Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease

We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.     

Reflex studies and MRI in the restless legs syndrome

Brainstem and spinal pathways of untreated patients with idiopathic restless legs syndrome (RLS) were examined using magnetic resonance imaging (MRI), blink reflex, first and second exteroceptive suppression (ES1, ES2) of temporalis muscle, and H reflex. MRI of 25 patients elicited no structural lesions beyond age-related atrophy or white matter lesions on proton density- and T2-weighted coronal and axial images. All patients showed a normal latency of the soleus H reflex (mean·SD latency=31.22·2.81 ms) and the H/M ratio was 48·17%. The duration and onset latency of the direct and indirect blink reflex responses were normal in all patients compared with those of controls (p>0.5). There was no significant difference in ES1 and ES2 latencies or duration between patients and controls (p>0.5). These results suggest that the etiology of RLS symptoms does not involve structural lesions.     

After-effects of pedaling exercise on spinal excitability and spinal reciprocal inhibition in patients with chronic stroke

Purpose of the study: To evaluate the after-effects of pedaling on spinal excitability and spinal reciprocal inhibition in patients with post-stroke spastic hemiparesis. Materials and methods: Twenty stroke patients with severe hemiparesis participated in this study and were instructed to perform 7 min of active pedaling and 7 min of passive pedaling with a recumbent ergometer at a comfortable speed. H reflexes and M waves of paretic soleus muscles were recorded at rest before, immediately after and 30 min after active and passive pedaling. The Hmax/Mmax ratio and H recruitment curve were measured. Reciprocal inhibition was assessed using the soleus H reflex conditioning test paradigm. Results: The Hmax/Mmax ratio was significantly decreased after active and passive pedaling exercise. The decreased Hmax/Mmax ratio after active pedaling lasted at least for 30 min. The H recruitment curve and reciprocal inhibition did not change significantly after active or passive pedaling exercise. Conclusions: Pedaling exercise decreased spinal excitability in patients with severe hemiparesis. Pedaling may be effective in rehabilitation following stroke.     

Effects of Transcutaneous Spinal Direct Current Stimulation in Idiopathic Restless Legs Patients

BackgroundTranscutaneous spinal direct current stimulation (tsDCS) is a new non-invasive technique to modulate spinal cord activity. The pathophysiological concept of primary RLS proposes increased spinal excitability.ObjectiveThis pilot study used tsDCS to reduce pathologically enhanced spinal excitability in RLS patients and to thereby ameliorate clinical symptoms.Methods20 patients with idiopathic RLS and 14 healthy subjects participated in this double-blinded, placebo-controlled study. All participants received one session of cathodal, anodal and sham stimulation of the thoracic spinal cord for 15 min (2.5 mA) each, in randomized order during their symptomatic phase in the evening. The soleus Hoffmann-reflex with Hmax/Mmax-ratio and seven different H2/H1-ratios (of two H-reflex responses to double stimuli) were measured. The RLS symptoms were assessed by a visual analogue scale (VAS). All parameters were measured before and twice after tsDCS.ResultsRLS patients showed increased H2/H1-ratios during their symptomatic phase in the evening. Application of anodal stimulation led to a decreased H2/H1-ratio for 0.2 and 0.3 s interstimulus intervals in patients. Furthermore, application of anodal and cathodal stimulation led to a reduction in restless legs symptoms on the VAS, whereas application of sham stimulation had no effects on either the VAS or on the H2/H1-ratio in patients. VAS changes did not correlate with changes of H2/H1-ratios.ConclusionsThis is the first tsDCS study in idiopathic RLS, which resulted in short-lasting clinical improvement. Furthermore, our results support the pathophysiological concept of spinal cord hyperexcitability in primary RLS and provide the basis for a new non-pharmacological treatment tool.     

H reflex latency in the healthy elderly

The purpose of this study was to evaluate prospectively and analyze the relationship of tibial nerve H reflex latency to age, sex, leg length, and skin temperature in a large healthy elderly population. The H reflex was recorded bilaterally in 92% of 103 carefully screened individuals aged 60–88 years. The mean H reflex latency was 30.8 (SD = 2.6) and 30.7 (SD = 2.6) ms for right and left legs, respectively. A high correlation (r = 0.55, P < 0.05) was present between H reflex latency and leg length. No significant correlation existed for H reflex latency and age. The upper normal limit for the difference between right and left H reflex latencies was 1.8 ms. This limit is greater than that reported in the literature for younger individuals due to a larger standard deviation. These findings suggest that aging increases the between-leg variability of H reflex latency in individuals. This greater difference must be taken into account when using side-to-side H reflex latency comparison to detect unilateral pathology in the elderly. © 1994 John Wiley & Sons, Inc.     

Alterations in excitatory and inhibitory brainstem interneuronal circuits in fibromyalgia: Evidence of brainstem dysfunction

ObjectivePatients with fibromyalgia syndrome (FMS) perceive stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role.MethodsBlink reflex, blink reflex excitability recovery, and prepulse inhibition of the blink reflex – representing brainstem excitability – were assessed in 10 female patients with FMS and 26 female healthy controls.ResultsUnconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls. Blink reflex excitability recovery was enhanced in patients versus controls at all intervals tested. Prepulses significantly suppressed R2 area and increased R2 latency in patients and controls. However, R2 area suppression was significantly less in patients than in controls (patients: to 80.0 ± 28.9%, controls: to 47.8 ± 21.7%). The general pattern of corresponding changes in R2c was similar.ConclusionsBlink reflex is normal, whereas blink reflex excitability recovery is enhanced and blink reflex prepulse inhibition is reduced in patients with FMS, suggesting functional changes at the brainstem level in FMS.SignificanceReduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.     

Electrophysiological findings in patients with restless legs syndrome

BackgroundRestless legs syndrome (RLS) manifests as an urge to move the body to relieve the discomfortable sensations, primarily when resting, sitting, laying down, or sleeping. Diagnosis of RLS relies on clinical criteria, and the immobilization test was the only instrumental tool with equivocal results.ObjectivesTo assess different electrophysiological findings in patients with RLS, and compare the diagnostic values of these parameters in the diagnosis of RLS.Methods30 patients with primary RLS and 30 controls who were matched for age and gender were studied. Participant's demographics, laboratory findings, and electrophysiological test, namely nerve conduction studies (NCS), cutaneous silent period (CSP), H reflex and sympathetic skin response (SSR), F-wave latency, amplitude, F-wave duration (FWD), and the ratio between FWD and duration of the corresponding compound muscle action potential (FWD/CMAPD) were analyzed.ResultsNone of the patients showed altered NCS data. FWD of upper (12.37 ± 2.77 ms) and lower limb (21.71 ± 5.24 ms) were significantly longer in patients. Also, FWD/CMAP duration of the upper (1.03 ± 0.2) and lower limb (2.02 ± 0.55) was longer in patients. Likewise, they exhibited delayed CSP latency from TA (110.62 ± 13.73 ms) and APB (77.35 ± 12.16 ms) whereas the CSP duration from TA and APB was decreased (37.36 ± 11.59 ms; 42.55 ± 7.97 ms, respectively). The SSR latency was not different, and right-sided H reflex amplitude (5.07 ± 3.98 mV) and H/M ratio (0.65 ± 1.81) were significantly increased in the patient group.ConclusionThe data suggest that there may be a dysfunction of the inhibitory/excitatory circuits at a spinal level; and no pathology in the peripheral nerves. The unilateral difference of H reflex amplitude and H/M ratio may suggest asymmetrical central inhibitory dysfunction. Further prospective studies with larger cohorts are now needed to evaluate the pathophysiology of RLS with different neurophysiological assessment tools.     

State dependent excitability changes of spinal flexor reflex in patients with restless legs syndrome secondary to chronic renal failure

OBJECTIVE: Periodic limb movement in sleep (PLMS) is a common dysfunction of motor control during sleep, occurring either in isolation or associated with a variety of neurological disorders including restless legs syndrome (RLS). Although the PLMS generators have not been established, their occurrence in patients with spinal cord injury and their clinical resemblance to the spinal cord flexor withdrawal reflex (FR) suggest that PLMS may originate in the circuitry that mediates the FR. The significantly increased spinal cord excitability noted in primary RLS/PLMS patients may play an important role in the pathophysiology of primary RLS. The aim of this study is to establish whether the enhanced spinal cord excitability, which is represented by a lower threshold and/or greater spatial spread of the FR, is also true for the RLS/PLMS patients whose RLS is secondary to chronic renal failure (CRF). METHODS: Twenty patients with RLS/PLMS secondary to CRF have been compared with matched controls according to the state dependent changes in FR excitability. All patients met the diagnostic criteria for RLS and PLMS. They had CRF for 5.2+/-3.5 years, and were under the hemodialysis treatment. Twenty healthy, age and sex matched subjects were tested as controls. The electrophysiological testing of the FR was performed during wakefulness (9:30-10:30 p.m.) and sleep (beginning of stage II, the first sleep cycle). RESULTS: A significant increase in FR excitability was found in RLS/PLMS patients with CRF. This abnormality was prominent during sleep, which was also true for the primary RLS. CONCLUSIONS: Our results suggest that similar neuronal pathways are involved in primary and secondary RLS/PLMS patients. Our results also support that RLS/PLMS and FR share a common spinal mechanism.     

Family recurrence and oligo-anuria predict uremic restless legs syndrome

Pizza F, Persici E, La Manna G, Campieri C, Plazzi G, Carretta E, Cappuccilli ML, Ferri B, Stefoni S, Montagna P. Family recurrence and oligo‐anuria predict uremic restless legs syndrome.
Acta Neurol Scand: 2012: 125: 403–409.
© 2011 John Wiley & Sons A/S. Objectives – To determine clinical and laboratory predictors of restless legs syndrome (RLS) in patients with end‐stage kidney disease (ESKD) undergoing long‐term hemodialysis (HD). Materials and Methods – One hundred and sixty‐two consecutive patients were assessed. History of sleep disturbances, neurological examination, clinical, and laboratory data were collected. Patients with and without RLS were compared, and a logistic regression model described the relations between independent predictors and RLS. Results – Fifty‐one patients (32%) currently had RLS (RLS+). RLS+ vs RLS? patients were more frequently women (49% vs 29%, P = 0.012), had first‐degree relative with RLS (22% vs 6%, P = 0.004), insomnia (59% vs 36%, P = 0.007), peripheral neuropathy (41% vs 21%, P = 0.006), and low residual diuresis (92% vs 68% with below 500 ml/24 h, P = 0.001). Low (OR = 8.71, CI = 2.27–33.41; P = 0.002) and absent (OR = 4.96, CI = 1.52–16.20; P = 0.008) residual diuresis, peripheral neuropathy (OR = 4.00, CI = 1.44–11.14; P = 0.008), and first‐degree relative with RLS (OR = 3.82, CI = 1.21–12.13; P = 0.023) significantly predicted RLS in ESKD patients undergoing HD. Conclusion – Positive family history for RLS together with reduced/absent residual renal function and peripheral neuropathy predicts the risk for RLS in ESKD patients undergoing HD. Longitudinal studies are warranted to correlate RLS occurrence with genetic and environmental factors.     

Interrogating interneurone function using threshold tracking of the H reflex in healthy subjects and patients with motor neurone disease

ObjectiveThe excitability of the lower motoneurone pool is traditionally tested using the H reflex and a constant-stimulus paradigm, which measures changes in the amplitude of the reflex response. This technique has limitations because reflex responses of different size must involve the recruitment or inhibition of different motoneurones. The threshold-tracking technique ensures that the changes in excitability occur for an identical population of motoneurones. We aimed to assess this technique and then apply it in patients with motor neurone disease (MND).MethodsThe threshold-tracking approach was assessed in 17 healthy subjects and 11 patients with MND. The soleus H reflex was conditioned by deep peroneal nerve stimulation producing reciprocal Ia and so-called D1 and D2 inhibitions, which are believed to reflect presynaptic inhibition of soleus Ia afferents.ResultsThreshold tracking was quicker than the constant-stimulus technique and reliable, properties that may be advantageous for clinical studies. D1 inhibition was significantly reduced in patients with MND.ConclusionsThreshold tracking is useful and may be preferable under some conditions for studying the excitability of the motoneurone pool. The decreased D1 inhibition in the patients suggests that presynaptic inhibition may be reduced in MND.SignificanceReduced presynaptic inhibition could be evidence of an interneuronopathy in MND. It is possible that the hyperreflexia is a spinal pre-motoneuronal disorder, and not definitive evidence of corticospinal involvement in MND.     

Periodic limb movements in sleep: state-dependent excitability of the spinal flexor reflex

OBJECTIVE: To test the hypothesis that periodic limb movements (PLMs) are related to spinal flexor reflexes (FRs), the authors compared the state-dependent changes in FR excitability in 10 patients with restless legs syndrome (RLS) and PLMs with those from matched controls. BACKGROUND: PLM is a disorder of motor control during sleep, frequently occurring in RLS. Clinically, PLMs resemble spinal FRs. METHODS: FRs were obtained by electrically stimulating the medial plantar nerve and recording from antagonist leg and thigh muscles bilaterally. RESULTS: Compared with controls, patients had significantly increased spinal cord excitability, as indicated by lower threshold and greater spatial spread of the FR, which was more prominent during sleep. Multiple late responses were seen during sleep in all patients and in some controls at higher threshold. The most prominent of these responses had a very long duration and a latency range of 250 to 800 msec, and because of its close temporal relationship to the FR stimulus, the authors considered it was a late, high-threshold component of the FR (FR3). The authors also found a similarity between the pattern of muscle recruitment and spatial spread of late components of the FR and those of spontaneous PLMs. CONCLUSIONS: The results support the hypothesis that PLMs in RLS and FRs share common spinal mechanisms and suggest that PLMs may result from enhanced spinal cord excitability in RLS patients. Because dopaminergic mechanisms are involved in spinal FR control, the results are consistent with the current view that RLS is a disorder of dopaminergic function.     

The effect of the GABA-agonist, progabide, on stretch and flexor reflexes and on voluntary power in spastic patients

ABSTRACT— The action of the GABA-receptor agonist, progabide, was investigated in a double-blind study with cross-over to placebo. The stretch and flexor reflexes and voluntary power were measured in 16 patients with spasticity. 2-week treatment periods were used; the median daily oral dosage of progabide was 24.3 mg/kg. The Achilles tendon (T) reflex was significantly suppressed whereas the Hoffmann (H) reflex remained unchanged: the T/H ratio was thus reduced. H_max/M (direct motor)_max ratio and the vibration-induced suppression of the T- and H-reflexes were unchanged. These findings indicate an effect of progabide on the spindles or on the controlling fusimotor system (probably acting on spinal interneurons), whereas influence on presynaptic inhibition and alpha-motoneuron excitability is unlikely. The flexor reflex threshold was increased during progabide treatment and latency at threshold decreased towards normal latency. This indicates some influence of progabide on flexor reflex activity attributed to reinforcement of action of GABAergic interneurons at the spinal level. Isokinetic measurement of voluntary power of knee extension revealed particularly good progress for the fastest movements during progabide treatment, whereas isometric measurement of sustained handgrip remained unchanged, probably reflecting a reduction of spasticity without reduction of voluntary power in non-spastic muscles.     

Cabergoline reverses cortical hyperexcitability in patients with restless legs syndrome

OBJECTIVE: To reverse the profile of abnormal intracortical excitability in patients with restless legs syndrome (RLS) by administering the dopaminergic agonist cabergoline. METHODS: The effects of this drug on motor cortex excitability were examined with a range of transcranial magnetic stimulation (TMS) protocols before and after administration of cabergoline over a period of 4 weeks in 14 patients with RLS and in 15 healthy volunteers. Measures of cortical excitability included central motor conduction time; resting and active motor threshold to TMS; duration of the cortical silent period; short latency intracortical inhibition (SICI) and intracortical facilitation using a paired-pulse TMS technique. RESULTS: Short latency intracortical inhibition was significantly reduced in RLS patients compared with the controls and this abnormal profile was reversed by treatment with cabergoline; the other TMS parameters did not differ significantly from the controls and remained unaffected after treatment with cabergoline. Cabergoline had no effect on cortical excitability of the normal subjects. CONCLUSIONS: As dopaminergic drugs are known to increase SICI, our findings suggest that RLS may be caused by a central nervous system dopaminergic dysfunction. This study demonstrates that the cortical hyperexcitability of RLS is reversed by cabergoline, and provides physiological evidence that this dopamine agonist may be a potentially efficacious option for the treatment of RLS.     

Restless legs syndrome in Friedreich ataxia: A polysomnographic study

Friedreich ataxia (FA) is the most common type of hereditary ataxia. Frataxin deficiency due to a GAA expansion in the first intron of chromosome 9 results in intramitochondrial iron accumulation. On the basis of the patients' complaints about sleep disturbance and pathophysiological considerations, we systematically assessed sleep history and polysomnography in FA. We included 16 consecutive FA patients (11 men, 5 women; mean age, 35.4 ± 11.1 years) with a mean disease duration of 16.5 ± 7.0 years. All patients underwent a standardized protocol including a detailed sleep history and polysomnographic recordings. Eight out of 16 patients were diagnosed with restless legs syndrome (RLS). In seven patients, RLS onset was after the onset of FA. Interestingly, FA patients with RLS had significantly lower serum ferritin levels than FA patients without RLS (76.3 ± 56.0 μg/L vs. 176.3 ± 100.7 μg/L; P = 0.043 after correction for sex and age). Moreover, periodic leg movements in wakefulness (PLMW) indices were significantly higher in FA patients with RLS than FA patients without RLS (FA with RLS, 118.1 ± 50.7; FA without RLS, 65.6 ± 44.2; P = 0.028). There was an inverse correlation between serum ferritin levels and PLMW indices obtained in all FA patients (rho ?0.538, P = 0.039). RLS is common in FA. Its frequency in this primarily spinal ataxia appears consistent with the concept of dysfunctional spinal sensorimotor integration in the pathophysiology of RLS. The finding that RLS is more frequent in the context of lower serum ferritin levels in FA is interesting, but requires further investigation in larger patient samples. © 2009 Movement Disorder Society.     

Altered Spinal Excitability in Patients with Primary Fibromyalgia: A Case-Control Study

Background and PurposeAbnormal excitability of the central nervous system, both spinal and supraspinal, has previously been described as a pathophysiological plastic mechanism for chronic pain syndromes. Primary fibromyalgia (FM) as one extreme of this spectrum of diseases. This case-control study aimed to determine the changes in the spinal excitability by investigating the Hoffman reflex (H-reflex) in patients with FM.MethodsThirty-eight patients with FM and 30 healthy controls participated in this case-control study. We measured the H-reflex bilaterally in the upper limbs (flexor carpi radialis) and the lower limbs (gastrocnemius and soleus). Moreover, pain-related variables were measured, including pain severity (using a visual analogue scale), pain duration, Widespread Pain Index, and the score on the Symptom Severity Scale. Various psychiatric comorbidities and quality-of-life parameters were measured for each patient, including scores on the Hamilton Depression Rating Scale, Taylor''s Manifest Anxiety Scale, and the Revised Fibromyalgia Impact Questionnaire.ResultsA significant increase in the ratio of the maximum baseline-to-peak amplitudes of H and M waves (H_max/M_max) but not in the H-wave minimum latency was found in patients with FM compared with healthy controls. There were no significant correlations between this ratio in both muscles and the various pain-related measures, psychiatric comorbidity, and quality of life in patients with FM. Patients with FM suffered more depression and anxiety than did the controls.ConclusionsWe found increased spinal excitability in patients with FM, which was not confined to the site of maximum pain. This information may help in the diagnosis of FM and supports the hypothesis of central sensitization.     

Cardiovascular risk factors in restless legs syndrome

We conducted a population‐based cross‐sectional study to assess prevalence of cardiovascular risk factors in subjects with and without restless legs syndrome (RLS). Adults attending their annual checkup completed the International RLS Study Group questionnaire and underwent an interview by a neurologist. Data from the annual checkup were compared between subjects with and without RLS. The prevalence of RLS was 6.7% (95% CI 5.45–7.95) among 1,537 responders. RLS subjects' blood tests showed significantly higher fasting blood glucose level (P = 0.029), higher prevalence of hypercholesterolemia (P = 0.029) and reduced renal function (P = 0.013), and increased prevalence of low hematocrit (P = 0.008). RLS subjects weighed more (P = 0.029), had a higher BMI (P = 0.033), larger hip circumference (P = 0.033), and were less fit (P = 0.010). To control for interactions among statistical predictors, we also employed multivariate logistic regression models adjusted for age, gender, smoking, BMI, hemoglobin, glucose, HDL/LDL cholesterol, triglycerides, and creatinine. We found that female gender (OR 2.16; 95% CI 1.11–4.17), smoking (OR 1.82; 95% CI, 1.10–3.00), and HDL/LDL cholesterol (OR 0.18; 95% CI 0.034–0.90) were significantly associated with RLS compared with subjects without RLS. RLS was associated with cardiovascular risk factors. © 2009 Movement Disorder Society     

Neurophysiological evaluation of areflexia in Holmes-Adie syndrome.

PURPOSE: To evaluate ankle areflexia in Holmes-Adie syndrome (HAS). PATIENTS AND METHODS: Hoffmann (H) and Tendon (T) soleus reflexes, tonic vibration reflex (TVR), and polysynaptic extension reflex of soleus muscle (PERS) were evaluated in eight patients with idiopathic HAS. Motor (MNCV) and sensory (SNCV) nerve conduction velocities, compound motor-action potential (CMAP), and sensory action potential (SAP) were also determined in upper and lower limbs. RESULTS: Soleus T reflex was obtained in one out of eight patients, and H-reflex was found in none of the patients. TVR was recorded in four out of eight patients, and PERS in all of the patients. MNCV, SNCV, CMAP and SAP showed normal values in all patients. In six out of the eight patients a late response following the tibial nerve stimulation showed constant latency, amplitude and morphology, with no recovery cycle or vibration inhibition. CONCLUSION: In this study, the neurophysiological spinal reflex circuitry evaluations support the view that HAS ankles areflexia is due to a selective impairement of monosynaptic connections of Ia afferents. A normal nuclear excitability is suggested by polysynaptic activation of the soleus motor nucleus.     

Can neck muscle spindle afferents activate fusimotor neurons of the lower limb?

Introduction: We investigated whether vibratory stimulation of the dorsal neck muscles activates fusimotor neurons of lower limb muscles in relaxed human subjects. Methods: The triceps surae (TS) muscles of seated subjects (n = 15) were conditioned to leave their muscle spindles in either an insensitive (hold‐long) or sensitive (hold‐short) state. A vibrator (80 HZ ) was applied to the dorsal neck muscles for 10 seconds. The tendon jerk was evoked from the right TS immediately before (during) or 5 seconds after (interposed) the offset of vibration. Results: The size of the reflex after hold‐long muscle conditioning and after neck vibration was significantly smaller than the control hold‐short reflex (P < 0.001). However, after hold‐short conditioning, neck vibration significantly increased tendon jerk amplitude, both during (P = 0.001) and interposed (P = 0.026). Conclusion: Dorsal neck vibration increases spinal reflex excitability of the TS in relaxed and seated subjects, but not through fusimotor excitation. Muscle Nerve, 2012     

Spinal and cortical inhibition in Huntington's chorea.

In this article we studied spinal and cortical inhibitory mechanisms in patients with Huntington's disease. To evaluate spinal cord inhibitory circuitries, we assessed reciprocal inhibition between antagonist forearm muscles and the recovery cycle of the H reflex in the flexor carpi radialis. Patients showed a significant decrease in the presynaptic phase of reciprocal inhibition reaching a minimum at the conditioning-test interval of 20 msec and an abnormal facilitation of the test H reflex at the conditioning test interval of 40 to 60 msec. Throughout its time course (10-200 msec), the H reflex recovery cycle showed a more prominent facilitation in patients than in control subjects. To assess whether the observed pathophysiological abnormalities might have arisen from an abnormal motor cortical excitability, we examined the recovery cycle of the motor potentials evoked by paired transcranial magnetic stimuli. We found that the inhibitory mechanisms controlling motor cortical excitability were normal. An interpretation of the spinal cord abnormalities is that the intrinsically normal but deafferentated motor cortex in Huntington's disease partly loses its inhibitory control, thus disinhibiting spinal cord circuitry. Our findings from paired transcranial magnetic stimulation suggest that cortical motor areas are not hyperexcitable in Huntington's disease. Hence, the postulated thalamocortical overactivity in experimental models of Huntington's disease needs to be reappraised.     

Abnormal dorsal premotor–motor inhibition in writer's cramp

The authors hypothesized that a deficient premotor–motor inhibitory network contributes to the unwanted involuntary movements in dystonia. The authors studied nine controls and nine patients with writer's cramp (WC). Dorsal premotor–motor cortical inhibition (dPMI) was tested by applying conditioning transcranial magnetic stimulation (TMS) to the dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6 ms. The authors used an H‐reflex in flexor carpi radialis paired with TMS over the premotor cortex to assess for spinal cord excitability change. Finally, the authors interrupted a choice reaction time task with TMS over dorsal premotor cortex to assess performance in a nondystonic task. The results showed that WC patients exhibited dPMI at rest (88.5%, the ratio of conditioned to unconditioned test pulse), in contrast to controls, who did not show dPMI (109.6%) (P = 0.0198). This difference between patients and controls persisted during contraction (100% vs. 112%) and pen‐holding (95.6% vs. 111%). The H‐reflex in the arm was not modulated by the premotor cortex stimulation. The WC patients made more errors, and the error rate improved with TMS over the premotor cortex. These results suggest that abnormal premotor–motor interactions may play a role in the pathophysiology of focal dystonia. The dPMI was not modulated by task in either group, but was constantly greater in the patients. The significance of the increased inhibition is likely to be compensatory. It appears to be a robust finding and, in combination with other features, could be further explored as a biomarker. © 2014 International Parkinson and Movement Disorder Society