Cranial Nerve Examination — Clinical Case

DCE Short Case — "Please examine this patient's cranial nerves"

Instruction

"Please examine this patient's cranial nerves. She has been complaining of a headache and double vision. You have 7 minutes for examination and 8 minutes for discussion." [1]

Patient brief (provided to examiner / simulated patient)

Patient: Mrs Eleanor Walsh, 58 years old, retired teacher, hypertensive. [1]

Findings the trainee elicits: The right eye is deviated down and out at rest with a complete ptosis. The right eye fails to adduct, elevate or depress; abduction is preserved. The right pupil is 6 millimetres and unresponsive to light; the left pupil is 3 millimetres and reactive. The swinging-flashlight test shows no relative afferent pupillary defect. The fundi, visual acuity, visual fields, facial nerve, hearing, palate, sternocleidomastoid, trapezius and tongue are all normal. Blood pressure 168/96. [1]

Systematic examination routine (model)

1. Set the stage: introduce, consent, position the patient sitting up at eye level, and state the plan to examine CN I to XII systematically.
2. Observe from the end of the bed: note the ptosis and the deviation of the right eye before touching the patient.
3. CN I: defer unless indicated.
4. CN II: acuity 6/6 both eyes; fields full by confrontation; pupils — note the anisocoria; swinging-flashlight test negative.
5. CN III, IV, VI: describe the ptosis, the down-and-out eye, the limitation of adduction, elevation and depression, and the fixed dilated pupil; abduction intact; no nystagmus; no diplopia complaint because the ptosis covers the eye.
6. CN V, VII, VIII, IX, X, XI, XII: all normal, stated and briefly tested.
7. Fundoscopy: normal discs. [1]

Presentation template (model)

"I examined Mrs Walsh, a 58-year-old woman with hypertension. On examination of the cranial nerves, the pupils are unequal: the right is 6 millimetres and unresponsive to light, the left is 3 millimetres and reactive, and there is no relative afferent pupillary defect. There is a complete ptosis on the right, and the right eye is deviated down and out. The right eye fails to adduct, elevate and depress, with abduction preserved. Visual acuity, fields and the fundi are normal, and the remaining cranial nerves are intact. [1]

In summary, this patient has a complete right third nerve palsy with the pupil involved. A pupil-involving complete palsy is compressive until proven otherwise; the classical cause is a posterior communicating artery aneurysm, and the headache raises the possibility of a sentinel leak. This is a neurosurgical emergency. My immediate step is urgent CT angiography of the intracranial circulation, neurosurgical referral, and blood pressure control." [1]

Discussion questions

Q: "Why is the pupil involved, and why does that matter?" [1]

"The parasympathetic fibres to the pupil travel on the surface of the third nerve, so they are the first to be affected by a compressive lesion pressing from outside. An expanding aneurysm at the posterior communicating artery to internal carotid junction, which lies beside the third nerve, picks off these surface fibres and dilates the pupil. A microvascular, ischaemic palsy infarcts the centre of the nerve and spares the surface fibres, so the pupil is spared. Pupil involvement matters because it marks the palsy as compressive and therefore potentially fatal if the aneurysm ruptures. So this patient is imaged and referred urgently, never observed." [1]

Q: "How would a pupil-sparing palsy change your management?" [1]

"A pupil-sparing, complete palsy in a patient with strong vascular risk factors is managed conservatively as a microvascular palsy — I confirm the risk factors, control the blood pressure and diabetes, and expect recovery over three months, because the nerve infarcts and then regenerates. But the rule is a guide, not a law: I would still re-examine the pupil over the first 24 to 48 hours for any change, and any pupillary involvement, any partial or evolving palsy, or any severe pain would prompt urgent imaging. The threshold to image is lower than the textbook suggests, because a compressive lesion can occasionally present with a pupil-sparing palsy early in its course." [1]

Q: "What is the role of the swinging-flashlight test here?" [1]

"It excludes an afferent (optic nerve) contribution to the pupillary abnormality. A relative afferent pupillary defect is the most sensitive sign of an optic neuropathy, demonstrated by a paradoxical dilation of both pupils when the light swings into the affected eye [4]. In this patient the test is negative, which tells me the pupillary abnormality is efferent — a third nerve lesion — rather than afferent. The fixed dilated pupil here is from loss of the parasympathetic constrictor, not from an optic nerve problem, and that localises the lesion precisely to the third nerve."

DCE Long Case — Lateral Medullary Stroke with Cranial-Nerve Findings

Patient brief (provided to trainee)

Patient: Mr Hiroshi Tanaka, 71 years old, retired engineer. [1]

Presenting complaint: Sudden onset of dizziness, slurred speech and difficulty swallowing, with numbness of the right face and the left limbs. [1]

History of presenting complaint: He woke this morning unable to walk straight, with the room spinning, nausea, and a hoarse voice. He coughed when he tried to drink water. He noticed his right face and his left arm and leg were numb. [1]

Past history: hypertension for 20 years, type 2 diabetes for 10 years, hyperlipidaemia, paroxysmal atrial fibrillation, a former smoker of 40 pack-years. [1]

Current medications: perindopril, amlodipine, metformin, atorvastatin, apixaban. [1]

Examination findings (trainee elicits):

• Alert, oriented, dysarthric with a hoarse (dysphonic) voice.
• CN V: reduced pinprick and temperature on the right face (V1 to V3); light touch preserved; corneal reflex intact.
• CN VIII: horizontal nystagmus beating left; unable to walk heel-to-toe; falls to the right on Romberg.
• CN IX, X: the palate elevates poorly; on saying ah the uvula deviates to the left (right vagal palsy); the gag reflex is diminished on the right.
• CN XI: slight weakness of the right sternocleidomastoid.
• Motor: mild right-sided limb ataxia, more than weakness; power 5 out of 5.
• Sensory: loss of pinprick and temperature on the left limbs and trunk (spinothalamic), with the right face affected as above.
• Horner: right partial ptosis and miosis with right facial anhidrosis.
• Blood pressure 176/98, pulse irregularly irregular. [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Tanaka is a 71-year-old man with hypertension, diabetes, hyperlipidaemia, paroxysmal atrial fibrillation and a significant smoking history, who presents with sudden dizziness, dysphagia, dysphonia and a crossed sensory loss — loss of pinprick on the right face and the left body. On examination he has a right Horner syndrome, a right vagal (ninth and tenth nerve) palsy with the uvula deviating left, right-sided cerebellar ataxia, nystagmus, and loss of pinprick and temperature on the right face and the left limbs. [1]

His main problems are:

1. An acute right lateral medullary (Wallenberg) syndrome from a posterior circulation stroke
2. Uncontrolled vascular risk factors and paroxysmal atrial fibrillation as the likely cause
3. Dysphagia with aspiration risk requiring speech-language and diet assessment [1]

This is a posterior circulation stroke. Because he is within the time window and has no contraindication, my immediate priority is stroke-pathway assessment for thrombolysis or thrombectomy, airway and swallow protection, blood pressure management, and secondary prevention." [1]

Management plan: [1]

1. Acute stroke pathway. Confirm the diagnosis with urgent CT then MRI brain with diffusion-weighted imaging, and CT angiography of the posterior circulation to look for vertebral or posterior inferior cerebellar artery occlusion. Assess for thrombolysis if within the time window and haemorrhage is excluded; thrombectomy is considered for a large-vessel posterior circulation occlusion.
2. Swallow and airway. Keep him nil by mouth until a formal swallow assessment; the right vagal palsy and dysphonia carry a high aspiration risk, so involve speech-language therapy early and consider nasogastric feeding.
3. Blood pressure and glucose. Manage permissively in the acute stroke window, then treat the hypertension and diabetes for secondary prevention.
4. Secondary prevention. Antiplatelet therapy (or anticoagulation if atrial fibrillation is judged the mechanism — he is already on apixaban, so review the indication and adherence), high-dose statin, smoking cessation, and stroke rehabilitation.
5. The Horner syndrome is part of the lateral medullary lesion and needs no separate treatment, but I document it as part of the localising picture. [1]

Examiner discussion questions

Q: "How do the cranial-nerve findings localise the stroke to the lateral medulla?" [1]

"The combination is characteristic. The right Horner syndrome (ptosis, miosis and anhidrosis) localises to the descending sympathetic tract in the lateral medulla. The right vagal palsy with the uvula deviating to the left, the diminished gag, and the dysphonia involve the nucleus ambiguus, which gives rise to the ninth and tenth nerves and lies in the lateral medulla. The loss of pinprick on the right face involves the spinal trigeminal tract, which descends into the lateral medulla, and the loss of pinprick on the left limbs involves the spinothalamic tract, which has already crossed. The right cerebellar ataxia involves the inferior cerebellar peduncle. Together these map precisely to the lateral medulla, supplied by the posterior inferior cerebellar artery, and the sudden onset in a vasculopathic patient with atrial fibrillation is an ischaemic stroke. The crossed sensory loss — ipsilateral face, contralateral body — is the signature of a brainstem lesion, because the facial sensory fibres cross in the brainstem while the body sensory fibres have already crossed in the cord." [1]

Q: "He is already on apixaban for atrial fibrillation. How does that affect your management?" [1]

"His presentation is an acute ischaemic stroke despite anticoagulation, which raises three questions. First, is the stroke cardioembolic from atrial fibrillation, or is it atherothrombotic from vertebral artery disease, given his smoking and vascular risk factors? The CT angiogram helps distinguish a vertebral origin stenosis or dissection from an embolic pattern. Second, is his anticoagulation adequate — is he adherent, and is the dose correct for his renal function? Third, he is on apixaban, so he is not a candidate for thrombolysis unless the anticoagulant effect can be shown to be absent, which is rarely reliable, so thrombolysis is usually withheld in a therapeutically anticoagulated patient. If a large-vessel posterior circulation occlusion is found, mechanical thrombectomy may still be considered. For secondary prevention, if atrial fibrillation is confirmed as the mechanism, I optimise the anticoagulant; if atherothrombotic disease is found, I add an antiplatelet once the haemorrhage risk is settled. The decision is individualised and made with the stroke team." [1]

Q: "Why is the uvula deviating to the left, and how does that differ from a tongue deviation?" [1]

"The uvula deviates away from the side of a vagal nerve lesion because the intact left side of the palate elevates and pulls the uvula toward it, away from the paralysed right side — the uvula deviates away from the lesion. The tongue, by contrast, deviates toward the side of a lower motor neuron hypoglossal lesion, because the intact genioglossus on the left pushes the tongue forward and across toward the weak right side. So the two direction rules are opposite: the uvula points away from the lesion, the tongue points toward it. In this patient the uvula deviates left because the lesion is on the right vagal nerve, and the tongue is midline because the hypoglossal pathway is spared." [1]