A Digital Atlas of the Dog Brain

There is a long history and a growing interest in the canine as a subject of study in neuroscience research and in translational neurology. In the last few years, anatomical and functional magnetic resonance imaging (MRI) studies of awake and anesthetized dogs have been reported. Such efforts can be enhanced by a population atlas of canine brain anatomy to implement group analyses. Here we present a canine brain atlas derived as the diffeomorphic average of a population of fifteen mesaticephalic dogs. The atlas includes: 1) A brain template derived from in-vivo, T1-weighted imaging at 1 mm isotropic resolution at 3 Tesla (with and without the soft tissues of the head); 2) A co-registered, high-resolution (0.33 mm isotropic) template created from imaging of ex-vivo brains at 7 Tesla; 3) A surface representation of the gray matter/white matter boundary of the high-resolution atlas (including labeling of gyral and sulcal features). The properties of the atlas are considered in relation to historical nomenclature and the evolutionary taxonomy of the Canini tribe. The atlas is available for download (https://cfn.upenn.edu/aguirre/wiki/public:data_plosone_2012_datta)

Anterograde Axonal Degeneration in Children with Vision Loss Secondary to NF1 Associated Optic Pathway Glioma (PDF)

The presence and evolution of anterograde axonal degeneration from an acquired optic neuropathy is an important feature to consider when designing treatment and neuroprotection strategies. We studied the association between measures of striate cortex volume and vision loss in children with optic pathway gliomas secondary to Neurofibromatosis type 1 (NF1-OPG)

The topography of visuospatial attention as revealed by a novel visual field mapping technique

& Previously, we and others have shown that attention can enhance visual processing in a spatially specific manner that is retinotopically mapped in the occipital cortex. However, it is difficult to appreciate the functional significance of the spatial pattern of cortical activation just by examining the brain maps. In this study, we visualize the neural representation of the ‘‘spotlight’ ’ of attention using a back-projection of attention-related brain activation onto a diagram of the visual field. In the two main experiments, we examine the topography of attentional activation in the occipital and parietal cortices. In retinotopic areas, attentional enhancement is strongest at the locations of the attended target, but also spreads to nearby locations and even weakly to restricted locations in the op-posite visual field. The dispersion of attentional effects around an attended site increases with the eccentricity of the target in a manner that roughly corresponds to a constant area of spread within the cortex. When averaged across multiple observers, these patterns appear consistent with a gradient model of spatial attention. However, individual observers exhibit com-plex variations that are unique but reproducible. Overall, these results suggest that the topography of visual attention for each individual is composed of a common theme plus a personal variation that may reflect their own unique ‘‘atten-tional style.’ ’ &amp

"Human visual cortex responses to rapid cone and melanopsin-directed flicker" (Spitschan et al.) – Data Supplement

<p><strong>"Human visual cortex responses to rapid cone and melanopsin-directed flicker" (Spitschan <i>et al.</i>)</strong></p> <p><b>Data Supplement</b></p><p><br></p><p><b>Figures</b> </p> <p><strong>Figure S1 [Figure_S1.pdf] | Echoplanar image intensity</strong>. Representative echoplanar images for each subject. The three views (sagittal, horizontal, and coronal) also include a colored overlay of the visual area ROIs (V1 and V2/V3, not restricted in eccentricity range). Image intensity is the mean of the set of spatially-aligned echoplanar images from a single scanning run and reflects signal-to-noise for a given spatial location. ROIs defined on the cortical surface were projected back to the volumetric space using FreeSurfer.</p> <p><strong>Figure S2 [Figure_S2.pdf] | Psychophysical nulling (average)</strong>. <em>a</em>, Perceptual nulling data for a 32% melanopsin (Mel*; non penumbral-cone silent) modulation in a population of subjects (n=15). Primary subjects (S01, S02, and S03) indicated with a star symbol. Ellipse indicates ±1SD across subjects. Some plot points are overlapping. <em>b</em>, Perceptual nulling data for a 32% cone directed (L+M+S) modulation in the same population of 15 subjects. Red error bar indicates ±1SD across subjects. Averages were obtained from the positive and negative arms shown in Fig. 3. All data are tabulated in Table S6.</p> <p><strong>Figure S3 [Figure_S3.pdf] | V2/V3, MT and LOC response to melanopsin modulations.</strong> BOLD amplitudes shown as average across the two ROI hemispheres and across ROI vertices in the relevant eccentricity range (inset). Format follows Fig. 5.</p> <p><strong>Figure S4 [Figure_S4.pdf] | Additional BOLD data.</strong> BOLD amplitudes shown as average across the two V1 hemispheres and across V1 vertices in the relevant eccentricity range (3°-13°). Subjects viewed 12 sec 4 Hz flicker with a dilated pupil. Experimental details and data analysis follows main experiments. Melanopsin and L+M+S modulations were nulled prior to the experiment. All modulations at ±32% contrast. Data shown were not included in the main report because of 1) equipment failure, preventing us from collecting behavioral responses during the attention task, 2) concern that subject S03 was sleeping in the scanner per his self report, 3) failure of the positive control modulation (light flux) to evoke a response in subject S03, and 4) the difficulty of interpreting any observed response to the melanopsin modulation, given that the modulation also stimulated the penumbral cones.</p> <p><b><br></b></p><p><b>Tables</b></p> <p><strong>Table S1 [Table_S1.xlsx] | Spreadsheet of spectral power distributions. </strong>All modulations are unsigned difference spectra. To derive the displayed stimulus, they would be added to the background. Spectral power distributions have been splined to 1 nm wavelength spacing (measured at 2 nm wavelength bands).</p> <p><strong>Table S2 [Table_S2.xlsx] | Spreadsheet of stimulus sequences (fMRI experiments)</strong>. Within a given BOLD fMRI run, subjects viewed 12 s segments. The order of frequencies was counterbalanced and is given in the columns. </p> <p><strong>Table S3 </strong><strong>[Table_S3.xlsx] | Spreadsheet of stimulus sequences (pupil experiments)</strong>. Within a given pupillometry run, subjects viewed 45 sec trials. The sequence is given in the rows, modulations and run types per column. </p> <p><strong>Table S4 [Table_S4.xlsx] | Demographic details about subjects.</strong></p> <p><strong>Table S5 [Table_S5.xlsx] | Individual subject pupil measures. </strong>Corresponds to data shown in graphical form in Fig. 3b.</p> <p><strong>Table S6 [Table_S6.xlsx] | Individual subject nulling measures.</strong> Corresponds to data shown in graphical form in Fig. 3a. Sheet 1 contains the nulling values for the ±32% L+M+S and melanopsin modulations (subjects S01-15). Sheet 2 contains the nulling values for the ±17% melanopsin modulations (subjects S01-03).</p><p><b><br></b></p><p><b>Data</b></p><p><b>Data S1 [Data_S1.tar.gz] | BOLD fMRI Data (L+M, L-M, S, 17% melanopsin, 2-64 Hz).</b> Beta effect size maps from each subject (as well as the mean EPI image), registered to the whole-brain, individual anatomical image in native subject space.<b> </b>See README.txt for details. [MD5 (Data_S1.tar.gz) = c17d1e8f872f78d2f7feefa860e7794d].</p><p><b>Data S2 [Data_S2.tar.gz] | BOLD fMRI Data (L+M, L-M, S, 17% melanopsin, 0.5-2 Hz).</b><b> </b>Beta effect size maps from each subject (as well as the mean EPI image), registered to the whole-brain, individual anatomical image in native subject space. See README.txt for details. [MD5 (Data_S2.tar.gz) = ce06eae027f0e550e077faf06871f27b].</p><p><b>Data S3 [Data_S3.tar.gz] | BOLD fMRI Data (L+M+S, 0.5-64 Hz).</b><b> </b>Beta effect size maps from each subject (as well as the mean EPI image), registered to the whole-brain, individual anatomical image in native subject space. See README.txt for details. [MD5 (Data_S3.tar.gz) = 8aa43a415a84bc09b56dbec8aa038e13].</p><p><b>Data S4 [Data_S4.tar.gz] | </b><b>BOLD fMRI Data (L*+M*, 2-64 Hz; scaled L+M, 0.5-64 Hz). </b>Beta effect size maps from each subject (as well as the mean EPI image), registered to the whole-brain, individual anatomical image in native subject space. See README.txt for details. [MD5 (Data_S4.tar.gz) = 8e8239784c5932ee7543cc335bdae046].</p><p><b>Data S5 [Data_S5.tar.gz] | </b><b>BOLD fMRI Data (Light flux, nulled and un-nulled melanopsin, L+M+S and L-M nulling contrast; 4 Hz). </b>Beta effect size maps from each subject (as well as the mean EPI image), registered to the whole-brain, individual anatomical image in native subject space. See README.txt for details. [MD5 (Data_S5.tar.gz) = 8b377ab28e99bf9eb9fbe8cb440ffc1c].</p

Migraine with aura is associated with an incomplete circle of willis: results of a prospective observational study.

To compare the prevalence of an incomplete circle of Willis in patients with migraine with aura, migraine without aura, and control subjects, and correlate circle of Willis variations with alterations in cerebral perfusion.Migraine with aura, migraine without aura, and control subjects were prospectively enrolled in a 1∶1∶1 ratio. Magnetic resonance angiography was performed to examine circle of Willis anatomy and arterial spin labeled perfusion magnetic resonance imaging to measure cerebral blood flow. A standardized template rating system was used to categorize circle of Willis variants. The primary pre-specified outcome measure was the frequency of an incomplete circle of Willis. The association between circle of Willis variations and cerebral blood flow was also analyzed.170 subjects were enrolled (56 migraine with aura, 61 migraine without aura, 53 controls). An incomplete circle of Willis was significantly more common in the migraine with aura compared to control group (73% vs. 51%, p = 0.02), with a similar trend for the migraine without aura group (67% vs. 51%, p = 0.08). Using a quantitative score of the burden of circle of Willis variants, migraine with aura subjects had a higher burden of variants than controls (p = 0.02). Compared to those with a complete circle, subjects with an incomplete circle had greater asymmetry in hemispheric cerebral blood flow (p = 0.05). Specific posterior cerebral artery variants were associated with greater asymmetries of blood flow in the posterior cerebral artery territory.An incomplete circle of Willis is more common in migraine with aura subjects than controls, and is associated with alterations in cerebral blood flow