Nerve Amplitude Research Articles

Peripheral neuropathy after viral eradication with direct-acting antivirals in chronic HCV hepatitis: A prospective study.

BackgroundHCV‐related extra‐hepatic complications include peripheral neuropathies, with important prevalence and impact. A recent metanalysis of previous intervention trials concluded for insufficient data to support evidence‐based treatments for this complication. In this longitudinal study, we assessed for the first time prevalence and outcome of neuropathy in a cohort of patients with chronic HCV, before and after direct‐acting antiviral agent (DAA) treatment.MethodNinety‐four patients (mean age 58.5 ± 9.9, infection duration 22.2 ± 6.3 years) without systemic and metabolic diseases, underwent neurological examination and electroneurography studies before (T0) and 10.4 ± 1.7 months after the end of DAA therapy (T1), and cryoglobulins (CG) assessment. Muscle strength was evaluated by Medical Research Council (MRC) score; neuropathic pain, sensory function, disability, quality of life were assessed by validated questionnaires (DN4, NPSI, SSS, INCAT and Euro‐QoL).ResultsAt T0, sensory‐motor neuropathy was detected in 22 patients (23%), reflexes were depressed in 32 (34%) with no association with infection duration, viral load, age, CG. Neuropathic pain (DN4 ≥4) was present in 37 patients (39%). At T1, out of the 22 patients with altered electroneurography, 3 had died or developed HCC, 4 showed normal electroneurography, and nerve amplitude parameters tended to improve in the whole group. Only 11 patients (12%) had depressed reflexes and 10 (11%) DN4 ≥4 (P < .05 compared to T0). Scores for MRC, questionnaires and Euro‐QoL improved significantly (P < .05).ConclusionOur study confirms the high prevalence of clinical and subclinical peripheral sensory‐motor neuropathy in patients with HCV infection and indicates improvement after eradication by DAA. These results support the need for larger intervention studies.

The long-term impact of ovariectomy on ventilation and expression of phrenic long-term facilitation in female rats.

New Findings What is the central question of this study? Would ovariectomy cause prolonged changes in ventilation and sustained loss of acute, intermittent hypoxia‐induced neuroplasticity or would these outcomes be restored with time? What is the main finding and its importance? Our main findings demonstrate that ovariectomy elicits minimal alteration in overall breathing function but impairs acute, intermittent hypoxia‐induced plasticity for ≤ 12 weeks. Sex hormones are necessary to enable respiratory neuroplasticity, including phrenic long‐term facilitation (pLTF), a form of respiratory motor plasticity elicited by acute, intermittent hypoxia (AIH). Female rats exhibit a progressive increase in phrenic nerve amplitude after AIH characteristic of pLTF only during pro‐oestrus, the stage of the oestrous cycle notable for elevated circulating oestradiol levels. Removal of the ovaries [ovariectomy (OVX)], the primary source of circulating oestradiol, also eliminates AIH‐induced pLTF after 1 week. Ovariectomy is used routinely as a model to examine the impact of sex hormones on CNS structure and function, but the long‐term impact of OVX is rarely examined. Extra‐ovarian sites of oestradiol synthesis, including multiple CNS sites, have been identified and might possess the capacity to restore oestradiol levels, in part, over time, impacting respiratory function and the expression of respiratory neuroplasticity. We examined both ventilation in awake, freely behaving female rats, using barometric plethysmography, and the expression of AIH‐induced pLTF in anaesthetized, ventilated female rats 2 and 12 weeks after OVX and compared them with age‐matched ovarian‐intact female rats. Our findings indicate that chronic OVX had little impact on baseline breathing or in the response to respiratory challenge (10% O2, 5% CO2, balance N2) during plethysmography. However, OVX rats at both 2 and 12 weeks demonstrated a persistent loss of AIH‐induced pLTF relative to control animals (P < 0.01), suggesting that other sources of oestradiol synthesis were insufficient to restore pLTF. These data are consistent with our previous work indicating that oestradiol plays a key role in expression of AIH‐induced respiratory neuroplasticity.

O-NE005. Electroneuromyography as a predictor of peripheral neuropathy symptoms after two years follow-up in farmers exposed to pesticide: A cohort study

Introduction . Farmer is one of the most common occupation in Indonesia. To increase crop production, they tend to use organophosphate or carbamate pesticides. These extensive pesticide uses could cause low cholinesterase levels in blood, and cause injury in peripheral nerve and neuropathy symptoms. With electroneuromyography (ENMG), subclinical neuropathy preceding its symptom could be found. The purpose of this study is to find association between any abnormality measurement in ENMG with neuropathic symptoms after two years. Methods . This was cohort prospective study. Farmers with history of pesticide exposure, without neuropathic symptoms in 2017, had low blood cholinesterase levels, and gave consent to have ENMG examination were recruited. Motor and sensory aspect of nerve was examined. For motor, we examined distal latency (DL), nerve conduction velocity (NCV), proximal amplitude (PA) and distal amplitude (DA) of median, ulnar, and tibial nerves. For sensory, we examined DL and PA of median, ulnar, and sural nerves. Neuropathic symptoms in 2 years follow up were determined from Total Neuropathic Symptoms Scale, with score > 0 diagnosed as having neuropathic symptoms. Results . There were 26 farmers included in this study. After statistical analyses, there were association between neuropathic symptoms after 2 years with motor NCV, motor PA and sensory DL of median nerve; motor NCV and motor PA of ulnar nerve (p-value > 0.05). After age, gender, working hour, pesticide spray duration adjustment, ENMG markers which had significant and independent association with neuropathy symptoms after two years were ulnar motor DL (p-value: 0.032), median motor NCV (p-value: 0.035), median motor PA (p-value: 0.043), and ulnar sensory DL (p-value: 0.010). Conclusion . From this study, we concluded that ENMG can be used as predictor for neuropathic symptoms in 2 years for asymptomatic farmers exposed to pesticide with low blood cholinesterase levels.

Nerve Conduction Studies (NCS) and Electromyography (EMG) P-NE002. The differences of vitamin D supplementation in nerve conduction studies based on diabetic duration and glycemic control in diabetic neuropathy

Introduction. Diabetic neuropathy (DN) is the most common form of neuropathy in developed countries. Diabetic duration and glycemic control are risk factors for DN. Evidence that vitamin D can improve glycemic control is still uncertain. In some literatures, there are conflicting reports on the effect of vitamin D on nerve conduction studies (NCSs). Aim: To assess the differences of vitamin D supplementation in NCSs based on diabetic duration and glycemic control in type 2 diabetes mellitus (T2DM) Indonesian patients. Methods. Twenty-five subjects with T2DM in Haji Adam Malik General Hospital Medan were studied. They were treated for 10 weeks with vitamin D (D3) supplementation of 50,000 IU/week. They were evaluated by HbA1c level and routine NCSs in the upper and lower limbs, before and 10 weeks after vitamin D supplementation. The differences of vitamin D supplementation in NCSs were based on diabetic duration and glycemic control. This was analyzed with dependent t-test. Results. There were significant differences of vitamin D supplementation in distal latency (DL) of all nerves, and amplitude (A) of motor median, ulnar, peroneal, and tibial nerves and sensory sural nerve based on diabetic duration. There were significant differences in A of motor and sensory median and ulnar nerves and motor peroneal and tibial nerves, and nerve conduction velocity (NCV) of all nerves. Conclusion. There were differences in vitamin D supplementation in NCSs based on diabetic duration and glycemic control in T2DM Indonesian patients.

P-PN006. Guillain barré syndrome treatment related fluctuation (GBS-TRF) following meningococcus vaccination: A case report

Introduction . GBS is an autoimmune neurological disorder, characterized by acute limb weakness and areflexia. The pathogenesis of GBS is triggered mostly by infection process. However, the consequence of vaccination can cause GBS has been widely discussed. Some studies address the potential relationship of GBS to influenza vaccination, while other vaccination is rarely described. In this study, we reported a case of GBS-TRF after administration of meningococcus vaccination. Case presentation: A 64-year-old man presented with glove-stocking hypoesthesia followed by flaccid tetraparesis, which occurred two weeks after meningococcus vaccination. There were no history of any infectious diseases preceding his symptoms. He and his family were administered these vaccinations, as the prerequisite for going to Umrah. After coming back of his Umrah, he was diagnosed with GBS based on history, clinical features and test results. Neurological examination revealed absent of knee and ankle reflexes. Nerve conduction studies indicated the decreased of sensory nerve action potential, amplitudes and conduction velocity, also prolongation of distal latency. He had six times therapeutic plasma exchange (TPE) and the symptoms slightly resolved at discharge. One month after plasma exchange, he was readmitted due to dyspnea, worsening of his weakness and severe hyponatremia. He was transferred to intensive care unit with mechanical ventilation. He was diagnosed as GBS-TRF. The treatment was intravenous immunoglobulin (IVIG) with full dose of 400 mg/kg/day. Unfortunately, the patient developed some complications during intensive care. He did not survive, suffering from cardiac arrythmia and septic shock, after IVIG treatment. Conclusion . Meningococcus vaccination may cause GBS as an unexpected abnormal autoimmune response. It is important to note the possibility of neurological complications after vaccine administration.

Prevalence and Characteristics of Polyneuropathy in Atypical Parkinsonian Syndromes: An Explorative Study

(1) Background: Peripheral nerve involvement is increasingly recognized in Parkinson’s disease (PD). Although non-motor symptoms and postural instability are early features of atypical parkinsonian syndromes (APS), peripheral neuropathies in APS have not been addressed in detail thus far. Therefore, the aim of this study was to investigate the prevalence and characteristics of polyneuropathies (PNP) in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), as representative syndromes of APS. (2) Methods: In total, 8 MSA and 6 PSP patients were comprehensively analyzed regarding subjective, clinical (motor and non-motor) and paraclinical PNP features using nerve conduction studies and high resolution nerve ultrasounds (HRUS). (3) Results: A total of 87.5% of MSA and 66.7% of PSP patients complained of at least one neuropathic symptom, with electrophysiological confirmation of PNP in 50.0% of both, MSA and PSP patients. PNP symptom severity in PSP and motor nerve amplitude in MSA were associated with compromised motor function. Morphologic nerve examination by HRUS showed few alterations according to the axonal type of PNP. (4) Conclusions: The overall high PNP symptom burden may be partially credited to the significant prevalence of electrophysiologically diagnosed PNP, and impact motor aspects of APS. The findings of this exploratory study reinforce further investigations on a larger scale, in order to elucidate peripheral nerve involvement and the underlying pathophysiological mechanisms of APS.

The role of abnormalities of lipoproteins and HDL functionality in small fibre dysfunction in people with severe obesity

Obesity and associated dyslipidemia may contribute to increased cardiovascular disease. Obesity has also been associated with neuropathy. We have investigated presence of peripheral nerve damage in patients with severe obesity without type 2 diabetes and the status of metabolic syndrome and lipoprotein abnormalities. 47participants with severe obesity and 30 age-matched healthy controls underwent detailed phenotyping of neuropathy and an assessment of lipoproteins and HDL-functionality. Participants with severe obesity had a higher neuropathy symptom profile, lower sural and peroneal nerve amplitudes, abnormal thermal thresholds, heart rate variability with deep breathing and corneal nerve parameters compared to healthy controls. Circulating apolipoprotein A1 (P = 0.009), HDL cholesterol (HDL-C) (P < 0.0001), cholesterol efflux (P = 0.002) and paroxonase-1 (PON-1) activity (P < 0.0001) were lower, and serum amyloid A (SAA) (P < 0.0001) was higher in participants with obesity compared to controls. Obese participants with small nerve fibre damage had higher serum triglycerides (P = 0.02), lower PON-1 activity (P = 0.002) and higher prevalence of metabolic syndrome (58% vs. 23%, P = 0.02) compared to those without. However, HDL-C (P = 0.8), cholesterol efflux (P = 0.08), apoA1 (P = 0.8) and SAA (P = 0.8) did not differ significantly between obese participants with and without small nerve fibre damage. Small nerve fibre damage occurs in people with severe obesity. Patients with obesity have deranged lipoproteins and compromised HDL functionality compared to controls. Obese patients with evidence of small nerve fibre damage, compared to those without, had significantly higher serum triglycerides, lower PON-1 activity and a higher prevalence of metabolic syndrome.

No evidence of improvement in neuropathy after renal transplantation in patients with end stage kidney disease.

To assess the impact of renal transplantation on peripheral nerve damage in patients with chronic kidney disease (CKD). Fifteen patients with CKD (eGFR <15 mL/min/1.73 m2 ) underwent longitudinal assessment after renal transplantation (age: 56.88 ± 2.53 years, eGFR: 46.82 ± 4.86) and were compared with 15 age-matched controls (age: 58.25 ± 2.18 years, eGFR: 86.0 ± 2.0). The neuropathy symptom profile (NSP), neuropathy disability score (NDS), vibration perception threshold (VPT), cold and warm sensation threshold (CST and WST), cold and heat induced pain (CIP and HIP), deep breathing heart rate variability (DB-HRV), nerve conduction studies and corneal confocal microscopy (CCM) to quantify small nerve fibre pathology, were undertaken within 1-month of renal transplantation (baseline) and at 6, 12 and 24 months of follow up. There was no significant difference in NSP (P=.1), NDS (P=.3), VPT (P=.6), CST (P=.2), CIP (P=.08), HIP (P=.1), DB-HRV (P=.9) and sural (P=.4) and peroneal (P=.1) nerve amplitude between patients with CKD and controls at baseline. However, sural (P=.04), peroneal (P=.002) and tibial (P=.007) nerve conduction velocity and tibial nerve amplitude (P=.03) were significantly lower, WST (P=.02) was significantly higher and corneal nerve fibre density (P=.004) was significantly lower in patients with CKD compared with controls. There was no significant change in NSP, NDS, quantitative sensory testing, DB-HRV, nerve conduction or CCM parameters 24 months after renal transplantation. There is evidence of small and large fibre neuropathy in patients with CKD, but no change up to 24 months after successful renal transplantation.

Feasibility of assessing progression of transthyretin amyloid polyneuropathy using nerve conduction studies: Findings from the Transthyretin Amyloidosis Outcomes Survey (THAOS).

Patients with transthyretin amyloid polyneuropathy (ATTR‐PN) show decreased motor and sensory nerve amplitudes and conduction. Electrophysiological changes over time may be sensitive indicators of progression. This analysis from the Transthyretin Amyloidosis Outcomes Survey (THAOS) assessed longitudinal changes in nerve conduction as signals of neurologic disease progression in patients with hereditary ATTR (ATTRv) amyloidosis. Patients with ATTRv in THAOS with recorded nerve conduction values were included (data cut‐off: January 6, 2020); changes in nerve amplitude and velocity over time were assessed. Patients (n = 1389) were 45.0% male; 80.4% were the Val30Met (p.Val50Met) genotype. Mean (SD) age at enrollment was 43.6 (14.5) years; duration of symptoms was 9.3 (6.4) years. Median (10th, 90th percentile) sural nerve amplitude and velocity was 18.0 (4.9, 35.0) μV and 50.7 (41.0, 57.9) m/s; peroneal conduction was 13.0 (4.4, 27.0) μV and 51.0 (41.7, 59.7) m/s, respectively. Median (10th, 90th percentile) percentage change from baseline in sural nerve amplitude was variable, but generally decreased over time from −7.4 (−43.2, 52.4) at year 1 to −14.4 (−76.9, 46.7) at year 8. Percent change from baseline in sural nerve velocity declined similarly: −0.1 (−14.5, 15.3) at year 1 and − 6.4 (−21.3, 10.5) at year 8. The decline was more pronounced in patients with greater disability at baseline. Similar patterns were observed for the peroneal nerve. These data show an association between nerve amplitudes and velocities and disease severity, suggesting progressive deterioration in nerve conduction may be an indicator of ATTRv amyloidosis disease progression.

The Long‐Term Impact of Ovariectomy on Ventilation and Expression of Phrenic Long‐Term Facilitation in Female Rats

Estrogen is necessary for the expression of phrenic long-term facilitation (pLTF) in female rats. pLTF, a well-studied model of respiratory neuroplasticity, is characterized by a progressive increase in phrenic nerve amplitude following acute intermittent hypoxia (AIH). Gonadally-intact, adult female rats only develop pLTF in stages of the estrous cycle with high levels of circulating estrogen. Removal of the ovaries (ovariectomy, OVX), the primary source of circulating estrogen in females, also prevents AIH-induced pLTF and estrogen supplementation is sufficient to restore pLTF in OVX rats, supporting a key role for estrogen in the development of pLTF. Respiratory neuroplasticity studies using OVX female rats are generally completed ~7-10 days post-OVX; a timeframe sufficient for surgery recovery and for circulating estrogen levels to significantly decline. However, few studies have explored the long-term impact of OVX on respiratory function or the development of respiratory neuroplasticity. Here, we examined ventilation in awake, freely behaving rats and the development of AIH-induced pLTF in adult female rats 12 weeks-post OVX (or sham control surgeries) and compared them to female rats 2 weeks-post OVX. Our hypothesis was that chronic OVX would have minimal long-term impact on ventilation but would continue to impair development of AIH-induced pLTF. Whole body plethysmography was used to measure baseline breathing (20.9% O2, N2 balance) and ventilatory responses to strong chemoreceptor stimulation (10% O2, 5% CO2, N2 balance). Respiratory measures including frequency, tidal volume, minute ventilation, and respiratory neural drive were measured and compared between groups. Following plethysmography, phrenic nerve recordings were used to quantify pLTF. Results indicate that chronic OVX had little impact on baseline breathing function and rats in all experimental groups responded appropriately to respiratory challenge during plethysmography. However, 12 week OVX rats showed a significant increase in tidal volume relative to baseline during respiratory challenge (p≤0.001), different from other groups. This increase in tidal volume production was also reflected in the calculation of tidal volume/inspiratory time, a measure of relative respiratory neural drive (p≤0.01) but not in minute ventilation. OVX had sustained effects on development of respiratory plasticity, as only rats in the 12 week sham control group displayed pLTF, indicated by significantly increased phrenic nerve amplitude 60-min following AIH (p≤0.001). This increase in amplitude was higher than both 12 week and 2 week OVX groups (p≤0.01). ELISA assays also showed a significant correlation between circulating estrogen levels and magnitude of pLTF (p= 0.039) In summary, OVX appears to limit the expression of respiratory neuroplasticity in female rats for up to 12 weeks. Since no significant changes in circulating estrogen are observed in OVX rats over that time, these data are consistent with our prior work indicating that estrogen plays a key role in development of respiratory neuroplasticity.

Immune Axonal Neuropathies Associated With Systemic Autoimmune Rheumatic Diseases.

Immune axonal neuropathies are a particular group of immune-mediated neuropathies that occasionally accompany systemic autoimmune rheumatic diseases such as connective tissue dissorders and primary systemic vasculitides. Apart from vasculitis of vasa nervorum, various other mechanisms are involved in their pathogenesis, with possible therapeutic implications. Immune axonal neuropathies have highly heterogeneous clinical presentation and course, ranging from mild chronic distal sensorimotor polyneuropathy to severe subacute mononeuritis multiplex with rapid progression and constitutional symptoms such as fever, malaise, weight loss and night sweats, underpinning a vasculitic process. Sensory neuronopathy (ganglionopathy), small fiber neuropathy (sensory and/or autonomic), axonal variants of Guillain-Barré syndrome and cranial neuropathies have also been reported. In contrast to demyelinating neuropathies, immune axonal neuropathies show absent or reduced nerve amplitudes with normal latencies and conduction velocities on nerve conduction studies. Diagnosis and initiation of treatment are often delayed, leading to accumulating disability. Considering the lack of validated diagnostic criteria and evidence-based treatment protocols for immune axonal neuropathies, this review offers a comprehensive perspective on etiopathogenesis, clinical and paraclinical findings as well as therapy guidance for assisting the clinician in approaching these patients. High quality clinical research is required in order to provide indications and follow up rules for treatment in immune axonal neuropathies related to systemic autoimmune rheumatic diseases.

Comparison of stimulating dissector and intermittent stimulating probe for the identification of recurrent laryngeal nerve in reoperative setting.

Recurrent laryngeal nerve (RLN) paralysis is one of the most devastating complications after thyroidectomy. Thyroid reoperation is a great challenge for surgeons due to anatomical distortion and fibrosis and associated with a higher risk of RLN injury. In this study, we aimed to compare stimulating dissector (SD) with intermittent stimulating probe (ISP) in thyroid reoperations. This study is the first one which compares the impact of different nerve stimulating devices in thyroid reoperations. Included in this randomized prospective study were patients who had a bilateral subtotal thyroidectomy and would undergo a completion thyroidectomy due to a diagnosis of thyroid papillary cancer between January 2015 and January 2017. Patients were divided into two groups as SD group and ISP group. Age, sex, nerve amplitudes, latencies, the first identification time of RLN and complications were compared in both groups. A total of 32 patients, 16 in both groups, were included in the study. The demographics, nerve signal amplitudes and latencies were similar in both groups (p > 0.05). The mean RLN identification time in the SD group was 17.4 ± 4.3min, which was significantly shorter than those in the ISP group (mean 21.3 ± 3.9) (p = 0.014). The first identification of RLN in the thyroid reoperations was faster with the use of SD than with the use of the ISP. Since the electromyographic amplitudes of RLN and vagus nerve with using SD were similar to the bipolar ISP, SD can be used safely for thyroid reoperations.

Intraoperative facial nerve electromyography parameters to optimize postoperative facial nerve outcome in patients with large unilateral vestibular schwannoma.

Decision-making for large sporadic vestibular schwannomas (VS) resection guided by the intraoperative change in supramaximal facial nerve (FN) amplitude and latency response to optimize post-operative FN outcome. Prospectively study of 43 patients, from January to December 2018, of large sporadic VS with preoperative normal FN function at our center. Tumors were removed through retrosigmoid (81%) or translabyrinthine (19%) approaches with FN monitoring. Intraoperative pre- and post-VS resection supramaximal (2 mA) amplitude and latency responses at the proximal FN root were recorded. Total, near-/subtotal VS resections (TR, NTR, STR) were achieved in 51%, 38%, and 11% of tumors, respectively, guided by no more than 40% decrease in supramaximal amplitude. Pre- and post-resection supramaximal amplitude and latency responses were lower and longer, respectively, in NTR+STR than in TR. At day 8, FN function was grade I-II in 77% of patients and grade III-V in 23%, and after 6 months, it was in grade I-II in 95% and grade III in 5%, and there was no significant difference between TR and NTR+STR. Facial palsy occurred in older patients and in the case of severe FN adhesion. At day 8, pre- and post-resection supramaximal amplitude but not latency responses were different between FN grade III-V and grade I-II. Serviceable hearing was preserved in 28% of large VS. Intraoperative FN monitoring guided VS resection in large VS so that 49% retained some residual tumor. Accordingly, 95% good postoperative FN function and significant hearing preservation were achieved after 6 months.

Effect of omalizumab treatment on peripheral nerves in patients with chronic spontaneous urticaria

Aim: Chronic spontaneous urticaria (CSU) is characterised by itchy, red and raised lesions that appear as an attack without any cause and last for six weeks or longer. Omalizumab is a humanised monoclonal antibody that selectively binds to the Ce3 moiety of circulating IgE and is indicated for the treatment of resistant CSU. In this study, we aimed to investigate whether there was peripheral nervous system involvement in patients with chronic urticaria receiving omalizumab treatment. Methods: Forty-seven patients who were treated with omalizumab for CSU were included in the study. Electrophysiological measurements were performed following a neurological examination before treatment and at three months after omalizumab treatment. In nerve conduction tests, eight different nerves were studied in four extremities (total 16 nerves). During these studies, two motor and two sensory nerves (median and ulnar) in the upper extremities, and two motor (tibial and common peroneal) and two sensory nerves (sural and superficial peroneal) in the lower extremities were analysed. Results: No pathological electrophysiological findings supporting neuropathy were detected in any of the measurements performed before and after treatment. When the nerve conduction velocity, amplitude and latency values ​​of all examined nerves were compared, no significant difference was found between the pre- and post-treatment values. Conclusions: It can be considered that omalizumab has no effect on peripheral nerves, and it is a safe and well tolerated agent in terms of both peripheral nerves and neurological structure.

Association of serum neurofilament light chain levels with clinicopathology of chronic inflammatory demyelinating polyneuropathy, including NF155 reactive patients

To clarify whether serum neurofilament light chains (NfLs) serve as a biomarker of axonal damage in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), especially in patients with anti-neurofascin 155 (NF155) antibodies. The Simoa system was used to examine serum NfL levels from 58 patients with CIDP, including 13 anti-NF155 antibody-positive patients, and from 14 age- and sex-matched healthy individuals. Serum NfL levels were evaluated before and after treatment in eight patients with anti-NF155 antibodies. Clinical features, electrophysiological findings, and cerebrospinal fluid (CSF) protein levels, were evaluated. The pathological features of sural nerves from 40 patients were also examined. Serum NfL levels were significantly higher in patients with CIDP than in healthy individuals (median 29.63 vs. 7.71pg/mL, p < 0.001) and were correlated with both modified Rankin Scale scores (r = 0.584, p < 0.001) and CSF protein levels (r = 0.432, p = 0.001). The NfL levels of anti-NF155 antibody-positive patients were higher than those of antibody-negative patients (p = 0.005). Serum NfL levels were negatively correlated with compound muscle action potential amplitudes of the tibial nerves (r = - 0.404, p = 0.004) and positively correlated with the degree of active axonal degeneration in the pathological findings (r = 0.485, p = 0.001). In the antibody-positive group, NfL levels and antibody titers decreased after treatment in all examined patients. Serum NfL correlated with pathological indices of axonal degeneration, and may serve as a biomarker that reflects active axonal damage of CIDP.

Critical illness polyneuropathy, myopathy and neuronal biomarkers in COVID-19 patients: A prospective study

ObjectiveThe aim was to characterize the electrophysiological features and plasma biomarkers of critical illness polyneuropathy (CIN) and myopathy (CIM) in coronavirus disease 2019 (COVID-19) patients with intensive care unit acquired weakness (ICUAW). MethodsAn observational ICU cohort study including adult patients admitted to the ICU at Uppsala University Hospital, Uppsala, Sweden, from March 13th to June 8th 2020. We compared the clinical, electrophysiological and plasma biomarker data between COVID-19 patients who developed CIN/CIM and those who did not. Electrophysiological characteristics were also compared between COVID-19 and non-COVID-19 ICU patients. Results111 COVID-19 patients were included, 11 of whom developed CIN/CIM. Patients with CIN/CIM had more severe illness; longer ICU stay, more thromboembolic events and were more frequently treated with invasive ventilation for longer than 2 weeks. In particular CIN was more frequent among COVID-19 patients with ICUAW (50%) compared with a non-COVID-19 cohort (0%, p = 0.008). Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAp) levels were higher in the CIN/CIM group compared with those that did not develop CIN/CIM (both p = 0.001) and correlated with nerve amplitudes. ConclusionsCIN/CIM was more prevalent among COVID-19 ICU patients with severe illness. SignificanceCOVID-19 patients who later developed CIN/CIM had significantly higher NfL and GFAp in the early phase of ICU care, suggesting their potential as predictive biomarkers for CIN/CIM.

A Prospective Study of Taxane-Induced Neuropathy with Breast Cancer: Proper Assessment Tool for Taxane-Induced Neuropathy.

Background Many chemotherapeutic agents, especially taxanes, can induce peripheral neuropathy. Aim To evaluate the clinical characteristics of taxane-induced neuropathy (TIN) and determine the proper assessment tool for TIN in patients with breast cancer. Setting and Design Single-center, observational, prospective study. Methods and Material Forty-three patients with breast cancer treated with taxanes were prospectively enrolled. The reduced version of the Total Neuropathy Score (TNSr) was performed at baseline and 3 months after enrollment. TIN was diagnosed if the difference between the baseline and 3-month TNSr was greater than 1. In patients with TIN, the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire— Chemotherapy-Induced Peripheral Neuropathy (20-item scale (EORTC-CIPN20) was also assessed 3 months after enrollment. Results Thirty-seven out of 43 (86.0%) patients were diagnosed with TIN. Sensory symptoms (64.9%) were the most frequent abnormality, followed by autonomic symptoms (54.1%). No patients reported motor symptoms or motor weakness. The TNSr sensory symptom score positively correlated with that of the EORTC-CIPN20. Nerve conduction studies showed reduced nerve conduction velocities and amplitudes after taxane treatment compared to those before chemotherapy in all tested nerves; however, only three (8.1%) patients had sural sensory nerve action potential amplitude outside normal limits. Conclusions TIN was predominantly sensory with normal nerve conduction studies which is the main feature of small fiber neuropathy. A combination scale comprising of a clinician-based scale and a patient-reported questionnaire and specialized tests for small nerve fibers should be considered as proper assessment tools to evaluate TIN.

The effectiveness of electroneuromyography in the early diagnosis of diabetic foot development

Objective: Diabetic foot is one of the first cause of lower extremity amputation. The aim of this study is to determine which of the nerve conduction disorders may be used predominantly for early diagnosis of diabetic foot development in the follow-up of diabetic patients. &#x0D; Material and Method: The study consists of 3 different groups (150) of patients diagnosed with type 2 diabetes (DM). 1. Group; 50 patients with diabetic foot complications (DA+), 2. Group; 50 patients without diabetic foot complications and with polyneuropathy (DA-/PNP+), 3. Group; 50 patients without diabetic foot complications and without polyneuropathy (DA-/PNP-). Diabetic foot wounds were grouped by pedis classification. &#x0D; Findings: Age, sex, diabetes duration, blood glucose, HbA1c values and electroneuromyography (ENMG) for nerve amplitude, velocity and latancy results were compared among the groups. A significant statistical difference was found between three groups when age, sex, HgbA1c, fasting blood glucose, diabetes duration were evaluated (p

Cardiovascular health and chronic axonal polyneuropathy: A population-based study.

Background and purposeChronic axonal polyneuropathy is a common, usually multifactorial, disease for which there is no treatment yet available. We investigated the association between cardiovascular health, defined by the health score of the American Heart Association, and chronic axonal polyneuropathy.MethodsBetween June 2013 and January 2017, we investigated participants of the Rotterdam Study, a population‐based cohort study. Participants were screened for polyneuropathy and categorized as having no, possible, probable or definite polyneuropathy. The cardiovascular health score (range 0–14; higher score reflecting better health) consisted of four health behaviours (diet, physical activity, smoking and body mass index) and three health factors (blood pressure, serum cholesterol and fasting glucose level).ResultsWe included 1919 participants, of whom 120 (6.3%) had definite polyneuropathy. The median (interquartile range [IQR]) age was 69.0 (58.6–73.7) years and 53.4% were women. A higher cardiovascular health score was associated with a lower prevalence of definite polyneuropathy (per point increase: odds ratio [OR] 0.90, 95% confidence interval [CI] 0.84–0.96). Optimal cardiovascular health (score≥10) was strongly associated with a lower prevalence of definite polyneuropathy (OR 0.55, 95% CI 0.32–0.90). An increase in health factors and health behaviour scores separately was associated with a lower prevalence of polyneuropathy (per point increase: OR 0.82, 95% CI 0.71–0.95 and OR 0.86, 95% CI 0.78–0.96, respectively). The association between a lower cardiovascular health score and lower sural nerve amplitude was not significant after correction for covariates (difference 0.07µV, 95% CI −0.02–0.17).ConclusionsBetter cardiovascular health, consisting of both modifiable health behaviours and health factors, is associated with a lower prevalence of chronic axonal polyneuropathy.

Greater small nerve fibre damage in the skin and cornea of type 1 diabetic patients with painful compared to painless diabetic neuropathy

Damage to small nociceptive fibres may contribute to painful diabetic neuropathy. We aimed to compare large and small nerve fibre measurements together with skin biopsy and corneal confocal microscopy in patients with type 1 diabetes and painful or painless diabetic neuropathy. We have assessed the McGill pain questionnaire, neuropathy disability score, vibration perception threshold, warm and cold sensation thresholds, electrophysiology, corneal confocal microscopy and skin biopsy in participants with type 1 diabetes and painful (n=41) or painless (n=50) diabetic neuropathy and control subjects (n=50). The duration of diabetes, body mass index, glycated haemoglobin (HbA1c), blood pressure and lipid profile did not differ between subjects with painful and painless neuropathy. Neuropathy disability score and vibration perception threshold were higher and sural nerve conduction velocity was lower, but sural nerve amplitude, peroneal nerve amplitude and conduction velocity and cold and warm sensation thresholds did not differ between patients with painful compared to painless diabetic neuropathy. However, intraepidermal nerve fibre density, corneal nerve fibre density, corneal nerve branch density and corneal nerve fibre length were significantly lower in subjects with painful compared to painless diabetic neuropathy. There is evidence of more severe neuropathy, particularly small fibre damage in the skin and cornea, of patients with painful compared to painless diabetic neuropathy.