570 POSTGkADUATE MEDICAL JOURNAL November I954 ment for patients with carcinoma of the breast and prostate who suffer extreme pain from metastases in bone. But relief of pain can now be assured in the majority of cases by bilateral adrenalectomy. Regression of the primary tumour occurs much less frequently than that of the metastases. Bilateral adrenalectomy is a practical proposition and no undue hardship is imposed upon the adrenalectomised patient. BIBLIOGRAPHY BEATSON, G. T. (I896), Lancet, ii, 104 and i62. BOYD, S. (1900), Brit. med. J., ii, 6 I. BURROWS, H., and HORNING, E. S. (I952), 'Oestrogens and Neoplasia', Blackwell, London. DARGENT, M. (I949), Brit. mred. -., ii, 54. FARROW, J. H., and WOODARD, H. Q. (I942), J. Amer. Med. Ass., xI8, 339. FOULDS, L. (I949), Brit. J. Cancer, 3, 240 and 345. GALTON, D. A. G. (950o), Brit. J. Cancer, 4, 20. HERRELL, W. E. (I937), Amer. J. Cancer, 39, 659. HUGGINS, C. C., and HODGES, C. V. (I94I), Cancer Res., I, 293. HUGGINS, C. C., and SCOTT,W. W. (I945), Ann. Surg., x22, Io3I. LATHROP, A. E. C and LOEB, L. (1916), J. Cancer Res., i, x. STOLL,3. i .. nd ELLIS, F. (1953), Brit. %Med. ., ii, 796. THROMBOSIS OF THE INTERNAL CAROTID ARTERY By SIMON BEHRMAN, B.Sc.(Hon.)Lond., M.R.C.P.Lond. Physician, Moorfields, Westminster and Central Eye Hospital; Consulting Neurologist S.E. and N.E. Metropolitan Regional Hospital Boards Numerous are the instances in the annals of medicine of discoveries made and subsequently forgotten, but this cycle seems to have recurred several times before angiography of the carotid artery revealed anew the frequency and the com- plications of occlusion of the internal carotid artery. The reasons for this recurring oblivion were twofold: I. Examination of carotids in the upper part of the neck and carotid canals is not usually per- formed in routine autopsy. 2. Ramsay Hunt in I914 gave the other reason for the neglect of this subject as follows: 'The assumption that the circle of Willis is sufficient to carry the blood into an obstructed vascular area when such obstruction is situated below the level of the anterior and posterior communicating arteries.'l This assumption was not only based on ana- tomical grounds but also on the experience of the effects of ligaturing these arteries. This operation was frequently performed during the I9th century for a variety of ' nervous disorders' such as epilepsy and trigeminal neuralgia, as is testified by the publication of four large series of cases col- lected during the second half of the century and quoted by Ramsay Hunt. In only i6 per cent. of some I,200 cases comprising a variety of con- ditions did cerebrovascular accidents supervene- and this before the days of asepsis! The present revival of interest in the subject of carotid thrombosis began after cerebral angio- graphy came into wide use, and confirmed Ramsay Hunt's contention that occlusion of carotid arteries was not uncommon. Pathology Frequency. On combining the three large pub- lished series pf unselected post-mortem examina- tions, which included a routine inspection of the carotid arteries in their entirety, the incidence of macroscopically visible thrombosis and embolism of this artery can be said to be approximately I.6 per cent.2a, 3,4 The incidence will to some ex- tent vary in accordance with the average age of the autopsy material. The following classification of the various con- ditions causing occlusion of the carotid artery either by thrombosis or embolism has been sug- gested by Hultquist: I. Trauma. 2. Morbid processes affecting the tissueb in the immediate relation of the carotid arteries. 3. Cardiovascular diseases. I. Trauma Non-penetrating injuries to the neck may oc- casionally be followed within 6 to 48 hours by rapid onset of hemiplegia due to spreading throm- bosis of the internal carotid artery. This was described by Northcroft and Morgan, and more recently the subject was reviewed by Schneider and Lemmen.5, 6 Cases of this nature simulate extradural and subdural haematomas, as is illus- Protected by copyright. on November 11, 2020 by guest. http://pmj.bmj.com/ Postgrad Med J: first published as 10.1136/pgmj.30.349.570 on 1 November 1954. Downloaded from
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570 POSTGkADUATE MEDICAL JOURNAL November I954
ment for patients with carcinoma of the breast andprostate who suffer extreme pain from metastasesin bone. But relief of pain can now be assured inthe majority of cases by bilateral adrenalectomy.Regression of the primary tumour occurs muchless frequently than that of the metastases.
Bilateral adrenalectomy is a practical propositionand no undue hardship is imposed upon theadrenalectomised patient.
BIBLIOGRAPHYBEATSON, G. T. (I896), Lancet, ii, 104 and i62.BOYD, S. (1900), Brit. med. J., ii, 6 I.BURROWS, H., and HORNING, E. S. (I952), 'Oestrogens and
Neoplasia', Blackwell, London.DARGENT, M. (I949), Brit. mred. -., ii, 54.FARROW, J. H., and WOODARD, H. Q. (I942), J. Amer. Med.
Ass., xI8, 339.FOULDS, L. (I949), Brit. J. Cancer, 3, 240 and 345.GALTON, D. A. G. (950o), Brit. J. Cancer, 4, 20.HERRELL, W. E. (I937), Amer. J. Cancer, 39, 659.HUGGINS, C. C., and HODGES, C. V. (I94I), Cancer Res., I, 293.HUGGINS, C. C., and SCOTT,W. W. (I945), Ann. Surg., x22, Io3I.LATHROP, A. E. C and LOEB, L. (1916), J. Cancer Res., i, x.STOLL,3. i .. nd ELLIS, F. (1953), Brit. %Med. ., ii, 796.
THROMBOSIS OF THE INTERNALCAROTID ARTERY
By SIMON BEHRMAN, B.Sc.(Hon.)Lond., M.R.C.P.Lond.Physician, Moorfields, Westminster and Central Eye Hospital; Consulting Neurologist S.E. and N.E. Metropolitan
Regional Hospital Boards
Numerous are the instances in the annals ofmedicine of discoveries made and subsequentlyforgotten, but this cycle seems to have recurredseveral times before angiography of the carotidartery revealed anew the frequency and the com-plications of occlusion of the internal carotidartery. The reasons for this recurring oblivionwere twofold:
I. Examination of carotids in the upper part ofthe neck and carotid canals is not usually per-formed in routine autopsy.
2. Ramsay Hunt in I914 gave the other reasonfor the neglect of this subject as follows: 'Theassumption that the circle of Willis is sufficient tocarry the blood into an obstructed vascular areawhen such obstruction is situated below the levelof the anterior and posterior communicatingarteries.'l
This assumption was not only based on ana-tomical grounds but also on the experience of theeffects of ligaturing these arteries. This operationwas frequently performed during the I9th centuryfor a variety of ' nervous disorders' such asepilepsy and trigeminal neuralgia, as is testified bythe publication of four large series of cases col-lected during the second half of the century andquoted by Ramsay Hunt. In only i6 per cent. ofsome I,200 cases comprising a variety of con-ditions did cerebrovascular accidents supervene-and this before the days of asepsis!The present revival of interest in the subject of
carotid thrombosis began after cerebral angio-
graphy came into wide use, and confirmed RamsayHunt's contention that occlusion of carotid arterieswas not uncommon.
PathologyFrequency. On combining the three large pub-
lished series pf unselected post-mortem examina-tions, which included a routine inspection of thecarotid arteries in their entirety, the incidence ofmacroscopically visible thrombosis and embolismof this artery can be said to be approximately I.6per cent.2a, 3,4 The incidence will to some ex-tent vary in accordance with the average age ofthe autopsy material.The following classification of the various con-
ditions causing occlusion of the carotid arteryeither by thrombosis or embolism has been sug-gested by Hultquist:
I. Trauma.2. Morbid processes affecting the tissueb in the
immediate relation of the carotid arteries.3. Cardiovascular diseases.
I. TraumaNon-penetrating injuries to the neck may oc-
casionally be followed within 6 to 48 hours byrapid onset of hemiplegia due to spreading throm-bosis of the internal carotid artery. This wasdescribed by Northcroft and Morgan, and morerecently the subject was reviewed by Schneiderand Lemmen.5, 6 Cases of this nature simulateextradural and subdural haematomas, as is illus-
572 POSTGRADUATE MEDICAL JOURNAL November I954trated by the following case reported by North-,croft and Morgan.
Case I. Male, aet. 31. A piece of loose ropehanging from the side of a passing lorry wounditself round the patient's neck, threw him to theground and then unwound itself without dragginghim along. He picked himself up and thoughfeeling faint was able to proceed on foot to theUnit Medical Officer, who noticed bruising of theleft side of the neck. About 24 hours after theaccident the patient had a right-sided epilepticfit followed by right flaccid paralysis and coma.He died 48 hours after the accident. Autopsysuggested that the original injury resulted inextravasation of blood into the media of the internalcarotid artery extensive enough to cause occlusionof the vessel. Intraluminal thrombosis was foundabove and below the level of the vessel injury, theupper thrombus extending upwards into themiddle cerebral vessels.
2. Morbid Processes Affecting Tissues in ImmediateRelation of the Carotid Arteries
(a) Inflammation. Otitis media with spread ofinfection to bony carotid canal. Meningitis withthrombosis of cavernous sinus. Peritonsilarabscess. Aseptic cavernous sinus thrombosis fol-lowed later by convulsions and contralateralhemiplegia.7
(b) Neoplasms. Sphenoidal ridge meningioma.Malignant tumours at the base of the skull.
3. Cardiovascular Diseases(a) Diseases of the carotid artery causing occlusion.
The incidence of atherosclerosis of the internalcarotid is high, as has been shown by severalpublications involving the examination of thisartery in series of unselected autopsies.8, 9 Thelocalization of atherosclerosis is probably relatedto the magnitude of the circumferential stretchingforce to which cfifferent portions of the vessel wallare subject.10° Broadly speaking this force can beexpressed by Laplace's Law, according to which itis proportional to intravascular pressure and theradius of the vessel. Atherosclerosis is minimalwhere the pressures within and outside the arteryare almost equal. This obtains in portions of theartery well supported by non-yielding surroundingstructures, e.g. the portion of the carotid withinthe bony canal. Experimentally these conditionshave been simulated by applying silver cuffs aboutthe circumference of short segments of arteries inrabbits. Willens noted that the enclosed arterywas not affected by atherosclerosis when animalswere fed with cholesterol.ll
According to Laplace's Law the circumferentialtension is proportional to the radius of the vessel.Two segments of internal carotid show antrum
like dilatations, viz., at the level of the carotidsinus and immediately after the emergence fromthe cavernous sinus. Atheromatous changes aremost pronounced in these situations where this-localized increase in the radii occurs.
Thromboangiitis obliterans and giant cellarteritis are two other vascular diseases liable tocause thrombosis of the internal carotid artery.l2
(b) Embolism. The lumen of the carotid can beoccluded by emboli originating in the heart, e.g.bacterial endocarditis and coronary infarction.l3Effect of Occlusion of the Internal CarotidArteryDye injected into the carotid artery is normatly
distributed only to the homolateral hemisphere,but should the contralateral common carotid becompressed during the angiographic procedure,the dye will be seen in the vascular systems of bothhemispheres in equal amounts. This angiographicevidence serves to confirm the well known fact thatocclusion of one carotid artery is immediately com-pensated and normally does not evoke anyabnormal symptoms. Even when the E.E.G. isused as an index of cerebral disturbance, noabnormalities can usually be detected on unilateralcarotid compression, provided stimulation of thecarotid sinus is avoided. Normal cerebral circula-tion under these conditions depends on the in-tegrity of the circle of Willis and the adequacy ofthe communicating vessels and of the remainingmain arteries of the brain. Provided these con-ditions obtain, spontaneous occlusion of one in-ternal carotid artery is also not fraught with anyabnormal symptoms. For compensation of suchocclusion, it is essential that a sufficient amount ofblood per unit of time should reach the portion ofthe cerebral hemisphere normally supplied by thisartery. This volume of blood has to be conveyedby the communicating arteries and anastomosingvessels. Since the volume of blood circulatingthrough a vessel per unit of time is, broadly speak-ing, governed by' Poiseuille's Law, two factorsdetermine whether such compensation can beeffected:
I. Diameter of the'vessel. The volume of flowper unit of time is proportional to the fourth powerof the diameter and therefore even slight narrowingof the concerned vessels by disease will consider-ably reduce the flow.
2. Since the flow is directly proportional to thepressure, this is also a factor which must be takeninto consideration. If under given conditions ofpressure the communicating and anastomosingvessels are, either through disease or maldevelop-ment, insufficient to compensate, a state of circu-latory insufficiency will result and, depending onits severity and duration, this will give rise to
NTovembcr I954 BEHRMAN: Thlrombosis of the Internal Carotid Artery 573
various signs and symptoms referable to theischaemic region of the hemisphere. Some ofthese disturbances may be caused by cerebralinfarction and may thus be permanent. In 60 ofIoo cases of fatal cerebral infarction Hicks andWarren were unable to find evidence of mechanicalocclusion of cerebral vessels.l4 Should the remain-ing main vessels be narrowed or occluded bydisease, then following occlusion of one internalcarotid artery, cerebral insufficiency may affectboth hemispheres. Recent studies of the effect ofligature of the internal carotid have provided someinformation to indicate that the subject of circula-tory insufficiency is far more complex than a simpleconsideration of Poiseuille's Law would suggest.Thus following ligature of the carotid not onlydoes the fall in pressure vary from individual toindividual, as was only to be expected, but resultsare subject to considerable variations in the sameindividual without any changes in the generalblood pressure to account for it. One of Dandy'spatients, for instance, tolerated complete closureof the internal carotid in the neck within oneweek of the first operation, when such closureevoked neurological signs of cerebral ischaemia.15Measurements of pressure within the carotiddistal to ligature may show striking differences inthe same i Rdividual, as was shown by Bakay andSweet.'6 Plressure fell to 23 per cent. of that priorto ligature. When the ligature was re-applied sixdays later it dropped only to 48 per cent. of theoriginal pressure. Serial pressure readingscarried on for as long as 60 minutes in other casesrevealed rise and also fall in pressures withoutcorresponding changes in blood pressure. Someof these pressure changes are no doubt due to theeffects of arterial spasm set up by the ligature.Clinical evidence of cerebral circulatory in-sufficiency following carotid ligation may appearabruptly or insidiously even after intervals as longas five to six days, and such symptoms can beabolished by the removal of the ligature thusproving the patency of the cerebral vessels in suchcases.
Break in the Circle of WillisAnatomical studies have revealed that the
anterior communicating artery is deficient in oper cent. and one of the post-communicatingarteries in 23 per cent.'7 Extension of thrombifrom the internal carotid artery, as also emboliarising from such thrombi, may cause a break inthe circle of Willis.
Consequences of Thrombosis of CarotidArteryAs has already been shown, cerebral circulation
is normally unaffected by occlusion of one of thecarotid arteries. However, in some cases cerebralcirculation may be critically dependent upon theintegrity of the carotids, and apoplexy may followocclusion of one carotid; in others complicationsmay arise after an interval. These may be causedby any of the following three processes, eithersingly or in combination:
I. Cerebral circulatory insufficiency (already re-viewed).
2. Spreading thrombosis so that thrombus ex-tends into the circle of Willis or cerebral arteries.Case I illustrates this.
3. Emboli which may become detached fromthe main thrombus of the internal carotid artery.The following case illustrates a massive embolismof this nature:
Case 2. Atheroma of left internal carotidartery-thrombosis-detached portion of throm-bus causing embolism of middle cerebral artery-thrombophlebitis of veins of legs-pulmonaryembolism.
Female, aet. 35. The patient had been inexcellent health until four weeks before admission.While having a meal she had twitching of the rightside of the face and developed uselessness of theright arm for a short time. She remained welluntil the day of admission when she suddenly lost
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FIG. I.--Ventriculogram showing considerable degreeof cerebral oedema in a proved case of thrombosisof left internal carotid artery (Mr. Ian McCaul'scase).
her speech, sat down, fell back and had a general-ized convulsion. Following this she was found tobe aphasic and paralyzed down the right side ofher body. She died suddenly one week afteradmission, following a brief period of breathless-ness and cyanosis; death was due to extensivepulmonary embolism.
Carotid artery showed organizing thrombusattached to the wall which, at the level of bifurca-tion, was the site of considerable atheromatousdeposits beneath the intima and had patchy areasof intimal hyperplasia. The thrombus was about7 cm. long with its centre approximately at thelevel of the bifurcation. A recent embolus in theleft middle cerebral artery, which was otherwisefree from disease, was responsible for extensiveinfarction of the left parietal and temporal lobes,together with the basal ganglia. The grossswelling of the brain substance had well-nighclosed the ventricular space.
Authors have differed in the relative importancethey have attached to these three factors. Cerebralcirculatory insufficiency has been stressed byCorday et al., spreading thrombosis by Hultquistand embolism by Chiari.l8 In any given case theassessment of the part played by these factorscannot be made on clinical grounds alone since,following cerebral embolism and cerebral throm-bosis, the paralytic phenomena may occasionally beonly transient and cerebral circulatory insufficiencymay cause irreversible cerebral damage. As abroad generalization, however, it can probably bestated that cerebral embolism and cerebral throm-bosis give rise to enduring disturbances and thatstereotyped recurrent paralytic episodes followedby recovery are most frequently due to cerebralcirculatory insufficiency. The following clinicaltypes can be recognized:Clinical Types
I. Massive apoplectiform hemiplegia, either dueto thrombosis or embolism of the main cerebralvessels or occlusion of the carotid in the presenceof a break in the circle of Willis.
2. Recurrent transient paralytic phenomenawith recovery-presumably due to cerebral cir-culatory insufficiency.
3. Various paralytic phenomena with onlypartial recovery-multiple embolic phenomena.
4. Progressive hemiparesis with or without fitssimulating tumour.
Clinical Features of Carotid OcclusionAs will be appreciated from the survey of the
complex nature of the factors responsible for theovert manifestations of carotid thrombosis, therange of symptoms and their degree of intensitymust, of necessity, be wide. Cerebral emboli may
be discreet or massive, cerebral circulatory in-sufficiency, according to circumstances, slight orgrave and the consequent symptomatology ex-ceedingly variable. The different clinical typeshave already been outlined and it only remains tomention briefly some of the symptoms mostfrequently seen with each type.
Type I. Hemiplegia with or without coma;often preceded by convulsions, predominantlyunilateral. In addition to hemiplegia there maybe unilateral sensory loss and hemianopia.
Type 2. Symptoms are of brief duration andtend to recur as evanescent episodes of stereotypednature. The commonest transient symptoms are:Monocular amaurosis, dysphasia, attacks of' dizziness,' monoplegia and sensory disturbancesin limbs.
Type 3. Every type of cerebral paralyticphenomena, either singly or in combination, canbe expected to occur and have been described inreported cases, a review of which reveals inaddition to such common forms of paresis as motoror sensory monoplegia or hemiplegia, dysphasia,dysgraphia, dyslexia and dyspraxia and also agreat variety of less common symptoms resultingfrom disturbance of cerebral function.
Type 4. This type is of particular importancebecause the clinical picture mimics that of cerebralneoplasm very closely. Progressive dementia canbe a feature in these cases.
In addition to the various cerebral paralytic andepileptic phenomena mentioned and the visualdisturbances about to be described, headache isthe only remaining important symptom. The in-cidence, severity and character would appear fromthe published and personal cases to be too variableto permit of a formulation of any definite pro-nouncement regarding pathogenesis. These head-aches are usually maximal on the affected side andmay well be due to dilatation and increased pulsa-tion of pial and cerebral vessels caused by cerebralcirculatory insufficiency. Dilatation of thesevessels in animals has been demonstrated in ex-perimental anoxaemia induced by various methodsand also when blood pressure has been lowered toa critical level.19, 20 Since headache of high in-tensity is a constant feature of active giant cellarteritis it constitutes one of the main symptoms ofcarotid thrombosis caused by this vascular dis-order.
Disturbances of VisionA discussion of some of the common ophthalmo-
logical manifestations of carotid thrombosis mustbe prefaced by stressing the following anatomicaland physiological facts:
I. Within the eyeball the pressure of the centralretinal artery is opposed by the intraocular pres-
November 1954 BEHRMAN: Thrombosis of the Internal Carotid Artery 575
sure of about 20 mm. Hg and therefore the effectiveintravascular pressure is reduced by this amount.A variety of 'blackouts' can be shown to beresulting from this physiological arrangement.21
2. There is free anastomosis between theophthalmic artery and branches of the externalcarotid artery so that occlusion of the ophthalmicartery does not as a rule lead to interruption ofcirculation through the central retinal artery.22
3. Sudden permanent unilateral amaurosis oc-curring in the course of carotid thrombosis usuallytakes place without any demonstrable lesion in thecourse of the ophthalmic artery.23, 24
Amaurosis in these cases can only be explainedon the basis of embolism or circulatory in-sufficiency and these two possible factors will nowbe considered in greater detail. We have seen thatthere is ample pathological evidence indicatingthat cerebral embolism is often a feature in carotidthrombosis and there is, therefore, reason to be-lieve that such emboli may -also reach the retinalvessels. Such embolism is most likely to give riseto enduring amaurosis owing to irreversibleretinal damage. In cases in which through mal-development or disease there is a break in thecircle of Willis, the fall of pressure in the internalcarotid following thrombosis may be considerable.After ligature of the internal carotid, as Strobosand Mount have shown, the pressure gradientbetween the internal carotid and ipsilateral smallcortical vessels is maintained.25 Assuming thatthis relationship also obtains between the internalcarotid and central retinal artery, then a 6o percent. fall of pressure will bring the pressurewithin the first branches of the central retinalartery from approximately 70 mm. down to 28 mm.Normal intraocular pressure will oppose thispressure and-impede retinal circulation, which maybecome insufficient to maintain retinal functionwith resulting amblyopia. A drop of pressure inthe internal carotid of 55 to 65 per cent. afterligation is compatible with normal cerebral func-tion, as has been shown by Strobos and Mountand also Sweet and Bennett.26 Thus it can besupposed that a fall of carotid pressure of certain'critical' value will give rise to amblyopia oramaurosis without symptoms indicative of dis-turbance of cerebral function. The fall of intra-ocular pressure which may result from this fall ofcarotid pressure may be one of the means wherebya dynamic adjustment can be effected. In thosecases of internal carotid thrombosis in which theposterior communicating artery contributes littletowards the ipsilateral cerebral circulation, com-pression of the unaffected carotid may result in aconsiderable fall of the carotid pressure.26 A fallof ' critical' magnitude under these circum-
stances would explain the observation made byDenny-Brown on one of his patients.27 On oneof the patients with thrombosis of the left internalcarotid artery, ' manual compression of the rightcarotid caused immediate blanching of the vesselsof the left fundus and marked pulsation of the rightfundus.' Under these conditions intraocularpressure presumably exceeded systolic pressure ofthe left and diastolic pressure of the right centralretinal arteries.
Absence of Carotid PulsationConsiderable diagnostic importance was at-
tached by Ramsay Hunt to loss of pulsation in theinternal carotid artery. However this is on thewhole an infrequent finding, partly because theocclusion may be distal to the cervical portion ofthe artery and partly because the thrust of eachpulse wave may be transmitted along the artery forsome distance beyond the embolus or thrombus.However Dunning claims that this examination isbest performed by feeling for pulsation on eachside of the pharynx.28
Paediactric AspectConsidering the infrequency of cerebrovascular
accidents in childhood the number of childrenamong the published cases of internal carotidthrombosis is surprisingly high.29, 30, 31, 32
Cave 3. Boy, aged 7. Generalized erythematousrash for three days associated with malaise. Twoweeks later severe headache and puffiness of eyes,followed on the next day by swelling of face andthe passing of deep red urine. One month laterdeveloped severe headache. On the following daywhen he awoke he was found to have right hemi-plegia. His speech was slowed and he noticed lossof left vision. During the following week he re-covered function of the right limbs. Peeling ofhands and feet was noticed at this time. Onexamination he showed left optic atrophy and righthemiparesis. Pulsation of left carotid artery couldbe hardly appreciated, whereas pulsation of rightcarotid was within normal limits. Blood pressure,90/60. Examination of urine, C.S.F. and radio-grams of the skull revealed no abnormality.
Radiological AbnormalitiesI. Angiography. Failure to visualize the con-
trast medium in the vessel does not necessarilymean it is thrombosed. Spasm provoked by themechanical stimulation by the needle may. producea similar effect and the following criteria are ofhelp in the differentiation between thrombosis andspasm of the internal carotid artery.
(a) Filling of the middle cerebral group ofvessels and perhaps of the carotid syphon about
four seconds after the injections (i.e. in thephlebogram).
(b) Repeated angiograms reveal partial fillingor absence of filling of the internal carotid.
(c) Contralateral angiogram visualizes cerebralvessels of both sides.
(d) Absence of filling of the syphon despitecompression of contralateral carotid, a procedurenot without danger.33
Conical narrowing of the stream of contrastmedium before it stops, as also narrowing of thevessel without interruption of the stream, arefeatures which suggest thrombosis. Very oc-casionally films taken subsequent to the arterio-graphy may reveal accumulation of some contrastmedium in the area of infarction.34
2. Pneumography. Ventriculography followingcarotid thrombosis may reveal in the early stage aconsiderable degree of ipsilateral cerebral oedema(Case 2, see Fig. I) or ipsilateral cerebral atrophyat a late stage.
ElectroencephalographyVarious E.E.G. abnormalities have been noted
in association with carotid thrombosis. However,slow delta waves localized to the ipsilateral fronto-temporal region is the commonest type of abnor-mality. In three out of four cases of carotidthrombosis Skillicorn and Aird have observed thatcompression of the non-affected common carotidartery resulted in the appearance of high voltageslow irregular waves, two to five per second fre-quency, usually in both hemispheres.35TreatmentAs has been indicated, the serious consequences
of carotid thrombosis are due to cerebral circula-tory insufficiency and cerebral embolism. Littlecan be done to overcome cerebral circulatoryinsufficiency, but much can be done by variousmedical procedures to aggravate it and theseshould be avoided if possible. Ventriculographyby raising intracranial pressure and angiographyby setting up spasm in the carotid tree may haveunfavourable effects. There are many instances inthe literature describing various cerebrovascularaccidents immediately following these investiga-tions which have been performed because of thesuspected possibility of intracranial neoplasm. Thedifferential diagnosis on clinical grounds alonebetween carotid thrombosis and intracranial neo-plasm may in certain cases be impossible and theseradiological aids to diagnosis have to be enlisted.Cerebral embolism constitutes a serious hazardand on theoretical grounds ligature distal to thesite of thrombosis can be justified. It is, however,not a practical measure in the majority of cases.It has been argued that the thrombosed segment
of the artery sets up irritation and thus provokesvasospasm peripheral to the point of occlusion andit has, therefore, been suggested that resection ordenervation of the affected segment may lead torelaxation of the distal arterial tree and this mayhelp to overcome cerebral circulatory insuf-ficiency.36 The available data are too meagre topermit of any definite conclusions as to the valueof this treatment.
Summaryi. Four main clinical types of internal carotid
thrombosis are described.2. These various clinical types are the result of
the interplay of the following three main causativefactors:
(a) Cerebral circulatory insufficiency resultingfrom a break in the circle of Willis, either con-genital or acquired.
(b) Spreading thrombosis so that the thrombusextends into the circle of Willis or cerebral arteries.
(c) Embolism originating from the main throm-bus of the internal carotid artery.
3. The mechanism for monocular amblyopia inthe absence of any simultaneous symptoms indica-tive of disturbance of cerebral function is dis-cussed. It is suggested that in the presence of alowered carotid pressure, intraocular pressure isthe main factor in the production of this syndrome.In some cases permanent monocular amaurosis isdue to embolism.
4. Analysis of the published case histories ofinternal carotid thrombosis reveals that the con-dition is not uncommon in children, and a furthercase is reported.Acknowledgment
I wish to thank Sir Russell Brain for permissionto publish details of Case 3.
REFERENCESI. HUNT, J. RAMSAY (1914), Amer. J. med. Sci., 147, 704.2. CHIARIS, H. (1905), Verhandl. d. deutsch. path. Gesellsch.,
9, 326.3. KRAYENBUHL, H., and WEBER, G. (1944), Helv. med.
Acta., 1, 289.4. HULTQUIST, G. T. (I942), 'Ueber Thrombose u. Embolie
d. Arteria Carotis u. hierbei vorkommende Gehirnstorungen,'Jena, Gustav Fischer.
5. NORTHCROFT, G. B., and MORGAN, A. D. (I944-5),Brit. J. Surg., 32, 105.
6. SCHNEIDER, R. C., and LEMMEN, L. J. (1952), J.Neurosurg., 9, 495.
7. WALSH, F. B., and SMITH (1952), Ibid., 9, 517.8. KEELE, C. A. (I933), Quart. J7. Med., 2, 2I3.9. HASSELBACH, H. (I93I), Beitz. z. path. Anat. u. z. ,allg.
path., 86, 369.io. WILLIS, G. C. (I954), J7. Canad. med. Ass., 70, I.i i. WILLENS, S. L. (1942), Amer. J. Path., IS, 63.12. GILMOUR (I94I), J. Path. Bact., 53, 263.I3. WINKELMAN and ECKEL (1930), Arch. Neurol. Psych., 23,
II6I.14. HICKS, S. P., and WARREN, S. (I95I), Arch. Path., 52, 403.I5. DANDY (I942), Arch. Surg., 45, 52I.I6. BAKAY, L., and SWEET, W. H. (I953), J. Neurosurg., 10, 353References continued on page 592
huge posterior penetrating duodenal ulcer in-volving the region of the bile ducts was found.The prepyloric region was opened and it wasfound that clear bile and no fresh blood came backfrom the duodenum, and so presumably thebleeding had ceased. After removing the antralmucosa, the sero-muscularis of the antrum wasclosed, and a partial gastrectomy performed.Following this he improved day by day, but onthe eighth day, massive melaena recurred. I feltthat the ulcer could hardly be active after thisspace of time and so we treated him conservativelythereafter. He died of repeated bleeding abouta week later.At autopsy, the ulcer indeed was found to have
practically healed (Fig. 28), the small unhealedpart being entirely occupied by a ruptured aneu-rysm, the rupture of which had no doubt led tothe repeated bleeding.Another conservative method for bleeding pos-
terior duodenal ulcer favoured at times and whichwe used for a period, was duodenotomy, arrest ofbleeding by suture together of the ulcer edges-followed by gastro-jejunostomy. I used this oneight occasions, but in two patients, the bleedingrecurred and one died of it. I do not use thismethod now.
After recounting my experiences with the variousregimes in the treatment of ulcer haemorrhage,you will see that I am inclined to favour surgery.That does not mean that I am advocating surgery
universally. There is a considerable variation inthe type of case treated in different places, and ourpreponderance of elderly gastric ulcer cases makessurgery particularly suitable. It is not withoutsignificance that we have such a volume of workthat we are able to keep in practice for theseoperations.
I have gone over a very wide field and so have,perhaps, only been able to give an over-all im-pression of our present practices in dealing withpeptic ulcer and its complications.
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