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The self-medication hypothesis suggests that patients diagnosed with schizophrenia might smoke as an attempt to self-medicate theirsymptoms. As a consequence, smoking cessation could worsen their clinical status.
Objectives
To assess the clinical changes associated with tobacco cessation in a sample of smoking outpatients with schizophrenia.
Methods
Sample: 63 smoking outpatients with DSM-IV Schizophrenia from three Mental Health Centers located in Northern Spain [77.0% males; mean age (SD) = 43.90 (8.72); average daily cigarette use (SD) = 27.99 (12.55)]. Instruments: (1) Clinical symptoms: Positive and Negative Symptoms Scale (PANSS), Hamilton Depression Rating Scale (HDRS), Clinical Global Impression (CGI). (2) Pattern of tobacco use: n° cigarettes/day; Expired carbon monoxide (CO ppm). Design: A quasi-experimental design with two groups was implemented: control group (GC − 18 patients not willing to stop smoking), and treatment group [TG − 45 patients in smoking cessation supported by nicotine patches or vareniclina (12 weeks)]. Patients were evaluated at baseline and at week 11 (end of program). Paired sample t-test was used to detect changes in clinical symptoms from baseline to follow-up.
Results
23.1% stopped smoking (from TG). No significant differences were found between baseline and follow-up scores (p>.05) among smokers and abstinent in PANSS subscales, HDRS and CGI.
Conclusions
Tobacco cessation did not have a significant effect on the clinical symptoms of this group of patients. Further studies should analyze the stability of these outcomes at longer follow-ups to confirm our results.
The self-medication hypothesis proposes that schizophrenia patients may smoke as an attempt to reduce their cognitive deficits, their symptoms or the antipsychotic side-effects.
Aim:
to identify the relationship between the smoking topography and psychopathology among outpatients with DSM-IV schizophrenia.
Method:
The sample included 26 smoking outpatients with DSM-IV schizophrenia from a Mental Health Center sited in the North of Spain [65.5% males; mean age (SD) = 44.66 (7.83)]. Instruments: (1) Psychopathology: Positive and Negative Syndrome Scales (PANSS); Clinical Global Impression of Severity (CGI-S); n° antipsychotic. (2) Pattern of tobacco use: n° cigarettes/day; Fargerstrom test for nicotine physical dependence; Glover-Nilsson test for nicotine psychological dependence; Expired carbon monoxide (CO ppm).
Results:
prevalence was 59.3% for non-heavy smokers [<30 cigarettes/day; Mean CO (SD)= 24 ppm (9.70)] and 40.7% for heavy smokers [≥30 cigarettes/day; Mean CO (SD) = 36 ppm (16.06)]. PANSS mean score (SD) = 54.07 (12.45); CGI-G mean score (SD) = 3.50 (1.17); Mean number of antipsychotic (SD) = 1.79 (0.88). No significant differences were found between the severity of the psychopatology (PANSS, CGI-S, n° antipsychotic) and all the variables of the pattern of tobacco use (n° cigarettes/day; expired carbon monoxide; Fargerstrom; Glover-Nilsson).
Conclusion:
In this sample of schizophrenia patients, there is no relation between the severity of psychopathology and the dependence of nicotine. However, the sample of this study is small.
Depression is a frequent mood disorder that affects around 33% of stroke patients and has been associated with both poorer outcome and increased mortality. Our aim was to test the possible association between inflammatory and neurotrophic molecular markers and the development of post-stroke depression.
Method
We studied 134 patients with a first episode of ischemic stroke without previous history of depression or speech disorders. We screened for the existence of major depression symptoms in accordance with DSM-IV criteria and a Yesavage Geriatric Depression Scale (GDS) score >11 at discharge and 1 month after stroke. At these times, serum levels of molecular markers of inflammation [interleukin (IL)−1β, IL-6, intracellular adhesion molecule 1 (ICAM-1), tumor necrosis factor (TNF)-α, leptin and high-sensitivity C-reactive protein (hs-CRP)] and neurotrophic factors [brain-derived neurotrophic factor (BDNF)] were measured by enzyme-linked immunosorbent assay (ELISA).
Results
Twenty-five patients (18.7%) were diagnosed as having major depression at discharge. Out of 104 patients who completed the follow-up period, 23 were depressed at 1 month (22.1%). Patients with major depression showed higher serum leptin levels at discharge [43.4 (23.4–60.2) v. 6.4 (3.7–16.8) ng/ml, p<0.001] and at 1 month after stroke [46.2 (34.0–117.7) v. 6.4 (3.4–12.2) ng/ml, p<0.001). Serum levels of leptin >20.7 ng/ml were independently associated with post-stroke depression [odds ratio (OR) 16.4, 95% confidence interval (CI) 5.2–51.5, p<0.0001]. Leptin levels were even higher in the eight patients who developed depression after discharge [114.6 (87.6–120.2) v. 7.2 (3.6–13.6) ng/ml, p<0.0001].
Conclusions
Serum leptin levels at discharge are found to be associated with post-stroke depression and may predict its development during the next month.
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