Polyneuropathy Patients Research Articles

P 160 Temporal discrimination and temporal discrimination motor thresholds – association with age, proprioception, and polyneuropathy

Introduction Temporal discrimination threshold (TDT) and temporal motor discrimination threshold (TMDT) are measures of somatosensory processing indicating the shortest time interval at which two stimuli applied to skin or muscle, respectively, are detected to be asynchronous. TDT and/or TDMT have been shown to be increased in patients with movement disorders, like essential tremor, dystonia, or Parkinson”s disease. However, the meaning of these findings is still quite unclear. Here, we assessed the association of TDT and TDMT with age, proprioception, and polyneuropathy (PNP). Materials and methods 54 healthy subjects (age 29–75 years) and 15 patients with neurophysiologically confirmed PNP were included. TDT was tested with surface electrodes placed over thenar or dorsal foot region, respectively. TDMT was measured via an insulated tungsten needle microelectrode inserted at the motor point of flexor carpi radialis (FCR) or tibialis anterior (TA) muscle. Pairs of subsequent electric stimuli with varying interstimulus intervals (ISI) were provided, and discrimination thresholds were defined as the shortest ISI at which subjects were able to identify two separate stimuli. Proprioception of upper and lower limbs was assessed by custom-built devices, basically consisting of a goniometer without direct visual feedback of the respective extremity and its movements (flexion/extension). Subjects were instructed (i) to point to LED markers attached to the outside of the device, (ii) to move in proportion to arrows of different length shown on a computer screen, and (iii) to estimate their limb position after passive hand movements. Part of the assessment was conducted under dual task condition (tone-counting task). Pointing (or estimation) error (in degree) was taken as a measure of proprioceptive performance. Results In healthy subjects higher age was associated with higher TDT in every tested condition (right hand [ r = 0.358, p r = 0.359, p r = 0.591, p r = 0.505, p r = 0.317, p = 0.05]). In PNP patients, TDMT and TDT were significantly higher at all sites as compared to controls ( p Discussion Our results point to an association between higher age and poorer capacity of discriminating somatosensory stimuli. The correlation of performance in a particular pointing task of the hand with lower TDMT suggests this measure as a potential surrogate marker of proprioceptive function. Both TDT and TDMT were markedly increased in PNP patients, indicating their clinical meaning in diseases with affection of the proprioceptive system. This might also be the pathophysiological link to previous findings of elevated thresholds in movement disorders.

Central conduction abnormalities in patients receiving levodopa-carbidopa intestinal gel infusion.

In recent years, several studies have reported a relatively high frequency of polyneuropathy in patients with Parkinson's disease (PD), in particular, in patients receiving levodopa-carbidopa intestinal gel (LCIG) infusion. In spite of the several patients investigated with nerve conduction studies, no study has prospectively explored a possible central nervous system involvement of patients receiving LCIG infusion. We prospectively evaluated eight PD patients receiving LCIG infusion, who underwent neurophysiological evaluations with nerve conduction studies, visual, somatosensory and motor evoked potentials before LCIG infusion, and 1 and 6months after. At 6months follow-up, we found significant reduction in sural nerve SNAP amplitude, increase of central sensory conduction time N22-P40, and increases of central motor conduction time recorded from I dorsal interosseous and tibialis anterior. In PD patients with LCIG infusion, we found a subclinical neurophysiological impairment of both peripheral and central nervous system.

Working hand syndrome: A new definition of non-classified polyneuropathy condition.

The aim of this paper was to define an unexplained non-classified polyneuropathy condition as a new neurological disease. This new diagnosis of occupation related polyneuropathy has been named as “WORKING HAND SYNDROME (WHS).”This study collected and compared clinic and electrophysiological analyze data from healthy controls, WHS patients, carpal tunnel syndrome (CTS) patients and polyneuropathy patients. The WHS patients presented to the clinic with pain, numbness, tingling, and burning sensations in their hands that increased significantly during rest and nighttime. However, there was no weakness in the muscles, and the deep tendon reflexes were normal in this disease. The patients had all been working in physically demanding jobs requiring the use of their hands/arms for at least 1 year, but no vibrating tools were used by the patients. All of the cases were men. I supposed that overload caused by an action repeated chronically by the hand/arm may impair the sensory nerves in mentioned hand/arm. In patients with these complaints, for a definitive diagnosis, similar diseases must be excluded. Nonetheless, the specific electrophysiological finding that the sural nerves are normal on the lower sides, as well as the occurrence of sensory axonal polyneuropathy in the sensory nerves without a significant effect on velocity and latency in the work-ups of the upper extremity are enough to make a diagnosis.In conclusion, WHS has been defined as a polyneuropathy and occupational disease. Patients with WHS present with pain, numbness, tingling, and burning sensations in their hands that increases significantly during rest and nighttime. They also use their arms/hands for jobs that require heavy labor. The neurological examinations of patients with WHS are normal. Only the sensory nerves in the upper extremities are affected. This article is suggested to serve as a resource for patients, health care professionals, and members of the neurology community at large.

Functional outcome of critical illness polyneuropathy in patients affected by severe brain injury.

Critical illness polyneuropathy and myopathy (CIPNM) frequently occur in intensive care unit (ICU) critically ill subjects; about 55-70% of subjects achieve full recovery. CIPNM can occur in ICU subjects with severe acquired brain injury (sABI), but no data have been reported regarding their outcome. The aim of the present study was to investigate the functional recovery in subjects suffering from both CIPNM and sABI and whether they had poorer outcome than those with sABI only. Prospective cohort study. Dedicated rehabilitation setting. Adult ICU subjects with sABI causing a disorder of consciousness graded 3-8 on the Glasgow Coma Scale admitted to a dedicated rehabilitative setting were enrolled from January 2015 to June 2016. The enrolled sample was divided in two groups: patients with CIPNM and coexistent sABI (CIPNM+sABI) and patients with sABI. Electromyography was performed in all subjects to ascertain CIPNM occurrence, at admission. Functional outcome was investigated using the Rancho Los Amigos Levels of Cognitive Functioning (LCF), Disability Rating Scale (DRS), Glasgow Outcome Scale (GOS) and modified Rankin Scale (mRS), at admission and discharge. Mortality and length of stay (LOS) were recorded. One-hundred and thirty-one patients (59 F, 72 M; mean age 54.7±15.8) were admitted to the rehabilitation setting, and 111 (47 F, 64 M; mean age: 53.6±18.4 years) were enrolled. Thirty-six (31.8%) had CIPNM+sABI, and 75 patients had isolated sABI. Significant functional outcomes in all assessment measures were observed after rehabilitation in all samples. The estimated mean scores (95% confidence interval) of LCF, DRS, GOS and mRS from a multivariate model adjusted for age, sex and time of ICU stay were: 2.85 (2.53-3.21) and 5.24 (4.81-5.71), 23.94 (22.37-25.62) and 16.04 (14.77-17.41), 2.86 (2.70-3.04) and 3.46 (3.28-3.65), and 4.91 (4.67-5.17) and 3.79 (3.58-4.02), at admission and at discharge, respectively. Despite functional improvement, CIPNM+sABI patients showed lesser improvement than those with sABI only. Furthermore, patients with both disorders had significantly higher median LOS than sABI subjects: 107 (q1-q3: 65-146), and 65 (q1-q3: 38-105) days (P=5.5x10-83), respectively. No statistically significant difference in mortality rates was found between groups. Subjects with CIPNM and coexistent sABI improved after rehabilitation, but had poorer recovery than those with solely sABI requiring a longer LOS. The rehabilitation process in subjects suffering from CINPM is challenging and no evidence support the use of specific rehabilitative approaches to improve function and activities of daily living.

Electrophysiological and neuromuscular stability of persons with chronic inflammatory demyelinating polyneuropathy

We assessed motor unit (MU) properties and neuromuscular stability in the tibialis anterior (TA) of chronic inflammatory demyelinating polyneuropathy (CIDP) patients using decomposition-based quantitative electromyography. Dorsiflexion strength was assessed, and surface and concentric needle electromyography were sampled from the TA. Estimates of MU numbers were derived using decomposition-based quantitative electromyography and spike-triggered averaging. Neuromuscular transmission stability was assessed from concentric needle-detected MU potentials. CIDP patients had 43% lower compound muscle action potential amplitude than controls, and despite near-maximum voluntary activation, were 37% weaker. CIDP had 27% fewer functioning MUs in the TA, and had 90% and 44% higher jiggle and jitter values, respectively compared with controls. CIDP had lower strength and compound muscle action potential values, moderately fewer numbers of MUs, and significant neuromuscular instability compared with controls. Thus, in addition to muscle atrophy, voluntary weakness is also due to limitations of peripheral neural transmission consistent with demyelination. Muscle Nerve 56: 413-420, 2017.

What's in the Literature?

In this edition of this column, we review new studies concerning the pathophysiology, treatment, and outcomes of patients with necrotizing myopathy, genetic testing in congenital myopathies, and limb girdle muscular dystrophies, and the incidence of polyneuropathy in the myotonic dystrophies. Various studies in myasthenia gravis, including those concerning antibody testing, clinical features, and quality of life are also reviewed as are recent findings in congenital myasthenic syndromes. Finally, 2 studies concerning polyneuropathy are discussed, including one on the association of polyneuropathy in patients with the metabolic syndrome and one on laboratory testing in patients with otherwise idiopathic small fiber polyneuropathy.

Therapeutic plasma exchange in chronic dysimmune peripheral neuropathies: A 10-year retrospective study.

Therapeutic plasma exchange (TPE) can be proposed in the treatment of chronic dysimmune peripheral neuropathies (CDPN). Actual guidelines are however based on few studies, and indications and protocols still remain to be clarified. We conducted a 10-year retrospective study in order to assess the effectiveness and tolerance of TPE in CDPN. All patients treated for CDPN with TPE from October 2006 to March 2016 in the university hospital of Angers were included. Patients were considered responders when they presented a clinical improvement substantial enough to continue the treatment. The Hughes functional grading score was also determined for each patient before and after TPE initiation. Among the 206 patients who received TPE during the study period, 30 (14.6%) met the diagnostic criteria of CDPN. Four of the five paraprotein neuropathies (PPN) patients (80%) and 8 of the 11 chronic inflammatory demyelinating polyneuropathies (CIDP) patients (72.7%) were responders, with a significant improvement of the Hughes score for the latter (P = 0.013). None of the three Lewis-Sumner and the two POEMS patients showed substantial improvement. Six of the nine anti-MAG neuropathy patients (66.7%) responded to treatment, with a trend towards improvement of the Hughes score (P = 0.072). TPE appears to be effective in CIDP and PPN, and ineffective in Lewis-Sumner and POEMS syndromes. Interestingly, anti-MAG neuropathy patients showed a good rate of response to TPE. Regarding these preliminary results, a randomized trial would be very worthwhile in this disease for which there is no evidence based treatment to date.

Frequency of Polyneuropathy in Patients on Long Term Peritoneal Dialysis Treatment.

Uremic polyneuropathy is very common among patients with Chronic Kidney Disease (CKD). The patients have electrophysiologic signs of impaired nerve function, although a lower percentage of patients are symptomatic. Electrophysiological parameters are quantitative indices of Polyneuropathy (PNP) severity. To assess the frequency of PNP in patients on long term Peritoneal Dialysis (PD) treatment. Twenty three PD patients were analysed, who were receiving dialysis for at least five years and the study population divided into two groups according to duration of PD treatment. Group 1 consisted of the patients who were dialysed for at least 10 years and Group 2 consisted of patients who were dialysed for five to nine years. Patients who switched from Haemodialysis (HD) to PD and patients with coexisting diseases that could lead to disturbances in nerve conduction were excluded from the study. PNP was diagnosed when slowing of Nerve Conduction Velocity (NCV) and/or lengthening of distal latencies and/or decrease in amplitude of muscle action potential were present in two or more nerves and longer F wave response was present in one or two nerves. Carpal Tunnel Syndrome (CTS) was diagnosed if slowing of NCV and/or decrease in amplitude of muscle action potential and/or lenghening of distal latency of either sensory or motor median nerve present. PNP was observed in 17 of the patients {73.9%; Group 1 (n=10) and Group 2 (n=7)}. Mixed type sensory motor neuropathy was diagnosed in nine patients from Group 1 and five patients from Group 2; one patient from Group 1 had demyelinating PNP affecting motor and sensory nerves; one patient from Group 2 had axonal PNP affecting motor and sensory nerves. From Group 1, two patients had CTS related to PNP and one patient had CTS without PNP. The results of motor conductivity testing showed lower conduction velocity for left popliteal nerve in Group 1 and Group 2 patients (13.85±2.17 ms, 4.80±1.11 ms, p=0.01). In both groups, mean motor and sensory latency, amplitude and velocity of other nerves were not found to be significantly different (p>0.05). PNP is a common complication in long term PD patients. Over five years of treatment, frequency of PNP and CTS do not increase with duration of dialysis.

Cardio-Ankle Vascular Index and Indices of Diabetic Polyneuropathy in Patients with Type 2 Diabetes.

The cardio-ankle vascular index (CAVI) is used to test vascular function and is an arterial stiffness marker and potential predictor of cardiovascular events. This study aimed to analyze the relation between objective indices of diabetic polyneuropathy (DPN) and the CAVI. One hundred sixty-six patients with type 2 diabetes mellitus were included in this study. We used nerve conduction studies (NCSs) and the coefficient of variation of the R-R interval to evaluate DPN. We estimated arteriosclerosis by the CAVI. Simple and multiple linear regression analyses were performed between neuropathy indices and the CAVI. In univariate analysis, the CAVI showed significant associations with sural sensory nerve conduction velocity and median F-wave conduction velocity. Multiple linear regression analysis for the CAVI showed that sural nerve conduction velocity and median F-wave conduction velocity were significant explanatory variables second only to age. In multiple linear regression analysis for sural nerve conduction velocity among neuropathy indices, the CAVI remained the most significant explanatory variable. In multiple linear regression analysis for median nerve F-wave conduction velocity among neuropathy indices, the CAVI remained the second most significant explanatory variable following HbA1c. These results suggest a close relationship between macroangiopathy and DPN.

Blink reflex role in algorithmic genetic testing of inherited polyneuropathies.

In severely affected inherited polyneuropathy patients, primary demyelination can be difficult to determine by routine extremity limb nerve conduction studies (NCS). Blink reflexes may help classify severe polyneuropathies as either axonal or demyelinating. However, blink reflex studies have not been studied systematically in any genetically confirmed cohort. Patients with a genetic diagnosis who had undergone blink reflex testing and extremity NCS were identified retrospectively. Blink reflex R1 latency, extremity NCS, and severity were compared. We identified 26 demyelinating and 23 axonal, genetically confirmed cases, including 20 with PMP22 duplications. In 12 (25%), the ulnar CMAP amplitude was ≤0.5 mV making electrophysiological classification difficult. However, the R1-latency cutoff of >13 ms (demyelinating) robustly classified all patients regardless of severity. We show that blink reflex studies are reliable for identification of inherited demyelinating polyneuropathy regardless of severity and can facilitate algorithmic decisions in genetic testing. Muscle Nerve 55: 316-322, 2017.

Involvement of Macrophages in the Pathogenesis of Familial Amyloid Polyneuropathy and Efficacy of Human iPS Cell-Derived Macrophages in Its Treatment.

We hypothesized that tissue-resident macrophages in familial amyloid polyneuropathy (FAP) patients will exhibit qualitative or quantitative abnormalities, that may accelerate transthyretin (TTR)-derived amyloid deposition. To evaluate this, we examined the number and subset of tissue-resident macrophages in heart tissue from amyloid-deposited FAP and control patients. In both FAP and control patients, tissue-resident macrophages in heart tissue were all Iba+/CD163+/CD206+ macrophages. However, the number of macrophages was significantly decreased in FAP patients compared with control patients. Furthermore, the proportion of intracellular TTR in CD14+ monocytes was reduced in peripheral blood compared with healthy donors. Based on these results, we next examined degradation and endocytosis of TTR in human induced pluripotent stem (iPS) cell-derived myeloid lineage cells (MLs), which function like macrophages. iPS-MLs express CD163 and CD206, and belong to the inhibitory macrophage category. In addition, iPS-MLs degrade both native and aggregated TTR in a cell-dependent manner in vitro. Further, iPS-MLs endocytose aggregated, and especially polymerized, TTR. These results suggest that decreased tissue-localized macrophages disrupt clearance of TTR-derived amyloid deposits, leading to progression of a pathological condition in FAP patients. To improve this situation, clinical application of pluripotent stem cell-derived MLs may be useful as an approach for FAP therapy.

Evaluation of vibration sensitivity violation as early diagnosis of diabetic distal polyneuropathy in patients with type 2 diabetes

Distal sensorimotor polyneuropathy (DSPN) is a severe complication and the most common form of peripheral neuropathies in patients with type 2 diabetes (T2D). Nowadays, interest in the DSPN has increased significantly due to the increase of incidence of T2D, as well as the severity of its clinical manifestations.This study aimed to assess the prevalence of DSPN in patients with T2D using Vibratip device as an alternative test for early diagnosis of vibration perception disorders.Design and methods. This study was a cross sectional observational design. Height, weight, body mass index (BMI), systolic and diastolic blood pressure measured according to standard protocol. The information about T2D duration and treatment, diabetic complications, concomitant diseases and its treatment, data about laboratory parameters (level of HbA1c during the last six months, total cholesterol and triglycerides) collected from local database. All participants examined with Vibratip on both feet. Vibratip is new device using standardized vibration for DSPN detection. Vibratip is applied to the patients feet, testing two sites on both feet (1st metatarsal head on the plantar surface and hallux pump) - once whilst non-vibrating and once whilst vibrating and the patients (with their eyes closed) is asked to indicate when they feel the vibration.Results. 2757 women and 1546 men aged 22-89 years selected from the six regions of the Republic of Belarus and Minsk-city. Among the 4303 subjects 7.78% (n=335) took place in this study aged less than 45 years (young patients), 65.4 % (n=2814) aged 45-65 years and 26.49 % (n=1140) aged more than 65 years old. Average age was 59 ±10.4; average body mass index (BMI) – 32.2±5.6 kg/m2. Participants with normal body mass index composed 9.02% (n=388), participants with superfluous body mass and obesity – 91% (n=3915). 710 (16.5%) participants were smoking, 2649 (61 %) suffered from high blood pressure. The most participants 1428 (33%) were treated by statins compared with fibrates 131 (3%). In patients with clinical symptoms of DSPN more often was pain (in 775 cases - 18.0%), burning (in 775 cases - 16.4%), numbness (in 1144 cases - 26.6%), feeling of pins and needles (in 921cases - 21.4%) and feeling of electric shock (in 235 cases - 5.5%). In patients with vibration sensitivity disorders were subjects with previous diagnosis of DSPN 1813 (42.13%) and subjects without previous diagnosis of DSPN 850 (19.75%). Amount subjects with asymptomatic vibration sensitivity disorder without clinical symptoms DSPN was 1640 (38.12%).Conclusions. In 20% of patients T2D with impaired vibration sensitivity, established with the device Vibratip, defined pre-clinical stage of DSPN. Given the ease of use of the device Vibratip advisable its use as a screening method for early diagnosis of DSPN in clinical practice.

Association of transketolase polymorphisms with measures of polyneuropathy in patients with recently diagnosed diabetes.

Shunting of glycolytic intermediates into the pentose phosphate pathway has been suggested to protect from hyperglycaemia-induced microvascular damage. We hypothesized that genetic variability in the gene encoding transketolase, a key pentose phosphate pathway enzyme, contributes to early nerve dysfunction in recent-onset diabetes. In this cross-sectional study, we assessed nine single nucleotide polymorphisms (SNPs) in the transketolase gene, plasma methylglyoxal concentrations, and clinical and quantitative measures of peripheral nerve function in 165 type 1 and 373 type 2 diabetic patients with a diabetes duration up to 1year. The Total Symptom Score was associated with transketolase SNPs rs7648309, rs62255988, and rs7633966, while peroneal motor nerve conduction velocity (MNCV) correlated only with rs7648309 (P < 0.01). Cold thermal detection threshold (TDT) (foot) was associated with transketolase SNPs rs11130362 and rs7648309, while warm TDT (hand) correlated with rs62255988 and rs7648309 (P < 0.01). After Bonferroni correction, the correlations of transketolase SNP rs7648309 with Total Symptom Score and rs62255988 with warm TDT (hand) remained statistically significant. Among subgroups, men with type 2 diabetes showed the strongest associations. No associations were observed between each of the nine tagged transketolase SNPs and plasma methylglyoxal concentrations. The observed associations of genetic variation in transketolase enzyme with neuropathic symptoms and reduced thermal sensation in recent-onset diabetes suggest a role of pathways metabolizing glycolytic intermediates in early diabetic neuropathy. Copyright © 2016 John Wiley & Sons, Ltd.

Trends in Outcome and Cost of Hospitalization in Chronic Inflammatory Demyelinating Polyneuropathy Patients Treated with IVIG, Versus Steroid or Other Treatments (2009-2013). A New York Statewide Planning and Research Cooperation System (SPARCS) Database Report (P2.270)

Trends in Outcome and Cost of Hospitalization in Chronic Inflammatory Demyelinating Polyneuropathy Patients Treated with IVIG, Versus Steroid or Other Treatments (2009-2013). A New York Statewide Planning and Research Cooperation System (SPARCS) Database Report (P2.270)

Alterations of Choroidal Thickness With Diabetic Neuropathy.

To evaluate the effect of diabetic polyneuropathy on choroidal thickness in type 2 diabetes patients. Forty-one diabetic polyneuropathy (DPN) patients with no or mild retinopathy, 50 non-DPN diabetic patients with no or mild retinopathy, and 42 healthy controls without any retinal complaint were included in the study. All participants underwent detailed ophthalmic examinations. Choroidal thickness (CT) measurements were performed by the same independent technician in the morning between 9 and 11 AM to avoid diurnal variations. Perpendicular CT was measured from the outer edge of the hyperreflective retinal pigment epithelium to the inner sclera at seven locations: the fovea; and 500, 1000, and 1500 μm temporally and nasally to the fovea. The groups were age and sex matched (P > 0.05). The mean subfoveal CT values were significantly different in groups with a thickening trend from control to non-DPN and DPN (P < 0.01). The mean values for subfoveal CT in control, non-DPN, and DPN groups were 241.12 ± 52.71, 279.82 ± 51.42, and 304.71 ± 54.92 μm, respectively. The same thickening trend was also evident in all other six measurement points with statistical significance (P < 0.01). Diabetic patients had increased CT compared to healthy controls. The presence of neuropathy in diabetes patients caused additional choroidal thickening, compared to nonneuropathic patients.

Contactin-1 IgG4 antibodies cause paranode dismantling and conduction defects.

Paranodal axoglial junctions formed by the association of contactin-1, contactin-associated protein 1, and neurofascin-155, play important functions in nerve impulse propagation along myelinated axons. Autoantibodies to contactin-1 and neurofascin-155 define chronic inflammatory demyelinating polyradiculoneuropathy subsets of patients with specific clinical features. These autoantibodies are mostly of the IgG4 isotype, but their pathogenicity has not been proven. Here, we investigated the mechanisms how IgG subclasses to contactin-1 affect conduction. We show that purified anti-contactin-1 IgG1 and IgG4 bind to paranodes. To determine whether these isotypes can pass the paranodal barrier, we incubated isolated sciatic nerves with the purified antibody or performed intraneural injections. We found that IgG4 diffused into the paranodal regions in vitro or after intraneural injections. IgG4 infiltration was slow and progressive. In 24 h, IgG4 accessed the paranode borders near the nodal lumen, and completely fill the paranodal segments by 3 days. By contrast, control IgG, anti-contactin-1 IgG1, or even anti-contactin-associated-protein-2 IgG4 did not pass the paranodal barrier. To determine whether chronic exposure to these antibodies is pathogenic, we passively transferred anti-contactin-1 IgG1 and IgG4 into Lewis rats immunized with P2 peptide. IgG4 to contactin-1, but not IgG1, induced progressive clinical deteriorations combined with gait ataxia. No demyelination, axonal degeneration, or immune infiltration were observed. Instead, these animals presented a selective loss of the paranodal specialization in motor neurons characterized by the disappearance of the contactin-associated protein 1/contactin-1/neurofascin-155 complex at paranodes. Paranode destruction did not affect nodal specialization, but resulted in a moderate node lengthening. The sensory nerves and dorsal root ganglion were not affected in these animals. Electrophysiological examination further supported these results and revealed strong nerve activity loss affecting predominantly small diameter or slow conducting motor axons. These deficits partly matched with those found in patients: proximal motor involvement, gait ataxia, and a demyelinating neuropathy that showed early axonal features. The animal model thus seemed to replicate the early deteriorations in these patients and pointed out that paranodal loss in mature fibres results in conduction defects, but not conduction slowing. Our findings indicate that IgG4 directed against contactin-1 are pathogenic and are reliable biomarkers of a specific subset of chronic inflammatory demyelinating polyneuropathy patients. These antibodies appear to loosen the paranodal barrier, thereby favouring antibody progression and causing paranodal collapse.

Autologous cytokine-induced killer (CIK) cell immunotherapy combined with cyclophosphamide in five patients with POEMS syndrome.

The primary objective of this study was to evaluate the safety and clinical efficacy of autologous cytokine-induced killer (CIK) cells combined with cyclophosphamide in the treatment of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome patients. We evaluated five POEMS syndrome patients treated with autologous CIK cell immunotherapy combined with cyclophosphamide from 1May 2012 to 30November 2014. The Overall Neuropathy Limitation Scale (ONLS), computed tomography of the chest and abdomen, ultrasound of the abdomen, serum vascular endothelial growth factor (VEGF) level and lymphocyte count findings in the five patients were recorded. The median age of the patients was 40 years (range: 25-62), and all the patients were male. CIK cells were generated routinely from peripheral blood mononuclear cells (PBMCs) of all five patients, and the numbers of CIK cells increased by approximately 105-fold after 14 days of culture. All five patients (100%) responded to their neuropathy treatment, the ONLS scores were reduced by at least 1 and a paired-sample t-test revealed a significant difference (t=5·715, P=0·003<0·01). The extravascular volume overload responses indicated partial remission (PR=60%) or stable disease (SD=40%), and no cases of progressive disease (PD) or complete remission (CR) were observed. During clinical treatment, the serum VEGF of patient 5 decreased after one cycle of transfusion within 1 month. The lymphocyte counts of all the patients increased significantly after CIK transfusion, and a paired-sample t-test revealed a significant difference (t=5·101, P=0·004<0·01). Autologous CIK cell infusion combined with cyclophosphamide was found to be highly safe and elicited no adverse reactions. CIK cells can improve both the symptoms and quality of life, decrease serum VEGF levels and increase lymphocyte counts in patients with POEMS syndrome.

Current aspects of treatment of diabetic polyneuropathy in patients with diabetes

The article is an overview of the prevalence, mechanisms of development, diagnosis and treatment of diabetic neuropathy as a complication of diabetes. It also tells about the pathogenetic aspects of treatment of diabetic polyneuropathy.

Effect of 850 nm He-Ne Laser Therapy on Nerve Conduction and Foot Planter Pressures Distribution of Painful Diabetic Neuropathy: A Randomized Controlled Trial

Introduction: Diabetic neuropathy patients are at very high risk for developing foot ulcer that may lead to lower extremity amputation and threaten the patient’s life. Objective: To evaluate the effects of scanning 850 nm He-Ne infrared laser on nerve conduction, pain intensity, and foot planter pressure distribution of painful diabetic polyneuropathy patients. Methods: Thirty diabetic neuropathy patients with pain and reduced nerve conduction velocity were randomly divided into two groups; an experimental group (active laser group, n=15) and a control group (placebo laser group, n=15). Peak static and dynamic planter pressure were measured under heel, big toe and little toe. Sural and Peroneal nerves conduction velocity and amplitude and pain level were measured before and after treatment in both groups. The active laser group had got scanning 850 nm He–Ne infrared laser on foot planter surface and lumbosacral area with 5.7 J/cm2 for 15 min/site/session, 3 session /week for four weeks. Results: All measured parameters improved significantly in the active laser group, while no significant changes obtained in the control group. Comparison of post treatment measurements between groups showed that sural nerve conduction velocity and amplitude, pain level, and peak static and dynamic planter pressure were significantly higher in the experimental group compared with the control group. On the other hand there was no significant difference between groups for peroneal nerve conduction velocity and amplitude. Conclusion: 850 nm He–Ne therapy with the applied parameter and technique was an effective modality for improving nerve conduction, redistributing foot plantar pressures and relieving pain of painful diabetic polyneuropathy patients.

Актуальные вопросы ведения пациентов с диабетической полинейропатией

Актуальные вопросы ведения пациентов с диабетической полинейропатией