САД HYPERLEXIA AND DYSLEXIA IN AUTISM : HITTING A MOVING TARGET

Дијагностичката историја на аутизмoт, дислексијатa и хиперлексијатa е комплексна. Затоа што овие состојби делат меѓу себе и конвергентни и дивергентни состојби, важно е да се разберат овие врски, особено во случај на истражување и на кој начин се интерпретираат студии кои поминуваат низ декади со променливи критериуми. Многу е важно да се синтетизира што е досега познато за морфологијата на овие состојби и да се подвлече што е сè уште непознато. Аутизмот и дислексијата, на пример, делат антиподни церебрални морфологии, како што се миниколумнарната густина, неурополната ширина, големината на клетките, волуменот на корпус калозум, гиралната комплексност, гиралната големина и церебралниот волумен, додека хиперлексијата не беше проучена на овој начин, иако таа има многу сличности со аутизмот. Во меѓувреме, флуктуацијата на критериумите на дислексијата The diagnostic histories of autism, dyslexia, and hyperlexia are complex. Because these conditions share both convergent and divergent properties, it is important to understand these relationships, especially in the case of research and how we interpret bodies of work which span decades of fluctuating criteria. It is also important to synthesize what we already know about the morphology of these conditions and pinpoint what we still don’t. Autism and dyslexia, for instance, share antipodal cerebral morphologies, such as minicolumnar density, neuropil width, cell size, corpus callosal volume, gyral complexity, gyral window size, and cerebral volume, while hyperlexia has not been studied in this fashion, although it shares much in common with autism. Meanwhile, the fluctuation in criteria of dyslexia

over the years, means that older studies, such as some of the most highly cited in postmortem research, have potentially used more heterogeneous groups of subjects than dyslexia research typically uses today.Considerably, these older studies are often the basis of current animal model and genetics research.In conclusion, in consideration of the continued flux in criteria, particularly the proposed change from "Reading Disorder" to the broader "Specific Learning Disorder" within the DSM-5, we strongly recommend a separation of the various reading disorders under their own headings to promote specificity of diagnosis and treatment, and to support better research.
developmental dyslexia occupy opposing extremes on a neuro-morphological distribution (8,9).Some individuals have questioned how autism and dyslexia display divergent etiologies and yet occur comorbidly.We suggest that while hyperlexia shares an etiology in common with the autism, when dyslexia appears in conjunction with an autistic spectrum condition (ASC) it is instead a secondary disorder that has more in common etiologically with the overarching ASC than with the form of dyslexia occurring separately.In lieu of this distinction, we refer to developmental dyslexia without comorbid autism as "primary dyslexia" and the comorbid form of dyslexia as "secondary dyslexia".

Морфологија на состојбите
The Morphology of the Conditions In order to understand the etiology of these conditions and how they converge and diverge behaviorally, studying the underlying morphology is imperative.From the postmortem examinations performed on those with autism, it is clear that a significant portion of cases display vestiges of aberrant neurogenesis.Casanova et al. (10) have found that the neocortex of autistic individuals exhibits increased numbers of minicolumns and that the cells within these minicolumns are smaller and less compact than their control counterparts.The neuropil space which lies between adjacent columns is also reduced in size.Overall, these attributes suggest a larger total population of cells, the result of either overproliferation of the founder population during the neurogenic stage or reduced apoptosis (11).Increased neuron number have been noted in other areas such as the hippocampus, the amygdala, and other portions of the limbic system, while it is suspected that the well-replicated finding of reduction in the Purkinje's cell number within the cerebellum is an acquired artifact (12,13).This is evidenced by the reactive gliosis frequently present in the cerebellum at the time of death, and by the fact that Purkinje's cells are a particularly vulnerable population же да објаснат зошто овие клетки покажуваат најголема загуба во бројност (13) to both hypoxia and seizures which may explain why these cells exhibit the greatest loss in numbers (13).In addition to the changes in the neuronal number, morphology and dispersion, white matter tracts are reduced in size in the ASC, with a concomitant rise in number of short-range fiber tracts (14).In relation to this change in connectivity, gyral complexity is increased and average gyral window volume, the area through which the arcuate tracts exit the gyrus and travel through the sub-cortex, in autism is decreased (9,15).Finally, at the gross level of comparison a minor yet significant portion of cases of autism falls within the macro cephalic range (16).
have suggested: dyslexics read for meaning, autistics read for sound.While the under connectivity in long-range fiber tracts in autism may underlie poor reading comprehension in hyperlexic and typical autism, average-to-above-average phonological skill may be due to local over connectivity (8).As a related example, synaethesia is more common in autistics than in the general population; it has recently been found that the capacity which underlies grapheme-color synaesthesia is related to greater connectivity in the inferior temporal cortex (49).We would expect similar findings in relevant areas within the hyperlexic brain, i.e., local over connectivity.Hopefully, future research will be able to explore this prediction.The relationship between autism and dyslexia is both an overlapping and dichotomous one.Dyslexia can be secondary to autism, while primary dyslexia exhibits cerebral morphology antipodal to the former.Meanwhile, hyperlexia presents with striking similarities to autism and may frequently be comorbid with the same.Although hyperlexia is often regarded as a super ability, it usually co-occurs with some form of reading deficit.And in fact, reading disorders are often found also in close family members (5,50).The imbrication with which these conditions present likely represents the point at which a common behavior overlaps two antipodal morphologies.Therefore, in order to determine whether this is the case, it is imperative that our definitions in the research are precise and consistent.
We commend the APA for including poor reading comprehension within the new criteria list, which will hopefully lend greater specificity than the previous criteria of Reading Disorder.However, the inclusion of several etiologically different reading disorders under a single heading may continue to promote similar confusions as before.Though the criteria are now separated, this new definition still blurs the line between a disorder of reading comprehension and classic dyslexia by subsuming them under the same diagnosis.Unfortunately, not only will diagnosis and treatment remain complex, it may continue to prove a challenge in studying etiological mechanisms of this heterogeneous group of conditions.Because structural and postmortem research already suggests divergent morphologies of the various reading disorders as our review of the postmortem and neuro-imaging literature illustrates, we would propose their separation rather than lump them under a single umbrella category.In this way, different reading disorders will be studied separately, the co-occurrence of secondary dyslexia with autism would be separated from primary dyslexia, and treatment modalities would be better suited to deal with the underlying deficits, e.g., reading comprehension versus word recognition.Thus, we would be better equipped to help deficient individuals improve their reading skills with precisely tailored programs, and research will not confound the study of etiology by including excessive heterogeneity within their samples.