Category Archives: vHIT

Wallenberg or lateral medullary syndrome

74yr woman with acute vestibular syndrome 10days old, but with still pronounced instability.
She has diabetes and hypertension.
On first day she was hypertensive 200mmHg and with described 3rd grade of Ny to the right. Because CT was ok she was dismissed.
On a second day again at emergency unit there was not described Ny nor any of neurological deficits.
She complains on instability, light headache at frontal part, weakness in left hand and left leg; hoarseness and difficult swallowing (feeling like she is going to choke, but she didn’t).

She can’t stand alone nor sit without support.
There’s no spontaneous Ny, but discrete gaze evoked to the left (when looking slight upwards) with slight torsional cw component.
Horner’s sign on the left side. (slight ptosis, with miosis and facial anhydrosis)
Left side of face was less sensitive and palatal reflex absent, but normal function of the vocal folds. Cerebellar sign showed bradikinesia at both sides and dysmetria at left side.
Head impulse test was slightly positive to the left (hardly visible, not obvious).

VHIT: showed slight reduction of the VOR to the left, but what was strange it varied (sometimes good, sometimes bad, but without compensatory saccades)

stroke-vhit-bad VHIT stroke PICA

VNG (tracking and saccades in horizontal plane): Saccades showed frequent hypometria and some increase in latency to the left, but smooth pursuit was normal at both sides, just slighly saccadic at high frequencies.
VNG hypometric saccades
MRI showed left medullary infarction and also diffuse hemosiderin deposit at left cerebellar hemisphere

Lateral medullary syndrome Lateral medullary infarction

Some comments on a case and advice:
CT scan has NO diagnostic value in evaluating patients with AVS.
Here’s the patient with AVS and risk factors for stroke.
Head impulse test wasn’t done at emergency unit.
Ny on a first day was mimicking Ny of peripheral origin, but it should be very suspicions not to have it on a second day!
Pronounced truncal ataxia is not characteristic for peripheral lesion.
Head impulse test can be positive in central lesions (stroke) as well, because ear get’s blood supply from AICA (sometimes PICA).
Gaze evoked Ny especially with torsional component should bring suspicion to central lesion.
Slight headache can be seen in patients with vestibular neuritis as well, but it’s more characteristic sign of central pathology, especially when it is pronounced.
Fully developed and pronounced neurological signs of Wallenberg syndrome like it is described in textbooks you would not see in the clinical practice.

Positive VHIT in pt with Cerebellar Ataxia

We interpret positive HIT to be due to peripheral vestibular deficit. But it can be seen in patients with cerebellar ataxia also.
False-Positive Head-Impulse Test in Cerebellar Ataxia
Abnormal Head Impulse Test in a Unilateral Cerebellar Lesion

It’s explained by deficit in floccular function.
Isolated floccular infarction: impaired vestibular responses to horizontal head impulse

Here’s a femail patient 59yr; her instability had started 2yr ago very progressively so she can’t walk, even sit unsupported; appendicular ataxia and dysarthria are also obvious signs of cerebellar dysfunction. MRI document marked cerebellar atrophy.

  • gaze evoked Ny
  • smooth pursuit: saccadic
  • very reduced OKN
  • bilaterally positive HIT
  • positive VVOR test

Very reduced VOR gain
Cerebellar_Atrophy_VHIT Cerebellar_Atrophy_VHIT_L
BUT caloric test is normal
Obviously, peripheral vestibular function is preserved. SPV is not elevated, meaning that nodular control of vestibular nuclei is preserved. Markedly reduced VOR gain could be explained by floccular dysfunction.

That means that in a regard of peripheral vestibular assessment in patients with cerebellar ataxia isn’t enough to perform just vhit, but also a caloric test.

Positive VVOR test was explained by three non-functioning compensatory mechanisams: smooth pursuit, OKR, VOR (first two as a sign of central vestibular dysfunction and third as peripheral vestibular dysfunction) and was considered as pathognomonic sign of CANVAS.