The uHot Stroke" and Transient VascularOcclusionsBY PHILIP R. YARNEU, M.D.,* MICHAEL P. EARNEST, M.D.,*

BOB SANDERS, M.D.,t AND DUNCAN BURDICK, M.D.t

Abstract:The "HotStroke"andTransientVascularOcclusions

• Two patients with left middle cerebral artery (MCA) distribution infarctions fulfilled the"hot stroke" criteria on sequential 99m Tc pertechnetate flow and static gamma camerastudies. The radioisotopic finding of a paradoxical relative increased flow to the affectedhemisphere correlated with serial angiography showing multiple MCA branch occlusionsbecoming patent with a vascular blush and early venous drainage. The angiographical finding oftransient vascular occlusions suggests embolism. Using the present cases together with priorobservations, some transient vascular occlusions can be diagnosed by finding an increase inrelative radioisotopic flow to the involved hemisphere within a few days to weeks of the infarc-tion. This finding should launch a search for a possible embolic source.

Additional Key Wordsembolism

gamma cameraradioisotopic flow

arterial branch occlusionscerebral infarct

• The "hot stroke" phenomenon1 has been defined asthe paradoxical transiently increased relativeradioisotopic perfusion to an area of cerebral infarc-tion as seen with 99m Tc pertechnetate gammacamera imaging. Other investigators also have seenthis finding.2 The angiographical correlation was avascular blush and/or early venous drainage of the in-volved area. Recently, patients serially studied bothradioisotopically and angiographically have providedthe first demonstration of the full evolution of a "hotstroke." With these cases as illustrative examples, weare able to correlate prior angiographical andradioisotopic observations and more strongly suggestetiological implications.

Case ReportsPATIENT NO. 1

A 62-year-old right-handed office worker slumped to thefloor at his job without losing consciousness. On admission(day 1) he was awake and able to follow simple commandsbut had a dense nonfluent aphasia. Examination revealed aright hemiparesis with maximal involvement of the arm,right extensor plantar reflex, right-sided inattention deficit,poor right lateral gaze movements and left ptosis and miosis.

There was a history of a myocardial infarction 12 yearsbefore with full recovery. Prior hypertension, which hadreturned to normotension for the last several years withoutmedication, had been recorded.

Laboratory evaluations were all consistent with acerebral ischemic infarction. Serial 99m Tc pertechnetateradioisotopic flow and static gamma camera studies andangiography documenting his left hemispheric infarction aresummarized in table 1 (figs. 1-3).

'Departments of Neurology and fRadiology, University ofColorado Medical School, Denver General Hospital, Denver,Colorado 80204.

The patient stabilized and was anticoagulated with war-farin sodium. At six weeks a benign-appearing atheroscle-rotic plaque was removed from his left carotid bifurcation.A few months later he had a reversible episode of paresis ofthe left hand. No vascular lesions were demonstrated in thesupply of his right hemisphere. He was placed on an-ticoagulation. His neurological residua included paralysis ofthe right hand and an expressive aphasia.

PATIENT NO. 2

A 61-year-old white man had an acute right-sided paresis,gaze deviation to the left, and inability to speak three daysafter aorto-coronary bypass graft surgery. He had a historyof a myocardial infarct three years prior with persistentangina, and a traumatic amputation of the right leg. Spinalfluid examination was unremarkable. Serial angiographicaland radioisotopic studies revealed a left parietal infarctionas well as clinically unsuspected right posterior circulationinfarcts. These studies are detailed in table 1 (figs. 4 and 5).He improved and was started on oral anticoagulants after aweek. On transfer to a rehabilitation hospital he was stillmute and had a right lower facial paresis with his tonguedeviating to the right.

DiscussionTransient middle cerebral artery (MCA) branchocclusions in cerebral infarction patients have beenrepeatedly verified angiographically by many in-vestigators.38 It has been stressed that the opportunityto see these transient occlusions is dependent on thetiming of the sequential angiograms, i.e., the earlierthe angiogram, the greater the frequency of findingocclusions.35'7 The movement or disappearance of anocclusive process on subsequent angiograms is con-sidered by some as diagnostic of intracranial em-boli.9'10 Dalai, Shah and Aiyar,4 in a hallmark study,were able to document restored middle cerebral cir-

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YARNELL, EARNEST, SANDIRS, MJRDICK

nouu i

Patient No. I: left carotid angiogram. Day 1. There is occlusion of the major part of the MCA circulation.Later films showed partial retrograde filling via anterior cerebral collaterals to the parietal area.

culation in 7 of 14 known cerebral emboli patients.These patients had their first arteriogram within 60hours of their ictus and then again within 100 hours ofthe first study.

Our patients with angiographical documentationof disappearing MCA proximal branch occlusionsover a seven-day to 13-day interval most likely hadcerebral embolism. In Patient No. 1, atheromatous ul-cer at the common carotid bifurcation at firstappeared to be the likely source.10'" In view of hissubsequent symptoms, his prior myocardial injury12 orother central lesions may be implicated. In PatientNo. 2 the infarcts may be a neurological complicationof the aorto-coronary bypass surgery13 or also may berelated to his antecedent heart disease.12 The serialradioisotopic flow and static images in Patient No. 1correlated with the vascular paucity on the initialarteriogram followed by the restored patency,vascular blush and early venous shunting in the in-farcted area shown later. In Patient No. 2, theradioisotopic flow study was first done on Day 4 andthus already demonstrated the relative increased flow,while the angiographical sequence was as in PatientNo. 1. Both patients had evidence of multiple sites ofinvolvement. Patient No. 1 had a later contralateralsymptom, while Patient No. 2 radioisotopicallydemonstrated left middle cerebral and right posteriorcirculation infarcts.

From our earlier study1 and subsequent obser-vations, the relative increased flow to the infarctedside usually does not appear at the clinical onset.Rather, the relative increased flow may be seen as

early as the second day and then persists for about twoweeks. This is consistent with the immediate

FIGUM 1

Patient No. I: left carotid angiogram, Day 13, subtraction view.The arrows outline the area of vascular blush seen on this latearterial (three-second) film. Most of the previously occluded middlecerebral branches are now patent. The early regional venousdrainage was best seen on the four-second film.

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"HOT STROKE" AND TtANSIINT VASCULAR OCCLUSIONS

TAU.I1

Angiographical and Radioisotopic Correlation

Anglogrwn Rodlollotop* Itudy

Patient No. 1Day 1: Arch and bilateral carotid angiograms

revealed multiple occluded L MCA branches(fig. 1). There was retrograde anteriorcerebral collateral circulation to the parietalarea. Atherosclerosis at the L CCA bifurcationwith a question of ulceration was noted.

Day 13: L carotid angiogram revealed that most ofpreviously occluded MCA branches were nowpatent. There was a vascular blush in the MCAsuprasylvian distribution (fig. 2), and earlyparietal and deep venous drainage, i.e.,a "luxury perfusion." Retrograde collateralswere no longer present. A definite L CCAbifurcation ulcer was seen.

Patient No. 2Day 1: L carotid angiogram revealed a filling defect

in the proximal posterior MCA trunk (fig. 4).There was a paucity of parietal brancheswith anterior cerebral retrograde fillingcollaterals to this area.

Day 7: L carotid angiogram showed a vascular blushand marked early venous drainage in theparietal area (fig. 5). Most of the previouslyoccluded MCA branches were now patent andfilled anterograde. The previously seen fillingdefect and collateral circulation were nolonger present.

Day 2: Slight decreased L flow.Normal static images.

Day 8: Increased L flow. Moderatestatic uptake L frontoparietaland anterior frontal areas.

Day 13: Increased L flow (fig. 3).Marked static uptake L.

Day 16: Regression of increased Lflow laterally with nowdecreased L flow medially(mixed pattern). Markedstatic uptake L.

Day 21: Decreased L flow. Moderatestatic uptake L frontoparietal.

8 mo: Decreased L flow, slightstatic uptake L frontoparietal.

Day 3: Static images —slight Lparietal uptake.

Day 4: Increased L MCA distributionflow.

Day 10: Increased L flow. Marked Lparietal, R occipital and Rposterior fossa static uptake.

Day 14: Slightly increased L flow.Static images as Day 10,i.e., marked L parietal andR posterior circulation staticuptakes.

6 wk: Decreased L flow. Trace Lparietal uptake residua only.

L = left, R = right, MCA = middle cerebral artery, CCA = common carotid artery, mo = month, wk = week.

angiographical finding of proximal middle cerebralbranch occlusions which then reopen and show luxuryperfusion on subsequent angiography. Pathologically,this fits the hypothesis that embolus lysis or distalmigration explains cerebral infarction withoutobserved occluded vessels, as proposed by Fisher andAdams.14 Furthermore, Lhermitte, Gautier and

Derouesnd18 in a pathological survey postulated thatembolism is a major cause of MCA territory infarc-tion. This was particularly true in the absence of mid-dle cerebral or internal carotid artery occlusion atpostmortem examination. However, it should benoted that embolus is still only an inferential diagnosiswhen transient vascular occlusions are either seen

noun 3Patient No. 1: vertex 99m Tc pertechnetate flow study. Day 13. In this sequence of successive four-second intervals, thereis a prominent relatively increased left-sided perfusion (the dot is on the patient's right)

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nouu 4Patient No. 2: left carotid angiogram, Day 1. There is a filling defect(arrow) in the proximal portion of the posterior trunk of the MCAwith branch occlusions. Later films showed partial retrograde fillingvia anterior cerebral collaterals to the parietal area.

angiographically or suspected pathologically. Theremay be other as yet undefined processes that causetemporary obstruction,16 such as possibly a non-

Patient No. 2: left carotid angiogram. Day 7, subtraction view. Thearrows outline the vascular stain area on this late arterial film.Some previously occluded branches now fill. Early regional venousdrainage also is present.

atherosclerotic thrombosis with subsequent lysis.Serial radioisotopic flow and static gamma

camera studies are a nontraumatic method of studyingcerebral infarction. Those patients who incur an in-crease in the relative flow to the infarcted hemisphereover a few days to weeks are believed to have had tran-sient vascular obstructions. This "hot stroke" evolu-tion should then launch a search for the source of thisprocess, especially seeking a source of emboli. Unfor-tunately, there will be a significant group of infarctpatients in whom the cause of obstruction remains"unknown"" using our current investigative tech-niques. This should serve to stimulate further develop-ment of methods to find the etiology of these transientvascular occlusions.

AcknowledgmentWe would like to acknowledge the radioisotopic technical excellenceof Ron Ficalora, N.M.R.T.

References1. Yarnell P, Burdick D, Sanders B: The hot stroke. Arch Neural

30:65-69, 19742. Snow RM, Keynes JW Jr: The "luxury-perfusion syndrome"

following a cerebrovascular accident demonstrated byradionuclide angiography. J Nucl Med 13:907-909, 1974

3. Bladin PF: A radiologic and pathologic study of embolism ofthe internal carotid-middle cerebral arterial axis. Radiology82:615-625, 1964

4. Dalai PM, Shah PM, Aiyar RR: Arteriographic study ofcerebral embolism. Lancet 2:358-361, 1965

5. Zati LM, lannone AM, Eckman PB, et al: Observations con-cerning intracerebral vascular occlusions. Neurology13:389-401, 1965

6. Allcock JM: Occlusion of the middle cerebral artery; serialangiography as guide to conservative therapy. J Neurosurg27:353-363, 1967

7. Fieschi C, Bozzao L Transient embolic occlusion of the middlecerebral and internal carotid arteries in cerebral apoplexy. JNeurol Neurosurg Psychiat 32:236-240, 1969

8. Sindermann F, Dichgans J, Bergleiter R: Occlusion of the mid-dle cerebral artery and its branches: Angiographic andclinical correlates. Brain 92:607-620, 1969

9. Ring BA: The Neglected Cause of Stroke. St. Louis, Missouri,Warren H. Green, Inc, pp 104-123, 1969

10. Kishore PRS, Chase NE, Kricheff II: Carotid stenosis and in-tracranial emboli. Radiology 100:351-356, 1971

11. Wood EH, Correll JW: Atheromatous ulceration in majorneck vessels as a cause of cerebral embolism. Acta RadiolDiagn 9:520-536, 1969

12. Vost A, Wolochow DA, Howell DA: Incidence of infarcts o<the brain in heart disease. J Path Bact 88:463-470, 1964

13. Spencer FC, Green GE, Tice DA, et ah Bypass grafting forocclusive disease of the coronary arteries. Ann Surg173:1029-1044, 1971

14. Fisher M, Adams RD: Observations on brain embolism withspecial reference to the mechanism of hemorrhagic infarc-tion, (abstract) J Neuropath Exp Neurol 10:92-94, 1951

15. Lhermitte F, Gautier JC, Derouesne C: Nature of occlusionsof the middle cerebral artery. Neurology 20:82-88, 1970

16. Fisher CM: Cerebral ischemia — less familiar types. ClinNeurosurg 18:267-336, 1970

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PHILIP R. YARNELL, MICHAEL P. EARNEST, BOB SANDERS and DUNCAN BURDICKThe "Hot Stroke" and Transient Vascular Occlusions

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1975 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.6.5.517

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