EM SAQs · Vertigo and dizziness
The acute vestibular syndrome — central or peripheral
An ACEM-style SAQ on the central HINTS pattern in the acute vestibular syndrome, the limitations of early CT and MRI, and the anticoagulated posterior-circulation stroke patient.
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Prompt
A 64-year-old man presents to the emergency department with four hours of continuous, severe rotational vertigo, nausea and vomiting. He cannot stand without stumbling to the right. He has type 2 diabetes, hypertension and paroxysmal atrial fibrillation, and takes apixaban. On examination he is alert. His head impulse test is normal. He has horizontal nystagmus that beats to the right on right gaze and to the left on left gaze. The alternate-cover test reveals a small vertical correction. A non-contrast CT of the brain is reported as normal. (a) What is the most likely diagnosis and what bedside findings support it? (4 marks). (b) Justify your imaging and disposition strategy despite the normal CT. (4 marks). (c) Outline the management implications of his apixaban. (3 marks).
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(a) Most likely diagnosis and supporting bedside findings (4 marks).
- The most likely diagnosis is an acute posterior-circulation ischaemic stroke (right cerebellar or brainstem, e.g. PICA or AICA territory) presenting as the acute vestibular syndrome — a "dizzy stroke".
- The bedside findings are a CENTRAL HINTS pattern, and the rule is that ANY one central sign is central:
- Normal head impulse test — the peripheral horizontal canal VOR is intact, localising centrally rather than to a peripheral vestibulopathy.
- Direction-changing (gaze-evoked) horizontal nystagmus — beats right on right gaze and left on left gaze, a central sign; peripheral nystagmus is direction-fixed, beating away from the affected ear.
- Positive skew deviation — the vertical correction on alternate-cover test indicates a brainstem otolith pathway lesion.
- The true gait ataxia (cannot stand, stumbles to the right) is an additional central red flag; peripheral vestibulopathy causes unsteadiness but the patient can usually walk.
- The paroxysmal atrial fibrillation marks him as high cardioembolic risk for a vertebral/basilar/posterior-cerebral occlusion. [1]
(b) Imaging and disposition despite the normal CT (4 marks).
- A normal non-contrast CT does not exclude posterior-circulation stroke. The petrous temporal bones produce beam-hardening artefact that obscures the posterior fossa, and early ischaemia is often invisible on CT for the first 24 to 48 hours.
- The HINTS examination is more sensitive than early imaging for stroke in AVS: Kattah 2009 found HINTS 100 per cent sensitive and 96 per cent specific for stroke, while even MRI DWI is falsely negative in roughly 12 per cent of strokes within the first 48 hours. A central HINTS pattern is therefore managed as stroke regardless of a normal CT or an early normal MRI.
- Disposition: admit to the stroke pathway / stroke unit with stroke-team review; arrange MRI with diffusion-weighted imaging (and consider CT or MR angiography of the posterior circulation) to localise the lesion and look for a vertebral or basilar large-vessel occlusion amenable to thrombectomy.
- Do NOT discharge the patient on the basis of a normal CT, and do NOT default to a vestibular neuritis diagnosis. The diagnosis of vestibular neuritis requires a PERIPHERAL HINTS pattern (abnormal head impulse, direction-fixed nystagmus, no skew). [1]
(c) Management implications of the apixaban (3 marks).
- The patient is on a direct oral anticoagulant (factor Xa inhibitor) for paroxysmal atrial fibrillation. In the setting of an acute posterior-circulation stroke this has three implications:
- He is excluded from intravenous alteplase unless the anticoagulant effect can be reliably excluded or reversed (last dose more than 48 hours, or reversal with andexanet alfa) — giving thrombolysis to an anticoagulated patient risks fatal intracranial haemorrhage.
- The mechanical thrombectomy window is unaffected — a basilar or vertebral large-vessel occlusion is a retrieval emergency even in the anticoagulated patient, and the interventional team should be activated in parallel.
- Check the time of the last apixaban dose, renal function and, where available, anti-factor Xa levels; involve haematology/stroke early to decide on reversal (andexanet alfa) and the timing of any reperfusion.
- Continue stroke-unit care (blood pressure permissive up to 220/120 unless thrombolysed, swallow screen, secondary prevention), and review long-term anticoagulation with the stroke team after the acute event. [1]
References2ShowHide
- [1]Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke, 2009.PMID 19762709
- [2]Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman-Toker DE. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ, 2011.PMID 21576300