Corresponding to lesions of left occipito-temporal (OT) regions in acquired cases, we found a dysfunction of this region in our developmental cases who failed to exhibit any responsiveness of left OT regions to the length of words and pseudowords.
Similar to acquired cases of letter-by-letter reading, the developmental cases exhibited an abnormal strong effect of length (i.e., number of letters) on response time for words and pseudowords.
Corresponding to lesions of left occipito-temporal (OT) regions in acquired cases, we found a dysfunction of this region in our developmental cases who failed to exhibit responsiveness of left OT regions to the length of words and pseudowords.
Similarly, one may hypothesize that the difficulty with fast fluent reading of developmental dyslexia cases may be caused by a congenital dysfunction of the OT cortex.
Interestingly, there was no abnormality in the left superior temporal cortex which corresponding to the onological deficit explanation is considered to be the prime locus of the reading difficulties of developmental dyslexia cases.
An abnormal word-length effect of developmental dyslexia cases was not only observed for latencies of reading aloud responses but also for visual inspection time in eye movement studies [5], [6].
However, developmental dyslexia cases suffer not only from an abnormal length effect for words, but they also exhibit inefficient sublexical processing of the unfamiliar letter strings of pseudowords (e.g., [8]), which may be attributed to frequent absence of larger sublexical multi-letter recognition units and adherence to serial grapheme-phoneme coding instead.
In the Introduction we hypothesized that the slow serial reading of our developmental dyslexia cases similar to the serial reading of acquired LBL readers may be due to a dysfunction of the left occipito-temporal (OT) cortex and specifically of the Visual Word Form Area (VWFA).
Due to the rareness of pure developmental dyscalculia cases, we could only test a small sample of participants.
The reasons for hip arthroplasty were primary osteoarthritis (7 cases), osteoarthritis secondary to developmental dysplasia (1 case), or osteoarthritis secondary to slipped upper femoral epiphysis (1 case).
