Lindsay-Hemenway Syndrome (LH syndrome)

Timothy C. Hain, MD Marcello Cherchi, MD, Ph.D. of Chicago Dizziness and Hearing. Page last modified: May 25, 2021

This site has many other pages on BPPV. There is also a comprehensive page on Vestibular neuritis.

The Lindsay-Hemenway syndrome is another name for vestibular neuritis followed by BPPV. We are not very enthusiastic about this syndrome -- here are the reasons why:

Why do we need another named syndrome with such a long/difficult name. Most clinicians just know that BPPV can occur after vestibular neuritis, and are not particularly helped by having a long name for a simple phenomenon.

Another question one might also reasonably ask why the syndrome is not named "Hemenway-Lindsay" as the first author on the paper was not Lindsay after all. Perhaps this was due to the greater prominence in the field of Lindsay, who was at one point the chairman of Otolaryngology at the University of Chicago, than the first author, Hemenway.

A third question is why are we naming a syndrome after these guys (Lindsay-Hemenway) when their index case was so unusual, and their explanation attributing this clinical syndrome uniformly to vascular injury is unproven.

Why does BPPV often follow Vestibular Neuritis ?

Current thought is that vestibular neuritis is a disorder of the vestibular nerve, which supplies the semicircular canals and the otolith organs. When the vestibular nerve is damaged, there may be damage to the utricle (one of the otolith organs), causing degeneration and otoconia to be dislodged. This can cause, in a delayed fashion, BPPV. It is necessary to assume that there is selective damage to the lateral canal (accounting for the typical pattern of vestibular neuritis nystagmus), and sparing of the posterior canal, which is needed to produce the characteristic nystagmus of BPPV.

Vestibular Nerve
Vestibular Nerve
Vascular supply
Schematic of circulation of inner ear, from Schuknecht's Pathology of the Ear. (Merchant and Nadol, 2010. The posterior vestibular artery is just to the right of the vestibulocochlear artery.


There is some apparent disagreement about whether or not the LH syndrome is due to selective damage to the anterior vestibular artery sparing the posterior vestibular artery, or whether this syndrome is due to selective damage to the portions of the vestibular nerve that goes to the top part of the inner ear, sparing the lower part of the inner ear. For example, see the discussion about the paper of Harada (1993) below.

Regarding whether it is differential damage to the nerve or the artery does not seem to be be very definitive in the literature. Logically, one would think that the explanation that there is selective damage to the anterior vestibular artery improbable, as the anterior and posterior vestibular arteries are of similar size and presumably similar vulnerability, and if really true, there should be a 50-50 split. This is certainly not the case. Goebel et al (2001) offered the most reasonable explanation -- namely: "The bony canal of the superior vestibular nerve is longer than the singular nerve canal. Additionally, the superior vestibular nerve and arteriole travel through a relatively narrower passage than the singular nerve and its vascular supply. From an anatomic standpoint, this renders the superior division of the vestibular nerve more susceptible to entrapment and possible ischemic labyrinthine changes."

Either explanation is sufficient to explain the clinical findings. We think that it is somewhat more plausible that the vestibular nerve has selective damage, but either explanation could be true. Autopsy of sufficient cases would be needed to be sure. These days, it is not very easy to obtain pathological material from the inner ear.


A simple search on Lindsay-Hemenway Syndrome returns almost nothing in Pubmed, which indicates how obscure this eponym is. Much of the literature is "off the grid" -- which is to say, not indexed in Pubmed. This is a strong sign that this syndrome is obscure and perhaps ignored (we think justifiably so).

The syndrome got its name from a paper by Hemenway and Lindsay, in 1965. Hemenway, probably a resident at the University of Chicago, and Lindsay who reported on the pathology of a single case, autopsied 13 years after symptoms. They noted that there was a "localized mass" of blood vessels connected with the vestibular nerve at Scarpa's ganglion, with resulting degeneration of part of the ganglion and the superior division of the vestibular nerve". This is a wildly unusual situation -- it is exceedingly rare to have a vascular malformation in the internal auditory canal. After presenting this single strange case, the authors go on to present a series of other cases that have no pathology, and presumably no vascular anomaly either. In the ensuing discussion, the authors do NOT make the connection between damage to the utricle and onset of BPPV. They mention many possibilities, none of which involve detached otoconia. So the index paper on this syndrome seems to have got it wrong.



Hemenway and Lindsay (1965). See discussion above. A single highly unusual case is followed by a muddled discussion. We don't think that this paper needs a syndrome.

Harada et al (1993) on discussing a series of 9 clinical cases, some of which had a very long delay between vestibular neuritis and BPPV. They stated "The first possibility is that the function of the posterior canal was not impaired in spite of the damage of the lateral canal. The fact that each canal differs in involvement in vestibular neuronitis may be explained by the difference in the blood supply or the innervation between lateral and posterior canals. If only the artery or nerve which is related to the lateral canal is damaged and the artery or nerve to the posterior canal is not involved, then the function of the posterior canal is preserved. "

Refoya et al (1998) reported "STUDY SUBJECTS: Ninety-eight patients with benign paroxysmal positional vertigo. RESULTS: Sixteen patients diagnosed as anterior vestibular artery syndrome were revised (16.3%). CONCLUSIONS: Although the literature is scarce, the incidence of Lindsay-Hemenway syndrome seems to be underestimated." We strongly agree - -but we just think that people don't bother to report this connection rather than someone is making mistakes. We are also dubious that all of these patients had :"anterior vestibular artery syndrome", as there was no pathological material.

Casani and colleagues (2018) reported two cases. They stated ". We report on two cases of Lindsay-Hemenway syndrome despite complete vestibular failure demonstrated by vestibular instrumental assessment. After making some critical considerations on these findings, we underline the importance of not disregarding the diagnosis of paroxysmal positional vertigo in an established complete labyrinthine loss of function." This is a bit hard to follow in as much if there was complete labyrinthine loss of function, by definition, there could also be no BPPV nystagmus (at least from that ear).

A recent review of LH syndrome in Romanian Journal of Rhinology was published in 2020 (Anghel et al). This article can be downloaded from ResearchGate, which is fortunate as this journal is not in Pubmed.