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(Stroke. 2002;33:702.)
© 2002 American Heart Association, Inc.
Original Contributions |
From the Department of Neurovascular Disorders of Lille and Institut dOrthophonie de Tours, Amiens, France.
Correspondence to O. Godefroy, Service de Neurologie, F-80054 Amiens, France. E-mail godefroy.olivier{at}chu-amiens.fr
| Abstract |
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Methods The study was performed in 308 patients consecutively assessed with a standardized aphasia battery.
Results Aphasia was observed in 207 patients; global and nonclassified aphasias accounted for 50% of aphasic syndromes at the acute stage, whereas classic aphasias (Wernickes, Brocas, transcortical, and subcortical aphasias) were less frequent. Age differed across aphasic syndromes in ischemic stroke patients only; patients with conduction aphasia were younger, and patients with subcortical aphasia were older. Sex did not significantly differ across aphasic syndromes. The presence of a previous stroke was more frequent in nonclassified aphasia.
Conclusions This study shows (1) that vascular aphasias are frequently severe or nonclassic at the acute stage, a finding explained in part by the presence of a previous stroke; (2) that the age effect is due mainly to its influence on infarct location; and (3) that the main determinant of aphasia characteristics is lesion location.
Key Words: aphasia neuropsychology
| Introduction |
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80 000 new cases of aphasia annually in the United States.5 The presence of aphasia is an index of poor prognosis, with more severe motor, cognitive, and social disability1,3,6 and higher mortality.3,4 Finally, aphasia outcome remains poor: 32% to 50% of aphasics still suffer from aphasia 6 months after stroke.3,4 Consequently, the need to evaluate and treat poststroke aphasia has been underlined.7 However, characteristics of vascular aphasias remain partly unknown for 3 main reasons. First, previous studies were performed before the stroke unit era, and characteristics of aphasia in patients admitted to acute stroke units have not been reported. Second, studies focusing on vascular aphasia have included either selected samples with extensive evaluation of language1,8,9 or large series of consecutive patients examined with shortened testing.210 Although the latter studies provide important findings, they usually focus on oral expression and do not determine the type of language disorder. This leads to confounding of very different disorders such as dysarthria and aphasia, or Brocas and global aphasias, which have different severities and outcomes. Third, factors determining the occurrence and severity of vascular aphasia remain a subject of controversy. Lesion location has long been regarded as the major determinant of aphasia characteristics. However, several CT-based studies have shown that an unexpectedly large proportion of aphasias deviate from classic clinical-anatomic correlations.1114 This suggests that other factors influence clinical outcome. A few studies have suggested age and sex, with a higher frequency of nonfluent aphasia in young patients,10,1517 a lower frequency of aphasia in women,2,18 and a better outcome in young patients.17,19,20 These results have been obtained in series of selected patients and were not replicated in other studies.4,8,21
The goal of the present study was to determine aphasia characteristics at the acute stage and the influence of general factors. The role of lesion location is examined in another study of a subgroup of 107 patients examined with MRI.22
| Subjects and Methods |
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Language was assessed when the neurological condition became favorable, usually within the first month after stroke. It used a battery based mainly on the Montreal-Toulouse battery24 and some subtests of the Boston Diagnosis Aphasia Examination2528 (Table 2). The battery could be administered within 1 hour and, if necessary, in the patients room. Criteria for classic aphasic syndromes (global, Brocas, Wernickes, conduction, transcortical motor and sensory, anomic) were those of the Montreal-Toulouse battery.24 We added the 2 following disorders: subcortical aphasia, when hypophonia was associated with a transcortical motor aphasia,11,29 and word-finding difficulties, when the sole abnormality consisted of mild impairment of picture naming. The aphasia was considered nonclassified when the disorder did not meet the criteria for any of the classic aphasic syndromes.
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| Results |
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Global and nonclassified aphasias accounted for 50% of all aphasic syndromes. Nonclassified aphasia included 37 patients (17.9%) with language disorders close to anomic aphasia associated with other impairments ("anomic-plus aphasia"). The remaining 18 patients (8.7%) had various combinations of impairments that did not correspond to a clearly established aphasic syndrome. Wernickes, Brocas, and subcortical and transcortical motor aphasias were less frequent, accounting for 40%. Other syndromes were rare. In the 207 aphasics, written language was assessable in 188 and was impaired in 168 patients (written expression, n=107; reading and comprehension, n=77).
Patients were examined within a mean delay of 11 days after stroke, and 11 patients were assessed after the first month mainly because they were referred from another hospital or suffered from vigilance disorders. The delay did not differ according to language status (P>0.2). Language disorders of referred patients did not differ (P>0.6) from those of directly admitted patients.
Performance on the aphasia battery was examined across aphasic syndromes (global, Wernickes, Brocas, subcortical, anomic, conduction, transcortical motor and sensory) by use of Fishers exact test (jargonaphasia, stereotyped utterances) and an analysis of variance (ANOVA; spontaneous verbal fluency, automatic series, repetition, and oral comprehension) with a rank transformation of scores.30 Posthoc analysis was performed with the Ryan Einot Gabriel Welsch test,31 and a value of P<0.0001 (corrected for multiple analysis) was regarded as significant. The results (Table 3) showed that the present battery allowed classification of the main aphasic syndromes. The word and sentence-picture matching subtest also assessed syntactic comprehension, and this accounted for the mild impairment observed in Brocas aphasia.
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We examined the effect of general factors (age, sex, handedness) and previous stroke on the occurrence and type of language disorders. The 13 patients with various disorders were excluded, and the analysis was performed in the remaining 295 patients with the Kruskal-Wallis test (age) and Fishers exact test (sex, handedness, previous stroke). Age (P=0.6), sex (P=0.8), and handedness (P=0.4) did not differ across syndromes (Table 1), whereas the presence of a previous stroke did differ (P=0.04) because of the higher frequency of previous stroke in nonclassified aphasia.
The absence of an age effect on the aphasic syndrome contrasted with findings from some previous reports10,1517 and was reexamined according to the 3 methods previously reported. First, age was compared across aphasic syndromes separately in men and women. No difference was observed in men (P=0.8) and women (P=0.5). Second, age was compared according to spontaneous verbal fluency (mutism or expression restricted to stereotyped utterances, n=51; nonfluent aphasia, n=59; fluent aphasia, n=97). Age did not differ (P=0.6) according to fluency (mutism, 61.2±17; nonfluent, 61±16; fluent, 63.7±15). Third, age was compared across aphasic syndromes separately in ischemic and hemorrhagic stroke patients by use of an ANOVA with the Ryan Einot Gabriel Welsch test31 as a posthoc test. Age differed across syndromes in ischemic stroke (P=0.04) but not in hemorrhagic stroke (P=0.5). In ischemic stroke, patients with a conduction aphasia were younger (mean age, 50±15 years), and patients with subcortical aphasia were older (mean age, 76.5±11 years). The absence of a significant difference between Brocas (mean age, 60.1±18 years) and Wernickes (mean age, 69.95±12.5 years) aphasias was due to correction for multiple comparisons because the direct comparison with a t test reached significance (P=0.05).
These results indicate (1) that age differed across aphasic syndromes in ischemic stroke only, with patients with conduction aphasia being younger and patients with subcortical aphasia being older; (2) that sex did not influence the variety of language disorder; and (3) that a previous stroke was more frequent in nonclassified aphasia.
| Discussion |
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The study was not designed to assess the frequency of aphasia in stroke. Thus, the finding of language disorder in
14% of patients at the acute stage may have underestimated the frequency of aphasia, reported in 16% to 25% of stroke patients.25 Because our primary aim was to examine aphasia characteristics encountered in daily practice, all stroke patients, including those with a previous stroke, were analyzed.
The first result of this study was that classic syndromes that represent the core of aphasiology such as Wernickes, Brocas, conduction, pure anomic, and transcortical aphasias accounted for only 40% of aphasias. Global aphasia accounted for a quarter of aphasic syndromes within the first weeks after stroke, indicating that stroke practitioners are more frequently confronted with severe or nonclassic disorders. The prominence of global aphasia, the most severe aphasic syndrome, has already been reported in series using an aphasia battery2,8,13,17 and is frequently underestimated on clinical grounds or shortened testing.24 This finding argues for the use of formal assessment of aphasia. In previous studies, the frequency of nonclassified aphasias varied from 0% to 45%2,8,13,14,32 and depended mainly on patient selection, the delay of assessment, and criteria of aphasic syndromes. In the present study, 25% of aphasia was not classifiable, which is explained by the use of restrictive criteria of anomic aphasia and by the inclusion of patients with previous stroke. If less restrictive criteria were used, 37 patients would have been classified as having anomic-plus aphasia, which represents a very important proportion of aphasics. From a practical point of view, the separation of pure anomia from anomic-plus aphasia is unclear and deserves further study. Nonclassified aphasia was more frequent in patients with previous stroke. This is likely a result of the unusual combination of language disorders in patients with several lesions.
Finally, this study supports an age effect on the aphasic syndrome in ischemic stroke only; patients with conduction aphasia were younger, and patients with subcortical aphasia were older. In addition, patients with Brocas aphasia were younger than those with Wernickes aphasia, but the difference did not reach significance after correction for multiple analyses. This result is consistent with studies suggesting a higher frequency of nonfluent aphasia, particularly Brocas aphasia, in young patients.10,13,1517 The age effect might be due to its influence on patterns of recovery, the cerebral organization of language areas, and infarct locations. The influence of age on patterns of recovery has been documented primarily after 3 months from onset,21 and this is unlikely to account for our findings that concerned the first month after stroke. Age-related changes in the organization of language areas predict different frequencies of aphasic syndromes regardless of brain pathology. This prediction was not matched by our findings of an age influence specific to ischemic stroke. Thus, our results strongly suggest that the age effect on aphasic syndromes at the acute stage is related to its influence on the vascular pathology and consequently on infarct locations. Such an interpretation is supported by the previous finding of a relation between age and the anterior-posterior location of infarcts in Brocas and Wernickes aphasias.10 These data and those obtained in the clinical-anatomical correlation study22 converge to support the finding that the main determinant of aphasia type is lesion location.
| Acknowledgments |
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Received April 17, 2001; revision received October 25, 2001; accepted November 29, 2001.
| References |
|---|
|
|
|---|
2.
Brust JCM, Shafer SQ, Richter RW, Bruun B. Aphasia in acute stroke. Stroke. 1976; 7: 167174.
3.
Wade DT, Hewer RL, David RM, Enderby PM. Aphasia after stroke: natural history and associated deficits. J Neurol Neurosurg Psychiatry. 1986; 49: 1116.
4. Pedersen PM, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Aphasia in acute stroke: incidence, determinants and recovery. Ann Neurol. 1995; 38: 659666.[CrossRef][Medline] [Order article via Infotrieve]
5. Holland AL, Fromm DS, DeRuyter F, Stein M. Treatment efficacy: aphasia. J Speech Hear Res. 1996; 39: S27S36.
6.
Pohjasvaara T, Erkinjuntti T, Ylikoski R, Hietanen M, Vataja R, Kaste M. Clinical determinants of poststroke dementia. Stroke. 1998; 29: 7581.
7. Aboderin I, Venables G. Stroke management in Europe: Pan European Consensus Meeting on Stroke Management. J Intern Med. 1996; 240: 173180.[CrossRef][Medline] [Order article via Infotrieve]
8.
Kertesz A, Sheppard A. The epidemiology of aphasic and cognitive impairment in stroke. Brain. 1981; 104: 117128.
9. Paolucci S, Antonucci G, Gialloreti LE, Traballesi M, Lubich S, Pratesi L, Palombi L. Predicting stroke inpatient rehabilitation outcome: the prominent role of neuropsychological disorders. Eur Neurol. 1996; 36: 385390.[CrossRef][Medline] [Order article via Infotrieve]
10. Ferro JM, Madureira S. Aphasia type, age and cerebral infarct localisation. J Neurol. 1997; 244: 505509.[CrossRef][Medline] [Order article via Infotrieve]
11. Puel M, Demonet JF, Cardebat D, Bonafe A, Gazounaud Y, Guiraud-Chaumeil B, Rascol A. Subcortical aphasia: neurolinguistic and x-ray computed tomography studies of 25 cases [in French]. Rev Neurol (Paris). 1984; 140: 695710.[Medline] [Order article via Infotrieve]
12. Basso A, Lecours AR, Moraschini S, Vanier M. Anatomoclinical correlations of the aphasias as defined through computerized tomography: exceptions. Brain Lang. 1985; 26: 201229.[CrossRef][Medline] [Order article via Infotrieve]
13. Annoni JM, Cot F, Ryalls J, Lecours AR. Profile of the aphasic population in a Montreal geriatric hospital: a 6-year study. Aphasiology. 1993; 7: 271284.
14.
Willmes K, Poeck K. To what extent can aphasic syndromes be localized ? Brain. 1993; 116: 15271540.
15. Obler LK, Albert ML, Goodglass H, Benson DF. Aphasia type and ageing. Brain Lang. 1978; 6: 318322.[CrossRef][Medline] [Order article via Infotrieve]
16. Basso A, Capitani E, Laiacona M, Luzzati C. Factors influencing type and severity of aphasia. Cortex. 1980; 16: 631636.[Medline] [Order article via Infotrieve]
17.
Ferro JM, Crespo M. Young adult stroke: neuropsychological dysfunction and recovery. Stroke. 1988; 19: 982986.
18. Hier DB, Yoon WB, Mohr JP, Price TR, Wolf PA. Gender and aphasia in the stroke data bank. Brain Lang. 1994; 47: 155167.[CrossRef][Medline] [Order article via Infotrieve]
19.
Kertesz A, McCabe P. Recovery patterns and prognosis in aphasia. Brain. 1977; 100: 118.
20. Basso A. Spontaneous recovery and language rehabilitation.In: Seron X, Deloche G, eds. Cognitive Approaches in Neuropsychological Rehabilitation. Hillsdale, NJ: Lawrence Erlbaum Associates Inc; 1989: 1738.
21. Coppens P. Why are Wernickes aphasia patients older than Brocas ? A critical view of the hypotheses. Aphasiology. 1991; 5: 279290.
22.
Kreisler A, Godefroy O, Delmaire C, Debachy B, Leclercq M, Pruvo JP, Leys D. The anatomy of aphasia revisited. Neurology. 2000; 54: 11171123.
23. The Members of the Lille Stroke Program. Misdiagnoses in 1250 consecutive patients admitted in an acute stroke unit. Cerebrovasc Dis. 1997; 7: 284288.
24. Nespoulous JL, Lecours AR, Lafond D, eds. Protocole Montréal-Toulouse de lexamen de laphasie: Module Standard Initial (Version Beta). Montréal, Canada: LOrtho Édition; 1986.
25. Goodglass H, Kaplan E, eds. The Assessment of Aphasia and Related Disorders. 2nd ed. Philadelphia, PA: Lea and Febiger; 1983.
26. Mazaux JM, Orgogozo JM, Henry P, Loiseau P. Troubles du langage au cours des lésions thalamiques: etude par le test de Goodglass et Kaplan. Rev Neurol (Paris). 1979; 135: 5964.[Medline] [Order article via Infotrieve]
27. De Renzi E, Faglioni P. Normative data and screening power of a shortened version of the token test. Cortex. 1978; 14: 4149.
28. Bachy-Langedock N, ed. Batterie dexamen des Troubles en Dénomination. Bruxelles, France: Edition du Centre de Psychologie Appliqué; 1989.
29.
Alexander MP, Naeser MA, Palumbo CL. Correlations of subcortical CT lesion sites and aphasia profiles. Brain. 1987; 110: 961991.
30. Conover WJ, Iman RL. Rank transformation as a bridge between parametric and nonparametric statistics. Am Stat. 1981; 35: 124129.[CrossRef]
31. SAS Users Guide, Version 6. Cary, NC: SAS Institute; 1990.
32.
Wertz RT, Weiss DG, Aten JL, Brookshire RH, Garcia-Bunuel L, Holland AL, Kurtzke JF, LaPointe LL, Milianti FJ, Brannegan R, et al. Comparison of clinic, home, and deferred language treatment for aphasia. Arch Neurol. 1986; 43: 653658.
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