|Year : 1984 | Volume
| Issue : 1 | Page : 9-12
Decompression of the perioptic meninges for relief of papilloedema in benign intracranial hypertension
P Subburam, VM Loganathan, G Baskara Rajan, M Natarajan
Department of Neurosurgery and Ophthalmology, Government Rajaji Hospital Madurai, India
Department of Neurosurgery & Ophthalmology, Government Rajaji Hospital Madurai- 625 020
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Subburam P, Loganathan V M, Rajan G B, Natarajan M. Decompression of the perioptic meninges for relief of papilloedema in benign intracranial hypertension. Indian J Ophthalmol 1984;32:9-12
Benign intracranial hypertension usually runs a self-limiting course with a good prognosis; but the long term prognosis with regard to vision is subject to variation in opinion,, Greer has reported permanent visual loss in 10 percent of patients with this syndrome. A prospective study of 25 cases of benign intracranial hypertension was made in the Departments of Neurosurgery and Ophthalmology Government Rajaji Hospital, Madurai during the period 1980-82. Twenty one patients responded well to usual conservative measures while four of them developed severe deterioration of vision. Further visual loss could be stopped only by decompressing the optic nerves through transorbital approach. This article describes a simple surgical approach to the optic nerve, and presents the results of the operation on four cases of benign intracranial hypertension.
| Material and methods|| |
Twenty five patients were diagnosed as having benign intracranial hypertension by doing all the possible investigations including fundus fluorescein angiography on all of them and CT Scan evaluation in six cases. Four of them developed visual deterioration in spite of adequate conservative treatment in the form of dehydrating agents, steroids, and serial lumbar punctures. Insertion of lumbar-the co-peritoneal shunt on three patients did not bring any relief, and they had lost vision almost completely in one of their eyes and developed progressive visual failure in the other. Transorbital decompression of the perioptic sheath on the eyes with persisting papilloedema resulted in clearance of the oedema. The fourth case, a 22 year-old obese lady, initially diagnosed as a case of benign ICT underwent decompression of the right optic nerve. But, 15 days after the operation she threw several attacks of generalised seizures and lapsed into coma. Contrast ventriculogram performed now showed evidence of dilated ventricular system and a filling defect in the cisterna magna. She regained consciousness after insertion of a ventriculo-peritoneal shunt. Subsequently the posterior fossa was explored and arachnoidal adhesions were found. Postoperatively she developed CSF leak and died of fulminant meningitis [Table - 1].
| Operative technique|| |
A fornix based conjunctival flap of 180° is fashioned on the nasal side of the globe and radial incisions are made at each end of the flap. Traction sutures are looped beneath the tendons of the superior and inferior rectus muscles. The medial rectus muscle is exposed and detached from the globe and marked with a stay suture. Firm anterolateral traction on the vertical rectus sutures will prolapse the globe; it is retracted laterally by means of an enucleation spoon. Operating spectacles are used at this stage. The orbital fat is retracted and the optic nerve exposed at the depths of the wound. The short ciliary vessels are displaced to expose the dural sheath; it is secured with a dural hook and a 3X5 mm window is excised from the sheath. The subarachnoid space is entered with ease because the dura and arachnoid are adherent. CSF will spurt if it is under tension. The retractors are removed, the medial rectus reattached to the globe, and the conjunctiva closed. antibiotic ointment is instilled into the conjunctival sac and the eye covered for 24 hours.
| Observations|| |
Oedema of the optic disc cleared and the venous engorgement subsided in all the four cases reported above, within two weeks after the operation. The progressive visual deterioration was stopped.
Complications of the operation are few and minor. There was transient pupillary dialatation in two cases probably from trauma to the posterior ciliary nerves. We did not observe proptosis. Chemosis and conjunctival swelling were no greater than would be expected from the operation itself.
| Discussion|| |
De Wecker in 1872 described an operation for the treatment of papilloedema. Through a lower temporal conjunctival incision, he identified the optic nerve by palpation, and incised its sheath blindly with a guarded knife. Papilloedema and symptoms of increased intracranial pressure were relieved in the two cases reported. In 1887, he reported his experience with unilateral optic nerve sheath decompression on four patients. Carter also adopted this method and achieved impressive results. But, Jack of detailed description and follow up make these and other early reports difficult to analyse. Although, usually effective, the procedure was eventually superseded by neurosurgical procedures.
Such a procedure on the optic nerve sheath was thereafter forgotten for 90 years until 1964 when Sohan Singh Hayreh employed the technique on monkeys to demonstrate that papilloedema due to raised intracranial pressure could be relieved by reducing the CSF pressure within the subarachnoid space of the optic nerve. Davidson reported five patients with papilloedema on whom unilateral optic nerve sheath decompression was performed through a lateral orbitotomy. He commented on the difficulty of identifying and exposing the optic nerve through the temporal approach. In 1969, Smith and his associates successfully relieved unilateral disc swelling in a patient who they speculated had a chronic "perioptic cystic hygroma"
They approached the optic nerve through the conjunctiva from the medial side after performing a Kr φnlein orbitotomy to allow lateral retraction of the globe. In 1974, Burde and his associates reported dramatic reversal of visual deficit in a case of pseudotumour cerebri with uncontrolled raise of ICP, papilloedema and visual loss, following bilateral optic nerve decompression. They commented that although the operation is technically less difficult with the optic nerve sheath expanded by increased CSF, the risks of general anaesthesia are increased, and therefore, they suggested that operation may be attempted under local anaesthesia. We adopted the approach described by Galbraith and Sullivan in 1973 along the medial side of the globe, under general anaesthesia and employed operating spectacles for controlled incision of the optic nerve sheath.
The exact mechanism of action of optic nerve decompression is still unclear., Hayreh, by means of experiments on monkeys, not only established that raised ICP was essential in the production of oedema of the disc, but he also showed the site of action of this raised ICP to be the retrobulbar portion of the optic nerve. Devidson suggested that the raised ICP is lowered due to a leak of CSF from the dural windows cut in the nerve sheaths. This hypothesis would explain the relief of symptoms noted to occur following optic nerve decompression and the improvement of papilloedema in the contralateral eye that 'has been reported following unilateral decompression. However, in an another article Davidson refuted his earlier hypothesis and postulated that the gap in the dura is soon plugged by fibroblastic proliferation extending from the subarachnoid space which prevents the transmission of the increased ICP along the subarachnoid space via the CSF.
The efficacy of transorbital retrobulbar incision of the optic nerve sheaths in relieving papilloedema is clear in the four cases reported. However, we could only arrest further progression of visual deterioration because this procedure was bone as a last resort when other measures failed to prevent the visual loss. Our results would have been better as reported by Galbraith and Sullivan had we operated on these cases before the onset of secondary optic atrophy.. Incidentally, the propensity for a case of benign intracranial hypertension to become a progressive neurosurgical condition is illustrated in case number 4.
We believe that optic nerve sheath decompression is a simple and safe procedure, especially in skilled hands, for preventing impending blindness from papilloedema when other attempts at controlling CSF pressure have failed.
| Summary|| |
Surgical intervention is rarely required in cases of Benign intracranial hypertension. This article describes the usefulness of transorbital decompression of the optic nerve sheath in relieving papilloedema when the conventional measures fail to reduce the CSF pressure.
| References|| |
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