Table 1.
Annett (1973) | Children with right hemiplegia have more speech deficits than a matched group with left hemiplegia |
Butters, Rosen, and Stein (1974) | Adult serial ablations of dorsolateral frontal cortex (but not orbitofrontal cortex) in monkeys preserve function as well as early-onset lesions to the same region |
Denckla (1973) | The association between dexterity and handedness is the same in children and adults, implying early left hemisphere specialization for skilled movements |
Dennis and Kohn (1975) | Early left lesions and left hemispherectomy produce deficits in the syntactic function of language that early right lesions and right hemispherectomy do not exhibit |
Douglas (1975) | Unilateral destruction of the hippocampus in infancy produces behavioral effects found only after bilateral lesions in the adult |
Glassman (1973) | Early (2–14 days) or late (5 months) destruction of sensorimotor cortex in cats affects placing and hopping independent of lesion age |
Goldman (1971) | Orbitofrontal lesions in the infant monkey produce similar functional effects to later lesions |
Goldman (1974a) | The strongest evidence for collateral sprouting after early-onset lesions in monkeys is in those subcortical structures and fiber tracts with the least behavioral sparing |
Goldman (1974b) | Differential development of frontal regions in monkeys accounts for the 1) rate of appearance of deficits after early dorsolateral lesions; 2) disappearance of deficits after early orbital lesions |
Goldman and Rosvold (1972) | 1) Deficits after anterodorsal caudate lesions in infant monkeys are as severe as those from adult lesions by one year of age; 2) Lesion extent relates to outcome similarly in infants and juveniles |
Gott (1973) | Hemispherectomy for childhood-onset disease causes more global lowering of function than adult onset hemispherectomy |
Hicks and D’Amato (1970) | 1) Hemispherectomy in rats produces contralateral loss of tactile placing response in both infants and adults; 2) deficits after infant lesions emerge only on the 7th postnatal day |
Isaacson (1975) | Damage to the infant brain produces greater anomalies of structure and behavior than are found after brain damage in juvenile or mature animals |
Johnson (1972) | Septal lesions at 7 days of age produce the same learning and social changes as lesions in the adult rat. |
Kohn and Dennis (1974) | Early right lesions and right hemispherectomy produce deficits in visuo-spatial function compared to early left lesions and left hemispherectomy |
Lawrence and Hopkins (1970) | Disruption of medullary pyramids in infancy produces the same deficits in finger dexterity found after similar damage in adult monkeys |
Milner (1974) | 1) Apparent sparing of language after early-onset lesions comes at the cost of right hemisphere functions; 2) Early-onset lesions in either hemisphere lower IQ |
Molfese, Freeman, and Palermo (1975) | Newborns and infants show EEG cerebral asymmetry for speech and music sounds |
Murphy and Stewart (1974) | Striate cortex lesions in the rabbit disrupt visual discrimination whether in infancy or in adulthood |
Nash (1971) | Neonatal irradiation affect mouse growth more than does irradiation later in life |
Nonneman and Isaacson (1973) | Neonatal hippocampal destruction produces extreme starting latencies in a passive avoidance task |
Rudel and Teuber (1971) | Brain-injured children are more impaired than brain-injured adults in egocentric route-finding |
Rudel, Teuber and Twitchell (1974) | 1) Early brain damage impairs oculomotor function, which is correlated with spatial deficits; 2) Lateralization of physical signs after early brain damage correlates with lateralized cognitive symptoms |
Schneider (1974) | Anomalous connections after early-onset lesions in hamsters may prevent sparing of function |
Schneider and Jhaveri (1974) | Neonatal visual cortex lesions retard learning in the hamster but adult lesions spare the same function |
Stein (1974) | Recovery of function occurs in mature rats, not only in rats with neonatal lesions |
Teuber (1971) | Children with brain injury show 1) increased starting position deficits compared to controls at all ages; 2) deficits righting from a tilted position younger than age 11 but not thereafter |
Thompson, Harlow, Blomquist and Schiltz (1971) | Lesions of the monkey dorsolateral prefrontal cortex at 5 months of age (when lesions do not influence delayed response) produce the same effects on oddity learning as do lesions later in life |
Twitchell (1974) | 1) Cerebral palsy delays sensory-motor maturation and produces hypertrophy of infantile reflexes; 2) Congenital encephalopathies suppress the development of fine finger movements |
Wada, Clarke, and Hamm (1975) | Asymmetry in the left hemisphere planum temporale exists in fetuses |
Witelson and Pallie (1973) | Neuroanatomical asymmetry exists in the left hemisphere language areas in newborns |
Woods and Teuber (1973) | Language is spared after early left hemisphere lesions but at the price of right hemisphere functions |