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17 recordsLinked to original sources
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↗
PubMed1977

Active avoidance in rats with unilateral hypothalamic and optic nerve lesions.

During the height of the contralateral sensorimotor deficit that follows unilateral hypothalamic lesions, rats demonstrate severe performance deficits when tested on a two-way active avoidance task which utilizes a visual conditioned stimulus. This deficit is observed whether or not the ipsilateral or contralateral optic nerve is sectioned in conjunction with the unilateral hypothalamic lesion. With the return of sensorimotor function contralateral to the lesion, animals that had been unable to avoid shock during their debillitated phase demonstrated significant savings when tested on the original task.

Animals↗
PubMed1979

Sign language aphasia in a non-deaf-mute.

A 19-year-old left-handed man, who was raised by deaf-mute parents and learned sign language concurrently with normal speech, sustained a traumatic cerebral contusion. He subsequently had no evidence of apraxic, visual-spatial, or sensorimotor deficits of the left limbs with which he was accustomed to use signs. Globally aphasic with a dense right hemiparesis, he initially recovered sign language to a greater degree than spoken language with a reversal on follow-up observations. Receptive skills improved to a greater degree than expressive skills with no marked difference between verbal and sign language, but with natural signs better preserved than finger spelling.

Adult↗
PubMed2023

Human mutations in high-confidence Tourette disorder genes affect sensorimotor behavior, reward learning, and striatal dopamine in mice.

UNLABELLED: Tourette disorder (TD) is poorly understood, despite affecting 1/160 children. A lack of animal models possessing construct, face, and predictive validity hinders progress in the field. We used CRISPR/Cas9 genome editing to generate mice with mutations orthologous to human de novo variants in two high-confidence Tourette genes, CELSR3 and WWC1 . Mice with human mutations in Celsr3 and Wwc1 exhibit cognitive and/or sensorimotor behavioral phenotypes consistent with TD. Sensorimotor gating deficits, as measured by acoustic prepulse inhibition, occur in both male and female Celsr3 TD models. Wwc1 mice show reduced prepulse inhibition only in females. Repetitive motor behaviors, common to Celsr3 mice and more pronounced in females, include vertical rearing and grooming. Sensorimotor gating deficits and rearing are attenuated by aripiprazole, a partial agonist at dopamine type II receptors. Unsupervised machine learning reveals numerous changes to spontaneous motor behavior and less predictable patterns of movement. Continuous fixed-ratio reinforcement shows Celsr3 TD mice have enhanced motor responding and reward learning. Electrically evoked striatal dopamine release, tested in one model, is greater. Brain development is otherwise grossly normal without signs of striatal interneuron loss. Altogether, mice expressing human mutations in high-confidence TD genes exhibit face and predictive validity. Reduced prepulse inhibition and repetitive motor behaviors are core behavioral phenotypes and are responsive to aripiprazole. Enhanced reward learning and motor responding occurs alongside greater evoked dopamine release. Phenotypes can also vary by sex and show stronger affection in females, an unexpected finding considering males are more frequently affected in TD. SIGNIFICANCE STATEMENT: We generated mouse models that express mutations in high-confidence genes linked to Tourette disorder (TD). These models show sensorimotor and cognitive behavioral phenotypes resembling TD-like behaviors. Sensorimotor gating deficits and repetitive motor behaviors are attenuated by drugs that act on dopamine. Reward learning and striatal dopamine is enhanced. Brain development is grossly normal, including cortical layering and patterning of major axon tracts. Further, no signs of striatal interneuron loss are detected. Interestingly, behavioral phenotypes in affected females can be more pronounced than in males, despite male sex bias in the diagnosis of TD. These novel mouse models with construct, face, and predictive validity provide a new resource to study neural substrates that cause tics and related behavioral phenotypes in TD.

Preprint↗
PubMed2024

Human mutations in high-confidence Tourette disorder genes affect sensorimotor behavior, reward learning, and striatal dopamine in mice.

Tourette disorder (TD) is poorly understood, despite affecting 1/160 children. A lack of animal models possessing construct, face, and predictive validity hinders progress in the field. We used CRISPR/Cas9 genome editing to generate mice with mutations orthologous to human de novo variants in two high-confidence Tourette genes, CELSR3 and WWC1. Mice with human mutations in Celsr3 and Wwc1 exhibit cognitive and/or sensorimotor behavioral phenotypes consistent with TD. Sensorimotor gating deficits, as measured by acoustic prepulse inhibition, occur in both male and female Celsr3 TD models. Wwc1 mice show reduced prepulse inhibition only in females. Repetitive motor behaviors, common to Celsr3 mice and more pronounced in females, include vertical rearing and grooming. Sensorimotor gating deficits and rearing are attenuated by aripiprazole, a partial agonist at dopamine type II receptors. Unsupervised machine learning reveals numerous changes to spontaneous motor behavior and less predictable patterns of movement. Continuous fixed-ratio reinforcement shows that Celsr3 TD mice have enhanced motor responding and reward learning. Electrically evoked striatal dopamine release, tested in one model, is greater. Brain development is otherwise grossly normal without signs of striatal interneuron loss. Altogether, mice expressing human mutations in high-confidence TD genes exhibit face and predictive validity. Reduced prepulse inhibition and repetitive motor behaviors are core behavioral phenotypes and are responsive to aripiprazole. Enhanced reward learning and motor responding occur alongside greater evoked dopamine release. Phenotypes can also vary by sex and show stronger affection in females, an unexpected finding considering males are more frequently affected in TD.

Animals↗
PubMed2026

Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined.

Animals↗
PubMedDate not supplied

Infant rats: sensorimotor ontogeny and effects of substantia nigra destruction.

The ontogeny of sensorimotor behaviors of albino rats were evaluated from birth through adulthood (Experiment 1). Sensorimotor behaviors (e.g., visual and tactile orientation, forelimb and hindlimb hopping, righting reflexes) achieved mature (adultlike) characteristics at various ages during ontogeny and a rostral-caudal developmental pattern was revealed. In Experiment 2, the substantia nigra was bilaterally or unilaterally destroyed in rats at 10 or 25 days of age and the ontogeny of sensorimotor and regulatory (feeding, drinking, body weight regulation) behaviors were evaluated. Bilateral destruction of the substantia nigra, zona compacta, at 10 and 25 days of age resulted in transient cessation of suckling and/or feeding and drinking followed by recovery. Male brain-damaged rats had reduced body weight through 150-170 days of age. Specific feeding and drinking tests revealed the presence of residual regulatory deficits which seemed permanent. Sensorimotor testing revealed transient dysfunction for a variety of sensorimotor behaviors, with eventual recovery of normal sensorimotor capacity. The results are related to sensorimotor ontogeny and recovery from infant brain damage.

Animals↗
PubMed1978

Polyneuropathy and folate deficiency.

We studied five patients (two men and three women, age between 58 and 76 years) with clinical and electrophysiological signs of polyneuropathy. Routine neurological, hematological, and gastroenterological studies as well as procedures to test fat malabsorption were performed. Folate determinations were done using both radioactive and Lactobacillus casei methods. Two patients displayed the signs of subacute combined degeneration of the spinal cord with polyneuropathy, while three had only signs of neuropathy. All had low serum folate concentration, long-standing gastrointestinal disease, and deficient folate intake. The D-xylose absorption test gave values in all patients, while none displayed the classical malabsorption syndrome. The patients had substantial improvement or recovered (according to clinical and electrophysiological measurements) after periods ranging from 9 to 39 months of folate therapy. Such acquired folate-responsive polyneuropathy has two principal characteristics: mixed sensorimotor with mainly sensory deficits, and involvement of one or both of the lower extremities much more extensively than the upper extremities.

Aged↗
PubMed1978

A behavioral analysis of complete unilateral section of the pyramidal tract at the medullary level in Macaca mulatta.

Ten Macaca mulatta monkeys were operantly conditioned to perform three motor paradigms designed to evaluate single and combination finger movements. Eight of these monkeys were retested after left medullary pyramidotomy; 2 monkeys underwent left medullary pyramidotomy prior to conditioning. All animals were tested for three years after operation. Monkeys with a completely sectioned medullary pyramid could, with time, perform difficult motor paradigms that required: (1) both individual and combination finger movements; (2) proximal upper extremity motor control; (3) thumb and index finger pincer grasp; and (4) the ability to preprogram and then execute a precision hand movement. The greater the extent of pyramidal tract destruction, the longer the time necessary for recovery of both discrete finger movement and pincer grasp, the greater the effort needed to attain recovery of hand function, and the weaker the affected musculature. The 2 animals in which pyramidotomy of at least 70% of the tract preceded efforts at operant conditioning learned and performed difficult motor paradigms. In all animals, neurological examination revealed that the most enduring and functionally most important deficit that interferes with hand function following pyramidotomy is loss of contactual hand orienting responses and failure of reflex sensorimotor adjustments.

Animals↗
PubMed1979

Lateralized hunger: ipsilateral attenuation of cortical spreading depression-induced feeding after unilateral 6-OHDA injection into the substantia nigra.

Unilateral injections of 6-hydroxydopamine into the substantia nigra in the rat significantly attenuated cortical spreading depression (CSD)-induced eating from the hemisphere ipsilateral but not contralateral to the lesion. The lateralized decrease in elicited feeding was correlated with postlesion body weight loss, striatal catecholamine depletion (dopamine, 94%; norepinephrine, 52%) and amphetamine-induced ipsilateral turning, and can be characterized as an inability of the lesioned nigrostriatal system to maintain the CSD-elicited response rather than a failure to induce it. The interhemispheric control procedure allows us to exclude various general sensory and motor deficits to account for the decrement of feeding, and to attribute the feeding deficit to a reduced nigrostriatal transmission. It is suggested that CSD-induced feeding is due to an activation of integrative sensorimotor systems (especially the nigrostriatal dopamine system), rather than to homeostatic imbalances.

Amphetamine↗
PubMed1977

Sensorimotor stroke due to thalamocapsular ischemia.

A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.

Cerebrovascular Disorders↗
PubMed2026

Motor coordination and behavioural deficits in a mouse model of KMT2B-related dystonia.

INTRODUCTION: Pathogenic variants in KMT2B cause early-onset dystonia, but a mouse model that has undergone comprehensive, dystonia-oriented phenotyping is lacking. METHODS: We conducted detailed phenotyping on heterozygous Kmt2b constitutive knockout mice and wild-type littermates, assessing growth, neurobehavioural traits, motor coordination, sensorimotor gating, social behaviour and metabolic parameters, combined with striatal RNA sequencing. RESULTS: Kmt2b knockout mice of both sexes were viable but significantly smaller and lighter than littermate controls. Knockouts were hyperlocomotive in the open field and showed approximately two-fold larger acoustic startle responses; unexpectedly, prepulse inhibition was enhanced rather than reduced at all prepulse intensities. On the balance beam, knockouts crossed more slowly and paused more frequently; female knockouts also paused more on the ladder rung task. Frame-by-frame video analysis revealed a claw-like hindpaw posture characterized by abnormal inward flexion of the digits. Knockout mice spent less time investigating a novel conspecific, while social recognition memory remained intact. Striatal RNA sequencing confirmed reduction of Kmt2b transcript to approximately half of control levels and identified 177 differentially expressed genes, including Maob, encoding monoamine oxidase B; gene set enrichment analysis implicated neurodevelopmental, glial and mitochondrial processes. Nociception, vision, body-weight-adjusted grip strength, and clinical chemistry and haematological measures were largely unaffected. CONCLUSION: Heterozygous Kmt2b knockout mice show hyperlocomotion, altered sensorimotor gating, impaired motor coordination with dystonic-like paw posturing and reduced sociability, alongside a striatal transcriptomic signature implicating neurodevelopmental processes. The model mirrors aspects of human KMT2B-related dystonia and provides a platform for mechanistic study; environmental or pharmacological challenge may be needed to unmask overt dystonic features.

Dystonia↗
PubMed1979

Acute homeostatic imbalances reinstate sensorimotor dysfunctions in rats with lateral hypothalamic lesions.

It has previously been demonstrated that rats recovered from aphagia and adipsia after large bilateral electrolytic lesions of the lateral hypothalamic area do not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glyol. The present work reveals that such homeostatic imbalances reinstate the profound sensorimotor impairments that are seen in the immediate postoperative period but abate in parallel with the gradual recovery of ingestive behaviors. Administration of alpha-methyltyrosine or spiroperidol produced sensory and motor dysfunctions in rats with lateral hypothalamic lesions that were similar to those observed after 2-deoxyglucose. These results suggest that the residual feeding and drinking deficits of rats with lateral hypothalamic lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. Instead, they may indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons.

Animals↗
PubMed1977

Sensorimotor organization in reach and prehension: a development model.

A model is presented to depict the organization of the reflex, visual, voluntary motor, and perceptual-cognitive systems in the development of reach and prehension during the first year of life. Five components of hand skills are identified based upon a review of infant scales and observational studies, and the sequential occurrence of behaviors leading to the development of these components is graphically presented. These sequences are juxtaposed to enable the reader to view the temporal relationship of the systems at various stages in the development of reach and prehension in the infant. Items in the models are operationally defined. An explanation is included to clarify the nature and the sequence of events involved in the culmination of mature hand skills. The model should be useful in the identification, analysis, and remediation of deficits in reach and prehension often noted in children with developmental disabilities.

Child Development↗
PubMed1979

Conditioning compensates the neglect due to unilateral 6-OHDA lesions of substantia nigra in rats.

The degree of the contralateral sensory neglect in rats with unilateral 6-OHDA lesions of substantia nigra was assessed by a conditioning procedure, employing lateralized CS. In the first experiment visual neglect (revealed by failure of the visually elicited placing reaction contralateral to the lesion) was shown to be accompanied by slower acquisition of a brightness discrimination task. The impairment was due to ipsilateral turning tendency rather then to visual deficit, however, since monocular relearning yielded equal savings with the ipsilateral and contralateral eyes. The second experiment showed that rats anesthetized with urethane reacted to noxious skin stimulation contralateral to the lesion with shorter-lasting EEG arousal than to ipsilateral stimulation of the same intensity. The electrophysiological asymmetry could be compensated by classical conditioning, i.e. by pairing habituated tactile stimuli with noxious tail shock. The conditioned arousal reaction could be elicited with the same efficiency from the neglected and intact body surface. It is concluded that neglect is due neither to a sensory nor to a motor failure, but that 6-OHDA lesions of substantia nigra in one hemisphere reduce the arousing efficiency of unconditioned stimuli and interfere with sensorimotor integrating mechanisms on the side contralateral to the lesion. Compensation of the neglect by conditioning indicates that the role of the nigrostriatal system can be partly substituted by other circuits.

Animals↗
PubMed2026

Optimizing focal vibration therapy for balance and gait: A systematic review.

OBJECTIVE: This systematic review evaluated the efficacy of focal (localized) vibration therapy (FVT) applied to muscles/tendons on balance, gait, and mobility, with a specific focus on defining optimal vibration protocols (frequency, amplitude, dosing) and muscle-targeting strategies to maximize sensorimotor recovery. METHODS: A systematic review was conducted across six databases (CINHAL, Embase, Medline, Web of Science, Scopus, CENTRAL) from January 2000 to May 2025. Studies were included if they involved human participants, applied FVT therapeutically, and reported balance, gait, or mobility outcomes. Data extraction included study characteristics, intervention protocols, and outcomes. Methodological quality was assessed using the PEDro scale. RESULTS: Sixty-two studies (n = 2090 participants) were included. Methodological quality assessment (PEDro scale) indicated 44% of studies met high-quality standards. Biomechanical analysis identified the quadriceps, gastrocnemius/soleus, and plantar muscles as the most effective vibration sites, given their critical roles in gait propulsion and postural stability. The synthesis of protocol data indicated a promising therapeutic window characterized by a vibration frequency of 80-120 Hz (primarily fixed sinusoidal waveforms at a single frequency) and an amplitude of 0.2-0.5 mm (reported only in 12 studies; amplitude was not reported in 23 studies), applied bilaterally for a minimum of 3 sessions per week over 4-12 weeks, which could lead to improved balance and gait performance with benefits sustained for up to 5 months. CONCLUSION: FVT shows potential to improve gait and balance, particularly when targeting lower-extremity muscles with optimized vibration parameters. To advance the field, future research must prioritize the development of standardized protocols and investigate neurophysiological mechanisms to refine FVT as a precision bioengineering solution for mobility deficits.

Humans↗
PubMed1979

Operant conditioning of EEG rhythms and ritalin in the treatment of hyperkinesis.

Enhanced voluntary motor inhibition regularly accompanies conditioned increases in the sensorimotor rhythm (SMR), a 12--14-Hz Rolandic EEG rhythm in cats.A similar rhythm, presumably SMR, has also been identified in the human EEG. The clinical effectiveness of SMR operant conditioning has been claimed for epilepsy, insomnia, and hyperkinesis concurrent with seizure disorders. The present report attempts to follow up and replicate preliminary findings that suggested the technique's successful application to hyperkinesis uncomplicated by a history of epilepsy. SMR was defined as 12--14-Hz EEG activity in the absence of high-voltage slow-wave activity between 4 and 7 Hz. Anticipated treatment effects were indexed by systematic behavioral assessments of undirected motor activity and short attention span in the classroom. EEG and behavioral indices were monitored in four hyperkinetic children under the following six conditions: (1) No Drug, (2) Drug Only, (3) Drug and SMR Training I, (4) Drug and SMR Reversal Training, (5) Drug and SMR Training II, (6) No Drug and SMR Training. All hyperkinetic subjects were maintained on a constant drug regimen throughout the phases employing chemotherapy. Contingent increases and decreases in SMR occurred in three of four training subjects and were associated with similar changes in classroom assessments of motor inactivity. Combining medication and SMR training resulted in substantial improvements that exceeded the effects of drugs alone and were sustained with SMR training after medication was withdrawn. In contrast, these physiological and behavioral changes were absent in one highly distractible subject who failed to acquire the SMR task. Finally, pretraining levels of SMR accurately reflected both the seve-ity of original motor deficits and the susceptibility of hyperkinetic subjects to both treatments. Although the procedure clearly reduced hyperkinetic behavior, a salient, specific therapeutic factor could not be identified due to the dual EEG contingency imposed combined with associated changes in EMG. Despite these and other qualifying factors, the findings suggested the prognostic and diagnostic value of the SMR in the disorder when overactivity rather than distractibility is the predominant behavioral deficit.

Biofeedback, Psychology↗