Apraxia of eyelid opening secondary to right hemisphere infarction

Johnston, James C.; Rosenbaum, Daniel M.; Picone, C. M.; Grotta, James C.

doi:10.1002/ana.410250615

Cited by 33 publications

(9 citation statements)

References 15 publications

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“…A recent study confirmed the view that a distributed network in the left hemisphere is involved in face eupraxia and pointed to a role of a similarly distributed network present also in the right hemisphere [9], especially associated with movements of the upper face. The possibility that the right hemisphere plays some role in face eupraxis is supported by evidence of eyelid opening apraxia secondary to right hemisphere infarction [30]. A few studies have also documented that even posterior lesions can cause face apraxia [8,9,27,28].…”

Section: Discussionmentioning

confidence: 99%

Upper and Lower Face and Ideomotor Apraxia in Patients with Alzheimer’s Disease

Capone

Sala

Spinnler

et al. 2002

Behavioural Neurology

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Introduction:Apraxia of face movement in Alzheimer's disease (AD) has been rarely investigated. This study aimed at investigating the frequency of lower (mouth, tongue and throat) and upper (eyes and eyebrows) face apraxia, in AD and its relationship with limb apraxia and severity of dementia.Methods:Fifty seven patients with AD were tested with a new standardised test of face apraxia including upper and lower face movements, which uses an item-difficulty weigthed scoring procedure, the IMA test, a test of ideomotor apraxia and the M.O.D.A., a means to assess dementia severity.Results:Thirteen (23%) and 19 (33%) participants were below cut-off respectively on the upper and lower face apraxia test. Both sections of the Face Apraxia Test correlated significantly with the Ideomotor Apraxia Test. However, double dissociations between different types of apraxia were observed. Both the upper and lower face apraxia tests correlated significantly with the measure of dementia severity.Conclusions:The finding show that a proportion of AD patients fails face apraxia tests. Their face apraxia is interlinked with ideomotor limb apraxia, although dissociations are possible. Severity of dementia deterioration accounts for a good proportion of the variability of AD patients’ performance on face apraxia tests.

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Section: Discussionmentioning

confidence: 99%

Upper and Lower Face and Ideomotor Apraxia in Patients with Alzheimer’s Disease

Capone

Sala

Spinnler

et al. 2002

Behavioural Neurology

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“…This syndrome has usually been reported in extrapyramidal disease [2,5,6], and less frequently after acute bilateral or nondominant hemisphere infarctions [3,4,8]. We report a man who developed AEO after an infarction of the dominant hemisphere.…”

mentioning

confidence: 83%

Apraxia of eyelid opening secondary to a dominant hemispheric infarction

Kaiboriboon¹,

Oliveira²,

Leira³

2002

Journal of Neurology

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Sirs: Apraxia of eyelid opening (AEO) is a nonparalytic inability to open eyes at will in the absence of orbicularis oculi contraction, and always associated with forceful frontalis muscle contraction [6]. This syndrome has usually been reported in extrapyramidal disease [2,5,6], and less frequently after acute bilateral or nondominant hemisphere infarctions [3,4,8]. We report a man who developed AEO after an infarction of the dominant hemisphere.A 60-year-old man with no significant past medical history woke up in the early morning and could not answer to his wife although he could understand her. Then he returned to sleep. The patient woke up two hours later with right leg weakness. A magnetic resonance imaging (MRI) of the brain showed a left anterior cerebral artery territory infarction (Fig. 1). Cerebral angiography demonstrated 40 % stenosis of left internal carotid artery, total occlusion of the right internal carotid artery, and the right and left subclavian arteries. There were reverse flow and steal phenomenon in both vertebral arteries. During a left carotid artery catheterization, he suddenly became globally aphasic. A middle cerebral artery thrombus was then visualized, and intraarterial thrombolysis was carried out. Subsequent MRI of the brain indicated the presence of a new infarction involving the left middle cerebral artery territory predominantly over the left periinsular, frontal operculum, and perirolandic region (Fig. 2).After the procedure, the patient was alert but did not speak or produce sounds, although he could follow commands. Pupils were symmetric and equally reactive. The patient had left conjugate gaze LETTER TO THE EDITORS JON 627 Fig. 1 Pre-left internal carotid angiogram, MRI fluid attenuated inversion-recovery (FLAIR) images show signal hyperintensity in the territory of the left anterior cerebral artery.Fig. 2 Post-left internal carotid angiogram, MRI diffusion-weighted images (DWI) demonstrate previously identified signal hyperintensity in the left anterior cerebral artery territory and a new focal area of signal hyperintensity involving the left middle cerebral artery territory.

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“…It may appear de novo in deteriorating patients. [36][37][38] Despite several attempts to date, 39,40 no clinical feature has been validated to reliably measure level of consciousness in this setting, nor has there been a good way of documenting the early changes in level of consciousness. (In several recent studies evaluating decompressive craniectomy, only item 1a of the National Institutes of Health Stroke Scale has been used to link decreased level of consciousness to brain swelling.)…”

Section: Hemispheric Strokementioning

confidence: 99%