Defective Somatosensory Inhibition and Plasticity Are Not Required to Develop Dystonia

Abstract

Background Dystonia may have different neuroanatomical substrates and pathophysiology. This is supported by studies on the motor system showing, for instance, that plasticity is abnormal in idiopathic dystonia, but not in dystonia secondary to basal ganglia lesions. Objective The aim of this study was to test whether somatosensory inhibition and plasticity abnormalities reported in patients with idiopathic dystonia also occur in patients with dystonia caused by basal ganglia damage. Methods Ten patients with acquired dystonia as a result of basal ganglia lesions and 12 healthy control subjects were recruited. They underwent electrophysiological testing at baseline and after a single 45‐minute session of high‐frequency repetitive somatosensory stimulation. Electrophysiological testing consisted of somatosensory temporal discrimination, somatosensory‐evoked potentials (including measurement of early and late high‐frequency oscillations and the spatial inhibition ratio of N20/25 and P14 components), the recovery cycle of paired‐pulse somatosensory‐evoked potentials, and primary motor cortex short‐interval intracortical inhibition. Results Unlike previous reports of patients with idiopathic dystonia, patients with acquired dystonia did not differ from healthy control subjects in any of the electrophysiological measures either before or after high‐frequency repetitive somatosensory stimulation, except for short‐interval intracortical inhibition, which was reduced at baseline in patients compared to control subjects. Conclusions The data show that reduced somatosensory inhibition and enhanced cortical plasticity are not required for the clinical expression of dystonia, and that the abnormalities reported in idiopathic dystonia are not necessarily linked to basal ganglia damage. © 2020 International Parkinson and Movement Disorder Society

Sensorimotor Integration in Childhood Dystonia and Dystonic Cerebral Palsy—A Developmental Perspective

“…In contrast to idiopathic or genetic dystonias, patients with acquired hemidystonia have shown normal responses to both PAS (44) and HF-RSS (45), suggesting that abnormal plasticity, at least in the form measured with these particular protocols, may not be essential for the development of dystonia (45). On the other hand, in patients with acquired dystonia secondary to basal ganglia lesions, there is usually a delay between the time of injury and the onset of dystonic symptoms (46), which would be consistent with a maladaptive plasticity response.…”

“…In contrast, in acquired dystonia due to perinatal brain injury, the "plasticity machinery" itself may be intact (44,45), but the consequence of reduced and atypical patterns of afferent feedback in early life induces a different form of maladaptive neuroplasticity. The "set-point" around which these processes function may well have been affected by the relative deprivation of afferent input induced by the lesion (30), even if this was only temporary.…”

Contribution of TMS and TMS-EEG to the Understanding of Mechanisms Underlying Physiological Brain Aging

“…Another important factor contributing to the inconsistency of ppTMS protocols is the choice of CS intensity, which can be calibrated either based on the RMT, or the active motor threshold (AMT). The intensities used vary considerably, usually ranging from 50% to 95% RMT [39,41,42,44,55,56] or from 70% to 90% AMT [73][74][75], and this variability may contribute to divergent findings in SICI studies. Another point to take into account is that ppTMS measures may have different sensitivity to coil orientation [66,76], and that this pattern of susceptibility to current direction might change according to the age of subjects.…”

“…These features of plasticity can be framed in the context of metaplasticity, which can be shortly defined as "the plasticity of synaptic plasticity"; this involves a wide range of mechanisms and, from a behavioral point of view, has an important role in the regulation of important brain functions, including memory and learning [27,180,181]. Metaplasticity in humans can be explored through different protocols, from priming an exogenous or endogenous plasticity-inducing protocol with NIBS, to delivering plasticity-inducing protocols with longer duration [64,73,75]. For instance, Opie and colleagues (2017) delivered iTBS 10 min after the application of sham TBS (sham TBS + iTBS), cTBS (cTBS + iTBS), or iTBS (iTBS + iTBS) in young and older participants.…”

Brainstem Reflexes in Idiopathic Cervical Dystonia: Does Medullary Dysfunction Play a Role?

“…1 A number of electrophysiological abnormalities have been demonstrated in dystonia, the most common being loss of finhibition, alterations of synaptic plasticity and sensory dysfunction. [2][3][4][5] However, limited reproducibility of these results has led some researchers to question their role as markers of dystonia. 6,7 Additionally, due to the fact that correlations between neurophysiological and clinical findings have rarely been confirmed, the pathophysiology of dystonia is still debated.…”