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Lenneberg’s Hypothesis (1967)

Lenneberg’s Hypothesis (1967). Hemisphere equipotentiality & progressive lateralization LH & RH functionally equivalent at birth. Only through experience they specialize (not unlike Broca (1865) argument) Evidence behind this idea: High incidence of aphasia in RHD children (Freud, 1891)

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Lenneberg’s Hypothesis (1967)

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  1. Lenneberg’s Hypothesis (1967) Hemisphere equipotentiality & progressive lateralization LH & RH functionally equivalent at birth. Only through experience they specialize (not unlike Broca (1865) argument) • Evidence behind this idea: • High incidence of aphasia in RHD children (Freud, 1891) • Basser (1962) reported on 34 child hemispherectomy cases for epilepsy. All but one developed normal speech. • Lashley (1950) principle of mass action: loss of learning is predicted by size of lesion rather than its location (in rats) • Adult difficulty in 2nd language acquisition (accents) • Language acquisition difficulty with feral children

  2. Lenneberg’s Hypothesis (1967) 35% of right hemispherectomy showed acquired speech disturbances (Basser, 1962) • but adult pattern seen in data >5y (Krashen, 1973) • selective reporting, lax criteria, & pre-antibiotic days often resulted in diffuse contralateral insults (Kinsbourne, 1975) • Modern data suggest 5% childhood RHD are aphasic Developmental invariance position (or irreversible determinism) • No distinct aphasic syndromes in children • Van Hout (1992) documents adult-like syndromes at 3y

  3. Lenneberg’s Hypothesis (1967) • Language recovery from LH hemispherectomy • but recovery incomplete! — impaired syntactic production • spatial impairments with RH missing as well • neuroplasticity greater in children, and still complex functions tend not to develop • LH damage= impaired math; RH=temperamental problems Additional evidence against Lenneberg • LH sensitivity to POA in neonates; other components (ERP) • Infant orientation tendency toward right side • Directed, target-related acts w/Rh (vs passive holding, reflexive) • Speech interferences with R hand activity most (13-28 mo) • Dichotic asymmetry at 3 wk or prenatal (habituation paradigms) • Blank slate =/= functional equivalency • Dichotic listening REAs remain constant across childhood Given immature cerebrum, due to subcortical asymmetries

  4. Language-base double dissociation in adults

  5. Dichotic listening for music and speech • Stable ear advantages across newborns to 6 mo old

  6. So you want to work with infants? (n=71 originally)

  7. Vocabulary (Lexicon) Development By age 2: a few hundred vocabulary words By age 6, >13,000 words (45/week)

  8. Token Test & Hemispherectomy

  9. NEXT

  10. Callosal Agenesis Sagittal, axial, and coronal T1WI show parallel lateral ventricles and absence of the corpus callosum

  11. ACC is an anomaly of ventral induction that occurs at 5-12 weeks gestation. Other anomalies in the same category include holoprosencephaly, septo-optic dysplasia, diencephalic cysts, cerebral hemihypoplasia/aplasia, and lobar hypoplasia. The inciting event in ACC is felt to be a defective lamina terminalis which could result from a number of intrauterine insults or chromosomal anomaly. Common associations include Aicardi syndrome, anterior encephalocele, craniofacial clefts, Dandy Walker malformations, chiari II malformation, and CC lipomas. Associated radiologic findings include no CC or cingulate gyrus, teardrop shaped occipital horns, parallel lateral vents, high riding 3rd vent, central cyst that extends to inner table, azygous/wandering ACA. The superomedial aspects of the lateral ventricles are indented by longitudinal WM tracts called "Probst bundles". Partial ACC is usually posterior and results from intrauterine injury.

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