Training Clinical Researchers with Design Thinking to To Develop Dementia Caregiving Research Initiatives.

Training healthcare professionals with Design Thinking (DT) can support patient-centred care by recognizing patient/care provider needs through empathizing. This article explored the Design Thinking in improving clinical researchers' understanding of relatively unexplored and understudied dementia caregiving problems. Following the Double-Diamond, a Design Thinking process model, we conducted a series of workshops and invited family caregivers of patients with dementia as active participants to provide training to clinical researchers on Design Thinking. We then evaluated the benefit of the workshops in improving clinical researchers' understanding of the caregiving problem and solution space through pre- and post-surveys. Our findings revealed researchers' overall perception of Design Thinking, their clear insights on dementia caregivers' challenges, and speculating caregiver-specific interventions. Our paper contributed to the health design community by exploring the benefit of Design Thinking in understudied areas by 1) Recognizing urgent matters in healthcare, 2) Revealing implicit needs through collective expertise and knowledge exchange, and 3) Producing original health care research and contributions. We hope this study inspires and supports training healthcare researchers to advance dementia caregiving and healthcare research initiatives by adopting the Double-Diamond process model.

Increased neural response to trauma scripts in posttraumatic stress disorder following paroxetine treatment: A pilot study.

Neuroimaging studies of individuals with posttraumatic stress disorder (PTSD) have revealed altered patterns of activity in medial prefrontal brain regions, including the anterior cingulate cortex (ACC), an area implicated in affect regulation. Selective serotonin reuptake inhibitors (SSRIs) have been shown to effectively treat PTSD symptoms, but there remains a lack of functional neuroimaging research examining the effects of psychopharmacological treatment on brain function in PTSD. The purpose of this pilot study was to assess the effects of the SSRI paroxetine on neural responses to traumatic memories in a small sample of patients with PTSD, as measured with PET imaging; we hypothesized that paroxetine treatment would be associated with increased regional cerebral blood flow (rCBF) in the medial prefrontal cortex. Thirteen participants with PTSD were given controlled-release paroxetine (paroxetine CR) or placebo in a randomized, double-blind fashion for 12 weeks. Participants underwent brain imaging using positron emission tomography (PET) before and at the end of treatment in conjunction with exposure to neutral scripts and personalized trauma scripts. Participants treated with paroxetine CR and placebo both exhibited significantly increased rCBF in the ACC during trauma versus neutral script presentations; however, we noted an increase in function in the orbitofrontal cortex (OFC) in paroxetine-treated (but not placebo-treated) participants. Participants in both groups showed decreases in overall PTSD symptomatology following treatment; paroxetine-treated participants showed a slightly greater percentage decrease in symptoms. These preliminary findings indicate that increased ACC function represents a nonspecific response to treatment, whereas increased OFC function is specifically associated with paroxetine treatment in PTSD. These pilot data reveal putative mechanisms for SSRI treatment in PTSD and substantiate the need for large-scale placebo-controlled studies investigating these effects.

Neuropsychological functioning in patients with posttraumatic stress disorder following short-term paroxetine treatment.

UNLABELLED: A previous study found improvements in verbal declarative memory in patients with Posttraumatic Stress Disorder (PTSD) following one year of open-label paroxetine treatment. The purpose of the present study was to replicate prior findings and to extend the previous study by comparing the effects of paroxetine versus placebo on cognition in patients with PTSD. METHODS: Eighteen participants with PTSD underwent assessment of neuropsychological function, following which they were randomized to receive controlled-release (CR) paroxetine or placebo, given in a variable dose in a double- blind manner for three months. Neuropsychological testing was then repeated. Subjects who had received placebo were then treated with open-label paroxetine CR and re-assessed. RESULTS: Paroxetine CR treatment resulted in a significant increase in verbal declarative memory function in the group as a whole, as measured by the Wechsler Memory Scale-Revised, the Selective Reminding Test, and novel paragraph recall, and explicit recall of neutral words. Although we found patterns of improved test performance with paroxetine versus placebo treatment, these differences were not statistically significant. CONCLUSION: These findings replicate an earlier finding that open label treatment with paroxetine CR is associated with improvements in verbal declarative memory function. The current study did not show a statistically significant difference between the effects of paroxetine and placebo on memory function, which may in part be related to our small sample size.

Effects of a cognitive stress challenge on myocardial perfusion and plasma cortisol in coronary heart disease patients with depression.

Although it is well established that coronary heart disease (CHD) patients with depression exhibit increased mortality compared with equally ill cardiac patients without depression, the mechanisms mediating this effect remain obscure. Depression is characterized by vulnerability to stress and heightened stress responsiveness, and stress can theoretically act through several biological pathways to contribute to excess mortality from CHD. Mechanisms connecting stress, depression and cardiovascular mortality have not been previously explored in detail. The purpose of this study was to assess the effects of stress and depression on myocardial perfusion and plasma cortisol concentrations in CHD patients. Patients with CHD with and without depression (n = 28) underwent single photon emission computed tomography imaging of myocardial perfusion at rest and during a stressful cognitive challenge. Severity of ischaemia was measured by summing perfusion defect scores across myocardial segments and subtracting out rest from stress scores. Plasma cortisol concentrations were measured at baseline and in response to the stressful challenge. There were no differences in stress-induced myocardial ischaemia or plasma cortisol response to stress between CHD patients with and without depression. Depressed CHD patients with a history of psychological trauma (n = 5) had an increase in stress-induced ischaemia scores [7; standard deviation (SD) = 5] compared with CHD patients with depression without a history of psychological trauma (2 SD = 2) and CHD patients without depression or psychological trauma (1; SD = 2) (F = 8.51; degree of freedom = 2,23; p = 0.007). Eighty per cent of CHD/depression trauma-exposed subjects had stress-induced ischaemia as opposed to 38 per cent of CHD/depression subjects without trauma exposure and 23 per cent of subjects with CHD without depression or trauma. Self-reported nervousness during the cognitive stressor was correlated with stress-induced ischaemia. These preliminary findings suggest that depression with a history of prior exposure to traumatic stress is associated with increased risk for stress-induced cardiovascular ischaemia.

Functional brain imaging alterations in acne patients treated with isotretinoin.

OBJECTIVE: Although there have been case reports suggesting a relationship between treatment with the acne medication isotretinoin and the development of depression and suicide, this topic remains controversial. In order for isotretinoin to cause depression, it must have an effect on the brain; however, the effects of isotretinoin on brain functioning in acne patients have not been established. The purpose of this study was to assess the effects of isotretinoin on brain functioning in acne patients. METHOD: Brain functioning in adults was measured with [(18)F]fluorodeoxyglucose positron emission tomography before and after 4 months of treatment with isotretinoin (N=13) or an antibiotic (N=15). RESULTS: Isotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression. There were no differences in the severity of depressive symptoms between the isotretinoin and antibiotic treatment groups before or after treatment. CONCLUSIONS: This study suggests that isotretinoin treatment is associated with changes in brain functioning.

Effects of phenytoin on memory, cognition and brain structure in post-traumatic stress disorder: a pilot study.

Phenytoin (Dilantin) is an anticonvulsant used in the treatment of epilepsy. It is believed to act by modulation of glutamatergic transmission. Because the neurobiology of post-traumatic stress disorder (PTSD) has been hypothesized to involve alterations in glutamatergic transmission with subsequention neurotoxicity, we assessed the effects of phenytoin on cognition and brain structure in PTSD patients. Phenytoin was administered in an open label fashion for 3 months to nine adult patients with PTSD related to a variety of traumas, including early abuse, combat and car accidents. Subjects underwent magnetic resonance imaging for measurement of whole brain and hippocampal volume, and neuropsychological testing of memory and cognition, before and after treatment. Phenytoin treatment resulted in a significant 6% increase in right brain volume (p < 0.05). Increased hippocampal volume was correlated with reductions in symptom severity as measured by the Clinician Administered PTSD Scale and improvements in executive function as measured by the Trails test. However, treatment associated improvements in memory and cognition did not achieve statistical significance. These findings suggest that phenytoin treatment may be associated with changes in brain structure in patients with PTSD.

Treatment of posttraumatic stress disorder with phenytoin: an open-label pilot study.

BACKGROUND: Phenytoin is an anticonvulsant used in the treatment of epilepsy. Its mechanism of action is incompletely understood but most likely involves modulation of glutamatergic transmission. The neurobiology of posttraumatic stress disorder (PTSD) has been hypothesized to involve, at least in part, alterations in glutamatergic transmission in the hippocampus and possibly other brain regions. The purpose of this study was to assess the effects of phenytoin on symptoms of PTSD. METHOD: Phenytoin was administered in an open-label fashion for 3 months to 9 adult male and female patients with DSM-IV PTSD related to a variety of traumas including childhood abuse, combat, and car accidents. Dosage was adjusted to maintain the therapeutic blood levels used in the treatment of epilepsy. Subjects were assessed before, during, and after treatment for PTSD with standardized dimensional measures of disease severity including the Clinician Administered PTSD Scale (CAPS), the Hamilton Rating Scale for Depression (HAM-D), and the Hamilton Rating Scale for Anxiety (HAM-A). Data were collected from November 2001 through June 2003. RESULTS: Phenytoin treatment resulted in a significant decrease in PTSD symptoms as measured with the CAPS (mean score = 65 pretreatment vs. 38 posttreatment) with reductions in each of the symptom clusters of intrusions, avoidance, and hyperarousal (p < .05). There were no significant decreases in symptoms of depression severity as measured with the HAM-D or anxiety severity as measured with the HAM-A. CONCLUSIONS: These findings suggest that phenytoin may be efficacious in the treatment of PTSD, possibly mediated through its antiglutamatergic effects. Randomized, controlled, double-blind clinical trials are indicated to further evaluate this medication in the treatment of PTSD.