Running head: BILINGUAL APHASIA: A PHYSIOLOGICAL OVERVIEW
Bilingual Aphasia: A Physiological, Theoretical, and Prognostic Overview
Garrett R. Harriman
Fort Lewis College
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Introduction
The relationship between language and the mind has long spurred philosophers, artists,
and scientists to seek answers regarding our unique human capacity for communication. In the
contemporary world, fruitful research in the realm of language disorders continues opening new
avenues of discussion and experimentation. Bilingual (Multilingual) aphasia is among the most
fascinating, and debilitating, of these disorders. This paper aims to introduce bilingual aphasia,
its neuroanatomical features, competing theories of linguistic representation, and distinctive
methods of therapy/recovery for those individuals living and coping with aphasic symptoms.
Defining Aphasia
Aphasia is a classification term for an umbrella of neurological disorders that minimally
to substantially affect systems and structures associated with the understanding and production of
language (“Clinical Topics: Aphasia,” 2013). In the United States, over 80,000 new aphasic
cases are reported annually with upwards of one million people currently living with aphasic
symptoms. As the majority of the global population speaks multiple languages, bilingual or
polyglot aphasia is the dominant incarnation of the aphasic spectrum of disorders (Fabbro, 2001).
Onset of aphasia is predominately the result of head trauma or injury sustained to the left
hemisphere, though people who are right-language dominant (right hemisphere) are not exempt
from aphasic damage (crossed aphasia). Strokes are the most common medical condition to elicit
aphasic symptoms, accounting for 25%-40% of diagnoses. Brain tumors, brain hemorrhages, and
dementia further account for aphasia onset. (“Clinical Topics: Aphasia,” 2013).
The broad range of aphasic symptoms has proven a difficult diagnostic challenge for
physicians to subdivide into discrete disorders. The two major language centers of the brain—
Wernicke’s area (language comprehension) and Broca’s area (language production)—provide a
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basis for diagnosis. Global aphasia implicates brain regions within or outside one or both of the
aforementioned areas, further muddying diagnosis. Aphasic cases in males tend to be more
Broca’s area-localized, with Wernicke’s and global aphasia more frequent among women.
Outside of these neuroanatomical zones, four categories of linguistic deficits are useful
for diagnosis and to isolate the unique neurolinguistic impairments and implicated brain areas of
aphasic sufferers. Many times aphasics will have deficits in multiple/overlapping categories:
1) Verbal expression: patients exhibit varying inability to produce speech and find
words (anomia), may omit small words (telegraphic speech), speak slowly, speak
with incorrect word order and syntax, speak in nonsense words (jargon), and speak in
long, unintelligible nonsense sentences.
2) Auditory comprehension: patients report trouble understanding speech, notably fast
speech, may require longer amounts of time to listen to speakers (receptive ability)
and generate responses (expressive ability), and often misinterpret their own speech
errors.
3) Reading comprehension (Alexia): patients can not recognize or sound out words,
substitute words for other words, and may find non-content/function words (if, the,
and) incomprehensible.
4) Written language: patients have difficulty writing or copying sentences, or alternately
produce nonsense word run-on sentences lacking proper syntax.
(“Clinical Topics: Aphasia,” 2013).
It is important to acknowledge that these “language modality” categories are fluid among
monolingual, and multilingual, victims of aphasia (Fabbro, 2001). Each new case presents
unique language impairments that must be identified and addressed throughout diagnosis and
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treatment. Often during recovery or relapse, aphasics move between categories into differential
and other impermanent diagnostic fields. Bilingual aphasics further complicate “concrete”
diagnoses, as each language they speak may undergo differential transformations, they may not
be fluent in one or more of their languages, or in fact exhibit distinct subcategories of language
modality deficits.
For example, a fluid bilingual speaker of English and Spanish may experience one or
more of the four broad impairment categories in one language with greater severity over the
other, or even experience completely dissimilar symptoms in either language. Evidence remains
convoluted, however, of “true” differential aphasia in both/multiple languages, e.g., Wernicke’s
aphasia in English, Broca’s aphasia in Spanish (Fabbro, 2001). Still, the real possibility of lexical
categorical differences and malleability during the course of multilingual aphasia, if not macrodistinctive physiological categorizations, creates complex challenges for care provides.
Irrespective of the flexibility of bilingual differential diagnoses, the trajectory of aphasic
phases follows a more reliable pattern. Again, from “Clinical Topics: Aphasia,” 2013:
1) Acute phase (4 weeks post-onset): Usually patients show a lessening of the diffuse
effects of aphasia across contralateral/ipsilateral brain areas/tissues affected by initial
trauma. A host of disorders may arise—temporary muteness, alternating antagonism
(difficulty retrieving words in languages), and/or selective aphasia (impairment in
using childhood-encoded language, i.e., L1).
2) Lesion phase (5 weeks – 5 months): More patterned and pronounced language
deficits emerge. This is the optimal time to administer clinical assessments in efforts
to isolate the systemic/physiological parameters of the patient’s aphasia.
3) Late phase (5 months – potentially remaining life): Depending on severity and depth
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of damage, this phase may be indistinguishable from the lesion phase (no
improvement) or, due to therapeutic intervention and recovery of surrounding brain
regions, various recovery patterns may emerge and evolve.
Of further note, aphasias (bilingual or otherwise) typically do not compromise motor
functioning in the patient. However, surrounding brain areas implicated during causal trauma
may trigger residual damage to develop. Aphasia is primarily a spectrum of disorders of
cognitive/linguistic functioning; motor deficits, if present or developed, are the product of faulty
secondary functioning that most often alleviate as treatment continues (Fabbro, 2001).
Implicated Brain Structures
Multiple brain structures/areas have been isolated via fMRI imaging as central to aphasia,
bilingual aphasia, and certain modes of recovery (e.g., compensatory recruitment). As will be
discussed in this and forthcoming sections, there is contention regarding aphasia type, recovery
type, and competing theories of language representation that make any isolated neuroanatomical
findings ever-rich subjects of scrutiny. The crux of these differences lies in the distinction (or
blurring) of damage incurred to language representational systems (language networks) and
control over these representations (neuroanatomical language control) (Green, 2008).
It bears restressing that cortical and subcortical damage to the language centers of the
brain are largely responsible for the large array of monolingual/polylingual aphasia typologies
(Kohnert, 2009). The most general brain sites linked to aphasia include damage to Broca’s
and/or Wernicke’s area, the left inferior frontal cortex, and the caudate nucleus and frontal basal
ganglia (Green, 2008). Certain brain structures and areas may also only be activated in certain
languages over others. For instance, the left inferior frontal cortex seems most tied to L1 (first
language learned) word production over secondary languages (L2s). Futhermore, L2 recovery
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gains, depending on the theoretical backdrop, are often described as having shared the linguistic
gains of L1 recovery, though conflicting results mar the phenomenon.
Other confirmatory neuroimaging studies have mapped more intricate patterns of damage
with specific language lapses and recovery deficits. For instance, Green (2008) found greater
blood flow to Broca’s, Wernicke’s, and select inferior/superior temporal lobe areas produced
greater naming improvements in aphasics, while auditory comprehension seems localized to
normalized blood flow in Wernicke’s area alone. A study of 20 aphasics (Non-Parallel
Recovery…) revealed further structural clues. Short term recovery/initial recovery is generally
associated with dominant (usually left) hemisphere activation; long-term recovery activation
involves the contralateral hemisphere, specifically homotopic frontal and thalamic areas.
Marangolo, Rizzi, Peran, Piras, & Sabatini (2009) found the left superior and middle
temporal gyrus, the left supramarginal gyrus, and the left inferior parietal lobe integral to
phonological processing. The study further collected evidence for differential brain activation
sites in different languages for one participant. After implementing a 6-month unilingual
recovery regimen for a bilingual speaker, both languages showed fMRI activation along the
bilateral precentral/postcentral gyrus, the right superior temporal gyrus, and
precentral/postcentral gyri, with single-language cortical activation observed in “peri-legional”
regions (the left inferior parietal lobe). As will be later debated, these differential activation
patterns somehow produced the same level of parallel recovery in both languages using a
monolingual treatment program. It can be inferred from this data that the same neural substrates
must be activated during aphasic language recovery while the recovery regimen may have less
direct causal influence than the brain’s tendency to recruit surrounding brain areas to aid in
compensatory linguistic performance
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Still other studies (Moore et al., 2005; Croft, Marshall, Pring, & Hardwick, 2011; Cocks,
Sautin, Kita, Morgan, & Zlotowitz, 2009). cite the basal ganglia and its surrounding “pre-SMA
(supplementary motor area)–dorsal caudate–ventral anterior thalamic loop” responsible for
specific word selection and generation in the dominant language hemisphere. The theory states
that the basal ganglia and its interacting loop subsystems facilitate word selection and speech by
ensuring right-prefrontal inactivation during left hemisphere word creation, performing as an
active suppression field to prevent competing cross-linguistic interference.
These brain areas and systems theories account for only a small sampling of potentially
implicated cortical candidates. Aphasia research is complex, as competing language theories,
language treatment regimens, individual damage profiles, and imaging studies routinely present
contravening information. The trend, however, slowly suggests a forthcoming limited consensus
regarding the neuroanatomical localization of language and aphasic centers in the brain.
Theories of Bilingual Language Representation
The integrated nature of brain anatomy and theories of language representation are
critical to past and current research of bilingual aphasia, as well as seminal in electing which
treatment measures with which to expose patients. Many of the most influential models of lexical
representation are described below. Applicable research affirming or casting doubt on each
theory is supplemented where appropriate.
Separate Lexicon Models (Localization)
A staple for nearly two decades, the Revised Hierarchical Model (RHM) offers one
possible explanation of language centers and conscious/unconscious linguistic representation.
Posited first by Kroll and Stewart (1994), the RHM claims that there exist multiple language
centers in the brain: one for every language a speaker knows. Under this theory, a speaker’s L1
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and L2 (and feasibly more languages) share no common lexical connections neurologically—no
universal word bank—and the many errors that occur during recovery are the result of
dissonance and interference between multiple language nuclei.
Reported cases of asymmetrical recovery in polyglot aphasics provide evidence for this
thesis. L2 functioning is often reclaimed at greater pace and depth than L1 recovery, signaling
researchers that L2 functioning is mediated by L1 functioning. The differential timescales
involved also point to discrete localizations of separate language banks (Croft et al., 2011).
Furthermore, connections a person makes from L1 to L2 equivalent words are often found to be
weaker than connections made from L2 to L1 words, which can change, morph, and strengthen
over time (Cross-Linguistic Lexical Connections). Integrated into cases of RHM is the
localizationalist stance, stating L1 and L2 forms and conceptualizations reside in different parts
of the brain, making recovery possible if one “space” is spared trauma (Green, 2008).
In discussing the RHM, cross-language lexical interference inevitably comes to light.
This refers to scenarios under which a multilingual speaker with aphasia cannot recall a word
used in their target (therapeutic) language, and so instead draws on the same/similar word in their
other language(s). This recovery patterns is recorded most between two non-native languages.
The theory posits that L2 words are learned in context from the L1 lexicon over “conceptual”
linkages that the patient’s languages share. These include cognates (words in two or more
languages which share phonological and morphological forms, as well as synonymous meanings)
and semantic/grammatical overlaps (for instance, both languages may share conjugation rules,
object-verb word order, etc.). It is due to faulty communication between the separate language
centers that accounts for strained recovery in bilingual aphasics, as L2 is viewed as wholly
dependent on L1 rules and lexical accumulation to function in the first place. (Cross-Linguistic
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Lexical Connections).
Shared Lexicon Models (Dynamic/Adaptive Networks)
Cross-language lexical interference is cited and explicated in different contexts within
another credible linguistic representational theory, the Bilingual Interactive Activation Model
(BIA). Based in large part on the “connectionist model of lexical representation” (Van Heuven,
Dijkstra, & Grainger, 1998), the BIA states that words are connected even at the letter level
across multiple languages in the mind; that one (or many) shared lexical pools are available to
polyglots; and that the compensatory L2-L1 paradoxical dynamic cited under RHM studies is
underdeveloped and erroneous (Goral, Levy, Obler, & Cohen, 2006).
Taking the BIA another phase further, the Multilingual Interactive Activation Model
(MIA) claims continual multi-lingual activation of languages in a polyglot’s mind. Both
languages are engaged and making connections even when only one is being used. In light of
this, there is not as narrowly selective a process underway for word selection as under the RHM
model, and the whole lexical pool is available for both or more languages at any time. This
shared lexical pool can keep expanding as both languages are used. As such, there should be
limited loss of selection speed or competitive discharge across languages (Goral et al., 2006).
Barring residual trauma of surrounding brain structures, the mental lexicon is a dynamic
and adaptive network. Different language recovery patterns are attributable, then, to different
areas of language control and are not the result of co-dependence between L2 formulation
hinging on L1 development. Whether damaged areas have caused partial, temporary, or
permanent damming of usage further directs the physiological activation chain (Green, 2008).
Many studies give credence to the BIA and MIA models. Green summarizes this single
adaptive language network theory handily. Regardless of greater L1 or L2 recovery, shared
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grammatical rules exist in structures/systems shared by both languages; therefore in the brain,
effect patterns in both languages, barring damage, should be the same. Concrete concepts are
more easily retrieved in both languages than abstract concepts. Morphological tasks (changing
tense of words) are also retrieved regardless of language. And verbs above nouns are harder to
generate in both L1 and L2 (though visual verbs scored better retrieval). These studies hint at an
underlying shared structure/tissue in the brain and that a common system represents multiple
languages up to a certain threshold of metalinguistic divergence.
A study by Fabbro (2001) presents another theoretical corroboration for an underlying
language locale. His patient spoke Friulian and Italian, each language rated as nonfluent aphasia,
and each sharing many morphological/syntactic rules. The mistakes made during therapy in both
languages were of the same nature—that is, similarly structured languages breed similar aphasic
mistakes. While more a theoretical grounding than categorical reality, the similar word
substitutions and morphosyntactic rules paralleled one other until diverging lines of logic and
usage unique to either language proved too dissimilar for superimposition.
Goral et al. (2006) cites studies showing that translation from a more proficient language
to a less proficient language is slower than less proficient to more proficient; however,
translation latency decreases with L2 usage and competency. Cognates are also cited as aiding
the speed and accuracy of translations across multiple languages above words that might share
meaning, but not form (e.g., house and casa). Shared “representation and processing” is
legitimized by such studies. Their own study of a trilingual aphasic (Hebrew, English, and
French) showcases specific shared lexical evidence. The subject spoke in 4-hour conversations in
all three of his languages with native speakers and was told to not actively suppress the use of
cognates and code-switching. His pauses during conversations were coded as the outward
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manifestation of shared lexical selection under his conscious control versus uninterrupted
speech-flow utilizing code-switching (speaking alternately in different languages). Though
usually able to suppress language interference or inappropriate translation equivalents, when
asked to actively inhibit his selections, the patient made more errors in his non-target language—
e.g., during a French conversation, he more routinely used similar words in English than finding
synonymous words in French. This pattern emerged most when asked to inhibit during
conversations in his least-recovered language.
The second phase of the study—specific word translation—yielded equally interesting
results. The subject was asked to translate across languages three categories of words (noncognates/cognates, abstract nouns/concrete nouns, words unique to particular language).
Response latencies served as measures of lexical awareness (single lexical pool). Cognate vs.
non-cognate translation yielded short latency for concrete cognates, shorter latency for concrete
non-cognate words. Contrary to other studies, however, there were no significant latency
differences between concrete and abstract words (Goral et al., 2006).
Several things may be inferred from this trilingual study, and offer extensions and
considerations beyond RHM and BIA models: 1) language proficiency significantly increases
performance 2) the “distance” of languages (their unique and unshared structures) seem to play a
predominant role in representation and recovery in trilingual aphasics, evidenced by the patient’s
most-recovered languages sharing less cognates, but languages more distant in recovery showing
equitable gains via cognates, and 3) it appears that L2 language selection and choice is more
mediated by L2 characteristics than original L1 encoding. This enticing yet conflicting study
further affirms that the patterns of overall language use are still indeterminate and signals the
need for more neuroimaging studies to rigorously test RHM, BIA, and latter-day branching
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theories (Goral et al., 2006).
Memory Models
There is also the circulating theory that separate memory systems are associated with
either L1 or L2 processing (Green, 2008). Evidence for this stance derives from dissociative
conditions, notably amnesia, wherein certain behaviors or skills are retained and others lost.
Declarative memory processes and stores facts, words, and events; procedural memory encodes
performing skills. Linguistically, “knowing how” to speak or form sentences is categorically
different than “knowing that” something is x, y, or z. The comparison is this: the more
ingrained/implicit aspects of language retention and learning can be equated as procedural
memories (language production) and thus employ different brain areas (striatum, cerebellum,
frontal zones) versus “knowing that” something is metalinguistically apart or similar to
something else (language comprehension), more likely involving the hippocampus and related
memory subsystems.
Taking this perspective, damage to either of these clustered cortical areas will produce
variable forms of damage. This could account for patients who retain competencies in L1 while
L2 gains somewhat lag, or who display distinctly different gains/losses in multiple languages. As
well, this declarative/procedural theory postulates that people who develop L2 competencies
much later than L1 declaratively rely on the procedural aspects of L1 to assist in L2; after
prolonged use, this reliance will appear subsumed and unconsciously unified. Conscious L1
metalinguistic practice may also guide L2 syntactic forms, not such that these competencies
occur simultaneously to become unconscious, but that conscious use of knowledge in one type of
system/memory directly effects development of L2 system/memory systems (Green, 2008).
Differential Recovery Patterns
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Bilingual aphasics are capable of undergoing a variety of recovery patterns. There
remains no unchallenged universal set of rules or unanimous evidence for any one model of
polyglot aphasia recovery/damage that encompasses all known cases. One of the earliest theories
stems from Ribot (1885) asserting that the first language learned is always the least aphasically
effected. A century later, Pitres (1985) formulated a contrasting hypothesis that the most used
language will be the one least aphasically affected, making way for linguist Noam Chomsky’s
(1986) idea that languages with similar structures and grammars more readily, and in tandem,
recover during therapy over more structurally dissimilar languages (Gil & Goral, 2004; Goral et
al., 2006). Pitres’s model postulates that language centers allow for language recovery if they are
not permanently damaged but only inhibited, and that the patient’s preferred language often
recovers because surrounding neural centers and pathways are more “invested,” so to say, in
serving that language (Fabbro, 2001).
Studies have confirmed and confuted this model: weaker neural connections and
functions are not as contributory to second/unfamiliar languages as they are to L1s. In Fabbro’s
own study (2001), bilingual patients displayed varying rates of language recovery. 13 out of 20
bilingual aphasics showed comparable language recovery in both their first and second
languages; four experienced greater impairment in their second language. The final three patients
showed greatest impairment in their native language. Today, no overwhelming correlations exist
between time of language acquisition and frequency of context use (concurrent, synchronic, or
familiarity), type of lesion (tumor, infarction, cerebral hemorrhage), the site of lesion (lobes,
language areas, etc.), or even syndrome typology, which consistently defy adequate groupings of
onset and recovery.
Parallel/Non-Parallel Recovery
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While no single model effectively accounts for the diversity of aphasic cases, several
patterns of recovery recur again and again in the literature—parallel and non-parallel recovery.
Parallel recovery describes bilingual aphasic suffers who display similar deficits in both
languages, and either through cross-generalizational (explained below) or spontaneous recovery,
both languages recover in unison. Non-parallel recovery essentially describes any pattern
tangential to parallel recovery—that is, one language appears less damaged or inhibited and thus
recovers faster. Notable subtypes of extended post-morbid polyglot non-parallel recovery
include:
1) Successive/Antagonistic Recovery (one language precedes recovery before others).
2) Selective Recovery (only one language seems eligible for recovery).
3) Alternate Pattern/Alternate Antagonism (victim vacillates language use daily).
4) Unintentional Language Switching (code-switch without patient volition).
(Gil & Goral, 2004)
Convergence Hypothesis and Threshold Elevation
What accounts for parallel/non-parallel recovery patterns is as convoluted as any other
component of bilingual aphasia. There appear, however, to be differences in the “neuroanatomic
convergence” of languages in patients. For example, Wartenberger et al. (2003) found very little
distinction in brain area activation with “early” bilinguals, i.e., those who leaned both languages
at a young age. There appears to be recruitment of more brain regions and resources in aphasics
whose second language was learned later (after age 6). This confirms Green & Abualebit’s
(2008) “convergence hypothesis”—if language proficiency increases, the distinctions between
L1 and L2 blend and merge; L2 is represented through L1 cognition and task performance. By
the same token, it has been speculated that so long as the neural connections allowing for
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language selection are mostly undamaged, as opposed to the amount of brain matter damaged,
the expected recovery pattern should be parallel. The more diffuse the damage, the more
probable is non-parallel recovery (Marangolo et al., 2009).
Green’s theory (1986, 1998) states it is not damage to the language centers themselves
that defers or prevents recovery, but a process of active inhibitory functioning to control the use
of a language; these patterns of activation/inhibition may account for nonparallel recovery. In
tandem, Paradis (1985, 1989) proposed the activation threshold hypothesis—as one word is used
(activated) more, its mental threshold for use decreases while other competing concepts/words,
even in another language, are not as regularly exercised, rendering their threshold higher. In this
view, “selective inactivation” and “threshold elevation” patterns account for the differential
patterns of recovery in polyglot aphasics. The integration of intra-hemisphere and extrahemisphere neural control networks during recovery—that is, if brain areas/networks are
associated with different languages—seems to indicate a more differential recovery. These recent
theories nest parallel and non-parallel recovery patterns within larger lexical brain systems per
language, and the partial inactivation/activation of one language during recovery of another
mediates the overarching course of recovery (Gil & Goral, 2004).
Treatments and Recovery
Bearing in mind the information so far presented, the following section consolidates and
summarizes several experimentally verified phenomena at work during bilingual aphasic
recovery. Popular and nascent recovery programs are also described alongside the standards and
practices speech language pathologists uphold during their sessions with aphasic sufferers.
Client/Language Factors Affecting Recovery
Speech-language pathologists are central figures in the screening, diagnosis, research,
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and education involved in bilingual aphasic cases. Aphasia recovery and prognosis are
individually tailored; contingent on the person’s lesion severity and physical location, there is no
standard recovery pattern. It has been shown that lesion site and size are the strongest indicators
of long-term recovery, with SES factors secondary, but weak, predictors (“Clinical Topics:
Aphasia,” 2013).
Proficiency of bilingual aphasics depends on a constellation of factors, including
acquisition history (age/context), language development opportunities, the social prestige
associated with using one or multiple tongues, and individual preferences and motivations for
usage. Client factors that should be considered when establishing recovery regimen include
number of languages spoken, the order they were learned in, their usage and proficiency, and the
type/severity of aphasia. Ideally, polyglot aphasics require the use of both languages, so
treatment options should prioritize as much as possible training and recovery for both languages
where applicable (Kohnert, 2009). Furthermore, most researchers believe that treating a bilingual
aphasic in both (or all) languages simultaneously has a stalling, if not negative effect on language
recovery. Standard protocol is to focus on one language at a time (Marangolo et al., 2009).
Cross-Language Generalization (C-LG)
The most intriguing experimental facets of bilingual aphasia involve the complex ways
conceptual language interaction affects treatment and subsequent recovery. Word retrieval in
bilingual aphasia patients prompts the question: Can monolingual naming therapy/recovery
techniques—specific word repairs that share grammatical/syntactic commonalities—create gains
in the patient’s second language, or are the gains isolated to the speaker’s dominant tongue? If
so, a process of cross-linguistic generalization (CL-G) has taken place. Croft et al.’s (2011) study
reiterates that semantic/phonological cues are hard to pinpoint, and studies suggest that only
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cognates produce the most reliable L1-L2 gains. Some evidence also exists in favor of semantic
therapy techniques over phonological ones benefitting L1 recovery more, as semantic to L1
connections/activations seem stronger than semantic to L2 connections.
Kohnert (2009), in an effort to isolate factors of cross-linguistic generalization, composed
a meta-study. Of the 12 articles investigated, 6 of 12 did not find valid C-LG; 4 of 12 showed
positive gains for both target and non-target language; and 2 found gains only for target
languages. His analysis shows the complexity of the problem, but also highlights areas that
should be studied to more conclusively show C-LG. Most studies showed little to modest gains,
and a general trend in favor of cognate usage, but several offer intriguing clues. A
Spanish/English study intimates that C-LG is most possible when “common processes” of each
language are targeted, and language-specific constructs are avoided. This transfer may be best
with L1 for phonological tasks only (e.g., rhyme judgments and syllable tasks) but both L1 and
L2 benefitted from lexical production tasks (word association/categorization). There is also a
controversial study stating that training in a patient’s non-dominant language may lead to better
cross-generalization gains overall, though most therapists still hold that the language decisions
that will most effect a client’s daily and life functions should be supported more, especially if the
client’s L2 is substantially weaker.
Kohnert concludes by listing language factors possibly attributing to C-LG gains:
linguistic aspects (retrieval vs. comprehension), typological differences in languages (tonal) and
structural similarities/differences (cognates). Selecting words during training for languages with
more phonological and typological overlap may facilitate C-LG over languages whose structural
and typological qualities are far more distant (e.g., English and Vietnamese).
The meta-analysis both reaffirms the complexity of the issue and sheds light on two
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treatment areas that can most benefit most bilingual aphasics. 1) that the facilitator of treatment
need not speak the same language as the client to effect gains; indirect methods of treatment (athome or computer-based strategies) help, and treatment in one language alone does not across
studies seem to limit or dampen overall recovery, and 2) areas of “cognitive linguistic overlap”
should be explored and exploited during treatment to possibly facilitate C-LG gains—this
includes structural (cognates) or computational (grammar) categories (Kohnert, 2009).
General Treatment Frameworks/Approaches
One widely-endorsed method of recovery is the WHOs ICF framework, which focuses on
health and contextual factors, overarching and overlapping. The Framework for Outcome
Measurement (FROM) includes four overlapping therapeutic domains: activities and
participation; personal factors and identity; body function and body structure; and environment
(barriers and facilitators). Though specific impairment treatments exist, the ultimate goal is to
help the aphasic’s quality of life and communication ability strengthen, hence mixing and
matching many approaches is common. Two broad categories of approaches are described
below:
1) Language-Impairment Based treatment: focus on spoken, written, and gesture
formation; increasing verbal output sans compensatory (code-switching) techniques;
melodic intonation therapy (MIT) relies on melody, rhythm and stress and
lengthening of speech; syntax, verb, and writing treatments.
2) Activities/Participation-Based Treatment: includes strategies for communication,
implements electronic aids, nonverbal cues, and gesture training; partner approaches
that encourage coaching and multimodal communication; and scripting conversations
and reversing listener/speaker roles (“Clinical Topics: Aphasia,” 2013).
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Gesture/Speech Integration
Speech and bodily/kinesic qualities are central to communication. One study (Cocks,
Sautin, Kita, Morgan, & Zlotowitz, 2009) of 20 Broca’s area bilingual aphasics found enticing
support for gesture-based therapies. Redundant gesture comprehension—a one-to-one body
motion corresponding to a speech act (e.g., brushing teeth gesture)—has been linked to greater
accuracy in aphasic comprehension. It has also been found that the more ambiguous a verbal
command or bit of information, the more aphasics rely on simple pointing gestures (pantomime)
to illicit more information. Regardless of aphasia severity, pantomime ability remains
unimpaired, and aphasics having sustained more posterior than anterior lesions produce it more
regularly. fMRI studies and theory suggest that multimodal gain—the information gained from
combined verbal and gesticular comprehension—is greater than gains reliant on a single
modality.
Hemispherical Transfer
A final compelling experiment (Moore et al., 2005) has exposed the role bilateral brain
activation might serve in aphasic cases, and lends credence to activation/suppression theories
described earlier. Two aphasic participants were asked to perform complex hand gestures with
their left hands (right-hemispherical activation) while simultaneously performing word
generation/recovery tasks (left-hemispherical activation). The participant who had yet to show
bilateral gains before treatment showed considerable bilateral activation above baseline
measures, indicating the transfer of lexical activation from left to right hemisphere, and the
concurrent activation of establishing word connections from the posterior left hemisphere in
newly formed right hemisphere word production capabilities. The patient who recovered showed
a reliance on the hand/speech methodology after initial gains, showing that this cross-lateral
BILINGUAL APHASIA: A PHYSIOLOGICAL OVERVIEW
20
treatment method might benefit aphasics with specific lesion severities and premorbid activation
patterns.
Considering Spontaneous Recovery
One thing to keep in mind with studies that claim parallel recovery of L1 and L2 solely
under L1 intervention is that spontaneous recovery—the sudden return to better/normal
functioning—is most associated with early stages of aphasia, and that these indices may be
conflated. The typical window in which spontaneous recovery occurs in bilingual aphasics is 6
months; during these weeks, distinguishing broad intervention technique gains, including crosslinguistic generalization, from spontaneous recovery, is virtually impossible. It remains unknown
if spontaneous recovery in bilingual aphasics affects both languages in the same manner.
Researchers must be vigilant when assessing the viability of their results during this window of
unmediated functional repair (Gil & Goral, 2004; Kohnert, 2009).
Further Research
There is much to be learned and continually confirmed in the field of bilingual aphasia
research. Just as dialects and languages are separated by murky divisions in linguistics,
neurologically and neuroanatomically, the hunt continues to discover if bilingual speakers’
brains contain and encode one language apart from the second, or if similar structures and areas
underlie both (Fabbro, 2001). Focusing on blood flow, depth of regional damage, and mapping
of these functional areas via imaging techniques will birth greater understanding into the
different systems underlying L1, L2, or their combined recovery pathway(s) in the brain. (Green,
2008).
Different languages may very well share overlapping computational subsystems—for
instance, word order or syntax may likely use same network/structures for multiple languages,
BILINGUAL APHASIA: A PHYSIOLOGICAL OVERVIEW
21
but within that network, there are likely to exist specific synaptic regions or pathways where
differential language usage diverges, and can eventually be tracked back (reverse engineered).
For example, specific neurons may be activated to produce a different vocabulary word in L2
even though the overall network is integrated. Evidence points to patients who can easily switch
or inhibit the use of one of their languages, but cannot control the usage of another. If speakers
have conscious knowledge of L2 usage that they lack in L1, their brain imaging should show
these computational differences compared against healthy bilinguals who have implicitly through
practice made these knowledge maps unconscious (Green, 2008). These are just a small swatch
of questions to be answered in the decades of research to come.
Conclusion
The complexity and depth of bilingual aphasic conditions has begotten competing
theories of language usage, integration, and conceptualization. In turn these theories have
spearheaded fantastic streams of technology, research, and invaluable insights into which
treatment methods provide sustainable results for those suffering under the spectrum of aphasia.
As each aphasic condition is a unique medical and neuroanatomical entity, overarching
generalizations about language deficits and gains must be avoided. Venturing as care
practitioners and researchers into the expanding gray of bilingual aphasia will be the way
forward toward a better understanding of human language production, loss, and above all the
refinement of individualized treatment plans for sufferers of bilingual aphasia.
BILINGUAL APHASIA: A PHYSIOLOGICAL OVERVIEW
22
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