El concepto de aprendizaje

Writing, due its complexity, is easily affected after brain lesions. Such disorders o f writing are called agraphias or dysgraphias. The term agraphia was first used by Benedick in 1865, but Ogle (1867) was one o f the first to describe the issues o f localization o f agraphia after his observations that aphasia and agraphia usually occur together. The first classification o f agraphias was by Nielsen (1946), when he proposed that agraphia can present in isolation without any other associated signs. However, this type o f agraphia is rare (Roeltegen, 1994). In the last decades two different approaches to classification o f written language disorders have been proposed, the neurological and the

neuropsychological. The neurological classification views agraphia as a syndrome with a cluster o f symptoms. Whereas in the neuropsychological classification, written language disorders are considered as an impairment o f one or more o f the components o f cognitive processes o f the model deseribed above. They hypothesize that eaeh processing model is also neurologically distinct and can therefore be selectively impaired by focal brain lesion. There are a lot o f similarities between the two approaches.

The neurological classification, as described by Roeltegen (1994), proposes five types o f agraphia, which are “pure agraphia”, “agraphia with alexia”, “aphasie agraphia”, “apraxic agraphia” and “spatial agraphia”. “Pure agraphia” is the disorder in which patients present with a selective agraphia in the absence o f any other language disturbance (Rosati & DeBastiani, 1981). The lesion sites associated with pure agraphia are variable including the Exner's area in the seeond left frontal gyrus (Vemea & Merory, 1975; Aimard et al, 1975), posterior perisylvian region (Rosati & DeBastiani, 1981), superior parietal lobe (Basso et al, 1978), left occipital lobe (Kapar & Lawton, 1983), posterior insula and posterior putamen (Roeltegen, 1989, 1991), and the basal ganglia (Laine & Marttila, 1981). This variability in localization o f selective writing impairment indicates that a single centre for writing is unlikely to exist. W riting itself is a complex task, which requires the dynamic participation o f multiple brain sites. “Agraphia with alexia” is also called parietal agraphia, because the two symptoms occur together in the absence o f aphasia usually in patients with parietal lobe lesions (Kaplan & Goodglass, 1981). This type o f agraphia is similar to that seen in patients with fluent aphasia and frequently these patients present with mild anomic aphasia (Benson & Cummings, 1985) and produce

poorly formed graphemes (Roeltegen, 1993). “Aphasie agraphia” is the type o f agraphia which is associated with a specific aphasie syndrome and its pattern in general has been reported to be similar to the disorder o f oral output (Benson & Cummings, 1985), although discrepancies have been reported (Roeltegen, 1993). The neurological lesion in patients with this type o f agraphia is thought to match the lesion site o f their aphasie syndrome, e.g. the lesions in patient with agraphia and B roca’s aphasia are similar to those found in patients with Broca’s aphasia (Roeltegen, 1994). In “Broca’s aphasia” two distinct subtypes o f agraphia have been described, one is characterized by difficulty in grapheme production and the other associated with agrammatism (Kaplan & Goodglass, 1981). In “conduction aphasia”, agraphia is characterized by poor word spelling, with real words spelled better than non-words (Marcie & Hecaen, 1979). In “W ernicke’s aphasia”, agraphia is characterized by having normal output with well formed graphemes and a decreased production o f substantive words and incorrect spelling (Benson & Cummings, 1985). In “transcortical motor aphasia” and in “transcortical sensory aphasia”, the agraphia is similar to the one presented in B roca’s and W ernicke’s aphasia respectively, while in “mixed transcortical aphasia”, patients are presenting with non­ fluent writing which improves with copying (Roeltegen, 1994). “Apraxic agraphia” is characterized by difficulty in forming graphemes when writing to dictation (Roeltegen, 1993). Alexander et al (1992) suggested that apraxic agraphia is a spatial disorder o f learned movements and is associated with lesions o f the superior parietal lobe. Also unilateral apraxic agraphia has been observed in patients with corpus collosum lesions (W atson & Heilman, 1983). “Spatial agraphia” is characterized by production o f duplicate strokes during grapheme formation, trouble with writing in a horizontal line

and, intrusions o f blank irregular spaces between graphemes (Roeltegen, 1994). This type o f agraphia is associated with lesions o f the non-dominant parietal lobe (Ellis et al, 1987). Although the above described types o f agraphias, as classified by the neurological approach, attempt to explain the behavioural and clinical-pathological aspects o f agraphias, inconsistencies and controversies do exist. For example one subtype o f agraphia may have similar behavioural disturbances as another type or be closer to another type. Furthermore in the last decade, the focus o f research has been shifted onto the neuropsychological processing models and the neuropsychological classification has dominated the recent literature on our understanding o f agraphia and overall writing impairments. So the notion o f syndrome has been criticized and reviewed in a way that has somewhat limited usefulness. Consequently in clinical practice, lesion localization using the terminology described above has restricted application (Basso & Maragnolo, 2000).

From a neuropsychological perspective, the classification o f agraphias is based on the theoretical model o f the writing processing. Its value can be judged by its ability to account for patterns o f abnormal performance often observed in clinical situation. Therefore different forms o f agraphia in neurologically impaired patients should be directly interpretable with reference to specific functional components o f the model described in Fig.l (Rapcsak & Beeson, 2000). According to this model, disorders o f written language are classified as central or peripheral dysgraphias. In central agraphias, the loci o f deficit are located in the central spelling routes such as the lexical semantic, lexical non-semantic and non-lexical resulting in lexical (or surface), phonological, deep,

semantic and graphemic buffer dysgraphias. In peripheral dysgraphias, the main difficulties involve the selection and/or production o f letters in handwriting and are described as allographic, apraxic, motor non-apraxic and afferent dysgraphias.

“Lexical or surface dysgraphia” is characterized by particular difficulty spelling irregular and ambiguous words due to damage o f graphemic output lexicon (Goodman & Caramazza, 1986). In such cases the aphasie agraphic person produces phonological plausible type errors and relies on the intact non-lexical route for spelling o f words. This type o f agraphia is most commonly associated with posterior temporal lesions (Goodman & Caramazza, 1986). Roeltegen & Heilman (1984) have proposed that the critical lesion site is located between the junction o f the posterior angular gyrus and the parietal lobule. Reduced metabolic activity in the left angular gyrus has also been revealed in patients with Alzheim er’s disease with impairment o f lexical spelling (Peniello, et al, 1995), making this region a possible neural substrate o f graphemic output lexicon.

In “phonological dysgraphia”, there is a marked impairment o f non-word spelling with selectively preserved real word spelling due to a dysfunction o f the non-lexical spelling route (Shallice, 1981). Errors in non-word spelling typically includes phonologically incorrect non-word responses and real words that have some visual or phonological similarity to the target as the lexical semantic route is mainly used for spelling. Phonological agraphia is typically seen following left perisylvanian lesions (Roeltegen et al, 1983). Roeltegen (1985) suggests that lesions in patients with this type o f agraphia overlap in the region o f the anterior supramarginal gyrus, concluding that this perisylvian

cortical area is important in spelling via the non-lexical route.

“Deep dysgraphia” has several linguistic characteristics in common with phonological dysgraphia, but it is distinguishable from phonological dysgraphia by the presence o f prominent semantic errors in writing (Hatfield, 1985). The type o f errors observed in this type o f agraphia is similar to phonological agraphia plus semantic errors, due to damage o f all three spelling routes. Rapcsak & Beeson (2000) suggest that these patients use the damaged lexical semantic route for spelling. Patients with deep agraphia have large left hemisphere lesions that typically involve most o f the perisylvian language zone. However, there is an intriguing possibility that in deep dysgraphia, writing is no longer controlled by the damaged left hemisphere, and that its characteristic features reflect the limitations o f the intact right hemisphere (Rapcsak et al, 1991).

“Semantic agraphia” is characterized by impairment in conceptually mediated writing tasks such as spontaneous writing and written naming while writing to dictation even o f familiar words is spared, yet their meaning can not be understood (Patterson, 1986). Semantic agraphia is due to damage to the lexical semantic route and the cases with this type o f dysgraphia have special difficulty with homophone words as they use the lexical non-semantic and the non-lexical routes for spelling. Patients with semantic agraphia constitute a homogenous group with respect to the lesion localization. Among the reported sites are various extraperisylvian lesions (Roeltegen et al, 1986), and posterior temporo-parietal sites as homophone errors have been observed in patients with lexical agraphia (Hatfield & Patterson, 1983). At the present time there is no conclusive

evidence o f the precise neuro-anatomical substrate o f this type o f agraphia.

Cases with “dysgraphia due to graphemic buffer impairment” present with errors of grapheme identity and order in all spelling tasks regardless o f word status affecting all output modalities (Miceli et al, 1985; Caramazza et al, 1987). A dysfunction o f the graphemic buffer involves a defective short term storage o f graphemic information, leading to errors o f letter substitution, deletion, addition and transposition. These errors are also related to the spatial location o f letters within the words. Lesion sites in patients with this type o f agraphia have been variable. Involvement o f left hemisphere fronto­ parietal cortical systems involved in working memory and spatial attention is common but more specific localization is not possible at this time (Rapscak & Beeson, 2000).

“Allographic dysgraphia” is characterized by an inability to generate or select the correct letter shapes in handwriting while oral spelling remains spared (Patterson & Wing, 1989). Cases with this type o f dysgraphia present with writing impairment specific to case (upper versus lower) or style (print versus cursive), case mixing errors and substitution o f physically similar letter forms due to defective assignment o f letter shapes to abstract graphemic representation held in the graphemic buffer. This can be either due to a production deficit - failure to create the appropriate letter because o f a failure to remember letter shapes (Kartsounis, 1992), or to a selection deficit- as an uncontrolled mixing o f the upper and lower case letters (DeBastiani & Barry, 1989). In the majority of cases with this type o f dysgraphia the responsible lesion has involved the left parieto­ occipital region (Rapscak & Beeson, 2000).

“Apraxic dysgraphia” is characterized by poor letter formation that can not be attributed to impaired letter shape knowledge or to sensorimotor, extrapyramidal or cerebellar dysfunction affecting the writing limb. These cases are unable to execute the sequences o f strokes necessary to produce the letter from the specified allographic code while oral spelling, typing ad spelling with anagrams is spared and letter imagery is preserved (Baxter & Warrington, 1986). These cases make gross errors o f letter morphology, spatial distortions, stroke insertions and deletions, which sometimes make writing completely illegible. This is due to destruction or disconnection o f graphic motor programs, or damage to systems responsible for translating these programs into graphic innervatory patterns. In apraxic agraphia, lesions are generally located in the hemisphere contralateral to the hand preferred for writing. However, the critical lesion site has been debatable as they have been reported cases with parietal lobe lesions- in the junction o f the angular gyrus and the superior lobule (Alexander et al, 1992), premotor cortical areas near the foot o f the second frontal convolution also known as Exner’s writing center (Hodges, 1991), and the supplementary motor area (Watson et al, 1986). Rapcsak & Beeson (2000) suggest, that the motor programming o f writing is mediated by a distributed neural network, which include both posterior and anterior cortical components with distinct functional roles. More specifically, they suggest that the parietal lobe is the area that graphic motor programs are stored, and that the frontal premotor areas are involved in translating these programs into graphic innervatory patterns. The critical role o f these areas is supported by functional neuroimaging studies in normal subjects (Seitz et al, 1997).

“Motor non-praxic dysgraphias” are characterized by defective regulation o f movement force, speed and amplitude in handwriting (Rapcsak & Beeson, 2000). A typical non- praxic dysgraphia is the micrographia observed in cases with Parkinson’s disease and the disjointed and irregular writing movements observed in cerebellar disorders. These dysgraphias are due to dysfunction o f motor systems involved in controlling the kinematic parameters o f writing. Brooks (1986) suggests that basal ganglia-thalamo- cortical and cortico-cerebellar motor loops are the possible neural substrates o f a distributed system that generates and modulates innervatory patterns for skilled limb movements, including innervatory patterns for writing movements. This has been supported by regional blood flow and PET studies (Seitz et al, 1997).

“Afferent dysgraphias” arise from lesions that interfere with the ability to utilize sensory feedback for the control and execution o f writing movements (Ellis, 1982; Lebrun, 1985). Errors in this type o f dysgraphia include duplications or omissions o f letters or strokes especially when writing sequences o f similar items, difficulty keeping the line o f writing straight and maintaining proper spacing between letters and words. This type o f dysgraphia is usually seen following right parietal lesions (Ellis, 1982; Lebrun, 1985) but also has been observed in association with cerebellar dysfunction (Silveri et al, 1997).