Aphemia: The Loss of Articulate Speech

Aphemia represents one of the foundational constructs in behavioral neurology, cognitive neuropsychology, and aphasiology, marking the precise historical intersection where localized brain pathology was first formally linked to the loss of articulate speech. Historically introduced by the French surgeon and anthropologist Paul Broca, the condition denotes an isolated, severe breakdown in the motor programming and execution of spoken language, occurring in the conspicuous absence of structural paralysis of the vocal apparatus or generalized linguistic deterioration. Understanding aphemia illuminates the delicate boundaries separating phonetic motor planning, syntactic-semantic comprehension, and peripheral neuromotor execution across human communication networks.

Aphemia

1. Concise Definition

Aphemia is an acquired neurological speech disorder characterized by the selective inability or profound impairment in the production of articulate speech, whereas auditory comprehension, reading comprehension, and written expression remain substantially preserved. Patients understand spoken language perfectly, recognize semantic and syntactic relationships, and can often communicate fluently through writing or gestures, yet they cannot coordinate the motor execution required to verbalize words.

In modern clinical neurology and cognitive neuropsychology, aphemia is frequently classified as a severe, isolated form of acquired apraxia of speech, pure motor aphasia, or cortical dysarthria. It differs fundamentally from classic multimodal Broca’s aphasia because it does not compromise the inner grammar, lexicon, or orthographic systems of the brain. The impairment is confined to the translational interface where abstract phonological representations are converted into coordinate motor-articulatory commands for the vocal tract, tongue, lips, and larynx.

2. Etymology & Linguistic Origin

The term aphemia derives directly from the Ancient Greek prefix a- (ἀ-), meaning “without,” “lacking,” or “deprived of,” and the Greek noun phēmē (φήμη), meaning “voice,” “speech,” “rumor,” or “utterance” (derived from the Proto-Indo-European root *bʰeh₂-, meaning “to speak”). When combined with the abstract noun suffix -ia (-ία), the composite term literally translates to “the condition of being without speech” or “absence of utterance.”

Paul Broca formally introduced the term to the academic medical community in 1861 during his presentations before the Société d’Anthropologie and the Société Anatomique de Paris. Broca deliberately selected aphémie to describe the unique clinical presentation of his famous patient Louis Victor Leborgne (widely known as “Tan”), who understood spoken communication but could utter only the single recurring syllable “tan.” Broca argued that the disorder did not reflect a loss of memory for words or an intellective deficit, but rather a loss of the special faculty of articulate language. Although French clinician Armand Trousseau subsequently argued in 1864 for the adoption of the term aphasia (from Greek aphasia, “speechlessness”), creating a lasting semantic controversy, modern aphasiologists preserved “aphemia” as a distinct nosological category indicating a pure, non-aphasic motor speech programming deficit.

3. Pronunciation & Grammatical Form

In contemporary English phonology, the standard pronunciation of aphemia is rendered phonetically as /əˈfiː.mi.ə/ (uh-FEE-mee-uh). Variant pronunciations occasionally heard in British and European medical traditions include /eɪˈfiː.mi.ə/ (ay-FEE-mee-uh).

Grammatically, aphemia operates as an uncountable abstract noun. The corresponding adjectival form is aphemic (/əˈfiː.mɪk/), used to describe speech patterns, lesions, or patients (e.g., “an aphemic deficit,” “the aphemic patient”). The plural form, when referring to distinct clinical cases or historical variations, is occasionally written as aphemias, though clinical literature predominantly treats the word as a non-count condition. Derived historical terms include aphemie (the original French spelling) and aphemist (a rare, archaic designation for an individual exhibiting the syndrome).

4. Detailed Conceptual Explanation

The conceptual framework of aphemia occupies a unique position in behavioral neurology because it challenges simplistic dichotomies between “central” linguistic processing and “peripheral” motor execution. Speech production requires a hierarchically organized cascade of cognitive and sensorimotor processes: conceptual formulation, lexical selection, phonological encoding, phonetic motor planning, and neuromuscular execution. Aphemia represents a selective dissociation specifically localized to the phonetic planning and motor programming phase—the bridge between phonology and peripheral neuromuscular innervation.

Clinically, an individual experiencing an acute onset of aphemia—most commonly secondary to an ischemic stroke, focal hemorrhage, or traumatic brain injury—initially presents with complete mutism. Unlike patients with generalized encephalopathy or abulia, the aphemic individual remains alert, highly oriented, and visibly distressed by their inability to articulate. Within days to weeks, the mutism typically transitions into severe, effortful, and telegraphic verbal output. The patient struggles with trial-and-error articulatory groping, characterized by visible and audible attempts to achieve correct phonetic posturing of the tongue, lips, and soft palate. Articulation is slow, characterized by syllable segregation, vowel prolongations, inconsistent phoneme substitution, distortion, and loss of normal prosodic melody (dysprosody).

Crucially, the scope and boundaries of aphemia are defined by strict exclusionary and inclusionary criteria:

• Preserved Linguistic Competence: The internal linguistic matrix remains fully functional. Patients demonstrate intact syntactic comprehension, lexical retrieval, and orthographic encoding. When handed a pen or a keyboard, they can compose coherent, grammatically complex, and semantically rich sentences, proving that language in its symbolic essence is intact.
• Absence of Significant Paralysis or Spasticity: The articulatory organs (tongue, lips, velum, pharynx) demonstrate normal strength, range of motion, and sensory perception during non-speech autonomic tasks, such as chewing, swallowing, and involuntary facial expressions. The deficit is not primarily bulbar or pseudobulbar in origin.
• Absence of Global Cognitive Decline: Working memory, executive functioning outside of verbalization, spatial processing, and episodic recall remain commensurate with premorbid functioning, isolating the impairment to the motor speech nexus.

Neuroanatomically, modern functional neuroimaging and lesion-mapping paradigms demonstrate that aphemia is typically caused by circumscribed damage to the left frontal speech network. Rather than reflecting massive lesions across the entire classic perisylvian language territory, aphemia is driven by focal damage to the lower portion of the left precentral gyrus (primary motor cortex corresponding to the face, lips, and tongue), the opercular portion of the inferior frontal gyrus (Broca’s area), the left anterior insula, or the subcortical white matter tracts linking these cortical hubs to the basal ganglia.

5. Historical Development

The history of aphemia is intrinsically linked to the birth of modern neuropsychology and cerebral localizationism during the nineteenth century. Prior to the mid-1800s, dominant scientific dogma—championed by researchers such as Marie Jean Pierre Flourens—held that the cerebral cortex operated as an equipotential, unitary organ without discrete functional specializations.

This paradigm shifted radically in April 1861 when Paul Broca presented the autopsy findings of Louis Victor Leborgne at the Société d’Anthropologie in Paris. Leborgne, who had been institutionalized for twenty-one years unable to speak any word other than “tan,” had suffered a localized lesion centered in the left posterior inferior frontal convolution. Broca coined the term aphémie to describe this state, asserting that Leborgne retained normal vocal apparatus function and linguistic comprehension but had lost the “memory of the coordinated movements needed to articulate words.” A second patient, Lazare Lelong, confirmed the association later that year.

In 1864, Armand Trousseau, an influential clinician at the Hôtel-Dieu in Paris, publicly criticized Broca’s nomenclature. Trousseau argued that aphémie in Greek was etymologically linked to infamy or bad reputation (confusing phēmē with aphemos) and proposed replacing it with aphasia. Broca fought vigorously to maintain the distinction, pointing out that aphasia historically implied a loss of speech through general debility or lack of ideas, whereas aphémie precisely isolated the motor-articulatory dimension. Broca wrote extensive defenses in the medical bulletins of 1864, but the broader medical community adopted Trousseau’s term, broadening “aphasia” to encompass diverse receptive and expressive deficits.

Throughout the twentieth century, several European neurologists revived aphemia to clarify taxonomic ambiguities. In 1906, Pierre Marie famously proclaimed that “Broca’s aphasia is simply Wernicke’s aphasia combined with anarthria,” using anarthria in a sense synonymous with Broca’s aphemia. In the 1960s and 1970s, pioneering aphasiologist Norman Geschwind and German neurologist D. Frank Benson demonstrated that patients with isolated lesions of the lower left precentral motor cortex or the pars opercularis manifested an isolated deficit in speech output without agraphia, naming the condition “aphemia” or “pure motor aphasia.” This work formally established aphemia as an independent diagnostic entity distinct from generalized Broca’s aphasia.

6. Theoretical Foundations

Theoretical interpretations of aphemia have evolved across distinct epochs of cognitive neuroscience, driven by connectionist models, psycholinguistic architectures, and contemporary computational sensorimotor control theories.

The earliest structural framework was provided by the nineteenth-century associationist school, formalized by Karl Wernicke, Ludwig Lichtheim, and later revived by Norman Geschwind. In the classic Lichtheim-Wernicke “house” model, language relies on interconnected sensory (auditory) memory centers, concept centers, and motor speech centers. Within this connectionist schema, aphemia was conceptualized as a subcortical or pure cortical lesion affecting exclusively the motor speech output node or its immediate projections to the primary motor strip, isolating the motor production center while leaving the conceptual hub, auditory sensory center, and orthographic pathways intact.

In modern psycholinguistics, Willem Levelt’s modular model of speech production provides a framework for decomposing aphemia. Levelt conceptualizes verbalization across stages: conceptualization (generating the message), formulation (grammatical and phonological encoding), and articulation (retrieving phonetic gestures and motor execution). Levelt postulated an intermediate structure known as the “mental syllabary”—a repository of pre-compiled motor programs for frequently uttered syllables. Contemporary researchers propose that aphemia arises from an inability to access the mental syllabary or to assemble novel phonetic motor scores online, forcing the brain to rely on cumbersome, segregate, and error-prone online movement construction.

More recently, computational neuroscience models such as the Directions Into Velocities of Articulators (DIVA) model, developed by Frank Guenther and colleagues, describe speech as a feedback and feedforward neurocomputational control system. The feedforward control system includes the left inferior frontal gyrus, anterior insula, and ventral premotor cortex, which store sensory-to-motor projections that coordinate rapid articulatory trajectories. Aphemia represents a catastrophic degradation of this feedforward motor controller. As a consequence, patients must rely on slow, imperfect auditory and somatosensory feedback loops to adjust their articulators, explaining the audible trial-and-error groping, prolonged transition intervals, and perceived foreign accent syndrome observed during recovery.

7. Key Components, Types & Dimensions

Aphemia is characterized by multidimensional acoustic, phonetic, neurological, and linguistic features:

• Initial Complete Mutism: In the immediate acute stage following neurovascular insult, patients typically experience a temporary period of total vocal suppression, during which they cannot produce phonation on command or generate automatic vocal sounds.
• Articulatory Groping and Phonetic Dissociation: As mutism subsides, patients exhibit visible struggle to position the tongue, lips, and jaw. Speech is marked by phonetic distortions, sound additions, transpositions, and inconsistent voicing errors (e.g., substituting voiceless stops for voiced stops).
• Disrupted Prosodic Architecture: Speech loses its natural melodic inflection. The vocal rate is profoundly slowed, characterized by equalized syllable stress, pauses between phonemes, and monotone pitch, giving speech a staccato or telegraphic quality.
• Intact Written Language (Absence of Agraphia): A definitive dimension of aphemia is the striking preservation of writing. Patients construct syntactically intact, grammatically rich, and accurately spelled written sentences, reflecting uncompromised lexical and syntactic processors.
• Intact Auditory and Reading Comprehension: Receptive capabilities remain unimpaired. Patients comprehend complex spoken instructions, metaphor, abstract semantics, and multisyllabic written texts without latency.
• Subcortical vs. Cortical Variants: Neurologists differentiate between cortical aphemia (associated with focal lesions confined to the frontal operculum, ventral precentral gyrus, or anterior insula) and subcortical aphemia (resulting from small lacunar infarctions in the internal capsule, striatum, or lenticular nucleus that disrupt white matter projections from the frontal cortex to lower motor nuclei).

8. Examples & Illustrative Cases

The clinical manifestations of aphemia are best understood through documented neuropsychological case presentations that capture both acute and chronic recovery trajectories.

Case Illustration 1: Acute Ischemic Stroke with Pure Aphemia
A 62-year-old right-handed retired professor suffered a focal acute ischemic infarction restricted to the left ventral precentral gyrus, with sparing of the superior temporal gyrus, angular gyrus, and subcortical periventricular white matter. Upon evaluation on post-stroke day two, the patient was completely mute. He displayed normal alertness and followed multi-step commands, such as “touch your left earlobe with your right thumb after closing your eyes.” When handed a clipboard, he immediately wrote: “I know exactly what you are asking me. I can think of every word clearly, but my mouth simply will not move to make the sounds. I feel completely trapped inside my own throat.” Over the subsequent four weeks, speech returned but was characterized by severe articulatory strain, prolonged vowel-consonant transitions, and marked phonetic distortions, while his written correspondence remained fluent and error-free.

Case Illustration 2: Traumatic Brain Injury and the Appearance of Pseudo-Foreign Accent
A 34-year-old engineer experienced a localized traumatic contusion over the left frontal operculum following a motor vehicle collision. Following an initial week of mutism, her recovery revealed speech output that sounded strikingly unfamiliar to her family. Her native American English vowels were flattened, consonants were uttered with unnatural tension, and syllable timing became syllable-timed rather than stress-timed. Her friends remarked that she sounded like a non-native speaker from Eastern Europe—a classic clinical manifestation of foreign accent syndrome, which is recognized as a mild or recovering variant of aphemia. Systematic testing demonstrated pristine syntactic comprehension, perfect written grammar, and normal non-speech oral motor control, confirming that the perceived foreign accent was secondary to damaged articulatory planning networks rather than genuine linguistic change.

9. Measurement & Assessment

Accurate diagnosis of aphemia necessitates a comprehensive, interdisciplinary evaluation combining standardized aphasiology batteries, motor speech assessments, structural and functional neuroimaging, and instrumental acoustic analysis.

Differential diagnosis relies on standardized neuropsychological instruments, including:

• Comprehensive Language Batteries: The Western Aphasia Battery-Revised (WAB-R) and the Boston Diagnostic Aphasia Examination (BDAE-3) are administered to quantify the dissociation between spoken output and other language modalities. An aphemic patient scores normally on auditory comprehension, written expression, and silent reading subtests, but exhibits severe impairments on spontaneous speech and repetition subtests.
• Motor Speech Inventories: The Apraxia Battery for Adults-Second Edition (ABA-2) evaluates limb and oral apraxia, latency and length effects during multisyllabic word production, articulatory posturing errors, and phonetic consistency across repeated trials.
• Instrumental Acoustic Phonetic Analysis: Digital acoustic software (such as Praat) is utilized to measure voice onset time (VOT), vowel formant trajectories, fundamental frequency variability, and syllable duration. Patients with aphemia show substantial dispersion and overlap in voice onset times for voiced versus voiceless stop consonants (/b/-/p/, /d/-/t/), demonstrating poor neuromotor coordination of laryngeal and supralaryngeal timing.
• High-Resolution Neuroimaging: Volumetric magnetic resonance imaging (MRI), diffusion tensor imaging (DTI), and computed tomography perfusion (CTP) map the spatial distribution of tissue damage. The diagnostic hallmark of aphemia is an isolated lesion in the left motor-speech network (ventral motor cortex, anterior insula, or lower frontal gyrus) with preservation of posterior language zones and subcortical basal ganglia circuits responsible for generalized language integration.

10. Applications & Practical Significance

The practical significance of understanding aphemia extends across acute neurocritical care, speech-language rehabilitation, technological interventions, and neurosurgical planning.

In acute neurology, the prompt identification of aphemia prevents diagnostic errors. Mute patients or those with severely restricted, distorted verbalization are frequently mislabeled as having broad “global aphasia” or severe cognitive deficits. Such misdiagnoses can lead to inappropriate clinical prognostication, premature institutionalization, or exclusion from active rehabilitation protocols. Recognizing that the patient’s internal intellect and linguistic cognition are intact allows clinicians, nurses, and family members to adopt appropriate non-verbal communication systems immediately.

In neurorehabilitation, speech-language pathologists employ specialized interventions designed to circumvent or retrain disrupted motor speech programming pathways. Common therapeutic protocols include:

• Melodic Intonation Therapy (MIT): Exploiting intact right-hemisphere prosodic and musical networks to bypass the damaged left-hemisphere motor planning channels by translating phrases into exaggerated intonational pitches and rhythmic tapping.
• Sound Production Treatment (SPT): A structured behavioral hierarchy emphasizing phonetic placement cues, verbal modeling, minimal word contrast drills (e.g., “pin” vs. “bin”), and visual feedback to re-establish stable sensorimotor representations.
• Augmentative and Alternative Communication (AAC): Because written language is fully intact, implementing high-tech communication devices—such as digital tablets equipped with text-to-speech software—allows aphemic patients to communicate and return to professional work despite ongoing verbal limitations.
• Intraoperative Awake Brain Mapping: During neurosurgical resections of brain tumors or epileptogenic foci near the left precentral gyrus, neurosurgeons apply direct cortical electrical stimulation while the patient speaks. Inducing transient speech arrests without agraphia alerts the surgical team to avoid resecting tissue critical to motor speech articulation, preventing permanent postoperative aphemia.

11. Research & Empirical Evidence

Over the past four decades, modern neuroimaging and clinical case registries have refined empirical knowledge regarding the pathophysiology, structural anatomy, and prognosis of aphemia.

A benchmark study by D. Frank Benson and colleagues (1973) evaluated patients with isolated speech arrest and dysarthria-like output who showed preservation of writing and auditory comprehension. Benson demonstrated that while Broca’s aphasia involves wide infarction across the superior division of the left middle cerebral artery territory, aphemia involves smaller, circumscribed lesions localized to the lower motor strip or subcortical white matter. Subsequent neuroimaging work by Nina Dronkers (1996) utilized voxel-based lesion-symptom mapping in stroke patients to reveal that the left anterior insula plays an indispensable role in motor planning for speech articulation, demonstrating that damage isolated to this subcortical opercular structure reliably predicted apraxic speech deficits consistent with aphemia.

Subsequent work by Josephs and colleagues (2006) investigated the clinical and radiological differences between progressive apraxia of speech (a primary degenerative form of aphemia) and classic non-fluent progressive aphasia. Their structural MRI and fluorodeoxyglucose positron emission tomography (FDG-PET) findings confirmed that pure speech planning deficits without linguistic decay correlate with isolated hypometabolism and gray matter atrophy within the superior premotor and supplementary motor areas, completely sparing the temporoparietal language networks.

Longitudinal studies tracking recovery trajectories in vascular aphemia have shown that the prognosis is favorable compared to classic Broca’s aphasia. Research by Schiff and colleagues documented that while initial recovery involves prolonged struggle and phonetic distortion, over 70% of patients with isolated, small-volume cortical or subcortical lesions regain functional verbal communication within six to twelve months, aided by neuroplastic reorganization in bilateral premotor networks.

12. Cultural & Cross-Cultural Considerations

Although the neurobiological substrates for motor speech programming are universal across human populations, the clinical expression, acoustic perception, and functional impact of aphemia vary depending on the phonological and prosodic structure of the patient’s native language.

In tonal languages such as Mandarin Chinese, Cantonese, and Vietnamese, pitch contours carry lexical meaning (distinguishing words with identical segmental phonemes). In patients with aphemia who speak tonal languages, researchers have observed a dissociation between segmental articulatory breakdown and lexical tone production. While patients experience severe distortion in producing consonant and vowel postures, tonal inflections modulated by sustained laryngeal tension can occasionally remain relatively preserved, or alternatively, become flattened, resulting in lexical ambiguity unique to tonal phonetic systems.

Furthermore, across languages with complex consonant clusters and long multisyllabic agglutinative morphology (such as Russian, German, or Finnish), aphemic patients encounter higher operational demands during speech formulation than speakers of languages with predominantly simple consonant-vowel-consonant (CVC) structures (such as Spanish or Japanese). In agglutinative languages, articulatory groping and phoneme substitutions occur more frequently, often causing clinicians to misdiagnose the patient with severe phonological aphasia unless careful written testing is performed.

Socio-cultural attitudes toward non-fluent speech and disability also influence patient outcomes. In cultures that heavily prioritize rapid conversational exchange, individuals with residual aphemic dysprosody face social isolation and occupational marginalization, highlighting the importance of access to culturally sensitive augmentative communication technology.

13. Criticisms, Debates & Limitations

The nosological classification and clinical boundaries of aphemia have been contested within neurology, neuropsychology, and speech-language pathology for over a century and a half.

The central debate concerns whether aphemia represents an independent diagnostic entity or merely a subtype or recovery stage of other conditions. Several prominent schools of thought illustrate these viewpoints:

• The Terminological Divide (Aphemia vs. Apraxia of Speech): In American speech-language pathology, the term aphemia is infrequently utilized in clinical reports, with practitioners favoring apraxia of speech (AOS) or verbal apraxia. Conversely, behavioral neurologists continue to use aphemia to emphasize the acute syndrome of mutism evolving into isolated articulatory failure following a vascular lesion, reserving AOS for both acquired and progressive manifestations.
• Aphemia vs. Cortical Dysarthria: A contentious neurological debate centers on whether aphemia should be classified as a motor planning disorder (apraxia) or an isolated upper motor neuron dysarthria restricted to the oral articulators (cortical dysarthria). Neurologists such as Marie and later modern researchers argued that focal lesions of the precentral gyrus produce subtle unilateral upper motor neuron paresis that impairs coordination without genuine cognitive-praxic breakdown.
• The “Pure” Syndrome Controversy: Some neuropsychologists argue that a truly “pure” aphemia is an idealization. Detailed psycholinguistic testing often reveals subtle subclinical receptive impairments or mild syntactic processing delays under high cognitive loads, suggesting that extensive damage rarely isolates articulatory planning from surrounding perisylvian language computation.

14. Related Terms & Distinctions

Differentiating aphemia from adjacent neurogenic speech and language disorders is essential for clinical diagnosis and scientific research. The primary distinctions include:

• Broca’s Aphasia: While aphemia involves an isolated motor-articulatory deficit with intact writing and preserved comprehension, Broca’s aphasia is a multimodal language disorder characterized by agrammatism, non-fluent speech, impaired repetition, and concomitant agraphia (writing is equally impaired).
• Dysarthria: Dysarthria refers to a group of neurogenic speech disorders caused by neuromuscular weakness, paralysis, ataxia, or abnormal tone affecting the muscles of respiration, phonation, resonance, and articulation. In dysarthria, involuntary and automatic motor functions (such as swallowing, coughing, or chewing) are frequently impaired, and speech errors are consistent and predictable, unlike the variable trial-and-error groping characteristic of aphemia.
• Apraxia of Speech (AOS): AOS is a disorder of phonetic motor programming. Many contemporary scholars treat aphemia as the severe, prototypical vascular presentation of acquired pure apraxia of speech. However, AOS can occur concurrently with significant aphasia, whereas aphemia by definition presents without linguistic impairment.
• Akinetic Mutism: Akinetic mutism is a condition of profound lack of motor and verbal initiation caused by bilateral medial frontal or thalamic-limbic damage. Unlike aphemic patients, individuals with akinetic mutism lack the drive or intent to communicate and do not attempt to write, gesture, or make visible efforts to speak.
• Selective Mutism: A psychiatric anxiety disorder occurring primarily in children, characterized by a persistent failure to speak in specific social situations despite speaking normally in familiar settings. It features no organic neuropathology or articulatory programming breakdown.

15. Summary & Key Takeaways

Aphemia remains an essential construct in clinical neuroscience, embodying the historic transition toward modern neuroanatomical localization and illuminating the cognitive architecture of human speech. Its essential features can be summarized as follows:

• Aphemia is an acquired speech disorder defined by the selective loss or severe impairment of articulate speech with full preservation of auditory comprehension, silent reading, and written language.
• First documented by Paul Broca in 1861 under the label aphémie, it served as the original clinical cornerstone for the localization of cerebral function in the human left hemisphere.
• The underlying mechanism is a breakdown in phonetic motor planning and execution—the computational translation of internal phonology into coordinate physical articulatory movements.
• Etiologies center on focal structural damage to the left ventral precentral gyrus, Broca’s area (pars opercularis), the anterior insula, or subcortical frontostriatal pathways, most frequently resulting from ischemic stroke.
• Diagnosis requires differentiating aphemia from Broca’s aphasia (which includes agraphia), dysarthria (which involves neuromuscular weakness across autonomic tasks), and abulic mutism.
• Recovery typically progresses from complete mutism to slow, effortful, dysprosodic verbalization, with rehabilitation methods such as Melodic Intonation Therapy and augmentative communication technologies playing pivotal roles in functional recovery.

References

• Benson, D. F. (1979). Aphasia, alexia, and agraphia. Clinical Neurology and Neurosurgery Monographs, Churchill Livingstone. https://pubmed.ncbi.nlm.nih.gov/540209/
• Broca, P. (1861). Remarques sur le siège de la faculté du langage articulé, suivies d’une observation d’aphémie (perte de la parole). Bulletin de la Société Anatomique de Paris, 36, 330–357. https://gallica.bnf.fr/ark:/12148/bpt6k297686p
• Dronkers, N. F. (1996). A new brain region for coordinating speech articulation. Nature, 384(6605), 159–161. https://doi.org/10.1038/384159a0
• Guenther, F. H. (2006). Cortical interactions underlying the production of speech sounds. Journal of Communication Disorders, 39(5), 350–365. https://doi.org/10.1016/j.jcomdis.2006.06.013
• Josephs, K. A., Duffy, J. R., Strand, E. A., Whitwell, J. L., Layton, K. F., Parisi, J. E., Hauser, M. F., Witte, R. J., & Boeve, B. F. (2006). Clinicopathological and imaging correlates of progressive apraxia of speech. Brain, 129(6), 1385–1398. https://doi.org/10.1093/brain/awl078