Writing is a system of communication in which conventional graphic signs are used to represent various elements of spoken language (i.e., words, syllables, or phonemes). In its fully developed form, writing is probably no more than 6000 years old—a relatively recent achievement in human evolution. The neuropsychological study of writing has an even shorter history that begins with the work of nineteenth-century European neurologists. These early investigators noted that although spoken and written expression were both frequently impaired following damage to the language-dominant hemisphere, disorders of writing, or agraphia, occasionally occurred

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in isolation. This important clinical observation led to the proposal that speech and writing may have distinct neuroanatomic substrates. The potential independence of writing from speech was cogently argued by William Ogle in a landmark paper published in 1867 which also included the first classification system of agraphia. Specifically, Ogle described a type of linguistic agraphia in which patients produced well-formed letters but spelling was inaccurate or one word was substituted for another. He also noted that in other patients, agraphia was characterized by defective motor execution resulting in poorly formed letters that were frequently unrecognizable. Although Ogle's views about the relationship between speech and writing drew criticism from many of his contemporaries, the proposed clinical distinction between linguistic and motor forms of agraphia was generally accepted.

Ogle's pioneering observations were soon followed by attempts to localize the brain areas involved in writing and to clarify their anatomical and functional interactions with the cortical speech centers identified by Broca and Wernicke (Fig. 1). These efforts, spearheaded by the so-called "diagram makers,'' culmi nated in neuroanatomical models that postulated two distinct cortical centers for writing. Following Dejer-ine's suggestion, orthographic information relevant to the correct spelling of words was believed to be stored in the dominant angular gyrus in the form of "optic word images.'' In contrast, the "motor graphic images'' responsible for controlling the execution of writing movements were localized to a premotor cortical area at the foot of the second frontal convolution, sometimes referred to as Exner's writing center. The act of writing presumably required the coordinated activity of the putative parietal and frontal cortical centers.

In addition to these anatomical considerations, the diagram makers also engaged in lively debates about the nature of the linguistic codes or representations used in writing. A central and often controversial topic concerned the role of phonology. The fact that writing is acquired relatively late in linguistic development, after oral language functions are firmly established, suggested to many that written expression was parasitic upon speech and that it involved obligatory phonological mediation. Consistent with this view, simple introspection reveals that writing is normally

Centro Cortical Exner

Figure 1 Cortical areas involved in speech and writing. B, Broca's area; W, Wernicke's area; E, Exner's writing center; AG, angular gyrus; PTC, posterior temporal cortex; SMG, supramarginal gyrus; SPL, superior parietal lobule [reproduced with permission from Nolte, J. (1998). The Human Brain: An Introduction to Its Functional Anatomy. Mosby, St. Louis, Missouri].

Figure 1 Cortical areas involved in speech and writing. B, Broca's area; W, Wernicke's area; E, Exner's writing center; AG, angular gyrus; PTC, posterior temporal cortex; SMG, supramarginal gyrus; SPL, superior parietal lobule [reproduced with permission from Nolte, J. (1998). The Human Brain: An Introduction to Its Functional Anatomy. Mosby, St. Louis, Missouri].

accompanied by "inner speech.'' Phonological theories of writing took two distinct forms. Some investigators explicitly denied the existence of word-specific orthographic representations and proposed that writing entailed segmenting spoken words into their constituent sounds, followed by the conversion of each sound into the appropriate letter (i.e., phonemegrapheme conversion). As we shall see, this hypothesis is falsified by patients who lose the ability to perform phoneme-grapheme conversion but who can nonetheless spell familiar words accurately. Another version of the phonological theory of writing allowed for the possibility of stored orthographic representations for familiar words but maintained that these representations could only be activated indirectly via the spoken form of the word. The problem with this proposal is the clinical observation that in some aphasic patients written expression is superior to or is qualitatively different from speech production. These findings demonstrate that access to orthography is possible even when the corresponding phonological representation of the word is unavailable and further suggest that lexical representations for written and spoken words are neuroanatomically distinct. Note, however, that although the neuropsychological evidence is clearly at odds with the view that writing involves obligatory phonological mediation, it need not imply that phonology plays no role in writing under normal circumstances.

Although the fundamental questions raised by nineteenth-century investigators about the neural substrates and linguistic mechanisms of writing are still relevant today, contemporary work on agraphia has also been strongly influenced by cognitive models of language processing. The cognitive method of analysis relies on an information processing approach and seeks to understand complex language skills by decomposing them into several potentially independent processing components with distinct functional roles. In order to interpret the performance of neurological patients within this type of a theoretical framework, it is necessary to make the additional assumption that the proposed processing modules are also neuroanatomically distinct and can therefore be selectively impaired by brain damage. Following this line of reasoning, we begin our discussion of agraphia by presenting a cognitive model of normal spelling and writing. Next, we describe the clinical characteristics and neuroanatomical correlates of various agraphia syndromes and attempt an explanation of abnormal writing performance in terms of damage to different functional components of the model.

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