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At least 901 records · Page 50Linked to original sources
PubMed2004

Mechanisms underlying recovery of motor function after stroke.

Stroke is the leading cause of long-term disability worldwide and a condition for which there is no universally accepted treatment. The development of new effective therapeutic strategies relies on a better understanding of the mechanisms underlying recovery of function. Noninvasive techniques to study brain function, including functional magnetic resonance imaging, positron emission tomography, transcranial magnetic stimulation, electroencephalography, and magnetoencephalography, led to recent studies that identified some of these operating mechanisms, resulting in the formulation of novel approaches to motor rehabilitation.

Humans↗
PubMed1986

The development and recovery of motor function in spinal cats. II. Pharmacological enhancement of recovery.

The effects of the gamma-aminobutyric acid (GABA) antagonist bicuculline (BCC) on hindlimb motor performance was examined in mature spinal cats with spinal cord transections made either on the day of birth or at approximately two weeks postpartum and in chronic adult cats with spinal transections made in adulthood. In those adult operates, whose pre-drug performance was poor compared to neonatal operates, treadmill locomotion and weight support were improved dramatically by BCC administration. In neonatal operates (examined as adults), BCC administration increased the force of extension to abnormal levels and this increase appeared to disrupt locomotion. Immunocytochemical localization of GABA's synthetic enzyme, glutamic acid decarboxylase (GAD) within the spinal cords of these animals revealed an abnormal distribution of GAD reaction product only in newborn operates. The behavioral results indicate that the full extent of recovery in adult operates is prevented by inhibitory influences and this may contribute to the comparatively superior performance of neonatal operates i.e., the infant lesion effect. The anatomical results suggest that one requirement for the normal development of some intrinsic spinal circuitry is transneuronal regulation mediated by the maturation of descending systems.

Aging↗
PubMed1995

School attainment, cognitive ability and motor function in a total Scottish very-low-birthweight population at eight years: a controlled study.

The prevalence of learning problems and of cognitive and motor impairment in a total geographically based very-low-birthweight population (N = 324) was compared at eight years of age with that in a population comprising two classroom peers, matched for gender and age (N = 590). 15 per cent of those with birthweights less than 1000g and 6 per cent of those weighing 1000 to 1499 g attended special schools. Index children in main-stream schools performed significantly less well in tests of neuromotor function than their comparison groups. Their mean IQs were 90.4 and 93.7 for those below and above 1000 g, respectively, while their comparison groups' IQs were 102.5 and 101.2. In all cognitive subscales apart from that testing short-term auditory sequential memory, both index groups were less competent. They were also less able in Word Reading and Basic Number Skills. These children placed heavy demands on mainstream schools, with 52 per cent and 37 per cent of the index groups, respectively, requiring learning support compared with 16 per cent in both comparison groups.

Achievement↗
PubMed2002

Role of thyrotrophin releasing hormone and corticotrophin releasing factor in stress related alterations of gastrointestinal motor function.

There is a growing body of experimental and clinical evidence to indicate that stress influences gastrointestinal motility. The most common pattern of gastrointestinal motor alterations induced by a variety of different stress factors is that of delayed gastric emptying and accelerated colonic transit. Central administration of corticotrophin releasing factor mimics both of these effects. This review focuses on the effects of two centrally acting peptides known to influence gastrointestinal motility and transit in experimental animals: thyrotrophin releasing hormone and corticotrophin releasing factor. The biological actions of these peptides are discussed in relation to the motility changes and pathways involved in their actions.

Animals↗
PubMed1987

Effect of cisapride, a new prokinetic agent, on esophageal motor function.

In this study, we assessed by a double-blinded, cross-over design the effect of intravenous and oral cisapride on esophageal motor activity during the late fed state in normal subjects. For the intravenous study, subjects were given placebo or 10 mg cisapride randomly, while in the oral study, they randomly received placebo or cisapride at 5, 10, or 20 mg. Cisapride given intravenously or orally caused a significant increase in resting LES pressure. The increase in LES pressure after oral administration was significant only after the 20 mg dose. Esophageal-body peristaltic amplitude, determined for all smooth-muscle sites, showed a modest but significant increase of approximately 10 mm Hg after intravenous cisapride, whereas no significant increase occurred after oral cisapride. Propagation time of peristalsis was unaffected by intravenous or oral cisapride. Side effects of treatment were minimal and at no time necessitated cessation of the study. We conclude that in healthy subjects during the late fed period, (1) cisapride at 10 mg intravenously or 20 mg orally increased resting LES pressure and (2) at 10 mg intravenously, but at no oral dose, cisapride increased peristaltic amplitude without affecting propagation time. The potentiating effect of cisapride on LES pressure suggests that cisapride could have an ancillary role in the therapy of gastroesophageal reflux disease.

Adult↗
PubMed2004

Possible mechanisms of involvement of the amygdaloid complex in the control of gastric motor function.

Electrophysiological and neuroanatomical experiments on Wistar rats were performed to study the mechanisms of the modulatory influences of the amygdaloid nuclei on reflex motor activity in the stomach. Electrical stimulation of the central nucleus was accompanied by reproducible changes in the ongoing motor activity of the stomach in activity evoked by activation of the vagovagal reflex arc. The most marked, and predominantly inhibitory, effects were seen in response to stimulation of the medial part of the nucleus. Microinjections of the anterograde neuron marker Phaseolus vulgaris leucoagglutinin (PHA-L) into the central nucleus of the amygdala revealed the existence of direct descending projections from its dorsomedial part to the area containing cells of the vagosolitary complex, associated with performance of the vagovagal reflexes of the stomach. Electrical stimulation of this part of the central nucleus led to changes in neuron responses in the bulbar "gastric" center evoked by stimulation of the vagus nerve. These features may underlie one of the mechanisms of the amygdalar modulation of the reflex activity of the stomach.

Amygdala↗
PubMed1990

Central nervous system action of peptides to influence gastrointestinal motor function.

The central action of peptides to influence GI motility in experimental animals is summarized in Table 1. TRH stimulates gastric, intestinal, and colonic contractility in rats and in several experimental species. A number of peptides including calcitonin, CGRP, neurotensin, NPY, and mu opioid peptides act centrally to induce a fasted MMC pattern of intestinal motility in fed animals while GRF and substance P shorten its duration. The dorsal vagal complex is site of action for TRH-, bombesin-, and somatostatin-induced stimulation of gastric contractility, and for CCK-, oxytocin- and substance P-induced decrease in gastric contractions or intraluminal pressure. The mechanisms through which TRH, bombesin, calcitonin, neurotensin, CCK, and oxytocin alter GI motility are vagally mediated. An involvement of central peptidergic neurons in the regulation of gut motility has recently been demonstrated in Aplysia, indicating that such regulatory mechanisms are important in the phylogenesis. Alterations of the pattern of GI motor activity are associated with functional changes in transit. TRH is so far the only centrally acting peptide stimulating simultaneously gastric, intestinal, and colonic transit in various animals species. Opioid peptides acting on mu receptor subtypes in the brain exert the opposite effect and inhibit concomitantly gastric, intestinal, and colonic transit. Bombesin and CRF were found to act centrally to inhibit gastric and intestinal transit and to stimulate colonic transit in the rat. The antitransit effect of calcitonin and CGRP is limited to the stomach and small intestine. The delay in GI transit is associated with reduced GI contractility for most of the peptides except central bombesin that increases GI motility. Nothing is known about brain sites through which these peptides act to alter gastric emptying and colonic transit. Regarding brain sites influencing intestinal transit, TRH-induced stimulation of intestinal transit in the rat is localized in the lateral and medial hypothalamus and medial septum. The periaqueductal gray matter is a responsive site for mu receptor agonist- and neurotensin-induced inhibition of intestinal transit. The neural pathways from the brain to the gut whereby these peptides express their stimulatory or inhibitory effects on GI transit is vagal dependent with the exception of calcitonin. It is not known whether the vagally mediated inhibition of GI transit by these peptides results from a decrease activity of vagal preganglionic fibers synapsing with excitatory myenteric neurons or an activation of vagal preganglionic neurons synapsing with inhibitory myenteric neurons. The lack of specific antagonists for these peptides has hampered the assessment of their physiological role.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Effect of aging on human skeletal muscle and motor function.

The percentage of Americans over the age of 65 yr is growing and this trend has heightened interest in aging research. In this review of human studies, comparisons, as a function of age, are made among the declines of VO2max, work endurance, muscle strength, total muscle cross-sectional area, muscle fiber number, spinal motor neuron number, and motor unit number. Declines in VO2max and total cross-sectional area of leg muscle begin in early adulthood. However, an accelerated loss of total muscle area and a decrease in muscle fiber number begins at about 50 yr of age. Losses in spinal motor neurons and motor units become apparent at about 60 yr of age. However, these findings were collected on different subjects. By better defining these temporal relationships in the same subjects, a more accurate cause and effect relationship may be obtained. Although muscle atrophy is attenuated by resistance training with aging, little is known about the effects of resistance training on the loss of spinal motor neurons, motor units, and muscle fiber number. The goal of this research would be to enhance the ability to promote as much function and independence of living as possible, i.e., increase the quality of life in our expanding elderly population.

Adult↗
PubMed2004

Sodium channel blockade with phenytoin protects spinal cord axons, enhances axonal conduction, and improves functional motor recovery after contusion SCI.

Accumulation of intracellular sodium through voltage-gated sodium channels (VGSCs) is an important event in the cascade leading to anatomic degeneration of spinal cord axons and poor functional outcome following traumatic spinal cord injury (SCI). In this study, we hypothesized that phenytoin, a sodium channel blocker, would result in protection of axons with concomitant improvement of functional recovery after SCI. Adult male Sprague-Dawley rats underwent T9 contusion SCI after being fed normal chow or chow containing phenytoin; serum levels of phenytoin were within therapeutic range at the time of injury. At various timepoints after injury, quantitative assessment of lesion volumes, axonal degeneration, axonal conduction, and functional locomotor recovery were performed. When compared to controls, phenytoin-treated animals demonstrated reductions in the degree of destruction of gray and white matter surrounding the lesion epicenter, sparing of axons within the dorsal corticospinal tract (dCST) and dorsal column (DC) system rostral to the lesion site, and within the dorsolateral funiculus (DLF) caudal to the lesion site, and enhanced axonal conduction across the lesion site. Improved performance in measures of skilled locomotor function was observed in phenytoin-treated animals. Based on these results, we conclude that phenytoin provides neuroprotection and improves functional outcome after experimental SCI, and that it merits further examination as a potential treatment strategy in human SCI.

Animals↗