Corrigendum to "Mobile intervention for emerging adults with regular cannabis use: a micro-randomized trial" [The Lancet Regional Health-Americas 2026; Volume 61: 101524; DOI: 10.1016/j.lana.2026.1015

Traumatic brain injury (TBI) impacts approximately 1.4 million Americans each year and is the leading cause of mortality and morbidity among individuals under 40 years old (; ; ; , ; ). Among the sequelae of TBI, psychotropic complications most commonly manifest as pain and depression. Meta-analyses indicate that chronic pain and depression symptoms are highly prevalent after TBI, occurring in 40-60% of moderate to severe TBI patients (; ; ; , ; ). Pain and depression symptoms are highly comorbid in the general population (; ), and remain closely linked and highly prevalent in the context of TBI (; ; ; ; ). Following TBI, these conditions can persist for decades contributing substantially to long-term morbidity (; ). For instance, a longitudinal prospective observational cohort study including more than 2000 patients over a 9-week period in an inpatient rehabilitation setting found that 70% of TBI patients remained on antidepressants and 40% continued to receive narcotics at week 9 (; ; ; ; ; ). Concerningly, TBI victims are ten times more likely than the general population to die from accidental overdoses, 70% of those involving opioids (). Systematic literature reviews indicate that TBI often results in a neuroinflammatory phenotype, including microglial activation, which likely influences the development of both pain and depressive symptoms that often accompany TBI (). This inflammatory response is characterized by sustained elevations in pro-inflammatory cytokines and chemokines, which can disrupt synaptic function and neural circuit integrity involved in the spinothalamic () and limbic pathways (), which regulate pain and depression. Importantly, the persistence of this neuroinflammatory state beyond the acute injury phase suggests a mechanistic link to chronic symptomatology rather than a transient response. However, the relationship between neuroinflammation and clinical outcomes is complex. Major depressive disorder (MDD) and chronic pain are highly heterogeneous conditions that arise from multiple biological mechanisms rather than a single pathophysiological process. Similarly, although neuroinflammation is a common consequence of TBI, not all individuals develop chronic pain, depression, or persistent inflammatory abnormalities following injury (; ). Indeed, there is ongoing debate as to whether inflammation should be viewed as merely an epiphenomenon or as a causal driver of depression (). With respect to TBI-pain, pain itself is recognized as one of the five cardinal signs of acute inflammation, alongside redness, heat, swelling, and loss of function, and it is both a consequence and remains a contributor to chronic pain states (). While not all individuals with chronic pain or depression exhibit inflammatory abnormalities (or vice versa), converging evidence suggests that immune and inflammatory mechanisms contribute to symptom development in biologically distinct subgroups of patients (; ; ). Accordingly, distinguishing such subgroups may help identify patients less likely to respond to standard pharmacotherapies alone, while also informing the selection of anti-inflammatory or immunomodulatory treatment strategies (; ). This inflammation-associated phenotype has become a major focus of investigation in both pain and depression research.