In a number of major medical illnesses depressive symptoms occur with such frequency as to become almost part of the disease. Contrariwise, in certain chronic and occult diseases, symptoms such as lassitude and fatigue may resemble and be mistaken for a depressive reaction. Hypothyroidism, infectious mononucleosis, hepatitis, lymphoma, myeloma, metastatic carcinoma, malnutrition, polymyalgia rheumatica, and frontal lobe tumors, especially meningiomas, may simulate depression for weeks or months before the diagnosis becomes evident. A special relationship to occult pancreatic or other abdominal cancers has been suggested but is difficult to understand. Sedative drugs, beta-adrenergic blocking agents, beta-interferons used for the treatment of multiple sclerosis and hepatitis, and the phenothiazines may also evoke a depressive reaction; corticosteroids can induce a peculiar psychiatric state in which confusion, insomnia, and either an elevation of mood or depression are combined, even to the point of psychoses. A depressed mood may also emerge during the tapering-off period of corticosteroid medication (a hypomanic state is more common in our experience during active use).
Of particular significance is the reactive depression that occurs on learning of a serious medical or neurologic disease. Often such an emotional reaction, which the physician may tend to ignore, is the dominant manifestation of a disease that threatens the life pattern and independence of the patient. Recognition by the patient that he has suffered a stroke or that he has cancer, multiple sclerosis, amyotrophic lateral sclerosis, or Parkinson disease, is almost always followed by some degree of reactive depression, often with an element of anxiety. A prime example is depression that follows myocardial infarction (Wishnie et al). Usually it begins toward the end of the patient’s stay in the hospital and attracts little attention. Once the patient is home, fatigability that approaches exhaustion may be the main complaint and interfere with accustomed activities and rehabilitation. It may be described as weakness and falsely attributed to heart failure. Symptoms of irritability, anxiety, and despondency are next in order of frequency, followed by insomnia and feelings of aimlessness and boredom. Although most of these patients ultimately recover without medical assistance the depression exacts a high toll in terms of mental suffering and some surveys suggest a relation of depression to poorer cardiovascular outcomes.
Depression following stroke and with degenerative neurologic disease An analogous depressive reaction occurs in some patients after stroke. Some studies have indicated that patients with left anterior cerebral lesions, involving predominantly the lateral frontal cortex or basal ganglia, have a greater frequency and severity of depression than do patients with lesions in other locations (Starkstein et al, 1987; Robinson). According to these authors, lesions of the right hemisphere do not show this correlation with depression but have a higher association with pathologic cheerfulness or mania. However, House and colleagues, in a British community-based study of stroke survivors, failed to confirm these findings, perhaps because the infarcts were small in size (more than half the patients had never been admitted to hospital) and many patients were examined for the first time only at 6 and 12 months after their strokes. Our colleagues Levine and Finkelstein reported the occurrence of psychotic depression with hallucinations and delusions in patients with right temporoparietal infarcts. Our own experience suggests an unsurprising relationship between the degree of motor and language disability and the severity of poststroke depression, but a less predictable relationship to the location of the lesion. The possible predisposing effects of minor previous episodes of depression, family history of depressive illness, and medications have not been studied systematically. These issues are also incorporated into Chap. 33.