Abnormality of motor cortex excitability in peripherally induced dystonia

Abstract

It is widely accepted that peripheral trauma such as soft tissue injuries can trigger dystonia, although little is known about the underlying mechanism. Because peripheral injury only rarely appears to elicit dystonia, a predisposing vulnerability in cortical motor areas might play a role. Using single and paired-pulse pulse transcranial magnetic stimulation, we evaluated motor cortex excitability of a hand muscle in a patient with peripherally induced foot dystonia, in her brother with craniocervical dystonia, and in her unaffected sister, and compared their results to those from a group of normal subjects. In the patient with peripherally induced dystonia, we found a paradoxical intracortical facilitation at short interstimulus intervals of 3 and 5 milliseconds, at which regular intracortical inhibition (ICI) occurred in healthy subjects. These findings suggest that the foot dystonia may have been precipitated as the result of a preexisting abnormality of motor cortex excitability. Furthermore, the abnormality of ICI in her brother and sister indicates that altered motor excitability may be a hereditary predisposition. The study demonstrates that the paired-pulse technique is a useful tool to assess individual vulnerability, which can be particularly relevant when the causal association between trauma and dystonia is less evident.

Primary and reversible Pisa syndrome in juvenile normal pressure hydrocephalus

“…And, blepharospasm, another focal dystonia with chronic afferent sensory dysfunction, also preceded PPS (13). These facts, along with the novel abnormalities found by us in patients with primary focal dystonia-associated peripheral nerve injury, assessed nauromagnetically (23), support the contention that peripheral trauma may precede PPS as well (14). Therefore, a new classification on Pisa syndrome emerges here that will help in offering better neuromodulatory approaches to improve the quality of life of these patients (Table).…”

“…Although the axial dystonia found in this unique case seemed to be due to central nervous system alterations, other movement disorders (e.g., parkinsonism), found very often in iNPH, when brain asymmetry is detected (21), present scoliosis, which is another type of focal dystonia thought to be part of abnormal movements associated with afferent sensory system injuries (22,23). Interestingly, three out of 18 patients with axial primary dystonia and an unexpected higher prevalence of previous peripheral trauma had scoliosis-like symptoms resembling PPS (24).…”

Galvanic vestibular stimulation: a novel modulatory countermeasure for vestibular-associated movement disorders

“…Of remark, GVS would also help to restore balance, gait, equilibrium and locomotion in humans affected not only by MS or SAS, but also by the sensory and motor mismatch following neurodegenerative conditions 27,56 . The fact that GVS improves the disordered sensorimotor activity by modulating the abnormal sensoperceptual 29,30 afferent information along with the disturbed motor output in patients with disabling neural disorders, including Parkinson's disease 59,60 , normal pressure hydrocephalus 61 (Leon-Sarmiento et al, unpublished observations), and focal dystonia 40,62 supports this view. To prove more efficiently these assumptions, we reana lyzed the results of the effects of GVS in a patient with cer vical dystonia 40 .…”

The motor evoked potential in aids and HAM/TSP State of the evidence

“…Besides the CMCT measurements discussed above, more sophisticated and sensitive TMS measures that detect early changes in thalamocortical-basal ganglia circuitry 20,83,84 such as cortical thresholds, recruitment curves, silent periods, and excitatory and inhibitory phenomena produced by short and long interval stimulation obtained by single and paired magnetic stimulation are worth trying in HIV asymptomatic patients as well as in HTLV-I carriers at times when the fastest corticospinal fibers remain uninvolved 11,12,24,76,[85][86][87][88][89] . This can be done in order to better understand cortico-cortical and neurotransmitter dysfunction early in disease development 90 , and it will also allow the application of more appropriate and effective neuromodulatory measures long before the fatal clinical AIDS or HAM/TSP appears.…”