Neuropsychiatric manifestations in rheumatoid arthritis

Joaquim, Andrei Fernandes; Appenzeller, Simone

doi:10.1016/j.autrev.2015.07.015

Cited by 67 publications

(50 citation statements)

References 85 publications

(160 reference statements)

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“…In support of this hypothesis, there have been numerous studies in patients with various inflammatory conditions including rheumatoid arthritis (Joaquim and Appenzeller, 2015 Matcham et al., 2015, Ryan and McGuire, 2015), multiple sclerosis (Hoang et al., 2016; Kallaur et al., 2015, Marrie et al., 2015), and psoriasis (Walker et al., 2011 Rabin et al., 2012, McDonough et al., 2014), demonstrating a relationship between inflammation and depressed mood. However, the relationship between depression and inflammation in humans is largely confounded by the likelihood that the symptoms of the disease themselves contribute to mood changes.…”

Section: Relationship Between Il-6 and Major Depressive Disordermentioning

confidence: 88%

Integrating Interleukin-6 into depression diagnosis and treatment

Hodes

Ménard

Russo

2016

Neurobiology of Stress

220

144

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There is growing evidence of a relationship between inflammation and psychiatric illness. In particular, the cytokine Interleukin-6 (IL-6) has been linked to stress-related disorders such as depression and anxiety. Here we discuss evidence from preclinical and clinical studies examining the role of IL-6 in mood disorders. We focus on the functional role of peripheral and central release of IL-6 on the development of stress susceptibility and depression-associated behavior. By examining the contribution of both peripheral and central IL-6 to manifestations of stress-related symptomatology, we hope to broaden the way the field thinks about diagnosing and treating mood disorders.

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Section: Relationship Between Il-6 and Major Depressive Disordermentioning

confidence: 88%

Integrating Interleukin-6 into depression diagnosis and treatment

Hodes

Ménard

Russo

2016

Neurobiology of Stress

220

144

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“…None of the three molecules taken from our patient was within the categories of drugs causing interaction with HCQ. Psychomotor agitation cannot be considered a manifestation of elderly-onset RA; neurological and psychiatric manifestations in the course of RA mostly depend on vasculitis, opportunistic infections, and accelerated atherosclerosis [27], all conditions excluded in our patient. Therefore, the RA was (at the time of the introduction of HCQ) in a minimal activity and typically there is a close relationship between disease activity and RA extra-articular manifestations.…”

Section: Discussionmentioning

confidence: 99%

Psychomotor Agitation Following Treatment with Hydroxychloroquine

Manzo¹,

Gareri²,

Castagna³

2017

Drug Saf - Case Rep

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We describe the case of an elderly woman with elderly-onset rheumatoid arthritis, where the use of 4 mg/kg/day of hydroxychloroquine (HCQ) was followed by the onset of psychomotor agitation with marked physical and verbal violence towards her partner, including throwing objects at her partner. No disturbance in sleep and no anxiety, nervousness, or irritability had emerged before the onset of her psychomotor agitation. The disappearance of agitation following targeted pharmacologic intervention and HCQ interruption, its re-onset after reintroduction of the drug, and the high score (9) of Naranjo’s algorithm are surely linked to the existence of a causal relationship between HCQ and psychomotor agitation. HCQ may produce undesirable effects on the central nervous system, mainly irritability, nervousness, emotional changes, and nightmares. To the best of our knowledge, there are only a few case reports of psychosis due to HCQ. No favoring condition such as pharmacokinetic interactions or a personal and family psychiatric history was present in our patient. The neuropsychiatric manifestations we observed could be considered a bizarre-type adverse drug reaction linked to an individual’s hypersensitivity.

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“…3) Rheumatoid arthritis : While the rate of motor or sensory neurological symptoms is relatively low in rheumatoid arthritis (RA) patients, the incidence of mood disorders is estimated to reach up to 70% 139 . Moreover, in independent studies, mild cognitive deficits were demonstrated in more than 70% of RA patients and were associated with MRI or biological signs of altered CNS tissue integrity 140, 141 .…”

Section: The Cns Is a Major Source Of Superautoantigensmentioning

confidence: 99%

Evolution, immunity and the emergence of brain superautoantigens

Nataf¹

2017

F1000Res

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While some autoimmune disorders remain extremely rare, others largely predominate the epidemiology of human autoimmunity. Notably, these include psoriasis, diabetes, vitiligo, thyroiditis, rheumatoid arthritis and multiple sclerosis. Thus, despite the quasi-infinite number of "self" antigens that could theoretically trigger autoimmune responses, only a limited set of antigens, referred here as superautoantigens, induce pathogenic adaptive responses. Several lines of evidence reviewed in this paper indicate that, irrespective of the targeted organ (e.g. thyroid, pancreas, joints, brain or skin), a significant proportion of superautoantigens are highly expressed in the synaptic compartment of the central nervous system (CNS). Such an observation applies notably for GAD65, AchR, ribonucleoproteins, heat shock proteins, collagen IV, laminin, tyrosine hydroxylase and the acetylcholinesterase domain of thyroglobulin. It is also argued that cognitive alterations have been described in a number of autoimmune disorders, including psoriasis, rheumatoid arthritis, lupus, Crohn's disease and autoimmune thyroiditis. Finally, the present paper points out that a great majority of the "incidental" autoimmune conditions notably triggered by neoplasms, vaccinations or microbial infections are targeting the synaptic or myelin compartments. On this basis, the concept of an immunological homunculus, proposed by Irun Cohen more than 25 years ago, is extended here in a model where physiological autoimmunity against brain superautoantigens confers both: i) a crucial evolutionary-determined advantage via cognition-promoting autoimmunity; and ii) a major evolutionary-determined vulnerability, leading to the emergence of autoimmune disorders in Homo sapiens. Moreover, in this theoretical framework, the so called co-development/co-evolution model, both the development (at the scale of an individual) and evolution (at the scale of species) of the antibody and T-cell repertoires are coupled to those of the neural repertoires (i.e. the distinct neuronal populations and synaptic circuits supporting cognitive and sensorimotor functions). Clinical implications and future experimental insights are also presented and discussed.

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Neuropsychiatric manifestations in rheumatoid arthritis

Cited by 67 publications

References 85 publications

Integrating Interleukin-6 into depression diagnosis and treatment

Integrating Interleukin-6 into depression diagnosis and treatment

Psychomotor Agitation Following Treatment with Hydroxychloroquine

Evolution, immunity and the emergence of brain superautoantigens

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