Faculty Bibliography

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)

Quetiapine fumarate is an atypical neuroleptic indicated for the treatment of schizophrenia. It is also used as both a monotherapy for the acute treatment of manic episodes and as an adjunct to treatment with lithium or divalproex associated with bipolar type 1 disorder. Pharmacologically, it is an antagonist at serotonin (5-HT)1A and 5-HT2, dopamine (D)1 and D2, histamine H1 and adrenergic alpha 1 and alpha 2 receptors. According to the package insert, in clinical trials of the drug there were small dose-related decreases in thyroid hormone, particularly total T4 and free T4; however, only 0.4% of subjects studied experienced significant increases in thyroid stimulating hormone (TSH) levels. In previously reported cases of quetiapine-induced hypothyroidism, most of the patients either had a history of compromised thyroid function or had normal TSH levels. In addition, no anti-thyroid antibody titers were measured in these studies. The following is a report of a depressed patient treated with quetiapine who developed hypothyroidism that remitted after drug discontinuation.

Wagstaff et al (2003) have summarized case reports of statin-induced memory problems in patients treated with simvastatin. This article presents a report of new-onset cognitive difficulties in an older patient after initiation of simvastatin therapy. A 64-year-old white male presented with memory problems shortly after initiation of simvastatin therapy. The man had a history of bipolar disorder, characterized predominantly by depressive episodes, which had been stable over the past 2 years. At the time of presentation, the patient's medications included venlafaxine, quetiapine fumarate, simvastatin, terazosin, and carbamazepine extended-release. Simvastatin had been initiated by the patient's primary care physician for dyslipidemia. Within 1 week of starting simvastatin, the patient complained of additional memory problems. The temporal sequence of events supports a highly probable association between simvastatin and cognitive decline in this patient.

Attention-deficit/hyperactivity disorder (ADHD), once considered to be a childhood disorder, is diagnosed in similar to 7 million adults in the United States, as reported by The National Comorbidity Study. Although it is now recognized that ADHD often persists into adulthood, the current diagnostic criteria is geared toward symptom identification in children. Symptoms of inattention, impulsivity, and hyperactivity evolve over the life cycle and present differently in adults. Further complicating diagnosis is that ADHD is associated with multiple functional impairments and comorbid psychiatric disorders. The Multi-Modal Treatment Study of ADHD reported that only 32% of the study population had ADHD alone; 29% had ADHD plus oppositional defiant disorder and/or conduct disorder, 14% had ADHD plus anxiety or depression, and 25% had all three disorders. Optimal treatment utilizes a multimodal approach including behavioral treatments combined with pharmacologic treatment strategies. Food and Drug Administration-approved medications for ADHD include the stimulants and nonstimulants, although tricyclic antidepressants and bupropion are also commonly used. In this monograph, Craig L. Donnelly, MD, reviews the history of ADHD and discusses the pathophysiologic progression of childhood symptoms into those commonly exhibited by adults. Next, Frederick W. Reimherr, MD, reviews comorbidity of ADHD and describes the Utah Criteria as a method of diagnosing adults through recollection of childhood problems. Finally, Joel L. Young, MD, reviews treatment approaches to adult ADHD and its comorbid conditions.

Venlafaxine is a serotonin norepinephrine reuptake inhibitor widely used for the treatment of depression, generalized anxiety disorder, and social anxiety disorder, as well as a number of other psychiatric conditions for which serotonergic antidepressants are often employed. Reported side effects for venlafaxine include nausea, somnolence, insomnia, dizziness, constipation, sweating, anorexia, asthenia, nervousness, dose-dependent blood pressure elevation, increased urinary frequency, and sexual dysfunction. The following is a report of venlafaxine-induced rapid and severe edema, otherwise known as anasarca.

While the exact pathophysiology of tinnitus remains unknown, possible causes include cochlear deterioration; an extra-auditory response to respiratory, vascular, or muscular stimuli; a drug reaction; microvascular compression of the eighth cranial nerve; and turbulent flow in the ipsilateral internal carotid artery. Regardless of the cause, tinnitus may result in significant diminution of quality of life. Proposed treatments include retraining therapy, maskers, hyperbaric oxygen, carotid artery stenting, selective cochlear neurotomy, and biofeedback, as well as pharmacotherapy with antidepressants, benzodiazepines, lidocaine, the calcium channel blocker nimodipine, or botulinum toxin. The double-blind, placebo-demonstrates the effectiveness of the selective serotonin reuptake inhibitor (SSRI) sertraline for the treatment of severe tinnitus. The findings support a possible role for sertraline, and likely other SSRIs, for the treatment of refractory tinnitus.