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Neurological consultation was requested 17 days after apparently uncomplicated coronary artery bypass grafting in a 73‐year old right‐handed woman who complained that she could no longer read properly. Blind from birth because of anophthalmia, she learned to read Braille at age 7 years using her left index finger, or middle finger if the index finger became “tired” (the right hemisphere may have better discrimination for complex spatial patterns4,7). She was a proficient Braille reader, normally reading 8–10 book chapters per day; however, on initial recovery from the operation, she could not read at all. Matters improved over the following days but her reading was still much slower than preoperatively (1–2 book chapters/day) and she reported making errors when reading, necessitating re‐reading, although she had no difficulty understanding what she read. Past medical history was unremarkable, aside from a right carotid endarterectomy performed several months previously.
On examination, her spoken language was fluent with no evidence of motor or sensory aphasia. There was no left‐sided sensory neglect or extinction, and no finger agnosia. Testing stereognosis in the left hand, she was able to identify a pen, ring, paper clip and watch, but was slow to identify a key, could not decide on the denomination of a coin (50p, heptagonal or 10p, circular) and thought a £1 coin was a badge, although she identified this immediately with the right hand. Two point discrimination was 3 mm on the pulp of the right index finger (minimum spacing possible between tines) but 5 mm on the pulp of the left index finger. As she had never learned letters or Arabic numerals, it was not possible to test for graphanaesthesia.
MRI of the brain showed a few punctate high signal hyperintense lesions on T2 weighted and FLAIR sequences in the subcortical white matter, thought to be ischaemic in origin, including one subjacent to the right motor cortex in the region of the internal watershed between the anterior and middle cerebral artery territories (fig 11).). In addition, there was marked acquired global brain atrophy, including the occipital lobes.
Three months later, she had still not returned to her previous level of reading fluency. A working diagnosis of Braille alexia due to an apperceptive tactile agnosia was made, of uncertain aetiology: acute onset and partial recovery strongly suggested a vascular event, supported by the structural brain imaging appearances, although neurodegenerative disorders first manifesting with acute postoperative language problems have been reported.8
Previous reports of Braille alexia are rare, and clinically heterogeneous with respect to early or late onset of blindness, premorbid fluency of Braille reading and presence or absence of additional neurological signs such as aphasia and hemiparesis, these differences reflecting lesion location and aetiology (vascular, neoplastic, neurodegenerative).1,2,3,4,5,6 Sensory limb symptoms, but without clinical or neurophysiological correlate, have been reported.5 In those cases undergoing neuroimaging, structural correlates have included bilateral occipital infarctions5 and selective calcarine atrophy in a patient with visual hallucinations,6 findings which correlate with functional imaging studies showing that visual cortical areas process tactile information in Braille readers.9 Dissociation between verbal and musical alexia in Braille has been reported following left middle cerebral artery infarction in a professional organist blind from childhood.3
Braille alexia, the tactile homologue of pure alexia (alexia without agraphia), a category specific visual agnosia, may result from disruption of different, possibly overlapping, psychoperceptual mechanisms, some analogous to those postulated in pure alexia.10 It may reflect problems integrating tactile information over the temporal or spatial domains, associative forms of agnosia (or tactile simultanagnosia). A frontal–parietal network may contribute to the integration of perception with action over time,11 and right hemisphere lesions may be associated with impaired integration of spatial information from multiple stimuli.12 Alternatively, Braille alexia may reflect perceptual impairment, an apperceptive form of agnosia. As Braille characters are close to the limits of normal perceptual resolution, impaired light touch perception following damage to the primary sensorimotor cortex or its connections may result in degraded tactile identification and slowed Braille reading speed.
Competing interests: None.