02
Module

The Bedside Examination

In skilled hands the eye exam outperforms early MRI for identifying posterior-circulation stroke. Here is how to do it.

Section 01

Approach to the dizzy patient

Dizziness accounts for ~3% of emergency-department visits. The most important branch-point is whether the presentation fits an acute vestibular syndrome (AVS) — rapid-onset vertigo lasting days, nausea/vomiting, gait unsteadiness, head-motion intolerance, spontaneous nystagmus. In AVS, the question becomes: is this peripheral (e.g., vestibular neuritis) or central (e.g., posterior fossa stroke)? The framework reframes the dizzy patient by Timing, Triggers and Targeted Exam — sorting presentations into four broad vestibular syndromes that drive very different workups.

Acute vestibular syndrome (AVS)
Duration: days–weeks
Trigger: spontaneous (continuous)
  • ·Vestibular neuritis
  • ·Labyrinthitis
  • ·Posterior fossa stroke
  • ·MS plaque
  • ·First migraine attack
Episodic vestibular syndrome — spontaneous
Duration: minutes–hours, recurrent
Trigger: no clear trigger
  • ·Vestibular migraine
  • ·Ménière's
  • ·TIA (vertebrobasilar)
  • ·Panic disorder
Episodic vestibular syndrome — triggered
Duration: seconds, with triggers
Trigger: head position changes
  • ·BPPV
  • ·Orthostatic hypotension
  • ·Central positional vertigo
  • ·SSCD (sound/pressure)
Chronic vestibular syndrome ()
Duration: weeks–months, persistent
Trigger: exacerbated by movement, upright posture, complex visual scenes
  • ·PPPD
  • ·Bilateral vestibulopathy
  • ·Cerebellar degeneration
  • ·Mal de débarquement syndrome
  • ·Post-concussive dizziness

is the bin most often missed in the emergency department because the patient is rarely in extremis: dizziness is constant but low-grade, and the bedside exam is often normal. These patients usually present to outpatient clinics, not the ED, and the diagnosis rests more on history pattern and vestibular function testing than on a single examination finding.

Section 02

Gross eye exam — what to look for first

  1. 1.
    Spontaneous nystagmus in primary gaze
    With fixation, then again after fixation is removed (Frenzel lenses, video-Frenzel, or look at the eyes with a +20 D lens / ophthalmoscope while the other eye fixates a target).
  2. 2.
    Range of EOM motion
    Test the 9 cardinal gaze positions. Look for an adduction deficit (INO), upgaze palsy (dorsal midbrain), or any restricted movement.
  3. 3.
    Ocular alignment
    Cover-uncover and alternate cover tests to detect tropias/phorias. Vertical misalignment (skew) is a central sign in AVS.
  4. 4.
    Pupils
    Anisocoria, light response, RAPD (Horner's accompanies Wallenberg lateral medullary syndrome).
  5. 5.
    Gaze-evoked nystagmus
    Hold gaze 15–20° eccentric for ≥10 seconds in 4 cardinal positions. A few unsustained beats at extremes = physiologic end-point; sustained = pathologic.
  6. 6.
    Saccades
    Quick gaze shifts between two targets. Look for slowing (INO, brainstem), inaccuracy (cerebellum: hypermetria), latency, or initiation difficulty.
  7. 7.
    Smooth pursuit
    Track a slowly moving finger. Saccadic ('cogwheel') pursuit = cerebellar/age/sedation.
Section 03

The head impulse test (Halmagyi-Curthoys)

With the patient fixating your nose, deliver a small (~15°), fast, and unpredictable head turn. Watch the eyes. A normal keeps the eyes locked on your nose (eyes counter-rotate equally to the head). An abnormal VOR produces a visible corrective ("catch-up") saccade back to the target after the head movement — the cardinal sign of peripheral vestibular hypofunction toward that side.

Examiner's nose (fixation target)
Phase: still · VOR gain: 1.00
Toggle sides to see the difference. The corrective saccade is the diagnostic finding — it tells you the VOR is impaired on the side the head was turned to.
What does it mean?
In a patient with acute vestibular syndrome, an abnormal head impulse test toward one side is REASSURING for peripheral disease (e.g., vestibular neuritis). A normal head impulse test in a patient with severe spontaneous vertigo and nystagmus is a DANGER sign — central causes (stroke) typically spare the VOR[1,2].
Section 04

Examining for nystagmus

To characterize nystagmus, observe in five conditions: primary gaze with fixation, primary gaze without fixation(Frenzel / video-Frenzel goggles), eccentric gaze in 4 directions, after head-shaking (15 cycles 2 Hz then watch), and in positions of provocation (Dix-Hallpike, roll test). Each tells you something different about where the lesion is.

Peripheral pattern
  • ·DIRECTION-FIXED (same fast-phase in all gaze)
  • ·Mixed horizontal-torsional
  • ·Suppressed by fixation
  • ·Intensity ↑ with gaze toward fast phase (Alexander)
  • ·Abnormal HIT on affected side
  • ·NO vertical or pure torsional nystagmus
Central pattern
  • ·DIRECTION-CHANGING (reverses with gaze)
  • ·Pure vertical or pure torsional
  • ·Not suppressed by fixation
  • ·Often accompanied by other signs (skew, dysmetria)
  • ·Normal HIT (usually)
  • ·Persistent positional without latency/fatigue
Congenital pattern
  • ·Lifelong history
  • ·Horizontal plane in ALL gaze (including vertical)
  • ·Increasing-velocity slow phase
  • ·Has a null zone (head turn adopted)
  • ·Dampens with convergence
Section 05

Test of skew — alternate cover test

Vertical ocular misalignment () is a hallmark of brainstem dysfunction, especially involving the otolith-ocular pathway from the utricle through the vestibular nuclei to the . Test by holding the patient's gaze on a target while alternately covering each eye every 1–2 seconds. A vertical refixation movement of the uncovered eye = skew.

TargetL eyeR eyeL eye covered → R eye visible refixates
In skew, when the cover moves from right to left eye, the previously covered eye refixates vertically. The pattern is conjugate (both eyes show similar offset) — distinct from a fourth-nerve palsy.
Skew vs CN IV palsy
Skew is comitant (similar magnitude in all positions) and lacks the torsional component and head tilt of fourth-nerve palsy. The hypertropic eye in skew often shows an excyclotorsion of the LOWER eye relative to the higher eye — opposite to trochlear palsy.
Section 06

Putting it together — HINTS+

= Head Impulse + Nystagmus + Test of Skew. In a patient with the, the combination distinguishes peripheral from central with sensitivity approaching 100% for stroke when performed by a trained clinician — exceeding early MRI-DWI[1]. "" adds a finger-rub hearing test (unilateral hearing loss in AVS suggests AICA stroke, since the cochlea is supplied by the internal auditory artery, a branch of AICA)[2,3].

TestPeripheral (benign)Central (dangerous)
Head Impulse TestABNORMAL — corrective saccade present (toward affected side)Normal — no corrective saccade
NystagmusDirection-fixed horizontal (with torsional component), suppressed by fixationDirection-changing, or pure vertical/torsional, not suppressed
Test of SkewAbsentPresent (vertical refixation on alternate cover test)
Hearing (the +)Symmetric (preserved)May have UNILATERAL hearing loss (AICA stroke)
A peripheral pattern requires ALL THREE to be benign. A central pattern is identified by ANY ONE dangerous feature.
Important caveats
  • HINTS is for AVS only — patients with acute, continuous vertigo + nystagmus + nausea. Do NOT use for episodic or triggered vertigo.
  • HINTS requires the examiner to be comfortable with all three components; sensitivity drops sharply in untrained hands.
  • An isolated cerebellar infarct without nystagmus or HIT abnormality may be missed — gait and truncal stability must also be tested[21,22].
  • HINTS does not replace neuroimaging when central signs are present.
Section 07

Dix-Hallpike maneuver

The diagnostic test for posterior (and anterior) canal BPPV. Move through the five steps; on the right is what you should see in the patient's eyes at each step.

head turned 45° to RIGHTPatient seated
Patient's eyes (close-up)

Patient seated. Patient sits with legs extended on table. Head turned 45° toward the side being tested (here: RIGHT).

Click the steps to walk through the maneuver and see what the eyes do.
Treatment: Epley maneuver
Once posterior canal BPPV is confirmed, Epley canalith repositioning is 80% effective on first attempt[4]. Sequence: Dix-Hallpike position (affected side) → rotate head 90° to opposite side (still supine) → roll body so head is face-down → sit up with head turned 45°. Hold each position 30–60 seconds[5].
Section 08

Supine roll test (Pagnini-McClure)

The horizontal canal is in the gravity plane when the patient is supine with head flexed ~30°. Rolling the head 90° to each side stimulates the affected horizontal canal. The nystagmus is purely horizontal[5,4].

Affected ear DOWN (geotropic)
Geotropic (canalithiasis): both directions provoke nystagmus beating toward the ground. The MORE intense side identifies the affected ear.
Affected ear DOWN (apogeotropic)
Apogeotropic (cupulolithiasis): both directions provoke nystagmus beating away from the ground. The LESS intense side identifies the affected ear.
Side identification
Geotropic: Affected side = side with STRONGER nystagmus on roll. Ewald's first law (ampullopetal flow excites the horizontal canal more strongly than ampullofugal).
Apogeotropic: Affected side = side with WEAKER nystagmus.
The "Bow & Lean" test (head pitched forward, then back, while seated) provides confirmatory lateralization in horizontal-canal BPPV.