Involuntary Muscle Activity Research Articles

Monitoring the insurgence of involuntary muscle activity and the development of spasticity after an ischemic stroke over a six-month period: a case study

Monitoring the insurgence of involuntary muscle activity and the development of spasticity after an ischemic stroke over a six-month period: a case study

Neurobiology of bruxism: The impact of stress (Review).

Bruxism is a non-functional involuntary muscle activity that affects more than one-third of the population at some point in their lives. A number of factors have been found to be related to the etiopathogenesis of bruxism; therefore, the condition is considered multifactorial. The most commonly accepted factor is stress. Stress has long been considered to increase muscle tone and to reduce the pain threshold. Current evidence indicates that exposure to chronic stress, distress and allostatic load ignite neurological degeneration and the attenuation of critical neuronal pathways that are highly implicated in the orofacial involuntary muscle activity. The present review discusses the negative effects that chronic stress exerts on certain parts of the central nervous system and the mechanisms through which these changes are involved in the etiopathogenesis of bruxism. The extent of these morphological and functional changes on nerves and neuronal tracts provides valuable insight into the obstacles that need to be overcome in order to achieve successful treatment. Additionally, particular emphasis is given on the effects of bruxism on the central nervous system, particularly the activation of the hypothalamic-pituitary-adrenal axis, as this subsequently induces an increase in circulating corticosterone levels, also evidenced by increased levels of salivary cortisol, thereby transforming bruxism into a self-reinforcing loop.

THE RELATIONSHIP BETWEEN AGE AND DURATION OF SURGERY WITH THE INCIDENCE OF POST ANESTHESIA SHIVERING IN SECTION CAESAREAN PATIENTS AT BENDAN HOSPITAL PEKALONGAN CITY

Background: Shivering is a physiological response to exposure to cold and the body's next steps to maintain heat after peripheral vasoconstriction. The incidence of shivering is caused by several factors including age and length of surgery. Postanesthesia shivering is involuntary oscillatory muscle activity during early recovery after anesthesia. Objective: This study aims to determine the relationship between age and duration of surgery with the incidence of shivering after anesthesia in caesarean section patients at Bendan Hospital, Pekalongan City. Methods: This research includes quantitative research with the type of analytical correlational observational research with a cross sectional approach. The subjects or samples used were 50 caesarean section patients. Determination of subjects was carried out using consecutive sampling technique. Data collection was carried out using an observation sheet for the degree of shivering. Result: Based on the research, the results of the Spearman rank test were obtained with a value of (p) 0.0004 < 0.05 between age and the incidence of shivering and p 0.000 < 0.05 between the length of operation and the incidence of shivering. Conclusion: The conclusion of this study is that there is a relationship between age and length of operation and the incidence of post-anesthesia shivering in caesarean section patients.

Changes in Spatiotemporal Variability of Muscular Response under the Influence of Post-stroke Spasticity.

Spasticity is characterized by involuntary muscle activation due to the hyperexcitability of the stretch reflex. However, the temporal pattern and spatial heterogeneity of motor unit recruitment in this activation are not fully understood. The aim of this study was to investigate changes in spatiotemporal variability in spastic muscle responses to passive stretch after stroke. We acquired high-density surface electromyography (HD-sEMG) signals from the biceps brachii in 21 stroke survivors, 10 age-matched old healthy controls, and 10 young healthy controls at velocities of 10°/s, 60°/s, 120°/s, and 180°/s. The average and distribution of fuzzy entropy extracted from HD-sEMG signals were used to characterize the spatiotemporal variability of muscle activation. Our results showed that the temporal variability of stroke survivors was significantly lower than that of old controls, while the latter was significantly lower than that of young controls. As velocity increased, only stroke survivors showed decreased activation variability and increased activation levels in specific region, and the distributions were similar across velocities. Notably, the activation variability and the size of regions with high activation levels were significantly negatively and positively correlated with the severity of spasticity, respectively. These findings provide entropy-based evidence for the contribution of greater silencing of motoneurons responsible for reflex inhibition to the synchronous recruitment of more motor units.

Effects of jaw clenching and mental stress on persistent inward currents estimated by two different methods.

Spinal motoneuron firing depends greatly on persistent inward currents (PICs), which in turn are facilitated by the neuromodulators serotonin and noradrenaline. The aim of this study was to determine whether jaw clenching (JC) and mental stress (MS), which may increase neuromodulator release, facilitate PICs in human motoneurons. The paired motor unit (MU) technique was used to estimate PIC contribution to motoneuron firing. Surface electromyograms were collected using a 32-channel matrix on gastrocnemius medialis (GM) during voluntary, ramp, plantar flexor contractions. MU discharges were identified, and delta frequency (ΔF), a measure of recruitment-derecruitment hysteresis, was calculated. Additionally, another technique was used (VibStim) that evokes involuntary contractions that persist after cessation of combined Achilles tendon vibration and triceps surae neuromuscular electrical stimulation. VibStim measures of plantar flexor torque and soleus activity may reflect PIC activation. ΔF was not significantly altered by JC (p = .679, n = 18, 9 females) or MS (p = .147, n = 14, 5 females). However, all VibStim variables quantifying involuntary torque and muscle activity during and after vibration cessation were significantly increased in JC (p < .011, n = 20, 10 females) and some, but not all, increased in MS (p = .017-.05, n = 19, 10 females). JC and MS significantly increased the magnitude of involuntary contractions (VibStim) but had no effect on GM ΔF during voluntary contractions. Effects of increased neuromodulator release on PIC contribution to motoneuron firing might differ between synergists or be context dependent. Based on these data, the background level of voluntary contraction and, hence, both neuromodulation and ionotropic inputs could influence neuromodulatory PIC enhancement.

Understanding corticomotor mechanisms for activation of non-target muscles during unilateral isometric contractions of leg muscles after stroke

Purpose Muscle activation often occurs in muscles ipsilateral to a voluntarily activated muscle and to a greater extent after stroke. In this study, we measured muscle activation in non-target, ipsilateral leg muscles and used transcranial magnetic stimulation (TMS) to provide insight into whether corticomotor pathways contribute to involuntary activation. Materials and methods Individuals with stroke performed unilateral isometric ankle dorsiflexion, ankle plantarflexion, knee extension, and knee flexion. To quantify involuntary muscle activation in non-target muscles, muscle activation was measured during contractions from the ipsilateral tibialis anterior (TA), medial gastrocnemius (MG), rectus femoris (RF), and biceps femoris (BF) and normalized to resting muscle activity. To provide insight into mechanisms of involuntary non-target muscle activation, TMS was applied to the contralateral hemisphere, and motor evoked potentials (MEPs) were recorded. Results We found significant muscle activation in nearly every non-target muscle during isometric unilateral contractions. MEPs were frequently observed in non-target muscles, but greater non-target MEP amplitude was not associated with greater non-target muscle activation. Conclusions Our results suggest that non-target muscle activation occurs frequently in individuals with chronic stroke. The lack of association between non-target TMS responses and non-target muscle activation suggests that non-target muscle activation may have a subcortical or spinal origin. Non-target muscle activation has important clinical implications because it may impair torque production, out-of-synergy movement, and muscle activation timing.

Evidence-based Considerations on Donor Nerve Selection and Ideal Muscle Weight in Long-standing Facial Paralysis – The Freiburg Algorithm

Introduction: Free functional muscle transfer (FMT) is the standard for smile reconstruction in long-standing facial paralysis. Using the contralateral NVII for innervation of the transferred muscle frequently produces satisfying results. However, axon counts of facial nerve branches used as donor nerves for cross-face nerve grafts (CFNG) generally decrease with age resulting in insufficient muscle contraction. Also, the volume of the transferred muscle segment necessary for symmetric oral excursion depends on the donor nerve. This study presents our algorithm for donor nerve selection and ideal muscle weight in long-standing facial paralysis. Materials and Methods: In a prospective cohort study, we evaluated facial palsy patients scheduled for dynamic smile reanimation preoperatively via EMG for involuntary masseter muscle activation upon smiling. Six months after noting the first muscle contraction, we assessed smile synchronicity and correlated the results with the EMG results. Furthermore, we correlated oral commissure amplitude with the weight of the muscle segment and the donor nerve used. Results: We recruited 30 patients for the prospective study and included 22 patients in the retrospective analysis. Postoperatively, all patients demonstrated a voluntary smile. The preoperative coactivation of the masseter muscle predicted the outcome regarding synchronicity of the smile with high sensitivity and specificity. Also, we observed a significant increase in oral commissure excursion with increasing muscle weight when using the NV. Conclusion: The lack of masseter coactivation upon smiling predicts the absence of a synchronous, involuntary smile after FMT using the masseteric nerve. The ideal muscle weight depends on the donor nerve and should be smaller for the NV.

Automatic Identification of Involuntary Muscle Activity in Subacute Patients with Upper Motor Neuron Lesion at Rest—A Validation Study

Sustained involuntary muscle activity (IMA) is a highly disabling phenomenon that arises in the acute phase of an upper motor neuron lesion (UMNL). Wearable probes for long-lasting surface EMG (sEMG) recordings have been recently recommended to detect IMA insurgence and to quantify its evolution over time, in conjunction with a complex algorithm for IMA automatic identification and classification. In this study, we computed sensitivity (Se), specificity (Sp), and overall accuracy (Acc) of this algorithm by comparing it with the classification provided by two expert assessors. Based on sample size estimation, 6020 10 s-long sEMG epochs were classified by both the algorithm and the assessors. Epochs were randomly extracted from long-lasting sEMG signals collected in-field from 14 biceps brachii (BB) muscles of 10 patients (5F, age range 50-71 years) hospitalized in an acute rehabilitation ward following a stroke or a post-anoxic coma and complete upper limb (UL) paralysis. Among the 14 BB muscles assessed, Se was 85.6% (83.6-87.4%); Sp was 89.7% (88.6-90.7%), and overall Acc was 88.5% (87.6-89.4%) and ranged between 78.6% and 98.7%. The presence of IMA was detected correctly in all patients. These results support the algorithm's use for in-field IMA assessment based on data acquired with wearable sensors. The assessment and monitoring of IMA in acute and subacute patients with UMNL could improve the quality of care needed by triggering early treatments to lessen long-term complications.

Lower-Extremity Neuromuscular Function Following Concussion: A Preliminary Examination

Neuromuscular function is altered acutely following concussion and theoretically linked to the subsequent postconcussion musculoskeletal injury risk. Existing research has only examined voluntary muscle activation, limiting mechanistic understanding. Therefore, our study aimed to examine voluntary and involuntary muscle activation between college-aged, concussed individuals when symptom-free and healthy matched controls. Prospective, cross-sectional cohort laboratory study. Concussed and healthy participants (n = 24; 58% male, age: 19.3 [1.1]y, mass: 70.3 [16.4]kg, height: 177.3 [12.7]cm) completed the superimposed burst (SB) neuromuscular assessment on their dominant limb within 72hours after self-reporting asymptomatic (22.4 [20.2]d postinjury). Unnormalized and bodyweight-normalized quadriceps maximal voluntary isometric contraction torque (in newton meters), unnormalized and bodyweight-normalized electrically stimulated SB torque, pain (numeric 1-10) during SB, and the central activation ratio (in percentage) were assessed via the SB. Parametric and nonparametric analyses, 95% confidence intervals (95% CIs), and Hedges g (parametric) and Spearman ρ (nonparametric) effect sizes were used to examine group differences (α = .05). The maximal voluntary isometric contraction torque (concussed: 635.60N·m [300.93] vs control: 556.27N·m [182.46]; 95% CI, -131.36 to 290.02; P = .443; d = 0.33), SB torque (concussed: 203.22N·m [97.17], control: 262.85N·m [159.07]; 95% CI, -171.22 to 51.97; P = .280; d = -0.47), and central activation ratio (concussed: 72.16% [17.16], control: 70.09% [12.63]; 95% CI, -10.68 to 14.83; P = .740; d = 0.14) did not differ between the concussed and control groups regardless of bodyweight normalization (P ≥ .344). Pain during the SB was significantly higher with a medium effect for participants with a concussion versus healthy controls (concussed: median = 7, control: median = 5; P = .046; ρ = -0.42). These findings suggest concussed participants do not have statistically altered voluntary or involuntary quadricep neuromuscular function once asymptomatic compared with controls. Therefore, the elevated postconcussion musculoskeletal injury risk may not be attributed to lower-extremity muscle activation. Concussed participants displayed greater pain perception during the SB, which suggests somatosensory or perception changes requiring further examination.

Motor overflow in the lower limb after stroke: Insights into mechanisms.

Motor overflow (involuntary muscle activation) is common after stroke, particularly in the non-paretic upper limb. Two potential cortical mechanisms are as follows: (1) The contralesional hemisphere controls both limbs, and (2) inhibition from the ipsilesional to the contralesional hemisphere is diminished. Few studies have differentiated between these hypotheses or investigated motor overflow in the lower limb after stroke. To investigate these potential mechanisms, individuals with chronic stroke performed unilateral isometric and dynamic dorsiflexion. Motor overflow was quantified in the contralateral, resting (non-target) ankle. Transcranial magnetic stimulation (TMS) was applied, and responses were measured in both legs. Relations between motor overflow, excitability of ipsilateral motor pathways, and interhemispheric inhibition were assessed. Non-target muscle activity (motor overflow) was greater during isometric and dynamic conditions than rest in both legs (p≤0.001) and was higher in the non-paretic than the paretic leg (p= 0.03). Some participants (25%) had motor overflow >4SD above the group mean in the non-paretic leg. Greater motor overflow in the non-paretic leg was associated with lesser inhibition from the ipsilesional to the contralesional hemisphere (p= 0.04). In both legs, non-target TMS responses were greater during the isometric and dynamic than the rest condition (p≤0.01) but not when normalized to background muscle activity. Overall, motor overflow occurred in both legs after stroke, suggesting a common bilateral mechanism. Our correlational results suggest that alterations in interhemispheric inhibition may contribute to motor overflow. Furthermore, the lack of differences in non-target motor evoked potentials MEPs between rest, isometric, and dynamic conditions suggests that subcortical and/or spinal pathways may contribute to motor overflow.

POST-COVID 19 ENCEPHALITIS IN PATIENT WITH DE NOVO MUTATION IN THE SCN1A GENE, A CASE REPORT

Seizures are defined as a transient occurrence of signs and symptoms due to an abnormal, excessive or synchronous neuronal activity in the brain, characterized by abrupt and involuntary skeletal muscle activity. The presence of cephalgic syndrome, infectious-toxic encephalopathy, hypo- and anosmia and ageusia are pathognomonic conditions in COVID-19 infected patients. Post-Covid 19 encephalitis develops to encephalopathy in children with epilepsy. Based on the clinical appearance and the parameters that showed past Covid-19 infection, a diagnosis of post-COVID19 encephalopathy was confirmed. To confirm the diagnosis, clinical examinations, MRI of the brain, electroencephalography, lumbar puncture, laboratory tests (including CBC, CRP, basic metabolic panel, liver panel, hemostasis with D-dimer) are necessary. Based on the brain changes registered on the EEG record, the physical findings and the presence of SARS CoV 2 IgG antibodies, it was concluded that a child with an initial diagnosis of epilepsy, developed encephalopathy after asymptomatic COVID 19 infection. Keywords: Post-COVID19 complications, encephalitis, Dravet syndrome, epilepsy, de novo mutation, children

The Correlation between Gross Motor Function Classification System and Spasticity in Children with Cerebral Palsy

Gross Motor Function Classification System (GMFCS) was used as a criterion to classify motor function in children with cerebral palsy. Spasticity is an increase in muscle resistance to passive stretching, which is an involuntary muscle activity associated with upper motor neuron paralysis that occurs in CP children so that it interferes with their activities. The purpose of this study was to determine the relationship between GMFCS and the level of spasticity assessed by the Ashworth scale in children with cerebral palsy. The analytical research method was observational with a cross sectional approach, the independent variable was assessed on the functional scale using the GMFCS and the dependent variable was assessed for spasticity using the Ashworth scale. The research sample was CP children at YPAC Semarang city. The results of this study are that the highest GMFCS level in children with cerebral palsy at SLB YPAC Semarang City is level III and IV as much as 25.0% while the assessment of spasticity using the ashworth scale obtained ashworth level 3 as much as 58.3% while the results of the calculation of the non-parametric Spearman correlation test were obtained. p value = 0.000 (p &lt; 0.05) with a value of r = 0.837. Therefore, it can be concluded that there is a positive correlation between GMFCS and the level of spasticity assessed using the Ashworth scale in children with cerebral palsy.

Clinical and Social Findings of Childhood Epilepsy

Background: Seizures are defined as a transient occurrence of signs and symptoms due to the abnormal, excessive, or synchronous neuronal activity in the brain characterized by abrupt and involuntary skeletal muscle activity. Seizure is related to specific risk factors like positive family history, fever, infections, neurological comorbidity, premature birth, mother’s alcohol abuse, and smoking in pregnancy. Epilepsy is the most frequent chronic neurologic condition in children. Studies have suggested declining incidence rates of childhood epilepsy in high-income countries during the last decades. Objective: To describe the clinical features and social findings of epilepsy in children, and to evaluate some risk factors associated with control of epilepsy. Patients and Methods: This cross-sectional study was conducted in the pediatric department of Albatool teaching hospital in Diyala province, Iraq. A total of 100 children were included in the study from February 2020 to May 2020. All children diagnosed with epilepsy in this study. Results: One hundred children with epilepsy, their mean age was 5.96± 3.33 years (range 1-14 years). Of the 48(48%) children were male and 52(52%). Of the total patients, 79% were free from seizure on AED, 21% of them were refractory to treatment.Patients without developmental delay (88.7%, p=0.012) can be controlled by AED. Patients who had idiopathic seizures (87.5%, p=0.04) can be controlled by AED. Patients who had seizure attacks can be controlled by AED more than patients who had weekly or monthly seizure attacks (97.4%) (p&lt;0.001). Patients who had been treated by monotherapy (94.7%, p=0.012) can be controlled more than patients who were treated by multidrug therapy. Affected social interaction and need more supervision were factors that detected more in patients with refractory epilepsy, p=0.04, 0.01 respectively. While there was no association between frightened other people and epilepsy control. Conclusion: Most of the patients are characterized by: treatment approach monotherapy, less affected by social interaction and need less supervision. Patients with refractory epilepsy had opposite factors. Keywords: Epilepsy, Albatool teaching hospital.

Present problem of neurororehabilitology: methods for quantitative assessment of pathological increased muscle tone

One of the urgent problems of neurorehabilitation is spasticity ― a motor disorder that depends on the rate of muscle stretching due to the enhancement of tonic stretch reflexes due to a violation of supraspinal inhibitory signals, which is manifested by intermittent or prolonged involuntary muscle activation. In addition to spasticity, the clinical forms of lesions of the upper motor neurons in the form of muscle hypertonicity include rigidity and dystonia.&#x0D; Although spasticity is one of the most common occurrences, its precise definition and pathophysiology remain unclear.&#x0D; Spasticity reduces the effectiveness of rehabilitation of patients with severe disabling diseases. With organic lesions of the brain, movement disorders are often caused by increased muscle tone, which makes it difficult to perform simple movements. For the correct setting of treatment goals for a patient with spasticity syndrome, including for the development of an individual rehabilitation program with a further assessment of its effectiveness, it is necessary to correctly determine the spasticity and its severity, differentiate from other forms of pathological changes in muscle tone (rigidity, plasticity, contractures), as well as to assess the impact on the active and passive function of the limb, daily life and quality of life of the patient.&#x0D; An important issue in the rehabilitation process is the method of quantitative assessment of the pathological increase in muscle tone, for which the collection of complaints and anamnesis, physical neurological examination, scales and various options for instrumental examination are used.&#x0D; The review article presents modern and traditional methods for quantifying muscle tone, as well as methods of therapy.

Monitoring Involuntary Muscle Activity in Acute Patients with Upper Motor Neuron Lesion by Wearable Sensors: A Feasibility Study.

Sustained involuntary muscle activity (IMA) is a highly disabling and not completely understood phenomenon that occurs after a central nervous system lesion. We tested the feasibility of in-field IMA measuring at an acute rehabilitation ward. We used wearable probes for single differential surface EMG (sEMG), inclusive of a 3D accelerometer, onboard memory and remote control. We collected 429 h of data from the biceps brachii of 10 patients with arm plegia. Data quality was first verified in the time and frequency domains. Next, IMA was automatically identified based on the steady presence of motor unit action potential (MUAP) trains at rest. Feasibility was excellent in terms of prep time and burden to the clinical staff. A total of 350.5 h of data (81.7%) were reliable. IMA was found in 85.9 h (25%). This was often present in the form of exceedingly long-lasting trains of one or a few MUAPs, with differences among patients and variability, both within and between days in terms of IMA duration, root mean square (RMS) and peak-to-peak amplitude. Our results proved the feasibility of using wearable probes for single differential sEMG to identify and quantify IMA in plegic muscles of bedridden acute neurological patients. Our results also suggest the need for long-lasting acquisitions to properly characterize IMA. The possibility of easily assessing IMA in acute inpatients can have a huge impact on the management of their postures, physiotherapy and treatments.

Evaluation of Changes in Depression Levels of Bruxism Patients Treated With Botulinum Toxin-A

Aim: Bruxism is defined as the involuntary recurrent masticatory muscle activity characterized by gnashing, grinding, clenching of teeth, and/or pushing the mandible. Factors creating its etiology are peripheral (morphological) or central (physiopathological and physiological), and exogenous. Recently, among physiological factors, depression and bruxism were considered to be related. A definitive treatment method does not exist for bruxism; however, botulinum toxin-A (BT-A) application is an up-to-date and effective way of treatment. The present study is aimed to evaluate the levels of depression in bruxism patients treated with BT-A application. Materials and Methods: A total of 25 individuals (23 females and 2 males) who were diagnosed as bruxism patients were included in the study. 25 U of BT-A for each masseter muscle was injected into the patients. Patients were prospectively observed for a possible change in depression levels by using Beck’s Depression Inventory. The inventory was implemented before and six months after the BT-A application. Depression levels before and six months after the injection were compared. A paired t-test was used to compare “before” and “after” treatment values. One-way analysis of variance and post-hoc Tukey tests were used to evaluate the change in Beck’s Depression Inventory scores according to age groups. Results: The mean total score was 7.80 ± 8.10 before the treatment and 7.16 ± 6.52 six months after the treatment. The decrease in the mean score was not statistically significant ( P &gt; .05). Conclusion: In conclusion, despite the decrease in the mean Beck’s Depression Inventory scores, a statistically significant decrease in the depression levels of patients was not observed.

Spastic movement disorder: should we forget hyperexcitable stretch reflexes and start talking about inappropriate prediction of sensory consequences of movement?

Spastic movement disorder is characterized by reduced ability to selectively activate muscles with significant co-activation of antagonist muscles. It has traditionally been thought that hyperexcitable stretch reflexes have a central role in the pathophysiology and the clinical manifestations of the disorder. Here we argue that the main functional challenges for persons with spastic movement disorder are related to contractures, paresis, weak muscles and inappropriate central motor commands, whereas hyperexcitable reflexes play no or only an insignificant functional role. Co-activation of antagonist muscles and stiff posture and gait may rather be adaptations that aim to ensure joint and postural stability due to insufficient muscle strength. Aberrant (involuntary) muscle activity is likely related to an inadequate prediction of the sensory consequences of movement and a resulting impairment of muscle coordination. We argue that improvement of functional muscle strength and muscle coordination following central motor lesions may be achieved by optimizing integration of somatosensory information into central feedforward motor programs, whereas anti-spastic therapy that aims to reduce reflex activity may be less efficient. This opens for novel investigations into new treatment strategies that may improve functional control of movement and prevent reduced joint mobility in people with brain lesions.

P35 Differences between voluntary and involuntary muscle activation in Parkinsonian patients

P35 Differences between voluntary and involuntary muscle activation in Parkinsonian patients

O-35 The Stiff Person Syndrome. Neurophysiological findings

Background Stiff Person Syndrome (SPS) an encephalomyelitis, is an immune-mediated disorder characterized by rigidity of the axial and proximal limb muscles with painful spasThis rare disease responds to immunotherapies and is frequently associated with other autoimmune diseases. More than 80% of SPS patients have autoantibodies to GAD65 and up to 15% have antibodies to glycinereceptor. Neurophysiological studies can help in the diagnosis by demonstrating the presence of continuous motor unit activity at rest, that the patient cannot voluntarily suppress. Material and methods We present a male patient 28 y/o with a history of weight loss, abdominal pain, ortostathic hypotension, ptosis and babinski sign, whith stiffness and painful spasms in both cuadriceps, tibialis anterior, gastronemius, rectus abdominis, thoracic and lumbar paraspinal muscles. Results EMG showed continuous, involuntary activity of normal motor unit potentials. Painful spasms of involuntary muscle activity, were also detected. No other abnormal spontaneus activity such as fibrilations, positive waves, miokimias, high frequency nor myotonic or neuromyotonic discharges were recorded. The SSR was absent en both hands. The Silent period was normal. ENG and SFEMG were normal. Antibodies to glycinereceptors were positive. After treatment with IvIg and plasma exchange the patient had moderate improvement and at present he is on baclofen, diazepam, methylprednisone and levetirazetam, with persistence of fluctuating stiffness and spas. Conclusions The neurophysiological studies play an important role in the differential diagnosis of the diseases associated with excess motor unit activity, leading in this patient to the diagnosis of encephalomyelitis with rigidity, variant of SPS.

Small amounts of involuntary muscle activity reduce passive joint range of motion.

When assessing passive joint range of motion in neurological conditions, concomitant involuntary muscle activity is generally regarded small enough to ignore. This assumption is untested. If false, many clinical and laboratory studies that rely on these assessments may be in error. We determined to what extent small amounts of involuntary muscle activity limit passive range of motion in 30 able-bodied adults. Subjects were seated with the knee flexed 90° and the ankle in neutral, and predicted maximal plantarflexion torque was determined using twitch interpolation. Next, with the knee flexed 90° or fully extended, the soleus muscle was continuously electrically stimulated to generate 1, 2.5, 5, 7.5, and 10% of predicted maximal torque, in random order, while the ankle was passively dorsiflexed to a torque of 9 N·m by a blinded investigator. A trial without stimulation was also performed. Ankle dorsiflexion torque-angle curves were obtained at each percent of predicted maximal torque. On average (mean, 95% confidence interval), each 1% increase in plantarflexion torque decreases ankle range of motion by 2.4° (2.0 to 2.7°; knee flexed 90°) and 2.3° (2.0 to 2.5°; knee fully extended). Thus 5% of involuntary plantarflexion torque, the amount usually considered small enough to ignore, decreases dorsiflexion range of motion by ~12°. Our results indicate that even small amounts of involuntary muscle activity will bias measures of passive range and hinder the differential diagnosis and treatment of neural and nonneural mechanisms of contracture. NEW & NOTEWORTHY The soleus muscle in able-bodied adults was tetanically stimulated while the ankle was passively dorsiflexed. Each 1% increase in involuntary plantarflexion torque at the ankle decreases the range of passive movement into dorsiflexion by >2°. Thus the range of ankle dorsiflexion decreases by ~12° when involuntary plantarflexion torque is 5% of maximum, a torque that is usually ignored. Thus very small amounts of involuntary muscle activity substantially limit passive joint range of motion.