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Background: Based on the lack of literature to support any treatment strategy in patients with foot drop due to peroneal nerve entrapment, a prospective study randomizing patients between surgery and conservative treatment is warranted. Since studies comparing surgery to no surgery are often challenging, we first examined the feasibility of such a randomized controlled trial. Methods/design: An internal feasibility pilot study was conducted to assess several aspects of process, resource, management, and scientific feasibility. The main objective was the assessment of the recruitment rate. The criterion to embark on a full study was the recruitment of at least 14 patients in 6 participating centers within 6 months. Cross-over rate, blinding measures, training strategies, and trial assessments were evaluated. The trial was entirely funded by the KCE Trials public funding program of the Belgian Health Care Knowledge Centre (ID KCE19-1232). Results: The initial duration was prolonged due to the COVID-19 pandemic. Between April 2021 and October 2022, we included 19 patients of which 15 were randomized. Fourteen patients were treated as randomized. One drop-out occurred after randomization, prior to surgery. We did not document any cross-over or accidental unblinding. Training strategies were successful. Patients perceived the quality of life questionnaire as the least relevant assessment. Assessment of ankle dorsiflexion range of motion was prone to interobserver variability. All other trial assessments were adequate. Discussion: Recruitment of the anticipated 14 patients was feasible although slower than expected. The Short-Form Health Survey (SF-36) and assessment of ankle dorsiflexion range of motion will no longer be included in the full-scale FOOTDROP trial. Conclusion: The FOOTDROP study is feasible. Trial registration: ClinicalTrials.gov, identifier NCT04695834 .Registered 4 January 2021., SCOPUS: ar.j, info:eu-repo/semantics/published

Recovery of motor function after peripheral nerve injury requires treatment of the neuromuscular junction (NMJ), as well as the injured nerve and skeletal muscle. The purpose of this study was to examine the effects of ultrasound (US) stimulation on NMJ degeneration after denervation using a rat model of peroneal nerve transection. Twelve-week-old male Wistar rats were randomly assigned to 3 groups: US stimulation, sham stimulation, and intact. US or sham stimulation was performed on the left tibialis anterior (TA) muscle starting the day after peroneal nerve transection for 5 minutes daily under anesthesia. Four weeks later, the number and morphology of the motor endplates were analyzed to assess NMJ in the TA muscle. The endplates were classified as normal, partially fragmented, or fully fragmented for morphometric analysis. In addition, the number of terminal Schwann cells (tSCs) per endplate and percentage of endplates with tSCs (tSC retention percentage) were calculated to evaluate the effect of tSCs on NMJs. Our results showed that endplates degenerated 4 weeks after transection, with a decrease in the normal type and an increase in the fully fragmented type in both the US and sham groups compared to the intact group. Furthermore, the US group showed significant suppression of the normal type decrease and a fully fragmented type increase compared to the sham group. These results suggest that US stimulation inhibits endplate degeneration in denervated TA muscles. In contrast, the number of endplates and tSC and tSC retention percentages were not significantly different between the US and sham groups. Further investigations are required to determine the molecular mechanisms by which US stimulation suppresses degeneration.

[Abstract] Background: Transcutaneous electrical nerve stimulation (TENS) is used to prevent venous stasis and thromboembolism. However, best electrostimulation parameters have yet to be established. The aim of the study was to compare the hemodynamic effects and the participants’ relative discomfort of 3 TENS sequences at the maximum tolerated intensity stimulus. Methods: Twenty-four healthy university students (50% male) participated in a cross-over, randomized study. Each participant received 2 TENS sequences on peroneal nerve at 1 and 5 Hz, and the third one on soleus muscle at 5 Hz. Popliteal flow volume (FV) and peak velocity (PV) were measured using Doppler ultrasound and the relative change from basal values was recorded. Discomfort questionnaires -visual analogue scale (VAS) and verbal rating scale (VRS)- were also administered to compare sensations among the three applications. Results: All interventions produced significant hemodynamic responses compared to baseline. Both 5 Hz applications obtained higher FV increments than 1 Hz TENS (P < .001). The muscle application resulted in the lowest PV increment (P < .001). TENS at 5 Hz on nerve location was the worst tolerated, with higher values in VRS (P = .056) and VAS (P = .11), although not significant. Conclusion: TENS at 5 Hz on soleus site may be the most appropriate protocol for enhancing venous return.

Obstructive sleep apnoea (OSA) is associated with an increase in the number of bursts of muscle sympathetic nerve activity (MSNA), leading to neurogenic hypertension. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment for preventing collapse of the upper airway in OSA. In addition to improving sleep, CPAP decreases daytime MSNA towards control levels. It remains unknown how this restoration of MSNA occurs, in particular whether CPAP treatment results in a simple readjustment in activity of those brain regions responsible for the initial increase in MSNA or whether other brain regions are recruited to over-ride aberrant brain activity. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI), we aimed to assess brain activity associated with each individual subject's patterns of MSNA prior to and following 6 months of CPAP treatment. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the common peroneal nerve in 13 newly diagnosed patients with OSA before and after 6 months of treatment with CPAP and in 15 healthy control subjects while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min). Fluctuations in BOLD signal intensity in multiple regions covaried with the intensity of the concurrently recorded bursts of MSNA. There was a significant fall in MSNA after 6 months of CPAP (39 ± 2 bursts/min). The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices. These data support our contention that functiona

Obstructive sleep apnoea (OSA) is associated with an increase in the number of bursts of muscle sympathetic nerve activity (MSNA), leading to neurogenic hypertension. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment for preventing collapse of the upper airway in OSA. In addition to improving sleep, CPAP decreases daytime MSNA towards control levels. It remains unknown how this restoration of MSNA occurs, in particular whether CPAP treatment results in a simple readjustment in activity of those brain regions responsible for the initial increase in MSNA or whether other brain regions are recruited to over-ride aberrant brain activity. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI), we aimed to assess brain activity associated with each individual subject's patterns of MSNA prior to and following 6 months of CPAP treatment. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the common peroneal nerve in 13 newly diagnosed patients with OSA before and after 6 months of treatment with CPAP and in 15 healthy control subjects while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min). Fluctuations in BOLD signal intensity in multiple regions covaried with the intensity of the concurrently recorded bursts of MSNA. There was a significant fall in MSNA after 6 months of CPAP (39 ± 2 bursts/min). The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices. These data support our contention that functiona

BackgroundMitochondrial dysfunction is a prominent hallmark of many sensory neuropathies. The purpose of this study was to assess the influence of mitochondrial DNA sequence variation on peripheral nerve function in the population-based Health, Aging, and Body Composition Study.MethodsWe investigated the role of common mitochondrial DNA variation (n = 1,580) and complete mitochondrial DNA sequences (n = 138) on peroneal motor nerve conduction velocity and amplitude, average vibration detection threshold, and monofilament sensitivity.ResultsNominal associations among common mitochondrial DNA variants and haplogroups were identified but were not statistically significant after adjustment for multiple comparisons. Sequence-based approaches were used to identify aggregate variant associations across the 16S rRNA (weighted-sum, p = 2E-05 and variable threshold, p = 9E-06) for nerve conduction velocity. Several of these rare 16S variants occurred at or near sites with earlier disease associations and are also in close proximity to the peptidyl transferase center, which is the catalytic center of the 16S rRNA CONCLUSIONS: These results suggest that sequence variation related to mitochondrial protein synthesis/assembly is associated with peripheral nerve function and may provide insight into targets for intervention or new clinical strategies to preserve nerve function in late life.

Muscle sympathetic nerve activity (MSNA) is greatly elevated in patients with obstructive sleep apnoea (OSA) during daytime wakefulness, leading to hypertension, but the underlying mechanisms are poorly understood. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI) of the brain we aimed to identify the central processes responsible for the sympathoexcitation. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted percutaneously into the common peroneal nerve in 17 OSA patients and 15 healthy controls lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. Fluctuations in BOLD signal intensity covaried with the intensity of the concurrently recorded bursts of MSNA. In both groups there was a positive correlation between MSNA and signal intensity in the left and right insulae, dorsolateral prefrontal cortex (dlPFC), dorsal precuneus, sensorimotor cortex and posterior temporal cortex, and the right mid-cingulate cortex and hypothalamus. In OSA the left and right dlPFC, medial PFC (mPFC), dorsal precuneus, anterior cingulate cortex, retrosplenial cortex and caudate nucleus showed augmented signal changes compared with controls, while the right hippocampus/parahippocampus signal intensity decreased in controls but did not change in the OSA subjects. In addition, there were significant increases in grey matter volume in the left mid-insula, the right insula, left and right primary motor cortices, left premotor cortex, left hippocampus and within the brainstem and cerebellum, and significant decreases in the mPFC, occipital lobe, right posterior cingulate cortex, left cerebellar cortex and the left and right amygdala in OSA, but there was no overlap between these structural changes and the functional changes in OSA. These data suggest that the elevated muscle vasoconstrictor drive in

Muscle sympathetic nerve activity (MSNA) is greatly elevated in patients with obstructive sleep apnoea (OSA) during daytime wakefulness, leading to hypertension, but the underlying mechanisms are poorly understood. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI) of the brain we aimed to identify the central processes responsible for the sympathoexcitation. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted percutaneously into the common peroneal nerve in 17 OSA patients and 15 healthy controls lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. Fluctuations in BOLD signal intensity covaried with the intensity of the concurrently recorded bursts of MSNA. In both groups there was a positive correlation between MSNA and signal intensity in the left and right insulae, dorsolateral prefrontal cortex (dlPFC), dorsal precuneus, sensorimotor cortex and posterior temporal cortex, and the right mid-cingulate cortex and hypothalamus. In OSA the left and right dlPFC, medial PFC (mPFC), dorsal precuneus, anterior cingulate cortex, retrosplenial cortex and caudate nucleus showed augmented signal changes compared with controls, while the right hippocampus/parahippocampus signal intensity decreased in controls but did not change in the OSA subjects. In addition, there were significant increases in grey matter volume in the left mid-insula, the right insula, left and right primary motor cortices, left premotor cortex, left hippocampus and within the brainstem and cerebellum, and significant decreases in the mPFC, occipital lobe, right posterior cingulate cortex, left cerebellar cortex and the left and right amygdala in OSA, but there was no overlap between these structural changes and the functional changes in OSA. These data suggest that the elevated muscle vasoconstrictor drive in

Objective: We aim to draw clinical-neurophysiological correlations in our cohort of patients affected by IgM-related neuropathy to investigate whether neurophysiological parameters may help differentiate the classical phenotype from atypical forms. Methods: We retrospectively evaluated patients with IgM-related neuropathy referred to our Institute from 1990 to 2011. All patients underwent extensive laboratory, clinical and neurophysiological evaluation. Results: A classic sensory-ataxic form was observed in 20 of 34 patients, while an atypical phenotype (multiple mononeuropathy, polyneuropathy with predominant motor impairment, painful small-fibre neuropathy) was identified in the remaining 14 cases. Nerve conduction studies revealed in almost all cases a pattern typical of demyelination. A reduced terminal latency index and a prolonged distal motor latency of median nerve, as well as a prolonged distal motor latency and a reduced motor conduction velocity of peroneal nerve when recorded from extensor digitorum brevis, were significantly associated with classic sensory-ataxic phenotype. Conversely, a compound muscle action potential amplitude reduction of peroneal nerve from the tibialis anterior, was mostly associated with atypical forms. Conclusions: No clear electrophysiological differences between classical forms and atypical cases can be identified in IgM-related neuropathy. Still, we demonstrated that demyelinating abnormalities are more often associated with classical phenotypes, while axonal impairment occurs more often in atypical clinical patterns. Significance: Performing correlations between clinical and neurophysiological findings in IgM-related neuropathy may help to better understand different disease mechanisms in this heterogeneous form of inflammatory neuropathy. © 2013 International Federation of Clinical Neurophysiology.

We aim to draw clinical-neurophysiological correlations in our cohort of patients affected by IgM-related neuropathy to investigate whether neurophysiological parameters may help differentiate the classical phenotype from atypical forms.

No abstract

The current gold standard for repair of a nerve injury is the interposition of an autologous nerve graft. This has several disadvantages, such as donor site morbidity, limited availability, size mismatch and painful neuroma formation. In addition, functional recovery rarely returns to pre-injury level. Therefore, the development and optimization of nerve conduits is an increasingly important focus in the field of peripheral nerve regeneration. One promising approach that may enhance nerve regeneration is the long term delivery of growth factors. However, accurate delivery and concentration maintenance of growth factors within the nerve conduit still pose problems. We therefore studied the long term release of nerve growth factor (NGF) using a microsphere delivery system. First, we evaluated the release of NGF from five different types of polymer microspheres both in vitro and in vivo. Next, we assessed the effect of both NGF and glial cellline derived neurotrophic factor (GDNF) releasing microspheres on functional regeneration using polymer nerve conduits., See also ADM002187. Proceedings of the Army Science Conference (26th) Held in Orlando, Florida on 1-4 December 2008, The original document contains color images.

Ultrasound imaging of peripheral nerves is increasingly used in the clinic for a wide range of applications. Although yet unapplied for experimental neuroscience, it also has potential value in this research area. This study explores the feasibility, possibilities and limitations of this technique in rabbits, with special focus on peripheral nerve regeneration after trauma. The peroneal nerve of 25 New Zealand White rabbits was imaged at varying time intervals after a crush lesion. The ultrasonic appearance of the nerve was determined, and recordings were validated with in vivo anatomy. Nerve swelling at the lesion site was estimated from ultrasound images and compared with anatomical parameters. The peroneal nerve could reliably be identified in all animals, and its course and anatomical variations agreed perfectly with anatomy. Nerve diameters from ultrasound were related to in vivo diameters (p < 0.001, R2 = 77%), although the prediction interval was rather wide. Nerve thickenings could be visualized and preliminary results indicate that ultrasound can differentiate between neuroma formation and external nerve thickening. The value of the technique for experimental neuroscience is discussed. We conclude that ultrasound imaging of the rabbit peroneal nerve is feasible and that it is a promising tool for different research areas within the field of experimental neuroscience.

Taxol, a natural extract with antineoplastic properties, is known to be neurotoxic in humans. Its neurotoxicity after systemic administration, however, has never been studied in detail at the morphological level in humans and in animals. In this study we administered taxol intraperitoneally to female Wistar rats and we performed an extended neurophysiological and morphological examination of the peripheral nerves, dorsal root ganglia, spinal rootlets, and spinal cord. The results obtained in this experimental model indicate that taxol induces pathological changes mainly in the peripheral nerves, but they are present also in the ventral and dorsal spinal rootlets and spinal dorsal column fibers. The dorsal root ganglia and spinal cord neurons were, on the contrary, unaffected. The most impressive change induced by systemic taxol administration was intraaxonal neurotubule accumulation. Schwann cells showed signs of "activation" but clear demyelination was not observed. We conclude that with the use of this model it is possible to induce a peripheral neuropathy in the Wistar rat which resembles that reported in humans and which can, therefore, be used to better understand the basic mechanism(s) of taxol toxicity and to evaluate protective strategies in an attempt to reduce it

The authors report a case of compression of the peroneal nerve by an intraneural ganglionic cyst. The chief complaint is generally a lateral upper leg pain occasionally associated with foot drop and swelling of the upper tibiofibular joint. In our case, the disease was revealed by a tentative intraarticular injection of betamethasone. Early microsurgical treatment remains the only way to avoid permanent motor sequellae.

Somatosensory evoked potentials (SEPs) were studied in 20 children with cerebral palsy and severe lower extremity spasticity before and after selective partial dorsal root rhizotomy of the lumbosacral cord. The potentials from stimulating nerves in the lower extremity were abnormal in two thirds of the children before the operation, whereas the potentials were generally normal from upper extremity nerves. Dorsal root rhizotomies caused an attenuation of nerve root entry volleys recorded over the lumbar cord but did not change SEPs recorded over the cortex. The exception to this was that the incidence of abnormal sural nerve SEPs decreased postoperatively. Lumbar cord functions measured by H-reflexes or by tendon jerks were depressed following the operation. These results indicate a significant degree of abnormality of somatosensory transmission from the lower extremity in a group of cerebral palsied children with severe spasticity. Moreover, selective sectioning of approximately 50% of the dorsal root fibers in the lumbosacral cord had little influence on cortical evoked potentials.

Somatosensory evoked potentials (SEPs) were studied in 20 children with cerebral palsy and severe lower extremity spasticity before and after selective partial dorsal root rhizotomy of the lumbosacral cord. The potentials from stimulating nerves in the lower extremity were abnormal in two thirds of the children before the operation, whereas the potentials were generally normal from upper extremity nerves. Dorsal root rhizotomies caused an attenuation of nerve root entry volleys recorded over the lumbar cord but did not change SEPs recorded over the cortex. The exception to this was that the incidence of abnormal sural nerve SEPs decreased postoperatively. Lumbar cord functions measured by H-reflexes or by tendon jerks were depressed following the operation. These results indicate a significant degree of abnormality of somatosensory transmission from the lower extremity in a group of cerebral palsied children with severe spasticity. Moreover, selective sectioning of approximately 50% of the dorsal root fibers in the lumbosacral cord had little influence on cortical evoked potentials.

Compound muscle action potentials of the extensor digitorum brevis were obtained in two groups of normal and uraemic subjects by stimulating the deep peroneal nerve at the ankle and at the capitulum fibulae. Particular attention was drawn to the index of desynchronisation supplied by the amplitude change in the muscle potential evoked by distal and proximal stimulation of the same nerve. Statistical studied confirmed the soundness of this index in the normal and in the pathological condition, and showed a significant increase of the values found in uraemic patients. The complex of the data pointed out the advantage of integrating the usual motor conduction velocity determination with the mentioned desynchronisation index