Preparar la cesación tabáquica en el trastorno mental grave: diagnóstico precoz y oportunidades de prevención / Prepare the smoking cessation in severe mental illness: Early diagnosis and prevention opportunities

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Smoking cessation opportunities in severe mental illness (tobacco intensive motivational and estimate risk - TIMER-): study protocol for a randomized controlled trial.

BACKGROUND: There is an increased risk of premature death in people with severe mental illness (SMI). Respiratory disorders and cardiovascular disease are leading causes of increased mortality rates in these patients, and tobacco consumption remains the most preventable risk factor involved. Developing new tools to motivate patients towards cessation of smoking is a high priority. Information on the motivational value of giving the lung age and prevention opportunities is unknown in this high-risk population. METHODS/DESIGN: This article describes in detail a protocol developed to evaluate an intensive motivational tool, based on the individual risks of pulmonary damage and prevention opportunities. It is designed as a randomized, 12-month, follow-up, multicenter study. A minimum of 204 smokers will be included, aged 40 years and older, all of whom are patients diagnosed with either schizophrenia or bipolar disorder (BD). Chronic obstructive pulmonary disease (COPD) will be evaluated using spirometry, and the diagnosis will then be validated by a pneumologist and the lung age estimated. Based on this value, a motivational message about prevention will be issued for the intervention group, which will be reinforced by individualized text messages over a period of 3 months. The efficacy of the method and the pulmonary damage variables will be evaluated: smoking cessation at the end of follow-up will be confirmed by cooximetry, and the COPD diagnosis and the severity of the staging for disease will be assessed. DISCUSSION: In the context of community care, screening and early detection of lung damage could potentially be used, together with mobile technology, in order to produce a prevention message, which may provide patients with SMI with a better chance of quitting smoking. TRIAL REGISTRATION: ClinicalTrials.gov, ID: NCT03583203 . Registered on 11 July 2018. Trial status: recruitment.

Effects of atypical antipsychotics on neurocognition in euthymic bipolar patients.

BACKGROUND: Different factors may influence cognitive functioning in bipolar disorder such as the effect of subsyndromal symptoms, the history of psychotic symptomatology or substance abuse, negative symptomatology, chronicity, sleep disturbances, and hormonal factors. The effect of pharmacologic treatment on cognition is still uncertain because of an insufficient number of studies examining this issue. OBJECTIVE: The aims of this study were to compare neuropsychologic performance of treated bipolar patients with that of controls, including unmedicated patients and healthy subjects, as well as to evaluate possible neurocognitive differences among 3 different atypical antipsychotics. RESEARCH DESIGN AND METHODS: A total of 119 subjects were included in the study. Of 79 Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition euthymic bipolar patients, 68 were treated with one atypical antipsychotic, quetiapine (n = 12), olanzapine (n = 26), or risperidone (n = 30). Sixteen patients were drug-free. The 4 groups were compared with a sample of drug-naïve patients and a healthy control group (n = 35) on several clinical and neuropsychologic variables, especially on the domains of attention, verbal memory, and executive functions. Euthymia was defined by a score of 6 or less at the Young Mania Rating Scale and a score of 8 or less at the Hamilton Depression Rating Scale for at least 6 months. RESULTS: The 5 groups did not differ in age, years of education, sex distribution, or estimated premorbid IQ. The 4 patients groups did not differ in chronicity, age of onset, total number of episodes, and number of hospitalizations. No differences were found regarding antipsychotic dosages between the groups. Bipolar patients performed poorly on most neuropsychologic measures as compared with healthy controls. After controlling for Hamilton Depression Rating Scale symptoms, no significant change in the results was observed. Because many patients with antipsychotic treatment had a history of psychotic symptoms, we performed multivariate analysis of covariance controlling for this variable. Bipolar patients taking 1 of the 3 antipsychotics presented with dose-independent significant deficits in most cognitive tasks compared with healthy controls. After several head-to-head group comparisons, the patients receiving quetiapine showed a better performance in learning task, short-term memory, and recognition task assessed with the California Verbal Learning Test and verbal fluency (P < .05). CONCLUSIONS: Our results confirm the findings of previous studies of cognitive deficits in bipolar disorder. Untreated euthymic patients showed better cognitive performance than did patients on atypical antipsychotics. Some iatrogenic-pharmacologic effect, therefore, cannot be excluded, but quetiapine seemed to be less associated with impairment in measures of verbal memory than olanzapine or risperidone. We suggest to use drugs in bipolar disorder with a lower risk of cognitive adverse effects. However, randomized controlled trials are urgently needed to give a definite answer to this critical problem.

Neurocognitive impairment in bipolar patients with and without history of psychosis.

OBJECTIVE: Little is known regarding the impact of psychotic symptoms on the cognitive functioning of bipolar patients. Findings from previous reports are controversial and mainly focused on current psychotic symptoms. The main aim of this study was to ascertain whether the history of psychotic symptoms was associated with greater cognitive impairment in euthymic bipolar patients. METHOD: Sixty-five euthymic bipolar disorder patients (DSM-IV criteria; 35 with a history of psychotic symptoms and 30 without such a history) were assessed through a neuropsychological battery targeting attention, psychomotor speed, verbal memory, and executive functions. Thirty-five healthy controls were also included in the study in order to compare the neuropsychological performance among groups. Multivariate analysis of covariance was performed controlling for the effect of residual depressive symptoms as a covariate. The study was conducted from June 2005 to June 2006. RESULTS: Bipolar patients with a history of psychotic symptoms showed a higher number of manic episodes and more hospitalizations than patients without such a history (both p < .001). Regarding neuropsychological performance, patients with a history of psychotic symptoms performed more poorly than those without such a history or controls in all verbal memory measures (p < .005). Furthermore, patients with a history of psychotic symptoms were more impaired on tasks related to executive functions compared to healthy controls (p < .05). History of psychotic symptoms was found to be a predictor of verbal memory impairment. CONCLUSIONS: Our findings suggest that the history of psychotic symptoms may partly account for the cognitive dysfunctions seen in euthymic bipolar patients, especially with regard to persistent verbal memory dysfunction, as well as with some executive dysfunctions.

Neurocognitive and clinical predictors of functional outcome in patients with schizophrenia and bipolar I disorder at one-year follow-up.

OBJECTIVE: Many studies have reported that cognitive ability may be predictive of the functional outcome for patients with schizophrenia. However, no study has prospectively examined these aspects in schizophrenia and bipolar disorders simultaneously. The present study attempted to analyze if neurocognition and clinical status predicts the real-life functioning for patients with schizophrenia or bipolar I disorder, using a longitudinal design. METHOD: Forty-seven schizophrenic and 43 bipolar I outpatients were assessed twice with a neurocognitive battery (Executive Functions, Working Memory, Verbal Memory, Visual Memory, Visual-Motor Processing, Vigilance, Vocabulary and Motor Speed tasks), clinical scales (the Positive and Negative Symptom Scale, the Hamilton Rating Scale for Depression and the Clinician Administered Rating Scale for Mania) and functional outcome measures (the Global Assessment of Functioning Scale, the WHO's Disability Assessment Scale and occupational adaptation level) over a one-year follow-up period. The cognitive performance of the patients was compared, at baseline and one year later, with that of 25 healthy subjects. RESULTS: In schizophrenia patients, global functioning one year later was predicted by a composite neurocognitive score and three specific domain (verbal memory, motor speed, vocabulary). Symptoms appeared to explain less of the variance in functioning. In bipolar I patients, changes in the composite neurocognitive score over one year, deficits in the visual/motor processing domain, severity of symptoms (psychotic, excitatory and affective symptoms) and premorbid adjustment at the first assessment were the variables that better predicted functioning or disability changes over follow-up period. CONCLUSIONS: Although the relationships between cognition, symptoms and functional capacity differ for schizophrenia or bipolar I patients, neuropsychological performance seems to be a principal longitudinal predictor of functioning in both disorders. Baseline neurocognition and cognitive changes over 12 months predicted changes in functioning over the same period, but only in bipolar I patients. These cognitive domains could be potential neurocognitive endophenotypes (endophenocognitypes) with regard to bipolar I disorder.

Persistent cognitive dysfunctions in bipolar I disorder and schizophrenic patients: a 3-year follow-up study.

BACKGROUND: Neurocognitive impairment has consistently been considered a central and stable feature in schizophrenia. As this possibility has been far less studied in bipolar disorder, we aimed to prospectively investigate the stability and specificity of cognitive performance in bipolar disorder compared to schizophrenia. METHODS: Fifteen DSM-IV bipolar type I patients and 15 schizophrenic patients were assessed twice with a comprehensive neuropsychological battery and the Positive and Negative Syndrome Scale over a 3-year follow-up. The cognitive performance of the groups was compared at baseline and 3 years later as a mean with that of 26 healthy volunteers. Endpoint and baseline assessments were also compared for each patient group in order to evaluate the stability of cognitive impairment. RESULTS: At both time points, bipolar and schizophrenic patients showed significant deficits on most of the cognitive tasks compared to healthy subjects. Overall, the cross-sectional cognitive profile was similar for both patient groups. Moreover, after controlling for age and length of illness, the two groups' cognitive function did not differ over time in any test. With the exception of the Stroop color-word interference task, performance at baseline for each test but neither length of illness nor diagnostic category predicted the endpoint performance. CONCLUSION: This preliminary study suggests that cognitive impairment is also mainly stable over time in bipolar I disorder and thus not specific to schizophrenia.

Specific executive/attentional deficits in patients with schizophrenia or bipolar disorder who have a positive family history of psychosis.

Neurocognitive impairments are well documented in patients with schizophrenia and their healthy first-degree biological relatives. Less is known about neuropsychological performance in bipolar disorders, but some studies indicate that, compared to schizophrenia, bipolar disorder displays a similar profile pattern with less severe deficits. The genetic and environmental contributions to the development of neurocognitive deficits are also unclear. This study explored the effect of a family history (FH) of psychotic disorders in first-degree relatives on a variety of cognitive domains (abstraction and flexibility, verbal fluency, verbal memory, motor activity and visual-motor processing/attention) in 30 patients with schizophrenia, and 24 type I bipolar patients. After adjusting the results for age, gender, education level and pre-morbid intelligence, patients with schizophrenia or bipolar disorder with positive FH (n=18) performed significantly worse than patients with negative FH (n=36) on the visual-motor processing/attention domain. These findings were independent of the specific diagnosis. Moreover, when logistic regression analysis was performed, poor Digit Symbol performance was the only predictor of belonging to the positive FH group. Our results are compatible with the existence of some common genetic factors between the illnesses, as well as the involvement of identical, or at least similar, disordered brain systems in both disorders. These findings are discussed within the context of the continuum model of psychosis.

Abnormal motor asymmetry only during bimanual movement in schizophrenic patients compared with healthy subjects.

In schizophrenia, research on motor asymmetry has focused on the direction and the degree of handedness using unimanual motor tests and tasks. However, typically both hands collaborate in the production of most manual movements. This study explored motor asymmetry exhibited during unimanual and bimanual tasks in schizophrenic and healthy subjects using a new experimental motor battery. Specifically, the authors investigated the motor indices of laterality during finger-tapping and hand-turning tasks in four unimanual and four bimanual conditions in 84 schizophrenic and 31 healthy subjects, all right-handed. The schizophrenic patients showed reduced motor asymmetries only during bimanual tapping compared with healthy subjects due to reduction in right-hand performance. These results stress the importance of considering bimanual conditions in the assessment of motor asymmetries, and suggest that it is necessary to use bimanual tasks to test hypotheses about abnormal motor lateralization in schizophrenia.