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Objective: Spasticity is common after spinal cord injury (SCI). Exaggerated tendon jerks, clonus, and spasms are key features of spasticity that result from hyperexcitability of the stretch reflex circuit. Here we studied the effects of vibration on the rectus femoris muscle (RF) on clinical and electrophysiological measures of spasticity in the leg., Methods: Nineteen SCI patients with spasticity and nine healthy subjects were studied at baseline and under stimulation (vibration at 50 Hz during 10 min on the thigh). Neurophysiological studies included evaluation of the soleus T wave and Hmax/Mmax ratio. Clinical measurements of spasticity were the score in the Modified Ashworth Scale (MAS), range of motion (ROM), and duration and frequency of clonus., Results: Patients with incomplete SCI (iSCI) presented higher number of cycles and longer duration of clonus than patients with complete SCI (cSCI). The Hmax/Mmax ratio and T wave amplitude at baseline were significantly larger in iSCI patients than in cSCI or healthy subjects. During vibration, we found a significant reduction of MAS and duration of clonus, and an increase in ROM, in all patients as a group. The Hmax/Mmax ratio and the T wave amplitude decreased significantly in both, patients and controls., Conclusions: Prolonged vibration on proximal lower extremity muscles decreased limb spasticity in patients with spinal cord injury, regardless of whether the lesion is complete or incomplete., Significance: Muscle vibration may be useful for physical therapy, by facilitating passive and active movements of the extremities in spastic SCI patients., (Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Axonal regeneration and organ reinnervation are the necessary steps for functional recovery after a nerve lesion. However, these processes are frequently accompanied by collateral events that may not be beneficial, such as: (1) Uncontrolled branching of growing axons at the lesion site. (2) Misdirection of axons and target organ reinnervation errors, (3) Enhancement of excitability of the parent neuron, and (4) Compensatory activity in non-damaged nerves. Each one of those possible problems or a combination of them can be the underlying pathophysiological mechanism for some clinical conditions seen as a consequence of a nerve lesion. Reinnervation-related motor disorders are more likely to occur with lesions affecting nerves which innervate muscles with antagonistic functions, such as the facial, the laryngeal and the ulnar nerves. Motor disorders are better demonstrated than sensory disturbances, which might follow similar patterns. In some instances, the available examination methods give only scarce evidence for the positive diagnosis of reinnervation-related disorders in humans and the diagnosis of such condition can only be based on clinical observation. Whatever the lesion, though, the restitution of complex functions such as fine motor control and sensory discrimination would require not only a successful regeneration process but also a central nervous system reorganization in order to integrate the newly formed peripheral nerve structure into the prepared motor programs and sensory patterns., (Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Objective: Spasticity with increased tone and spasms is frequent in patients after spinal cord injury (SCI). Damage to descending corticospinal pathways that normally exert spinal segmental control is thought to play an important causal role in spasticity. The authors examined whether the modulation of excitability of the primary motor cortex with high-frequency repetitive transcranial magnetic stimulation (rTMS) could modify lower limb spasticity in patients with incomplete SCI., Methods: Patients were assessed by the Modified Ashworth Scale, Visual Analogue Scale, and the Spinal Cord Injury Spasticity Evaluation Tool (SCI-SET) and neurophysiologically with measures of corticospinal and segmental excitability by the H(max)/M(max), T reflex, and withdrawal reflex. Fifteen patients received 5 days of daily sessions of active (n = 14) or sham (n = 7) rTMS to the leg motor area (20 trains of 40 pulses at 20 Hz and an intensity of 90% of resting motor threshold for the biceps brachii muscle)., Result: A significant clinical improvement in lower limb spasticity was observed in patients following active rTMS but not after sham stimulation.This improvement lasted for at least 1 week following the intervention. Neurophysiological studies did not change., Conclusions: High-frequency rTMS over the leg motor area can improve aspects of spasticity in patients with incomplete SCI.

Imagining motor actions is enough to enhance cortical motor excitability. However, the fact that execution of the motor task has to be inhibited should have a correlate on the extent of cortical excitability enhancement. Therefore, we examined the possible differences between real and motor imagery of simple reaction time tasks (SRT) in the facilitation of the motor-evoked potential (MEP) to transcranial magnetic stimulation (TMS) and in the reduction of short-interval intracortical inhibition (SICI) taking place before the movement onset. Thirteen healthy volunteers were requested to perform visual real or imaginary SRT tasks (rSRT and iSRT) with their dominant hand. For rSRT, subjects had to perform a rapid isometric squeeze as soon as possible after the imperative signal. For iSRT they had to imagine the same movement without actually doing it. Electromyographic (EMG) signals were recorded from the first dorsal interosseus (FDI) muscle. The mean EMG onset was calculated for each subject in rSRT trials. Single-and paired-pulse TMS (at an interstimulus interval of 2.5 ms) were applied at rest and at time intervals of -25, -50, -75, -100 and -125 ms before the expected real (rSRT) mean EMG onset. In rSRT there was a significant increase of MEP to single-pulseTMS at the intervals of -50 and -25 ms, and in iSRT at -50 ms in comparison to the rest condition. % SICI changes were significantly reduced at the intervals of -75, -50 and -25 ms, before EMG the onset in rSRT and at -50 and -25 in iSRT (P < 0.05) in comparison to % SICI changes at rest. The differences between MEPs to spTMS and MEP to ppTMS were significantly larger at rest, -125 and -100 ms intervals in rSRT, and at all intervals in iSRT. Imagining to move causes an increase in corticospinal excitability and a decrease in intracortical inhibition that follow a temporal profile similar to those observed with real movements. However, complete removal of SICI happened only in rSRT at the shortest intervals before the EMG onset. Such action may delineate new tool in motor rehabilitation of patients who have limitation to move.

Psychogenic tremor (PT) is visually indistinguishable from voluntarily mimicked tremor. Healthy volunteers have difficulties with carrying out simultaneously two tasks due to the phenomenon known as dual task interference. Therefore, performing voluntary rhythmic movements would be a burden for carrying out fast ballistic movements with the contralateral hand. We hypothesized that, similarly to healthy volunteers performing rhythmic movements, patients with PT should show the effects of dual task interference, and this may distinguish them from patients with other types of tremor. We studied 6 patients with PT, 9 with Parkinson's disease (PD) and predominantly unilateral tremor, 11 with essential tremor (ET), and 10 normal volunteers (NV) mimicking tremor. They were requested to perform a unilateral simple reaction time task (SRT) to a visual imperative signal in two different conditions: at rest (rSRT) and during contralateral hand tremor (tSRT). Reaction time was significantly longer in tSRT than in rSRT in PT and in NV groups (P < 0.01 for both groups). However, no significant differences were observed between rSRT and tSRT in PD and ET. The delay of unilateral tSRT with respect to rSRT suggests an effect of tremorlike oscillatory movements on reaction time that is consistent with the concept of dual-task interference in NV or PT patients but not in PD or ET. These observations may be useful in the evaluation of psychogenic movement disorders., ((c) 2007 Movement Disorder Society.)

Performing unlearned unimanual tasks when simultaneously carrying out another task with the contralateral hand is known to be difficult. The dual task interference theory predicts that reaction time will be delayed if the investigated task is performed in the course of ongoing contralateral movements. Ballistic movements can be performed at maximal speed in simple reaction time (SRT) experiments when subjects have adequately prepared the motor system needed for movement execution. When fully prepared, activation of subcortical motor pathways by a startling auditory stimulus (SAS) triggers the whole reaction. In this study, we have examined dual task interference with reaction time in eight healthy volunteers. They were presented with a visual imperative signal to perform unilateral SRT either in a baseline condition (control trials) or while carrying out contralateral rhythmic oscillatory movements (test trials). A SAS was introduced in 25% of the trials in both conditions. SRT was significantly delayed in the interference test trial when compared to control trials either with or without SAS (P<0.001). Control and test trials with SAS were significantly faster than those without SAS in both conditions (P<0.001). However, there were no significant differences in the percentage SRT shortening induced by SAS or in the percentage SRT delay observed in the test trials. Our results suggest that performing rhythmic oscillatory movements with one limb slows SRT in the contralateral limb and that this effect is likely related to motor preparation changes. The effect described here can be of interest for physiological studies of interlimb coordination and the mechanisms underlying the dual task interference phenomenon.

Context: Subthalamic nucleus (STN) stimulation may be effective in ameliorating parkinsonian symptoms even to the extent to permit levodopa withdrawal., Objectives: To analyze the efficacy of STN stimulation in patients with Parkinson disease (PD) and to determine if levodopa may be withdrawn after surgery., Design: Before-after trial., Setting: Referral center, hospitalized care., Patients: Fifteen patients with advanced PD., Interventions: Microelectrode-guided bilateral STN high-frequency stimulation., Outcome Measures: Before surgery patients were evaluated in off-medication and on-medication conditions. Dopaminergic drug dosages were reduced after surgery, aiming for complete withdrawal. Six months after surgery, patients were reeavaluated in off- and on-medication conditions, with the stimulation turned on and off., Results: Total Unified Parkinson's Disease Rating Scale (UPDRS) motor score in the off-medication condition improved by 65.9%; and axial symptoms, bradykinesia, rigidity, and tremor improved by 65.8%, 60.4%, 66.1%, and 81.1%, respectively. UPDRS part II scores were reduced by 71.8% and Schwab and England scores improved by 45.3%. Levodopa was withdrawn in 8 patients and the overall levodopa dose was reduced 80.4%. "Off" time was reduced 89.7% and the severity of dyskinesias decreased 80.6% after surgery. All results reached significance (P<.001). Stimulation of the STN achieved antiparkinsonian effect similar to that of treatment with levodopa. No life-threatening adverse effects occurred., Conclusions: Bilateral STN stimulation safely improves all parkinsonian symptoms, decreases or eliminates the need for levodopa, and ameliorates motor fluctuations and dyskinesias. Complete withdrawal of levodopa is feasible with this technique and the overall motor effect of STN stimulation is quantitatively comparable to that obtained with levodopa.

A functional disorder of facial muscle activity commonly occurs in patients after recovery from Bell's palsy with axonal degeneration. The postparalytic facial dysfunction is probably related to the aberrant growing of regenerating axons, although other theories such as ephaptic transmission, spontaneous generation of impulses, and enhancement of motoneuron excitability should also be considered. In this work, we have carried out a comparative electrophysiological study of both sides of the face in 23 patients who had recovered from a unilateral Bell's palsy with axonal degeneration. At rest, spontaneous firing of motor units was observed in muscles of the previously paralyzed side. Direct motor responses to facial nerve stimulation were smaller in the muscles of the previously paralyzed side, but reflex responses obtained in the same muscles by stimulation of either the facial or trigeminal nerve were larger when compared with those of the contralateral side. These data indicate that patients with "postparalytic facial dysfunction" may have an increased background muscle activity, as well as an enhanced recruitment of facial motoneurons to reflex activation in the side of the previous paralysis. These findings are compatible with an enhanced level of motoneuron excitability in the facial nucleus.

We report the electrophysiological study of a patient with carpal tunnel syndrome who, besides the features of median nerve entrapment at the wrist, showed an aberrant motor innervation of Martin-Gruber type and an unusual distribution of the sensory innervation of the fingers. Studies based on collision between sensory volleys showed that the fibers supplying the anomalous innervation did not follow the same path as the aberrant motor fibers. This finding is consistent with the hypothesis that Martin-Gruber anastomosis is made up of motor axons only, and supports the idea that other abnormalities of innervation may be found in patients with Martin-Gruber anastomosis.

Although the impairment of autonomic function has been described in alcoholic subjects, there is no evidence for such a dysfunction to be due to damage of autonomic centers or peripheral small caliber fibers. To investigate the function of peripheral fibres of the autonomic nervous system, we have carried out an electrophysiological study of the sympathetic skin response (SSR) in the hands and feet in 70 alcoholic and in 33 non-alcoholic subjects. In the hand, SSR recordings were done simultaneously in the palm and finger tip by stimulating the median nerve at the wrist. A conventional electrophysiological study performed in the same patients was used to classify them according to the presence or absence of electrophysiological criteria for peripheral polyneuropathy (ECPN). In analyzing the results of the SSR test, we found absent responses in the finger tip with present responses in the palm in 18 patients, 13 of them with ECPN. Absent responses in the feet were observed in 37 patients, 28 of them with ECPN. From our findings, it is concluded that alcoholics suffer from a dysfunction of sympathetic sudomotor activity due to axonal involvement of the most distal segments of the nerves.

A pure sensory neuropathy due to neuronal damage in the gasserian and spinal ganglia has been described in patients with Sjögren's syndrome. Conventional electromyographic (EMG) studies can demonstrate the selective involvement of the sensory pathways but they do not provide definite evidence for the site of the lesion. Noting that the trigeminal sensory neurons carrying cutaneous and muscular afferents are differentially located in the gasserian and mesencephalic nuclei, respectively, we carried out an electrophysiological study of the trigeminofacial and trigeminotrigeminal reflexes in 5 patients with Sjögren's syndrome and pure sensory neuropathy, in 10 patients with sensory-motor neuropathies of other causes, and in 10 healthy subjects. Our results show that patients with Sjögren's syndrome and pure sensory neuropathy who exhibited abnormal blink reflexes and an abnormal, cutaneous-induced masseter silent period had normal jaw jerks, whereas patients with sensory-motor neuropathies who exhibited abnormal cutaneous responses had abnormal jaw jerks. These findings suggest that the lesion in pure sensory neuropathy involves damage to the neurons of the gasserian ganglia and not to the trigeminal axons, since an axonal lesion would be expected to involve the large axons from muscle spindle receptors.

We studied electrically elicited blink reflex responses in patients with hemifacial spasm (HFS) by applying single isolated, as well as paired (conditioning and test), stimuli at both sides of the face. Responses after single stimuli were of larger size on the side of the spasm compared with the uninvolved side and controls. With paired stimuli, the inhibitory effect of the conditioning stimuli upon the test stimuli late response (R2), which was always observed in normals, was significantly less pronounced at short interstimuli intervals. This resulted in an enhanced recovery curve of R2, which was observed on the side of the spasm and the contralateral, clinically normal side. Patients with longer disease duration showed more striking abnormalities of the recovery curve. We suggest that there is enhanced excitability of facial motoneurons and of those brainstem interneurons that mediate the blink reflex pathway in patients with HFS.