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Reversed Robin Hood Syndrome in a Patient With Luxury Perfusion After Acute Ischemic Stroke

2011; Lippincott Williams & Wilkins; Volume: 123; Issue: 7 Linguagem: Inglês

10.1161/circulationaha.110.972000

1524-4539

Vijay K. Sharma, Hock Luen Teoh, Prakash Paliwal, Vincent Chong, Bernard P.L. Chan, Arvind Sinha,

Advanced Neuroimaging Techniques and Applications

HomeCirculationVol. 123, No. 7Reversed Robin Hood Syndrome in a Patient With Luxury Perfusion After Acute Ischemic Stroke Free AccessBrief ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessBrief ReportPDF/EPUBReversed Robin Hood Syndrome in a Patient With Luxury Perfusion After Acute Ischemic Stroke Vijay K. Sharma, Hock Luen Teoh, Prakash R. Paliwal, Vincent F. Chong, Bernard P.L. Chan and Arvind K. Sinha Vijay K. SharmaVijay K. Sharma From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. , Hock Luen TeohHock Luen Teoh From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. , Prakash R. PaliwalPrakash R. Paliwal From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. , Vincent F. ChongVincent F. Chong From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. , Bernard P.L. ChanBernard P.L. Chan From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. and Arvind K. SinhaArvind K. Sinha From the Division of Neurology (V.K.S., H.L.T., P.R.P., B.P.L.C.) and Department of Diagnostic Imaging (V.F.C., A.K.S.), National University Hospital, Singapore. Originally published22 Feb 2011https://doi.org/10.1161/CIRCULATIONAHA.110.972000Circulation. 2011;123:e243–e244A 49-year-old man presented with a 1-day history of multiple transient episodes of right-sided weakness. The episodes were stereotypical, precipitated by exertion, and lasted 5 to 10 minutes. He denied any chest pain, palpitation, headache, or injury. He was a chronic smoker (40 cigarettes per day for 20 years) and denied any past or family history of hypertension, diabetes mellitus, dyslipidemia, stroke, or ischemic heart disease.On arrival, he was fully conscious and oriented and had regular pulse (65 bpm), and blood pressure (145/90 mm Hg). Some word-finding difficulties and mild right-sided weakness (power, Medical Research Council grade 4) were noted (National Institute of Health Stroke Scale score, 4 points). Magnetic resonance imaging of the brain (Figure 1A) revealed multiple areas of restricted diffusion in the left middle cerebral artery (MCA) territory. Although the classic ultrasonographic findings were not seen on carotid duplex, the absence of significant atherosclerotic plaques and smooth tapering with severe luminal narrowing of internal carotid artery (ICA) strongly suggested a possible arterial dissection. The findings were confirmed on digital subtraction angiography (Figure 1B). Transcranial Doppler ultrasonography revealed anterior cross-filling of the left MCA via a patent anterior communicating artery. No spontaneous microembolic signals were noted on extended monitoring. Vasomotor reactivity1 was evaluated during voluntary breath holding for 30 seconds with simultaneous recording of both MCAs. Normal flow acceleration was noted in the right MCA during breath holding, but at the same time, the left MCA demonstrated a paradoxical reduction in flow velocities resulting from the intracranial steal phenomenon (Figure 2), the so-called reversed Robin Hood syndrome.2Download figureDownload PowerPointFigure 1. Neuroimaging findings in a patient with severe steno-occlusive disease of left ICA. Diffusion-weighted magnetic resonance imaging (A) shows multiple areas of restricted diffusion in the left MCA. Severe luminal narrowing of the left ICA with smooth tapering seen on digital subtraction angiography (B) suggests an arterial dissection. Increased cerebral blood volume (CBV) and cerebral blood flow (CBF) are noted in the left MCA territory despite an elevated mean transit time (MTT) on computed tomographic perfusion imaging (C through F). Baseline technetium-99–hexamethylpropyleneamine oxime single-photon emission computed tomography imaging (G) shows significantly increased perfusion in the left MCA territory despite multiple ischemic infarcts and severe ICA disease (luxury perfusion). Single-photon emission computed tomography imaging after acetazolamide (Diamox) challenge (H) shows a paradoxical reduction in the left MCA territory perfusion resulting from the reversed Robin Hood syndrome.Download figureDownload PowerPointFigure 2. Continuous transcranial Doppler monitoring of both MCAs during voluntary breath holding for 30 seconds. During breath holding, right MCA (RMCA) mean flow velocity increased significantly (from 40 to 58 cm/s). During the same period, the left MCA (LMCA) showed a paradoxical reduction in mean flow velocity (from 44 to 38 cm/s). Bottom, Overall trend of the flow velocities in both MCAs.Metabolic perfusion and cerebral vasodilatory reserve were evaluated by acetazolamide-challenged technetium-99–hexamethylpropyleneamine oxime single-photon emission computed tomography.3 Significantly increased perfusion (Figure 1G) in the left MCA territory despite multiple ischemic infarctions and severe ICA steno-occlusive disease suggested "luxury perfusion." However, a paradoxical reduction in the metabolic perfusion in the left MCA territory (Figure 1H) occurred after the vasodilatory challenge with acetazolamide, consistent with reversed Robin Hood syndrome on transcranial Doppler ultrasonography. Power in the patient's right extremities deteriorated transiently (to Medical Research Council grade 3, lasting ≈10 minutes) during the acetazolamide challenge.In addition to administering aspirin and statins, we kept our patient in the "head-down" position and provided liberal intravenous fluids to facilitate cerebral perfusion.4 Although we did not observe sleep apnea, nocturnal desaturation, or significant blood pressure reductions, he continued to have neurological fluctuations during the first week, especially on awakening. We hypothesize that the vicious cycles of transient hypoventilation-hypercapnia-intracranial steal phenomenon, occurring several times during sleep, accounted for his diurnal fluctuations. He made a slow but satisfactory recovery and was discharged after 3 weeks (modified Rankin Scale score, 0). Despite persistent and severe ICA steno-occlusive disease, he has remained symptom free during 4 months of follow-up. Normal vasomotor reactivity (and no reversed Robin Hood syndrome) was noted on transcranial Doppler ultrasonography reassessment at 3 months.In conclusion, we present a patient with acute ischemic infarctions in the MCA territory caused by spontaneous ICA dissection. Luxury perfusion is an uncommon brain imaging abnormality, usually seen after 3 to 7 days of infarction, and represents the failure of cerebrovascular autoregulation. Reversed Robin Hood syndrome in such cases might aggravate the tissue injury and should be considered if neurological fluctuations are noted during the early poststroke period.DisclosuresNone.FootnotesCorrespondence to Vijay K. Sharma, MD, Division of Neurology, Department of Medicine, 5 Lower Kent Ridge Rd, National University Hospital, Singapore 119074. E-mail [email protected]com.sgReferences1. Markus HS, Harrison MJ. Estimation of cerebrovascular reactivity using transcranial Doppler, including the use of breath-holding as the vasodilatory stimulus. Stroke. 1992; 23:668–673.LinkGoogle Scholar2. Alexandrov AV, Sharma VK, Lao AY, Tsivgoulis G, Malkoff MD, Alexandrov AW. Reversed Robin Hood syndrome in acute ischemic stroke patients. Stroke. 2007; 38:3045–3048.LinkGoogle Scholar3. Hirano T, Minematsu K, Hasegawa Y, Tanaka Y, Hayashida K, Yamaguchi T. Acetazolamide reactivity on 123I-IMP single photon emission computed tomography in patients with major cerebral artery occlusive disease: correlation with positron emission tomography parameters. J Cereb Blood Flow Metab. 1994; 14:763–770.CrossrefMedlineGoogle Scholar4. Wojner-Alexander AW, Garami Z, Chernyshev OY, Alexandrov AV. Heads down: flat positioning improves blood flow velocity in acute ischemic stroke. Neurology. 2005; 64:1354–1357.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Golovkova-Kucheriavaia М, Yanishevskiy S, Bochkarev М, Korostovtseva L and Sviryaev Y (2022) Pathogenetic links between ischemic stroke and sleep-disordered breathing, "Arterial'naya Gipertenziya" ("Arterial Hypertension"), 10.18705/1607-419X-2022-28-3-224-234, 28:3, (224-234) Bernard F, Barsan W, Diaz-Arrastia R, Merck L, Yeatts S and Shutter L (2022) Brain Oxygen Optimization in Severe Traumatic Brain Injury (BOOST-3): a multicentre, randomised, blinded-endpoint, comparative effectiveness study of brain tissue oxygen and intracranial pressure monitoring versus intracranial pressure alone, BMJ Open, 10.1136/bmjopen-2021-060188, 12:3, (e060188), Online publication date: 1-Mar-2022. Sivakumar S and Hakimi R (2022) Reversed Robin Hood Syndrome and Ischemic Stroke: Usefulness of Transcranial Doppler (TCD/TCCS) to Real-Time Monitoring Neurosonology in Critical Care, 10.1007/978-3-030-81419-9_33, (569-580), . Kepplinger J, Barlinn K, Kolieskova S, Shahripour R, Pallesen L, Schrempf W, Graehlert X, Schwanebeck U, Sisson A, Zerna C, Puetz V, Reichmann H, Albright K, Alexandrov A, Vosko M, Mikulik R, Bodechtel U and Alexandrov A (2013) Reversal of the neurological deficit in acute stroke with the signal of efficacy trial of auto-BPAP to limit damage from suspected sleep apnea (Reverse-STEAL): study protocol for a randomized controlled trial, Trials, 10.1186/1745-6215-14-252, 14:1, (252), . Barlinn K and Alexandrov A (2012) Sleep apnea and acute stroke deterioration Sleep, Stroke and Cardiovascular Disease, 10.1017/CBO9781139061056.011, (104-114) Tsivgoulis G, Apostolidou N, Giannopoulos S and Sharma V (2012) Hemodynamic causes of deterioration in acute ischemic stroke, Perspectives in Medicine, 10.1016/j.permed.2012.02.015, 1:1-12, (177-184), Online publication date: 1-Sep-2012. February 22, 2011Vol 123, Issue 7 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.110.972000PMID: 21343588 Originally publishedFebruary 22, 2011 PDF download Advertisement SubjectsIschemic StrokeNuclear Cardiology and PETUltrasoundVascular Biology