-
The Cochrane Database of Systematic... Nov 2023A panic attack is a discrete period of fear or anxiety that has a rapid onset and reaches a peak within 10 minutes. The main symptoms involve bodily systems, such as... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
A panic attack is a discrete period of fear or anxiety that has a rapid onset and reaches a peak within 10 minutes. The main symptoms involve bodily systems, such as racing heart, chest pain, sweating, shaking, dizziness, flushing, churning stomach, faintness and breathlessness. Other recognised panic attack symptoms involve fearful cognitions, such as the fear of collapse, going mad or dying, and derealisation (the sensation that the world is unreal). Panic disorder is common in the general population with a prevalence of 1% to 4%. The treatment of panic disorder includes psychological and pharmacological interventions, including antidepressants and benzodiazepines.
OBJECTIVES
To compare, via network meta-analysis, individual drugs (antidepressants and benzodiazepines) or placebo in terms of efficacy and acceptability in the acute treatment of panic disorder, with or without agoraphobia. To rank individual active drugs for panic disorder (antidepressants, benzodiazepines and placebo) according to their effectiveness and acceptability. To rank drug classes for panic disorder (selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), mono-amine oxidase inhibitors (MAOIs) and benzodiazepines (BDZs) and placebo) according to their effectiveness and acceptability. To explore heterogeneity and inconsistency between direct and indirect evidence in a network meta-analysis.
SEARCH METHODS
We searched the Cochrane Common Mental Disorders Specialised Register, CENTRAL, CDSR, MEDLINE, Ovid Embase and PsycINFO to 26 May 2022.
SELECTION CRITERIA
We included randomised controlled trials (RCTs) of people aged 18 years or older of either sex and any ethnicity with clinically diagnosed panic disorder, with or without agoraphobia. We included trials that compared the effectiveness of antidepressants and benzodiazepines with each other or with a placebo.
DATA COLLECTION AND ANALYSIS
Two authors independently screened titles/abstracts and full texts, extracted data and assessed risk of bias. We analysed dichotomous data and continuous data as risk ratios (RRs), mean differences (MD) or standardised mean differences (SMD): response to treatment (i.e. substantial improvement from baseline as defined by the original investigators: dichotomous outcome), total number of dropouts due to any reason (as a proxy measure of treatment acceptability: dichotomous outcome), remission (i.e. satisfactory end state as defined by global judgement of the original investigators: dichotomous outcome), panic symptom scales and global judgement (continuous outcome), frequency of panic attacks (as recorded, for example, by a panic diary; continuous outcome), agoraphobia (dichotomous outcome). We assessed the certainty of evidence using threshold analyses.
MAIN RESULTS
Overall, we included 70 trials in this review. Sample sizes ranged between 5 and 445 participants in each arm, and the total sample size per study ranged from 10 to 1168. Thirty-five studies included sample sizes of over 100 participants. There is evidence from 48 RCTs (N = 10,118) that most medications are more effective in the response outcome than placebo. In particular, diazepam, alprazolam, clonazepam, paroxetine, venlafaxine, clomipramine, fluoxetine and adinazolam showed the strongest effect, with diazepam, alprazolam and clonazepam ranking as the most effective. We found heterogeneity in most of the comparisons, but our threshold analyses suggest that this is unlikely to impact the findings of the network meta-analysis. Results from 64 RCTs (N = 12,310) suggest that most medications are associated with either a reduced or similar risk of dropouts to placebo. Alprazolam and diazepam were associated with a lower dropout rate compared to placebo and were ranked as the most tolerated of all the medications examined. Thirty-two RCTs (N = 8569) were included in the remission outcome. Most medications were more effective than placebo, namely desipramine, fluoxetine, clonazepam, diazepam, fluvoxamine, imipramine, venlafaxine and paroxetine, and their effects were clinically meaningful. Amongst these medications, desipramine and alprazolam were ranked highest. Thirty-five RCTs (N = 8826) are included in the continuous outcome reduction in panic scale scores. Brofaromine, clonazepam and reboxetine had the strongest reductions in panic symptoms compared to placebo, but results were based on either one trial or very small trials. Forty-one RCTs (N = 7853) are included in the frequency of panic attack outcome. Only clonazepam and alprazolam showed a strong reduction in the frequency of panic attacks compared to placebo, and were ranked highest. Twenty-six RCTs (N = 7044) provided data for agoraphobia. The strongest reductions in agoraphobia symptoms were found for citalopram, reboxetine, escitalopram, clomipramine and diazepam, compared to placebo. For the pooled intervention classes, we examined the two primary outcomes (response and dropout). The classes of medication were: SSRIs, SNRIs, TCAs, MAOIs and BDZs. For the response outcome, all classes of medications examined were more effective than placebo. TCAs as a class ranked as the most effective, followed by BDZs and MAOIs. SSRIs as a class ranked fifth on average, while SNRIs were ranked lowest. When we compared classes of medication with each other for the response outcome, we found no difference between classes. Comparisons between MAOIs and TCAs and between BDZs and TCAs also suggested no differences between these medications, but the results were imprecise. For the dropout outcome, BDZs were the only class associated with a lower dropout compared to placebo and were ranked first in terms of tolerability. The other classes did not show any difference in dropouts compared to placebo. In terms of ranking, TCAs are on average second to BDZs, followed by SNRIs, then by SSRIs and lastly by MAOIs. BDZs were associated with lower dropout rates compared to SSRIs, SNRIs and TCAs. The quality of the studies comparing antidepressants with placebo was moderate, while the quality of the studies comparing BDZs with placebo and antidepressants was low.
AUTHORS' CONCLUSIONS
In terms of efficacy, SSRIs, SNRIs (venlafaxine), TCAs, MAOIs and BDZs may be effective, with little difference between classes. However, it is important to note that the reliability of these findings may be limited due to the overall low quality of the studies, with all having unclear or high risk of bias across multiple domains. Within classes, some differences emerged. For example, amongst the SSRIs paroxetine and fluoxetine seem to have stronger evidence of efficacy than sertraline. Benzodiazepines appear to have a small but significant advantage in terms of tolerability (incidence of dropouts) over other classes.
Topics: Adult; Humans; Panic Disorder; Selective Serotonin Reuptake Inhibitors; Paroxetine; Fluoxetine; Venlafaxine Hydrochloride; Serotonin and Noradrenaline Reuptake Inhibitors; Alprazolam; Clomipramine; Reboxetine; Clonazepam; Desipramine; Network Meta-Analysis; Antidepressive Agents; Antidepressive Agents, Tricyclic; Benzodiazepines; Diazepam
PubMed: 38014714
DOI: 10.1002/14651858.CD012729.pub3 -
Epilepsy & Behavior Reports 2024A 51-year-old woman showed structural epilepsy following an atypical, nontraumatic intracranial hemorrhage in the right frontal area. Despite successful seizure control...
A 51-year-old woman showed structural epilepsy following an atypical, nontraumatic intracranial hemorrhage in the right frontal area. Despite successful seizure control with lamotrigine, she developed severe morning anxiety and panic attacks, leading to agoraphobia, social withdrawal, and psychogenic nonepileptic seizures. Neuropsychiatric and psychological assessments confirmed an anxiety disorder with no significant symptoms of depression. The patient received various psychopharmacological treatments with limited success. This case report illustrates that managing panic disorder in patients with structural epilepsy requires a comprehensive treatment approach that includes pharmacotherapy and psychotherapy. Differential diagnosis and accurate treatment are crucial because of the symptom overlap between panic attacks and -ictal fear. Screenings instruments such as the Panic and Agoraphobia Scale (PAS) can aid in assessing anxiety-related symptoms. First-line pharmacotherapy with selective serotonin reuptake inhibitors, especially sertraline, or venlafaxine can effectively reduce panic attacks and can be recommended in patients with epilepsy. Psychotherapy, particularly cognitive-behavioral therapy, is the treatment of choice. Referral to a psychiatrist is indicated when symptoms are severe or refractory to treatment.
PubMed: 38299123
DOI: 10.1016/j.ebr.2024.100646 -
Journal of Affective Disorders Oct 2023Maternal and paternal perinatal depression and anxiety are theorised to adversely impact infant development. Yet, few studies have assessed both mental health symptoms...
BACKGROUND
Maternal and paternal perinatal depression and anxiety are theorised to adversely impact infant development. Yet, few studies have assessed both mental health symptoms and clinical diagnoses within the one study. Moreover, research on fathers is limited. This study therefore aimed to examine the association between symptoms and diagnoses of maternal and paternal perinatal depression and anxiety with infant development.
METHOD
Data were from the Triple B Pregnancy Cohort Study. Participants included 1539 mothers and 793 partners. Depressive and anxiety symptoms were assessed using the Edinburgh Postnatal Depression Scale and Depression Anxiety Stress Scales. Major depressive disorder, generalized anxiety disorder, social anxiety disorder, panic disorder, and agoraphobia were assessed using the Composite International Diagnostic Interview in trimester three. Infant development was assessed at 12-months using the Bayley Scales of Infant and Toddler Development.
RESULTS
Antepartum, maternal depressive and anxiety symptoms were associated with poorer infant social-emotional (d = -0.11, p = .025) and language development (d = -0.16, p = .001). At 8-weeks postpartum, maternal anxiety symptoms were associated with poorer overall development (d = -0.11, p = .030). No association was observed for clinical diagnoses in mothers, nor paternal depressive and anxiety symptoms or clinical diagnoses; albeit risk estimates were largely in the expected direction of adverse effects on infant development.
CONCLUSIONS
Evidence suggests that maternal perinatal depression and anxiety symptoms may adversely impact infant development. Effects were small but findings underscore the importance of prevention, early screening and intervention, alongside consideration of other risk factors during early critical periods.
Topics: Male; Female; Pregnancy; Infant; Humans; Longitudinal Studies; Depression; Cohort Studies; Depressive Disorder, Major; Anxiety; Anxiety Disorders; Fathers; Mothers; Depression, Postpartum
PubMed: 37302506
DOI: 10.1016/j.jad.2023.06.020 -
Comprehensive Psychiatry Apr 2024Impulsivity is a common cognitive issue across several psychiatric illnesses but is most frequently associated with the DSM-5 Disruptive, Impulse Control and Conduct...
PURPOSE
Impulsivity is a common cognitive issue across several psychiatric illnesses but is most frequently associated with the DSM-5 Disruptive, Impulse Control and Conduct Disorders, ADHD, and addictive disorders. We hypothesized that a wide range of psychiatric disorders would be associated with elevated impulsivity, not just those commonly linked to impulsiveness. This study aimed to explore the relationship between impulsivity and various psychiatric disorders in young adults.
PROCEDURES
700 non-treatment seeking participants (aged 18-29 years) were enrolled from the general community, provided demographic information, and underwent a psychiatric evaluation to screen for various psychiatric disorders. Each participant then completed the Barratt Impulsiveness Scale (BIS), a self-report measure of impulsivity, followed by the Stop Signal Task (SST), a computerized stop-attention task that measures impulse control. Impulsivity levels across psychiatric disorders were examined by analyzing z-scores relative to controls.
MAIN FINDINGS
Patients with bulimia nervosa, comorbid panic disorder with agoraphobia, and borderline personality disorder showed the highest levels of attentional, motor, and non-planning impulsivity, respectively. The effect size of the difference in total BIS impulsivity was large (d > 0.8) for several conditions including eating, personality, addictive, and mood disorders. The effect size of the difference in impulsivity was not large for any of the measures of ADHD. As compared to other psychiatric disorders analyzed, trichotillomania showed the greatest levels of impulsivity as measured by SST.
PRINCIPAL CONCLUSIONS
This data indicates that a wide range of psychiatric disorders exhibit heightened impulsivity with findings differing across various cognitive domains. Comorbidity resulted in unique findings of elevated impulsivity. This may suggest utility in viewing impulsivity as a transdiagnostic factor for a broad range of psychiatric disorders. Future studies should analyze comorbidities and whether patient psychiatric medication impacts these findings.
Topics: Humans; Young Adult; Impulsive Behavior; Personality Disorders; Mood Disorders; Trichotillomania; Behavior, Addictive
PubMed: 38184857
DOI: 10.1016/j.comppsych.2023.152449 -
Frontiers in Psychology 2023A number of case studies describing hypnotherapy in the treatment of anxiety disorder patients have already been published. Only a few randomized controlled trials...
UNLABELLED
A number of case studies describing hypnotherapy in the treatment of anxiety disorder patients have already been published. Only a few randomized controlled trials (RCTs) investigated the efficacy of hypnotherapy but focused mainly on symptoms rather than specific mental disorders. The goal of this study was to investigate whether hypnotherapy (HT) was superior to a waitlist control group (WL) in the reduction of agoraphobia-related symptoms. Further goals were to report the feasibility of hypnotherapy as well as attrition and completion rates and detect (epi-)genetic variables, which might play a role in treatment outcome. This pilot study was based on a monocentric two-armed randomized controlled rater-blind clinical trial that was conducted between 2018 and 2020 with a waitlist control group. A total of 36 patients diagnosed with agoraphobia were randomized to either HT or WL. Patients in HT received individual outpatient treatment with hypnotherapy with 8 to 12 sessions for a period of 3 months. Patients in WL received HT after 3 months. Agoraphobia-related symptoms were assessed at baseline, after the treatment, and 3 months later in both groups with a clinician rating. The primary hypothesis concerning the difference between groups in the individual percentage symptom reduction could be confirmed in the intention-to-treat, not the per-protocol sample. Additionally, we applied repeated-measures analyses of variance and found a higher symptom decrease in HT compared with WL patients in three of the five imputed datasets. The dropout rate was low, and satisfaction with the treatment was high. HT patients experienced a strong symptom reduction after receiving hypnotherapy. WL patients improved slightly during the waiting period. The ValMet genotype had an effect on the agoraphobia-related symptoms as well as on DNA methylation levels. This is the first study to indicate that hypnotherapy performed better than a waitlist control group regarding the reduction in anxiety symptoms in an RCT. Future studies should confirm the efficacy of hypnotherapy and compare the treatment with a standard treatment for anxiety disorders in a larger trial. Future studies should also investigate whether hypnotic susceptibility is associated with ValMet genotype and could predict treatment success for HT.
CLINICAL TRIAL REGISTRATION
https://classic.clinicaltrials.gov/ct2/show/NCT03684577, identifier: NCT03684577.
PubMed: 37637902
DOI: 10.3389/fpsyg.2023.1213792 -
BMC Medicine Aug 2023Comorbidity is the rule rather than the exception for childhood and adolescent onset mental disorders, but we cannot predict its occurrence and do not know the neural...
Neurodevelopmental risk and adaptation as a model for comorbidity among internalizing and externalizing disorders: genomics and cell-specific expression enriched morphometric study.
BACKGROUND
Comorbidity is the rule rather than the exception for childhood and adolescent onset mental disorders, but we cannot predict its occurrence and do not know the neural mechanisms underlying comorbidity. We investigate if the effects of comorbid internalizing and externalizing disorders on anatomical differences represent a simple aggregate of the effects on each disorder and if these comorbidity-associated cortical surface differences relate to a distinct genetic underpinning.
METHODS
We studied the cortical surface area (SA) and thickness (CT) of 11,878 preadolescents (9-10 years) from the Adolescent Brain and Cognitive Development Study. Linear mixed models were implemented in comparative and association analyses among internalizing (dysthymia, major depressive disorder, disruptive mood dysregulation disorder, agoraphobia, panic disorder, specific phobia, separation anxiety disorder, social anxiety disorder, generalized anxiety disorder, post-traumatic stress disorder), externalizing (attention-deficit/hyperactivity disorder, oppositional defiant disorder, conduct disorder) diagnostic groups, a group with comorbidity of the two and a healthy control group. Genome-wide association analysis (GWAS) and cell type specificity analysis were performed on 4468 unrelated European participants from this cohort.
RESULTS
Smaller cortical surface area but higher thickness was noted across patient groups when compared to controls. Children with comorbid internalizing and externalizing disorders had more pronounced areal reduction than those without comorbidity, indicating an additive burden. In contrast, cortical thickness had a non-linear effect with comorbidity: the comorbid group had no significant CT differences, while those patient groups without comorbidity had significantly higher thickness compare to healthy controls. Distinct biological pathways were implicated in regional SA and CT differences. Specifically, CT differences were associated with immune-related processes implicating astrocytes and oligodendrocytes, while SA-related differences related mainly to inhibitory neurons.
CONCLUSION
The emergence of comorbidity across distinct clusters of psychopathology is unlikely to be due to a simple additive neurobiological effect alone. Distinct developmental risk moderated by immune-related adaptation processes, with unique genetic and cell-specific factors, may contribute to underlying SA and CT differences. Children with the highest risk but lowest resilience, both captured in their developmental morphometry, may develop a comorbid illness pattern.
Topics: Humans; Depressive Disorder, Major; Genome-Wide Association Study; Anxiety Disorders; Attention Deficit Disorder with Hyperactivity; Comorbidity; Genomics
PubMed: 37542243
DOI: 10.1186/s12916-023-02920-9