close

Вход

Забыли?

вход по аккаунту

?

Deterioration of naming nouns versus verbs in primary progressive aphasia.

код для вставкиСкачать
Deterioration of Naming Nouns versus
Verbs in Primary Progressive Aphasia
Argye E. Hillis, MD, Sangjin Oh, MD, and Lynda Ken
Disproportionate impairment of naming nouns versus verbs and the opposite pattern have been reported in cases of focal
brain damage or degenerative disease, indicating that processing of nouns and verbs may rely on different brain regions.
However, it has not been clear whether it is the spoken word forms or the meanings (or both) of nouns and verbs that
depend on separate neural regions. We tested oral and written naming of nouns and verbs, matched in difficulty, in
patients with nonfluent primary progressive aphasia (nonfluent PPA; n ⴝ 15), fluent primary progressive aphasia (fluent
PPA; n ⴝ 7), and amyotrophic lateral sclerosis with frontotemporal dementia (ALS-FTD; n ⴝ 6). Patients with nonfluent PPA and ALS-FTD, both individually and as groups, were significantly more impaired on verb naming than on
noun naming and significantly more impaired on oral naming than written naming. Patients with fluent PPA showed the
opposite pattern for both word class and modality, significantly more impaired naming of nouns versus verbs and
significantly more impaired written versus oral naming. Results indicate that separate regions of the brain are essential
for access to oral and written word forms of verbs and nouns, and that these neural regions can be differentially damaged
in separate forms of PPA.
Ann Neurol 2004;55:268 –275
Primary progressive aphasia (PPA) is a degenerative
condition characterized by deterioration in language for
at least 2 years, without deterioration in other cognitive
domains other than praxis.1,2 It is now considered one
of a family of disorders known as frontotemporal lobar
degeneration, frontotemporal dementia, Pick’s disease,
or Pick’s complex.3– 6 PPA is observed in two very different forms: nonfluent PPA (with halting, agrammatic
speech, effortful articulation, and relatively preserved
comprehension) and fluent PPA (with fluent, paragrammatic speech, intact articulation, and severe impairment of comprehension and naming).7 The
former, nonfluent PPA, is sometimes the presenting
clinical syndrome in patients who eventually develop
amyotrophic lateral sclerosis with frontotemporal dementia (ALS-FTD, also known as motor neuron
disease-dementia-aphasia syndrome8). It has been proposed that nonfluent PPA and ALS-FTD reflect dysfunction or atrophy predominantly of the left posterior, inferior frontal lobe and/or left premotor cortex,
and insula,9,10 and fluent PPA (also called posterior
progressive aphasia) reflects dysfunction or atrophy of
the left posterior, superior temporal lobe, and angular
gyrus.7,10 The terms semantic dementia or temporal
variant frontotemporal dementia are sometimes used
From the Johns Hopkins University School of Medicine, Department of Neurology, Johns Hopkins University Department of Cognitive Science; University of Maryland School of Medicine, Department of Neurology; and Johns Hopkins University, Department of
Neuroscience, Baltimore, MD
Received Aug 1, 2003, and in revised form Sep 8. Accepted for
publication Sep 16, 2003.
268
synonymously with fluent PPA or used only when the
syndrome includes associative agnosia or impaired semantic memory for objects. The latter syndrome most
frequently has been associated with dysfunction or atrophy in the left temporal pole or inferior temporal
gyrus,9 –16 although associated atrophy of surrounding
regions also has been reported.9,11,17 Because the neural dysfunction in PPA is not necessarily confined to a
particular vascular territory (as in stroke), these cases
allow a unique opportunity to evaluate hypotheses
about brain/language relationships, and about how language deteriorates over time with progressive disease of
the left frontal and temporal lobes.
One such hypothesis that can be uniquely evaluated
in PPA is the proposal that there are distinct neural
regions essential for accessing representations of object
names (nouns) versus action names (verbs). Reported
cases of selective impairment in naming verbs, relative
to nouns, and the opposite dissociation (impairment in
naming nouns relative to verbs) due to stroke18 –25 or
dementia26 –30 provide evidence that some neural regions are more critical for naming one word class or
the other. Some position emission tomography studies,31,32 but not others,33,34 show distinct regions of
activation when naming nouns versus verbs. Most le-
Address correspondence to Dr Hillis, Department of Neurology,
Johns Hopkins Hospital, Meyer 5-185, 600 N. Wolfe Street, Baltimore, MD 21287.
E-mail: argye@JHMI.edu
© 2004 American Neurological Association
Published by Wiley-Liss, Inc., through Wiley Subscription Services
sion studies suggest that frontal damage generally
causes more problems naming verbs, whereas temporal
damage causes more problems naming nouns.27,35–38
Repetitive transcranial magnetic stimulation of left
frontal regions also affects verb more than noun production.39,40 Likewise, functional imaging studies show
more frontal activation when naming verbs and
tools41– 43 and more temporal activation in naming
nouns other than tools.31
Most of the naming studies have not distinguished
whether the regions that are more critical for naming
verbs versus nouns are components of semantic networks (for word meaning) or networks for accessing
spoken and written word form representations. Prevailing models of the cognitive processes underlying naming postulate that naming requires access to both the
semantic representation and the word form representation (phonological word form for spoken naming and
orthographic word form for written naming44,45). In
some patients with focal lesions or dementia, the dissociation between nouns and verbs seems to be caused
by disproportionately impaired meaning of one word
class.26,27,46 One study reported that patients with
ALS-FTD were more impaired, as a group, on verbs
than nouns in semantic tasks, but none of the individual subjects showed a significant difference between
nouns and verbs.8 A relatively large study of word/picture verification, which requires access to semantic representations, in patients with FTD reported more difficulty with verbs than nouns in all subtypes of FTD.47
Interestingly, however, impaired performance with verb
stimuli correlated with scores on different tests for the
three subgroups. Verb comprehension correlated with
time to completion on tests of executive function in
patients with dysexecutive syndrome, correlated with
sentence comprehension in patients with nonfluent
PPA, and correlated with neither in patients with semantic dementia. These results indicated that failure
on verb comprehension may have reflected different
deficits in the three groups.47 Bak reported that patients with nonfluent PPA showed progressive deterioration in semantics of verbs relative to nouns, whereas
patients with semantic dementia showed deterioration
of nouns relative to verbs (in a picture-matching
task).48 Although there are some divergent conclusions
from these two studies, both provide evidence of semantic deterioration of verbs relative to nouns in at
least some patients with PPA. These results suggest that
semantic representations of verbs and nouns might entail somewhat different neural substrates, because they
can be differentially impaired by brain damage. Consistent with this proposal, recent functional magnetic
resonance imaging studies have demonstrated distinct
areas of activation associated with meanings of motion
verbs versus nouns.49,50
Impaired semantics of verbs might account for poor
verb naming in patients who show equivalent impairment in oral and written naming of verbs and verb
comprehension. However, several single-case studies of
patients with chronic stroke,23,24 acute stroke,37 or
nonfluent PPA30 have reported disproportionate impairment for verbs versus nouns (or the opposite)25 in
one modality of output, speaking or writing, and preserved naming of both nouns and verbs in the other
modality. These cases indicate that some distinct neural
mechanisms underlying noun versus verb naming are
components of neural networks for accessing spoken
and written word forms, rather than components of semantic networks, because a deficit in accessing semantic representations of one word class should affect spoken and written naming equally.
We sought to confirm this observation from singlecase studies, by conducting a group study of oral and
written naming and comprehension of nouns and verbs
in patients with nonfluent PPA (n ⫽ 15), fluent PPA
(n ⫽ 7), and ALS-FTD (n ⫽ 6). We hypothesized that
patients with nonfluent PPA and ALS-FTD (who are
thought to have more frontal lobe dysfunction than
those with fluent PPA), both individually and as a
group, would be significantly more impaired in naming
verbs than nouns. We also hypothesized that patients
with fluent PPA (who are thought to have more temporal lobe dysfunction), both individually and a group,
would show the opposite pattern: significantly more
impairment in naming nouns than verbs. Furthermore,
we hypothesized that nonfluent PPA patients would
show the word class-specific naming impairment only
in spoken naming, indicating that at least some mechanisms specific to verbs versus nouns are components
of networks underlying access to word form representations.
Subjects and Methods
Subjects
We studied a consecutive series of 28 patients who presented
to Johns Hopkins Hospital, were native English speakers,
and met the criteria for the clinical diagnosis of PPA or ALSFTD. PPA was defined as progressive deterioration in language out of proportion to other cognitive functions (except
praxis) for at least 2 years.1,2 PPA patients then were subdivided into (1) nonfluent PPA, characterized by effortful,
agrammatic speech, with short phrase length and distorted
articulation (n ⫽ 15), and (2) fluent PPA, characterized by
effortless, grammatical or paragrammatic speech with normal
phrase length and normal articulation, but limited content
(n ⫽ 7).7 Patients with ALS-FTD met clinical and neurometric criteria for ALS, as well as clinical criteria for FTD
(n ⫽ 6).4 All patients in the last group had presented with a
nonfluent PPA (for more than 2 years) but had developed
some other cognitive deficits by the time of the current
study. Cognition initially was evaluated with a battery of
neuropsychological tests, including the Mini-Mental State
Examination,51 Digit Span (forward and backward), Orien-
Hillis et al: Naming in Progressive Aphasia
269
tation and Information subtest of the Weschler Memory
Scale,52 Rey Complex Figure Test (copying and immediate
and delayed recall),53 Rey Auditory Verbal Naming Test
(Western Psychological Services, 1996), Boston Naming
Test,54 Controlled Oral Word Association Test,55 Grooved
Pegboard (Psychological Assessment Resources, 1999),
Stroop Test,56 and the Trails Test.57 Although results are
somewhat difficult to interpret in patients with PPA because
the tests rely on verbal directions, verbal stimuli, and/or verbal responses, these tests were used primarily to exclude patients with deficits in cognitive domains other than language
(eg, impaired performance on the Rey Complex Figure copy
or recall) from the PPA groups. Approximate disease duration (from reported onset of symptoms) ranged from 24 to
120 months. Age ranged from 45 to 81 years; 69% were
female. All were right-handed. All were independent in activities of daily living and had preserved insight regarding
their deficits. All patients had magnetic resonance imaging
scans showing asymmetric frontal and/or temporal atrophy.
This study was approved by the Johns Hopkins Institutional Review Board.
Procedures
Patients were administered tasks of oral and written naming
of 30 “pure” nouns and 30 “pure” verbs, matched for word
frequency, pictured as black and white line drawings that
elicited a high degree of name agreement in pilot testing.22
The term pure here means that the word is used exclusively
(or almost exclusively) as a noun or a verb in English.22
Stimuli were presented in a counterbalanced A1 B2 B1 A2
design. Nouns (A) were administered first in half of the patients, and verbs (B) were administered first in the other half.
Modalities (1 and 2) were randomly assigned. We also administered tests of word-picture verification (described previously in Hillis and colleagues30) and repetition of the same
nouns and verbs in a separate session. Because these tasks are
not matched in “difficulty” to the naming test, performance
on these tests are noted only in the illustrative cases.
Differences between word classes and modalities for each
test were evaluated with nonparametric tests because of the
low number of patients in each group. The Wilcoxon ranksum test and signs test were used for paired comparisons
across word class and modalities within groups, and the
Mann–Whitney u test was used for unpaired comparisons
across groups. Fisher’s exact tests were used to identify word
class and modality effects for individual patients.
Results
Across-Group Comparisons
There were no differences across groups for MiniMental State Examination score (nonfluent PPA: mean
23.9 ⫾ 5, median 26; fluent PPA: mean 16 ⫾ 5, median ⫽ 20; ALS-FTD: mean 16 ⫾ 5, median ⫽ 24).
In contrast, there were significant differences across
groups on naming tests. Median scores on oral and
written naming of nouns and verbs for each group are
summarized in Figure 1; mean scores are reported in
the text (ie, the figures and text provide complementary data). Patients with nonfluent PPA were signifi-
270
Annals of Neurology
Vol 55
No 2
February 2004
Fig 1. Median scores for oral and written naming in each
group. PPA ⫽ primary progressive aphosia; ALS ⫽ amyotrophic lateral sclerosis; FTD ⫽ frontotemporal dementia.
cantly more impaired than patients with fluent PPA in
oral naming of verbs (mean, 54.5 ⫾ 30 vs 79.2 ⫾ 24
correct; Z ⫽ ⫺2.1; p ⬍ 0.04). The same trend was
observed for written naming of verbs (mean, 31.5 ⫾
29 vs 61.6 ⫾ 34; Z ⫽ ⫺1.8; p ⫽ 0.08). In contrast,
patients with fluent PPA were significantly more impaired than patients with nonfluent PPA in oral naming of nouns (64.7 ⫾ 26 vs 81.9 ⫾ 22; Z ⫽ ⫺1.9;
p ⫽ 0.05) and in written naming of nouns (39.6 ⫾ 35
vs 82.4 ⫾ 19; Z ⫽ ⫺2.6; p ⬍ 0.01). There were no
significant differences between patients with ALS-FTD
and those with nonfluent PPA on any test (Z ⫽
⫺0.711 to ⫺0.826; p ⬎ 0.4 for all). There was a trend
for patients with ALS-FTD to be more impaired in
oral naming of verbs, compared with patients with fluent PPA (42.4 ⫾ 42 vs 81.9 ⫾ 22; Z ⫽ ⫺1.8; p ⫽
0.07).
Within-Group Comparisons
PRIMARY PROGRESSIVE APHASIA. As a
group, patients with nonfluent PPA showed significantly more impaired oral naming of verbs than nouns
(54.5 ⫾ 30.3 vs 81.9 ⫾ 22.1% correct; Z ⫽ ⫺3.4;
p ⬍ 0.002; Sign’s test: p ⬍ 0.0001). They were also
significantly more impaired in written naming of verbs
than nouns (61.6 ⫾ 33.9 vs 82.4 ⫾ 18.7% correct;
Z ⫽ ⫺2.9; p ⬍ 0.004; sign’s test: p ⬍ 0.002). This
group also showed more impaired oral than written
naming of verbs (54.5 ⫾ 30.3 vs 61.6 ⫾ 33.9%) but
relatively intact oral and written naming of nouns
(81.9 ⫾ 22.1% vs 82.4 ⫾ 18.7%), with no significant
difference between modalities for nouns. More importantly, individual analyses showed that all patients with
nonfluent PPA showed more impaired oral naming of
verbs relative to nouns, and this difference was signifNONFLUENT
icant in 6 of 15 patients (Fisher’s exact test: p ⬍ 0.04
to p ⬍ 0.00001; Fig 2). Furthermore, all patients with
nonfluent PPA also showed more impaired oral than
written naming, and this difference was significant in 6
of 15 patients (Fisher’s exact test: p ⬍ 0.03 to p ⬍
0.00001). All but two patients showed a significant difference between nouns and verbs in at least one modality of output.
Although all of these patients had somewhat effortful
articulation and slightly distorted speech sounds, they
were able to repeat both nouns and verbs with 100%
accuracy (distorted speech sounds were not penalized
in either oral naming or repetition, as long as the word
was clearly intelligible). Their errors in oral naming
were predominantly semantic paraphasias, substituting
nouns for the target verbs (eg, “book” for “read”) or
more general verbs for the target verbs (eg, “talk” for
“teach”), or “I don’t know” responses. Furthermore,
these patients were able to orally name the nouns,
which equally required motor speech. Therefore, impaired oral naming of verbs was not caused by the motor speech impairment itself. Errors in oral naming of
verbs also could not, in most cases, be attributed to
impaired recognition of the picture stimuli or impaired
semantic representations of the verbs, because many of
the patients could write the target verbs in response to
the same pictures. Therefore, at least in most cases, impaired oral naming of verbs can be accounted for by
impaired access to the spoken word forms (phonological representations) of verbs. However, we cannot rule
out some contribution of subtly impaired semantics of
verbs in cases with impaired oral and written naming
of verbs.
AMYOTROPHIC LATERAL SCLEROSIS WITH FRONTOTEMPORAL DEMENTIA. Patients with ALS-FTD showed
the same pattern as patients with nonfluent PPA, with
significantly more impaired naming of verbs than
nouns in both oral naming (42.4 ⫾ 41.5 vs 57.1 ⫾
41.5% correct; Z ⫽ ⫺2.0; p ⬍ 0.05) and written
naming (56.0 ⫾ 30.9% vs 70.7 ⫾ 35.8% Z ⫽ ⫺2.0;
p ⬍ 0.05). Patients with ALS-FTD were also more impaired in oral than written naming of nouns (57.1 ⫾
41.5% vs 70.7 ⫾ 35.8%) and verbs (42.4 ⫾ 41.5% vs
56.0 ⫾ 30.9% correct), although the difference was
not significant because of the low number of patients
or the variability within the group. Individual analysis
showed that all of the patients with ALS-FTD showed
the same pattern as the group: more impairment in
naming verbs than nouns (Fisher’s exact test: p ⬍ 0.05
Fig 2. Individual scores for oral naming of nouns and verbs in patients with nonfluent primary progressive aphasia.
Hillis et al: Naming in Progressive Aphasia
271
to p ⬍ 0.00001) and more impairment in oral than
written naming (significant in five of five patients who
were able to write at all; Fisher’s exact test: p ⬍ 0.05 to
p ⬍ 0.00001) (Fig 3). However, it is unclear whether
the greater impairment in oral than written naming in
two patients was caused by impaired access to the phonological word forms or caused by the motor speech
impairment, or both, because these two patients were
also unable to repeat words they could not produce in
oral naming. The other five patients repeated nouns
and verbs with 100% accuracy. Two patients with
ALS-FTD were unable to write because of limb weakness. Thus, although the cases with ALS-FTD showed
the same pattern of naming performance as the patients with nonfluent PPA, the former group had a
more complicated picture, because their motor deficits
(limb weakness and dysarthria) frequently interfered
with oral and/or written naming.
Patients with
fluent PPA showed the opposite pattern for word class
and modality (Fig 4). As a group, they were more impaired in oral naming of nouns than verbs: 64.7 ⫾
26.0 versus 79.2 ⫾ 23.7% correct; Z ⫽ ⫺2.4; p ⬍
0.02. They were also more impaired in written than
oral naming for both nouns (39.6 ⫾ 35.1 vs 64.7 ⫾
26.0% correct; Z ⫽ ⫺2.0; p ⬍ 0.05) and verbs
(31.5 ⫾ 28.8 vs 79.2 ⫾ 23.7% correct; Z ⫽ ⫺2.2;
p ⬍ 0.03). Individual analyses showed that all seven
patients with fluent PPA showed the same pattern as
the group, with more impairment for nouns than verbs
in oral naming (significant in three of seven; Fisher’s
exact test: p ⬍ 0.05 to p ⬍ 0.001), and more impairment in written than oral naming (significant three of
seven; Fisher’s exact test: p ⬍ 0.05 to p ⬍ 0.001). Because of the patients had deficits in both oral and writ-
Fig 4. Individual scores for oral naming of nouns and verbs
in patients with fluent primary progressive aphasia.
FLUENT PRIMARY PROGRESSIVE APHASIA.
Fig 3. Individual scores for oral naming of nouns and verbs
in patients with amyotrophic lateral sclerosis with Frontotemporal dementia. For cases marked with asterisks, scores on
written naming are shown, because these patients were mute.
272
Annals of Neurology
Vol 55
No 2
February 2004
ten naming, it is unclear whether their disproportionate naming of nouns than verbs was caused by
impaired access to the phonological and orthographic
word forms or the semantic representations of nouns,
or all of the above.
Longitudinal Studies
Longitudinal studies of three patients with nonfluent
PPA who participated in this study showed the identical pattern of deterioration across patients: oral naming
of verbs deteriorated first, then oral naming of nouns,
then written naming of verbs, followed by written
naming of nouns.30 Additional longitudinal testing, beyond what was previously reported, was conducted
with one of these three subjects with nonfluent PPA.
We administered the experimental stimuli once per
year, over 4 years. Her accuracy in oral and written
naming of nouns and verbs is shown in Figure 5. Results show continuation of the previously reported progression of impairment: oral naming of verbs, then oral
naming of nouns, then written naming of verbs, then
written naming of nouns. Her performance on spoken
word/picture verification was 100% accurate for nouns
and verbs referring to objects and actions, although by
the last session she made occasional errors in pointing
to named colors, letters, numbers, and geometric forms
on the Boston Diagnostic Aphasia Examination.58 By
the time of the last session, her communication output
was limited to writing occasional nouns, although she
could still repeat one to two syllable words of all word
classes. In contrast, longitudinal study of a patient with
fluent PPA using the same stimuli and methods
showed the opposite pattern of deterioration: written
naming and oral naming of nouns were impaired first;
oral naming of verbs deteriorated last (Fig 6). Comprehension, tested with word/picture verification, was im-
Fig 5. Longitudinal scores on oral and written naming of a
patient with nonfluent primary progressive aphasia.
paired from the second session (when he was 83% accurate on nouns, 100% accurate on verbs).
Discussion
Results of this study provide evidence that patients
with nonfluent PPA and ALS-FTD show disproportionately impaired oral naming of verbs, compared
with oral naming of nouns and compared with written
naming of either word class. This pattern of deterioration is not limited to occasional cases but was quite
consistent across a series of consecutive patients. Patients with fluent PPA consistently showed the opposite pattern of deterioration, with initial impairment in
naming of nouns relative to verbs, and in written naming relative to oral naming. However, the word class
effect (verb naming worse than noun naming) was
more marked and consistent than the modality effect
in the nonfluent and ALS-FTD patients, and the modality effect (written worse than oral naming) was
much more marked than the word class effect in the
fluent patients. Because we were not able to carefully
localize the atrophy or hypometabolism in these patients, conclusions about the brain regions responsible
for these selective naming deficits cannot be made on
the basis of our results. The unique contribution of
this study is the consistency of the word class and modality effects in a consecutive series of patients with
PPA.
Another unique contribution of this study is the
evaluation of both oral and written naming in both
word classes, which showed modality-specific word
class effects in a total of 12 patients. Four nonfluent
patients showed impaired oral naming of verbs, relative
to nouns, but intact written naming of both word
classes. This pattern cannot be attributed to impaired
semantic representations of verbs, because such an impairment should equally affect spoken and written
naming of verbs. We believe this pattern of dissociation is the pattern likely to be seen early in the course
of nonfluent PPA (and perhaps ALS-FTD), based on
longitudinal studies of three patients who showed this
pattern early in the course and went on to show deterioration in spoken naming of nouns, then written
naming of verbs, and then written naming of nouns.30
In our cross-sectional study, all patients with nonfluent
PPA showed one of three patterns, which would be
expected along the hypothesized course of deterioration: (1) disproportionately impaired oral naming of
verbs, with relatively spared written naming of nouns
and verbs; (2) disproportionately impaired naming of
verbs relative to nouns in both oral and written naming, but more severe impairment in oral than written
naming for both word classes; or (3) disproportionately
impaired written naming of verbs relative to nouns and
uniformly poor oral naming of both nouns and verbs.
Of the fluent patients, seven of seven showed disproportionately spared oral naming of verbs, with more
impairment in oral naming of nouns and written naming of both word classes. These results provide evidence for impaired access to phonological and/or semantic representations of nouns, along with impaired
access to orthographic representations of both nouns
and verbs.
All subjects with nonfluent PPA or FTD-ALS had
some degree of motor speech impairment (effortful articulation with distorted consonants). However, it is
unlikely that the motor speech impairment was responsible for the disproportionate difficulty with naming
verbs, because the motor speech impairment affected
articulation of verbs and nouns equally. The disproportionately impaired verb naming was more likely caused
by impaired access to phonological (and orthographic)
word forms of verbs, either because word forms of
verbs and nouns are processed in separate regions of
cortex, or because access to the word forms of verbs
requires access to a particular morphological form,
which may depend on more anterior regions.59 That is,
producing a verb in response to a picture of someone
drinking requires selection of the morphological form
(drinking vs drinks vs drink), any of which would be
Fig 6. Longitudinal scores on oral and written naming of a
patient with fluent primary progressive aphasia.
Hillis et al: Naming in Progressive Aphasia
273
scored as correct. In contrast, producing a noun in response to a pictured object does not require such a
selection, because only one morphological form is correct in English. Another explanation of the dissociation
between noun and verb naming is that the nouns we
used (object names) are more concrete or have higher
imagability than the verbs we used (action names), because some functional imaging studies have shown that
abstract nouns and verbs recruit more premotor cortex
(and posteriolateral temporal cortex) than concrete
nouns.32,38
One limitation of this study is that although noun
and verb stimuli were matched for frequency, they
were not matched for age of acquisition, visual complexity, or familiarity (or concreteness, as discussed earlier), which are factors that might influence naming accuracy. However, it is unlikely that verbs were simply
“harder” than nouns, because the patients with fluent
PPA were more accurate for verbs. Also, studies of
stroke patients using the same stimuli have shown cases
with more errors on the verbs and other cases with
more errors on the nouns.22,30,36 Another limitation
was the low numbers of subjects with fluent PPA and
ALS-FTD. Nevertheless, the results of this study provide evidence that access to orthographic and phonological word forms of nouns and verbs can be differentially affected in various forms of frontotemporal
dementia or Pick’s complex.
Results of this study, if confirmed in a larger study,
may have clinical implications as well. The data indicate that performance in naming nouns relative to
verbs may help distinguish nonfluent from fluent PPA
early in the course, when both types of PPA present as
anomia. This distinction may be important for prognosis, because the course and most likely sites of pathology (and possibly the type of pathology) differ. For
instance, patients with nonfluent PPA are more likely
to eventually develop signs of corticobasal degeneration, including asymmetric rigidity, apraxia, cortical
sensory loss, myoclonus, and tremor.60 – 62 Patients
with fluent PPA are more likely to develop other signs
of semantic dementia, including associative agnosia.63
In sum, there are distinct patterns of deterioration in
oral and written naming of nouns versus verbs in PPA
that provide evidence for proposing distinct neural
mechanisms necessary for accessing orthographic and
phonological word forms of verbs relative to nouns,
and that provide a basis for distinguishing nonfluent
and fluent PPA early in the course.
This research was supported by gifts for research funds from E.
Mack and W. Mack.
References
1. Mesulam MM. Slowly progressive aphasia without generalized
dementia. Ann Neurol 1982;11:592–598.
274
Annals of Neurology
Vol 55
No 2
February 2004
2. Mesulam MM. Primary progressive aphasia. Ann Neurol 2001;
49:425– 432.
3. Neary D, Snowden JS, Gustafson L, et al. Frontotemporal lobar
degeneration—a consensus on clinical diagnostic criteria. Neurology 1998;51:1546 –1554.
4. McKhann GM, Albert MS, Grossman M, et al. Clinical and
pathological diagnosis of frontotemporal dementia. Arch Neurol 2001;58:1803–1809.
5. Perry RJ, Hodges JR. Differentiating frontal and temporal variant frontal temporal dementia from Alzheimer’s disease. Neurology 2000;54:2277–2284.
6. Kertesz A, Munoz DG, Hillis AE. Frontotemporal degeneration, Pick’s disease, Pick complex, and Ravel. Ann Neurol
2003;54(suppl 5):S1–S2.
7. Mesulam MM, Grossman M, Hillis AE, et al. The core and
halo of primary progressive aphasia and semantic dementia.
Ann Neurol 2003;54(suppl 5):S11–S14.
8. Bak TH, O’Donovan DG, Xuereb JH, et al. Selective impairment of verb processing associated with pathological changes in
Brodmann areas 44 and 45 in the motor neuron diseasedementia-aphasia syndrome. Brain 2001;124:103–120.
9. Rosen HJ, Gorno-Tempini ML, Goldman WP, et al. Patterns
of brain atrophy in frontotemporal dementia and semantic dementia. Neurology 2002;58:198 –208.
10. Gorno-Tempini ML, Dronkers N, Rankin K, et al. Anatomy
and behavior in three variants of progressive aphasia. Neurology
2003;60(suppl.1):A263.
11. Chan D, Fox NC, Scahill RI, et al. Patterns of temporal lobe
atrophy in semantic dementia and Alzheimer’s disease. Ann
Neurol 2001;49:433– 442.
12. Hodges JR, Patterson K, Oxbury S, Funnell E. Semantic dementia. Progressive aphasia with temporal lobe atrophy. Brain
1992;115:1783–1806.
13. Neary D, Snowden JS, Mann DM. Familial progressive
aphasia: its relationship to other forms of lobar atrophy. J Neurol Neurosurg Pshychiatry 1993;56:1122–1125.
14. Edwards-Lee T, Miller BL, Benson DF, et al. The temporal
variant of frontotemporal dementia. Brain 1997;120:
1027–1040.
15. Mummery CJ, Patterson K, Price CJ, et al. A voxel-based morphometry study of semantic dementia: relationship between
temporal lobe atrophy and semantic memory. Ann Neurol
2000;47:36 – 45.
16. Snowden JS, Goulding PJ, Neary D. Semantic dementia: a
form of circumscribed cerebral atrophy. Behav Neurol 1989;2:
167–182.
17. Galton CJ, Patterson K, Graham K, et al. Semantic knowledge
and episodic memory for faces in semantic dementia. Neuropsychology 2001;15:10 –14.
18. Miceli G, Silveri MC, Villa G, Caramazza A. On the basis of
agrammatic’s difficulty in producing main verbs. Cortex 1984;
20:217–220.
19. Zingeser LB, Berndt RS. Grammatical class and context effects
in a case of pure anomia: implications for models of language
production. Cogn Neuropsychol 1988;5:473–516.
20. Zingeser LB, Berndt RS. Retrieval of nouns and verbs in
agrammatism and anomia. Brain Lang 1990;39:14 –32.
21. Damasio AR, Tranel D. Nouns and verbs are retrieved with
differently distributed neural systems. Proc Natl Acad Sci USA
1993;90:4957– 4960.
22. Berndt RS, Mitchum CC, Haendiges AN, Sandson J. Verb retrieval in aphasia. Brain Lang 1997;56:68 –106.
23. Caramazza A, Hillis AE. Lexical organization of nouns and
verbs in the brain. Nature 1991;349:788 –790.
24. Rapp BC, Benzing L, Caramazza A. The autonomy of lexical
orthographic representations. Cogn Neuropsychol 1997;14:
71–104.
25. Hillis AE, Caramazza A. The representation of grammatical categories of words in the brain. J Cogn Neurosci 1995;7:
396 – 407.
26. McCarthy RA, Warrington EK. Category specificity in an
agrammatic patient: the relative impairment of verb retrieval
and comprehension. Neuropsychologia 1985;23:709 –723.
27. Daniele A, Giustolisi L, Silver MC, et al. Evidence for a possible neuroanatomical basis for lexical processing of nouns and
verbs. Neuropsychologia 1994;32:1325–1334.
28. Kertesz A, Davidson W, McCabe P. Primary progressive
aphasia: a case study. J Int Neuropsychol Soc 1998;4:388 –398.
29. Cappa S, Binetti G, Pezzini A, et al. Object and action naming
in Alzheimer’s disease and frontotemporal dementia. Neurology
1998;50:351–355.
30. Hillis AE, Tuffiash E, Caramazza A. Modality specific deterioration in oral naming of verbs. J Cogn Neurosci 2002;14:
1099 –1108.
31. Tranel D, Damasio H, Damasio A. On the neurology of naming. In: Goodglass H, ed. Anomia. London: Academic Press,
1997.
32. Perani D, Cappa SF, Schnur T, et al. The neural correlates of
verb and noun processing. A PET study. Brain 1999;122:
2337–2344.
33. Tyler LK, Russell R, Fadili J, Moss HE. The neural representation of nouns and verbs: PET studies. Brain 2001;124:
1619 –1634.
34. Warburton E, Wise R, Price C, et al. Noun and verb retrieval
by normal subjects with PET. Brain 1996;119:159 –179.
35. Tranel D, Adolphs R, Damasio H, Damasio AR. A neural basis
for the retrieval of words for actions. Cogn Neuropsychol 2001;
18:655– 670.
36. Hillis AE, Tuffiash E, Wityk RJ, Barker PB. Regions of neural
dysfunction associated with impaired naming of actions and objects in acute stroke. Cogn Neuropsychol 2002;19:523–534.
37. Hillis AE, Wityk R, Barker PB, Caramazza A. Neural regions
essential for writing verbs. Nat Neurosci 2003;6:9 –20.
38. Bird H, Howard D, Franklin S. Why is a verb like an inanimate object? Grammatical category and semantic category deficits. Brain Lang 2000;72:246 –309.
39. Shapiro KA, Pascual-Leone A, Mottaghy FM, et al. Grammatical distinctions in the left frontal cortex. J Cogn Neurosci
2001;13:713–720.
40. Cappa SF, Sandrini M, Rossini PM, et al. The role of the left
frontal lobe in action naming: rTMS evidence. Neurology
2002;59:720 –723.
41. Damasio H, Grabowski TJ, Tranel D, et al. Neural correlates
of naming actions and naming spatial relations. Neuroimage
2001;13:1053–1064.
42. Grabowski TJ, Damasio H, Damasio AR. Premotor and prefrontal correlates of category-related lexical retrieval. Neuroimage 1998;7:232–243.
43. Grafton ST, Fadiga L, Arbib MA, Rizzolatti G. Premotor cortex activation during observation and naming of familiar tools.
Neuroimage 1997;6:231–236.
44. Goodglass H, Wingfield A. Word-finding deficits in aphasia:
brain-behavior relations and symptomatology. Anomia 1997:
5–30.
45. Hillis AE, Rapp BC, Caramazza A. When a rose is a rose in
speaking but a tulip in writing. Cortex 1999;35:337–356.
46. Silveri MC, DiBetta AM. Noun-verb dissociations in braindamaged patients: further evidence. Neurocase 1997;3:
477– 488.
47. Rhee J, Antiquena P, Grossman M. Verb comprehension in
frontotemporal degeneration: the role of grammatical, semantic
and executive components. Neurocase 2001;7:173–184.
48. Bak TH. Knowledge of objects and actions in frontal and temporal dementia. Paper presented at: the World Federation of
Neurology Research Group on Aphasia and Cognitive
Disorders; 2000. Salvador, Brazil.
49. Kable JW, Lease-Spellmeyer J, Chatterjee A. Neural substrates
of action event knowledge. J Cogn Neurosci 2002;14:795– 805.
50. Grossman M, Koenig P, Devita C, et al. Neural representation
of verb meaning: an fMRI study. Hum Brain Mapp 2002;15:
124 –134.
51. Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”: a
practical method for grading the mental state of patients for the
clinician. J Psychiatr Res 1975;12:189 –198.
52. Weschler D. The Weschler Memory Scale. New York: The Psychological Corporation, 1945.
53. Osterrieth PA. Le test de copie d’une figure complex: contribution a l’étude de la perception et de la mémoire. Arch Psychol
1944;30:286 –356.
54. Goodglass H, Kaplan E, Weintraub S. The Revised Boston
Naming Test. Philadelphia: Lea & Febiger, 1983.
55. Spreen O, Benton AL. Neurosensory Center Comprehensive
Examination for Aphasia (NCCEA). Victoria: University of
Victoria Neuropsychology Laboratory, 1969, 1977.
56. Golden JC. Stroop color and word test. Chicago: Stoelting,
1978.
57. Partington JE, Leither RG. Partington’s pathway test. Psychol
Service Bull 1949;1:9 –20.
58. Goodglass H, Kaplan E. The Boston Diagnostic Aphasia Examination. Philadelphia: Lea & Febiger, 1972.
59. Shapiro K, Caramazza A. The organization of lexical knowledge
in the brain: the grammatical dimension. In: Gazzaniga M, ed.
The new cognitive neurosciences. Cambridge, MA: MIT Press
(in press).
60. Boeve BF, Lang AE, Litivan I. Corticobasal degeneration and
its relationship to progressive supranuclear palsy and frontotemporal dementia. Ann Neurol 2003;54(suppl 5):S15–S19.
61. Frattali CM, Grafman J, Patronas N, et al. Language disturbances in corticobasal degeneration. Neurology 2000;54:
990 –992.
62. Kertesz A, Martinez-Lage P, Davidson W, Munoz DG. The
corticobasal degeneration syndrome overlaps progressive aphasia
and frontotemporal dementia. Neurology 2000;55:1368 –1375.
63. Hodges JR. Frontotemporal dementia (Pick’s disease): clinical
features and assessment. Neurol 2001;56(suppl 4):S6 –S10.
Hillis et al: Naming in Progressive Aphasia
275
Документ
Категория
Без категории
Просмотров
5
Размер файла
317 Кб
Теги
progressive, aphasia, verbs, deterioration, primary, versus, naming, nouns
1/--страниц
Пожаловаться на содержимое документа