Depression and Hemispheric Site of Cerebral Vascular Accident

Transcription

1 Archrves o/cl~nrcalh;europsycholog.v. Vol. I, pp , /86 $3.00 Printed in the USA. All nghtr reserved. Copyright C 1987 Nawanal Academy of Clinical NeuropsycholOgists Brief Report Depression and Hemispheric Site of Cerebral Vascular Accident j. Michael Williams, Marsha M. little, and Kimberly Klein Department of Psychology, Memphis State University In order to investigate the possible role of left and right hemisphere neural structures in the manifestation of depression, 50 left brain damaged and 50 right brain damaged stroke inpatients were administered the Zung Depression Scale (20 S) during the course of the rehabilitation phase of their treatment. These subjects were randomly chosen from all stroke patients receiving rehabilitation services who could be administered the ZDS. Approximately 30% of these subjects, regardless of the site of lesion, were clinically depressed. The severity of depression was independent of demographic factors and time since injury. Right brain damaged patients reported sigm@antly more sleep disturbance, psychomotor agitation and pervasive sense of sadness. These results were discussed in light of previous findings that damage to the left hemisphere results in greater depression. A model of reactive depression that results from neurological disability was proposed to partially account for these findings. Many investigators have examined the relationship between mood disorder associated with cerebral vascular accident and the hemispheric site of the brain lesion. Clinical observations of stroke patients with left-hemisphere lesions suggested that they experienced a greater frequency of depressive catastrophic reactions (Goldstein, 1939). Others have observed that righthemisphere strokes are associated with apathy and indifference (Denny- Brown, Meyer, & Horenstein, 1952). Experimental studies of these phenomena have generally supported these observations. Studies of patients submitted to unilateral Amytal injection indicated that sedation of the left-hemisphere resulted in depressive catastrophic reactions whereas sedation of the right-hemisphere resulted in eu- Requests for reprints should be addressed to J. Michael Williams, Department of Psychology, Memphis State University, Memphis, TN

2 394 J. M. Williams, M. M. Little, and K. Klein phoric reactions (Terzian, 1964; Rossi & Rosadini, 1967). However, Milner (1967) did not find a particular pattern of mood disorder associated with hemispheric side of inactivation. Robinson and coworkers (Robinson & Szetela, 198 1; Robinson & Benson, 1981; Robinson, Kubos, Starr, Rao, & Price, 1984; Lipsey, Robinson, Pearlson, Rao, & Price, 1983) found that almost 50% of all stroke patients suffer clinically significant depression in the early stages of recovery and many of the symptoms last up to 9 months post injury. Further, the manifestations of depression are more severe in patients suffering left-hemisphere lesions and those suffering frontal left hemisphere lesions are most affected. Similarly, Gainotti (1972) found a greater incidence of catastrophic reactions in patients who had suffered a left-hemisphere lesion. He also found that this reaction was more strongly associated with expressive aphasia. In contrast, Folstein, Maiberger, and McHugh (1975) found right-hemisphere stroke patients to be more depressed and Dikmen and Reitan (1974) found no relationship between depression and hemispheric site of lesion. Two explanations have been proposed to account for the results of studies using stroke patients. The first is that unilateral cerebral vascular accident results in disruption of catecolamine systems that regulate mood (Robinson, 1979; Robinson, Shoemaker, Schlumpf, Valk, & Bloom, 1975). The second is that degree of depression is related to the extent of neurological disability and people who suffer left-hemisphere stroke have disabilities that result in greater functional limitations (Benson, 1973; Heilman, 1974). The following study was conducted in an attempt to replicate these previous findings and further examine the manifestations of mood disorder in patients suffering cerebral vascular accident. METHOD One hundred patients who had recently suffered hemorrhagic, thrombotic or embolic completed cerebral vascular accident participated in this study (Table 1). They were all inpatients of the Regional Rehabilitation Center of Baptist Hospital in Memphis, Tennessee and were therefore medically stable and engaged in rehabilitation treatment. Fifty each of left- and right-hemisphere cerebral vascular accident were administered the Zung Depression Scale (Zung, 1965). Aphasic patients who could not comprehend the ZDS items were not included in this study. The hemispheric side of cerebral infarct was determined from CT scan findings, angiogram or neurological evaluation. Differences between lesion site groups on the ZDS were examined using Multivariate Analysis of Variance (MANOVA), in order to control for multiple comparisons, and univariate paired f-tests.

3 Brief Report 395 TABLE 1 Demographic Chsmcteristics Right Lesion Site Left M SD M SD As 69 yrs yrs Education 10.3 yrs yrs. 3.8 Time Since Injury 3.1 mos mos. 2.8 Sex 24M 26F 23M 27F Note: Paired t-test comparisons revealed no significant differences between the groups. RESULTS Table 1 presents the comparison of stroke groups on demographic variables and the time elapsed since onset of the stroke. Univariate paired t-test analyses revealed that there were no significant differences between lesion site groups on any demographic variables or time since injury. As can be seen in Table 2, the incidence of significant depression in this sample of stroke patients was approximately 30%, which was determined using a cut-off score of 50 on the ZDS (Zung, 1983). This is comparable to the high incidence of depression others have observed in this population (Robinson & Price, 1982). The overall MANOVA results were statistically significant for the ZDS items [Multivariate F(20, 79)=2.12, p<.ol], although the groups were not significantly different on the total score from the ZDS, when the means were examined using univariate C-tests. The right hemisphere lesioned group endorsed significantly greater depression on 3 of the 20 ZDS items. These were: pervasive sadness (item. l), sleep disturbance (item.4) and restlessness or agitation (item.13). DISCUSSION These results clearly support other studies which have found a high incidence of depressive symptoms among patients who have recently sustained a cerebral vascular accident (Benson, 1973; Robinson & Benson, 1981). Clearly depression is a common result of this type of brain injury and it strongly affects rehabilitation outcome (Oradei & Waite, 1974; Schwab, 1972). However, virtually none of these patients receive treatment for their depression (Robinson & Price, 1982). This study and others suggest that this complication is significant and potentially debilitating, thus deserving treatment. Folstein et al. (1975) found that imipramine was effective in treating the depression of one stroke patient in their study. It has yet to be determined if

4 396 J. M. Williatns, M. M. Little, and K. Klein TABLE 2 Zung Depression Scale Comparison for Hemispheric Site of Stroke ZDS Items Right Left M SD M SD t(98) I. Pervasive Sadness 2. Feel Best In Morning 3. Crying Spells 4. Trouble Sleeping 5. Same Appetite 6. Attracted IO Other Sex 7. Losing Weight 8. Constipation 9. Heart Beats Faster IO. Tired I I. Mind Is Clear 12. Easy To Do Things 13. Restless 14. Hopeful 15. Irritable 16. Easy To Make Decisions 17. Feel Needed 18. Life Is Full 19. Better Off Dead 20. Still Enjoy Things Total Depression Score I I ; I.4.I 1.7 I.1 I.7 1.o o 2.0 I o I I I.o I I * I.8.9 I I 2.3 I I I Note: The ZDS ranges from I, None of the Time, IO 4, All or most of the Time. *p<.o5 **p<.ol, MultivariateF(20, 79)=2.12,p<.Ol. other treatments for depression, such as cognitive behavior therapy (e.g., Beck, 1970), will likewise be effective in this group. This study discovered that right-hemisphere lesions were associated with slightly greater depressive symptoms of pervasive sadness, sleep disturbance and agitation. These results are similar to those of Folstein et al. (1977). However, the results stand in stark contrast to numerous investigations (e.g., Gainotti, 1972; Robinson & Price, 1982; Robinson & Szetala, 1980) that found greater depression among subjects with left hemisphere injury. All of the patients in the present sample suffered considerable physical and cognitive limitations imposed by the stroke. Most of these subjects were assessed within four months of their injury. Their depressive symptoms may be due to the acute reactive effects of debilitating illness (Benson, 1973). This reaction may be sufficiently severe in the early stages of recovery that they mask the potentially endogenous depression that is suggested from the results of studies by Robinson & Price (1982) and Gainotti (1972). All of the subjects in these previous studies were assessed well after the initial trauma and the persistent endogenous effects of mood disorder could therefore be observed. Thus both reactive and endogenous processes might operate to

5 Brief Report 397 produce the depression observed in all these studies and might explain the occurrence of the apparently conflicting findings regarding lesion site and depressive symptoms. In order to assess these effects, future studies should include some measure of disability status and symptoms similar to the control exercised by Folstein, Maiberger, and McHugh (1977), who compared stroke patients to orthopedic patients. However, future studies must additionally control for the extent of aphasic and cognitive symptoms as well as physical limitations. Also of interest are the patient s perception of the cause of their depressive symptoms and the interaction of the patient s disability with everyday demands. If depression in stroke represents a reaction of the patient to perceived disabilities, then future studies should directly examine this relationship and control for these effects in studying the relationship between brain lesion site and depression symptomatology. An investigation of the reactive component of depression in stroke may also lead to the evaluation of psychotherapy intervention strategies that have hitherto been neglected as studies have focused only on the lesion site of stroke and the possible endogenous nature of the resulting depression. REFERENCES Beck, A. T. (1970). Cognitive Therapy: Nature and relation to behavior therapy. Behavior Therapy, 1, Benson, D. F. (1973). Psychiatric aspects of aphasia. British Journal of Psychiatry, 123, Denny-Brown, D., Meyer, J. S., & Horenstein, S. (1952). The significance of perceptual rivalry resulting from parietal lesion. Bruin, 75, Dikmen, S., & Reitan, R. (1974). Minnesota Multiphasic Personality Inventory correlates of dysphasic language disturbance. Journal of Abnormal Psychology, Folstein, M. F., Mailberger, R., & McHugh, P. R. (1975). Mood disorder as a specific complication of stroke. Journul of Neurology, Neurosurgery and Psychiutry, 40, Gainotti, G. (1972). Emotional behavior and hemispheric side of lesion. Corfex, 8, Goldstein, K. (1939). The effects of brain damage on the personality. Psychiatry, 15, Heilman, K. (1974). Neuropsychologic changes in the stroke patient. Geriatrics, 29, Lipsey, J. R., Robinson, R. G., Pearlson, G. D., Rao, K., & Price, T. R. (1983). Mood changes following bilateral hemisphere brain injury. British Journul of Psychiatry, 143, Mimer, B. (1967). Discussion of the subject: Experimental analysis of cerebral dominance in man. In C. H. Millikan and F. L. Darley (Eds.) Bruin Mechanisms Underlying Speech and Lunguge, New York: Grune & Stratton. Oradei, D., & Waite, N. S. (1974). Group psychotherapy with stroke patients during the immediate recovery phase. American Journal of Orthopsychiufry, 44, Robinson, R. G. (1979). Differential behavioral and biochemical effects of right and left hemispheric cerebral infarction in the rat. Science, 205, Robinson, R. G., & Benson, D. F. (1981). Depression in aphasic patients: Frequency, severity, and clinical-pathological correlations. Bruin and Language, 14, Robinson, R. G., Kubos, K. L., Starr, L. B., Rao, K., & Price, T. R. (1984). Mood disorders in stroke patients. The importance of lesion location. Bruin, 107,

6 398 J. M. Williams, M. M. Little, and K. Klein Robinson, R. G., & Price, T. R. (1982). Post-stroke depressive disorders: a follow-up study of 103 patients. Stroke, 13, Robinson, R. G., Shoemaker, W. J., Schlumpf, M., Valk, T., & Bloom, F. E. (1975). Effect of experimental cerebral infarction in rat brain on catecholamines and behavior. Nofure, 255, Robinson, R. G., & Szetala, B. (1981). Mood change following left hemispheric brain injury. Annuls of Neurology, 9, Rossi, G. F., & Rosadini, G. (1967). Experimental analysis of cerebral dominance in man. In C. H. Millikan & F. L. Darley (Eds.), Bruin mechanisms underlying speech and lunguoge. New York: Grune & Stratton. Schwab, J. J. (1972). Emotional considerations in cancer and stroke. New York Store Journalof Medicine, 72, Terzian, H. (1964). Behavioral and EEG effects of intracarotid sodium amytal injection. Acre Neurochir, Zung, W. W. K. (1%5). A self-rating depression scale. Archives of General Psychiatry, 12, Zung, W. W. K. (1983). Self-rating scales for psychopathology. In T. Crook, S. Ferris, & R. Bartus (Eds.), Assessment in geriutic psychopharmacology. Connecticut: Mark Powley Associates.