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Results for “sensorimotor function”

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PubMed2001

Functional magnetic resonance imaging of reorganization in rat brain after stroke.

Functional recovery after stroke has been associated with brain plasticity; however, the exact relationship is unknown. We performed behavioral tests, functional MRI, and histology in a rat stroke model to assess the correlation between temporal changes in sensorimotor function, brain activation patterns, cerebral ischemic damage, and cerebrovascular reactivity. Unilateral stroke induced a large ipsilateral infarct and acute dysfunction of the contralateral forelimb, which significantly recovered at later stages. Forelimb impairment was accompanied by loss of stimulus-induced activation in the ipsilesional sensorimotor cortex; however, local tissue and perfusion were only moderately affected and cerebrovascular reactivity was preserved in this area. At 3 days after stroke, extensive activation-induced responses were detected in the contralesional hemisphere. After 14 days, we found reduced involvement of the contralesional hemisphere, and significant responses in the infarction periphery. Our data suggest that limb dysfunction is related to loss of brain activation in the ipsilesional sensorimotor cortex and that restoration of function is associated with biphasic recruitment of peri- and contralesional functional fields in the brain.

Animals↗

PubMed2005

Differentiation of hamstring short latency versus medium latency responses after tibia translation.

After injuries to the anterior cruciate ligament (ACL) a functional instability is frequently observed which has been attributed to a disturbed sensorimotor function. In light of the clinical importance of ACL injuries and the resulting functional instability, it is of enormous clinical interest to elucidate the role of sensorimotor pathways that involve the ACL. In animals and humans a direct reflex pathway between the ACL and the hamstrings has been shown. The onset latencies of responses reported after ventral tibia translation were around 40-50 ms (range 17.9-65) and were regarded as medium latency responses (MLR). However, ventral tibia translation should also induce a stretch of the hamstring muscles and evoke a short latency response (SLR). Before any muscle response after ventral tibia translation can be ascribed to anatomical structures, it is crucial to analyze the obtained muscle responses carefully. The aim of the present study was the development of an algorithm to differentiate SLR and MLR responses after ventral tibia translation. In ten healthy subjects reflex responses of the hamstrings after anterior tibia translation and after tendon taps on the biceps femoris tendon were evaluated. To investigate the influence of skin afferents, control experiments were performed after lidocain injection of the dorsal calf. The mean onset latency of the tendon jerk reflex was 21.9 +/- 3.1 ms (range 17.3 - 28.7 ms). Both SLR responses (mean onset latency: 20.3 +/- 3.5 ms; range 15.4 - 25.8) and MLR responses (mean onset latency: 38.9 +/- 4.2 ms; range 32.9 - 46.7) were obtained in all subjects. Skin afferents from the calf do not play a major role. The development of an evaluation algorithm is presented that allows a safe differentiation between these partly superimposed SLR and MLR components. It is demonstrated that by measuring the first part of the SLR from the onset to the first peak the end of the SLR can be predicted and that the onset latency of the MLR component can be assessed reliably. Possible reasons are discussed why previous studies only reported responses at MLR latencies. The fact that both SLR and MLR components can be observed after anterior tibia translation underlines the necessity to differentiate the responses before they can be ascribed to any anatomical structures. As a basis for future work the algorithm presented may become a useful tool to differentiate which afferent pathways play a role in initiating hamstring activity.

Adult↗

PubMed1998

The functional emergence of prefrontally-guided working memory systems in four- to eight-year-old children.

The neural processes that underlie the functional emergence of human cognitive functions, particularly those associated with the prefrontal cortex (PFC), are of growing interest to developmental psychologists and neuroscientists. Specifically, working memory functions have been correlated with PFC activity in nonhuman primates and adult humans but have not been extensively studied in children. We examined the developmental emergence of functions involved in working memory through the use of the Cambridge Neuropsychological Test Automated Battery (CANTAB), a computerized battery of nonverbal visually-presented neuropsychological tests designed to dissociate frontal from temporal lobe behavioral functions. Participants were normal children, aged 4-8 (n = 181) and a small group of young adults (n = 24) who completed measures of Spatial Memory Span, Spatial Working Memory, the Tower of London planning task, Visual Pattern and Spatial Recognition tasks, and a Set-Shifting task. Findings indicate a general age-related progression in ability levels on frontal lobe tasks, with 4-year-olds performing worse than 5- to 7-year-olds on all measures. Eight-year-olds are superior to younger children in their ability to solve complex problems but have not yet reached adult levels of performance on the most difficult items of the Tower of London and Spatial Working Memory tasks. We conclude that the development of working memory functions proceeds dimensionally, starting with refinement of basic perceptual and sensorimotor functions and culminating with the physiological maturation of widespread neural networks that integrate complex processing demands inherent to working memory tasks.

Adolescent↗

PubMed1998

Quadriceps weakness in osteoarthritis.

Involvement of the quadriceps muscle group in knee osteoarthritis is receiving increasing research interest. The motor and sensory functions of muscle are intimately linked, and deficits in the sensorimotor functions of the quadriceps have been identified and proposed as possible factors in the pathogenesis of knee osteoarthritis or as consequences of the disease. Weakness of the quadriceps as a clinical feature of knee osteoarthritis has been well recognized for some time, but causes for this weakness and its significance as a determinant of the patient's disability is only now being investigated. Rehabilitation regimens that increase quadriceps weakness also effect improvements in the patient's disability, but the length and cost most of these research regimens would be impractical in the clinical setting. More clinically practicable rehabilitation regimens need to be devised that could be implemented in the community, if the management of this chronic, prevalent condition is to be managed effectively and cost-effectively.

Disability Evaluation↗

PubMedDate not supplied

A functional fatiguing protocol and deceleration time of the shoulder from an internal rotation perturbation.

CONTEXT: Muscular fatigue impedes sensorimotor function and may increase the risk of shoulder injury during activity. The effects of fatigue on the sensorimotor system of the shoulder have been studied with various results. Deceleration times have been used to study neuromuscular control of the shoulder; however, no studies involving the effects of fatigue on deceleration times have been reported. OBJECTIVE: To compare shoulder deceleration times after a shoulder internal rotation perturbation before and after a repetitive throwing exercise protocol. DESIGN: A 2 x 2 repeated-measures design. SETTING: Exercise and sport injury laboratory. PATIENTS OR OTHER PARTICIPANTS: Twenty healthy, recreationally active men (age = 24.76 +/- 4.03 years, height = 178.41 +/- 8.36 cm, mass = 80.16 +/- 15.20 kg) volunteered to participate in the study. To ensure familiarity with the overhead motion, all subjects chosen had previously participated in an overhead throwing sport. INTERVENTION(S): The independent variables were time (preintervention and postintervention) and session (experimental and control). The intervention consisted of continuous overhead throwing. The subjects were considered fatigued when a 10% decrease in velocity was noted on 3 consecutive pitches. MAIN OUTCOME MEASURE(S): Time necessary to decelerate from an internal rotation perturbation. RESULTS: Deceleration time was significantly increased by the fatiguing intervention ( P = .001). CONCLUSIONS: The decreased ability to decelerate may be an adaptive response by the subjects to dissipate a lower percentage of force per second.

Journal Article↗

PubMed2005

Reduced basal activity and increased functional homogeneity in sensorimotor and striatum of a Parkinson's disease rat model: a functional MRI study.

Functional neuro-imaging studies of Parkinson's disease (PD) patients and animal models show inconsistent cortical responses to sensory stimulation: some present increased sensorimotor cortex activation contradicting classical basal ganglia-cortex circuitry models, whereas others show decreased activation. As functional neuro-imaging activation is defined as the signal difference between stimulation ON and stimulation OFF, reduced 'activation' can point to either increased neuronal activity during stimulation ON or to decreased basal neuronal activity during stimulation OFF. A unique non-invasive method that uses the temporal and the spatial variances of functional magnetic resonance imaging signal is employed here to compare basal neuronal activity levels and 'functional homogeneity' between groups. Based on the assumption that the temporal variance reflects average neuronal activity, the variance of activity within a predefined region is defined as the region's 'functional homogeneity', which is assumed to estimate neuronal synchronization. Comparison of temporal and spatial variances of the sensorimotor cortex and the striatum in the 6-hydroxydopamine (6-OHDA) PD rat model and a control rat group show bilaterally decreased temporal and spatial variances in the 6-OHDA rat group, suggesting bilateral reduction of basal neuronal activity levels together with an increase in local neuronal synchronization in line with classical basal ganglia-cortex circuit models.

Adrenergic Agents↗

PubMed2003

Delayed transplantation of fibroblasts genetically modified to secrete BDNF and NT-3 into a spinal cord injury site is associated with limited recovery of function.

Delivery of neurotrophic factors in acute models of spinal cord injury in adult rats can rescue axotomized neurons, promote axonal growth, and partially restore function. The extent to which repair and recovery of function can be achieved after chronic injury has received less attention. In the companion paper we show that transplanting fibroblasts genetically modified to produce neurotrophic factors into chronic (6-week) hemisection injuries results in sprouting, partial neuroprotection, but only limited regeneration. Here we describe functional consequences of this treatment using a series of behavioral tests. Adult rats received a complete unilateral C3/C4 hemisection and recovery from the injury was assessed over 5 weeks. At 6 weeks postoperative, the experimental group received grafts of a combination of fibroblasts modified to secrete BDNF or NT-3. The operated control groups received grafts of either gelfoam or gelfoam with fibroblasts expressing GFP into the lesion site. Behavioral recovery in the three groups was assessed over the next 10 weeks. Severe deficits with no recovery in any of the groups were observed in several tests (BBB, limb preference, narrow beam, horizontal rope test) that measure primarily motor function. Recovery was observed in the grid test, a measure of sensorimotor function, and the von Frey test, a measure of response to mechanical stimulation, but there were no differences between the operated control or experimental groups. Both groups also showed recovery from heat-induced hyperalgesia, with the experimental group exhibiting greater recovery than the operated control groups. In this test, delivery of neurotrophic factors from transplanted fibroblasts does not worsen responses to nociceptive stimuli and in fact appears to reduce hypersensitivity. Our data also demonstrate that additional damage to the spinal cord upon placement of a graft further compromises behavioral recovery for locomotor and postural function. Additional therapeutic interventions will be necessary to provide greater levels of recovery after chronic injuries.

Animals↗

PubMed1996

Benefits of aerobic exercise after stroke.

The debilitating loss of function after a stroke has both primary and secondary effects on sensorimotor function. Primary effects include paresis, paralysis, spasticity, and sensory-perceptual dysfunction due to upper motor neuron damage. Secondary effects, contractures and disuse muscle atrophy, are also debilitating. This paper presents theoretical and empirical benefits of aerobic exercise after stroke, issues relevant to measuring peak capacity, exercise training protocols, and the clinical use of aerobic exercise in this patient population. A stroke, and resulting hemiparesis, produces physiological changes in muscle fibres and muscle metabolism during exercise. These changes, along with comorbid cardiovascular disease, must be considered when exercising stroke patients. While few studies have measured peak exercise capacity in hemiparetic populations, it has been consistently observed in these studies that stroke patients have a lower functional capacity than healthy populations. Hemiparetic patients have low peak exercise responses probably due to a reduced number of motor units available for recruitment during dynamic exercise, the reduced oxidative capacity of paretic muscle, and decreased overall endurance. Consequently, traditional methods to predict aerobic capacity are not appropriate for use with stroke patients. Endurance exercise training is increasingly recognised as an important component in rehabilitation. An average improvement in maximal oxygen consumption (VO2max) of 13.3% in stroke patients who participated in a 10-week aerobic exercise training programme has been reported compared with controls. This study underscored the potential benefits of aerobic exercise training in stroke patients. In this paper, advantages and disadvantages of exercise modalities are discussed in relation to stroke patients. Recommendations are presented to maximise physical performance and minimise potential cardiac risks during exercise.

Cerebrovascular Disorders↗

PubMed2004

Hypoxic preconditioning confers long-term reduction of brain injury and improvement of neurological ability in immature rats.

Exposure to preconditioning (PC) hypoxia 24 h before a severe hypoxic-ischemic (HI) insult reduces development of injury in the immature brain. Several protective regimens have proved effective in the short-term but not in the long-term perspective. The aim of the present study, therefore, was to evaluate the PC effect on long-term morphologic and neurologic outcome in the developing brain. Six-day-old rats were subjected to hypoxia (36 degrees C, 8.0% O2; PC/HI group) and sham controls to normoxia (36 degrees C; HI group) for 3 h. Twenty-four hours later, all rats were exposed to cerebral HI produced by unilateral carotid artery occlusion combined with 1 h, 15 min of hypoxia (36 degrees C, 7.7% O2). A cylinder test was used to evaluate forelimb asymmetry to determine sensorimotor function at 4, 6, and 8 wk of age. Spatial/cognitive ability was assessed by Morris water maze trials at 7 wk of recovery. Neuropathologic analysis was performed 8 wk after insult. Brain damage was reduced (p<0.0001) in PC/HI (45.0+/-11.1 mm3) in comparison with HI (159.3+/-12.2 mm3) rats. A bias for using the ipsilateral forelimb in wall movements was observed in the cylinder test in HI compared with PC/HI rats at 4 (p<0.001), 6 (p<0.01), and 8 (p<0.0001) wk of age. Results of the Morris water maze test revealed differences (p<0.0001) in average path length between groups on the third and fourth day of trials. Hypoxic PC before HI reduced brain injury by 72% at 8 wk after the insult and provided long-term improvement of sensorimotor and spatial/cognitive functions.

Animals↗

PubMed1986

Age-related regional loss of caudate-putamen dopamine receptors revealed by quantitative autoradiography.

Senescent (26-28 months) Fischer 344 rats were shown to have a lower density of D2 sites (-36%) without any change in affinity in membranes prepared from homogenized caudate-putamen (CPU), as compared to young adult (5-6 months) rats. In additional rats prepared for quantitative autoradiography of [3H]spiroperidol binding, the loss was shown to be specific for and quite extensive (50-60%) in the lateral to ventrolateral region of the CPU. The region of the CPU that shows the major age-related loss of D2 sites is critically involved in sensorimotor functions; therefore this regional loss of D2 sites may contribute importantly to the sensorimotor deficits in aged rats.

Aging↗

PubMed1981

Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas.

The postoperative progress of 3 patients with spinal epidural hemorrhage, but without spinal fracture or dislocation, is presented. From the literature, 158 cases were collected of spontaneous spinal epidural hematoma treated surgically. Postoperative return of motor function was noted in 95.3%, 87%, and 45.3% of the patients with incomplete sensorimotor, incomplete sensory but complete motor, and complete sensorimotor lesions, respectively. Complete sensorimotor recovery occurred in 41.9%, 26.1%, and 11.3% of these 3 groups of patients, respectively. Recovery following surgical treatment depends on the severity of neurological deficits before treatment. However, the absence of motor or sensorimotor functions preoperatively does not necessarily indicate a poor prognosis.

Adult↗

PubMed2005

Functional MRI localizing in the cerebellum.

Mapping of cerebellar function by functional MRI now enables us not only to re-establish older anatomic findings of somatotopic representations but to gain new insights in the function of the cerebellum and its intimate relations of cerebral regions to serving sensorimotor function, sensory discrimination, and cognitive processing. Consequently, it will change our understanding of neurologic and psychologic failures in patients with inborn errors or neurodegenerative diseases or after neurosurgical procedures.

Brain Mapping↗

PubMed1992

Comparison of screening approaches.

Neurobehavioral techniques have been used extensively in animal toxicology studies because, in many cases, such procedures are designed to evaluate neurobiological functions thought to be affected in chemical-exposed humans, e.g., changes in sensorimotor function. Procedures used to identify or screen for the presence of neurotoxicity are usually designed to test large numbers of animals and are not considered to be as sensitive to subtle effects as more specialized tests for neurobiological dysfunction. For purposes of screening, the use of a functional observational battery (FOB) is now generally accepted. In general, FOB evaluations in animals are similar to clinical neurological examinations in humans in that they rate the presence and, in some cases, the severity of behavioral and neurological signs. A number of batteries containing different observations and measurements have been developed in several laboratories for rodents, dogs, and non-human primates. Frequently, the FOB is used in conjunction with other measures of neurotoxicity, i.e., neuropathology or sensory evoked potentials. FOB used in screening typically assess several neurobiological domains including neuromuscular (i.e., weakness, incoordination, abnormal movements, gait, motor seizures, myoclonia, rigidity and tremor), sensory (i.e., auditory, visual and somatosensory) and autonomic (i.e., pupil response, salivation) functions. Most FOB used for screening do not assess cognitive function (i.e., learning and memory). FOB evaluations can yield important information concerning dose-response characteristics and data on the onset, duration and persistence of an effect. FOB should be able to differentiate neurotoxicants from non-neurotoxicants and neurotoxicants having different mechanism(s) or site(s) of action.

Animals↗

PubMed2005

Talampanel improves the functional deficit after transient focal cerebral ischemia in rats. A 30-day follow up study.

The neuroprotective effect of talampanel, a negative allosteric modulator of alpha-amino-3-hydroxy-methyl-4-isoxazolyl-propionic acid (AMPA) receptors has been described previously. However, in these studies the histological changes and not the functional consequences of the brain damage were evaluated. The aim of present investigation was to analyze the sensorimotor function after stroke and to test the influence of talampanel (GYKI-53773, LY-300164) by 30-day monitoring in rats. After 1h middle cerebral artery occlusion (MCAO) general 'well-being', neurological status, spontaneous motor activity, rotation, motor coordination, balancing, muscle strength and reaction time were followed for 1 month. Talampanel (6 x 10 mg/kg i.p. given on the day of stroke) improved the motor coordination in rotarod (p < 0.01) and beam walking (p < 0.01) tests, reduced the number of stroke-induced rotations (p < 0.05), shortened the reflex time on the forelimb contralateral to brain ischemia and improved the survival rate comparing with vehicle treated control. After stroke, serious sensorimotor deficits appeared in rats but they showed partial spontaneous recovery after 30 days. Talampanel treatment enhanced the rate of functional improvement without changing the morphology at the end of the experiment. Our results indicate that modulation of AMPA receptors by talampanel can be a promising therapeutic approach to the treatment of stroke.

Animals↗

PubMed2003

The behavioral effects of magnesium therapy on recovery of function following bilateral anterior medial cortex lesions in the rat.

Magnesium (Mg(++)) therapy has been shown to be neuroprotective and to facilitate recovery of motor and sensorimotor function in a variety of animal models of traumatic brain injury. However, few studies have investigated the efficacy of Mg(++) therapy on cognitive impairments following injury. The present study evaluated the ability of magnesium chloride (MgCl(2)) to facilitate recovery of function following bilateral anterior medial cortex lesions (bAMC). Rats received electrolytic bAMC lesions or sham surgery and were then treated with 1 mmol/kg, i.p. MgCl(2), 2 mmol/kg, i.p. MgCl(2), or 1.0 ml/kg, i.p. 0.9% saline. Drug treatment was administered 15 min following injury with subsequent injections administered at 24 and 72 h. Rats were tested on a battery of behavioral tests that measured both cognitive (reference and working memory in the Morris Water Maze (MWM) and spatial delayed matching-to-sample (DMTS)) and sensorimotor performance (bilateral tactile adhesive removal). The results indicated that bAMC lesions produced significant cognitive impairments in reference memory and working memory in the MWM, DMTS and sensorimotor impairments compared to shams. Mg(++) therapy exhibited a dose-dependent effect in facilitating recovery of function. Administration of 2mmol of MgCl(2) significantly improved performance on the bilateral adhesive tactile removal test, DMTS and working memory tests. The 1 mmol dose of MgCl(2) reduced the initial deficit on the tactile adhesive removal test and reduced the working memory impairment on the second day of testing. These results suggest Mg(++) therapy improves cognitive performance following injury in a dose-dependent manner.

Analysis of Variance↗

PubMed2006

Mechanisms of oral somatosensory and motor functions and their clinical correlates.

This article provides a review of somatosensory and motor pathways and processes involved in oral sensorimotor function and dysfunction. It reviews somatosensory processes in peripheral tissues, brainstem and higher brain centres such as thalamus and cerebral cortex, with a particular emphasis on nociceptive mechanisms. It also outlines some of the circuits and processes involved in reflexes and motor control. In addition, it emphasizes the concept of neuroplasticity and its applicability to oro-facial pain, to motor control and motor learning, and to adaptation to changes in the oral sensory environment such as may occur with the placement of dental implants.

Animals↗

PubMed2001

Behavioral and anatomical correlates of chronic episodic hypoxia during sleep in the rat.

The role played by chronic episodic hypoxia (EHYP) in the neurocognitive morbidity of obstructive sleep apnea (OSA) is unknown. Sleep recordings, Morris water maze experiments, and immunohistochemistry for NMDA NR1 glutamate receptor, c-fos protein, and apoptosis [nuclear immunoreactivity for single-stranded DNA and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling assay] were conducted in EHYP-exposed Sprague Dawley male rats. Exposures consisted of up to14 d in an environmental chamber in which O(2) concentrations were cycled between 10 and 21% every 90 sec or 30 min during 12 hr of daylight. For the remaining 12 hr, EHYP rats breathed room air, while controls spent 14 d in room air. Although EHYP induced significant disruption of sleep architecture during the initial day of exposure, sleep patterns normalized thereafter. Marked increases in apoptosis occurred in the CA1 hippocampal region (sevenfold) and cortex (Cx; eightfold) after 1-2 d of EHYP but not in CA3 and were followed by decreases toward normoxic levels by 14 d. Double labeling for NMDA NR1 and c-fos revealed marked architectural disorganization in CA1 and Cx with increases in c-fos over time. Rats exposed to EHYP displayed significantly longer escape latencies and swim path lengths to escape a hidden platform during 12 training trials given over 2 d. Differences in the performances of EHYP and control rats, although reduced, persisted after 14 d of recovery. We conclude that EHYP is associated with marked cellular changes over time within neural regions associated with cognitive functions. Furthermore, EHYP impaired performance during acquisition of a cognitive spatial task without affecting sensorimotor function. Such changes may underlie components of the learning and memory impairments found in OSA.

Animals↗

PubMed1997

Studies on neuroprotective and regenerative effects of GDNF in a partial lesion model of Parkinson's disease.

Intrastriatal 6-hydroxydopamine injections in rats induce partial lesions of the nigrostriatal dopamine (DA) system which are accompanied by a delayed and protracted degeneration of DA neurons within the substantia nigra. By careful selection of the dose and placement of the toxin it is possible to obtain reproducible and regionally defined partial lesions which are well correlated with stable functional deficits, not only in drug-induced behaviors but also in spontaneous motoric and sensorimotoric function, which are analogous to the symptoms seen in patients during early stages of Parkinson's disease. The intrastriatal partial lesion model has proved to be particularly useful for studies on the mechanisms of action of neurotrophic factors since it offers opportunities to investigate both protection of degenerating DA neurons during the acute phases after the lesion and stimulation of regeneration and functional recovery during the chronic phase of the postlesion period when a subset of the spared nigral DA neurons persist in an atrophic and dysfunctional state. In the in vivo experiments performed in this model glial cell line-derived neurotrophic factor (GDNF) has been shown to exert neurotrophic effects both at the level of the cell bodies in the substantia nigra and at the level of the axon terminals in the striatum. Intrastriatal administration of GDNF appears to be a particularly effective site for induction of axonal sprouting and regeneration accompanied by recovery of spontaneous sensorimotor behaviors in the chronically lesioned nigrostriatal dopamine system.

Animals↗