62ournal ofNeurology, Neurosurgery, and Psychiatry 1993;56:672-678

Depression in acute and chronic aphasia:symptoms, pathoanatomical-clinical correlationsand functional implications

Manfred Herrmann, Claudius Bartels, Claus-W Wallesch

AbstractDepressive alterations were investigatedin 21 acute and 21 chronic aphasicpatients with single left sided strokes.The assessment of depression was basedon a psychometrically evaluated Germanversion of the Cornell Scale forDepression (CDS) and the ResearchDiagnostic Criteria (RDC). No signifi-cant difference was found concerningdepression sumscores between the twoaphasic groups. The acute group, howev-er, exhibited significandy higher ratingsin items related to physical signs ofdepression and disturbances of cyclicfunctions. Patients corresponding to theRDC-syndrome of major depressionwere only found in the acute group.Neither age, sex nor degree of hemipare-sis discriminated the patients on theseverity of depressive symptoms. In theacute patient group, nonfluency of apha-sia was the only parameter that could beidentified which had an effect on themood symptom scores. A CT scan analy-sis in the acute patient group showed anassociation between the severity ofdepression and anterior lesions. A signif-icant correlation was found betweenCDS sum-scores and the proximity ofthe anterior border of the lesion to thefrontal pole of the hemisphere whereasthe volume of lesions seemed to have noeffect on depressive alterations in acuteaphasic patients. Superimposition of thelesions of the aphasic patients with majordepressive disorders showed a commonsubcortical lesion area involving putami-nal and external pallidal structures.

Freiburg University,Freiburg, GermanyDepartment ofRehabilitationPsychologyM HerrmannDepartment ofNeurologyC BartelsResearch Programmein Neuropsychologyand NeurolinguisticsC-W WalleschCorrespondence to:Dr Herrmann, Departmentof RehabilitationPsychology, FreiburgUniversity, Belfortstrasse 16,7800 Freiburg i Br,GermanyReceived 1O January 1992and in final revised form27 July 1992.Accepted 31 July 1992

Neurol Neurosurg Psychiatry 1993;56:672-678)

In the past decade, depressive mood changesafter stroke gained importance both for our

understanding of the mechanisms underlyingimpairment and for rehabilitation. Despiteintensive research concerning aetiology,pathogenesis and differential diagnosis ofdepressive disorders following brain insults,the results and conclusions of the variousstudies differ greatly. The extent of the varia-tion in the data on the prevalence of post-stroke depression (PSD) indicates thatheterogeneous and in some aspects incompat-ible research designs were applied. Lipsey etall found "clinically significant depression" tooccur in 30-60% of patients suffering from

the consequences of brain infarction, whereasHouse et al2 reported a prevalence of "majordepressive disorders" in only 11 % one monthand 5% one year post stroke. The reliabilityand comparability of various investigationsare hampered by differences in study designtwo of which are briefly outlined:

1) Research strategies are based upon atleast three different theories concerning aeti-ology and pathogenesis of depressive changesfollowing stroke. Recent research focusing onPSD as a correlate of the neuropathologicalconsequences of stroke describes depressionas a mental disease in the terminology of psy-chiatric classification systems.' In contrast tothis view, the concept of "grief response"4views the depressive reaction as a natural,non-pathological phase of the coping processwhereas the concept of "(depressive-) cata-strophic reaction"56 describes an entirely dif-ferent entity of emotional-affective reactions.

2) In a number of studies, depressivechanges following stroke have been evaluatedusing standardised instruments taken frompsychiatric research on depressive disorders.Furthermore, psychiatric classification sys-tems were often used (for example, DSM-III-R7; or RDC).5 Only exceptionally, validityand applicability have been investigated forstroke patient populations.

This aspect is of special importance for theassessment of depressive changes in aphasicpatients. It seems highly doubtful thatpatients with relevant (written language)comprehension impairment can be reliablyand validly evaluated by standard self ratingscales or assessment procedures that rely onintensive verbal communication. Con-sequently, asphasic patients, although a quan-titatively important sub-population of strokepatients, have frequently been excluded fromstudies concerned with PSD.The present state of research on depression

in stroke, and in aphasic patients in particu-lar, is hall-marked by the contributions ofRobinson and Starkstein, who claim thatmajor depressive disorders are a frequentresult of cerebrovascular insults that mayalready be present in the acute phase andusually last for one to two years.9-"1 Furtherresults indicate that depressive changes aremore frequent with left hemisphere lesionsand that their degree correlates negativelywith the distance between the frontal poleand the anterior border of the lesion, bothwith respect to its cortical and subcorticalaspects.'2 13 However, House et aP andothers'4 15 were unable to replicate the

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significant correlation of degree of depressionwith the proximity of the lesion to the frontalpole.

This study compares depressive changes inacute and chronic aphasic patients. The studyaimed: 1) at differences in degree and profileof depressive, symptoms, and 2) at associa-tions of depressive changes with type of apha-sia, lesion localisation and volume.

Patients and methodsPatientsTwenty one patients with acute (less than 3months post onset) and 21 with chronic(more than 6 months post onset) aphasia ofvascular origin were included. Selection crite-ria were:1) Aphasia diagnosed on the basis of theAachen Aphasia-Test.'62) Vascular aetiology (ischaemic or secon-dary haemorrhagic stroke).3) Presence of a single demarcated lesion inthe CT.4) No history of alcohol or drug abuse orpsychiatric disorder.The groups were comparable for type and

degree of language deficit, age, income andeducational status. Table 1 gives details of theclinical and demographic data of both patientgroups.

MethodsPsychiatic assessmentsA psychometrically evaluated German adap-tation of the Cornell Depression Scale(CDS),"7 was used. The CDS was originallyconstructed for the assessment of dementedpatients and has been evaluated for this pop-ulation. The scale consists of 19 items thatwere selected to take into account the specificcognitive and somatic impairments of patientswith brain disease. Five levels of observationare included: A) mood related signs; B)behavioural disturbances; C) physical signs;D) cyclic functions and E) ideational distur-bances. The instrument focuses on observers'ratings but also includes information derivedfrom a short interview and case history. Theinterrater-reliability was good for various

Table 1 Clinical data of the acute and chronic patientgroups

Acute Chronicpatients patients

Number of patients 21 21Age (Median/Range [years]) 62/26-81 62/27-79Sex (Female/Male) 6/15 10/11MPO (Median/Range [months]) 1 0/0 5-2-5 35/7-132Type of Pathology:

Ischaemic 15 17Secondary haemorrhage 6 4

Type of Aphasia':Amnestic 2 2Wemicke 5 5Broca 7 8Global 3 4Non Classifiable 4 2

Hemiparesis 16 11Apraxia 6 5

'according to Aachen Aphasia-Test criteria (AAT"6).

aphasic populations and rater groups (Spear-man's Rho = 76-84 (p < 0-01); Kendall'sW = 0-75-0-85 (p < 0-001)). Its internal con-sistency (Cronbach alpha = 0-80, KR-20 =0 82) and congruent validity (compared withthe Montgomery-Asberg-Scale'8 (Spearman'sRho = 0-81 p < 001) reflect a high method-ological quality of the instrument for theinvestigation of aphasic patients. In addition,the power to differentiate degrees of impair-ment (discriminant validity: Mann-WhitneyU: p = 0-0002-0 0182) seemed satisfactory.

All patients were classified for depressivedisorders on the basis of the RDC-classifica-tion8 which was used to allow for a compari-son of our data with the psychometricevaluation of Alexopoulos et al."7

Radiological assessmentsOnly CT scans of the acute aphasic patientsare considered in our investigation. Con-siderable differences in slice thickness andangle precluded comparative analysis of theCT scans in the chronic group. The scans ofthe acute patients group were performedabout 15 days post stroke in standardisedslices without contrast enhancement. Asdescribed by Poeck et al,19 site and extent oflesion was measured in the original CT pho-tographs and then transposed into a set of 9standardised grids based on the brain sectionsof Matsui and Hirano.20 These grids wereanalysed by a computer program developedin our laboratory that computes lesion vol-umes and produces superimposition diagramsand analyses.The average distance from the frontal pole

in per cent of overall anterior-posterior dis-tance was calculated and the lesions wereclassified as anterior or posterior based on theapproach of Robinson et al.'2 For each case,these data were collected independently bytwo CT evaluators. The interrater-reliabilitywas highly satisfactory both for evaluation ofthe original scans and the standard templates(Spearmnan's Rho = 096; p < 0-001).Data analysis was conducted by non-

parametric procedures (Mann-Whitney-U-Tests, rank correlations, values corrected forties) with the SPSS-X statistical package.

ResultsPsychiatric statusFor the acute and the chronic group, theanalysis of the depression-scores revealedskewed distributions (acute patients: CDS:Mdn = 6, Range = 0-21; chronic patients;CDS: Mdn = 5, Range = 0-13). Numericallyhigher scores were found with the acutepatients, but statistical significance was notreached (Mann-Whitney U-test: CDS:U = 195, p = 0-5193). With the exception ofa non-significant higher frequency with theitem "sadness" in the acute group (66-6%acute vs 42-8% chronic patients), no differ-ences were found for the CDS-level of obser-vation "mood related signs". Symptoms ofanxiety were noted in about half of thepatients in both groups (42-8% acute vs

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47-6% chronic patients). Lack of reactivity inresponse to pleasant events was rarelyobserved. There was also no significant differ-ence between the acute and chronic group forsymptoms of "behavioural disturbances".Half of the chronic aphasics exhibited symp-toms of agitation and unrest (47-6% chronicvs 28-6% acute patients; ns), whereas morethan half of the acute patients showedpsychomotor retardation (61 9% acute vs52-4% chronic patients). The "physicalsigns" of loss of weight and appetite were sig-nificantly more frequently observed inpatients with acute aphasia. The most promi-nent symptom of this group is "lack of ener-gy", which was exhibited by a majority ofpatients from both groups, although morefrequently by the acute aphasics (71-4% acutevs 52-4% chronic aphasics; ns). The statisti-cally most marked differences between thetwo groups were found for "disturbances ofcyclic functions". With each symptom20-25% of the acute, but less than 5% of thechronic aphasics received positive ratings("Diurnal variation of mood": 28-6% acute vs4-8% chronic patients; p < 005; "Difficultyfalling asleep": 23-8% acute vs 4-8% chronicpatients; ns.; "Multiple awakenings": 28-6%acute vs 0% chronic patients; p < 0 01;"Early morning awakening": 28-6% acute vs0% chronic patients; p < 001). No signifi-cant difference between groups occurred forthe level of "ideational disturbances":Suicidal ideas, self depreciation and pes-simism were more frequently noted with thechronic patients. Mood congruent delusionswere exhibited by one acute and one chronicaphasic.A comparison of the CDS profiles revealed

that the patients with chronic aphasiareceived higher ratings with items that can beinterpreted as symptoms of a depressive reac-tion to stroke-related impairment (physicalcomplaints, suicidal ideas, poor self-esteem,pessimism). The higher scores of the acutegroup for physical signs of depression andcyclic dysfunctions cannot be interpretedunequivocally. They could represent endoge-nously induced symptoms of depression orreflect reactions to either acute severe diseaseor to the special inpatient conditions.However, the acute fluent patients withaphasia who were subject to the same inpa-tient conditions as the acute nonfluentpatients exhibited significantly lower scoresfor "physical signs" and disturbances of"cyclic functions".

The relationship between speech pathology,neurological impairment and psychiatric statusAn analysis of differences in the distributionof CDS sumscores for patient groups dividedaccording to sex, age, and degree of hemi-paresis revealed no significant effects. Type ofaphasia (fluent (Wernicke and anomic) vsnonfluent (Broca and global)) was the onlysignificant parameter which separated theaphasic patients with respect to the degree ofdepression. Patients with nonfluent aphasiaexhibited significantly higher depression

scores (all patients: p = 0 0074; Mann-Whitney U-Test). Closer analysis revealedthat this difference is only valid for the acutepatients (p = 00014), but breaks down whenonly the chronic aphasic patients are consid-ered (p = 0-9317).

All patients were then classified accordingto the RDC-criteria into the categories of "nodepressive disorder", "minor depressive dis-order", "probable major depressive disorder"and "definite major depressive disorder".This analysis supports the findings obtainedwith the CDS sumscores. In the acute group,7 patients with nonfluent aphasia and onepatient with non-classifiable speech pathologyshowed depressive disorders, 5 of which ful-filled the criteria for definite major depres-sion. In the chronic group, no patient wasrated as having probable or definite majordepression. Minor depressive disorders werefound in 3 nonfluent and 1 fluent chronicaphasic.

CT scan findingsThe patients included in the acute group hadbeen investigated by CT scan 9-43 days afterstroke (MDN: 15 days). The presence of awell-defined lesion was required for inclusion.Three patients showed predominantly corti-cal lesions without involvement of the subcor-tical nuclei, in 7 the cortex was spared, and in11 patients both cortical and subcorticalstructures were involved. A total of 15patients had suffered from ischaemic infarc-tion and 6 from secondary cerebral haemor-rhage. (1 patient was excluded from furtheranalysis because of marked midline shift andleft sided ventricular enlargement). Themedian distance of the anterior lesion bound-ary from the frontal pole was calculated36 1% (Range = 13-1%-86-2%) and themedian lesion volume in per cent of forebrainvolume was calculated 2-75% (Range =0-8%-19-7%). Unsurprisingly, all patientswith posterior and none with anterior lesionsexhibited fluent aphasia. Three patients withanterior lesions were non-classifiable by thefluent/nonfluent division, and two nonfluentpatients showed non-classifiable lesions.

Figure 1 shows a scattergram of thecorrelation between CDS sumscores and theproximity of the lesion to the frontal pole.The correlation between the proximity of

the lesion and the CDS sumscore was numer-ically low but significant (Rho = 0 445 (p <0 05). Its value was considerably below corre-lations reported by the Baltimore group'0 1221and others), but higher than the correlationreported by House et al.2 Our data are com-parable to those calculated by Starkstein etaP3 in a combined analysis of cortical andsubcortical lesions.House et aP' suggested that the proximity

effect could represent an epiphenomenon of alesion volume effect with larger lesions tend-ing to coincide with more anterior bound-aries. In our study, no interaction was foundbetween lesion volume and proximity of thelesion (Spearman's Rho = 0-043; ns). Therewas also no correlation between lesion

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Figure 1 Scatterplot ofthe correlation betweenproximity of the lesion andCDS-sumscores.

Correlation between ANTPER and CDS-Sumscores100 r

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volume and degree of depressive changes(Rho = 0d152; ns). These results suggest thatthe presence of a depressive disorder ratherreflects the effect of a specific lesion type or

location than a volume effect.In fig 2, the lesions of those 6 patients with

acute aphasia that fulfilled the RDC-criteriafor "probable or definite major Depression"(MD) were superimposed and compared witha superposition of 6 other acute patients with-out signs of a depressive disorder that hadlesions of comparable size (NSD). This sec-

ond group consisted of patients with a CDSsumscore of less than 5 (maximum = 38)who exhibited no symptoms of depressivemood (that is, no positive ratings in the items"sadness" and "loss of interest") and who didnot comply with the RDC criteria of major or

minor depression.The anatomical lesions were analysed by

comparison with the templates of Damasioand Damasio.3 Figure 2 shows that the MDgroup consisted of patients with predomi-nantly fronto-parietal lesions with a maximaloverlap in paramedian subcortical structures.Conversely, the NSD patients showed a

rather diffuse distribution of more posteriorlylocated lesions without clear overlap and thecore lesion of the MD aphasics was hardlyinvolved at all.The anatomical analysis of the MD core

lesion suggests that it includes basal aspectsof the lentiform nucleus, the medial part ofthe posterior limb of the internal capsule andlarge parts of pallidum and putamen, corpusnuclei caudati and parietal periventricularwhite matter. The thalamus is probablyspared, but due to the low resolution of thegrid matrix, an involvement of the most later-al aspects of the ventrolateral nuclei cannotbe ruled out. In summary, the superimposedlesions of patients with acute aphasia withmajor depression show an area of overlap inthe region of the left lenticular nucleus. Thisoverlap area is supplied by lateral and medial

lenticular branches of the middle cerebralartery and the anterior choroideal artery(according to Damasio and Damasio22 andGhika et a123).

DiscussionWe found no overall difference in degree ofdepressive changes between two groups ofpatients with acute and chronic aphasia thatwere comparable for the degree of languageimpairment. However, there were significantdifferences for the profile of depressive symp-toms: those with acute aphasia received sig-nificantly higher scores on ratings of "physicalsigns" of depression and "disturbances ofcyclic functions".An obvious first approach at interpretation,

especially for the acutely aphasic patients,would be to assign the depressive symptoma-tology to an acute depressive reaction towardsacute severe illness/impairment or as an arte-fact of the inpatient condition. However, thesymptom profile of the acute patients fulfill-ing the criteria of probable or definite majordepression in our study is parallel to the pat-terns described by Lipsey et al,24 for strokepatients with major depression. Theseauthors were able to demonstrate that therewere no significant differences between theprofiles of depressive symptoms related tostroke and functional major depressive disor-ders. We assume that post stroke depressionin acute patients cannot be interpreted on thebasis of "increased emotionalism"2 but is par-allel to the psychiatric disorder of majordepression.

Patients corresponding to the RDC criteriaof major depression were exclusively foundamong the acute aphasic patients and majordepressive disorders were significantly associ-ated with nonfluency of aphasia. This findingsupports similar results of previous studies.525However, Gainotti5 and Robinson andBenson25 interpreted their findings differently.

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Figure 2 Superimposedlesions of six patients withmajor depression (MD)and six patients with nosigns of depression (NSD).

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Gainotti's concept of "(depressive)-cata-strophic reactions" rather corresponds to the"increased emotionalism" of House et al.2With this line of interpretation the higherincidence and greater degree of depressivesymptoms in patients with anterior lesionscould be explained as psychoreactive to theirmore distressing nonfluent language disorders(compared with patients with posteriorlesions and fluent language disorder) and

hemiparesis. At least in the postacute andchronic stages of aphasia, psychosocial andcoping factors are relevant for the develop-ment of reactive depression. We have dis-cussed these interactions in a multitime andmultifactor model of depression in aphasiaelsewhere.26

Conversely, Robinson et al assume ananatomically based coincidence of depressionand nonfluent aphasia. Our CT scan analysis

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for the acute aphasic patients supports thissecond interpretation. We found a low butsignificant correlation between the anteriorlesion boundary and the degree of depressionin acute aphasia, but no interaction withlesion size.The following pathogenetic considerations

are based only on the results of our acutepatients. The correlation between degree ofdepression and the proximity of the lesion assuch gives only scanty evidence on the under-lying anatomical or physiological basis ofdepressive disorders in aphasic strokepatients. Detailed analysis reveals that thecorrelation mainly stems from the corticalextent of lesions of patients suffering frominfarctions including the anterior group ofbranches of the middle cerebral artery. Withrespect to the anatomical structures involved,all acute aphasic patients with "MajorDepression" in our study had either entirelysubcortical CT lesions (N = 3) or lesionsinvolving both subcortical and cortical struc-tures (N = 3). Superposition of the lesions ofthis patient group revealed a core lesion areain the region of the left basal ganglia. The lowcorrelation between degree of depression andthe proximity of the lesion may thereforemerely reflect a secondary aspect of thepathology that caused a lesion in this corearea but have no further explanatory value ofits own on the pathogenesis of post-strokedepression. If depressive disorders in acuteaphasic patients result from certain focal sub-cortical lesions, then the lesion volume can-not have much relevance in pathogenesis. Inaccordance with this assumption, no correla-tion was found between lesion size anddegree of depression.The view that post-stroke depression

results from specific subcortical damage iscollaterally supported by modem models ofdepression pathogenesis. Robinson et alP2 32

favour the monoamine deficit hypothesis as apathophysiological explanation of post-strokedepression. They point out that more anteri-orly located lesions affect noradrenergic andserotonergic projections ascending from thetegmentum pontis to the forebrain cortexmore proximally and therefore to a greaterextent than posterior lesions. This hypothesisis supported by studies on neurochemicalchanges of receptor sensitivity for biogenicamines after stroke.2728 These recent findings,however, contribute little to our understand-ing of the possible role of the subcorticalnuclei in the pathogenesis of depression inleft hemisphere stroke.

Another line of evidence indicates thatlesions of subcortical structures could indeedbe of crucial importance in the pathogenesisof post-stroke depression. In their study ofsubcortical aphasia, Alexander and LoVerme'9 reported marked or severe depres-sion in two of nine cases with thalamic lesionsand in four of six patients with putaminalpathology. Starkstein et al3 established aninteraction between the anteriority of thelesion and the degree of depression also forpatients with left hemisphere subcortical

lesions. A reanalysis of their data3 revealed asignificantly higher prevalence of majordepressive disorders in patients with basalganglia than with thalamic lesions.Furthermore, these authors were able to showthat patients with left basal ganglia lesionsexhibited more severe depressive changesthan patients with right sided basal ganglia orthalamic lesions of either side.30 Finally,Starkstein et al31 reported that basal ganglialesions occurred more frequently in patientswith major depression than in a control groupsuffering from generalised anxiety disorders.The authors offer a number of explanatorymodels for these findings: a) subcorticallesions could cause prefrontal hypometabo-lism as a remote effect; b) ascendingmonoaminergic pathways could be affected;c) the basal ganglia lesion itself could berelated to depression genesis.The latter hypothesis is supported by

theories concerning the role of the ventralstriatum as a central component of a cortico-striato-pallido-thalamo-cortical loop in theregulation of emotional processes. The struc-ture of the "anterior cingulate loop" ofAlexander et a132 predicts that the interrup-tion of the striato-pallidal pathway would leadto dysregulations of emotional functions. Themore elaborated model of Swerdlow andKoob33 contains three functionally indepen-dent loop systems between limbic cortex,basal ganglia, the dorsomedial nucleus of thethalamus and brainstem structures. The corelesion of patients with major depressiondescribed in this study interrupts bothascending dopaminergic pathways from theventral tegmentum and striato-pallidal pro-jections. In the Swerdlow and Koob model, itwould lead to a tonic disinhibition of thecortico-thalamo-cortical reverberation loopand, as the behavioural correlate of the neu-rochemical dysregulation, to "psychomotorretardation, paucity of affect, cognitive perse-veration, and anhedonia in depression"(Swerdlow and Koob33).

Swerdlow and Koob's model is also consis-tent with numerous reports that isolated thal-amic lesions may result in multipleneuropsychological dysfunctions but onlyrarely in depressive changes (for example,34)and the improvement of depression followingdorsomedial thalamotomy.3

Although the results of our study are ham-pered by a number of reservations, especiallysmall sample size, a number of conclusionscan be drawn: 1) differences in the depressivesymptom profile between acute and chronicaphasics and the presence of a specific corelesion with acute aphasic patients with majordepressive disorder indicate an endogenousgenesis of depression in acutely aphasic strokepatients. Aphasia and depression can beviewed as coincident consequences resultingfrom a common type of underlying vascularpathology; 2) the analysis of the commonlesion found in acute aphasic patients withmajor depression indicates a special role ofthe basal ganglia and their surrounding whitematter in the pathogenesis of poststroke left

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hemisphere depression; 3) moderately andseverely aphasic patients are an importantsubpopulation in investigations of poststrokedepression that must not be disregarded byexclusion for methodological reasons.

This work was supported in part by the DeutscheForschungsgemeinschaft, grant He 1756 (MH), and by theWilhelm Sander-Stiftung, grant 90-065 (CB). During thepreparation of the manuscript, Professor Wallesch wassupported by the Hermann- and Lilly-Schilling-Foundation.The authors wish to express their gratitude to Professor UKoch-Gromus, Dr K H Hagel, Dr J C Haas, H Johannsen-Horbach and C Wenz for their cooperation and to an anony-mous reviewer of the first version of our manuscript for theirhelpful comments.

1 Lipsey JR, Robinson RG, Pearlson GD, Rao K, Price TR.The dexamethasone suppression test and mood follow-ing stroke. AmJIPsychiatry 1985;142:318-23.

2 House A, Dennis M, Warlow C, Hawton K, Molyneux A.Mood disorders after stroke and their relation to lesionlocation-A CT scan study. Brain 1990;113:1113-29.

3 Starkstein SE, Robinson RG. Aphasia and depression.Aphasiology 1988;2:1-20.

4 Tanner DC, Gerstenberger DL. The grief response inneuropathologies of speech and language. Aphasiology1988;2:79-84.

5 Gainotti G. Emotional behavior and hemispheric side ofthe lesion. Cortex 1972;8:41-55.

6 Benson DF. Aphasia, alexia, and agraphia. New York:Churchill Livingstone 1979: 174-80.

7 American Psychiatric Association. Diagnostic and statisticalmanual of mental disorders, 3rd ed. Washington, DC:American Psychiatric Association, 1987.

8 Spitzer RL, Endicott J, Robins E. Research diagnostic cri-teria: Rationale and reliability. Archives of GeneralPsychiatry 1978;35:773-82.

9 Robinson RG, Starr LB, Kubos KIb Price TR. A two-yearlongitudinal study of post-stroke mood disorders:findings during the initial evaluation. Stroke1983;14:736-41.

10 Robinson RG, Starr LB, Lipsey JR, Rao K, Price TR. Atwo-year longitudinal study of poststroke mood disor-ders: dynamic changes in associated variables over thefirst six months of follow-up. Stroke 1984;15:510-17.

11 Robinson RG, Bolduc PI, Price TR. Two year longitudi-nal study of poststroke mood disorders: Diagncsis andoutcome at one and two years. Stroke 1987;18:837-43.

12 Robinson RG, Kubos Kb, Starr LB, Rao K, Price TR.Mood disorders in stroke patients-importance oflocation of lesion. Brain 1984;107:81-93.

13 Starkstein SE, Robinson RG, Price TR. Comparison ofcortical and subcortical lesions in the production ofpoststroke mood disorders. Brain 1987;110: 1045-59.

14 Sharpe M, Hawton K, House A, et al. Mood disorders inlong-term survivors of stroke: Associations with brainlesion location and volume. Psychological Medicine1990;20:815-28.

15 Wade DT, Legh-Smith JE, Hewer RA. Depressed mood

after stroke: A community study of its frequency Br JPsychiatry 1987;151:200-5.

16 Huber W, Poeck K, Weniger D, Willmes K. AachenerAphasie Test. Gottingen: Hogrefe, 1983.

17 Alexopoulos GS, Abrams RC, Young RC, Shamoian CA.Use of the Cornell Scale in nondemented patients.JAmGeriatric Soc 1988-36:230-6.

18 Montgomery SA, Xsberg M. A new depression scaledesigned to be sensitive to change. Br J Psychiatry1979;134:382-9.

19 Poeck K, De Bleser R, von Keyserlingk D. Computedtomography localization of standard aphasic syndromes.In: Rose FC, ed. Progress in aphasiology. New York:Raven, 1984:71-90.

20 Matsui T, Hirano A. An atlas of the human brain for com-puterized tomography. New York: Igaku-Shoin, 1978.

21 Robinson RG, Szetela B. Mood change following lefthemispheric brain injury. Ann Neurol 1981;9:447-53.

22 Damasio H, Damasio AR. Lesion analysis in neuropsycholo-gy. New York: Oxford University Press, 1989.

23 Ghika JA, Bogousslavsky J, Regli F. Deep perforatorsfrom the carotid system-Template of the vascular terri-tories. Arch Neurol 1990;47:1097-100.

24 Lipsey JR, Spencer WC, Rabins PV, Robinson RG.Phenomenological comparison of poststroke depressionand functional depression. Am J Psychiatry 1986;143:527-9.

25 Robinson RG, Benson DF. Depression in aphasicpatients: frequency, severity, and clinical-pathologicalcorrelations. Brain and Language 1981;14:282-9 1.

26 Herrmann M, Wallesch CW. Depressive changes in strokepatients. Disability and Rehabilitation (in press)

27 Mayberg HS, Robinson RG, Wong DF, et al. PET imag-ing of cortical S2-serotonin receptors after stroke-later-alized changes and relationship to depression. Am JPsychiatry 1988;145:937-43.

28 Barry S, Dinan TG. Alpha-2 adrenergic receptor functionin post-stroke depression. Psychological Medicine 1990;20:305-9.

29 Alexander MP, Lo Verme SR. Aphasia after left hemi-spheric intracerebral hemorrhage. Neurology 1980;30:1193-202.

30 Starkstein SE, Robinson RG, Berthier ML, Parikh RM,Price TR. Differential mood changes following basalganglia vs. thalamic lesions. Arch Neurol 1988;45:725-30.

31 Starkstein SE, Cohen BS, Fedoroff P, Parikh RM, PriceTR, Robinson RG. Relationship between anxiety disor-ders and depressive disorders in patients with cere-brovascular injury. Arch Gen Psychiatry 1990;47:246-5 1.

32 Alexander GE, De-Long MR, Strick PL. Parallel organiza-tion of functionally segregated circuits linking basal gan-glia and cortex. Ann Rev Neurosci 1986;9:357-81.

33 Swerdlow NR, Koob GE. Dopamine, schizophrenia,mania, and depression: Toward a unified hypothesis incortico-striato-paflido-thalamic function. Behavioral andBrain Sciences 1987;10:197-245.

34 Graff-Radford NR, Eslinger PJ, Damasio AR, Yamada T.Nonhemorrhagic infarction of the thalamus: Behavioral,anatomic, and physiologic correlates. Neurology 1984;34:14-23.

35 Spiegel EA, Wycis HT, Freed H, Orchinik C. The centralmechanism of the emotions (Experiences with circum-scribed thalamic lesions). Am J Psychiatry 1951;108:426-32.

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