Acquired Dyslexias Flashcards
DEJERINE: MONSIEUR C. (1892)
- 68yo; unable to read post stroke
- oral language/spelling = intact
- object/face/drawing/number recognition largely preserved
- tactile/gestural letter/word recognition remains intact
- post-mortem = pure verbal blindness (aka. pure alexia w/o agraphia) results from disconnection between primary visual areas/other occipital areas dealing specifically w/letters/words
COHEN ET AL. (2000) - now we know this region is located in ventral occipito-temporal region
CLASSIFICATIONS
PERIPHERAL DYSLEXIAS
- any reading disorder in which seeing word as stable orthographic object fails (PRE linguistic relevance failure)
CENTRAL DYSLEXIAS
- any reading disorder in which impairment occurs POST stage of visual word form (aka. reading system so psycho/neurolinguistic in nature)
PERIPHERAL DYSLEXIAS
DEJERINE (1892)
- pure alexia/alexia w/o agraphia/letter-by-letter reading
SHALLICE & WARRINGTON (1977)
- attentional dyslexia
ELLIS, FLUDE & YOUNG (1987)
- neglect dyslexia
CENTRAL DYSLEXIAS
BEAUVOIS & DEROUESNE (1979)
- phonological dyslexia
MARSHALL & NEWCOMBE (1973)
- deep dyslexia
- surface dyslexia
SCHWARTZ ET AL. (1980)
- semantic dyslexia
PURE ALEXIA
- “alexia w/o agraphia” (ie. no concurrent spelling impairment)
- many cases described
- substantial length effect/almost linear relation between length in letters/reading time
- readers = heavily affected by whether the font = ambiguous at first lvl aka. contextual info (ie. “s_ile”) doesn’t help
MAIN SYMPTOM - word identification = impossible except via explicit sequential identification of individual letters (slowly & w/effort)
PURE ALEXIA: THE SAFFRAN EFFECT
SAFFRAN & COSLETT (1998)
- pure alexias = well above chance in categorising meaning of word (is it an animal?)/lexial status of letter string (is it a real world?) despite inability to consciously identify word
- cerebral area involved; visual word form area (VMFA; ventral occipito-temporal region) = damaged/disconnected
HEMI-ALEXIA: MOLKO ET AL. (2002)
- info from left visual hemi-field initially processed in right hemisphere needs to cross to left hemisphere to combine w/right hemi-field info in visual word-form area
- BUT if corpus callosum (which allows communication between hemispheres) = damaged then transfer may no longer be possible
- result = patient has difficulty reading only words presented in left visual field aka. hemi-alexia
- NOT hemi-neglect dyslexia
- patient AC = visual word-form area is NOT activated by strings presented in left visual field
ATTENTIONAL DYSLEXIA: SHALLICE & WARRINGTON (1977)
- v rare; associated w/left parietal lesion
- difficulty in identifying letters/words when flanked by other items of same category
- BUT naming of letter/word in isolation = preserved:
1) “o” is fine BUT error-prone in “word”
2) “word” is fine BUT error-prone in “when the word is in a sentence” - aka. highly sensitive to crowding from same-lvl items (ie. words from words)
ATTENTIONAL DYSLEXIA: WARRINGTON (1993)
- migration of letters to analogous position (info within-word letter position = preserved despite attentional deficit) in other words (ie. left hemisphere > heft hemisphere)
- disorder of attentional filter = larger window of attention > target part of visual field; lets in other info
- specific to reading as doesn’t hold for pics
- flankers’ nature modulates manifestation of disorders; less interference w/dif category than w/same category distractors
NEGLECT DYSLEXIA: KINSBOURNE & WARRINGTON (1962)
- NOT attentional dyslexia
- oft not necessarily associated w/spatial neglect
- typically contralateral parietal lesion
- most common form = initial portion of word is problematic (ie. right lesion)
- aka. lend > end; wine > mine; oat > boat
MAIN SYMPTOM - failure to identify initial/final letters of word/group of words resulting in omissions/substitutions/additions
NEGLECT DYSLEXIA: ERRONEOUS LETTERS
- many erroneous letters to left/right of neglect point as neglected letters in target
- ie. car > bar; enigma > stigma (opposed to sigma)
- aka. some processing of neglected letters occurs; suggests that position = preserved BUT identity = lost
NEGLECT DYSLEXIA: IMPAIRMENT
- disorder of orientation of spatial attention but various lvls possible:
1) impairment tied to left visual hemi-field - ie. end x blend
2) impairment tied to left stimulus part irrespective of horizontal location in visual field - ie. end x end BUT (vertical) blend
3) impairment tied to onset word part irrespective of orientation (most abstract form of impairment) - ie. (vertical) end x (horizontal) end x (opposite vertical) end
PHONOLOGICAL DYSLEXIA
- lesion of temporal lobe of dominant hemisphere
- BUT reading words/visual letter string processing/immediate nonword repetition = relatively intact/perfect
- some patients read concrete words better than abstract words/show difficulty w/function (opposed to content) words
MAIN SYMPTOM - impaired ability to read new/made up words/nonwords or to sound out individual graphemes
PHONOLOGICAL DYSLEXIA: BEAUVOIS & DEROUESNE (1979)
- complex correspondences between letters group & 1 individual sound (ie. complex graphemes (“igh” read as “ai”) acquired late in reading development
- their less secured knowledge is therefore first to go compared to simple graphemes (ie. P read “p”)
- BUT sound familiarity to existing words improves reading performance on nonwords (ie. “brane”) as whole-word knowledge of existing homophone can compensate for failure to apply correspondence rules
PHONOLOGICAL DYSLEXIA: DRC
- explains poor performance on pseudowords by impairment (slowing down) of grapho-phonological conversion mechanism
DEEP DYSLEXIA: MARSHALL & NEWCOMBE (1973)
- associated w/extensive damage to dominant (left) hemisphere; consists of:
1) inability to read nonwords
2) semantically related errors (ill > sick; bush > tree; bad > liar)
3) visual errors (life > wife; sword > words); could be compensation by lexical knowledge for imprecise grapheme-phoneme conversion
4) derivational errors (card > cards; fleeing > flee; beg > beggar)
5) effect of syntactical class (nouns > adjectives > verbs > functors); shared w/phonological dyslexia
6) effect of imageability (concrete > abstract words); shared w/phonological dyslexia
DEEP DYSLEXIA: COMMON EXPLANATION
- reading only by semantic lexical route
- all other routes (nonsemantic lexical/graphophonological) = impaired
- interpretation of this symptomatology in DRC would implicate damage to both nonlexical route/direct nonsemantic lexical route
- the only way to retrieve pronunciation is via semantic system
DEEP DYSLEXIA: SEMANTIC ERRORS
- semantic route = by default inaccurate w/selecting words for speech production
- patient has no info about target word other than meaning
- would explain imageability effect & low performance on functors
- NOT sign of damage to semantic system; just sign that this may be only source of knowledge available to achieve pronunciation
SURFACE DYSLEXIA: MARSHALLL & NEWCOMBE (1973)
MAIN SYMTPOMS
- regularisations (typical pronunciation chosen) esp. for low frequency irregular words (ie. pint rhyming w/mint)
- stress shift (ie. guiTAR > GUItar)
- comprehension based on pronunciation (ie. bear = alcoholic beverage (beer))
- failures to apply contextual rules (ie. insect > insist; guest > just)
- incomplete decoding of diagram vowels (ie. niece > nice)
SURFACE DYSLEXIA: ARGUMENT FOR NONLEXICAL ROUTE
- reading regular words/nonwords = spared
- traditional interpretation = impairment of lexical route; reading primarily reflects reliance on nonlexical route & thus GPC reliance
- strong sensitivity to regularity = critical variable
- better performance on frequent > rare irregular words interpreted into -> representations of rare irregular words are more likely to go > frequent irregular words
- aka. surface dyslexia = argument for nonlexical route existence
SURFACE DYSLEXIA: DRC
- at least 3 possible functional loci:
1) orthographic input lexicon (or access to it)
2) pathway between orthographic input/phonological output lexica
3) phonological output lexicon (or its connection w/lower speech lvls)
SURFACE DYSLEXIA: LIMITATIONS TO NONLEXICAL ROUTE ARGUMENT
- DRC doesn’t explain lexical errors that aren’t just regulations (ie. incense > increase; barge > bargain)
- surface dyslexia possibly reflects compensatory strategy given slowness of reading/occasional use of letter names
LAMBON-RALPH & PATTERSON (2005) - damage to lexical route doesn’t explain why surface dyslexia tends to be associated w/semantic dyslexia
SEMANTIC DYSLEXIA
- aka. reading w/o meaning
- disorder associated w/neurological disease (ie. Alzheimer’s/semantic dementia)
- most patients evolve towards surface dyslexia (itself associated w/semantic disorders)
- damage to semantic system = most straightforward explanation in DRC
MAIN SYMPTOM - ability of patients to read fast/fluently (even irregular words in some patients) BUT inability to comprehend what they’re reading
SEMANTIC DYSLEXIA: SCHWARTZ ET AL. (1980)
- case of WLP (patient w/semantic dementia)
- can:
1) read pseudowords
2) match spoken word (“brain”) w/written pseudohomophone (brane”
3) read aloud irregular words (pint) which by contrast she cannot define/match w/picture - BUT fails at object naming task (1/70) though she can mimic use of certain objects (-> poor conceptual knowledge)
- aka. DRC w/o semantic system
- WLP -> drastic revision of dual-route theory; needed to include direct (non-semantic) lexical route to explain good performance on irregular words in absence of semantic access
SEMANTIC DYSLEXIA: PRE WLP
- reading was thought to involve only semantic route & grapho-phonological route
- reading irregular words w/o comprehension was impossible for this concept
- semantic dyslexia patients forced to distinguish:
1) within lexical system
2) between access to meaning
3) access to pronounciation - aka. DRC became TRC (three-route reading theory)
