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Subacute Neurological Deterioration with Selective Axonal Injury in Patients with Acute Ischemic Stroke following Reperfusion of Middle Cerebral Artery Occlusion.
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PMID:  22087099     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
To date, the long-term effects of reperfusion on the salvaged brain tissues have not been addressed in the literature. We report 4 cases presenting subacute neurological deteriorations with selective axonal injury following reperfusion therapies for acute ischemic stroke. Our case series based on 4 patients showed common features distinct from those of early reperfusion injury in that (1) the neurological symptoms developed after 1-2 months of reperfusion therapies, (2) these symptoms were accompanied by the subcortical white matter changes on brain MRI, and (3) these findings were mostly reversible with time. This suggests that axons in the reperfused brain may be vulnerable to further neurological injury.
Authors:
Yang-Ha Hwang; Yong-Won Kim; Jongyeol Kim; Yong-Sun Kim; Sung-Pa Park; Chung-Kyu Suh
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Publication Detail:
Type:  Journal Article     Date:  2011-09-07
Journal Detail:
Title:  Case reports in neurology     Volume:  3     ISSN:  1662-680X     ISO Abbreviation:  Case Rep Neurol     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-11-17     Completed Date:  2011-11-23     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  101517693     Medline TA:  Case Rep Neurol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  199-202     Citation Subset:  -    
Affiliation:
Department of Neurology, Kyungpook National University Hospital, Daegu, Republic of Korea, Lubbock, Tex., USA.
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Journal ID (nlm-ta): Case Rep Neurol
Journal ID (publisher-id): CRN
ISSN: 1662-680X
Publisher: S. Karger AG, Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.ch
Article Information
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Copyright © 2011 by S. Karger AG, Basel
open-access:
collection publication date: Season: Sep-Dec Year: 2011
Electronic publication date: Day: 7 Month: 9 Year: 2011
pmc-release publication date: Day: 7 Month: 9 Year: 2011
Volume: 3 Issue: 3
First Page: 199 Last Page: 202
ID: 3214670
PubMed Id: 22087099
DOI: 10.1159/000331450
Publisher Id: crn0003-0199

Subacute Neurological Deterioration with Selective Axonal Injury in Patients with Acute Ischemic Stroke following Reperfusion of Middle Cerebral Artery Occlusion
Yang-Ha Hwangac*
Yong-Won Kimac
Jongyeol Kimd
Yong-Sun Kimbc
Sung-Pa Parka
Chung-Kyu Suhac
aDepartment of Neurology, Kyungpook National University Hospital, Daegu, Republic of Korea, Lubbock, Tex., USA
bDepartment of Neuroradiology, Kyungpook National University Hospital, Daegu, Republic of Korea, Lubbock, Tex., USA
cDepartment of Daegu-Gyeongbuk Cardio-Cerebrovascular Center, Kyungpook National University Hospital, Daegu, Republic of Korea, Lubbock, Tex., USA
dDepartment of Texas Tech University Health Sciences Center, Lubbock, Tex., USA
Correspondence: *Yang-Ha Hwang, MD, Department of Neurology and Daegu-Gyeongbuk Cardio-Cerebrovascular Center, Kyungpook National University Hospital, 200 Dongduk-ro, Jung-gu, Daegu 700-721 (Republic of Korea), Tel. +82 53 420 5758, E-Mail yangha.hwang@gmail.com

Introduction

Reopening of occluded vessels in patients with acute ischemic stroke has been one of the therapeutic options, which improves clinical outcome through regional reperfusion and salvage of threatened brain tissues [1]. Reperfusion, however, sometimes carries certain risks known as ‘cerebral reperfusion injury’ including no reflow phenomenon, postischemic hyperperfusion, or brain hemorrhage and edema associated with the breakdown of the blood-brain barrier, which mostly occur within 1 week after reperfusion [2, 3]. We herein report 4 cases that showed subacute neurological deterioration combined with newly developed brain white matter (WM) lesions presumably associated with selective axonal injury following reperfusion of occluded vessels after 1-2 months of index stroke.


Case Report
Illustrative Case (Case 1)

A 68-year-old, right-handed woman was admitted with gradual onset of speech disturbance. About 50 days prior to admission, she underwent intra-arterial reperfusion therapy for acute ischemic stroke due to left middle cerebral artery occlusion. With successful recanalization, her global aphasia and right arm weakness rapidly improved, and she regained excellent functional recovery with subtle right arm weakness. Two weeks before admission, she developed progressive onset of speech disturbance – she was not able to form words. Neurological examination showed expressive aphasia without any weakness of extremities. The brain MRI revealed increased signal intensities of the left subcortical WMs on T2WI, FLAIR, and DWI without any concomitant vascular occlusion of the corresponding artery. During hospitalization, she showed some improvement in spontaneous speech. One month after discharge, she recovered to her previous functional status with nearly complete resolution of speech disturbance. Follow-up brain MRI about 3 months following the second admission, showed decreased signal intensities of the left subcortical WMs on the same MRI sequences (fig.1). Details of the 4 cases are summarized in table1.


Discussion

To our knowledge, this is the first case report addressing the chronic effects of reperfusion, the so-called ‘delayed selective axonal injury in reperfused brain’, in cases with acute ischemic stroke due to middle cerebral artery occlusion. Moreover, neurological adverse events related to reperfusion in human ischemic stroke were reported within several days from onset [4, 5]. This type of reperfusion injury was expressed as brain hemorrhage or secondary ischemia associated with disruption of the blood-brain barrier, no reflow phenomenon, and postischemic hyperperfusion [2, 3, 6]. Our case series, however, have some common features distinct from those of early reperfusion injury in that (1) the neurological symptoms appeared after 1-2 months of reperfusion therapies, (2) these symptoms were accompanied by the subcortical WM changes on brain MRI, and (3) these findings were mostly reversible with time.

Microscopic cellular damage can occur in the reperfused brain. In general, neurons are more vulnerable than glial cells or blood vessels, and oligodendroglia are more vulnerable than astrocytes and microglia in the global ischemia model [7]. Our proposed explanation for delayed selective axonal injury in reperfused brain was as follows: during the first hours of focal ischemia, the neurons are more vulnerable to ischemia than axonal structures, so ischemia resistant axons have greater chance to survive with reperfusion. However, some survived axons can be damaged in the microenvironmental levels, and after passing the silent period, clinical deterioration and subcortical WM lesions may occur in some cases. Our findings may suggest that the reperfused brain may be susceptible after acute stages of ischemic stroke. Accordingly, long-term follow-up imaging might be needed to elucidate the real frequency and clinical features in the consecutive thrombolysis registry.


Disclosure Statement

The authors of the present study have no financial, personal, or professional relationships with other people or organizations that could reasonably be perceived as conflicts of interest or as potentially influencing or biasing their work.


References
1. Rha JH,JL Saver. The impact of recanalization on ischemic stroke outcome: a meta-analysisStrokeYear: 20073896797317272772
2. Pan J,Konstas AA,Bateman B,Ortolano GA,Pile-Spellman J. Reperfusion injury following cerebral ischemia: pathophysiology, MR imaging, and potential therapiesNeuroradiologyYear: 2007499310217177065
3. Schaller B,Graf R. Cerebral ischemia and reperfusion: the pathophysiologic concept as a basis for clinical therapyJ Cereb Blood Flow MetabYear: 20042435137115087705
4. Kidwell CS,Saver JL,Mattiello J,Starkman S,Vinuela F,Duckwiler G,Gobin YP,Jahan R,Vespa P,Villablanca JP,Liebeskind DS,Woods RP,Alger JR. Diffusion-perfusion MRI characterization of post-recanalization hyperperfusion in humansNeurologyYear: 2001572015202111739819
5. Kidwell CS,Saver JL,Starkman S,Duckwiler G,Jahan R,Vespa P,Villablanca JP,Liebeskind DS,Gobin YP,Vinuela F,Alger JR. Late secondary ischemic injury in patients receiving intraarterial thrombolysisAnn NeurolYear: 20025269870312447922
6. White BC,Sullivan JM,DeGracia DJ,O'Neil BJ,Neumar RW,Grossman LI,Rafols JA,Krause GS. Brain ischemia and reperfusion: molecular mechanisms of neuronal injuryJ Neurol SciYear: 200017913311054482
7. Garcia JH,Lassen NA,Weiller C,Sperling B,Nakagawara J. Ischemic stroke and incomplete infarctionStrokeYear: 1996277617658614945

Article Categories:
  • Published: September 2011

Keywords: Key Words Reperfusion, Acute ischemic stroke, Neurological deterioration.

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