To assess the efficacy and safety of topiramate in treating binge eating disorder (BED), using a systematic review and meta-analysis of the available randomized clinical trials (RCTs).

The RCTs assessing topiramate vs placebo with or without adjunctive psychotherapy in BED were reviewed using a systematic search in the PubMed, Web of Science, PsycINFO, Cochrane Database of Systematic Review, and ClinicalTrials.gov search Websites, from inception to November 2019. Main outcomes were the changes in binge frequency, quality of life, and weight, respectively. Effect estimates were pooled using random-effect models and presented as risk ratios (RRs) or mean differences (MDs) and their 95% confidence interval (95% CI). Data extraction was performed by two independent reviewers.

Three studies were eligible for inclusion, involving 528 BED patients. Topiramate was found to be significantly more efficacious than placebo in reducing: (a) the number of binge episodes per week (MD = −1.31; 95% CI = −2.58 to −0.03; I2 = 94%); (b) the number of binge days per week (MD = −0.98; 95% CI = −1.80 to −0.16; I2 = 94%); and (c) weight (MD = −4.91 kg; 95% CI = −6.42 to −3.41; I2 = 10%). However, participants in the topiramate groups withdrew significantly more frequently for safety reasons, relative to placebo participants (RR = 1.90; 95% CI = 1.13-3.18, I2 = 0%).

Preliminary findings support a possible efficacy of topiramate for the treatment of BED, even if safety concerns could limit the practical use of this treatment in BED subjects.

Psychiatric prescribers typically assess adherence by patient or caregiver self-report. A new digital medicine (DM) technology provides objective data on adherence by using an ingestible event monitoring (IEM) sensor embedded within oral medication to track ingestion. Despite likely clinical benefit, adoption by prescribers will in part depend on attitudes toward and experience with digital health technology, learning style preference (LSP), and how the technology s utility and value are described.

is to identify attitudes, experiences, and proclivities toward DM platforms that may affect adoption of the IEM platform and provide direction on tailoring educational materials to maximize adoption. Methods A survey of prescribers treating seriously mentally ill patients was conducted to assess drivers/barriers to IEM adoption. Factor analysis was performed on 13 items representing prior experience with and attitudes toward DM. Factor scores were correlated with prescriber characteristics including attitude and experience with digital technologies, LSP, and level of focus on healthcare cost.

A total of 127 prescribers (56% female, 76% physicians, mean age 48.1yrs.) completed the survey. Over 90% agreed medication adherence is important, visits allow enough time to monitor adherence (84.1%), and tailoring treatment to level of adherence would be beneficial (92.9%). The majority (65.9%) preferred relying upon outcomes data as their learning style while 15.9% preferred opinion leader recommendations and 18.3% information about how the technology would affect practice efficiency. Factor analysis revealed four dimensions: Level of comfort with EHR; Concern over current ability to monitor medication adherence; Attitudes about value of DM applications; and Benefits vs cost of DM for payers. Women scored higher on attitudes about the value of digital applications (p<0.01). Providers who perceive non-adherence as costly, and those who believe DM could benefit providers and patients scored higher on the value of DM (p<.05). Those whose LSP focuses on improving efficiency and prescribers with a higher proportion of Medicaid/ uninsured patients displayed concern about their ability to monitor adherence (p<0.05). Willingness to be a Beta Test site for DM applications was positively correlated with concern about their ability to monitor adherence and attitudes about the value of DM (p <0.01).

Prescriber characteristics including LSP, focus on healthcare costs, and attitudes toward DM may be related to adoption of the IEM platform. Those with more Medicaid/ uninsured patients were more concerned about ability to monitor adherence while those focused-on cost and benefit to providers and patients viewed DM as part of a solution for managing outcomes and cost. Overall, LSP, patient panel size by payer type, and focus on healthcare cost containment should be considered when developing IEM provider training materials.

Otsuka Pharmaceutical Development & Commercialization, Inc.

The delusion of being a living animate non-animal object has not heretofore been reported.

A 21-year-old right-handed cisgender female, two months prior to presentation, noted stiffness and difficulty with ambulation. One-month prior to admission, she experienced recurrent depression with myriad vegetative and nonvegetative symptoms of depression. On admission her chief complaint was I am a tree, standing motionless and minimally responding to query. After treatment with quetiapine, mirtazapine and hydroxyzine for a one-week period, her perception of being a tree fully resolved.

Abnormalities in Mental Status Examination: Anxious mood repeatedly stating, I am a tree. Standing still for long periods of time, refusing blood pressure to be obtained and expressing fear of constricting flow. Neuropsychiatric Testing: Beck Depression Inventory Type II: 33 (severe depression)

The rapid response to risperidone is consistent with Cotard’s syndrome, which has been noted to respond rapidly to neuroleptics (Sharma, 2014). However, in Cotard’s syndrome, replacement by a living non-animal object has not hitherto been reported. Body infestation with animate objects, as in Ekbom syndrome, only includes animals not botanicals (Chaudhary, 2019). This could be viewed as Reverse Inanimate Capgras Syndrome: instead of an imposter replacing a close friend, who then is inserted into the sufferer; a tree has replaced the sufferer. Peradventure, this may fit into the construct of Intermetamorphosis, a misidentification syndrome associated with the belief that individuals have transformed into other persons (Jariwala, 2017). Botanical Intermetamorphosis, the belief by the sufferer that the other individual is transformed from a person into a plant has not been described. Reverse Intermetamorphosis is the projection of an external individual into the person suffering or a syndrome of altered physical and psychological identities of the self (Silva, 1990). However, in this situation, the objects are all human or animate animals not botanicals. In Fregoli syndrome, there is an altered physical identity of others. In Reverse Fregoli syndrome, the sufferer assumes the physical but not the psychological identity of the stranger (Silva, 1990). But in this instance, the stranger is human as opposed to a plant life form. In the current case there is only altered physical identity (into a tree) not psychological identity. The current case may also be interpreted as a Botanical Variant of Interparietal Syndrome. In this condition, parts of the body are perceived to be lifeless, due to lesions of the inferior parietal lobe including supramarginalis gyrus, angular gyrus and the basalis parietalis area (Angyal, 1935). Investigation for those whom have Intermetamorphosis, Fregoli syndrome, Capgras syndrome, Interparietal syndrome, and Cotard’s syndrome for the presence of delusions involving plant life is warranted.

For some time now, there has been a strong consensus that the migration process can influence the onset, course, development, outcome, and clinical aspects of psychiatric pathologies.

In this study, we have analyzed the influence of the migration process on the clinical expression of heroin use disorder (HUD). In a naturalistic case–control study, we compared, both at univariate and multivariate level, 30 migrant HUD (M-HUD) patients with 30 age/gender-matched Italian HUD (IT-HUD) patients. We also analyzed demographic data, drug addiction history, psychopathological symptoms, addictive behavior, and emotional reactivity to life events.

Compared with IT-HUD pairs, at HUD Agonist Opioid Treatment, M-HUD patients were characterized by inadequate income and the presence of legal problems. They were more frequently at stage 3 of heroin addiction, with a concomitantly less frequent use of stimulants. Their age at the onset of heroin use was greater than that of subjects in the IT-HUD group. HUD post-traumatic stress disorder spectrum was present and was more severe in all M-HUD patients, but grief reactions and maladaptive behavior were the most discriminant traits. No differences were found in terms of addictive behaviors related to heroin craving or with respect to the severity/typology of psychopathology specific to HUD.

The migratory process does not seem to be correlated with addictive behaviors or with psychopathology specific to HUD. It partly affects HUD history, and specifically correlates with emotional reactivity to loss and traumatic life events, so suggesting that in M-HUD individuals, the link between the migratory syndrome and HUD is very close.

Most antidepressants have a delayed onset of action and must be administered for several weeks to generate therapeutic effects. Trazodone is a serotonin antagonist and reuptake inhibitor approved for the treatment of major depressive disorder. The once-a-day (OAD) formulation of trazodone has an improved tolerability profile compared to its conventional formulations. In this study, we systematically reviewed the evidence available for the antidepressant efficacy and early improvement in depressive symptoms with trazodone OAD treatment.

We conducted a PubMed database search for randomized controlled trials published from 2005 to 2020.

Two studies, a placebo-controlled and an active-comparator (venlafaxine extended-release or XR) study were found. Both the studies demonstrated that trazodone exhibits antidepressant activity at a starting dose of 150 mg/day and results in statistically significant greater reduction in Hamilton Depression Rating Scale (HAM-D17) scores within 1 week of starting treatment compared to placebo or venlafaxine XR (P < .05). Trazodone also resulted in significant early improvement in the HAM-D17 sleep disturbance factor compared to placebo or venlafaxine XR at day 7 (P < .05). This clinical effect is supported by in vitro proprietary data for the affinity of trazodone for different target receptors. Activity at these receptors may underlie trazodone’s fast antidepressant action.

Trazodone, if properly dosed, can be an effective antidepressant with early onset of action and good tolerability. Future studies designed to specifically evaluate onset and timing of improvement of depressive symptoms remain necessary to confirm and extend these results.

To assess the effects of treatment with lurasidone on risk for metabolic syndrome (MetS) in patients with schizophrenia.

Rates of metabolic syndrome during treatment with lurasidone (40-160 mg/d) were analyzed using pooled, short-term data from three randomized, double-blind, placebo-controlled studies (vs olanzapine and quetiapine XR); long-term data from two active-comparator-controlled studies (vs risperidone and quetiapine XR); and data from two open-label studies in which patients were switched from olanzapine or risperidone to lurasidone.

MetS was defined based on the National Cholesterol Education Program criteria. In short-term studies, the odds of meeting criteria for MetS at week 6 LOCF (adjusted for baseline metabolic syndrome status) was similar for the lurasidone and placebo groups (OR = 1.18; [95% CI, 0.81-1.71]; P = .39), but the odds (vs placebo) were significantly greater for olanzapine (OR = 2.81; [95% CI, 1.53-5.15]; P < .001) and quetiapine (OR = 3.49; [95% CI, 1.93-6.29]; P < .0001). No dose effect was observed for lurasidone across the dose range of 40-160 mg/d. In long-term studies, the odds of MetS after 12 months of treatment was significantly higher for risperidone compared with lurasidone (OR = 2.12; 95% CI, 1.15-3.90; P = .016) and for quetiapine XR compared with lurasidone (OR = 3.92; 95% CI, 1.15-13.40; P = .029). In open-label extension studies, the rate of MetS decreased in patients switched to lurasidone after 6 weeks of treatment with olanzapine or 12 months of treatment with risperidone.

In this analysis of lurasidone clinical trials, the odds of developing metabolic syndrome were minimal during short- and long-term treatment with lurasidone (40-160 mg/d).

Prazosin has been an accepted treatment for patients with post-traumatic stress disorder (PTSD) who experience sleep disturbances, including nightmares. Results of a recent large randomized control trial did not find benefit of prazosin vs placebo in improving such outcomes. A meta-analysis that includes this most recent trial was conducted to examine the pooled effect of prazosin vs placebo on sleep disturbances and overall PTSD symptoms in patients with PTSD.

A systematic review of the published literature on trials comparing prazosin vs placebo for improvement of overall PTSD scores, nightmares, and sleep quality was conducted. Hedges’ g standardized mean differences (SMD) between prazosin and placebo were calculated for each outcome across studies.

Six randomized placebo-controlled studies representing 429 patients were included in the analysis, including two studies with a crossover design. Results showed prazosin significantly improved overall PTSD scores (SMD = −0.31; 95% confidence intervals [CI]: −0.62, −0.01), nightmares (SMD = −0.75; 95% CI: −1.24, −0.27), and sleep quality (SMD = −0.57; 95% CI: −1.02, −0.13). In the largest trial, prazosin showed a reduction in clinical outcome measures similar to past studies, but a relatively large placebo effect size, particularly for nightmares, contributed to no treatment differences.

Despite the results of a recent, large randomized study, pooled effect estimates show that prazosin has a statistically significant benefit on PTSD symptoms and sleep disturbances. Limitations that should be considered include heterogeneity of study design and study populations as well as the small number of studies conducted and included in this meta-analysis.

The aim of this fixed-dose study was to evaluate the efficacy and safety of dasotraline in the treatment of patients with binge-eating disorder (BED).

Patients meeting Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria for BED were randomized to 12 weeks of double-blind treatment with fixed doses of dasotraline (4 and 6 mg/d), or placebo. The primary efficacy endpoint was change in number of binge-eating (BE) days per week at week 12. Secondary efficacy endpoints included week 12 change on the BE CGI-Severity Scale (BE-CGI-S) and the Yale-Brown Obsessive–Compulsive Scale Modified for BE (YBOCS-BE).

At week 12, treatment with dasotraline was associated with significant improvement in number of BE days per week on the dose of 6 mg/d (N = 162) vs placebo (N = 162; −3.47 vs −2.92; P = .0045), but not 4 mg/d (N = 161; −3.21). Improvement vs placebo was observed for dasotraline 6 and 4 mg/d, respectively, on the BE-CGI-S (effect size [ES]: 0.37 and 0.27) and on the YBOCS-BE total score (ES: 0.43 and 0.29). The most common adverse events on dasotraline were insomnia, dry mouth, headache, decreased appetite, nausea, and anxiety. Changes in blood pressure and pulse were minimal.

Treatment with dasotraline 6 mg/d (but not 4 mg/d) was associated with significantly greater reduction in BE days per week. Both doses of dasotraline were generally safe and well-tolerated and resulted in global improvement on the BE-CGI-S, as well as improvement in BE related obsessional thoughts and compulsive behaviors on the YBOCS-BE. These results confirm the findings of a previous flexible dose study.

The main objectives of this case study are 1. Clinicians facing symptoms that are difficult to interpret should exercise caution in diagnosing conversion disorder. 2. Increasing awareness about rare neurological conditions may appear as psychogenic illnesses. 3. Clinicians be advocate for their patients.

Conversion disorder is a mental condition in which a person present with one or more symptoms of altered voluntary motor or sensory function, or other neurologic symptoms that cannot be explained by medical evaluation. Stiff person syndrome (SPS) is a disabling autoimmune central nervous system disorder characterized by progressive muscle rigidity, gait impairment, with superimposed painful spasms. SPS is commonly associated with high anti-glutamic acid decarboxylase (GAD) antibody titers. The dominant antigen recognized by these antibodies is the GABA-synthesizing enzyme GAD.

Patient X, a 17-year-old Hispanic American female who presented to the Child and Adolescent Psychiatry Clinic with the complaint of ataxia & aphasia associated with anxiety. Patient was referred by the neurology clinic after they could not establish any organic cause of her ataxia or aphasia. After thorough evaluation at the child psychiatry clinic she was given the diagnosis of anxiety secondary to ataxia and aphasia and r/o Conversion Disorder. She was initiated treatment with sertraline for her anxiety. Her sertraline dose was increased gradually up to 100 mg daily. From the beginning the patient also received counseling & physical therapy. With these combination of treatments, patient’s symptoms did not get any better. Her symptoms actually got worse over time. At this point, the Child Psychiatry Clinic sent a message to the neurology clinic for further evaluation of patient due to her progressive gait and speech impairments.

The neurology clinic saw the patient again and did further testing. The patient was positive for high titers of anti-glutamic acid decarboxylase antibodies (Anti-GAD). At this point, the patient was given the diagnosis of Stiff Person Syndrome. Patient was admitted to the hospital for further management. She was treated with benzodiazepines, IV immune globulin, & steroid. Soon after discharge from the hospital, the patient was seen at the Child Psychiatric Clinic. The patient’s mother reported, after the in-patient treatment, the patient’s symptoms improved.

It is essential for clinicians to look for neurologic & other general medical conditions while evaluating a patient with possible conversion disorder. A systematic review of 27 studies found that among 1466 patients initially diagnosed with conversion symptoms, the frequency of misdiagnosis was approximately 4 percent.

References. BMJ. 2005;331(7523):989. Epub Oct 13. Childhood onset of stiff-man syndrome. JAMA Neurol. 2013;70(12):1531. J Neurol Neurosurg Psychiatry. 2015 Aug; 86(8):840–8. Epub 2014 Dec 15.

Depression is considered to be the most difficult to treat phase of bipolar disorder as patients experience residual symptoms causing long-term disability. This work aims to explore the role of add-on stimulant and stimulant-like medication in resistant bipolar depression patients.

Systematic review of add-on stimulants and stimulant-like drugs in resistant bipolar depression by following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Analysis was performed using the random-effects models. Heterogeneity was evaluated with Cochran’s Q and I2 statistics.

Six randomized controlled trials of add-on modafinil, armodafinil, and lisdexamphetamine (LDX) (n = 813) vs placebo (n = 815) in the treatment of resistant bipolar depression were included. These drugs were more likely to induce remission from an episode of resistant bipolar depression (relative risk [RR] = 1.37; 95% confidence interval [CI]: 1.06-1.77; number needed to treat for an additional beneficial outcome = 16). Moreover, they did not induce more dropouts than placebo (RR = 1.04; 95% CI: 0.91-1.18), nor did they increase the risk of adverse effects (53/772 vs 41/771) at the end of treatment (RR = 1.30; 95% CI: 0.81-2.10; number needed to treat for an additional harmful outcome = 62). Suicidality and manic switch were not affected by active treatment. Heterogeneity was low (Cochran’s Q: P > .05), but sometimes with a large CI.

LDX, modafinil, and armodafinil seem to offer a reasonably well-tolerated and safe treatment in resistant bipolar depression. Treatment guidelines should, therefore, be revised to include these medications earlier in the therapeutic algorithm for resistant acute bipolar depression. Further research is, however, necessary for the elucidation of the clinical usefulness of these and other similar compounds.

To explore relationships among post-traumatic stress disorder (PTSD), depressive spectrum symptoms, and intrusiveness in subjects who survived the crash of a train derailed carrying liquefied petroleum gas and exploded causing a fire.

A sample of 111 subjects was enrolled in Viareggio, Italy. AMOS version 21 (IBM Corp, 2012) was utilized for a structural equation model-path analysis to model the direct and indirect links between the exposure to the traumatic event, the occurrence of depressive symptoms, and intrusiveness. Subjects were administered with the SCID-IV (Structured Clinical Interview for DSM-IV), the Questionnaire for Mood Spectrum (MOODS-SR)-Last Month version, the Trauma and Loss Spectrum Questionnaire (TALS-SR), and the Impact of Event Scale-Revised version (IES-R).

Sixty-six (66/111; 59.4%) subjects met SCID-IV criteria for PTSD. Indices of goodness of fit were as followed: χ2/df = 0.2 P = .6; comparative fit index = 1 and root mean square error of approximation = 0.0001. A significant path coefficient for direct effect of potential traumatic events on depressive symptoms (β = 0.25; P < .04) and from depressive symptoms to intrusiveness (β = 0.34; P < .003) was found. An indirect effect was also observed: standardized value of potential traumatic events on intrusiveness was 0.86. The mediating factor of this indirect effect path was represented by depressive symptoms. Potential traumatic events explained 6.2% of the variance of depressive symptoms; 11.8% of the variance of intrusiveness was accounted for traumatic event and depressive symptoms.

Path analysis led us to speculate that depression symptoms might have mediated the relationship between the exposure to potential traumatic events and intrusiveness for the onset of PTSD.

To (1) confirm whether the Habit, Reward, and Fear Scale is able to generate a 3-factor solution in a population of obsessive-compulsive disorder and alcohol use disorder (AUD) patients; (2) compare these clinical groups in their habit, reward, and fear motivations; and (3) investigate whether homogenous subgroups can be identified to resolve heterogeneity within and across disorders based on the motivations driving ritualistic and drinking behaviors.

One hundred and thirty-four obsessive-compulsive disorder (n = 76) or AUD (n = 58) patients were assessed with a battery of scales including the Habit, Reward, and Fear Scale, the Yale-Brown Obsessive-Compulsive Scale, the Alcohol Dependence Scale, the Behavioral Inhibition/Activation System Scale, and the Urgency, (lack of ) Premeditation, (lack of ) Perseverance, Sensation Seeking, and Positive Urgency Impulsive Behavior Scale.

A 3-factor solution reflecting habit, reward, and fear subscores explained 56.6% of the total variance of the Habit, Reward, and Fear Scale. Although the habit and fear subscores were significantly higher in obsessive-compulsive disorder (OCD) and the reward subscores were significantly greater in AUD patients, a cluster analysis identified that the 3 clusters were each characterized by differing proportions of OCD and AUD patients.

While affective (reward- and fear-driven) and nonaffective (habitual) motivations for repetitive behaviors seem dissociable from each other, it is possible to identify subgroups in a transdiagnostic manner based on motivations that do not match perfectly motivations that usually described in OCD and AUD patients.