BRAIN

AND

LANGUAGE

42, 77-88 (1992)

The Usefulness of the Western Aphasia Battery for Differential Diagnosis of Alzheimer Dementia and Focal Stroke Syndromes: Preliminary Evidence JENNIFER HORNER,* DEBORAH V. DAWSON,~ ALBERT HEYMAN,$ AND ALICE MCGORMAN FISH§ *The Center for Speech and Hearing Disorders, Department of Surgery, and the Center for the Study of Aging and Human Development, &he Center for Speech and Hearing Disorders, tthe Division of Biometry, Department of Family and Community Medicine, and $the Division of Neurology, Department of Medicine, Duke University Medical Center, Durham, North Carolina

We assessedthe usefulness of the Western Aphasia Battery for distinguishing the language disturbances caused by Alzheimer dementia (AD) from those caused by stroke. Using discrimant function analyses, the multiple variable “aphasia quotient-reading quotient-writing quotient” classified 29 (72.5%) of the 40 patients correctly. These 29 patients included 8 of 10 patients with left hemisphere infarction and fluent aphasia; 6 of 10 with AD; 5 of 10 patients with right hemisphere infarction; and all 10 of the neurologically normal control subjects. The patients with AD and those with right hemisphere stroke were the most difficult to classify using the aphasia battery. o IYZ Academic press. 1nc.

Few studies compare the language disturbances seen in early Alzheimer dementia (AD) with those caused by right and left hemisphere stroke (Horner, 1985; Nicholas, Obler, Albert, & Helm-Estabrooks, 1985; Tikofsky, Glatt, Hoffman, Allen, & Befera, 1986; Horner, Lathrop, Fish, & Dawson, 1987; Bayles, Boone, Tomoeda, Slauson, & Kaszniak, 1989; Fromm & Holland, 1989). The usefulness of the Western Aphasia Buttery for differential diagnosis among the linguistic changes caused by these disorders is not known. The authors express their appreciation and thanks to Joseph R. Duffy, Ph.D. (Mayo Clinic, Rochester MN) for his critique of our prepublication manuscript. This work was presented in part at the 41st annual meeting of the American Academy of Neurology, Chicago, IL. Address all correspondence and reprint requests to Jennifer Horner, Duke University Medical Center, Department of Surgery, Box 3887, Durham, NC 27710. 77 0093-934X/92 $3.00 Copyright 0 1992 by Academic Press, Inc. All rights of reproduction in any form reserved.

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Several lines of evidence from the literature motivated us to explore the usefulness of language evaluation of patients with AD. First, aphasia has predictive validity for 1Zmonth ratings of global functioning (Berg, Danziger, Storandt, et al., 1984; Berg, Miller, Storandt, et al., 1988) may predict familial AD (Folstein, & Breitner, 1981), may signal a rapidly progressing course (Knesevich, Toro, Morris, & LaBarge, 1985), and may predict mortality (Kaszniak, Fox, Gandell, et al., 1978). Second, aphasia is more prevalent in early onset AD than late onset AD (Seltzer & Sherwin, 1983; Chui, Teng, Henderson, & Moy, 1985; Filley, Kelly, & Heaton, 1986). Third, aphasia is present in all cases of AD, some argue, and should be included as a diagnostic criterion (Cummings, Benson, Hill, & Read, 1985; Murdoch, Chenery, Wilks, & Boyle, 1987). Fourth, aphasia may appear as an isolated or prominent feature in early dementing illness (Wechsler, 1977; Mesulam, 1982; Foster, Chase, Fedio, Patronas, Brooks, & DiChiro, 1983; Heath, Kennedy, & Kapur, 1983; Kirshner, Webb, Kelly, & Wells, 1984; Chawluk, Mesulam, Hurtig, et al., 1986; Duffy, 1987; Green, Morris, Sandson, McKeel, & Miller, 1990)-as distinct from prominent nonlanguage signs (Crystal, Horoupian, Katzman, & Jotkowitz, 1982; Mayeux, Stern, & Spanton, 1985; DeRenzi, 1986; Martin, Brouwers, Lalonde, et al., 1986)-that later progresses to global dementia. A fifth reason for comprehensive language evaluation (perhaps the most compelling) is to compare the effects of different pathological conditions on language. Appell, Kertesz, and Fisman (1982), using the Western Aphasia Battery, compared the language performance of advanced AD patients with that of historical controls, both left hemisphere stroke patients and non-brain-damaged controls. AD subjects performed significantly below controls on all dimensions of the Aphasia Quotient (fluency, information content, comprehension, repetition, and naming). In contrast, AD subjects differed significantly from left hemisphere stroke aphasic subjects in speech fluency and comprehension. AD subjects achieved higher fluency ratings and demonstrated poorer comprehension. Whereas only 20% of the stroke sample were characterized as Wernicke’s or Transcortical Sensory aphasia, a full 44% of the AD sample had these types of fluent aphasia. The overall naming subscore did not differentiate these subject groups. However, Appell and colleagues note that “naming” difficulty in AD subjects was characterized by relatively well preserved object naming while word fluency was always poor. In summary, this important study of the language impairment in AD showed how distinct disease processes can have distinctly different effects on basic language abilities. AD patients were notable for their preserved speech fluency, relatively poor comprehension, and uniformly poor word fluency. The reasons for comparing and contrasting different etiologic groups are both practical and theoretical (Bayles & Kaszniak, 1987; Duffy & Myers, 1991). One practical reason is to assessthe discriminative power

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of the assessment procedure (Wertz, Dronkers, & Deal, 1985; Tierney, Snow, Reid, Zorzitto, & Fisher, 1987) as we attempt in the present study. A second practical reason is to make accurate clinical diagnoses. In clinical practice, neurologists see a number of elderly individuals in whom it is likely that AD and cerebral infarction cooccur (Hier, Hagenlocker, & Shindler, 1985; Chui, 1989) and although rare, may see patients with progressive focal neurologic signs with AD (Jagust, Davies, Tiller-Borcich, & Reed, 1990). A third practical reason for language evaluation is to discern the patient’s functional communication profile (Fromm & Holland, 1989), which in turn may guide family counselling. Our specific research question was stimulated by Bayles and Kaszniak’s (1987) clinical observation that problems in communication seen in early AD may be most difficult to distinguish from those of fluently speaking individuals with focal infarction of either cerebral hemisphere. To study this differential diagnostic question, we compared the Western Aphasia Battery performance of four groups of fluent speakers. METHODS Subjecrs. We examined 40 fluently speaking individuals, 10 each from the following four groups: (1) patients with probable early AD based on NINCDS-ADRDA criteria (McKhann, Drachman, Folstein, et al., 1984); (2) patients with cerebral infarction localized to the left hemisphere, resulting in fluent aphasia; (3) patients with a history of cerebral infarction localized to the right hemisphere; and (4) neurologically normal adults with education similar to that of the patients with AD. Based on history, neurologic examination, and neuroradiologic evidence, the individuals with cerebral infarction had single lesions. The duration of illness was much shorter in the patients with stroke than in those with AD (p = .OOOl). There were differences in the frequency of visual field defects and hemiparesis (see details in the footnote of Table 1). There was no statistical evidence that the four groups differed in the distribution of age, sex, or years of educational attainment. All patients with AD had mild memory problems and difficulty in word finding; they were well groomed, socially appropriate, and lived at home. Procedure. We chose to test language using the Western Aphasia Battery (Kertesz, 1979, 1982) because this instrument is standardized and has good reliability and validity (Shewan & Kertesz, 1980), and because we wanted to compare our results with those of Appell et al. (1982). A broad range of language functions is tested by this battery which yields four possible summary scores, each expressed as a “quotient” (each 100.0 maximum points). The four quotients and their subtests are as follows: (1) an Aphasia Quotient (AQ) derived from scores for spontaneous speech content, spontaneous speech fluency, comprehension, repetition, and naming:(2) a Reading Quotient (RQ) derived from tests of comprehension of paragraphs, and oral and silent comprehension of sentences, words, and spelling; (3) a Writing Quotient (WQ) derived from spontaneous writing, word, letter, number, and sentence dictation, serial writing (alphabet, numerals), and copying; and (4) a Language Quotient (LQ) derived from those scores comprising the Aphasia, Reading, and Writing quotients. Shewan (1986) developed the LQ by weighting Western Aphasia Barrery scores as follows: spontaneous speech (20%), auditory comprehension (20%), repetition (lo%), naming (lo%), reading (20%), and writing (20%). Srarisrical procedures. Correlational analyses among demographic variables and measures of language performance were carried out using Spearman rank-order correlation coefficients. Nonparametric procedures based on ranks were used to compare the distribution of

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HORNER ET AL. TABLE 1

CHARACTERISTICS OF PATIENTS WITH ALZHEIMER DEMENTIA (AD), LEFT HEMISPHERE STROKE (LHS), RIGHT HEMISPHERE STROKE (RHS), AND NEUROLOGICALLY NORMAL ADULTS(NL)

(NAplO) Age (years)

61.1

WI

Education (years)

13.6

Duration (months)

29.6’ [19.4] 4:6

Sex (male : female) Neurologic signs Visual signs

i1.81

-

LHS (N = 10)

RHS (N = 10)

62.0 [IO.21 12.8 ]I.91 4.1

58.8 16.51 12.2 l1.91 2.2 i3.81 713 10 Left 7d

WI

713 6 Right 3

(N tLIO) 46.8 [16.2] 14.0

P.11 7:3 -

Note. Values shown are means with standard deviations in brackets.

’ All patients were right handed. All had fluent, melodic speech. b The duration of illness was significantly longer in AD (p < .OOl) than in LHS or RHS groups. ’ One patient had right visual neglect; two patients, right homonymous hemianopsia. d Five patients had left visual neglect; two patients, left homonymous hemianopsia.

Aphasia, Reading, Writing, and Language quotients among the four diagnostic groups. The Kruskal-Wallis test (Conover, 1980) was used to evaluate all four groups simultaneously. Because of modest sample sizes, pairwise comparisons among groups were made using the Wilcoxon-Mann-Whitney test (Conover, 1980). Significance probabilities associated with pairwise comparisons among groups for categorical variables were calculated according to the Exact method of Pagan0 and Halvorsen (1981). Adjustment for multiple comparisons specifying an overall 5% level of statistical significance was made for each score of interest by the Bonferroni method (Neter & Wasserman, 1973). Single variable discriminant function analysis procedures were used to assessthe ability of the Aphasia, Reading, Writing, and Language quotients to classify the subjects by diagnosis. Because of the normality assumptions inherent in the discriminant methods, power transformations of these quotients were determined using the method of Box and Cox (1964).

RESULTS Language Performance

Table 2 shows results of the Western Aphasia Battery in terms of four summary scores: AQ, RQ, WQ, and the derivative LQ. All pairwise comparisons were statistically significant for the AQ and LQ, with the exception of patients with AD versus those with right hemisphere infarction. Pairwise comparisons were statistically significant for the RQ for AD vs normal subjects and left hemisphere infarction versus normal subjects. Pairwise comparisons were statistically significant for the WQ for normal versus both left and right hemisphere infarction subjects (see Table 2 footnote).

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TABLE 2 WESTERNAPHASIA BATTERY PERFORMANCE:SUMMARY SCORESOF PATIENTSWITH ALZHEIMER DEMENTIA (AD), LEFT HEMISPHERESTROKE (LHS), RIGHT HEMISPHERESTROKE(RHS), AND NEUROLOGICALLYNORMAL ADULTS (NL)

Subject group (N = 10 each)

Aphasia Quotient (AQ) Reading Quotient (RQ) Writing Quotient (WQ) Language Quotient (LO)

DAT

LHS

RHS

NL

89.0 14.11 88.9 [11.6] 88.9 [11.6] 79.1 [ 16.51

66.9 [14.9] 69.2 (20.81 64.3 [17.1] 68.0 [15.9]

92.5 i5.11 85.4 [17.4] 71.9 [12.4] 88.3 16.91

98.9

Note. Values shown are means, with standard deviations in brackets. AQ, comparisons are significant (p < .Ol) except DAT vs RHS. RQ, select pairwise are significant: DAT vs NL (p < .Ol); LHS vs NL (p < .Ol). WQ, select pairwise are significant: LHS vs NL (p < .Ol); RHS vs NL (p < .Ol). LQ, all pairwise are significant (p < .Ol) except DAT vs RHS.

Il.01

99.0 2.5 92.4 l5.61 97.7

Il.61 all pairwise comparisons comparisons comparisons

Aphasia Quotient Subscores Table 3 shows the subscores comprising the AQ, and Table 4 shows the statistically significant differences among the five subscores. As defined TABLE 3 MEANS AND STANDARD DEVIATIONS FOR “APHASIA QUOTIENT” SUBSCORESFOR THE FOUR ETIOLOGIC GROUPS: ALZHEIMER DEMENTIA (AD), LEFT HEMISPHERE STROKE (LHS), RIGHT HEMISPHERESTROKE (RHS), AND NEUROL~CICALLY NORMAL ADULTS (NL)

Subject group (N = 10 each) Aphasia Quotient subscore” Speech content Speech fluency Comprehension Repetition Naming

AD

LHS

RHS

8.9 [0.74] 8.6 [0.97] 9.1 [0.88] 9.0 [1.03] 8.8 [0.39]

7.8 [1.69] 6.4 [1.07] 7.8 [1.90]

8.8 [1.03] 9.2 [0.63] 9.5 [0.76] 9.6 [0.43] 9.0 [0.50]

[::;s] 5.5 [2.61]

NL 10.0

PW

9.9 [0.32] 10.0 [0.08] 9.97 [0.07] 9.7 [0.37]

a The Aphasia Quotient is composed of over 200 discrete responses, from which five subscores arc derived using formulae described by Kertesz (1979, 1982). Performance scores within each subtest are adjusted to a subscore maximum of 10.0 points.

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HORNER ET AL. TABLE 4

RESULTS OF STATISTICAL TESTS COMPARING THE DISTRIBUTION OF APHASIA QUOTIENT SUBSCORESFORTHE SIX POSSIBLEPAIRWISECOMPARISONSOF FOUR DIAGNOSTIC GROUPS:ALZHEIMER DEMENTIA (AD), LEFT HEMISPHERE STROKE (LHS), NORMAL CONTROLS (NL), AND RIGHT HEMISPHERESTROKE (RHS)

Significance probabilities (p values) Speech content

Speech fluency

Comprehension

Overall: comparison

.0005

.OOOl

.ooo3

Naming .Oool

Repetition JO01

DAT DAT DAT LHS LHS RHS

N.S. ** N.S. ***

*** *** N.S. ***

N.S. **

*** N.S.

N.S. ** N.S. *** ** N.S.

** ** N.S. *** *** **

*** *** N.S. *** ***

vs LHS vs NL vs RHS vs NL vs RHS vs NL

N.S.

” Overall tests simultaneously compare the distribution of scores for all four groups using the Kruskal-Wallis nonparametric method; paitwise comparisons are made using the Wilcoxon-Mann-Whitney test and Exact tables. In each case the null hypothesis posits that the distribution of the scores is the same for each of the diagnostic groups of interest. * p < .05. ** p < .Ol.

*** p < ,001.

by the Western Aphasia Battery, the subscores of fluency, comprehension, repetition, and naming can be used to classify patients by type of aphasia. Language profiles obtained from these subscores revealed that among patients with left hemisphere infarction, four had conduction aphasia, two had Wernicke aphasia, and four had anemic aphasia. In contrast, all patients with AD showed “anemic aphasia” using the Western Aphasia Battery taxonomy, while among patients with right hemisphere infarction, four patients fit an “anemic” classification due to poor word fluency (rapid category naming), and six performed within normal limits. By virtue of achieving an AQ of 93.8 or better (Kertesz, 1979), all neurologically normal subjects performed within normal limits. Discriminant

Function

Single and multiple variable discriminant functions (Table 5) differed in their successin classifying patients correctly into their diagnostic groups. Using single variables, overall correct classifications were as follows: AQ, 27 of 40 (67.5%); RQ, 17 or 40 (42.5%); WQ, 19 of 40 (47.5%); and, LQ, 24 of 40 (60.0%). The best discriminant was the multiple variable AQ-RQ-WQ: Of 40 subjects, 29 (72.57)o were classified correctly. Finally, Table 6 shows the actual successes and failures of the multiple variable discriminant function analysis.

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TABLE 5 CORRECTCLASSIFICATIONOF 40 PATIENTS USINGTHE WESTERN APHASIA BATTERY BY DISCRIMINANT FUNCTION ANALYSES FOR FOUR ETIOL~GIC GROUPS: ALZHEIMER DEMENTIA, LEFT HEMISPHERESTROKE, RIGHT HEMISPHERESTROKE, AND NEUROLOGICALLY NORMALADULTS

Variable

Percentage correctly classified

Single Aphasia Quotient Reading Quotient Writing Quotient Derivative: Language Quotient

67.5% 42.5% 47.5% 60.0%

Multiple Aphasia Quotient-Reading Quotient-Writing

72.5%

Quotient

DISCUSSION

The findings of this study partially confirm the observation of Bayles and Kaszniak (1987) that the problems in communication seen in early AD may be difficult to distinguish from fluently speaking individuals with focal lesions of either cerebral hemisphere. In our examination of four groups of subjects, those with AD and anomia were more readily distinguished from patients with left hemisphere infarction and fluent aphasia than from patients with right cerebral infarction and no aphasia. All patients were easily distinguished from the neurologically normal group. The discriminant function analyses showed that individuals with AD and those with right cerebral infarction were difficult to classify, whereas individuals with left cerebral infarction and normal subjects were both classified with relative success. The multiple variable AQ-RQ-WQ discriminant (with 29 successful classifications) was only marginally better than the single variable AQ (with 27 successful classifications). Although the TABLE 6 PREDICTEDVERSUSACTUAL CLASSIFICATIONSUSING THE MULTIPLE VARIABLE DISCRIMINANT “APHASIA QUOTIENT-READING QUOTIENT-WRITING QUOTIENT” FROMTHE WESTERN APHASIA BATTERY FORFOUR ETIOLOGICGROUPS,10 INDIVIDUALS IN EACH GROUP: ALZHEIMER DEMENTIA (AD), LEFT HEMISPHERESTROKEWITH FLUENT APHASIA (LHS), RIGHT HEMISPHERESTROKE (RHS), AND NEUROL~GICALLY NORMAL ADULTS (NL)

Predicted Actual

DAT

LHS

RHS

NL

DAT LHS RHS NL

6 2 3 0

0 8 0 0

4 0 5 0

0 0 2 10

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ET AL.

multiple variable discriminant was the “best,” only 19 (about 63%) of 30 individuals with cerebral disorders were classified correctly. Further studies are needed to determine if this less than optimal result is related to the small number of subjects or to the testing instrument. The patients selected for this study were all fluent speakers, i.e., showed preserved melodic line and articulatory agility. All individuals with AD or with left cerebral infarction demonstrated anemic hesitations and circumlocutory responses, while six patients with left cerebral infarction (those with conduction and Wernicke aphasia) showed additional aphasic signs such as phonemic paraphasias, semantic paraphasias, and/or paragrammatisms. These focal aphasic signs (reflected in lower speech fluency, oral repetition, and oral naming scores) distinguished the subjects with fluent aphasia due to left cerebral infarction from patients with early, primarily anemic AD. In contrast, patients with right cerebral infarction did not differ significantly from patients with AD on any of the scores comprising the AQ. As Appell and colleagues (1982) observed, AD patients fail to show classic focal aphasic signs such as phonemic paraphasias, semantic paraphasias, and morphosyntactic deviations. A similar “failure” by patients with right cerebral infarction helps explain why AD and right cerebral infarction groups do not differ significantly on the aphasia battery. Our results modify Bayles and Kaszniak’s (1987) observation that communication problems in early AD may be most difficult to distinguish from fluently speaking individuals with focal infarction of either cerebral hemisphere. Our data show that AD patients are most difficult to distinguish from fluently speaking individuals who have sustained right cerebral infarction, but are distinguished relatively well from left cerebral infarction patients with fluent aphasia. With regard to Aphasia Quotient profiles (Table 3), we did not replicate the observation by Appell and colleagues that AD patients show relatively preserved speech fluency and relatively impaired comprehension by comparison to those of the left cerebral infarction patients. This is probably due to differences in the stage of AD patients examined, as well as to our a priori control on speech fluency across the groups of interest. Several possibilities for further study of the differential diagnostic characteristics of these disorders are suggested by our findings. As clinicians familiar with these disorders know, the communication abilities within groups of AD, left hemisphere fluent aphasia, and right hemisphere infarction individuals (and even within a normal sample) are heterogeneous. To examine Bayles and Kaszniak’s (1987) observation, our main a priori selection criterion was the presence of fluent speech. Further studies might address our question by limiting the selection of left hemisphere aphasia subjects to “anemic aphasia.” An alternative approach would be to stratify subjects by type of fluent aphasia (anemic, Wernicke, conduction, transcortical sensory aphasia) and to control, in all subgroups of interest, the

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severity of communication disability. Finally, slow word retrieval on the controlled oral naming task (“word fluency”) has been shown to be ubiquitous in brain damaged individuals of all types and not pathognomonic. The fact that right hemisphere patients and AD patients performed similarly, and resisted classification by discriminant function analysis, might simply reflect the fact that neither group was “aphasic” as classically defined. The Western Aphasia Battery was designed to discriminate aphasic from normal language, and our study confirmed the battery’s usefulness for this purpose. However, the Western Aphasia Battery failed to discriminate robustly among language performance disorders due to diverse etiologies. Although we recognize that a comprehensive, standardized neuropsychological battery comprised of language and nonlanguage cognitive abilities may be the “best” approach for differential diagnosis among the four groups we studied, the contrastive effect of cortical disease OIZlunguuge remains an important question. In addition to the clinically practical reasons for intergroup comparisons outlined in the introduction, there are several compelling theoretical reasons for such comparisons. By systematic assessment of language using reliable and valid standardized tests, Duffy and Myers (1991) suggest we can modify existing classifications (subtyping); we can track both subtle and gross changes during disease progression (staging); and, we can evaluate theories about the nature of the deficits both within and across etiologic groups. The heterogeneity of individuals with AD in general (Chui et al., 1985; Chui, 1989; Jagust et al., 1990) and the language disorder of dementia in particular (Joynt, 1984) calls for a standard, replicable approach. Some reject, explicitly or implicitly, the notion of using standardized aphasia batteries in dementia research (Wertz, 1982; Smith, Murdoch, & Chenery, 1987; Swindell, Boller, & Holland, 1988; Bayles et al., 1989; Kovesi, 1989). Others think this is a reasonable approach (Appell et al., 1982; Kirshner et al., 1984; Cummings et al., 1985; Horner, 1985; Tikofsky et al., 1986; Murdoch et al., 1987). Appell et al. (1982) provided the first comprehensive study of late stage AD using the Western Aphasia Battery. Others have studied AD with the Neurosensory Center Comprehensive Buttery for Aphasia (Murdoch et al., 1987) and the complete Boston Diagnostic Aphasia Examination (Kirshner et al., 1984; Cummings et al., 1985). The Boston Diagnostic Aphasia Examination is frequently cited but only selected portions of this battery are given or reported (Foster et al., 1983; Knesevich et al., 1985; Kaszniak, Wilson, Fox, & Stebbins, 1986; Berg et al., 1988; Morris & Fulling, 1988). While the descriptive information from isolated subtests may be useful, administering selected subtests potentially undermines the reliability and validity of the test battery. This practice may lead to either false negative or false positive rates of identification of language disorders in AD (Schmitt, Ranseen, &

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DeKosky, 1989). We suggest that further studies are needed using complete aphasia batteries with known reliability and validity if researchers hope to identify the presence and degree of language impairment, to differentiate among types and subtypes of the disorder, and to differentially diagnose focal neurobehavioral syndromes from diffuse dementing illnesses such as AD. REFERENCES Appell, J., Kertesz, A., & Fisman, M. 1982. A study of language functioning in Alzheimer patients. Brain and Language, 17, 73-91. Bayles, K. A., Boone, D. R., Tomoeda, C. K., Slauson, T. J., & Kaszniak, A. W. 1989. Differentiating Alzheimer’s patients from the normal elderly and stroke patients with aphasia. Journal of Speech and Hearing Disorders 34, 74-87. Bayles, K. A., & Kaszniak, A. W. 1987. Communication and cognition in normal aging and dementia. Boston: College-Hill/Little Brown. Berg, L., Danziger, W. L., Storandt, M., et al. 1984. Predictive features in mild senile dementia of the Alzheimer type. Neurology (Cleveland), 34, 563-569. Berg, L., Miller, J. P., Storandt, M., et al. 1988. Mild senile dementia of the Alzheimer type: 2 Longitudinal assessment. Annals of Neurology, 23, 477-484. Box, G. E. P., & Cox, D. R. 1964. An analysis of transformations. Journal of the Royal Statistical Society, 26, 211-252.

Chawluk, J. B., Mesulam, M-M., Hurtig, H., & et al. 1986. Slowly progressive aphasia without generalized dementia: Studies with positron emission tomography. Annals of Neurology,

19, 68-74.

Chui, H. C. 1989. Dementia: A review emphasizing clinicopathologic correlation and brainbehavior relationships. Archives of Neurology, 44, 720-722. Chui, H. C., Teng, E. L., Henderson, V. W., & Moy, A. C. 1985. Clinical subtypes of dementia of the Alzheimer type. Neurology, 35, 1544-1550. Conover, W. B. 1980. Practical nonparametric statistics. New York: Wiley. Second ed. Crystal, H. A., Horoupian, D. S., Katzman, R., & Jotkowitz, S. 1982. Biopsy-proved Alzheimer disease presenting as a right parietal lobe syndrome. Annals of Neurology, 12, 186-188. Cummings, J. L., Benson, F., Hill, M. A., & Read, S. 1985. Aphasia in dementia of the Alzheimer type. Neurology, 35, 394-397. DeRenzi, E. 1986. Slowly progressive visual agnosia or apraxia without dementia. Cortex, 22, 171-180. Duffy, J. R. 1987. Slowly progressive aphasia. In R. H. Brookshire (Ed.), Clinical aphasiology. Minneapolis: BRK Pub. Vol. 17, Pp. 349-356. Duffy, J. R., & Myers, P. S. 1991. Group comparisons across neurologic communication disorders: Some methodological issues. In T. E. Prescott (Ed.), Clinical aphasiology. Austin TX: Pro-Ed. Vol. 19, Pp. 1-14. Filley, C. M., Kelly, J., & Heaton, R. K. 1986. Neuropsychological features of early- and late-onset Alzheimer’s disease. Archives of Neurology, 43, 574-576. Folstein, M. F., & Breitner, J. C. S. 1981. Language disorder predicts familial Alzheimer disease. Johns Hopkins Medical Journal, 149, 145-147. Foster, N. L., Chase, T. N., Fedio, P., Patronas, N. J., Brooks, R. A., & DiChiro, G. 1983. Alzheimer’s disease: Focal cortical changes shown by positron emission tomography. Neurology (Cleveland), 33, 961-965. Fromm, D., & Holland, A. L. 1989. Functional communication in Alzheimer’s disease. Journal of Speech and Hearing Disorders,

54, 535-540.

USEFULNESS OF WESTERN APHASIA

BATTERY

87

Green, J., Morris, J. C., Sandson, J., McKee], D. W., & Miller, J. W. 1990. Progressive aphasia: A precursor of global dementia? Neurology, 40, 423-429. Heath, P. D., Kennedy, P., & Kapur, N. 1983. Slowly progressive aphasia without generalized dementia. Annals of Neurology, 13, 687-699. Hier, D. B., Hagenlocker, K., & Shindler, A. G. 198.5.Language disintegration in dementia: Effects of etiology and severity. Brain and Language, 25, 117-133. Horner, J. 1985. Language disorder associated with Alzheimer’s dementia, left hemisphere stroke, and progressive illness of uncertain etiology. In R. H. Brookshire (Ed.), Clinical aphasiology. Minneapolis: BRK Pub. Vol. 15, Pp. 149-158. Horner. J., Lathrop, D. L., Fish, A. M., & Dawson, D. V. 1987. Agraphia in left and right hemisphere stroke and Alzheimer dementia patients. In R. H. Brookshire (Ed.), Clinical aphasiology. Minneapolis: BRK Pub. Vol. 17, Pp. 73-83. Jagust, W. J., Davies, P., Tiller-Borcich, J. K., & Reed, B. R. 1990. Focal Alzheimer’s disease. Neurology, 40, 14-19. Joynt, R. J. 1984. The language of dementia. In F. C. Rose (Ed.), Advances in neurology. New York: Raven Press. Vol. 42, Pp. 65-69. Kaszniak, A. W., Fox, J., Gandell, D. L., et al. 1978. Predictors of mortality in presenile and senile dementia. Annals of Neurology, 3, 246-252. Kaszniak, A. W., Wilson, R. S., Fox, J. H.. & Stebbins, G. T. 1986. Cognitive assessment in Alzheimer’s disease: Cross-sectional and longitudinal perspectives. Canadian Journal of Neurological

Sciences, 13, 420-423.

Kertesz, A. 1979. Aphasia and associated disorders. New York: Grune & Stratton. Kertesz, A. 1982. Western Aphasia Battery. New York: Grune & Stratton. Kirshner, H. S., Webb. W. G., Kelly, M. P., & Wells, C. E. 1984. Language disturbance: An initial symptom of cortical degeneration and dementia. Archives of Neurology, 41, 491-496. Knesevich; J. W., Toro, F. R., Morris, J. C., & LaBarge, E. 1985. Aphasia, family history, and the longitudinal course of senile dementia of the Alzheimer type. Psychiatry Besearch, 14, 255-263.

Kovesi, C. 1989. The application of language tasks to the identification of senile dementia. Australian Journal of Human Communication Disorders, 17, 17-32. McKhann, G., Drachman, D., Folstein, M., et al. 1984. Clinical diagnosis of Alzheimer’s disease: Report of the NINCDS-ADRDA Work Group under the auspices of the Department of Health and Human Services Task Force on Alzheimer’s disease. Neurology, 34, 939-944.

Martin, A., Brouwers, P., Lalonde, F., et al. 1986. Towards a behavioral typology of Alzheimer’s patients. Journal of Clinical and Experimental Neuropsychology, 8, 594610. Mayeux, R., Stern, Y., & Spanton, S. 1985. Heterogeneity in dementia of the Alzheimer type: Evidence of subgroups. Neurology, 35, 453-461. Mesulam, M-M. 1982. Slowly progressive aphasia without generalized dementia. Annals of Neurology,

11, 592-598.

Morris, J. C., & Fulling, K. 1988. Early Alzheimer’s disease: Diagnostic considerations. Archives of Neurology,

45, 345-349.

Murdoch, B. E., Chenery, H. J., Wilks, V., & Boyle, R. S. 1987. Language disorders in dementia of the Alzheimer type. Brain and Language, 31, 122-137. Neter, J., & Wasserman, W. 1973. Applied linear statistical models. Homewood IL: Irwin. Nicholas, M., Obler, L. K., Albert, M. L., & Helm-Estabrooks, N. 1985. Empty speech in Alzheimer’s disease and fluent aphasia. Journal of Speech and Hearing Research, 28, 405-410. Pagano, M., & Halvorsen, K. T. 1981. An algorithm for finding the exact significance levels

HORNER ET AL.

88

of r X c contingency tables. Journal of the American Statistical Association, 76, 931934. Schmitt, F. A., Ranseen, J. D., & DeKosky, S. T. 1989. Cognitive mental status examinations. Clinics in Geriafric Medicine, 5, 545-564. Seltzer, B., & Sherwin, I. 1983. A comparison of features in early- and late-onset primary degenerative dementia: One entity or two? Archives of Neurology, 40, 143-146. Shewan, C. M. 1986. The language quotient (La): A new measure for the Western Aphasia Battery. Journal of Communication

Disorders,

19, 427-439.

Shewan, C. M., & Kertesz, A. 1980. Reliability and validity characteristics of the Western Aphasia Battery (WAB).

Journal of Speech and Hearing Disorders,

45, 308-324.

Smith, S. R., Murdoch, B. E., & Chenery, H. J. 1987. Language disorders associated with dementia of the Alzheimer type: A review. Australian Journal of Human Communication Disorders, 15, 49-69. Swindell, C. S., Boller, F., & Holland, A. L. 1988. Expressive language characteristics in probable Alzheimer’s disease. Aphasiology, 2, 411-416. Tierney, M. C., Snow, G., Reid, D. W., Zorzitto, M. L., & Fisher, R. H. 1987. Psychometric differentiation of dementia: Replication and extension of the findings of Storandt and co-workers. Archives of Neurology, 44, 720-722. Tikofsky, R. S., Glatt, S. J., Hoffman, R. G., Allen, P. A., & Befera, M. 1986. Performance characteristics of demented patients on the Western Aphasia Battery and Boston Naming Test. Journal of Clinical and Experimental Neuropsychology, 8, 139-140. [Abstract] Wechsler, A. F. 1977. Presenile dementia presenting as aphasia. Journal of Neurology, Neurosurgery,

and Psychiatry,

40, 303-305.

Wertz, R. T. 1982. Language deficit in aphasia and dementia: The same as, different from, or both? In R. H. Brookshire (Ed.), Clinical aphasiology. Minneapolis: BRK Pub. Vol. 12, Pp. 350-359. Wertz, R. T., Dronkers, N. F., & Deal, J. L. 1985. Language and localization: A comparison of left, right, and bilaterally brain-damaged patients. In R. H. Brookshire (Ed.), Clinical aphasiology. Minneapolis: BRK Pub. Vol. Pp. 141-148.