The diagnostic criteria of Asperger's syndrome (AS), considered a part of the autistic spectrum disorder, are still unclear. A critical marker, which distinguishes AS from autism, is the presence of language. The ability of a child with AS to acquire and use language early results in the fact that AS usually is diagnosed much later than autism. Autism is not usually diagnosed until around the age of 3, whereas AS usually is not diagnosed until the child is 6 or 7 years of age. In the present article, using Eshkol-Wachman movement notation, we present evidence that abnormal movement patterns can be detected in AS in infancy. This finding suggests that AS can be diagnosed very early, independent of the presence of language. As shown earlier by us, almost all of the movement disturbances in autism can be interpreted as infantile reflexes ''gone astray''; i.e., some reflexes are not inhibited at the appropriate age in development, whereas others fail to appear when they should. This phenomenon appears to apply to AS as well. Based on preliminary results, a simple test using one such reflex is proposed for the early detection of a subgroup of children with AS or autism.

Performance of a motor task is improved by practicing a specific task with added “challenges” to a training regimen. We tested the hypothesis that in the absence of brain control the performance of a motor task is enhanced by training using specific variations of that task. We utilized modifications of step performance training to improve the ability of spinal rats to forward step. After a complete thoracic spinal cord transection, 20 adult rats were divided randomly to bipedally step on a treadmill in the forward, sideward, or backward direction for 28 sessions (20 min, 5d/week) and subsequently tested for their ability to step in the forward direction. Although the animals from all trained groups showed improvement, the rats in the sideward trained and backward trained groups had greater step consistency and coordination along with higher peak amplitudes and total integrated activity of the rectified electromyography signals from selected hindlimb muscles per step during forward stepping than the rats in the forward trained group. Our results demonstrate that by retaining the fundamental features of a motor task (bipedal stepping) the ability to perform that motor task can be enhanced by the addition of specific contextual variations to the task (direction of stepping). Our data suggest that the forward stepping neuronal locomotor networks are partially complemented by synchronous activation of interneuronal/motoneuronal populations that are also a part of the sideward or backward stepping locomotor networks. Accordingly, the overlap and interaction of neuronal elements may play a critical role in positive task transference.

Can lower limb motor function be improved after a spinal cord lesion by re-engaging functional activity of the upper limbs? We addressed this issue by training the forelimbs in conjunction with the hindlimbs after a thoracic spinal cord hemisection in adult rats. The spinal circuitries were more excitable, and behavioural and electrophysiological analyses showed improved hindlimb function when the forelimbs were engaged simultaneously with the hindlimbs during treadmill step-training as opposed to training only the hindlimbs. Neuronal retrograde labelling demonstrated a greater number of propriospinal labelled neurons above and below the thoracic lesion site in quadrupedally versus bipedally trained rats. The results provide strong evidence that actively engaging the forelimbs improves hindlimb function and that one likely mechanism underlying these effects is the reorganization and re-engagement of rostrocaudal spinal interneuronal networks. For the first time, we provide evidence that the spinal interneuronal networks linking the forelimbs and hindlimbs are amenable to a rehabilitation training paradigm. Identification of this phenomenon provides a strong rationale for proceeding toward preclinical studies for determining whether training paradigms involving upper arm training in concert with lower extremity training can enhance locomotor recovery after neurological damage.

Study design: A cross-sectional study design. Objectives: To characterize and specifically quantify impairments in muscle function after chronic incomplete spinal cord injury (SCI). Setting: University of Florida, Gainesville, FL, USA. Methods: Voluntary and electrically elicited contractile measurements were performed and voluntary activation deficits were quantitatively determined in the knee extensor and ankle plantar flexor muscle groups in 10 individuals with chronic incomplete SCI (C5-T8, ASIA C or D) and age-, gender-, height-and body weight matched healthy controls. Results: Persons with incomplete-SCI were able to produce only 36 and 24% of the knee extensor torque and 38 and 26% of the plantar flexor torque generated by noninjured controls in the self-reported less-involved and more-involved limbs, respectively (Po0.05). In addition, both indices of explosive or instantaneous muscle strength, torque 200 (absolute torque reached at 200 ms) and the average rate of torque development (ARTD) were dramatically reduced in the ankle plantar flexor and knee extensor muscle groups in persons with incomplete-SCI. However, the deficit in instantaneous muscle strength was most pronounced in the ankle plantar flexor muscles, with an 11.7-fold difference between the torque 200 measured in the self-reported more involved limb and a 5-fold difference in the less-involved limb compared to control muscles. Voluntary activation deficits ranged between 42 and 66% in both muscle groups. Interestingly, electrically elicited contractile properties did not differ between the groups. Conclusion: The resultant impact of incomplete-SCI is that affected muscles not only become weak, but slow to develop voluntary torque. We speculate that the large deficit in torque 200 and ARTD in the ankle plantar flexors muscles of persons with incomplete-SCI may limit locomotor function. The results presented in this study provide a quantitative and sensitive assessment of muscle function upon which future research examining rehabilitation programs aimed at restoring muscle function and promoting functional recovery after incomplete-SCI may be based.

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Muscle atrophy is clearly related to a loss of muscle torque, but the reduction in muscle size cannot entirely account for the decrease in muscle torque. Reduced neural input to muscle has been proposed to account for much of the remaining torque deficits after disuse or immobilization. The purpose of this investigation was to assess the relative contributions of voluntary muscle activation failure and muscle atrophy to loss of plantarflexor muscle torque after immobilization. Nine subjects (ages 19-23) years with unilateral ankle malleolar fractures were treated by open reduction-internal fixation and 7 weeks of cast immobilization. Subjects participated in 10 weeks of rehabilitation that focused on both strength and endurance of the plantarflexors. Magnetic resonance imaging, isometric plantarflexor muscle torque and activation (interpolated twitch technique) measurements were performed at 0, 5, and 10 weeks of rehabilitation. Following immobilization, voluntary muscle activation (56.8 AE 16.3%), maximal cross-sectional area (CSA) (35.3 AE 7.6cm 2 ), and peak torque (26.2 AE 12.7N-m) were all significantly decreased ( p < 0.0056) compared to the uninvolved limb (98.0 AE 2.3%, 48.0 AE 6.8 cm 2 , and 105.2 AE 27.0 N-m, respectively). During 10 weeks of rehabilitation, muscle activation alone accounted for 56.1% of the variance in torque ( p < 0.01) and muscle CSA alone accounted for 35.5% of the variance in torque ( p < 0.01). Together, CSA and muscle activation accounted for 61.5% of the variance in torque ( p < 0.01). The greatest gains in muscle activation were made during the first 5 weeks of rehabilitation. Both increases in voluntary muscle activation and muscle hypertrophy contributed to the recovery in muscle strength following immobilization, with large gains in activation during the first 5 weeks of rehabilitation. In contrast, muscle CSA showed fairly comparable gains throughout both the early and later phase of rehabilitation. ß

Dyshomeostasis of both ceramides and sphingosine-1-phosphate (S1P) in the brain has been implicated in aging-associated neurodegenerative disorders in humans. However, mechanisms that maintain the homeostasis of these bioactive sphingolipids in the brain remain unclear. Mouse alkaline ceramidase 3 (Acer3), which preferentially catalyzes the hydrolysis of C18:1-ceramide, a major unsaturated long-chain ceramide species in the brain, is upregulated with age in the mouse brain. Acer3 knockout causes an age-dependent accumulation of various ceramides and C18:1-monohexosylceramide and abolishes the age-related increase in the levels of sphingosine and S1P in the brain; thereby resulting in Purkinje cell degeneration in the cerebellum and deficits in motor coordination and balance. Our results indicate that Acer3 plays critically protective roles in controlling the homeostasis of various sphingolipids, including ceramides, sphingosine, S1P, and certain complex sphingolipids in the brain and protects Purkinje cells from premature degeneration.

BackgroundEpidural stimulation of the spinal cord can be used to enable stepping on a treadmill (electrical enabling motor control, eEmc) after a complete mid-thoracic spinal cord transection in adult rats. Herein we have studied the effects of eEmc using a sub-threshold intensity of stimulation combined with spontaneous load-bearing proprioception to facilitate hindlimb stepping and standing during daily cage activity in paralyzed rats.MethodsWe hypothesized that eEmc combined with spontaneous cage activity would greatly increase the frequency and level of activation of the locomotor circuits in paralyzed rats. Spontaneous cage activity was recorded using a specially designed swivel connector to record EMG signals and an IR based camcorder to record video.Results and conclusionThe spinal rats initially were very lethargic in their cages showing little movement. Without eEmc, the rats remained rather inactive with the torso rarely being elevated from the cage floor. When the rats used their forelimbs to move, the hindlimbs were extended and dragged behind with little or no flexion. In contrast, with eEmc the rats were highly active and the hindlimbs showed robust alternating flexion and extension resulting in step-like movements during forelimb-facilitated locomotion and often would stand using the sides of the cages as support. The mean and summed integrated EMG levels in both a hindlimb flexor and extensor muscle were higher with than without eEmc. These data suggest that eEmc, in combination with the associated proprioceptive input, can modulate the spinal networks to significantly amplify the amount and robustness of spontaneous motor activity in paralyzed rats.