Makindo Medical Notes

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🧠 Introduction

Foster Kennedy Syndrome is a rare neurological disorder defined by a striking combination of findings — optic atrophy in one eye and papilloedema in the other. It reflects both local compressive damage and raised intracranial pressure (ICP), classically from a frontal lobe or olfactory groove tumour such as a meningioma.

📚 Key Pathophysiology

• 👁️ Ipsilateral optic atrophy: Direct compression of the optic nerve by the mass leads to loss of axons and pallor of the optic disc on the same side as the lesion.
• 👁️ Contralateral papilloedema: Raised intracranial pressure causes venous congestion and swelling of the optic disc in the opposite eye, where the optic nerve is not compressed.
• 🧩 The combination is diagnostic — one disc pale (atrophic) and one swollen (oedematous).

🎯 Common Causes

• Olfactory groove meningioma — the classic cause; the tumour compresses the ipsilateral optic nerve and elevates intracranial pressure.
• Medial sphenoid wing meningioma — second most common location.
• Less commonly: frontal lobe glioma, craniopharyngioma, aneurysm, or metastatic lesion.

👀 Clinical Features

• Progressive unilateral visual loss (from optic atrophy).
• Contralateral visual blurring or headaches from raised ICP.
• Anosmia (loss of smell) if olfactory nerve compressed.
• Headache, nausea, and vomiting due to increased ICP.
• On fundoscopy:
  • Atrophic disc (pale, flat) on the side of the tumour.
  • Papilloedema (swollen disc margins, hyperaemia, blurred edges) on the opposite side.

🔎 Investigations

• Ophthalmic Assessment:
  • Fundoscopy — confirm optic atrophy vs papilloedema pattern.
  • Visual acuity and visual field testing (commonly central scotoma or field constriction).
• Imaging:
  • MRI brain with contrast — gold standard for defining mass lesion and relation to optic nerves.
  • CT scan — useful for identifying calcification or hyperostosis (typical in meningioma).
• ICP Assessment:
  • Indirectly via clinical and imaging markers (ventricular dilation, peritumoural oedema).
  • Formal ICP monitoring only if diagnosis unclear or perioperative guidance required.
• Neurological Examination: Evaluate cranial nerves I–VI, motor and sensory function, and higher cortical signs to localise lesion.

🧩 Differential Diagnosis

• Pseudo–Foster Kennedy Syndrome: Sequential optic neuritis or bilateral papilloedema with optic atrophy in one eye following chronic raised ICP (without a mass).
• Anterior ischaemic optic neuropathy or optic nerve glioma may mimic the appearance.

🩺 Management

• 🎯 Definitive Treatment – Neurosurgical:
  • Surgical resection of the meningioma (often via transcranial or endoscopic approach) to relieve compression and restore CSF dynamics.
  • Goal: decompress optic apparatus and reduce ICP.
  • Postoperative radiotherapy may be considered for residual tumour.
• 🧴 ICP Control (Pre- and Peri-operative):
  • Mannitol and dexamethasone to reduce oedema.
  • Optimise positioning (head elevated 30°), maintain normocapnia and euvolaemia.
• 📅 Follow-up and Monitoring:
  • Regular neuro-ophthalmologic review to monitor visual fields and disc changes.
  • Postoperative MRI scans to detect recurrence or residual tumour.
  • Long-term rehabilitation for persistent visual loss or olfactory deficits.

💡 Teaching Points

• Foster Kennedy Syndrome = optic atrophy + papilloedema = think frontal meningioma.
• Always exclude a mass lesion before assuming benign raised ICP (idiopathic intracranial hypertension).
• “Pseudo–Foster Kennedy” describes a similar optic appearance but without a space-occupying lesion.
• Early recognition allows curative surgery before irreversible optic damage occurs.

🧩 Summary: Foster Kennedy Syndrome is a distinct neuro-ophthalmological sign complex signalling a frontal intracranial mass. Multidisciplinary management involving neurology, neurosurgery, and ophthalmology is vital for preserving vision and preventing recurrence.