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Timothy C. Hain, MD 
Page last modified:
May 17, 2008
Head-shaking nystagmus is the nystagmus that follows sinusoidal movement of the head. It was probably first described by Vogel (1932) in the old German literature. Moritz called it "kopfschutteinnystagmus" (1951).
There are three variants: Horizontal head-shaking -- rotation of the head in the horizontal plane, vertical head-shaking -- rotation in the vertical plane, and circular head-shaking -- rotation of the head so that the nose traces out a circle in the coronal plane. The usual duration is 20 cycles, aiming for a horizontal or vertical movement of about 30-45 degrees, and a frequency of roughly one cycle/sec.
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| Head-Shaking Nystagmus -- position trace. The head is shaken as is described in the text, after which a nystagmus ensues, typically for about 15 seconds, with a peak velocity of about 15 deg/sec. (Wei et al, 1989) |
Horizontal head-shaking is generally performed by the examiner who moves the patient's head back and forth at about a frequency of 2 hz, for 20 cycles. The usual excursion is +-30 degrees, as tolerated. Horizontal HSN is often encountered in persons with unilateral vestibular lesions (e.g. Hain et al, 1987). HSN is not very specific or sensitive to caloric weakness (Wei et al, 1989).
Vertical head-shaking is perfomed similarly in the vertical plane. Vertical HSN is less useful than horizontal. Its main utility is when a horizontal or torsional nystagmus follows vertical head-shaking, which either reflects a "latent" nystagmus, or a central cross-coupling (Hain et al, 1993).
of Head-shaking Nystagmus
Patterns of HSNHead-shaking nystagmus in the horizontal and vertical planes is abnormal. A well adjusted vestibular system doesn't produce head-shaking nystagmus, at least not for more than a second or so, because it reflects a unidirectional output for a sinusoidal input. This is abnormal and either means that the vestibular-ocular motor system is rectifying the input (clipping it in one direction), or that the system is being perturbed by the input. One would expect HSN to beat away from the "bad" side. One would also expect HSN to be followed by a secondary or "reversal" phase, caused by adaptation of the vestibular system. This is indeed often the case.
Unfortunately, HSN is not 100% reliable, being neither always appropriately directed nor present. The details of this are reviewed by Hain/Spindler (1993). Recent papers have suggested that HSN has insufficient sensitivity to be useful as a clinical test (Humphriss et al, 2003).
HSN, like the head-impulse test (HIT) , is a method of measuring asymmetries in vestibular gain. The asymmetry in vestibular gain was first observed by Ewald (Ewald 1892), and is referred to as Ewald’s second law. In its specific form it states that ampullopetal endolymph flow in the horizontal canal causes a greater response than ampullofugal endolymph flow (Ewald 1892; Baloh and Honrubia 2001). In its general form it states that excitation is a relatively better vestibular stimulus than is inhibition (Leigh and Zee 2006). Ewald’s second law is thought to be due to the inability of inhibitory stimuli to decrease vestibular nerve firing rates to less than zero (Baloh, Honrubia et al. 1977; Hain and Spindler 1993). This phenomenon may be caused by an ensemble of vestibular neurons, all having somewhat different tonic rates, gradually being driven into inhibitory cutoff.
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| Bilateral mathematical model of vestibular processing from Hain (Hain, Fetter et al. 1987). This early model does not include acceleration in the canal transfer function, but otherwise contains the general features described below. |
We can take these ideas and convert them into a more quantitative form. We will not do this formally, but just try to get the general concepts converted into a mathematical form. First, firing rate in the vestibular nerve is mainly proportional to head velocity, but there is also a component due to head acceleration. So one can (approximately) say that:
Firing rate = K0+Kv*head-velocity
(Vestibular physiologists would shudder at this oversimplification). Continuing, because firing rate has a lower limit of 0 spikes/second, there is a saturation of the overall response for the nerve. In the diagram above, this is the little box with the curved line (nonlinearity) inside of it.
Net firing rate = saturation*Firing rate
The vestibular system is hooked up in "push-pull" so that the firing rate for one side is subtracted from the other. In other words:
central firing rate = right-left.
This is the circle with the +- in the center. When both vestibular nerves are working, net firing rate (right-left) shows a saturation in both direction.
When just one vestibular nerve is working, there is a strong response for rotation in that excites the remaining nerve (i.e. contralateral to the lesion for the lateral canal), and a weaker response for rotation for rotation towards the lesion.
The cross-connected boxes that implement velocity storage. This stores the asymmetry and explains the decay when the eyes stop.
This (fairly) simple theory explains the HSN in quantative terms.
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HSN in four patients with acoustic neuroma. Horizontal head shaking elicits an initial slow-phase velocity beating away from the paretic side.
Vertical head-shaking elicits an initial slow-phase velocity towards the paretic side. |
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HSN in patient with acoustic neuroma. A (long) video of HSN in a patient with unilateral loss is here. |
Patients with unilateral vestibular loss do indeed exhibit head-shaking nystagmus. In the adjacent figure adapted from Hain et al, 1997, a strong HSN is illustrated in patient with unilateral vestibular loss caused by an acoustic neuroma. As mentioned above, HSN generally beats away from the "bad" side and has a reversal phase. One would also expect HSN to be followed by a secondary or "reversal" phase, caused by adaptation of the vestibular system.
HSN is somewhat erratic. As illustrated by the figure below on the left, in patients with complete unilateral loss, while the direction is consistent, the size and duration varies.
In general, HSN should result from any vestibular nonlinearity , whether it be peripheral or central, and could also result from interactions from neck afferents which are, of course, also stimulated by head-shaking.
In theory, for HSN to be generated, the nonlinearity must also be accompanied by some dynamics to average and retain the clipped input. In the past we have proposed that the velocity storage mechanism performs this function.
Central HSN
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Another possible source of head-shaking nystagmus is simply a response of the system to any perturbation. In the old German literature, this was called "latent nystagmus". From a systems analysis perspective, this also derives from nonlinearity, but it need not necessarily scale with the size of the input
Situations where it seems likely that HSN is simply a result of perturbation are generally central ones. In the figure above entitled "lateral medullary syndrome", an extremely powerful HSN is produced, which is inconsistent with the amount of nystagmus produced in complete peripheral vestibular lesions. This could in theory be either due to a more drastic central nonlinearity in this patient with a vestibular nucleus infarct, or from perturbation. In the figure above entitled "cerebellar degeneration" is an example of a strong head-shaking nystagmus is given where the reversal phase is larger than the primary phase.
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| Model of HSN caused by a perturbation (Hain and Spindler, 1993) | Simulation |
These two figures are suggestions for a central mechanism for HSN. Head-shaking opens a switch in the velocity storage mechanism, creating a transient central nystagmus.
Circular head-shaking, first described by Hain and Spindler (1993), is performed by moving the head so that the nose follows the outline of a circle, in front of the patient's head. If this is done for 10 cycles fairly briskly, on stopping a very brisk rotatory nystagmus can be seen with frenzel goggles or any other method of observing the eyes. Circular HSN is mainly a torsional eye movement, which is commonly found in normal subjects and reflects a post-rotatory nystagmus (Hain et al, 1993; Haslwanter and Minor, 1999).
Unlike the horizontal and vertical HSN discussed above, this so-called "circular HSN" occurs quite reproducably in normal individuals. It can be shown (with some effort) that circular-HSN is a consequence of geometry. In this type of movement, the head is in-effect rotating about the front-back axis of the head (without getting twisted off !). When the head-stops, what ensues is simply a post-rotatory nystagmus.Loss of circular HSN is probably abnormal and expected in persons with bilateral vestibular loss.
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| Method of Circular Head Shaking | Recording of Circular Head Shaking Nystagmus |
Head-shaking nystagmus is an indication of asymmetrical vestibular function. Kristindottir et al (2000) rcently reported that there is a higher frequency of HSN in hip fracture subjects than halthy subjects.
| © Copyright May 22, 2008 , Timothy C. Hain, M.D. All rights reserved. Last saved on May 22, 2008 |