RESUMO
Fibromyalgia is characterised by widespread musculoskeletal pain, which may present with fatigue, depression, anxiety, sleep and cognitive disturbances. It is the second most prevalent rheumatic disease. An accurate diagnosis is challenging, since its symptoms may resemble diverse conditions such as carpal tunnel syndrome, Raynaud syndrome, Sjögren syndrome, amongst others. Neuropathic pain and autonomic dysfunction in fibromyalgia suggest the involvement of the nervous system. Ion channels, neurotransmitters and neuromodulators may play a role. Small fibre neuropathy (SFN) may also cause chronic widespread pain. SFN may occur in 50% of fibromyalgia patients, but its role in the disease is unknown. Despite several efforts to synthesise the evidence on the mechanisms for pain in fibromyalgia, there are few studies applying an integrative perspective of neurochemical, immunological, and neuroanatomical characteristics, and their relevance to the disease. This protocol aims to clarify the mechanisms of the central and peripheral nervous system associated with pain in fibromyalgia. We will retrieve published studies from Web of Science, MEDLINE, Scopus, EBSCOhost, Ovid and Google Scholar. All clinical studies or experimental models of fibromyalgia reporting imaging, neurophysiological, anatomical, structural, neurochemical, or immunological characteristics of the central or peripheral nervous systems associated with pain will be included. Exclusion criteria will eliminate studies evaluating pain without a standardised measure, studies written in languages different from Spanish or English that could not be appropriately translated, and studies whose full-text files could not be retrieved after all efforts made. A narrative synthesis will be performed.
Assuntos
Dor Crônica , Fibromialgia , Neuralgia , Doenças Reumáticas , Humanos , Fibromialgia/diagnóstico , Dor Crônica/etiologiaRESUMO
BACKGROUND: Changes in quantitative sensory testing (QST) parameters following topical anaesthesia could contribute to better elucidate underlying mechanisms of somatosensory alterations in temporomandibular disorder (TMD) pain patients. This placebo-controlled crossover investigation compared the somatosensory profile following topical anaesthesia between TMD patients (n = 20) and healthy participants (n = 20). METHODS: Cold detection threshold, warm detection threshold, cold pain threshold, heat pain threshold, mechanical detection threshold, mechanical pain threshold, wind-up ratio and pressure pain threshold were assessed on the skin overlying the masseter at three consecutive days (baseline and immediately after lidocaine 4%/placebo cream). Mixed ANOVA and a coding system that accounts for the diversity of types of peripheral axons associated with the somatosensory parameters were applied for data analysis. RESULTS: The lidocaine application caused no changes in the somatosensory sensitivity in the masseter region in TMD patients (P > .050), but sensitivity to cold, cold pain, touch and pinprick stimuli were reduced after topical anaesthesia in healthy participants (P < .050). Also, the degree of topical anaesthesia was greater in healthy participants (P = .008). The coding system suggested that TMD patients presented only Aδ-fibre block, whereas a combination of either Aß- and/or C-fibre block was observed in 35% of healthy participants in addition to Aδ-fibre block following lidocaine application. CONCLUSION: Quantitative sensory testing can be successfully applied to identify meaningful differences in the degree of hypoalgesia and hypoesthesia following short-time topical anaesthesia.
Assuntos
Anestesia Local , Lidocaína , Limiar da Dor , Transtornos da Articulação Temporomandibular , Humanos , Dor , Medição da DorRESUMO
BACKGROUND: Central sensitisation pain is a predominant mechanism in a proportion of individuals with non-specific chronic low back pain and is associated with poor outcomes. It is proposed that the pre-morbid experiences and contexts may be related to the development of central sensitisation. OBJECTIVES: The objective of this study was to explore the pre-morbid experiences and personal characteristics of participants with central sensitisation pain from a non-specific chronic low back pain population. METHODS: This was a qualitative, exploratory study, using a concurrent nested design within a mixed methods protocol. n=9 participants were recruited purposively based on sensory profiles and trait anxiety-related personality types. Data were collected through semi structured interviews, managed using QSR NVivo 10 software and analysed using theoretical thematic analysis. RESULTS: Four themes emerged: developmental learning experiences, personal characteristics, sensitivity and trauma. Reported was lack of confidence, low esteem and a need to please others, physical hyper-sensitivities (smell, light, sound) and emotional sensitivity (anxiety) as well as physical hypo-sensitivity. Participants had also suffered emotional and/or physical trauma. Learning difficulties, sensory sensitivities and trauma are associated with autonomic stress responses, which in turn have been linked to physiological changes seen in central sensitisation pain. CONCLUSION: Central sensitisation pain developed in the context of sensory processing differences related to learning difficulties, sensitivities and trauma, and personal characteristics of low confidence and control, in a group of participants with non-specific chronic low back pain. The role of pre-existing sensory processing differences, as a component of altered central nervous system function, in relation to central sensitisation pain warrants further investigation.