Altered Sensory Processing Research Articles

Altered Sensory Processing in People Attending Specialist Orthopaedic Consultation for Management of Persistent Shoulder Pain: An Observational Cross-Sectional Study.

OBJECTIVES: The primary objective was to compare sensory processing measures in people attending specialist orthopaedic consultation for management of persistent shoulder pain with control participants. The secondary objective was to compare the groups' sociodemographic, clinical, general health and lifestyle, and psychological characteristics. DESIGN: Observational cross-sectional. METHODS: Participants with shoulder pain for ≥3 months, who attended a public hospital orthopaedic department (n = 119), and community participants without shoulder pain (n = 44) underwent a standardized quantitative sensory testing protocol, measuring pressure pain threshold, temporal summation, and conditioned pain modulation. Sociodemographic, clinical, general health and lifestyle, and psychological characteristics were also collected. RESULTS: Participants with shoulder pain had significantly lower pressure pain thresholds at all sites (ie, local and widespread mechanical hyperalgesia) and significantly decreased conditioned pain modulation effect (ie, descending inhibition of nociception) than control participants. There was no significant difference between groups for temporal summation. Participants with shoulder pain had decreased general health and function, less healthy lifestyles, and poorer psychological health compared with controls. CONCLUSION: People referred to specialist orthopaedic care for management of persistent shoulder pain had clinical signs of altered sensory processing and poor health outcomes. J Orthop Sports Phys Ther 2024;54(10):1-10. Epub 25 July 2024. doi:10.2519/jospt.2024.12512.

Хроническая боль в спине: от патогенеза к адекватной фармакотерапии

Chronic back pain is an actual problem of clinical medicine, the pathogenesis of which includes peripheral nociceptive stimulation, peripheral and/or central inflammation, abnormality of the central pain modulation network and mixed onset of various pathological mechanisms. Sources of nociceptive signal generation include the intervertebral disc, muscles, fasciae, facet joints, sacroiliac joints, pubic symphysis, ligaments and joint capsule, and other structures that contain nociceptors. Any event that causes tissue degeneration activates a massive inflammatory response that infiltrates the MPD, joints, muscles, fascia and other tissues, stimulates nociceptive receptors to produce inflammatory substances, which directly damages the nerve root and causes pain. Simultaneously, the damaged MPD and endplate stimulate pathological and invasive growth and proliferation of vessels and nerves in the MPD. Increasing evidence also suggests that systemic inflammation plays a crucial role in the pathogenesis of chronic back pain. The central mechanism of back pain involves altered sensory processing in the brain. Dysfunction of the descending pain modulation system results in amplification of pain information in the brain. Since monotherapy for chronic back pain is not optimal, it is necessary to promote the comprehensive treatment recommended by current international clinical guidelines and it is reasonable to combine several therapies to improve the clinical effect of therapy. The combination of Tizanidine and Mirtazapine is an effective pharmacotherapy for chronic back pain. KEYWORDS: Chronic back pain, pathogenesis of dorsalgia, Tizanidine, Mirtazapine

Hallucination Proneness Alters Sensory Feedback Processing in Self-voice Production.

Sensory suppression occurs when hearing one's self-generated voice, as opposed to passively listening to one's own voice. Quality changes in sensory feedback to the self-generated voice can increase attentional control. These changes affect the self-other voice distinction and might lead to hearing voices in the absence of an external source (ie, auditory verbal hallucinations). However, it is unclear how changes in sensory feedback processing and attention allocation interact and how this interaction might relate to hallucination proneness (HP). Participants varying in HP self-generated (via a button-press) and passively listened to their voice that varied in emotional quality and certainty of recognition-100% neutral, 60%-40% neutral-angry, 50%-50% neutral-angry, 40%-60% neutral-angry, 100% angry, during electroencephalography (EEG) recordings. The N1 auditory evoked potential was more suppressed for self-generated than externally generated voices. Increased HP was associated with (1) an increased N1 response to the self- compared with externally generated voices, (2) a reduced N1 response for angry compared with neutral voices, and (3) a reduced N2 response to unexpected voice quality in sensory feedback (60%-40% neutral-angry) compared with neutral voices. The current study highlights an association between increased HP and systematic changes in the emotional quality and certainty in sensory feedback processing (N1) and attentional control (N2) in self-voice production in a nonclinical population. Considering that voice hearers also display these changes, these findings support the continuum hypothesis.

Population-based detection of children ASD/ADHD comorbidity from atypical sensory processing

Comorbidity between neurodevelopmental disorders is common, especially between autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD). This study aimed to detect overlapped sensory processing alterations in a sample of children and adolescents diagnosed with both ASD and ADHD. A collection of 42 standard and 8 proposed machine learning classifiers, 22 feature selection methods and 19 unbalanced classification strategies were applied on the 6 standard question groups of the Sensory Profile-2 questionnaire. The relatively low performance achieved by state-of-the-art classifiers led us to propose the feature population sum classifier, a probabilistic method based on class and feature value populations, designed for datasets where features are discrete numeric answers to questions in a questionnaire. The proposed method achieves the best kappa and accuracy, 60% and 82.5%, respectively, reaching 68% and 86.5% combined with backward sequential feature selection, with false positive and negative rates below 15%. Since the SP2 questionnaire can be filled by parents for children from three years, our prediction can alert the clinicians with an early diagnosis in order to apply early interventions.

Brain circuits in autonomous sensory meridian response and related phenomena.

Autonomous sensory meridian response (ASMR) is characterized by a tingling sensation with a feeling of relaxation and a state of flow. We explore the neural underpinnings and comorbidities of ASMR and related phenomena with altered sensory processing. These phenomena include sensory processing sensitivity (SPS), synaesthesia, Alice in Wonderland syndrome and misophonia. The objective of this article is to uncover the shared neural substrates and distinctive features of ASMR and its counterparts. ASMR, SPS and misophonia exhibit common activations in the brain regions associated with social cognition, emotion regulation and empathy. Nevertheless, ASMR responders display reduced connectivity in the salience network (SN), while individuals with SPS exhibit increased connectivity in the SN. Furthermore, ASMR induces relaxation and temporarily reduces symptoms of depression, in contrast to SPS and misophonia, which are linked to depression. These observations lead us to propose that ASMR is a distinct phenomenon owing to its attention dispatch mechanism and its connection with emotion regulation. We suggest that increased activations in the insula, along with reduction inconnectivity within the salience and default mode networks in ASMR responders, may account for their experiences of relaxation and flow states. This article is part of the theme issue 'Sensing and feeling: an integrative approach to sensory processing and emotional experience'.

Neuroimmunological effects of omega-3 fatty acids on migraine: a review.

Migraine is a highly prevalent disease worldwide, imposing enormous clinical and economic burdens on individuals and societies. Current treatments exhibit limited efficacy and acceptability, highlighting the need for more effective and safety prophylactic approaches, including the use of nutraceuticals for migraine treatment. Migraine involves interactions within the central and peripheral nervous systems, with significant activation and sensitization of the trigeminovascular system (TVS) in pain generation and transmission. The condition is influenced by genetic predispositions and environmental factors, leading to altered sensory processing. The neuroinflammatory response is increasingly recognized as a key event underpinning the pathophysiology of migraine, involving a complex neuro-glio-vascular interplay. This interplay is partially mediated by neuropeptides such as calcitonin gene receptor peptide (CGRP), pituitary adenylate cyclase activating polypeptide (PACAP) and/or cortical spreading depression (CSD) and involves oxidative stress, mitochondrial dysfunction, nucleotide-binding domain-like receptor family pyrin domain containing-3 (NLRP3) inflammasome formation, activated microglia, and reactive astrocytes. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), crucial for the nervous system, mediate various physiological functions. Omega-3 PUFAs offer cardiovascular, neurological, and psychiatric benefits due to their potent anti-inflammatory, anti-nociceptive, antioxidant, and neuromodulatory properties, which modulate neuroinflammation, neurogenic inflammation, pain transmission, enhance mitochondrial stability, and mood regulation. Moreover, specialized pro-resolving mediators (SPMs), a class of PUFA-derived lipid mediators, regulate pro-inflammatory and resolution pathways, playing significant anti-inflammatory and neurological roles, which in turn may be beneficial in alleviating the symptomatology of migraine. Omega-3 PUFAs impact various neurobiological pathways and have demonstrated a lack of major adverse events, underscoring their multifaceted approach and safety in migraine management. Although not all omega-3 PUFAs trials have shown beneficial in reducing the symptomatology of migraine, further research is needed to fully establish their clinical efficacy and understand the precise molecular mechanisms underlying the effects of omega-3 PUFAs and PUFA-derived lipid mediators, SPMs on migraine pathophysiology and progression. This review highlights their potential in modulating brain functions, such as neuroimmunological effects, and suggests their promise as candidates for effective migraine prophylaxis.

Pathophysiology of Migraine.

This article provides an overview of the current understanding of migraine pathophysiology through insights gained from the extended symptom spectrum of migraine, neuroanatomy, migraine neurochemistry, and therapeutics. Recent advances in human migraine research, including human experimental migraine models and functional neuroimaging, have provided novel insights into migraine attack initiation, neurochemistry, neuroanatomy, and therapeutic substrates. It has become clear that migraine is a neural disorder, in which a wide range of brain areas and neurochemical systems are implicated, producing a heterogeneous clinical phenotype. Many of these neural pathways are monoaminergic and peptidergic, such as those involving calcitonin gene-related peptide and pituitary adenylate cyclase-activating polypeptide. We are currently witnessing an exciting era in which specific drugs targeting these pathways have shown promise in treating migraine, including some studies suggesting efficacy before headache has even started. Migraine is a brain disorder involving both headache and altered sensory, limbic, and homeostatic processing. A complex interplay between neurotransmitter systems, physiologic systems, and pain processing likely occurs. Targeting various therapeutic substrates within these networks provides an exciting avenue for future migraine therapeutics.

Autistic Traits and Somatic Symptom Disorders: What Is the Link?

Alterations in sensory processing, a key component of autism spectrum disorder (ASD), have recently attracted increasing attention as they result in peculiar responses to sensory stimuli, possibly representing a risk factor for the development of somatic symptom disorder (SSD). Contextually, other features also associated with ASD, such as alexithymia, camouflaging and altered verbal, and non-verbal communication, have been suggested to represent risk factors for the occurrence and worsening of somatic symptomatology. The aim of this work was to review the available literature about the association between SSD and the autism spectrum. The results highlighted not only a higher prevalence of autistic features in patients suffering from SSD and a higher prevalence of reported somatic symptomatology in subjects with ASD but also how ASD subjects with co-occurrent somatic symptoms exhibit more severe autism-linked symptomatology. From the paper reviewed also emerged many shared features between the two conditions, such as alexithymia, altered sensitivity to sensory stimuli, cognitive inflexibility, intolerance of uncertainty, and an increased risk of experiencing stressful life events, which may provide an explanation for the correlation reported. Even though studies on the topic are still scant, the evidence reported suggests the importance of further assessing the correlation between the two disorders.

From synaptic dysfunction to atypical emotional processing in autism.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition mainly characterized by social impairments and repetitive behaviors. Among these core symptoms, a notable aspect of ASD is the presence of emotional complexities, including high rates of anxiety disorders. The inherent heterogeneity of ASD poses a unique challenge in understanding its etiological origins, yet the utilization of diverse animal models replicating ASD traits has enabled researchers to dissect the intricate relationship between autism and atypical emotional processing. In this review, we delve into the general findings about the neural circuits underpinning one of the most extensively researched and evolutionarily conserved emotional states: fear and anxiety. Additionally, we explore how distinct ASD animal models exhibit various anxiety phenotypes, making them a crucial tool for dissecting ASD's multifaceted nature. Overall, to a proper display of fear response, it is crucial to properly process and integrate sensorial and visceral cues to the fear-induced stimuli. ASD individuals exhibit altered sensory processing, possibly contributing to the emergence of atypical phobias, a prevailing anxiety disorder manifested in this population. Moreover, these individuals display distinctive alterations in a pivotal fear and anxiety processing hub, the amygdala. By examining the neurobiological mechanisms underlying fear and anxiety regulation, we can gain insights into the factors contributing to the distinctive emotional profile observed in individuals with ASD. Such insights hold the potential to pave the way for more targeted interventions and therapies that address the emotional challenges faced by individuals within the autism spectrum.

Degraded inferior colliculus responses to complex sounds in prenatally exposed VPA rats

BackgroundIndividuals with autism spectrum disorders (ASD) often exhibit altered sensory processing and deficits in language development. Prenatal exposure to valproic acid (VPA) increases the risk for ASD and impairs both receptive and expressive language. Like individuals with ASD, rodents prenatally exposed to VPA exhibit degraded auditory cortical processing and abnormal neural activity to sounds. Disrupted neuronal morphology has been documented in earlier processing areas of the auditory pathway in VPA-exposed rodents, but there are no studies documenting early auditory pathway physiology. Therefore, the objective of this study is to characterize inferior colliculus (IC) responses to different sounds in rats prenatally exposed to VPA compared to saline-exposed rats.MethodsIn vivo extracellular multiunit recordings from the inferior colliculus were collected in response to tones, speech sounds, and noise burst trains.ResultsOur results indicate that the overall response to speech sounds was degraded in VPA-exposed rats compared to saline-exposed controls, but responses to tones and noise burst trains were unaltered.ConclusionsThese results are consistent with observations in individuals with autism that neural responses to complex sounds, like speech, are often altered, and lays the foundation for future studies of potential therapeutics to improve auditory processing in the VPA rat model of ASD.

First-episode psychosis and autism spectrum disorder: a scoping review and a guide to overcome diagnostic challenges

Background Undiagnosed Autism Spectrum Disorder (ASD) may represent a diagnostic challenge in people who refer to specialized services for first-episode psychosis (FEP). Similarly, individuals with ASD can present newly-onset psychotic symptoms. Aims The present review aimed to summarize the literature available on ASD and FEP to guide differential diagnosis between the two conditions and discuss the impact of ASD-FEP comorbidity on recovery. Methods The PRISMA-ScR guidelines were followed. After conducting a comprehensive literature search, we screened 204 papers including participants with: (1) a comorbid diagnosis of FEP and ASD; (2) FEP and autistic traits; (3) separate groups of FEP and ASD. Results A total of 18 studies were discussed and confirmed the high prevalence of ASD or autistic traits in people referring to FEP services (up to 9% and 35% of FEP, respectively), which could negatively impact pathways to care, clinical presentation, and outcomes. Due to some similarities in ASD and FEP presentation (e.g., difficulties in social functioning), a differential diagnosis could be challenging. The features more suggestive of ASD rather than a primary FEP include illogical and concrete thinking, and a longstanding social interaction difficulty. Aberrant salience and suspiciousness can manifest in ASD, but are usually more transient, and stress-related than in FEP. Also, perceptual abnormalities are due to altered sensory processing rather than pathological hallucinations. The co-occurrence of ASD symptoms is associated with a reduced probability of clinical and functional recovery in FEP, a higher risk of suicidal behaviors, and higher unemployment rates. Conclusions The kaleidoscopic manifestations of FEP require an adequate differential diagnosis that should include ASD. FEP services ought to be equipped for an adequate assessment and diagnostic formulation, which can result particularly challenging should symptoms of autism be present in adult patients.

Effects of Introvision, a self-regulation method with a mindfulness-based perception technique in migraine prevention: a monocentric randomized waiting-list controlled study (IntroMig Study)

BackgroundMigraine is a brain disorder with recurrent headache attacks and altered sensory processing. Introvision is a self-regulation method based on mindfulness-like perception techniques, developed at the University of Hamburg. Here, we examined the effect of Introvision in migraine prevention.MethodsMigraineurs with at least five headache days per month were block-randomized to the experimental group (EG) or waiting list group (WL), the latter starting Introvision training six weeks after the EG. Participants learned Introvision in six weekly on-site group sessions with video-conference support followed by three individual video-conference sessions. Headache diaries and questionnaires were obtained before Introvision training and three months after the last individual Introvision session.ResultsFifty-one patients completed the study. The primary outcome, headache days of the EG after Introvision training compared to those of the WL before the training, showed no significant effect (10.6 ± 7.7, n = 22; vs. 10.9 ± 6.3, n = 29, p = 0.63; Mann–Whitney-U-Test). The secondary outcome, comparing pooled EG and WL data before and after Introvision training, revealed a significant reduction of headache days (from 11.7 ± 6.5 to 9.8 ± 7.0; p = 0.003; Wilcoxon-paired-Test) as well as of acute medication intake and Headache-Impact-Test 6 (HIT-6) scores and increased self-efficacy as quantified by increased FKMS-scores (FKMS: german short form of the Headache Management Self-Efficacy Scale (HMSE)).ConclusionAlthough the study did not reach its primary endpoint, several secondary outcome parameters in the pooled (non-controlled) pre-post analysis showed an improvement with a decrease in monthly headache days by 1.9 days/ month. A larger randomized controlled trial has to corroborate these preliminary findings.Trial registrationNCT03507400, Registration date 09.03.2018.

Sensory Processing Differences in Individuals With Autism Spectrum Disorder: A Narrative Review of Underlying Mechanisms and Sensory-Based Interventions.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by difficulties with social interaction and restricted, repetitive patterns of behavior. Altered sensory processing and perception are consideredcharacteristics of ASD. Sensory processing differences (SPDs) are commonly observed in individuals with ASD, leading to atypical responses to sensory stimuli.SPDs refer to the way in which individuals receive, process, and respond to sensory information from the environment. People with SPDs may be hypersensitive (over-reactive) or hyposensitive (under-reactive) to sensory input, or they may experience fragmented or distorted perceptions. These differences can make it difficult for individuals with SPDs to filter out irrelevant sensory information, and to integrate sensory information from different sources. This study intends to investigate the underlying mechanisms contributing to SPDs in individuals with autism and determine the effectiveness of sensory-based therapies in addressing these challenges. The literature suggests that altered neural pathways, sensory gating dysfunction, and atypical sensory modulation contribute to SPDs in individuals with ASD. Assistive technology, environmental changes, and sensory-based interventions like sensory integration therapy (SIT) have all shown promise in improving sensory functioning and reducing associated behavioral issues. However, further research is needed to improve our understanding of sensory processing in autism and to optimize interventions for individuals with ASD.

Exploratory evidence for differences in GABAergic regulation of auditory processing in autism spectrum disorder

Altered reactivity and responses to auditory input are core to the diagnosis of autism spectrum disorder (ASD). Preclinical models implicate ϒ-aminobutyric acid (GABA) in this process. However, the link between GABA and auditory processing in humans (with or without ASD) is largely correlational. As part of a study of potential biosignatures of GABA function in ASD to inform future clinical trials, we evaluated the role of GABA in auditory repetition suppression in 66 adults (n = 28 with ASD). Neurophysiological responses (temporal and frequency domains) to repetitive standard tones and novel deviants presented in an oddball paradigm were compared after double-blind, randomized administration of placebo, 15 or 30 mg of arbaclofen (STX209), a GABA type B (GABAB) receptor agonist. We first established that temporal mismatch negativity was comparable between participants with ASD and those with typical development (TD). Next, we showed that temporal and spectral responses to repetitive standards were suppressed relative to responses to deviants in the two groups, but suppression was significantly weaker in individuals with ASD at baseline. Arbaclofen reversed weaker suppression of spectral responses in ASD but disrupted suppression in TD. A post hoc analysis showed that arbaclofen-elicited shift in suppression was correlated with autistic symptomatology measured using the Autism Quotient across the entire group, though not in the smaller sample of the ASD and TD group when examined separately. Thus, our results confirm: GABAergic dysfunction contributes to the neurophysiology of auditory sensory processing alterations in ASD, and can be modulated by targeting GABAB activity. These GABA-dependent sensory differences may be upstream of more complex autistic phenotypes.

Drugs prescribed for Phelan-McDermid syndrome differentially impact sensory behaviors in shank3 zebrafish models.

Background: Altered sensory processing is a pervasive symptom in individuals with Autism Spectrum Disorders (ASD); people with Phelan McDermid syndrome (PMS), in particular, show reduced responses to sensory stimuli. PMS is caused by deletions of the terminal end of chromosome 22 or point mutations in Shank3. People with PMS can present with an array of symptoms including ASD, epilepsy, gastrointestinal distress, and reduced responses to sensory stimuli. People with PMS are often medicated to manage behaviors like aggression and/or self-harm and/or epilepsy, and it remains unclear how these medications might impact perception/sensory processing. Here we test this using zebrafish mutant shank3ab PMS models that likewise show reduced sensory responses in a visual motor response (VMR) assay, in which increased locomotion is triggered by light to dark transitions. Methods: We screened three medications, risperidone, lithium chloride (LiCl), and carbamazepine (CBZ), prescribed to people with PMS and one drug, 2-methyl-6-(phenylethynyl) pyridine (MPEP) tested in rodent models of PMS, for their effects on a sensory-induced behavior in two zebrafish PMS models with frameshift mutations in either the N- or C- termini. To test how pharmacological treatments affect the VMR, we exposed larvae to selected drugs for 24 hours and then quantified their locomotion during four ten-minute cycles of lights on-to-off stimuli. Results: We found that risperidone normalized the VMR in shank3 models. LiCl and CBZ had no effect on the VMR in any of the three genotypes. MPEP reduced the VMR in wildtype (WT) to levels seen in shank3 models but caused no changes in either shank3 model. Finally, shank3 mutants showed resistance to the seizure-inducing drug pentylenetetrazol (PTZ), at a dosage that results in hyperactive swimming in WT zebrafish. Conclusions: Our work shows that the effects of drugs on sensory processing are varied in ways that can be highly genotype- and drug-dependent.

Vasopressin as Possible Treatment Option in Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is rather common, presenting with prevalent early problems in social communication and accompanied by repetitive behavior. As vasopressin was implicated not only in salt-water homeostasis and stress-axis regulation, but also in social behavior, its role in the development of ASD might be suggested. In this review, we summarized a wide range of problems associated with ASD to which vasopressin might contribute, from social skills to communication, motor function problems, autonomous nervous system alterations as well as sleep disturbances, and altered sensory information processing. Beside functional connections between vasopressin and ASD, we draw attention to the anatomical background, highlighting several brain areas, including the paraventricular nucleus of the hypothalamus, medial preoptic area, lateral septum, bed nucleus of stria terminalis, amygdala, hippocampus, olfactory bulb and even the cerebellum, either producing vasopressin or containing vasopressinergic receptors (presumably V1a). Sex differences in the vasopressinergic system might underline the male prevalence of ASD. Moreover, vasopressin might contribute to the effectiveness of available off-label therapies as well as serve as a possible target for intervention. In this sense, vasopressin, but paradoxically also V1a receptor antagonist, were found to be effective in some clinical trials. We concluded that although vasopressin might be an effective candidate for ASD treatment, we might assume that only a subgroup (e.g., with stress-axis disturbances), a certain sex (most probably males) and a certain brain area (targeting by means of virus vectors) would benefit from this therapy.

Exploring sensory sensitivity, cortical excitability, and habituation in episodic migraine, as a function of age and disease severity, using the pattern-reversal task

BackgroundMigraine is a cyclic, neurosensory disorder characterized by recurrent headaches and altered sensory processing. The latter is manifested in hypersensitivity to visual stimuli, measured with questionnaires and sensory thresholds, as well as in abnormal cortical excitability and a lack of habituation, assessed with visual evoked potentials elicited by pattern-reversal stimulation. Here, the goal was to determine whether factors such as age and/or disease severity may exert a modulatory influence on sensory sensitivity, cortical excitability, and habituation.MethodsTwo similar experiments were carried out, the first comparing 24 young, episodic migraine patients and 28 healthy age- and gender-matched controls and the second 36 middle-aged, episodic migraine patients and 30 healthy age- and gender-matched controls. A neurologist confirmed the diagnoses. Migraine phases were obtained using eDiaries. Sensory sensitivity was assessed with the Sensory Perception Quotient and group comparisons were carried out. We obtained pattern-reversal visual evoked potentials and calculated the N1-P1 Peak-to-Peak amplitude. Two linear mixed-effects models were fitted to these data. The first model had Block (first block, last block) and Group (patients, controls) as fixed factors, whereas the second model had Trial (all trials) and Group as fixed factors. Participant was included as a random factor in both. N1-P1 first block amplitude was used to assess cortical excitability and habituation was defined as a decrease of N1-P1 amplitude across Blocks/Trials. Both experiments were performed interictally.ResultsThe final samples consisted of 18 patients with episodic migraine and 27 headache-free controls (first experiment) and 19 patients and 29 controls (second experiment). In both experiments, patients reported increased visual hypersensitivity on the Sensory Perception Quotient as compared to controls. Regarding N1-P1 peak-to-peak data, there was no main effect of Group, indicating no differences in cortical excitability between groups. Finally, significant main effects of both Block and Trial were found indicating habituation in both groups, regardless of age and headache frequency.ConclusionsThe results of this study yielded evidence for significant hypersensitivity in patients but no significant differences in either habituation or cortical excitability, as compared to headache-free controls. Although the alterations in patients may be less pronounced than originally anticipated they demonstrate the need for the definition and standardization of optimal methodological parameters.

A review of dietary and nutritional interventions available for management of autism spectrum disorder symptoms in children and adolescents - Kenya

Research on the challenges of raising a child with autism is mostly reported from Europe, North America and Australia. There is limited autism spectrum disorder (ASD) research in Kenya and families lack support as the etiology is linked to witchcraft and sorcery. Research indicates an increase in ASD prevalence globally and in Africa. Malnutrition and neuro-disability are major public health problems in Africa. Approximately one billion people, 15% of the world’s population, have a disability of some kind and 80% live in Low- and Middle-Income countries (LMICs). Of these, 53 million are children aged below 5 years living in sub-Saharan Africa. In Kenya, 2.2% (0.9 million people) live with some form of disability. Children diagnosed with autism spectrum disorder (ASD) suffer from neuro disabilities eliciting: altered sensory processing, restricted interests, and behavioral rigidity. Autism spectrum disorders have no cure, management is by use of interventional targeting autistic symptoms such as linguistic development, non-verbal cognitive development, and motor development. The objectives of this review were: to identify dietary and nutritional interventions available for the management of ASD symptoms in children and adolescents - Kenya, and to analyze the results of existing research in this area in order to understand and describe the characteristics and results of these studies to enable their use in the management of ASD symptoms. Cochrane Library, PubMed, PMC, Google scholar, and Free Full databases were searched to identify studies published between September 2011 and September 2021. Included were studies on nutrition or dietary interventions given to ASD children and adolescents that assessed autistic behavior and/or gastrointestinal symptoms. Excluded were those articles that evaluated surrogate outcomes as the primary outcome such as urinary peptide excretion and other neuro-disabilities other than ASD. Eighteen articles were included: 12 randomized case-control trials, 3 open-label trials, one 2×2 factorial study, and 2 cross-over trials. The following dietary and nutritional interventions were evaluated: gluten and casein-free diet, ketogenic diets; probiotic supplements, specific carbohydrate diets, polyunsaturated fatty acids, vitamin and mineral supplantation (A, B6, B12, D, magnesium, folic acid), and alternative diets. Authors report improvements in the symptoms associated with ASD individuals receiving nutritional interventions such as vitamin and mineral supplementation however, their safety and efficacy needs to be evaluated. The study findings will help policymakers and implementers to understand the consistency and precision and impact of these interventions. These findings will contribute to improving the safety and efficacy of these interventions, positively impacting the health and nutrition outcomes of children and adolescents with ASD. These study findings indicate that more research targeting ASD dietary and Nutritional Interventions for management of ASD symptoms is required in Kenya and other resource constrained settings. Key words: autism spectrum disorder, nutritional intervention, diet therapy, child, adolescent, Kenya

Excitation-Inhibition Imbalance in Migraine: From Neurotransmitters to Brain Oscillations.

Migraine is among the most common and debilitating neurological disorders typically affecting people of working age. It is characterised by a unilateral, pulsating headache often associated with severe pain. Despite the intensive research, there is still little understanding of the pathophysiology of migraine. At the electrophysiological level, altered oscillatory parameters have been reported within the alpha and gamma bands. At the molecular level, altered glutamate and GABA concentrations have been reported. However, there has been little cross-talk between these lines of research. Thus, the relationship between oscillatory activity and neurotransmitter concentrations remains to be empirically traced. Importantly, how these indices link back to altered sensory processing has to be clearly established as yet. Accordingly, pharmacologic treatments have been mostly symptom-based, and yet sometimes proving ineffective in resolving pain or related issues. This review provides an integrative theoretical framework of excitation-inhibition imbalance for the understanding of current evidence and to address outstanding questions concerning the pathophysiology of migraine. We propose the use of computational modelling for the rigorous formulation of testable hypotheses on mechanisms of homeostatic imbalance and for the development of mechanism-based pharmacological treatments and neurostimulation interventions.

Are clinical outcomes associated with baseline sensory profiles in people with musculoskeletal shoulder pain? Protocol for a prospective longitudinal observational study.

Musculoskeletal shoulder pain is a common problem and its symptoms often become persistent. The experience of pain is multidimensional, and therefore, a range of patient characteristics may influence treatment response. An altered sensory processing has been associated with persistent musculoskeletal pain states and may contribute to outcomes in patients with musculoskeletal shoulder pain. The presence and potential impact of altered sensory processing in this patient cohort is not currently known. The aim of this prospective longitudinal cohort study is to investigate if baseline sensory characteristics are associated with clinical outcomes in patients presenting to a tertiary hospital with persistent musculoskeletal shoulder pain. If found, a relationship between sensory characteristics and outcome may lead to the creation of more effective treatment strategies and improvements in risk adjustment and prognosis. This is a single-centre prospective cohort study with 6-, 12- and 24-month follow-up. A total of 120 participants aged ≥18years with persistent musculoskeletal shoulder pain (≥3months) will be recruited from an Australian public tertiary hospital orthopaedic department. Baseline assessments, including quantitative sensory tests and a standardised physical examination, will be performed. In addition, information will be obtained from patient interviews, self-report questionnaires and medical records. Follow-up outcome measures will comprise information from the Shoulder Pain and Disability Index and a six-point Global Rating of Change scale. Descriptive statistics will be used to report baseline characteristics and outcome measures over time. Change in outcome measures at the primary endpoint of sixmonths from baseline will be calculated using paired t-tests. Associations between baseline characteristics and outcomes at a 6-month follow-up will be reported using multivariable linear and logistic regression models. Understanding the relationship between sensory profile and the variable response to treatment in people with persistent musculoskeletal shoulder pain may enhance our understanding of the mechanisms contributing to the presentation. In addition, through better understanding of the contributing factors, the results of this study may contribute to the development of an individualised, patient-centred approach to treatment for people with this highly prevalent and debilitating condition.