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Psychiatric Times. Vol. 18 No. 6
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Treating the Patient as a Whole Person

By Elizabeth Fried Ellen, LICSW | June 1, 2001

Stroke

An estimated 10% to 27% of American stroke patients experience major depression each year. That translates to between 60,000 and 162,000 people, three-quarters of whom are over the age of 65. An additional 15% to 40% will suffer depressive symptoms within two months of suffering a stroke.

If the emotional suffering inherent in depression were not incentive enough to treat the disorder, researchers have discovered that untreated depression in this population can seriously impede patients' chances of recovery. A growing body of research strongly indicates that depression in stroke patients leads to poorer outcomes, both in cognitive functioning (Kimura et al., 2000) and in the recovery of the ability to perform activities of daily living (ADLs) (Chemerinski et al., 2001).

"Patients tend to report that they're depressed because they've had a stroke," Robert Robinson, M.D., head of the psychiatry department at the University of Iowa College of Medicine, explained to PT. "Physicians in those circumstances will often just regard it as an understandable, reactive depression and not realize what a profound effect this depression has on [the patients'] recovery and survival."

Assessing depression in a stroke patient can present unique clinical challenges. Stroke can cause apathy and/or crying spells, interfere with a patient's awareness of objectively observable neurovegetative signs, and impair their ability to express or describe emotion (Black, 1995).

If a patient's ability to process verbal or written language has not been impaired, a normal mental status exam can provide reliable and valuable diagnostic information when combined with a comprehensive interview and direct observation of depressive symptomatology. For patients whose language processing skills have been affected, Robinson said a presumptive diagnosis of depression generally is made in the presence of neurovegetative signs such as crying, withdrawal and sleep and/or appetite disturbance.

Robinson believes that when depressed stroke patients are treated, they are most likely to receive SSRIs, regardless of the demonstrated effectiveness and relative safety of the tricyclic antidepressant nortriptyline(Drug information on nortriptyline) (Aventyl, Pamelor) in this patient group. In a placebo-controlled, double-blind study published last year (Robinson et al., 2000), nortriptyline bested fluoxetine(Drug information on fluoxetine) (Prozac) in the treatment of post-stroke depression, improving recovery of ADLs and reducing anxiety symptoms.

Still, "there are psychiatrists who just don't have any experience with these medications, even though they're effective," said Robinson. "In patients who can't take nortriptyline, citalopram(Drug information on citalopram) (Celexa) may be a good idea," particularly for patients with cardiac conduction abnormalities. Robinson firmly believes that cardiovascular disease is not necessarily a contraindication for the use of tricyclics and said that if a stroke patient's electrocardiogram shows no conduction problems six to 12 months after an MI, he feels confident about prescribing nortriptyline. Regardless of the antidepressant, Robinson believes that treatment should continue for a full year; he bases this recommendation on research he is conducting that suggests depressed stroke patients may be at increased risk for mortality for up to five years following the stroke.

Parkinson's Disease

As many as two out of three Americans afflicted with Parkinson's disease may suffer from depression. While common in this population, depression can be hard to diagnose because some PD symptoms (such as psychomotor retardation, appetite disturbance and affective flatness) can mimic it. Depressed patients with PD have higher rates of anxiety and are more likely to experience sadness without guilt or self-blame than depressed patients who do not have the disease. Looking at phenomena such as sleep disturbance -- a chronic problem in PD patients -- in conjunction with feelings of hopelessness, worthlessness, anhedonia and suicidal ideation is a better way to assess depression in this population, according to William McDonald, M.D., professor of psychiatry and behavioral science at Emory University and director of the Fuqua Center for Late-Life Depression.

The SSRIs have been used safely and effectively to treat depression in patients with PD. An exception is patients taking selegiline(Drug information on selegiline) (Eldepryl), an antiparkinson agent, in whom the combination may lead to serotonin syndrome.

Otherwise, McDonald told PT, "There's absolutely no reason not to give them a trial of antidepressant. My clinical experience tells me that they have great responses and you clearly do not worsen their Parkinson's symptoms I think when you get into the area of medical comorbidity, psychiatrists tend to be a little less willing to use medication for fear they'll make things worse."

The phenomenon known as off-period depression is another PD-related problem that can be successfully treated with medication, according to Kevin J. Black, M.D., assistant professor of psychiatry, neurology and radiology at the Washington University School of Medicine. Off-period depression occurs when a dose of levodopa (Sinemet) or a dopamine agonist (e.g., pramipexole [Mirapex], pergolide [Permax], ropinirole(Drug information on ropinirole) [Requip], bromocriptine(Drug information on bromocriptine) [Parlodel]) wears off. Black told fPT it affects between 5% and 10% of patients with PD at some time during the course of their illness. These patients are not otherwise depressed and their clinical presentation can be striking. Black recalled meeting one patient with a 10- to 15-year history of the disease who talked of a wish to die; after taking a dose of levodopa(Drug information on levodopa) 30 minutes later, all depressive signs vanished and were replaced by cheerful affect. Increasing the amount or frequency of levodopa doses can be of considerable help, said Black. Other alternatives include the addition of selegiline or catechol-O-methyltransferase inhibitors such as entacapone(Drug information on entacapone) (Comtan), which enhance and extend the effects of levodopa.

Black has found electroconvulsive therapy (ECT) to be helpful in patients with PD with psychotic depression and with hallucinations that often occur in later stages of the disease. Black recommends that ECT be performed only twice per week in these patients due to an increased tendency to become confused after treatment.

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References
1.Black KJ (1995), Diagnosing depression after stroke. South Med J 88(7):699-708.
2.Chemerinski E, Robinson RG, Kosier JT (2001), Improved recovery in activities of daily living associated with remission of poststroke depression. Stroke 32(1):113-117.
3.Frasure-Smith N, Lesperance F, Juneau M et al. (1999), Gender, depression, and one-year prognosis after myocardial infarction. Psychosom Med 61(1):26-37 [see comment pp18-20].
4.Goodnick PJ, Hernandez M (2000), Treatment of depression in comorbid medical illness. Exp Opin Pharmacother 1(7):1367-1384.
5.Kimura M, Robinson RG, Kosier JT (2000), Treatment of cognitive impairment after poststroke depression: a double-blind treatment trial. Stroke 31(7):1482-1486.
6.Moon MA (2001), Growing evidence links depression to heart disease. Clinical Psychiatry News, March, p1.
7.NIMH (1999), Co-occurrence of depression with heart disease. Fact Sheet. Available at: www.nimh.nih.gov/publicat/heart.cfm. Accessed April 26, 2001.
8.Robinson RG, Krishnan KRR (in press), Depression and the medically ill. In: Neuropsychopharmacology: The Fifth Generation of Progress. Davis K, Charney D, Coyle J, Nemeroff C, eds. New York: Lippincott, Williams & Wilkins.
9.Robinson RG, Schultz SK, Castillo C et al. (2000), Nortriptyline versus fluoxetine in the treatment of depression and in short-term recovery after stroke: a placebo-controlled, double-blind study. Am J Psychiatry 157(3):351-359,157(3):351-359.
10.Wulsin LR, Singal B (2000), Is depression a risk factor for coronary artery disease onset? A meta-analysis. No. 26. Presented at the 153rd Annual Meeting of the American Psychiatric Association. Chicago; May 13-18.


 
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