No description available.

Understanding these neurodevelopmental disorders will help oral health professionals provide safe and effective care.

The purpose of the study was to explore sensory processing patterns with children ages 5 to 12 years who are diagnosed with two subtypes of ADHD, inattention and hyperactive- impulsive and with children who do not have ADHD. The study delineated children with ADHD from a control group of children without ADHD and how sensory processing issues affect the population with ADHD. The participants were parents or caregivers of children aged 5 to 12 years diagnosed with ADHD and parents or caregivers of children aged 5 to 12 years without a diagnosis of ADHD. The participants totaled 45 with 26 participants in the ADHD group and 19 participants in the non ADHD group. Parents or caregivers completed the SSP Caregiver Questionnaire, the Sensory Processing Measure [SPM], and the Connors Parent Rating Scale-Revised: Short Form. The independent t-test was the statistical procedure used to determine whether the means of the ADHD and non-ADHD groups were statistically different from each other. A Pearson correlation was calculated to measure the degree of association between the children with ADHD and non-ADHD with the types of sensory processing patterns. Finding suggested that children who score high on these ADHD scales have more sensory processing difficulties. Children with hyperactivity ADHD scored a significantly higher mean then children with inattention on an auditory subtest and on a under responsive subtest. Children with inattentive ADHD scored a significantly higher mean than children with hyperactivity on a touch subtest. / Occupational Therapy

Every second throughout life, cortical circuitry efficiently compresses and interprets huge volumes of incoming sensory information. This high fidelity sensory processing guides normal brain development and is essential for animals’ successful interaction with the environment. Low-level sensory perceptual disturbance is nearly ubiquitous in Autism Spectrum Disorder (ASD), but despite the potential to offer crucial insight into the abnormal development of higher brain function is poorly understood. Fragile X Syndrome (FXS) is the most common heritable cause of ASD. Previous studies in the Fmr1-KO mouse model of FXS report cell-intrinsic, synaptic and local connectivity abnormalities in the neuronal physiology of primary sensory cortices. This suggests that sensory perceptual dysfunction could emerge from interacting circuit-wide pathophysiology to impair neural adaptations that support high fidelity sensory information processing. However, there is little mechanistic consensus about how this might occur. To address this, in this thesis I use brain slice electrophysiology and computer modelling to provide a bottom-up description of how thalamocortical (TC) responses, the principal cortical input for ascending sensory information, are mis-interpreted in the somatosensory Layer 4 (L4) circuit in Fmr1-KOs at a crucial developmental transition to active sensory processing. Recruitment of intracortical L4 network activity could be atypically evoked by lower frequency thalamic stimulation in Fmr1-KO slices. Furthermore, profound alterations to single-cell and network response dynamics were observed, in particular loss of spike timing precision considered critical for sensory circuit performance. These network phenomena were supported by interacting single-cell and local circuitry pathophysiology, including hyperexcitable cortical neurons and temporally distorted feed forward and feedback inhibition. Together, these data demonstrate cortical hypersensitivity to TC inputs and abnormal recruitment of network activity in critical period Fmr1-KO somatosensory cortical circuits. The hyperresponsiveness of intracortical circuitry may underlie tactile hyperexcitability and distorted sensory perception in FXS patients. Interestingly, modelling suggests that many of the alterations of synaptic and neuronal function are compensatory, thus minimizing the impact of the genetic lesion. Thus, this study shows for the first time that circuit level dysfunction emerges in the Fmr1-KO mouse from an accumulation of effects at the synaptic and cellular level; however, it also highlights the challenge of understanding which of these changes are pathological and which are compensatory.

Being knowledgeable about sensory processing disorders can help dental teams provide effective care and improve the oral health of this patient population.

No description available.

The incidence of autism has increased from an average of one in 88 to one in 110 (Center for Disease Control, 2010; ADDM Network, 2012). Autism spectrum disorders are an important health and educational problem affecting many areas of daily living, (CDC, 2012; Cermak, S., et al, 2010). Over 80 percent of children diagnosed with autism demonstrate sensory modulation symptoms and related behaviors such as sensory seeking, sensory avoiding, self-stimulation, etc, (Kintwell, et al, 2011; Ben-Sasson, et al, 2009; Tomchek & Dunn, 2006). There is some beginning evidence found in the literature that sensory processing of children on the autism spectrum interferes with their daily routines (Nadon, et al, 2011; Stein, et al, 2011/2012; Schaff, et al, 2011), and there is a paucity of research which addresses the impact sensory processing has on the daily routine of eating. This study will contribute to this expanding body of knowledge. Eating difficulties are a frequent problem for children on the autism spectrum (Nadon, et al, 2011; Schreck & Williams, 2006) which impacts their physical health (Lukens & Linscheid, 2008), their functioning in the family (Schaff, et al, 2001) and their functioning in educational settings (Koenig & Rudney, 2010). This study assesses the differences in sensory processing and eating problem behaviors between two groups of children, aged 5 -12 years, those identified on the autism spectrum (N=34) and those typically developing (N=34). Data was collected through parent and child questionnaires that assessed sensory processing and eating behaviors (BAMBI, Short Sensory Profile, Sensory Eating Checklist, and Touch Inventory for Elementary-Aged Children). Results of the t test, anovas and correlation analyses revealed statistically significant differences on all measures between both samples (p

Behavioral and psychological symptoms of dementia create challenges for those living with neurodegenerative cognitive impairment and their care partners. Pharmacological approaches for treatment of challenging behaviors seen in dementia have limited success and serious side effects. Because of this, nonpharmacological approaches are being investigated with increasing frequency. Of particular interest are nonpharmacological approaches involving environmental stimulation to change behaviors. Success of such approaches relies on sensory processing systems, personal preferences, and environmental congruence. There is limited evidence describing behaviors of persons with cognitive impairment in relation to these components. Currently, there is no guiding model for implementation of environmental and sensory-based strategies with this population. The overall goal of this project is to elaborate on an emerging model describing the relationship among environment, behavior, sensation, and cognitive impairment for community-dwelling adults with mild cognitive impairment or dementia. Three studies allow for deeper understanding of this relationship. Study one compared behaviors seen in autism spectrum disorder (ASD) with exhibited behaviors of individuals with mild cognitive impairment or dementia. Of neurological conditions similar to dementia, ASD has been chosen as an exemplar for comparison of behavioral expression because evidence supports sensory-based theory and interventions to improve behaviors for those with ASD. Results indicate that ASD behaviors are reported in those assessed, with highest rates of behaviors in those with young age of onset and advanced cognitive impairment severity. Study two described presentation of behavior, sensory processing, and environment for community-dwelling adults with cognitive impairment in the context of the caregiver situation. Findings reflect dyadic experiences for the person with cognitive impairment and the primary care partner. Emergent themes included consideration of the passage of time, environmental contexts, behavioral adjustments while aging, and overall influences of living with cognitive impairment. Sensory processing assessment using the Adult Sensory Profile identified that all participants had some atypical sensory processing patterns, highlighting a need for attention to environmental congruence to promote adaptive behaviors. Using data collected in study one and study two, a model was created describing interactions among the person with cognitive impairment, sensation, and the environment as these interactions evolve over time. Areas for future research are conceptualized for implementation of the model. Future research is needed for assessment of the model to test for validity and reliability. Creation of an instrument is needed to place individuals within the model given their behavior and cognitive impairment progression. And, future research is needed to create and test interventions in order to aid in environmental congruence. Long-term goals are to improve care for adults with cognitive impairment and dementia via environmental interventions.

This study tested the prediction that a group of dyslexic children (n = 70) would be less sensitive to auditory and visual temporal stimuli than a control group (n = 52). In the auditory domain, detection thresholds for 2 Hz FM, 2 Hz AM and 20 Hz AM were assessed. The modulations in these stimuli are detected on the basis of temporal cues. In contrast, the modulations in the control stimulus 240 Hz FM modulate too rapidly to be detected with temporal cues. The dyslexic group were significantly less sensitive than the control group to the temporal and non-temporal measures at initial testing (Phase 1) and again nine months later (Phase 4). These data demonstrated that the auditory deficit in the dyslexic group was more general in nature than had previously been suggested. In the visual domain, sensitivity to global coherent motion was assessed. The dyslexic group were significantly less sensitive than the control group on this measure at both phases of the study. Despite the overall between group differences, the magnitude of the effects were low to moderate. There was also substantial overlap between the performance of the two groups on the sensory processing measures. A deviance analysis was conducted to determine the proportion of dyslexic individuals who had sensory processing deficits. When data from each phase was examined separately, the incidence of sensory processing deficits in the dyslexic group was comparable to previous studies. However, when the data from both phases was combined, only 5-18% of the dyslexic group had impairments on any of the sensory tasks that were stable across time. Nevertheless, these results do not preclude sensory processing making a contribution to reading difficulties in some children. When the relationship between sensory processing thresholds and reading ability was considered, sensitivity to auditory and visual temporal measures accounted for significant unique variance in phonological processing, orthographic coding and overall reading skill, even after accounting for IQ and vigilance. This study was also tested the prediction that visual attention can explain the link between visual temporal processing and reading. Vidyasagar (1999) proposed that the magnocellular (M) system, which processes temporal stimuli (e.g., motion), is also important for efficient functioning of an attentional spotlight. This spotlight is proposed to arise in parietal cortex (a major endpoint of the M system), and is involved in highlighting areas for detailed visual processing when performing visual tasks, such as visual search or reading. It was predicted that only those dyslexic participants with motion detection impairments would also be impaired on a serial search task that required the attentional spotlight. On average, the dyslexic group had significantly slower serial search than the control group. However, the magnitude of effect was small and a deviance analysis demonstrated that only 8.5% of the dyslexic group had stable impairments relative to the control group. Furthermore, only one of the six dyslexic participants with a visual attention impairment had a co-existing deficit in detecting coherent motion. Thus, visual attention deficits of this type appear to exist independently of coherent motion deficits. This study also provided important evidence on the reliability of measurement for the sensory processing tasks. The data showed that the test-retest reliability of the sensory measures was only moderate over a nine month period. Test-retest for other cognitive measures over the same time frame was high - including that for an orthographic coding task, which had similar procedure and task demands to the sensory measures. The results also demonstrated that a high proportion of participants in both groups performed inconsistently across time (i.e., they had a threshold indicative of a deficit at one phase and performance within normal limits at the other). Up to 32% of the dyslexic group and 19% of the control group had inconsistent performance on the sensory measures across time. The importance of developing more reliable methods of estimating sensory sensitivity is discussed, as is the need for normative data on sensory processing tasks in order to more accurately make decisions about the incidence of sensory deficits. In summary, this study provided evidence for a relationship between sensory processing and reading. However, the current data demonstrated that sensory processing deficits are not characteristic of all dyslexic individuals. Future research should focus on explaining why only a sub-group of dyslexics have sensory deficits, and also why some control participants have deficits.

The medial geniculate body (MGB) is the thalamic nucleus situated between the inferior colliculus (IC) and auditory cortex (AC) in the ascending auditory pathway. It has classically been thought of as a relay station for auditory stimuli; however, we now know that is capable of significantly influencing incoming auditory information. As aging occurs, there is a loss of auditory signal fidelity as well as a disruption in the accurate coding of acoustic information. In order to compensate for the age-related loss of auditory signal quality, additional cortical resources play a role in knowledge-based optimization of input. This top-down processing is mediated in part by cholinergic systems, which direct attention to relevant incoming sensory information. The primary cholinergic input to the MGB is a large cholinergic projection from the pontomesencephalic tegmentum. The PMT is a brainstem structure composed of the pedunculopontine nucleus and laterodorsal tegmental nuclei. These structures provide acetylcholine (ACh) to the auditory thalamus and midbrain thereby playing a role in sustaining attention, sensory gating, and arousal. Acetylcholine may then act at pre- and postsynaptic receptors at the level of MGB and function to assign salience to auditory stimuli. The central goal of these studies is to examine the location of nAChRs in the local MGB circuitry, their subunit composition, physiology, and how these properties are impacted with age. We have found that ACh produces significant excitatory postsynaptic actions on young MGB neurons, likely mediated by β2-containing heteromeric nAChRs. Use of the β2-selective nAChR antagonist, dihydro-β-erythroidine, suggests that loss of cholinergic efficacy may also be due to an age-related subunit switch from high affinity β2-containing nAChRs to low affinity β4-containing nAChRs, in addition to a loss of total nAChR number. This age-related nAChR dysfunction may partially underpin the attentional deficits which contribute to the loss of speech understanding in the elderly. Activation of presynaptic nAChRs potentiated responses evoked by stimulation of excitatory corticothalamic terminals and inhibitory tectothalamic terminals. Conversely, application of ACh appeared to have no consistent effects on paired-pulse responses evoked from stimulation of excitatory tectothalamic terminals and inhibitory projections from the thalamic reticular nucleus. Responses to nAChR activation at excitatory corticothalamic and inhibitory tectothalamic inputs were attenuated by aging. The present findings suggest that the increased output from the cholinergic pedunculopontine neurons onto MGB neurons following presentation of difficult to identify stimuli or arousal increases the strength of tectothalamic inhibitory projections likely improving signal-to-noise ratio and enhancing signal detection, while increasing gain on corticothalamic excitatory signals facilitating top-down identification of the unknown stimulus. Thus, cholinergic inputs to MGB are positioned to maximize sensory processing by dynamically adjusting both top-down and bottom-up mechanisms in conditions of attention/arousal.