Articles: pain-clinics.
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Pain with bladder filling remains an unexplained clinical presentation with limited treatment options. Here, we aim to establish the clinical significance of bladder filling pain using a standardized test and the associated neural signature. We studied individuals diagnosed with urologic chronic pelvic pain syndrome (UCPPS) recruited as part of the multidisciplinary approach to the study of chronic pelvic pain (MAPP) study. ⋯ The UCPPS subtype with bladder-filling pain (BFP+) had altered morphology and increased functional activity in brain areas involved in sensory and pain processing. Bladder-filling pain positive status predicted increased symptom flare-ups and healthcare utilization over the subsequent 18 months when controlling for symptom severity and a self-reported history of bladder-filling pain. These results both highlight the importance of assessing bladder filling pain in heterogeneous populations and demonstrate that persistent bladder-filling pain profoundly affects the brain.
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Migraine oscillates between different states in association with internal homeostatic functions and biological rhythms that become more easily dysregulated in genetically susceptible individuals. Clinical and pre-clinical data on migraine pathophysiology support a primary role of the central nervous system (CNS) through 'dysexcitability' of certain brain networks, and a critical contribution of the peripheral sensory and autonomic signalling from the intracranial meningeal innervation. This review focuses on the most relevant back and forward translational studies devoted to the assessment of CNS dysfunctions involved in primary headaches and discusses the role they play in rendering the brain susceptible to headache states. ⋯ This review focuses on the most relevant back and forward translational studies showing the crucial role of top-down brain modulation in triggering and maintaining primary headache states and how these central dysfunctions may interact with personalized pain management strategies.
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Background Pain after a SARS-CoV-2 acute infection (post-COVID pain) is becoming a new healthcare emergency but remains underestimated and most likely undertreated due to a lack of recognition of the phenomenon and knowledge of the underlying pain mechanisms. Evidence supporting any particular treatment approach for the management of post-COVID pain is lacking. Large variability in the patient response to any standard pain treatments is clinically observed, which has led to calls for a personalized, tailored approach to treating patients with chronic post-COVID pain (i.e. 'precision pain medicine'). ⋯ Further, the consideration of other factors, such as gender, comorbidities, treatments received at the acute phase of infection for onset-associated COVID-19 symptoms, factors during hospitalization or the presence of emotional disturbances should be implemented into a treatment programme. Conclusions Accordingly, considering these factors, management of post-COVID pain should include multimodal pharmacological and non-pharmacological modalities targeting emotional/cognitive aspects (i.e. psychological and/or coping strategies), central sensitization-associated mechanisms (i.e. pain neuroscience education), exercise programmes as well as lifestyle interventions (e.g. nutritional support and sleep management). SIGNIFICANCE: This position paper presents an evidence-based clinical reasoning approach for precision management of post-COVID pain.
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Depression is prevalent among patients with chronic pain and may impact pain management. An accurate assessment is, however, complicated by overlapping symptoms. This study investigated how patients with high-impact chronic pain interpreted and responded to the Patient Health Questionnaire 9 (PHQ-9) to identify problematic items and causes hereof. ⋯ Problematic items limit the construct validity of the PHQ-9, leaving an increased risk of inflated depression scores in high-impact chronic pain. Identified problems should guide future revisions to enhance validity and screening accuracy for the benefit of both research and clinical practice.
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Referred sensation (RS) as a specific clinical phenomenon has been known for a long time, although the underlying mechanisms remain unclear. The aims of this study were to assess if (1) healthy individuals who experienced RS had a less active endogenous pain system when compared with those who did not; (2) activation of descending pain inhibition mechanisms can modulate RS parameters; and finally, (3) a transient decrease in peripheral afferent input because of a local anesthetic (LA) block in the masseter muscle can modulate RS parameters. To assess these, 50 healthy participants were assessed in 3 different sessions. ⋯ In the second and third sessions, participants had their mechanical sensitivity and RS assessed before and after receiving an injection of 2 mL of LA and isotonic saline into the masseter muscle. The main findings of this study were (1) participants who experienced RS during standardized palpation exhibited increased mechanical sensitivity ( P < 0.05, Tukey post hoc test) and decreased CPM ( P < 0.05, Tukey post hoc test) when compared with those who did not; RS incidence ( P < 0.05, Cochran Q test), frequency ( P < 0.05; Friedman test), intensity ( P < 0.05, Tukey post hoc test), and area ( P < 0.05, Tukey post hoc test) were all significantly reduced when assessed (2) during a painful conditioning stimulus and (3) after LA block. These novel findings highlight that RS in the orofacial region are strongly modified by both peripheral and central nervous system factors.