Assessment of the gait-related acceleration patterns in adults with autism spectrum disorder.

Individuals with autism spectrum disorder (ASD) can exhibit a range of movement issues, which are often characterized by a general slowing of movement responses that can extend to walking speed. The current study was designed to examine the spatio-temporal features and pattern of acceleration for the trunk, neck and head during walking for a cohort of adults with ASD compared to neurotypical individuals. Twenty young adults with ASD and 20 age-matched neurotypical adults participated in this study. Participants performed five walking trials across a 20ft Protokinetics pressure sensitive surface at their preferred walking speed. Accelerations were collected using three triaxial accelerometers affixed to the head, neck, and lower trunk. Comparisons of acceleration amplitude (i.e., RMS), frequency, segmental gain and regularity (i.e., SampEn) during the walking tasks were performed. Results revealed that the adults with ASD walked slower than the neurotypical persons with a greater proportion of time spent in double stance. Despite walking at a slower pace overall, the adults with ASD exhibited a decreased ability to attenuate gait-related oscillations from the trunk to the head. Overall, these findings suggest that adults with ASD exhibited a decreased ability to accommodate and dampen those accelerations related to walking. As declines in gait speed are often linked with loss of head control, one suggestion is that the inability to appropriately compensate for gait-related oscillations may, in part, explain why persons with ASD walk slower.

Activation of cholinergic and adrenergic receptors increases the concentration of extracellular adenosine in the cerebral cortex of unanesthetized rat.

Adenosine is an inhibitory neuromodulator in the CNS. For extracellular adenosine to play a physiological role in the brain, it must be present at effective concentrations. Acetylcholine and noradrenaline are known to play an important role in modulating the activity of cortical neurons, and they might have a role also in the release of adenosine in the cerebral cortex in vivo. We examined whether activation of cholinergic and adrenergic receptors affects extracellular adenosine levels in the cerebral cortex of unanesthetized rats using in vivo microdialysis. All drugs were administered locally within the cortex by reverse dialysis. Both acetylcholine and the acetylcholinesterase inhibitor neostigmine increased extracellular adenosine levels, and the effect of neostigmine was blocked by the nicotinic receptor antagonist mecamylamine. Both nicotine and the nicotinic receptor agonist epibatidine increased the concentration of extracellular adenosine. Activation of muscarinic receptors using the nonselective agonist oxotremorine and a selective M1 receptor agonist also increased extracellular adenosine levels. Noradrenaline and the noradrenergic reuptake inhibitor desipramine increased extracellular adenosine levels. The alpha(1)-adrenergic receptor agonist phenylephrine and the beta-adrenergic agonist isoproterenol increased extracellular adenosine levels, whereas the alpha(2)-adrenergic receptor agonist clonidine did not have an effect. These findings indicate that activation of specific cholinergic and adrenergic receptors can increase extracellular levels of adenosine in the cortex, and suggest that cholinergic and adrenergic receptor-mediated regulation of adenosine levels may represent a mechanism for controlling the excitability of cortical neurons.

Activation of metabotropic glutamate receptors increases extracellular adenosine in vivo.

In order to identify the mechanisms that would lead to increased levels of the inhibitory neuromodulator adenosine in the brain, we tested metabotropic glutamate receptor agonists for their ability to increase extracellular adenosine in the cortex of unanesthetized rat using in vivo microdialysis. The group I/II metabotropic glutamate receptor agonist trans-(+/-)- 1-amino-(1S,3R)-cyclopenyanedicarboxylic acid (I mM) increased extracellular adenosine as did the specific group I agonist (S)- 3,5-dihydroxyphenylglycine (DHPG; 1 mM). The evoked increase of adenosine by 1 mM DHPG was reduced by the group I antagonist (RS)- 1-aminoindan-1,5,-dicarboxylic acid. Activation of group II or III metabotropic receptors did not affect extracellular adenosine. These results suggest that activation of group I metabotropic receptors contributes to elevated extracellular adenosine levels in vivo.

Immunohistochemical localization of caffeine-induced c-Fos protein expression in the rat brain.

Although caffeine is the most widely used central nervous system stimulant, the neuronal populations and pathways mediating its stimulant effects are not well understood. Using c-Fos protein as a marker for neuronal activation, the present study investigated the pattern of c-Fos induction at 2 hours after low locomotor-stimulant doses (1, 5, 10, and 30 mg/kg, i.p.) of caffeine and compared them with those after a higher dose (75 mg/kg, i.p.) or saline injection in adult male rats. Fos-immunoreactive neurons were counted in selected nuclei across the entire brain. Caffeine induced an increase in locomotor activity in a dose-dependent manner up to doses of 30 mg/kg and a decline at 75 mg/kg. Quantitative analysis of Fos-immunoreactive neurons indicated that no structures showed significant Fos expression at doses below 75 mg/kg or a biphasic pattern of Fos expression, as in locomotion. In contrast, caffeine at 75 mg/kg induced a significant increase compared with the saline condition in the number of Fos-immunoreactive neurons in the majority of structures examined. The structures included the striatum, nucleus accumbens, globus pallidus, and substantia nigra pars reticulata and autonomic and limbic structures including the basolateral and central nuclei of the amygdala, paraventricular and supraoptic hypothalamic nuclei, periventricular hypothalamus, paraventricular thalamic nuclei, parabrachial nuclei, locus coeruleus, and nucleus of the solitary tract. The locomotor-enhancing effects of low doses of caffeine did not appear to be associated with significant Fos expression in the rat brain.

The teething virus.

A prospective study was carried out on 500 teething infants which demonstrated that a new infectious agent, the human teething virus, is responsible for the febrile response that accompanies the eruption of deciduous teeth. Speculations are made concerning whether or not primary care physicians will began prescribing amoxicillin instead of Jack Daniel's to treat teething infants and their parents.

The student's dilemma.

This section is reserved for commentaries and brief essays dealing with matters of interest to physicians. Material for consideration should not exceed five double-spaced typewritten pages. An honorarium of $75 is offered at the time of publication. Submissions should be addressed to: Editor, POSTGRADUATE MEDICINE, 4530 W 77th St, Minneapolis, MN 55435.