Neurobiology of Reading and Dyslexia Flashcards

The visual word form area (VWFA) in the left fusiform gyrus is consistently underactivated in individuals with dyslexia on fMRI. Beyond general visual processing, which specific functional role does this underactivation most directly impair?

Answer: Rapid, automatic holistic recognition of stored orthographic word forms

The VWFA (approximately left fusiform gyrus, BA37) supports fast, automatic access to whole-word orthographic representations — the 'lexical' or 'sight word' route. Its underactivation in dyslexia specifically disrupts reading fluency and automaticity, not sequential decoding, which relies more on the dorsal temporo-parietal pathway. Compensated dyslexic adults often achieve accuracy by over-relying on the slower dorsal phonological route precisely because the VWFA pathway remains underactivated.

DCDC2, one of the most replicated genetic risk loci for dyslexia, confers risk primarily through its effect on which neurobiological process during brain development?

Answer: Radial neuronal migration during cortical lamination

DCDC2 encodes a doublecortin domain-containing protein that regulates radial migration of neurons through the developing cortical plate. Risk variants disrupt proper cortical lamination, consistent with the focal ectopias and cortical microgyria found in postmortem studies of dyslexic brains (e.g., Galaburda et al.). This developmental migration failure — not postnatal myelination or synaptic pruning — is the mechanistic link from gene to atypical cortical organization.

Psychophysical research testing the magnocellular (M-pathway) deficit hypothesis in dyslexia predicts impaired sensitivity to which specific stimulus properties?

Answer: Low spatial frequency, low contrast, rapidly moving stimuli

Magnocellular neurons in the lateral geniculate nucleus are tuned to low spatial frequencies, low luminance contrast, and high temporal frequencies (rapidly changing or moving stimuli). They are largely contrast-insensitive and color-blind. The M-deficit hypothesis predicts — and multiple psychophysical studies confirm — that individuals with dyslexia show selectively reduced thresholds for exactly these low-contrast, low-spatial-frequency, rapidly moving stimuli, leaving parvocellular (high-contrast, static, fine-detail) processing relatively intact.

Neuroimaging of compensated adult dyslexic readers — those who are accurate but slow — reveals a distinctive activation pattern. Which pattern is most consistently reported in the literature?

Answer: Persistent underactivation of left temporoparietal and occipito-temporal regions with increased right-hemisphere and left inferior frontal activation

Studies by Shaywitz, Pugh, and others consistently show that compensated dyslexic adults maintain the core neural signature of dyslexia — underactivation of the left posterior reading network (temporoparietal and occipito-temporal regions) — but recruit compensatory resources: right-hemisphere homologs of these regions and left inferior frontal gyrus (Broca's area). This right-shifted, anterior-weighted pattern is distinct from both typical readers and uncompensated dyslexics, explaining why these individuals can achieve accuracy through effortful, slower processing.

Diffusion tensor imaging (DTI) studies most consistently identify reduced fractional anisotropy (FA) in which white matter tract in individuals with dyslexia, and what reading process does this specifically compromise?

Answer: Left arcuate fasciculus; phonological-to-orthographic mapping in the dorsal reading pathway

The left arcuate fasciculus (part of the superior longitudinal fasciculus) is the primary white matter connection between posterior superior temporal language regions and left inferior frontal regions. Its reduced FA in dyslexia reflects degraded structural connectivity along the dorsal phonological reading pathway. This specifically impairs phonological assembly — the ability to map phonemes onto graphemes during decoding — which is the core deficit in dyslexia. Numerous DTI studies (Klingberg, Beaulieu, Odegard) have replicated this finding.

The cerebellar deficit hypothesis (Nicolson & Fawcett) attributes dyslexia partly to cerebellar dysfunction affecting procedural learning and automatization. Which evidence most directly challenges the cerebellar deficit as a PRIMARY causal explanation for phonological processing deficits in dyslexia?

Answer: Phonological awareness deficits are detectable in pre-readers before reading instruction and automaticity demands begin

The cerebellar hypothesis posits that impaired automatization (a cerebellar function) causes reading to remain effortful, degrading phonological skills over time. The strongest counterargument is developmental timing: longitudinal studies show that children later diagnosed with dyslexia exhibit phonological awareness deficits in preschool, before any reading instruction has begun and before the automatization demands that would engage cerebellar consolidation exist. This temporal precedence of phonological deficits suggests they are neurologically upstream of cerebellar processes, not a downstream consequence of failed automatization.