Search Results (19)

Background/Objectives: Cochlear implants (CIs) constitute a viable method for auditory rehabilitation in patients with profound sensorineural hearing loss after temporal bone fractures (TBFs). These patients comprise a challenging population due to the anatomical deformity and neural injury. Methods: By performing this systematic review, we attempted to evaluate the viability of CIs in the context of TBF. The literature search, across Pubmed/MEDLINE, Scopus and Google Scholar, was performed under the PRISMA guidelines. The selected time period was from December 1995 to September 2025. The final analysis included 11 manuscripts. The majority of the studies were retrospective case series with a moderate risk of bias. Results: The primary outcome was postoperative auditory function, evaluated with speech perception tasks and aided sound-field pure-tone audiometry. The secondary outcomes were the report of radiological and electrophysiologic prognosticators of implants’ viability, timing of surgery, procedural feasibility and complications. Across the studies, CIs conferred meaningful auditory benefit when the cochlear nerve was intact. High-Resolution Computed Tomography (CT) was utilized for TBF classification and cochlear patency, whereas Magnetic Resonance Imaging (MRI) and a promontory test were crucial for the assessment of neural integrity. Prompt placement, optimally within 12 months after trauma, was related to improved outcomes by limiting cochlear fibrosis and ossification. Despite patients’ impedance fluctuation, restricted speech perception in noise and frequent abnormal facial nerve excitation, the overall audiologic and speech discrimination results are comparable to non-trauma recipients. Conclusions: A CI appears to be the choice of treatment over auditory brainstem implants, as long as the cochlear nerve remains intact. Rapid implantation in well-selected patients coupled with ordinal mapping and follow-up can restore dysfunctional hearing and improve patients’ quality of life. Full article

Background/Objectives: Acute lateral ankle sprain (ALAS) affects balance, often assessed by changes in traditional center of pressure (COP) parameters. Spatiotemporal measures of COP and time-to-boundary (TTB) analysis may offer improved sensitivity in detecting postural deviations associated with ALAS. However, the neurophysiological mechanism underlying these changes remains unknown. This study aimed to explore the effects of ALAS on spinal reflex excitability in the fibularis longus (FL) during single-leg balance and TTB parameters following ALAS. Methods: Fourteen participants with and without ALAS were recruited within 14 days from the onset of the injury. We assessed FL spinal reflex excitability and postural control during a single-leg stance. The primary outcomes included the H/M ratio, H-latency, and TTB parameters. For H-reflex testing, the peripheral electrical stimulation was delivered at the sciatic nerve before bifurcating into the tibial and common fibular nerve while participants maintained a single-leg balance position with the involved side of the limb. The TTB parameters of the medial–lateral (ML) and anterior–posterior (AP) directions of the mean, SD, and minimum were assessed, which indicate postural correction and strategies. Results: Patients with ALAS had a significantly lower AP-TTB minimum compared with healthy uninjured controls, with a moderate effect size (p = 0.039; d = −0.83). However, there was no significant difference in the H/M ratio (ALAS: 0.29 ± 0.16 vs. CON: 0.24 ± 0.10; p = 0.258) and H-reflex latency (ALAS: 34.6 ± 1.92 vs. CON: 33.8 ± 1.75 ms; p = 0.277); Conclusions: These results indicate that reflex control at the spinal level may have a minimal role in response to balance deficits following ALAS. Full article

Background/Objectives: Before a cochlear implant is considered, patients undergo various audiological tests to assess their suitability. One key test measures the auditory brainstem response (ABR) to acoustic stimuli. However, in some cases, even with maximum sound stimulation, no response is detected. Methods: The promontory test involves electrical stimulation near the auditory nerve, allowing patients to associate the sensation. Ideally, the electrode is placed in the middle ear after opening the eardrum. This method, along with trans-tympanic electrically evoked ABR in local anesthesia (LA-TT-EABR) and the cortical equivalent (LA-TT-EALR), helps assess the auditory nerve’s existence and excitability. The TympEALR test, utilizing a “tympanic LA-TT-EALR”, provides an alternative measurement. Previous research has shown the possibility of deriving brainstem and cortical potentials through trans-tympanic electrical stimulation, allowing for objective assessment of the auditory nerve’s integrity and potentially objectifying patient sensations. Results: Sixteen patients have been tested using TympEALR. In seven of these, we found a positive response. The morphology was similar to other electrically evoked cortical auditory responses (EALR), e.g., using cochlear implants or trans-tympanic stimulation electrodes. We observed a higher influence of electrical artifacts than in other EALRs. Conclusions: TympEALR showed positive results in nearly half of the study participants, potentially avoiding invasive procedures. TympEALR can be a valuable alternative to trans-tympanic methods. More research is needed to determine if a negative result suggests against cochlear implantation. Full article

In vitro experiments performed on dissociated dorsal root ganglion (DRG) neurons suggest the involvement of the hyperpolarization-activated cation current (I_h) in enhancing neuronal excitability, potentially contributing to neuropathic pain. However, the more confirmative in vivo information about how nerve injury interacts with I_h is lacking. In this study, I_h was recorded in vivo using the dynamic single-electrode voltage clamp (dSEVC) technique on L5 DRG neurons of normal rats and those seven days after spinal nerve axotomy (SNA). Compared to normal rats, SNA unexpectedly inhibited the activity of I_h channels on A-fiber DRG neurons: (a) the I_h current magnitude, density, and conductance were consistently diminished; and (b) the I_h activation velocity was slowed and the voltage for I_h activation was hyperpolarized. The half-activation voltage (V_0.5) exhibited a negative shift, and the time constant for I_h activation was prolonged across all test potentials, indicating the reduced availability of I_h after SNA. To further investigate the mechanisms of SNA on I_h, the underlying HCN channels and the correlated mRNA were quantified and compared. The mRNA expression level of HCN1-4 was uniformly enhanced after SNA, which might have contributed to the increased cytoplasmic HCN1 intensity observed in both medium- and large-sized DRG neurons. This finding contradicted the functional reduction of I_h after SNA. Surprisingly, the HCN labeling pattern was altered after SNA: the labeling area of HCN1 and HCN2 at the membranous ring region of the axotomized large neurons became significantly thinner or absent. We concluded that the diminished ring immunoreactivity for HCN1 and HCN2 correlated with a reduced availability of I_h channels, elucidating the observed decrease in I_h in axotomized A-fiber neurons. Full article

Obstructive sleep apnea (OSA) is a heterogenous disease process that cannot be adequately categorized by AHI alone. There is a significant prevalence of OSA in the general population with ongoing efforts to evaluate the risk factors contributing to OSA and its associated clinical implications. Only by improving our understanding of OSA can we advance our methods in the diagnosis and treatment of OSA. For this article, the authors reviewed keywords of obstructive sleep apnea diagnosis and therapy in the databases of Embase, Medline, and Medline ePub over the past 3 years, excluding any articles that only addressed sleep apnea in children under age 17 years. This review article is divided into three main sections. First, we will investigate the use of novel screening tools, biomarkers, anthropometric measurements, and novel wearable technologies that show promise in improving the diagnosis of OSA. There is mention of comorbid conditions seen in OSA patients since certain disease combinations can significantly worsen health and should raise our awareness to diagnose and manage those concomitant disorders. The second section will look at the current and developing treatment options for OSA. These include positive airway therapy (PAP), mandibular advancement device (MAD), exciting new findings in certain medications, orofacial myofunctional therapy (OMT), hypoglossal nerve stimulation therapy (HGNS), and other surgical options. We will conclude with a section reviewing the current Clinical Practice Guidelines for Diagnostic Testing in Adults with Obstructive Sleep Apnea from 2017, which strongly advises polysomnography (PSG) or home sleep apnea testing (HSAT), along with comprehensive sleep evaluation for uncomplicated patients with a clinical presentation of OSA. Full article

Purpose: Our aim was to use intracortical recording to enable the tracking of ischemic infarct development over the first few critical hours of ischemia with a high time resolution in pigs. We employed electrophysiological measurements to obtain quick feedback on neural function, which might be useful for screening, e.g., for the optimal dosage and timing of agents prior to further pre-clinical evaluation. Methods: Micro-electrode arrays containing 16 (animal 1) or 32 electrodes (animal 2–7) were implanted in the primary somatosensory cortex of seven female pigs, and continuous electrical stimulation was applied at 0.2 Hz to a cuff electrode implanted on the ulnar nerve. Ischemic stroke was induced after 30 min of baseline recording by injection of endothelin-1 onto the cortex adjacent to the micro-electrode array. Evoked responses were extracted over a moving window of 180 s and averaged across channels as a measure of cortical excitability. Results: Across the animals, the cortical excitability was significantly reduced in all seven 30 min segments following endothelin-1 injection, as compared to the 30 min preceding this intervention. This difference was not explained by changes in the anesthesia, ventilation, end-tidal CO₂, mean blood pressure, heart rate, blood oxygenation, or core temperature, which all remained stable throughout the experiment. Conclusions: The animal model may assist in maturing neuroprotective approaches by testing them in an accessible model of resemblance to human neural and cardiovascular physiology and body size. This would constitute an intermediate step for translating positive results from rodent studies into human application, by more efficiently enabling effective optimization prior to chronic pre-clinical studies in large animals. Full article

Background: The reduction of muscular hypertonia is important in the treatment of various diseases or rehabilitation. This study aims to test the efficacy of a 5 Hz mechanical muscle stimulation (tapotement massage) in comparison to a 5 Hz repetitive peripheral magnetic stimulation (rPMS) on the neuromuscular reflex response. Methods: In a randomized control trial, 15 healthy volunteers were administered with either 5 Hz rPMS, tapotement massage, or rPMS sham stimulation. The posterior tibial nerve was stimulated with rPMS and sham stimulation. The Achilles tendon was exposed to a mechanically applied high-amplitude 5 Hz repetitive tendon tapotement massage (rTTM). The tendon reflex (TR) was measured for the spinal response of the soleus muscle. Results: After rPMS, there was a reduction of the TR response (−9.8%, p ≤ 0.034) with no significant changes after sham stimulation. Likewise, TR decreased significantly (−17.4%, p ≤ 0.002) after Achilles tendon tapotement intervention. Conclusions: These findings support the hypothesis that both afferent 5 Hz sensory stimulations contributed to a modulation within the spinal and/or supraspinal circuits, which resulted in a reduction of the spinal reflex excitability. The effects could be beneficial for patients with muscle hypertonia and could improve the functional results of rehabilitation programs. Full article

The hyperexcitability of the anterior cingulate cortex (ACC) has been implicated in the development of chronic pain. As one of the key causes of ACC hyperexcitation, disinhibition of the ACC may be closely related to the dysfunction of inhibitory parvalbumin (PV)-expressing interneurons (PV-INs). However, the molecular mechanism underlying the ACC PV-INs injury remains unclear. The present study demonstrates that spared sciatic nerve injury (SNI) induces an imbalance in the excitation and inhibition (E/I) of the ACC. To test whether tumor necrosis factor-α (TNF-α) upregulation in the ACC after SNI activates necroptosis and participates in PV-INs damage, we performed a differential analysis of transcriptome sequencing using data from neuropathic pain models and found that the expression of genes key to the TNF-α-necroptosis pathway were upregulated. TNF-α immunoreactivity (IR) signals in the ACCs of SNI rats were co-located with p-RIP3- and PV-IR, or p-MLKL- and PV-IR signals. We then systematically detected the expression and cell localization of necroptosis-related proteins, including kinase RIP1, RIP3, MLKL, and their phosphorylated states, in the ACC of SNI rats. Except for RIP1 and MLKL, the levels of these proteins were significantly elevated in the contralateral ACC and mainly expressed in PV-INs. Blocking the ACC TNF-α-necroptosis pathway by microinjecting TNF-α neutralizing antibody or using an siRNA knockdown to block expression of MLKL in the ACC alleviated SNI-induced pain hypersensitivity and inhibited the upregulation of TNF-α and p-MLKL. Targeting TNF-α-triggered necroptosis within ACC PV-INs may help to correct PV-INs injury and E/I imbalance in the ACC in neuropathic pain. Full article

The anatomical complexity of brachial plexus injury requires specialized in-depth diagnostics. The clinical examination should include clinical neurophysiology tests, especially with reference to the proximal part, with innovative devices used as sources of precise functional diagnostics. However, the principles and clinical usefulness of this technique are not fully described. The aim of this study was to reinvestigate the clinical usefulness of motor evoked potential (MEP) induced by a magnetic field applied over the vertebrae and at Erb’s point to assess the neural transmission of brachial plexus motor fibers. Seventy-five volunteer subjects were randomly chosen to participate in the research. The clinical studies included an evaluation of the upper extremity sensory perception in dermatomes C5–C8 based on von Frey’s tactile monofilament method, and proximal and distal muscle strength by Lovett’s scale. Finally, 42 healthy people met the inclusion criteria. Magnetic and electrical stimuli were applied to assess the motor function of the peripheral nerves of the upper extremity and magnetic stimulus was applied to study the neural transmission from the C5–C8 spinal roots. The parameters of compound muscle action potential (CMAP) recorded during electroneurography and MEP induced by magnetic stimulation were analyzed. Because the conduction parameters for the groups of women and men were comparable, the final statistical analysis covered 84 tests. The parameters of the potentials generated by electrical stimulus were comparable to those of the potentials induced by magnetic impulse at Erb’s point. The amplitude of the CMAP was significantly higher following electrical stimulation than that of the MEP following magnetic stimulation for all the examined nerves, in the range of 3–7%. The differences in the potential latency values evaluated in CMAP and MEP did not exceed 5%. The results show a significantly higher amplitude of potentials after stimulation of the cervical roots compared to potentials evoked at Erb’s point (C5, C6 level). At the C8 level, the amplitude was lower than the potentials evoked at Erb’s point, varying in the range of 9–16%. We conclude that magnetic field stimulation enables the recording of the supramaximal potential, similar to that evoked by an electric impulse, which is a novel result. Both types of excitation can be used interchangeably during an examination, which is essential for clinical application. Magnetic stimulation was painless in comparison with electrical stimulation according to the results of a pain visual analog scale (3 vs. 5.5 on average). MEP studies with advanced sensor technology allow evaluation of the proximal part of the peripheral motor pathway (between the cervical root level and Erb’s point, and via trunks of the brachial plexus to the target muscles) following the application of stimulus over the vertebrae. Full article

Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Increased activity of the sympathetic nervous system (SNS) plays a role in the development and progression of metabolic diseases; however, despite the importance of the central circuits, the excitability of pre-sympathetic liver-related neurons remains to be determined. Here, we tested the hypothesis that the activity of liver-related neurons in the PVN and VLM/VMM is altered in diet-induced obese mice, as well as their response to insulin. Patch-clamp recordings were conducted from liver-related PVN neurons, VLM-projecting PVN neurons, and pre-sympathetic liver-related neurons in the ventral brainstem. Our data demonstrate that the excitability of liver-related PVN neurons increased in high-fat diet (HFD)-fed mice compared to mice fed with control diet. Insulin receptor expression was detected in a population of liver-related neurons, and insulin suppressed the firing activity of liver-related PVN and pre-sympathetic VLM/VMM neurons in HFD mice; however, it did not affect VLM-projecting liver-related PVN neurons. These findings further suggest that HFD alters the excitability of pre-autonomic neurons as well as their response to insulin. Full article

Peripheral nerve injuries induce long-lasting physiological and severe functional impairment due to motor, sensory, and autonomic denervation. Preclinical models allow us to study the process of nerve damage, evaluate the capacity of the peripheral nervous system for spontaneous recovery, and test diagnostic tools to assess the damage and subsequent recovery. Methods: In this study on Sprague–Dawley rats, we: (1) compared the use of two different anesthetics (isoflurane and urethane) for the evaluation of motor evoked potentials (MEPs) induced by trans-spinal magnetic stimulation (TSMS) in gastrocnemius and brachioradialis muscles; (2) monitored the evolution of gastrocnemius MEPs by applying paired-pulse stimulation to evaluate the neuromuscular junction activity; and (3) evaluated the MEP amplitude before and after left tibialis nerve crush (up to 7 days post-injury under isoflurane anesthesia). The results showed that muscle MEPs had higher amplitudes under isoflurane anesthesia, as compared with urethane anesthesia in the rats, demonstrating higher motoneuronal excitability under isoflurane anesthesia evaluated by TSMS. Following tibial nerve crush, a significant reduction in gastrocnemius MEP amplitude was observed on the injured side, mainly due to axonal damage from the initial crush. No spontaneous recovery of MEP amplitude in gastrocnemius muscles was observed up to 7 days post-crush; even a nerve section did not induce any variation in residual MEP amplitude, suggesting that the initial crush effectively severed the axonal fibers. These observations were confirmed histologically by a drastic reduction in the remaining myelinated fibers in the crushed tibial nerve. These data demonstrate that TSMS can be reliably used to noninvasively evaluate peripheral nerve function in rats. This method could therefore readily be applied to evaluate nerve conductance in the clinical environment. Full article

Oxaliplatin (OHP)-induced peripheral neurotoxicity (OIPN) is a frequent adverse event of colorectal cancer treatment. OIPN encompasses a chronic and an acute syndrome. The latter consists of transient axonal hyperexcitability, due to unbalance in Na⁺ voltage-operated channels (Na⁺VOC). This leads to sustained depolarisation which can activate the reverse mode of the Na⁺/Ca²⁺ exchanger 2 (NCX2), resulting in toxic Ca²⁺ accumulation and axonal damage (ADa). We explored the role of NCX2 in in vitro and in vivo settings. Embryonic rat Dorsal Root Ganglia (DRG) organotypic cultures treated with SEA0400 (SEA), a NCX inhibitor, were used to assess neuroprotection in a proof-of-concept and pilot study to exploit NCX modulation to prevent ADa. In vivo, OHP treated mice (7 mg/Kg, i.v., once a week for 8 weeks) were compared with a vehicle-treated group (n = 12 each). Neurophysiological and behavioural testing were performed to characterise acute and chronic OIPN, and morphological analyses were performed to detect ADa. Immunohistochemistry, immunofluorescence, and western blotting (WB) analyses were also performed to demonstrate changes in NCX2 immunoreactivity and protein expression. In vitro, NCX inhibition was matched by ADa mitigation. In the in vivo part, after verifyingboth acute and chronic OIPN had ensued, we confirmed via immunohistochemistry, immunofluorescence, and WB that a significant NCX2 alteration had ensued in the OHP group. Our data suggest NCX2 involvement in ADa development, paving the way to a new line of research to prevent OIPN. Full article

Neural changes in the ankle stabilizing muscles following ankle sprains are thought to be one contributing factor to persistent ankle dysfunction. However, empirical evidence is limited. Therefore, we aimed to examine spinal reflex excitability of lower leg muscles following acute ankle sprains (AAS). We performed a case-control study with 2 groups consisting of 30 young adults with AAS and 30 aged-matched uninjured controls. Hoffmann reflex (H-reflex) testing was performed to estimate spinal reflex excitability of lower leg muscles: soleus, fibularis longus (FL), tibialis anterior (TA). Maximal H-reflex (H_max) and motor responses (M_max) were determined by delivering a series of electrical stimuli at the sciatic nerve. H_max/M_max ratios were calculated to represent normalized spinal reflex excitability. Separate group-by-limb analyses of variance (ANOVA) with repeated measures found there were no significant interactions for any of the muscles (SL: F_1,56 = 0.95, p = 0.33, FL: F_1,51 = 0.65, p = 0.42, TA: F_1,51 = 1.87, p = 0.18), but there was a significant main effect of group in the soleus (F_1,56 = 6.56, p = 0.013), indicating the H_max/M_max ratio of soleus in the AAS group was significantly lower bilaterally (AAS = 0.56 ± 0.19, control = 0.68 ± 0.17, p = 0.013), with no significant group differences in the other muscles (FL: F_1,51 = 0.26, p = 0.61, TA: F_1,51 = 0.93, p = 0.34). The bilateral inhibition of the soleus spinal reflex excitability following AAS may be significant in that it may explain bilateral sensorimotor deficits (postural control deficits) following unilateral injury, and provide insights into additional therapies aimed at the neural change. Full article

Psoriasis is a complex immune-mediated inflammatory disorder that generates enormous interest within the scientific communities worldwide, with new therapeutic targets being constantly identified and tested. Despite the numerous topical and systemic medications available for the treatment of psoriasis, alternative therapies are still needed for the optimal management of some patients who present with localized, resistant lesions. Novel insights into the contribution of cutaneous neurogenic inflammation in the pathogenesis of psoriasis have yielded exciting new potential roles of nerve-targeting treatments, namely botulinum toxin type A (BoNT-A), for the management of this disease. This paper aims to review the existing literature on knowledge regarding the potential role of BoNT-A in psoriasis treatment, with a focus on its ability to interfere with the immunopathogenetic aspects of psoriatic disease. Furthermore, in our paper, we are also including the first report of psoriatic lesions remission following local BoNT-A injections that were administered for treating upper limb spasticity, in a patient that concomitantly suffered from psoriasis and post-stroke spasticity. Full article

The long-term impact of neurotological symptoms after a temporal bone fracture (TBF), including facial nerve palsy (FP), hearing loss, tinnitus, and dizziness on the quality of life of patients is often underevaluated. Thus, we retrospectively assessed 30 patients with TBF (26 men and 4 women) in our university tertiary referral center. They participated from injury onset to the final follow-up, over an 18-month period. Quality of life was estimated using validated questionnaires, such as the Facial Disability Index (FDI: physical and social), Hearing Handicap Inventory (HHI), Tinnitus Handicap Inventory (THI), and Dizziness Handicap Inventory (DHI). The FDI score was significantly worse in patients with severe initial (for physical FDI) and final facial palsy (for both physical and social FDI), mainly with immediate onset. The HHI score was statistically worse in patients with mixed hearing loss compared to those with conductive or sensorineural hearing loss and in those with profound hearing loss vs. normal hearing. The mixed TBF and the severity of hearing loss (especially profound hearing loss) were correlated with HHI, THI and DHI score values. In the long-term period after a TBF, moderate or severe facial palsy, mainly with immediate onset, may cause psychological distress, more easily resulting in social disability than functional impairment. Mixed TBF and mixed or profound hearing loss may also negatively influence quality of life. Full article