Cooper, S.A.

Hadley, D.M.

Joshi, A.C.

Leigh, R.J.

Metcalfe, R.A.

Muir, K.W.

Seenan, P.J.

English

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Enlighten – Research publications by members of the University of Glasgow http://eprints.gla.ac.uk        Cooper, S.A., Joshi, A.C., Seenan, P.J., Hadley, D.M., Muir, K.W., Leigh, R.J., and Metcalfe, R.A. (2012) Akinetopsia: acute presentation and evidence for persisting defects in motion vision. Journal of Neurology, Neurosurgery & Psychiatry 83 (2). pp. 229-230. ISSN 0022-3050       0B0Bhttp://eprints.gla.ac.uk/61428/     Deposited on: 10 April 2012   Funding GG was funded by the Stroke Association.Competing interests None.Ethics approval This study was conducted with theapproval of the St George’s University EthicalCommittee.Provenance and peer review Not commissioned;externally peer reviewed.Received 24 June 2010Revised 15 October 2010Accepted 19 November 2010Published Online First 4 January 2011J Neurol Neurosurg Psychiatry 2012;83:228e229.doi:10.1136/jnnp.2010.222091REFERENCES1. Rothwell PM, Giles MF, Chandratheva A, et al. Effectof urgent treatment of transient ischaemic attack andminor stroke on early recurrent stroke (EXPRESSstudy): a prospective population-based sequentialcomparison. Lancet 2007;370:1432e42.2. Kothari RU, Pancioli A, Liu T, et al. Cincinnatiprehospital stroke scale: reproducibility and validity.Ann Emerg Med 1999;33:373e8.3. Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al.Validation and refinement of scores to predict veryearly stroke risk after transient ischaemic attack.Lancet 2007;369:283e92.4. Gulli G, Khan S, Markus HS. Vertebrobasilarstenosis predicts high early recurrent stroke risk inposterior circulation stroke and TIA. Stroke2009;40:2732e7.5. Harbison J, Hossain O, Jenkinson D, et al. Diagnosticaccuracy of stroke referrals from primary care,emergency room physicians, and ambulance staffusing the face arm speech test. Stroke2003;34:71e6.Akinetopsia: acute presentationand evidence for persistingdefects in motion visionAkinetopsiadselective loss of motionvisiondis rarely described.1 2 Currentevidence indicates that the brain treatsmoving stimuli as a distinct feature ofvision.2 3 Thus, electrophysiological studieshave identiﬁed cortical areas in the macaquemonkey that encode the direction and speedof moving visual stimuli in visual area V5and adjacent medial superior temporal visualarea (MST).2 3 Inactivating V5/MST inmacaque monkeys induces defects of motionvision that are evident with psychophysicaltesting or measurement of ocular tracking.2 3Akinetopsia in patients after lesions such asstroke rarely persists, probably becauseseveral cortical areas contribute to humanperception.2 Here, we present a patient’spersonal account of acute transient akine-topsia following stroke, and report howa patient with transient akinetopsia duea stroke 23 years previously still showsevidence of abnormal motion vision, basedon his ocular tracking.Patient 1 is a 61-year-old woman whosought medical advice the morning aftersudden onset of visual disturbance. She hadbeen well, apart from a mild bi-frontalheadache until leaving work the precedingday. Travelling home she suddenly noticedthat, although static objects appearednormal, smooth movements of people wereseen as a series of discontinuous ‘freezeframes’. The opening of a train door was‘broken up’ and those nearby appeared to‘move in slow motion’. She was startledwhen surrounding passengers ‘suddenlymoved’. Recognition of people or objects andvisual acuity was preserved. These symp-toms were unchanged when admitted tohospital 22 h later. She was an ex-smoker of22 years with an unremarkable past medicalhistory. Her only medication was celecoxibfor osteoarthritis. Her account can be foundin the accompanying online video.Her general examination was normal;blood pressure was 167/69. Pursuit andsaccadic eye movements were intact onexamination but not measured. ColourFigure 1 Ocular tracking responses of Patient 2. (AeD) Tracking of small laser target. When thetarget was stepped into his right visual hemifield and ramped either to the left (A) or right (B), inboth cases, his initial saccade was appropriate in size for the step but did not take into account thesubsequent ramp so that his eye landed off target (grey arrows). When the target was stepped intohis left visual hemifield and ramped either to the right (C) or left (D), his initial saccade wasaccurate (grey arrows), indicating that both the step and ramp were taken into account. (E,F)Ocular following responses (OFRs) of a vertically moving grating, with spatial frequency 0.17degrees/cycle. (E) Mean responses for Patient 2 when he viewed the display presented in hiscentral visual field (PC), left visual hemifield (PL) or right visual hemifield (PR). Also shown aremean responses of a representative control subject when he viewed the display in his central visualfield (CC). All responses of Patient 2 are smaller than those of the control subject, especiallydownwards, and the smallest responses occur during stimulation of his right visual hemifield. (F)Comparison of upward OFR of Patient 2 during the three viewing conditions and six control subjectsduring central viewing; percentiles of this box plot are indicated on the left. All of the patient’sresponses are significantly smaller than those of control subjects, and responses during stimulationof Patient 2’s right visual hemifield are significantly smaller than any other set of responses(p<0.02, ManneWhitney rank sum test).J Neurol Neurosurg Psychiatry February 2012 Vol 83 No 2 229PostScript group.bmj.com on April 10, 2012 - Published by jnnp.bmj.comDownloaded from vision and visual ﬁelds were normal. Herneurological examination was unremarkable.After 2 days her symptoms improved andhad resolved by day ﬁve. MRI demonstratedtiny multifocal areas of restricted diffusion(hyperintensity on diffusion-weightedimaging (DWI) and hypointensity onapparent diffusion coefﬁcient map) consis-tent with recent infarcts in the cortex andsubcortical white matter of the inferiorparietal lobe and parietaleoccipital junctionon the right (online supplementary ﬁgure 1).Lesions were not detected in her left cerebralhemisphere.Patient 2 is a 79-year-old former engineerwho suffered a left posterior hemisphericstroke at the age of 56, in 1986, causingdyslexia and dyscalculia (see online supple-mentary data).4 Soon afterwards, he becameaware that objects moving in his right visualhemiﬁeld appeared to jump from one loca-tion to the next. Thus, when he watchedbirds ﬂying outside his hospital window, ifthey appeared in his right visual hemiﬁeld,they seemed to jump rather than movesmoothly. All symptoms improved withina month, although he is still aware of milddifﬁculties estimating the speed of objects inhis right visual hemiﬁeld. When studied in1986, he showed a defect of both saccade andpursuit tracking of targets moving in hisright, but not in his left, visual hemiﬁeld.4This defect was similar to that reportedfollowing experimental lesions of extrafovealV5,2 3 and MRI demonstrated a left-sidedhemorrhagic infarction affecting Brodmannareas 37 and 19.4When re-evaluated in 2009, uncorrectedvisual acuitywas 20/20ODand 20/50OS andhe had a homonymous, partial, right superiorvisual quadrant defect; however, he couldeasily see the visual stimuli we used. Wemeasured (search coil) ocular tracking of stepand step-rampmotion of a small target (ﬁgure1AeD and online supplementary data).5 Ifthe stimulus moved in his right visual hemi-ﬁeld, the initial saccade was inaccurate;however, saccades to targets moving in hisleft visual hemiﬁeld were generally on target.Saccades to appearance of static targets ineither hemiﬁeld showed no signiﬁcant asym-metry. Thus, his retinotopic tracking defectpersisted after 23 years.4 We also testedmotion vision in his central ﬁeld, and eachhemiﬁeld, by measuring the ocular followingresponse (OFR) to vertically moving sine-wave gratings.5 Comparisons of Patient 2’smean OFRwith those of a control subject aredisplayed in ﬁgure 1E; all of his responses aresmaller than those of the control subject, andresponses during stimulation of his rightvisual hemiﬁeld are smallest. Comparison ofall upward OFRs from Patient 2 and sixcontrol subjects are shown in ﬁgure 1F.Patient 2’s OFRs during stimulation of hisright visual hemiﬁeld were signiﬁcantlysmaller than during stimulation of his left orcentral visual ﬁelds, and all of his responseswere smaller than those of control subjects.These two patients with akinetopsiadocument several features of this raredisorder. Patient 1 demonstrated how akine-topsia may present as a spectacular andisolated visual disturbance, affecting thewhole visual ﬁeld. The cerebral lesionscausing her global akinetopsia were detectedin only the right hemisphere. Signal changeson MRI affected her right inferior parietallobe and parietaleoccipital junction, butspared the homologue of V5. These ﬁndingsare consistent with studies indicating thatrostro-dorsal parietal, occipito-parietal andsuperior parietal cortex may all contribute toglobal motion processing.2 3 However, thepattern of scattered tiny foci of DWIhyperintensity is consistent with sponta-neous fragmentation of thrombus andreperfusion. Without perfusion imagingshortly after the ictus, it remains possiblethat the initial ischaemic insult was moreextensive, or even bilateral. Thus, our MRIﬁndings cannot deﬁnitively localise theanatomical substrate for her akinetopsia.Patient 2 reported disturbance of motionvision restricted to his right visual hemiﬁeld,and his left-hemisphere lesion encompassedmodern estimates of the human homologuefor V5.4 Twenty-three years later, he reportedonly minor, persisting disturbance of motionvision, but showed a persisting retinotopicdefect of tracking (ﬁgure 1) consistent withan extrafoveal V5 lesion.2 His OFR was moreimpaired for stimuli presented in his rightvisual hemiﬁeld.In summary, akinetopsia can present as anacute but transient phenomenon affectingthe complete visual ﬁeld due to unilateralcerebral lesions at more than one site. Longafter symptomatic akinetopsia has resolved,disturbance of motion vision may be detectedby abnormal tracking eye movements.Sarah A Cooper,1 Anand C Joshi,2,3Pamela J Seenan,4 Donald M Hadley,5Keith W Muir,6 R John Leigh,2,3Richard A Metcalfe11Department of Neurology, Institute of NeurologicalSciences, Southern General Hospital, Glasgow, UK;2Department of Neurology, Veterans Affairs MedicalCenter and Case Western Reserve University, Cleveland,Ohio, USA; 3Department of Biomedical Engineering,Veterans Affairs Medical Center and Case WesternReserve University, Cleveland, Ohio, USA; 4GartnavelGeneral Hospital, Great Western Road, Glasgow, UK;5Department of Neuroradiology, Institute of NeurologicalSciences, Southern General Hospital, Glasgow, UK;6Division of Clinical Neurosciences, University ofGlasgow, Southern General Hospital, Glasgow, UKCorrespondence to Dr Richard Metcalfe, Institute ofNeurological Sciences, Southern General Hospital,Glasgow, G51 4TF, UK; Richard.Metcalfe@glasgow.ac.uk< Additional materials are published online only. To viewthese files please visit the journal online (http://jnnp.bmj.com/content/83/2.toc).Competing interests None.Patient consent Obtained.Provenance and peer review Not commissioned;externally peer reviewed.Received 13 July 2010Revised 18 November 2010Accepted 20 November 2010Published Online First 8 January 2011J Neurol Neurosurg Psychiatry 2012;83:229e230.doi:10.1136/jnnp.2010.223727REFERENCES1. Barton JJS. Disorders of higher visual function. In:Kennard C, Leigh RJ, eds. Handbook of Neurology;Neuro-Ophthalmology. London: Elsevier, 2011.2. Shipp S, de Jong BM, Zihl J, et al. The brain activityrelated to residual motion vision in a patient withbilateral lesions of V5. Brain 1994;117:1023e38.3. Leigh RJ, Zee DS. The Neurology of Eye Movements.4th edn. New York: Oxford University Press, 2006.4. Thurston SE, Leigh RJ, Crawford T, et al. Two distinctdeficits of visual tracking caused by unilateral lesions ofcerebral cortex in humans. Ann Neurol1988;23:266e73.5. Joshi AC, Riley DE, Mustari MJ, et al. Selectivedefects of visual tracking in progressive supranuclearpalsy (PSP): implications for mechanisms of motionvision. Vision Res 2010;50:761e71.Cerebellar-type multiple systematrophy presenting withleucoencephalopathyIn June 2004, a 52-year-old woman wasadmitted to our department with a walkingimpairment and scanning speech that hadpersisted over the previous few months. Aneurological examination revealed exclu-sively cerebellar signs with gait ataxia, slightoculomotor dysfunction and impaired coor-dination. Known medical and family historywere unremarkable up to this point(however, no information could be providedon the patient’s father). MRI scans showeda severe cerebellar atrophy of both hemi-spheres without any additional pathologies.Electrophysiological (evoked potentials) andblood examination, including vitamin E,vitamin B12, antineuronal antibodies andgenetic testing for spinocerebellar ataxiagenotypes 1, 2, 3 and 6, were negative forpathological ﬁndings. Over the followingmonths the patient developed neurogenicbladder dysfunction with urge incontinenceand incomplete bladder release, thusfulﬁlling the consensus criteria for probablemultiple system atrophy of the cerebellartype (MSA-C).1We initiated a single photon emissiontomography investigation, which revealeda striatal dopaminergic deﬁcit and down-regulation of postsynaptic dopamine recep-tors; MIBG scans of the heart remainednormal. The patient was treated with aman-tadine up to 300 mg/day without showingany signiﬁcant improvement. Over time, thedisease slowly progressed: the patient neededconstant support when walking and shecomplained of cognitive deﬁcits but therewere still no signs of parkinsonism. As theinitial MRI scans lacked characteristic ﬁnd-ings for MSA-C,2 we repeated the MRI scansat the end of 2006. As expected, cerebellar230 J Neurol Neurosurg Psychiatry February 2012 Vol 83 No 2PostScript group.bmj.com on April 10, 2012 - Published by jnnp.bmj.comDownloaded from doi: 10.1136/jnnp.2010.223727online January 8, 2011 2012 83: 229-230 originally publishedJ Neurol Neurosurg Psychiatry Sarah A Cooper, Anand C Joshi, Pamela J Seenan, et al. visionevidence for persisting defects in motion Akinetopsia: acute presentation and http://jnnp.bmj.com/content/83/2/229.full.htmlUpdated information and services can be found at: These include:References http://jnnp.bmj.com/content/83/2/229.full.html#ref-list-1This article cites 3 articles, 1 of which can be accessed free at:serviceEmail alertingthe box at the top right corner of the online article.Receive free email alerts when new articles cite this article. Sign up inNotes http://group.bmj.com/group/rights-licensing/permissionsTo request permissions go to: http://journals.bmj.com/cgi/reprintformTo order reprints go to: http://group.bmj.com/subscribe/To subscribe to BMJ go to: group.bmj.com on April 10, 2012 - Published by jnnp.bmj.comDownloaded from 

Akinetopsia: acute presentation and evidence for persisting defects in motion vision

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Akinetopsia: acute presentation and evidence for persisting defects in motion vision

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