Agraphia (or dysgraphia) is the term used to describe an acquired impairment of writing. The impairment may result from damage to any of the cognitive, linguistic, or sensorimotor processes that normally support the ability to spell and write. These procedures can be conceptualized within the framework of a cognitive model of language processing such as that shown in Figure 1 (Ellis, 1988; Shallice, 1988; Rapcsak and Beeson, 2000). According to the model, the writing process can be divided into central and peripheral components. The central components are linguistic in nature and are responsible for the retrieval of appropriate words and provision of information about their correct spelling. Peripheral procedures serve to translate spelling knowledge into handwriting, and to guide the motor control for appropriate movements of the hand.

Figure 1..  

A simplified model of single-word writing. Semantic system refers to knowledge of word meanings. Orthographic output lexicon refers to memory store of learned spellings. Phoneme-grapheme conversion is the process of spelling by converting units of sound to corresponding letters. Graphemic buffer denotes a working memory system that temporarily stores orthographic representations while they are being converted into output for handwriting (or typing or oral spelling). Allographic conversion is the process by which abstract orthographic representations are converted into appropriate physical letter shapes. Graphic motor programs are spatiotemporal codes for writing movements that contain information about the sequence, position, direction, and relative size of the strokes necessary to create different letters. Graphic innervatory patterns are motor commands to specific muscle systems specifying the appropriate force, speed, and amplitude of movement. Phonological output lexicon is the memory store of sound patterns for familiar words used in speech production. Phonological buffer is a working memory system for phonological information.

When the system is working normally and an individual wants to write a familiar word, the relevant concepts in the semantic system activate representations in the memory store for learned spellings (i.e., the orthographic output lexicon). Access to this lexicon via the semantic system is referred to as the lexical-semantic spelling route. In contrast, when the individual attempts to spell unfamiliar words or pronounceable nonwords (such as flig), reliance on knowledge of sound-to-letter correspondences allows the assembly of plausible spellings by a process referred to as phoneme-grapheme conversion. This alternative means of spelling is depicted in Figure 1 by the arrow from the phonological buffer (where phonological information is held) to the graphemic buffer (where the assembled spelling is held). Spelling in this manner is considered a nonlexical process, because spellings are not retrieved as whole words from the lexicon. Spellings generated by the lexical-semantic and nonlexical spelling routes are subsequently processed in the graphemic buffer. This buffer serves as an interface between central spelling processes and the peripheral procedures that support the production of handwriting. Peripheral writing procedures are accomplished through a series of hierarchically organized stages that include letter selection (referred to as allographic conversion), motor programming, and the generation of graphic innervatory patterns.

Clinical assessment of spelling and writing provides an understanding of the nature and degree of impairment to specific processes as well as the availability of residual abilities (Kay, Lesser, and Coltheart, 1992; Beeson and Hillis, 2001; Beeson and Rapcsak, 2002). Damage to specific components of the spelling process may result in identifiable agraphia syndromes with relatively predictable lesion sites (Roeltgen, 1993, 1994; Rapcsak and Beeson, 2000, 2002). Central agraphia syndromes reflect damage to the lexical-semantic or nonlexical spelling routes, or the graphemic buffer, and result in similar impairments across different modalities of output (e.g., written spelling, oral spelling, typing). Central agraphia syndromes include lexical agraphia, phonological agraphia, deep agraphia, and graphemic buffer agraphia. Peripheral agraphia syndromes reflect damage to writing processes that are distal to the graphemic buffer. Dysfunction primarily affects the selection or production of letters in handwriting. These syndromes include allographic disorders, apraxic agraphia, and nonapraxic disorders of neuromuscular execution (Roeltgen, 1993; Rapcsak, 1997; Rapcsak and Beeson, 2000). An individual may have impairment to multiple components of the writing process so that the agraphia profile does not conform to a recognized syndrome.

Lexical agraphia (also called surface agraphia) is a central agraphia syndrome that results from damage to the lexical-semantic spelling route. It is characterized by the loss or unavailability of orthographic knowledge, so that spelling is accomplished by phoneme-grapheme conversion and words are spelled as they sound. Spelling accuracy is strongly influenced by orthographic regularity in that regular words (e.g., bake) and nonwords are spelled correctly, but attempts to spell words with irregular sound-to-spelling relationships result in phonologically plausible errors (e.g., cough—coff). Low-frequency, irregular words are especially vulnerable to error. In addition, if the semantic influence on spelling is impaired, there is difficulty writing homophonic words that cannot be spelled correctly without reference to meaning (e.g., dear—deer). Lexical agraphia is typically seen following damage to left extrasylvian temporoparietal regions. The syndrome has also been described in patients with Alzheimer's disease and in semantic dementia.

Phonological agraphia and deep agraphia are central agraphia syndromes attributable to dysfunction of the nonlexical spelling route. In both syndromes, spelling is accomplished primarily via a lexical-semantic strategy, and individuals have difficulty using phoneme-grapheme conversion to spell unfamiliar words or nonwords. In phonological agraphia, the spelling of familiar words, both regular and irregular, may be relatively spared; however, in deep agraphia, there is concomitant impairment of the lexical-semantic spelling route, so that semantic errors are prevalent (e.g., boy—girl). In both syndromes, spelling accuracy is better for highly frequent, concrete words (e.g., house) than for low-frequency, abstract words (e.g., honor). There is also an influence of grammatical word class in that nouns are easier to spell than function words such as prepositions, pronouns, and articles. Other spelling errors may include morphological errors (talked—talking) and functor substitutions (as—with). As in any of the central agraphia syndromes, patients may recall only some of the letters of the target word, reflecting partial orthographic knowledge. Phonological and deep agraphia are associated with damage to the perisylvian language areas, including Broca's area, Wernicke's area, and the supramarginal gyrus. Deep agraphia in patients with extensive left hemisphere lesions may reflect reliance on the right hemisphere for writing (Rapcsak, Beeson, and Rubens, 1991).

Graphemic buffer agraphia reflects impairment of the ability to retain orthographic representations in short-term memory as the appropriate graphic motor programs are selected and implemented. Damage to the graphemic buffer leads to abnormally rapid decay of information relevant to the order and identity of stored graphemes. Spelling accuracy is notably affected by word length because each additional grapheme increases the demand on limited storage capacity. In contrast to other central agraphia syndromes, spelling in graphemic buffer agraphia is not significantly influenced by lexical status (words versus nonwords), lexical-semantic features (frequency, concreteness, grammatical class), or orthographic regularity. Characteristic spelling errors include letter substitutions, additions, deletions, and transpositions (e.g., garden—garned). These errors are observed in all spelling tasks and across all modalities of output (writing, oral spelling, typing). Lesion sites in patients with graphemic buffer agraphia have been variable, but left parietal and frontal cortical involvement is common.

Allographic disorders are peripheral writing impairments that reflect the breakdown of procedures by which orthographic representations are mapped to letter-specific graphic motor programs. Allographic disorders are characterized by an inability to activate or select appropriate letter shapes, whereas oral spelling is preserved. Patients may have difficulty that is specific to writing upper-or lowercase letters, or they may produce case-mixing errors (e.g., pApeR). Other patients produce well-formed letter substitution errors that bear physical similarity to the target. Allographic disorders are usually associated with damage to the left parieto-occipital region.

Apraxia agraphia is a peripheral writing impairment caused by damage to graphic motor programs, or it may reflect an inability to translate information contained in these programs into specific motor commands. Apraxic agraphia is characterized by poor letter formation that cannot be attributed to sensorimotor impairment (i.e., weakness, deafferentation) or damage to the basal ganglia (i.e., tremor, rigidity) or cerebellum (i.e., ataxia, dysmetria). Typical errors of letter morphology include spatial distortions and stroke omissions or additions, which may result in illegible handwriting. Spelling by other modalities (e.g., oral spelling) is typically spared. In right-handers, apraxic agraphia is associated with damage to a left hemisphere cortical network dedicated to the motor programming of handwriting movements. The major functional components of this neural network include posterior-superior parietal cortex (including the region of the intraparietal sulcus), dorsolateral premotor cortex, and the supplementary motor area (SMA). Callosal lesions in right-handers may be accompanied by unilateral apraxic agraphia of the left hand.

Writing disorders attributable to impaired neuromuscular execution are caused by damage to motor systems involved in generating graphic innervatory patterns. Poor motor control results in defective control of writing force, speed, and amplitude. Such writing disorders reflect the specific underlying disease or locus of damage. In the case of Parkinson's disease, micrographia results from reduced force and amplitude of movements of the hand. In patients with cerebellar dysfunction, movements of the pen may be disjointed and erratic. Breakdown of graphomotor control in these neurological conditions suggests that the basal ganglia and the cerebellum, working in concert with dorsolateral premotor cortex and the SMA, are critically involved in the selection and implementation of kinematic parameters for writing movements. Obviously, patients with hemiparesis often have weakness and spasticity of the hand and limb that markedly impairs their ability to write with the preferred hand.

Behavioral treatments for agraphia may target central or peripheral components of the writing process (Behrmann and Byng, 1992; Carlomagno, Iavarone, and Colombo, 1994; Hillis and Caramazza, 1994; Patterson, 1994; Beeson and Hillis, 2001; Beeson and Rapcsak, 2002). Treatments for central agraphias may be directed toward the lexical-semantic or nonlexical spelling procedures. In contrast, treatments for peripheral agraphias are designed to improve the selection and implementation of graphic motor programs for writing. In general, agraphia treatments are designed to strengthen damaged processes and take advantage of residual abilities.

See also alexia; phonological analysis of language disorders in aphasia; phonology and adult aphasia.