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Intracisternal antisense oligonucleotide to growth associated protein-43 blocks the recovery-promoting effects of basic fibroblast growth factor after focal stroke.

Focal infarction (stroke) of the lateral cerebral cortex of rats (including the sensorimotor cortex) produces deficits in sensorimotor function of the contralateral limbs that recover partially over time. In previous studies, we found that the intracisternal injection of basic fibroblast growth factor (bFGF), a potent neurotrophic growth factor, starting at 1 day after stroke, significantly enhanced recovery of sensorimotor function of the contralateral forelimb and hindlimb. Moreover, immunoreactivity (IR) for growth-associated protein-43 (GAP-43), a molecular marker of new axonal growth, was increased in the intact contralateral sensorimotor cortex following bFGF treatment. In the current study, we found that the intracisternal administration of antisense, but not missense, oligonucleotide to GAP-43 blocked the recovery-enhancing effects of bFGF and blocked the increase in GAP-43 IR in the contralateral cortex. These results suggest that upregulation of GAP-43 expression and consequent enhanced axonal sprouting in intact uninjured parts of the brain are likely mechanisms for the recovery-promoting effects of bFGF.

Animals↗

Gait and balance dysfunction: a model of the interaction of age and disease.

This article reviews age-associated changes in gait, balance, and sensorimotor function and contrasts them to the changes that occur as a result of disease. Strength peaks in the mid-20s but declines only modestly until the fifth decade, after which there is rapid decline. All aspects of sensory function diminish with age, resulting in modest sensory changes in older patients. Gait speed is stable until the seventh decade and thereafter slows modestly. Age-related changes in the balance of older persons result in an effective response that meets routine needs but may be ineffective under demanding circumstances capable of producing response. Thus, these modest age-related decrements may be an element in the increased incidence of falls in older people. The loss of function caused by disease is of greater magnitude as well as being superimposed on that caused by age and thus may lead to a failure of mobility. Neurologic diseases that impair sensorimotor function compromise mobility in a manner consistent with the deficits that they produce. In mobility dysfunction caused by white matter lesions, the gait/balance abnormalities may not have unique clinical features, making diagnosis difficult. We used quantitative MRI to study the brains of older subjects with mobility impairment. The volume of white matter lesions in mobility-impaired subjects was double that of controls and was unrelated to increasing age, suggesting that white matter lesions are a disease-related rather than an age-related occurrence. We also used stance perturbation evoked potentials to demonstrate delayed conduction in some mobility-impaired older subjects. Prolonged sensory conduction may contribute to maladaptive balance and thus may be useful for diagnosis. Contemporary imaging and neurophysiology thus provides insight into the pathophysiology of mobility impairment and allows for more accurate diagnosis.

Aging↗

Human bone marrow stem cells exhibit neural phenotypes and ameliorate neurological deficits after grafting into the ischemic brain of rats.

There is now evidence to suggest that bone marrow mesenchymal stem cells (MSCs) not only differentiate into mesodermal cells, but can also adopt the fate of endodermal and ectodermal cell types. In this study, we addressed the hypotheses that human MSCs can differentiate into neural cells when implanted in the brain and restore sensorimotor function after experimental stroke. Purified human MSCs were grafted into the cortex surrounding the area of infarction 1 week after cortical brain ischemia in rats. Two and 6 weeks after transplantation animals were assessed for sensorimotor function and then sacrificed for histological examination. Ischemic rats that received human MSCs exhibited significantly improved functional performance in limb placement test. Histological analyses revealed that transplanted human MSCs expressed markers for astrocytes (GFAP(+)), oligodendroglia (GalC(+)), and neurons (beta III(+), NF160(+), NF200(+), hNSE(+), and hNF70(+)). The morphological features of the grafted cells, however, were spherical in nature with few processes. Therefore, it is unlikely that the functional recovery observed by the ischemic rats with human MSC grafts was mediated by the integration of new "neuronal" cells into the circuitry of the host brain. The observed functional improvement might have been mediated by proteins secreted by transplanted hMSCs, which could have upregulated host brain plasticity in response to experimental stroke.

Adolescent↗

[Allocation of cognitive resources during the simultaneous performance of cognitive and sensorimotor tasks].

We review research on the allocation of cognitive resources during the simultaneous performance of cognitive and sensorimotor tasks. From the developmental and clinical perspectives,we emphasize: (1) the distinction between the availability and the allocation of resources, (2) lifespan changes in relation to the environmental validity of sensorimotor functions, and (3) the potentials and limitations for an individuals' adaptations to multi-task constraints. These aspects can be operationalized within the framework of selection, optimization, and compensation (SOC). Related studies focus on older individuals' selective resource allocation and compensatory processes as adaptive means in the context of reduced resources and decreased sensorimotor functioning. Results show that older adults must invest increasing amounts of their cognitive resources into the coordination of bodily functions such as balance and gait. SOC research on Alzheimer's patients provides new insights into the increased risks of falling. We argue that adaptive resource allocation in everyday sensorimotor performance is an instance of intelligent behavior that is insufficiently represented in extant psychometric tests.

Accidental Falls↗

Parallel and serial processing of haptic information in man: effects of parietal lesions on sensorimotor hand function.

Recent animal studies have shown that there is an evolutionary shift within the order of primates from parallel to serial processing of haptic information. In an attempt to determine whether there is also evidence of serial processing in humans 10 patients with parietal cortical lesions, three patients with subcortical lesions and one patient after hemispherectomy, were examined. Case-by-case and across subject analysis of lesion type, sensorimotor profile and electrophysiological findings showed that in unihemispheric lesions: (a) there is little impairment of thermesthesia, nociception and vibration sense: (b) two-point discrimination and integrity of the N20 somatosensory component are highly correlated; (c) a loss of the N20 component is accompanied by a severe impairment of stereognosis; (d) conversely, in more posterior lesions astereognosis can occur with an intact N20 component; and (e) if the lesion is in the right hemisphere there is frequently impairment of graphesthesia in both hands. These data are taken to indicate serial processing from SI (as evidenced by an intact N20 component) to posterior parietal cortex allowing progressive spatial and temporal integration. In graphesthesia our data suggest an integrative function of the right parietal cortex for both sides of the body. Other sensory qualities like vibration nociception and thermesthesia are apparently processed in a non-serial, probably parallel way involving both hemispheres. The effects of cerebral lesions in our series suggest parallel as well as serial processing of somesthetic information in man underlying the perception of different haptic features.

Adult↗

Effects of duodenal lipids on gastric sensitivity and relaxation in patients with ulcer-like and dysmotility-like dyspepsia.

BACKGROUND/AIMS: Functional dyspepsia (FD) according to Rome II is divided into ulcer-like dyspepsia (ULD) and dysmotility-like dyspepsia (DLD). The rationale behind this is the assumption that the underlying pathophysiology is different, but this is largely unexplored. Our aim was to elucidate the differences in gastric sensorimotor function in these subgroups of FD. 13 healthy controls (HC) and 20 patients with FD, 10 ULD and 10 DLD, were included. METHODS: A feeding tube was placed fluoroscopically in the proximal duodenum and a barostat balloon was placed in the proximal stomach. Sensory thresholds to gastric distention for first sensation, bloating and discomfort were assessed before and after duodenal lipid infusion (2 kcal/min, 60 min). RESULTS: Volume changes in the balloon were recorded as a measure of gastric tone. In FD patients, sensory thresholds in the fasting state were significantly lower than in HC, mostly due to gastric hypersensitivity in ULD. After lipid infusion, 95% of FD patients fell outside the normal range of HC for first sensation, bloating and/or discomfort, compared with 65% in the fasting state. Patients with ULD but not DLD had impaired fundic relaxation after duodenal lipids compared with HC. CONCLUSIONS: Investigating gastric sensorimotor function after duodenal lipid infusion, FD patients can accurately be differentiated from HC. Impaired fundic relaxation seems to be more common in patients with ULD.

Adult↗

Recovery of function and basal ganglia [14C]2-deoxyglucose uptake after nigrostriatal injury.

Rats with unilateral 6-hydroxydopamine injections along the mesotelencephalic dopaminergic projection showed a profound impairment in localizing somatosensory stimuli on the contralateral body surface at 3 days postoperatively. Approximately one-half of the affected animals recovered the ability to localize tactile stimuli during 6 weeks postoperatively, whereas the remainder did not. When it occurred, the recovery of sensorimotor function began between the third and fifth day postoperatively and plateaued between days 14 and 21. Unilateral damage to these dopaminergic neurons resulted in hemispheric asymmetries of [14C]2-deoxyglucose incorporation at 3 days postoperatively. For structures that normally receive a dopaminergic innervation (e.g., neostriatum, nucleus accumbens septi, olfactory tubercle) the autoradiographic density of the injured side was decreased relative to the intact hemisphere. For structures that receive striatal inputs (globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata), the autoradiographic density was increased on the side of the injury. This pattern of altered [14C]2-deoxyglucose incorporation was still present at 6 weeks postoperatively in animals that showed no recovery of somatosensory localization during that time. In contrast, rats that did recover showed no hemispheric asymmetries within the anterior neostriatum, globus pallidus, or substantia nigra pars reticulata at 6 weeks postoperatively, and the time course of normalization of metabolic activity in these structures was similar to that for behavioral restoration. These results directly demonstrate the importance of the neostriatum and particular structures efferent to it in the recovery of sensorimotor functions after striatal dopamine depletion. The types of neuronal plasticity within this basal ganglia circuitry responsible for the normalization of [14C]2-deoxyglucose incorporation and behavior are discussed.

Afferent Pathways↗

Efficacy of Prophylactic Ankle Support: An Experimental Perspective.

OBJECTIVE: To provide a comprehensive review of the literature regarding the role of external ankle support on joint kinematics, joint kinetics, sensorimotor function, and functional performance. DATA SOURCES: We searched MEDLINE and SPORT Discus databases from 1960-2001 for the key words ankle bracing, ankle support, ankle taping, and ankle prophylaxes. We also used personal libraries based on our own research to complement the existing literature. DATA SYNTHESIS: The effects of external ankle support have been studied on a plethora of dependent measures. Here, we specifically discuss the role of external ankle support on joint kinematics, joint kinetics, sensorimotor function, and functional performance and present a general consensus regarding the overall effects of these prophylactic devices. CONCLUSIONS/RECOMMENDATIONS: The effects of ankle support on joint kinematics during static joint assessment and on traditional functional-performance measures (ie, agility, sprint speed, vertical jump height) are well understood. However, the potential effects of ankle support on joint kinetics, joint kinematics during dynamic activity (eg, a cutting maneuver), and various sensorimotor measures are not well known. Future research investigating the role of external ankle bracing needs to focus on these areas.

Journal Article↗

MEG response to median nerve stimulation correlates with recovery of sensory and motor function after stroke.

OBJECTIVE: Hemiparesis due to damage by stroke in primary motor cortex (MI) or its underlying projections presents a problem for functional neuroimaging technologies that attempt to evaluate the neurophysiological basis for restoration of motor function. Traditional assessments of MI function require patients to move their fingers, hands, or limbs, which can be either impossible or markedly compromised after stroke. We recently demonstrated in normal subjects that magnetoencephalography (MEG), a non-invasive neuromagnetic functional imaging technique, detects neuronal response elicited by electrical median nerve stimulation in MI, as well as primary somatosensory cortex (SI). In the present study, we used the MEG response from median nerve stimulation to investigate the recovery of primary motor and somatosensory in acute ischemic stroke patients. METHODS: Twelve patients with unilateral ischemic strokes that affected sensorimotor functions of their hand were studied in the acute stage (4.4+/-1.2 days, mean+/-SD) and during a 1-month follow-up (38.6+/-5.6 days, except for one patient's follow-up done 6 month after stroke). RESULTS: Among the multiple cortical sources localized after median nerve stimulation, one source localized to SI and another localized to the vicinity of MI. Changes in the source strengths of the first component post-stimulus of MI and SI correlated with the extent of recovery of sensorimotor functions as determined by neurological exams. CONCLUSIONS: This study provides a novel way of indirectly assessing MI function using MEG during the acute stroke phase, when many patients often cannot perform motor tasks due to paralysis.

Adult↗

Human umbilical cord blood cells do not improve sensorimotor or cognitive outcome following transient middle cerebral artery occlusion in rats.

The present study investigated effects of human umbilical cord blood (HUCB) cells on sensorimotor, cognitive, and histological outcome in rats subjected to transient middle cerebral artery occlusion (MCAO). Halothane anesthetized adult male Wistar rats were subjected to transient MCAO for 2 h. HUCB cells (mononuclear 1-5x10(7) or Lin(-) cells 1-5x10(5)) were administered intravenously after 24 h recovery. The limb-placing test was performed on postoperative days 2, 4, 6, 9, 12, 16, and 20. In addition, beam-walking and cylinder tests were used to assess sensorimotor function at baseline, and on postoperative days 4, 12, and 20. Morris water-maze was used to assess cognitive performance on postoperative days 22-24. Subsequently, rats were perfused for measurement of infarct volumes and detection of HUCB cells by immunohistochemistry (MAB1281). MCAO rats showed a partial spontaneous recovery in sensorimotor function during the follow-up. However, the recovery profile was similar in MCAO controls and in MCAO rats that received HUCB cells. HUCB did not affect impaired water-maze performance of MCAO rats. Only few human nuclei-specific MAB1281-positive cells were detected in the ipsilateral hemisphere in MCAO rats that received HUCB cells. Infarct volumes did not differ between the experimental groups. A group of additional rats were used to further study biodistribution of intravenously given (111)In-oxine-labelled mononuclear HUCB cells in MCAO and sham-operated rats. SPECT imaging data indicated a high tracer uptake in the lung, liver, spleen, and kidney, but not in the brain immediately after administration or 24 h post-administration. The present study suggests that HUCB cells do not improve functional recovery or histological outcome in MCAO rats after systemic administration because of limited migration of cells in the ischemic brain.

Analysis of Variance↗

Posture-independent sensorimotor analysis of inter-hemispheric receptor asymmetries in neostriatum.

Nigrostriatal dopaminergic neurons are thought to be critically important for somato-sensorimotor behavior. Following unilateral irreversible elimination of these neurons, an animal shows an ipsiversive postural bias and permanently fails to orient its head toward tactile stimuli placed on the contralateral side of the body. In response to apomorphine, a dopamine agonist, these rats display contraversive circling. This effect is thought to reflect denervation-induced proliferation of dopamine receptors in the ipsilateral striatum. We have developed a sensitive procedure that measures sensorimotor function independent of postural and circling biases. We record the latencies to remove small pieces of adhesive stimuli placed onto the snout or radial surface of the forelimbs. The stimuli are placed symmetrically and simultaneously, which is analogous to tactile-extinction procedures used clinically. In the first study we found that rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the nigrostriatal pathway showed a contralateral sensorimotor bias in response to doses of apomorphine below those necessary to produce contraversive circling. In a second study, unilateral striatal microinjections of kainic acid (KA) were used to destroy the neurons on which the postsynaptic dopaminergic receptors of the nigrostriatal system are contained. Compared to 6-OHDA, KA produced unexpected results in standard orientation tests. None of the KA-treated rats showed contralateral neglect, and some even showed ipsilateral deficits. However, the standard orientation tests are confounded by postural asymmetries, which were irregular in the KA-treated group. Using again the posture-independent sensorimotor procedure, we found that all KA-treated rats, like the 6-OHDA-treated rats, uniformly displayed ipsilateral sensorimotor biases. Sensorimotor function relating to inter-striatal asymmetries may be more specifically assessed with the bilateral-adhesive tests.

Animals↗

Parvalbumin-containing GABAergic neurons in the basal ganglia output system of the rat.

The output of the basal ganglia is directed through the entopeduncular nucleus (EPN) and the substantia nigra pars reticulata (SNR) and pars lateralis (SNL), which provide a gamma-aminobutyric acidergic (GABAergic) projection to various nuclei of the thalamus and brainstem. Although many neurons within the SNR and EPN have been described as modality specific, the morphological and neurochemical similarities preclude their precise identification. In the present study, the immunocytochemical localization of parvalbumin, a calcium-binding protein, is used in combination with axonal tracing to verify neuronal heterogeneity within the SNR, SNL, and EPN. The results reveal that the majority of neurons in all three centers contain parvalbumin. The parvalbumin-containing neurons are distributed in the caudal two-thirds of the EPN, the rostral part of the SNL, and the lateral two-thirds of the entire rostrocaudal extent of the SNR, the areas involved in sensorimotor function of the basal ganglia. Moreover, the nigrothalamic, nigrocollicular, and EPN-thalamic neurons possess parvalbumin immunoreactivity, whereas the EPN-habenular neurons are devoid of parvalbumin immunoreactivity. The results indicate a neurochemical heterogeneity within the GABAergic output neurons of the basal ganglia and suggest that the parvalbumin-containing neurons of the SNR, SNL, and EPN are the tonically active output neurons that form a major link in the disinhibitory neuronal circuit of the basal ganglia, especially that concerned with sensorimotor function.

Animals↗

Chronic lithium administration alters behavioral recovery from nigrostriatal injury: effects on neostriatal [3H]spiroperidol binding sites.

Unilateral damage to the mesotelencephalic dopaminergic projection of the rat produces impairments in sensorimotor functions, including an inability to localize contralateral somatosensory stimuli. Many rats with 6 hydroxydopamine injections along this pathway show a gradual improvement in somatosensory localization during the first post-operative month. One mechanism that may contribute to this behavioral recovery is the proliferation of dopamine receptor sites in the affected neostriatum. The role of these binding site changes in the recovery was tested by chronic administration of lithium to rats. Rats given lithium in their drinking water for 4 weeks after the 6-hydroxydopamine injection showed a greatly attenuated recovery of sensorimotor functions, compared to brain-damaged rats drinking unadulterated water. When rats that were given lithium for the first four postoperative weeks were subsequently given unadulterated water to drink, they recovered normally. Lithium treatment did not prevent the augmentation of [3H]spiroperidol binding in the neostriatum ipsilateral to the lesion, relative to the contralateral control neostriatum, at 4 or 8 weeks post-operatively. Thus, lithium treatment dissociates behavioral recovery after nigrostriatal injury from the lesion-induced relative proliferation of neostriatal [3H]spiroperidol binding sites. However, the lithium treatment decreased the absolute amount of specific [3H]spiroperidol binding to both the ipsilateral and contralateral neostriata. The significance of these findings for the neural mechanism underlying this recovery sequence is discussed.

Animals↗

Prehension movements and motor development in children.

The maturation of manual dexterity and other sensorimotor functions was assessed with various behavioural tests. In healthy children (age 4-5 years) and in adults, the kinematics of reaching and grasping, a bimanual task and fast repetitive tapping movements were analysed. Furthermore a comprehensive motor function score (MOT), probing agility and balance, was evaluated. In the prehension task, the straightness of the reaching trajectories increased with age. Children opened their grip relatively wider than adults, thus grasping with a higher safety margin. The speed of both tapping and bimanual movements increased with age, and higher scores were reached in the MOT. Although the different behavioural tests sensitively indicated maturational changes, their results were generally not correlated, i.e. the outcome of a particular test could not predict the results of other tasks. Hence there is no simple and uniform relationship between different behavioural data describing maturation of sensorimotor functions.

Adult↗

Chronic infusion of GABA into the nucleus basalis magnocellularis or frontal cortex of rats: a behavioral and histological study.

In order to determine the influence of the nucleus basalis magnocellularis (NBM) on the sensorimotor function of the frontal cortex (FCx) of the rat, GABA at various concentrations (10, 50 or 100 micrograms.microliters-1) was administered into these structures. GABA was infused for four consecutive days after which saline was infused for another four. On the contralateral side the order of administration was reversed. Each structure received GABA while its homologous on the contralateral side received saline. Before, during and after drug infusion, the animals were weighted and their performance in two non-reinforced behavioral tasks (beam walking and spontaneous rotation) was examined. When GABA was infused into the FCx, a dose-dependent and reversible sensorimotor deficit was observed along with a behavioral withdrawal syndrome upon GABA discontinuation. When GABA was administered into the NBM, a reversible sensorimotor deficit was observed only when GABA was infused at the highest concentration. In this case no behavioral changes were observed upon GABA discontinuation. Histologically, a gliosis was observed in the NBM in which GABA was infused at the two highest concentrations without saline pretreatment; these effects were not observed when GABA was infused without saline pretreatment into the FCx. In relation to our previous findings, these results suggest that i) the FCx is directly involved in the expression of sensorimotor functions, while the influence of the NBM on these functions appears only after severe subcortical damage, ii) a GABA withdrawal syndrome is observed following GABA administration in the FCx but not in the NBM, and iii) "tonic" effects of GABA are dose-related and partially dependent upon pretreatment conditions and the brain region infused.

Analysis of Variance↗

Gonadectomy impairs T-maze acquisition in adult male rats.

Recent studies have shown that chronic gonadectomy increases the density of dopaminergic axons in prefrontal but not sensorimotor cortices in adult male rats. Since supranormal prefrontal cortical dopamine stimulation is known to impair rats' performance in T-maze delayed alternation paradigms, we tested whether long-term gonadectomy might also impair T-maze performance. For comparison, sensorimotor functions were also assessed. Adult male rats were gonadectomized and placebo-, estradiol-, or testosterone propionate-treated or were sham operated and placebo-treated. Four weeks after surgery, the subjects were tested using a rotorod apparatus and in the acquisition of a T-maze delayed alternation paradigm. Gonadectomized placebo-treated and estradiol-treated rats took significantly longer to acquire the T-maze rule than controls, and gonadectomized, testosterone-treated rats acquired the task within the same time frame as controls. No group differences were detected in rotorod performance. Thus, chronic gonadectomy induced testosterone-sensitive, estradiol-insensitive acquisition deficits in a spatial learning task but had no demonstrable effects on the sensorimotor functions tested.

Animals↗

Protective effects of moderate hypothermia after neonatal hypoxia-ischemia: short- and long-term outcome.

We have previously shown that mild hypothermia applied after hypoxia-ischemia in newborn piglets and rats reduces brain injury evaluated 3-7 d after the insult. The aim of the present study was to assess the neuroprotective efficacy of hypothermia with respect to short- (neuropathology) and long-term (neuropathology and sensorimotor function) outcome after hypoxia-ischemia in 7-d-old rats. One hundred fourteen animals from 13 litters survived either 1 or 6 wk after a hypoxic-ischemic insult. The animals were randomized to either 1) normothermic recovery for the whole 1- or 6-wk period or 2) cooling to a rectal temperature of 32.0 degrees C for the first 6 h followed by normothermic recovery with the dam. Hypothermia offered a uniform protection of 27, 35, 28, and 25% in cerebral cortex, hippocampus, basal ganglia, and thalamus, respectively, in the 1-wk survivors (n = 32). The corresponding values for the 6-wk survivors (n = 61) were 22, 28, 37, and 35%. There was a significant correlation between sensorimotor performance and infarct volume (r = 0.66; p < 0.001). However, the sensorimotor function was not significantly improved by hypothermia if all animals were included, but in female pups the total functional score was higher in the hypothermia group (150 +/- 35 versus 100 +/- 34, p < 0.0007) which corresponded to a marked (51%) reduction of the neuropathology score in this subgroup. This is the first neonatal study to show a long-term histopathologic protection of the brain after posthypoxic hypothermia.

Animals↗

Exercise can reverse quadriceps sensorimotor dysfunction that is associated with rheumatoid arthritis without exacerbating disease activity.

OBJECTIVES: To compare quadriceps sensorimotor function, lower limb functional performance and disability in patients with rheumatoid arthritis (RA) and healthy subjects, and to investigate the efficacy and safety of a brief rehabilitation regime. METHODS: Quadriceps strength, voluntary activation, proprioceptive acuity and the aggregate time [aggregate functional performance time (AFPT)] taken to perform four common activities [aggregate functional performance time (AFPT)] were compared between 103 RA patients who had lower limb involvement and 25 healthy subjects. In addition, disability (Health Assessment Questionnaire), clinical disease activity and the plasma concentration of proinflammatory cytokines were measured in the RA patients. In a follow-on randomized controlled trial of rehabilitation, these variables were used as baseline data for 93 of the RA patients, who were randomized to a rehabilitation or a control group. Changes in the variables were analysed within and between groups. RESULTS: Compared with healthy subjects, RA patients had weaker quadriceps [mean difference 157 N; 95% confidence interval (CI) 125-189], poorer activation (8%, 95% CI 4.5-15) and proprioceptive acuity (0.8 degrees, 95% CI 0.4-1.3) and took longer to perform the AFPT (34 s, CI 23.5-44.8). Rehabilitation increased quadriceps strength (mean increase 61 N, 95% CI 28-95) and voluntary activation (8%, 95% CI 3-12.4) and decreased the AFPT (12.3 s, 95% CI -2 to 27.7) and subjective disability (0.21 HAQ points, 95% CI 0-0.35) without exacerbating disease activity. All the improvements were maintained at the 6-month follow-up. There was no change during the control period. CONCLUSIONS: Patients with RA that affected their lower limb had quadriceps sensorimotor deficits that were associated with lower limb disability. A clinically applicable rehabilitation regime increased quadriceps sensorimotor function and decreased lower limb disability without exacerbating pain or disease activity. For patients with well-controlled RA that causes lower limb involvement, the regime is effective and safe.

Adult↗