Optic Nerve Compression

Damage to the optic nerve by a mass, enlarged tissue or bone within the orbit, optic canal or intracranial space, causing progressive or acute visual loss. The orbital apex and canal are crowded spaces where small lesions cause large effects.

• Causes:
  • Orbital: thyroid eye disease (enlarged muscles), idiopathic orbital inflammation, tumour (optic nerve sheath meningioma, optic glioma, haemangioma, lymphoma, metastasis), abscess, haematoma, mucocele, orbital apex fracture.
  • Bony: fibrous dysplasia, hyperostosing sphenoid wing meningioma, Paget disease, osteopetrosis, craniosynostosis, optic canal fracture.
  • Intracranial: pituitary adenoma, suprasellar meningioma, craniopharyngioma, internal carotid or ophthalmic artery aneurysm, dolichoectasia.
• Acute: haematoma, abscess, thyroid disease (dysthyroid optic neuropathy), sinus mucocele; chronic: tumour, bony.

• Painless, progressive unilateral loss of acuity, dyschromatopsia (red desaturation), relative afferent pupillary defect, and visual field defects (central scotoma, arcuate, altitudinal or temporal depending on level).
• Optic disc: swelling (anterior compression), normal early, or atrophy (late); optociliary shunt vessels in meningioma; choroidal folds and hyperopic shift.
• Proptosis, restricted motility, ptosis, periorbital swelling, pain (inflammation, infection).
• Chiasmal compression: bitemporal field loss, headache, endocrine features.
• Compressive neuropathy in thyroid disease may occur with minimal proptosis, with limited motility and lid retraction.

• Visual acuity, colour vision (Ishihara), pupils, fields (Humphrey 24-2 and 30-2 or Goldmann), fundus, optical coherence tomography (retinal nerve fibre layer, ganglion cell complex), visual evoked potentials.
• MRI orbits and brain with contrast and fat suppression: tumour, muscle enlargement, optic nerve sheath thickening, intracranial compression; CT orbits for bone, canal, fracture and calcification; CT angiography or MR angiography for aneurysm.
• Blood tests: thyroid function and antibodies, ESR, CRP, ANCA, ACE, IgG4, pituitary hormones.
• Biopsy for tissue diagnosis when the mass is accessible and cause unknown.
• Exclude optic neuritis, glaucoma, ischaemic optic neuropathy, and toxic and nutritional neuropathy.

• Dysthyroid optic neuropathy: intravenous methylprednisolone 500 mg to 1 g daily for 3 days (or alternate days), followed by oral prednisolone 60 to 80 mg tapered; orbital decompression urgently if no improvement within 1 to 2 weeks or if vision is rapidly worsening; radiotherapy or teprotumumab as adjuncts.
• Tumour: surgery when the lesion is accessible without damaging the nerve (cavernous haemangioma, schwannoma), radiotherapy for optic nerve sheath meningioma (stereotactic fractionated 50.4 to 54 Gy), chemotherapy for glioma and lymphoma, hormone therapy and surgery for pituitary tumours (cabergoline 0.25 mg twice weekly for prolactinoma, increasing to 1 mg weekly).
• Inflammatory: oral prednisolone 1 to 1.5 mg/kg daily, with steroid sparing agents.
• Aneurysm: endovascular coiling or neurosurgical clipping.
• Infection and haematoma: drainage and antibiotics.
• Fibrous dysplasia: observation when asymptomatic; optic canal decompression only for documented progressive visual loss (prophylactic decompression is not indicated).
• Trauma: observation, steroid use controversial, decompression only in selected progressive cases.
• Visual recovery is better with earlier treatment; follow with acuity, fields and optical coherence tomography every 1 to 3 months.