Izchak Kohen

Serotonin syndrome in elderly patients treated for psychotic depression with atypical antipsychotics and antidepressants: two case reports.

We report two cases of serotonin syndrome in elderly patients during treatment of psychotic depression with atypical antipsychotics and antidepressants. The first case is a 69-year-old man who was admitted for depression with psychosis and treated with trazodone, risperidone, and sertraline. Subsequently, he developed myoclonus, tremor, cogwheel rigidity, and diaphoresis. The second case is a 72-year-old female initially admitted to a medical inpatient unit for a change in mental status that presented as increased confusion, lethargy, slurred speech, and a fever of 101.5 degrees. She had been on phenelzine and quetiapine. In both cases, all symptoms resolved within 24 hours of the psychotropics being stopped. In both cases, we believe that serotonin syndrome was produced by a combination of an antidepressant and an atypical antipsychotic. There have been several case reports of serotonin syndrome from similar combinations of antidepressant and atypical antipsychotic treatment. Clinicians treating elderly patients with a combination of serotonergic antidepressants and atypical antipsychotics for psychotic depression should be aware of the potential for serotonin syndrome.

Bitemporal electroconvulsive therapy for depression in a Parkinson disease patient with a deep-brain stimulator.

We report the successful treatment of an episode of major depression with psychotic features with electroconvulsive therapy (ECT) in a 78-year-old woman with advanced Parkinson disease who had a left subthalamic nucleus deep-brain stimulator (DBS) in place. Electroconvulsive therapy effectively and safely treated the patients depression without harming the patient or damaging the DBS hardware. We offer additional evidence about the safety and efficacy of electroconvulsive therapy in patients with DBS.

Rapidly Developing Hyperglycemia During Treatment with Olanzapine

OBJECTIVE: To report a case of rapidly occurring hyperglycemia that occurred in a geriatric patient 3 days after treatment with olanzapine. CASE SUMMARY: An 89-year-old man was admitted for dementia with behavioral disturbance and psychosis and was started on olanzapine 2.5 mg twice daily. Due to paranoia and agitation, the dose was increased to 5 mg twice daily after 2 days. Subsequently, he developed hyperglycemia (fasting blood glucose 138 mg/dL) that resolved when olanzapine was stopped and recurred (fasting blood glucose 150 mg/dL) after 2 days of rechallenge with olanzapine 2.5 mg twice daily. In addition, his overall medical status worsened, as he developed concurrent acute renal failure and became more confused and lethargic. The hyperglycemia once again resolved with discontinuation of the drug. DISCUSSION: We postulate that the rapid onset of hyperglycemia and the resulting medical sequelae were due to olanzapine. An objective causality assessment revealed that the adverse drug event was probable. There have been numerous case reports of hyperglycemia with olanzapine in the literature, but none reported hyperglycemia within days of initiation of the medication. Although weight gain often coincides with hyperglycemia in patients taking atypical antipsychotics, it does not seem to be a necessary causal factor. Recent data in animal studies have indicated that olanzapine and clozapine rapidly impair whole-body insulin sensitivity in a dose-dependent manner. CONCLUSIONS: Clinicians treating elderly patients with olanzapine should be aware of the potential for rapidly developing hyperglycemia and monitor such patients accordingly.

Central Sleep Apnea in a Geriatric Patient Treated With Aripiprazole

We report a case of central sleep apnea in a geriatric patient that was associated with treatment with aripiprazole for an episode of major depressive disorder with psychotic features. The patient was a 72-year-old man who was started on aripiprazole and developed central sleep apnea that improved significantly when the medication was stopped. A rechallenge with aripiprazole led to a worsening of the central sleep apnea, which again improved off the aripiprazole. We postulate that the central sleep apnea was due to aripiprazole. There have been numerous case reports in the literature of obstructive sleep apnea associated with atypical antipsychotics. To our knowledge, this is the first published case of central sleep apnea. We caution clinicians to be aware that there is potential risk of atypical antipsychotics like aripiprazole inducing or exacerbating central sleep apnea.

Antipsychotic-induced hyponatremia: case report and literature review.

We report a case of hyponatremia in a patient that occurred 3 days after initiation of treatment with aripiprazole. The patient was a 50-year-old man admitted to an inpatient psychiatric unit for exacerbation of schizophrenia. He was started on aripiprazole and developed hyponatremia that resolved when the medication was stopped. We postulate that the hyponatremia was due to an aripiprazole-induced syndrome of inappropriate secretion of antidiuretic hormone. There have been numerous case reports in the literature of hyponatremia in the literature associated with atypical antipsychotics. We caution clinicians to be aware that the potential hyponatremic-inducing effects of atypical antipsychotics can occur rapidly after initiation of the medications.

Increases in C-Reactive Protein May Predict Recurrence of Clozapine-Induced Fever

OBJECTIVE To report a case of recurrent clozapine-induced fever that was associated with a rise in C-reactive protein (CRP). CASE SUMMARY A 73-year-old man with Lewy Body dementia was admitted for psychosis. He was treated with clozapine (initial dose 12.5 mg/day, titrated to 75 mg/day over 15 days). On day 15 of clozapine therapy, he developed a benign fever (maximum 38.4 °C) that was associated with a rise in the CRP level (3.96 mg/dL). The level normalized when clozapine was discontinued. However, when the patient was rechallenged with clozapine, the CRP level became elevated (4.36 mg/dL) after 3 days of therapy, with a subsequent recurrence of fever (38.7 °C). DISCUSSION We postulate that the elevation in CRP levels and the subsequent fever were caused by the effects of clozapine on the cytokine system via interleukin-6 and tumor necrosis factor-α, resulting in an inflammatory response with an acute phase reaction. This case is unique, as it is the first reported in the literature associating a recurrence of clozapine-induced fever with the known immunomodulatory effects of clozapine on cytokines and CRP level. According to the Naranjo probability scale, this adverse effect is probably associated with clozapine. CONCLUSIONS Clozapine-related fever is generally benign but difficult to assess and manage, as it can be confused with much more serious conditions. Further research is needed to study whether CRP is a useful tool in predicting and managing clozapine fever.

Quetiapine-associated dysphagia

We report a case of quetiapine-induced dysphagia in a geriatric patient which improved with discontinuation of the antipsychotic. The patient had developed dysphagia while being treated with antipsychotics for bipolar disorder. The patients dysphagia showed significant improvement when she was taken off quetiapine. We review the available literature on antipsychotic-related dysphagia and suggest that clinicans need to be aware of the potential for this syndrome even with lower potency antipsychotics.

Mirtazapine in bupropion-induced dyskinesias: a case report.

Therefore, a 500-U vial should contain 12.5 ng. An important consideration for the REAL DOSE Study not considered by Kingswell and colleagues is the fact that each patient evaluated in the study was his or her own control. Kingswell and colleagues have incorrectly interpreted that 86.4% of all patients have received treatment for more than 5 years. While it is true that the majority of patients (83.3%) reported the duration of their conditions being longer than 5 years, no information obtained during this study would allow the authors to assume that these patients have been treated for more than 5 years. In addition, Kingswell and colleagues also suggest a possible bias in the reporting as most of the patients started on Dysport before switching to Botox. Along these same lines, if there were indeed a bias, it would likely manifest itself in the postswitch group (Botox in our case) because adverse events are likely to be reported during the titration period postswitch. For the REAL DOSE Study, reported side effects were lower with the Botox group compared to the Dysport group. The REAL DOSE Study was conducted to evaluate the utilization of Botox and Dysport in a real-world/clinical setting for patients with cervical dystonia or blepharospasm. Although approximately 21% of patients fall into the 3:1 ratio grouping, it is clear that the majority of patients do not. We have concluded from our findings that no single ratio or conversion factor exists and when switching a patient from one toxin to the other, each patient is unique and should be titrated to the appropriate dose based on individual therapeutic needs.

Rapidly Worsening Hypertriglyceridemia During Treatment with Risperidone

To report a case of rapidly worsening hypertriglyceridemia in a geriatric patient that occurred 2 weeks after treatment with risperidone. The patient is a 70-year-old morbidly obese woman admitted to an inpatient psychiatric unit for exacerbation of schizophrenia. She had a pre-existing metabolic syndrome at baseline with a baseline triglyceride level of 188 mg/dL (>150 mg/dL), high-density lipoprotein of 34 mg/dL (<50 mg/dL), and fasting blood glucose of 100 mg/dL. She was started on risperidone and rapidly developed worsening hypertriglyceridemia after 2 weeks of being on the medication without any associated weight gain. Two weeks after admission, a repeat fasting lipid profile revealed serum triglycerides of 395 mg/dL with a direct low-density lipoprotein of 79 mg/dL, high-density lipoprotein of 21 mg/dL, and total serum cholesterol of 155 mg/dL. The hypertriglyceridemia improved when the medication was stopped. We postulate that the worsening hypertriglyceridemia was due to the effects of risperidone. An objective causality assessment revealed that the adverse drug event was probable. There have been numerous reports in the literature of hypertriglyceridemia without weight gain associated with atypical antipsychotics. None of the published cases had reported a rapidly occurring hypertriglyceridemia within 2 weeks of starting an atypical antipsychotic. It is possible that baseline obesity and baseline metabolic disorder may be risk factors for worsening hypertriglyceridemia in patients started on atypical antipsychotics. Clinicians treating elderly patients with risperidone should be aware of the potential for rapidly developing hypertriglyceridemia and monitor such patients accordingly. We caution clinicians to be aware that hypertriglyceridemia can worsen rapidly after initiation of atypical antipsychotics even in the first 2 weeks of treatment. Further studies are needed to see whether pre-existing metabolic syndrome is a possible risk factor for developing rapid hypertriglyceridemia in patients started on atypical antipsychotic drugs.

A case report of quetiapine withdrawal syndrome in a geriatric patient

We report a possible case of withdrawal syndrome from quetiapine with a discussion of its treatment and possible causal mechanisms. The case is of a geriatric patient who had symptoms of suspected quetiapine withdrawal due to a rapid taper of the medication. The patient’s symptoms resolved when quetiapine was reinstituted with a slower taper. This case raises awareness that clinicians may consider tapering quetiapine slowly to minimize the possibility of a discontinuation syndrome. Ms C, 65-year-old woman with paranoid schizophrenia, was admitted to the inpatient unit with an acute exacerbation of psychotic symptoms. She was treated as an outpatient prior to admission with quetiapine 400 mg in two divided doses and was compliant with the medication per report of family. She presented with paranoid delusions, disorganized speech and auditory hallucinations. Due to its ineffectiveness, the patient was taken off quetiapine with a 7-day taper beginning on admission. Risperidone was started at 0.5 mg daily on day of admission and increased to 1 mg daily on day 3. Two days after stopping the quetiapine, she began to complain of nausea and vomiting with poor PO intake. She was afebrile but her BP was elevated at 160/90 (she had been normotensive up to that point) but was not tachycardic or bradycardic. She also felt anxious and lightheaded. She was given several doses of intramuscular prochlorperazine 5 mg as needed for nausea with no improvement. There was no exacerbation of her psychosis. The patient was restarted on quetiapine at 100 mg at bedtime dose with resolution of symptoms in one day. A slower quetiapine taper was initiated with no further reported psychotic symptoms. No other medications were changed. The patient had not been prescribed benzodiazepines at home and her urine toxicology was negative. A MEDLINE literature search (using terms ‘‘quetiapine’’ and ‘‘withdrawal’’) revealed two previous cases of quetiapine withdrawal in the literature. In both of those cases, the patients had similar symptoms of nausea, dizziness and anxiety following a rapid taper of quetiapine (Thurstone and Alahi 2000; Kim and Staab 2005). One possible mechanism may be supersensitivity to acetylcholine. Dopamine antagonists can inhibit acetylcholine release and cause an upregulation of cholinergic receptors. The symptoms of emesis, nausea, nervousness and hypertension would be consistent with possible cholinergic rebound. Dopamine antagonism’s effect on postsynaptic acetylcholine may explain the resolution of cholinergic rebound when quetiapine was restarted (Dilsaver and Alessi 1988; Thurstone and Alahi 2000). In addition, the short half-life of quetiapine (around 6 8 h) may also be a factor in the cholinergic rebound leading to withdrawal symptoms (Tranter and Healy 1998). This case report provides further evidence that quetiapine may cause significant withdrawal symptoms in individuals if the medication is tapered too rapidly. This case raises awareness that clinician