Proprioceptive and tactile processing in individuals with Friedreich ataxia: an fMRI study

ObjectiveFriedreich ataxia (FA) neuropathology affects dorsal root ganglia, posterior columns in the spinal cord, the spinocerebellar tracts, and cerebellar dentate nuclei. The impact of the somatosensory system on ataxic symptoms remains debated. This study aims to better evaluate the contribution of somatosensory processing to ataxia clinical severity by simultaneously investigating passive movement and tactile pneumatic stimulation in individuals with FA.MethodsTwenty patients with FA and 20 healthy participants were included. All subjects underwent two 6 min block-design functional magnetic resonance imaging (fMRI) paradigms consisting of twelve 30 s alternating blocks (10 brain volumes per block, 120 brain volumes per paradigm) of a tactile oddball paradigm and a passive movement paradigm. Spearman rank correlation tests were used for correlations between BOLD levels and ataxia severity.ResultsThe passive movement paradigm led to the lower activation of primary (cSI) and secondary somatosensory cortices (cSII) in FA compared with healthy subjects (respectively 1.1 ± 0.78 vs. 0.61 ± 1.02, p = 0.04, and 0.69 ± 0.5 vs. 0.3 ± 0.41, p = 0.005). In the tactile paradigm, there was no significant difference between cSI and cSII activation levels in healthy controls and FA (respectively 0.88 ± 0.73 vs. 1.14 ± 0.99, p = 0.33, and 0.54 ± 0.37 vs. 0.55 ± 0.54, p = 0.93). Correlation analysis showed a significant correlation between cSI activation levels in the tactile paradigm and the clinical severity (R = 0.481, p = 0.032).InterpretationOur study captured the difference between tactile and proprioceptive impairments in FA using somatosensory fMRI paradigms. The lack of correlation between the proprioceptive paradigm and ataxia clinical parameters supports a low contribution of afferent ataxia to FA clinical severity

BOLD signal in sensorimotor regions reveals differential encoding of passive forefinger velocity and displacement amplitude

Peripheral encoding of movement kinematics has been well-characterized, but there is little understanding of the relationship between movement kinematics and associated brain activation. We hypothesized that kinematics of passive movement is differentially represented in the sensorimotor network, reflecting the well-studied afferent responses to movement. A robotic forefinger manipulandum was used to induce passive kinematic stimuli and monitor interaction force in 41 healthy participants during whole-brain functional magnetic resonance imaging (fMRI). Levels of forefinger displacement amplitude and velocity were presented in flexion and extension. Increases in velocity were linearly associated with activation in contralateral primary somatosensory cortex (S1), bilateral secondary somatosensory cortex (S2), primary motor cortex, and supplementary motor area. No difference in activation was found for direction of the finger movement. Unexpectedly, S1 and S2 activation decreased nonlinearly with increasing displacement amplitude. We conclude that while straightforward relations were found with velocity, the complex neural representation of displacement amplitude suggests a more nuanced relationship between peripheral responses to kinematic stimuli and sensorimotor network activity. Here we present a novel, systematic characterization of the whole-brain response to passive movement kinematics