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We read with interest the short report by Leker and Biran,1 describing unidirectional dyslexia in a polyglot, and would like to offer alternative hypotheses for the symptomatology.
The case describes alexia while reading Hebrew, but not when reading English. This is a recognised neuro-ophthalmic phenomenon, which we have encountered in our practice in patients reading the Urdu language, another script written right to left.
The extent of reading difficulties in patients with hemianopia is well described.2 Patients with a right hemianopia cannot see letters following those already deciphered. Patients with a left hemianopia can read without difficulty, until they have to refixate the beginning of the next line which is in the hemianopic field, and their place in the text is then lost. It would be interesting to know if this was the case with this patient while reading English. Turning the page through 90° allows reading in the intact hemifield, and is standard advice to all patients with hemianopia.2 Also by turning a page through 180° the Hebrew text would have been readable and comprehensible, as this would allow horizontal reading in a left to right direction.
The process of reading consists of repetitive small saccadic eye movements alternating with periods of fixation. Semantic identification of word strings occurs during these pauses between the saccades. At the end of a line, a large saccade in the opposite direction, to the beginning of the next line occurs and the pattern of small saccades is repeated.3
Horizontal saccadic eye movements for reading are generated to peripheral visual stimuli (letters following those already interpreted). If the stimulus is in the hemianopic field, there is a primary inability to initiate the saccade (saccades can be generated without a target, but tend to be inaccurate4). Also, the parietal eye fields are involved in horizontal saccadic eye movements, and may be implicated in the reported case given the anatomical location of the haematoma. Parietal eye field neurons discharge while executing visually guided saccades, and during learned saccadic tasks, which may be important during reading,4 and parietal lesions are known to cause saccadic defects. Vertical saccades are mediated via a separate system.
In true alexia, reading error results from an inability to interpret written material. The anatomical basis of alexia without agraphia is well described. This usually occurs in association with a right hemianopia, colour anomia, cerebral dyschromatopsia, and prosopagnosia, and is seen in left occipital lesions with damage to the contralateral visual association fibres which cross in the splenium of the corpus callosum.5 Reading pathways are well defined from visual cortex to auditory cortex via the dominant left angular gyrus, and such lesions have essentially isolated the angular gyrus from visual input. We think that the reported case describes “pseudoalexia”5 or “hemianopic dyslexia”,1 where a fixation splitting hemianopia causes difficulty reading by obscuring parts of words.
Visual hallucinations are common in patients with hemianopias despite being rarely mentioned,5 and in this case represent a release phenomenon, as ictal activity and pharmacological causes were excluded. They are a prognostically favourable sign.2Palinopsia is also seen in hemianopic fields. It would be interesting to know what palinoptic imagery was seen in this case, and under what circumstances. Was it perseveration of the hallucinations, or “blindsight” imagery of objects in motion being detected in the blind hemifield (the Riddoch phenomenon).
The “fluttering” described in the intact visual field of the reported case may reflect the “bilateral effect” seen from unilateral occipital lesions, which affect the primary visual and extrastriate cortex. Such damage is thought to alter interhemispheric connections along their presplenial course and cause disturbance of visual attention.2 The effects are usually subtle relative to the hemianopia but often functionally significant.
We think that all the symptoms in the reported case can be accounted for within the realms of established knowledge, without postulating the existence of novel language associated neuronal networks in the right hemisphere.
The authors reply:
We thank Mohamed, Elsherbiny, and Goulding for their insightful comments regarding our paper.1-1 We also think that the essence of this case is the distinction between a peripheral and a central processing defect causing the lexical phenomenon encountered by our patient. Mohamed et al suggest saccadic dysfunction as a mechanism for explaining the unidirectional dyslexia in our patient. However, whereas such a mechanism can explain right to left dyslexia when reading sentences, our patient had the same language abnormalities when reading isolated words when such saccadic mechanisms are not as important. We agree with Mohamed et althat visual hallucinations in the hemianopic field represent a favourable sign as indeed exemplified by the favourable outcome in our patient. Furthermore, we concede that the fluttering motion probably contributed to our patient's lexical difficulties. As pointed out by Mohamed et al such motion results from alterations in interhemispheric (occipital) connections.1-2This favours a more central processing abnormality. Moreover, the persistence of the unidirectional dyslexia while the visual fields returned to normal, as well as the dissociation between reading Yiddish (written in Hebrew letters from right to left), which was preserved, to reading Hebrew which was abnormal both support a higher hierarchical disorder.
Last but not least, the role of the right hemisphere in language functions as suggested by our case is supported by recent observations on aphasia recovery after stroke.1-3
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