01 NRDC Dyslexia 1-88 update - Texthelp

Developmental dyslexia in adults: a research review 63
variable (Klein & Farmer, 1995). There have been indications that temporal processing deficits
occur frequently in dyslexics and might be an important consideration for investigating the
underlying causes of dyslexia. Nevertheless, even if an association between temporal
processing deficits and dyslexia is accepted and the plausibility of a causal path from the
former to the latter recognised, the hypothesis that temporal processing deficits are the root
cause of some cases of dyslexia may be far from established (Farmer & Klein, 1995).
The temporal processing deficit theory proposes that dyslexia might be caused by
inefficiency in processing rapid sequences of very brief stimuli.
Do dyslexics have a temporal deficit in visual processing?
At one time, dyslexia was explained in terms of a visual deficit (Orton, 1937). This explanation
imbued dyslexia with ‘a certain exotic quality, manifested most prominently in the popular
belief that children so afflicted literally perceive letters backward and frequently reverse them
in their printing and writing’ (Vellutino, 1979). Popular or not, this belief may be mistaken if it
requires written reversals to be consistent, since observation shows that they are erratic.
However, the implausibility of one kind of visual deficit does not exclude the possibility of a
different kind of visual deficit in dyslexia. Because of the heterogeneity in reading disability,
the validity of other explanations ought not to exclude the possibility of a valid visual-deficit
explanation in some cases if not in all of them.
What, then, is the evidence for a visual deficit in dyslexia? Converging lines of evidence have
shown that about three in four dyslexics have normal visual sustained system functioning but
deficient visual transient system sensitivity (Lovegrove, 1994). Such a deficit might be only a
correlate of dyslexia, but it raises the possibility of a more general deficit underlying systems
processing temporal stimuli (Solan, 1999). Differences between groups may be attributable to
a minority of dyslexics, but data from some tasks are consistent with deficits within the visual
transient system (Everatt et al., 1999).
Against a visual transient system deficit, it has been argued that reading problems caused by
a defect in the transient system would create most difficulty in reading prose and least
difficulty in reading single, isolated words, whereas ‘retarded’ readers show a profound and
intransigent impairment in word recognition skills (Hulme, 1988). If such an impairment were
caused by neurological immaturity, there might be associated impairments on many tasks
where deviation is unrelated to reading difficulty (Hulme, 1988); however, maturational
impairments might not persist into adulthood (Bruck, 1998).
Alternatively, deficits in visual perception might result from inappropriate strategy decisions
rather than any organic dysfunction (Geiger et al., 1992). Since normal reading ability appears
to be compatible with the visual persistence across spatial frequency found in dyslexics
(Slaghuis et al., 1993), it may be either that this problem is remediable or that a different
pattern of impairment affects only a minority of dyslexics (Mattis et al., 1975). A further
possibility is that the impairments originate not in the visual system but in the executive
functions. However, with experimental control for attention and memory problems, visual
deficits have not been observed (Bruck, 1998).
Yet again, it appears that only phonological dyslexics, not ‘ordinary’ poor readers (or ‘surface
dyslexics’), are impaired on some if not all visual tasks (Cestnick & Coltheart, 1999). Poor
readers described as ‘dyseidetic’ or ‘surface dyslexic’ (who by definition have no phonological