Behavior of chronically decerebrated kittens

Kittens were decerebrated within 1 wk after birth and the subsequent development of functional capacity of these mesencephalic animals was observed for up to 2 mo. The only detectable immediate deficit was that sucking behavior was abolished. Ingestion of solid foods and lapping of milk, however, developed at weaning age. These were reflex in nature and and required contact of the lips with the food. Development of temperature regulation was impaired only slightly. Auditory reflexes, placing reactions, defense reactions, and many other types of behavior except visual recognition and socialization developed in nearly normal chronological order. In most animals some aspects of behavior were exaggerated. Hyperkinesis, hypermetria, compulsive climbing, and exaggerated prey behavior were frequently observed. The findings suggest that many aspects of behavior and regulatory processes generally thought to be organized primarily in the prosencephalon originate instead in the mesencephalon and more caudal structures and, during ontogeny, become increasingly dependent upon subsequently developing descending synaptic inputs.     

Activation by high intensity peripheral nerve stimulation of adrenergic and opioidergic inhibition of a spinal reflex in the decerebrated rabbit

The short-latency sural to gastrocnemius reflex in the decerebrated rabbit was depressed for 20-30 min following high intensity conditioning stimulation of the common peroneal nerve. This effect was observed in animals with or without spinal section, but was greater in non-spinalized preparations. Graded conditioning stimuli showed that it was necessary to activate fine myelinated common peroneal axons to inhibit the reflex. In spinalized rabbits, maximal inhibition was achieved with conditioning stimulation of fine myelinated axons and was completely reversed by the opioid antagonist naloxone. In non-spinalized rabbits, maximal inhibition was only obtained with conditioning stimuli which activated non-myelinated axons. In these preparations the effects of common peroneal nerve stimuli were only blocked by co-administration of naloxone with the alpha 2-adrenoceptor antagonist idazoxan. Thus high intensity peripheral nerve stimuli activated a segmental opioidergic and a supraspinal adrenergic suppression of the sural-gastrocnemius withdrawal reflex. Such long-lasting suppression of reflex excitability may contribute to recovery from intensely noxious stimuli.     

Postural development in rats

Mammals adopt a limited number of postures during their day-to-day activities. These stereotyped skeletal configurations are functionally adequate and limit the number of degrees of freedom to be controlled by the central nervous system. The temporal pattern of emergence of these configurations in altricial mammals is unknown. We therefore carried out an X-ray study in unrestrained rats from birth (P0) until postnatal day 23 (P23). The X-rays showed that many of the skeletal configurations described in adult rodents were already present at birth. By contrast, limb placement changed abruptly at around P10. These skeletal configurations, observed in anesthetized pups, required the maintenance of precise motor control. On the other hand, motor control continued to mature, as shown by progressive changes in resting posture and head movements from P0 to P23. We suggest that a few innate skeletal configurations provide the necessary frames of reference for the gradual construction of an adult motor repertoire in altricial mammals, such as the rat. The apparent absence of a requirement for external sensorial cues in the maturation of this repertoire may account for the maturation of postural and motor control in utero in precocial mammals (Muir et al., 2000 for a review on the locomotor behavior of altricial and precocial animals).     

Postural deformities in Parkinson's disease

Postural deformities are frequent and disabling complications of Parkinson's disease (PD) and atypical parkinsonism. These deformities include camptocormia, antecollis, Pisa syndrome, and scoliosis. Recognition of specific postural syndromes might have differential diagnostic value in patients presenting with parkinsonism. The evidence to date suggests that postural deformities have a multifactorial pathophysiology. Contributing factors include muscular rigidity; axial dystonia; weakness caused by myopathy; body scheme defects due to centrally impaired proprioception; and structural changes in the spine. The relative contribution of these different factors varies between patients and across specific syndromes. Improved understanding of the mechanisms underlying postural deformities in PD might ultimately lead us to more effective management strategies for these disabling and drug-refractory complications.     

Postural inflexibility in parkinsonian subjects.

In order to identify the types of postural deficits seen in parkinsonian patients with postural instability, we compared the performance of parkinsonian subjects with young and old control subjects in 3 aspects of postural control: (1) the use of sensory information for postural orientation, (2) the coordination of postural movement patterns in response to surface displacements, and (3) the flexible modification of postural response patterns to changes in support conditions. Parkinsonian subjects had very small sway, even under altered sensory conditions. Postural response latencies to displacements were also normal. Postural instability was associated with abnormal patterns of postural responses including excessive antagonist activity and inflexibility in adapting to changing support conditions. Some parkinsonian subjects appeared to have difficulty sequencing motor programs for postural correction. The parkinsonian subjects appeared stiffer since the rate-of-change of sway in response to displacements was reduced. Levodopa improved postural coordination but not the flexible adaptation to changing support conditions.     

Postural control in children with autism

Postural control was evaluated in samples of autistic, normal, and mentally retarded children in this pilot study using a recently developed, computerized posturographic procedure. A battery of postural positions was administered including postures involving some degree of stress (e.g., occluded vision or standing on pads). The postural patterns of children with autism differed from those observed in normal children, in mentally retarded children, and in adults with vestibular disorders. In comparison to normal children the autistic subjects were less likely to exhibit age-related changes in postural performance and postures were more variable and less stable with more lateral sway. Autistic subjects also exhibited a paradoxical response of greater stability with more stressful postures, putting excessive weight on one foot, one toe, or one heel. The implications for neuroanatomical models of autism are discussed.This work was supported in part by grant NS25026 from the National Institute of Health.     

Postural hypotension in chronically medicated schizophrenics

Blood pressure readings at rest and on standing in 196 chronic schizophrenic patients on stable long-term antipsychotic treatment were compared with those in unmedicated healthy controls. Patients recorded significantly lower resting blood pressure and significantly higher prevalence of postural hypotension than controls. The prevalence of postural hypotension in patients was 77% at 1 minute and 16.8% at 3 minutes after standing compared with absence of postural hypotension in controls at both time points. Prevalence of postural hypotension was unaffected by age or sex and was poorly correlated with drug dose, except in young patients. alpha 1-Receptor binding affinity of antipsychotic drugs was not predictive of postural hypotension. The possible significance of such persistent postural hypotension in chronically medicated patients is discussed.     

Reduction in excessive muscle tone by selective depletion of serotonin in intercollicularly decerebrated rats

Intercollicular decerebration in animals induces sustained facilitation of muscle tone of the limbs and this animal model has been used to assess centrally acting muscle relaxants. We have examined the involvement of central and spinal cord serotonergic pathways in the onset of excessive muscle tone in an intercollicularly decerebrated rat. Descending serotonergic pathways are known to modulate, directly or indirectly, the excitability of spinal cord motoneurons and it is inferred that serotonin (5-HT) plays an important role in locomotion. Alteration of muscle tone has been investigated in 5-HT-depleted rats with a neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT) after pretreatment with desipramine. Intracerebroventricular (i.c.v.) administration of 5,7-DHT reduced 5-HT content in the forebrain to 50.5% and that in the spinal cord to 10.5%, while intrathecal (i.t.) administration of 5,7-DHT decreased 5-HT content in the spinal cord to 8.9% without causing any change in the forebrain. In contrast, noradrenaline or dopamine content was not affected by the neurotoxin in both tissues. These treatments significantly attenuated the muscle tone in the animal models. Moreover, the measurement of 5-HT and 5-hydroxyindoleacetic acid content in intact rats after decerebration showed that facilitation of the 5-HT turnover in the spinal cord, but not in the forebrain, was enhanced compared with sham-operated rats. These findings suggest that the descending serotonergic pathways are essential to induce excessive muscle tone in the intercollicular decerebrated rats and that 5-HT antagonists might be candidates for centrally acting muscle relaxants.     

Postural induced‐tremor in psychiatry

Postural tremor is the most common movement disorder in psychiatry, and often a difficult problem for clinicians. It can be classified as physiological, essential, drug‐induced, and postural tremor in Parkinson's disease. Drugs used in psychiatry that can produce postural tremor, include lithium, valproic acid, lamotrigine, antidepressants, and neuroleptics. Clinical characteristics of postural tremor induced by each of these drugs are described. Pharmacological strategies for therapy in disabling drug‐induced tremor include beta‐blockers, primidone, gabapentin, topiramate, and benzodiazepines; their utility, doses and side‐effects are also discussed.     

Postural control in dyslexic and non-dyslexic children

Postural control relies to visual-motion processing (afferent or efferent) and this is thought to be deficient in dyslexics. There is a controversy between clinic and fundamental studies as to the presence of posture abnormalities in dyslexics. To explore further this issue, this study examines posture stability in quite stance in 13 dyslexics (mean age: 13.5 years) and in 13 non-dyslexics (mean age: 13 years). Experiment 1 shows that, similarly to adults and elderly, all children (dyslexics and non-dyslexics), present better stability at near distance (i.e. smaller surface area of the COP, smaller lateral and antero-posterior oscillations). This could be due to reduced angular size of retinal motion signals at far, but also to convergence relaxation. Importantly, the surface area of the COP, lateral and antero-posterior oscillations are significantly higher in dyslexics. Experiment 2 examines posture stability while subjects make active vergence movements between a far and a near target. For many dyslexics, moving the eyes back and forth in depth rather improved postural stability. The only significant difference was that the lateral oscillations were still higher in dyslexics. Experiment 3 uses eye movement recordings (video-oculography) and demonstrates that dyslexics have problems with maintaining stable the angle of vergence for a prolonged period. We conclude that mild postural instability may exist in dyslexics but it could be improved by oculomotor and attention processes.     

Postural balance in children with cerebral palsy

Postural control deficits have been suggested to be a major component of gait disorders in cerebral palsy (CP). Standing balance was investigated in 23 ambulatory children and adolescents with spastic diplegic CP, ages 5 to 18 years, and compared with values of 92 children without disability, ages 5 to 18 years, while they stood on a force plate with eyes open or eyes closed. The measurements included center of pressure calculations of path length per second, average radial displacement, mean frequency of sway, and Brownian random motion measures of the short-term diffusion coefficient, and the long-term scaling exponent. In the majority of children with CP (14 of 23) all standing balance values were normal. However, approximately one-third of the children with CP (eight of 23) had abnormal values in at least two of the six center of pressure measures. Thus, mean values for path length, average radial displacement, and diffusion coefficient were higher for participants with CP compared with control individuals with eyes open and closed (p<0.05). Mean values for frequency of sway and the long-term scaling exponent were lower for participants with CP compared with control participants (p<0.05). Increased average radial displacement was the most common (nine of 23) postural control deficit. There was no increase in abnormal values with eyes closed compared with eyes open for participants with CP, indicating that most participants with CP had normal dependence on visual feedback to maintain balance. Identification of those children with impaired standing balance can delineate factors that contribute to the patient's gait disorder and help to guide treatment.     

Postural instability precedes motion sickness

We evaluated the hypothesis that postural instability precedes the onset of motion sickness. Subjects standing in a "moving room" were exposed to nearly global oscillating optical flow. In the experimental condition, the optical oscillations were a complex sum-of-sines between 0.1 and 0.3 Hz, with an excursion of 1.8 cm. This optical motion was of such low frequency and magnitude that it was sometimes not noticed by subjects. However, in two experiments, exposure to the moving room produced significant increases in scores on a standard motion sickness questionnaire. In addition, approximately half of subjects reported motion sickness. Analysis of postural motion during exposure to the moving room revealed increases in postural sway before the onset of subjective motion sickness symptoms. This confirms a key prediction of the postural instability theory of motion sickness.