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To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2008.00327.x Byline: M. Riverol (1), L. Samaranch (1), B. Pascual (1), P. Pastor (1), J. Irigoyen (1), M.A. Pastor (1), P. de Castro (1), J.C. Masdeu (1) Keywords: Hereditary spastic paraparesis with thin corpus callosum; SPG11; spatacsin; magnetic resonance imaging (MRI); forceps minor of the corpus callosum Abstract: ABSTRACT BACKGROUND AND PURPOSE A thin corpus callosum on magnetic resonance imaging (MRI) characterizes a type of autosomal recessive disorder with progressive spastic paraparesis and cognitive impairment. Known as Hereditary Spastic Paraparesis with Thin Corpus Callosum (HSP-TCC), it has been associated with mutations of the SPG11 gene. No other specific MRI findings have been reported. METHODS We studied with MRI four patients from three families with HSP-TCC who had identified causal mutations in the SPG11 gene. RESULTS In all individuals studied the region of the forceps minor of the corpus callosum, corresponding to the genu fibers, appeared bright on T2-weighted and dark on T1-weighted images. On axial sections, the frontal horn region bore a remarkable resemblance to the ears of a lynx, with the areas of abnormal signal reminiscent of the tufts of hair crowning the tips of the ears of this animal. Less specific findings included a box-shape appearance of the calloso-caudate angle and diffusely increased signal in the hemispheric white matter. CONCLUSION Abnormal MRI signal in the region of the forceps minor of the corpus callosum is a characteristic early imaging finding of HSP-TCC with SPG11 mutations. Author Affiliation: (1)From the Department of Neurology and Neurosurgery (MR, PP, MAP, PC, JCM); Clinica Universitaria de Navarra, and the Neuroimaging (JI, BP); and Neurogenetics Laboratories (LS), Division of Neurosciences, Center for Applied Medical Research, University of Navarra, and the 'Centro de Investigacion Biomedica en Red (CIBER)' (PP, BP, JI, MAP, JCM), Pamplona, Spain. Article History: Acceptance: Received April 12, 2008, and in revised form August 13, 2008. Accepted for publication September 25, 2008. Article note: Correspondence: Address correspondence to Joseph C. Masdeu, MD, PhD, Department of Neurology and Neurosurgery, Pio XII 36, 31008 Pamplona (Navarra), Spain, E-mail: masdeu@unav.es

Study design:Several causes of Brown-Sequard syndrome have been described. Endovascular embolization can be used to treat symptomatic vertebral hemangiomas. We describe a previously undocumented case of Brown-Sequard syndrome followed by endovascular embolization with microcoils of a vertebral hemangioma. We also provide a clinical-radiological correlation of this finding and review the relevant literature.Case report:A 39-year-old male was referred to our hospital for endovascular treatment of a right T9 hemivertebral hemangioma with compromise of the spinal canal. Fifteen minutes after the procedure, the patient developed right lower limb weakness and numbness on the left leg. The emergency magnetic resonance imaging (MRI) of the spine showed no abnormalities. Five days later, a new spinal MRI revealed an infarction in the right half of the spinal cord at T6 and T7 level. This stroke was probably caused by a microcoil ended up in the right sulcocommisural artery. One week after surgery, the patient was able to raise the right leg against gravity, but sensory deficit showed no improvement.Conclusions:To the best of our knowledge this is the first case of a Brown-Sequard syndrome related to vertebral hemangioma embolization, a relatively safe technique with no important complications made known until this report. Clinicians should always weight the benefits with the potential devastating complications of this therapeutic option. [ABSTRACT FROM AUTHOR]

Abstract: Normalization of neuroimaging studies to a stereotaxic space allows the utilization of standard volumes of interest (VOIs) and voxel-based analysis (SPM). Such spatial normalization of PET and MRI studies requires a high quality template image. The aim of this study was to create new MRI and PET templates of 18F-DOPA and 11C-(+)-α-dihydrotetrabenazine (11C-DTBZ) of the Macaca fascicularis brain, an important animal model of Parkinson''s disease. MRI template was constructed as a smoothed average of the scans of 15 healthy animals, previously transformed into the space of one representative MRI. In order to create the PET templates, 18F-DOPA and 11C-DTBZ PET of the same subjects were acquired in a dedicated small animal PET scanner and transformed to the created MRI template space. To validate these templates for PET quantification, parametric values obtained with a standard VOI-map applied after spatial normalization to each template were statistically compared to results computed using individual VOIs drawn for each animal. The high correlation between both procedures validated the utilization of all the templates, improving the reproducibility of PET analysis. To prove the utility of the templates for voxel-based quantification, dopamine striatal depletion in a representative monkey treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was assessed by SPM analysis of 11C-DTBZ PET. A symmetric reduction in striatal 11C-DTBZ uptake was detected in accordance with the induced lesion. In conclusion, templates of M. fascicularis brain have been constructed and validated for reproducible and automated PET quantification. All templates are electronically available via the internet. [Copyright &y& Elsevier]