vHIT Atlas

Two ways to ask the same question

The standard vHIT — what most clinicians mean by "vHIT" — uses an earth-fixed target. The patient stares at a dot on the wall while you thrust their head. A working VOR moves the eyes opposite to the head, keeping gaze on the wall target. This is the HIMP paradigm: head impulse paradigm.

In 2016 MacDougall and Curthoys introduced an alternative: SHIMP — suppression head impulse paradigm^{[MacDougall HG 2016]}. SHIMP uses a head-fixed laser target. The patient stares at a dot projected from the goggles onto the wall, which moves with their head. A working VOR — which moves the eyes opposite the head — would carry the eyes off the target. To stay on the head-fixed target, the patient has to actively cancel their own VOR with a compensating saccade. This saccade is the anti-compensatory saccade: it goes in the same direction as the head movement, catching up to the head-fixed laser.

What each paradigm shows in the four scenarios

The simulator below shows traces for the same patient in HIMP and SHIMP across four clinical situations. Toggle between them and notice how they complement each other.

Clinical scenario:

HIMP

earth-fixed target

SHIMP

head-fixed laser target

HIMP gain

0.95 (Normal)

Saccades: none

SHIMP gain

0.92 (Normal)

Saccades: anti-comp

What this scenario teaches

Normal subject

HIMP shows preserved gain with no corrective saccades (eye tracks head perfectly opposite). SHIMP shows the same intact VOR, so a large anti-compensatory saccade is needed to catch up to the head-fixed laser target. Anti-compensatory saccades in healthy SHIMP are the signature of a working VOR.

How the two paradigms differ

HIMP

Patient fixates an earth-fixed target. Intact VOR → eye moves opposite head, gaze stays on target. Deficient VOR → eye lags, then a compensatory saccade brings gaze back.

SHIMP

Patient fixates a head-fixed laser target. Intact VOR → eye still moves opposite head, so an anti-compensatory saccade is needed to catch the head-fixed target. Deficient VOR → eye stays with head, no anti-compensatory saccade needed.

Read across the simulator scenarios and a pattern emerges:

Normal subject: HIMP gain ≈ 1, no saccades. SHIMP gain ≈ 1 with a large anti-compensatory saccade.
Acute unilateral loss: HIMP shows low gain with overt compensatory saccades. SHIMP shows low gain with no anti-compensatory saccade — the patient cannot generate one because there's no VOR to suppress.
Compensated unilateral loss: HIMP shows reduced gain with covert saccades that may make the bedside picture look almost normal. SHIMP unmasks the residual deficit with small or absent anti-compensatory saccades.
Bilateral vestibulopathy: both paradigms show low gain. SHIMP shows no anti-compensatory saccades bilaterally.

Why SHIMP matters clinically

The principal contribution of SHIMP is that it dissociates central compensation from residual peripheral functionin a way HIMP cannot. A patient one year out from superior vestibular neuritis may show a HIMP picture that looks reassuring: gains in the 0.7 range, with covert saccades doing most of the compensatory work and very few visible overt saccades. On the bedside head impulse test, you can't see anything wrong. But the same patient's SHIMP will show absent or markedly diminished anti-compensatory saccades on the affected side — direct evidence that the underlying canal function is still impaired, regardless of how well the brain has learned to hide it^{[MacDougall HG 2016]}.

SHIMP peak velocity as a quantitative marker

In the original SHIMP description, MacDougall and colleagues quantified the test by measuring the peak velocity of the anti-compensatory saccade. In healthy subjects this peak velocity ranges from approximately 150 to 250°/s. A peak velocity below about 75°/s on the lateral canal is highly suggestive of significant residual canal deficit, even when HIMP gain has recovered into the "mild loss" or "normal" range^{[MacDougall HG 2016]}.

A practical clinical question — "has this patient's VOR actually recovered, or just their bedside picture?" — is therefore best answered with SHIMP rather than HIMP alone. In vestibular rehabilitation, where the question is whether to step down the intensity of gaze-stabilisation exercises, the SHIMP gain is arguably a better guide than the HIMP gain.

When SHIMP doesn't add information

For untreated acute vestibulopathy, SHIMP and HIMP carry the same information. The two paradigms genuinely diverge only when central compensation has had time to occur — typically weeks to months after the lesion. For acute presentations and the differentiation of stroke from neuritis (HINTS), HIMP alone is what you need. SHIMP becomes useful when the clinical question is about chronic residual deficit and rehabilitation planning.

Key teaching points

HIMP uses an earth-fixed target. SHIMP uses a head-fixed laser.
Healthy SHIMP shows a vigorous anti-compensatory saccade — that's the sign of an intact VOR.
SHIMP unmasks residual canal deficit hidden by covert-saccade compensation in chronic vestibulopathy.
For acute presentations, HIMP is enough. SHIMP adds value in chronic and rehab contexts.