1. American Psychiatric Association. (1980): Diagnostic and Statistical Manual of Mental Disorders, 3rd. ed. American Psychiatric Association, Washington, D.C. 2. Angst, J. (1985): In: Drug Treatment of Neurotic Disorders: Focus on Alprazolam, edited by M. H. Lader and H. C. Davies, pp. 70-75. Churchill Livingstone, New York. 3. Barlow, D. H., Di Nardo, P. A., Vermicyea, В . В ., et al. (1986): J. New. Ment. Dis., 174:63-72. 4. Beck-Friis, J., Kjellman, В ., Aperia, F„ et al. (1985): Acta Psychiatr. Scand, 71:319-330. 5. Beckman, H., and Goodwin, F. K. (1980): Neuropsychobiology, 6:91-100. 6. Bremer, A., Charney, D. S., and Heninger, G. R. (1984): Arch. Gen. Psychiatry, 41:1129-1135. 7. Brown, G. L., Goodwin, F. K., and Bunney, W. E. (1982): In: Serotonin in Biological Psychiatry, edited by B. T. Ho, J. С Schoolar, and E. Usdin, pp. 287-307. Raven Press, New York. 8. Brown, W. A., and Shuey, I. (1980): Arch. Gen. Psychiatry, 37:737-751. 9. Buchsbaum, M. S., Mayer, D. J., and Murphy, A. L. (1977): Acta Psychiatr. Scand, 56:69-79. 10. Bunney, W. E., Fawcett, J. A., Davies, J. M., et al. (1969): Arch. Gen. Psychiatry, 21:138-150. 11. Carrol, B. J. (1979): In: Lithium: Controversies and Unresolved Issues, edited by Т . В . Cooper, S. Gershon, N. S. Kline, and M. Schou, pp. 171-197. Excerpta Medica, Amsterdam. 12. Cassano, G. B. (1983): In: The Benzodiazepines: From Molecular Biology to Clinical Practice, edited by E. Costa, pp. 287-293. Raven Press, New York. 13. Cazzullo, С L., Sacchetti, E., Allaria, E., et al. (1982): In: Typical and Atypical Antidepressants. Clinical Practice, edited by E. Costa and G. Racagni, pp. 237-247. Raven Press, New York. 14. Cazzullo, С . L„ Sacchetti, E., Vita, A., et al. (1984): IRCS Med. Set., 12:917-918. 15. Cazzullo, С L., Smeraldi, E., and Sacchetti, E. (1979): Prog. Neuropsychopharmacol. Biol. Psy­chiatry, 3:25-38. 16. Charney, D. S., and Nelson, J. С (1981): Am. J. Psychiatry, 138:328-333. 17. Conte, G., Vita, A., Alciati, A., et al. (1984): In: Current Trends in Lithium and Rubidium Therapy, edited by G. U. Corsini, pp. 211-221. MTP Press, Lancaster. 18. Covi, L., and Lipman, R. S. (1984): Clin. NeuropharmacoL 7S 1:924-925. 19. Fawcett, J. A., Maas, J. W., and Dekirmenjan, H. (1972): Arch. Gen. Psychiatry, 26:246-251. 20. Feighner, J. P., Robins, E., Guze, S., et al. (1972): Arch. Gen. Psychiatry, 26:57-63. 21. Freud, S. (1894): Collected Works, I. Hogarth Press and Institute of Psychoanalysis, London. 22. Glassman, A. H., Kantor, S. J., and Shostak, M. (1975): Am. J. Psychiatry, 132:716-719. 23. Goldberg, D., Rickels, K, Downing, R., and Hesbacher, P. (1976): Br. J. Psychiatry, 129:61-67. 24. Goldberg, D., and Simpson, N. (1986): In: Drug Treatment of Neurotic Disorders: Focus on Alprazolam, edited by M. H. Lader and H. С Davies, pp. 76-82. Churchill-Livingstone, New York. 25. Goodwin, F. K., Cowdry, R. W., and Webster, M. H. (1978): In: Psychopharmacology: A Gen­eration of Progress, edited by M. A. Lipton, A. DiMascio, and K. F. Killam, pp. 1277-1288. Raven Press, New York. 26. Hamilton, M. (1960): Neurol. Neurosurg. Psychiatry, 23:56-62. 27. Hamilton, M. (1983): Br. J. Clin. Pharmacol., 15:165S-169S. 28. Invernizzi, G, and Sacchetti, E. (1985): In: Proceedings of the IVth National Congress of the Italian Society of Biological Psychiatry (Pavia, Italy, 19-20 October 1985), edited by G. Nappi, P. Pinelli, and D. Kemali, pp. 75-80. Emi Ras, Pavia, Italy. 29. Kraepelin, E. (1921): Manic Depressive Insanity and Paranoia. E. & S. Livingstone, Edinburgh. 30. Krauthammer, C, and Klerman, G. (1979): In: Manic Illness, edited by B. Shopshin, pp. 11-28. Raven Press, New York. 31. Maas, J. W. (1983): MHPG: Basic Mechanisms and Psychopathology. Academic Press, New York. 32. Maas, J. W., Fawcett, J. A., and Dekirmenjian, H. (1968): Arch. Gen. Psychiatry, 19:129-134. 33. Mendels, J., Weinstein, N.. and Cochrane, С (1972): Arch. Gen. Psychiatry, 27:649-653. 34. Montgomery, S. A., and Montgomery, D. B. (1982): In: Typical and Atypical Antidepressants: Clinical Practice, edited by E. Costa and G. Racagni, pp. 347-358. Raven Press, New York. 35. Nasrallah, H. A., McCalley-Whitters, M., and Chapman, S. (1984): Am. J. Psychiatry, 141:919. 36. Nelson, J. C, and Bowers, M. B. (1978): Arch. Gen. Psychiatry, 35:1321-1328. 37. Nelson, W. H., Khan, A., and Orr, W. W. (1984): J. Affective Disord., 6:297-306. 38. Owen, F., Cross, A. J., Crow, T. J., et al. (1983): Lancet, ii:1286. 39. Raskin, A., Schulterbrandt, J. G., Boothe, H., et al. (1972): In: Recent Advances in the Psycho-biology of the Depressive Illnesses, edited by T. A. Williams, M. M. Katz, and J. A. Shield, pp. 315-329. U.S. Government Printing Office, Washington, D.C. 40. Roose, S. P., Glassman, A. H., Walsh, В . Т ., et al. (1983): Am. J. Psychiatry, 140:1159-1162. 41. Rosenbaum, A. H., Toshihiko, M., Schatzberg, A. P., et al. (1983): Am. J. Psychiatry, 140:314-318. 42. Sacchetti, E., Allaria, E., Negri, F., et al. (1979): Biol. Psychiatry, 14:473-484. 43. Sacchetti, E., Conte, G, Pennati, A., et al. (1985): J. Psychiatr. Res., 19:579-586. 44. Sacchetti, E., and Smeraldi, E. (1980): In: La Depressione come Problema Psicobiologico, edited by E. Smeraldi and E. Sacchetti, pp. 49-79. Edi Ermes, Milan. 45. Sacchetti, E., Vita, A., Conte, G., et al. (1984): In: Current Trends in Lithium and Rubidium Therapy, edited by G U. Corsini, pp. 165-187. MTP Press, Lancaster. 46. Sacchetti, E., Vita, A., Conte, G, et al. (1986): IRCS Med. Scl, 14:407-412. 47. Schatzberg, A. F., Orsulak, P. J., Rosenbaum, A. H., et al. (1983): In: Treatment of Depression: Old Controversies and New Approaches, edited by P. J. Clayton and J. E. Barrett, pp. 53-59. Raven Press, New York. 48. Schulsinger, F„ Kety, S. S., Rosenthal, D., and Wender, P. H. (1979): In: Origins, Prevention and Treatment of Affective Disorders, edited by M. Schou and E. Stromgren, pp. 277-287. Ac­ademic Press London. 49. Smeraldi, E., Gasperini, M., Macciardi, F., et al. (1983): J. Psychiatr. Res., 17:309-317. 50. Stanley, M. (1983): Lancet, i:214. 51. Targum, S. D., Rosen, L. N., DeLisi, L. E., et al. (1983): Biol. Psychiatry, 18:329-336. 52. Traskman, L., Asberg, M., Bertilsson, L., et al. (1981): Arch. Gen. Psychiatry, 38:831-836. 53. Vita, A., Sacchetti, E., Conte, G, et al. (1985): L’Encephale, 11:71-77. 54. Weissmann, M. M., Leckmann, J. F., Merikangas, K. R., et al. (1984): Arch. Gen. Psychiatry, 41:845-852. 55. Winokur, G. (1978): In: Psychopharmacology: A Generation of Progress, edited by M. A. Lipton, A. DiMascio, and K. F. Killam, pp. 1213-1221. Raven Press, New York. 56. Zis, A. P., Grof, P., and Goodwin, F. K. (1979): In: Lithium: Controversies and Unresolved Issues, edited by T. B. Cooper, S. Gershon, N. S. Kline, and M. Schou, pp. 381-398. Excerpta Medica, Amsterdam. /> Read the rest of this entry »

These early findings appeared promising, but thereafter the picture became much more complex. We next turned our attention to response to MAO inhib­itors. The literature on this relies very much on the concept of atypical depression, another depressive classification that overlaps with anxious depression. The first clear published description of atypical depression was in a study by West and Dally (39) working with Sargant at St. Thomas’s Hospital. Responders to iproni-azid were described as showing a syndrome that included longer illness, phobic and generalized anxiety, fatigue, evening worsening, hysterical symptoms; absence of self-reproach, of morning worsening, and of early wakening; and sometimes an impression of life-long inadequate personality, although on close examina­tion premorbid personality was nonneurotic. There have been many subse­quent papers. When we came to look over the literature we were impressed that there were three different meanings that had been used by different authors when referring to atypical depression (22). The first one was that of marked anxiety and phobic symptoms, either accompanied by depression or assumed to have some relation to an underlying depression, as indicated, for instance, by diurnal variation. This is much the same as anxious depression. It would include the influential views of Tyrer (37) that MAO inhibitors are "delayed psycho-stimulants" indicated for agoraphobia, anxiety neurosis, anergia, and mixed anxiety depressions rather than pure depressions. The second meaning is what Pollitt (25) describes as reversed functional shift, i.e., depression with a diurnal pattern of evening worsening, insomnia of early rather than late kind, or increased sleep, increased appetite and weight, all in the opposite directions to the physiological changes said to characterize endog­enous depression. In the United States Klein and colleagues (15) assigned prin­cipal importance in their selection criteria to increased sleep, increased weight, and reactivity of mood and have found some evidence that atypical depressives so defined respond better to phenelzine than to imipramine. A third usage of the term atypical depression is a wide one of nonendogenous depression in general. In the United States a systematic series of studies of MAO inhibitors has been carried out by Robinson, Nies, and Ravaris. They have derived a diagnostic index for typical and atypical depression (29) that assigns high weights for typical depression to suicidal ideation, weight loss, depressed mood, agitation, retardation, guilt, hallucinations, and nihilistic delusions; high weights for atypical depression to psychic and somatic anxiety, initial insomnia. These three meanings are separate and do not necessarily identify the same patients. We assigned a mixed sample of outpatient depressives to a wide variety of different classificatory systems (22). We examined the relationships between diagnostic systems using Cramers’ V, a nonparametric measure of association. Using separate classifications based on marked anxiety symptoms, reversed functional shift, and nonendogenous depression, we found that these three criteria related poorly, and tended to select quite different patients. We had to conclude that the concept of atypical depression was imprecise. It would be better to specify which aspect was under consideration. Our main interest was in the response to MAO inhibitors. Here previous studies have not been clear-cut. The best evidence that type of depression predicts response comes from controlled trials of phenelzine against placebo (20), among which studies in outpatients, likely to include milder, more neurotic patients, have tended to show drugs superior to placebo, whereas inpatient studies have not. There are also positive studies in phobics. In a predictor study (20), we found better response in outpatients, patients who were less severely ill, not retarded, showed an admixture of anxiety symp­toms, and scored at the atypical end of the Nies-Robinson Diagnostic Index. The earlier cluster analytic typology did not predict. However, this was an open study without placebo or tricyclic comparison groups. We therefore undertook a controlled trial in outpatient depressives (24,33). One hundred and thirty-one outpatients with depression and mixed anxiety depression were randomly assigned to 6 weeks of treatment with phenelzine rising to a dose of 60 to 75 mg daily, amitriptyline 150 mg daily, or placebo. On global measures and total severity scores, both drugs were found to be clearly superior to placebo and to much the same extent. In a predominantly neurotic sample of the type in which tricyclics have often been thought not to be useful, they appeared to be of considerable benefit. When we examined individual symptom ratings to see which symptoms were predominantly affected it was clear that both drugs had their main effects on the classical symptoms of depres­sion, including depressed mood and depressed thought content (33). On anxiety measures, effects of both drugs were quite weak. There was, however, a slightly better effect on anxiety measures from phenelzine than from amitriptyline. We classified these patients in a variety of ways, reflecting the three different concepts of atypical depression, and looked for differential drug responses. We found relatively little evidence of patient groups responding specifically to phen­elzine or amitriptyline rather than responding well to both drugs (24). We found no interactions greater than chance significance in two-way analyses of covariance between drug effects and diagnostic subtypes based either on atypical functional shift or a broad concept of nonendogenous depression. We did find a little evi­dence of interactions in subgroups based on the additional presence of anxiety, such that phenelzine produced its best effect in patients with an admixture of anxiety with their depression. However, this effect was only found with certain classifications, and amitriptyline was also clearly superior to placebo in anxious depressives, although a little less so than phenelzine. Overall, the findings of this study did not indicate that tricyclics are without value in anxious depression, when the comparison is made with placebo so that the true contribution of the drug effect can be measured. Rather they tended to suggest that tricyclics have a broad spectrum of antidepressant effects.

Differences in individual responses to psychopharmacological therapy may be assumed to be phenotypical indicators of distinct underlying pathogenetic dis­orders if it is also certain that these differences are not reflecting pharmacokinetic factors. This assumption has been the basis of many significant efforts to verify whether patients who do and do not respond to various antidepressants or lithium salts can be classified into actually distinct subgroups of the major affective dis­orders. As far as lithium therapy is concerned, the consensus is that lithium responders have more relatives with major affective disorders than do nonresponders, thus suggesting that familial factors are important in distinguishing between the two subgroups (11,15). The differences between the two, however, do not appear to be limited to this factor alone. We are beginning to gather evidence (even though further studies will be required) that lithium nonresponders appear to be more likely to be high urinary MHPG excretors and to have ventricular enlargement; further, they are more likely to have had a late disease onset, a history of delusional depression, suicidal behavior, short episode cycling, and drug-induced mood switches (11,17,43,46). In addition, they seem to have qualitatively distinct pat­terns of response to tricyclic antidepressants (45). We compared the outcome to lithium prophylaxis of 14 definitely anxious depressive patients with that of 18 definitely nonanxious major depressives. The differences between the responsiveness of the two groups to long-term lithium treatment were very striking. None of the definitely anxious patients had been satisfactorily stabilized, whereas over 22% of the definitely nonanxious, 13 of the total of 18, had clearly benefited from the treatment (x 2 = 14.2; p < 0.001). Undoubtedly it would be both reasonable and easy to say that the real strength of the association between a poor lithium response and the presence of a definitely anxious pattern of depression is really weaker than that observed in this particular patient sample. Despite this, however, the results obtained still seem promising, not only from the theoretical viewpoint, but also from the clinical one. Knowing that it is possible to have a reliable early screening of major depression with different lithium treatment prospects, we can more readily plan alternative in­dividualized stabilizing programs on a rational, less hit-or-miss basis. A sizable body of evidence indicates that age at disease onset is a good index for recognizing distinct subtypes of major affective disorder. As compared to patients with early onset, those with late onset have been shown to have: higher MHPG excretion (5,13,42,53); lower alpha-2-adrenoceptor density upon platelets (43); enlarged ventricular size (14,28); a poorer response to long-term lithium therapy (45,46); fewer relatives with major affective disorders (49,55); lowered chances for manic episodes (30); an increased recurrence rate (56); and, when bipolar, higher chances for drug-induced switches into mania (17). In view of the above, it seemed worthwhile to us to explore whether there is a relationship between age at onset and definite anxiety in major depression. Among the 88 patients for whom it was possible to securely ascertain age at onset, those classified as definitely anxious had their first depressive episode later than those who were definitely nonanxious (39.8 ± 11.9 vs. 33.5 ± 12 years; Student Mest = 2.41, p < 0.02). Further, the dichotomy between early and late onset patients (cut-off age: 40 years) provided a satisfactory basis for distinguishing between major depressives with anxiety symptoms from those without anxiety. As many as 27 of the 35 late onset patients and only 22 of the 49 early onset patients were anxious (X 2 = 8.7; p < 0.003). These results do not appear to be mere indirect effects of age or polarity: the anxious and nonanxious major depressives were of comparable age (51.5 ± 10.3 vs. 50.3 ± 11.1 years), and there was an analogous incidence of bipolar disorders among them (34% and 53%, respectively; x 2 = 3.07, p = NS). Delusions On the whole, research on delusional depression strongly points to the pos­sibility that this term actually does denote and circumscribe a specific subtype of the major affective disorders. This not only is characterized by extremely virulent symptoms (evidence compatible with the hypothesis of a severity con­tinuum in depression), but also by specific biological and pharmacological fea­tures. As compared to nondelusional depressives, those with delusions not only are at higher risk for suicidal behavior (40), but also have greater chance for both abnormal dilation of the lateral cerebral ventricles (28,51) and a dysfunction of hypothalamic-pituitary-adrenal axis activity (16). Further, delusional depres­sives show a poor response to tricyclic antidepressants (TAD) given alone, benefit from TAD neuroleptics cotherapies or electroconvulsive therapy (22,36,37), and do not become adequately stabilized by lithium therapy (46). This picture of delusional depression aroused our interest in attempting to determine whether definite anxiety and delusion in major depressives are inter­twined phenomena. In the group of 68 patients studied, only 3 of the 31 (9.6%) nonanxious depressives were also unerringly delusional. Clear delusional states, however, were found in 12 of the 37 (32%) definitely anxious patients (x 2 = 5.08, p = 0.023). In the latter group, the relative risk of mood-congruent delusions was 4.5 times higher than that in the former. These data clearly indicate that the anxiety-delusions association in major depression is not merely fortuitous, despite the high incidence of false positives (37%), which is at least partially secondary to an overrepresentation of anxious versus delusional cases in the total study group.

Over Living in the Community

Experience Sampling
In spite of the agreement about the importance of environmental factors in anxiety, panic, and depression, we know little about the diurnal and temporal aspects of affect and anxiety, and their interaction in daily life. The ambulatory monitoring of patients is ideally suited to clarify these issues. Recent studies employing such methods have compared the shape of circadian rhythms of de­pressed and normal persons and demonstrated that variations in affective symp­toms are universal. In these studies the difference between well and ill groups is ore a difference of degree rather than kind. In Maastricht we use the ES tech-nique, which employs random, repeated self-report measures. Developed in the for seventies and early eighties by the author and others (4,11), the ES method has today taken its place with other substantiated assessment methods in the social and psychological sciences (8,26). ES uses a "beeper" to randomly, within 90-min periods, signal subjects to fill out self-reports 10 times per day for 1 week in the context of a person’s natural environment. This method of interrupting experience provides a representative sample of a person’s mental state. In this way we have examined the temporal characteristics, situational dependence, and time budget aspects of mental state, as well as the variability and stability of symptoms over time in a number of disorders. When the beeper signals, the respondent writes down information concerning his or her momentary situation and psychological condition. This record becomes the basic data of ES. The questionnaire form is designed to take no more than a few minutes to complete. Respondents carry all the forms in booklets. The forms used in this study had the objective of seeking a comprehensive coverage of external and internal situations as well as functioning as a repeated diagnostic instrument. Items are included that assess the time at which the form is filled out, whom the subject is with, where he or she is, and what activities he or she is involved in. Nine open-ended questions assess the social and physical context as well as the content of thoughts and activities. Further assessments of mental state are made using 25 Likert-type scales based on the mental status exam and grouped in modules for evaluating thought (17), affect (18), the presence of somatic and psychological complaints, and the level of motivation. These mod­ules have been validated by factor analysis. Added to these questions about the general properties of mental state, a pathology subsection has been added eliciting specific questions about anxiety. These questions were derived from cross-sec­tional diagnostic descriptions of anxiety, such as those offered by Spielberger et al. (27), DSM-III (1), and Marks and Mathews (23). Data were gathered at two levels. There were one time, cross-sectional measures gathered at the start of the study. These include illness severity ratings, diagnosis, demographic data, and other psychological assessments such as Zung and Spiel­berger rating scales. These diagnostic measures are in part incorporated into the Psychopathology subsection of the self-report forms. The second type of data gathered was the within-day repeated self-report measures previously described, filled in 10 times a day for 6 days. Skepticism about the application of this approach with ill persons generally arises around four central issues: (a) the adequacy of the sampling of ill persons, (b) the adequacy of the sampling of experience, (c) the experimental effects of the method, and (d) the construct validity of the self-reports. Full discussion of these methodological issues, as well as of the validity and reliability of the ap­proach, has recently been published (5,16). Most surprisingly, compliance across sampled disordered groups, ranging from pain to schizophrenia, as well as across developmental stages, from adolescents to the elderly, has been generally high and sometimes greater than that achieved with normal controls. In order to assure the acquisition of moment-to-moment information, reports are discarded if the beep is not responded to within 10 minutes. In general, the method has validity. The time allocation questions asking who, what, or where a person is favorably match reports from larger time-budget studies (29). In studies of distinct diagnostic disorders, ES data have discriminated diagnostic groups from one another and from normals (6). Reactivity and practice effects have also proved less problematic than expected, as shown by the very small differences in split week means from the end to the beginning of the week. Further pre- and posttest differences in subject self-consciousness measures, ap­plied to determine if psychological reactivity to the ES procedure takes place, have demonstrated negligible effects of the procedure (16). The research alliance is the key to increasing and maintaining compliance as well as the validity and reliability of the research. In this sense, ES is not a survey instrument, but a labor-intensive research method that requires the full coop­eration of the subject. In summary, past research suggests that the beeper method can be used with a wide array of people and that reports can be obtained on nearly all their experience. Studies also suggest that the effects of the method on what it is measuring are minimal and that the self-reports have construct validity. Studies have further shown that it can be used with adolescents, children as young as the sixth grade, and even severely psychotic individuals. It is useful to consider the method in light of traditional paper and pencil and interview meth­ods. It makes use of psychometric research instruments as they do, but unlike them, it does not rely on people’s ability to recollect and reconstruct their past experience. The ES method is capable of sensitively capturing mood and anxiety fluctu­ations over time and in different contexts in clinical populations. For example, previous studies have shown depression to co-occur with a variety of disorders when measured in daily life, such as bulimia and anorexia (7,19), and multiple personalities (22). Further, behavioral aspects of disorders have been elucidated and discussed for anxiety (12) and in schizophrenics (6,7-11). The assessment of affect by ES has correlated significantly with aspects of psychopathology, mo­tivation, and thought while still retaining its independent factor structure. For the study reported here, this means that affect and aspects of anxiety are differ-entiable by a number of the ES variables and, therefore, the study of their interplay in daily life could be successfully explored using the ES method. We thus aim to illustrate variations in time allocation, self-report of mental states, and temporal properties of anxious and depressed subjects. Read the rest of this entry »

Table 1 shows the segregation analyses results when all relatives with Major Affective Disorders and Affective Spectrum Disorders are included. These results thus represent the maximum likelihood estimates for each group of families according to the different transmission hypotheses. The likelihood values within each group can be compared, but it is not possible to make intergroup comparisons because the absolute values of the likelihoods are related to the number of subjects in the three groups, all of which vary in this respect. The discussed hypotheses are those for which the program could reach a max­imum likelihood estimate. The estimated likelihood values obtained allow us to rule out the hypothesis of no genetic transmission. For the group of tricyclic drug responders, the Mendelian model appears to be the most suitable. A good fit also is obtained under the SML additive transmission hypothesis. The model that best fits the group of poor responders is the polygenic one, whereas for the nonresponders, the best fit appears to be the SML hypothesis with transmission probability estimate (for heterozygotic genotype). The incorporated population prevalence values were calculated from the data
Read the rest of this entry »

Diurnal patterns in anxiety and depression scores in the highly and medium depressed groups were explored applying a linear regression technique to the entire sequence of beeps per subject and collapsed over subjects per group. For the moderately depressed group, no daily pattern was found for anxiety or depression symptoms, but for the highly depressed group, a within-day significant fluctuation was found for depression (t = -2.06, p < 0.04). This significant effect was produced by one subject who demonstrated a strong late in the day mood upswing (t = -3.93, p < 0.001). This finding was supported by a trend in the other four subjects. Interday differences per subject were also detected, but at the group level this effect disappeared. We next asked if we could separate the two groups on other temporal dimen­sions such as the recovery rate or decay time from high anxiety or low mood states. To demonstrate this, we tracked the flow of the symptom within the day from a point minimally one SD below that individual’s mean mental state on anxiety or depression. The "symptom event" was followed over subsequent sig­nals that day to manufacture a recovery or decay curve of intense emotional anxiety episodes for each group. Figures 2 to 4 show these recovery curves in the course of the day in relation to the group mean. Figure 2 depicts temporal pattern of recovery from anxiety states in medium and highly depressed subjects. On this graph we see that the high depression group recovers from anxiety more slowly. We also note that at the end of the day, a rebound or a diurnal decrease in anxiety is reported by the high depression group. This finding is greater than may be expected from the regression to the mean shown by the moderately depressed group. In Fig. 3, the recovery from a depressive episode is depicted for both high and medium groups. In contrast to anxiety, a more rapid recovery is noted in both groups as well as a more erratic recovery pattern that does not distinguish the groups from each other. Since the two groups are differentiated by the degree of depression scores, it is interesting to note that the temporal moment-to-moment recovery from a depressive episode is not altered by increased severity. On the other hand, it is anxiety that recovers more slowly in the highly depressed group in addition to showing a late-day rebound. This suggests at least an interplay in daily life between the effects of anxiety and affect. Affect perhaps predisposes the individual to problems in the experience of and coping with anxiety.
Read the rest of this entry »

Department of Psychiatry, Umea University, S-901 85 Umea, Sweden
Over time, our knowledge has increased about the classification and delineation of the affective psychoses. A distinction between unipolar affective disorders and bipolar affective disorders has been suggested by Perris (12) and Angst (3). Di­agnostic criteria for major depression and bipolar disorders have been presented in DSM-III (2). As concerns the nonpsychotic depressive disorders, there are still many un­solved problems, and there are no generally accepted diagnostic criteria delin­eating specific diagnostic subgroups. At the Department of Psychiatry at Umea University, we have used an op­erational definition of a subgroup called neurotic-reactive depression. The di­agnostic criteria have been used in a series of studies over the last 15 years. According to the diagnostic definition, the patients must have shown a clear-cut depressive symptomatology of a neurotic, nonpsychotic dimension, i.e., with unimpaired evaluation of reality during the whole course of the depressive dis­order. Furthermore, the condition must have arisen as a reaction to external events or represent an acute breakdown in patients with unstable personalities and a tendency to react with depressive, anxious, or psychosomatic symptoms under the influence of stress in relatively ordinary life situations (5). This definition somewhat resembles the definition of neurotic depression used by the World Health Organization (23). A neurotic disorder characterized by disproportionate depression which has usually recognizably ensued on a distressing experience; it does not include among its features delusions or hallucinations, and there is often preoccupation with the psychic trauma Which preceded the illness, e.g., loss of a cherished person or possession. Anxiety is also frequently present and mixed states of anxiety and depression should be included ere. The distinction between depressive neuroses and psychosis should be made ot only upon the degree of depression but also on the presence or absence of other eurotic and psychotic characteristics and upon the degree of disturbance of the patient’s behaviour. Read the rest of this entry »

In our family studies, it is obvious that patients with neurotic-reactive depres­sion have a low morbidity risk of bipolar affective disorders in their first-degree relatives (Table 4) (13). Thus both neurotic-reactive depression and unipolar affective disorders seem to be distinct categories from bipolar affective disorders as concerns family studies. Furthermore, there is no significant difference in morbidity risk for alcoholism or schizophrenia between the first-degree relatives of patients with neurotic-reactive depression and patients with unipolar affective disorders. The only significant difference found is a significantly higher morbidity risk for nonbipolar affective disorders in the first-degree relatives of patients with unipolar affective disorders, as compared to the first-degree relatives of patients with neurotic-reactive depression. The results seem to indicate a higher genetic component in unipolar affective disorders than in patients with neurotic-reactive depression. The results are comparable to results from other studies presented earlier (Table 5) (13).

1. American Psychiatric Association. (1980): Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. American Psychiatric Association, Washington, D.C. 2. Clerget-Darpoux, F., Bonaiti-Pellie, C, and Feingold, N. (1984): In: Hystocompatibility Testing, edited by E. D. Albert et al., pp. 664-665. Springer Verlag, Berlin. 3. Goldin, L. R., Gershon, E. S., Targum, S. D., Sparkes, R. S., and McGinnis, M. (1983): Am. J. Hum. Genet., 35:274-287. 4. Heimbuch, R. C, Matthysse, S., and Kidd, К . К . (1980): Am. J. Hum. Genet., 32:564-574. 5. Kidd, К . К . (1983): Paper presented at The Aino Hospital Foundation International Conference on Genetic Aspects of Human Behavior. November 5-6, Kobe, Japan. 6. Kruger, S. D., Turner, W. J., and Kidd, К . К . (1982): Biol. Psychiatry, 17:1081-1099. 7. Ott, J. (1984): Am. J. Hum. Genet., 26:588-597. 8. Smeraldi, E., and Bellodi, L. (1981): Am. J. Psychiatry, 138:1232-1234. 9. Smeraldi, E., Negri, F., Melica, A. M., Scorza-Smeraldi, R., Fabio, G., Bonara, P., Bellodi, L., Sacchetti, E., Sabbadini-Villa, M. G., Cazzullo, С L., and Zanussi, С (1978): Neuropsychobiology, 4:344-352. 10. Smeraldi, E., Petroccione, A., Gasperini, M., Macciardi, F., and Orsini, A. (1984): J. Affective Disord., 7:99-107. 11. Smeraldi, E., Petroccione, A., Gasperini, M., Macciardi, F., Orsini, A., and Kidd, К . К . (1984): J. Affective Disord. ,6:139-151. 12. Smeraldi, E., Scorza-Smeraldi, R., and Cazzullo, С L. (1979): In: Biological Psychiatry Today, edited by J. Obiols et al., pp. 90-95. Elsevier, Amsterdam. 13. Suarez, В . К , and Reich, T. (1984): Arch. Gen. Psychiatry, 41:22-27. 14. Targum, S. D., Gershon, E. S., Van Eerdewegh, M., and Rogentin, N. (1979): Biol. Psychiatry, 14:615-636. 15. Tiwari, J. L., and Terasaky, P. I. (1985): Hla and Disease Associations. Springer Verlag, New York.
Read the rest of this entry »