Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:238-242

Entrapment of the temporal horn: a form of focalobstructive hydrocephalusRS MAURICE-WILLIAMS, M CHOKSEY

From the Royal Free Hospital and School of Medicine, London, UK

SUMMARY Three cases of a form of focal hydrocephalus are described which the authors term"entrapment of the temporal horn". Obstruction of one lateral ventricle in the region of the trigoneisolates the temporal horn. Continued secretion of cerebrospinal fluid within the temporal horncauses it to behave as a mass lesion. In the cases described the causes of the condition were recurrentglioma, previous tuberculous meningitis and surgical excision of an arteriovenous malformationwhich extended into the trigone. Shunting of the trapped temporal horn provides satisfactorytreatment.

We describe three cases of a syndrome in whichobstruction of the trigone of the lateral ventricle sealsoff the temporal horn from the rest of the ventricularsystem. Continued secretion of cerebro-spinal fluid bythe choroid plexus within the temporal horn leads it toexpand into a cyst which behaves as a mass lesion.This entity which we have termed "entrapment of thetemporal horn" is a form of focal hydrocephalus,which has previously attracted little notice. It isdistinct from two other rare but well recognised formsof partial hydrocephalus: unilateral hydrocephaluscaused by obstruction of one foramen of Monro andseptation of the ventricular system after infantilemeningitis.

Case reports

Case 1This 23-year-old woman had undergone resection of a righttemporal malignant glioma 2 l/2 years previously followed bya course of radiotherapy. Eighteen months later a localrecurrence of her tumour had been treated by further surgicalresection and chemotherapy. At neither operation had theventricular system been entered and she had been left with noneurological defect. One year later she developed severeprogressive headache and drowsiness over a period of threedays. On admission she was found to be confused and irri-table with a marked left facio-brachial weakness and a tensesub-temporal decompression. On re-exploration there wasfound to be very little recurrent tumour within the temporallobe but there was a cystic expansion of the right temporal

Address for reprint requests: Mr RS Maurice-Williams, Royal FreeHospital, Pond Street, London NW3 2QG, UK.

Received 21 May 1985 and in revised form 18 July 1985.Accepted 23 July 1985

horn which contained 60 ml of clear colourless fluid resem-bling cerebro-spinal fluid. The communication of the tempo-ral horn and the trigone was severely narrowed by fibroustissue. This stenosis was opened up so that the temporal horncommunicated freely with the trigone. After operation shemade a rapid recovery although she was left with a left lowerfacial weakness and a homonymous lower quadrantinopia.She remained well until six months later when she died froma recurrence of her tumour.

Fig I Case 2. CT scan showing expanded right temporalhorn displacing the lateral ventricles to the left.

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Entrapment of the temporal horn: a form offocal obstructive hydrocephalus

Case 2This 35-year-old Asian housewife, had been treated for twomonths for tuberculous meningitis but had persistent head-

aches and had had two epileptic fits. A CT scan showed anarea oflow attenuation around the trigone of the right lateralventricle. The headache improved spontaneously but a

month later it recurred and she developed a slight left sidedweakness. Over the next few days she became increasinglydrowsy and was referred to the neurosurgical department.On examination she had a temperature of 36°C and no signsof meningeal irritation. She was well orientated but drowsywith a left homonymous hemianopia and a left hemiparesis,more marked in the arm than the leg. Haemoglobin was 14 1gm, white cell count 7000/mm3 and sedimentation rate 25mm in the first hour. CT scan (fig 1) showed expansion of thetemporal horn of the right lateral ventricle with low attenu-ation of the surrounding white matter and a shift of themidline structures to the left. The choroid plexus of the rightlateral ventricle was prominent. A right temporal crani-otomy was carried out and the right middle temporal gyrus

was incised to enter an expanded temporal horn which was

4cm across. Communication with the trigone was obstructedby an engorged choroid plexus. The choroid plexus was

largely destroyed with diathermy and it was hoped that theencysted temporal horn would drain through the corticalincision into the subarachnoid space. However, after oper-

ation she became progressively drowsy and the left hemi-paresis worsened. A repeat CT scan showed that the cyst hadre-formed and that there was considerable oedema of thesurrounding white matter. The cyst was shunted into theright atrium through a Pudenz valve system. Thereafter thepatient made an uneventful recovery. CT scan three weeksafter insertion of the shunt showed that the cyst had resolvedand six months later the patient remained symptom-free andhad no neurological deficit.

Fig 2 (a) Case 3. CT scan: expanded lefi temporal horncompressing the remainder of the left lateral ventricle andcausing midline shift. (b) Case 3. CT scan showingappearance after shunting of trapped temporal horn.

Fig 3 Case 3. CT scan showing position and extent ofencysted temporal horn in the sagittal plane.

Fig 4 Case 3. CT scan showing position of encystedtemporal horn in the coronal plane.

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Case 3This 30-year-old housewife had a subarachnoid hae-morrhage when 32 weeks pregnant. On admission to hospitalshe had hesitancy of speech, a mild right hemiparesis andsensory inattention of the right limbs. CT scan showed bloodin the lateral and third ventricles and a small left parietalintracerebral haematoma. Angiography revealed a 5 cmdiameter left parietal arterio-venous malformation fed byenlarged terminal branches of the middle cerebral artery anddraining into the superior sagittal sinus. Seven days after thehaemorrhage, craniotomy and complete excision of the mal-formation was carried out. A deep extension of the mal-formation into the trigone of the left lateral ventricle wasfound and in this region small patches of muslin were usedto obtain haemostasis. Check angiography three days latershowed no residual malformation. Seventeen days afteroperation she went into labour and a healthy child wasdelivered by Caesarean section. After excision of the mal-formation, there was some improvement in her pre-operativeneurological deficit but this fluctuated and CT scan showedthat the bed of the malformation was occupied by a cysticcollection of fluid extending into the temporal lobe and caus-ing displacement ofthe midline structures. This cyst persisteddespite three aspirations of brownish muddy fluid throughthe craniotomy incision. The craniotomy was then reopenedand 40 ml of slightly cloudy colourless fluid was aspiratedfrom beneath the site of the malformation through the pre-vious cortical incision. This further procedure producedsome improvement but her condition then levelled out andshe was left with a marked expressive dysphasia and a spasticweakness of the right arm. Subsequent scans showed a per-sistent and well defined expansion of the left temporal hornwhich was causing considerable cerebral displacement (figs 2,3 and 4). It was thought that scarring within the trigone ofthe lateral ventricle, perhaps partly provoked by the muslinpatches, had obstructed the egress of cerebro-spinal fluidfrom the temporal horn. It was now three months sinceremoval of her malformation. A Holter medium pressureshunt system was inserted so as to drain the entrapped tem-poral horn into the peritoneal cavity. This led to a rapid andmarked neurological recovery. A scan four days after theshunt showed that the cyst had resolved and that there wasno longer any cerebral shift. One year later she was lookingafter her family without any functional disability. She had anoccasional slight hesitancy of speech and a right hom-onymous hemianopia but otherwise no residual neurologicaldeficit. CT scan at this time showed no re-formation of thecyst but there was a small dense nodule in the region of theleft trigone which was thought to represent calcifying muslin.

Discussion

Hydrocephalus results when the flow of cerebro-spinal fluid is impeded. When the block lies within theventricular system, it is termed "obstructive hydro-cephalus". Both active secretion of cerebro-spinalfluid by the choroid plexus and the pulse waves fromthe plexus expand the trapped part of the ventricularsystem, ' 2 for the brain parenchyma has only a limitedcapacity to absorb cerebro-spinal fluid.3 Obstructivehydrocephalus usually results from compression of, or

Maurice- Williams, Choksey

a block within, the fourth ventricle, the aqueduct ofSylvius, or the third ventricle, leading to symmetricaldilatation of the lateral ventricles.

If part of the ventricular system is closed off fromthe rest, and if the sealed off section contains choroidplexus, a partial or focal hydrocephalus may result.This is a rare event but may occur in two circum-stances. First, obstruction of one foramen of Munromay cause hydrocephalus confined to one lateral ven-tricle. This so-called unilateral hydrocephalus leads tothe symptoms of raised intracranial pressure accom-panied by the features of dysfunction of the affectedcerebral hemisphere. Unilateral hydrocephalus maybe caused by a wide range of lesions in the region ofthe foramen of Monro, including colloid cysts of thethird ventricle, tumours of the septum pellucidum andthalamus, cysticercosis, congenital gliotic atresia ofthe foramen of Munro and after ventriculitis or sur-gical procedures within the lateral ventricle.48 If theobstruction cannot be removed, the condition istreated by shunting the affected ventricle.The second situation where partial hydrocephalus

may occur is after meningitis in infancy. If the infec-tion has involved the ventricles, and especially if it hasbeen caused by a gram negative organism, the patientmay develop a number of thin veils or septa within theventricles separating them into a number of compart-ments.9 -12 These septa may progress after the infec-tion has been overcome.'3 They consist of thin trans-lucent veils of tissue which are most often situated inthe lateral ventricles just behind the foramina ofMonro,'0 though there may be multiple septathroughout the ventricular system.9 Their patho-genesis is uncertain but it has been suggested that theyarise from tufts of glial tissue which grow out fromareas of the ventricular wall which have been denudedof ependyma by the preceding ventriculitis.9 This so-called compartmentalised or multi-loculated hydro-cephalus is difficult to treat. Ventricular shunts bythemselves often fail and open ventriculostomy maybe required to divide the septa." 13 Cerebral endo-scopy has also been used as a lesser procedure toachieve the same end. 14 However, regardless of treat-ment, the condition is associated with a very poorprognosis. Most of the affected children die and a highproportion of the survivors are left with a severe psy-chomotor retardation.'0 11

These two examples of partial hydrocephalusshould be distinguished from the situation where acyst projects into the brain from the wall of one ven-tricle in association with hydrocephalus.15 Thisoccurs most often when a generalised hydrocephalusis associated with a focal brain injury. This may hap-pen in infantile hydrocephalus, after an injury in adultlife, or from a cerebral haemorrhage which has causedhydrocephalus as well as a focal disruption of brain

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Entrapment of the temporal horn: a form offocal obstructive hydrocephalustissue. Tearing of the ependyma at the point of focalinjury permits the growth of a diverticulum from theventricular system into the damaged white matter atthat point. Such a porencephalic cyst communicatesfreely with the ventricle and it can be treated by asingle shunt placed anywhere within the ventricularsystem.The entity which we describe here is quite different

from these syndromes. It consists of obstruction ofthetrigone of one lateral ventricle so that the trapped orisolated temporal horn containing choroid plexusexpands into a cyst. This gives rise to the symptoms ofraised intracranial pressure as well as appropriate fea-tures of focal cerebral dysfunction such as dysphasiaor a contralateral hemiparesis. In normal individuals,the ventricles of the brain are narrow slit-like cavitiesrather than the full-bodied chambers which their dia-grammatic representations often suggest. Indeed theopposing wall of the ventricles often adhere so thattheir extreme lateral angles may be pinched off. 6 Thetrigonal part of the lateral ventricle is further nar-rowed by the bulk of the choroid plexus. It does notseem surprising that obstruction can occur at thispoint and many neurosurgeons must have experi-enced the phenomenon we describe, yet it does notseem to have been reported previously as a definedclinico-pathological entity other than by Cairns andcolleagues in 1941.17 They described three patientswith the syndrome. In two patients the temporal hornentrapment resulted from a penetrating wound of thebrain which had entered the ventricle. In the remain-ing case, an infant, the ventricular obstruction wascaused by a subependymal haemorrhage.The aetiology of the condition was different in each

of our three patients. In the first case the trigone wasstenosed by a limited recurrence of a glioma aroundthe ventricle. The expansion of the temporal hornmimicked a solid recurrence of the tumour. Drainageof the cyst into the main body of the ventricle sufficedto give a remission for several months until thetumour recurred. In case 2, the trigone was obstructedfrom within by a swollen choroid plexus after tuber-culous meningitis. Ventriculostomy into the sub-arachnoid space failed and a shunt was required. Inthe third case, entrapment of the temporal horn fol-lowed excision of an arteriovenous malformationwhich extended into the trigone. Fibrosis around mus-lin squares placed in the trigone to obtain haemostasismay have contributed to the obstruction.

Entrapment of the temporal horn should be sus-pected in patients who develop symptoms of anexpanding temporal lobe mass after a condition whichhas involved the region of the trigone of the lateralventricle. Our first patient was treated before thedevelopment of the CT scan, an investigation whichshould make the diagnosis of this condition easy by

showing a large low attenuation cyst in the temporo-parietal region in the position of the normal temporalhorn. Judging from our experience there seems little tobe said for attempted aspiration or open explorationof such cysts and drainage through a shunt systemseems a satisfactory method of treatment.

We thank Mr R Campbell Connolly for permission toreport the first patient who was treated under his careat St Bartholomew's Hospital.

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