Bupropion Overdose Complicated by Cardiogenic Shock Requiring Vasopressor Support and Lipid Emulsion Therapy

BackgroundBupropion overdose is a commonly encountered presentation in the emergency department (ED). While the majority of cases resolve with supportive care, serious adverse effects, including seizures, cardiogenic shock, and death, can occur. Intravenous lipid emulsion (ILE) therapy has been utilized for a multitude of poisonings with varying levels of success. Although a number of cases suggest the value of ILE therapy in cases of bupropion overdose, more recent data propose that its role may be overstated.Case ReportA young woman presented to the ED with altered mental status complicated by seizure after bupropion overdose. She subsequently developed cardiogenic shock requiring vasopressor support. Bedside echocardiogram revealed a decreased left ventricular ejection fraction (LVEF). She received ILE therapy with significant improvement in both hemodynamic status and LVEF by bedside ultrasound.Why Should an Emergency Physician Be Aware of This?Although the majority of patients presenting with bupropion overdose improve with supportive care, life-threatening sequelae are possible. ILE therapy has shown promise in a variety of different overdose situations, although the evidence in cases of bupropion poisoning has been varied, and it has traditionally been utilized as a last-line rescue modality. Based on hemodynamic parameters and bedside ultrasound, this case suggests that early initiation of ILE therapy should be considered in these cases, as the potential benefits likely outweigh the theoretical risks.     

Bupropion improved apathy in behavioral variant frontotemporal dementia: a case report

ABSTRACT

Apathy is a common neurobehavioral sign in cases of behavioral variant frontotemporal dementia. However, there is still no established sustained effective treatment. We present the case of a 65-year-old man with behavioral variant frontotemporal dementia who suffered from severe apathy, but his apathy improved after a 10-month period of bupropion treatment. His single photon emission computed tomography report also showed slight improvement. To the best of our knowledge, such a case with imaging evidence has never been reported. Further studies to correlate the effects of bupropion on apathy in behavioral variant frontotemporal dementia patients are clearly needed.     

Restoration of Serotonin Neuronal Firing Following Long-Term Administration of Bupropion but Not Paroxetine in Olfactory Bulbectomized Rats

Background:

Olfactory bulbectomized rats generally manifest many of the neurochemical, physiological, and behavioral features of major depressive disorder in humans. Another interesting feature of this model is that it responds to chronic but not acute antidepressant treatments, including selective serotonin reuptake inhibitors. The purpose of the present study was first to characterize the firing activity of dorsal raphe serotonin neurons in olfactory bulbectomized rats and then examine the effects of 2 antidepressants, bupropion and paroxetine.

Methods:

Olfactory bulbectomy was performed by aspirating olfactory bulbs in anesthetized rats. Vehicle and drugs were delivered for 2 and 14 days via subcutaneously implanted minipumps. In vivo electrophysiological recordings were carried out in male anesthetized Sprague-Dawley rats.

Results:

Following ablation of olfactory bulbs, the firing rate of serotonin neurons was decreased by 36%, leaving those of norepinephrine and dopamine neurons unchanged. In olfactory bulbectomized rats, bupropion (30mg/kg/d) restored the firing rate of serotonin neurons to the control level following 2- and 14-day administration and also induced an increase in the tonic activation of serotonin_1A receptors; paroxetine (10mg/kg/d) did not result in a return to normal of the attenuated firing of serotonin neurons in olfactory bulbectomized rats. In the hippocampus, although at a higher dose of WAY 100635 than that required in bupropion-treated animals, paroxetine administration also resulted in an increase in the tonic activation of serotonin_1A receptors.

Conclusions:

The present results indicate that unlike paroxetine, bupropion administration normalized serotonin neuronal activity and increased tonic activation of the serotonin_1A receptors in hippocampus.     

Efficacy of bupropion for relapse prevention in smokers with and without a past history of major depression

BACKGROUND: This study evaluated the efficacy of bupropion for relapse prevention in smokers with and without a past history of major depressive disorder. Changes in depressive symptoms were also examined. DESIGN: Data were gathered prospectively from a randomized, double-blind relapse prevention trial of bupropion conducted at five study sites. A total of 784 smokers (54% female, 97% white) were enrolled. Using the Structured Clinical Interview for Depression, 17% of the subjects reported a past history of major depressive disorder at baseline. All subjects received open-label bupropion SR (300 mg/d) for 7 weeks. Subjects abstinent from smoking at the end of 7 weeks (N = 429) were randomized to bupropion SR (300 mg/d) or placebo for the remainder of the year and followed for 1 year off medication. The primary outcome measures were median time to relapse to smoking and the 7-day point-prevalence smoking abstinence rate. Self-reported abstinence from smoking was verified by expired air carbon monoxide. The Beck Depression Inventory was used to assess depressive symptoms at baseline and at weeks 8 and 12. RESULTS: Median time to relapse did not differ by past history of major depressive disorder. Bupropion was associated with higher point-prevalence smoking abstinence at the end of medication compared to placebo (P = .007), independent of a past history of major depressive disorder. Moreover, change in depressive symptoms during the double-blind phase did not differ for those with and without a past history of major depressive disorder. CONCLUSIONS: Extended use of bupropion for relapse prevention is effective for smokers with and without a history of major depression.     

Speaker Abstracts

Narcolepsy is a rare disorder characterised by sleep disturbances, cataplexy, sleep paralysis and hypnagogic, hypnopompic hallucinations. Although several treatment modalities, such as tricyclic antidepressants or selective serotonin reuptake inhibitors, have been used to treat different symptoms, there is no definite treatment for narcolepsy. Modafinil or amphetamine-like stimulants, such as dexamphetamine or methylphenidate, are used to treat sleepiness. Our case was a 58-year-old woman who was diagnosed as narcolepsy cataplexy syndrome. Her Epworth Sleepiness Scale (ESS) score was 14 and Beck Depression Inventory (BDI) score was 29 in the first evaluation. Imipramine and modafinil were begun for the treatment, but there was no improvement in her symptoms. Subsequently, bupropion was started at 150 mg/day and then dosage was increased to 300 mg/day. She was asymptomatic at the end of 3 months. To our knowledge, this is the second depressive narcoleptic patient who has responded to 300 mg/day of bupropion.