Spinal cord embolism · Vascular accidents involving the spinal cord, in contrast to the brain, are extremely rare. Damage to the spinal cord fromverified emboli seems to be an even

J. Neurol. Neurosurg. Psychiat., 1967, 30, 446

Spinal cord embolismLIONEL WOLMAN AND PETER BRADSHAW

From the Departments of Neuropathology and Neurology, United Sheffield Hospitals

Vascular accidents involving the spinal cord, incontrast to the brain, are extremely rare. Damageto the spinal cord from verified emboli seems to bean even greater rarity and no examples were foundby Blackwood (1958) in a series of 3,737 post-mortem reports from the National Hospital, QueenSquare, London. Embolic myelomalacia has beenreported in bacterial endocarditis and other formsof heart disease such as mitral stenosis and coronaryocclusion. When caisson disease and air embolismare excluded, the paucity of the literature on thesubject indicates that spinal embolism is very un-common, and in some reports confirmation of theemboli and the site of their impaction has beenlacking. The purpose of this paper is to record twofurther examples of the syndrome and to presentdetails of the nature and origin of the emboli andthe lesions produced.

CASE REPORTS

CASE 1 T.D., a man aged 59, early in March, 1966,noticed progressive weakness first of the right and, a fewdays later, of the left lower limb. The disability wasslight until six weeks later when he awoke with paralysisof both lower limbs and numbness up to the waist. Thefollowing morning he was unable to pass urine. He hadsuffered from a cough dating from bronchitis 20 yearspreviously but otherwise the past and family historiescontributed nothing. On May 2, he was admitted tohospital elsewhere and transferred to the neurologicaldepartment on 26 May 1966.On examination the spine, cranial nerves, and special

senses were intact. Inconspicuous but coarse fascicu-lation was observed over the shoulder girdles and arms,but the upper limbs were otherwise normal. There wasflaccid paralysis of both lower limbs. The deep tendonreflexes were normal in the upper and depressed in thelower limbs, the abdominal responses were absent andboth plantars were extensor. Vibration sense was absentbelow and including the pelvis and joint position sensewas absent in the toes and defective in the ankles. Therewas a cutaneous sensory impairment to pin prick, tem-perature and touch below the second dorsal segment andincluding the sacral area on both sides. There was re-tention of urine which necessitated the use of an indwell-ing catheter and numerous deep pressure sores over thesacrum, buttocks, and legs. General examination was

unremarkable and the blood pressure was 190/90 mm.Hg.A plain radiograph of the chest revealed evidence ofan

old right basal pleurisy. Radiographs of cervical anddorsal spines were normal. A full blood count wasnormal but the erythrocyte sedimentation rate (E.S.R.)was 50 mm./hr. The lumbar cerebrospinal fluid pressureand manometric observations were normal and the fluidcontained no white cells, 7 red cells/c.mm., protein 35mg./100 ml.; Lange no change. The Wassermann reaction(W.R.) was negative in the blood and cerebrospinal fluid.A myelogram showed no abnormality between the lumbarsac and the foramen magnum.

In view of the negative results of investigation, it wasthought that the patient was probably suffering from theeffects of metastatic carcinoma, possibly arising from thebronchus. The patient's condition deteriorated and thecourse was complicated by both pulmonary and renalinfections and by anaemia. He died on 10 August 1966within five months of the onset.Necropsy findings The body was that of a thin, wasted

male whose appearance was older than the stated age.Extensive pressure sores were present over the sacrum,lateral aspects of both thighs and left heel. The leftpleural cavity was obliterated by old dense adhesions.There was a severe terminal bilateral bronchopneumonia.The heart was of normal size and appearance and thecoronary arteries showed minimal atheroma. The wholeof the aorta was extremely atheromatous with manylarge erosions of the intimal surface on several of whichfleshy fibrin thrombus had been deposited (Fig. 1). Thelower abdominal aorta was most severely affected butthe ascending aorta, the arch adjacent to the origin of theleft common carotid artery, and the posterior aspect ofthe descending aorta round the openings of the lowerintercostal and lumbar branches were similarly involved.Both common carotid arteries were very atheromatousand the origins of both internal carotid arteries werestenosed by fibrin thrombus deposited on severely athero-matous areas. The subclavian and vertebral arteriesappeared healthy. The renal, coeliac, and mesentericarteries were widely patent and only slightly athero-matous. The kidneys showed no gross abnormality andthe urinary tract was free from infection. The otherviscera appeared healthy.The brain (weight 1,455 g.) showed bilateral frontal

cortical atrophy with widened sulci. The vessels at itsbase showed only patchy atheroma at their junctions.There was slight ex-vacuo dilatation of the ventricles. Thespinal cord showed slight swelling in the upper thoracic

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Spinal cord embolism

FIG. 1.Severe diffuseatheroma ofthe aorta witherosions in thearch andabdominalpart (x ith).

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region and there was congestion of the pial vessels onthe surface. The pia arachnoid was not thickened andthere was no evidence of tumour infiltration or of anymetastatic deposits in the extradural tissue or in thevertebral bodies.

Histology Although no lesions were recognized in thebrain on naked-eye examination, several scattered minuteareas of old softening were found in the routine sections.These were situated in the cortex of the frontal lobe andin the cortex on either side of the central sulcus, in thehead of the caudate nucleus and in the putamen on theright side. They consisted of areas of dense gliosis, wedgeshaped in the cortex, in which an occasional lymphocyteand histiocyte could be recognized. No thrombosedvessels were seen in relation to these infarcts.

Sections were examined from each segmental level ofthe cord and the upper thoracic segments were cutserially in view of the history of a sensory level at D.2.The sections were stained by haematoxylin and eosin,Nissl, Mallory's phosphotungstic acid haematoxylin,Masson's trichrome combined with Verhoef's elastictissue, Holmes' silver impregnation, and Weigert's myelinmethod. In the cervical region and D.1 segment therewas ascending degeneration in the posterior and antero-lateral columns. At D.2 there,was a wedge-shaped areaof necrosis involving the right anterolateral column ofwhite matter extending from the surface into the super-ficial part of the anterior horn (Fig. 2). At D.3 the areawas of similar shape but was separated from the antero-lateral surface by a thin band of intact tissue. At D.4 thearea was much larger, extending dorsally in the lateralcolumn, and was accompanied by a transversely elon-gated area of necrosis in the centre of the posteriorcolumns. This latter area became much more prominentat D.5, extending across the right posterior horn to link

*. FIG. 2. Transverse section ofJr- X right half of spinal cord at D.2

showing necrotic area inanterolateral column.(myelin x 15).

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Lionel Wolman and Peter Bradshaw

up with an elongated area in the right lateral column.At D.6 there were three discrete areas of necrosis invol-ving a large wedge-shaped area in the right anterolateralcolumn, a transversely elongated area involving theposterior columns and right posterior horn and a smallwedge-shaped area in the dorsal part of the left lateralcolumn. At D.7 the area in the right anterolateralcolumn had become small and wedge-shaped beneaththe surface, whilst extending across the posterior columns,left posterior horn, and left lateral column was a largecrescentic area of necrosis separated from the surface bya thick band of intact white matter (Fig. 3). This cre-scentic-shaped lesion also involved D.8 becoming smallerand split into posterior and lateral components (Fig. 4).These extended into the D.9 segment only on the leftside, whilst at D.10 the necrosis was confined solely tothe left lateral column. Below this level the cord wasintact apart from descending degeneration in the dorsalhalf of the lateral columns. The infarcted areas had asimilar appearance consisting of pale-staining, vacuo-lated necrotic tissue in which were numerous histiocytesand scanty lymphocytes. In only one small intramedullaryartery in the necrotic area on the right side at D.6 wasfibrinous embolic material seen in the lumen of thevessel. The anterior and posterior spinal arteries andtheir branches seen in all these sections were patent,healthy, and free from atheroma.The aorta was removed at necropsy together with the

paravertebral tissues. Several of the pairs of intercostaland lumbar arteries were dissected out from their originsin the aorta and sectioned serially, some transversely andothers longitudinally. Although the lumbar arteriesoriginated in severely eroded areas of the aorta so thatit was difficult to see their openings with the naked eye,the sections surprisingly showed the lumen to be widelypatent and the atheromatous process either did notextend into the vessel or if it did it was minimal. In allthe sections examined, however, embolic atheromatousmaterial was seen lying free in the lumen or occasionallyloosely attached to the wall (Fig. 5). Most of this mate-rial was eosinophilic and structureless, staining positivewith P.A.S. and Luxol fast blue, and resembling in itsappearance the soft grumous material lying on thesurface of the eroded areas in the aorta. A few smallcholesterol crystal clefts were seen in the embolicmaterial (Fig. 6).Although the kidneys appeared healthy, microscopi-

cally there were several minute wedge-shaped corticalinfarcts and small arteries in relation to these containedcholesterol emboli (Fig. 7).

The subacute onset of paraparesis in a middle-agedman with a chronic cough, followed after six weeksby flaccid paralysis of the lower limbs and a sensorylevel over the trunk, suggested metastatic carcinoma.However, no primary carcinoma was detected, plainradiographs and myelography excluded spinal com-pression, and the normality of the cerebrospinalfluid pointed away from subacute necrotic myelitis.At necropsy the detection of intense atheroma

of the aorta suggested that it had blocked the

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FIG. 3. Transverse section of D.7 showing crescenticarea of infarction extending round spinal cord (myelinx 7).

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FIG. 4. Transverse section at D.8 showing necrotic areasin lateral and posterior columns (myelin x 7).

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FIG. 5. Longitudinal section of lower intercostal arteryshowing masses of atheromatous material lying free in thelumen (haematoxylin and eosin x 150).

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FIG. 6. Section of radicular branch of the upper lumbarartery showing a few small cholesterol crystal clefts inatheromatous embolic material in the lumen (haematoxylinand eosin x 150).

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FIG. 7. Section ofkidney showing cholesterol emboli in asmall artery adjacent to a glomerulus (haematoxylin andeosin x 150).

openings of the lumbar or intercostal arteries orhad extended into these branches. However, micro-scopy showed that this was not so and the walls ofthese small vessels, together with the anterior andposterior spinal arteries, were healthy. Instead,numerous small atheromatous emboli lay in thelumina of the lumbar and intercostal arteries. Thespinal cord contained many small areas of infarc-tion between D.2 and D.1O. At the upper and lowerlimits these were wedge-shaped and confined to theanterolateral columns. Over the remainder of theaffected cord, areas of infarction were crescentic andlay in the watershed territory between tissues supp-lied by the central branches of the anterior spinalartery and the penetrating branches of the peri-pheral circumferential pial vessels, extending betweenthe posterior and anterior spinal arteries (Hassler,1966). As both these spinal arteries originate fromthe radicular arteries, especially in the thoraco-lumbar region, atheromatous emboli would tend tobe held up at the proximal origin and at the distalbifurcations of the radicular arteries, before migra-ting distally as has been demonstrated in the cerebralcirculation. Only one small intramedullary vesselwas found to contain embolic material in thepresent case but it is likely that showers of embolihad occurred, resulting in ischaemic myelopathy.Evidence of extraspinal embolism was detected inthe brain and kidney.

CASE 2 A.B., a woman aged 65, early in March 1961noticed progressive weakness of both lower limbs, un-steadiness of gait, and a sensation that she was walkingon cotton wool. In July, she complained of slightclumsiness and weakness of the right hand withoutsensory disturbance. On 7 August, after a fall, sheexperienced urgency and hesitancy of micturition. Therewas no relevant past or family history and she wasadmitted to the neurological department on 12 August1961.On examination the spine, cranial nerves, special

senses, and upper limbs were intact. There was relativeweakness of both lower limbs without alteration of tone.The deep tendon reflexes were normal but the abdominalresponses were absent and the plantars were equivocal.Vibration sense was absent in the toes, present at theankles, and the threshold for joint position sense waselevated in the great toes. There was relative hypalgesia,thermalgesia, and hypaesthesia below the fourth dorsalsegment and including the sacral area on both sides.General examination was unremarkable and the bloodpressure was 150/80 mm. Hg.

Plain radiographs of the chest, cervical, dorsal, andlumbar spines were normal, together with a full bloodcount, E.S.R., urine analysis, and the serum electrolytes,urea, plasma acid, and alkaline phosphatases. There wasa histamine-fast achlorhydria but the serum B12 levelwas 466ppg./100 ml. On 3 September painful swellingof the left calf was detected which was attributed to a

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deep vein thrombosis. This was treated by rest and apressure bandage but no anticoagulants were given. On ;II19 September, the pain and swelling had subsided. Re-examination then showed a severe spastic paraparesiswith increased deep tendon reflexes and bilaterally Aextensor plantar responses. There was a dense cutaneoussensory loss, to all modalities, below the level ofD.4.aThe lumbar cerebrospinal fluid pressure and manometricobservations were normal, and the fluid contained nowhite cells, 7 red cells/c.mm., protein 25 mg./lOOml.;Lange no change. The Wassermann reaction was nega-tive in the blood and cerebrospinal fluid. A myelogramshowed no abnormality between the lumbar sac and theforamen magnum. On 24 September, the patient had amajor fit, collapsed, and never regained consciousness.She died on 26 September, six months after the onset ofsymptoms. FIG. 9. Transverse section at C.4 showing necrot

Necropsy findings The body was that of a thin, wasted in right anterolateral column with ascending degenfemale whose appearance was older than the stated age. in posterior columns (myelin x 7).Small superficial pressure ulcers were present over thesacrum and the left hip. A pulmonary embolus whichhad originated in the left calf was a terminal factor in thedeath. A mass of fibrin thrombus was adherent to themedial wall of the left auricle near its apex. Thecoronary and carotid arteries showed patchy atheromabut there was very severe atheroma of the aorta,especially in its lower abdominal part extending intothe iliac vessels. Several small cysts were present in thecortex of the kidneys, the surface of which was granu-laro Some small uterine fibroids and a large yellow infarctof the lower half of the spleen were found.,<~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

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FIG. 8. Section from left atrium showing fibrin depositon myxoma (haematoxylin and eosin x 150).

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FIG. IL Transverse section at D. 7 showing large infarctextending across the midline (myelin x 7).



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The brain (weight 1,300 g.) was swollen, with flattenedconvolutions and narrowed sulci. The vessels at its baseshowed severe patchy atheroma at their junctions. Theupper part of the brainstem appeared swollen, softened,and haemorrhagic, and these haemorrhages had extendedinto the tegmentum of the pons on either side in itslateral part. The lateral and third ventricles were narrowedbut showed no displacement. There were some smallcalcified plaques in the pia arachnoid over the posterioraspect of the lumbosacral cord but no other grossabnormalities were recognized.

Histology A section of the mass of fibrin thrombusattached to the wall of the left auricle showed that thishad been deposited on a small myxoma growing on themedial wall of the auricle (Fig. 8). There was no evidenceof infarction of the septal wall in this region. Several ofthe splenic vessels in the margin of the infarct wereoccluded with fibrin thrombus.There was haemorrhagic necrosis of the tectum and

tegmentum of the midbrain with numerous small hae-morrhages scattered throughout the necrotic tissue inwhich were many foci of polymorphs, mainly aroundvessels. The haemorrhages had ruptured into the aque-duct. The basilar artery appeared healthy, patent andfree from atheroma but several of the small perforatingvessels had necrotic walls. The haemorrhages extendedinto the dorsal half of the upper pons and upwards to thesubependymal tissue in the walls of the third ventricle.Small recent wedge-shaped infarcts were seen in thecortex of the cerebellum, right insula, left frontal andtemporal lobes and right central region. No cellularreaction had occurred in these areas and no occludedvessels were seen.The spinal cord showed several discrete areas of

infarction of longer duration. At C.4 there was an areainvolving the right anterolateral column extending fromthe ventral nerve roots into the anterior horn of greymatter (Fig. 9). Many histiocytes were present betweenproliferated capillary vessels in the necrotic region.Ascending degeneration was prominent in the posteriorcolumns. At C.6 a wedge-shaped area of necrosis waspresent in both lateral columns. A much larger wedge-shaped area of necrosis of more recent origin waspresent in the right lateral column at D.1 (Fig. 10) whichextended into the anterior horn at D.2-3 and tapered outat D.4. At D.7 there was a large infarct involving thelateral and ventral column on the right side as well asthe anterior horn and extending across the ventromedianfissure to include the medial part of the left ventralcolumn and left anterior horn (Fig. 11). Similar but lessextensive involvement was present at D.8. The remainingthoracic segments were intact, apart from D.12 (Fig. 12),where both lateral columns and the ventral part of theposterior columns contained infarcts which extended onthe left side into L.1 (Fig. 13). In the lower lumbarsegments the infarction was confined to the medial partof the ventral columns and anterior horns as well as theventral part of the posterior columns in the territorysupplied by the anterior spinal artery (Fig. 14).The anterior and posterior spinal arteries were patent

and free from atheroma. Several small intramedullaryvessels in the infarcts had necrotic walls and numerous

FIG. 12. Transverse section at D.12 showing bilateralareas of infarction extending across the ventral part of theposterior columns (myelin x 7).

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FIG. 13. Transverse section at L.J showing infarcted areaextending across the left posterior horn (myelin x 7).

FIG. 14. Transverse section at L.3 showing infarctionmainly in the territory supplied by the anterior spinalartery (myelin x 7).

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FIG. 15. Section of spinal cord in area of infarction at

L.1 showing organizing thrombus in the lumen of a small

intramedullary artery with intense perivascular lympho-

cytic reaction and numerous histiocytes in surrounding

tissue (haematoxylin and eosin x 285).

lymphocytes and occasional polymorphs cuffed many of

these vessels, some of which were filled with fibrin

thrombus or with a cellular mass, interpreted as organi-

zation by endothelial reaction rather than by tumour cell

emboli (Fig. 15).

This patient developed weakness and paraes-

thesiae of both lower limbs and, five months after

the onset, exhibited a flaccid paraparesis with a

sensory level at DA. Investigations failed to establish

a diagnosis. The condition deteriorated, spasticity

developed in the lower limbs, and she died six

months from the commencement of symptoms.

Although the atheroma of the aorta was severe in

this case also, especially in the lower abdominal

portion, and may have contributed to the spinalcord damage, the myxoma of the left auricle was

probably the major source of emboli. Unfortunately

the intercostal and lumbar arteries were not exa-

mined but the presence of multiple infarcts in the

cerebral and cerebellar cortex, brainstem, cervical

cord, and spleen, as well as in the thoracolumbarsegments, supports the cardiac origin of the emboli.No myxomatous material was recognized in vessels

in relation to the infarcts and it may well be thatonly the fibrinous deposit on the tumour acted asembolic material. Many of the vessels in or near theinfarcts had become necrotic and haemorrhage intothe surrounding tissue in the case of the brainsteminfarct had resulted in death.The spinal cord infarcts were much more discrete,

widely separated, and diffusely scattered than in theprevious case. In addition they were more variablein their appearance, age, and situation. Thus in thecervical and upper thoracic cord they involvedwedge-shaped areas in the lateral columns, whereasin the lower lumbar segments the infarct was con-fined to the anterior spinal artery territory. Only atthe thoracolumbar junction had the infarctionoccurred in the arcuate watershed territory.

DISCUSSION AND CONCLUSIONS

The symptoms and signs relating to two patientswith paraparesis due to spinal embolism have beenpresented. Although certain features were commonto both, nothing came to light during life by whichthe correct diagnosis could have been achieved.Their ages were 59 and 65 respectively and neitherdisplayed clinical evidence of significant hypertensionatheroma, or cardiac disease. Symptoms commencedinsidiously and consisted of weakness of the lowerlimbs and impairment of urinary sphincter control.In case 2, there was progressive paraparesis; in case1 there was sudden flaccid paraplegia within sixweeks of the onset. Initial examination of bothpatients showed a flaccid paraparesis, without anyincrease in the deep tendon reflexes, and a sensorylevel extending to the upper dorsal region. Thestriking absence of spasticity, despite the presenceof severe weakness, might at first have been attri-butable to spinal shock in case 1, but this featureremained throughout the course of the illness. Itsuggested the presence of a lesion extending overmany segments of the spinal cord that had interrup-ted reflex arcs concerned with muscle stretch.Investigations served only to exclude more commonpathologies; there was no evidence of primarycarcinoma or of metastases; spinal compression wasruled out by the negative myelogram; and the nor-mality of the spinal cerebrospinal fluid pointed awayfrom a diagnosis of subacute necrotic myelitis. It ispossible that an aortogram might have shown areduction in the number of segmental vessels but,even with hindsight, it is difficult to determine howthe nature of the vascular occlusions could havebeen revealed.The concept that atheromatous material may

become embolic has been attributed to Panum(1862), who quoted the gross necropsy findings in

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the case of the Danish sculptor, Thorwaldsen, andascribed the sudden death to rupture of an athero-matous plaque in a coronary artery with occlusionof that vessel. No microscopic confirmation wasrecorded. In recent years microscopic proof of theoccurrence of atheromatous emboli in almost everyorgan of the body, especially the abdominal viscera,the lower limbs, and the brain, has been demon-strated. The interest and thoroughness of theinvestigator appear to be important factors in deter-mining where such lesions are found. Mention of thespinal cord, apart from a few exceptions, is curiouslylacking. PWrier, Demanet, Henneaux, and NunesVincente (1960) described two examples of necrosisof the spinal cord in the territory supplied by theposterior spinal arteries. In the first the state of theaorta was not mentioned, but in the second, a man of65, obstruction of the posterior spinal arteries by em-boli of atheromatous material from a thoracic aorticaneurysm was demonstrated. Soloway and Aronson(1964) reported on 16 cases of atheromatous embolito the c,entral nervous system. In two of these, emboliwere observed in vessels supplying the spinal cordthough there was no associated myelomalacia.However, only three routine sections of the cordwere examined.

Chronic myelopathy is seldom recognized as aconsequence of aortic atheroma (Wells, 1966) butthe condition may be commoner than these tworeports indicate. This is suggested by the examplescollected by Corbin (1961) and by Gruner andLapresle (1962). Garland, Greenberg, and Harri-man (1966) also raised the possibility of an emboliccausation of the necrosis of the spinal cord in theircases where it was associated with aortic diseasebut they were unable to prove this. They stressed theimportance of examining thoroughly the full extentof the blood vessels supplying the spinal cord fromthe aorta in addition to the spinal arteries and theirbranches in the leptomeninges.

Severe atheroma of the aorta, especially in itsabdominal part above the bifurcation, is a commoncondition whereas atheromatous embolism is appa-rently relatively rare. Several explanations couldaccount for this discrepancy. Smaller emboli may,be without clinical significance or they may migratethrough the vasculature in a solitary fashion andlarger leptomeningeal arteries may dilate in responseto emboli contained therein, as has been observedby Luessenhop, Gibbs, and Velasquez (1962) in thebrain. Further, the long and tedious examinationof the spinal cord and the tracing of its blood supplyfrom the aorta which is required to prove theembolic process has deterred many from compre-hensive necropsy study. The other factors concerndifficulties in recognizing the embolic material which

is eosinophilic, grumous, and structureless, resem-bling fibrin. It may not contain definite cholesterolcrystal clefts or they may be most conspicuous. Theforeign body giant cell reaction to these crystalsusually disappears after a few days and the reactionwhich persists is an intense inflammatory reactionin the vessel wall and extending into the surroundingtissue, in which eosinophils predominate. In thespinal cord this panarteritis could be easily mis-interpreted as a form of myelitis.Thus if atheromatous embolization of the spinal

cord can occur in cases of severe aortic atheroma, itought to be more commonly found and may wellaccount for the slowly progressive spinal cord syn-dromes found in older patients. If the watershedterritory is mainly affected then unilateral or, morelikely, bilateral, motor or sensory symptoms mayensue.

Involvement of the nervous system by embolifrom cardiac tumours is a much less common eventowing to the rarity of these growths, which arepredominantly myxoma arising in the left atrium.Thus in a recent review, Joynt, Zimmerman, andKhalifeh (1965) were able to collect from the litera-ture 11 cases of cardiac tumours with cerebralemboli of tumour fragments and to add one of theirown. Six additional cases with cerebral infarcts butno definitely identified tumour emboli were alsofound. In our second case multiple embolic softe-nings were found in the brain and spinal cord aswell as in the spleen. No tumour fragments werefound in relation to these but several vessels wereoccluded with fibrin thrombus. This was not sur-prising in view of the large amount of clot depositedon the surface of the myxoma. Progressive throm-bosis of blood with organization on the surface ofthese tumours is a common occurrence so thatmany have been regarded as organized muralthrombi. The necrotic damage to vessel walls inmost of the infarcts was in striking contrast to thefirst case. The associated perivascular cellular in-filtration resembled that seen in myelitis, but itappears to be a non-specific response as vasculitis hasbeen reported with other types of embolic materialsuch as cholesterol and fibrocartilage (Feigin,Popoff, and Adachi 1965).

SUMMARY

A clinical-pathological study of two patients withspinal cord embolism is described.

In the first, the embolic material originated insevere eroding atheroma of the aorta and consistedmainly of grumous material containing some chole-sterol crystals. It was found in the intercostal andlumbar arteries which were themselves free from

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atheroma. It is suggested that owing to the frequencyof aortic atheroma compared with the infrequentfinding of atheroma of spinal arteries this mechanismmay be more prevalent in producing chronic is-chaemic myelopathy.

In the second case the emboli consisted of fibrinoriginating from a mass deposited on a myxoma ofthe left atrium.

Several similar patterns of infarction in the spinalcord were seen in both cases. They consisted of a

wedge-shaped area extending in from the lateralsurface, or a central area incorporating both ventralcolumns, but a crescentic area in the watershedterritory between anterior and posterior spinalarteries was the most typical. It would account forboth the motor and sensory aspects of the syndrome.

It is a pleasure to express our thanks to our colleagues,Dr. N. A. Lewtas and Dr. R. G. Grainger, for reportingon the plain radiographs and myelograms.

REFERENCES

Blackwood, W. (1958). Discussion on vascular disease of the spinalcord. Proc. roy. Soc. Med., 51, 543-547.

Corbin, J. L. (1961). Recherches anatomiques sur la vascularisationarterielle Leur contribution a l'6tude de I 'isch6mie medullaired'origine art6rielle. These de la Faculte de Medecine deParis. Masson, Paris.

Feigin, I., Popoff, N., and Adachi, M. (1965). Fibrocartilagenousvenous emboli to the spinal cord with necrotic myelopathy.J. Neuropath. exp. Neurol., 24, 63-74.

Garland, H., Greenberg, J., and Harriman, D. G. F. (1966). Infarctionof the spinal cord. Brain, 89, 645-662.

Gruner, J., and Lapresle, J. (1962). ttude anatomo-pathologique desmedullopathies d'origine vasculaire. Rev. neurol. ,106, 592-631.

Hassler, 0. (1966). Blood supply to human spinal cord. A micro-angiographic study. Arch. Neurol. (Chic.), 15, 302-307.

Joynt, R. J., Zimmerman, G., and Khalifeh, R. (1965). Cerebralemboli from cardiac tumors. Ibid., 12, 84-91.

Luessenhop, A. J., Gibbs, M., and Velasquez, A. C. (1962). Cerebro-vascular response to emboli: observations in patients witharteriovenous malformations. Ibid., 7, 264-374.

Panum, P. L. (1862). Experimentelle Beitrage zur Lehre von derEmbolie. Virchow's Arch. path Anat., 25, 308-3 10.

Nrier, O., Demanet, J. D., Henneaux, J., and Nunes Vincente, A.(1960). Existe-t-il un syndrome des arteres spinales posterie-ures? A propos de deux observations anatomo-cliniques.Rev. neurol., 103, 396409.

Soloway, H. B., and Aronson, S. M. (1964). Atheromatous emboli tocentral nervous system: report of 16 cases. Arch. Neurol.(Chic.), 11, 657-667.

Wells, C. E. C. (1966). Clinical aspects of spinovascular disease.Proc. roy. Soc. Med., 59, 790-796.

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Documents

Spinal cord embolism · Vascular accidents involving the spinal cord, in contrast to the brain, are extremely rare. Damage to the spinal cord fromverified emboli seems to be an even