Biomedical subjects

Cristina M Del-Ben

Publications and source records attributed to Cristina M Del-Ben.

5 recordsLinked to original sources

PubMed2005

Does the panic attack activate the hypothalamic-pituitary-adrenal axis?

A bibliographic search has been performed in MEDLINE using cortisol and panic as key-words, occurring in the title and/or in the abstract. Human studies were selected, with no time limit. The following publications were excluded: review articles, case reports, panic attacks in disorders other than panic disorder, and studies on changes that occurred in-between panic attacks. The results showed that real-life panic attacks as well as those induced by selective panicogenic agents such as lactate and carbon dioxide do not activate the hypothalamic-pituitary-adrenal (HPA) axis. Agonists of the colecystokinin receptor B, such as the colecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a panic attack and thus, seem to activate the HPA axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increased anxiety in both normal subjects and panic patients raised stress hormone levels; among them are the alpha2-adrenergic antagonist yohimbine, the serotonergic agents 1-(m-chlorophenyl) piperazine (mCPP) and fenfluramine, as well as the psychostimulant agent caffeine. Therefore, the panic attack does not seem to activate the HPAaxis, in contrast to anticipatory anxiety.

Anxiety↗

PubMed2005

Subjective and neurovegetative changes in healthy volunteers and panic patients performing simulated public speaking.

Drug-free symptomatic panic patients, drug-treated nonsymptomatic patients and healthy controls were submitted to simulated public speaking. Subjective anxiety, cognitive impairment and discomfort measured by the visual analog mood scale as well as skin conductance level were higher in symptomatic patients than in controls at the beginning of the experimental session, nonsymptomatic patients lying in between. Subjective sedation, spontaneous fluctuations of skin conductance, heart rate and blood pressure were similar in the three groups. Preparation and performance of speech decreased sedation while increasing anxiety, cognitive impairment, level and fluctuations of skin conductance, heart rate and blood pressure. Anxiety, cognitive impairment and conductance level were less increased in symptomatic patients than in controls. Electrodermal activity, but not cardiovascular measures of sympathetic arousal correlated with anticipatory anxiety. Chronic treatment with serotonin uptake inhibitors attenuated the differences between panic patients and controls, supporting the participation of serotonin in panic disorder.

Adult↗

PubMed2005

Anxiety and salivary cortisol in symptomatic and nonsymptomatic panic patients and healthy volunteers performing simulated public speaking.

Anxiety and salivary cortisol were measured in subjects performing simulated public speaking (SPS), a procedure that has been neurobiologically related to panic disorder. The subjects were divided into three groups: 18 symptomatic panic patients, 16 nonsymptomatic, drug-treated panic patients, and 17 healthy controls. In the experimental session, subjective anxiety (Visual Analogue Mood Scale) and the total score of the Bodily Symptom Scale (BSS) were higher in symptomatic patients than in controls, with nonsymptomatic patients in between. Measures of cortisol taken at home showed that the level was higher at 9:00 h than at 23:00 h in every group, indicating a normal circadian regulation of the hypothalamic-pituitary-adrenal (HPA) axis in panic patients. Also in every group, the level of cortisol was high at the beginning of the experimental session and decreased after 70 min. This fall parallels the decrease in anxiety and BSS ratings, and appears to reflect habituation of initial, anticipatory anxiety. Preparation and performance of speech raised anxiety and BSS scores to the initial levels, but failed to increase cortisol measured over 60 min, starting at the end of the speech. Therefore, SPS does not seem to activate the HPA axis, as reported in panic attacks.

Adult↗

PubMed2005

The effect of citalopram pretreatment on neuronal responses to neuropsychological tasks in normal volunteers: an FMRI study.

Changes in serotonin neurotransmission have also been implicated in the etiology and treatment of impulse control disorders, depression, and anxiety. We have investigated the effect of enhancing serotonin function on fundamental brain processes that we have proposed are abnormal in these disorders. In all, 12 male volunteers received citalopram (7.5 mg intravenously) and placebo pretreatment in a single-blind crossover design before undertaking Go/No-go, Loss/No-loss, and covert (aversive) face emotion recognition tasks during functional magnetic resonance imaging (fMRI). Blood oxygenation level dependent responses were analyzed using Statistical Parametric Mapping (SPM2). The tasks activated prefrontal and subcortical regions generally consistent with literature with lateral orbitofrontal cortex (BA47) common to the three tasks. Citalopram pretreatment enhanced the right BA47 responses to the No-go condition, but attenuated this response to aversive faces. Attenuations were seen following citalopram in the medial orbitofrontal (BA11) responses to the No-go and No-loss (ie relative reward compared with Loss) conditions. The right amygdala response to aversive faces was attenuated by citalopram. These results support the involvement of serotonin in modulating basic processes involved in psychiatric disorders but argue for a process-specific, rather than general effect. The technique of combining drug challenge with fMRI (pharmacoMRI) has promise for investigating human psychiatric disorders.

Adult↗

PubMedDate not supplied

Stability of the diagnosis of first-episode psychosis made in an emergency setting.

OBJECTIVE: This study aimed at evaluating the stability of the first psychotic episode diagnosis in the emergency context. METHODS: Fifty-nine patients were selected during a 15-month period and were followed for an average of 19.35 +/- 6.12 months. The admission and discharge emergency diagnosis were compared with the longitudinal diagnosis, obtained by the application of Structured Clinical Interview for DSM-IV Axis I Disorders--clinical version at the end of the follow-up. Severity rating scales (Brief Psychiatric Rating Scale, Young Mania Rating Scale and Hamilton Rating Scale for Depression) were applied in the emergency assessment. RESULTS: Agreement between admission emergency diagnosis and longitudinal diagnosis was unsatisfactory (k=0.25), whereas that between emergency discharge and longitudinal diagnosis was satisfactory (k=0.57). Brief psychotic disorder diagnosis presented higher sensitivity rates but low specificity, comprising several false positives. Bipolar disorder had the highest rates of specificity. CONCLUSION: Brief psychotic disorder may not be a useful concept in the emergency assessment. A short period of observation can improve emergency psychiatric diagnosis.

Adolescent↗