Continuing Education Activity

Conduction aphasia is a relatively rare form of fluent aphasia characterized by the inability to repeat sentences, defective use of phonemes, and impaired naming ability. By far, the most common antecedent of conduction aphasia is a cerebrovascular event (stroke). According to the classical categorization of aphasic syndromes, frontal lesions cause motor aphasias (impaired language production,) and temporal–parietal lesions produce sensory aphasias (impaired language comprehension), while lesions connecting the frontal and temporal lobes through the white matter tract known as the arcuate fasciculus cause conduction aphasia. Language production and auditory comprehension remain relatively preserved in conduction aphasia, distinguishing it from the more familiar non-fluent (Broca's) and semantic (Wernicke's) aphasias. 

This activity reviews the underlying etiology and pathophysiology of conduction aphasia, examines when conduction aphasia should be considered in the differential diagnosis of aphasia, and clarifies how to evaluate conduction aphasia properly. This activity provides healthcare professionals the knowledge and tools to improve patient care for this complex condition. 

Objectives:

• Identify the different neuroanatomical lesions that can cause conduction aphasia.

• Differentiate between conduction aphasia and the more common Wernicke and Broca aphasia.

• Evaluate the role of different neuroimaging studies in determining the etiology of conduction aphasia.

• Apply effective strategies to improve care coordination among members of the clinical team to improve the outcome of patients with conduction aphasia. 

Introduction

Aphasia describes a disturbance of language function resulting from brain injury, typically an ischemic stroke. Traditionally, clinicians characterize aphasia as either a Broca aphasia—a so-called motor or expressive aphasia, with decreased verbal fluency—or Wernicke aphasia—a so-called sensory or receptive aphasia, with decreased comprehension—depending on symptoms and the location of the underlying brain lesion.[1] Conduction aphasia is a much rarer aphasia wherein both expression and comprehension are relatively preserved, but the patient demonstrates phonological sequencing errors, especially when repeating polysyllabic sentences.[2][3] Affected individuals often struggle to repeat nonwords, are prone to phonemic paraphasic errors and neologisms, have difficulty naming objects, and may also show some features of Wernicke aphasia, albeit usually mild. 

Carl Wernicke first proposed in the mid-1870s that a disconnection between the 2 language systems in the para-Sylvian dominant hemisphere (Broca's area in the frontal lobe and Wernicke's area in the posterior region of the superior temporal gyrus) leads to this unique condition.[4] During the first half of the 20th century, Ludwig Lichtheim and Norman Geschwind expanded on Wernicke's work.[5]  In the Lichtheim-Geschwind model, conduction aphasia arises from a lesion in the arcuate fasciculus, a white matter fiber tract that connects the two language centers.[6] 

More recent work suggests that the classical model is insufficient. Functional MRI (fMRI) and diffusion tensor imaging (DTI) studies have identified gray matter lesions, now termed the area Spt, between the superior-posterior temporal and inferior parietal lobe in patients demonstrating classical conduction aphasia. Due to these findings, current aphasia models now emphasize that language processing occurs in interdependent dual "dorsal" and "ventral" pathways.[7][8][9][10] The dorsal pathway mediates phonological information, and the ventral pathway mediates semantic information. The area Spt may serve as a gray matter hub. According to this model, conduction aphasia likely represents a parietotemporal disconnection syndrome impacting cortical area Spt and its associated white matter circuits of the frontal lobe, as opposed to being purely a disconnection of the arcuate fasciculus.[11]

Etiology

Hallmarks of conduction aphasia include spontaneous verbal output that is relatively fluent albeit paraphasic, accompanied by mostly preserved auditory comprehension and disproportionately impaired ability to repeat sentences or phrases. As noted, recent fMRI evidence suggests that lesions of the left superior temporal gyrus, the left supramarginal gyrus, the left inferior parietal lobe (Brodmann area 40), the left primary auditory cortices (Brodmann area 41 and 42), and the insula, all can lead to this condition.[12] Thus, lesions in multiple areas surrounding the Sylvian fissure may impair repetition. This likely represents the interconnectivity of the language areas of the brain. fMRI studies have shown that the other important area involved in conduction aphasia is probably the area Spt, a region in the most posterior area of the left planum temporale.[8] Atrophy of the posterior segment of this indirect pathway in the Spt correlates well with the degree of conduction deficits.[13]

The most common cause of aphasia, including conduction aphasia, is an acute ischemic stroke in the territory of the dominant (usually left) middle cerebral artery (MCA). While blockade of the anterior branch of the left MCA typically causes motor weakness of the contralateral face and arms and Broca type of aphasia, both conduction and Wernicke aphasias are usually caused by blockade of the posterior branch of the left MCA. Other causes of conduction aphasia tend to have a more insidious onset with slow progression. These include degenerative etiologies such as Alzheimer disease, frontotemporal dementia, primary progressive aphasia, and corticobasal degeneration. A tumor, especially a left hemisphere glioma, may cause an aphasic syndrome, including conduction aphasia.[14] Conduction aphasia has also been associated with acute COVID-19 infection, although case reports report concomitant left hemisphere infarction.[15][16]

Epidemiology

Conduction aphasia is generally recognized as being a relatively uncommon presentation in stroke, but epidemiologic data specific to conduction aphasia are lacking.

Broca and Wernicke's aphasias are relatively common in strokes affecting the distribution of the middle cerebral artery in the dominant hemisphere. A recent European study reported an incidence of 31 cases of aphasia in stroke per 100,000 person-years, adjusted to the European Standard Population (95% CI: 25-38 per 100,000 person-years). This constitutes a notable decrease of approximately 30% compared to incidence levels from roughly a decade earlier. The overall proportion of patients with aphasia at stroke onset remained roughly stable at 30%, suggesting that the reduction in incidence is not specific to aphasia.[17] 

A recent study reported the impact of social determinants of health on naming performance in individuals with aphasia, finding that, relative to individuals with Wernicke aphasia, individuals with conduction aphasia performed better on a standard test of naming ability. The study found no correlation between naming ability and age, but it did note that higher income levels and larger family sizes were correlated with better naming ability, suggesting that social determinants of health also contribute to the epidemiology of conduction aphasia.[18]

Pathophysiology

The areas that mediate language in the brain lie in the dominant hemisphere. In most people, this is the left hemisphere of the brain. Broca's area resides in the inferior frontal lobe in Brodmann areas 44 and 45. Wernicke's area is in the superior temporal gyrus in Brodmann area 22. The white matter tract known as the arcuate fasciculus connects these 2 regions. The classical explanation for conduction aphasia is that damage to the arcuate fasciculus impairs the transmission of information between the Wernicke and Broca areas. This injury leads to impaired repetition. Thus, the patient can comprehend the speech but cannot transmit the information to the speech production centers in the Broca area to allow repetition. Recent research with fMRI or DTI of the anatomically distributed modular networks shows that patients with conduction aphasia clinically often have lesions in the dominant peri-Sylvian inferior parietal and superior temporal region (Spt). These studies underscore the lack of precision of any single neuroanatomical lesion or site as the pathological site for conduction aphasia.[19]

Recent work conducted by cognitive neuroscientists classifies conduction aphasia as a post-lexical deficit in which primary impairments lie in phonological encoding (phoneme sequences and representations) and the phonological output buffer that maintains phonological representations in short-term memory.[20]

Finally, the frontal and temporoparietal regions that form the neural substrate for language comprehension and production involve large, distributed networks of neurons, so diaschisis must be considered. Diaschisis refers to the loss of afferent inputs due to major damage (stroke, mass lesion, trauma, neurodegeneration) to connected and interdependent regions of the brain, which in turn inhibits firing and leads to a silence that approximates dead neurons. However, over time (usually months), synaptic modification creates new afferent inputs, and the neurons recover all or part of their normal physiology and function. In aphasia caused by stroke, diaschisis usually resolves in 6 to 12 months.[2] 

History and Physical

A patient with conduction aphasia typically presents with frequent language and speech errors, characterized by significantly impaired repetition, frequent phonemic paraphasic errors (and frequent attempts at self-correction), impaired naming, and phonological short-term memory impairment.

During the assessment of aphasia, the clinician should examine the patient's verbal fluency (number of words per minute), pausing, effort, prosody, phrase length, grammar and syntax, lexical retrieval, comprehension, repetition, reading, writing, and naming.[21]

Individuals with conduction aphasia frequently display a prominent impairment in repetition, accompanied by milder difficulty with naming due to paraphasic errors and writing. The ability to read out loud is often compromised, but reading silently for comprehension is usually preserved. Patients may display well-articulated responses similar to the target word and continue to repeat words or phrases to correct the error, resulting in a progressively closer approximation of the target word(s). This has been described as conduit d’approache. Patients with conduction aphasia may exhibit ideomotor apraxia, a type of voluntary–automatic dissociation typified by the inability to perform a variety of task-oriented physical movements (eg, the use of a pretend tool, like a comb), despite the preservation of normal motor strength. The rest of the neurological exam (cranial nerves, motor, sensory, reflexes, gait, coordination) may be normal or reflect deficits associated with an underlying stroke.[22]

A person with conduction aphasia asked to repeat the phrase "The president lives in Washington" may attempt repetition by saying "The predident libs in Washton ton."[2] When presented with a picture of a family enjoying a picnic at a beach and asked to describe it, a patient with conduction aphasia may say, "I see a bunch of people. There's a tree and a car and a house and water and the pier. Guy's fishing, and a couple o' guys that are saying hi to the sail's person. And a guy washing something next to a hail of sand and grass. A flag—is that a flag?— And the wind and the pole and some more grass."

Current theories suggest that patients with conduction aphasia must rely on nonverbatim, semantic routes to information because they can no longer access the phonological trace. This theory also helps to explain the difficulty persons with conduction aphasia have when asked to repeat a nonsense word, which by definition has no semantic meaning, which prevents the use of a paraphrase or synonym and leads to repetition failure. 

Evaluation

The finding of conduction aphasia at the bedside suggests the possibility of a lesion in the dominant hemisphere of the brain, specifically the peri-Sylvian areas. Any structural lesion in the left superior temporal gyrus, the left supramarginal gyrus, or the left inferior parietal lobe may cause conduction aphasia. The clinician should perform neuro-imaging to look for a stroke, tumor, infection, or another pathology in the setting of conduction aphasia. A noncontrast CT of the head is quick to obtain; if stroke is possible, it should be undertaken with high urgency and speed. A brain MRI of the brain is the imaging modality of choice for ascertainment of the lesion's location and extent. Gadolinium contrast should be used if there is suspicion of infection or mass lesion. Depending on the results, further testing may be necessary to determine the precise etiology. For specification of the nature and extent of the aphasia, examination by a neuropsychologist or speech therapist can be helpful. 

An aphasia rapid test (ART) has been developed as a simple, reliable, and reproducible language function testing to assess the severity of aphasia. ART also has good sensitivity and specificity in predicting the 3-month verbal communication outcome. This 26-item testing battery[23] takes only a few minutes of testing time with good inter-rater reliability. Other testing batteries have been developed for patients speaking different languages, such as Tamil, India.[24] ART may serve as a template for other languages.

Treatment / Management

There is no standard treatment for aphasia. Speech and language therapy is the core mainstay of care for patients with aphasia. The therapist should tailor the treatment to the individual needs of the patient.

Aphasia is an important part of any rehabilitation program. Recent developments include therapist-guided tablet-based telerehabilitation programs with promising outcomes.[25][26][27] Acupuncture as a treatment modality has been studied recently.[28] Complementary approaches, such as using mental imagery to support naming, have also recently been explored, including via digital data acquisition.[29] Speech pathologists have also piloted approaches to language and communication in unstructured, participant-led conversations guided by therapists and report reduced aphasia severity measured by the Western Aphasia Battery-Revised at posttreatment or maintenance.[30]

Conduction aphasia is a relatively mild language impairment, and most patients can return to normal daily life activities. No medical or surgical treatment improves the outcome in patients with aphasia. However, if the underlying lesion is an infection or tumor, removing the offending lesion may prevent the worsening of the deficit.

Differential Diagnosis

Aphasia differs from dysarthria, which results from impaired articulation of speech. Dysarthria is a motor dysfunction due to disrupted innervation to the face, tongue, or soft palate, resulting in slurred speech.

Conduction aphasia differs from Wernicke and Broca aphasia in that there is a prominent inability to repeat. Neurodegenerative disorders such as primary progressive aphasia lead to a gradual loss of language function.[31] However, this condition affects all aspects of language. Trans-cortical motor and sensory aphasias do not involve repetition. Anomic aphasia affects only the ability to name objects and does not affect repetition. 

Prognosis

The prognosis for conduction aphasia depends on the underlying cause. If the cause is a stroke, patients can make a good recovery but may have persistent deficits. Speech therapy may be helpful for the remediation of the effects of aphasia and the restoration of normal function.

Some researchers posit a relationship between premorbid intelligence and aphasia severity but not aphasia recovery. Therefore, although there may be an association between measures of intelligence and aphasia severity, recovery of language function does not seem to depend on premorbid intelligence.[32]

Diffusion tensor tractography has been used to study recovery mechanisms in aphasia, including conduction aphasia. Indeed, most extant studies have focused on the arcuate fasciculus, suggesting that decreased functional anisotropy may be a biomarker of improved language ability.[6][33]

Complications

Aphasia can affect the quality of life in a significant way because communication in day-to-day life can be compromised. Communication difficulty may affect a patient's daily functional ability, relationships, and job performance. Communication barriers may lead to social embarrassment, depression, and relationship issues. Some studies, now quite old, have reported complications such as a right-sided pseudothalamic pain syndrome as a complication of conduction aphasia.[34] 

Consultations

Consultation with neuropsychology, speech therapy, and rehabilitation medicine may be salubrious. 

Deterrence and Patient Education

Conduction aphasia is often less disabling than other types of aphasia. However, it still may cause issues with communication. Education regarding the patient's condition should involve the patient, family, and caregivers.

Pearls and Other Issues

When patients complain of stumbling over words, clinicians need to ask the patient to repeat simple phrases to test for conduction aphasia. The impaired repetition suggests a lesion in the para-Sylvian region of the dominant hemisphere. Therefore, the clinician should get neuro-imaging to look for pathology affecting this brain region.

Enhancing Healthcare Team Outcomes

Conduction aphasia is a language disorder characterized by impaired repetition despite fluent spontaneous speech. Clinicians should recognize its distinct features, such as paraphasic errors and intact comprehension. Diagnosing conduction aphasia involves assessing the disconnect between comprehension and repetition abilities. Management focuses on speech therapy to improve repetition skills and utilize compensatory strategies. Regular monitoring of language function is essential. This summary emphasizes early identification, differentiation from other aphasias, and a targeted therapeutic approach to enhance clinicians' ability to provide optimal care for individuals with conduction aphasia, addressing both diagnostic intricacies and tailored intervention strategies.

Patients with conduction aphasia may take weeks to months to recover. The patient, family, caregivers, and all treatment team members need to know of the patient's deficits and support the recovery efforts to maximize recovery. Patients should continue to engage in social and leisure activities to avoid social isolation. Importantly, patients with conduction aphasia rarely have intellectual deficits but only an isolated difficulty in repetition.