Alexia with Agraphia: Loss of Written Language

Language embodies the pinnacle of human cognitive architecture, binding sensory perception, motor execution, and abstract symbolic manipulation into a coherent communicative matrix. When focal brain pathology disrupts the neural networks sustaining written communication, individuals may experience alexia with agraphia—a profound, acquired syndrome characterized by the simultaneous loss of the ability to read and write, typically occurring despite relatively preserved spoken speech and auditory comprehension. This neurobehavioral syndrome offers a crucial window into how the human cerebral cortex encodes, processes, and reproduces orthographic representations.

Alexia with Agraphia

1. Concise Definition

Alexia with agraphia, historically termed parietal alexia or central alexia, is an acquired neurocognitive disorder marked by the co-occurring impairment of both reading comprehension (alexia) and written expression (agraphia), resulting from damage to brain regions essential for orthographic representation, most notably the left angular gyrus. Unlike peripheral reading disorders, this condition compromises the core central linguistic mechanisms governing literacy, meaning the patient can neither decode visually presented text nor encode orthographic forms across all modalities of writing.

In classical aphasiology, alexia with agraphia is distinguished from “pure alexia” (alexia without agraphia) because the deficit in the former is not restricted to visual input pathways. Patients with alexia with agraphia cannot read words, letters, or numbers, and they are equally incapable of spontaneous writing, writing to dictation, or transcribing words. Spoken auditory comprehension and oral language production frequently remain remarkably fluent or only mildly impaired, creating a striking clinical dissociation between spoken and written language facilities.

Neuroanatomically, this syndrome reflects the disintegration of the polymodal association hubs responsible for mediating between phonological auditory tokens, visual orthographic forms, and graphomotor execution programs. Consequently, it represents a breakdown in the cross-modal synthesis of linguistic symbols rather than an elementary sensory or motor failure.

2. Etymology & Linguistic Origin

The term is formed from classical Greek linguistic roots combined with negative prefixes to denote acquired functional loss. The component alexia derives from the Ancient Greek privative prefix a- (ἀ-, meaning “without” or “lacking”) attached to lexis (λέξις), meaning “word,” “speech,” or “diction,” which itself stems from the verb legein (λέγειν, “to speak” or “to gather”). In late nineteenth-century clinical neurology, alexia was formally adopted to indicate an acquired inability to comprehend written language, distinguishing it from developmental dyslexia.

The companion term agraphia similarly incorporates the Greek privative a- (ἀ-) and the root noun graphē (γραφή), meaning “writing,” “drawing,” or “carving,” which traces to the verb graphein (γράφειν, “to scratch, engrave, or write”). Agraphia entered the medical nomenclature to signify the acquired impairment of writing ability following cerebral insult.

Synthesizing these terms creates a diagnostic designation indicating a dual deficit: the concurrent elimination of reading reception and written production. In early French and German neurological treatises, the condition was frequently designated as cécité et surdité verbales (word blindness combined with graphic dissolution) or Wortblindheit mit Agraphie before the standardized Greco-Latin composite achieved universal diagnostic consensus.

3. Pronunciation & Grammatical Form

Pronunciation: /eɪˈlɛksiə wɪθ eɪˈɡræfiə/ (General American); /əˈlɛksiə wɪð əˈɡræfiə/ (Received Pronunciation).

Grammatical Form: Compound noun phrase. The construct functions as a singular clinical diagnosis. Derivative adjective forms include alexic-agraphic (e.g., “an alexic-agraphic profile”), while an individual exhibiting the condition is occasionally referred to clinically as an alexic with agraphia, though contemporary person-first nomenclature prefers “an individual with alexia and agraphia.”

4. Detailed Conceptual Explanation

To understand alexia with agraphia, one must appreciate how literate brains process orthography. Literacy is an evolutionary newcomer; the human brain contains no innate, genetically predetermined reading or writing organ. Instead, reading and writing rely on a culturally recycled neural network linking visual analysis systems in the occipitotemporal cortex with phonological and semantic networks in the temporal and frontal lobes, and motor execution systems in the premotor cortex. Alexia with agraphia occurs when the critical convergence zone that integrates these heterogeneous modalities sustains structural damage.

At the center of this integration lies the left inferior parietal lobule, specifically the angular gyrus (Brodmann area 39). The angular gyrus occupies an anatomical crossroads at the confluence of visual, somatosensory, and auditory association cortices. It serves as an orthographic clearinghouse: it translates the visual patterns of written letters into phonemes (grapheme-to-phoneme conversion), maps sounds to written symbols (phoneme-to-grapheme conversion), and connects orthographic forms directly to mental lexicons and semantic concepts. When this structure or its subcortical white matter pathways are injured, the internal representation of written language is extinguished.

Clinically, this destruction produces a catastrophic breakdown across all dimensions of written language. The individual cannot read aloud or silently for comprehension. Unlike individuals with pure alexia, who can recognize words spelled aloud to them or identify letters traced onto their palms via tactile kinesthesia, patients with alexia with agraphia exhibit deficits across every sensory modality. They cannot comprehend tactile or auditory spelling, nor can they reconstruct words using physical plastic letters or letter blocks. This confirms that the deficit is not an input processing failure, but a complete dissolution of the internal orthographic processor.

Writing is compromised in an identical fashion. Patients can neither generate spontaneous narrative text nor transcribe dictated phonemes. Their attempts to write letters result in illegible scribbles, letter substitutions (paragraphias), literal omissions, or completely malformed graphemic sequences. Importantly, mechanical motor execution is preserved; the motor apraxia of the hand is absent, and patients can routinely copy geometric shapes or draw recognizable figures. Copying text, however, is heavily degraded. Patients may reduce copying to a laborious, stroke-by-stroke drawing process, frequently transcribing uppercase letters without recognizing their identity, or fail the task completely.

Crucially, spontaneous oral language is typically spared or only mildly affected. Patients may participate in conversational speech with fluent phrasing, intact syntactic structures, and preserved auditory comprehension. Mild word-finding difficulties (anomia) and occasional phonemic or semantic paraphasias may emerge, but the contrast between the patient’s spoken fluency and their total illiteracy is one of the most remarkable dissociations in clinical neurology.

5. Historical Development

The clinical identification of alexia with agraphia played a pivotal role in the emergence of nineteenth-century localizationist neurology. Prior to systematic clinicopathological studies, language deficits were often viewed holistically as general intellectual declines or variants of Broca’s motor aphasia.

The foundational breakthrough occurred in 1891, when the French neurologist Joseph Jules Dejerine described the index case of Madame C. She was an educated woman who, following a cerebrovascular accident, suddenly lost the capacity to read and write while retaining articulate speech and auditory comprehension. Dejerine observed that her writing was severely disorganized, characterized by severe paragraphia, and she could not decipher her own previous journals or the words spoken aloud to her via letter names. Post-mortem pathological examination revealed a discrete infarct localized to the left angular gyrus (the plica poliformis) extending into the neighboring white matter. Dejerine deduced that the angular gyrus was the structural substrate for the “visual image of words” (centre de la mémoire visuelle des mots).

One year later, in 1892, Dejerine encountered another landmark patient, Monsieur C., who could write fluently but could not read anything at all, not even his own handwriting. Dejerine’s post-mortem analysis of this second case revealed lesions in the left visual cortex and the splenium of the corpus callosum, preserving the angular gyrus. By juxtaposing these two cases, Dejerine firmly established the classic dichotomy: alexia without agraphia (pure alexia) resulting from disconnection of intact orthographic regions from visual input, versus alexia with agraphia (parietal alexia) resulting from destruction of the central orthographic representations within the angular gyrus itself.

Throughout the mid-twentieth century, the American neurologist Norman Geschwind integrated Dejerine’s observations into his influential neo-associationist framework. Geschwind characterized the angular gyrus as an evolutionary “association area of association areas,” uniquely expanded in humans to enable cross-modal associations between auditory and visual stimuli. Geschwind posited that alexia with agraphia resulted from the disruption of this polymodal integration hub, which permanently decoupled spoken linguistic streams from graphic visual representations.

In the modern neuroimaging era, functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have refined this classic picture. While verifying the pivotal role of the left inferior parietal lobule, modern cognitive neuroscience emphasizes that the angular gyrus operates within an extended distributed network. This network connects the Visual Word Form Area (VWFA) in the left fusiform gyrus with Wernicke’s area in the superior temporal gyrus and Exner’s area in the frontal motor cortex, demonstrating that the syndrome can arise not only from isolated cortical lesions but also from disconnection within this broader subcortical circuitry.

6. Theoretical Foundations

The cognitive and computational architecture underlying alexia with agraphia is primarily explained through two influential models: the classical neuroanatomical disconnectionist model and the modern dual-route cognitive neuropsychological model of reading and writing.

The disconnectionist framework, pioneered by Dejerine and refined by Geschwind, posits that acquired reading and writing require intact sensory pathways feeding into a localized cross-modal dictionary. In this model, reading visual input travels from the primary visual cortex (Brodmann area 17) to secondary visual areas, and then projects directly to the angular gyrus. There, visual word forms are linked to auditory equivalents stored in Wernicke’s area. For writing, thoughts originating across the cerebral cortex are transformed into linguistic form within Wernicke’s area, transmitted to the angular gyrus to activate graphemic representations, and relayed via the superior longitudinal fasciculus to Exner’s area and the primary motor cortex to guide hand movements. A lesion directly inside the angular gyrus simultaneously destroys the visual word storehouse and the graphemic translation engine, producing alexia and agraphia together.

In contrast, cognitive neuropsychology explains the syndrome through the dual-route model of orthographic processing. This model posits that reading and writing proceed via two parallel processing routes:

• The Lexical-Semantic Route: Direct access from the orthographic input lexicon to the semantic system and out to the orthographic output lexicon. This route is required for recognizing and writing irregular, exception words (such as yacht, colonel, or choir).
• The Sublexical / Non-Lexical Phonological Route: Indirect rule-based conversion between graphemes and phonemes via the grapheme-to-phoneme conversion mechanism (for reading) and phoneme-to-grapheme conversion (for spelling). This pathway is required for sounding out and writing novel words or pseudowords (such as blonk or frad).

In classical alexia with agraphia, both routes are typically impaired. The collapse of the orthographic input lexicon and the grapheme-to-phoneme conversion engine obliterates reading comprehension for both regular and irregular forms. Concurrently, the collapse of the orthographic output lexicon and the phoneme-to-grapheme converter degrades writing across all lexical classes. Depending on the exact lesion boundary, patients may exhibit profiles mimicking severe deep dyslexia/dysgraphia or complete global orthographic disintegration.

7. Key Components, Types & Dimensions

Alexia with agraphia presents across a spectrum of neurobehavioral manifestations, classified by clinical severity, cognitive mechanisms, and accompanying neurological deficits:

• Parietal (Angular Gyrus) Alexia with Agraphia: The classic syndrome described by Dejerine. Characterized by severe reading and writing deficits across all modalities, accompanied by fluent or near-fluent spontaneous speech, with visual spatial deficits and varying degrees of the Gerstmann syndrome tetrad (acalculia, finger agnosia, left-right disorientation, and agraphia).
• Temporal-Parietal Alexia-Agraphia: Occurs when lesions extend ventrally toward the superior and middle temporal gyri. This variant incorporates more pronounced auditory comprehension deficits and prominent paraphasias, overlapping with Wernicke’s aphasia.
• Occipital (Subcortical) Alexia with Agraphia: Arises from subcortical white matter lesions beneath the parietal and occipital lobes that isolate orthographic networks from visual input and graphomotor planning channels, mimicking cortical damage.
• Deep Alexia with Deep Agraphia: A subtype in which the non-lexical (phonological) route is entirely abolished while the lexical-semantic route functions with severe error rates. Patients produce semantic reading errors (e.g., reading the word forest as “trees”) and comparable semantic paragraphias in their written output, accompanied by an absolute inability to read or write pseudowords.
• Surface Alexia with Surface Agraphia: Characterized by the breakdown of the lexical-semantic pathway with a relatively intact phonological route. The patient reads and writes strictly by phoneme-to-grapheme correspondence, resulting in successful decoding of phonetically regular words but catastrophic errors with irregular words (e.g., writing busy as “bizee” or reading knife as “k-neef”).
• Global Central Alexia-Agraphia: The most severe presentation, in which the patient loses all capacity to identify letters, sounds, or written symbols. Copying is completely lost or reduced to fragmented scribbling, with total failure on both lexical and phonological assessments.

8. Examples & Illustrative Cases

The following anonymized clinical cases illustrate how alexia with agraphia manifests in practical neurocognitive evaluations:

Case 1: The Classic Vascular Presentation
A 64-year-old retired accountant presented to the emergency department following an acute embolic occlusion of the angular branch of the left middle cerebral artery. On examination, his spoken conversational fluency was preserved, his speech was grammatically correct, and he comprehended spoken queries without difficulty. However, when handed a newspaper, he looked at the print with confusion, stating that the letters appeared completely unrecognizable. He could not read headlines, short monosyllabic words, or even individual letters of the alphabet.

When asked to write his name, home address, or a simple sentence to dictation (“The sun shines brightly”), the patient gripped the pen correctly but produced a distorted sequence of illegible squiggles interspersed with incorrect, perseverative letter fragments (e.g., writing “Te son ss…”). Spontaneous writing was equally fragmented. When examiners spelled the word “C-A-T” out loud to him, he could not recognize it, and he could not identify letters traced onto the palm of his hand. Neuropsychological evaluation revealed concurrent acalculia and right-left disorientation, confirming a localized infarct of the left angular gyrus producing alexia with agraphia alongside Gerstmann syndrome.

Case 2: The Evolving Neoplastic Profile
A 52-year-old schoolteacher presented with a four-week history of subtle changes in text comprehension and writing. Her family noticed she had stopped reading books and was making bizarre spelling errors on grocery lists. Neurocognitive testing demonstrated that while her visual fields were intact and her spoken vocabulary was pristine, her reading comprehension had plummeted. Presented with the word yacht, she sounded it out phonetically as “yatcht” and admitted she had no idea what it meant. In spontaneous writing, she exhibited severe surface agraphia, spelling words such as laugh as “laf” and neighbor as “naybor.” Over the following month, she lost the capacity to spell novel nonwords entirely. Contrast-enhanced MRI revealed an expanding high-grade glioma within the left temporoparietal junction, illustrating the transition from isolated lexical-orthographic breakdown to comprehensive central alexia with agraphia.

9. Measurement & Assessment

Assessing alexia with agraphia requires a structured neurobehavioral examination to evaluate all linguistic channels and differentiate the syndrome from other aphasic or visual disorders. Assessment focuses on oral reading, reading comprehension, writing to dictation, spontaneous writing, written copying, and tactile/auditory letter recognition.

Standardized diagnostic batteries typically employed include:

• The Boston Diagnostic Aphasia Examination (BDAE-3): Contains specialized subtests evaluating reading of letters, regular words, irregular exception words, and pseudowords, along with parallel tasks assessing written mechanics, spelling to dictation, and narrative writing.
• The Western Aphasia Battery-Revised (WAB-R): Provides dedicated reading and writing sections calculating a Reading/Writing Quotient to quantify literacy impairment separate from the overall Aphasia Quotient.
• The Psycholinguistic Assessments of Language Processing in Adult Aphasia (PALPA): A cognitive neuropsychological battery that isolates specific pathways within the dual-route reading and writing architecture. It tests the effects of lexical variables, including word frequency, imageability, grammatical class, regularity, and word length, systematically mapping the patient’s functional impairments.
• Johns Hopkins Dyslexia and Dysgraphia Batteries: Granular diagnostic tools engineered to systematically identify errors such as phonemic paragraphias, semantic substitutions, and letter transpositions across regular, irregular, and non-lexical target items.

To establish a definitive diagnosis of alexia with agraphia, clinicians must exclude several differential diagnoses. The absence of homonymous hemianopia or visual object agnosia must be verified via perimetry testing and object identification tasks. Letter identification via alternative modalities (auditory spelling and tactile skin-tracing) must be administered: intact recognition supports a diagnosis of alexia without agraphia, whereas failure across these non-visual modalities confirms central alexia with agraphia.

10. Applications & Practical Significance

The diagnosis of alexia with agraphia carries critical clinical, functional, and rehabilitation consequences. In modern literate societies, losing the ability to read and write severely compromises functional independence, rendering individuals unable to manage medications, operate digital devices, manage personal finances, read road signs, or maintain professional employment.

In speech-language pathology and neurorehabilitation, identifying central alexia with agraphia requires distinct therapeutic approaches. Rehabilitation cannot rely on shifting reading input to other sensory channels (such as tracing letters or auditory spelling), as these compensatory mechanisms are viable only in pure alexia. Instead, therapy must rebuild core orthographic representations or deploy non-orthographic adaptive strategies:

• Lexical Re-training Approaches: Utilizing Copy and Recall Therapy (CART) to restore a functional sight-word vocabulary. Patients systematically practice writing personally relevant high-frequency words using visual cues, repetitive copying, and delayed recall to re-establish orthographic representations.
• Phonological Treatment Protocols: Training phoneme-to-grapheme and grapheme-to-phoneme conversion routines. Patients use key-word association techniques to re-learn lost graphemic connections, improving their capacity to decode and generate regular orthographic forms.
• Assistive Technology Interventions: Leveraging digital technologies, such as speech-to-text and text-to-speech software, optical character recognition (OCR) readers, and icon-based communication applications. By bypassing written text entirely, these tools allow patients to communicate and consume information using their preserved auditory and oral language faculties.

11. Research & Empirical Evidence

Modern empirical investigations using voxel-based lesion-symptom mapping (VLSM), diffusion tensor tractography, and functional neuroimaging have re-evaluated the classic anatomical model of alexia with agraphia. While Dejerine’s focus on the angular gyrus remains a cornerstone of neurology, contemporary research paints a more nuanced picture of distributed network connectivity.

In landmark VLSM studies led by researchers such as Argyropoulos and colleagues, as well as classic functional investigations by Philip H. Beeson and colleagues, lesions isolated strictly to the cortical gray matter of the angular gyrus were found to produce varying degrees of orthographic impairment. Many patients with classic, enduring alexia with agraphia exhibited lesions extending deeper into the subcortical white matter. These subcortical lesions interrupt the superior longitudinal fasciculus, the arcuate fasciculus, and the inferior fronto-occipital fasciculus, severing functional communication between the temporal auditory systems, the visual word form area (VWFA) in the ventral occipitotemporal cortex, and the frontal motor regions.

Moreover, functional neuroimaging studies of healthy adults reveal that reading and writing recruit a distributed, bilateral network with left-hemisphere dominance. The angular gyrus serves as a polymodal hub that binds semantic concepts to their corresponding orthographic and phonological symbols. Research confirms that when this hub sustains structural damage, neuroplastic reorganization often requires recruitment of the contralateral homologous right angular gyrus and adjacent perilesional tissue. Functional recovery is frequently slower and less complete than recovery from isolated motor speech impairments, highlighting the computational complexity of the human orthographic system.

12. Cultural & Cross-Cultural Considerations

The clinical presentation of alexia with agraphia is heavily influenced by the orthographic depth and structural typology of the language an individual reads and writes. Orthographies vary dramatically in their regularity and visual complexity, altering how neurological lesions manifest clinically:

• Opaque (Deep) vs. Transparent (Shallow) Alphabetic Systems: In transparent orthographies like Spanish, Italian, and Finnish, letter-to-sound correspondences are highly regular and consistent. Patients with central lesions in these language communities may retain functional reading aloud through their preserved phonological processing systems, but demonstrate profound deficits in comprehension and regular writing. Conversely, in deep orthographies like English or French, which contain numerous irregular exception words, central damage produces severe, immediate reading and writing breakdowns across everyday vocabulary.
• Logographic vs. Syllabic Scripts (The Japanese Model): Japanese provides an exceptional cross-linguistic paradigm because it integrates two writing systems: Kanji (morphographic/logographic characters derived from Chinese, conveying meaning directly) and Kana (a phonologically transparent syllabic script). Neuropsychological studies show that lesions of the left angular gyrus can produce double dissociations between these scripts. Patients with angular gyrus lesions frequently exhibit marked impairment in reading and writing Kana (syllabic phonology), while their ability to read and write familiar Kanji (visual-semantic) characters may remain relatively preserved—or, conversely, Kanji can be selectively abolished depending on whether ventral occipitotemporal or posterior parietal pathways are predominantly damaged.
• Literacy Level and Premorbid Education: The functional impact of alexia with agraphia varies with an individual’s premorbid literacy level. In societies or demographics with lower baseline literacy, central orthographic deficits may be missed during superficial clinical examinations unless formal reading and writing evaluations are administered.

13. Criticisms, Debates & Limitations

Despite its long-standing acceptance, the syndrome of alexia with agraphia remains a subject of ongoing theoretical debate within behavioral neurology and cognitive neuropsychology.

The primary controversy centers on the anatomical specificity of the angular gyrus. Several modern researchers dispute Dejerine’s original assertion that the angular gyrus is the sole visual memory repository for words. Lesion studies using modern structural imaging have demonstrated that discrete, isolated lesions limited strictly to the angular gyrus do not always cause enduring, complete alexia with agraphia. Some patients recover reading fluency quickly, leaving only persistent agraphia or Gerstmann syndrome deficits. These findings suggest that the most severe, chronic forms of the syndrome occur when lesions disrupt both the angular gyrus and the surrounding white matter tracts connecting it to the ventral occipitotemporal system and superior temporal regions.

A second major debate concerns whether alexia with agraphia should be categorized as an autonomous syndrome or viewed as an evolving manifestation of a broader aphasic disorder, specifically mild Wernicke’s or transcortical sensory aphasia. Critics point out that patients with alexia with agraphia frequently exhibit subtle semantic, syntactic, or lexical retrieval deficits on sensitive neuropsychological testing, suggesting that the disorder is part of a generalized central linguistic impairment rather than an isolated literacy defect. Proponents counter that the severe, disproportionate collapse of reading and writing alongside fluent, functional conversational speech justifies its status as a distinct clinical entity.

14. Related Terms & Distinctions

Understanding alexia with agraphia requires distinguishing it from other acquired language, reading, and motor disorders:

• Pure Alexia (Alexia without Agraphia): The most critical clinical distinction. Patients with pure alexia cannot read visual text, but their writing abilities are preserved (though they cannot read what they have written). Tactile and auditory letter recognition remain completely intact, and the lesion is typically localized to the left visual cortex and splenium of the corpus callosum, sparing the angular gyrus.
• Pure Agraphia: An isolated writing impairment occurring in the total absence of reading deficits, spoken language disturbances, or motor apraxia. This rare condition is typically caused by focal lesions within the left superior frontal lobe (Exner’s area) or the superior parietal lobule.
• Wernicke’s Aphasia: While patients with Wernicke’s aphasia exhibit severe reading and writing impairments, they also suffer from profound deficits in spoken auditory comprehension, accompanied by paraphasic, neologistic spoken output (jargon aphasia), whereas spoken output and auditory comprehension are largely preserved in classic alexia with agraphia.
• Apraxic Agraphia: A localized motor planning disorder of writing where orthographic knowledge is intact, but the patient cannot execute the motor programs required to form letters with a pen. These individuals spell accurately when using letter tiles, typing, or spelling aloud, unlike individuals with central agraphia.
• Developmental Dyslexia and Dysgraphia: Neurodevelopmental difficulties in acquiring reading and writing skills in the absence of acquired neurological trauma, contrasting directly with the acquired, catastrophic loss seen in alexia with agraphia.

15. Summary / Key Takeaways

Alexia with agraphia is a classical neurobehavioral syndrome characterized by the simultaneous loss of reading and writing capacities resulting from acquired damage to central orthographic processing networks, most characteristically the left angular gyrus (Brodmann area 39). Unlike pure alexia, this condition is a central linguistic disorder that disrupts the internal representations of written language across all sensory modalities, rendering patients unable to read or write via visual, auditory, or tactile channels. Spoken language production and auditory comprehension, however, remain relatively preserved. First identified clinicopathologically by Joseph Jules Dejerine in 1891, the disorder illustrates the brain’s specialized architecture for cultural literacy and serves as an important diagnostic sign of left parietal pathology. Effective management requires comprehensive neuropsychological assessment to differentiate it from peripheral sensory or motor apraxias, followed by structured, interdisciplinary neurorehabilitation using compensatory technologies and targeted cognitive retraining.

References

• Beeson, P. M., & Rapcsak, S. Z. (2003). Clinical diagnosis and treatment of spelling disorders. Topics in Language Disorders, 23(4), 314–328. https://doi.org/10.1097/00011363-200310000-00007
• Binder, J. R., & Desai, R. H. (2011). The neurobiology of semantic memory. Trends in Cognitive Sciences, 15(11), 527–536. https://doi.org/10.1016/j.tics.2011.10.001
• Dejerine, J. (1891). Sur un cas de cécité verbale avec agraphie, suivi d’autopsie. Mémoires de la Société de Biologie, 43, 197–201.
• Geschwind, N. (1965). Disconnexion syndromes in animals and man. Brain, 88(2), 237–294. https://doi.org/10.1093/brain/88.2.237
• Rapcsak, S. Z., & Beeson, P. M. (2004). The role of left posterior inferior temporal cortex in spelling and reading: A neural substrate for the orthographic lexicon. Brain and Language, 89(1), 164–178. https://doi.org/10.1016/S0093-934X(03)00346-6