSIONS: Although FTD and SemD are associated with different overall patterns of brain atrophy, regions of gray matter tissue loss in the orbital frontal, insular, and anterior cingulate regions are present in both groups. The authors suggest that pathology in the areas of atrophy associated with both FTD and SemD may underlie some the behavioral symptoms seen in the two disorders.     

The effect of meditation on brain structure: cortical thickness mapping and diffusion tensor imaging

A convergent line of neuroscientific evidence suggests that meditation alters the functional and structural plasticity of distributed neural processes underlying attention and emotion. The purpose of this study was to examine the brain structural differences between a well-matched sample of long-term meditators and controls. We employed whole-brain cortical thickness analysis based on magnetic resonance imaging, and diffusion tensor imaging to quantify white matter integrity in the brains of 46 experienced meditators compared with 46 matched meditation-naïve volunteers. Meditators, compared with controls, showed significantly greater cortical thickness in the anterior regions of the brain, located in frontal and temporal areas, including the medial prefrontal cortex, superior frontal cortex, temporal pole and the middle and interior temporal cortices. Significantly thinner cortical thickness was found in the posterior regions of the brain, located in the parietal and occipital areas, including the postcentral cortex, inferior parietal cortex, middle occipital cortex and posterior cingulate cortex. Moreover, in the region adjacent to the medial prefrontal cortex, both higher fractional anisotropy values and greater cortical thickness were observed. Our findings suggest that long-term meditators have structural differences in both gray and white matter.     

Episodic memory and regional atrophy in frontotemporal lobar degeneration

It has been unclear to what extent memory is affected in frontotemporal lobar degeneration (FTLD). Since patients usually have atrophy in regions implicated in memory function, the frontal and/or temporal lobes, one would expect some memory impairment, and that the degree of atrophy in these regions would be inversely related to memory function. The purposes of this study were (1) to assess episodic memory function in FTLD, and more specifically patients' ability to episodically re-experience an event, and determine its source; (2) to examine whether memory performance is related to quantified regional brain atrophy. FTLD patients (n=18) and healthy comparison subjects (n=14) were assessed with cued recall, recognition, "remember/know" (self-reported re-experiencing) and source recall, at 30 min and 24h after encoding. Regional gray matter volumes were assessed with high resolution structural MRI concurrently to testing. Patients performed worse than comparison subjects on all memory measures. Gray matter volume in the left medial temporal lobe was positively correlated with recognition, re-experiencing, and source recall. Gray matter volume in the left posterior temporal lobe correlated significantly with recognition, at 30 min and 24h, and with source recall at 30 min. Estimated familiarity at 30 min was positively correlated with gray matter volume in the left inferior parietal lobe. In summary, episodic memory deficits in FTLD may be more common than previously thought, particularly in patients with left medial and posterior temporal atrophy.     

How common is brain atrophy in patients with medial temporal lobe epilepsy?

Purpose: It is unclear whether extrahippocampal brain damage in patients with medial temporal lobe epilepsy (MTLE) is a homogeneous phenomenon, as most data relates to the average volume reduction in groups of patients. This study aimed to evaluate where and how much atrophy is to be expected in an individual patient with MTLE. Methods: High‐resolution T₁ magnetic resonance imaging (MRI) was obtained from 23 consecutive patients with unilateral MTLE and from a matched control group. Parametric tests of voxel‐based gray matter volume evaluated mean regional atrophy in MTLE compared with controls. Gray matter images were then submitted to a voxel by voxel calculation of the fitted receiver operating characteristic (ROC) curve area, plotting the sensitivity versus 1–specificity for a binary classifier (MTLE vs. controls). The area under the curve (AUC) was calculated for each voxel and a resulting three‐dimensional map of gray matter voxel‐wise AUCs was obtained. Results: On average, patients with MTLE showed atrophy in the ipsilateral hippocampus and on a limbic network. Elevated AUC was demonstrated in the ipsilateral hippocampus and medial temporal lobe, the ipsilateral thalamus and occipitotemporal cortex, the ipsilateral cerebellum, the cingulate, the contralateral insula, and the occipitoparietal and dorsolateral prefrontal cortex. Conclusion: This study suggests that the medial temporal lobe, occipitotemporal areas, the cerebellum, the cingulate cortex, the ipsilateral insula, and thalamus are more likely to be atrophied in randomly selected patients with MTLE. Structures such as the orbitofrontal cortex, the contralateral medial temporal areas and insula, the putamen, and the caudate may be atrophied, but not as consistently.     

Imaging of amyloid beta in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism

BACKGROUND: Amyloid-beta (Abeta) plaque formation is a hallmark of Alzheimer's disease (AD) and precedes the onset of dementia. Abeta imaging should allow earlier diagnosis, but clinical application is hindered by the short decay half-life of current Abeta-specific ligands. (18)F-BAY94-9172 is an Abeta ligand that, due to the half-life of (18)F, is suitable for clinical use. We thus studied the effectiveness of this ligand in identifying patients with AD. METHODS: 15 patients with mild AD, 15 healthy elderly controls, and five individuals with frontotemporal lobar degeneration (FTLD) were studied. (18)F-BAY94-9172 binding was quantified by use of the standardised uptake value ratio (SUVR), which was calculated for the neocortex by use of the cerebellum as reference region. SUVR images were visually rated as normal or AD. FINDINGS: (18)F-BAY94-9172 binding matched the reported post-mortem distribution of Abeta plaques. All AD patients showed widespread neocortical binding, which was greater in the precuneus/posterior cingulate and frontal cortex than in the lateral temporal and parietal cortex. There was relative sparing of sensorimotor, occipital, and medial temporal cortex. Healthy controls and FTLD patients showed only white-matter binding, although three controls and one FTLD patient had mild uptake in frontal and precuneus cortex. At 90-120 min after injection, higher neocortical SUVR was observed in AD patients (2.0 [SD 0.3]) than in healthy controls (1.3 [SD 0.2]; p<0.0001) or FTLD patients (1.2 [SD 0.2]; p=0.009). Visual interpretation was 100% sensitive and 90% specific for detection of AD. INTERPRETATION: (18)F-BAY94-9172 PET discriminates between AD and FTLD or healthy controls and might facilitate integration of Abeta imaging into clinical practice.     

Cerebral blood flow in corticobasal degeneration and progressive supranuclear palsy

To compare brain perfusion between corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), we investigated regional cerebral blood flow (rCBF) semiquantitatively with single-photon emission computed tomography and [123I]iodoamphetamine in six patients with CBD and five with PSP. Compared with 12 age-matched control subjects, the average of the left and right rCBF values for the CBD patients was significantly reduced in the inferior prefrontal, anterior cingulate, medial premotor, sensorimotor, posterior parietal, and superior temporal cortices as well as in the basal ganglia and thalamus, whereas only the medial premotor cortex was significantly hypoperfused in the PSP patients. Compared with the PSP patients, the CBD patients showed significantly decreased rCBF in the inferior prefrontal, sensorimotor, and posterior parietal cortices, but not in the subcortical regions. Compared with the controls, interhemispheric differences of rCBF were significant in the inferior prefrontal, sensorimotor, and posterior parietal cortices of the CBD patients but in only the medial prefrontal cortex of the PSP patients. These results indicate that rCBF reductions are more extensive and asymmetric in CBD than in PSP, although the two diseases share medial frontal involvement.     

Posterior cortical atrophy and Alzheimer’s disease: a meta-analytic review of neuropsychological and brain morphometry studies

This paper presents the first systematic review and meta-analysis of neuropsychological and brain morphometry studies comparing posterior cortical atrophy (PCA) to typical Alzheimer’s disease (tAD). Literature searches were conducted for brain morphometry and neuropsychological studies including a PCA and a tAD group. Compared to healthy controls (HC), PCA patients exhibited significant decreases in temporal, occipital and parietal gray matter (GM) volumes, whereas tAD patients showed extensive left temporal atrophy. Compared to tAD patients, participants with PCA showed greater GM volume reduction in the right occipital gyrus extending to the posterior lobule. In addition, PCA patients showed less GM volume loss in the left parahippocampal gyrus and left hippocampus than tAD patients. PCA patients exhibit significantly greater impairment in Immediate Visuospatial Memory as well as Visuoperceptual and Visuospatial Abilities than patients with tAD. However, tAD patients showed greater impairment in Delayed Auditory/Verbal Memory than patients with PCA. PCA is characterized by significant atrophy of the occipital and parietal regions and severe impairments in visuospatial functioning.     

A multiparametric MRI study of structural brain damage in dementia with lewy bodies: A comparison with Alzheimer's disease

IntroductionDifferential diagnosis between dementia with Lewy bodies (DLB) and Alzheimer's disease (AD) is crucial for an adequate patients' management but might be challenging. We investigated with advanced MRI techniques gray (GM) and white matter (WM) damage in DLB patients compared to those with AD.Methods24 DLB patients, 26 age- and disease severity-matched AD patients, and 20 age and sex-matched controls performed clinical and neuropsychological assessment, and brain structural and diffusion-tensor MRI. We measured GM atrophy using voxel-based morphometry, WM hyperintensities (WMH) using a local thresholding segmentation technique, and normal-appearing WM (NAWM) damage using tract-based spatial statistic.ResultsDLB and AD patients exhibited mild-to-moderate-stage dementia. Compared to controls, GM damage was diffuse in AD, while limited to bilateral thalamus and temporal regions in DLB. Compared to DLB, AD patients exhibited GM atrophy in bilateral fronto-temporal and occipital regions. DLB and AD patients showed higher WMH load than controls, with no differences among each other. WMH in DLB were diffuse with relative prevalence in posterior parietal-occipital regions. Compared to controls, both DLB and AD patients showed reduced microstructural integrity of the main supratentorial and infratentorial NAWM tracts. AD patients exhibited greater posterior NAWM damage than DLB.ConclusionsDLB showed prominent WM degeneration compared to the limited GM atrophy, while in AD both tissue compartments were severely involved. In DLB, NAWM microstructural degeneration was independent of WMH, thus revealing two possible underlying processes. Different pathophysiological mechanisms are likely to drive GM and WM damage distribution in DLB and AD.     

Correlations between MRI-assessed volumes of the thalamus and cortical Brodmann's areas in schizophrenia

BACKGROUND: We compared the thalamic-cortical volumetric correlational patterns in patients with schizophrenia and normal comparison subjects, and evaluated their relations to outcome. METHODS: High-resolution MR images were acquired in patients with schizophrenia (n=106) and normal comparison subjects (n=42). Patients were divided into good-outcome (n=52) and poor-outcome (Kraepelinian, n=54) subtypes based on their ability for self-care. Correlations between the relative gray and white matter volumes of the individual cortical Brodmann's areas and five dorsoventral levels of the thalamus were assessed. RESULTS: Compared to normal subjects, schizophrenia patients lacked significant thalamic gray matter volume correlations with the prefrontal and medial temporal cortical regions in the right hemisphere, and with frontal, cingulate, posterior parietal and occipital regions in the left hemisphere, while normal white matter volume cortical-thalamic correlations along the cingulate gyrus and in the temporal lobe were not found in schizophrenia patients in both hemispheres. In contrast to both normal comparison subjects and good-outcome group, schizophrenia patients with poor outcomes showed significant bilateral gray matter volume correlations between the dorsal thalamus and ventral prefrontal cortex, while the group differences in the white matter volume correlations were mostly restricted to the cingulate arch. CONCLUSIONS: Whereas patients with schizophrenia exhibit deficiencies in cortical-thalamic correlational patterns, poor outcome is associated with abnormal interregional correlations not observed in either normal subjects or patients with good outcomes. This latter finding may be explained by a core neurodevelopmental disturbance that results in aberrant cortical-thalamic connectivity in poor-outcome schizophrenia.     

White matter integrity and cortical metabolic associations in aging and dementia

BackgroundStudies show that white matter hyperintensities, regardless of location, primarily affect frontal lobe metabolism and function. This report investigated how regional white matter integrity (measured as fractional anisotropy [FA]) relates to brain metabolism, to unravel the complex relationship between white matter changes and brain metabolism.ObjectiveTo elucidate the relationship between white matter integrity and gray matter metabolism using diffusion tensor imaging and fluorodeoxyglucose-positron emission tomography in a cohort of 16 subjects ranging from normal to demented (age, >55 years).MethodsMean FA values from white matter regions underlying the medial prefrontal, inferior-lateral prefrontal, parietal association, and posterior temporal areas and the corpus callosum were regressed with glucose metabolism (by positron emission tomography), using statistical parametric mapping (P < 0.005; voxel cluster, >100). Regional cerebral glucose metabolism was the primary outcome measure. According to our hypothesis, those hypometabolic cortical regions affected by Alzheimer's disease would correlate with a lower FA of associated tracks.ResultsOur data show inter-regional positive correlations between FA and gray matter metabolism for the prefrontal cortex, temporal, and parietal regions. Our results suggest that left prefrontal FA is associated with left temporal and parietal metabolism. Further, left posterior temporal FA correlated with left prefrontal metabolism. Finally, bilateral parietal FA correlated with bilateral temporal metabolism.ConclusionsThese regions are associated with cognitive processes affected in Alzheimer's disease and cerebrovascular disease, suggesting a link with white matter degeneration and gray matter hypometabolism. Therefore, cortical function and white matter degeneration are related in aging and dementia.     

Anatomical differences between CBS‐corticobasal degeneration and CBS‐Alzheimer's disease

We compare patterns of gray matter loss on MRI in subjects presenting as corticobasal syndrome (CBS) with Alzheimer disease pathology (CBS‐AD) to those presenting as CBS with corticobasal degeneration pathology (CBS‐CBD). Voxel‐based morphometry was used to compare patterns of gray matter loss in pathologically confirmed CBS‐AD subjects (n = 5) and CBS‐CBD subjects (n = 6) to a group of healthy controls (n = 20), and to each other. Atlas based parcellation using the automated anatomic labeling atlas was also utilized in a region‐of‐interest analysis to account for laterality. The CBS‐AD subjects were younger at the time of scan when compared with CBS‐CBD subjects (median: 60 years vs. 69; P = 0.04). After adjusting for age at time of MRI scan, the CBS‐AD subjects showed loss in posterior frontal, temporal, and superior and inferior parietal lobes, while CBS‐CBD showed more focal loss predominantly in the posterior frontal lobes when compared with controls. In both CBS‐AD and CBS‐CBD groups, there was basal ganglia volume loss, yet relative sparing of hippocampi. On direct comparisons between the two subject groups, CBS‐AD showed greater loss in both temporal and inferior parietal cortices than CBS‐CBD. No regions showed greater loss in the CBS‐CBD group compared to the CBS‐AD group. These findings persisted when laterality was taken into account. In subjects presenting with CBS, prominent temporoparietal, especially posterior temporal and inferior parietal, atrophy may be a clue to the presence of underlying AD pathology. © 2010 Movement Disorder Society     

Basal forebrain atrophy is a distinctive pattern in dementia with Lewy bodies

We determined brain atrophy patterns in dementia with Lewy bodies and Alzheimer's disease using voxel-based morphometry, an indirect volumetry. Ten patients with dementia with Lewy bodies, 10 patients with Alzheimer's disease and 10 controls were included. All groups were matched for age; sex and global differences in voxel intensities were included as confounding covariates. We observed basal forebrain atrophy discriminating dementia with Lewy bodies from Alzheimer's disease. Compared to controls, atrophy of lateral prefrontal cortex and left premotor cortex was seen in dementia with Lewy bodies whereas atrophy of the medial temporal cortex, posterior parietal cortex, thalamus and temporo-occipital areas was observed in Alzheimer's disease. Atrophy of insular cortex was found in both patient groups.     

A high-resolution single photon emission computed tomography study of verbal recognition memory in Alzheimer's disease

BACKGROUND: In view of the recent technological advances and its ease of availability, we used single photon emission computed tomography (SPECT) to examine the performance of early Alzheimer's disease (AD) subjects on a verbal recognition memory task. METHODS: Eighteen early AD and 10 matched healthy control subjects underwent split-dose (99m)Tc-HMPAO (Ceretec) SPECT using a verbal recognition memory and control task. SPECT images co-registered with MRI scans were used to determine relative regional cerebral blood flow (rCBF) changes in regions of interest. RESULTS: In healthy control subjects, verbal recognition increased rCBF in the right occipital region, thalamus, left prefrontal pole, posterior parietal region and cerebellum, and decreased rCBF in the right hippocampus. AD subjects showed bilateral prefrontal, posterior parietal and occipital increases, unilateral increase in the left posterior temporal region, and bilateral reductions in the hippocampus. Although activation was significantly different between the two groups in the right thalamus and left medial prefrontal region, the verbal recognition task did not enhance discrimination between groups. CONCLUSIONS: Compared with controls, AD subjects activate a similar but more extensive bilateral network during verbal recognition, possibly reflecting an attempt to compensate for impaired processing.     

Corticolimbic gray matter loss in Parkinson’s disease without dementia

Background: The relationship between corticolimbic involvement and cognitive dysfunction in non‐demented Parkinson’s disease (PD) patients has not yet been elucidated. Objectives: To delineate involvement of the cerebral cortex and limbic structures in non‐demented PD and to clarify distributional differences of gray matter loss between non‐demented PD with impaired cognition (PD‐CI) and without cognitive impairment (PD‐NC). Methods: Operational criteria based on the Clinical Dementia Rating were used to identify PD‐CI. Of 40 consecutive non‐demented patients with PD, 13 were classified as PD‐CI and 27 as PD‐NC. Comparisons of regional gray matter volume (rGMV) were made amongst the PD‐CI, PD‐NC, and control groups using voxel‐based morphometry. Results: Gray matter loss was found extensively in the frontal, temporal, parietal, and occipital cortices in the present non‐demented patients with PD. rGMV in the medial frontal and medial occipital cortices was reduced comparably in the PD‐NC and PD‐CI groups. The severity of gray matter loss in the perisylvian cortices increased in order from the control, to the PD‐NC, to the PD‐CI groups. rGMV reduction in the lateral and orbital frontal, medial and lateral temporal, medial and lateral parietal, and lateral occipital cortices and cerebellum was found specifically in PD‐CI. Conclusions: Our results suggest that corticolimbic degeneration occurs in non‐demented patients with PD, and extensive involvement of the limbic and posterior cortical regions as well as the frontal cortices is associated with cognitive impairment in PD.     

The pattern of cortical atrophy in patients with Parkinson's disease according to cognitive status

Background: Cognitive dysfunction is common in Parkinson's disease (PD), and along with PD with dementia (PDD), the concept of mild cognitive impairment in PD (PD‐MCI) has been introduced. Methods: To identify structural candidates according to cognitive status in PD, we compared gray matter (GM) density across PD‐intact cognition (PD‐IC, n = 23), PD‐MCI (n = 27), and PDD (n = 18) using voxel‐based morphometry. Results: The demographic data among PD subjects were similar, however, general cognition and disease duration were more severe in PD‐MCI and PDD than in PD‐IC. Compared with controls, GM density was significantly decreased in the left occipital area in PD‐IC; the bilateral temporal, left prefrontal and insular, and right occipital areas in PD‐MCI; and in widespread brain areas in PDD. Compared with PD‐IC, patients with PD‐MCI had significantly decreased GM density in the right middle frontal area, and those with PDD had decreased GM density in the right parietal, middle frontal, insular, and lentiform areas. GM density in patients with PDD was significantly decreased in the bilateral middle temporal, right inferior temporal, and left middle and superior prefrontal areas. PDD patients with shorter disease duration before dementia (<5 year) showed greater GM atrophy in the posterior cingulate area than did those with longer disease duration (≥5 year). Conclusions: These data suggest that cortical atrophy in PD exhibits a greater extent with increasing levels of cognitive impairment, and different anatomical substrates would correspond to each cognitive status. © 2011 Movement Disorder Society     

In vivo mapping of incremental cortical atrophy from incipient to overt Alzheimer’s disease

Progressive brain atrophy is believed to be the Alzheimer’s disease (AD) marker with the greatest evidence for validity. Mapping the topography of cortical atrophy throughout the stages of severity may allow the neural networks affected to be identified. Twenty healthy elderly persons (OH, MMSE 29.1 ± 1.0), 11 patients with incipient AD (iAD, 26.5 ± 2.0), 15 with mild AD (miAD, 23.5 ± 2.2), and 15 with moderate AD (moAD, 16.5 ± 2.0) underwent 3D magnetic resonance. Cortical pattern matching analysis was performed and maps of percent differences in gray matter distribution were computed between the following groups: iAD versus OH, miAD versus iAD, and moAD versus miAD. Compared to OH, iAD patients exhibited a mean cortical gray matter loss of 9–20% in areas encompassing the polysynaptic hippocampal pathway (posterior cingulate/retrosplenial and medial temporal cortex) and subgenual/orbitofrontal cortices, and a less widespread loss of 5–11% in other neocortical areas. Compared to iAD, miAD featured widespread mean gray matter loss of 14–19% in areas encompassing the direct hippocampal pathway (temporal pole, temporoparietal association cortex, and dorsal prefrontal cortex), sensorimotor, and visual cortex, with a less marked loss (7–9%) in the polysynaptic pathway areas. Compared to miAD, only atrophy in the primary sensorimotor cortex was still relatively marked in moAD, with a mean gray matter loss of 10–11%; the loss in other regions was generally below 10%. These findings suggest that the polysynaptic hippocampal pathway is affected in iAD, the direct pathway and sensorimotor and visual networks are affected in moAD, and the sensorimotor network is affected in moAD. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Localized volume reduction in prefrontal, temporolimbic, and paralimbic regions in schizophrenia: an MRI parcellation study

Functional and structural abnormalities of the anterior cingulate gyrus (ACG) in patients with schizophrenia have been repeatedly reported. However, one remaining issue is whether gray matter volume reduction in ACG exists to an extent comparable with, or even in excess of, that in other prefrontal and temporolimbic regions. High-spatial-resolution magnetic resonance imaging was performed on patients with schizophrenia (n=27) and on age-, gender-, and parental socioeconomic-status-matched healthy control subjects (n=27). After the gray and white matter were semiautomatically segmented, whole prefrontal and temporal lobes were manually parceled into 15 subregions-by-two hemispheres (30 regions of interest) constituting seven prefrontal gray matter regions, six temporal gray matter regions, the prefrontal white matter, and the temporal white matter. Compared with healthy subjects, schizophrenic patients showed significant gray matter volume reduction in the bilateral ACG, this being the largest effect size (left, 0.84; right, 0.56) among all the regions examined. There were also significant gray matter volume reductions in the bilateral posterior STG, bilateral inferior frontal gyrus, left posterior amygdala-hippocampal complex (mostly hippocampus), and the left insula. These results suggest that gray matter volume reductions in the ACG are prominent among prefrontal and temporolimbic regions in patients with schizophrenia. These findings indicate the importance of ACG abnormalities in the pathophysiology of schizophrenia.     

后部皮质萎缩的临床及影像学特点

目的后部皮质萎缩(posterior cortical atrophy,PCA)是以视觉障碍为突出表现,并伴进行性认知功能受损的神经系统退行性疾病。PCA的临床表现以视觉加工、计算力下降、阅读书写能力受损为主,患者的视觉认知损害突出,而情景记忆、语言能力和自知力相对保留。本文结合我院收治PCA病例,总结PCA的临床及影像学特征,以期为该病的早期诊治提供参考。方法收集2013年至2018年于宣武医院神经内科确诊的后部皮质萎缩8例患者的临床表现、神经心理学检查、影像学资料等各项检查结果并进行回顾性分析。结果8例PCA患者起病均为隐袭起病,病情进展缓慢,其中有5例符合背侧型后部皮质萎缩特点,临床表现为巴林特综合征、视空间功能障碍以及格茨曼综合征特点,头MRI显示顶枕叶皮质萎缩为主;另3例符合腹侧型后部皮质萎缩特点,临床表现主要为面孔失认、视觉忽视,头MRI显示双侧颞枕叶皮质萎缩为主,而内侧颞叶和海马萎缩程度相对较轻。8例患者均行SPECT检查,显示大脑后部包括顶叶、颞枕叶皮质血流低灌注现象。3例患者行18F FDG PET检查显示大脑后部枕叶、顶叶、颞叶皮质葡萄糖代谢降低。结论对于存在视觉障碍和后部皮质相关认知功能损害的患者,临床医生要考虑到PCA的诊断,特别注意进行视觉相关的全面的神经心理学评估及PET检查,以辅助进行PCA的诊断。