Behavioural and neurophysiological markers reveal differential sensitivity to homeostatic interactions between centrally and peripherally applied passive stimulation

Repetitive transcranial magnetic stimulation (rTMS) is an effective tool for inducing functional plastic changes in the brain. rTMS can also potentiate the effects of other interventions such as tactile coactivation, a form of repetitive stimulation, when both are applied simultaneously. In this study, we investigated the interaction of these techniques in affecting tactile acuity and cortical excitability, measured with somatosensory evoked potentials after paired median nerve stimulation. We first applied a session of 5‐Hz rTMS, followed by a session of tactile repetitive stimulation, consisting of intermittent high‐frequency tactile stimulation (iHFS) to a group of 15 healthy volunteers (“rTMS + iHFS” group). In a second group (“rTMS w/o iHFS”), rTMS was applied without iHFS, with a third assessment performed after a similar wait period. In the rTMS w/o iHFS group, the 5‐Hz rTMS induced an increase in cortical excitability that continued to build for at least 25 min after stimulation, with the effect on excitability after the wait period being inversely correlated to the baseline state. In the rTMS + iHFS group, the second intervention prevented the continued increase in excitability after rTMS. In contrast to the effect on cortical excitability, rTMS produced an improvement in tactile acuity that remained stable until the last assessment, independent of the presence or absence of iHFS. Our results show that these methods can interact homeostatically when used consecutively, and suggest that different measures of cortical plasticity are differentially susceptible to homeostatic interactions.     

A Retrospective View of a Sexual Dysfunction Clinic, 1980–83

Case notes of 337 couples attending a well-established sexual dysfunction clinic between 1980 and 1983 were surveyed. The distribution of various types of sexual dysfunction was compared with similar studies reported from the U.K. Among males secondary erectile dysfunction was the commonest presenting cause and general unresponsiveness among the females. The majority of the referrals were from general practitioners. The drop-out rates in each category were high. The reasons for this are discussed and suggestions for further research made.     

The acute effects of light on murine sleep during the dark phase: importance of melanopsin for maintenance of light‐induced sleep

Light exerts a direct effect on sleep and wakefulness in nocturnal and diurnal animals, with a light pulse during the dark phase suppressing locomotor activity and promoting sleep in the former. In the present study, we investigated this direct effect of light on various sleep parameters by exposing mice to a broad range of illuminances (0.2–200 μW/cm²; equivalent to 1–1000 lux) for 1 h during the dark phase (zeitgeber time 13–14). Fitting the data with a three‐parameter log model indicated that ～0.1 μW/cm² can generate half the sleep response observed at 200 μW/cm². We observed decreases in total sleep time during the 1 h following the end of the light pulse. Light reduced the latency to sleep from ~30 min in darkness (baseline) to ~10 min at the highest intensity, although this effect was invariant across the light intensities used. We then assessed the role of melanopsin during the rapid transition from wakefulness to sleep at the onset of a light pulse and the maintenance of sleep with a 6‐h 20 μW/cm² light pulse. Even though the melanopsin knockout mice had robust induction of sleep (~35 min) during the first hour of the pulse, it was not maintained. Total sleep decreased by almost 65% by the third hour in comparison with the first hour of the pulse in mice lacking melanopsin, whereas only an 8% decrease was observed in wild‐type mice. Collectively, our findings highlight the selective effects of light on murine sleep, and suggest that melanopsin‐based photoreception is primarily involved in sustaining light‐induced sleep.     

A symptom network model of misophonia: From heightened sensory sensitivity to clinical comorbidity

Objectives

Misophonia—an unusually strong intolerance of certain sounds—can cause significant distress and disruption to those who have it but is an enigma in terms of our scientific understanding. A key challenge for explaining misophonia is that, as with other disorders, it is likely to emerge from an interaction of traits that also occur in the general population (e.g., sensory sensitivity and anxiety) and that are transdiagnostic in nature (i.e., shared with other disorders).

Methods

In this preregistered study with a large sample of participants (N = 1430), we performed a cluster analysis (based on responses to questions relating to misophonia) and identified two misophonia subgroups differing in severity, as well as a third group without misophonia. A subset of this sample (N = 419) then completed a battery of measures designed to assess sensory sensitivity and clinical comorbidities.

Results

Clinical symptoms were limited to the most severe group of misophonics (including autistic traits, migraine with visual aura, anxiety sensitivity, obsessive-compulsive traits). Both the moderate and severe groups showed elevated attention-to-detail and hypersensitivity (across multiple senses). A novel symptom network model of the data shows the presence of a central hub linking misophonia to sensory sensitivity which, in turn, connects to other symptoms in the network (relating to autism, anxiety, etc.).

Conclusion

The core features of misophonia are sensory-attentional in nature with severity linked strongly to comorbidities.     

Assessment of proxy-reported responses as predictors of motor and sensory peripheral neuropathy in children with B-lymphoblastic leukemia

Chemotherapy-induced peripheral neuropathy (CIPN), a common condition in children with acute lymphoblastic leukemia, can be challenging to diagnose. Using data from Children's Oncology Group AALL0932 physical function study, we sought to determine if parent/guardian proxy-reported responses from the Pediatric Outcomes Data Collection Instrument could identify children with motor or sensory CIPN diagnosed by physical/occupational therapists (PT/OT). Four variables moderately discriminated between children with and without motor CIPN (c-index 0.76, 95% confidence interval [CI]: 0.64–0.84), but sensory and optimism-corrected models had weak discrimination (c-index sensory models 0.65, 95% CI: 0.54–0.74). New proxy-report measures are needed to identify children with PT/OT diagnosed CIPN.     

Cellular distribution of the Fragile X mental retardation protein in the inner ear: a developmental and comparative study in the mouse,rat, gerbil,and chicken

The Fragile X mental retardation protein (FMRP) is an mRNA binding protein that is essential for neural circuit assembly and synaptic plasticity. Loss of functional FMRP leads to Fragile X syndrome (FXS), a neurodevelopmental disorder characterized by sensory dysfunction including abnormal auditory processing. While the central mechanisms of FMRP regulation have been studied in the brain, whether FMRP is expressed in the auditory periphery and how it develops and functions remains unknown. In this study, we characterized the spatiotemporal distribution pattern of FMRP immunoreactivity in the inner ear of mice, rats, gerbils, and chickens. Across species, FMRP was expressed in hair cells and supporting cells, with a particularly high level in immature hair cells during the prehearing period. Interestingly, the distribution of cytoplasmic FMRP displayed an age-dependent translocation in hair cells, and this feature was conserved across species. In the auditory ganglion (AG), FMRP immunoreactivity was detected in neuronal cell bodies as well as their peripheral and central processes. Distinct from hair cells, FMRP intensity in AG neurons was high both during development and after maturation. Additionally, FMRP was evident in mature glial cells surrounding AG neurons. Together, these observations demonstrate distinct developmental trajectories across cell types in the auditory periphery. Given the importance of peripheral inputs to the maturation of auditory circuits, these findings implicate involvement of FMRP in inner ear development as well as a potential contribution of periphery FMRP to the generation of auditory dysfunction in FXS.