Neurobiology of Reading and Dyslexia Flashcards

Diffusion tensor imaging (DTI) studies in individuals with dyslexia have consistently identified reduced fractional anisotropy in which white matter tract, and what functional consequence does this most directly predict?

Answer: Left arcuate fasciculus; disrupted phonological-orthographic integration between temporal and frontal language areas

Reduced fractional anisotropy in the left arcuate fasciculus is one of the most replicated DTI findings in dyslexia. This tract connects Wernicke's area (posterior superior temporal) with Broca's area (inferior frontal), and its structural integrity is directly tied to phonological processing efficiency — the core deficit in most dyslexia profiles. The other tracts listed play roles in language but are not the primary locus of dyslexia-related white matter pathology.

The DCDC2 gene on chromosome 6p22 is one of the most replicated genetic risk factors for dyslexia. What is the primary neurodevelopmental mechanism by which DCDC2 variants are hypothesized to disrupt reading circuitry?

Answer: Impaired neuronal radial migration during cortical development, disrupting laminar organization in left perisylvian regions

DCDC2 encodes a doublecortin domain-containing protein that regulates radial neuronal migration along glial fibers during cortical development. Variants that reduce DCDC2 expression cause ectopic neurons and disorganized cortical lamination, particularly in left hemisphere perisylvian areas critical for phonological and reading development. This is consistent with postmortem findings of cortical ectopias and microgyria in brains of individuals with dyslexia.

Neuroimaging studies comparing dyslexic and typical readers across languages with transparent orthographies (e.g., Italian, Finnish) versus opaque orthographies (e.g., English) have produced a nuanced finding. Which best characterizes the cross-linguistic pattern?

Answer: Dyslexic readers of transparent orthographies display the same left posterior hypoactivation as English dyslexics, but their behavioral deficit manifests primarily as reading-rate impairment rather than accuracy errors

Paulesu et al. (2001, Science) demonstrated that Italian, French, and English dyslexics all showed hypoactivation in the left posterior reading system (particularly the occipito-temporal and parieto-temporal regions), suggesting a universal neurobiological signature. However, because transparent orthographies offer reliable grapheme-phoneme correspondences, Italian and Finnish dyslexics achieve near-normal accuracy at the cost of greatly slowed reading speed — the error profile differs even though the neural substrate dysfunction is comparable.

The 'double-deficit hypothesis' (Wolf & Bowers, 1999) posits two independent core deficits in dyslexia. Neurobiologically, the phonological deficit and the naming-speed (RAN) deficit are dissociable because they map to distinct neural systems. Which pairing best reflects the current neuroimaging evidence?

Answer: Phonological deficit → left parieto-temporal and inferior frontal circuits; RAN deficit → left occipito-temporal 'word form area' automaticity and cerebellar timing networks

The phonological deficit is associated with dysfunction in left parieto-temporal cortex (supramarginal gyrus, angular gyrus, posterior superior temporal) and left inferior frontal gyrus (Broca's area). The RAN deficit implicates a separate circuit involving the left occipito-temporal cortex (visual word form area) — responsible for rapid, automatic orthographic recognition — and cerebellar timing networks that support the rapid, serial, timed retrieval required for naming tasks. Children with deficits in both systems form the most severe subgroup.

Compensated adults with dyslexia — those who attain functional reading accuracy through intensive instruction or effort — consistently show a distinctive neural pattern compared to typical fluent readers. Which fMRI finding best describes this compensatory profile?

Answer: Persistent underactivation of left posterior systems (parieto-temporal and occipito-temporal), with increased reliance on right-hemisphere homologues and left inferior frontal regions

Studies by Shaywitz et al. and subsequent replication work show that compensated dyslexics maintain the dyslexic neural signature — left posterior hypoactivation — despite behaviorally adequate reading. They compensate through two alternate routes: (1) right-hemisphere homologues of temporal and occipital language areas, and (2) increased left inferior frontal (Broca's area) activation, reflecting greater phonological effort and subvocal rehearsal. This profile explains why compensated dyslexics often read accurately but slowly and with high cognitive load.

The magnocellular theory of dyslexia (Stein & Walsh) proposes that deficient M-pathway processing disrupts reading through a specific cascade. Which sequence most accurately describes the proposed causal chain from magnocellular deficit to reading failure?

Answer: Impaired temporal sampling of visual input → unstable binocular fixation and disrupted letter position encoding → degraded orthographic input to phonological decoding systems

The magnocellular pathway (M-pathway, dorsal stream) is specialized for low spatial frequency, high temporal frequency processing, and is critical for detecting rapid changes in the visual field. The magnocellular theory proposes that a deficit in this system impairs temporal sampling — the ability to parse rapidly changing visual information — leading to unstable fixation, poor letter position coding, and unreliable input to the orthographic processing systems that feed phonological decoding. This is distinct from a simple contrast sensitivity deficit (which involves the parvocellular system) and from eye-tracking mechanics per se.