Articles: chronic.
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British medical bulletin · Sep 2024
ReviewPharmacological management of secondary chronic spinal cord injury: a systematic review.
Spinal cord injury (SCI) may bring lifelong consequences for affected patients and a high financial burden to the health care system. ⋯ Different approaches exist for the pharmacological management of secondary chronic SCI. One of the most investigated drugs, 4-aminopyridine, improves central motor conduction and shows improvement in neurological signs. Positive results in different areas have been observed in patients receiving the anti-spastic drugs tizanidine and baclofen or Granulocyte colony-stimulating factor. Growth hormone showed only minimal or no significant effects, and the therapy of secondary chronic SCI with riluzole has been poorly researched to date.
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Traumatic brain injury (TBI) annually impacts 69 million individuals worldwide. Mild TBI constitutes approximately 90% of all TBIs. Chronic pain post-mTBI occurs in 29% to 58% of patients. ⋯ The optimized predictive model demonstrated high efficacy, with an accuracy of 83%, a sensitivity of 92%, and an area under the receiver operating characteristic curve of 0.8. Our findings indicate feasibility in predicting chronic post-MVA pain within the critical 72-hour window postinjury using simple bedside metrics. This approach offers a promising avenue for the early detection of individuals at increased risk for chronic pain, enabling the implementation of targeted early interventions.
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Chronic pain disorders are among the most common and affect approximately 20% of the US population, leading to disproportionately high medical expenditures and negative economic impact. Behavioral factors of pain catastrophizing and perceived injustice are associated with pain intensity in chronic pain. Diminished heart rate variability (HRV) is also strongly associated with chronic pain. These factors have been less explored earlier in the pain experience and it is unclear whether they play a role in the transition from acute to chronic pain. The aim of this study was to determine the relationship between pain catastrophizing, perceived injustice, pain intensity and HRV in naturally occurring acute pain. ⋯ While greater chronic pain intensity is associated with lower HRV, the relationship is reversed in the setting of acute pain. These findings highlight the need to better understand the unique factors that contribute to lower HRV in the acute phase.
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Persistent or chronic pain is the primary reason people seek medical care, yet current therapies are either limited in efficacy or cause intolerable side effects. Diverse mechanisms contribute to the basic phenomena of nociceptor hyperexcitability that initiates and maintains pain. Two prominent players in the modulation of nociceptor hyperexcitability are the transient receptor potential vanilloid type 1 (TRPV1) ligand-gated ion channel and the voltage-gated potassium channel, Kv7.2/3, that reciprocally regulate neuronal excitability. ⋯ Importantly, this specific MOA is not associated with any previously described Kv7.2/3 or TRPV1 class-specific side effects. We suggest that the therapeutic potential of this MOA is derived from the selective and specific targeting of a subpopulation of nociceptors found in rodents and humans. This efficacy and safety profile supports the advancement of dual TRPV1-Kv7.2/3 modulating compounds into preclinical and clinical development for the treatment of chronic pain.
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Chronic postoperative pain is present in approximately 20% of patients undergoing total knee arthroplasty. Studies indicate that pain mechanisms are associated with development and maintenance of chronic postoperative pain. The current study assessed pain sensitivity, inflammation, microRNAs, and psychological factors and combined these in a network to describe chronic postoperative pain. ⋯ The reduction of the number of parameters stabilized the models and reduced the explanatory value to 69% and 51%. This is the first study to use the DIABLO model for chronic postoperative pain and to demonstrate how different pain mechanisms form a pain mechanistic network. The complex model explained 81% of the variability of clinical pain intensity, whereas the less complex model explained 51% of the variability of clinical pain intensity.