post-traumatic complications of arachnoid cysts … · a cavity in the anterior middle fossa. the...

Journal of Neurology, Neurosurgery, and Psychiatry, 1981, 44, 29-34

Post-traumatic complications of arachnoidcysts and temporal lobe agenesisT R K VARMA, C B SEDZIMIR, AND J B MILES

From the Department of Medical and Surgical Neurology, Walton Hospital, Liverpool

S UM MARY Six patients with arachnoidal cysts of the middle cranial fossa who presented withraised intracranial pressure are described. All of them had a history of trauma though in twoof them it was a remote incident. They all showed radiological changes of an expanded middlecranial fossa and temporal lobe agenesis. The relationship of trauma to these congenital lesionsis discussed.

Cysts overlying the temporal lobes have been welldescribed in the literature. These are often associ-ated with agenesis of the temporal lobe and theirassociation with epilepsy and asymmetry of theskull is well known. We report our experience withsix such cases, all of whom sustained minortrauma and suffered haemorrhagic complications.

Case IA 24 year old male nurse was admitted to a medicalward with a three day history of severe headachesand vomiting. He had marked nuchal rigidity withKernig's sign. There were no lateralising signs orpapilloedema. A provisional diagnosis of subarachnoidhaemorrhage was confirmed when the CSF obtainedat lumbar puncture was found to be xanthochromic.On later questioning he recalled a blow to the righttemporal region sustained during a game of footballa year previously. He had not lost consciousness orbeen otherwise disturbed.Skull radiographs showed thinning and outward bulg-ing of the right temporal bone with expansion of themiddle cranial fossa.Right carotid angiogram showed medial shift of themiddle cerebral artery with appearances suggestive ofa right temporal extracerebral collection.Operation A right temporal burr hole was made andon incising the dura xanthochromic fluid gushed outunder pressure. A right temporal craniotomy was thenperformed and a cystic cavity exposed. The super-ficial part of the cyst wall was adherent to the duraand the deep layer to arachnoid from which it waseasily stripped. There appeared to be a direct com-munication between the cyst and the chiasmaticAddress for reprint requests: Mr TRK Varma, Department of Neuro-surgery, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF.

Accepted 30 July 1980

cistern. The temporal lobe was hypoplastic and theinternal carotid artery, the optic nerve and the thirdnerve were easily visible without retraction. Thepatient recovered completely and ten years later wassymptom free.

Case 2A 7 year old boy was admitted with a six weekshistory of headaches and vomiting. Two days priorto the onset of symptoms he had fallen from a fenceand bumped his head. He had not lost consciousnessand was not taken to hospital. There was no signifi-cant past illness and his development had been normal.He was fully conscious but had bilateral papilloedemathough no lateralising signs.Skull radiographs showed expansion of the rightmiddle cranial fossa with outward bulging of thesquamous temporal bone.Bilateral carotid angiogram showed the midlinevessels to be shifted to the left with evidence of anextracerebral collection in the right front temporalregion.Operation A right temporal burr hole was made andon opening the dura xanthochromic fluid gushed out.The chiid improved after this procedure but there wasa persistent collection of fluid under the scalp woundwhich required repeated aspiration. Four months latera temporal craniotomy was performed. A cystic cavitywas present replacing the tip of the agenetic temporallobe. The walls of the cyst were easily stripped fromthe dura superficially and arachnoid on its inneraspect. The cyst appeared to communicate withgeneral subarachnoid space by a "valvular" arrange-ment and by stripping its walls a good communicationwas established with the chiasmatic cistern. The childrecovered well from the operation apart from awound infection which was treated with anti-biotics.He was well two years later.

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T R K Varma, C B Sedzimir, and J B Miles

Case 3A 7 year old male child was admitted with ahistory of headache and vomiting for five weeks. Hewas the first born of twins and had no birth trauma.His development and intellect were normal. A fewdays after hospitalisation the mother recalled that thechild had been knocked down by a slow moving taxiabout twelve months prior to the onset of his symp-toms. He had not lost consciousness and was nottaken to hospital. On admission he was drowsy witha mild hemiparesis and early papilloedema.Skull radiographs were at first thought to be normalbut review showed there wvas thinning and outwardbulging of the left squamous temporal bone with ex-pansion of the middle cranial fossa.Isotope brain scan was normal.Carotid angiography showed a large extracerebralcollection on the left side with elevation of the middlecerebral artery and shift of midline vessels.Operation Three burr holes were made and on open-ing the dura 75 ml of golden yellow fluid was drained.The cortical surface was about 15 cm from the innertable. There was a rapid improvement in his levelof consciousness and relief from headache. However,there was a persistent collection of fluid over the burrholes. A week later a craniotomy was carried out anda large cyst found in the middle fossa replacing thetip of the temporal lobe. The cy3t appeared to com-

municate with the subarachnoid space through a val-vular arrangement. The walls of the cyst were strippedexposing a large Sylvian fissure with a clear view ofthe optic chiasma and internal carotid artery. Thepatient had an uneventful recovery and remains wellone year later.

Case 5A 17 year old male was admitted complaining offrontal headache for two weeks. Five weeks prior tothe onset of headache, after a game of rugby football,he had noticed a large bruise over the left supraorbitalregion. He attributed this to bumping his head in atackle but he had not lost consciousness and did notgo to hospital. He was found to have bilateral papil-loedema and a mild right hemiparesis.Skull radiographs showed expansion of the rightmiddle fossa with outward bulging of the squamoustemporal bone.Carotid angiogram showed evidence of a right sidedextracerebral collection.Operation A right temporal craniotomy was carriedout. A lightly bloodstained subdural collection offluid was found with a 2 cm defect connecting itthrough a layer of apparently thickened arachnoid toa cavity in the anterior middle fossa. The anteriorpole of the right temporal lobe was deficient but theexposed gyri appeared normal. The cyst was drained

Fig 1 Operative photograph showing cyst wall with a tear in it. The temporal lobe is deficient in itsanterior part leaving the sylvian fissure widely open.

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Fig 2 Same case as fig 1 after stripping off the cyst wall.

and the walls excised (figs I and 2). The patient hadan uneventful recovery and was symptom free twoyears later.

Case 5A 21 year old male, who was initially seen as anoutpatient with a history of severe headache for oneweek. Four months prior to this he had fallen from hismotorcycle but did not think he had banged his head.He was seen in hospital and treated for bruises of hisback. At this stage he had no neurological deficitexcept for an equivocal plantar reaction on the leftside. When seen again two weeks later the headacheswere worse and he now had bilateral papilloedemawith left hemiparesis.Skull radiographs showed asymmetrical bulging of theright middle cranial fossa with thinning of the tem-poral bone.Isotope brain scan was normal.Right carotid angiography showed a large extra-cerebral collection on the right side.Operation A large subdural haematoma containingblack fluid was found overlying the parietal region.In the temporal region there was a tense cyst con-taining clear fluid and the tip of the temporal lobewas deficient. There was no connection between thetwo cavities though the haematoma did partially over-lie the posterior edge of the cyst. The arachnoidal cvst

did not appear to communicate with the general sub-arachnoid space. The walls of the cyst were strippedeasily from the arachnoid and dura. The patient hadan uneventful recovery and was well one year later.

Case 6A 13 year old boy was admitted with a two monthhistory of headache, which in the last two weeks hadbecome severe and was associated with vomiting. Priorto the onset of symptoms the child had fallen from askateboard but had not lost consciousness. He wasconscious with hyper-reflexia and impaired sensationin the left limbs. He had florid bilateral papilloedema.Skull radiographs showed expansion of the rightmiddle fossa with outward bulging of the right tem-poral bone.CA T scan showed small lateral ventricles displacedfrom the right by a large CSF density lesion in thefrontal and temporal region associated with a bulgeof the skull (figs 3 and 4).Operation Right fronto-temporal craniotomy was per-formed. All the bones here were thin suggesting along standing pressure on this part of the skull. Under-lying the dura was an enormous cystic collection ofhaemorrhagic fluid contained in two cavities. Thecapsule of the cyst was adherent to the dura on thelateral aspect and to the arachnoid on the deep aspect,with a similar membrane partitioning the two cavities.

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Fig 3, 4 CAT scan showing expansion of rightmiddle cranial fossa with a low density arachnoidalcyst

The tip of the right temporal lobe was deficient. Thewalls of the cyst were excised to produce a free com-munication between the "cyst" and the general cerebrospinal fluid circulation. The patient recovered satis-factorily and was well two years later.

Discussion

Cysts overlying the cerebral hemispheres havebeen well recorded in literature and various aeti-ological factors suggested including trauma, in-fection and a congenital maldevelopment. Oursix cases show four common features-their situ-ation in the middle cranial fossa, the association

with agenesis of the temporal lobe, asymmetry ofthe skull and a history of trauma.

Reynolds,l 2 Naffziger3 and Frazier4 have re-corded cases of patients with collections of fluidin the temporal region. Robinson5 reported twocases who presented with localised bulging of theskull in the temporal region and were found tohave a collection of fluid in the anterior part ofthe middle fossa. The absence of the temporallobe left the insula exposed. He analysed the 15cases in the literature at that time and suggestedthat in these cases the tip of the temporal lobewas congenitally absent and the space was occu-pied by a cystic collection of fluid. Later Robin-son6 suggested that these cases had the "temporallobe agenesis" syndrome and he discussed in detailthe postmortem findings in one such case (case 10).The exact relationship of the cyst to the men-

inges and their communication with the generalsubarachnoid space has been a matter of debate.Starkman et al,7 reporting the gross pathologyand histopathology of four cases of cysts overlyingthe cerebral hemispheres, concluded that they aresituated between two layers of arachnoid andseparated from the pia mater by the subarachnoidspace. However, Robinson,5 6 in his papers main-tains that they are subarachnoidal in position andregards it as a true "external hydrocephalus." Atoperation the "cyst" appears to lie between thedura and the arachnoid. The walls, which appearmacroscopically similar to the membrane arounda chronic subdural haematoma, microscopicallyconsist of a "vascular membrane." But this shedsno light on the origin of the membrane or itslocation.Trauma as a precipitating factor has been a

common finding in many cases in the literature.Robinson5 in his review of cases in the literatureat that time found a history of trauma in sevenout of the 15 cases. Tiberin and Gruzkiewicz8described a 10 year old boy with an arachnoidalcyst who had sustained a minor though signifi-cant head injury when he was two years old.Gruss et a19 reported a case of a 5 year oldchild with an arachnoidal cyst and temporal lobeagenesis. The child had sustained a severe headinjury when he was one and a half years old butthey felt this had no relevance to the developmentof the cyst. Four cases described by Torma andHeiskanenlo had a history of head injuries, onefour years and the other four months prior toclinical presentation.

In our series all six cases had a history of headinjury with varying time intervals prior to presen-tation. Two (cases I and II), like those quoted in

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the literature, had sustained the injury a year ormore prior to the onset of symptoms. In each ofthese the head injury had been slight and not re-quiring medical attention. At operation fluid hadbeen xanthocromic indicating that haemorrhagehad been a factor in the presentation but whetherthis was traumatic or a spontaneous event seems amatter for speculation. The other four casessuffered a definite head injury more recently andthese incidents would seem very likely to be ofsignificance. The trauma was of a minor natureand only one was seen in hospital as a direct re-sult of the injury.Asymmetry of the skull as seen on skull radio-

graphs was a characteristic feature of all ourcases. In the earlier cases it was identified only inretrospect but later was recognised early andalerted us to the possibility of a temporal lobeagenesis and the possibility of a subdural collec-tion. The radiological features that were noticedwere the outward bulging of the squamous tem-poral bone and greater wing of the sphenoidwhich was seen best on the axial view (fig 5). Thelateral view shows an anterior expansion of themiddle cranial fossa by a forward displacementof the lesser and greater wings of the sphenoid(fig 6). Hardman"' discussed asymmetry of the

Fig 5 Axial skull x-ray showing bulging of lefttemporal bone

skull in relation to subdural collection of fluidand described three cases, two of which were sub-dural haematomas and the other a "subduralhydroma." All three presented after trauma butone had noticed the swelling seven years prior tothe injury. Childe12 reported eight cases of "sub-dural hydromas," with localised thinning andbulging of the middle fossa and in these cases theswelling was the presenting symptom. In 10 ofthe 15 cases reviewed by Robinson5 the patientshad themselves noticed the bulging of the skull;in eight of them it was the only clinical finding.The two cases he reported in 1955 presented witha temporal swelling, in one it was noticed aftertrauma and in the other appeared spontaneously.In his latest paper" he considered the thinningand bulging of the temporal bone to be a diagnos-tic feature of the "temporal lobe agenesis" syn-drome. Anderson and Landing13 discussed cere-bral arachnoidal cysts in nine patients, eight ofwhom were children. All showed radiological thin-ning and expansion of the temporal bone but itwas clinically distinguishable in only four of them.He suggested that such cysts were a common causeof rapid enlargements of the head in infants.The actual cause of the expansion of the skull

overlying these cysts is uncertain. Dr List,12 inhis discussion on Childe's paper, suggested that itwas due to the pulsating pressure of the localisedcollection of fluid. Robinson5 6 suggests that themaldevelopment of the temporal lobe leaves acapacious subarachnoid space and suggests that

Fig 6 Lateral skull x-ray showing anterior expansionof middle cranial fossa

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the skull is expanded by its pulsation. This wouldhave to occur before the skull is fully developedand suggests that the basic abnormality is morelikely to be congenital.

Various clinical presentations of arachnoidalcysts of the middle fossa have been described, thecommonest being epilepsy. All our cases exceptone presented with symptoms and signs of raisedintracranial pressure and space occupation. Case 1presented with subarachnoid haemorrhage. Tormaand Heiskanen'0 described a similar case in a47 year old female, who presented as a verifiedsubarachnoid haemorrhage with the history of aconcussion suffered 11 months earlier. Robinsonhad a similar case in his series. These cysts mayremain asymptomatic and be found at necropsyfollowing death due to other causes.5 6

Conclusions

The six cases in our opinion, are examples of con-

genital agenesis of the temporal lobe and its sus-ceptibility to haemorrhagic complications evenwith minor trauma.

It is likely that in most or all the cases minortrauma in some way provoked an increase in thesize of the cyst. It is likely that trauma can giverise to haemorrhage within the cyst, causing thisto expand. The source of the bleeding may be thevessels in the arachnoid or the cyst capsule. Thecyst wall might also tear giving rise to a subduralcollection of haemorrhagic fluid as was seen un-

equivoLally in case 5. It is also possible thattear of the deeper layer of the cyst wall gives riseto a valvular arrangement whereby CSF flowsone way causing a gradual increase in the size ofthe cyst. It appears that these patients have an

increased susceptibility to trivial trauma, an

opinion also expressed in Greenfield's Neuropath-ology.'4 The exact reason for this is not clear butit may be because of the altered anatomy of themiddle cranial fossa. This may be similar to theincreased vulnerability to trauma seen in hydro-cephalus or in cerebral atrophy. There is evidenceto suggest that the basic defect, that is either thecyst or the temporal lobe agenesis, is congential


in origin. The expanded middle fossa certainlysuggests long standing or life long abnormality.These changes can be seen on the plain radio-graphs. The haemorrhagic complication of a longstanding abnormality may thus be recognised atan early stage.Craniotomy and excision of the cyst walls would

appear to be the ideal treatment. Drainage of thecyst through burr holes may be followed by re-current accumulation of fluid as was seen in twoof our cases.

References

1 Reynolds CE. Infective external hydrocephalus:shifting epilepsy. Br Med J 1921; 2:66-70.

2 Reynolds CE. Further observation upon externalhydrocephalus. Br Med J 1922; 1:950.

3 Naffziger HC. Subdural fluid accumulations fol-lowing head injury. JAMA 1924; 82:1751-2.

4 Frazier CH. Cerebral pseudotumours. ArchNeurol 1930; 24:1117-32.

5 Robinson RG. Intracranial collections of fluidwith local bulging of the skull. J Neurosurg1955; 12:345-53.

6 Robinson RG. The temporal lobe agenesis syn-drome. Brain 1964; 88:87-106.

7 Starkman SP, Brown TC, Lunell MD. Cerebralarachnoid cysts. J Neuropathol Exp Neurol 1958;17:484-500.

8 Tiberin P, Gruzkewicz J. Chronic arachnoidalcysts of the middle cranial possa and theirrelation to trauma. J Neurol NeurosurgPsych;atry 1961; 24:86-91.

9 Gruss P, Auer-Doinet G. Genesis of temporalarachnoid cysts. Neuropaediatrie 1974; 5:175-80.

10 Torma T, Heiskanen 0. Chronic subarachnoidalcyst in the middle cranial fossa. Acta NeurolScand 1962; 38:166-70.

11 Hardman J. Asymmetry of the skull in relationto subdural collections of fluid. B J Radiol 1939;12:455-61.

12 Childe AE. Localised thinning and enlargementof the cranium with special reference to themiddle fossa. Am J Roentgenol 1953; 70:1-22.

13 Anderson FM, Landing BH. Cerebral arachnoidcysts in infants. J Paediatr 1975; 68:88-96.

14 Urich H. In: Backwood W & Corsellis JAN(ed) Greenfield's Neuropathology, London:Edward Arnold 1976; 394.



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