chronic abscess of the brain stem · although classical brain stem syndromes occur in only a few...

Journal ofNeurology, Neurosurgery, and Psychiatry, 1977, 40, 625--629

Chronic abscess of the brain stemJ. A. RUSSELL AND M. D. M. SHAW

From the Institute of Neurological Sciences, Southern General Hospital, Glasgow, Scotland

SUM M A R Y The incidence of solitary brain stem abscess is less than 4%0 of all posterior fossaabscesses, and probably less than 100 of all intracranial abscesses. Two cases are reported, bothpresenting as chronic progressive clinical problems and initially diagnosed as gliomas. It is sug-gested that aspiration is a more suitable treatment than excision, and that in cases secondary tootogenic disease, radical mastoidectomy might have been an adequate method of prophylaxis.

In Gowers' (1893) experience abscesses of thebrain stem were rare (1.7% -that is, four out of231 abscesses): pontine abscesses were more com-mon than medullary abscesses. More recentreports (Van Gilder et al., 1974; Danziger et al.,1974) suggest that brain stem abscess remains arare condition, and each report one case of sur-vival after surgery.The purpose of this report is to describe two

cases of brain stem abscess, both of which pre-sented as chronic brain stem masses which wereinitially thought to be gliomas, and one of whomsurvived after surgery.

Case 1

MR, a 60 year old woman, was first seen inSeptember 1965. She had a 15 year history oftinnitus with a progressive sensori-neural deafnessover the final year. Within the preceding monthsshe had developed occipital headaches, numbnessof the right side of the face and tongue for fourweeks, and sudden onset of a right lower motorneurone facial weakness. Examination confirmedthe deficits, but strength duration curves showedsome conduction in the seventh nerve which onsubsequent recordings appeared to improve. Skullradiographs were normal, as was the fourth ven-tricle judged by ventriculography with sodiumiophendylate. A lumbar pneumoencephalogramshowed only slight dilatation of the lateral ventri-cular system: the lumbar CSF contained 600white blood cells per c.mm (80% polymorphs), 6g/l protein and 4.0 mmol/l glucose.She was readmitted in May 1966 complaining

of continuing headaches, but on examination hercondition was unchanged. Lumbar pneumoen-cephalography again confirmed the increase in theAccepted 1 I January 1977

size of the lateral ventricles: the CSF now con-tained 40 monocytes per c.mm and a protein levelof 8.3 g/l.

Suddenly in August 1967 she developed a lefthemiplegia, which had been preceded for onemonth by more severe headaches associated withvomiting, and transient episodes of complete lossof vision for a few seconds. She was drowsy, hadpapilloedema, nystagmus on lateral and upwardsgaze, and a flaccid left hemiplegia. The cranialnerve signs were unchanged. lophendylate ventri-culography now revealed a thinned aqueductwhich was displaced backwards and to the left. Itwas felt that the clinical history and the investiga-tions indicated an intrinsic glioma of the brainstem. She died in December 1967, and postmortemexamination revealed a well encapsulated abscess(40X35X40 mm) in the pons. There was noevidence of a primary source of infection.

Case 2

CS, a 10 year old girl, was first seen in May 1975,some five months after a febrile illness. She com-plained of headache and disturbance of vision fortwo months, and for several months her right earhad been discharging pus. On examinationpapilloedema, diplopia on left lateral gaze, andataxia of the lower limbs were found. Keratindebris and a possible perforation in the attic ofthe right ear werc present. The ear was cleanedand treated with ampicillin. CT scan (EMI scan)demonstrated dilatation of the whole ventricularsystem. This was confirmed by meglumine iothala-mate (retro Conray 3501, w/v; May and Baker)ventriculography (Fig. la), which showed ob-struction of the outflow foramina of the fourthiventricle. Ventriculo-peritoneal drainagexwas there-fore established, and after this she progressed well.

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Fig. 1 Ventriculograms showing (a) non-communicating hydrocephalus, and (b) blocked aqueduct threemonths later.



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In August 1975 she suddenly developed a rightfacial weakness, together with pain over the rightmastoid and headache and had to be readmittedto hospital. Meglumine iothalamate ventriculo-graphy (Fig. ib) showed an obstruction at theupper end of the aqueduct and lumbar pneumo-encephalography suggested some enlargement ofthe pons: CSF contained 263 white cells per c.mmof which the majority were lymphocytes andmonocytes. Vertebral angiography was not helpful.Review of the radiology at this time seemed toindicate adhesions around the brain stem and inthe aqueduct after a meningitic illness which wassecondary to ear disease. A right radicalmastoidectomy was carried out when a largeamount of cholesteatoma was found, but themiddle fossa dura mater was seen to be healthy.She improved after the operation except for theright seventh nerve palsy.

In March 1976 she was readmitted because shehad become less active and was tending to fall tothe left. Examination showed a left third nerveparesis, right sixth, seventh, ninth, tenth, andtwelfth nerve palsies, and a spastic left hemi-paresis. Four vessel angiography was not helpful,but after revision of the shunt she improvedslowly. The original diagnosis was modified: wefelt that in addition she now had a pontine glioma.

In September 1976 she presented in a state ofdepressed responsiveness after a seizure. She hadalso been dysphagic for three days. A CT scan(Fig. 2a) demonstrated a mass, which enhancedwith sodium iothalamate 70% w/v (Conray 420:May and Baker), in the brain stem extending intothe right cerebello-pontine angle and supra-tentorially into the medial posterior temporalregion. Posterior fossa exploration confirmed thepresence of a mass which on smear biopsy wasthought initially to be a glioma. Subsequent paraf-fin sections did not confirm this diagnosis, andcombined posterior fossa and right sided trans-tentorial approach was made to the mid-brainand the pons, which were grossly enlarged andhard. Aspiration obtained 3 ml pus from withinthe pons but microscopy and culture failed toidentify any organisms.

Postoperatively she improved over a few daysto the stage where she was alert, able to walk, eat,was continent, and could speak intelligibly. Aftera four week course of chloramphenicol, a repeatCT scan (Fig. 2b) suggested that (even though thepositioning of the patient was not quite com-parable with that of the CT scan before surgery)the fourth ventricle had returned almost to themidline and there was only minimal evidence ofany area of enhancement. On the advice of a

Fig. 2 Enhanced CT scans showing (a) brain stemmass, and (b) its resolution six weeks later.

bacteriologist, antibiotic treatment was continuedfor a further month; this consisted of a course ofclindamycin and ampicillin followed by one oferythromycin. The patient continued to improve,and three months after the operation she has afixed deficit consisting of a right hemiparesis, aright sixth nerve palsy, and is dysarthric thoughclearly understandable.

Discussion

Hulme (1961) suggested that the incidence ofsolitary brain stem abscesses was less than 3%,but even this is almost twice that estimated by

B

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Gowers (1893). During the 26 year period fromDecember 1950, 54 cases of posterior fossaabscesses (51 cerebellar, two brain stem, and onesubdural) have been admitted to the Institute ofNeurological Sciences in Glasgow which acts as asecondary neurosurgical referral service for apopulation of approximately three million. There-fore, the incidence of brain stem abscesses is lessthan 4% of all posterior fossa abscesses. Temporallobe abscesses are twice as common as cerebellarabscesses (Wright and Grimaldi, 1973). Othersupratentorial sites-for example, frontal andparieto-occipital-are at present over twice ascommonly affected as the temporal lobe (Martin,1973; Sampson and Clark, 1973), and with thecontinuing decline in the incidence of abscesssecondary to otogenic infective disease (Carey etal., 1972; Martin, 1973; Sampson and Clark, 1973;Wright and Grimaldi, 1973) will become relativelymore common. The incidence of solitary brainstem abscess is, therefore, likely to be appreciablyless than 1%: indeed several large series do notcontain such a case (Loeser and Scheinburg, 1957;Le Beau et al., 1973; Morgan et al., 1973). SinceWeickhardt and Davis's review of the literature(1964) we have found detailed reports of fivefurther brain stem abscesses (Corbella et al., 1967;Mazars et al., 1972; Van Gilder et al., 1974;Danziger et al., 1974; Robert et al., 1975), andseven in which no further details are given(Krayenbuhl, 1967; Gurdjian and Thomas, 1969;Carey et al., 1972; Sampson and Clark, 1973).Most of the cases previously reported have short

neurological histories (Weickhardt and Watts,1944; Hulme, 1961; Weickhardt and Davis, 1964;Van Gilder et al., 1974). Death usually ensuesquickly, often in days. However, this is notinevitable: Weickhardt and Watts (1944) quote apatient described by Moniz (1934) who survivedsix months, and one of Abercrombie's (1836) whosurvived three months (case 7); Weickhardt andDavis (1964) had one patient who survived foreight months (case 3). Danziger et al. (1974) des-cribed a case which was similar to the two reportedhere in that the working diagnosis was that of abrain stem glioma and the correct diagnosis wasnot made until some four and a half months afterthe onset of neurological symptoms.Although classical brain stem syndromes occur

in only a few patients (Weickhardt and Davis,1964), the high frequency of cranial nerve lesions,and especially facial weakness and dysphagia,together with headache and fever, commonlyallows an accurate anatomical localisation, but thepathological diagnosis remains difficult in bothacute and chronic cases. Particularly in the latter

group, there is a slow indolent progression ofbrain stem dysfunction which often leads to thediagnosis of a glioma. Both brain stem gliomas(White, 1963) and abscesses (Weickhardt andDavis, 1964) not uncommonly cause multiplecranial nerve lesions without producing longtract signs until later in the natural history of thedisease. In the case of the abscess this may beexplained by the macroscopic pathology.Abscesses at other sites in the brain are usuallyglobular but in the brain stem, they are elongatedand will tend to displace rather than interrupt thelong tracts. Case 1 in this report survived 26months after the onset of neurological symptomswithout any definite treatment, and was able tocarry on a relatively normal life for the first 21months. Case 2 improved dramatically particu-larly with respect to responsive level and longtract function after aspiration of the abscess.The difficulty of diagnosis is compounded by

the lack of any apparent infective source in 37%of cases (Weickhardt and Davis, 1964), whichobscures a clue to the possibility of an intra-cranial infective process. Case 1 was such a case.Weickhardt and Davis (1964) reported also that34% of pontine abscesses in the literature resultedfrom haematogenous spread, whereas 29% re-sulted from direct extension, 91% of these latterfrom otogenic disease. Furthermore, a non-communicating hydrocephalus which results fromfourth ventricular outlet blockage which issecondary to post-meningitic adhesions may pre-cede the development of a pontine abscess (case 2).Thus if a non-communicating hydrocephalus pro-gresses to involve the aqueduct, and particularlyif there is any suggestion of enlargement of thebrain stem, investigation for abscess should beundertaken even though the clinical diagnosis isalmost certainly a glioma. Computed tomographyis of value in demonstrating an abscess (Shaw andRussell, 1977), but the appearances are not specificand, therefore, surgical exploration should becarried out if there is any doubt about thediagnosis.

Recently Van Gilder et al. (1974) and Danzigeret al. (1974) have both described survivors aftersurgery for pontine abscess. In the former's casethe abscess was drained after which the patientmade a good functional recovery and was able toreturn to work. Robert et al. (1975) similarlyaspirated a pontine abscess which was followedinitially by an improvement in the patient's re-sponsive level. However, sudden death occurredeight days after the operation, probably because itwas not appreciated that the abscess was multi-locular. Danziger et al. (1974) were more radical,

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and excised the abscess almost completely, but al-though the child survived, she is severely disabled.Though there is little experience upon which tojudge, it would seem that aspiration is more satis-factory than excision as the former should resultin less severe neurological deficit. Internal drain-age of cerebrospinal fluid may be required tocontrol the hydrocephalus.Though brain stem abscess is a rare condition,

its devastating nature is a further argument infavour of a very radical surgical approach toinfective middle ear disease (Wright and Grimaldi,1973; Shaw and Russell, 1975), as a prophylaxisagainst the development of secondary intracranialsuppuration.

We wish to thank Miss H. Wilson for typing themanuscript.

References

Abercrombie, J. (1836). Pathological and PracticalResearches on Diseases of the Brain and SpinalCord. 3rd Edition. John Carfrae and Son: Edinburgh.

Carey, M. E., Chou. S. N., and French, L. A. (1972).Experience with brain abscess. Journal of Neuro-surgery, 36, 1-9.

Corbella, T., Mamoli, A., and Terzi, G. F. (1967).Raro caso di abcesso del tronco cerebrali. Rivista diNeurologia, 37, 515-528.

Danziger, J., Allen, K. L., and Bloch, S. (1974). Brainstem abscess in childhood. Case report. Journal ofNeurosurgery, 40, 391-393.

Gowers, W. R. (1893). A Manual of Diseases of theNervous System. 2nd Edition, Volume 2. J. and A.Churchill: London.

Gurdjian, E. S., and Thomas, L. M. (1969). Surgicaltreatment of cranial and intracranial infections. InCranial and Intracranial Suppuration. Chapter I.Edited by E. S. Gurdjian. Charles C. Thomas:Springfield, Illinois.

Hulme, A. (1961). Suppurative lesions of the brainstem. Journal of Neurology, Neurosurgery, andPsychiatry, 24, 291-293.

Krayenbuhl. H. A. (1967). Abscess of the brain.Clinical Neurosurgery, 14, 25-44.

Le Beau, J., Creissard, P., Harispe, L., and Redondo,A. (1973). Surgical treatment of brain abscess andsubdural empyema. Journal of Neurosurgery, 38,198-203.

Loeser. E., and Scheinburg, L. (1957). Brain abscess.A review of 99 cases. Neurology (Minneapolis), 7,601-609.

Martin, G. (1973). Non-otogenic cerebral abscess.Journal of Neurology, Neurosurgery, and Psy-chiatry, 36, 607-610.

Mazars, G., Merienne, L., Veron, J. P., and Poirier,J. (1972). Abcs solitaire du bulbe. Nouvelle PresseMedicale, 1, 3115-3117.

Moniz, E. (1934). Abces isole du bulbe. Revue d' Oto-neuro-ophtalmologie, 12, 568-570.

Morgan, H., Wood, M. W., and Murphey, F. (1973).Experience with 88 consecutive cases of brain ab-scess. Journal of Neurosurgery, 38, 698-704.

Robert, C. M., Stern, W. E., Brown, W. J., Greenfield,M. A., and Bentson, J. R. (1975). Brain stem ab-scess treated surgically with special note upon theemployment of thorium dioxide. Surgical Neurology,3, 153-160.

Sampson, D. S., and Clark, K. (1973). A current re-view of brain abscess. American Journal of Medi-cine, 54, 201-210.

Shaw, M. D. M.. and Russell, J. A. (1975). Cerebellarabscess. A review of 47 cases. Journal of Neurology,Neurosurgery, and Psychiatry, 38, 429-435.

Shaw, M. D. M., and Russell, J. A. (1977). Value ofcomputed tomography in the diagnosis of intra-cranial infection. Journal of Neurology, Neuro-surgery, and Psychiatry, 40, 214-220.

Van Gilder, J. C., Allen, W. E., and Lesser, J. A.(1974). Pontine abscess: Survival following surgicaldrainage. Case report. Journal of Neurosurgery, 40,386-390.

Weickhardt, G. D., and Davis, R. L. (1964). Solitaryabscess of the brain stem. Neurology (Minneapolis),14, 918-925.

Weickhardt, G. D., and Watts, J. W. (1944). Abscessof the medulla oblongata. Report of a case. Archivesof Neurology and Psychiatry (Chicago), 51, 282-284.

White, H. H. (1963). Brain stem tumors occurring inadults. Neurology (Minneapolis), 13, 292-300.

Wright, J. L. W., and Grimaldi, P. M. G. B. (1973).Otogenic intracranial complications. Journal ofLaryngology and Otology, 87, 1085-1096.

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