(Stroke. 1995;26:850-856.)
© 1995 American Heart Association, Inc.
Articles |
Poststroke Depression
Is There a Pathoanatomic Correlate for Depression in the Postacute Stage of Stroke?
From the Research Program on Neuropsychology and Neurolinguistics (M.H.), the Department of Rehabilitation Psychology (M.H.), and the Department of Neuroradiology (M.S.), University of Freiburg; and the Department of Neurology, University of Magdeburg (C.B., C.-W.W.) (Germany).
Correspondence to Manfred Herrmann, MD, PhD, Research Program on Neuropsychology and Neurolinguistics, University of Freiburg, Belfortstrasse 16, D-79085 Freiburg, Germany. E-mail herrmann@psychologie.uni-freiburg.de.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose This study is aimed at the pathoanatomic correlates of depression in the postacute stage of patients with stroke.
Methods Of a consecutive series of 104 stroke patients, a subgroup of 47 patients with single demarcated unilateral lesions was selected. Clinical examination, neuroradiological CT scan examination, and psychiatric assessment were performed within a 2-month period after the acute stroke. Depression was assessed with the Cornell Depression Scale, the Montgomery-Åsberg Depression Rating Scale, and according to modified DSM-III-R criteria. The neuroradiological examination of all patients was performed on the same scanner, and lesion location, lesion volume, and ventricle-to-brain ratio were analyzed.
Results We found no significant differences in depression scores between patients with left and right hemisphere lesions and no correlation between the severity of depression and the anteriority and the volume of lesion or brain atrophy. Major depressive disorders were only found in nine patients with left hemisphere lesions, all involving the basal ganglia, whereas none of the patients with right hemisphere stroke exhibited major depression.
Conclusions Lesions in the vicinity of the left hemisphere basal ganglia tend to play a crucial role in the development of major depression after the acute stage of stroke. The pathophysiological implications of this finding are discussed.
Key Words: depression • neuroanatomy • neuropsychology • tomography
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Depressive alterations after stroke have been a subject of widespread interest in the last decade. Although various hypotheses exist concerning the etiology of poststroke mood disorders, there is increasing evidence that poststroke depressive changes may have an organic basis due to biochemical derangement. Depressive stroke patients exhibit alterations of cortical receptor sensitivity1 2 and neurotransmitter metabolite concentrations in cerebrospinal fluid3 as well as abnormalities in electrophysiological parameters (eg, shortening of rapid eye movement latency4 ). Grasso et al5 were able to demonstrate a local decrease of cerebral blood flow in poststroke depressed patients. Interest in the relationship between lesion location and type and severity of depression has motivated a series of studies focusing on the pathoanatomic correlates of depressive disorders. Robinson and coworkers6 7 8 demonstrated in a series of articles that left hemisphere (LH) lesions may be associated with a higher incidence of depression and that within the LH, severity of depression may be correlated with the distance between lesion and anterior pole of the hemisphere. Some groups were able to replicate these findings9 10 ; others found no significant correlation between lesion location and depressive alterations after stroke.11 12 13 On the other hand, some data indicate a higher incidence of depression after right hemisphere (RH) lesions.14 15 Lesions localized in the left frontal lobe or basal ganglia seem to be more often associated with severe depressive disorders than lesions localized in other brain areas.16 17 18 Other pathoanatomic parameters such as volume of lesion19 20 21 22 or cortical/subcortical atrophy10 23 showed no clear-cut association with type or severity of depressive disorders.
Critical problems in interpreting these data are posed by wide differences in the patient groups involved, time span from onset of stroke to investigation, definition of terms, measurements, and neuroradiological equipment. Some groups use the same type of measurement with different definitions (eg, the distance of the lesion to the anterior pole of the brain8 20 ), while other groups use the same term with different measurements (eg, "brain atrophy," an index based on planimetric measurements23 or on diagnostics by evidence10 ).
The following study is aimed at the correlation of poststroke depression with well-defined pathoanatomic parameters in a homogeneous subgroup of patients in the postacute stage of stroke. We addressed the following questions: Are there differences between lesion location and type and severity of poststroke depressive disorders? Does the severity of depression correlate with the distance of the lesion to the anterior pole of the brain, the volume of the lesion, and/or preexisting cortical/subcortical atrophy? Do patients who develop depression after stroke share a common lesion configuration?
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Subjects
Patients included in this study were selected from a consecutive series of 104 patients from our stroke data bank. Criteria of inclusion were the following: (1) no history of psychiatric diagnosis or alcohol or drug abuse; (2) first single unilateral stroke event (no transient ischemic attack or prolonged reversible ischemic neurological deficit); and (3) no severe or consumptive concomitant disease. The main group was narrowed down to a subgroup of 47 patients who had been examined in the first 2 months after the stroke event and who fulfilled the following neuroradiological criteria: (1) all CT scans had been acquired with the same scanner and the same protocol; (2) all patients showed a single clearly demarcated lesion and no other signs of brain disease; and (3) the hemisphere contralateral to the lesion was not affected (no signs of space occupation due to midline shift or edema). All patients were initially admitted to the Freiburg University Clinic. Most examinations were performed during inpatient treatment at the Neurological Clinic; some patients were examined in a secondary referral center. The group consisted of 31 male and 16 female patients. Fifteen suffered from RH and 32 from LH stroke. The median age was 62 years (Table 1
). None of the patients was treated with antidepressant
medication or any drug with depression as a known side effect.
|
Methods
All patients were assessed with detailed neurological
examinations and neuropsychological tests, which are not the subject of
the present report. Relevant demographic, psychiatric, and
neuroradiological data are described in Table 1
.
Psychiatric Examinations
All patients were examined with the Cornell Depression Scale
(CDS24 ), which was considered an adequate instrument for
the assessment of the severity of depressive disorders in brain-damaged
patients because of its lower weighting of cognitive and somatic items.
Psychometric properties of this scale in brain-damaged patients have
been reported elsewhere.22 We used the Montgomery-Åsberg
Depression Rating Scale (MAS25 ) as an external validation
criterion. Furthermore, all patients were classified according to the
Diagnostic and Statistical Manual of Mental Disorders,
edition 3, revised (DSM-III-R) criteria26 (whenever
possible with the use of the Structured Clinical Interview for
DSM-III-R27 ). In the diagnosis of a dysthymic depression
we had to ignore the 2-year criterion of DSM-III-R classification.
Therefore, we use the operatively defined term "minor
depression," which indicates that the respective patients otherwise
fulfilled the DSM-III-R criteria of a dysthymic disorder with symptoms
lasting less than 2 months.
Neuroradiological Examinations
All patients were studied with the same CT scanner (Siemens
Somatom-ART) under standardized conditions of data acquisition (four
infratentorial and eight supratentorial slices parallel to the
orbitomeatal line; nonenhanced CTs). Data were transferred to a Silicon
Graphics Indigo work station and processed with ANALYZE
software (Mayo Foundation Computer Research Center). Software developed
in our laboratories was used to superimpose lesions in standardized
slices. The demarcated infarctions were analyzed with respect to the
topography of lesion configuration (based on Matsui and
Hirano28 and Talairach and Tournoux29 ) and
territories of vascular supply (based on Damasio and
Damasio,30 including the territories of the deep
perforators of the carotid system of Ghika et al31 ). We
calculated the average distances of the anterior and posterior lesion
borders to the frontal pole of the brain in each slice that contained a
demarcated lesion. Lesions were classified as anterior, posterior, or
nonclassifiable according to the definitions of Robinson et
al.8 Furthermore, the mean distance from the anterior
lesion border to the frontal pole in percentage of overall
anterior-posterior distance in each slice was calculated (ANTPER). For
the assessment of cortical/subcortical atrophy, we performed
planimetric measurements on the original CT data and calculated the
lateral ventricle-to-brain ratio (VBR) contralateral to the side of the
stroke lesion (according to the method of Starkstein et
al23 ). VBR measurements were performed on the slice that
showed the greatest width of the body of the lateral ventricles. Areas
of interest were marked by setting density thresholds of cerebrospinal
fluid and brain tissue. Lesion volume was calculated in percentage of
forebrain volume on standardized slices. We established interrater
reliability for all neuroradiological measurements. The reliability
coefficients obtained ranged between r=.85
(P<.001) for planimetric indexes and r=.98
(P<.001) for ANTPER measurements and classifications of
lesion location.
Statistical Analysis
Data analysis was performed by nonparametric procedures with
the use of rank correlation coefficients, Mann-Whitney U
statistics, and 
2 tests. All probability values
are two-tailed and corrected for ties.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Six patients (12.7%) showed a primary or secondary hemorrhagic stroke event; all others showed ischemic lesions. Sixty-three percent of all patients exhibited hemiparesis and 62% sensory disturbances. A visual field defect was diagnosed in 31% of the patients, and 62% exhibited facial weakness. There were no significant group differences between patients with RH and LH lesions with respect to motor or sensory deficits or visual field defects. Eighty-four percent of the patients with LH lesions showed aphasia, whereas none of the patients with RH stroke was aphasic. According to the Aachen aphasia test32 performed 1 month after aphasia onset, 15.6% of the LH group exhibited amnestic or Wernicke's aphasia, 25% exhibited Broca's aphasia, 18.8% exhibited global aphasia, and 9.4% demonstrated a nonclassifiable aphasic syndrome. There was no significant effect between groups in demographic variables such as age, education, or time since stroke.
Psychiatric Findings
A summary of the depression ratings is presented in Table 1. The median score on all rating scales was low, but a
wide range indicated a bimodal distribution. We found a high
correlation between CDS and MAS (r=.80, P<.001)
but no significant difference of depression scores between LH and RH
lesions. According to the DSM-III-R criteria as modified above, 8
patients (17%) exhibited minor depression (5 [33%] RH lesions and 3
[9%] LH lesions), and 9 patients (19%) were diagnosed as major
depressive; the latter all had LH lesions. To analyze the relationship
between the clinical diagnosis and the severity rating of depression,
we performed a cross-tabulation, which is presented in Table 2. Patients with a clinical diagnosis of depression
scored higher on both rating scales. A Mann-Whitney U test
revealed a significant difference between both groups with a clinical
diagnosis of depression and the nondepressive group (CDS,
P<.001; MAS, P<.05), whereas no significance
could be established between the depression groups concerning the
distribution of CDS or MAS scores.
|
Neuroradiological Findings
The median of slices that presented demarcated lesions was 4
(range, 1 to 8). There was no substantial difference in lesion
topography between LH and RH lesions (Table 1) except for a greater
temporal lobe involvement in patients with RH lesions
(2=7.5, df=1, P<.05). The
thalamus was spared in all patients. Damaged brain tissue had mainly
been supplied by branches of the carotid system, predominantly by the
middle cerebral artery. Twenty percent of patients in both groups (LH
and RH stroke) demonstrated lesions in territories supplied by the
posterior cerebral artery. According to the definitions described
above, 21 (45%) patients had anterior lesions, 14 (30%) had posterior
lesions, and in 12 patients the lesion was not classifiable. The ANTPER
value was 39 (range, 13 to 86). The median of lesion volume as a
percentage of forebrain volume was calculated as 2.1% (range, 0.06%
to 18.6%). Significant differences between LH and RH lesions were not
found. The median value of VBR was 11 (range, 3 to 29). The VBR values
were considerably higher than those reported by Starkstein and
colleagues.23 This result could be explained by the
assessment procedure. As the borders of the areas of interest (body of
the lateral ventricle contralateral to the side of the lesion and
surrounding brain tissue) were not traced but marked by setting density
thresholds, the inclusion of ventricle ependyma, cortical gray matter,
and partial volumes was reduced. This results in a higher ratio of
cerebrospinal fluid to brain tissue. There was no significant
difference between patients with RH and LH lesions.
Associations Between Pathoanatomic Parameters and Depression
With respect to the lesion dichotomy as defined by Robinson et
al,8 we found that patients with lesions classified as
anterior showed significantly higher depression scores than patients
with posterior lesions in both CDS and MAS rating scales (anterior
lesions: CDS, median=10 [range, 0 to 21]; MAS, median=13 [range, 2
to 35]; posterior lesions: CDS, median=4.5 [range, 0 to 17]; MAS,
median=8.5 [range, 0 to 22]; P<.05 for both rating scales
[Mann-Whitney U test]). Separate analysis of LH and RH
lesions revealed that only patients with LH anterior lesions scored
significantly higher in the respective depression scales (Mann-Whitney
U test, P<.05). Fig 1 shows
scatterplots of CDS sum scores and ANTPER, volume of lesion, and VBR
measurements.
|
We found a low but significant negative correlation (r=-.29, P<.05) between ANTPER and CDS sum score, thus replicating data of the Baltimore group.7 8 16 Surprisingly, this correlation could be maintained only in patients with RH lesions (r=-.55, P<.05), whereas an isolated analysis of the LH group showed no significant effect (r=-.19, P=NS). Neither volume of lesion (r=.02, P=NS) nor VBR (r=-.07, P=NS) was associated with severity of depression as measured by the CDS. Furthermore, we found no significant intercorrelations among the pathoanatomic variables.
The correlation analyses described above included all patients and the entire range of depression scores. One could argue that, particularly in the postacute stage of stroke, physical or neuropsychological symptoms related to the stroke event and symptoms produced by depression are highly confounded, and that low depression scores do not reflect any degree of depression at all. We investigated this problem and the psychometric properties of depression rating scales used in studies with stroke patients elsewhere.33 In the present study we reanalyzed our data excluding all patients scoring on fewer than three CDS scales and presenting fewer than six positive scores. Twenty-eight patients (18 with LH and 10 with RH lesions) remained in the statistical analysis. The correlation coefficients obtained did not differ from the data reported above: We found no significant correlation between the anteriority of lesion (total group, r=-.08; LH, r=.03; RH, r=-.38), lesion volume (total group, r=-.05; LH, r=-.07; RH, r=.03), or VBR (total group, r=-.08; LH, r=.13; RH, r=-.47) (all P=NS) and CDS sum scores.
As described above, we found major depressive disorders only in
patients with LH lesions. In an additional step, we evaluated the
lesion topography of those patients. This patient group consisted of 6
men and 3 women with a median age of 58 years (range, 43 to 79 years)
and a median CDS score of 12 (range, 7 to 21). Fig 2
demonstrates the lesion configurations. Seven lesions were classified
as anterior, and two lesions were nonclassifiable. Lesion volume ranged
from 0.22% to 18.66% (median, 2.02%).
|
All lesions were located in the territory of vascular supply of the
middle cerebral artery. The templates show that some lesions damaged
cortical areas, whereas all lesions involved parts of the basal
ganglia. To analyze the core lesion areas we performed superimpositions
in standardized templates. Fig 3 demonstrates the
superimposed lesions of 9 patients with major depression and LH stroke
in comparison to 5 patients with minor depression and RH stroke.
|
Superimposition revealed an area of maximal overlap in the left lenticular nucleus that was included in the lesions of 6 patients with LH lesions and major depressive disorders. Patients with RH lesions and minor depression also presented an overlap in subcortical (mainly in opercular) areas but no clear-cut maximum.
Accordingly, patients with lesions of the LH basal ganglia or lesions
in the LH lenticulostriate or anterior choroidal artery area of
vascular supply showed a significantly higher frequency of major
depressive disorders (2=10.7, df=1,
P<.01) and scored significantly higher on depression rating
scales (CDS, Mann-Whitney U=114.5, P<.001; MAS,
Mann-Whitney U=60, P<.01) compared with patients
with lesions in all other territories of vascular supply.
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
This study analyzed the relationship between depressive disorders in the postacute stage of stroke with pathoanatomic data and measurements based on CT scan examinations. We found no significant differences between depression scores in LH and RH lesions and no remarkable correlation between the severity of depression and the anteriority or the volume of lesion or cortical/subcortical brain atrophy. However, there was an association between lesion location and DSM-III-R diagnosis of major depressive disorders. Nine of 13 patients with LH lesions that involved the lentiform nucleus exhibited major depression.
Before attempting a further discussion of these findings, several limitations of the present study should be noted. Because we examined a highly selected population of patients, our results cannot be generalized to the population of stroke patients. We investigated only patients within a 2-month period after the acute stroke event. Because we insisted on including only patients who were examined with the same neuroradiological procedure and who showed a first unilateral single demarcated lesion, our series became small. Additionally, male patients were overrepresented in our study, and the patient group was relatively young compared with epidemiological data. Although these limitations impair the generalizability of our results, the questions we addressed in our study required a homogeneous subgroup that was carefully selected according to the described inclusion criteria.
One interesting result of our present study was that we found no differences in depression severity between RH and LH lesions, whereas major depressive disorders were only found in patients with LH stroke. Furthermore, we found no essential correlation between pathoanatomic measurements and depression severity ratings. The degree of depressive changes in the postacute stage of stroke was not associated with the degree of preexisting brain atrophy. This result conflicts with the data presented by Starkstein and coworkers,23 who demonstrated that patients diagnosed as major depressive show significantly more brain atrophy. Åström et al,10 however, found no significant association between depression and brain atrophy in the postacute stage of stroke, whereas in a follow-up study 3 years later brain atrophy was demonstrated to contribute significantly to major depressive alterations. The most critical point of the study of Åström et al, however, is that brain atrophy was based on diagnoses by evidence. The results of all correlations between degree of depression and pathoanatomic measurements in the present study indicate that the occurrence of depressive disorders after stroke reflects neither a pure "left frontal pathology" nor a simple volume effect of the brain tissue damaged. A measurement such as anteriority of lesion location does not reflect neuroanatomic data and seems somewhat superficial. However, specific lesion location may prominently determine the pathogenesis of poststroke depressive alterations. The most striking result of our present study is the finding that lesions of the LH basal ganglia seem to play a crucial role in the production of major depressive disorders in the postacute stage after stroke. This result replicates the findings of a previous study of our group22 that reported a significant overlap of lesions in LH basal ganglia structures in acute stroke patients with aphasia and major depression. Although the configuration of the core lesion in that study differed from the lesion configuration reported in the present study, the left basal ganglia were involved in all acute aphasics with depressive disorders. Some other studies have assigned an important role to lesions of the basal ganglia in poststroke depression. Alexander and Lo Verme34 investigated patients with subcortical aphasia and found that only 2 of 9 patients with thalamic lesions but 4 of 6 patients with putaminal lesions showed medium to severe depressive disorders. Starkstein et al17 demonstrated that patients with a stroke in the area of the LH basal ganglia exhibit significantly higher depression scores compared with RH basal ganglia or LH and RH thalamic lesions. Moreover, patients with a pure depressive disorder after stroke more often demonstrate an involvement of the LH basal ganglia compared with patients with poststroke anxiety disorders.18
What might be the role of lesions of the LH basal ganglia and/or their surrounding white matter in the pathophysiology of poststroke depression? The modern view of functional neuroanatomy of emotional behavior favors complex and multiple interactions of cortical and subcortical brain structures.35 36 Within these networks of neuronal activity not only may specific lesions of the cortex or subcortical ganglia evoke disorders of emotional behavior but also the disruption of ascending or descending neuronal pathways. Noradrenergic activation,8 neurochemical changes of serotonergic receptors,1 and the interruption of dopaminergic pathways ascending from the ventral tegmental area22 have been implicated in the pathogenesis of poststroke depressive disorders. Moreover, treatment studies of poststroke depressive disorders confirmed the therapeutic use of different antidepressant agents.37 38 39 40 41 42 At the present time there is no conclusive evidence that one neurotransmission system plays a dominant role in the development of poststroke depression. However, most of the implied neuronal pathways have to transit the basal ganglia and surrounding white matter. Therefore, lesions of the basal ganglia and their vicinity affect different neurotransmission systems and may cause serious cortical remote effects.5 Damage of the basal ganglia and surrounding white matter may produce a significantly higher frequency of depressive disorders simply because these structures are the most important subcortical/cortical gateway. This hypothesis, however, does not explain the finding of higher frequencies of depressive alterations after LH basal ganglia lesions. A positron emission tomographic study based on 5-hydroxytryptamine receptor binding demonstrated a significantly lower (compensatory) upregulation of cortical 5-hydroxytryptamine receptors in patients with LH compared with RH lesions.1 The authors hypothesize that RH lesions lead to a greater depletion of biogenic amines that results in an ipsilateral compensatory upregulation, whereas no or only moderate upregulation occurs after LH lesions. However, presently there is little corroborative evidence for a lateralized effect of biochemical changes after cerebral lesions, and the lateralization of depressive disorders after basal ganglia lesions still remains unclear.
In the present study we were able to demonstrate that patients with LH basal ganglia lesions are more likely to exhibit major depression than patients with RH lesions. This result shows that at least in the postacute stage after stroke, depressive alterations can be mediated by organic factors. Moreover, our data show that simple dichotomies such as anterior or posterior lesions do not have a significant value in terms of pathoanatomic considerations of poststroke mood disorders. However, other variables also influence the development of depression after stroke. Illness perception, coping styles, or psychosocial changes all can lead to psychoreactive induced depression. We have discussed these variables in a multitime and multifactor model of depression after stroke elsewhere.43
|
Acknowledgments |
|---|
This study was supported in part by grants from the Deutsche Forschungsgemeinschaft (DFG He 1756/1-2; Dr Herrmann) and the Wilhelm Sander-Stiftung (WSS 90.065/1-2; Drs Herrmann and Wallesch). The authors wish to thank an anonymous reviewer of a previous version of the manuscript for his helpful comments.
Received December 13, 1994; revision received February 13, 1995; accepted February 17, 1995.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Mayberg HS, Robinson RG, Wong DF, Parikh R, Bolduc P, Starkstein SE, Price T, Dannals RF, Links JM, Wilson AA, Ravert HT, Wagner HN. PET imaging of cortical S2 serotonin receptors after stroke: lateralized changes and relationship to depression. Am J Psychiatry. 1988;145:937-943.
2. Barry S, Dinan TG. Alpha-2 adrenergic receptor function in post-stroke depression. Psychol Med. 1990;20:305-309. [Medline] [Order article via Infotrieve]
3.
Bryer JB, Starkstein SE, Votypka V, Parikh RM, Price
TR, Robinson RG. Reduction of CSF monoamine metabolites in
poststroke depression: a preliminary report. J
Neuropsychiatry Clin Neurosci. 1992;4:440-442.
4. Kapen S, Greiffenstein M. Stroke and depression: the cholinergic REM sleep induction test. In: Horne J, ed. Sleep '88. New York, NY: Gustav Fischer; 1989:238-240.
5. Grasso MG, Pantano P, Ricci M, Iniso DF, Pace A, Padovani A, Orzi F, Pozzilli C, Lenzi GL. Mesial temporal cortex hypoperfusion is associated with depression in subcortical stroke. Stroke. 1994;25:980-985. [Abstract]
6.
Robinson RG, Price TR. Post-stroke depressive
disorders: a follow-up study of 103 patients.
Stroke. 1982;13:635-641.
7. Robinson RG, Kubos KL, Starr LB, Rao K, Price TR. Mood changes in stroke patients: relationship to lesion location. Compr Psychiatry. 1983;24:555-566. [Medline] [Order article via Infotrieve]
8.
Robinson RG, Kubos KL, Starr LB, Rao K, Price TR.
Mood disorders in stroke patients: importance of location of
lesion. Brain. 1984;107:81-93.
9. Finklestein S, Benowitz LJ, Baldessarini RG, Arana GW, Levine D, Woo E, Bear D, Moya K, Stoll AL. Mood, vegetative disturbance and dexamethasone suppression test after stroke. Ann Neurol. 1982;12:463-468. [Medline] [Order article via Infotrieve]
10.
Åström M, Adolfsson R, Asplund K. Major
depression in stroke patients: a 3-year longitudinal study.
Stroke. 1993;24:976-982.
11.
Sinyor D, Jacques P, Kaloupek DB, Becker R, Goldenberg
M, Coopersmith HM. Post-stroke depression and lesion location:
an attempted replication. Brain. 1986;109:537-546.
12. Sharpe M, Hawton K, House A, Molyneux A, Sandercock P, Bamford J, Warlow C. Mood disorders in long-term survivors of stroke: associations with brain lesion location and volume. Psychol Med. 1990;20:815-828. [Medline] [Order article via Infotrieve]
13.
Ebrahim S, Barer KD, Nouri F. Affective illness
after stroke. Br J Psychiatry. 1987;151:52-56.
14. Dam H, Peterson HE, Ahlgren P. Depression among patients with stroke. Acta Psychiatr Scand. 1989;80:118-124. [Medline] [Order article via Infotrieve]
15. Williams JM, Little MM, Klein K. Depression and hemispheric site of cerebral vascular accident. Arch Clin Neuropsychol. 1986;1:393-398. [Medline] [Order article via Infotrieve]
16.
Starkstein SE, Robinson RG, Price TR. Comparison
of cortical and subcortical lesions in the production of poststroke
mood disorders. Brain. 1987;110:1045-1059.
17.
Starkstein SE, Robinson RG, Berthier ML, Parikh RM,
Price TR. Differential mood changes following basal ganglia vs
thalamic lesions. Arch Neurol. 1988;45:725-730.
18.
Starkstein SE, Cohen BS, Fedoroff P, Parikh RM, Price
TR, Robinson RG. Relationship between anxiety disorders and
depressive disorders in patients with cerebrovascular injury.
Arch Gen Psychiatry. 1990;47:246-251.
19. Robinson RG, Benson DF. Depression in aphasic patients: frequency, severity, and clinical-pathological correlations. Brain Lang. 1981;14:282-291. [Medline] [Order article via Infotrieve]
20.
House A, Dennis M, Warlow C, Hawton K, Molyneux A.
Mood disorders after stroke and their relation to lesion
location: a CT scan study. Brain. 1990;113:1113-1129.
21.
Eastwood MR, Rifat SL, Nobbs H, Ruderman J.
Mood disorders following cerebrovascular accident.
Br J Psychiatry. 1989;154:195-200.
22.
Herrmann M, Bartels C, Wallesch CW. Depression
in acute and chronic aphasia: symptoms, pathoanatomo-clinical
correlations, and functional implications. J Neurol
Neurosurg Psychiatry. 1993;56:672-678.
23.
Starkstein SE, Robinson RG, Price TR. Comparison
of patients with and without post-stroke major depression matched for
size and location of lesion. Arch Gen Psychiatry. 1988;45:247-252.
24. Alexopoulos GS, Abrams RC, Young RC, Shamoian CA. Cornell scale for depression in dementia. Biol Psychiatry. 1988;23:271-284. [Medline] [Order article via Infotrieve]
25.
Montgomery SA, Åsberg M. A new depression scale
designed to be sensitive to change. Br J Psychiatry. 1979;134:382-389.
26. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed, revised. Washington, DC: American Psychiatric Association; 1987.
27. Spitzer RL, Williams JB, Gibbon M. Instruction Manual for the Structured Clinical Interview for DSM-IIIR. New York, NY: Biometrics Research Dept, Psychiatric Institute, New York; 1986.
28. Matsui T, Hirano A. An Atlas of the Human Brain for Computerized Tomography. New York, NY: Igaku-Shoin; 1978.
29. Talairach J, Tournoux P. Co-Planar Stereotaxic Atlas of the Human Brain. New York, NY: Thieme Medical Publishers, Inc; 1988.
30. Damasio H, Damasio AR. Lesion Analysis in Neuropsychology. New York, NY: Oxford University Press; 1989.
31.
Ghika JA, Bogousslavsky J, Regli F. Deep
perforators from the carotid system: template of the vascular
territories. Arch Neurol. 1990;47:1097-1100.
32.
Huber W, Poeck K, Weniger D, Willmes K.
Aachener Aphasie Test. G
ttingen,
Germany: Hogrefe; 1983.
33. Herrmann M, Bartels C, Keller A, Borchardt D, Wallesch CW. Die Cornell Depressionsskala: Ein Verfahren zur Fremdbeurteilung depressiver Veränderungen bei Patienten mit hirnorganischen Läsionen? Psychometrische Gütekriterien [The Cornell Depression Scale: An Instrument to Assess Depressive Changes of Patients Following Cerebral Lesions? Psychometric Properties; in German]. Z Neuropsychol. In press.
34.
Alexander MP, Lo Verme SR. Aphasia after left
hemispheric intracerebral hemorrhage. Neurology. 1980;30:1193-1202.
35. Swerdlow NR, Koob GF. Dopamine, schizophrenia, mania, and depression: toward a unified hypothesis in cortico-striato-pallido-thalamic function. Behav Brain Sci. 1987;10:197-245.
36. Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu Rev Neurosci. 1986;9:357-381. [Medline] [Order article via Infotrieve]
37.
Reding MJ, Orto LA, Winter SW, Fortuna IM, DiPonte P,
McDowell FN. Antidepressant therapy after stroke: a double-blind
trial. Arch Neurol. 1986;43:763-765.
38. Lipsey JR, Robinson RG, Pearlson GD, Rao K, Price TR. Nortriptyline treatment of post-stroke depression: a double blind treatment trial. Lancet. 1984;1:297-300. [Medline] [Order article via Infotrieve]
39. Fedoroff JP, Robinson RG. Tricyclic antidepressants in the treatment of poststroke depression. J Clin Psychiatry. 1989;50:18-23.
40.
Masand P, Murray GB, Pickett P. Psychostimulants
in post-stroke depression. J Neuropsychiatry Clin
Neurosci. 1991;3:23-27.
41. Finklestein SP, Weintraub RJ, Karmouz N. Antidepressant drug treatment for post-stroke depression: a retrospective study. Arch Phys Med Rehabil. 1987;68:772-776. [Medline] [Order article via Infotrieve]
42. Andersen G, Veestergard K, Lauritzen L. Effective treatment of poststroke depression with the selective serotonin reuptake inhibitor citalopram. Stroke. 1994;25:1099-1104. [Abstract]
43. Herrmann M, Wallesch CW. Depressive changes in stroke patients. Disabil Rehabil. 1993;150:55-66.
This article has been cited by other articles:
 |
|
 |
|
  E. Townend, M. Brady, and K. McLaughlan A Systematic Evaluation of the Adaptation of Depression Diagnostic Methods for Stroke Survivors Who Have Aphasia Stroke, November 1, 2007; 38(11): 3076 - 3083. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. L. Hackett, C. Yapa, V. Parag, and C. S. Anderson Frequency of Depression After Stroke: A Systematic Review of Observational Studies Stroke, June 1, 2005; 36(6): 1330 - 1340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. K. Bhogal, R. Teasell, N. Foley, and M. Speechley Lesion Location and Poststroke Depression: Systematic Review of the Methodological Limitations in the Literature Stroke, March 1, 2004; 35(3): 794 - 802. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Narushima, J. T. Kosier, and R. G. Robinson A Reappraisal of Poststroke Depression, Intra- and Inter-Hemispheric Lesion Location Using Meta-Analysis J Neuropsychiatry Clin Neurosci, November 1, 2003; 15(4): 422 - 430. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Berg, H. Palomaki, M. Lehtihalmes, J. Lonnqvist, and M. Kaste Poststroke Depression: An 18-Month Follow-Up Stroke, January 1, 2003; 34(1): 138 - 143. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Beblo and M. Driessen No Melancholia in Poststroke Depression? A Phenomenologic Comparison of Primary and Poststroke Depression J Geriatr Psychiatry Neurol, April 1, 2002; 15(1): 44 - 49. [Abstract] [PDF]
|
|
|
|
 |
|
 R. Vataja, T. Pohjasvaara, A. Leppavuori, R. Mantyla, H. J. Aronen, O. Salonen, M. Kaste, and T. Erkinjuntti Magnetic Resonance Imaging Correlates of Depression After Ischemic Stroke Arch Gen Psychiatry, October 1, 2001; 58(10): 925 - 931. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Kim and S. Choi-Kwon Poststroke depression and emotional incontinence: Correlation with lesion location Neurology, May 9, 2000; 54(9): 1805 - 1810. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Singh, S. E. Black, N. Herrmann, F. S. Leibovitch, P. L. Ebert, J. Lawrence, and J. P. Szalai Functional and Neuroanatomic Correlations in Poststroke Depression : The Sunnybrook Stroke Study Stroke, March 1, 2000; 31(3): 637 - 644. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Gesztelyi, I. Fekete, M. Kellermann, L. Csiba, and D. Bereczki Screening for Depressive Symptoms among Post-Stroke Outpatients in Eastern Hungary J Geriatr Psychiatry Neurol, December 1, 1999; 12(4): 194 - 199. [Abstract] [PDF]
|
|
|
|
 |
|
 B.-P. Bejjani, P. Damier, I. Arnulf, L. Thivard, A.-M. Bonnet, D. Dormont, P. Cornu, B. Pidoux, Y. Samson, and Y. Agid Transient Acute Depression Induced by High-Frequency Deep-Brain Stimulation N. Engl. J. Med., May 13, 1999; 340(19): 1476 - 1480. [Full Text] [PDF]
|
|
|
|
|
|
F. Ghika-Schmid, G. van Melle, P. Guex, and J. Bogousslavsky Subjective experience and behavior in acute stroke: The Lausanne Emotion in Acute Stroke Study Neurology, January 1, 1999; 52(1): 22 - 22. [Abstract] [Full Text]
|
|
|
|
 |
|
 L M Sutcliffe and N B Lincoln The assessment of depression in aphasic stroke patients: the development of the Stroke Aphasic Depression Questionnaire Clinical Rehabilitation, June 1, 1998; 12(6): 506 - 513. [Abstract] [PDF]
|
|
|
|
|
|
S. Paradiso and R. G. Robinson Gender Differences in Poststroke Depression J Neuropsychiatry Clin Neurosci, February 1, 1998; 10(1): 41 - 47. [Abstract] [Full Text]
|
|
|
|
 |
|
 M. Alexander A 36-Year-Old Woman Recuperating From a Stroke JAMA, June 25, 1997; 277(24): 1970 - 1976. [Abstract] [PDF]
|
|
|
|
|
|
J.-L. Fuh, H.-C. Liu, S.-J. Wang, C.-Y. Liu, and P.-N. Wang Poststroke Depression Among the Chinese Elderly in a Rural Community Stroke, June 1, 1997; 28(6): 1126 - 1129. [Abstract] [Full Text]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||