Faculty Bibliography

Dopamine acts to inhibit the release of prolactin, a hormone that initiates and sustains lactation. In women, prolactin elevation can cause galactorrhea, amenorrhea, cessation of normal cyclic ovarian function, loss of libido, hirsutism, and increased long-term risk of osteoporosis and breast cancer. Presented here is a case of hyperprolactinemia and galactorrhea associated with sequential use of the serotnin norepinephrine reuptake inhibitors (SNRIs) venlafaxine and duloxetine A 40-year-old Caucasian female with three children and without any history of endocrine or reproductive pathology presented with dysthymic disorder. The patient appears to represent the first published case of SNRI-induced, dose-dependent, nonmenstrual vaginal spotting and galactorrhea accompanied by prolactin elevation. Since serum levels were not obtained it is not known if use of bupropion ER resulted in elevated levels of venlafaxine or duloxetine. Interestingly, the dopaminergic effects of bupropion were not enough to offset this patient's hyperprolactinemia, although it is possible but unproved that it may have attenuated it.

This is a report of a patient with an acute schizoaffective episode who developed severe cervical dystonia while being treated with a combination of quetiapine and valproic acid. A 60-year-old woman with schizoaffective disorder was admitted to the inpatient psychiatry unit at the University Hospital in Basel, Switzerland due to symptoms of mania and psychosis. She had recently been discharged from the hospital on quetiapine monotherapy 500 mg/day, which led her to remission and had been well tolerated. During that last hospitalization, she suffered two generalized seizures. She discontinued the quetiapine on her own, resulting in a rapid return of psychotic symptoms. She developed paranoia about being poisoned, as manifested by her persistent refusal of food and fluid intake. Upon readmission to the hospital, quetiapine was rapidly increased to 800 mg/day. The cervical dystonia improved with biperiden and resolved totally after reduction of both quetiapine and valproic acid. The patient was discharged on a combination of olanzapine and valproic acid.

Presents a case of bilateral complicated cataract and glaucoma following large-dose methylphenidate use for 2 years. A 10-year-old boy presented with progressive blurred vision in both eyes over the past year. He had no history of systemic disease, ocular trauma, or ocular disorder except myopia before this episode. Three months before the current visit, decreased visual acuity had been noted during a routine school physical check-up. Glaucoma and cataract were diagnosed at the ophthalmic clinic. History revealed that the patient had ADHD and had been taking methylphenidate hydrochloride 40 mg/day in two divided doses as prescribed by his psychiatrist. Over the prior 2 years, however, at the instruction of his mother, the patient had been taking 60 mg/day. A diagnosis was made of methylphenidate-associated cataract and glaucoma. Methylphenidate was discontinued. Despite maximal anti-glaucomatous medication, IOP still could not be controlled. The patient then received combined cataract and glaucoma surgery, with intraocular lens implantation for both eyes. Postoperatively, visual acuity improved with IOP within normal limits in both eyes. These improvements were sustained at 1 year follow-up.

Presents the first published report of bilateral eyelid edema in association with use of olanzapine. A 41-year-old previously healthy man experienced a first psychotic episode and attempted suicide by opening the veins of his forearm. This act was motivated by the delusional idea that he was infected with human immunodeficiency virus (HIV). He was diagnosed with schizoaffective disorder. Over the weeks, trials of risperidone, aripiprazole, and venlafaxine failed. With a combination of duloxetine 90 mg/day and amisulpride 400 mg/day, psychotic and depressive symptoms improved. Within 24 hours of the first (evening) dose of olanzapine 5 mg, the patient complained of a 'swollen face,' with his eyelids found to be turgid. After 10 days, olanzapine was discontinued and the eyelid swelling disappeared completely the following day. The temporal course of events described suggests an association between olanzapine and the development of bilateral eyelid edema.

The following is a report of two patients who developed reversible facial myoclonus in association with use of topiramate. The first patient was a 28-year-old man with posttraumatic frontal lobe epilepsy who was switched to topiramate monotherapy after failure on phenytoin. Topiramate was initiated at 25 mg/day, then increased by 25 mg every week. The second patient was a 49-year-old woman who presented with new-onset complex partial seizures. In both patients described above, facial myoclonus appears to be a dose-related adverse event associated with topiramate.

Previous Psychopharmacology Reviews have discussed the association between serotonin reuptake inhibitors (SRIs) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which is characterized by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary gland. The norepinephrine reuptake inhibitor reboxetine, approved in Europe for the treatment of depression, has also been associated with SIADH. Other medications associated with SIADH include tricyclic antidepressants (TCAs), bupropion, neuroleptics, carbarnazepine, sodium divalproex, vincristine, and cyclophosphamide.

The occurrence and duration of paroxysmal atrial fibrillation are influenced by vagal tone. The selective serotonin reuptake inhibitor (SSRI) paroxetine can modulate vagal tone at the level of the mid-brain and inhibit the vasovagal reflex. Paroxysm of refractory neurally mediated syncope has been reduced with paroxetine. That finding supports the notion that paroxetine may modulate the occurrence of atrial fibrillation that is under the influence of the vagus nerve. In one study, oral paroxetine 10 mg/day was administered to nine patients with multidrug-resistant paroxysmal atrial fibrillation. Conventional antiarrhythmic drugs were used for all the patients for a minimum of 2 weeks, and, in the case of amiodarone, at least 3 months. These agents decreased the frequency of arrhythmia events by < 30% in all patients. In contrast, the frequency decreased significantly in all patients after paroxetine was added. Notably, in three patients, atrial fibrillation resolved completely. In three other patients, the daily doses of antiarrhythmic drugs were decreased by 33% to 50%, although the frequency of atrial fibrillation still remained low. For the group as a whole, the mean atrial fibrillation frequency declined from a baseline of 13.2 to 1.0 episodes per month. These preliminary results indicate that some patients with atrial fibrillation may respond very favorably to oral treatment with paroxetine. While the pathophysiology underlying this effect is not known, several possibilities exist, including modulation of central serotonin metabolism at the level of the mid-brain and anxiolysis resulting in decreased myocardial irritability. Whether the reputed benefit of paroxetine or other SSRIs in the treatment of atrial fibrillation depends upon the presence of comorbid depression is a question worthy of further study.

Anxiety disorders are common in depressed patients. Several studies of the full range of Diagnostic and Statistical Manual of Mental Disoroters-defined anxiety disorders in depressed psychiatric outpatients each found that when diagnoses are based on semi-structured diagnostic interviews >40% of the patients had a comorbid anxiety disorder. The recognition of comorbidity is not simply of academic interest, but it has important clinical significance. Epidemiological studies, such as the National Comorbidity Study, have demonstrated that depressed individuals with a history of anxiety disorders are at increased risk for hospitalization, suicide attempt, and greater impairment from the depression. The co-occurrence of anxiety disorders in depressed patients has been associated with a more chronic course of depression in psychiatric patients, primary care patients, and epidemiological samples. Recent research has suggested that clinicians underrecognize anxiety disorder comorbidity in depressed patients. The clinical significance of this underrecognition is highlighted by the finding that patients often want treatment to address their anxiety disorder comorbidity. When anxiety disorders are detected they often influence clinicians' selection of antidepressant medication, though some of clinicians' prescribing biases are not supported by empirical data. In this monograph, Iwona Chelminski, PhD, reviews the significance of anxiety in patients with depression as well as diagnostic instruments for recognizing this comorbidity. Next, Mark Zimmerman, MD, addresses the factors that affect the clinician's choice of antidepressant, focusing on the influence of comorbid anxiety. Finally, Sidney Zisook, MD, discusses the differential efficacy of antidepressants as well as the role of psychotherapy in patients with comorbid anxiety and depression. (journal abstract)