Spontaneous Ischemic Infarction ofthe Spinal Cord with Traumatic SequelaBY CHARLES BURTON, M.D.

Abstract:SpontaneousIschemicInfarction ofthe Spinal Cordwith TraumaticSequela

• What is believed to have been spontaneous infarction of the spinal cord isreported in two individuals with known chronic cardiovascular diseaseapparently causing paraparesis while driving motor vehicles. Although blunttrauma to the spinal cord cannot be ruled out, there was no objective evidenceof such. The history of spontaneous onset of paraplegia prior to trauma is clearin the first case but could only be inferred in the second case.

ADDITIONAL KEY WORDSvascular accidents

cardiovascular disease paraplegiaautomobile accidents

• Vascular accidents of the spinal cord havealways been considered a rare occurrence.Blackwood found only nine examples ofobstructive vascular lesions in a review of3,737 postmortem reports from the NationalHospital, Queens Square, London, in 1958.1

Innovations in diagnostic neuroradiology2 andmicrosurgery8 have initiated a resurgence ofinterest in spinal cord circulatory dynamicsresulting in a more astute appreciation ofvascular pathology and its clinical presenta-tions. This has been reflected in a number ofexcellent reviews4'B and case reports6-7 whichindicate that the incidence of spinal cordvascular disease remains to be determined.

Two cases of apparent spontaneous spinal"stroke" are presented in this communication.In both instances the vascular accident appearsto have been causally related to coincidentautomobile accidents.

CASE 1

A 67-year-old former seaman had a history ofrecent myocardial infarction, chronic "heartdisease," and thrombophlebitis for which he wastaking Coumadin. He was apparently doing welluntil, while driving on a clear day, he suddenly

From the Neurosurgical Service, United States PublicHealth Service Hospital, Seattle, Washington 98114.

Author's present address: Department of Neuro-surgery, Temple University Health Sciences Center,Broad and Ontario Streets, Philadelphia, Pennsylvania19140.

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lost the use of his legs, causing the car to run offthe road and crash. The accident did not involveanother person or vehicle. At time of admission tothe hospital, there was a complete paraplegia andpartial paralysis of the upper extremities with C5to 6 motor and sensory levels. The patient wasslightly disoriented as to time and speech wassomewhat slurred. External evidences of traumawere lacking and there was no complaint of heador neck pain. Skull and cervical spine x-rays werenormal. Chest x-rays disclosed an enlarged heartwith clear lung fields; serial EKGs were allabnormal, showing first degree AV and rightbundle block, frequent premature ventricularcontractions and left ventricular hypertrophy. Onlumbar puncture the opening pressure was 65 mmH2O, the fluid was clear, and manometrics werenormal. Two cubic centimeters of Pantopaque(ethyl iodophenylundecanoate) were injectedintrathecally and an incomplete myelographicalblock was seen in the Tl to 4 area suggestingspinal cord enlargement. Contrast media passedalong the left lateral gutter to the cervical area(fig. 1).

Although there was no direct evidence of aneck injury, it was deemed wise to place thepatient in Cone-Barton skull tongs with 8 lbtraction. Exploratory decompressive laminectomywas felt to be indicated but was not performedbecause of a prothrombin time of 14% and a poorresponse to Mephyton (phytonadione) therapy.Repeat cervical spine x-rays with special viewswere normal and the tongs were removed on theninth hospital day. On the thirteenth hospital daythe patient became febrile to 103°F due to a gramnegative urinary tract infection which responded

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FIGURE 1

Thoracic field of Pantopaque myelogram showing in-complete block beginning at arrow (T-6). This ex-tended in irregular fashion to about the C-7 segment.

to antibiotic therapy. Repeat myelographyperformed on the twenty-seventh hospital dayrevealed a filling pattern exactly similar to thepattern shown in figure 1.

The severity of the hematological andinfectious complications referred to above forcedpostponement of a C5 to T3 exploratorylaminectomy until the fifty-seventh day ofhospitalization during which time the neurologicaldeficit remained unchanged. Upon opening thedura, the cord was found to be grossly swollen.Dorsal myelotomy revealed complete liqueficationof the cord to the Tl level. No old clot orhemosiderin staining was present.

The initial postoperative course was benign,but the patient began to run a low-gTade feverwith progressive cardiac and renal failure whichdid not respond to therapy, and he died on theninety-third hospital day.

Autopsy revealed the cause of death to bepulmonary edema due to severe coronary arterio-sclerosis, and acute myocardial infarction withextensive interstitial myocardial fibrosis. Sections

of the spinal cord revealed very little tissue withinthe meninges identifiable as spinal cord from theC7 to T6 levels within the intact pia as it appearedgrossly as a sac filled with thin milky fluid.

CASE 2A 38-year-old Negro male USAF T Sargeant hada history of "pericarditis" 14, 12 and eight yearsprior to admission, as well as chronic hyperten-sion and a known episode of atrial fibrillation. Hewas otherwise active and in good health untilinvolvement in an automobile accident occurringunder peculiar circumstances. While he wasdriving alone on a highway at noon on a clear andsunny day, his car suddenly left the road along astraight section, rolled down an embankment, andcrashed. No cause for the accident could be foundby the police.

The patient was initially admitted to anotherhospital where he was alert and oriented butamnesic regarding the accident. Frontal andoccipital lacerations were sutured. The patient wasparaplegic and unable to void and had been so

FIGURE 2

Thoracic field of Pantopaque myelogram showingfusiform enlargement of spinal cord shadow at T5to T6 levels.

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INFARCTION OF THE SPINAL CORD

VERTEIRAL

VERTEIRAL

ASC. CERVICAL

SUP. INTERCOSTAL

INTERCOSTAL

ARTERIAMAGMA

FIGURE 3

Schematic illustration (redrawn from Doppman*)showing the spinal cord outline with the thoracic"watershed" zone in heavy dots and the relativearterial input on the right side. The descending arrowon the left indicates the extent of the physiologicaldeficit from a thoracic "watershed" zone lesion.

since the accident. X-rays of the cervical andthoracic spine were normal.

He was referred to the USPHS Hospital,Seattle, the following day, where he was noted tobe alert but slightly confused as to time and place.Blood pressure was 160/110 mm Hg and pulsewas 104 bpm and regular. Other than the scalplacerations and a trimalleolar fracture of the leftankle there were no other external evidences oftrauma. Flaccid paraplegia and C5 to 6 to 7 armweakness with a T4 sensory level were presentwith preservation of cremasteric reflexes. ABabinski sign was not present. EKG wasabnormal with nonspecific T wave changes.

X-rays of the cervical, thoracic, and lumbarspine, including tomography, were normal. Onlumbar puncture the opening pressure was 160mm H2O with grossly clear fluid and sluggishmanometrics. Cell count revealed 4,200 RBCs and

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one WBC per cubic millimeter. Treatment withparenteral Dextran and intramuscular Decadron(dexamethasone) was instituted. Panmyelographyperformed on the second hospital day revealed aT5 to 6 defect (figure 2), consistent withintramedullary swelling of the spinal cord. Thecontrast media were not removed.

Four days later the patient was transferred toMadigan Army Hospital where repeat fluoroscopyrevealed a complete myelographical block at T6and an exploratory thoracic decompressive lami-nectomy was performed. Upon opening the dura,the spinal cord was found to be grossly swollen.Dorsal myelotomy revealed infarcted spinal cordof "toothpaste" consistency which extrudedthrough the incision. No evidence of osseous-ligamentous trauma or hemorrhage was encoun-tered.

DiscussionThe first accurate accounts of spinal bloodsupply have been credited to Adamkiewicz8 andKadyi.9 Although Bastian10 extended Rey-nold's11 thoughts regarding the relationshipbetween vascular occlusion and cerebral soft-ening to include similar softenings in the cord,it was not until the development of arteriog-raphy (Moniz12) that such relationships couldbe documented occasionally. But even withcareful arteriography and postmortem examina-tion the diagnosis of spinal stroke has veryoften remained only a clinical impression.

This is also due in part to the greatamount of anatomical variation in the locationand dynamics of the major feeding arteries tothe spinal cord. Figure 3 illustrates diagram-matically the major arterial inputs to the spinalcord. The area in heavy dots represents the T4level where the vascular supply is tenuous,creating a "watershed" zone most susceptibleto ischemia.

In the cases presented it is believed thatthe spontaneous infarction of the cord occurredin the watershed zone, producing clinical deficitbeginning at the uppermost level of involve-ment. The presentation of such infarctions inindividuals with cardiovascular disease hasbeen reviewed by Henson and Parsons4 andrelates well to the cases presented here.

The history of spontaneous onset ofparaplegia was clear from the history obtainedin case 1, while it is inferred in case 2, due tothe unusual circumstances of the accident. Inboth cases there was focal necrosis of the spinalcord in the watershed zone. Clinical examina-

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tion and operative exploration revealed noevidence of gross trauma or tissue injury. Nohemorrhage or hemosiderin staining of thespinal cord or its coverings was found in eithercase.

AcknowledgmentThe author would like to express his appreciation toDrs. John T. West and Willard Johnson for theirassistance and support and to Dr. Randall Smith forproviding the follow-up history in case 2.

References1. Blackwood W: Discussion on vascular disease.

Proc Roy Soc Med 5 1 : 543-547, 19582. Doppman JL, DiChiro G, Ommaya AK:

Selective Arteriography of the Spinal Cord. St.Louis, W. H. Green, 1969

3. Yasargil MG: Microneurosurgery. New York,Academic Press, 1969

4. Henson RA, Parsons M: Ischemic lesions ofthe spinal cord: An illustrated review. Quart JMed 142: 205-222, 1967

5. Wolman L, Bradshaw P: Spinal cord embo-lism. J Neurol Neurosurg Psychiat 30: 446-454, 1967

6. Aach R, Kissan J (ed) : Clinicopathologic confer-ence. Amer J Med 44: 430-440, 1968

7. Skillman JJ, Zervas NT, Weintraub RM, et a l :Paraplegia after resection of aneurysms of theabdominal aorta. New Eng J Med 281: 422-424, 1969

8. Adamkiewicz A: Die Blutgefdsse des men-schlichen Ruckenmarkes oberflache. II Theil:Die Gefdsse der Ruckenmarkober fldche. Sitz-ungsb d k Acad d Wissensch Math—naturw. cl.85: 101-130, 1882

9. Kadyi H: Ober die Blutgefdsse des menschli-chen Ruckenmarkes: Nach einer im XV:Bande der Denkschaften der math, naturw.Classe der Akademie der Wissenschafrenimkra'kau erschienenen Monographic, aus demPolnischen ubersetzt vom Verfasser. Lemberg,Gubrynowicz and Schmidt, 1 889

10. Bastian HC: In Quain R (ed) : Dictionary ofMedicine. 1st edition, Part I I . London, Long-mans, Green and Co., p 1456-1499, 1882

11. Reynolds JR, Bashan HC: System of Medicine.2nd edition, Philadelphia, JB Lippmcott andCo., p 446-490, 1872

12. Moniz E: L'encephalographie artenelle, sonimportance dans a la localization des tumeurscerebrales. Rev Neurol 2: 72-90, 1927

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CHARLES BURTONSpontaneous Ischemic Infarction of the Spinal Cord with Traumatic Sequela

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1970 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.1.6.397

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