Archives of Psychiatric Nursing 28 (2014) 368–371

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A Survey on 465 Patients With Post-Stroke Depression in China Ning Sun a, Qiu-Jie Li b,⁎, Dong-Mei Lv a, Jing Man c, Xue-Song Liu a, Mei-Ling Sun a a b c

Department of Nursing, The Second Affiliated Hospital of Harbin Medical University, School of Nursing, Harbin Medical University, Harbin, P. R. China School of Nursing, Harbin Medical University, Harbin, P. R. China Neurology Department, The Second Affiliated Hospital of Harbin Medical University, Harbin, P. R. China

a b s t r a c t The incidence of PSD patients is very high. To analyze the related factors and incidence of post-stroke depression (PSD). A total of 465 stroke patients were evaluated by a self-designed questionnaire, Self-Rating Depression Scale (SDS) and Hamilton Depression Rating Scale (HAMD). The neurologic deficit score was tested using the National Institute of Health stroke scale (NIHSS). A multiple factor analysis with the logistic regression method was carried out to analyze related factors of PSD. A total of 146 cases (31.4%) were identified as suffering from PSD. In addition the stepwise regression analysis showed that important risk factors of PSD included of sex, lesion location, the course of post-stroke and degree of neurological deficit score (all P b 0.05). Above mentioned factors about the patients of PSD are very significant and may provide reference for further treating. © 2014 Published by Elsevier Inc.

Depression is a distressing illness and is associated with a substantial reduction in quality of life and increased risk of suicide (Saarni, Suvisaari, Sintonen, et al., 2007; Teasdale & Engberg, 2001). Poststroke depression (PSD) is among the most frequent neuropsychiatric consequence of stroke. PSD occurs in at least one third of patients within the first year of stroke onset (Hackett & Anderson, 2005), being associated with significant social and cognitive impairment, poor rehabilitation outcomes and high mortality rates (Starkstein, Mizrahi, & Power, 2008). Depression is a distressing illness and is associated with a substantial reduction in quality of life and increased risk of suicide (Saarni et al., 2007; Teasdale & Engberg, 2001). PSD occurs in up to 50% of all stroke survivors (Robinson, 1998; Wiart, Petit, Joseph, et al., 2000) with prevalence peaking approximately 6 months after the vascular event (Dafaer, Rao, Shareef, et al., 2008). PSD is often inadequately diagnosed and treated, despite an evidence base for effective treatments (Dafaer et al., 2008). The etiology of the development of PSD is complex and remains incompletely understood. One of the main questions remaining controversial to the current time is the relationship between the location of the focal lesion and the development of post-stroke depression (Gordon & Hubbard, 1997; Neau, Ingrand, Mouille-Brachet, et al., 1998). PSD is believed to arise most frequently when focal lesions are located in the left frontal area or the adjacent basal nuclei. A role for the subcortical ganglia of the right hemisphere has been demonstrated. The development of post-stroke depression correlates with histories of depressive episodes, the extent of functional disorders, age, education, the family situation, gender, and the presence of a history of stroke.

⁎ Corresponding Author: Qiu-jie Li, PhD, RN, School of Nursing, Harbin Medical University. Harbin, P. R. China, 150040. E-mail addresses: [email protected] (N. Sun), [email protected] (Q.-J. Li). http://dx.doi.org/10.1016/j.apnu.2014.08.007 0883-9417/© 2014 Published by Elsevier Inc.

Prospective observations of patients with PSD have shown that affective symptoms persist in the long term if left untreated. Thus, the symptoms of major depression identified in 27% of stroke patients persisted for 1 year, while the symptoms of minor depression seen in 20% of patients persisted for more than 2 years (Morris, Robinson, & Raphael, 1990; Robinson & Price, 1982). In their recent studies of 100 patients for 18 months, Berg, Palomäki, Lehtihalmes, Lönnqvist, and Kaste (2003) showed that depression occurred in 46% of patients within the first 2 months of stroke, while the first symptoms appeared only at 12 months in 12% of patients. The incidence of post-stroke depression among patients admitted for treatment was 40.4%, compared with 37.4% among out-patients 3 years after stroke (Bogolepova, 2003). The incidence of depression was maximal in the late recovery period following is chemic stroke, reaching 72.2%. Post-stroke depression developed more frequently in older patients and those with marked focal neurological lesions. Bogolepova (2003) indicate that risk factors for the development of post-stroke depression in the long-term poststroke period are being female, being elderly, having a right hemisphere lesion, and having poor recovery of self-care ability. The objective is to evaluate the factors associated with PSD as assessed with the Hamilton Depression Scale (HAMD) and Self-rating depression scale (SDS). METHOD Study Population Four hundred sixty-five patients who first visited the department of Neurology in the Second Affiliated Hospital of Harbin Medical University were enrolled from 1 July 2012 to 31 August 2013. Diagnostic criteria were agreement with the China 4th National Cerebrovascular Meeting's diagnostic criteria for stroke. CT-scan and MRI were used to diagnose the patients finally.

N. Sun et al. / Archives of Psychiatric Nursing 28 (2014) 368–371

Other inclusion criteria are: (1) being conscious and no cognitive disorder; (2) being less than 6 months post stroke; (3) being 30 years or older; and (4) having sufficient communication skills. Exclusion criteria are: (1) co-morbidity that might affect outcome (e.g., cancer or major psychiatric illnesses for which psychological treatment is given at the moment of inclusion); (2) a major depression diagnosis requiring medication; and (3) a pre-morbid major depression diagnosis, or having received psychiatric care for depression. Measures The Demographic Data Questionnaire was designed by the researchers and collected information about the gender, age, job category, marital status, education level, history of hypertension, history of diabetes, history of coronary heart disease, stroke classification, side of lesion from the CT report, and course of disease. The dynamics of depressive disorders were assessed using the SelfRating Depression Scale (SDS). The depressive disorders were diagnosed if the score was higher than 40. Post-stroke depression was diagnosed in accordance with IDC-10 criteria. The severity of the depressive state was evaluated using the Hamilton Depression Rating Scale (HAMD) (17 items) (Aben, Verhey, Lousberg, Lodder, & Honig, 2002). Mild depression was defined if the score was higher than 7; Moderate depression was defined if the score was higher than 17; severe depression was defined if the score was higher than 24. The questionnaires were finished by two neurologists who were trained 2 weeks before the research. The neurologic deficit score was tested using the National Institute of Health stroke scale (NIHSS). The scale was finished by two neurologists. The two neurologists were trained 2 weeks before the study. An obligatory condition was informed consent from the patient. Data Analysis The data were analyzed using SPSS 15.0 software. Descriptive statistics (mean and standard deviation) were used to summarize data. Independent samples t tests were used to compare means for continuous variables with 2 groups, one-way ANOVAs for continuous variables with more than 2 groups and two test for categorical variables. Stepwise multiple regression analysis was used to test the influence of the demographic variables to depression. The differences were considered to be statistically significant if P b 0.05. RESULTS A total of 465 patients agreed to participate in the study. Demographic data included as following: male 198, female 267; the average age is 65.57 ± 10.16; married 424; unemployed or retirement 336; urban residents 446, rural residents 19; higher educators 26, secondary education and below 439; hypertension 403, diabetes 367, coronary heart disease 122; stroke type: cerebral infarction 385, cerebral hemorrhage 80; diseased location: left hemisphere stroke 118, right hemisphere stroke 127 and bilateral hemisphere stroke 22; course of disease: less than 1 month 320, more than 1 month 145. Neurologic deficit score: mild (0–15), 105; moderate (16–30), 153; severe (31–45), 207. There were 146 PSD patients, with the female 65 and male 81. The scores of SDS were 50.26 ± 7.65 points. The scores of HAMD were all higher than 7. The scores of HAMD were 15.77 ± 5.45 points. The prevalence of PSD was 31.4%. The single factor analysis for depression is showed in Table 1. According to the multiple regression analysis, the important risk factors of PSD included of sex, lesion location, the course of post-stroke and degree of neurological deficit score (Table 2).

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Table 1 The Single Factor Analysis Between PSD and Non-PSD (N = 465). PSD (n) Gender Male Female Age ≥60 b60 Job category Be on the job Unemployed and retire Residence City Village Marital status Married Spinsterhood Education level Higher educators Secondary education and below Past medical history Hypertension Diabetes Coronary heart disease Stroke history Stroke type Cerebral infarction Cerebral hemorrhage Diseased location Left hemisphere stroke Right hemisphere stroke Bilateral hemisphere stroke Course of disease Less than 1 month More than 1 month Neurologic deficit score Mild (0–15) Moderate (16–30) Severe (31–45)

χ2

P

11.87

0.001

Non-PSD (n)

65 81

133 186

88 58

180 139

62 84

67 252

142 4

304 15

128 18

296 23

12 134

14 305

87 89 33 108

316 278 89 297

128 18

257 62

60 55 31

58 72 189

58 88

262 57

36 62 48

69 91 159

0.801

0.398

0.004

0.955

3.016

0.079

0.914

0.313

0.524

0.431

3.792 3.108 3.346 3.579 3.869

0.062 0.091 0.068 0.068 0.054

16.987

0.006

69.892

0.000

27.987

0.002

DISCUSSION The mean prevalence of PSD has been estimated to be around 30–35%, ranging from 20 to 60% 16. The prevalence of PSD in our study was 31.4%, consistent with some studies in Western countries (Hackett & Anderson, 2005; Paolucci et al., 2005). The mean HAMD score in the patients was 15.77 ± 5.45 points. The HAMD diagnosed mild depression in 58 patients (39.7%) and moderate depression in 78 patients (53%). Risk factors related to PSD are constitutional (female gender), clinical (previous stroke, previous depressive or psychiatric episode, cognitive impairment or aphasia), functional (severity of disability); environmental (premorbid neurotic personality and social isolation), and biological (family history of depression). Other risk factors such as education level, previous stroke, stroke severity, apathy, denial reaction at the acute stage, and cerebral atrophy have been alternatively found to be associated with PSD (Paolucci et al., 2005; Whyte & Mulsant, 2002). Our data indicate that risk factors for the development of post-stroke depression are being female, having a diseased hemisphere lesion, having longer course of disease and having neurologic deficit (Table 1). The

Table 2 Stepwise Multiple Regression of Predictor Values Explaining Depression. Variable Gender Diseased location Course of disease Neurologic deficit score

B

Beta

t

P

0.65 0.24 −0.286 0.05

0.19 0.07 0.15 0.03

11.74 7.36 5.09 5.87

0.001 0.004 0.003 0.015

R2 = 0.116, adjusted R2 = 0.215, F = 36.508, P b 0.0001.

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results were consistent with Bogolepova's (2003) study. Stepwise multiple regression analysis was used to test the influence of the demographic variables on PSD. Stepwise multiple regression revealed that 21.5% of the variance in depression was explained by a combination of gender, diseased location, course of disease and neurologic deficit (Table 2). Our results indicated that the risk factors are female, left lesion, longer course of disease and neurologic deficit. The etiology of the development of post-stroke depression is complex and remains incompletely understood. One of the main questions remaining controversial to the current time is the relationship between the gender and the development of post-stroke depression (Kotila, Numminen, Waltimo, & Kaste, 1998). Our results indicated that being female is associated with PSD, consistent with Kotila et al.'s (1998) study. Another of the main questions remaining controversial to the current time is the relationship between the location of the focal lesion and the development of PSD (Neau et al., 1998). With regard to biological mechanism, there are the following statements: on the one hand the historical association (Robinson, Starkstein, & Price, 1988) TR between lesion in the left frontal pole and PSD (also with PSD severity) was not confirmed by other authors (Vataja et al., 2004); on the other hand, a correlation between PSD and right hemispheric lesion was shown (Machale, O’Rourke, & Dennis, 1998). Patients with left hemisphere lesions more often showed more marked sleep disturbances and a predominance of verbal expressions of the depressed state. Our results indicated that the left hemisphere lesions are associated with PSD, consistent with Robinson et al.'s (1988) study. Studies performed at various times have demonstrated that its incidence can reach 79% (Gustafson, Nilsson, Mattsson, et al., 1995) and it can develop at both the early and late post-stroke periods (Huff, Steckel, & Sitzer, 2003). However, the vast majority of cases of PSD are encountered in patients during the recovery phase, 3–6 months after stroke (Alexopoulos, Meyers, & Young, 1997). In their recent studies of 100 patients for 18 months, Berg et al. (2003) showed that depression occurred in 46% of patients within the first 2 months of stroke, while the first symptoms appeared only at 12 months in 12% of patients. Among patients with early onsets of post-stroke depression, symptoms persisted for 12 and 18 months. Our results indicated that the longer course of the disease is associated with PSD, consistent with some studies in the West (Berg et al., 2003). From the clinical point of view, it is important that 2–3% of patients show depressive symptoms without depressive mood (“masking” of depression). The main manifestations of this depression may be impairments of biological rhythms (sleeplessness, hypersomnia) and somatizing disorders, particularly autonomic vascular dystonia, vertigo, various algic phenomena, etc. The symptom profile of vascular depression has been described as consisting of prominent psychomotor retardation, cognitive impairment, and disability with limited depressive ideation, insight, and depressed mood (Fedoroff, Starkstein, Parikh, Price, & Robinson, 1991; Fujikawa, Yamawaki, & Touhouda, 1994). While poststroke depression could be considered a subtype of vascular depression, its symptom profile appears more similar to that of functional depression than that of vascular depression (Paradiso, Ohkubo, & Robinson, 1997). In our study, all patients had relatively moderate focal neurological deficits (42.4%). The neurologic deficits are associated with PSD, consistent with some studies in Western (Fujikawa et al., 1994).

CONCLUSION Depression is a frequent and serious complication after stroke for the possible negative repercussions on patients' recovery. The incidence of PSD among patients admitted was 31.4%. PSD developed more frequently in female patients and those with marked focal neurological lesions. Our data indicate that risk factors for the development of PSD are

sex, lesion location, the course of post-stroke and degree of neurological deficit score. Acknowledgment The authors would like to thank the patients who participated in the study, and Professor Li Kang for statistical assistance, who are working in the Department of Public Health, Harbin Medical University, China. Conflict of interest The authors declare that they have no conflict of interests. There are no possible conflicts of interest including financial support, corporate involvement, patent holdings, etc. Ethical approval Permission to conduct the study and to obtain entry for the purpose of gathering the data was obtained from the researchers' academic institution and the appropriate administrative person of each hospital. Author contributions NS and DML were responsible for the study conception and design. JM and XSL performed the data collection. NS, DML and QJL performed the data analysis. NS, DML, JM, MLS and QJL were responsible for the drafting of the manuscript and made critical revisions to the paper for important intellectual content. NS and JM provided statistical expertise. QJL obtained funding. MLS provided administrative, technical or material support. MLS, XSL and QJL supervised the study. NS, DML and JM provided other contributions. Financial disclosure None reported. References Aben, I., Verhey, F., Lousberg, R., Lodder, J., & Honig, A. (2002). Validity of the beck depression inventory, hospital anxiety and depression scale, SCL-90, and hamilton depression rating scale as screening instruments for depression in stroke patients. Psychosomatics, 43, 386–393. Alexopoulos, G., Meyers, B., & Young, R. (1997). Clinically defined vascular depression. The American Journal of Psychiatry, 154, 562–565. Berg, A., Palomäki, H., Lehtihalmes, M., Lönnqvist, J., & Kaste, M. (2003). Poststroke depression. An 18-month follow-up. Stroke, 34, 138–143. Bogolepova, A. N. (2003). Criteria for the Diagnosis and Prognosis of Ischemic Stroke (A ClinicalNeuropsychological Study). [in Russian]. Author’s Abstract of Doctoral Thesis, Moscow. Dafaer, R. M., Rao, M., Shareef, A., et al. (2008). Poststroke Depression. Stroke Rehabilitation, 15(1), 13–21. Fedoroff, J., Starkstein, S., Parikh, R., Price, T., & Robinson, R. (1991). Are depressive symptoms nonspecific in patients with acute stroke? The American Journal of Psychiatry, 148(9), 1172–1176. Fujikawa, T., Yamawaki, S., & Touhouda, Y. (1994). Background factors and clinical symptoms of major depression with silent cerebral infarction. Stroke, 25, 798–801. Gordon, W. A., & Hubbard, M. R. (1997). Poststroke depression: an examination of the literature. Archives of Physical Medicine and Rehabilitation, 78, 658–663. Gustafson, Y., Nilsson, I., Mattsson, M., et al. (1995). Epidemiology and treatment of poststroke depression. Drugs & Aging, 7, 298–309. Hackett, M. L., & Anderson, C. S. (2005). Predictors of depression after stroke: A systematic review of observational studies. Stroke, 36, 2296–2301. Huff, W., Steckel, R., & Sitzer, M. (2003). Poststroke depression: risk factors and effects on the course of the stroke. Nervenarzt, 74, 104–114. Kotila, M., Numminen, H., Waltimo, O., & Kaste, M. (1998). Depression after stroke: Results of the finnstroke study. Stroke, 29, 368–372. Machale, S. M., O’Rourke, S. J., & Dennis, M. S. (1998). Depression and its relation to lesion location after stroke. Journal of Neurology, Neurosurgery, and Psychiatry, 64, 371–374. Morris, P. L., Robinson, R. G., & Raphael, B. (1990). Prevalence and course of depressive disorders in hospitalized stroke patients. International Journal of Psychiatry in Medicine, 20, 349–364. Neau, J. P., Ingrand, P., Mouille-Brachet, C., et al. (1998). Functional recovery and social outcome after cerebral infarction in young adults. Cerebrovascular, 8(5), 296–302. Paolucci, S., Gandolfo, C., Provinciali, L., Torta, R., Sommacal, S., Toso, V., & DESTRO Study Group (2005). Quantification of the risk of post-stroke depression: the Italian multicenter study DESTRO. Acta Psychiatrica Scandinavica, 112, 272–278. Paradiso, S., Ohkubo, T., & Robinson, R. (1997). Vegetative and psychological symptoms associated with depressed mood over the first two years after stroke. International Journal of Psychiatry in Medicine, 27(2), 137–157. Robinson, R. G. (1998). Treatment issues in poststoke depression. Depression and Anxiety, 8, 85–90. Robinson, R. G., & Price, T. R. (1982). Post-stroke depressive disorders: a follow-up study of 103 outpatients. Stroke, 13, 635–641. Robinson, R. G., Starkstein, S. E., & Price, T. R. (1988). Post-stroke depression and lesion location. Stroke, 19, 125–126.

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