Neuropathy In Rheumatoid Arthritis Research Articles

Demyelinating neuropathy requires differential diagnosis with vasculitic neuropathy in rheumatoid arthritis: Significance of sural nerve electrophysiology findings

AbstractObjectivesNeuropathy is considered a complication of rheumatoid arthritis (RA), whose underlying mechanisms are mainly entrapment, drug‐induced and rheumatoid vasculitis (RV). At Tokyo Women's Medical University, for the purpose of diagnosing vasculitic neuropathy, we carried out nerve and muscle biopsies in nine RA patients. Unexpectedly, we found three cases of demyelinating neuropathy, together with six cases of RV. Our aim was to investigate the neurophysiological features of demyelinating neuropathy in patients with RA, compared with those of patients with RV.MethodsWe reviewed the pathological, clinical and electrophysiological findings in patients with RA who underwent nerve and muscle biopsies. We compared patient demographics and nerve conduction study findings between patients with RV and other patients.ResultsThe histological findings showed necrotizing vasculitis in six of nine patients. Vasculitis was absent in the other three patients, which showed evidence of demyelination and remyelination. The absence of a sensory nerve action potential and compound motor action potential were observed more frequently in the RV cohort. Sural sparing, shown as the sural‐to‐median sensory nerve action potential ratio, was significantly higher in demyelinating neuropathy patients. Treatment was corticosteroid and cyclophosphamide in RV patients, and intravenous immunoglobulin was administered to three demyelinating neuropathy patients. Treatment response was satisfactory in seven of the nine patients.ConclusionDemyelinating neuropathy was found more often in patients with RA neuropathy than expected. Sural nerve sparing, as well as the absence of sensory nerve action potential or compound motor action potential, are useful for the differential diagnosis of demyelinating neuropathy with RV in RA patients with neuropathy.

Autonomic neuropathy in Rheumatoid Arthritis: Relationship with seropositivity of Rheumatoid factor and disease activity

Background: Autonomic neuropathy (AN) has been recognized as a strong predictor of sudden cardiac death in Rheumatoid Arthritis (RA). Autonomic neuropathy may be assessed by five cardiovascular reflex tests. Objective: To find out the prevalence and severity of AN in RA and also to assess the correlation of inflammatory markers, disease severity and serological factor, Rheumatoid factor (RF) with autonomic reflex test parameters. Method: This cross sectional study was conducted on sixty (60) female RA patients, age range 18-50 years enrolled from the Out- Patient Department of Rheumatology Wing, Department of Medicine, of Bangabandhu Sheikh Mujib Medical University (BSMMU). Age matched 30 apparently healthy females were control. Cardiac autonomic reactivity was assessed by five cardiovascular reflex tests as described by Ewing include heart rate response to standing, deep breathing, valsalva maneuver and blood pressure response to standing and sustained hand grip. Inflammatory activity in RA was assessed by serum rheumatoid factor (RF)level which was estimated by the latex agglutination test ,C-reactive protein(CRP) and ESR and marker of disease activity was assessed by Disease activity score(DAS- 28 score) value. For statistical analysis, independent sample ‘t’ test chi-square test, pearson correlation coefficient test, spearman correlation test were used. Results: Among 60 RA patients, 43 (71.6%) patients were RF positive. Frequency of AN in RA patients was significantly higher (p< 0.001) compared to control. AN was detected in 78% of RA patients. Among the RA patients 17.38% showed severe,13.04% showed definite, 54.35% showed early involvement and 17.38% showed evidence of atypical pattern of AN. In addition, valsalva ratio and difference between maximum and minimum heart rate during deep breathing showed significant(p<0.05) negative correlation with autoantibody Rheumatoid factor(RF) whereas no significant correlation of autonomic nerve reactivity parameters with DAS- 28, CRP and ESR were found. Conclusion: Autonomic neuropathy was associated with RA. Autonomic neuropathy may be related to the presence of autoantibody RF in RA patients. J Bngladesh Soc Physiol 2021;16(1): 70-76

Advances in imaging technologies for the assessment of peripheral neuropathies in rheumatoid arthritis.

Peripheral neuropathy in patients with rheumatoid arthritis is associated with a maladaptive autoimmune response that may cause chronic pain and disability. Nerve conduction studies are the routine method performed when rheumatologists presume its presence. However, this approach is invasive, may not reveal subtle malfunctions in the early stages of the disease, and does not expose abnormalities in structures surrounding the nerves and muscles, limiting the possibility of a timely diagnosis. This work aims to present a narrative review of new technologies for the clinical assessment of peripheral neuropathy in Rheumatoid Arthritis. Through a bibliographic search carried out in five repositories, from 1990 to 2020, we identified three technologies that could detect peripheral nerve lesions and perform quantitative evaluations: (1) magnetic resonance neurography, (2) functional magnetic resonance imaging, and (3) high-resolution ultrasonography of peripheral nerves. We found these tools can overcome the main constraints imposed by the previous electrophysiologic methods, enabling early diagnosis.

Ultrasonographic measurement of the peroneal and tibial nerves in patients with rheumatoid arthritis with symptoms or signs of polyneuropathy: A cross-sectional study

Background: Drug toxicity, vasculitis, entrapment neuropathy, and amyloidosis are among the various different reasons of peripheral neuropathy in rheumatoid arthritis (RA). We aimed to determine the cross-sectional areas (CSA) of the peroneal and tibial nerves in patients with RA who had neuropathic symptoms, and to determine a cutoff value for peroneal and tibial nerves CSA by ultrasonography (USG) to diagnose polyneuropathy (PN) in patients with RA. Materials and Methods: Sixty-nine patients with RA and thirty healthy controls were included in this cross-sectional study. According to nerve conduction study (NCS) test, patients with RA were divided into two groups, diagnosed as having PN or not. Demographic data, laboratory findings, CSA of bilateral peroneal and tibial nerves, NCS values, and painDETECT (PD-Q) scores of all patients were assessed. Disease duration, disease activity score 28, duration of neuropathic symptoms, and Health Assessment Questionnaire of patients with RA were also determined. Results: No statistically significant difference was found among the groups in terms of age, gender, and laboratory findings. However, a statistically significant difference was found among these three groups in comparison with PD-Q, NCS values, and nerve CSA (P Conclusion: USG can be used as a noninvasive diagnostic modality in the assessment of RA-associated PN.

Tumor necrosis factor-alpha blockade with etanercept improves autonomic dysfunction in rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune and chronic inflammatory disease associated with autonomic neuropathy. There is no specific treatment recommendation for autonomic neuropathy (AN) in rheumatic diseases. In addition, there is no study demonstrating therapeutic efficacy of TNF-inhibitor (TNFi) etanercept on autonomic neuropathy in RA. This is the first reported observation of improvement in AN with blockade of TNFi-etanercept in RA. We report a case of a 46-year-old female with severe disease activity treated with subcutaneous etanercept 50mg once a week along with methotrexate 15 mg/week. A significant improvement in cardiovascular autonomic neuropathy and sudomotor function was noted after 6 weeks of treatment.

Cardiovascular autonomic neuropathy in rheumatoid arthritis assessed by cardiovascular autonomic function tests: A cross-sectional survey.

Objective:In this study, we aimed to evaluate cardiovascular autonomic neuropathy (CAN) in RA patients by cardiovascular autonomic function tests. Because CAN was reported of patients with automimmune rheumatic diseases those may in sudden death or myocardial infarction.Methods:A total of 44 patients with RA and 44 age-and sex-matched healthy volunteers participated in this cross-sectional study. Assessment of CAN was performed using cardiovascular reflex tests. These five tests were: 1) beat-to-beat heart rate variation during deep breathing; 2) heart rate response to standing up; 3) heart rate response to the Valsalva maneuver; 4) blood pressure response to standing up; and 5) blood pressure response to sustained handgrip.Results:The mean age was 43.15 (SD, 12.18) years (range, 23-68 years) in the RA group, and 38 were women. In beat-to-beat heart rate variation during deep breathing, expiration-to-inspiration ratio was abnormal in 3 cases with RA (6.8%) but in 1 (2.3%) control subject (p=0.3), and maximum minus minimum heart rate was abnormal in 8 patients (18.2%) and in 3 (6.8%) control subjects (p=0.1). 2) In heart rate response to standing up, all patients and controls had normal results. Valsalva ratio was abnormal in 7 RA patients (15.9%) and in 7 control subjects (15.9%). Blood pressure response to standing up was normal in RA patients but abnormal in 1 (2.3%) control subject (p=0.4). Blood pressure response to sustained handgrip was abnormal in 5 RA patients (11.4%) and 2 (4.6%) control subjects (p=0.2).Conclusion:Our study failed to show any statistically significant difference between cardiovascular autonomic function tests in RA patients with control subjects by our test done.

Disease-modifying anti-rheumatic drugs improve autonomic neuropathy in arthritis: DIANA study.

Autonomic neuropathy (AN) is a risk predictor for sudden cardiac death in rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, the impact of most commonly employed disease-modifying anti-rheumatic drug (DMARD) therapy on autonomic neuropathy in rheumatic diseases is not known. Hence, we investigated the efficacy of DMARDs on autonomic neuropathy in RA and AS. We performed autonomic function assessment in 60 patients in this open-label, 12-week pilot study including 42 patients with RA, 18 with AS, and 30 aged-matched healthy subjects. The methodology included assessment of cardiovascular autonomic reflex tests according to Ewing. Parasympathetic dysfunction was established by performing three tests: heart rate response to deep breathing, standing, and Valsalva tests. Sympathetic dysfunction was examined by applying two tests: blood pressure response to standing and handgrip tests. Sudomotor function was assessed by Sudoscan. Cardiovascular reflex tests were impaired significantly among the patients as compared to healthy subjects (p < 0.05). Autonomic neuropathy was more pronounced in biologic-naive RA and AS patients. After treatment with combination synthetic DMARDs, parasympathetic, and sudomotor dysfunction significantly (p < 0.05) improved in RA and AS. Biologic DMARDs significantly improved parasympathetic, sympathetic and peripheral sympathetic autonomic neuropathy (p < 0.05) in biologic-naive RA and AS patients. In conclusion, synthetic DMARDs improved parasympathetic and sudomotor dysfunction in both DMARD-naive RA and AS patients. However, biologic DMARDs improved parasympathetic, sympathetic and sudomotor dysfunction to a greater extent than synthetic DMARDs in both RA and AS patients.

AB0309 The impact of modern antirheumatic therapy on the neuropathic component of pain in patients with ra

BackgroundThe main objective of Rheumatoid arthritis treatment is the achievement of permanent remission and suppression of symptoms of arthritis and extraarticular symptoms, prevention of destruction, dysfunction and deformation of joints,...

AB0718 Ultrasonographic assessment of subclinical median and ulnar nerve involvement in rheumatoid arthritis

BackgroundThe prevalence of subclinical neuropathy in Rheumatoid Arthritis (RA) is 65-85% (1). It has been shown that RA patients may have electrophysiological or histological abnormalities even in the absence of...

P69 To study the frequency of subclinical neuropathy in rheumatoid arthritis and its relation to duration of disease

P69 To study the frequency of subclinical neuropathy in rheumatoid arthritis and its relation to duration of disease

A Case of Peripheral Neuropathy in a Patient with Rheumatoid Arthritis Treated with Leflunomide

Leflunomide is a new disease-modifying drug licensed for treatment of rheumatoid arthritis. Recently, neuropathy has been reported with leflunomide. We report a case of peripheral neuropathy in rheumatoid arthritis treated with leflunomide. Nerve conduction study and electromyogram show sensory-motor polyneuropathy of both upper and lower limbs. Leflunomide medication was discontinued and cholestryamine washout was performed with some improvement in a couple of weeks.

A clinical, electrophysiological, and pathological study of neuropathy in rheumatoid arthritis

Neuropathy in rheumatoid arthritis (RA) may result secondary to entrapment, vasculitis, and drug toxicity. We aimed to study clinical and electrophysiological neuropathy and pathological changes in sural nerve in patients with RA. One hundred eight patients of RA, fulfilling American College of Rheumatology 1987 criteria (mean age, 45.83 years; M/F 1:3, 80.3% seropositive) were examined clinically and electrophysiologically for evidence of peripheral neuropathy. Sural nerve biopsies were performed in the involved cases. In all RA patient medications, disease activity, results of blood tests, and X-rays of affected joints were recorded. Twenty-three patients complained of paresthesias in the extremities. Vibration sensations were decreased in 9, and tendon reflexes were decreased or absent in 28 patients. Sixty-two (57.4%) patients had electrophysiologic evidence of neuropathy. Of these 53 (85.5%) patients had pure sensory or sensory motor axonal neuropathy (mononeuritis multiplex, n = 7), while 9 (14.5%) had demyelinating neuropathy (chronic inflammatory demyelinating polyneuropathy, n = 1). Carpal tunnel syndrome was seen in 11 (10.1%) patients (associated with neuropathy in 6). Of 23 sural nerve biopsies available, perineurial thickening (n = 5, amyloid deposits n = 4), perivascular lymphomononuclear cell infiltrate (n = 4), loss of myelin fibers (n = 2), and necrotizing vasculitis (n = 1) were found. Clinically, however, seven patients had evidence of cutaneous vasculitis. Comparing the clinical characteristics of the patients with or without electrophysiological neuropathy, absence of deep tendon jerks (p < 0.005) and presence of extra articular manifestations (p < 0.01) were conspicuous in the neuropathic group. There was no relation of neuropathy with the duration of RA, seropositivity, joint erosions, joint deformities, prior disease-modifying anti-rheumatic drugs or glucocorticoid intake, and 28-joint disease activity score. Neuropathy in RA was mostly subclinical and predominantly axonal. Pathologically, neuropathy secondary to amyloid infiltration was second only to vasculitic neuropathy. Absence of deep tendon jerks and presence of vasculitis were more commonly observed in patients with neuropathy.

P6 A clinical, electrophysiological and pathological study of neuropathy in rheumatoid arthritis

P6 A clinical, electrophysiological and pathological study of neuropathy in rheumatoid arthritis

Cranial and peripheral neuropathy in rheumatoid arthritis with special emphasis to II, V, VII, VIII and XI cranial nerves

AbstractBackground: Cranial neuropathy in rheumatoid arthritis (RA) is relatively rare compared to the frequently reported peripheral neuropathy.Methods: We investigated the occurrence of subclinical cranial and peripheral nerve involvement in 55 patients with RA.Results: Patients had a mean age of 43.1 years and a mean duration of illness of 6.4 years. All patients presented with electrophysiological findings suggestive of peripheral neuropathy. In addition, 69.1% of them had entrapment neuropathies, in which carpal tunnel syndrome was the most common (54.6%). Sensorimotor neuropathy at sites other than usual entrapment sites was diagnosed in 70.9%, while bilateral distal sensory neuropathy in lower limbs was identified in 29.1%. Among cranial nerves examined, optic and vestibulocochlear neuropathies were common (29.1% of eyes and 40% of ears examined). Spinal accessory neuropathy was reported in 21.8% of records. Neither facial nor trigeminal nerves were affected. Electrophysiological characteristics of neuropathies were indicative of axon loss. Significant association was identified between neuropathy and patients’ ages (P &lt; 0.01), duration of the illness (P &lt; 0.001), presence of rheumatoid nodules (P &lt; 0.001) and disease stages (P &lt; 0.001).Conclusions: Our results indicate that cranial and non‐compressive neuropathies are not uncommon in RA. This extends the pathologic disease spectrum. We do not confirm, but suggest the contribution of chronic immune‐mediated vasculitis and/or neurotoxicity in RA neuropathies. Of clinical importance, subclinical neuropathy may never progress and/or be of clinical significance, which contradicts that of comparable diseases, such as systemic lupus erythematosus. Advances in genetics implicate a complex immune genetics which controls susceptibilities and adaptive molecular mechanisms as a culprit of phenotypical heterogenicity among related diseases.

Clinical and electrophysiological evaluation of peripheral neuropathy in rheumatoid arthritis

Clinical and electrophysiological evaluation of peripheral neuropathy in rheumatoid arthritis

Combined Femoral Ncuropathy and Obturator Neuropathy in Rheumatoid Arthritis with Cervical Subluxation After Operation

Combined Femoral Ncuropathy and Obturator Neuropathy in Rheumatoid Arthritis with Cervical Subluxation After Operation

Antibodies To Neuroblastoma Cells In Rheumatoid Arthritis: A Potential Marker For Neuropathy

OBJECTIVE: To investigate the prevalence of antibodies to neuroblastoma cells in patients with rheumatoid arthritis (RA) complicated by peripheral neuropathy (PN), and to determine whether there is any relationship of these antibodies with the severity of neuropathy. METHODS: The study was carried out on 28 patients with RA complicated by PN, 29 RA patients without PN mid 28 healthy volunteers (HV). A cell‐based ELISA method was used to test sera for the presence of IgG and IgM anti‐neuroblastoma cell antibodies. Localisation and characterisation of neuroblastoma antigens recognised by patient's sera was carried out by immunofluorescent microscopy and Western blotting. RESULTS: Elevated levels of IgG anti‐neuroblastoma cell antibodies were found in 10 (36%) neuropathic patients and in 1 (3%) RA control (chi2 = 9.53, P = 0.002), while significant levels of IgM anti‐neuroblastoma cell antibodies were demonstrated in 10 (36%) neuropathic patients and in 2 (7%) RA controls (chi2 = 7.12, P = 0.008). Overall, the levels of antibodies in healthy volunteers were significantly lower than in RA controls and patients with PN. No significant relationship was found between the level of anti‐neuroblastoma cell antibodies and severity of RA or neuropathy. Immunofluorescence staining of neuroblastoma cells with sera from 18 neuropathic patients demonstrated cytoplasmic and/or nuclear‐patterns. Western blotting demonstrated reactivity with a heterogeneous group of neuroblastoma antigens. Little or no reactivity was seen with RA control or HV sera. CONCLUSION: Antibodies against neuroblastoma cells are more prevalent in RA patients with peripheral neuropathy than in RA patients without peripheral nerve involvement. Such antibodies may be useful diagnostic markers for peripheral neuropathy in RA.

Pyridoxine and Penicillamine

Excerpt To the editor: I read with interest the brief report on penicillamine-induced neuropathy in rheumatoid arthritis (1). This report emphasizes the need for a physician to become familiar with...

ILEAL PERFORATION AND ACUTE PERIPHERAL NEUROPATHY IN RHEUMATOID ARTHRITIS.

ILEAL PERFORATION AND ACUTE PERIPHERAL NEUROPATHY IN RHEUMATOID ARTHRITIS.