Abnormal Motor Activity Research Articles

Peripheral neuropathy in stable chronic obstructive pulmonary disease: Is the phrenic nerve more affected compared with other peripheral nerves?

Background Chronic obstructive pulmonary disease (COPD) is a multicomponent disease with extrapulmonary manifestation. Peripheral nerve affection may be one of the results or mechanism of COPD. Objective The aim of this study was to evaluate peripheral neuropathy in patients with stable COPD and whether these changes are more or less marked in the phrenic nerve when compared with other peripheral nerves. Patients and methods Eighty patients with COPD and 60 healthy individuals as a control group were included. All were subjected to the following: (i) full history taking; (ii) clinical and neurological examination; (iii) chest radiography; (iv) high-resol ution computed tomography scanning of the chest; (v) arterial blood gases analysis at room air; and (vi) spirometric tests. Results There was a statistically significant increase in smoking packs/year, respiratory rate, hemoglobin, and white blood cells in the COPD group. There was a significant decrease in oxygen saturation, pH, arterial oxygen tension, forced expiratory volume in 1 s, forced expiratory volume in 1 s/forced vital capacity, and forced vital capacity% in the study group when compared with the control group, whereas there was a significant increase in CO2 tension in the COPD group. There was a significant increase in the distal latency of all nerves and a significant decrease in the amplitude and conduction velocity of all nerves, except the amplitude of the phrenic nerve in the COPD group. The difference for phrenic nerve amplitude was statistically nonsignificant. In the COPD group, abnormal motor activity in the median, ulnar, common peroneal, and phrenic nerves of 30, 22.5, 35, and 22.5%, respectively, was reported, whereas abnormal sensory activity in the median, ulnar, and sural nerves of 30.0, 27.5, and 42.5%, respectively, was reported. Finally, we found a statistically significant increase in nerve abnormalities with increased severity of the disease. Conclusion COPD had a significant affection on peripheral nerves, either motor or sensory. In addition, COPD had a significant affection on the phrenic nerve and muscle of the diaphragm. However, this affection of the phrenic nerve was confined to grades III and IV and was the least affection of studied nerves.

Focal task specific dystonia: a review and update

In this review, we summarize recent advances in understanding the etiology, risk factors and pathophysiology of focal task specific dystonia (FTSD), movement disorders characterized by abnormal motor activation during the performance of specific, repetitive actions. We focus on two common FTSD, musician’s dystonia and writer’s cramp. FTSD may pose a threat to the patient’s livelihood, and improved therapeutic treatments are needed.

FMRP Expression Levels in Mouse Central Nervous System Neurons Determine Behavioral Phenotype.

Fragile X mental retardation protein (FMRP) is absent or highly reduced in Fragile X Syndrome, a genetic disorder causing cognitive impairment and autistic behaviors. Previous proof-of-principle studies have demonstrated that restoring FMRP in the brain using viral vectors can improve pathological abnormalities in mouse models of fragile X. However, unlike small molecule drugs where the dose can readily be adjusted during treatment, viral vector–based biological therapeutic drugs present challenges in terms of achieving optimal dosing and expression levels. The objective of this study was to investigate the consequences of expressing varying levels of FMRP selectively in neurons of Fmr1 knockout and wild-type (WT) mice. A wide range of neuronal FMRP transgene levels was achieved in individual mice after intra-cerebroventricular administration of adeno-associated viral vectors coding for FMRP. In all treated knockout mice, prominent FMRP transgene expression was observed in forebrain structures, whereas lower levels were present in more caudal regions of the brain. Reduced levels of the synaptic protein PSD-95, elevated levels of the transcriptional modulator MeCP2, and abnormal motor activity, anxiety, and acoustic startle responses in Fmr1 knockout mice were fully or partially rescued after expression of FMRP at about 35–115% of WT expression, depending on the brain region examined. In the WT mouse, moderate FMRP over-expression of up to about twofold had little or no effect on PSD-95 and MeCP2 levels or on behavioral endophenotypes. In contrast, excessive over-expression in the Fmr1 knockout mouse forebrain (approximately 2.5–6-fold over WT) induced pathological motor hyperactivity and suppressed the startle response relative to WT mice. These results delineate a range of FMRP expression levels in the central nervous system that confer phenotypic improvement in fragile X mice. Collectively, these findings are pertinent to the development of long-term curative gene therapy strategies for treating Fragile X Syndrome and other neurodevelopmental disorders.

ID 30 – Influence of M1 hand knob ischemic stroke on motor activation: An fMRI study in chronic stage

Objective To evaluate whether stroke lesion focused on the primary motor cortex hand knob re-localizes the hand motor area in the affected hemisphere. Methods The study included 8 right-handed chronic ischemic stroke patients (2 females, age range: 48–68 years) with hand knob localized lesion (2 left hemisphere, 6 right hemisphere, at least 2 years from stroke). Block-design fMRI was performed using a 3T MR scanner during finger tapping task to both hemispheres. For the analysis, images with left hemisphere lesions were flipped. Differences between affected and unaffected hemispheres were tested with a paired t-test using a threshold of p T = 4.79), uncorrected for multiple comparisons. Results Significantly reduced motor activation in the affected hemisphere versus unaffected hemisphere was observed in the posterior part of precentral gyrus (hand-knob), pars opercularis and pars triangularis of the inferior frontal gyrus, inferior parietal cortex, intraparietal sulcus and lobule VI in cerebellum. Conclusions Reduction in the hand motor activation was observed in M1 in the affected hemisphere. Key message fMRI is capable to detect abnormal motor activation after focal stroke on hand knob area.

Abnormal Motor Activity and Thermoregulation in a Schizophrenia Rat Model for Translational Science.

BackgroundSchizophrenia is accompanied by altered motor activity and abnormal thermoregulation; therefore, the presence of these symptoms can enhance the face validity of a schizophrenia animal model. The goal was to characterize these parameters in freely moving condition of a new substrain of rats showing several schizophrenia-related alterations.MethodsMale Wistar rats were used: the new substrain housed individually (for four weeks) and treated subchronically with ketamine, and naive animals without any manipulations. Adult animals were implanted with E-Mitter transponders intraabdominally to record body temperature and locomotor activity continuously. The circadian rhythm of these parameters and the acute effects of changes in light conditions were analyzed under undisturbed circumstances, and the effects of different interventions (handling, bed changing or intraperitoneal vehicle injection) were also determined.ResultsDecreased motor activity with fragmented pattern was observed in the new substrain. However, these animals had higher body temperature during the active phase, and they showed wider range of its alterations, too. The changes in light conditions and different interventions produced blunted hyperactivity and altered body temperature responses in the new substrain. Poincaré plot analysis of body temperature revealed enhanced short- and long-term variabilities during the active phase compared to the inactive phase in both groups. Furthermore, the new substrain showed increased short- and long-term variabilities with lower degree of asymmetry suggesting autonomic dysregulation.ConclusionsIn summary, the new substrain with schizophrenia-related phenomena showed disturbed motor activity and thermoregulation suggesting that these objectively determined parameters can be biomarkers in translational research.

Pitx3 deficiency produces decreased dopamine signaling and induces motor deficits in Pitx3(−/−) mice

Midbrain dopamine (DA) neurons are involved in cognition, control of motor activity, and emotion-related behaviors. Degeneration of DA neurons particularly in the substantia nigra is a hallmark of Parkinson's disease. The homeobox transcription factor, Pitx3, plays a critical role in the development, function, and maintenance of midbrain DA neurons. We found that in young adult Pitx3-null mice, Pitx3(−/−), there was decreased tyrosine hydroxylase staining, indicating a loss of DA neurons particularly in the substantia nigra. In addition, fast-scan cyclic voltammetry and microdialysis assays of DA release indicated that the lack of Pitx3 caused a significant reduction of striatal DA release. Tonic DA release was impaired more significantly than the phasic DA release induced by burst firing of DA neurons. Furthermore, behavioral tests revealed that Pitx3(−/−) mice displayed abnormal motor activities, including impaired motor coordination and decreased locomotion. In summary, these data provide further evidence that Pitx3 is specifically required for DA-related function and, if impaired, Pitx3 could contribute during the pathogenesis of Parkinson's disease.

Spontaneous epileptic seizures in transgenic rats harboring a human ADNFLE missense mutation in the β2-subunit of the nicotinic acetylcholine receptor

We generated a transgenic rat strain with a missense mutation in V286L (V286L-TG), in the gene encoding the neuronal nicotinic acetylcholine receptor β2 subunit (CHRNB2) found in patients with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). To confirm that V286L-TG rats exhibit seizures similar to those observed in humans, gene expression patterns and behavioral phenotypes were analyzed. In situ hybridization using a V286L Chrnb2-selective probe indicated that the transgene was expressed at higher levels in the cortex, hippocampus, and cerebellum of V286L-TG than wild-type littermates (non-TG). Spontaneous epileptic seizures with ictal discharges in electroencephalograms were detected in 45% of V286L-TG rats and the frequency of seizures was 0.73 times a week. This seizure type is similar to “paroxysmal arousals” that are observed in human ADNFLE. V286L-TG rats displayed nicotine-induced abnormal motor activity including seizures in comparison to non-TGs. Response time following nicotine administration occurred faster in V286L-TG than in non-TG rats.V286L-TG rats demonstrated spontaneous epileptic seizures, which are similar to human ADNFLE, and also showed a higher sensitivity to nicotine administration. Thus, the V286L-TG rat model could be a valuable tool for developing novel mechanism-driven treatment strategies for epilepsy and provide a better understanding of ADNFLE.

Lack of neuronal nitric oxide synthase results in attention deficit hyperactivity disorder-like behaviors in mice.

Nitric oxide (NO) is an important molecule for the proper development and function of the central nervous system. In this study, we investigated the behavioral alterations in the neuronal NO synthase knockout mice (NOS1 KO) with a deficient NO production mechanism in the brain, characterizing it as a potential rodent model for attention deficit hyperactivity disorder (ADHD). NOS1 KO exhibited higher locomotor activity than their wildtype counterparts in a novel environment, as measured by open field (OF) test. In a 2-way active avoidance paradigm (TWAA), we found sex-dependent effects, where male KO displayed deficits in avoidance and escape behavior, sustained higher incidences of shuttle crossings, and higher incidences of intertrial interval crossings, suggesting learning, and/or performance impairments. On the other hand, female KO demonstrated few deficits in TWAA. Molsidomine (MSD), a NO donor, rescued TWAA deficits in male KO when acutely administered before training. In a passive avoidance paradigm, KO of both sexes displayed significantly shorter step-through latencies after training. Further, abnormal spontaneous motor activity rhythms were found in the KO during the dark phase of the day, indicating dysregulation of rhythmic activities. These data indicate that NOS1 KO mimics certain ADHD-like behaviors and could potentially serve as a novel rodent model for ADHD.

Mechanism of gastrointestinal abnormal motor activity induced by cisplatin in conscious dogs.

To investigate whether 5-hydroxytryptamine (serotonin; 5-HT) is involved in mediating abnormal motor activity in dogs after cisplatin administration. After the dogs had been given a 2-wk recovery period, all of them were administered cisplatin, and the motor activity was recorded using strain gauge force transducers. Blood and intestinal fluid samples were collected to measure 5-HT for 24 h. To determine whether 5-HT in plasma or that in intestinal fluids is more closely related to abnormal motor activity we injected 5-HT into the bloodstream and the intestinal tract of the dogs. Cisplatin given intravenously produced abnormal motor activity that lasted up to 5 h. From 3 to 4 h after cisplatin administration, normal intact dogs exhibited retropropagation of motor activity accompanied by emesis. The concentration of 5-HT in plasma reached the peak at 4 h, and that in intestinal fluids reached the peak at 3 h. In normal intact dogs with resection of the vagus nerve that were administered kytril, cisplatin given intravenously did not produce abnormal motor activity. Intestinal serotonin administration did not produce abnormal motor activity, but intravenous serotonin administration did. After the intravenous administration of cisplatin, abnormal motor activity was produced in the involved vagus nerve and in the involved serotonergic neurons via another pathway. This study was the first to determine the relationship between 5-HT and emesis-induced motor activity.

Sleep bruxism and masseter muscle activity during rem sleep of rem sleep behavior disorder patients: a case control study

Introduction Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by abnormal and excessive motor activity in electromyographic (EMG) during REM sleep. Presence of sleep bBruxism (SB)/tooth grinding and oromandibular myoclonus (OMM) were investigated in RBD patients not taking medications in comparison to age matched control subjects (CTRL). Materials and methods Polygraphy sleep and oromotor activity data from 9 RBD patients (68.22 ± 3.63 y.o.) and 9 healthy CTRL (65.11 ± 3.95 y.o.) were analyzed. RBD patients were diagnosed by a neurologist and confirmed by sleep laboratory recording. Rhythmic masticatory muscle activity (RMMA), a marker of sleep bruxism, and oromandibular myoclonus were scored from jaw electromyographic recordings during sleep using published criteria (Lavigne 1996; Kato 1999). Results RBD patients had significantly higher index of RMMA/SB than CTRL during sleep (p 0.01). During REM sleep, RBD patients had significantly higher index of RMMA/SB episodes and bursts than CTRL subjects (p 0.001). During non-REM sleep, no significantly difference between RBD and CTRL was observed (p = 0.12). Compared to controls, the OMM episode and burst indexes were significantly higher in RBD patients (p = 0.04 and 0.03, respectively). Conclusion RBD patient’s not taking medication had significantly higher RMMA activity, a proxy of sleep bruxism diagnosis, than CTRL subjects over night and during REM sleep. The higher index of RMMA/SB during REM sleep of RBD patients suggest that activity in jaw closing muscles can be scored during sleep of suspected RBD patients. Furthermore, sleep bruxism occurring during REM may be a concomitant finding influencing the diagnosis and management of both SB and RBD. Acknowledgements (Supported by the Canadian Institutes of Health Research. grant from CIHR).

REM sleep behavior disorder and periodic leg movements in sleep in patients with amyotrophic lateral sclerosis

In the last few years, it has been increasingly recognized that patients with amyotrophic lateral sclerosis (ALS) frequently suffer of sleep-related complaints, including insomnia, restless legs syndrome, and daytime sleepiness, although, in the past, many of the nocturnal symptoms have been mainly ascribed to chronic respiratory insufficiency and hypoventilation. In addition, excluding few single cases reported, polysomnographic studies did not look for abnormal motor activity during sleep that could be indicative of Rapid Eye Movements (REM) sleep behavior disorder (RBD) and REM sleep without atonia (RSWA), which are highly prevalent in other neurodegenerative disorders with brainstem involvement. Finally, data on the presence of periodic leg movements in sleep (PLMS) in patients with ALS are sparse. We sought to assess sleep characteristics and the occurrence of abnormal muscle activity during sleep, such as RSWA, RBD, and PLMS in patients with ALS. Forty-one patients with ALS and 26 healthy subjects were submitted to clinical interview and overnight video-polysomnography. Twenty-two patients with ALS (53.6%) reported poor sleep quality. Polysomnographic studies showed that patients with ALS had reduced total time of sleep, increased wakefulness after sleep onset, shortened REM and slow wave sleep, and decreased sleep efficiency compared to control subjects. Polysomnographic abnormalities were not different in patients reporting good or poor sleep, and were not correlated to clinical and demographic variables. PLMS index was significantly higher in patients with ALS than in healthy subjects, and 22 patients (53.6%) showed a PLMS index > 15, vs 4 (15.4%) control subjects ( p < 0.001). Finally, two patients with ALS (4.9%) had RBD, and two more patients presented RSWA (4.9%), whereas no control subjects showed abnormalities of REM sleep. Patients with ALS frequently present abnormalities of sleep that can be documented both at the clinical interview and at the polysomnographic evaluation, including insomnia, fragmented sleep, and increased PLMS. Moreover, abnormalities of REM sleep can sometimes be found in these patients. The authors would like to thank Dr. A. Mattaliano, Ospedale Civico ARNAS of Palermo, Dr. V. La Bella, University of Palermo-Italy, and Dr. G. Borghero, University of Cagliari-Italy, for their important contribution.

Pallidal stimulation for cervical dystonia does not correct abnormal temporal discrimination

We investigated whether clinical improvement observed after deep brain stimulation (DBS) of the globus pallidus internus (GPi) in cervical dystonia (CD) is paralleled by the normalisation of temporal discrimination thresholds (TDTs), a marker of abnormal sensory processing in CD. TDT was tested in 11 patients with CD after they received DBS and was compared with TDT scores from 24 patients with CD and a group of 61 controls. A clear clinical response to GPi-DBS was demonstrated (total Toronto Western Spasmodic Torticollis Rating Scale scores fell from 50 to 18; P < 0.001). In contrast, TDT remained abnormal in the CD-DBS group (P < 0.001) and was not significantly different from the abnormal TDT range observed in CD. Underlying sensory abnormalities in temporal discrimination observed in dystonia do not seem to be corrected by successful GPi-DBS. This adds further data to the ongoing debate regarding which pathophysiological abnormalities observed in dystonia are likely to be causal in the genesis of the disease rather than epiphenomena observed secondary to abnormal motor activity.

Enteric dysmotility/acquired chronic intestinal pseudoobstruction (ED/CIPO): relationship between symptoms, small intestinal manometric abnormalities and neurohistopathological findings

IntroductionEnteric dysmotility is an important clinical subgroup of the gastrointestinal neuromuscular disorders.1 Of a personal series of 130 patients recorded on our data base 89 have undergone both 24 h...

Long-lasting effects of social isolation and NMDA-antagonist treatment on thermoregulation and motor activity.

Event Abstract Back to Event Long-lasting effects of social isolation and NMDA-antagonist treatment on thermoregulation and motor activity. G. Horvath1, G. Adam1, Z. Petrovszki1 and G. Benedek1 1 University of Szeged, Department of Physiology, Hungary Clinical studies have proved that schizophrenia can be accompanied by abnormal thermoregulation and motor activity. We induced schizophrenia-related alterations in rats to examine their effects on the motor activity and body temperature in awake, freely moving rats. Methods: Male Wistar rats (day 21 of age) were either housed individually and treated with ketamine for 4 weeks or grouped without any treatments. At the age between 4 and 6 month animals were implanted with Mini-Mitter biotelemeters, and after one week recovery period core body temperature and activity were recorded for six days (12 h LD cycle) in temperature controlled room. Results: Both groups showed circadian rhythm of body temperature and motor activity, however, body temperature of schizophrenic rats was significantly lower compared to control animals during the active period. As regards the locomotor activity, a trend for decreased activity was observed in the active phase in treated animals. In new environment both groups showed increased activity for about 30 min and an enhanced body temperature for about 1 hour. The treated group showed significantly decreased temperature at the first 10 min. Our results suggest that this treatment paradigm produced sustained alterations in these parameters, and highlight the importance of juvenile period in the development of thermoregulation and motor activity. Acknowledgements This work was supported by the TÁMOP 4.2.2.-08/01-2008-0002 and a Hungarian Research Grant (OTKA, K68594). Keywords: Behaviour and cognition, Neuroscience Conference: 13th Conference of the Hungarian Neuroscience Society (MITT), Budapest, Hungary, 20 Jan - 22 Jan, 2011. Presentation Type: Abstract Topic: Behaviour and cognition Citation: Horvath G, Adam G, Petrovszki Z and Benedek G (2011). Long-lasting effects of social isolation and NMDA-antagonist treatment on thermoregulation and motor activity.. Front. Neurosci. Conference Abstract: 13th Conference of the Hungarian Neuroscience Society (MITT). doi: 10.3389/conf.fnins.2011.84.00138 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Mar 2011; Published Online: 23 Mar 2011. Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers G. Horvath G. Adam Z. Petrovszki G. Benedek Google G. Horvath G. Adam Z. Petrovszki G. Benedek Google Scholar G. Horvath G. Adam Z. Petrovszki G. Benedek PubMed G. Horvath G. Adam Z. Petrovszki G. Benedek Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Abnormal motor activity during anaesthesia in a dog: a case report

Seizures or convulsions that occur during anaesthesia in veterinary patients are infrequently reported in the literature. Consequently, the incidence of such events is unknown. Several drugs commonly used in clinical veterinary anaesthesia have been shown to induce epileptiform activity in both human clinical patients and experimental candidates. The present case report describes convulsions in a four-year old male Bernese mountain dog during maintenance of anaesthesia with isoflurane after premedication with acepromazine and methadone followed by co-induction with propofol and ketamine. The dog had no history of previous convulsions. The use of several sedative and anaesthetic drugs makes it difficult to find one single causative pharmaceutical.

Resting Electromyographic Activity of Deep Thoracic Transversospinalis Muscles Identified as Abnormal With Palpation

In the 1940s, osteopathic researchers suggested that paraspinal tissue abnormality was associated with spontaneous muscle activity, but few studies have since re-examined these reports. To determine whether abnormal motor activity plays a role in deep paraspinal tissues that appear abnormal to palpation. Using an observational study design, the PVG of participants with thoracic pain were palpated by two examiners for consensus on the most marked level of tissue abnormality. Dual fine-wire, intramuscular electrodes were inserted into the deep transversospinalis (multifidus, rotatores) muscles at the abnormal level and at two normal sites (above and below the abnormal level). Surface electrodes were placed over the erector spinae muscles adjacent to each intramuscular electrode site. Electromyography signals were recorded during initial prone resting, three maximal voluntary isometric contractions (MVIC), and a second prone resting. The area under the curve for a 2-second period was analyzed for each condition, and values were normalized and reported as a percentage of MVIC. Data were analyzed using a 2-factor repeated-measures analysis of variance. Twenty-five participants with mean (SD) thoracic pain of 3.3 (1.9) on a 0 to 10 visual analog pain scale completed the study protocol. There were no statistically significant differences in normalized resting activity between the three intramuscular sites (P=.25) or between the three surface sites (P=.33). Substantial variability in normalized resting activity at each of the three intramuscular sites was evident (mean [SD] percent of MVIC: abnormal 7.83 [8.76]; normal 9.47 [8.45], 6.65 [7.39]). No statistically significant differences existed in the intramuscular EMG values between the two resting baseline periods (P=.10). The lack of statistically significant differences between EMG activity at the abnormal and normal paraspinal sites suggests that factors other than muscle activity are responsible for the apparent abnormality of these tissues to palpation. Investigation of these regions for increased tissue fluid and inflammatory mediators is recommended.

Gastrointestinal system

The functions of the gastrointestinal (GI) tract include digestion, absorption, excretion, and protection. In this review, we focus on the electrical activity of the stomach and small intestine, which underlies the motility of these organs, and where the most detailed systems descriptions and computational models have been based to date. Much of this discussion is also applicable to the rest of the GI tract. This review covers four major spatial scales: cell, tissue, organ, and torso, and discusses the methods of investigation and the challenges associated with each. We begin by describing the origin of the electrical activity in the interstitial cells of Cajal, and its spread to smooth muscle cells. The spread of electrical activity through the stomach and small intestine is then described, followed by the resultant electrical and magnetic activity that may be recorded on the body surface. A number of common and highly symptomatic GI conditions involve abnormal electrical and/or motor activity, which are often termed functional disorders. In the last section of this review we address approaches being used to characterize and diagnose abnormalities in the electrical activity and how these might be applied in the clinical setting. The understanding of electrophysiology and motility of the GI system remains a challenging field, and the review discusses how biophysically based mathematical models can help to bridge gaps in our current knowledge, through integration of otherwise separate concepts.

Identification of abnormal motor cortex activation patterns in children with cerebral palsy by functional near-infrared spectroscopy.

We demonstrate the utility of functional near-infrared spectroscopy (fNIRS) as a tool for physicians to study cortical plasticity in children with cerebral palsy (CP). Motor cortex activation patterns were studied in five healthy children and five children with CP (8.4+/-2.3 years old in both groups) performing a finger-tapping protocol. Spatial (distance from center and area difference) and temporal (duration and time-to-peak) image metrics are proposed as potential biomarkers for differentiating abnormal cortical activation in children with CP from healthy pediatric controls. In addition, a similarity image-analysis concept is presented that unveils areas that have similar activation patterns as that of the maximum activation area, but are not discernible by visual inspection of standard activation images. Metrics derived from the images presenting areas of similarity are shown to be sensitive identifiers of abnormal activation patterns in children with CP. Importantly, the proposed similarity concept and related metrics may be applicable to other studies for the identification of cortical activation patterns by fNIRS.

Understanding Motor Impairment in the Paretic Lower Limb After a Stroke: A Review of the Literature

In addition to muscle weakness caused by injury to supraspinal centers, several mechanisms may contribute to motor impairment in the paretic lower limb following a stroke. Physiological changes in the paretic muscles and their motor units, passive or active restraint of agonist activation, and abnormal muscle activation patterns have been shown to occur after a stroke and to reduce muscle force generation. Other factors such as increased passive tone may impede agonist and antagonist muscle torque generation, while abnormal motor activation and altered motor control of muscles can produce abnormal gait patterns. Co-activation of opposing lower limb muscles contributes to joint stiffness and postural stability; abnormal co-activation in paretic lower limbs can lead to deficits in postural stabilization. Abnormal timing of muscle activation can also yield reduced muscle work output and, in turn, reduced limb function. When sensory deficits accompany muscle weakness, impaired processing of afferent signals may contribute to abnormal muscle activation, abnormal gait patterns, and abnormal responses to perturbation during gait and stance. This article reviews the impact of these various factors, individually and in combination, on impaired motor function in the paretic lower limb after a stroke.

Normal interhemispheric inhibition in persistent developmental stuttering

Imaging studies suggest a right hemispheric (pre)motor overactivity in patients with persistent developmental stuttering (PDS). The interhemispheric inhibition (IHI) studied with transcranial magnetic stimulation is an established measure of the interplay between right and left motor areas. We assessed IHI in 15 young male adults with PDS and 15 age-matched fluent-speaking subjects. We additionally studied the ipsilateral silent period (iSP) duration. We found no significant between-group difference for IHI or for iSP duration. We conclude that the interplay between the primary motor cortices is normal in patients with PDS. The abnormal right motor and premotor activity observed in functional imaging studies on PDS are not likely to reflect altered primary motor cortex excitability, but are likely to have a different origin.