Impaired intracortical inhibition in the primary somatosensory cortex in focal hand dystonia

Abstract

Somesthetic temporal discrimination (STD) is impaired in focal hand dystonia (FHD). We explored the electrophysiological correlate of the STD deficit to assess whether this is due to dysfunction of temporal inhibition in the somatosensory inhibitory pathway or due to dysfunction in structures responsible for nonmodality-specific timing integration. Eleven FHD patients and 11 healthy volunteers were studied. STD threshold was investigated as the time interval required for perceiving a pair of stimuli as two separate stimuli in time. We also examined the somatosensory-evoked potential (SEP) in a paired-pulse paradigm. We compared STD threshold and recovery function of SEP between the groups. STD thresholds were significantly greater in FHD than in healthy volunteers. The amount of P27 suppression in the 5 ms-ISI condition was significantly less in FHD. It was also found that the STD threshold and P27 suppression were significantly correlated: the greater the STD threshold, the less the P27 suppression. Significantly less suppression of P27 with a lack of significant change in N20 indicates that the impairment of somatosensory information processing in the time domain is due to dysfunction within the primary somatosensory cortex, suggesting that that the STD deficit in FHD is more attributable to dysfunction in the somatosensory pathway.

Reduced Motor Cortex Deactivation in Individuals Who Suffer from Writer's Cramp

“…This implies that the somatosensory processing from the peripheral to primary somatosensory cortex in patients with WC is relatively preserved. However, loss of somatosensory inhibition at spinal and cortical levels in patients with WC was discovered under paired-pulse with an interstimulus interval of 5 to 40 ms [40], [41]. In present study, the interstimulus interval is 3 s. The N20m and P35m deflections might have been able to recover fully after each stimulus after such a time interval [42].…”

Somatosensory temporal discrimination in patients with primary focal dystonia

“…In healthy subjects, active movements reduce the amplitude of somatosensory evoked potentials (pre-movement gating) but in patients with hand dystonia, pre-movement gating is absent, suggesting an abnormality in the interaction between motor and sensory cortical areas 22. Furthermore, studies investigating the inhibitory functions of the sensory system with the technique of somatosensory evoked potentials reported altered inhibitory functions within the somatosensory system and, in particular, a loss of short latency inhibitory mechanisms in primary sensory cortex, leading to impaired afferent–input gating in dystonia 23 24. Afferent–input gating plays a role in the spatio-temporal separation of two incoming stimuli and allows information to be processed separately 25.…”

Sensory functions in dystonia: Insights from behavioral studies

“…26,[29][30][31] Sensory Discrimination Paradigms in Primary Adult Onset Dystonia Several studies have revealed an abnormal tactile TDT in generalized and focal dystonias, including blepharospasm, cervical and focal hand dystonia. [24][25][26][27][28][29][30][31][32][33] TDT alterations were observed not only in the affected body regions but also in parts remote from dystonic symptoms. These findings hint at a disorder in processing cutaneous inputs and may relate to deficits of kinesthesia, graphesthesia and stereognosis found in dystonia.…”

“…[19][20][21][22][23] Recent behavioral studies have shown that these sensory functions are compromised in patients with several forms of primary dystonia. Changes have been found in: (1) temporal discrimination and integration of sensory signals [24][25][26][27][28][29][30][31][32][33] ; (2) spatial discrimination of tactile stimuli 28,[34][35][36][37][38] ; (3) vibration-induced illusion of movements [39][40][41][42] ; and (4) movement representation and learning. [43][44][45][46] In this review, we focus on the possible role of abnormal sensory processing in the pathophysiology of primary dystonia, highlighting potential implications for innovative therapeutic strategies to aid functional recovery.…”