Chronic Sensory Deafferentation results in cerebellar and basal ganglia structural abnormalities. (P6.090)

OBJECTIVE: To characterize cerebral structural abnormalities in patients with chronic Sensory neuronopathy (SN). BACKGROUND: SN is characterized by severe sensory loss and proprioceptive ataxia. Sensory-motor integration is impaired in the disease, but little is known about the location and extent of structural modifications. DESIGN/METHODS:Sixteen consecutive patients with clinical and neurophysiological criteria for SN (8 women; 50.8±7.5 years old) and 16 control subjects (8 women; 51.0±7.3 years old) were enrolled. We acquired T1-weighted images in a 3T scanner, with voxel size of 1x1x1mm³, matrix size of 240 x 240, TR=7ms, TE=3.2ms and flip angle = 8°. We used the VBM8 toolbox to analyze the images. VBM is a method used to compare gray/white matter concentration in brain regions by analyzing the signal intensity in the images. Statistics were performed with SPM8 and images from both groups were compared using a two-sample t-test. Exploratory results were obtained with no corrections for multiple comparisons, an alpha level of 0.001 and a cluster size threshold of 25 voxels. RESULTS:Mean disease duration was 15.1 ± 8.4years and 10 patients had idiopathic SN, despite extensive investigation. In the SN group, we found regions with both increased and decreased gray matter volumes. There was volumetric increase in VII and VIII areas of the right cerebellum, right putamen, right caudate, left caudate head, bilateral internal and external globus pallidus, thalamus and superior colliculus. In contrast, we found gray matter atrophy in medial temporal and parahippocampal gyri. White matter atrophy was identified in the inferior cerebellar peduncle. CONCLUSIONS: Chronic sensory deafferentation leads to gross structural abnormalities in the brain, including basal ganglia and cerebellar volumetric increase. Such modifications are probably compensatory phenomena to account for the loss of sensory input. Further studies are needed to evaluate the potential therapeutic usefulness of neuromodulation targeted at these structures. Disclosure: Dr. Martinez has nothing to disclose. Dr. Casseb has nothing to disclose. Dr. Paiva has nothing to disclose. Dr. Campos has nothing to disclose. Dr. Beltramini has nothing to disclose. Dr. Castellano has nothing to disclose. Dr. Nucci has nothing to disclose. Dr. Franca, Jr. has nothing to disclose.