Acquired dyslexia, epilepsy, traumatic brain injury, cerebral palsy,











Acquired Dyslexia: Its Causes and Effects




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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 letter-by-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,

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.