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64yr male with the main complain of instability for three years; when he stands up something push him backwards and he has a feeling like walking on sponge.
About a year ago he has started to miss lines while reading and has a problem with sight when bending or looking upwards.
He has diabetes and peripheral neuropathy and depression.
On exam pronounced gaze palsy in vertical plane, saccadic pursuit in horizontal plane and slightly reduced VOR gain to the left.
This is an interesting case of a 48yr woman with a 2year complaint of missing lines when reading and blurring when focusing on something or someone. She has frequent fluttering of the right eye lasting less than a minute and feeling like right eye is crossing over left one.
The only thing I found in this patient was an objective flutter of the right eye, unpredictable, sometimes stronger sometimes less pronounced, more often when looking downward. Please look at this video with series of very discrete ocular flutter with mainly torsional movement.
The reason of this uniocular rotatory nystagmus usually is neurovascular conflict between the Trochlear nerve and superior cerebellar artery. But there are more etiologies described, so the MRI is obligatory to perform in this patients.
Here’s a very peculiar case of a 63yr male with acute vertical diplopia, more pronounced when looking down which makes him feel dizzy and unstable all the time especially when looking downwards. He came to my office 7 days after the beginning of his symptoms.
The only thing I’ve noticed was skew deviation discovered at cross cover test with the hyperphoria of the right eye and hypophoria of the left eye.
I’ve asked for MRI which disclosed a punktiform lesion at mesencephalon.
Man 49yr with tinnitus and hearing loss at right ear lasting for 5-6years. Two times per year he has episodes of positional vertigo usually lasting about 7 days (last time a month ago). He doesn’t have vertigo on sounds.
tympanograms type A
But cVEMP shows good vestibulo-cervical reflex at both sides.
Because of present cVEMP, the hearing loss is pseudoconductive. Also, the bone conductive tone thresholds are elevated. We’re looking for dehiscence at temporal bone CT. And here we can see high jugular bulb at right side and dehiscent posterior canal to jugular bulb. Please, click on a picture for better view.
Dehiscence is usually on superior semicircular canal. But dehiscence of the posterior canal is described in the literature as well and usually is a consequence of high jugular bulb like in this patient.
Audiological parameters which suggest the dehiscence are conductive hearing loss with good tympanograms, elevated bone conduction threshold and finaly present cVEMP which confirms that hearing loss isn’t conductive but pseudoconductive. In patient with conductive hearing loss, cVEMPs are absent.
The only unusual thing is that amplitude of the vestibulo-cervical reflex is not larger than on the opposite side (almost the same). In patients with third window lesions we expect larger amplitude and decreased VEMP threshold on the affected side.
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)
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.
MRI showed left medullary infarction and also diffuse hemosiderin deposit at left cerebellar hemisphere
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.
Woman 66yr with symptoms of acute vestibular syndrome comes three weeks later to our office with complaints of slight instability, oscillopsia and vertigo with abrupt head movements.
No spont Ny, head-impulse neg. positional tests neg.
VHIT, calotic test and cVEMP didn’t show any pathological finding
BUT oVEMP showed left utricular deficit. SVV also confirmed it: -2.7
VNG and MRI excluded any central pathology.
In this patient acute vestibular syndrome can be ascribed to isolated acute utricular lesion. Lesion of the left utriculus is proven by pathological oVEMP and SVV while other tests showed good function of the semicircular canals and sacculus. Central pathology was excluded by VNG and MRI showing normal findings. We regret we didn’t have an opportunity to record ocular fundus for cyclotorsion.
Patients with acute vestibular syndrome but with good results on VHIT and caloric test should be tested by VEMPs for otolithic function also. Isolated acute utricular lesion might not be so rare cause of acute vestibular syndrome, as it is probably often unrecognized.
Except looking for oculomotor signs in patient with acute vestibular syndrome the attention should be payed to head position as lateropulsion might be a sign of utricular lesion.
Something on this topic:
1. Magliulo G, Iannella G, Gagliardi S, Re M. A 1-year follow-up study with C-VEMPs, O-VEMPs and video head impulse testing in vestibular neuritis. Eur Arch Otorhinolaryngol. 2015;272(11):3277-81.
2. Blödow A, Helbig R, Bloching M, Walther LE. Isolated functional loss of the lateral semicircular canal in vestibular neuritis. HNO. 2013;61(1):46-51.
3. Manzari L, Burgess AM, Curthoys IS. Does unilateral utricular dysfunction cause horizontal spontaneous nystagmus? Eur Arch Otorhinolaryngol. 2012;269(11):2441-5.
4. Manzari L, Burgess AM, MacDougall HG, Curthoys IS. Superior canal dehiscence reveals concomitant unilateral utricular loss (UUL). Acta Otolaryngol. 2015;135(6):557-64.
5. Manzari L, MacDougall HG, Burgess AM, Curthoys IS. Selective otolith dysfunctions objectively verified. J Vestib Res. 2014;24(5-6):365-73.
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In head impulse test, patient is looking at earth fixed target while passive and unpredictable movement quickly turns his head. In subjects with preserved VOR function the vision stays at target regarding eye movement at same velocity but opposite direction. While in patients with deficient VOR function eyes don’t move, or eyes velocity lag head velocity and after finishing quick head turn, eyes make corrective saccadic movement in order to regain the target. So, video head impulse test measures eye and head velocity and calculates the gain and also detects the corrective saccades if present.
On contrary, during suppression head impulse test, patient is looking at head fixed target. During unpredictable and passive quick head turn in subjects with unaffected VOR, eyes moves at same velocity but different direction. In order to regain target which moved with head, eyes have to make anticompensatory saccadic movement in head direction. While in patients with absent VOR eyes moves with head and because there’s nothing to distract them from looking at head fixed target, after the head turn there’s no need for any corrective saccade. If anything of VOR is preserved it will drive eyes to move in opposite direction of head and make at least small anticompensatory saccade. This idea makes this test indicator of any VOR residual function. Also during suppression head impulse test the camera records eye and head movement and equipment calculate the gain, anticompensatory saccades emerge after the head movement making it easier to calculate the gain without saccades during head movement as can be the case in video head impulse test where covert saccades emerge during head movement.
|HIMP unaffected side||HIMP affected side|
|SHIMP unaffected side||SHIMP affected side|
To recap.: in suppression head impulse test, normal subjects are the one who have saccades after head turn. And this anticompensatory saccades are the one who mark functioning VOR. While reduction of anticompensatory saccades and their absence are the sign of deficient or absent VOR.
27yr old male with AVS (Acute Vestibular Syndrome) and aural fullness in the right ear which started three days ago.
Nothing would be so peculiar that he had Ny to the left. But he had Ny to the right !?! Nystagmus was present just without fixation.
It is possible to see nystagmus to the affected side but usually on the first day. But in this case it’s already third day and caloric test and VHIT demonstrate obvious vestibular asymmetry (right side deficient).
Also, what’s interesting he has BPPV on the right side also. Dix-Hallpike to the right resolved much stronger horizontal ny but without vertigo, but after latency of about 10sec vertigo has started and torsional ccw component added to spont ny. Epley.