Sign · 1
Nystagmus
Rhythmic eye-jerking is the first and most diagnostic sign of vertigo. Its plane, direction, and modulation by gaze and fixation tell you whether the lesion is in the labyrinth or the brain.
A gallery of patterns
Nystagmus is a slow drift of the eyes away from the target followed by a quick corrective jerk back. The direction of the quick (fast) phase names the nystagmus — “right-beating”, “downbeating”, and so on.
Peripheral inner-ear nystagmus jerks in one fixed direction, gets quieter when the patient stares at a target (visual fixation), and stronger on looking the way the fast phase beats. Central — brain — nystagmus often does the opposite: vertical, torsional, or changing direction with gaze, and not easily quietened by fixation.
Spontaneous nystagmus. Vestibular neuritis and acute labyrinthitis give unidirectional, horizontal-torsional jerk nystagmus with the fast phase away from the affected ear. It is augmented on gaze toward the fast phase (Alexander's law), suppressed by fixation, and fades over days to weeks as the CNS compensates.
Central spontaneous nystagmus can be vertical (downbeat or upbeat), purely torsional, or direction-changing with gaze; it tends to resist fixation suppression and is not constrained by Alexander's law.1 Downbeat nystagmus points to the flocculus/nodulus or craniocervical junction (Chiari, MS, paraneoplastic) and may improve with aminopyridines.5
Gaze-evoked nystagmus (GEN) appears or worsens on eccentric gaze and reflects a failing neural integrator — the cerebellar–brainstem circuit that holds the eyes off-centre. Bilateral symmetric GEN points to the cerebellum; direction-changing GEN in acute vertigo is a HINTS central flag.2,3
Distinguishing peripheral from central is a question of pattern recognition across multiple modulators: spontaneous direction, change with gaze, effect of fixation suppression, response to head-shaking, and the head impulse test. Direction-changing nystagmus on lateral gaze, vertical or purely torsional patterns, and failure of fixation suppression each independently raise the central probability.2 Video-oculography documents subtle drift velocities and waveform shapes lost at the bedside.
The classical floccular ablation studies provide the substrate: removal of the flocculus/paraflocculus impairs VOR gain calibration, fixation suppression, and smooth pursuit — producing the GEN, downbeat, and saccadic-pursuit pattern of cerebellar disease.6
Right-beating horizontal
Unidirectional horizontal-torsional jerk; fast phase away from the lesioned ear; suppressed by fixation; obeys Alexander's law.
Right-beating
Slow leftward drift, fast rightward jerk — the conventional peripheral pattern.
Central positional nystagmus — the BPPV mimic
Most positional vertigo is benign — BPPV — caused by tiny crystals (otoconia) loose in a semicircular canal. A small fraction is central, due to a cerebellar or brainstem lesion, and can mimic BPPV closely. The give-aways are timing and response: central positional nystagmus starts immediately, doesn't fade, and ignores Epley.
Central positional nystagmus is immediate (no latency), non-fatiguing, persistent for as long as the position is held, and often direction-changing or purely vertical. Pure downbeat on head-hanging strongly suggests a craniocervical-junction or cerebellar lesion; direction-changing horizontal nystagmus on roll testing without the BPPV crescendo–decrescendo pattern should not be treated as BPPV.4
A common clinical trap is the patient with concurrent BPPV and a posterior- fossa lesion. A negative Dix–Hallpike or persistent nystagmus after successful repositioning does not exclude a central process; cerebellar signs (dysmetria, ataxia, dysarthria) and the HINTS pattern matter more than the bare positional test. Recognise the pattern, image early.
Direction-changing positional nystagmus, sustained downbeat on head-hanging, or persistence beyond the BPPV time-course should prompt MRI of the posterior fossa.