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centre, of individuals identified with homonymous visual field loss post ischaemic stroke. Exclusion criteria were bilateral ischaemia, anterior / pregeniculate visual pathway affected and other pathology with the potential to effect visual fields. The following were extracted from the medical records; demographics, location of stroke, visual field mean deviation, and OCT measurements (>3 months post-stroke). A total of 15 individuals were included in the study, nine with hemianopia and six with quadrantanopia. Over half (53%), and all >2.5 years post-stroke, had more than 10% difference between the hemifields on the affected and unaffected sides. The degree of atrophy significantly correlated with time since stroke but not age or mean deviation on 24-2 SITA Fast. The authors describe three cases with serial OCTs and report the annual rate of atrophy of the ganglion cell layer plus inner plexiform layer in the affected hemifield. In view of not all cases developing threshold hemiatrophy, the authors have highlighted the need for further longitudinal studies. The authors acknowledge limitations including the small sample size and retrospective methodology. Transsynaptic retrograde degeneration can occur as early as six months post-stroke but often several years to develop. There is a possibility of using these findings to identify longstanding stroke related visual field loss if the individual did not present at the time of onset.

Transsynaptic ganglion cell degeneration in adult patients after occipital lobe stroke.
Donaldson L, Chen M, Margolin E.
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Lauren R Hepworth

University of Liverpool; Honorary Stroke Specialist Clinical Orthoptist, Northern Care Alliance NHS Foundation Trust; St Helen’s and Knowsley NHS Foundation Trust, UK.

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