Research conducted with the best available assessment instruments shows that a significant minority of children and adolescents develop PTSD after trauma exposure, with those exposed to interpersonal trauma and girls at particular risk. The estimates provide a benchmark for DSM-5 and ICD-11.
The aim of the study was to reveal the incidence and time course of depressive symptoms following acute spinal cord injury (SCI) in relation to clinical outcomes for comparison to other neurological disorders with severe impairment. In patients with acute traumatic SCI (n = 130), combined follow up assessments of neurological and functional outcomes, pain and patient-rated affective factors (e.g. mood, anxiety) were prospectively (1, 3, 6, 12 months after injury) collected during rehabilitation and follow up in out-patient clinics. We related these to the severity of depressive symptoms (no, mild, moderate and severe) based on the Beck Depression Inventory (BDI) scores. The mean 65% of patients showed no depressive symptoms and 30% mild depressive symptoms, while less than 5% presented moderate to severe depressive symptoms. The group findings and symptoms in individual patients remained stable over 1 year though patients revealed significant clinical recovery. Although two-thirds of the patients experienced pain, BDI scores were not related to pain intensity. BDI mean scores were only slightly higher than in control populations, but rather low compared to patients with other neurological disorders (e.g. stroke and multiple sclerosis) that are also associated with severe functional impairment. The prevalence of depressive symptoms following acute SCI is rather low and remains stable within the first year after injury despite the severe neurological impairment and loss of independency. In comparison to other neurological disorders that also involve brain function SCI patients seem to be less challenged by depressive symptoms that constitute additional burdens to respond to the severe functional impairments.
There is growing evidence that fear learning abnormalities are involved in the development of posttraumatic stress disorder (PTSD) and chronic pain. More than 50% of PTSD patients suffer from chronic pain. This study aimed to examine the role of fear-learning deficits in the link between pain perception and PTSD. We included 19 subjects with PTSD and 21 age- and sex-matched healthy control subjects in a fear-conditioning experiment. The conditioned stimulus (CS) consisted of visual signs flashed upon a screen in front of each subject. The unconditioned stimulus was either a low or high temperature impulse delivered through a thermal contact thermode on the subjects’ hand. A designation of ‘CS−’ was assigned to CS always followed by nonpainful low-temperature stimuli; a designation of ‘CS+’ was given to CS that were randomly followed by either a low or a more painful high temperature. Skin conductance was used as a physiological marker of fear. In healthy control subjects, CS+ induced more fear than CS−, and a low-temperature stimulus induced less subjective pain after CS− than after CS+. PTSD subjects failed to demonstrate such adaptive conditioning. Fear ratings after CS presentation were significantly higher in the PTSD group than in the control group. There were significant interaction effects between group and the type of CS on fear and pain ratings. Fear-learning deficits are a potentially promising, specific psychopathological factor in altered pain perception associated with PTSD. Deficits in safety learning may increase fear and, consequently, pain sensations. These findings may contribute to elucidating the pathogenesis behind the highly prevalent comorbidity that exists between PTSD and pain disorders, and to developing new treatments.
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