Acquired Dyslexia

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Acquired Dyslexia: Its Causes and Effects
By
Marie Claire Sammut
Bachelor of Psychology: Learning Disabilities
INE 3622
Acquired Dyslexia: Its Causes and Effects
Learning disabilities is an umbrella term for a variety of neurologically-based processing
problems. These disorders can make it challenging for a person to learn as fast, or in the similar
way, as someone who is not affected by a learning disability. One of the most common, and
best known, learning disabilities, is dyslexia. According to the International Dyslexia
Association (2002), dyslexia is a language-based learning disability which refers to a cluster of
symptoms that result in people having difficulties with specific language skills, particularly in
reading. There are two types of dyslexia, developmental and acquired dyslexia. Developmental
dyslexia is a neurological based disorder which interferes with the processing and acquisition
of language. (Orton Dyslexia Society, 1995). Most dyslexia is developmental, but dyslexia can
also be acquired.
Acquired Dyslexia is an acquired disturbance in reading ability that has been previously learnt.
This can result from a traumatic brain injury or stroke to the areas of the brain responsible for
learning written language. The extensive damage causes the loss or impairment to comprehend
written language even if it has already been previously learnt. Cherney (2004) said that
generally, visual processing problems are caused by disturbances coming from right brain
damage, whereas left-brain damage usually results in a linguistic deficit (Cherney, 2004).
Another word for acquired dyslexia is alexia. Alexia is the term used when a person loses the
ability to read or understand words. Some causes of acquired dyslexia are; intraventricular
haemorrhage (from strokes), periventricular leukomalacia dyslexia, epilepsy, traumatic brain
injury, cerebral palsy, foetal alcohol syndrome and all conditions associated with damaged
magnocells. Some differences between acquired dyslexia and developmental dyslexia are; that
acquired dyslexia is much rarer, it is not genetic, unlike developmental dyslexia, and it is due
to localised, and not whole brain damage. Despite these differences, the strategies that help
developmental dyslexia also seem to help individuals with acquired dyslexia. There are many
different types of acquired dyslexia depending on where the damage is caused. The type of
dyslexia depends not only on the specific area damaged but also on the particular injury or
pathology affecting this area. This is the reason why some strategies may work on some people
and not on others. Evidence from brain imaging has shown that there is a brain area which is
hypothesised to be specialised in recognising words and letters, called the visual word form
area. This is the area that is usually seen to be damaged in individuals with acquired
dyslexia. There are 2 categorical types of acquired dyslexia; peripheral dyslexia and central
dyslexia. These categories are also split into several other types of acquired dyslexia.
Peripheral dyslexia is characterised by a visual deficit in word processing and the inability to
match familiar words to its stored visual from in the brain as a result of brain injury. Peripheral
dyslexia is split up into subgroups which include; pure dyslexia, neglect dyslexia and
attentional dyslexia (Coslett, 2000). Pure dyslexia, also known as phonologically-based
dyslexia, dyslexia without agraphia or pure word blindness, is having difficulty in recognizing
all types of words; novel, regular and irregular, especially in sequence. Words are read letterby-letter as the word cannot be recognised as a whole. It is considered to be ‘pure’, as it does
not cause speech, handwriting, language or comprehension impairments. The affected
individual can write, but cannot read. As stated by Coslett (2000), pure dyslexia is caused by
legions in the corpus colostrum or in the left visual cortex (Coslett, 2000). In neglect dyslexia,
the reader has a problem with reading the first letter of words. The first letter is either skipped
or misread, for example ‘plane’ is read as ‘lane’. Neglect dyslexia is associated with lesions in
the right parietal lobe. In attention dyslexia, the individual sees letters crowded and blending
into one. The lack of spacing between words makes reading slow. The other subgroup of
peripheral dyslexia is attentional dyslexia. Attentional dyslexia is a reading deficit where letters
appear to migrate between words next to each other. Letter migration is caused by failure of
the letter to word binding system. An individual with attentional dyslexia can read words but
find it difficult to read individual letters. Reading is much easier if the letter or word is
presented in isolation rather than when presented in a sentence. There is barely any research
about what brain damage causes this type of dyslexia but it is typically correlated with damage
to the left parietal lobe.
Central dyslexia involves impairments in lexical or sub-lexical processing and the individuals
affected will also have a general language disorder. These impairments affect the cognitive
processing operations occurring in the central nervous system after the words have been
visually analysed. Besides not being able to read very well, the individual will also have
problems with writing. Subtypes of this dyslexia are; surface, deep, phonological and semantic
dyslexia (Coslett, 2000).
Surface dyslexia, first defined by Marshall and Newcombe (1973), is characterised by the
incapability to read ‘irregular’ words where the letters written are not consistent with the sound
they make and do not follow traditional pronunciation rules. (Marshall. J, & Newcombe. F,
1973). Regular words and non-words are read correctly but surface dyslexics are impaired to
reading irregular or exception words. People with surface dyslexia have problems reading
words like yacht, island and pint. Surface dyslexics can read some irregular words correctly if
they are high frequency words and are seen very often, for example words like ‘some’ and
‘said’ (Coslett, 2002). Since irregular words are what cause problems to the individual, and not
regular or non-words, it shows that the brain damage is caused by an impairment in the lexical
route. The lexical route is a process in the dual-route theory of reading aloud, first described in
the 1970s, where readers can recognise known words by sight from a mental database.
Deep dyslexia involves having problems with reading unfamiliar words non-words. Another
problem which deep dyslexics encounter is semantic reading errors. For example, they would
read the word ship as boat. When deep dyslexics read individual words out loud, with no
context, what they actually say is semantically associated to the word that is trying to be read
but not orthographically or phonologically associated (Frackowiak, Friston, Howard,
Patterson, Price & Warburton, 1998). The cause of this reading deficit is typically associated
with extensive damage in the left hemisphere. For this reason, individuals with deep dyslexia
use their right hemisphere for reading. There are various hypotheses for how much reading is
actually done by the right hemisphere. No researcher has ever stated that deep dyslexics rely
solely on their right hemisphere to read. But, it is agreed upon that reading out loud, in deep
dyslexics, is accomplished by 3 processing steps; orthography processing, semantic processing
and phonological processing. Once any one of these processes cannot be carried out by the left
hemisphere, due to brain damage, then right hemisphere reading mechanism takes place. Some
evidence consistent with the right hemisphere hypothesis was reported by Patterson et al.
(1989), where they studied a girl who had her left hemisphere surgically removed. Two years
later, she had all the symptoms of a deep dyslexia.
Phonological dyslexia is the extreme difficulty to read which is a result of phonological
impairment. A person with phonological dyslexia cannot read unfamiliar words or non-words
because they struggle to manipulate the basic sounds of language and so, cannot sound words
out. This is very similar to deep dyslexia. The key difference between the two is that
phonological dyslexics are not prone to make semantic errors like a deep dyslexic would.
According to the dual-route cascaded model, the central problem in phonological dyslexia is
the individual’s inability to use the grapheme-phoneme conversion. Support for the dual-route
model comes from a study done by Caccappolo-van Vliet et al in 2004.
People who suffer from semantic dyslexia are incapable to properly match words to their
meanings in both reading and speech. They might say a synonym or a similar word instead of
the proper word they mean to say. Semantic dyslexia is usually paired with semantic dementia
as they have very similar symptoms. Semantic dementia is a neurodegenerative disorder
distinguished by the loss of semantic memory.
Cherney (2004), argued that there are very limited studies that have well defined and researched
into acquired dyslexia. The majority of the research conducted is about developmental
dyslexia, as it far more common. Since the legions in the brain associated with acquired
dyslexia vary, even from person to person, there are less studies which are well defined and
critically evaluated (Cherney, 2004). Phonological and surface dyslexia are researched quite
well in developmental dyslexia with many neuroimaging studies being conducted, which are
critical to be able to come up with treatment strategies to best assist dyslexic children in
learning to read. Perhaps the knowledge learned from studying developmental dyslexia could
be better utilised in the future to assist in also understanding and applying the knowledge
discovered, to further investing the causes of acquired dyslexia.
Reference list
Coltheart, M. (2000). Deep Dyslexia Is Right-Hemisphere Reading. Brain and Language, 71,
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https://brainaacn.org/alexia/
Imamović, K., Mrkonjić, Z., Sinanović, O., Vidović, M., & Zukić, S. (2011). Post-stroke
language disorders. Acta Clin Croat, 50(1), 79-94.
Luzzatti, C. (2008) Acquired Reading and Writing disorders. In Stemmer, B & Whitaker, H.A.
(Ed) Handbook of the Neuroscience of Language.
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Transactions
Of
The
Royal
Society
B-Biological
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