Anger attacks in seasonal affective disorder

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1 International Journal of Neuropsychopharmacology (2006), 9, Copyright f 2005 CINP doi: /s First published online 8 July 2005 Anger attacks in seasonal affective disorder Dietmar Winkler 1, Edda Pjrek 1, Anastasios Konstantinidis 1, Nicole Praschak-Rieder 2, Matthäus Willeit 2,Jürgen Stastny 1 and Siegfried Kasper 1 BRIEF REPORT 1 Department of General Psychiatry, Medical University of Vienna, Austria 2 Centre of Addiction and Mental Health, Toronto, Canada Abstract Previous research has linked aggression especially anger attacks with depression. The objective of the present study was to examine the prevalence and clinical picture of anger attacks in seasonal affective disorder (SAD) in comparison to non-seasonal depression. Thirty-six SAD patients and 24 non-seasonally depressed controls were included in this evaluation. Anger attacks were assessed with the Anger Attacks Questionnaire. The prevalence of anger attacks did not differ statistically significantly between seasonally and non-seasonally depressed subjects. However, the monthly number of anger attacks was significantly higher in SAD patients (p=0.009) and they presented with more vegetative symptoms and behavioural outbursts during the anger attacks (p=0.006). SAD patients with anger attacks had significantly lower age of onset (p=0.021) and obtained lower global seasonality scores than SAD patients without anger attacks (p=0.001). Anger attacks are experienced as particularly intense in SAD patients and seem to contribute considerably to their symptomatology. Received 15 February 2005; Reviewed 16 March 2005; Revised 23 March 2005; Accepted 27 March 2005 Key words: Aggression, anger attacks, seasonal affective disorder. Introduction Previous research has suggested that depressed patients often suppress aggression (Brody et al., 1999). In contrast to these findings recent studies have found that depressed subjects are more likely to express anger than patients with other psychiatric disorders (Koh et al., 2002). Aggression in the form of anger attacks, seems to be particularly prevalent in major depression (Fava et al., 1993). Anger attacks are sudden spells of inappropriate anger accompanied by vegetative hyperarousal similar to panic attacks. Anger attacks obtain clinical significance, not only because they increase personal suffering and compromise social functioning; Mammen et al. (1997) have reported that they were associated with lower treatment adherence in a sample of pregnant and postpartum women. Furthermore, anger attacks have been shown to increase cardiovascular risk (Fava et al., 1996a) and to have a deleterious impact on the wellbeing of patients offspring (Alpert et al., 2003). Address for correspondence: D. Winkler, M.D., Department of General Psychiatry, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. Tel.: Fax: dietmar.winkler@meduniwien.ac.at According to the DSM-IV (APA, 2000) seasonal affective disorder (SAD), winter type is a subtype of mood disorder with recurrent major depressive episodes in autumn or winter occasionally followed by hypomanic or manic episodes during the successive spring/summer period. The prevalence of this disorder is up to 10% in the general population, and the rate of subjects suffering from the subsyndromal variant of SAD is even higher (Magnusson, 2000). Several lines of evidence suggest that the serotonergic system is involved in the pathophysiology of both anger attacks and SAD; anger attacks have been found to respond very well to treatment with SSRIs (Fava et al., 1993; Mammen et al., 2004), and patients suffering from these attacks exhibit a greater central serotonergic dysregulation than depressed patients without anger attacks as measured by neuroendocrine challenge tests (Fava et al., 2000). Likewise monoamine depletion studies (Neumeister et al., 1997), challenge tests (Schwartz et al., 1997) and neuroimaging studies (Willeit et al., 2000) have repeatedly demonstrated abnormalities in brain serotonin function in SAD. The present research project was aimed to assess the prevalence, frequency and symptom pattern of anger attacks in SAD and to compare our findings to non-seasonally depressed control subjects. Based on preceding clinical reports yielding particularly high

2 216 D. Winkler et al. levels of irritability in SAD patients (Winkler et al., 2002b) we formulated the a-priori hypothesis of higher rates of anger attacks in SAD. Method Study subjects were consecutively recruited at the outpatient clinic of the Department of General Psychiatry (Medical University of Vienna) and underwent semi-structured diagnostic interviews according to DSM-IV (First et al., 1996). SAD patients fulfilled the Rosenthal (Rosenthal et al., 1984) and DSM-IV criteria (APA, 2000) for SAD. The control group consisted of patients with non-seasonal (recurrent) major depressive disorder according to DSM-IV. SAD patients and controls were clinically depressed at the time of the interview. Subjects with past mania or hypomania or present psychiatric comorbidity were excluded. Patients completed the German version of the Seasonal Pattern Assessment Questionnaire (Rosenthal et al., 1987) to obtain the Global Seasonality Score (GSS). A GSS of o10 was required for SAD patients; Controls with a GSS of >6 were excluded by the protocol. Anger attacks were assessed in all subjects with the Anger Attacks Questionnaire (Fava et al., 1991). According to this questionnaire study subjects were classified as suffering from anger attacks, if they fulfilled all of the following criteria during the last 6 months of their current depressive episode: (1) irritability, (2) overreaction to minor annoyances, (3) at least one anger attack per month, (4) at least four of 13 autonomic arousal symptoms and behavioural outbursts during the anger attacks. Both groups were examined during the same time of the year, i.e. during autumn and winter. The psychiatric assessments for this study were approved by the Ethics Committee of the Medical University of Vienna. All subjects gave informed consent prior to the study procedures. Statistical analysis was carried out with SPSS for Windows (SPSS Inc., Chicago, IL, USA). We used Fisher s exact test, and Student s t test to assess group differences. The pf0.05 level of significance was adopted in this report (unless otherwise specified). All statistical comparisons were two-tailed. Results Thirty-six SAD patients (24 women, 12 men) and 24 controls with non-seasonal depression (14 women, 10 men) were included in this study. The mean age ( S.D.) of SAD patients ( yr) and control subjects ( yr) was not statistically significantly different (t=x1.594, d.f.=58, p=0.116). There was a numerically but statistically insignificant difference in the prevalence of anger attacks (i.e. the rate of patients who fulfilled the above-mentioned criteria for anger attacks) between seasonal [41.7%, 95% confidence interval (CI) ] and nonseasonal depression (29.2%, 95% CI , p=0.416). The monthly number of anger attacks was significantly higher in SAD patients with anger attacks ( ) than in non-seasonal major depression with anger attacks ( ; t=2.932, d.f.=17.102, p=0.009). Additionally, SAD patients reported a significantly higher number of vegetative and behavioural symptoms (item 5, a-m of the Anger Attacks Questionnaire) during the anger attacks ( vs ; t=3.111, d.f.=20, p=0.006; Figure 1). Anger attacks in our sample were characterized most frequently by the following symptoms: feeling like attacking others (86.4%), palpitations or tachycardia (81.8%), feeling out of control (81.8%), dyspnoea (68.2%), tremor (68.2%) and hyperhidrosis (59.1%). A total of 72.7% experienced these anger attacks as uncharacteristic, 86.4% regretted these symptoms afterwards. The prevalence (females 31.6%, males 45.5%, p=0.405) and monthly number of anger attacks (females , males ; t=x1.043, d.f.= 20, p=0.309) were numerically higher in males than in females, but gender differences were not statistically significant. In the SAD sample patients with anger attacks had significantly lower age of onset of illness ( yr) than those without anger attacks ( yr; t=2.437, d.f.=29.178, p=0.021) and they had a longer course of illness until diagnosed with SAD ( vs yr; t=x2.221, d.f.=33, p=0.033). Interestingly, SAD patients with anger attacks obtained a lower mean GSS ( ) than those without anger attacks ( ; t=3.761, d.f.=33, p=0.001). We examined the subitems of the GSS to identify the source of variation between the groups employing a Bonferroni-type corrected level of statistical significance (p<0.006) to obviate inflation of type I error: there were no significant differences in regard to duration of sleep (t=0.987, d.f.=34, p=0.330), social activity (t=x0.197, d.f.=34, p=0.845), mood (t=x0.197, d.f.=34, p=0.845) and energy (t=x0.114, d.f.=34, p=0.910); However, SAD patients without anger attacks reported significantly more often changes in appetite (t=4.549, d.f.=34, p<0.0001) and weight (t=4.274, d.f.=34, p=0.0001) than those with anger attacks present. Further analysis confirmed that patients without anger attacks suffered more frequently from increased appetite (p=0.0001); however, there were no significant group differences in regard to reduced appetite (p=0.046).

3 Anger attacks in SAD 217 Feeling like attacking others Palpitations or tachycardia Feeling out of control Shortness of breath Shaking or trembling Sweating Lightheadedness or dizziness Fear, panic, or anxiety Hot flushes Attacking physically or verbally Chest tightness or pressure Limb numbness or tingling Throwing or destroying objects Anger attacks as uncharacteristic Guilt or regret after attacks 0% 20% 40% 60% 80% 100% Rate in group of patients with anger attacks present Figure 1. Clinical features of anger attacks in 15 SAD patients (dark grey bars) and seven non-seasonally depressed patients (light grey bars). Symptoms are derived from item 5, a-m of the Anger Attacks Questionnaire (Fava et al., 1991). Asymmetrical 95% confidence intervals are presented with the percentage of patients suffering from different symptoms. Discussion To the best of our knowledge this is the first report on anger attacks in SAD. We found higher rates of anger attacks in SAD compared to non-seasonal depression, but this difference did not reach the level of statistical significance. This could be due to limited sample size and points out the necessity to carry out similar studies in larger samples. The mean monthly number of anger attacks in SAD patients significantly exceeded the frequency in non-seasonally depressed subjects. SAD patients were also more likely to report a larger number of accompanying symptoms during the anger attacks, suggesting that they experience the anger attacks as particularly intense. When comparing SAD patients with and without anger attacks it became apparent that the subgroup with anger attacks had a markedly lower age of onset of illness. This could be indicative of a higher predisposition towards mood disorders. The longer diagnostic latency in these subjects on the other hand may be explained by the social stigma that is associated with aggressive impulses. It has previously been reported that anger attacks are more frequent in depressed patients with comorbid personality disorder (Tedlow et al., 1999). We have tried to exclude any study subjects with categorically defined personality disorder. However, if personality is viewed as a dimensional construct, it cannot be completely ruled out that some of our patients exhibited greater personality pathology, which could have influenced our results. Previous research has likewise found that anger attacks are more prevalent in bipolar disorder than in unipolar depression (Perlis et al., 2004). We intended only to include patients with a strictly unipolar course of illness to accomplish valid intra-group comparisons, however, this may have posed methodological difficulties, since it has been argued before that major depressive disorder with anger attacks is associated with bipolar variables (e.g. positive family history for bipolar disorder) and might be considered midway between unipolar depression without anger attacks and bipolar II disorder (Benazzi, 2003). Our data does not support the idea of gender differences as previously reported for a sample of nonseasonally depressed in-patients (Winkler et al., 2005). It is nevertheless quite possible that our study lacked statistical power (type-ii error) to recognize a true difference between groups. Our secondary finding of a lower GSS in SAD patients with anger attacks

4 218 D. Winkler et al. indicates that these patients were less seasonal than those without anger attacks. Probably patients with anger attacks attribute their symptoms rather to psychosocial factors (e.g. problems with the family or the spouse) than to a seasonal change. It would also be interesting, if SAD patients with anger attacks are more likely to experience non-seasonal affective episodes during their further course of illness. It was surprising for us to see that the difference in the GSS between the groups was almost entirely due to the subitems appetite and weight. Patients with anger attacks had fewer seasonal changes in regard to these symptoms than patients without anger attacks. Few studies have compared the effects of specific emotions such as sadness and anger on eating responses. However, research on the regulation of appetite in healthy persons (Macht et al., 2002) and studies in eating disorders (Deaver et al., 2003; Stickney and Miltenberger, 1999) have identified at least two complex types of emotion-induced changes of eating; decreased eating induced by negative emotions may be a consequence of an emotion-congruent modulation. The affect regulation model on the other hand provides evidence that increased eating occurs because it provides momentary relief from negative affect. This mood control eating may be present in the majority of SAD patients, who suffer from atypical depressive symptoms such as hyperphagia (Winkler et al., 2002a). However, in line with the theory of emotion-congruent modulation intense affects such as aggression have repeatedly been shown to lower food intake in rodents (Greeno and Wing, 1994; Krebs et al., 1996; Robbins and Fray, 1980), which could explain the lower rate of increased appetite and weight gain in our subgroup with anger attacks. In summary this study demonstrates that anger attacks play an important role in the clinical picture of SAD. Compared to other studies investigating anger attacks in outpatients with unipolar major depression (Fava et al., 1996b, 1991, 1997) we have found a rather high prevalence in SAD patients, which is relevant as anger attacks are a major source of the burden of depression. Because of the potentially severe psychosocial consequences of anger attacks, clinicians have to be increasingly aware of these symptoms. Up to now studies investigating the efficacy of light therapy have not established if the presence of anger attacks in SAD influences the outcome. As light therapy has been suggested as treatment of choice for SAD (Partonen and Loennqvist, 1998), it would be worthwhile to investigate the differential response of SAD patients with and without anger attacks to bright-light therapy in comparison to psychopharmacological treatment with SSRIs, which have already been shown to be an effective strategy for treating anger attacks (Fava et al., 1993; Mammen et al., 2004). Acknowledgements None. Statement of Interest None. References Alpert JE, Petersen T, Roffi PA, Papakostas GI, Freed R, Smith MM, Spector AR, Nierenberg AA, Rosenbaum JF, Fava M (2003). Behavioral and emotional disturbances in the offspring of depressed parents with anger attacks. Psychotherapy and Psychosomatics 72, APA (2000). Diagnostic and Statistical Manual of Mental Disorder (4th edn, text revision) (DSM-IV-TR). Washington, DC: American Psychiatric Press. Benazzi F (2003). Major depressive disorder with anger: a bipolar spectrum disorder? Psychotherapy and Psychosomatics 72, Brody CL, Haaga DA, Kirk L, Solomon A (1999). Experiences of anger in people who have recovered from depression and never-depressed people. Journal of Nervous and Mental Disease 187, Deaver CM, Miltenberger RG, Smyth J, Meidinger A, Crosby R (2003). An evaluation of affect and binge eating. Behavior Modification 27, Fava M, Abraham M, Pava J, Shuster J, Rosenbaum J (1996a). Cardiovascular risk factors in depression. The role of anxiety and anger. Psychosomatics 37, Fava M, Alpert J, Nierenberg AA, Ghaemi N, O Sullivan R, Tedlow J, Worthington J, Rosenbaum JF (1996b). Fluoxetine treatment of anger attacks: a replication study. Annals of Clinical Psychiatry 8, Fava M, Nierenberg AA, Quitkin FM, Zisook S (1997). A preliminary study on the efficacy of sertraline and imipramine on anger attacks in atypical depression and dysthymia. Psychopharmacology Bulletin 33, Fava M, Rosenbaum JF, McCarthy M, Pava J, Steingard R, Bless E (1991). Anger attacks in depressed outpatients and their response to fluoxetine. Psychopharmacology Bulletin 27, Fava M, Rosenbaum JF, Pava JA, McCarthy MK, Steingard RJ, Bouffides E (1993). Anger attacks in unipolar depression, Part 1: Clinical correlates and response to fluoxetine treatment. American Journal of Psychiatry 150, Fava M, Vuolo RD, Wright EC, Nierenberg AA, Alpert JE, Rosenbaum JF (2000). Fenfluramine challenge in unipolar depression with and without anger attacks. Psychiatry Research 94, 9 18.

5 Anger attacks in SAD 219 First MB, Spitzer RL, Gibbon M, Williams JB (1996). Structured Clinical Interview for DSM-IV Axis I Disorders Patient Edition. SCID-I/P, version 2.0. New York, NY: New York State Psychiatric Institute, Biometric Research Department. Greeno GG, Wing RR (1994). Stress-induced eating. Psychological Bulletin 115, Koh KB, Kim CH, Park JK (2002). Predominance of anger in depressive disorders compared with anxiety disorders and somatoform disorders. Journal of Clinical Psychiatry 63, Krebs H, Macht M, Weyers P, Weijers HG, Janke W (1996). Effects of stressful noise on eating and non-eating behavior in rats. Appetite 26, Macht M, Roth S, Ellgring H (2002). Chocolate eating in healthy men during experimentally induced sadness and joy. Appetite 39, Magnusson A (2000). An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica 101, Mammen O, Shear K, Greeno C, Wheeler S, Hughes C (1997). Anger attacks and treatment nonadherence in a perinatal psychiatry clinic. Psychopharmacology Bulletin 33, Mammen OK, Pilkonis PA, Chengappa KN, Kupfer DJ (2004). Anger attacks in bipolar depression: predictors and response to citalopram added to mood stabilizers. Journal of Clinical Psychiatry 65, Neumeister A, Praschak-Rieder N, Besselmann B, Rao ML, Gluck J, Kasper S (1997). Effects of tryptophan depletion on drug-free patients with seasonal affective disorder during a stable response to bright light therapy. Archives of General Psychiatry 54, Partonen T, Loennqvist J (1998). Seasonal affective disorder: a guide to diagnosis and management. CNS Drugs 9, Perlis RH, Smoller JW, Fava M, Rosenbaum JF, Nierenberg AA, Sachs GS (2004). The prevalence and clinical correlates of anger attacks during depressive episodes in bipolar disorder. Journal of Affective Disorders 79, Robbins TW, Fray PJ (1980). Stress-induced eating: fact, fiction or misunderstanding? Appetite 1, Rosenthal NE, Bradt GH, Wehr TA (1987). Seasonal Pattern Assessment Questionnaire. Washington, DC: National Institute of Mental Health. Rosenthal NE, Sack DA, Gillin JC, Lewy AJ, Goodwin FK, Davenport Y, Mueller PS, Newsome DA, Wehr TA (1984). Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy. Archives of General Psychiatry 41, Schwartz PJ, Murphy DL, Wehr TA, Garcia-Borreguero D, Oren DA, Moul DE, Ozaki N, Snelbaker AJ, Rosenthal NE (1997). Effects of Meta-chlorophenylpiperazine infusions in patients with seasonal affective disorder and healthy control subjects: diurnal responses and nocturnal regulatory mechanisms. Archives of General Psychiatry 54, Stickney MI, Miltenberger RG (1999). Evaluating direct and indirect measures for the functional assessment of binge eating. International Journal of Eating Disorders 26, Tedlow J, Leslie V, Keefe BR, Alpert J, Nierenberg AA, Rosenbaum JF, Fava M (1999). Axis I and Axis II disorder comorbidity in unipolar depression with anger attacks. Journal of Affective Disorders 52, Willeit M, Praschak-Rieder N, Neumeister A, Pirker W, Asenbaum S, Vitouch O, Tauscher J, Hilger E, Stastny J, Brucke T, Kasper S (2000). [ 123 I]-beta-CIT SPECT imaging shows reduced brain serotonin transporter availability in drug-free depressed patients with seasonal affective disorder. Biological Psychiatry 47, Winkler D, Pjrek E, Kasper S (2005). Anger attacks in depression evidence for a male depressive syndrome. Psychotherapy and Psychosomatics. doi: / Winkler D, Praschak-Rieder N, Willeit M, Lucht MJ, Hilger E, Konstantinidis A, Stastny J, Thierry N, Pjrek E, Neumeister A, Moller HJ, Kasper S (2002a). Seasonal affective depression in 2 German speaking university centers: Bonn, Vienna. Clinical and demographic characteristics. Nervenarzt 73, Winkler D, Willeit M, Praschak-Rieder N, Lucht MJ, Hilger E, Konstantinidis A, Stastny J, Thierry N, Pjrek E, Neumeister A, Moller HJ, Kasper S (2002b). Changes of clinical pattern in seasonal affective disorder (SAD) over time in a German-speaking sample. European Archives of Psychiatry and Clinical Neuroscience 252,

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