Unusual association of diseases/symptoms

CASE REPORT

Dystypia in acute stroke not attributable to aphasia
or neglect
Fabian Alexander Blyth Cook,1 Stephen D J Makin,2 Joanna Wardlaw,3
Martin S Dennis3
1

University of Edinburgh,
Edinburgh, UK
2
Division of Clinical
Neuroimaging Sciences,
Western General Hospital,
Edinburgh, UK
3
Department of Clinical
Neurosciences,
Western General Hospital,
Edinburgh, UK
Correspondence to
Fabian Alexander Blyth Cook,
f.a.b.cook@sms.ed.ac.uk

SUMMARY
A 68-year-old right-handed man had a sudden onset of
impaired typing ability due to an ischaemic stroke that
recovered over 2 months. The typing impairment was
grossly out of proportion to his transient handwriting
disturbance. Diffusion MRI showed a recent acute left
temporoparietal infarct. There was no evidence of
aphasia, alexia, agraphia, visuospatial inattention,
sensory loss, neglect or poor coordination that could
account for his isolated typing impairment. This example
of a stroke that disproportionately affected typing more
than handwriting abilities has practical implications for
what deficits to look for in patients with stroke when
assessing their fitness for work and rehabilitation
requirements.
BACKGROUND

To cite: Cook FAB,
Makin SDJ, Wardlaw J, et al.
BMJ Case Rep Published
online: [ please include Day
Month Year] doi:10.1136/
bcr-2013-200257

Keyboard typing is a multifunctional task. To type
a familiar word such as ‘ball’ requires first accessing
some linguistic representation of the object,
whether orthographic or phonological. Next is the
conversion of this information into specific procedural motor functions. Typing differs from writing
in that one must be able to read the letters on the
keyboard to know which one to press. Alternatively
it requires some form of visuospatial memory that
maps each specific letter to a location on the keyboard, as is the case with ‘touch typing’. Lastly,
intact visual fields and visual-spatial attention along
with coordination and control of the fingers is
needed to push the correct keys.
There is likely to be a substantial overlap
between the processes required to write and type
and yet few studies have examined whether writing
and typing can actually be impaired separately.1–3
Recent work has shown that different patterns of
agraphia can be reversibly induced by electrical
stimulation during surgery of the left superior parietal gyrus with similar impairments in typing and
writing but minimal or no effects on oral spelling.1
The finding that a stroke can disproportionately
affect typing more than handwriting has practical
implications for assessing patients’’ fitness for work
after a stroke, particularly in an increasingly computerised society. It also may help us elucidate the
anatomical brain locations involved in the typing
process.

Figure 1 Handwriting sample written 1 day after his
stroke showing the words ‘Bell street’.
tried to use his computer. He had difficulty navigating the menu items and when he opened a word
processing programme he typed jumbled words.
His hand did not feel ‘normal’ when he wrote but
he was able to write with occasional difficulty. He
presented to hospital 1 day after his stroke with
impaired typing ability that took 2 months to
recover to baseline, while his handwriting was neat
and legible (figures 1–3). The patient was an
experienced typist who previously typed very well
with a ‘two finger’ technique without looking at
the keys.
The patient had a 2-year history of Parkinson’s
disease and associated micrographia. His writing
was legible and there was little change from his
prior ability when he presented to the hospital. His
Parkinsonian symptoms were well controlled on
cocareldopa. He had hypertension and was taking
ramipril, aspirin and a fibrate.

Examination findings
On neurological examination his coordination was
intact and he had no dysdiadokinesia. He was also
able to follow three-stage commands involving
taking a piece of paper in the right hand, folding it
and placing it on the ground. He also performed
the finger-to-nose test with no dysmetria or intention tremor. His resting tremor was well controlled.
He could write legibly showing intact fine motor
control. His cranial nerves II–XII were normal and
he did not show gaze preponderance, visual field
defects or spatial inattention in the doublesimultaneous stimulation test. This implies that
visual–spatial neglect was not the cause of his
typing errors. Upper and lower limb neurological
examination were normal and there were no other
examination findings.

CASE PRESENTATION
A 68-year-old man presented with a sudden onset,
1-day history of typing difficulty. Prior to presentation he had awoken from an afternoon nap and

Cook FAB, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200257

Figure 2 Typing sample 1 day after his stroke. There
are a further series of emails showing gradual
improvement for a further 2 months.
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Unusual association of diseases/symptoms

Figure 3 Typing sample 4 days after his stroke.

Four weeks poststroke he underwent further neurological
assessment and scored 28/30 on the mini-mental state examination, 88/100 on the Addenbrooke’s Cognitive Examinationrevised version (attention and orientation 17/18; memory 22/
26; verbal fluency 8/14; language 26/26; visual spatial 15/16)
and he scored 50/50 on the National Adult Reading Test. He
was only able to list seven words beginning with the letter ‘‘T’
and only 10 animals in 1 min which accounted for his reduced
verbal fluency. He did not show neglect or visual spatial impairment when copying pentagons, cubes and clock drawing as part
of the Addenbrooke’s. He could also count the number of dots
and correctly identify masked letters.

INVESTIGATIONS
Two days after his stroke, an MRI scan at 1.5 T showed a
recent left temporoparietal infarct consistent with his symptoms
(figure 4). Diffusion, FLAIR and T2-weighted imaging showed
scattered areas of increased signal in the left posterior insular
cortex involving a small area of the transverse temporal gyrus. In
addition there were extensive white matter hyperintensities in
keeping with background small vessel changes which were beginning to coalesce. There was also an old cortical infarct in the
right frontal cortex but no haemorrhage or microhaemorrhage.
A Speech and Language Therapy (SALT) assessment was
carried out at 3 weeks poststroke and showed that his typing
impairment was disproportionately worse than his writing.
This suggests that it was not just agraphia. His handwriting
was legible although micrographic with no spelling errors and
the same standard as before his stroke. There was also no deterioration for low frequency, irregular spelling words or
non-word-spelling. Irregular word spelling demonstrated that he
could store and use ‘whole-word’ representations. Whereas his
non-word spelling showed that his phonological processing was
intact. In comparison his spelling on the keyboard was significantly worse and the errors made were typically an additional
stroke of an adjacent key causing an incorrect letter insertion, or
a letter order error, for example, seize becomes ‘sieze’.
Importantly the errors were not confined to any one part of the

keyboard as they might have been if they were the result of
visual-spatial neglect. Neglect is also more commonly the result
of right-sided parietal lesions. He was able to construct fully
grammatical paragraphs. He demonstrated insight and was
aware of the mistakes in his typing and could correct them.
The typing deficit was not attributable to alexia. The patient
was able to read the newspaper and hospital forms and he
reported his reading ability was unaffected by his stroke. His
SALT assessment confirmed that he was able to read aloud fluently and scored 40/40 on the Western Aphasia Battery paragraph reading section. His visual scanning was slightly slowed
but he performed well in the letter identification task and continued to proofread writing for other people frequently in his
spare time.
The patient’s speech showed slight hesitation but was otherwise normal. He spoke in full grammatical sentences with no
obvious word finding difficulty or semantic or phonological
paraphasic errors. He described a loss of confidence with
fluency of his verbal expression but this was present before the
stroke. He was only able to list 10 animals in 1 min and listed
seven words beginning with the letter ‘T’. It was the opinion of
the speech and language therapist that this was an example of
thought freezing that he experienced under pressure. His auditory comprehension was unaffected. He was able to follow
complex sequential commands, retain and repeat complex sentences and showed no difficulty with right or left orientation.

DIFFERENTIAL DIAGNOSIS
The appearance on diffusion MRI—the signal change and lesion
distribution—as well as the appearance on the other sequences
were pathognomonic of a recent cortical infarct. There is no differential diagnosis for this particular MR appearance.

TREATMENT
Secondary stroke prevention in line with current guidelines
including early mobilisation and lifestyle advice. The patient is
already on aspirin, a fibrate and an ACE-inhibitor.

Figure 4 Two images from MRI,
diffusion imaging at 36 h after onset
showed an acute 21 mm infarct in the
left posterior insular cortex involving a
small area of the transverse temporal
gyrus. There was also an old cortical
infarct in the right frontal cortex.

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Cook FAB, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200257

Unusual association of diseases/symptoms
OUTCOME AND FOLLOW-UP
The patient’s typing fully recovered after 2 months evidenced
by a series of emails and self-report.

DISCUSSION
There are only a handful of studies that report a specific typing
impairment that is not attributable to agraphia, alexia, aphasia
or neglect. Only two of these studies to date have localised the
lesion on MRI.2 3 One of these is a recent case from Korea
showing a left frontal subcortical infarct on an MRI.2 The
authors suggest that damage to the dorsolateral prefrontal
cortex, the posterior parietal cortex or the connecting networks
between them may result in impairment in visual-spatial
memory for the position of the individual keys. Indeed there is
good evidence from cognitive neuroscience that the hippocampus and frontoparietal network play an important role in visualspatial memory.4 This explanation is compatible with our
patient where there is a temporoparietal infarct which could
interrupt this network. The other report is of a case from Japan
where the infarct is in a different area of the left frontal lobe.3
Interestingly, studies of ‘agraphia’ for pictograms have also
shown the lesion to be in the left frontal lobes.5 6 Unfortunately
the value of comparing these studies to our own is limited by
the individuals communicating in different languages. Korean
and Japanese both use pictograms rather than letters.
The first case report to describe a case of isolated typing
impairment was an American touch typist who had a left parietal infarct.7 However, this was only demonstrated on a CT
scan and she also presented with a mild aphasia and multiple
lesions. They argued that the parietal infarct caused a failure of
somatosensory monitoring on the grounds that when the patient
used her intact visual system to monitor typing she made far
fewer errors. There are other compatible explanations, for
example when the individuals looked at the keys, they no longer
had to rely on their visual–spatial memory that matches each
separate letter to a location on the keyboard. Rhu et al2 posit
that a loss of visuospatial memory, particularly for the keyboard
arrangement, is the reason for an isolated typing deficit in their
Korean patient. They showed that their patient had reduced performance on the ‘Rey-Osterrieth Complex Figure Test’ and the
‘Fill-in Keyboard Test’. These may be more relevant tests of
visuospatial memory than the ones that we used because our
patient scored 15/16 on the visual–spatial component of the
Addenbrook’s Cognitive Examination.
Recent work demonstrated that a small glioblastoma in the
left parietal lobe of an Italian patient resulted in a combined
agraphia for handwriting and typewriting.1 Furthermore electrical stimulation of the left superior parietal gyrus during
surgery could reversibly induce different patterns of agraphia
including written spelling errors or a complete cessation of
writing with minimal or no effects on oral spelling.1 Magrassi
et al1 argue that handwriting and typing share a working
memory grapheme buffer. However, the mechanisms associated
with visuospatial memory for typing are not fully understood
and there may be other processes involved. Our patient’s stroke
may have resulted in a further pattern of agraphia that disproportionately affects typing more than handwriting.
Our patient was impaired in semantic ( participants have to say
as many words from the category ‘animals’ in 60 s) and phonemic (as above but naming words beginning with the letter ‘T’)

Cook FAB, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200257

fluency. Parkinson’s disease patients are usually significantly more
impaired on semantic compared to phonemic fluency.8
Therefore, the deficit could be related to the ‘dystypia’ or alternatively white matter disease present prior to his stroke. A further
possibility is that the isolated typing impairment may be a selective form of apraxia that was not detected in the investigations but
he could perform three stage commands, imitate gestures (eg,
cough, stick out tongue) and reported no functional difficulties
except for his typing.

CONCLUSION
The patient is an example of a stroke that disproportionately
affected typing more than handwriting. This has practical implications for the deficits that we look for in patients with stroke
to assess their fitness for work.

Learning points
▸ The patient is an example of a stroke that disproportionately
affected typing more than handwriting. This has practical
implications for the deficits that we look for in stroke
patients when assessing their fitness for work.
▸ The increasing and near-universal dependence on computer
skills and communication through typing—email, text,
tweets, data entries—means that such deficits are likely to
become more common.
▸ Typing skills should be considered as part of rehabilitation
after stroke or other focal brain injury.

Acknowledgements The authors would like to give special thanks for the
Wellcome Trust funding.
Contributors SDJM was the research supervisor on this case report and has
provided invaluable advice over the past 2 years. He was the doctor who examined
the patient with sudden onset difficulty typing the day he presented to the hospital.
JW and MSD provided invaluable advice and support throughout the process.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
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2

3
4
5
6
7
8

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Otsuki M, Soma Y, Arihiro S, et al. Dystypia: isolated typing impairment without
aphasia, apraxia or visuospatial impairment. Eur Neurol 2002;47:136–40.
Pierrot-Deseilligny C, Müri RM, Rivaud-Pechoux S, et al. Cortical control of spatial
memory in humans: the visuooculomotor model. Ann Neurol 2002;52:10–19.
Tohgi H, Saitoh K, Takahashi S, et al. Agraphia and acalculia after a left prefrontal
(F1, F2) infarction. J Neurol Neurosurg Psychiatry 1995;58:629–32.
Sakurai Y, Matsumura K, Iwatsubo T, et al. Frontal pure agraphia for kanji or kana:
dissociation between morphology and phonology. Neurology 1997;49:946–52.
Boyle M, Canter GJ. Neuropsychological analysis of a typewriting disturbance
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Henry JD, Crawford JR. Verbal fluency in Parkinson’s disease: a meta-analysis.
J Neuropsychol Soc 2004;10:608–22.

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Unusual association of diseases/symptoms

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Cook FAB, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200257