Neurodevelopmental disorders are disorders wherein impairments in neural development lead to deficits in various cognitive and/or social abilities (Reynolds & Goldstein, 1999). Historically, researchers have often assumed that human cognition is served by numerous “modules”, each of which performs a specific cognitive function. It is typically argued that each module is supported by a specific brain region whose evolutionarily-defined characteristics confer neural properties that facilitate module-appropriate cognitive operations (Buss, 2010). Accordingly, many neurodevelopmental disorders have historically been viewed as deficits that arise in consequence of the abnormal development of a particular module (e.g. Baron-Cohen et al., 1985). The neuroconstructivist position (Karmiloff-Smith, 1998, 2009, 2010) rejects this account of neurodevelopmental disorders.
Contrary to the view that specific brain regions are evolutionarily constrained to serve specific functions, the …show more content…
Cognitive impairments displayed by individuals who have suffered brain lesions have typically been interpreted as the observable manifestation of damage to the module that the lesioned region underpins (Kandel et al., 2001). For instance, in 1861, Paul Broca discovered a patient with impairments in speech production and damage to the left inferior frontal gyrus (LIFG), leading him to conclude that the LIFG was the neural locus of human speech production abilities (Dronkers et al., 2007). The same logic has been used to infer neural function on the basis of lesion-induced impairments for the last 150 years (e.g. Duncan, 2010). Thus, adult neuropsychological models have typically explained the effects of brain lesions in terms damage to the modules underpinned by the lesioned regions (Burgess et al.,
Contrary to the view that specific brain regions are evolutionarily constrained to serve specific functions, the …show more content…
Cognitive impairments displayed by individuals who have suffered brain lesions have typically been interpreted as the observable manifestation of damage to the module that the lesioned region underpins (Kandel et al., 2001). For instance, in 1861, Paul Broca discovered a patient with impairments in speech production and damage to the left inferior frontal gyrus (LIFG), leading him to conclude that the LIFG was the neural locus of human speech production abilities (Dronkers et al., 2007). The same logic has been used to infer neural function on the basis of lesion-induced impairments for the last 150 years (e.g. Duncan, 2010). Thus, adult neuropsychological models have typically explained the effects of brain lesions in terms damage to the modules underpinned by the lesioned regions (Burgess et al.,