What causes dyslexia?: comment on Goswami

Finding an underlying deﬁcit that links the disparateimpairments associated with dyslexia would be majorbreakthrough. In a recent article in TiCS, Goswami [1]offers a viable candidate for such a deﬁcit – and has done aremarkable job of ﬁnding links that are plausible if stillmostly circumstantial. Her stimulating article raises nu-merous directions for future research.The epidemiology of dyslexia is poorly documented.Although many deﬁcits have been reported [2], how oftenthey occur and co-occur at different ages in different lan-guages is still unknown. Goswami’s descriptions of what isfoundindyslexiashouldbereadaswhatwasfoundinsomestudies.Morefactsareneeded;forexample,withrespecttothe greater sensitivity of dyslexics to allophonic variation(which is crucial to Goswami’s account of phoneme-leveldifﬁculties), many have sought this effect, and some havefound it. The null results, however, get ﬁled away.Studies testing the Temporal Sampling Framework(TSF) need to beconducted more widely and with a varietyof methods, together with tests of other putative deﬁcits.The challenge is not only to establish closer mechanistic,causal connections between the hypothesized deﬁcit anddiverse behavioral impairments, but also to explain thedistribution of impairments. The theory also needs toaccommodate strong evidence for mainly left-hemispheresubcortical anomalies in dyslexia [3,4].Short of a large-scale international epidemiologicalstudy, researchers (both of brain and behavior) need to testthesame subjects usingeach other’smeasures,and postallresults, both positive and negative. An online archive inwhich researchers could deposit their stimulus materialswould make this possible. Perhaps a major funding agencycould see the value in this undertaking.Becausereadingisacomplextaskdrawingonnumerouscapacities, it is unsurprising that multiple genetic poly-morphisms are apparently involved. The TSF would bestronger if there were a reason why various genetic anom-alies converge on low-frequency oscillation in the righthemisphere.I would be inclined to search for anomalies in braindevelopment that have, as one highly salient consequence,the deﬁcit that Goswami has identiﬁed. I present thefollowing speculative sketch to illustrate the type of multi-level theory to which we might aspire.(i) Prominent candidate genes for dyslexia are implicat-ed in cell migration [5].(ii) Disorders of brain development often involve distur-bances of interneuron migration and integration [6].(iii) AnomaliesinthemigrationofGABAergic(inhibitory)interneuronsmayunderlieavarietyofdevelopmentaldisorders.Suchanomaliescanberegionalratherthanglobal [7].(iv) GABAergic interneuron pathology impairs lateralinhibition, affecting discrimination of competingtypes of sensory information [8].(v) Auditory processing at multiple time and frequencyscales in parallel requires resolution of such compet-ing information, and similarly for vision.(vi) For some unknown reason, the processing of lowertemporal frequency auditory information is particu-larly vulnerable,(vii) From which deﬁcits on tasks that rely on thisinformation follow.Therefore, rather than the auditory-processing deﬁcitcausing associated impairments in vision, motor perform-ance, attention, learning, memory, and so on, all theseimpairments arise from a common source: an attestedtype of neurodevelopmental anomaly, caused by multiplegenes, creating the observed variability in the phenotypicoutcome. Processing of low temporal frequency auditorysignals might be especially affected, with multiple down-stream consequences.Goswami’s article is an interesting addition to the liter-ature and her theory will stimulate much valuable re-search. However, much remains to be learned.