Depression. Aaron T. Beck, M.D.

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Depressive Equivalents

      Many writers attempted to spread the umbrella of depression to cover cases showing clinical symptoms or behaviors different from those generally indicative of depression. The term depressive equivalents was introduced by Kennedy and Wiesel³⁸ to describe patients who had various somatic complaints but did not show any apparent mood depression. They reported three cases characterized by somatic pain, sleep disturbance, and weight loss, all of whom recovered completely after a course of ECT.

      A number of other terms have been applied at various times to designate such cases of concealed depression. These include incomplete depression, latent depression, atypical depression, and masked depression. Various psychosomatic disorders, hypochondriacal reactions, anxiety reactions, phobic reactions, and obsessive-compulsive reactions have also been implicated as masking the typical picture of depressive reactions.³⁹

TABLE 4-4. Diagnostic Criteria for Mood Disorder Due to General Medical Condition

A.	A prominent and persistent disturbance in mood predominates in the clinical picture and is characterized by either (or both) of the following:
	(1) depressed mood or markedly diminished interest or pleasure in all, or almost all, activities; (2) elevated, expansive, or irritable mood.
B.	There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition.
C.	The disturbance is not better accounted for by another mental disorder (e.g., adjustment disorder with depressed mood in response to the stress of having a general medical condition).
D.	The disturbance does not occur exclusively during the course of a delirium.
E.	The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

      Adapted from DSM-IV-TR.

      The use of such a term as depressive equivalents raised several difficult conceptual, semantic, and diagnostic problems. (1) How could a syndrome substitute for a depressive reaction? (2) Since the usual indices of depression are lacking, how can the diagnosis of masked depression, etc. be made? (3) Since the concept of depressive equivalent is so loose, it could be stretched to encompass practically any psychiatric or somatic syndrome.

      One of the main criteria for diagnosing a depressive equivalent has been the response of patients with formerly intractable symptoms to ECT.³⁸ Denison and Yaskin,⁴⁰ in a report titled “Medical and Surgical Masquerades of the Depressed State,” listed several criteria for the diagnosis of an underlying depression. These include previous attacks of somatic complaints similar to the present attack, with complete recovery after several months; disturbance of sleep cycle; loss of appetite; loss of energy disproportionate to the somatic complaints; diurnal variation in intensity of somatic symptoms; and feeling of unreality. In the consideration of disguised depressions, it is worth emphasizing the truism that depression may mask organic disease as well as vice versa.

Depressions Secondary to Somatic Disorders

      It has long been understood that depressions are associated with a wide variety of nonpsychiatric disorders. In some instances, the depression appears to be a manifestation of the physiological disturbance caused by structural disease or toxic agents. The current American Psychiatric Association criteria for diagnosing depressions secondary to somatic disorders are in Table 4-4. In other instances, the depression seems to be a psychological reaction to being acutely or chronically ill—that is, the illness is a nonspecific precipitating factor. In either event, the depressive symptomatology per se, is not distinguishable from that observed in primary depressions.^1,41

      Conditions that specifically impair the normal functioning of the nervous system have long been known to produce depression.⁴² These conditions may be acute (the acute brain syndromes) such as those associated with alcohol, drugs, head trauma, or post-ictal states. Or the conditions may be chronic (chronic brain syndromes) such as those associated with cerebral arteriosclerosis, dementia, neurosyphilis, multiple sclerosis, malnutrition, and various vitamin deficiency syndromes.

      Depression as a complication of the use of the tranquilizing drugs has frequently been reported. Early reports of the use of reserpine in the treatment of hypertension implicated this drug as a causative agent in many depressions. Also, the phenothiazines have been suspected. Simonson,⁴³ for instance, interviewed 480 patients who were having their first acknowledged depression. He found that 146 (30 percent) had been taking a phenothiazine prior to the depression. Ayd,⁴⁴ however, was skeptical of the role of tranquilizers in producing a depression. He studied 47 cases of so-called drug-induced depression, and concluded that each case presented a history of predisposition to psychic disturbance and of physical and psychological stresses that helped precipitate the depression. This is not surprising, since the people in this study were presumably prescribed the tranquilizers due to some identified “psychic disturbance” in the first place.

      Depressive symptomatology was found in a substantial proportion of patients hospitalized for medical disorders.⁴⁵ Yaskin⁴⁶ and Yaskin et al.⁴⁷ reported a high frequency in patients with organic disease of the abdominal organs, particularly carcinoma of the pancreas. Dovenmuehle and Verwoerdt⁴⁸ reported that 64 percent of 62 patients hospitalized for definitely diagnosed cardiac disease had depressive symptoms of moderate or severe degree.

      Other types of generalized somatic disorders that, according to Castelnuovo-Tedesco, are likely to be complicated by depression are (1) certain infectious diseases—especially infectious hepatitis, influenza, infectious mononucleosis, atypical pneumonia, rheumatic fever, and tuberculosis; (2) so-called psychosomatic disorders such as ulcerative colitis, asthma, neurodermatitis, and rheumatoid arthritis; (3) anemias; (4) malignancies; and (5) endocrine disturbances.

      In view of the longstanding theory that primary depression is caused by an endocrine disturbance, it is interesting that certain diseases of the endocrine glands are associated with a high frequency of depression. Michael and Gibbons⁴⁹ pointed out that the adrenocortical hyperfunction of Cushing’s syndrome is almost always accompanied by mood change. The alteration in mood is generally depressive, but it may also be characterized by emotional lability and overreactiveness. In their review of the reports of psychiatric disturbance related to Cushing’s syndrome, Michael and Gibbons stated that the incidence of psychiatric disturbance generally exceeded 50 percent. Severe mental disturbance, extreme enough to warrant the label psychotic, was found in 15–20 percent of the cases. In one series, 12 of 13 patients with Cushing’s syndrome were reported to be consistently or intermittently depressed. There was, however, no close correlation between the symptoms of depression and the steroid output.

      Michael and Gibbons also reviewed the incidence of depression in Addison’s disease. They noted that depression occurred in 25 percent of the cases, and, somewhat surprisingly, euphoria occurred in 50 percent. Psychiatric disturbances have also been reported in cases of hypopituitarism. In longstanding untreated cases, the symptoms may appear in an extreme form. The most prominent symptom tends to be apathy and inactivity. Mild depression, occasionally interrupted by brief episodes of irritability and quarrelsomeness, is also prominent. Additional studies on the biological aspects are reviewed in Chapter 9.

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