BRAIN AND LANGUAGE 60, 335–346 (1997)

ARTICLE NO. BL971796

A Perspective on the Neurobiology of Language

Sheila E. Blumstein
Department of Cognitive and Linguistic Sciences, Brown University; and Aphasia Research
Center, Boston University School of Medicine

This paper provides a perspective on current issues and challenges in the investi-
gation of the neurobiology of language. It is proposed that the speech/language
deficits of aphasic patients reflect impairments in the processing components in-
volved in accessing language. More specifically, it is hypothesized that many of
these deficits result from changes in the activation level of word candidates in the
lexicon. Because word recognition and lexical access processes are crucially in-
volved in virtually all aspects of language processing, such an impairment has reper-
cussions throughout the components of the linguistic grammar. It is suggested that
the intersection of such language behaviors with the identification of underlying
neural systems will define future research directions. Methodological and technolog-
ical issues are discussed as they impact on current and future research.  1997
Academic Press

The goal of this paper is to provide a perspective on current issues and

challenges in the investigation of the neurobiology of language.1 In recent
years, a theoretical framework has been developed in our lab in collaboration
with William Milberg which serves as a basis for characterizing much of
the speech/language processing deficits in aphasia. Although our research
has focused particularly on language deficits in Broca’s and Wernicke’s
aphasia, it is our expectation (as elaborated more fully below) that this frame-
work will elucidate the neural systems underlying many aspects of speech
and language processing deficits and thus will pertain to aphasic patients
more broadly.
We have proposed that the speech/language deficits of aphasic patients
reflect impairments in the processing components involved in accessing lan-
guage. Specifically, we hypothesize that these deficits are reflected in the

Address correspondence and reprint requests to Sheila E. Blumstein, Department of Cogni-

tive and Linguistic Sciences, Brown University, Box 1978, Providence, RI 02912.
This research was supported in part by NIH Grant NIDCD00314 to Brown University and
by NIDCD0081 to the Boston University School of Medicine.
1
Text based on keynote address presented at the 33rd Annual Meeting of the Academy of
Aphasia, San Diego, California, November, 1995.
335
0093-934X/97 $25.00
Copyright  1997 by Academic Press
All rights of reproduction in any form reserved.
336 SHEILA E. BLUMSTEIN

activation level of word candidates in the lexicon. Because word recognition

and lexical access processes are crucially involved in virtually all aspects of
language processing (that is, lexical access serves as the entry point for
higher levels of language processing, including identifying word candidates
from the sound structure, deriving meanings of individual words, and build-
ing up syntactic representations based on the syntactic functions of the lexical
entries), this impairment will have repercussions throughout the components
of the linguistic grammar. Thus, we would expect potential impairments in
how the sound properties of language contact the lexicon, how an individual
lexical entry and its lexical network are activated and thus contact meaning,
and perhaps even how the syntactic structure of an utterance is ultimately
derived. In this view, then, the profiles of speech and language impairments
that characterize the aphasias which appear to reflect language deficits in
various linguistic components or linguistic modules—phonological, lexical,
and syntactic—derive from a single processing impairment. Moreover, the
impairment is linguistic only in the sense that it relates to the activation of
lexical candidates and thus to the activation of the language system. It is not
linguistic in the sense that specific linguistic operations relating to particular
components of the grammar are impaired. Thus, we do not believe that many
of the aphasic deficits are selective with respect to the components of the
grammar, nor do we believe that linguistic representations or, more broadly,
specific linguistic processes are impaired.
Let us review some of the evidence. In the 1970s and early 1980s, research
on language deficits in aphasia explored whether the different profiles of
language displayed by the traditional aphasia syndromes reflected impair-
ments to different underlying mechanisms. Results were, in general, disap-
pointing. While differences were found in severity of impairment as a func-
tion of aphasia syndrome (i.e., the quantity of errors differed across aphasia
groups), the patterns of language deficit were for the most part the same.
These deficits emerged whether focusing on phonology, morphology, or syn-
tax and whether one focused on production or on comprehension. For exam-
ple, investigations of speech production revealed that although the quantity
of errors varied as a function of aphasia syndrome, patients from differ-
ent diagnostic groups showed similar phonological patterns of deficit
(Blumstein, 1973). Similarly, in speech perception, the patterns of perceptual
errors were the same across groups, and even more disappointingly they did
not seem to relate in a systematic way to the auditory comprehension deficits
of the patients (Blumstein, Baker, & Goodglass, 1977; Blumstein, 1994).
With respect to production and comprehension of morphology, similar pat-
terns were also shown across groups (Goodglass, 1968; Lesser, 1978). And
finally, similar patterns in sentence comprehension were found when as-
sessed in terms of parameters of syntactic complexity (Caplan, Baker, &
Dehaut, 1985), as were similar patterns in the production of grammatical
errors by patients diagnosed as agrammatic or paragrammatic (cf., Bates,
 NEUROBIOLOGY OF LANGUAGE 337

Wulfeck, & MacWhinney, 1991 for a review; Goodglass and Menn, 1985).
In many ways, these results should not have been surprising. Most of the
parameters investigated were based on structural properties of the grammar,
and all patients showed greater impairments as structural complexity in-
creased. Even normals show a similar hierarchy of difficulty as do patients,
not because they are incipient aphasics, but because those aspects of lan-
guage which are structurally more complex are inherently more difficult to
either produce or comprehend.
As a result of this failure to distinguish among the aphasia groups on the
basis of linguistic parameters, two different approaches to the study of lan-
guage deficits in aphasia emerged. One approach rejected the use of the tradi-
tional aphasia syndromes, arguing that the failure to find differences among
the aphasia groups reflected the fact that the traditional classification schema
did not hold any theoretical significance in determining the basis for language
impairments (Caramazza, 1984, 1986; Schwartz, 1984; Shallice, 1979). Pro-
ponents of this approach also argued that group investigations in general
were fundamentally flawed, in part, because of the difficulties of determining
a theoretical basis for classification. Instead, this research strategy turned to
a detailed investigation of single-case studies. Another approach, and the
one taken in our research, used as a working hypothesis that the failure to
find differences among the aphasia groups reflected in part the selection of
inappropriate language variables and research methodologies for studying
them. We are still committed to the view that the study of language deficits
using the traditional aphasia syndromes provides an important framework
for study, since these groups show different profiles of language ability (cf.
Goodglass, 1993) and, perhaps more importantly, also have a well-delimited
lesion localization (Geschwind, 1965; Damasio, 1991). These different struc-
tural lesions presumably define the neural systems underlying the language
deficits of aphasic patients. It is the understanding of these neural systems,
not of the clinical syndromes per se, that underlies our emphasis on the explo-
ration of language deficits in Broca’s and Wernicke’s aphasics.
This change in theoretical perspective began when we started to consider
language comprehension and production not as static end-states, but rather
when we began to consider language as a dynamic process with language
comprehension and production the result of a number of time-limited pro-
cessing operations. Language deficits in aphasia then might reflect impair-
ments in any of a number of these processing operations. Such deficits could
affect access to linguistic representations or the integration of sources of
information contributed by various linguistic components. This approach re-
quired a change in research methodology to one that allowed an examination
of the unfolding of the language comprehension or language production pro-
cess. To that end, we applied on-line techniques as a means of examining
the dynamics of the language comprehension process. One technique that
we have used is the lexical decision task. Subjects are required to make a
338 SHEILA E. BLUMSTEIN

lexical decision to either a visually or an auditorily presented stimulus target.

Both accuracy and reaction time measures are taken.
In a series of experiments (Milberg & Blumstein, 1981; Blumstein, Mil-
berg, & Shrier, 1982; Milberg, Blumstein, & Dworetzky, 1988; Milberg,
Blumstein, Saffran, Hourihan, & Brown, 1995), we explored whether apha-
sic patients show, as do normals, semantic facilitation in a lexical decision
task. Investigations with normal subjects indicate that they show faster reac-
tion time latencies to lexical decision targets when they are preceded by
semantically related words, e.g., cat–dog, than when they are preceded by
either semantically unrelated words e.g., chair–dog, or nonwords, e.g., plub–
dog. These results have been interpreted as reflecting the spreading of activa-
tion in a lexical network. In particular, most current models of the semantic
priming phenomenon assume that different semantic concepts or lexical
items are represented as nodes organized within a network-like architecture.
Presumably, every node has a resting state, a maximal level of activation
which is reached over some specified time frame, and a decay function over
some time frame until the lexical node returns to its resting state (see Fig.
1). Models of the semantic priming phenomenon assume that the presentation
of a word changes the resting state of its lexical node. It also changes the
activation level of those lexical nodes that are a part of its lexical network.
Thus, not only the lexical node corresponding to a target word is activated
but so are words which are semantically related to it, thus resulting in shorter
reaction time latencies when they are presented as lexical decision targets.
Returning to the aphasic patients, results were interesting and unexpected.
We found systematic differences in performance between Wernicke’s and
Broca’s aphasics. Wernicke’s aphasics showed semantic facilitation, despite
the fact that they were unable to judge in an off-line task whether the same
words used in the lexical decision task were semantically related; that is,
they were unable to reliably say whether two words such as cat–dog were
related. Surprisingly, Broca’s aphasics did not show this semantic facilitation
effect as consistently as did patients with Wernicke’s aphasia, although they
were always able to judge whether pairs of words were semantically related.
Under some experimental conditions, Broca’s aphasics showed evidence of
priming, while under others they did not. A close examination of these differ-
ent studies shows that when words are presented in pairs and their relation-
ship can be invoked using heuristic strategies, Broca’s aphasics show statisti-
cally reliable semantic facilitation (Blumstein et al., 1982; Katz, 1988;
Chenery, Ingram, & Murdoch 1990; Hagoort, 1990) (see Fig. 2). When the
stimuli are not paired and are presented either in list form, where the subjects
must respond to each individual stimuli, or in such a way that they cannot
predict what the target word might be, Broca’s aphasics fail as a group to
show statistically reliable semantic facilitation (Milberg & Blumstein, 1981;
Prather, Zurif, Stern, & Rosen, 1992; see Milberg, et al., 1988, 1995 for a
review of this issue).
 NEUROBIOLOGY OF LANGUAGE 339

FIG. 1. Schematic of theoretical activation of a lexical node.

Several conclusions were drawn from these studies. Because of the evi-
dence of semantic facilitation in Wernicke’s aphasics, it was concluded that
at least some aspects of the representation of word meaning were preserved.
The language comprehension deficit of these patients appeared to reflect their
inability to overtly access, use, or manipulate semantic information, rather
than a loss of the underlying semantic representation of words. The failure
of Broca’s aphasics to show systematic semantic facilitation suggests that
they have a lexical processing impairment, one which we have proposed is
attributable to the activation of the lexical network. In particular, we have
suggested that in Broca’s aphasics there is a reduction in the activation level
of the lexical entry (Milberg et al., 1995). Thus, a lexical target will not
activate its lexical node to the same extent as in normals, affecting not only
the activation of the lexical node itself but also its lexical network (see Fig.
3). The most obvious consequence of such a reduction in maximum activa-
340 SHEILA E. BLUMSTEIN

FIG. 2. Experimental designs which have resulted in priming in Broca’s aphasics and those
which have not. Targets which are predictable based on the preceding prime show priming
when the prime–target pairs are either semantic associates or the prime is an ambiguous word.
Nonpredictable pairs fail to show semantic priming in Broca’s aphasics.

tion would be a less consistent and/or a smaller magnitude of semantic facili-

tation, unless the patient can invoke heuristic strategies and attentional re-
sources during the task.
Broca’s aphasics’ overreliance on heuristic strategies is evident in a recent
study exploring the role of top-down processing on phonetic categorization
(Blumstein, Burton, Baum, Waldstein, & Katz, 1994). In this study, we in-
vestigated the so-called lexical effect—a phenomenon shown in normal sub-
jects whereby the lexical status of a stimulus affects the phonetic boundary
of an acoustic continuum. For example, subjects perceive more /d/’s when
presented with a voice onset time [d-t] continuum in which the [d]-endpoint
stimulus is a word such as dash and the [t]-endpoint stimulus is a nonword
such as tash, compared to when the [d]-endpoint stimulus is a nonword such
as dask and the [t]-endpoint stimulus is a word such as task. Interestingly,
Broca’s aphasics show a larger than normal lexical effect, whereas Wer-
nicke’s aphasics show no lexical effect at all. These results underscore the
overreliance of Broca’s aphasics on heuristic strategies, in this case having
a lexical bias.
The hypothesis that a basis of the speech/language processing deficits of
Broca’s aphasics may be due to an underactivation of lexical entries would
suggest ramifications not only throughout the lexical network but also in the
activation of lexical entries by the sound properties of language. The results
 NEUROBIOLOGY OF LANGUAGE 341

FIG. 3. Schematic of spreading activation in a lexical network. (Top) Activation for a nor-
mal. (Bottom) Hypothesized activation when the activation level of lexical entries are reduced
as proposed for Broca’s aphasics.

of a series of studies that we have conducted and are currently conducting

support this view (Milberg et al., 1988; Aydelott & Blumstein, 1995). Bro-
ca’s aphasics show a reduced activation of lexical entries by the sound prop-
erties of language not only at the phonological level but also at the acoustic
level. With respect to the phonological level, normal subjects show a de-
crease in semantic facilitation, as a prime stimulus is phonologically more
distant from a real word prime which is semantically related to a target.
For example, there is systematically less semantic facilitation compared to
a baseline cat–dog, if the initial consonant of the prime word has been
changed by one feature, e.g., gat–dog, and even less semantic facilitation is
obtained if the initial consonant of the prime is more than one feature away,
e.g., wat–dog. The patterns of performance of the aphasic patients are sys-
tematically different from those of normal controls. Broca’s aphasics and,
in particular, nonfluent patients fail to show any semantic facilitation for the
342 SHEILA E. BLUMSTEIN

phonologically altered targets, whereas Wernicke’s aphasics and, in particu-

lar, fluent aphasics show facilitation for all of the phonologically altered
variants.
These results suggest that for Wernicke’s aphasics there seems to be an
overactivation of lexical entries, such that phonologically altered stimuli gain
access to the lexicon to the same extent as do phonologically correct lexical
entries. As to Broca’s aphasics, the results are consistent with the view that
for these patients lexical entries are underactivated, and, as a consequence,
phonologically altered stimuli simply do not contact the lexicon as they do
for normals. That this effect also obtains for Broca’s aphasics using poor
acoustic–phonetic exemplars of a phonetic category, namely a phonetically
altered [p*] in pear–fruit compared to a phonetically unaltered [p] in pear–
fruit, further supports the view that there is a reduction in the activation of
lexical candidates, and as such poor phonetic prototypes fail to activate the
lexical entry as they do for normals (Aydelott and Blumstein, 1995).
The dissociations in performance obtained in Broca’s and Wernicke’s
aphasics fail to tell us what is it about the patients in these clinical categories
that produces these results. In other words, it is important to get beyond the
labels of the clinical categories and examine what it is about Broca’s and
Wernicke’s aphasia that contributes to these different language processing
impairments. In our view, the basis for these disorders most assuredly lies
in the neural systems contributing to normal language processing. Thus it
is essential, and will become increasingly more so, to chart the underlying
neuropathology of patients to begin to identify these neural systems. Two
examples will suffice, examples which show that to focus solely on the ‘‘cog-
nitive architecture’’ of these deficits in the absence of exploration of the
neural systems underlying them will ultimately fail to provide a means of
understanding the neurobiology of language. In several recent experiments,
we have found that certain patients classified clinically as Broca’s aphasics
have not shown the same pattern of performance as other patients in the
group. Further analysis has revealed that these patients have had structural
lesions that differed from the rest of the patients in the group. For example,
voice-onset time impairments in speech production which typically emerge
in Broca’s aphasics did not emerge in a clinically diagnosed Broca’s patient
whose lesion did not include Broca’s area, the anterior limb of the internal
capsule, and the lower motor cortex areas for larynx and tongue (Baum,
Blumstein, Naeser, & Palumbo, 1990). In a second study, we found that the
overreliance on heuristic strategies in the phonetic categorization of speech
that characterizes Broca’s aphasics failed to emerge in a patient classified
clinically as a Broca’s aphasic but whose lesion showed considerable poste-
rior extension including parietal areas and Wernicke’s area (Blumstein et
al., 1994).
What is the nature of these neural systems? At this stage we do not know.
However, these systems will probably not correspond to a single site, but
 NEUROBIOLOGY OF LANGUAGE 343

rather will correspond to a network that though distributed will have a clear
neural substrate. The nature of the neural system that underlies the processing
impairments that we have identified for Broca’s and Wernicke’s aphasics is
not yet clear; however, it will likely include a broader array of patients who
may not be classified clinically as Broca’s or Wernicke’s aphasics but who
will share a common neural substrate. Work toward this goal will be accom-
plished only if careful attention is paid to the underlying neuropathology of
the patients.
It is this intersection of language behavior with the identification of neural
systems that will likely mark the future direction of research for the field.
This research direction will undoubtedly shore up the study of neuropsychol-
ogy. Not only have our views about language ‘‘behavior’’ evolved, but also
have our views about the nature of the neural mechanisms underlying lan-
guage and cognition. Put in the context of the revolution in the field of brain
imaging, the stage is set for a new and exciting frontier of research that will
guide us in the decades to come. Another important research frontier that
will also have great influence on research on the neurobiology of language
is the application of brain imaging and electrophysiological techniques in
normals as well as neural modeling of language processing. As important,
exciting, and influential as these new areas are and will continue to be, the
study of the neurobehavior of normal subjects will probably not supplant
the study of brain-damaged patients, in part because progress will be made
only as a partnership. Nearly all of the neuroimaging studies with normals
use the knowledge base that has been accrued from investigations with brain-
damaged patients as the framework from which to elucidate the findings.
Importantly, as new and unexpected areas of the brain ‘‘light up,’’ as it were,
in the context of some cognitive or language function in normals, researchers
are seeking behavioral correlates in brain-damaged patients. Some interest-
ing insights have recently been made in this vein with respect to the role of
the cerebellum, largely ignored in past research in terms of its potential role
in higher cognitive processing (cf. Schmahmann, 1991 for review; Fiez,
Petersen, & Raichle, 1990).
Having said this, two cautionary notes are important to make, one concern-
ing methodology and the other concerning technology—both of which may
impact more directly than perhaps they should on the theoretical underpin-
nings driving much of the research in this field. As to methodology, put
simply, there is no one methodology that will provide the true path to the
understanding of the neurobiology of language. In my view, our field has
become unnecessarily fixated on, in fact, mired in the single-case versus
group study debate, and, as a result, attention has been diverted away from
many substantive research issues. Worse, to the outsider (such as colleagues
in neuroscience, cognitive neuroscience, and peer review panels), the field
looks to be in disarray—with so-called colleagues demeaning work which
does not come out of the ‘‘politically correct’’ camp and showing such a
344 SHEILA E. BLUMSTEIN

lack of respect for the research of their colleagues that it looks as though
the field is in an intellectual vacuum. As a consequence, the field has not
done justice to itself.
Without discussing the details of the methodological arguments that we
have been deluged with in the past decade, it is the case that each and every
methodology is flawed and has limitations. The group study approach has
limitations. So has the single-case approach. For example, a number of the
major experimental phenomena contributing to theories of language pro-
cessing emerge only as statistical effects in normal subjects. As examples,
categorical perception in speech perception, lexical effects in phonetic cate-
gorization, semantic facilitation in lexical decision tasks, and even right ear
laterality for speech and language in dichotic listening are all phenomena
which have importantly shaped current views on the nature of speech and
language processing. Many normal subjects fail to show these effects and,
perhaps even worse, may show them one time and fail to show them another
time, even though in the aggregate there is a statistically reliable effect from
a group of subjects (cf. Blumstein, Goodglass, & Tartter 1975). Thus, these
effects cannot be explored with the single-case approach, if the absence of an
effect is attributed to brain damage. It is precisely because of the limitations
inherent in any single methodology that all of scientific inquiry ultimately
requires multiple approaches. Each approach provides a different vantage
point, and taken together, the various methodologies provide converging evi-
dence on a particular research question.
Turning to the second cautionary note. Technology will be playing an
increasingly greater role in our research. The technological advances of neu-
roimaging and neural modeling provide new and exciting tools which prom-
ise advances and discoveries in the field. Nonetheless, just as in the case of
methodologies, every technology has its limitations and provides a window
constrained by the limits of that technology. We must take care not to mistake
the technology of today for a theoretical insight, nor to build a theoretical
framework that is in essence a metaphor for the technology itself. An exam-
ple from speech research will suffice. The sound spectrogram, invented in
the 1940s, revolutionized speech research, for it provided a visual representa-
tion of the sounds of speech over time. To some this display reflected the
way the listener analyzed and perceived speech—referring to the representa-
tion of speech in terms of a ‘‘neural spectrogram.’’ Because bursts and transi-
tions were visually isolable on a spectrogram, they were considered to pro-
vide separate and separable cues to speech. Researchers for decades
investigated speech almost exclusively in these terms and failed to consider
speech processing in terms of the integration of spectral information over
the frequency/amplitude/time domain.
In sum, there is cause for great optimism about the future and for the
possibilities of solving what is one of the most exciting and to date intractable
mysteries of the mind—the nature of human language. Although each indi-
 NEUROBIOLOGY OF LANGUAGE 345

vidual’s language system is shaped differently as a function of inheritance

and experience, we share a common biological and neurological substrate
that constrains the nature of human language and its ultimate realization. It
is this quest which will drive research efforts in the decades to come.

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