Increased central gain in aging 5xFAD mice resulted in deficits in hearing sound pips within noisy contexts, consistent with the auditory processing disorder (CAPD) profile frequently observed in Alzheimer's disease (AD) sufferers. The auditory cortex of both mouse strains exhibited amyloid plaque deposits, as revealed by histological study. Only in 5xFAD mice, but not in APP/PS1 mice, was plaque formation evident in the upper auditory brainstem, encompassing the inferior colliculus (IC) and the medial geniculate body (MGB). Schmidtea mediterranea Plaque distribution shows a parallel trend to histological findings from human subjects with Alzheimer's disease, and this correlation is evident with increasing central gain in older individuals. We posit that auditory modifications in amyloidosis mouse models are intertwined with amyloid plaque development within the auditory brainstem, a phenomenon that may be potentially reversed through the enhancement of cholinergic signaling. ABR recording patterns that shift, alongside rising central gain, preceding AD-related hearing deficits, point towards its potential as an early biomarker of AD.
The combination of Single-Sided Deafness (SSD) and Asymmetrical Hearing Loss (AHL) frequently presents with tinnitus as a symptom. Besides the distressing tinnitus in their less-favored ear, these patients often experience difficulties comprehending speech amidst background noise and locating sounds accurately. Cochlear implantation, bone conduction devices, and contralateral routing of signal (CROS) hearing aids are the standard, established options for these patients to enhance their auditory abilities. The recently established benefit of cochlear implantation for AHL/SSD-linked tinnitus was shown to be greater than that achievable through the other two treatment modalities. A conceivable explanation for the modest impact on tinnitus perception lies in the inadequate stimulation provided to the disadvantaged ear in these recent approaches. In the realm of hearing technology, the StereoBiCROS system's novel design combines the ear-to-ear sound redirection of the CROS system with traditional sound amplification to simultaneously stimulate both the weaker and the stronger ears. G Protein activator This study's goal was to explore the repercussions of applying this new device to tinnitus. Tinnitus sufferers among 12 AHL and 2 SSD patients, aged between 70 and 77 years, received bilateral hearing aids with three distinct programs: Stereophonic, BiCROS, and StereoBiCROS, which integrated CROS technology with bilateral amplification. A tinnitus Loudness Visual Analog Scale (VAS) and the Tinnitus Handicap Inventory (THI) were respectively utilized to evaluate the short-term and long-term consequences of the approach on tinnitus. Prior to and one month following the hearing aid fitting, both the VAS and the THI were employed. The StereoBiCROS program was utilized most frequently (818205% of the time) among the 14 patients who wore their hearing aids daily (12616 hours each day). The one-month trial showed a significant decline in average THI total score (47 (22) to 15 (16), p=0.0002) and VAS-Loudness score (7 (1) to 2 (2), p < 0.0001). StereoBiCROS stimulation, as a whole, demonstrates the potential to offer a helpful solution for tinnitus-related challenges such as reduced handicap and decreased loudness perception in patients with AHL/SSD and tinnitus. The effect could be a result of the less effective ear's sound enhancement.
Transcranial magnetic stimulation (TMS) serves as a prevalent method for exploring central nervous system mechanisms associated with motor control. In spite of the numerous studies utilizing transcranial magnetic stimulation (TMS) to study the neurophysiological basis of corticomotor control for distal muscles, there is a dearth of research focusing on the control of axial muscles, notably those in the low back region. Still, variations in corticomotor control between low back and distal muscles (like gross and fine motor control) imply discrepancies in the neural circuits. To detail the organizational structure and neural mechanisms involved in corticomotor control of low back muscles, this systematic review analyzes the relevant literature, focusing on studies utilizing TMS in healthy humans.
A comprehensive literature search, spanning from the beginning to May 2022, encompassed four databases: CINAHL, Embase, Medline (Ovid), and Web of Science. The research studies included utilized TMS in tandem with EMG recordings from paraspinal muscles situated within the spinal column's T12 to L5 region for healthy test subjects. To synthesize the quantitative study results, a weighted average was employed.
After the application of the selection criteria, forty-four articles were identified. Electromyographic studies using transcranial magnetic stimulation (TMS) on the low back muscles provided consistent evidence of both contralateral and ipsilateral motor evoked potentials (with prolonged ipsilateral latencies) as well as short-latency intracortical inhibition/facilitation. However, a limited number of studies investigated alternative paired pulse designs, such as extended intracortical inhibition and interhemispheric inhibition. Furthermore, no investigation examined the interplay between various cortical regions utilizing a dual transcranial magnetic stimulation coil protocol (e.g., connecting the primary motor cortex and supplementary motor area).
The distinct cortical influence on low back muscles is quite different from the cortical control over hand muscles. Our investigation reveals that projections from each individual primary motor cortex are bilateral, with potentially distinct mechanisms governing contralateral (monosynaptic) and ipsilateral (oligo/polysynaptic) tracts. Furthermore, the presence of intracortical inhibitory and excitatory circuits within M1 modulates the excitability of contralateral corticospinal cells innervating lumbar muscles. Insight into these mechanisms is significant for improving our comprehension of neuromuscular function in the back's lower muscles and for enhancing treatment options for patient populations experiencing conditions like low back pain and stroke.
Low back muscle activation via corticomotor pathways is distinct from the corticomotor control of hand muscles. The most important finding demonstrates (i) dual projections from each primary motor cortex, where contralateral and ipsilateral tracts probably vary in their synaptic structure (contralateral, monosynaptic; ipsilateral, oligo/polysynaptic), and (ii) the presence of intracortical inhibitory and excitatory pathways within M1, which modulate the excitability of the contralateral corticospinal neurons projecting to the low back musculature. A critical understanding of these mechanisms is imperative for progressing our understanding of neuromuscular function within the low back muscles, and consequently, improving the management of clinical populations, such as those with low back pain or stroke.
A substantial portion of the population, estimated between 10 and 20 percent, experiences tinnitus. Individuals who are significantly impacted by their tinnitus's presence have their attention constantly directed toward and are distracted by the sound of their tinnitus. Though many approaches to alleviate tinnitus have been tried, none have been clinically validated. To investigate tinnitus, this study leveraged an established rat model of tinnitus, induced by noise exposure, to (1) determine the effects of tinnitus on the function of nicotinic acetylcholine receptors (nAChRs) in layer 5 pyramidal neurons (PNs) and vasoactive intestinal peptide (VIP) neurons within the primary auditory cortex (A1), and (2) evaluate sazetidine-A and varenicline, partial nAChR desensitizing agonists, as potential tinnitus treatments. We theorized that the decline in attentional resources observed in this animal model (Brozoski et al., 2019) might be explained by alterations in layer 5 nAChR responses linked to tinnitus. Whole-cell patch-clamp studies in vitro previously demonstrated a substantial tinnitus-linked decrease in excitatory postsynaptic currents triggered by nAChRs in layer 5 A1 pyramidal neurons. Opposite to the findings in control animals, VIP neurons from animals exhibiting tinnitus behavior showed a considerable rise in nAChR-evoked excitability. Our research proposes that sazetidine-A and varenicline might provide therapeutic efficacy for individuals experiencing phantom auditory perceptions and having difficulty detaching their attention. The GABAergic input current reductions in A1 layer 5 principal neurons attributable to tinnitus were ameliorated by sazetidine-A or varenicline. Using our tinnitus animal model, sazetidine-A and varenicline were then tested in an effort to manage tinnitus. Chemical-defined medium Rats receiving subcutaneous injections of sazetidine-A or varenicline, an hour before tinnitus testing, showed a dose-dependent decrease in behavioral tinnitus evidence. Given these results, a call for more clinical trials exploring the use of sazetidine-A and varenicline, partial desensitizing nAChR agonists, in the management of tinnitus is justified.
A common, progressive, and inescapable neurodegenerative illness, Alzheimer's disease (AD), unfortunately, is marked by a rapidly escalating worldwide incidence. Extensive research on the magnetic resonance imaging (MRI) of white matter (WM) in AD has been documented, yet a bibliometric analysis investigating this phenomenon is still nonexistent. Therefore, this investigation sought to provide a broad perspective on the current condition, key regions, and evolving directions in MRI studies of white matter in AD.
We undertook a search of the Web of Science Core Collection (WOSCC) database for MRI studies of white matter (WM) in Alzheimer's Disease (AD) conducted between 1990 and 2022. For the execution of bibliometric analyses, CiteSpace (version 51.R8) and VOSviewer (version 16.19) software packages were employed.
A total of 2199 articles resulted from this study's investigation.