Background: A number of neurophysiological characteristics demonstrated in autism share the common theme of under-connectivity in the cerebral cortex. One of the prominent theories of the cause of the dysfunctional connectivity in autism is based on distinct anatomical structures that differ between the autistic and the neurotypical cortex. The functional minicolumn has been identified as occupying a much smaller space in the cortex of people with autism as compared to neurotypical controls, and this aberration in architecture has been proposed to lead to under-connectivity at the local or withinmacrocolumn level, which in turn leads to dysfunctional connectivity globally across cortical areas in persons with autism. Numerous reports have indicated reduced synchronization of activity on a large scale in the brains of people with autism. We hypothesized that if the larger-scale aberrant dynamics in autism were due -at least in part -to a widespread propagation of the errors introduced at the level of local connectivity between minicolumns, then aberrations in local functional connectivity should also be detectable in autism.

While it is well known that skin physiology – and consequently sensitivity to peripheral stimuli – degrades with age, what is less appreciated is that centrally mediated mechanisms allow for maintenance of the same degree of functionality in processing these peripheral inputs and interacting with the external environment. In order to demonstrate this concept, we obtained observations of processing speed, sensitivity (thresholds), discriminative capacity, and adaptation metrics on subjects ranging in age from 18 to 70. The results indicate that although reaction speed and sensory thresholds change with age, discriminative capacity, and adaptation metrics do not. The significance of these findings is that similar metrics of adaptation have been demonstrated to change significantly when the central nervous system (CNS) is compromised. Such compromise has been demonstrated in subject populations with autism, chronic pain, acute NMDA receptor block, concussion, and with tactile–thermal interactions. If the metric of adaptation parallels cortical plasticity, the results of the current study suggest that the CNS in the aging population is still capable of plastic changes, and this cortical plasticity could be the mechanism that compensates for the degradations that are known to naturally occur with age. Thus, these quantitative measures – since they can be obtained efficiently and objectively, and appear to deviate from normative values significantly with systemic cortical alterations – could be useful indicators of cerebral cortical health.

Adults with autism exhibit inhibitory deficits that are often manifested in behavioral modifications, such as repetitive behaviors, and/or sensory hyper-responsiveness. If such behaviors are the result of a generalized deficiency in inhibitory neurotransmission, then it stands to reason that deficits involving localized cortical-cortical interactions – such as in sensory discrimination tasks – could be detected and quantified. This study exemplifies a newly developed method for quantifying sensory testing metrics. Our novel sensory discrimination tests may provide (a) an effective means for biobehavioral assessment of deficits specific to autism and (b) an efficient and sensitive measure of change following treatment. The sensory discriminative capacity of 10 subjects with autism and 10 controls was compared both before and after short duration adapting stimuli. Specifically, vibrotactile amplitude discriminative capacity was obtained both in the presence and absence of 1 sec adapting stimuli that were delivered 1 sec prior to the comparison stimuli. Although adaptation had a pronounced effect on the amplitude discriminative capacity of the control subjects, little or no impact was observed on the sensory discriminative capacity of the subjects with autism. This lack of impact of the adapting stimuli on the responses of the subjects with autism was interpreted to be consistent with the reduced GABAergic mediated inhibition described in previous reports. One significant aspect of this study is that the methods could prove to be a useful and efficient way to detect specific neural deficits and monitor the efficacy of pharmacological or behavioral treatments in autism.

Background: A subject's ability to differentiate the loci of two points on the skin depends on the stimulus-evoked pericolumnar lateral inhibitory interactions which increase the spatial contrast between regions of SI cortex that are activated by stimulus-evoked afferent drive. Nevertheless, there is very little known about the impact that neuronal interactions -such as those evoked by mechanical skin stimuli that project to and coordinate synchronized activity in adjacent and/or near-adjacent cortical columns -could have on sensory information processing.

Objective To investigate the clinical correlates of central nervous system (CNS) alterations among women with vulvodynia. Altered central sensitization has been linked to dysfunction in CNS inhibitory pathways (e.g. GABAergic), and metrics of sensory adaptation, a centrally mediated process that is sensitive to this dysfunction, could potentially be used to identify women at risk of treatment failure using conventional approaches. Methods Twelve women with vulvodynia and twenty age-matched controls participated in this study, which was conducted by sensory testing of the right hand’s index and middle fingers. The following sensory precepts were assessed: 1) vibrotactile detection threshold; 2) amplitude discrimination capacity (defined as the ability to detect differences in intensity of simultaneously delivered stimuli to two fingers); and 3) a metric of adaptation (determined by the impact that applying conditioning stimuli have on amplitude discriminative capacity). Results Participants did not differ on key demographic variables, vibrotactile detection threshold, and amplitude discrimination capacity. However, we found significant differences from controls in adaptation metrics in one subgroup of vulvodynia patients. Compared to healthy controls and women with a shorter history of pain (n=5; duration (yr) = 3.4 ± 1.3), those with a longer history (n=7; duration (yr) = 9.3 ±1.4)) were found to be less likely to have adaptation metrics similar to control values. Discussion Chronic pain is thought to lead to altered central sensitization, and adaptation is a centrally mediated process that is sensitive to this condition. This report suggests that similar alterations exist in a subgroup of vulvodynia patients.