Yu Lee

Association between Serotonin Transporter Gene Polymorphism and Eating Disorders: A Meta-Analytic Study

OBJECTIVE Compelling evidence has suggested a role for serotonin system dysfunction in the pathogenesis of eating disorders (EDs), including anorexia nervosa (AN) and bulimia nervosa (BN). Studies have examined the association between EDs and a functional polymorphism of the serotonin transporter gene promoter (5-HTTLPR). These studies have yielded inconsistent results. The present study aimed to determine conclusively whether there is an association by using a meta-analytic method. METHOD Data of over 2,000 participants from eight independent case-controlassociation studies were pooled by using a random effects model. RESULTS AN was found to be significantly associated with the S allele (p < .001) and S carrier (SS + LS) genotype (p = .007). However, BN was associated neither with the S allele (p = .49) nor with the S carrier genotype (p = .33). DISCUSSION These results suggested that the genetic variance of the serotonin transporter gene promoter contributed to the susceptibility of AN.

Low-dose escitalopram for 2 days associated with corrected QT interval prolongation in a middle-aged woman: a case report and literature review

Prolongation of the corrected QT interval (QTc) on the electrocardiography is an important clinical condition because it increases the risk of torsade de pointes, a medical emergency that can cause sudden cardiac death. QTc prolongation can be induced by many drugs, including antipsychotics and tricyclic antidepressants (TCAs). Compared with TCAs, use of selective serotonin reuptake inhibitors (SSRIs) was less likely to cause severe cardiac adverse effects. Escitalopram, one of the SSRIs, has shown significant antidepressant efficacy and well tolerability. Here, we present one female patient showing QTc prolongation induced by low-dose (5 mg/day) treatment of escitalopram for 2 days. The QTc returned to normal soon after discontinuation of escitalopram. Clinicians should be cautious about cardiac effects when using a SSRI, even in a low dose.

Ziprasidone-induced tardive laryngeal dystonia: a case report

Tardive laryngeal dystonia, a rare form of dystonic syndrome, was only reported to be induced by typical antipsychotics. Here, we report one case of ziprasidone-induced tardive laryngeal dystonia in a schizophrenic female patient, who showed dysphonia, hoarseness and dyspnea after taking ziprasidone 120 mg/day for 8 months. These symptoms were significantly improved after discontinuing ziprasidone and increasing the dose of trihexyphenidyl for 1 week. Although atypical antipsychotics are associated with a lower risk of extrapyramidal symptoms, caution should be taken for any tardive dystonic movement when using these medications.

Duloxetine-related tardive dystonia and tardive dyskinesia: a case report

Tardive dyskinesia and tardive dystonia are caused by dopamine receptor blocking agents, mostly antipsychotics and sometimes antidepressants or calcium channel blockers. Duloxetine-related tardive syndrome is rarely reported in the literature. We report one case of tardive dystonia and tardive dyskinesia occurring in a 58-year-old female with major depressive disorder, who developed distressing oral dyskinesia, mandibular dystonia with trismus and dystonia over left neck after treatment of duloxetine (30-60 mg per day) for 18 months. Despite discontinuation of duloxetine, she only obtained partial remission. Even though this association has been rarely reported, duloxetine may pose a potential risk of inducing tardive syndrome. Clinicians should cautiously detect early signs of movement abnormality when prescribing antidepressants.

Prevalence and risk factors of depressive disorder in caregivers of patients with head and neck cancer

The purpose of this study is to examine the prevalence and risk factors of depressive disorder in caregivers of patients with head and neck cancer.

Tardive dystonia and tardive sensory syndrome related to trazodone: A case report

Dystonia is a movement disorder characterized by involuntary, patterned, directional, and often sustained muscle contractions that produce abnormal postures or repetitive movements. Dystonia can be reduced by a tactile or proprioceptive sensory trick. For example, voluntary activities, such as talking or chewing, could suppress eye closure in blepharospasm or jaw opening in oromandibular dystonia. Tardive dystonia is often associated with dopamine-receptor blocking agents such as antipsychotic drugs, during or within 2 months after drug treatment (Burke et al., 1982). When pain or sensory discomfort coexists with tardive dystonia, it is known as tardive sensory syndrome (Jankovic, 1995). In recent years, antidepressants, such as serotonin reuptake inhibitors, are reported to cause tardive syndromes (Sandler, 1996; Boffa and Lofchy, 2000). Trazodone is a potent antagonist of serotonin 5-HT2A and 5-HT2C receptors, aweak inhibitor of serotonin reuptake, a moderate to highly potent α-adrenoceptor antagonist (especially to α1), and a moderate histaminergic (H1) antagonist. Trazodone can also inhibit recombinant T-type calcium channels (Kraus et al., 2007). Trazodone was observed to induce acute dystonia in two case reports (Kramer et al.,1986; Lewis et al., 1997). To our knowledge, therewas no previous report of tardive dystonia or tardive sensory syndrome associated with trazodone.

Electroconvulsive therapy without consent from patients: One‐year follow‐up study

No previous study has been designed to analyze the reasons for electroconvulsive therapy (ECT) without patients’ consent. In the present study we compared the clinical characteristics and one‐year outcomes between patients with refusal to undergo ECT and patients without competency for ECT consent.

Antidepressant-induced Tardive Syndrome: a Retrospective Epidemiological Study

INTRODUCTION The impact of using antidepressant on the occurrence of tardive syndrome is rarely studied. Here we aimed to investigate the prevalence of various types of antidepressant induced tardive syndrome. METHODS This study was conducted by means of a retrospective survey. Subjects receiving antidepressant(s) for over 6 months, but no other agents that may cause involuntary movements, were consecutively recruited. Tardive syndrome was evaluated in every included subject. Possible confounding medical conditions were carefully ruled out. RESULTS Of the 158 included subjects, 22 (14.0 %) were found to have at least one tardive syndrome. The prevalence of subtypes of tardive syndromes was: tardive dystonia: 10.8 %, tardive dykinesia: 3.2 %, tardive tremor: 1.3 %, tardive parkinsonism: 1.3 %, tardive tics: 1.3 %, tardive sensory syndrome: 1.3 %, and tardive myoclonus: 0.6 %. Using serotonin-norepinephrine reuptake inhibitors and previous marital status significantly increase the risk of tardive syndrome. DISCUSSION This study showed that antidepressants may induce various types of tardive syndrome, of which tardive dystonia is the predominant form. Clinicians should be cautious of this infrequent but distressing adverse effect when using antidepressants.

Repeated suicide attempts among suicidal cases: Outcome of one-year follow-up

To assess the mortality rates and risk factors involved in repeated suicide attempts.

A Case Report of Catatonia and Neuroleptic Malignant Syndrome With Multiple Treatment Modalities: Short Communication and Literature Review.

AbstractWe describe a case with complicated clinical presentations who was difficult to treat. We described the possible etiologies and differential diagnosis of neuroleptic malignant syndrome (NMS), catatonia, and infection, in details. This patient was also referred to neuro-intensive care unit for extensive workup and treatments by neurologist guidelines. In addition, we also used lorazepam–diazepam protocol and antipsychotics, but both failed to completely relieve her symptoms. She eventually responded to electroconvulsive therapy (ECT).A 60-year-old female patient with schizophrenia was diagnosed to suspected pneumonia, urinary tract infection, and retarded catatonia at first. The brain computed tomography revealed no significant finding. She developed NMS caused by the administration of low-dose quetiapine (200 mg) after carbamazepine was discontinued. The Francis–Yacoub NMS rating scale (F-Y scale) total score was 90. We utilized lorazepam–diazepam protocol and prescribed bromocriptine and amantadine, but NMS was not improved. Meanwhile, we arranged the brain magnetic resonance imaging to survey the physical problem, which revealed agenesis of septum pellucidum and dilated lateral ventricles. She was then transferred to the neuro-intensive care unit on the 15th hospital day for complete study. The results of cerebrospinal fluid study and electroencephalography were unremarkable. She was transferred back to psychiatric ward on the 21st hospital day with residual catatonic and parkinsonian symptoms of NMS, and the F-Y scale total score was 63. Finally, her residual catatonic condition that followed NMS got improved after 11 sessions of ECT. On the 47th hospital day, the F-Y scale total score was 9.This report underscores that the ECT is an effective treatment for a patient of NMS when other treatments have failed.