Trichotillomania is characterized by recurrent pulling of one’s hair despite attempts of stopping, resulting in hair loss. Previously classified as impulse control disorder, it is now considered an obsessive-compulsive related disorder in DSM-5. First-line therapy is cognitive behavioural therapy (CBT), with strong support for habit reversal training. For pharmacological therapy, selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed. Clomipramine has been used but is limited by its side effect profile. Many patients continue to experience distressing symptoms despite current treatment methods.

Lamotrigine, an anticonvulsant medication, is frequently utilized by psychiatrists to treat conditions like Bipolar Disorder. However, its utility in treating Trichotillomania has not been explored. We are interested to find out if it could benefit patients who have not responded adequately to current available treatment.

We report a case of a lady suffering from Trichotillomania for many years with limited improvement despite active treatment. We follow her progress after being started on Lamotrigine for six months.

In our case, a lady with longstanding Trichotillomania has previously been treated with SSRIs and Chlomipramine with limited response. An incidental trial of Lamotrigine after stopping her other medications has led to sustained improvement and stabilization of her condition. A possible hypothesis on how Lamotrigine’s mode of action could have led to this improvement will explored in this paper.

This case illustrates the potential of Lamotrigine to treat Trichotillomania in someone who has not responded adequately to usual treatment and could be an area worth looking into for future research.

No significant relationships.

The significant clinical efficacy of lithium and lamotrigine in the described patients is consistent with the hypothesis that microdeletion of the SHANK3 gene may be associated with bipolar disorder.

The described phenotypes were characterized by intellectual disability, general speech underdevelopment, muscle hypotonia, and developmental dyspraxia. Their causal relationships with epileptic encephalopathy, schizophrenia, bipolar and hyperkinetic disorders have been analyzed.

Prospective studies of two patients with Phelan McDermid syndrome (22q13.3 microdeletions of the SHANK3 gene) within 10-12 years after genome scanning allowed describing the clinical polymorphism of developmental disorders. The sensitivity of psychotic symptoms to antipsychotic and mood stabilizer therapy has also been studied.

Manifest psychotic disorders in patients did not reveal an affinity for therapy with amisulpride, haloperidol, quetiapine, which demonstrated a partial therapeutic response to treatment with aripiprazole, which cast doubt on the possibility of qualifying psychotic symptoms in patients as the debut of schizophrenia. The partial therapeutic efficacy of combination therapy with aripiprazole and benzodiazepines (clonazepam/diazepam) qualified psychotic episodes in two patients with 22q13.3 syndrome as pediatric delirium. The significant clinical efficacy of lithium and lamotrigine in the described patients is consistent with the hypothesis that microdeletion of the SHANK3 gene may be associated with bipolar disorder.

The combination of lithium and lamotrigine may be recommended for the treatment of polymorbid mental disorders in patients with ASD and 22q13.3 syndrome. If lithium salts are poorly tolerated, a combination of lamotrigine and aripiprazole may be used to treat polymorbid mental disorders with confusion and catatonic symptoms in ASD.

No significant relationships.

Depressive episodes are common in bipolar illness. Treatment of bipolar depression is often problematic because standard antidepressants carry a number of disadvantages: apparent lower efficacy than in unipolar depression; risk of inducing mania; risk of inducing rapid cycling. Anticonvulsants such as carbamazepine, valproate and lamotrigine are useful in the management of bipolar disorder and they can prevent episodes of depression. There is less evidence that they have antidepressant efficacy but lamotrigine was shown to produce antidepressant effects in a placebo-controlled trial in bipolar depressed patients. Lamotrigine has a role in acute management of bipolar depression and is probably free of a risk of inducing mania or rapid cycling.

To determine the efficacy of lamotrigine in treatment of patients with bipolar depression.

Investigation of lamotrigine efficacy with bipolar depression in 3 month-follow-up and 6 months follow-up treatment with lamotrigine.

The sample consisted of 30 patients with bipolar depression, age range between 26 and 58. All subjects received monotherapy with lamotrigine in the period of six months. Subjects were assessed prior to therapy and in 3 and 6 months follow-up using the following instruments: The Clinical Global Impressions scale (CGI), and Hamilton Depression Rating Scale (HAM-D-21).

The difference between three assessments on CGI was statistically significant. The results indicate statistically significant reduction of depression on HAMD-21 following six months treatment with lamotrigine.

Lamotrigine proved to be efficient in the treatment of patients with bipolar depression for the subjects in this study.

Lamotrigine is a commonly used drug in the treatment of bipolar disorder. Although there are reports of its effectiveness in the management of bipolar disorder and comorbid obsessive-compulsive disorder (OCD), lamotrigine has also been associated with obsessionality in patients with bipolar disorder.

Charts of 8 patients with bipolar disorder who had de novo onset of obsessions and compulsions after the use of lamotrigine were reviewed. The Naranjo scale was used to assess the likelihood of patients developing OCD due to lamotrigine use.

Two to 8 months after the initiation of lamotrigine, patients with no such prior history developed obsessions and compulsions meeting the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for medication-induced OCD. In all except 1 patient, the symptoms resolved within a month of lamotrigine discontinuation.

Some patients with bipolar disorder may develop OCD after initiation of lamotrigine. Due to the inherent limitations of a case series, the findings should be interpreted with caution.

To meta-analytically summarize lamotrigine’s effectiveness and safety in unipolar and bipolar depression.

We conducted systematic PubMed and SCOPUS reviews (last search =10/01/2015) of randomized controlled trials comparing lamotrigine to placebo or other agents with antidepressant activity in unipolar or bipolar depression. We performed a random-effects meta-analysis of depression ratings, response, remission, and adverse effects calculating standardized mean difference (SMD) and risk ratio (RR) ±95% confidence intervals (CIs).

Eighteen studies (n=2152, duration=9.83 weeks) in patients with unipolar depression (studies=4, n=187; monotherapy vs lithium=1, augmentation of antidepressants vs placebo=3) or bipolar depression (studies=14, n=1965; monotherapy vs placebo=5, monotherapy vs lithium or olanzapine+fluoxetine=2, augmentation of antidepressants vs placebo=1, augmentation of mood stabilizers vs placebo=3, augmentation of mood stabilizers vs trancylpromine, citalopram, or inositol=3) were meta-analyzed. Lamotrigine’s efficacy for depressive symptoms did not differ significantly in monotherapy vs augmentation studies (vs. placebo: p=0.98, I2=0%; vs active agents: p=0.48, I2=0%) or in unipolar vs bipolar patients (vs placebo: p=0.60, I2=0%), allowing pooling of each placebo-controlled and active-controlled trials. Lamotrigine outperformed placebo regarding depressive symptoms (studies=11, n=713 vs n=696; SMD=–0.15, 95% CI=–0.27, –0.02, p=0.02, heterogeneity: p=0.24) and response (after removing one extreme outlier; RR=1.42, 95% CI=1.13–1.78; p=0.003, heterogeneity: p=0.08). Conversely, lamotrigine did not differ regarding efficacy on depressive symptoms, response, or remission from lithium, olanzapine+fluoxetine, citalopram, or inositol (studies=6, n=306 vs n=318, p-values=0.85–0.92). Adverse effects and all-cause/specific-cause discontinuation were similar across all comparisons.

Lamotrigine was superior to placebo in improving unipolar and bipolar depressive symptoms, without causing more frequent adverse effects/discontinuations. Lamotrigine did not differ from lithium, olanzapine+fluoxetine, citalopram, or inositol.

There have been no previous factor analytic studies of the Hamilton Depression Rating Scale (HDRS) in samples with bipolar I depression, and no investigations of the utility of any derived factors in determining treatment response in this condition. This study aimed to identify and compare factors of a 31-item version of the HDRS (HDRS-31) in large samples of patients with bipolar depression and Major Depressive Disorder (MDD), then examine the responsiveness of such factors to lamotrigine compared with placebo in the bipolar depressed sample.

This multivariate analytical study was performed on 2 large depressed samples (one bipolar and the other MDD) that had been recruited for separate, contemporaneous, double-blind placebo-controlled trials of lamotrigine. The 2 studies had similar designs and assessment tools, the major measures being the Montgomery–Asberg Depression Rating Scale (MADRS) and HDRS-31. To identify the constructs underlying the scale, exploratory factor analyses were conducted using HDRS-31 baseline scores. Treatment responsiveness in the bipolar depressed sample—as indicated by improvement in the total MADRS and HDRS-31, as well as HDRS factors—were examined using both a mixed-effects analysis and individual time-point t-tests.

Seven factors of the HDRS-31 were identified: I—“depressive cognitions,” II—“psychomotor retardation,” III—“insomnia,” IV—“hypersomnia,” V—“appetite and weight change,” VI—“anxiety,” and VII—“anergia.” A significant therapeutic effect of lamotrigine in bipolar depression was found for the “depressive cognitions” factor (from week 3) and “psychomotor retardation” (from week 4).

This study has identified 7 factors of the HDRS in a large sample of patients with bipolar depression. The results suggest that that the clinical benefits of lamotrigine in acute bipolar depression are primarily upon depressive cognitions and psychomotor slowing.