SUMMARY1. A method to assess changes in presynaptic inhibition of I a afferent terminals in man is proposed. The soleus H reflex was facilitated by a heteronymous Ia volley from quadriceps and the amount of reflex facilitation was used to estimate the size of the conditioning I a excitatory post-synaptic potential (e.p.s.p.). It is argued that the size of this e.p.s.p. as measured by the resulting amount of reflex facilitation reflects the amount of presynaptic inhibition on the corresponding Ia fibres. A decrease in the reflex facilitation may then be ascribed to an increase in presynaptic inhibition of the Ia fibres mediating the conditioning volley.2. That the heteronymous Ia facilitation from quadriceps to soleus is caused by a purely monosynaptic e.p.s.p. is a prerequisite for the validity of the method. Experimental evidence is therefore given in an Appendix that in man the earliest part (first 0-5 ms) of this heteronymous I a facilitation is mediated through a monosynaptic pathway. Evidence is also given that this earliest facilitation is not yet contaminated by any polysynaptic effects from Ia or Ib afferents.3. The validity of the method was established in animal experiments in which presynaptic inhibition of I a fibres and post-synaptic events in motoneurones could be assessed by direct tests. It was found that the amount of test reflex facilitation produced by a conditioning I a volley was decreased when I a fibres were subjected to presynaptic inhibition but remained unchanged when the motoneurone pool in which the test reflex was elicited received pure post-synaptic inhibition.4. In man, presynaptic inhibition of I a fibres was evoked by a short-lasting (three H. HULTBORN AND OTHERS 5. The short-lasting tibialis anterior vibration used here evoked a long-lasting (300-500 ms) depression of soleus and quadriceps H reflexes. Even though several mechanisms contribute to this depression, it is argued that presynaptic inhibition of I a fibres mediating the afferent volley of the reflex is the only mechanism responsible for the reflex depression when the test reflex is evoked 40-60 ms after the onset of vibration. Within this time interval, therefore, the measurement of the vibratory inhibition of the H reflex assesses the excitability of the interneurones mediating presynaptic inhibition of homonymous I a extensor fibres.

SUMMARY1. Two independent methods were used, in man, to assess changes in presynaptic inhibition of Ia terminals at the onset of selective voluntary contractions: (1) measurement of the amount of heteronymous monosynaptic I a facilitation (from the quadriceps muscle to soleus motoneurones) to provide an assessment of the amount of ongoing presynaptic inhibition exerted on the la fibres responsible for the facilitation; (2) measurement of the inhibition of H reflexes 40-60 ms after a short vibration to the tibialis anterior tendon to estimate the excitability of the interneurones mediating presynaptic inhibition from tibialis anterior Ia afferents to the Ia afferents of the test H reflex (soleus or quadriceps).2. At the onset of an isolated voluntary plantar flexion of the foot (gastrocnemius-soleus contraction) the heteronymous facilitation from quadriceps to soleus was increased, reflecting a decreased presynaptic inhibition of the quadriceps Ia terminals on soleus motoneurones. Vibratory inhibition of the soleus H reflex was decreased, reflecting an inhibition of transmission of presynaptic inhibition to homonymous soleus Ia afferent terminals.3. At the onset of the same gastrocnemius-soleus contraction there was, on the contrary, an increased vibratory inhibition of the quadriceps H reflex indicating a facilitation of transmission of presynaptic inhibition to homonymous quadriceps la afferent terminals.4. At the onset of an isolated voluntary knee extension (quadriceps contraction) the opposite pattern was seen: the heteronymous facilitation from quadriceps to soleus was decreased and the vibratory inhibition of a soleus H reflex was increased, whereas the vibratory inhibition of the quadriceps H reflex was decreased.5. These results indicate that presynaptic inhibition of Ia afferent terminals on motoneurones of contracting muscles is decreased, permitting Ia activity to contribute to excitation of voluntarily activated motoneurones. On the contrary, presynaptic inhibition of Ia fibres to motoneurones of muscles not involved in the

Introduction Chronic unimanual motor practice increases the motor output not only in the trained but also in the non-exercised homologous muscle in the opposite limb. We examined the hypothesis that adaptations in motor cortical excitability of the non-trained primary motor cortex (iM1) and in interhemispheric inhibition (IHI) from the trained to the non-trained M1 mediate this inter-limb cross education. Methods Healthy, young volunteers (n = 12) performed 1000 submaximal voluntary contractions (MVC) of the right first dorsal interosseus (FDI) at 80% MVC over 20 sessions. Results Trained FDI’s MVC increased 49.9% and the untrained FDI’s MVC increased 28.1%. Although corticospinal excitability in iM1, measured with magnetic brain stimulation (TMS) before and after every 5th session, increased 6% at rest, these changes, as those in intracortical inhibition and facilitation, did not correlate with cross education. When weak and strong TMS of iM1 were, respectively, delivered on a background of a weak and strong muscle contraction of the right FDI, excitability of iM1 increased dramatically after 20 sessions. IHI decreased 8.9% acutely within sessions and 30.9% chronically over 20 sessions and these chronic reductions progressively became more strongly associated with cross education. There were no changes in force or TMS measures in the trained group’s left ADM nor were there changes in a non-exercising control group (n = 8). Conclusions The findings provide the first evidence for plasticity of interhemispheric connections to mediate cross education produced by a simple motor task.

Dystonia has a wide clinical spectrum from early-onset generalized to late-onset sporadic, task-specific forms. The genetic origin of the former has been clearly established. A critical role of repetitive skilled motor tasks has been put forward for the latter, while underlying vulnerability traits are still being searched for. Using magnetoencephalography, we looked for structural abnormalities reflecting a preexisting dysfunction. We studied finger representations of both hands in the primary sensory cortex, as compared in 23 patients with unilateral task-specific dystonia and 20 control subjects. A dramatic disorganization of the nondystonic hand representation was found in all patients, and its amount paralleled the severity of the dystonic limb motor impairment. Abnormalities were also observed in the cortex coding the dystonic limb representation, but they were important only in the most severely affected patients. The abnormal cortical finger representations from the nondystonic limb appear to be endophenotypic traits of dystonia. That finger representations from the dystonic limb were almost normal for the less severely affected patients may be due to intrinsic beneficial remapping in reaction against the primary disorder.

This review will consider the knowledge that neuroimaging studies have provided to the understanding of the anatomy of dystonia. Major advances have occurred in the use of neuroimaging for dystonia in the past 2 decades. At present, the most developed imaging approaches include whole-brain or region-specific studies of structural or diffusion changes, functional imaging using fMRI or positron emission tomography (PET), and metabolic imaging using fluorodeoxyglucose PET. These techniques have provided evidence that regions other than the basal ganglia are involved in dystonia. In particular, there is increasing evidence that primary dystonia can be viewed as a circuit disorder, involving the basal ganglia-thalamo-cortical and cerebello-thalamo-cortical pathways. This suggests that a better understanding of the dysfunction in each region in the network and their interactions are important topics to address. Current views of interpretation of imaging data as cause or consequence of dystonia, and the postmortem correlates of imaging data are presented. The application of imaging as a tool to monitor therapy and its use as an outcome measure will be discussed. © 2013 Movement Disorder Society.

A role for the cerebellum in causing ataxia, a disorder characterized by uncoordinated movement, is widely accepted. Recent work has suggested that alterations in activity, connectivity, and structure of the cerebellum are also associated with dystonia, a neurological disorder characterized by abnormal and sustained muscle contractions often leading to abnormal maintained postures. In this manuscript, the authors discuss their views on how the cerebellum may play a role in dystonia. The following topics are discussed: The relationships between neuronal/network dysfunctions and motor abnormalities in rodent models of dystonia.Data about brain structure, cerebellar metabolism, cerebellar connections, and noninvasive cerebellar stimulation that support (or not) a role for the cerebellum in human dystonia.Connections between the cerebellum and motor cortical and sub-cortical structures that could support a role for the cerebellum in dystonia. Overall points of consensus include: Neuronal dysfunction originating in the cerebellum can drive dystonic movements in rodent model systems.Imaging and neurophysiological studies in humans suggest that the cerebellum plays a role in the pathophysiology of dystonia, but do not provide conclusive evidence that the cerebellum is the primary or sole neuroanatomical site of origin.

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These results demonstrate in writer's cramp the presence of structural abnormalities in brain structures interconnected within the sensorimotor network including the cerebellum and the cortical representation of the affected hand. These abnormalities may be related to the pathophysiology of writer's cramp, questioning the role of the cerebellum, or to maladaptive plasticity in a task-related dystonia.