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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 59, Num. 4, 2011, pp. 542-547

Neurology India, Vol. 59, No. 4, July-August, 2011, pp. 542-547

Original Article

Management outcome of the transcallosal, transforaminal approach to colloid cysts of the anterior third ventricle:  An analysis of 78 cases

Nigel Peter Symss, Ravi Ramamurthi, Santosh Mohan Rao, Madabushi C Vasudevan, Pradeep Kumar Jain, Anil Pande

Post Graduate Institute of Neurological Surgery, Dr. A. Lakshmipathi Neurosurgical Centre, VHS Hospital, Chennai, India
Correspondence Address: Nigel Peter Symss, Post Graduate Institute of Neurological Surgery, Dr. A. Lakshmipathi Neurosurgical Centre, VHS Hospital, IT Corridor, Taramani Main Road, Chennai - 600 113, India, nigelpetersymss@gmail.com

Date of Submission: 14-Feb-2011
Date of Decision: 09-Mar-2011
Date of Acceptance: 29-Apr-2011

Code Number: ni11167

PMID: 21891930

DOI: 10.4103/0028-3886.84334

Abstract

Background: Colloid cysts are not common brain lesions and account for 0.2-2.0% of all brain lesions. Transcallosal, transforaminal approach is a safe route and the most direct path to excise third ventricular colloid cyst, without dependence on hydrocephalus.
Aim: To assess the surgical outcome of patients with colloid cysts of the anterior third ventricle treated by the transcallosal, transforaminal approach.
Patients and Methods: Seventy-eight patients operated by the above approach over a period of 20 years were analyzed. A pre- and postoperative neurological assessment was done in all the patients. Neuro-cognitive evaluation of corpus callosum function was done in the last 20 patients. Computer tomography scan of the brain was done in all patients pre- and postoperatively.
Results:
Clinical features of raised intracranial pressure without localizing signs were the commonest presenting feature in 52 (66.7%) patients. Hydrocephalus was present in 65 (83.3%) patients. All patients underwent the transcallosal, transforaminal approach, and total excision of the lesion was achieved in 77 patients and subtotal in 1. Four patients required a postoperative shunt for acute hydrocephalus. There was no incidence of postoperative disconnection syndrome. In two patients, there was recurrence of the lesion after 2 and 6 years, respectively. Two patients died in the postoperative period.
Conclusion:
Colloid cyst is surgically curable. Early detection and total excision of the lesion can be a permanent cure with low mortality and minimum morbidity, when compared to the natural history of the disease. The limited anterior callosotomy does not result in disconnection syndromes or behavioral disturbance.

Keywords: Anterior third ventricle, colloid cyst, disconnection syndrome, transcallosal, transforaminal

Introduction

Colloid cysts are not common brain lesions, accounting for 0.2-2.0% of all brain lesions. In 1921, Dandy was the first neurosurgeon who successfully removed a colloid cyst from the third ventricle through a posterior transcallosal approach, and stated that no treatment short of total removal could have any possible value in the treatment of tumors in this region. [1] The anterior transcallosal approach was suggested by Ehni who used this approach for different pathological entities. [2] We report our experience of treating colloid cysts of anterior third ventricle by the transcallosal, transforaminal approach in 78 patients.

Patients and Methods

This was a retrospective study of patients with colloid cyst of anterior third ventricle treated by transcallosal, transforaminal approach from 1988 to 1999, and a prospective study from 2000 to 2010. Exclusion criteria were patients operated by the transcortical transventricular approach and those undergoing only a cerebrospinal fluid (CSF) diversion. The data analyzed were age, gender, and clinical features. Pre- and postoperative neuro-cognitive assessment was done in the last 20 patients. Postoperative assessment was done on the sixth postoperative day and on follow-up. Abattery of bedside clinical tests was performed to assess the interhemispheric somatosensory and motor transfer of information and memory function. Each patient underwent mini-mental status examination (MMSE) and specific tasks defined for assessing corpus callosal function, namely, volitional saccades, transfer functions, stereognosis and coin sorting tasks. Twenty patients with other intracranial lesions were also analyzed as a control group. Brain computer tomography (CT) scan was done in all the patients pre- and postoperatively, and magnetic resonance imaging (MRI) scan was done whenever feasible. The size of the lesion, density/intensity, contrast enhancement, and presence of hydrocephalus were analyzed.

Results

Clinical characteristics

There were 43 male patients; the youngest patient was 14 years old and the oldest 62 years; and maximum number of patients was in the 3 rd to 5 th decade [Table - 1]. The duration of symptoms ranged from 15 days to 8 years. The commonest mode of presentation was headache, persistent or paroxysmal, in 70 patients, vomiting in 52, and visual disturbances in 33 patients [Table - 2]. Episodic loss of consciousness with arousal with a change in posture suggestive of acute hydrocephalus was seen in seven patients. The commonest clinical sign was papilledema observed in 52 patients [Table - 3].

Of the 20 patients who had pre- and postoperative neuro-cognitive assessment, 14 patients were found to have deficits in the tasks done, while only 5 controls had the abnormalities. Analysis of the results is as follows: 9 patients had impairment in all the four tasks, 2 had in three tasks, and 1 in two tasks. Stereognosis/tactile anomia and cross replication of finger positions (transfer functions) were the most commonly affected tasks, especially in the left hand. Decreased memory was seen, especially transient impairment of immediate recall in 8 patients compared pre-operatively. Mood disorders such as depression were seen in six patients and elevation in seven patients, and these resolved by 2 weeks. MMSE score ranged between 27 and 30 in these patients. Pre-op mean MMSE was 28.30, post-op mean MMSE was 28.12.

Radiology

CT features were as follows. The lesion was hyperdense to brain in 60 patients, 39 were contrast enhancing and 21 were non-enhancing with contrast. In 8 patients, the lesion was hypodense, 6 were contrast enhancing and 2 were non-enhancing. In 10 patients, the lesion was isodense to brain, and all were contrast enhancing [Table - 4]. The hypodense and isodense lesions had viscous colloid material, which could be aspirated. Sixty-five patients had associated hydrocephalus. Brain MRI scan was done in 26 patients. On T1W image, the lesion was hyperintense in 11 patients, hypointense in 3 patients, and isointense in 10. On T2W image, the lesion was hyperintense in 12 patients, hypointense in 3 and isointense in 9. In two patients, the lesion was hypointense on T1W images, with a peripheral rim of isointensity, and on T2W images the lesion remained hypointense but the rim was hyperintense.

Surgical treatment

Of the 65 patients who had preoperative hydrocephalus, a right VP shunt with a left frontal burr hole was done in 16 patients. This was the protocol followed in the initial years in patients with papilledema and significant hydrocephalus. All the patients underwent a right fronto-parietal midline craniotomy, anterior transcallosal, transforaminal approach and excision of the lesion [Figure - 1]a, b. In 67 patients, the lesion was seen at the foramen of Munro occluding it. In 11 patients, it was situated posterior to the foramen of Munro, bulging into the septum pellucidum. When the lesion was located at the foramen of Munro, the transforaminal entry into the third ventricle was facilitated by a large lesion which widened the foramen. Even when the lesion was a little posterior to the foramen, it was possible to excise the cyst through the same approach. The foramen was never made wider by incision of the brain tissue. Total excision of the lesion was achieved in 77 patients, and in 1 patient, only subtotal excision of the lesion could be achieved as it was densely adherent to the posterior wall of the third ventricle [Figure - 2]a, b and [Figure - 3]a, b. The septum pellucidum was fenestrated in all the patients, allowing inspection of the opposite side foramen, and to communicate the two ventricles. In two patients, there was rupture of a branch of the pericallosal artery during dissection. In one patient, a posterior cortical vein draining into the superior saggital sinus ruptured and the patient developed seizures with hemiparesis.

Complications

The postoperative complications encountered included seizures in six patients, venous cortical infarct in four [Figure - 4], acute hydrocephalus in four requiring a CSF diversion [Figure - 5], transient hemiparesis due to retraction edema in four, transient memory impairment especially immediate recall in nine, mutism in one, subdural hematoma requiring evacuation in one, meningitis in three, and tension pneumocephalus in one. There were two mortalities. Both the patients developed a basal ganglia hemorrhagic infarct [Table - 5]. The majority of the complications occurred during the initial years.

Recurrence

Recurrence of the lesion was seen in two patients (4.35%) after 2 and 6 years of operation, one in the patient with subtotal excision and the other in the patient who underwent re-transcallosal approach and total excision of the lesion. This patient had hydrocephalus and underwent only shunt revision as he was medically unfit for a major surgery.

Follow-up

Seventy-two patients (92.3%) were followed up for a period of 1 month to 6 years, with a mean follow-up of 1.18 years. Six patients did not return for follow-up. Sixty-eight patients (95%) had no deficits during the follow-up. One patient had shunt infection at 1 month follow-up which required removal of the shunt tube. One patient had generalized tonic clonic seizures at 6 months follow-up. One patient had residual hemiparesis. Three patients had impaired recent memory at follow-up of 3 months, 1 year, and 5 years. None of the patients had a disconnection syndrome.

Discussion

Colloid cysts have always provoked interest in neurosurgeons because of their controversial origin, benign histology, dramatic clinical presentations and the variety of possible treatment options. Of the 36 patients in Dandy's series, 31 were diagnosed at autopsy, thus confirming the belief that sudden death can be a common initial presentation. [3] Ryder et al.[4] analyzed 56 cases of colloid cysts having suffered sudden death and postulated that the reflex effects involving the cardiovascular centers near the third ventricle might have contributed to the sudden death. In patients with colloid cyst of anterior third ventricle, the symptoms are primarily those of increased intracranial pressure and are non-localizing as seen in our series. [5],[6],[7],[8] These symptoms are not specific for colloid cyst, and any midline mass may present with these features. However, this presentation should suggest the diagnostic possibility of colloid cyst. [6]

Kondziolka and Lunsford [9],[10] reviewed radiology of 122 cases in the literature and related density directly to the viscosity of the cystic contents and found that hyperdense cysts were unlikely to be aspirated successfully. The analysis of Donaldson and Simsons [11] found sodium, magnesium and calcium within the mucin of the cyst and they suggested that the calcium bound to prealbumin may contribute to the density. Mader et al.[12] attributed the viscosity to the cholesterol content of the cyst. Most colloid cysts show hyperintensity on T1W and T2W images, which often correlates with the increased protein content of colloid cysts. Wilms et al.[13] reported another group of colloid cysts with mixed signal intensities on T1W and T2W images. These cysts are usually large. [13] Ahmadi et al. [14] found that cystic fluid that is hypointense on T1W and hyperintense on T2W images tends to be watery and easily aspirated.

Apuzzo et al.[15] reviewed 100 angiograms, analyzing the parasagittal venous tributaries, and stressed the importance of proper planning of the dural flap. The corpus callosum is incised in the midline between the pericallosal arteries for a length of 1.5-2.5 cm in the sagittal plane in the anterior corpus callosum. Woiciechowsky et al.[16] found that 3.7% of their patients had an azygous pericallosal artery, requiring a callosotomy lateral to the pericallosal arteries. Hernesniemi [17] has found that the far lateral corpus callosal incision has been valuable in avoiding memory disturbances and the foramen of Munro is never made wider by incision of brain tissue.

Transient amnesia, probably due to forniceal manipulation during surgery, is not an unusual postoperative complication. [15],[18],[19],[20] Memory deficits may also arise from trauma to the basal forebrain nuclei, thalamic nuclei, septal nuclei, and inferior thalamic peduncle. [21],[22],[23],[24] Some studies find little influence of one forniceal lesion on recent memory if the contralateral fornix is intact. [16] Nakasu et al.[25] stated that injury to adjacent structures such as cingulate gyrus, trauma to the wall of the anterior III ventricle and floor of the lateral ventricle and damage to the dominant supplementary motor cortex may lead to postoperative mutism. Bellotti et al.[26] reported mutism as the most frequent complication in their series. We routinely give anticonvulsants postoperatively because of the frontal lobe retraction. However, some neurosurgeons do not give anticonvulsants, as a cortical incision is avoided. [27] The incidence of postoperative seizures in the transcortical transventricular approach in some series ranges from 11 to 13%. [5],[21],[28],[29] Motor deficits may be due to pericallosal artery branch injury, venous infarct, and retraction edema. Prolonged lateral retraction can result in frontal lobe swelling, and excessive medial retraction on the superior sagittal sinus can lead to sinus thrombosis. [30] Cerebral venous infarct secondary to cortical vein occlusion causes serious neurological deficits. [5],[7],[15],[17],[18],[30],[31],[32] Arterial injury may occur during lateral dissection, which may injure the small branches of the pericallosal arteries. [2]

We had two (2.6%) postoperative deaths. Both the patients developed a basal ganglia hemorrhagic infarct with intraventricular bleed due to vascular injury. Hernesniemi [17] had reported a mortality of 13%. Recurrence of colloid cyst is rare. [17],[18],[21] This may occur due to leaving a fragment of the capsule behind.

During the follow-up, three patients had impaired recent memory and none had a disconnection syndrome. An incision of up to 2.5 cm in the anterior body of the corpus callosum, which is necessary for the exposure of the ventricular system, does not result in any disconnection disorder. [3],[33],[34],[35],[36],[37],[38],[39],[40],[41] Jeeves et al.[42] have found impairment in the transfer of tactile data. Bogen [43] concluded that interhemispheric transfer of information is preserved as long as the splenium remained intact. Regarding the transcortical transventricular approach, Solaroglu et al. treated 26 patients by the transcortical transventricular approach. They had no surgical mortality and the main morbidity was seizures in two patients. Their overall outcome was good. [44] Sudden deterioration followed by death has not been reported in patients with a colloid cyst of less than 1 cm in size. [4],[5],[45] Patients with a colloid cyst larger than 1.5 cm should be considered for surgical excision as these cysts are more likely to become symptomatic. [46] We are reluctant to recommend conservative management for incidentally discovered colloid cysts.

In conclusion, transcallosal, transforaminal approach is a safe route and the most direct path to excise third ventricular colloid cyst, without dependence on hydrocephalus. There are no major permanent deficits in memory or intellectual function with the limited anterior callosotomy and forniceal handling. The approach does not result in disconnection syndromes or behavioral abnormalities.

References

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