Cranial Nerve Examination — Written Clinical Reasoning

SAQ 1 — A Pupil-Involving Third Nerve Palsy (15 marks, 20 minutes)

Prompt: Describe your immediate assessment, the localising interpretation of the findings, the urgent investigations, and the initial management of this patient. Justify the role of the pupil and the urgency of each step. [1]

Model Answer

Recognition and localisation (3 marks): [1]

This patient has an acute, complete right third (oculomotor) nerve palsy with the pupil involved. The eye is down and out at rest because the unopposed lateral rectus (CN VI) abducts the eye and the unopposed superior oblique (CN IV) depresses it; the complete ptosis follows paralysis of the levator palpebrae supplied by CN III; and the fixed dilated pupil reflects loss of the parasympathetic constrictor fibres. The decisive finding is pupil involvement. The parasympathetic pupillary fibres travel on the surface of the third nerve, so a lesion that dilates the pupil is compressive until proven otherwise. The commonest and most dangerous cause is an expanding aneurysm at the junction of the posterior communicating artery and the internal carotid artery, which lies beside the third nerve. The sudden severe periorbital headache is consistent with a sentinel leak or expansion before rupture, and the risk is catastrophic subarachnoid haemorrhage. This is a neurosurgical emergency. [1]

Urgent investigations (5 marks): [1]

1. Urgent CT angiography of the intracranial circulation is the first and pivotal investigation. The priority is to identify a posterior communicating artery aneurysm (or other compressive lesion) before it ruptures. CT angiography has high sensitivity for aneurysms above 3 millimetres and is rapid and widely available. If it confirms an aneurysm, the patient is referred immediately to neurosurgery and neurointervention for securing by endovascular coiling or surgical clipping.
2. Non-contrast CT brain is performed at the same time to look for subarachnoid blood if the headache suggests a leak, and to exclude a mass or haemorrhage.
3. If the CT angiogram is negative but clinical suspicion remains (a painful pupil-involving palsy), proceed to digital subtraction angiography, the gold standard, which can detect smaller aneurysms missed by CTA.
4. Blood tests include a full blood count, coagulation profile, electrolytes, glucose and lipids, and a group-and-save, because the patient may proceed to intervention or theatre.
5. A lumbar puncture is considered only if subarachnoid haemorrhage is suspected and the CT is negative, looking for xanthochromia; it is not the first test when a compressive lesion is the priority. [1]

Initial management (5 marks): [1]

1. Neurosurgical and neurointervention referral immediately on confirmation or strong suspicion of an aneurysm. Do not wait for all results.
2. Blood pressure control is important but must be balanced: avoid hypertension that could precipitate rupture, but do not cause hypotension that could worsen any ischaemia. Treat the documented hypertension (168/96) with a titratable agent such as labetalol if needed, while awaiting definitive management.
3. Analgesia for the headache and antiemetics if needed, avoiding agents that depress consciousness and obscure the neurological examination.
4. Nimodipine 60 milligrams every four hours is started if subarachnoid haemorrhage is confirmed, to reduce vasospasm.
5. Eye protection is less of an issue here because the ptosis covers the eye, but if the lid is later lifted the cornea must be protected with lubricants. Monitor the conscious state and the pupils for any change. [1]

Why the rule of the pupil is a guide, not a law (2 marks): [1]

The classic teaching is that a pupil-sparing, complete palsy in a vasculopathic patient is microvascular (ischaemic) and managed conservatively, while a pupil-involving palsy is compressive and imaged urgently. This patient has a pupil-involving palsy and must be imaged. However, the rule has exceptions: a pupil-involving palsy can rarely be microvascular (especially in diabetes), and a pupil-sparing palsy can rarely be compressive, particularly if partial, painful or evolving. Modern neuro-ophthalmological practice therefore tends to image any new third nerve palsy that does not fit the textbook microvascular pattern, and to re-examine a pupil-sparing palsy over the first 24 to 48 hours for any pupillary change. The safe position at viva is: this pupil is involved, so I image now. [1]

SAQ 2 — UMN versus LMN Facial Palsy: Reasoning and Management (10 marks, 15 minutes)

Prompt: A 33-year-old otherwise well man wakes with painless drooping of the left side of his face. On examination the left forehead is smooth and cannot be wrinkled, the left eye cannot be closed (the globe rolls upward on the attempt), and the left mouth angle droops. There is reduced taste on the anterior left tongue. The ear canal, the parotid and the limbs are normal. Outline your classification, the differential diagnosis, the management, and the prognosis. [1]

Model Answer

Classification (2 marks): [1]

This is a lower motor neuron facial nerve (CN VII) palsy because the entire left hemiface is affected, including the forehead (which cannot be wrinkled) and the eye (which cannot be closed). The upper facial muscles receive bilateral cortical innervation, so an upper motor neuron lesion spares the forehead; here the forehead is paralysed, so the lesion is in the nerve itself, distal to the nucleus. The reduced taste on the anterior tongue places the lesion proximal to the origin of the chorda tympani. [1]

Differential diagnosis (2 marks): [1]

With no vesicles in the ear, no middle-ear disease, no parotid mass, and no preceding illness, this is most likely Bell palsy (idiopathic facial nerve palsy), the commonest cause of an acute unilateral LMN facial palsy. The alternatives to exclude by history and examination are: Ramsey Hunt syndrome (herpes zoster oticus, with vesicles in the ear canal or on the palate and a worse prognosis); otitis media or cholesteatoma; a parotid tumour or post-surgical injury; a skull base fracture; Lyme disease (especially with a tick exposure or erythema migrans); and, less commonly, sarcoidosis or HIV seroconversion. I have examined the ear and the parotid, which are normal, supporting Bell palsy. [1]

Management (4 marks): [1]

1. Oral corticosteroids started within 72 hours of onset are the evidence-based treatment. The Sullivan 2007 NEJM factorial trial demonstrated that prednisolone significantly improved the proportion of patients with complete recovery (83 per cent versus 64 per cent at 3 months), whereas aciclovir added no benefit [1]. A typical regimen is prednisolone 60 milligrams daily for five days, tapering over the following five days. The Cochrane review confirms that corticosteroids improve the likelihood of complete recovery [2].
2. Antivirals are not routinely added, as they confer no meaningful additional benefit over corticosteroids alone. They may be considered if Ramsey Hunt syndrome is suspected.
3. Eye protection is mandatory because the eye cannot close. Prescribe preservative-free lubricant drops during the day and ointment and taping of the lid at night, and refer to ophthalmology if there is any sign of exposure keratopathy.
4. Reassure and follow up. Most patients recover, but those with severe palsy at onset, Ramsey Hunt, diabetes, or pregnancy have a worse prognosis and warrant early referral to a facial-nerve service for consideration of electroneuronography and, rarely, decompression.

Prognosis (2 marks): [1]

About 70 per cent of patients recover completely without treatment, and corticosteroids within 72 hours improve this further. Residual sequelae include synkinesis (abnormal movements such as eye closure on smiling), contracture, and persistent facial weakness, which are more likely with severe palsy at onset, older age, diabetes, and pregnancy. I would warn the patient that recovery takes weeks to months, counsel them on eye care, and arrange review at one week and at three months, with urgent return if the eye becomes painful or red. [1]