Timothy C. Hain, MD • Page last modified: March 15, 2020
This page is an attempt to organize positional nystagmus (PN) by it's ENG findings, rather than point out what kind of positional nystagmus occurs in various disorders.
Positional nystagmus of low velocity (about 2 deg/sec) is common. Some sort of positional nystagmus (i.e. any direction) was reported in 76-88% of middle aged subjects (Martens et al, 2015; Jeffrey et al, 2017). This is not all that informative as it lumps together everything into one basket, and we are rather dubious about the Marten's report in particular as it doesn't fit our own clinical experience. Well anyway, Jeffrey et al (2017) proposed that reasonable normal limits should be > 3 deg/sec for horizontal and >7 deg/sec for vertical. Norms for torsional nystagmus appear to be sparse, perhaps because as of 2018, most recording systems cannot quantify torsional nystagmus.
A logical conclusion of the fact that PN is common, is that a small amount of horizontal or vertical positional nystagmus is "normal". The exception is torsional nystagmus, where nobody seems to know.
This is an example of an unusually strong posterior canal type BPPV. Note that the "LV" trace develops a very powerful upbeating about 10 seconds into this recording. Other than being much bigger than usual, this is pretty typical of the BPPV pattern of UBN.
UPN indicates upbeating nystagmus elicited by lying supine, generally with the head tilted to one or the other side (the Dix-Hallpike). It is generally accompanied by geotropic torsion, and often is due to posterior canal BPPV. If upbeating nystagmus is present in all positions (and at least upright), then it is just called UBN, as it is not positional. See this page for another ENG positive for BPPV. Nystagmus that is purely upbeating (without torsion) is generally little discussed. It may be "normal" in the sense discussed above.
Martens et al (2015) reported weak UPN in about 55% of their 75 normal middle aged subjects. We haven't noticed this ourselves however. We think that the prevalence is about 1%. Usually one also combines a judgement process involving whether or not it is one ear only (e.g. more likely to be mild BPPV), and whether it is present in all positions (e.g. more likely to be central). UBN can be found in smokers as nicotine induces UBN.
DPN indicates downbeating nystagmus elicited by lying supine. If it is present in all positions -- then it is not a positional nystagmus but just DBN. Generally it doesn't matter if the head is tilted to the side -- it works in any position. This is generally unaccompanied by torsion. Sometimes it is due to anterior canal BPPV, sometimes from cerebellar disorders, but most often it is found in otherwise normal older people, who have no complaints at all.
Our guess (and thats all it is) is that about 50% of 70+ year olds, with a history of dizziness, have transient downbeating nystagmus on assuming supine. We base this on a huge experience in dizzy patients.
Martens et al (2015) reported DPN in 20% of their normal middle-aged subjects. We are a little dubious about this, particularly because of the odd findings they reported with UBN. Again, a judgement process is needed to decide whether it is pathologic or a normal variant. DBN that is only present to one side, would be less likely to be "normal" than nystagmus provoked by simply being supine (or forward). DBN that increases on lateral gaze would be more likely to be cerebellar.
Data from Martens et al (2015) shows that lateral positional nystagmus is usually weak in normal middle aged persons.
LPN refers to side-beating nystagmus elicited by lying supine, and not modulated to any great extent by turning the head to one side or the other. This nystagmus is of usually of uncertain origin, but reasonable possibilities include central positional nystagmus syndromes. Weak lateral positional nystagmus, according to Martens et al, is common in normal people (about 40%).
The term DCPN is always used to refer to a horizontal nystagmus that changes direction, while the person is supine, depending on whether the person's head is turned to the right or left. This nystagmus is generally due to lateral canal BPPV. It can also be central or be an insufficiently characterized cervical nystagmus. Horizontal direction changing nystagmus is much less common than unidirectional nystagmus (according to Martens et al, 2015).
There are two variants of DCPN -- geotrophic (the common one), and ageotrophic (the uncommon one).
For example, when people have PC BPPV, their nystagmus does reverse on sitting -- it becomes downbeating for about 10 seconds. This is very common.
In theory, people with anterior canal BPPV should have DBN on supine, and UBN on sitting. Practically, this is exceedingly rare. It never reversed in normal subjects (Martens, 2015).
In persons with lateral canal BPPV, the lateral canal is tilted in the head so debris can roll one way when they are down, and another way when they are sitting.
This refers to a twisting of the eyes elicited by having the person lie supine. It is nearly always geotropic -- twisting so that the fast phase is downward in space.
The origin of this common pattern is unclear. It is sometimes seen in persons with pontine injuries, sometimes in persons with bilateral BPPV, and most comonly in persons with Migraine associated vertigo. In the central forms, presumably it is associated with abnormal processing of otolithic signals.
There are several movies concerning cervical vertigo on the list of resources.
Cervical vertigo basically means dizziness that is a function of the position of the head on the trunk (i.e. neck). Cervical nystagmus is a nystagmus that always goes the same direction no matter how the head is oriented to gravity.
The "core" test for cervical vertigo is called the "vertebral artery test". It is nothing complex - -with the person sitting upright, just turn the head to the end of rotation on the trunk, hold it there long enough (about 20 seconds), and look for nystagmus (with the eye in the center, in complete darkness). The PT literature talks quite a bit about this test, as a screen for vertebral artery disease (it doesn't do this very well). However, the procedure itself may produce nystagmus -- usually it is weak and beats directed towards the direction of head rotation. Most people with this pattern have a herniated cervical disk. This is most commonly associated with a herniated disk around C5, and is diagnostic of diskogenic cervical vertigo.
Occasionally it is strong and beats in some other direction. Most people with this pattern are undiagnosed, but their symptoms are attributed to vertebral artery compression anyway.
You might wonder why people with the strong nystagmus are usually undiagnosed - -the reason is that radiologists are reluctant to turn the head far enough to one side -- perhaps because they are afraid of a stroke and being sued - -so there is a "catch 22" with this particular syndrome.
There are numerous variants of this simple procedure that are much harder to interpret. Perhaps they are valuable, but usually they simply seem to muddy the water.
Method #1 -- compare supine head-R and head-L with prone head-R and head-L. Cervical should stay the same, ear or brain should "flip".
Method #2 -- compare supine head-R and head-L with body R and body L. Cervical should go away with body
Method #3 -- have the person sit on a swivel chair, hold their head still, and have them rotate their body under the head. Any nystagmus here should be cervical.
Practically -- I have discarded most of these methods in favor of the simple and straightforward procedure that I first listed.
In the usual case of vestibular neuritis, there is a strong horizontal nystagmus beating away from the damaged ear. This appears in any position. It is thought that these patients generally have damage to the superior division of the vestibular nerve, causing both loss of lateral canal function and utricular function on that side. While the nystagmus continues supine, there is often more nystagmus with the "bad ear down" and less with the "good ear up", first reported by Fluur (1973). This is also called "homolateral excitation and contralateral inhibition". Not much is known about this other than it obviously reflects an interaction between the remaining utricle and lateral canal. There is presently no data concerning utricular sparing and the effect on this as well. At this writing, this sign has little diagnostic value. Presumably though, individuals with horizontal nystagmus from a different mechanism, such as central nystagmus, might show a different pattern.