Agraphia

Abstract

Agraphia is an acquired loss of the ability to write, caused by brain damage rather than any weakness of the hand. Medical Subject Headings classifies it under Specific Learning Disorder and, more broadly, among the Language Disorders, reflecting its dual life as an acquired neurological syndrome and a developmental condition. Because writing is a chain of processes — retrieving a word’s spelling, holding its ordered letters in mind, and shaping each into movement — it can break at many points, and each break produces a different clinical picture. This article treats agraphia as a window onto the cognitive architecture of spelling: the two spelling routes, the short-term graphemic buffer that holds a letter string during output, and the perceptual-motor stages that render it. Three interactive demonstrations trace writing from spelling route to lesion site.

Keywords: agraphia, dysgraphia, spelling, graphemic buffer, lexical and phonological routes

Writing is among the most recently acquired of human abilities, culturally invented rather than biologically given, and it is assembled in each individual from parts that evolved for other purposes — spoken language, visual object recognition, and skilled movement. That assembled quality is exactly what makes writing so informative when it fails. A stroke, a degenerative disease, or an atypical developmental trajectory rarely abolishes writing wholesale; far more often it removes one component and spares the rest, so that a person may write real words but not invented ones, or spell aloud perfectly yet form illegible letters (Roeltgen & Heilman, 1984). The pattern of what is lost and what is kept is a natural experiment on the structure of the writing system.

The term agraphia denotes an acquired impairment of writing due to brain injury; dysgraphia is used both for the developmental failure of writing to emerge normally in childhood and, in much of the literature, interchangeably with agraphia for the acquired forms (McCloskey & Rapp, 2017). Either way, the object of study is the same: the mental machinery that converts a meaning into an ordered string of letters and then into marks on a page. Cognitive neuropsychology has used the dissociations of agraphia to reverse-engineer that machinery in some detail, and the resulting model — two spelling routes feeding a common short-term buffer, which in turn feeds the peripheral processes of letter shape and hand movement — is one of the field’s more complete accounts of a complex skill.

What Agraphia Is

Agraphia is the loss or degradation of writing ability resulting from neurological damage, in a person who had learned to write and whose hand and arm remain mechanically capable of the movements (Roeltgen & Heilman, 1984). The qualification matters: an inability to write because of a paralysed or tremulous hand is not agraphia, because the deficit is in the effector, not in the mental processes that specify what to write. True agraphia is a disorder of the central and perceptual-motor operations of spelling and letter production, and it can occur with the writing hand entirely intact — a patient may be unable to write a word to dictation with the right hand yet unable to do so with the left either, or unable to spell the word with letter tiles, showing that the problem lies upstream of any particular limb.

It is essential to separate agraphia from the disorders it commonly accompanies. Writing frequently fails alongside reading, because the two share the orthographic knowledge stored in the brain; the acquired reading disorder is alexia, and the two often co-occur, as in the classical syndrome of *alexia with agraphia*. Writing also fails alongside speaking in most aphasias, since a disturbance of language will usually disturb its written as well as its spoken expression. But agraphia can also occur in relative isolation — pure agraphia, a disproportionate loss of writing with reading and speech comparatively spared — and it is these purer cases, together with the selective dissociations within writing, that have been most revealing about the architecture of the spelling system (Rapcsak et al., 2009).

The systematic study of agraphia begins in the late nineteenth century with the French-Swiss neurologist Joseph Jules Dejerine, who localised acquired reading and writing loss to the left parietal region and its junction with the occipital and temporal lobes, founding the clinical neurology of written language. Modern cognitive neuropsychology inherited that clinical tradition but reframed the question: rather than asking only *where* the lesion sits, it asks *which processing component* has been removed, and reads the answer from the precise pattern of preserved and impaired writing.

The Two Routes to Spelling

The central discovery of the cognitive study of writing is that there are two independent ways to produce a spelling, and that brain damage can knock out one while sparing the other. The first is the lexical route: for a word the writer already knows, its spelling is stored as a whole entry in an *orthographic long-term memory* — a mental lexicon of known letter strings — and writing the word is a matter of retrieving that entry. The second is the phonological route (also called the sublexical or sound-to-spelling route): for a word the writer does *not* know, or an invented nonword, a plausible spelling can be assembled by converting the word’s sounds into their most probable letters, using learned regularities of the language’s sound-to-spelling correspondences (Roeltgen & Heilman, 1984).

In a language such as English, whose spelling is only partly regular, the two routes make different predictions and can be pried apart by the right words. Consider an irregular word such as *yacht*: it cannot be spelled correctly by sounding it out — a phonological assembly would yield something like *yot* — so it requires the stored lexical entry. Now consider an invented nonword such as *blorp*: it has no lexical entry, so it can only be spelled by the phonological route. A writer who can spell *blorp* but not *yacht* has a working phonological route and a damaged lexical one; a writer who can spell *yacht* but not *blorp* has the opposite. These two mirror-image syndromes are exactly what the clinic finds.

Lexical (or surface) agraphia is the loss of the lexical route. Because the writer must now fall back on phonological assembly, regular words and nonwords are spelled well, but irregular words are spelled as if they were regular — *yacht* becomes *yot*, *island* becomes *iland* — producing phonologically plausible errors (Roeltgen & Heilman, 1984). Phonological agraphia is the reverse: the phonological route is lost, so familiar words of any spelling regularity are written well from their stored entries, but the writer cannot assemble a spelling for an unfamiliar word or a nonword, because the sound-to-letter mechanism is gone (Rapcsak et al., 2009). The double dissociation — each ability lost while the other is spared, in different patients — is the strongest kind of evidence that the two routes are genuinely separate mechanisms rather than two ends of a single process.

The Graphemic Buffer

Whichever route supplies a spelling, the result is an ordered sequence of abstract letter identities — *graphemes* — that must be held in mind while they are written or spelled out one at a time. Writing even a short word takes seconds, far longer than the sequence can be produced in a single instant, so the system needs a short-term store to keep the letters and their order available during output. This store is the graphemic buffer, and its existence was demonstrated by Alfonso Caramazza and colleagues in a landmark 1987 single-case study of a patient whose writing showed a very particular signature (Caramazza, Miceli, Villa, & Romani, 1987).

The signature has two parts. First, a length effect: the patient’s error rate rose steeply with the number of letters in the word, because a longer string must be held in the buffer longer and has more positions to lose. Second, a characteristic serial-position curve: errors were not spread evenly but concentrated in the *middle* of the word, with the first and last letters best preserved — a bow-shaped distribution that is the fingerprint of a decaying ordered store rather than of a failure to retrieve the spelling in the first place. Crucially, this pattern appeared for regular words, irregular words, and nonwords alike, and in writing, oral spelling, and typing — showing that the damaged component sits *after* both spelling routes have done their work and is shared by every form of output. That route-independence is what makes the buffer a distinct processing stage rather than a part of either route (Caramazza et al., 1987).

The errors themselves are informative: they are substitutions, deletions, insertions, and transpositions of individual letters (*graphemic buffer* damage yields *graphmeic* or *grahemic*), not phonologically plausible whole-word errors. The letters are the right ones for the word; it is their identity-in-position that decays. Contemporary work has mapped this orthographic working memory onto its own neural substrate, distinct from the orthographic *long-term* memory that stores the spellings themselves, showing that the storage of a known spelling and the momentary holding of that spelling during output are dissociable both cognitively and in the brain (Rapp, Purcell, Hillis, Capasso, & Miceli, 2016).

Central and Peripheral Agraphias

The lexical route, the phonological route, and the graphemic buffer are the central components of spelling — they specify *which letters, in which order*. Downstream of the buffer lie the peripheral components, which specify *how each letter is physically produced*: selecting the particular shape of the letter (its case and style, its *allograph*), programming the sequence of strokes, and driving the hand. Agraphias divide cleanly into central and peripheral kinds, and a large meta-analysis of the neuroimaging of written word production confirms that these two families recruit partly separate brain networks (Purcell, Turkeltaub, Eden, & Rapp, 2011).

The central agraphias are the route and buffer disorders already described — lexical, phonological, and graphemic buffer agraphia — plus deep agraphia, a severe form in which the phonological route is lost and the damaged lexical route produces *semantic errors* in writing, such as writing *chair* for *table*. Their common feature is that the error is in the spelling itself, and it appears whatever the output modality: a patient with a central agraphia will make the same errors writing by hand, spelling aloud, and arranging letter tiles, because the fault lies in the abstract letter string, not its physical rendering. Rarer still is ideational agraphia, in which single words can still be spelled to dictation but the capacity to compose connected written language breaks down, pointing to a disturbance above the level of the spelling routes themselves (Baxter & Warrington, 1986).

The peripheral agraphias leave the abstract spelling intact but corrupt its execution. In apraxic agraphia, the writer knows the correct letters — and can often spell the word aloud or select it from tiles perfectly — but cannot form the letter shapes, producing malformed, illegible script from a loss of the learned motor programs for writing (Roux et al., 2009). In allographic agraphia, the fault is in selecting the right letter form: a patient may mix upper- and lower-case letters, or substitute one well-formed letter for another, while the underlying spelling is correct. Table 1 sets out the principal subtypes and their signatures.

Table 1

Principal Subtypes of Agraphia and Their Signatures

The Neural Bases of Writing

Because writing recruits vision, language, and skilled movement, its neural substrate is distributed across several left-hemisphere regions, each aligned with one stage of the model. Orthographic long-term memory — the store of known spellings — depends on the left fusiform gyrus in the ventral occipitotemporal cortex, the same region implicated in visual word recognition. Kyriaki Tsapkini and Brenda Rapp showed that damage here impairs the orthography-specific functions of the region, and that its role is specific to written language rather than a general visual or semantic function (Tsapkini & Rapp, 2010). The graphemic buffer and orthographic working memory, by contrast, depend more on parietal and frontal regions, and lesion-mapping in dysgraphic patients has begun to separate the neural bases of orthographic long-term memory from those of orthographic working memory (Rapp et al., 2016).

The peripheral, motor side of writing has its own dedicated cortex. In 1881 the neurologist Sigmund Exner proposed a “writing centre” in the posterior middle frontal gyrus, and although the idea was long disputed, direct cortical stimulation during awake neurosurgery has confirmed a graphemic/motor frontal area — Exner’s area revisited — whose stimulation disrupts writing while sparing other movements and language (Roux et al., 2009). Converging meta-analyses of neuroimaging localise the handwriting network to this frontal region together with the superior parietal lobule and the cerebellum, distinguishing the specifically *graphomotor* processes from the more central *orthographic* ones (Planton, Jucla, Roux, & Démonet, 2013). More recent functional imaging has asked how *specialised* these writing regions really are, finding that some respond during drawing and oral spelling as well as handwriting, so the network is partly, but not wholly, writing-specific (Planton, Longcamp, Péran, Démonet, & Jucla, 2017).

A striking demonstration of how focal these substrates can be comes from the frontal lobe. Steven Anderson, Antonio Damasio, and Hanna Damasio described a patient with damage to the left frontal cortex who was selectively impaired at writing *letters* while remaining able to write *numbers* — “troubled letters but not numbers” — a domain-specific dissociation that would be inexplicable if writing were a single undifferentiated skill (Anderson, Damasio, & Damasio, 1990). Findings like this are the neural counterpart of the cognitive dissociations: they show that the components the model proposes are not merely convenient abstractions but are separately localisable in the brain.

Worked Example

The single most diagnostic quantitative signature in agraphia is the length effect produced by damage to the graphemic buffer, and it follows directly from what the buffer does. Suppose the buffer holds each letter of a word in an ordered slot, and that damage gives each occupied slot some fixed, independent probability of surviving intact until it is written out. Call that per-letter survival probability $p$. Because a word is spelled correctly only if *every* one of its letters survives, the probability of writing an $n$-letter word correctly is

$$P(\text{correct}) = p^{\,n},$$

and the expected error rate is $1 - p^{\,n}$. The error rate therefore does not rise linearly with length but accelerates, because each additional letter multiplies in another chance of failure.

Take a plausible per-letter survival of $p = 0.90$ — a buffer that keeps any given letter nine times in ten. The model then predicts the error rates in Table 2. A three-letter word is misspelled about a quarter of the time; an eight-letter word more than half the time. This steep, curved rise with length — flat for the shortest words, climbing sharply for the longest — is exactly the pattern Caramazza and colleagues found, and it distinguishes a buffer disorder from a lexical-retrieval one, where error rate depends on a word’s familiarity and regularity rather than on its raw length (Caramazza et al., 1987).

Table 2

Predicted Spelling Error Rate by Word Length, Graphemic Buffer Model (per-letter survival p = 0.90)

The second half of the signature — *where* in the word the errors fall — is not captured by this simplest model, which treats every position alike. In real graphemic-buffer patients the surviving probability is not flat across positions but bowed: the first and last letters of a word are the most robust and the middle letters the most vulnerable, giving the characteristic inverted-U of errors by position. The interactive demonstration below varies both the per-letter survival and the word length, so that the two halves of the signature — the accelerating length effect and the mid-word concentration of errors — emerge together.

Assessment and Treatment

Because agraphia is not one disorder but a family of component failures, both assessment and treatment are organised around *identifying which component is broken* and addressing that component specifically. Assessment contrasts writing across carefully chosen word types — regular words, irregular words, and nonwords — and across output modes — handwriting, oral spelling, typing, and letter-tile arrangement — because it is the *pattern* across these conditions, not the overall error rate, that localises the deficit. A patient who fails irregular words but not nonwords has a lexical-route problem; one who fails handwriting but spells aloud perfectly has a peripheral, graphomotor one.

Treatment follows the same logic. Pelagie Beeson showed that a patient with a degraded orthographic lexicon can be helped by systematically strengthening the graphemic representations of a targeted set of functionally important words, through repeated copy-and-recall practice that rebuilds the stored spellings (Beeson, 1999). For patients whose phonological route is the weak link, a different, staged approach rebuilds sound-to-spelling correspondences: Pelagie Beeson, Kindle Rising, Esther Kim, and Steven Rapcsak developed a treatment sequence for phonological alexia and agraphia that reteaches letter-sound relationships and then trains the patient to use them to build and check spellings, with gains that transfer to untrained words (Beeson, Rising, Kim, & Rapcsak, 2010). The matching of a specific treatment to a specific broken component is the clinical payoff of the cognitive model: the same overall symptom — poor writing — calls for opposite therapies depending on which route or store has failed.

Discussion

Agraphia occupies a special place in cognitive neuropsychology because writing is a *constructed* skill whose parts are unusually visible when they come apart. Where a more evolutionarily basic ability might fail as a whole, writing fails in pieces, and each piece — the lexical route, the phonological route, the graphemic buffer, the graphomotor programs — announces itself through a distinct and replicable pattern of spared and impaired performance. The double dissociations between these patterns are the classic evidence for a modular architecture: if lexical and phonological spelling can each be lost while the other survives, they cannot be two aspects of one undifferentiated process (Roeltgen & Heilman, 1984).

The model also illustrates a deep point about the relationship between reading and writing. The two share the orthographic knowledge in the fusiform gyrus, which is why alexia and agraphia so often co-occur, yet they are not simply the same competence run in two directions: patients exist who read far better than they write, or the reverse, so the shared store feeds partly separate input and output processes (Tsapkini & Rapp, 2010). The graphemic buffer makes a similar point within writing itself, dissociating the *long-term* storage of a spelling from its *momentary* maintenance during output — two functions that intuition would fuse but that damage cleanly separates (Rapp et al., 2016).

Cognitive Implications

Beyond the clinic, the study of agraphia has shaped how cognitive science thinks about skilled sequential behaviour in general. The graphemic buffer is a concrete, well-specified example of an *output buffer* — a short-term store that holds an ordered plan while it is executed piece by piece — and its length effect and bowed serial-position curve are properties that any such buffer, whether for spelling, speaking, or typing, might be expected to show. The buffer thus connects the specific problem of spelling to the general problem of how the mind holds and unspools ordered sequences, a problem that runs through working memory and the phonological loop as much as through writing.

The two-route structure of spelling, too, is an instance of a recurring motif in cognition: the coexistence of a fast, memory-based path for the familiar and a slower, rule-based path for the novel. The same dual-route logic organises the cognitive account of reading, where lexical and sublexical routes explain the analogous dissociations of the acquired dyslexias, and the parallel between the two is not accidental — reading and writing draw on a common orthographic system and exhibit mirror-image breakdowns (Rapcsak et al., 2009). Agraphia, in this light, is not a narrow clinical curiosity but a particularly legible case of how the mind builds a complex skill from separable, individually vulnerable parts.

Current Directions

Current research on agraphia and dysgraphia is moving on several fronts. One is the sharpening of the neural map of the spelling system: lesion-symptom mapping and functional imaging are increasingly able to separate the substrate of orthographic long-term memory from that of orthographic working memory, and to ask how writing-specific each node of the network really is, rather than treating “the writing centre” as a single place (Rapp et al., 2016); (Planton et al., 2017). The answer emerging is that writing borrows heavily from regions shared with drawing, reading, and general motor control, with only a few nodes doing genuinely writing-specific work.

A second front is developmental dysgraphia, which has historically lagged behind its acquired counterpart. Michael McCloskey and Brenda Rapp have argued that the mature cognitive model of spelling can and should be applied to children whose writing fails to develop normally, providing a framework in which developmental dysgraphia is analysed, like the acquired forms, in terms of *which component* has failed to mature (McCloskey & Rapp, 2017). A related question is the relationship between developmental dysgraphia and developmental dyslexia — whether the reading and spelling difficulties of childhood share a common cause or are partly independent — which remains actively debated (Döhla & Heim, 2016). A third front is treatment: building on the component-specific therapies above, current work asks how to maximise *generalisation* from trained to untrained words and how to match a given patient’s deficit profile to the therapy most likely to help (Beeson et al., 2010).

Common Misconceptions

Agraphia just means bad handwriting.

No. Agraphia is a loss of the mental processes of spelling and writing, not of penmanship. Many people with agraphia have perfectly capable hands; some spell aloud or with letter tiles no better than they write, showing the deficit is central, not motor. Poor letter formation is only one, peripheral, form of the disorder (Roux et al., 2009).

Agraphia is simply the writing side of aphasia.

Not necessarily. Writing does fail in most aphasias, but agraphia can occur in relative isolation, with speech and even reading comparatively spared, and its internal pattern can dissociate from the spoken-language deficit. Pure agraphia is precisely a writing loss that is not reducible to the aphasia (Rapcsak et al., 2009).

There is one kind of agraphia.

No. Agraphia is a family of dissociable disorders — lexical, phonological, deep, graphemic-buffer, apraxic, and allographic — each reflecting a different broken component of the spelling system, and each with its own signature and its own indicated treatment (Caramazza et al., 1987).

Someone who spells irregular words wrong just never learned them.

Not in acquired lexical agraphia. These patients could once spell the words and now cannot, falling back on phonological assembly and producing plausible misspellings (yacht → yot). The knowledge was lost through brain damage to the lexical route, not never acquired (Roeltgen & Heilman, 1984).

Glossary

Agraphia.

An acquired loss or impairment of writing caused by brain damage, in a person whose hand remains mechanically capable of the movements.

Alexia.

An acquired loss of reading from brain damage; frequently co-occurs with agraphia because the two share stored orthographic knowledge.

Allographic agraphia.

A peripheral agraphia in which the correct letter shape cannot be selected, producing case mixing or letter substitutions while the spelling itself is intact.

Apraxic agraphia.

A peripheral agraphia in which the learned motor programs for forming letters are lost, yielding illegible writing despite intact knowledge of the spelling.

Deep agraphia.

A severe central agraphia combining loss of the phonological route with semantic errors in writing, such as writing chair for table.

Dysgraphia.

A writing disorder; used for the developmental failure of writing to emerge normally and, in much of the literature, interchangeably with acquired agraphia.

Exner’s area.

A region of the posterior middle frontal gyrus, the graphemic/motor frontal area, whose stimulation selectively disrupts handwriting.

Grapheme.

An abstract letter identity, independent of its physical shape, that is the unit stored and manipulated by the central spelling system.

Graphemic buffer.

A short-term store that holds the ordered letters of a word during writing; its damage produces a length effect and mid-word errors across all word types.

Length effect.

The steep, accelerating rise in spelling error rate with the number of letters in a word, the signature of graphemic buffer damage.

Lexical (surface) agraphia.

Loss of the lexical route, so irregular words are misspelled by phonological assembly (yacht → yot) while nonwords are spared.

Lexical route.

The spelling pathway that retrieves a familiar word’s whole stored spelling from orthographic long-term memory.

Orthographic long-term memory.

The mental lexicon of known word spellings, drawn on by the lexical route and dependent on the left fusiform gyrus.

Phonological agraphia.

Loss of the phonological route, so unfamiliar words and nonwords cannot be spelled while familiar real words are written from their stored entries.

Phonological route.

The spelling pathway that assembles a plausible spelling from a word’s sound using learned sound-to-letter correspondences; also called the sublexical route.

Pure agraphia.

A disproportionate loss of writing with reading and speech comparatively spared; historically central to isolating the writing system.

Serial-position curve.

The bow-shaped distribution of errors across letter positions — first and last letters best preserved, middle letters worst — typical of graphemic buffer damage.

Key Researchers

Pelagie M. Beeson

Professor of Speech, Language, and Hearing Sciences at the University of Arizona, whose research established evidence-based, component-specific treatments for acquired agraphia, from strengthening graphemic representations to a staged sequence for phonological alexia and agraphia. ORCID - Google Scholar

Alfonso Caramazza

Professor of Psychology at Harvard University, whose 1987 single-case study of a patient with a selective length-and-position error pattern demonstrated the graphemic buffer as a distinct working-memory stage in spelling. ORCID - Google Scholar - Faculty Page

Joseph Jules Dejerine

(1849–1917). French-Swiss neurologist at the Salpêtrière whose studies of alexia and agraphia in the 1890s first localised acquired reading and writing loss to the left parietal cortex, founding the clinical neurology of written language. Wikipedia - Wikidata

Kenneth M. Heilman

(1938–2024). Behavioral neurologist at the University of Florida who, with David Roeltgen, distinguished lexical from phonological agraphia, grounding the two-route model of spelling in dissociable lesion syndromes. Wikipedia - Google Scholar

Argye E. Hillis

Professor of Neurology at the Johns Hopkins University School of Medicine, a leader in lesion-symptom mapping of written- and spoken-language deficits and co-author on the neural bases of orthographic memory in dysgraphia. ORCID

Steven Z. Rapcsak

Professor of Neurology at the University of Arizona, whose work established the cognitive mechanisms and neural substrates of phonological dyslexia and dysgraphia and their shared reliance on phonological processing. ORCID - Faculty Page

Brenda Rapp

Professor of Cognitive Science at Johns Hopkins University, whose research anchors the modern cognitive and neural model of spelling — the dissociation of orthographic long-term from working memory, and a framework for developmental dysgraphia. ORCID - Google Scholar - Faculty Page

Frequently Asked Questions

What exactly is agraphia?

Agraphia is a loss or impairment of the ability to write that results from brain damage, in a person who had learned to write and whose hand is still mechanically able to move. It is a disorder of the mental processes of spelling and letter production, not of the muscles, so it can occur with a perfectly capable hand.

How is agraphia different from dysgraphia?

The terms overlap. Agraphia usually refers to an acquired loss of writing after brain injury in someone who could previously write; dysgraphia usually refers to a developmental difficulty in which writing never develops normally in childhood, though many authors use the two words interchangeably for the acquired forms.

Why can some people write real words but not made-up ones?

Because spelling can be reached by two routes. Familiar words can be retrieved whole from a mental store of known spellings, while unfamiliar words and nonwords must be assembled from their sounds. If the sound-to-spelling route is damaged (phonological agraphia), real words survive but invented ones cannot be spelled.

Why do longer words cause more errors in some patients?

This is the signature of damage to the graphemic buffer, the short-term store that holds a word’s ordered letters while they are written. A longer word must be held longer and has more letter positions to lose, so the error rate climbs steeply with length, and errors bunch in the middle of the word.

Can someone have agraphia but still read normally?

Yes, though reading and writing often fail together because they share stored knowledge of spellings. Some patients read far better than they write, or the reverse, which shows that the shared orthographic store feeds partly separate processes for recognising and producing written words.

Is agraphia the same as aphasia?

No. Aphasia is a disorder of language that usually affects writing along with speech, but agraphia can occur in relative isolation, with speech and even reading comparatively spared, and its internal pattern can differ from the spoken-language impairment. Pure agraphia is a writing loss not reducible to aphasia.

Can agraphia be treated?

Yes. Treatment is targeted at the specific broken component identified by assessment. A degraded store of spellings can be rebuilt by focused copy-and-recall practice on important words; a failed sound-to-spelling route can be addressed by a staged programme that reteaches letter-sound relationships, with gains that can transfer to untrained words.

What part of the brain is damaged in agraphia?

It depends on the type. Loss of stored spellings involves the left fusiform gyrus; the short-term letter buffer involves parietal and frontal regions; and the motor production of letters involves a frontal “writing area” (Exner’s area) with the superior parietal lobule and cerebellum. Different lesions produce different agraphias.

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