Writer's cramp: Increased dorsal premotor activity during intended writing

Simple writer's cramp (WC) is a task‐specific form of dystonia, characterized by abnormal movements and postures of the hand during writing. It is extremely task‐specific, since dystonic symptoms can occur when a patient uses a pencil for writing, but not when it is used for sharpening. Maladaptive plasticity, loss of inhibition, and abnormal sensory processing are important pathophysiological elements of WC. However, it remains unclear how those elements can account for its task‐specificity. We used fMRI to isolate cerebral alterations associated with the task‐specificity of simple WC. Subjects (13 simple WC patients, 20 matched controls) imagined grasping a pencil to either write with it or sharpen it. On each trial, we manipulated the pencil's position and the number of imagined movements, while monitoring variations in motor output with electromyography. We show that simple WC is characterized by abnormally increased activity in the dorsal premotor cortex (PMd) when imagined actions are specifically related to writing. This cerebral effect was independent from the known deficits in dystonia in generating focal motor output and in processing somatosensory feedback. This abnormal activity of the PMd suggests that the task‐specific element of simple WC is primarily due to alterations at the planning level, in the computations that transform a desired action outcome into the motor commands leading to that action. These findings open the way for testing the therapeutic value of interventions that take into account the computational substrate of task‐specificity in simple WC, e.g. modulations of PMd activity during the planning phase of writing. Hum Brain Mapp, 2013. © 2011 Wiley Periodicals, Inc.     

White matter abnormalities in Parkinson's disease patients with glucocerebrosidase gene mutations

Glucocerebrosidase gene mutations represent a genetic risk factor for the development of Parkinson's disease. This study investigated brain alterations in Parkinson's disease patients carrying heterozygous glucocerebrosidase gene mutations using structural and diffusion tensor magnetic resonance imaging. Among 360 Parkinson's disease patients screened for glucocerebrosidase gene mutations, 19 heterozygous mutation carriers (5.3%) were identified. Of these, 15 patients underwent a neuropsychological evaluation and a magnetic resonance imaging scan. Sixteen age‐ and sex‐matched healthy controls and 14 idiopathic Parkinson's disease patients without glucocerebrosidase gene mutations were also studied. Tract‐based spatial statistics was used to perform a white matter voxel‐wise analysis of diffusion tensor magnetic resonance imaging metrics. Mean fractional anisotropy values were obtained from white matter tracts of interest. Voxel‐based morphometry was used to assess gray‐matter atrophy. Cognitive deficits were found in 9 mutation carrier patients (60%). Compared with controls, Parkinson's disease patients carrying glucocerebrosidase gene mutations showed decreased fractional anisotropy in the olfactory tracts, corpus callosum, and anterior limb of the internal capsule bilaterally, as well as in the right anterior external capsule, and left cingulum, parahippocampal tract, parietal portion of the superior longitudinal fasciculus, and occipital white matter. Mutation carrier patients also had decreased fractional anisotropy of the majority of white matter tracts compared with Parkinson's disease patients with no mutations. No white matter abnormalities were found in Parkinson's disease patients without glucocerebrosidase gene mutations. No gray matter difference was found between patients and controls. In Parkinson's disease patients, verbal fluency scores correlated with white matter abnormalities. Parkinson's disease patients carrying glucocerebrosidase gene mutations experience a distributed pattern of white matter abnormalities involving the interhemispheric, frontal corticocortical, and parahippocampal tracts. White matter pathology in these patients may have an impact on the clinical manifestations of the disease, including cognitive impairment. © 2013 Movement Disorder Society     

18F－FDGPET／CT显像对颞叶癫痫灶定位的价值

目的探讨以18氟-2-脱氧葡萄糖为显影剂的正电子发射断层扫描／计算机断层成像（18F-FDGPET／CT）对颞叶癫痫（TLE）灶的定位价值。方法本研究回顾分析被确诊为TLE的24例患者的临床资料,将术前18F-FDGPET／CT、MRI、视频脑电图（VEEG）与术中颅内电极脑电图和术后病理学检查结果进行对比研究。结果24例TLE患者中,18F-FDGPET／CT准确定位致痫灶21例,MRI准确定位10例,VEEG准确定位10例。18F-FDGPET／CT对TLE致痫灶的敏感性为87．5％（21／24）,其中对内侧颢叶癫痫（MTLE）致痫灶为88．9％（16／18）,对外侧颞叶癫痫（LTLE）致痫灶为83．3％（5／6）。MRI对TLE致痫灶的敏感性为41．7％（10／24）,其中对MTLE致痫灶为55．5％（10／18）,对LTLE致痫灶为0。VEEG对TLE致痫灶的敏感性为41．7％（10／24）,其中对MTLE致痫灶为50．5％（9／18）,对LTLE致痫灶为16．7（1／6）。18F-FDGPET／CT对TLE（包括MTLE和LTME）致痫灶的敏感性均显著高于MRI和VEEG（P〈0．05）,而MRI和VEEG对TLE致痫灶的敏感性无显著差异（P〉0．05）。结论18F-FDGPET／CT对于TLE致痫灶定位具有独特的优势。     

Seeking huntington disease biomarkers by multimodal,cross‐sectional basal ganglia imaging

Neurodegeneration of the striatum in Huntington disease (HD) is characterized by loss of medium‐spiny neurons, huntingtin nuclear inclusions, reactive gliosis, and iron accumulation. Neuroimaging allows in vivo detection of the macro‐ and micro‐structural changes that occur from presymptomatic stages of the disease (preHD). The aim of our study was to evaluate the reliability of multimodal imaging as an in vivo biomarker of vulnerability and development of the disease and to characterize macro‐ and micro‐structural changes in subcortical nuclei in HD. Macrostructure (T₁‐weighted images), microstructure (diffusion tensor imaging), and iron content (R relaxometry) of subcortical nuclei and medial temporal lobe structures were evaluated by a 3 T scanner in 17 preHD carriers, 12 early‐stage patients and 29 matched controls. We observed a volume reduction and microstructural changes in the basal ganglia (caudate, putamen, and globus pallidus) and iron accumulation in the globus pallidus in both preHD and symptomatic subjects; all these features were significantly more pronounced in patients, in whom degeneration extended to the other subcortical nuclei (i.e., thalamus and accumbens). Mean diffusivity (MD) was the most powerful predictor in models explaining more than 50% of the variability in HD development in the caudate, putamen, and thalamus. These findings suggest that the measurement of MD may further enhance the well‐known predictive value of striatal volume to assess disease progression as it is highly sensitive to tissue microimpairment. Multimodal imaging may detect brain changes even in preHD stages. Hum Brain Mapp, 2013. © 2012 Wiley Periodicals, Inc.     

Right,left, and center: How does cerebral asymmetry mix with callosal connectivity?

Background: Prior research has shown that cerebral asymmetry is associated with differences in corpus callosum connectivity. Such associations were detected in histological and anatomical studies investigating callosal fiber size and density, in neuroimaging investigations based on structural and diffusion tensor imaging, as well as in neuropsychological experiments. However, little is known about typical associations between these factors, and even less about the relative influences of magnitude and direction of cerebral asymmetries. Here, we investigated relationships between callosal connectivity and cerebral asymmetry using precise measures of callosal thickness and selected cerebral structures. We considered both the direction and magnitude of the asymmetries. Methods: Associations between cerebral asymmetry and callosal thickness were investigated in 348 cognitively healthy older individuals. Results: The magnitude and direction of cerebral lateralization were significant independent predictors of callosal thickness. However, associations were small. Leftward asymmetry and increased magnitude of asymmetry were generally associated with increased callosal thickness, mostly in the callosal midbody and isthmus. Conclusions: When a large sample of normal individuals is considered, cerebral asymmetries are only subtly associated with callosal thickness. Hum Brain Mapp, 2013. © 2012 Wiley Periodicals, Inc.     

Resting‐state networks show dynamic functional connectivity in awake humans and anesthetized macaques

Characterization of large‐scale brain networks using blood‐oxygenation‐level‐dependent functional magnetic resonance imaging is typically based on the assumption of network stationarity across the duration of scan. Recent studies in humans have questioned this assumption by showing that within‐network functional connectivity fluctuates on the order of seconds to minutes. Time‐varying profiles of resting‐state networks (RSNs) may relate to spontaneously shifting, electrophysiological network states and are thus mechanistically of particular importance. However, because these studies acquired data from awake subjects, the fluctuating connectivity could reflect various forms of conscious brain processing such as passive mind wandering, active monitoring, memory formation, or changes in attention and arousal during image acquisition. Here, we characterize RSN dynamics of anesthetized macaques that control for these accounts, and compare them to awake human subjects. We find that functional connectivity among nodes comprising the “oculomotor (OCM) network” strongly fluctuated over time during awake as well as anaesthetized states. For time dependent analysis with short windows (<60 s), periods of positive functional correlations alternated with prominent anticorrelations that were missed when assessed with longer time windows. Similarly, the analysis identified network nodes that transiently link to the OCM network and did not emerge in average RSN analysis. Furthermore, time‐dependent analysis reliably revealed transient states of large‐scale synchronization that spanned all seeds. The results illustrate that resting‐state functional connectivity is not static and that RSNs can exhibit nonstationary, spontaneous relationships irrespective of conscious, cognitive processing. The findings imply that mechanistically important network information can be missed when using average functional connectivity as the single network measure. Hum Brain Mapp 34:2154–2177, 2013. © 2011 Wiley Periodicals, Inc.