904 STROKE VOL 15, No 5, SEPTEMBER-OCTOBER 1984

This new physical sign, the elimination of a subjec-tive bruit with occlusion of ipsilateral temporal artery,indicates augmented flow due to ipsilateral internalcarotid obstruction. If a subjective bruit is not present,insertion of the finger into the ear canal may bring outthe bruit.

It is not certain how often this sign will be presentwithout any other physical evidence of augmentedflow through the external carotid system. The absenceof this sign does not rule-out significant stenosis orocclusion of the internal carotid artery. Caution shouldbe exercised in eliciting this sign: marginal blood sup-ply through the external carotid artery may be presentand the appearance of ocular or cerebral symptoms

with pressure over the temporal artery calls for imme-diate termination of the maneuver.

References1. Countee RW, Gnanadev A, Chavis P. Dilated episcleral arteries —

A significant physical finding in assessment of patients with cerebro-vascular insufficiency. Stroke 9: 42-45, 1978

2. Pessin MS, Panis W, Prager RJ, et al: Ascultation of cervical andocular bruits in extracranial carotid occlusive disease: clinical andangiographic study. Stroke 14: 246-249, 1983

3. Fisher CM: Facial pulses in internal carotid artery occlusion Neu-rology 20: 476-478, 1970

4. Millikan CH: A new sign of occlusion of the origin of the internalcarotid artery. Stroke 7: 546, 1976

5. Hardison JE, Smith RB, Crawley IS, et al: Self-heard venous hums.JAMA 245: 1146-1147, 1981

Massive Intracerebral Hemorrhage ComplicatingCardiac Catheterization with Ergonovine

AdministrationJOSEPH H. PIATT, J R . , M.D.

SUMMARY Massive Intracerebral hemorrhage Is reported as a complication of cardiac catheterizationwith ergonovine administration. Possible mechanisms relating stroke to cardiac catheterization are re-viewed. Patients who suffer neurologic deterioration after this procedure require prompt evaluation includ-ing computed tomography.

Stroke Vol 15, No 5, 1984

STROKE is a recognized but infrequent complicationof cardiac catheterization. In large series and surveysof catheterizations published in the last decade, theincidence of new, lasting neurologic deficits has beenreported between 0.02% and 0.2%,'~5 and several se-ries have been entirely free of this complication.6-7 Themechanism has been thought to be embolization ofthrombus stripped from the catheter tip or guidewire ordislodged from the endocardial surface, while somereports have stressed atheroembolism from plaques inthe aortic arch.8 In only a few cases has the pathologybeen defined by radiographic studies, operative inter-vention or autopsy.9"12 These cases have been charac-terized by embolic occlusion of a major cerebral arterywith infarction, often hemorrhagic, in the territory ofthe occluded vessel. In contradistinction to hemor-rhagic infarction, I was unable to discover a previousreport of massive intracerebral hemorrhage (ICH)complicating cardiac catheterization.

From the Division of Neurosurgery, Duke University Medical Cen-ter, Durham, North Carolina. During preparation of this mansucript,Dr. Piatt was supported in part by a training grant from the Neurobehav-ioral Science Research Training Program, NIMH Grant #MH15177.

Address correspondence to: Dr. Joseph H. Piatt, Jr., Box 31101,Duke University Medical Center, Durham, North Carolina 27710.

Received December 14, 1983: revision #1 accepted February 22,1984.

Case ReportThe patient is a 51 year old right-handed white

woman who was admitted for evaluation of chest pain.About one month earlier she had developed a dull,substemal pain radiating to the back and to both arms.Her pain was precipitated by exertion and was associ-ated with dyspnea. It lasted 5 to 10 minutes, and it wasameliorated by leaning forward, by rest and by nitro-glycerin. A treadmill test had been positive. There wasno history of diabetes or hypertension. She described achronic, bifrontal and bitemporal headache exacerbat-ed by anxiety and at the time of her menses. Theheadache was throbbing and infrequently associatedwith nausea and vomiting. It typically lasted severalhours at a time.

The brachial blood pressure was 125/85, and prior tocardiac catheterization it ranged no higher than 160torr systolic or 85 torr diastolic. The patient's weightwas 52 kg. The fundi were normal. There was a softsystolic bruit at the angle of the mandible on the left;the carotid pulses were normal. The cardiac rhythmwas regular. SI and S2 were normal, and there were nogallops. There was a grade 2/6 systolic murmur bestheard over the pulmonic area with radiation to the leftsternal border and to the apex. Peripheral pulses werenormal. The neurological examination was normal.

Routine laboratory work was normal. Specifically,

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HEMORRHAGE WITH ERGONOVWEJPiatt 905

the platelet count was 352,OOO/mm3; the prothrombintime was 10.3 s; the partial thromboplastin time was22.8 s; the erythrocyte sedimentation rate (Wester-gren) was 20 mm/hr. The electrocardiogram and chestx-ray were normal.

The patient was submitted to cardiac catheterizationfor evaluation of what was considered to be atypicalchest pain. A # 7 French pigtail catheter was intro-duced percutaneously into the right femoral artery andwas advanced retrograde across the aortic valve intothe left ventricle. The aortic blood pressure was 170/80. Heparin 2000 U. was administered intravenously.Left ventriculography and coronary angiography werecompletely normal. Ergonovine maleate 0.05 mg wasthen administered intravenously. This initial dose didnot produce symptoms, and 3 minutes later a seconddose of 0.1 mg was administered. The blood pressurerose transiently to 200/95. The patient, who had beenexperiencing her usual headache throughout the proce-dure, suddenly complained of a more severe headacheand then became unresponsive. She remained unre-sponsive for about 60 seconds, and during this period itwas noted that her eyes were deviated to the right.When consciousness was restored, sublingual nitro-glycerin was administered. The procedure was termi-nated, and upon returning to her room the patient wasobeying commands, moving all four extremities andcomplaining of a severe headache and nausea.

About 5 hours after the catheterization the patientwas found to be obtunded. She opened her eyes to loudverbal stimuli. Her speech was unintelligible, and sheobeyed no commands. There was a right hemiparesisaffecting the face and upper extremity more than thelower extremity. Right-sided hyperreflexia was noted,and the plantar response was extensor on the right. Acomputed tomographic (CT) scan of the brain withoutenhancement demonstrated a large frontoparietal intra-cerebral hematoma on the left with apparent ruptureinto the ipsilateral subdural space (fig. 1). The epicen-ter of the hematoma was in subcortical white matter,and it did not involve the basal ganglia. A left commoncarotid angiogram demonstrated only depression of theleft Sylvian point and a round shift of the anteriorcerebral artery from left to right; no abnormal vesselswere seen, nor were there any intraluminal filling de-fects. Because of the patient's declining level of con-sciousness and because of the mass effect evident onthe CT scan, an emergency craniotomy was performedfor evacuation of the intraparenchymal and subduralhematomas. The hematoma cavity was carefully in-spected for tumor or vascular malformation. No suchlesion was seen, and biopsies were taken from the wallof the cavity and from the cortical surface where it hadbeen breached by the hematoma. Upon awakeningfrom anesthesia the patient obeyed commands, and hersubsequent postoperative course was unremarkable.

FIGURE I. A CT scan without enhancement through the level of the frontal horns showed a crescentic, high-density,extracerebral collection over the left hemisphere with swelling of the underlying brain and shift of midline structures(left). At a higher level was a globular, high-density mass abutting the cortical surface on the same side as theextracerebral collection (right). At operation a large intraparenchymal hematoma was found to have ruptured into thesubdural space.

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906 STROKE VOL 15, No 5, SEPTEMBER-OCTOBER 1984

At the time of discharge her neurological examinationshowed an anomic dysphasia and a monoparesis of herright upper extremity. Microscopic examination of thebiopsies showed no tumor. The blood vessels includedin the specimen were normally formed. There was noamyloid or inflammatory infiltration of the vessels;Congo red staining was negative.

DiscussionSeveral different neurologic syndromes can compli-

cate cardiac catheterization, and specific diagnosis isnecessary for intelligent management. Angiographiccontrast material can by itself cause alterations of con-sciousness, seizures and focal neurologic deficits suchas cortical blindness.8- " These reactions are often tran-sient, and with modern contrast agents they are nowvery infrequent. Hypotension and dehydration can pre-cipitate thrombosis of a major cerebral vessel.8- " Morecommonly there is embolization of the cerebral circu-lation as a consequence of catheter-related mishaps:thrombus, atheroma and air have all been implicatedin the generation of transient or permanent focal neu-rologic deficits in the course of cardiac catheteriza-tion.8"14 To this list of complications affecting the cen-tral nervous system, massive intracerebral hemorrhagemust now be added.

In this case the intracerebral hemorrhage appearedto arise in subcortical white matter without involvingthe basal ganglia or thalamus. These characteristicsdefine a "lobar" hemorrhage.1516 It is generallythought that patients with lobar hemorrhage have ahistory of hypertension less frequently than patientswith hemorrhage in other locations.15"18 One autopsyseries reported that in less than 8% of patients withlobar hemorrhage was hypertension the sole predispos-ing condition; the comparable figure for ganglionichemorrhage was 4 8 % . " Coagulopathy and blooddyscrasia, angiopathy, tumor, angiitis, aneurysm andvascular malformation account for variable portions ofclinical series of spontaneous lobar hemorrhages, butin the remaining 27-38% no etiology can bedetermined."-17

There was no evidence for chronic hypertension inthis case, but it seems reasonable to suspect that tran-sient arterial hypertension caused by the discomfort ofthe procedure and by the infusion of ergonovine20"23

may have acted in conjunction with some other under-lying condition to produce the consequent stroke.

There was no evidence in the admission laboratorydata to suggest that our patient had a preexisting co-agulopathy or blood dyscrasia, but she did receiveheparin 2000 U. at the start of the procedure. Walkerand associates studied the effects of comparable dosesof heparin in this setting and found prolongation of theLee-White clotting time 2 to 10 times normal for theduration of the catheterization.24 Nevertheless, the useof heparin to inhibit thrombus formation on the cath-eter and guidewire has become a standard techniqueand has been associated with infrequent, clinically sig-nificant hemorrhage.

The remaining recognized causes of lobar intracere-

bral hemorrhage were investigated appropriately andcan with reasonable assurance be eliminated from con-sideration. Microscopic examination of the biopsy ofthe wall of the hematoma cavity provided no supportfor diagnoses of amyloid angiopathy, angiitis or neo-plasia. An underlying vascular malformation wassought by angiography, by careful inspection of thehematoma cavity and by biopsy; none was found.

It is clear that the information available does notpermit assigning our patient's intracerebral hemor-rhage to a certain cause, and logic compels consider-ation of the possibility that this complication was acoincidence, a "pseudocomplication".7 Against thisconsideration is the patient's utter lack of predisposingconditions and the conjunction of two iatrogenicstresses: transient hypertension and anticoagulation.These stresses are common concomitants of cardiaccatheterization with ergonovine administration. Thefrequent performance of this procedure and the appar-ent absence from the literature of previous reports ofmassive ICH complicating it testify to its relative safe-ty. However, our experiences with this case indicatethat patients who suffer neurological changes after car-diac catheterization require prompt evaluation includ-ing a CT scan. Not all such patients are the victims ofcerebral embolism; some have suffered massive intra-cerebral hemorrhage and may require immediate neu-rosurgical attention.

AcknowledgmentsI wish to thank Dr. Wesley A. Cook, Jr. for permitting me to report

his patient and Dr. Peter C Burger for performing special stains of thebiopsy specimens.

References1. Abrams H, Adams D: The complications of coronary arteriog-

raphy. Circulation 52: 11-27, 1975 (abstr)2. Davis K, Kennedy J, Kemp H, Judkins M, Gosselin A, Killip T:

Complications of coronary arteriography from the CollaborativeStudy of Coronary Artery Surgery (CASS). Circulation 59: 1105-1112, 1979

3. Gwost J. Stoebe T, Chesler E, Weir E. Analysis of the complica-tions of cardiac catheterization over nine years. Cathet CardiovascDiagn 8: 13-21, 1982

4. Hansing C: The risk and cost of coronary angiography. II The riskof coronary angiography in Washington State. JAMA 242: 735-738, 1979

5. Kennedy J: Complications associated with cardiac catheterizationand angiography. Cathet Cardiovasc Diagn 8: 5-11, 1982

6. Bourassa M, Noble J: Complication rate of coronary arteriography.A review of 5250 cases studied by a percutaneous femoral tech-nique. Circulation 53: 106-114, 1976

7. Hildner F, Javier R, Tolentino A, Samet P: Pseudocomplicationsof cardiac catheterization: update. Cathet Cardiovasc Diagn 8: 43-47, 1982

8. Dawson D, Fischer E: Neurologic complications of cardiac cath-eterization. Neurology (Minneap) 27: 496-497, 1977

9. Giddings J, See J, Lewis R, Cosby R: Thromboembolism follow-ing coronary arteriography. Chest 61: 235-239, 1972

10. Stumer W, Mierzwiak D, Daniel C: Cerebral embolism with in-farction and death from dislodged thrombus during retrograde fem-oral arterial catheterization. J Forensic Sci 16: 484-492, 1971

11. Swan H: Complications involving the nervous system. Circulation37: III-42-III-45, 1968

12. Terplan K: Patterns of brain damage in infants and children withcongenital heart disease. Am J Dis Child 125: 175-185, 1973

13. Calverly R. Dodds W, Trapp W. Jenkins L: Hyperbaric treatment

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of cerebral air embolism: a report of a case following cardiaccathetenzation. Can Anaesth Soc J 18: 665-674, 1971

14. Murphy T, Piper C, Anderson C: Complications of left heart cath-eterization. Am Surg 37: 472^*75, 1971

15. Ropper A, Davis K: Lobar cerebral hemorrhages: acute clinicalsyndromes in 26 cases. Ann Neurol 8: 141-147, 1980

16. KaseC, Williams J, Wyatt D, MohrJ: Lobar intracerebral hemato-mas: clinical and CT analysis of 22 cases. Neurology (NY) 32:1146-1150, 1982

17. Weisberg L: Computerized tomography in intracranial hemor-rhage. Arch Neurol 36: 422^»26, 1979

18. Mohr J, Caplan L, Melski J, et al.: The Harvard CooperativeStroke Registry: a prospective registry. Neurology (Minneap) 28:754-762, 1978

19. McCormick W, Rosenfield D: Massive brain hemorrhage: a reviewof 144 cases and an examination of their causes. Stroke 4: 946-954, 1973

20 Clark B, Chu D, Aellig W: Actions on the heart and circulation. In:Berde B, Schild H, eds., Ergot Alkaloids and Related Compounds(Handbook of Experimental Pharmacology, Vol 49). New York,Springer-Verlag, 321-420, 1978

21. Casady G, Moore D, Bridenbaugh L: Post-partum hypertensionafter use of vasoconstrictor and oxytocic drugs. JAMA 172: 1011-1015, 1960

22. Heupler F, Proudfit W, Razavi M, Shirey E, Greenstreet R, Shel-don W: Ergonovine maleate provocative test for coronary arteryspasm. Am Heart J 41: 631-640, 1978

23 Curry C, PepineC, SabonaM, etal.: Hemodynamic and myocardi-al effects of ergonovine in patients with chest pain. Circulation 58:648-654, 1978

24. Walker W, Mundall S, Broderick H, Prasad B, Kim J, Ravi J:Systemic heparinization for femoral percutaneous coronary arteri-ography. N Engl J Med 288: 826-827, 1973

The Terminology of Transient Visual Loss Due toVascular Insufficiency

THOMAS R. HEDGES, M.D.

SUMMARY Transient visual loss due to cerebro-ocular vascular disease is a common symptom. Thepurpose of this paper is to present a unified terminology of the monocular vs. binocular or homonymoustypes. Lack of proper identification may lead to mis-diagnosis and improper management of these entities.Monocular blurred vision must be investigated since its origin is so commonly due to atherosclerosis of thecarotid system. Binocular blurred vision due to vertebro-basilar insufficiency is managed conservatively inalmost all instances.

Stroke Vol 15, No 5. 1984

IT IS UNIVERSALLY acknowledged that the mostreliable indicator of impending ischemic stroke is atransient ischemic attack.' The semantics of the ocularsymptomatology have become confusing and are oftenmerely referred to as transient visual obscurations. It isthe purpose of this communication to attempt to clarifythis matter.

The first distinction one must make in describing theocular symptoms is whether they are monocular orbinocular. The monocular attacks are designated asamaurosis fugax and transient monocular blindnessand are due to vascular insufficiency in the optic nerveand retina, whereas transient binocular blindness indi-cates involvement of the posterior visual pathways.Secondly, one should ascertain the duration of the at-tacks. Accompanying neurologic signs or symptomsprovide additional evidence as to the localization of theischemic process in the visual system.

Amaurosis fugax is a monocular fleeting attack ofpartial to total (rare) blindness lasting from seconds toa few minutes. It is usually considered to be due toemboli but may be due to a perfusion deficit at thenerve head as in papilledema or incipient anterior isch-

From the Ophthalmology Section, Pennsylvania Hospital, 8th andSpruce Streets, Philadelphia, Pennsylvania 19107

Address correspondence to: Thomas R Hedges, M.D., Ophthalmol-ogy Section, Pennsylvania Hospital, 8th and Spruce Streets, Philadel-phia, Pennsylvania 19107.

Received December 6, 1983; revision # I accepted March 21, 1984.

emic neuropathy. The word obscuration means veryfleeting loss of vision (few seconds). Transient visualobscurations may be most aptly applied to this phe-nomenon seen with papilledema; thus, as in pseudo-tumor cerebri especially and rarely in brain tumor,these attacks can be characteristic and associated withheadache and other neurologic signs or symptoms.

Transient Monocular Blindness is an episode oftransient visual obscuration longer in duration thanamaurosis fugax which may be partial or total. Partialblindness may take the form of a shadow coming frombelow up, from above down, or from the side (usuallytemporal). It may progress towards fixation and thenregress. A "shutter" effect may constrict the field andthen disappear. These attacks may last many minutes,hours and rarely several days. These episodes are prob-ably related to hemodynamic changes such as in hyper-tension or some hematological cause. Migraine is anuncommon cause of monocular visual loss. Patientswith bilateral carotid disease causing orbital hypoxiaeither due to retinal or optic nerve hypoperfusion canget transient visual loss but this is not simultaneous orbinocular.

Transient Binocular Blindness is usually due to ce-rebral ischemia affecting the calcarine cortex. It is bi-lateral and involves either the homonymous field, theinferior or superior altitudinal fields or the centralfields. These episodes usually last 5 to 30 minutes andoccasionally as long as several hours. They may exact-

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J H Piatt, Jradministration.

Massive intracerebral hemorrhage complicating cardiac catheterization with ergonovine

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1984 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.15.5.904

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