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Akinetopsia: acute presentation and evidence for persisting defects in motion vision
  1. Sarah A Cooper1,
  2. Anand C Joshi2,3,
  3. Pamela J Seenan4,
  4. Donald M Hadley5,
  5. Keith W Muir6,
  6. R John Leigh2,3,
  7. Richard A Metcalfe1
  1. 1Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK
  2. 2Department of Neurology, Veterans Affairs Medical Center and Case Western Reserve University, Cleveland, Ohio, USA
  3. 3Department of Biomedical Engineering, Veterans Affairs Medical Center and Case Western Reserve University, Cleveland, Ohio, USA
  4. 4Gartnavel General Hospital, Great Western Road, Glasgow, UK
  5. 5Department of Neuroradiology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK
  6. 6Division of Clinical Neurosciences, University of Glasgow, Southern General Hospital, Glasgow, UK
  1. Correspondence to Dr Richard Metcalfe, Institute of Neurological Sciences, Southern General Hospital, Glasgow, G51 4TF, UK; Richard.Metcalfe{at}glasgow.ac.uk

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Akinetopsia—selective loss of motion vision—is rarely described.1 2 Current evidence indicates that the brain treats moving stimuli as a distinct feature of vision.2 3 Thus, electrophysiological studies have identified cortical areas in the macaque monkey that encode the direction and speed of moving visual stimuli in visual area V5 and adjacent medial superior temporal visual area (MST).2 3 Inactivating V5/MST in macaque monkeys induces defects of motion vision that are evident with psychophysical testing or measurement of ocular tracking.2 3 Akinetopsia in patients after lesions such as stroke rarely persists, probably because several cortical areas contribute to human perception.2 Here, we present a patient's personal account of acute transient akinetopsia following stroke, and report how a patient with transient akinetopsia due a stroke 23 years previously still shows evidence of abnormal motion vision, based on his ocular tracking.

Patient 1 is a 61-year-old woman who sought medical advice the morning after sudden onset of visual disturbance. She had been well, apart from a mild bi-frontal headache until leaving work the preceding day. Travelling home she suddenly noticed that, although static objects appeared normal, smooth movements of people were seen as a series of discontinuous ‘freeze frames’. The opening of a train door was ‘broken up’ and those nearby appeared to ‘move in slow motion’. She was startled when surrounding passengers ‘suddenly moved’. Recognition of people or objects and visual acuity was preserved. These symptoms were unchanged when admitted to hospital 22 h later. She was an ex-smoker of 22 years with an unremarkable past medical …

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