A Superadditive-Impairment Theory of Optic Aphasia
Authors: Michael Mozer, Mark Sitton, Martha J. Farah
Published in: Advances in Neural Information Processing Systems 10  (NIPS 1997) (Main Conference Track), 1997

Abstract: Accounts  of  neurological  disorders  often  posit  damage  to  a  specific  functional  pathway of the brain.  Farah (1990) has  proposed an  alterna(cid:173) tive  class  of explanations  involving  partial  damage  to  multiple  path(cid:173) ways. We explore this explanation for optic aphasia, a disorder in which  severe  perfonnance  deficits  are  observed  when  patients  are  asked  to  name  visually  presented objects, but  surprisingly,  performance  is  rela(cid:173) tively  nonnal  on  naming  objects  from  auditory  cues  and  on  gesturing  the appropriate use  of visually  presented objects.  We  model  this  highly  specific deficit through partial damage to two pathways-one that maps  visual  input to  semantics, and  the other that maps semantics  to  naming  responses.  The  effect  of  this  damage  is  superadditive,  meaning  that  tasks  which  require  one  pathway  or the  other show  little  or  no  perfor(cid:173) mance  deficit,  but the  damage  is  manifested  when  a  task  requires  both  pathways (i.e.,  naming  visually  presented objects).  Our model explains  other  phenomena  associated  with  optic  aphasia,  and  makes  testable  experimental predictions. 
Neuropsychology is the study of disrupted cognition resulting from  damage to functional  systems in the brain. Generally, accounts of neuropsychological disorders posit damage to  a  particular  functional  system  or  a  disconnection  between  systems.  Farah  (1990)  sug(cid:173) gested an alternative class of explanations for  neuropsychological disorders:  partial  dam(cid:173) age  to  multiple  systems,  which  is  manifested  through  interactions  among  the  loci  of  damage. We explore this explanation for the neuropsychological disorder of optic aphasia.  Optic aphasia, arising from unilateral left posterior lesions, including occipital cortex  and  the splenium of the corpus callosum (Schnider,  Benson, &  Scharre,  1994),  is  marked  by  a deficit  in  naming  visually  presented objects,  hereafter referred  to  as  visual naming  (Farah,  1990).  However,  patients  can  demonstrate  recognition  of  visually  presented  objects nonverbally,  for  example, by gesturing the appropriate use  of an object or sorting  visual  items  into  their  proper  superordinate  categories  (hereafter,  visual  gesturing).  Patients  can  also  name  objects  by  nonvisual  cues  such  as  a  verbal  definition  or  typical  sounds made by  the objects (hereafter, auditory naming). The highly specific nature of the  deficit rules out an explanation in terms of damage to a single pathway in a standard model  of visual naming (Figure  1), suggesting that a more complex model  is required, involving 
A Superadditive-Impainnent Theory of Optic Aphasia 
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FIGURE  1.  A  standard  box-and-arrow  model  of visual  naming. The  boxes  denote  levels  of  representation,  and  the  arrows  denote pathways mapping from one level of  representation  to  another.  Although  optic  aphasia cannot be explained by damage to  the  vision-to-semantics  pathway  or  the  semantics-ta-naming  Farah  (1990) proposed an explanation in terms of  partial damage to both pathways (the X's).