Discontinuation Of Escitalopram Research Articles

0840 Be Wary Of Adjustment Disorder with Anxiety In Patient With Insomnia And Discomfort With Positive Pressure Airway Therapy

Abstract Introduction Insomnia is a common complaint. When it occurs in the context of treatment with continuous positive airway pressure (CPAP), it can complicate treatment and lead to dissatisfaction with CPAP therapy. Adjustment disorder with anxiety (ADWA) is a condition that develops following an identifiable stressor and can be associated with insomnia. We describe a case of ADWA causing disrupted sleep and dissatisfaction with CPAP therapy. Report of Cases: The patient is an 80-year-old man with history of severe obstructive sleep apnea (OSA) and chronic obstructive lung disease, under stable management with CPAP. During a routine follow up visit, he reported the recent onset of frequent, and often prolonged, nocturnal awakenings associated with daytime sleepiness and fatigue. Insomnia was associated with discomfort with breathing, especially during exhalation, while using CPAP. His machine report indicated a significant decrement in compliance. Upon questioning, he reported that a few of his family members had died unexpectedly, following which he began to experience significant anxiety. His wife noted that he had become moody and irritable. On examination, the patient was visibly anxious; his speech was accelerated and animated, and he displayed psychomotor activation. Affect also displayed despondency. The patient was diagnosed with ADWA leading to insomnia and discomfort with CPAP use. He was prescribed buspirone 10 mg twice daily. On two week follow up patient reported no improvement in symptoms and was switched to escitalopram 10 mg daily. Following approximately three weeks, his clinical evaluation revealed significant improvement in mood; anxiety had dissipated, and sleep was more continuous with infrequent and brief awakenings. Daytime alertness had been restored. Of interest was the temporary return of anxiety and insomnia symptoms following the brief discontinuation of escitalopram because of hospitalization. Conclusion ADWA can occur in the setting of recent stressors and can result in sudden onset of insomnia, compromise CPAP adherence and decrease subjective benefit from PAP therapy. This case highlights the importance of questioning patients for the possibility of recent stressors and traumatic events when they develop difficulties with PAP use. These may indicate the presence of ADWA, whose management can restore CPAP compliance and improve sleep quality and daytime functioning. Support (If Any)

Nystagmus as a discontinuation symptom after antidepressant therapy: a case report.

To the Editor: I present a patient with recurrent depression who experienced remission on a fixed daily dose of 150 mg of venlafaxine in the first episode and 15 mg of escitalopram in the second episode. Postural nystagmus appeared after discontinuation of treatment in each episode. Case report. Mr A, a 56-year-old married man, had a 6-year history of recurrent major depressive disorder (MDD) according to the DSM-5. His first episode had begun by January 2007 when he was 50 years old. His depressive symptoms began to appear slowly and were characterized by depressed mood, irritability, diminished interest and pleasure in his everyday activities, loss of appetite, lack of energy, poor concentration, early morning waking, and recurrent thoughts such as, “It is not interesting being alive.” These symptoms led to impaired work and social functioning. His parents and sister had a history of symptoms of depression. Extended-release venlafaxine was started with 37.5 mg/d and was increased gradually to 150 mg/d in 4 weeks with no adverse effects. The patient experienced important symptomatic relief by week 4 and reached remission in 8 weeks. Functionality was completely restored by August 2007. For the next 18 months, Mr A was on the same treatment regimen with full MDD remission. Remarkably, 10 days after completion of slow antidepressant discontinuation (ie, taper for 2 months), Mr A, who had no medical history of eye problems, started experiencing position vertical and lateral nystagmus, usually at its worst in the morning. The symptom was ameliorated during the day, almost disappearing by night. No other visual problem was related by the patient or detected. The symptom persisted for 3 weeks but disappeared slowly at the end of the fifth week. In January 2010, MDD reappeared, characterized by similar symptoms as previously described but with the emergence of symptoms of anxiety and fatigue (both severely worsening in the morning) and serious impairment of social functioning. Escitalopram was administered at 5 mg/d, reaching 15 mg/d in 3 weeks with no unwanted effects. After 6 weeks, depression had remitted. During follow-up (18 months), there was no relapse. After slow discontinuation of escitalopram for 6 weeks, the patient experienced nystagmus with the same characteristics as described earlier, disappearing by 4 to 5 weeks. The literature includes only 1 report of positional nystagmus associated with amitriptyline withdrawal.1 There is another case report of a patient who manifested signs of serotonin syndrome during an intravenous anesthetic with remifentanil and propofol. The patient displayed nystagmus, lower extremity clonus, and diaphoresis. At the time of surgery, the patient was being treated with 60 mg of fluoxetine for severe MDD. His symptoms resolved in the surgical care unit without incident. Investigators have shown that fluoxetine2,3 and sertraline4 can induce oculomotor abnormalities during sleep in depressed patients. It is suggested that these abnormalities are likely to be the result of increased availability of serotonin5,6 and secondary dopaminergic effects.7–9 As the use of antidepressants continues to increase, the incidence of withdrawal symptoms is also likely to increase. Patients treated with antidepressants should be questioned specifically during the discontinuation phase about the presence of this unwanted effect. It is important to recognize its clinical features as well as the benign course after a few weeks of follow-up.

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.

Recurrent escitalopram-induced hyponatremia in an elderly woman with dementia with Lewy bodies

We report the development of hyponatremia following initiation of escitalopram therapy in a 73-year-old woman. The patient, with a history of dementia with Lewy bodies, had presented with multiple neuropsychiatric symptoms. Within 2 months of escitalopram, she became delirious with a serum sodium level of 122 mmol/L. After discontinuation of escitalopram, her consciousness improved with resolving hyponatremia. Delirium and hyponatremia (122 mmol/L), however, recurred after escitalopram was rechallenged. Apart from eight other cases to date, this is the only one with recurrent hyponatremia. Rechallenge of the same antidepressant is discouraged especially in patients at risk of developing hyponatremia.

Syndrome sérotoninergique consécutif à l’association d’escitalopram et de cyclosporine chez une patiente de 84 ans

Due to the stimulation of central and peripheral 5-hydroxytryptamine receptors, the serotonin syndrome is a potentially lethal situation. The large variety of its clinical manifestations leads to a difficult diagnosis. We describe the case of a serotonin syndrome induced by the combined escitalopram and cyclosporine administration. An 84-year-old woman was hospitalized with a history of delirium associated with hyperthermia. The diagnosis of serotonin syndrome was suspected with the combination of the clinical features: the absence of infection, the selective serotonin reuptake inhibitor administration, and the absence of other metabolic and cerebral aetiology. After the discontinuation of escitalopram, the patient's condition improved rapidly. This report is a reminder of the clinical and pharmacological features of the serotonin syndrome from a recent literature review.

Resolution of Late-Onset Hypomania After Repair of Carotid Artery Stenosis

3Further research has described the relationship between right-sided lesions and secondary mania. 4 We describe the resolution of hypomanic symptoms after bilateral carotid endarterectomy in a patient with long-standing unipolar depression who developed late-onset hypomania with MRI white matter hyperintensities. Case report. Mr. A, a 67-year-old left-handed man with long-standing diabetes mellitus and coronary artery disease, was diagnosed with unipolar recurrent depression 40 years ago. Three years ago, he developed decreased sleep, increased energy, racing thoughts, and prominent irritability while taking his long-standing maintenance antidepressant, escitalopram 20 mg q.d. These symptoms responded only partially to the addition of lamotrigine, aripiprazole, and daily clonazepam and the eventual discontinuation of escitalopram. His diagnosis was subsequently changed to DSM-IV bipolar II disorder. Two separate attempts to taper off both the aripiprazole and the clonazepam failed when the patient experienced worsening insomnia and extreme irritability. The patient remained stable, but with subsyndromal symptoms, on this medication regimen for approximately 2 years. He then underwent a right carotid endarterectomy for critical stenosis of the right internal carotid artery followed 3 months later by a left carotid endarterectomy for occlusion of the cervical segment of the internal carotid artery, both discovered when he developed episodic aphasia. Prior to surgery, he had an MRI with contrast that revealed small foci of white matter hyperintensity in the right periventricular subependymal region, in the right superior frontal gyrus, and in the left cingulate gyrus. There were no infarcts observed. Within 3 weeks after his first surgery, he reported a dramatic improvement in his mood, and 1 month after his second surgery, his symptoms completely remitted, and he felt himself again. Aripiprazole and clonazepam were discontinued, and at his 4-month follow-up, he remains well, taking lamotrigine, without any irritability or difficulties sleeping. The temporal relationship between the resolution of this patient’s symptoms and his surgeries suggests that his irritability and insomnia, the cornerstones of his bipolar II diagnosis, were at least in part mediated by decreased cerebral blood flow due to carotid stenosis. When the blood flow was restored, his symptoms abated. The MRI findings are consistent with previous research that demonstrated a relationship between right-sided lesions and secondary mania 4 as well as a correlation between bipolar disorder and hyperintensities in the subependymal region, deep white matter, and subcortical gray

Syndrome of Inappropriate Antidiuretic Hormone Associated with Escitalopram Therapy

Escitalopram is the selective serotonin reuptake inhibitor (SSRI) most recently approved for use in the United States. It is structurally related to citalopram, but is felt to have a more tolerable side-effect profile than its parent compound. Side effects are not generally serious and include headache, diarrhea, and nausea. While hyponatremia and the syndrome of inappropriate antidiuretic hormone (SIADH) have been associated with treatment with other SSRIs, there has only been one case of escitalopram-induced SIADH reported in the literature to date. We now report another case of a patient who developed SIADH after being treated with escitalopram for 4 weeks. The patient's hyponatremia improved following the discontinuation of escitalopram. Clinicians should be aware of this uncommon but significant side effect of SSRIs and monitor high-risk patients for the development of SIADH.

Renal Tubular Defects from Antidepressant Use in an Older Adult

Adverse drug reactions are common and contribute to significant mortality and morbidity. We report a case study of an elderly woman who manifested with uncommon reversible renal tubular defects following the use of escitalopram. She was initially seen for worsening symptoms of depression and started on escitalopram in addition to her regular medications, which included donepezil, hydrochlorothiazide and mirtazapine. Three weeks later, she became increasingly confused and manifested recurrent falls. Laboratory evaluation showed hyponatraemia and evidence of renal tubular absorption defects. The patient's symptoms and laboratory abnormalities improved upon discontinuation of escitalopram as well as of mirtazapine and hydrochlorthiazide. This case illustrates the possibility of rare but reversible renal tubular defects associated with the use of antidepressant medications.