A Brief Mind-body Intervention Is Feasible and May Prevent Persistent Pain After Acute Orthopaedic Traumas: A Randomized Controlled Trial.
Authors: Vranceanu AM, Jochimsen KN, Brewer JR, Briskin EA, Parker RA, Macklin EA, Ring D, Jacobs C, Ly T, Archer KR, Conley CEW, Harris M, Matuszewski PE, Obremskey WT, Laverty D, Bakhshaie J, the TOR Study Team
Journal: Clinical orthopaedics and related research
mental health
psychology
open access
Abstract
Sickle cell disease (SCD) is a hemoglobinopathy associated with hemolytic anemia, acute and chronic pain, chronic organ damage, and increased mortality. Pain is the most common symptom experienced by individuals with SCD. Acute recurrent episodes of pain, known as vaso-occlusive crises (VOCs), may start as early as 4 – 6 months of age and occur throughout life. The frequency of pain increases with age, with many patients developing chronic pain. VOCs are the primary reason for SCD-related emergency department (ED) visits and hospitalization with annual health care costs of 1.1 billion dollars. SCD-related pain profoundly impacts quality of life and remains a significant challenge for patients, families, and treating healthcare providers. Individuals with SCD are also at risk for mental health difficulties such as anxiety and depressive symptoms. These affective comorbidities are associated with use of maladaptive strategies for coping with pain and poorer SCD management, which have the potential to lead to greater healthcare utilization. There is evidence that children with SCD who report more anxiety symptoms have higher admission rates for pain and longer hospital stays. In adults with SCD, depressive symptoms have been associated with higher healthcare utilization including increased ED use and hospitalizations for pain. Emotional functioning plays an important role in both processing one’s own pain and implementing coping strategies that may influence healthcare outcomes. SCD also contributes to direct and deleterious neurological effects that can lead to impairments in neurocognitive functioning. The most substantive neurocognitive impairments typically result from overt stroke, though deficits are also associated with the presence of silent cerebral infarcts. Moreover, mounting evidence suggests that even patients with SCD without a history of cerebral infarct are at risk for neurocognitive deficits through varied pathways. Robust data highlights an association between neurocognitive performance and hemoglobin and hematocrit and recent studies point to a role for other biomarkers of disease severity such as cerebral blood flow, oxygen extraction, inflammatory cytokines, and platelets. Worsening neurocognitive functioning poses significant risks to patient health and quality of life due to potential for increased difficulty managing one’s disease (e.g., adhering to treatment recommendations, navigating transition to adult health care).