Neuropsychiatric debut as a presentation of Guillain-Barré Syndrome: An atypical clinical case and literature review.

INTRODUCTION: Guillain Barré Syndrome (GBS) is an acute immune-mediated polyneuropathy most frequently presenting two to four weeks after an acute mild-moderately severe infection as progressive muscular weakness of the lower limbs extending proximally with dysreflexia and autonomic dysfunction. While GBS is typically believed to be isolated to the Peripheral Nervous System, Central Nervous System (CNS) and psychiatric manifestations as a sequela of the disease have been described in different imaging and clinical studies. Many variants of presentation of GBS have been recognized, however a case presenting with primarily psychiatric and autonomic dysfunction preceding muscle weakness has not been cited in the literatures to date. CASE PRESENTATION: We describe a 24-year-old previously healthy male presenting with behavioral symptoms including depression, anxiety, and amnesia, and autonomic dysfunction which preceded muscle weakness by two weeks. CNS imaging and blood work results were unremarkable. GBS was confirmed upon cerebral spinal fluid analysis remarkable for an important cytoalbuminologic dissociation and markedly elevated protein concentration. The patient responded well to five cycles of inpatient plasmapheresis and short-term selective serotonin reuptake inhibitor treatment with complete recovery of both neurological and behavioral symptoms. CONCLUSION: Though GBS is typically considered a peripheral neuropathy, evidence for CNS involvement exists; GBS should be considered within the differential diagnosis, and neurological features should be monitored, in a patient with new onset unclear psychiatric and CNS symptoms.

Modafinil Treatment of Cocaine Dependence: A Systematic Review and Meta-Analysis.

BACKGROUND: Currently, there is none FDA-approved medication to treat cocaine dependency. Studies conducted with various medications, including antipsychotics, antidepressants, anticonvulsants, and others, revealed inconsistent results. OBJECTIVES: To meta-analytically investigate the efficacy and safety of modafinil in the treatment of cocaine-dependent patients. METHODS: Randomized controlled trials with ≥20 subjects comparing the numerical therapeutic outcomes of modafinil with placebo were identified in databases, such as PUBMED, psycINFO, EMBASE, and Clinicaltrials.gov. Relevant data on efficacy and safety were extracted. Relative risk (RR) and standardized mean difference were applied for reporting dichotomous and continuous outcomes respectively. Random effects, subgroup, and meta-regression analyses were conducted to further explore the results and evaluate for any moderators. RESULTS: In total, 11 studies (participants = 896, duration = 6.7 ± 1.9 weeks) comparing modafinil with placebo were systematically analyzed, which indicated that modafinil was not superior to placebo in improving the treatment retention rate (studies = 11, participants = 891, RR = 1.030, 95% CI = 0.918-1.156, p = .613). Similarly, data from 7/11 studies did not evidence superiority of modafinil in achieving cocaine abstinence (participants = 696, RR = 1.259, 95% CI = 0.813-1.949, p = .302). However, subgroup analysis of six studies conducted in the United States demonstrated superiority of modafinil in cocaine abstinence rate (studies = 6, participants = 669, 95% CI = 1.027-2.020, p = 0.035). In addition, no evidence suggested modafinil-related discontinuation or specific adverse events than placebo. CONCLUSIONS: Overall, there is no evidence to conclude superiority of modafinil in increasing cocaine abstinence and treatment retention rate. However, promising result in subgroup analysis of cocaine abstinence, secondary outcomes, and good safety profile urged the need of larger studies to derive more conclusive results.

Clozapine Treatment of Olanzapine-induced Tardive Dyskinesia: A Case Report.

Tardive dyskinesias (TD) are serious, often irreversible side effects of dopamine blocking agents, most commonly first-generation antipsychotics. No definitive treatment exists, with different interventions showing inconsistent results. We report a case of TD presenting after 12 years of olanzapine therapy in a 66-year-old Hispanic male with paranoid schizophrenia. The TD symptoms were successfully treated within a few weeks by switching to clozapine. Two cases of olanzapine-induced TD treated with clozapine have previously been reported, but in those cases, the symptom onset was quicker, ranging from a few months to a few years after initiation of olanzapine therapy, and the treatment response was relatively slower. Clinicians should carefully monitor for symptoms of TD after prolonged treatment with olanzapine and other antipsychotics. If otherwise indicated for psychiatric treatment, clozapine can be considered a good choice for patients with TD in preventing or reversing the debilitating consequences of this condition.

Safety and tolerability of antidepressant co-treatment in acute major depressive disorder: results from a systematic review and exploratory meta-analysis.

INTRODUCTION: Although antidepressant (AD) monotherapy is recommended first-line for major depressive disorder (MDD), AD + AD co-treatment is common. AREAS COVERED: We conducted the first systematic review searching PubMed/MEDLINE/PsycInfo/Embase from database inception until 1 June 2015 for acute randomized trials in ≥ 20 adults with MDD comparing AD monotherapy with AD + AD co-treatment that reported quantitative data on adverse events (AEs). Meta-analyzing 23 studies (n = 2435, duration = 6.6 weeks) AD monotherapy and AD + AD co-treatment were similar regarding intolerability-related discontinuation (risk ratio [RR] = 1.38, 95% CI = 0.89 - 1.10) and frequency of ≥ 1 AE (RR = 1.19, 95% CI = 0.95 - 1.49). Nevertheless, AD + AD co-treatment was associated with significantly greater burden regarding 4/25 AEs (tremor: RR = 1.55, 95% CI = 1.01 - 2.38; sweating: RR = 1.95, 95% CI = 1.13 -3.38, ≥ 7% weight gain: RR = 3.15, 95% CI = 1.34 - 7.41; weight gain = 2.17, 95% CI = 0.71 - 3.63 kg), but not more CNS, gastrointestinal, sexual or alertness-related AEs. However, 11/25 AEs (44.0%) were reported in only 1 - 2 studies. Adding noradrenergic and specific serotonergic antidepressants (NaSSA) or tricyclic antidepressants (TCA) to selective serotonin reuptake inhibitors (SSRIs) was specifically associated with more AEs. EXPERT OPINION: The potential for increased AEs with AD + AD co-treatment needs to be considered vis-à-vis unclear efficacy benefits of this strategy. In particular, NaSSAs and TCAs should be added to SSRIs with caution. Clearly, more data on side-effect burden of AD + AD co-treatment are needed.