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(Last Updated: October 24, 2021)

Expressive aphasia (a.k.a. Broca’s aphasia) is a disorder of language resulting in non-fluent, effortful speech alongside difficulty repeating phrases and naming objects (Spreen & Risser, 2003). About 125,000 Canadians are estimated to live with some type of aphasia at any time. Historically, Broca’s aphasia yields great significance as the first disorder to be defined by a specific cortical lesion in the brain: Broca’s area (Lazar & Mohr, 2011). In addition to non-fluent speech, many patients must cope with grammatical impairments when trying to speak. Wide-ranging speech impairments complicate classification of the disorder; however, they also highlight the importance of Broca’s area for many processing tasks unrelated to speech.

Patient “Tan” – the first documented case of Broca’s aphasia – suddenly lost the ability to speak except for the ability to repeat a single-word: “Tan” (Mohammed et al., 2018). French physician Paul Broca followed “Tan” clinically for some time, eventually documenting extensive damage within the inferior frontal gyrus (IFG) after his death (Lazar & Mohr, 2011). The IFG is a hub for motor speech planning in the brain, appropriately called Broca’s area (Lazar & Mohr, 2011). While commonly located within the left hemisphere (Black et al., 2015), lateralization effects sometimes result in a contra-lateral presentation of the IFG in the Right hemisphere of the brain (Van der Haegen et al., 2012). Irrespective of lateralization effects, Broca’s area consists of two underlying structures with distinct features: the pars triangularis and pars opercularis (Skipper et al., 2007) – illustrated via Figure 1.

Cardinal Signs & Symptoms
Broca’s aphasia produces non-fluent speech without substantial impairment in language comprehension. Objective measures of speech fluency include the rate of speech, pauses and missing words in addition to the ‘quality of speech’ like melody and prosody (Fridriksson et al., 2015).
Prosody describes the appropriate intonation and rhythm of speech to produce meaning (Zumbansen et al., 2014). While disrupted prosody is quite noticeable, the severity of this impairment is difficult to quantify aside from human interpretation and description.
Although there are many types of non-fluent speech disorders, Broca’s aphasia is the pre-dominant sub-type of expressive aphasia. These terms are used interchangeably in this article.
Of note, expressive aphasias may also resemble (but are distinct from) other motor speech disorders like dysarthria and apraxia of speech:
- Dysarthria – often marked by slurred speech – is a disorder caused by poor coordination of speech muscles. (Dysarthria is often associated with cerebellar impairments, and psychiatric concerns.)
- Apraxia of speech involves incorrect translation of speech to motor commands. (Apraxia is often associated with developmental or neurological disorders, such as autism or Parkinson’s Disease.)
Kuschmann et al. (2014) note that dysarthria and apraxia only approximate speech non-fluency. Meanwhile, most people with expressive aphasia have notable deficits in grammar – or syntactical processing – which further obstructs the formulation motor speech plans in the brain (Grodzinsky, 2000). Speech non-fluency is a primary hallmark of expressive aphasias.
Agrammatism creates barriers to expressive language, both written and oral (Grodzinsky, 2000; Skipper et al., 2007). This is because people must codify, parse and store verbal information in working memory to speak fluently (Burton et al., 2000).
As illustrated in the YouTube vignette (above), persons with expressive aphasia often seek out more simplistic grammatical forms (e.g. sentence structures) to enhance speech fluency. They may speak using simple sentences (Faroqi-Shah & Thompson, 2007) and conceptually similar words in each sentence (Kennedy et al., 2019). More complex grammatical forms – like backward anaphora – would typically result in referential errors that further impede speech production and comprehension among persons with lesions to the pars triangularis (Matchin et al., 2014). Therefore, limits on syntactical processing explain many speech eccentricities seen in mild expressive aphasias.
Even mild forms of agrammatism can impact normal speech by interfering with verb conjugation and word finding (Thompson & Lee, 2009). This is likely because the process of codification relies upon the pars orbicularis, a key region within Broca’s area (Skipper et al., 2007). Agrammatism can cause something known as telegraphic speech (Friedmann, 2006). Telegraphic speech is highly suggestive of expressive aphasia, marked by the omission of non-critical words and suffixes (American Psychological Association, 2020).
Common Neurobiological Causes
Damage to Broca’s area is the first described cause (but, not the only cause) of Broca’s aphasia. Figure 4 illustrates how lesions to Broca’s area are causally associated to Broca’s aphasia.

As the left medial cerebral artery (MCA) perfuses a significant portion of the inferior frontal lobe, Left MCA stroke frequently causes Broca’s aphasia (Mazza et al., 2012). A retrospective matched case-control study, Levine et al. (2003) examined the causes of expressive aphasia following stroke. Over 53% of Broca’s infarcts resulted from cardioembolic causes, which was a significantly higher proportion than matched controls (Levine et al., 2003). As a result, Levine et al. (2003) concluded that cardiac conditions (such as Atrial Fibrillation) significantly increased the risk of developing Broca’s aphasia post-stroke.
Given the varied causes of brain injury, expressive aphasias are largely underreported and underdiagnosed. For example, persons with schizophrenia also have a notable loss of grey matter volume within the pars triangularis region, suggesting transient or mild forms of Broca’s aphasia coincide with many severe, persistent psychiatric disorders (Iwashiro et al., 2016). Hillis (2018) also note other common causes of aphasia, including:
- traumatic head injury
- brain tumours
- intracranial hemorrhage
- major neurocognitive disorders
- epilepsy

Regardless of initiating event, expressive aphasia affects more than motor speech planning – see Figure 5. For example, the process of action mirroring (e.g. imitation) also depends upon Broca’s area (Skipper et al., 2007). Following a meta-analysis of multiple fMRI studies, Papitto et al. (2020) concluded that Broca’s area activation is associated with action imitation and motor imagery in addition to motor speech tasks. Burton et al. (2000) also concluded that related speech tasks (such as phonological segmentation) were not dependent on Broca’s area activation. Confirming this, Hickok et al. (2011) administered language comprehension tasks to participants with lesions to Broca’s area. Independent of motor speech ability, language comprehension was globally preserved among many Broca’s aphasiacs (Hickok et al., 2011). Finally, IFG lesions are marked by multiple syntactic – but not semantic – deficits which predict impairments in speech fluency and comprehension (Friedmann, 2006).
Emerging evidence supports a grammatical view of motor speech planning, because speech plans require accurate syntactical processing abilities within Broca’s area (Grodzinsky, 2000).
Syntactical Tree Pruning is one such theory, suggesting that Broca’s aphasiacs have difficulty recognizing nodal phrases to establish hierarchical relationships between words (Friedmann, 2006). These syntactical errors, in turn, produce non-fluent speech (Aboitiz et al., 2006; Grodzinsky, 2000). Increased distance between a noun phrase and verb within a sentence is also known to create an untraceable linkage that impairs speech in expressive aphasia (Drai, 2006).
The Trace Deletion Hypothesis also explains why IFG lesions interfere with the processing of past tense regular verbs, even after priming effects (Faroqi-Shah & Thompson, 2007; Grodzinsky, 2000; Justus et al., 2011). Recent evidence also suggests that common symptoms of motor speech defects – such as disrupted prosody – do not cause the grammatical impairments observed among Broca’s aphasiacs (Gavarro & Salmons, 2013). In this way, non-fluent speech in expressive aphasia stems from syntactic processing deficits.

As neuroscience methods improved, so too did neuropsychological understandings of aphasia. For example, motor speech planning is now understood to occur simultaneously and not consecutively in the brain (Conner et al., 2019; Gorisek et al., 2016) – see Figure 6.
Tate et al. (2014) produced a cortical map of speech during direct cortical stimulation during surgery. Cortical mapping showed far greater integration of motor speech tasks than was previously believed, among an unusually large sample of 165 participants (Tate et al., 2014).
In an fMRI study of healthy participants, Lee et al. (2012) note that the IFG is active during categorical speech processing, suggesting integration with other cortical structures. Broca’s area is also known to influence language comprehension tasks traditionally associated with Wernicke’s area (Poeppel et al., 2008). Finally, the IFG remains a critical node within the larger multiple demand (MD) network (Fedorenko & Blank, 2020). As a neural hub for problem solving (Crittenden et al., 2016), Broca’s area is as much as contributor to MD functions as it is a centre for speech (Duffau, 2018; Fedorenko & Blank, 2020) – see Figure 7.

This more integrative view suggests the pars opercularis is a terminal node for auditory mapping in addition to speech (Nasios et al., 2019). Often left lateralized, the dorsal auditory stream is almost exclusively focused on speech production (Nasios et al., 2019). Since multiple structures of the dorsal stream also exist in close proximity to Broca’s area, localization of speech production tasks solely to the IFG is unlikely (Sakreida et al., 2019). However, there is considerable support that the IFG controls an integrated general-domain language network within the dominant hemisphere (Conner et al., 2019; Duffau, 2018; Gorisek et al., 2016). Therefore, damage to the IFG is likely to cause desynchronization of auditory and language processing.
Differential Diagnosis & Prognosis

It is possible to diagnose expressive aphasias without direct evidence of any acquired brain injury. However, Figure 8 shows a simplified diagnostic classification of expressive aphasia which links to common signs and symptoms.
Although not included in this classification, there are also other forms of non-fluent aphasia – such as anomic aphasia – which are related to (but, different from) Broca’s aphasia (Spreen & Risser, 2003). Expressive aphasias are primarily marked by impoverished speech where the person also has great difficultly repeating phrases and naming objects (Spreen & Risser, 2003).
- The Boston Diagnostic Aphasia Examination (BDAE) is a common tool used to differentiate and diagnose different types of aphasia (Roth, 2011). Although different versions of the tool exist, all versions of the BDAE categorize expressive aphasias as non-fluent speech disorders (Roth, 2011). Compared to other tools, like the Bilingual Aphasia Test (BAT), the short-form BDAE has comparable internal reliability and consistency (Peristeri & Tsapkini, 2011). However, the BAT – a shorter and less involved measure of aphasia – appears to be a more sensitive measure of specific language impairments that occur with expressive aphasia, especially among non-English speakers (Peristeri & Tsapkini, 2011).
- The Western Aphasia Battery (WAB) is a widely-endorsed neuropsychological assessment for diagnosing expressive aphasia (Woods et al., 2017). A close relative to the BDAE, the WAB has strong construct validity and a key feature of this scale is its ability to measure the overall severity of expressive aphasia (Spreen & Risser, 2003). Because of these features, the WAB is a commonly employed measure in research settings (Ochfeld et al., 2010). However, while Spreen and Risser (2003) argue that both the BDAE and WAB are comprehensive assessments, they may be too onerous for bedside use.
Brief screening tools for specific aphasias also exist, including:
- Amsterdam-Nijmegen Everyday Language Test (ANELT)
- American Speech-Language Hearing Association – Functional Assessment of Communication Skills for Adults (ASHA-FACS)
- Boston Naming Test
- Frenchay Aphasia Screening Test (FAST)

Although Broca’s aphasia is a common post-stroke outcome, neither MRI nor Computed Tomography (CT) can independently diagnose this disease (Spreen & Risser, 2003). Rather, diagnostic imaging would only confirm the diagnosis (Mazza et al., 2012). Figure 9 illustrates a typical MRI showing an infarct to Broca’s area following a left MCA stroke. One explanation for this phenomena is that brain plasticity produces a time-confounding effect for diagnosis of aphasia via MRI and CT scans. For example, there is a substantially reduced correlation between lesions to Broca’s area and symptoms of aphasia about six months after the initial injurious event (Ochfeld et al., 2010). It is also common for activity within the IFG to shift to the contralateral brain region after a left MCA stroke (Qiu et al., 2017), which is a positive adaptation empowered by brain plasticity.
As illustrated in Figure 10, Lazar and Mohr (2011) note that the severity of structural injury to the IFG does not predict aphasia severity. While brain plasticity can help people recover from expressive aphasia, this regenerative process limits the clinical utility of diagnostic imaging for measuring progression of disease long-term.

Finally, current diagnostic classification systems for aphasia do not account for the fact that specific aphasias often co-occur with other brain disorders (Vigliecca, 2016). Many diagnostic classifications of Broca’s aphasia overlook emerging understandings on the functional integration between speech centers and other neuropsychological processes, like working memory (Aboitiz et al., 2006). Even Paul Broca’s model case had sustained damage to several cortical areas adjacent to the IFG (Devinsky & Samuels, 2016). Observing these cross-over effects, Lazar and Mohr (2011) noted:
“By contrast, the lesion required to produce the extensive motor aphasia in Broca’s case… was associated with a much larger region of injury, including Broca area, insula, and adjacent cortex, with the site of occlusion in the proximal portion of the upper division of the left middle cerebral artery.”
(Lazar & Mohr, 2011, p. 238)
While a pure case of Broca’s aphasia is likely to result from impairment to syntactical processing, measurement concerns abound from the frequent co-occurrence of other brain disorders among people affected by this symptom (Vigliecca, 2016). One possible solution is to measure global functioning, like conversational speech, in a ‘real world’ environment (Carragher et al., 2015; Vigliecca, 2016). In this way, future diagnostic classifications of aphasia would better approximate observable functional impairments.
Conventional & Emerging Treatments
In a recent Cochrane systematic review, structured Speech and Language Therapy (SLT) significantly improved speech fluency (SMD 1.28) and writing ability (SMD 0.41) among persons with expressive aphasia post-stroke (Brady et al., 2016). Specific results are illustrated in Figure 11.

However, social support groups were superior to structured SLT in improving overall speaking ability and word fluency (Brady et al., 2016). Compared to no treatment, structured SLT also failed to show long-term effectiveness (Brady et al., 2016). While there are many different structured SLT’s, evidence suggests that traditional therapeutic approaches require significant effort for incremental benefits (Boo & Rose, 2011; Franco de Santana et al., 2018; Wardana et al., 2019). Meanwhile, social supports provide cumulative benefits with less substantial investment.
There are two emerging therapies that hold great promise for recovery from expressive aphasia:
Speech Entrainment
The IFG is the main brain region governing the process of mirroring or mimicry, formally known as “action mirroring” (Papitto et al., 2020; Skipper et al., 2007). Speech entrainment utilizes the process of mirroring – a.k.a. mimicking – to augment the return of expressive speech (Fridriksson et al., 2012). Following a 6-week course of treatment, a small-scale trial (n=13) found that speech entrainment resulted in several improvements on fMRI alongside substantial improvements in speech fluency (Fridriksson et al., 2012). Following a larger study among 44 participants, Fridriksson et al. (2015) confirmed that speech entrainment significantly improved expressive language abilities among persons with expressive aphasia but not other aphasias. These findings suggest participants with left IFG injury would experience clinical benefit from speech entrainment as a psychological intervention (Fridriksson et al., 2015).
Hypothetically, it is also assumed that action imitation is an unexplored process within social support groups for expressive aphasia. Tarrant et al. (2016) evaluated patient experiences after concluding a group singing session for expressive aphasia, noting that participants reported more confidence that they could participate in future social interactions requiring melodic and rhythmic work (Tarrant et al., 2016). More extensive study is required on group interaction effects, although it is assumed that speech entrainment could occur naturally during routine social interactions as part of observational or action learning processes (Fridriksson et al., 2012). In this way, group speech entrainment for Broca’s aphasia may provide an opportunity for future research.
Direct Stimulation of Broca’s Area
Despite evidence discussed on the high level of integration between cortical structures for speech, expressive aphasias remain associated with localized damage to the IFG (Lazar & Mohr, 2011). Direct stimulation of this area using Transcranial Magnetic Stimulation (TMS) or transcranial Direct Current Stimulation (tDCS) is hypothesized to stimulate the IFG and, therefore, enhance speech fluency (Kindler et al., 2012; Rosso et al., 2014; Saadi et al., 2019). While distinct therapies, both tDCS and TMS aim to directly stimulate Broca’s area:
- TMS involves applying short but repeated magnetic pulses to specific locations on the scalp.
- tDCS applies a low-amplitude of direct electrical current to the scalp.
Overall, TMS shows great potential for enhancing speech fluency. Among eighteen patients with aphasia post-stroke, Kindler et al. (2012) conducted a randomized cross-over trial on pulse TMS applied to Broca’s area. Participants performed significantly better on naming tasks with less time latency compared to a sham therapy (Kindler et al., 2012). There was also evidence to suggest TMS worked better in the active recovery phase after stroke (Kindler et al., 2012). Conversely, Wheat et al. (2013) attempted to stimulate Broca’s area using fMRI-guided TMS therapy among persons diagnosed with aphasia. In this case, investigators did not observe any appreciable effect of TMS on reaction times during naming and reading tasks (Wheat et al., 2013). While this study contradicts earlier results, the study by Kindler et al. (2012) used a specific type of TMS treatment among a larger and more appropriate sample of patients.
Meanwhile, results are less promising for tDCS. One randomized controlled trial determined that tDCS applied to the left IFG resulted in greater resting state brain activity – measured by EEG power – while simultaneously improving performance on a task measuring cognitive-verbal ability (Saadi et al., 2019). However, these results have little clinical significance, as only a small magnitude of change was observed in digit span performance with no improvement in syntactical processing (Saadi et al., 2019). Meanwhile, another study by Rosso et al. (2014) found that persons with IFG lesions did not demonstrate any significant change in resting state activity following tDCS. While tDCS is an emerging theory, it does not appear to hold the same promise as TMS in the treatment of Broca’s aphasia.
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