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Results for “sensorimotor deficits”

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PubMedDate not supplied

Children with sensorimotor deficits: a special risk group.

Children with spina bifida, cerebral palsy, mental retardation, developmental delays, and seizure states are handicapped with sensorimotor deficits, including gait or coordination instability, temperature insensitivity, and mental simplicity. These handicaps make this distinct and unpretentious population more susceptible to lethal burns. A 30-year review was conducted in a pediatric burn center to examine the relationships between pediatric sensorimotor deficit and burn injury. Of the 4874 acute burn admissions, 66 children were identified with preexisting sensorimotor deficits. Data indicate that children with sensorimotor deficit are more prone to burn injury from both their physical impairment and poorly supervised environments. In addition to extended hospitalizations, these children bear significantly higher mortality risks. Had the special supervisions and protection required by such handicapped children been provided, 80% of the burn injuries could have been prevented. Results emphasize that the future of these special children with sensorimotor deficits relies on health care providers playing a greater role in educating parents and caregivers.

Burns↗

PubMed1983

Residual sensorimotor deficits in the adult head-injured patient. A treatment approach.

Deficits in sensorimotor integration, cognition, and psychosocial behavior may lead to a characteristic set of problems in the head-injured adult. An inpatient Sensorimotor Integration Class for ambulatory head-injured patients was developed to introduce challenging sensorimotor activities before these patients established avoidance patterns. The class includes perceptual motor, sensory integration, and sports activities. Clinical observations suggest that the class leads to improved quality of movement for participants. Objective research is needed to document clinical observations.

Adult↗

PubMed1989

Continued administration of GM1 ganglioside is required to maintain recovery from neuroleptic-induced sensorimotor deficits in MPTP-treated mice.

Injection of a dose of haloperidol that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and sensory neglect in MPTP-treated mice. Chronic GM1 ganglioside administration improves the behavioral impairments, partially restores striatal dopamine (DA) content and prevents DA D-2 receptor up-regulation. Discontinuation of GM1 ganglioside treatment results in a time-dependent decline of striatal DA content to pretreatment pathological levels, return of haloperidol-induced sensorimotor deficits and a rise of DA D-2 receptor density in the striatum. Apparently, continuous administration of GM1 ganglioside is necessary to maintain the biochemical and behavioral recovery in the MPTP-treated mouse. These observations may provide useful cues for understanding the mechanism of action of GM1 ganglioside.

Animals↗

PubMed1992

Hyperactivity, hyper-reactivity, and sensorimotor deficits induced by low doses of the N-methyl-D-aspartate non-competitive channel blocker MK801.

Three doses of MK801 (0.05 mg/kg, 0.3 mg/kg and 1.0 mg/kg) were given systemically to adult male rats, which were then tested on a battery of previously learned, reactive and spontaneous behaviors. Hyperactivity, hyper-reactivity, reductions in rearing behavior and deficits in tongue extension were found at the 0.05 mg/kg dose. Similar, but more severe results were found at the 0.3 mg/kg dose, with the addition of difficulties in climbing, balancing on a beam, and abnormalities in orienting to tactile stimuli. A number of tasks could not be performed at the 1.0 mg/kg dose including tongue extension, orienting, balancing on a beam, and climbing. Additionally, abnormal postures, gaits, and swimming behaviors were observed at this dose. These results characterize the behavioral effects of MK801 as a syndrome of hyperactivity, hyper-reactivity, and sensorimotor deficits. Evidence of this syndrome was present at all three doses, including the 0.05 mg/kg dose, which previously has been claimed to induce deficits similar to hippocampal lesions. Learning literature employing MK801 is discussed in the context of the behavioral deficits found in this study.

Animals↗

PubMed1988

'Disengage' sensorimotor deficit following apparent recovery from unilateral dopamine depletion.

Sensorimotor behavior in Long-Evans rats was evaluated acutely and chronically after unilateral dopamine depletion caused by infusions of 6-hydroxydopamine into the nigrostriatal system. In each rat, control infusions were delivered to the opposite hemisphere and a noradrenaline uptake blocker was used as a pretreatment to help protect noradrenaline cells. During the first few postoperative weeks, head movement reactions to repetitive tactile-perioral stimulation contralateral to the dopamine-depleted hemisphere were delayed but not eliminated. With recovery, facilitated by special training, the rats were able to respond quickly. However, two lasting abnormalities were observed. First, the types of head-orienting movements directed toward contralateral stimulation were different from that directed toward ipsilateral stimulation. Second, when the animals were engaged in eating behavior there was a complete failure to orient to contralateral stimulation, whereas they instantly disengaged from eating to orient to ipsilateral stimulation. When not eating, orienting was rapid and reliable to stimulation of either side of the body. These data may have implications for the role of the striatum and connected structures in the organization and integration of sensorimotor and ingestive behavior.

Animals↗

PubMed1985

Sensorimotor deficits related to postural stability. Implications for falling in the elderly.

The effects of age-related sensorimotor and central processing deficits on postural control are reviewed, and the paucity of knowledge about proprioceptive changes with age is noted. A model of processing stages in the production of responses to postural instability is outlined. Even slight response slowing produces disproportionate increases in clinically slow responses. Many aspects of postural responses are "cognitively penetrable". Research on falls should examine learned as well as automated behaviors.

Accidents↗

PubMed1989

Photochemical stroke model: flunarizine prevents sensorimotor deficits after neocortical infarcts in rats.

We produced unilateral photochemical infarcts in the hindlimb sensorimotor neocortex of 186 rats by intravenous injection of the fluorescein derivative rose bengal and focal illumination of the intact skull surface. Infarcted rats showed specific, long-lasting deficits in tactile and proprioceptive placing reactions of the contralateral limbs, mostly the hindlimb. Placing deficits were most prominent during transition to immobility and/or when independent limb movements were required. Administration of flunarizine, a Class IV calcium antagonist, 30 minutes after infarction resulted in marked sparing of sensorimotor function in 30 rats. In contrast to 20 vehicle-treated rats, which remained deficient for at least 21 days, 15 (75%) of the rats treated with 1.25 mg/kg i.v. flunarizine showed normal placing on Day 1 after infarction, whereas the remaining five (25%) recovered within 5 days. Oral treatment of 10 rats with 40 mg/kg flunarizine was also effective. Neocortical infarct volume and thalamic gliosis, assessed 21 days after infarction, did not differ between 30 flunarizine- and 30 vehicle-treated rats. However, when 4-hour-old infarcts were measured in 16 rats, posttreatment with intravenous flunarizine reduced infarct size by 31%. In combination with appropriate behavioral analyses, photochemical thrombosis may constitute a relevant stroke model, in which flunarizine preserved behavioral function during a critical period, corresponding to the spread of ischemic damage.

Animals↗

PubMed1993

Amelioration of sensory attention and sensorimotor deficits by chromaffin cell grafts to the cerebral cortex of nucleus basalis magnocellularis lesioned rats.

Rats that have received lesions to the nucleus basalis magnocellularis display with a variety of behavioral deficits; among these are decreases in performance of maze tests as well as deficiencies on measures of general health, sensory attention and sensorimotor abilities. We have previously shown that grafts of chromaffin cells placed in the cerebral cortex of nucleus basalis magnocellularis lesioned rats can ameliorate the lesion-induced deficits in performance of a task involving spatial memory. In the present study, we find that lesion-induced deficits in the sensory attention measure of exploration of the environment (head scanning) as well as the sensorimotor behavior involving a rat righting itself when placed nose down on an inclined grid are evident at 8 weeks post-lesion in lesioned-alone rats; these deficits are significantly ameliorated by chromaffin cell grafts in the cerebral cortex placed two weeks following the lesion procedure. These findings may have relevance to the use of chromaffin cells for grafting in neurodegenerative disorders in which sensorimotor or attention deficit components are involved.

Acetylcholinesterase↗

PubMed1988

Acute stress or neuroleptics elicit sensorimotor deficits in MPTP-treated mice.

The present study evaluates the effects of MPTP-induced striatal DA depletions on sensorimotor behavior in mice. While MPTP produces no obvious behavioral deficits under normal conditions, acute stress (cold swim) or injection of low doses of haloperidol results in marked akinesia, catalepsy, and sensory neglect. Thus, significant behavioral impairments do accompany the neurotoxicity observed after MPTP administration in mice and render this a valuable animal model for studying mechanisms underlying Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1985

Ibotenic acid lesions of the lateral hypothalamus: comparison with 6-hydroxydopamine-induced sensorimotor deficits.

Three groups of rats received unilateral injections of ibotenic acid, 6-hydroxydopamine or vehicle control into the lateral hypothalamic area, and were given a range of tests of sensorimotor capacity. As expected from previous reports, the 6-hydroxydopamine injections induced a marked sensorimotor impairment to the contralateral side of the body. By contrast, the ibotenic acid injections produced no detectable sensorimotor changes, although the parameters and histological extent of the lesion were identical to those which produce aphagia, adipsia and sustained regulatory impairments when administered bilaterally. These results dissociate the classic electrolytic lesion of the lateral hypothalamus into homeostatic impairments following damage to intrinsic hypothalamic neurones, and sensorimotor impairments dependent only on damage to passing catecholamine fibre systems.

Animals↗

PubMed1994

Unilateral AMPA lesions of nucleus basalis magnocellularis induce a sensorimotor deficit which is differentially altered by arecoline and nicotine.

One week after unilateral alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) lesions of nucleus basalis magnocellularis, rats showed significant lateralised bias in spontaneous turning and in turning induced by tail pinch or by placing the rat on a 45 degrees grid. Turning was biased to the lesioned side and this side also showed increased responsiveness to pin-prick stimulation of the skin (somaesthesia), snout and whisker stimulation and ammonia olfaction. Arecoline (0.5 mg/kg), at a dose which did not affect responses to sensorimotor stimulation in sham-operated rats, corrected the lesion-induced biased turning to tail pinch and the 45 degrees grid test and reduced the bias in the open field. In contrast, nicotine (0.05 mg/kg), at a dose which also did not substantially affect responses to sensorimotor stimulation in sham-operated rats, switched the lesion-induced turning bias towards the contralateral side. Neither cholinoceptor agonist reduced the lesion-induced increased sensory responsiveness. The effects of nicotine were blocked by the centrally acting nicotinic antagonist, mecamylamine (1.0 mg/kg), but not by hexamethonium (1.0 mg/kg), or ondansetron (0.01 mg/kg). Amphetamine (up to 1.0 mg/kg) did not affect the lesion-induced motor asymmetry. The results confirm that the basal forebrain cholinergic system plays a role in sensorimotor cortical functions, but suggest different functional roles for muscarinic and nicotinic receptors.

Afferent Pathways↗

PubMed1979

Sensorimotor deficits produced by phenytoin and chlorpromazine in unanesthetized cats.

Unanesthetized adult cats were evaluated for suprasegmental reflex activity and motor skills before and after administration of chlorpromazine (0.0625--0.5 mg/kg) alone and in combination with phenytoin (20 mg/kg). The greatest deficits were seen in the tests of balance and corrdination in which half the animals failed to match their control responses after administration of chlorpromazine and phenytoin. The impairment was most noticeable with the most stringent test (walking a 4 cm wide beam), and the effects of the two drugs were additive. Although there was no effect of either drug on muscle strength, the two drugs in combination depressed the animals' motivational state, making them less willing to work against imposed loads. Neither drug, alone or in combination, altered responses to the flexor reflex, blind placing, the hopping response or visually aided placing. It is concluded that the effects of chlorpromazine and phenytoin on motor control are selective for the CNS loci which control balance and coordination. Although the two drugs produce additive responses, the deficits occur only at doses which are well above those needed for clinical efficacy and thus may not pose a problem in their long term clinical use.

Animals↗

PubMed1988

Administration of GM1 ganglioside eliminates neuroleptic-induced sensorimotor deficits in MPTP-treated mice.

Injection of a low dose of haloperidol, that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and sensory neglect in MPTP-treated mice. GM1 ganglioside treatment eliminates all of these behavioral impairments and also partially restores striatal dopamine content. These observations suggest that the MPTP-treated mouse may be a valuable model for studying mechanisms underlying parkinsonism and that administration of GM1 ganglioside may be an effective therapy.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1997

Cysteamine blocks amphetamine-induced deficits in sensorimotor gating.

Somatostatin is a neuropeptide that has been shown to interact with dopamine. Low concentrations of cysteamine selectively depletes somatostatin and has been used to investigate the role of endogenous somatostatin in lieu of an available selective receptor antagonist. We examined the effects of various doses of subcutaneous cysteamine on baseline and amphetamine-disrupted sensorimotor gating as measured by prepulse inhibition of the acoustic startle reflex. Cysteamine in doses ranging from 50-300 mg/kg reversed decreases in PPI induced by systemic injections of amphetamine (2 mg/kg). Cysteamine had no effect on the amplitude of the acoustic startle reflex itself. The results lend further support to a somatostatin-dopamine interaction within the brain in which endogenous somatostatin facilitates dopaminergic activity. These findings also suggest that endogenous somatostatin might play a significant role in regulation of sensorimotor gating deficits. This has clinical implications as deficient prepulse inhibition is recorded in humans suffering from neuropsychiatric conditions such as schizophrenia.

Acoustic Stimulation↗

PubMed1998

Chronic treatment with haloperidol diminishes the phencyclidine-induced sensorimotor gating deficit in rats.

Prepulse inhibition is a model in which a weak subthreshold stimulus (prepulse), presented to an individual before a strong stimulus (pulse), inhibits a startle response to the latter. A deficit of prepulse inhibition induced by dopaminomimetics and antagonists of NMDA receptors has been suggested as an animal model of the sensorimotor deficit in schizophrenia. The aim of the present study was to examine the effect of chronic treatment with the classic neuroleptic haloperidol on the disruption of prepulse inhibition induced by the uncompetitive antagonist of NMDA receptors phencyclidine (PCP, 5 mg/kg sc). Haloperidol in a dose of 1 mg/kg/day was given to rats in drinking water for 3 months. The PCP-induced reduction in prepulse inhibition was not reversed by short-term (4-day) haloperidol administration. In contrast, long-term treatment with haloperidol (6 weeks or 3 months) diminished the PCP-induced effect. The present study suggests that the improvement in sensorimotor gating in the PCP model in rats by prolonged treatment with haloperidol may reflect its antipsychotic action.

Animals↗

PubMed1997

The modulation of sensorimotor gating deficits by mesolimbic cholecystokinin.

The effects of cholecystokinin (CCK) in an animal model of sensorimotor-gating deficits with strong face, construct and predictive validity for schizophrenia were investigated. Prepulse inhibition (PPI) occurs when a weak acoustic lead stimulus inhibits the startle response to a loud startling stimulus. Infusions of sulfated CCK-8 in the posterior nucleus accumbens potentiated apomorphine-induced disruption of PPI but had no effect on baseline PPI or the amplitude of acoustic startle reflex itself. The results provide evidence that mesolimbic CCK may play a role in regulating sensorimotor gating deficits but contradict earlier notions that CCK agonists may have antipsychotic properties and upon which clinical trials of CCK agonists in schizophrenia were based. Rather, these results suggest that antagonists of CCK may display neuroleptic-like actions on deficits in PPI and may hold greater promise as antipsychotics.

Acoustic Stimulation↗

PubMed1997

Ladder beam and camera video recording system for evaluating forelimb and hindlimb deficits after sensorimotor cortex injury in rats.

Hindlimb and forelimb deficits in rats caused by sensorimotor cortex lesions are frequently tested by using the narrow flat beam (hindlimb), the narrow pegged beam (hindlimb and forelimb) or the grid-walking (forelimb) tests. Although these are excellent tests, the narrow flat beam generates non-parametric data so that using more powerful parametric statistical analyses are prohibited. All these tests can be difficult to score if the rat is moving rapidly. Foot misplacements, especially on the grid-walking test, are indicative of an ongoing deficit, but have not been reliably and accurately described and quantified previously. In this paper we present an easy to construct and use horizontal ladder-beam with a camera system on rails which can be used to evaluate both hindlimb and forelimb deficits in a single test. By slow motion videotape playback we were able to quantify and demonstrate foot misplacements which go beyond the recovery period usually seen using more conventional measures (i.e. footslips and footfaults). This convenient system provides a rapid and reliable method for recording and evaluating rat performance on any type of beam and may be useful for measuring sensorimotor recovery following brain injury.

Animals↗

PubMed1997

Pro-dopamine effects of neurotensin on sensorimotor gating deficits.

Neurotensin is a neuropeptide which coexists with mesolimbic dopamine and has exhibited neuroleptic-like activity in the nucleus accumbens. This study examined the effects of neurotensin infused into the nucleus accumbens on prepulse inhibition (PPI) of the rat's acoustic startle reflex, a measure which is relevant to the sensorimotor gating deficits seen in schizophrenia. Neurotensin (5 micrograms) had no effect on the amplitude of the acoustic startle reflex nor on baseline PPI, but it potentiated the disruption of PPI produced by amphetamine and apomorphine. This is the first report of a pro-dopamine action for intra-accumbens neurotensin, and suggests that a complex behavioral pharmacology is associated with this neuropeptide.

Acoustic Stimulation↗