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Volume 14, Issue 12,
, Pages 1116-1122
Rheumatoid arthritis (RA) is a chronic disease characterized by persistent synovitis, systemic inflammation, and the presence of autoantibodies. Neuropsychiatric manifestations are quite common in RA, including depression, cognitive dysfunction, behavior changes, spinal cord compression and peripheral nerve involvement. Potential causes include systemic inflammatory process, neural compression due to bone and joint destruction, side effects of medications and copying difficulties due to the chronicity of the disease. A high level of suspicious is required for an adequate diagnosis and treatment. In this review, we will discuss topographically the main neuropsychiatric manifestations described in RA patients, in an attempt to help in the management of these complex and multifaceted disease.
Rheumatoid arthritis (RA) is a chronic disease characterized by persistent synovitis, systemic inflammation, and autoantibodies (particularly to rheumatoid factor and citrullinated peptide) . Extra-articular features are observed in up to 40% of patients and are associated with increased morbimortality , . The estimate incidence of neurological symptoms in rheumatic diseases is about 11%, but in RA it can reach up to 70% when mood disorders are included , , , , . Extra-articular manifestations are associated with disease severity, disease duration, presence of autoantibodies and comorbidities (e.g. smoking) , . With earlier diagnosis and more aggressive treatment many extra-articular manifestations such as rheumatoid nodules, have been declining , , . However little is known about neuropsychiatric manifestations. In a recent study, rheumatoid vasculitis has been shown to remain a serious complication of RA and associated with significant mortality .
Some of the reasons for a higher incidence of neurological symptoms in RA patients compared with the normal population are:
RA disease by itself, with inflammation, autoantibodies, pain, fatigue and disability leading to psychiatric diseases , .
The systemic inflammatory processes involving all organs and systems, which can involve the neural tissue (e.g. pachimeningitis or vasculitis) .
Joint and bone destruction leading to neural compression (e.g. cervical myelopathy symptoms caused by destruction of the atlanto-axial joints and subsequent atlantoaxial subluxation) or the presence of rheumatoid nodules compressing peripheral nerves , , , .
Potential side effects of the medication used to obtain disease control, such as corticosteroids, disease modifying drugs (DMARDS) and biological agents (BA) .
Accelerated atherosclerosis associated with systemic inflammation and autoantibodies , .
Clinical presentation of neurological symptoms may vary from a sudden and emergent vertebrobasilar stroke to a slowly and insidious process of peripheral neuropathy. The intensity of the symptoms is influenced by the degree of the inflammatory process, the size of the vessel involved, medication and comorbidities , .
To better understand and treat neurological diseases in patients with RA it is important to identify the primary cause of the symptoms, which may not be an easy task .
In this review, we discussed the most common neurological manifestations during the course of RA as well as their most probably etiology, in an attempt to help physicians in the management of these complex and multifaceted disease. The clinical manifestations are presented topographically, according to the main involved site.
We performed a review in the MedLine Database (National Library of Medicine), without time restriction. The following search strategy was used: (“Rheumatoid arthritis” AND “Neurological” OR “Neural” OR “Central Nervous System” OR “Spinal Cord” OR “Peripheral nerves” OR “Cognitive impairment” OR “Vasculitis” OR “Seizure” OR “Depression” OR “Anxiety” OR “Stoke”).
Abstracts were then reviewed and we included articles in English language discussing about the incidence, prevalence, diagnosis and
The exact incidence of brain involvement in RA is not known but is probably low compared with spine and peripheral nerve involvement.
Neurological and psychiatric manifestations in RA patients are common. Brain symptoms may occur due to vasculitis, inflammatory meningitis, opportunistic infections, atherosclerosis and side effects of RA medication.
Cervical spine instabilities, especially AAS, are one of the most common causes of myelopathy in RA patients. Peripheral neuropathy can occur by nerve entrapment or secondary to other causes, such as side effects of medication or vasculitis.
It is of paramount importance for
RA can course with neuropsychiatric symptoms caused by neural compression secondary to damage on joints and bones, the diffuse and systemic inflammatory process and also for side effects of the drugs used for disease control.
Brain involvement can be secondary to vasculitis or inflammatory meningitis, as well as opportunistic infections and side effects of RA medication for disease control. Depression and cognitive dysfunction are quite common, potential related to the disease itself and its
- A. Malipeddi et al.Posterior interosseous nerve palsy: an unusual complication of rheumatoid arthritis: case report and review of the literature
Semin Arthritis Rheum
- N. Massy-Westropp et al.A systematic review of the clinical diagnostic tests for carpal tunnel syndrome
J Hand Surg
- T. Sakai et al.Radiological features of lumbar spinal lesions in patients with rheumatoid arthritis with special reference to the changes around intervertebral discs
- E. Kaltsonoudis et al.Demyelination and other neurological adverse events after anti-TNF therapy
- B. Richioud et al.Rheumatoid arthritis and meningeal nodules
Rev Neurol (Paris)
- D. Guadalupe Loya-de la Cerda et al.Isolated rheumatoid arthritis-associated cerebral vasculitis: a diagnostic challenge
Joint Bone Spine
- F. Cantini et al.Guidance for the management of patients with latent tuberculosis infection requiring biologic therapy in rheumatology and dermatology clinical practice
- H.X. Zhou et al.Cryptococcosis of lumbar vertebra in a patient with rheumatoid arthritis and scleroderma: case report and literature review
BMC Infect Dis
- A.L. Lopresti et al.A review of peripheral biomarkers in major depression: the potential of inflammatory and oxidative stress biomarkers
Prog Neuropsychopharmacol Biol Psychiatry
- Y. Liu et al.The role of interleukin (IL)-17 in anxiety and depression of patients with rheumatoid arthritis
Int J Rheum Dis
Clin Psychol Rev
Gen Hosp Psychiatry
Am J Med
Occurrence of extraarticular disease manifestations is associated with excess mortality in a community based cohort of patients with rheumatoid arthritis
Rheumatoid arthritis of the craniovertebral junction
Depression and anxiety in patients with rheumatoid arthritis: prevalence rates based on a comparison of the Depression, Anxiety and Stress Scale (DASS) and the hospital, Anxiety and Depression Scale (HADS)
Anti tumor necrosis factor therapy is associated with less frequent mood and anxiety disorders in patients with rheumatoid arthritis
Psychiatry Clin Neurosci
Tripartite model of anxiety and depression: psychometric evidence and taxonomic implications
J Abnorm Psychol
Are behaviour and motor performances of rheumatoid arthritis patients influenced by subclinical cognitive impairments? A clinical and neuroimaging study
Clin Exp Rheumatol
Cognitive impairment in rheumatoid arthritis
Methods Find Exp Clin Pharmacol
Vasculitis associated with rheumatoid arthritis: a case–control study
An unusual central nervous system involvement in rheumatoid arthritis: combination of pachymeningitis and cerebral vasculitis
Beyond the joints: neurological involvement in rheumatoid arthritis
Peripheral nerve entrapment syndromes: diagnosis and management
Br J Hosp Med
Radiological evaluation of cervical spine involvement in rheumatoid arthritis
Cardiovascular risk in rheumatoid arthritis: pathogenesis, diagnosis, and management
J Clin Rheumatol
Cardiovascular death in rheumatoid arthritis: a population-based study
Overt psychopathology in rheumatoid arthritis. A fifteen-year follow-up study
Scand J Rheumatol
Psychological aspects of rheumatoid arthritis
Psychological well being in rheumatoid arthritis: a review of the literature
Depression in rheumatoid arthritis: a systematic review of the literature with meta-analysis
Predicting depression in rheumatoid arthritis: the signal importance of pain extent and fatigue, and comorbidity
Arthritis Care Res
Poststroke depression: a review
Can J Psychiatry
Risk of developing depressive disorders following rheumatoid arthritis: a nationwide population-based study
The prevalence of depression in rheumatoid arthritis: a systematic review and meta-analysis
Suicides in persons suffering from rheumatoid arthritis
Concurrent psychiatric disorders are associated with significantly poorer quality of life in patients with rheumatoid arthritis
Scand J Rheumatol
Major depressive episodes are associated with poor concordance with therapy in rheumatoid arthritis patients: the impact on disease outcomes
Clin Exp Rheumatol
Corticosteroid-related central nervous system side effects
J Pharmacol Pharmacother
Depression in rheumatoid arthritis
The psychosocial impact of systemic lupus erythematosus and rheumatoid arthritis
Cognitive impairment in persons with rheumatoid arthritis
Arthritis Care Res (Hoboken)
Tocilizumab treatment safety in rheumatoid arthritis in a patient with multiple sclerosis: a case report
BMC Res Notes
A biochemical perspective of methotrexate neurotoxicity with insight on nonfolate rescue modalities
J Investig Med
- Neuropsychiatric disorders: An immunological perspective
2021, Advances in Immunology
Neuropsychiatric diseases have traditionally been studied from brain, and mind-centric perspectives. However, mounting epidemiological and clinical evidence shows a strong correlation of neuropsychiatric manifestations with immune system activation, suggesting a likely mechanistic interaction between the immune and nervous systems in mediating neuropsychiatric disease. Indeed, immune mediators such as cytokines, antibodies, and complement proteins have been shown to affect various cellular members of the central nervous system in multitudinous ways, such as by modulating neuronal firing rates, inducing cellular apoptosis, or triggering synaptic pruning. These observations have in turn led to the exciting development of clinical therapies aiming to harness this neuro-immune interaction for the treatment of neuropsychiatric disease and symptoms. Besides the clinic, important theoretical fundamentals can be drawn from the immune system and applied to our understanding of the brain and neuropsychiatric disease. These new frameworks could lead to novel insights in the field and further potentiate the development of future therapies to treat neuropsychiatric disease.(Video) Forum LIVE: Precision medicine in rheumatoid arthritis
- The cytokine network in the pathogenesis of major depressive disorder. Close to translation?
2020, Autoimmunity Reviews
Major depressive disorder (MDD) is a common condition that afflicts the general population across a broad spectrum of ages and social backgrounds. MDD has been identified by the World Health Organization as a leading cause of disability worldwide.
Approximately 30% of patients are poor responsive to standard of care (SOC) treatment and novel therapeutic approaches are warranted.
Since chronic inflammation, as it is often observed in certain cancers, type 2 diabetes, psoriasis and chronic arthritis, are accompanied by depression, it has been suggested that immunoinflammatory processes may be involved in the pathogenesis of MDD.
Cytokines are a group of glycoproteins secreted from lymphoid and non-lymphoid cells that orchestrate immune responses. It has been suggested that a dysregulated production of cytokines may be implicated in the pathogenesis and maintenance of MDD. On the basis of their functions, cytokines can be subdivided in pro-inflammatory and anti-inflammatory cytokines. Since abnormal blood and cerebrospinal fluid of both pro and anti-inflammatory cytokines are altered in MDD, it has been suggested that abnormal cytokine homeostasis may be implicated in the pathogenesis of MDD and possibly to induction of therapeutic resistance.
We review current data that indicate that cytokines may represent a useful tool to identify MDD patients that may benefit from tailored immunotherapeutic approaches and may represent a potential tailored therapeutic target.
- Microglial A20 Protects the Brain from CD8 T-Cell-Mediated Immunopathology
2020, Cell Reports
Tumor-necrosis-factor-alpha-induced protein 3 (TNFAIP3), or A20, is a ubiquitin-modifying protein and negative regulator of canonical nuclear factor κB (NF-κB) signaling. Several single-nucleotide polymorphisms in TNFAIP3 are associated with autoimmune diseases, suggesting a role in tissue inflammation. While the role of A20 in peripheral immune cells has been well investigated, less is known about its role in the central nervous system (CNS). Here, we show that microglial A20 is crucial for maintaining brain homeostasis. Without microglial A20, CD8+ Tcells spontaneously infiltrate the CNS and acquire a viral response signature. The combination of infiltrating CD8+ Tcells and activated A20-deficient microglia leads to an increase in VGLUT1+ terminals and frequency of spontaneous excitatory currents. Ultimately, A20-deficient microglia upregulate genes associated with the antiviral response and neurodegenerative diseases. Together, our data suggest that microglial A20 acts as a sensor for viral infection and a master regulator of CNS homeostasis.
- Autoimmune and autoantibody-associated encephalomyelopathies
2019, The Autoimmune Diseases
Autoimmune central nervous system (CNS) affection comprises an expanding group of potentially treatable disorders that should be included in the differential diagnosis of any type of encephalitis or myelitis.
The extent of CNS involvement in systemic immunopathic disorders such as lupus erythematosus, rheumatoid arthritis (RA), or sarcoidosis has been recognized since long. However, the identification of underlying pathogenic mechanisms has led to the development of revolutionary antibody (Ab)-based therapies improving the prognosis of this group of patients.
Further advances in autoimmune involvement of the nervous system have led to the identification of new clinical syndromes, associated with antineuronal Abs that have transformed the diagnostic and therapeutic approach to these disorders. Starting with auto-Abs to the acetylcholine receptor for myasthenia gravis and against intracellular antineuronal nuclear Ab 1 (ANNA-1) (Hu) antigen, there is still a continuous expansion of the number of cell surface, synaptic, and intracellular molecules, which expose antigenic epitopes for autoimmune neurological disorders. Numerous of these Abs were associated with an extraneural malignancy, causing “paraneoplastic neurological syndromes,” while others occur as primary autoimmune diseases. Furthermore, identification of several Abs targeting glial antigens, such as aquaporin-4 (AQP4), has enabled the classification of these disorders as distinct clinical entities.
The particular focus of this chapter is on autoimmune disorders associated with encephalitis or myelitis, subdivided into two groups: (1) systemic diseases with CNS manifestations and (2) Ab-associated disorders of the CNS.
- Central nervous system involvement in rheumatoid arthritis patients and the potential implications of using biological agents
2018, Best Practice and Research: Clinical Rheumatology
Finally, folate consumption by the use of methotrexate (MTX) should be carefully pointed out in each case of neurocognitive deterioration . Joakquim et al. have highlighted the relatively high frequency of neuropsychiatric disorders in patients with RA, including depression, cognitive dysfunction, headache and meningitis, which may be due to the inflammatory process, concomitant medications and/or opportunistic infections . They estimated that the prevalence of anxiety/depression among patients with RA with mild to moderate symptoms was about 40%, in line with that of other chronic pathologies.
Central nervous system (CNS) involvement is quite unusual in patients with rheumatoid arthritis (RA), although cerebral vasculitis, rheumatoid nodules and meningitis have all been reported, and patients with RA may also have CNS comorbidities such as stroke and neuro-degenerative and demyelinating syndromes. It has been found that biological drugs, especially anti-tumour necrosis factor-alpha (anti-TNF-α) drugs, slightly increase the risk of developing demyelinating diseases, and they are consequently discouraged in patients with multiple sclerosis and related disorders. Furthermore, the risk of opportunistic CNS infections is increased in immunosuppressed patients.
To review the current literature concerning CNS involvement in patients with RA (including RA-related forms and comorbidities) and the incidence of new-onset CNS diseases in patients with RA undergoing biological treatment (anti-TNF or non-anti-TNF drugs), the Medline database was searched using the key words ‘rheumatoid arthritis’, ‘central nervous system’, ‘anti-TNF’, ‘abatacept’, ‘tocilizumab’, ‘rituximab’ and ‘anakinra’. Abstracts not in English were excluded.
We selected 76 articles published between 1989 and 2017, which were divided into four groups on the basis of whether CNS involvement was RA-related or not and according to the type of biological agent used (TNF inhibitors or other agents). The RA-related diseases included aseptic meningitis, vasculitis and cerebral rheumatoid nodules, which benefit from immunosuppressive treatments. CNS comorbidities included stroke, seizures, dementia and neuropsychiatric disorders, which have been frequently described in biological agent-naïve patients with RA, and other rarely reported neurological diseases, such as extra-pyramidal syndromes and demyelinating disorders. CNS comorbidities are relatively frequent among patients with RA and may be related to systemic inflammation or concomitant medications. The use of anti-TNF drugs is associated with the risk of developing demyelinating diseases, and CNS infections have been described in patients treated with anti-TNF and non-anti-TNF agents. Non-anti-TNF drugs may be preferred in the case of demyelinating diseases, cerebral vasculitis or neurolupus.
Patients with RA may suffer from CNS involvement as a manifestation of RA or as a comorbidity. The treatment of such medical conditions should be guided on the basis of their etiopathogenesis: steroids and immunosuppressants are useful in the case of RA-related CNS diseases but are often detrimental in other situations. Similarly, the choice of biological agents in patients with RA with CNS complications should be guided by a correct diagnosis in order to prevent further complications.
- Olfactory function in systemic lupus erythematosus and systemic sclerosis. A longitudinal study and review of the literature
2018, Autoimmunity Reviews
Central nervous system (CNS) manifestations are often observed in autoimmune rheumatic diseases, and are associated with higher mortality and worse quality of life [1–4].
To evaluate olfactory function in systemic lupus erythematosus (SLE), systemic sclerosis (SSc) and healthy controls over a 2-year period, and to determine the association of olfactory dysfunction with age, disease activity, disease damage, treatment, anxiety and depression symptoms and limbic structures volumes.
Consecutive SLE and SSc patients were enrolled in this study. Clinical, laboratory disease activity and damage were assessed according to diseases specific guidelines. Olfactory functions were evaluated using the Sniffin' Sticks test (TDI). Volumetric magnetic resonance imaging (MRI) was obtained in a 3T Phillips scanner. Amygdalae and hippocampi volumes were analyzed using FreeSurfer® software.
We included 143 SLE, 57 SSc and 166 healthy volunteers. Olfactory dysfunction was observed in 78 (54.5%) SLE, 35 (59.3%) SSc patients and in 24 (14.45%) controls (p<0.001) at study entry. SLE and SSc patients had significantly lower mean in all three phases (TDI) of the olfactory assessment when compared with healthy volunteers. In SLE, the presence of olfactory dysfunction was associated with older age, disease activity, higher anxiety and depression symptoms score, smaller left hippocampus volume, smaller left and right amygdalae volume and the presence of anti-ribosomal P (anti-P) antibodies. In SSc the presence of olfactory impairment was associated with older age, disease activity, smaller left and right hippocampi volumes and smaller right amygdala volume. Olfactory function was repeated after a 2-year period in 90 SLE, 35 SSc and 62 controls and was stable in all three groups.
Both SLE and SSc patients with longstanding disease had significant reduction in all stages of TDI that maintained stable over a 2-year period. Olfactory dysfunction was associated with age, inflammation and hippocampi and amygdalae volumes. In SLE, additional association with anti-P, anxiety and depression symptoms was observed.
Research articleA 4-year observation in lupus nephritis patients treated with an intensified B-lymphocyte depletion without immunosuppressive maintenance treatment—Clinical response compared to literature and immunological re-assessment(Video) Neurological Manifestations of Lupus and Other Systemic Rheumatologic Disorders
Autoimmunity Reviews, Volume 14, Issue 12, 2015, pp. 1123-1130
B cells (BC) play a critical role in systemic lupus erythematosus (SLE). BC depletion therapy still remains an attractive option, despite the disappointing results of randomized controlled trials (RTCs).
Twelve patients with SLE [3 males, mean age 43.8yrs (25–55)] with severe multiorgan involvement all including kidney (3 patients with Class IV, 4 with Class III/V and 5 with Class V, according to the International Society of Nephrology/Renal Pathology Society glomerulonephritis classification), skin lesions , severe polyarthralgias with arthritis , polyserositis , and lymphadenopathy  have been prospectively treated with an intensified B cell depletion therapy (IBCDT) protocol due to their resistance or intolerance to previous therapy (six cases) or as a front line immunosuppressive treatment in 6 women with unsatisfactory therapeutic compliance or as a specific request of a short-time immunosuppression for gestational perspectives. Protocol: Rituximab (RTX) 375mg/sm on days 1, 8, 15, 22, and 2 more doses after 1 and 2months, associated with 2 IV administrations of 10mg/kg of cyclophosphamide and 3 methylprednisolone pulses (15mg/kg) followed by oral prednisone (0.8mg/kg/day, rapidly tapered to 5mg/day by the end of the 3rd month after RTX). No further immunosuppressive maintenance therapy has been given.
Patients had been followed-up for a mean of 44.5 (24–93)months. Significant decreases (p<0.05) were found in the levels of ESR (baseline mean value: 55.0mm; 3months: 36; end of follow-up: 13), anti-dsDNA antibodies (baseline: 185 U; 3months: 107; end of follow-up: 15), and proteinuria (baseline: 4.9g/24h; 3months: 0.97; end of follow-up: 0.22). C4 values (baseline 11mg/dl) significantly increased (p<0.05) after 3months (22mg/dl) and at the end of the follow-up (20mg/dl). Of the 12 patients, 9 (75%) have remained well after one cycle of IBCDT, with no flare (mean 51.6months [25–93]). Three patients relapsed after 36, 41, and 72months, respectively. Following re-treatment, they again showed complete remission over 18–48months of observation.
A promising role of RTX in an intensified protocol of induction therapy can be envisaged in patients for whom avoiding immunosuppressive maintenance therapy and sparing steroids are particularly appealing. Moreover, our data confirm in one of the longest follow-up available, the opportunity to reconsider the regimens of BL depletion in the treatment of the most severe or refractory forms of SLE despite the disappointing results of RCTs.
Research articleAuto-reactions, autoimmunity and psoriatic arthritis
Autoimmunity Reviews, Volume 14, Issue 12, 2015, pp. 1142-1146
Evidence from the literature suggests that autoimmune processes may drive features of psoriatic arthritis (PsA). Such hypothesis is supported by the evidence that class I major histocompatibility complex (MHC) genes are associated with susceptibility to develop PsA and auto-reactive cells, such as CD8 T cells, T helper (h) 17 and plasma cells, have been demonstrated in PsA. However, no autoantigens have ever been demonstrated in PsA. The presence of a new autoantibody system, anti-carbamylated protein (anti-CarP) antibodies, has been identified in rheumatoid arthritis (RA) patients. These autoantibodies have been associated with a worse disease progression independent of anti-citrulline antibodies (ACPA). In PsA, anti-CarP antibodies have not been evaluated yet. We aimed at analyzing, for the first time, the anti-CarP antibodies in sera of patients with active PsA who were negative for ACPA in order to explore both their presence and their relationship with disease activity. A total of 70 individuals, 30 patients with diagnosis of PsA (according to CASPAR criteria) and 40 healthy controls (HC) were enrolled. We found significantly increased levels of anti-CarP antibodies in PsA patients compared with HC (P<0.0001). Our findings indicate that anti-CarP antibodies are detectable with high specificity and sensibility in PsA patients suggesting an autoimmune background of PsA. Anti-CarP antibodies can be useful in improving the diagnosis of PsA and are correlated with disease activity.
Research articleAutoimmune neuropathies associated to rheumatic diseases
Autoimmunity Reviews, Volume 16, Issue 4, 2017, pp. 335-342
Systemic manifestations are frequent in autoimmune rheumatic diseases and include peripheral nervous system damage. Neuron cell body, axons and myelin sheath may all be affected in this context. This involvement results in severe and sometimes disabling symptoms. Sensory, motor and autonomic features may be present in different patterns that emerge as peculiar clinical pictures. Prompt recognition of these neuropathies is pivotal to guide treatment and reduce the risks of long term disability. In this review, we aim to describe the main immune-mediated neuropathies associated to rheumatic diseases: sensory neuronopathies, multiple mononeuropathies and chronic inflammatory demyelinating polyradiculoneuropathy, with an emphasis on clinical features and therapeutic options.
Research articleRheumatoid arthritis, spondyloarthropathies, and relapsing polychondritis
Handbook of Clinical Neurology, Volume 119, 2014, pp. 449-461
The neurologic complications of rheumatic disease are highly variable and their manifestations are linked to the pathogenesis and clinical phenotype of the specific rheumatologic syndrome. In active rheumatoid arthritis (RA), the peripheral nervous system is most commonly involved and mononeuritis multiplex, nerve entrapment and vascultitic sensorimotor neuropathy are not uncommon. Central nervous system complications such as pachymeningitis and cerebral vasculitis are rare. TNF blockade therapy of RA is rarely associated with demyelinating syndromes. In the spondyloarthropathies, especially ankylosing spondylitis (AS), neurologic complications are more frequent in long-standing, advanced disease and include atlantoaxial subluxation, cauda equina syndrome, spinal stenosis, and acute vertebral fractures. Peripheral nervous system involvement in any of the spondyloarthropaties is rare. Relapsing polychondritis (RP) is characterized by recurring bouts of inflammation, destruction of cartilaginous structures, and systemic and rarely central nervous system vasculitis. Visual-oculo and auditory complications are common. Definitive treatment of the neurologic complications and prevention of subsequent ones is dependent upon effective treatment of RA, AS or RP.
Research articlePsychological distress across twelve months in patients with rheumatoid arthritis: The role of disease activity, disability, and mindfulness
Journal of Psychosomatic Research, Volume 78, Issue 2, 2015, pp. 162-167
Mindfulness may diminish effects of adversities on psychological well-being in medical patients, but studies are scarce, especially in patients with rheumatoid arthritis (RA). The purpose was to examine the prospective moderating effect of mindfulness regarding psychological distress associated with disease activity and disability in patients with RA.
Two-hundred-and-one patients with RA (mean age 57.4±11.7, 55% women) completed questionnaires at baseline and at six and twelve month follow-up. Disease activity score was assessed by the rheumatologist.
Controlled for potential confounders, mixed linear model analyses showed a strong prospective association of higher baseline mindfulness with lower psychological distress up to the twelve month follow-up (p<.001). In addition, a mindfulness by disability by time interaction showed that higher baseline mindfulness was associated with lower disability related psychological distress at follow-up (p=.022).
Findings are in line with the hypothesis that mindfulness may protect against psychological distress associated with disability in RA. Potential benefits of mindfulness-based interventions for prevention should be examined in this population.
Research articleBurden of disease in treated rheumatoid arthritis patients: Going beyond the joint
Seminars in Arthritis and Rheumatism, Volume 43, Issue 4, 2014, pp. 479-488
The disease burden in rheumatoid arthritis (RA) extends beyond the joint. This article evaluates the physical and psychosocial extra-articular burden of treated RA and relationships among diverse disease manifestations.
MEDLINE searches identified papers published in English from January 2003 to December 2012 that evaluated systemic complications and psychosocial aspects associated with RA. Preference was given to studies with randomized cohorts and large (>100) sample sizes. Of 378 articles identified in the initial search, 118 were selected for inclusion.
RA is associated with multiple comorbidities and psychosocial impairments, including cardiovascular disease, osteoporosis, interstitial lung disease, infection, malignancies, fatigue, depression, cognitive dysfunction, reduced work performance, work disability, and decreased health-related quality of life. The etiology of the extra-articular burden may reflect the systemic inflammation and immune system alteration associated with RA, metabolic imbalances and side effects related to treatment, or the influence of comorbidities. Strategies that may help to reduce the extra-articular disease burden include personalized medicine and the potential introduction of treatments with new mechanisms of action.
Despite improvements in treating joint disease, the extra-articular burden in RA remains substantial, encompassing multiple comorbidities and psychosocial impairments.
Copyright © 2015 Elsevier B.V. All rights reserved.
RA patients are more prone to have anxiety, depression and cognitive impairment compared to the general healthy population. Those mental health conditions contribute to less responsiveness to treatment and higher disease activity in RA mainly due to fatigue and bodily pain.
Rheumatoid arthritis (RA) is associated with various nonarticular manifestations, including a range of neurologic abnormalities, such as cervical spine instability, compressive neuropathy (eg, of the median nerve at the wrist, which results in carpal tunnel syndrome [CTS]), and an often subclinical sensory or ...
A lot of people with rheumatoid arthritis (RA) report having trouble with memory, attention, and mental focus. They forget names and appointments, struggle to find the right words and have trouble making and carrying out plans.
People with all types of arthritis are at high risk of depression and anxiety. If you have been diagnosed with rheumatoid arthritis and are feeling depressed or are worried about developing depression, it's important to talk to your doctor.
Many adults with arthritis have anxiety and depression. Learn how arthritis and mental health are connected. Learn about programs that can improve mood and well-being, and ease arthritis symptoms. About 1 in 5 US adults with arthritis has symptoms of anxiety or depression.
Psoriatic arthritis is a type of arthritis that affects some people with the skin condition psoriasis. It typically causes affected joints to become swollen, stiff and painful. Like psoriasis, psoriatic arthritis is a long-term condition that can get progressively worse.
Neurological disorders are medically defined as disorders that affect the brain as well as the nerves found throughout the human body and the spinal cord. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms.
Remember, RA causes your body's immune system to attack the lining between your joints, which causes inflammation and swelling. That swelling can alter the way the nerves in your brain communicate. Inflammation in the brain, with or without other RA-related neurologic changes, can lead to brain fog.
Inflammatory central nervous system lesions are infrequent in RA. Cerebral rheumatoid vasculitis is an uncommon and serious complication of RA. Most reported cases have led to the death of the patient especially when cerebral vasculitis was associated with systemic rheumatoid vasculitis (Table1).
Psychosis and its Association with Rheumatoid Arthritis
The disease onset for rheumatoid arthritis is less as compared to schizophrenia and bipolar disorder . The incidence of rheumatoid arthritis lowers/raises the risk of bipolar disorder and schizophrenia [76,77].
Rheumatoid arthritis (RA) is a chronic inflammatory joint condition and an autoimmune disease that can be caused by stress, according to research. Stress triggers rheumatoid arthritis by setting off the immune system's inflammatory response in which cytokines are released.
The patients investigated in the two disease groups represent an unselected population with regard to psychological abnormalities (from two internistic rheumatism outpatient clinics); the results can thus be considered to be representative and permit the following conclusions to be drawn: RA is not a psychosomatic ...
Unlike a normal headache, a neck arthritis headache typically begins with pain in your neck. From there, the pain will move up the back of your head until it reaches the top. In addition, the pain will usually be worse on one side of your head, and you won't have pain in your temple region.
Neurological effects of systemic inflammation
Systemic inflammation can lead to immune responses in the brain that show up in many ways. People may experience cognitive symptoms such as memory lapses or confusion. Other common symptoms, known as “sickness behavior,” may include: Depression.
Rheumatoid arthritis (RA) is an autoimmune disorder that not only attacks your joints, but can lead to brain fog. Cognitive issues can develop when proteins called cytokines increase inflammation in your brain.
- Pain or aching in more than one joint.
- Stiffness in more than one joint.
- Tenderness and swelling in more than one joint.
- The same symptoms on both sides of the body (such as in both hands or both knees)
- Weight loss.
- Fatigue or tiredness.
Background. Symptoms of anxiety and depression are more prevalent in rheumatoid arthritis (RA) patients than in the general population [1, 2]. Studies have shown that 26–46% of RA patients have anxiety symptoms, and 14.8–34.2% have depression symptoms .
Rheumatoid arthritis can take a toll on your mental health. The disease is known for causing pain, stiff joints, and fatigue, but it can also lead to depression. In fact, if you have RA, you're two to four times as likely to have depression as someone who doesn't have it.
The causes of mood swings for people with rheumatoid arthritis are similar to the causes of depression. The chronic inflammation, pain, fatigue, and other symptoms can make it harder for you to withstand stress, so you may react more intensely to certain stressors or situations.
Rheumatoid arthritis can at times put a strain on social relationships. Pain and loss of independence can make people feel frustrated, angry, and depressed, which can in turn affect other members of the family.
Psychosis and its Association with Rheumatoid Arthritis
The disease onset for rheumatoid arthritis is less as compared to schizophrenia and bipolar disorder . The incidence of rheumatoid arthritis lowers/raises the risk of bipolar disorder and schizophrenia [76,77].
- Tell your doctor how you feel. They may want to change your medications or their doses. ...
- Take a breathing break. ...
- Keep doing things you enjoy. ...
- Use heat, cold, and massage. ...
- Notice your emotions. ...
- Join a support group. ...
- Exercise. ...
- Eat a balanced diet.
A study published in July 2018 in Arthritis Care & Research found that people who have rheumatoid arthritis (RA) are more likely to experience depression, anxiety, and bipolar disorder in their lifetimes than those who have not been diagnosed with the autoimmune disease.
Rheumatoid arthritis and brain fog
Rheumatoid arthritis (RA) is best known for causing painful, swollen joints. But many people with RA say they also have to deal with symptoms like forgetfulness, trouble concentrating, and difficulty thinking clearly.
This study revealed that patients with RA were at a higher risk of subsequent bipolar disorder.
- Osteoporosis. ...
- Rheumatoid nodules. ...
- Dry eyes and mouth. ...
- Infections. ...
- Abnormal body composition. ...
- Carpal tunnel syndrome. ...
- Heart problems. ...
- Lung disease.
- Not Seeing a Rheumatologist. Your regular doctor may have diagnosed your RA. ...
- Too Much Couch Time. You need rest, just not too much. ...
- Canceling Doctor Appointments. When you feel good, do you stop seeing your doctor? ...
- Not Taking All Your Medications. ...
- Skipping Medication When You Feel Good. ...
- Overlooking Your Mood.
Rheumatoid arthritis can be life changing. You may need long-term treatment to control the symptoms and joint damage. Depending on how much pain and stiffness you feel and how much joint damage you have, simple daily tasks may become difficult or take longer to do.
Disease-specific familial risks were similar to what has been shown in previous studies. A family history of RA was associated with a tripled risk for RA (HR = 3.4, 95% CI = 3.2–3.6), and a family history of schizophrenia was associated with an 8-fold risk of schizophrenia (HR = 8.2, 95% CI = 7.6–8.8).
One study found a 16% lifetime prevalence rate of anxiety disorders in individuals with RA,24 and in an analysis of survey data, an estimated 11.2% of patients with arthritis reported panic attacks and 5.6% reported receiving a diagnosis of generalized anxiety disorder, though this latter study did not delineate ...
Autoimmune encephalitis is a collection of related conditions in which the body's immune system attacks the brain, causing inflammation. The immune system produces substances called antibodies that mistakenly attack brain cells.
- Talk with your doctor or nurse. ...
- Take time to rest during the day. ...
- Try to relax. ...
- Learn special techniques like yoga and meditation. ...
- Reach out for support from friends, family, and co-workers.
- Join a class or support group.
|abatacept (Orencia)||selective T cell costimulation modulator|
|adalimumab (Humira)||tumor necrosis factor (TNF) blocker|
|anakinra (Kineret)||interleukin-1 receptor antagonist|
|infliximab (Remicade)||tumor necrosis factor (TNF) blocker|
While rheumatoid arthritis is not considered life-threatening, if you die from something linked to your condition, your life cover will payout. A life insurance policy will pay out a cash lump sum to your family if you pass away for almost any reason.