Journal of Ear, Nose and Throat Disorders

The Lyndsay-Hemenway Syndrome: Two Case Reports. Review and Comments

Case Report | Open Access

  • 1. Department of Otorhinolaryngology, University of Athens, Greece
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Corresponding Authors
Eleni Zoe Gkoritsa, Department of Otorhinolaryngology, University of Athens, Greece, ENT Surgeon, 21, Petrou Mpoua str. Tripoli Greece, Zip: 22100

The syndrome of Lindsay and Hemenway i.e. vestibular neuritis with Benign Paroxysmal Positional Vertigo (BPPV) as a clinical sequel is believed to be not frequent. However the careful observation of the patient in the course of several months reveals a higher incidence in reality.

Aim of the study is the presentation of two case reports of patients with different clinical occurrences of the same syndrome.

In the first case the initial vestibular neuritis occurs a few months before the occurrence of BPPV and BPPV is resistant to treatment with repositioning maneuvers. In the second case BPPV occurs as an immediate sequel of vestibular neuritis and responds to treatment.

The syndrome of Lindsay and Hemenway is an interesting clinical entity the existence of which the clinician should be aware of, in order to be able to combine repositioning maneuvers for the treatment of BPPV with vestibular rehabilitation targeting the treatment of a defective central compensation due to unilateral labyrinthine paresis.


Gkoritsa EZ (2016) The Lyndsay-Hemenway Syndrome: Two Case Reports. Review and Comments. J Ear Nose Throat Disord 1(1): 1014.


The syndrome of Lindsay-Hemenway is vestibular neuritis having Benign Paroxysmal Positional Vertigo as a sequel. It is attributed to a thrombosis of the anterior vestibular artery irrigating the anterior and lateral semicircular canals and the utricle. Consequently ischemia in this territory can lead to classical symptoms of vestibular neuritis together with the detachment of otoconia from the gelatinous layer of the utricular macula. This latter event is the pathophysiological basis of Benign Paroxysmal Positional Vertigo. Given the fact that the function of the posterior semicircular canal is not abolished, because the canal ampulla is spared, a further translocation of otoconia into the canal lumen is the generative cause of clinical occurrence of Benign Paroxysmal Positional Vertigo.

Two case reports will be presented in this study. They concern two elderly males, but the clinical course of the syndrome is different in each one of them.


A 75 year old male patient with a strong sensation of imbalance was examined in a vertigo clinic seven months ago. He reported a progressive (during one month and a half before consultation) deterioration of his gait and sensation of dizziness at the movements of the head. He did not report any rotatory vertigo. His clinical examination is shown on (Table 1). He received cinnarizine oral solution (75 mg) once in the evening and followed a vestibular rehabilitation program with Cowthorne- Cooksey [1,2] exercises. A month later he reported a satisfactory improvement of his symptoms. Four months later he came back, complaining of a relapse of his unsteadiness with concomitant rotatory vertigo on lying and rolling over in bed. His symptoms were worse in the morning as he stood up from bed. The clinical findings are reported on table 1. The patient had a medical history of diabetes type I treated with insulin.

Lindsay-Hemenway (L-H) syndrome was suspected and the modified Epley maneuver (Canalith Repositioning Procedure, CRP) [3] was performed on the right side as a cure. He was reexamined five days later, to find a persisting positive DixHallpike test [4] on the right. Epley maneuver was repeated, but it didn’t succeed for a second time. Five days later, the Semont liberatory maneuver [5] was performed, three consecutive times at the same session. Ten days later, he was assessed with a persistent positive right Dix-Hallpike test, but Unterberger (stepping) test was improved (body did not turn at all) and he reported diminution of his symptoms. Due to persistence of positional vertigo he was investigated with CT scan of the brain, which was normal. He was given Brandt and Daroff [6] habituation exercises and was advised to walk up and down two or three steps of a staircase and to practice on tandem gait, in order to improve the feeling of moderate instability that he still reported. Two months later the patient reports a considerable improvement of both symptoms of instability and vertigo in bed.

Table 1: The clinical and laboratory investigations of patient 1. Empty cells signify no change comparing to previous.

  Consultation 1:
One month and a half after beginning of symptoms
Consultation 2:
Four months after first consultation
Consultation 3:
5 days after 1st Epley treatment
Consultation 4:
5 days after 2nd Epley treatment
10 days after
Semont treatment
Spontaneous nystagmus Absent Absent      
Vestibular Ocular Reflex (VOR) Sinusoidal testing Reduced on the right Normal      
VOR suppression Normal Normal      
Halmagyi Head Impulse Test Positive on the right Positive on the right      
Smooth pursuit Normal Normal      
Saccades Normal Normal      
Optokinetic nystagmus (OKN) Normal Normal      
Romberg test Normal, but feels unsure Normal      
Tandem Romberg Unstable Unstable      
Unterberger (Fukuda) Stepping test Deviation of the body to the right A small Deviation of the body to the right     Normal: No body deviation
Walking Normal Normal      
Tandem gait Unstable Unstable, turns toes out of the line to broaden the base of support     Unstable, turns toes out of the line to broaden the base of support
Dix-Hallpike test Positive on the right Positive on the right Positive on the right Positive on the right Positive on the right
Supine Roll test Negative Negative      
Otoscopy Normal Normal      
Bithermal Caloric irrigation of the labyrinth Important labyrinth paresis on the right Important labyrinth paresis on the right      
Brain CT-scan         normal
Treatment Cowthorne-Cooksey Epley CRP Epley CRP Semont LP Brandt-Daroff Step climbing Tandem gait



An 80 year old patient was seen in a vertigo clinic, reporting a feeling of “dizziness inside his head” particularly when he moved his head or eyes. He also reported a slight feeling of rotatory vertigo on lying in bed. A month earlier he had experienced a strong vertiginous episode, for which he was seen in hospital casualties. Vertigo then was rotatory, strong and accompanied by serious nausea. He was prescribed dimenhydrinate capsules but he did not take more than two, due to stomach-ache. Rotatory vertigo stopped after three days, but he kept feeling dizzy. The patient’s clinical examination findings are reported on (Table 2). Dix-Hallpike triggering position on the right revealed intense nystagmus with nausea. The patient was not able to undergo the complete maneuver of Epley, so he was prescribed dimenhydrinate capsules in order to reduce the symptoms and come back the next day to repeat the Dix-Hallpike test and continue with the therapeutic modified Epley maneuver. The therapeutic maneuver was performed the day after with success. On a following assessment ten days later, Dix-Hallpike was negative and the patient reported an important reduction of his dizziness. Clinical examination showed improvement of Unterberger test (he could make twenty steps, but still there was an obvious and repeatable turn of the body to the right side).

He was put on Cowthorne Cooksey exercises at home. Twenty days later, on re-examination he performed even better with a minor turn of the body at the Unterberger test.


The vascularization of the internal ear [7] [Figure 1], belongs to the vertebrobasilar system. The anterior inferior cebellar artery (AICA) derives from the basilar artery. The common labyrinthine artery (or internal auditory artery) derives from the AICA. The common labyrinthine artery divides into two rami: The common cochlear artery and the anterior vestibular artery. The anterior vestibular artery irrigates the anterior and lateral semicircular canal ampullae, the utricular macula and a part of the saccule. The common cochlear artery divides into the main cochlear artery and the cochleovestibular artery, which gives off the posterior vestibular artery and cochlear branches.

The main cochlear artery irrigates the modiolus and three quarters of the cochlea. The basal quarter of the cochlea receives blood circulation from the cochlear branches of the cochleovestibular artery. The posterior vestibular artery irrigates the rest of the saccule and the posterior semicircular canal ampulla. All branches are terminal and a flow interruption leads to rapid functional loss. Lyndsay and Hemenway syndrome refers to interruption of the blood flow of the anterior vestibular artery.

The syndrome was described in 1956 by J.R. Lindsay and W.G. Hemenway [8], although H.F. Schuknecht discovered its vascular origin. It is a particular form of vestibular neuritis, beginning with major vertigo as described in the typical form, but which is followed by true BPPV of the posterior semicircular canal after an amount of time, ranging from a few days to several months. It is more frequent in patients over 60 years of age particularly if there are risk factors for arterial thrombosis. Hearing is spared, the labyrinth damage is major as measured in caloric irrigation, but in a few days to weeks, posterior canal BPPV is evident on the affected side. BPPV is a testimony of the utricular macular degeneration, which results in the dislocation of otoliths. At the same time however, BPPV marks the survival of posterior canal function. The explanation of the syndrome can be vascular thrombosis of the anterior vestibular artery, or a virus affecting the upper branch of the vestibular nerve, resulting in disruption of the homeostasis of the calcium carbonate crystals on the gelatinous macula of the utricle. Since the lower branch of the nerve is left intact, it can be excited by the dislodged otoconia, producing the symptoms of BPPV [Table 3].

A long term cohort study [9] found a 10% of patients with vestibular neuritis, presenting BPPV of the affected ear. It occurred predominantly to patients who had not fully recovered from the vestibular neuritis and was more difficult to treat, as it happened with the first patient of this study. Another study [10], seeking to detect L-H syndrome among patients consulting for BPPV, reported a prevalence of 16.3% of the syndrome among BPPV patients. Harada et al. (1993) [11], report that time interval between vestibular neuritis and BPPV onset ranged from 2 weeks to 20 years and assume that in case BPPV appears soon after vestibular neuritis, there is a possibility that the posterior canal has been spared from the beginning of the incident. In case it appears later, a possible initial lesion is assumed, followed by a progressive recovery of the posterior canal function later.

The present series of two patients is of particular value, because it is an example of the two possibilities of BPPV occurrence: either immediately after the symptoms of vestibular neuritis subside (one month time in the second case) or some time later (four months in the first case). Another particularity that has to be mentioned is the progressiveness of the initial symptoms of the first patient, who had diabetes i.e. an important risk of vascular thrombosis. Boffi [12] refers to the possibility of vestibular neuritis to occur without rotatory vertigo, but with a persistent feeling of unsteadiness. Pardal et al. [10], report the possibility of slowly progressive installation of the vestibular lesion preceding BPPV in Lindsay-Hemenway syndrome. One possible interpretation is a slow formation of a thrombus in the anterior vestibular artery, diminishing the patency of the vessel in a gradual fashion, leading to progressive loss of vestibular function.

The differential diagnosis of the syndrome comprises a wide variety of diseases [10]. Practically the clinician has to do differential diagnosis for two clinical entities. Multiple sclerosis and ischemic or tumoric lesions of the cerebellum have to be excluded with caution. Exclusion of central lesions will be based on the identification of benign (peripheral)characteristics of positional vertigo, the presence of a positive Halmagyi Head Impulse Test, the ability of the patient to stand with eyes closed (Romberg test) [Table3]. In general this is possible by the careful registration of medical history of the patient and clinical examination. Caloric irrigation should show lateral canal paresis (or important hypofunction), Playtone Audiometry should not be showing alterations of the hearing function of the patient. Air Conducted Cervical Vestibular evoked myogenic potentials (AC-VEMP) should be either present or absent in the initial incident, but should reappear in the case of BPPV. This is the case because air conducted VEMP measure the function of the saccule, which should be recovering function together with the posterior semicircular canal (or be spared from the beginning) as both structures are irrigated from the posterior vestibular artery. In cases of elderly people in whom degeneration of the saccular macula could have already taken place, AC- VEMP should be absent [13]. Imaging with CT scan or MRI is justified if treatment for BPPV is not successful and/or if clinical findings are suspicious for a central lesion. Due to the ischemic nature of underlying pathology, a full cardiovascular control is also mandatory in these patients.

Table 2: The clinical and laboratory investigations of patient 2. Empty cells signify no change comparing to previous.

Clinical and laboratory investigations of patient 2
  Consultation 1:
One month after beginning of symptoms
Consultation 2
24hours later, with sedatives
Consultation 3:
10 days after first consultation
 (results after Epley)
Consultation 4
20 days later
Spontaneous nystagmus Absent   Absent  
Vestibular Ocular Reflex (VOR) Sinusoidal testing Reduced on the right   Normal  
VOR suppression Normal   Normal  
Halmagyi Head Impulse Test Positive on the right   Positive on the right  
Smooth pursuit Normal   Normal  
Saccades Normal   Normal  
Optokinetic nystagmus (OKN) Normal   Normal  
Romberg test Normal, but feels unsure   Normal  
Tandem Romberg Unstable   Unstable  
Unterberger (Fukuda) Stepping test Unstable after 10 steps   Deviation of the body to the right Minor deviation to the right
Walking Normal   Normal  
Tandem gait Normal   Normal  
Dix-Hallpike test Positive on the right, very nauseous, intense nystagmus Positive on the right, no nausea Negative Negative
Supine Roll test Negative   Negative  
Otoscopy Normal   Normal  
Bithermal Caloric irrigation of the labyrinth Important labyrinth paresis on the right   Important labyrinth paresis on the right  
Treatment sedatives of labyrinth Epley CRP Cowthorne-Cooksey  

Table 3: The clinical and laboratory findings of Vestibular Neuritis in the very acute phase and Benign Paroxysmal Positional Vertigo (BPPV), presented as separate clinical entities. In patients with L-H syndrome, as BPPV occurs after some time, central compensation of the vestibular imbalance taking place in the mean time, can alter some of the clinical findings, i.e. disappearance of spontaneous nystagmus, VOR gain increase at the side of the lesion (Sinusoidal testing), Body deviation towards the healthy side at the Fukuda stepping test.

Clinical findings Vestibular Neuritis BPPV
Nystagmus Occurence Non dependent on head positions (spontaneous) Dependent on head position relative to gravity (positioning/positional)
Nystagmus Direction Horizontal (with torsional component when all canal function is abolished unilaterally) Torsional upbeating (PC-BPPV) or Horizontal(LC-BPPV)
  One directional One directional (PC-BPPV) Direction changing on contralateral side(LC-BPPV)
Nystagmus Duration Continuous (lasting from hours to days) Paroxysmal (Beginning-crescendo-subsiding) lasting up to 40(PC-BPPV) or 60 seconds (LC-BPPV)
Nystagmus Intensity Intensity affected by direction of gaze (Alexander’s law) Rotational or vertical component more obvious according to gaze direction(PC-BPPV)
Fixation More pronounced without fixation More pronounced without fixation
Vestibular Ocular Reflex (VOR) Sinusoidal testing Reduced on side of lesion Normal
Halmagyi Head Impulse Test Positive on side of lesion Normal
Romberg test Body leaning to side of lesion with tendency to fall Usually Normal
Unterberger (Fukuda) Stepping test Body deviates to side of lesion Usually Normal
Dix-Hallpike test/Supine roll test Negative (spontaneous nystagmus still present) Positive on side of lesion (PC-BPPV) Positive bilaterally with direction changing horizontal nystagmus(LC-BPPV)
Laboratory findings
Bithermal Caloric irrigation Canal Paresis Normal for PC-BPPV Occasionally hypofunction in case of LC-BPPV
AC-VEMP Absent or present Absent or present
PC-BPPV: Posterior Canal BPPV; LC-BPPV: Lateral Canal BPPV; AC-VEMP: Air Conducted Cervical Vestibular Evoked Myogenic Potentials.



Lyndsay-Hemenway syndrome is a clinical entity associating vestibular neuritis with BPPV. It manifests with a variety of symptoms, but in the majority of cases it is characterized by abrupt intense vertigo and nystagmus, followed by posterior canal BPPV after a variable amount of time. Clinicians dealing with vertigo should be aware of this clinical entity in order to diagnose it and reassure the patients accordingly and to help them with treatment combining vestibular rehabilitation and otoconia repositioning maneuvers.


1. Cawthorne T. Vestibular injuries. Proc R Soc Med. 1946; 39: 270-273.

2. Cooksey FS. Rehabilitation in vestibular injuries. Proc R Soc Med. 1946; 39: 273-278.

3. Epley JM. The Canalith Repositioning Procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngology-Head and Neck Surgery. 1992; 107: 399-404.

4. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Annals of Otology, Rhinology and Laryngology. 1952; 61: 987-1016.

5. Semont A, Freyss G, Vitte E. Curing the BPPV with a liberatory maneuver. Advances in Oto-Rhino-Laryngology. 1988; 42: 290-293.

6. Brandt T, Steddin S, Daroff RB. Therapy for benign paroxysmal positioning vertigo, revisited. Neurology. 1994; 44: 796-800.

7. Sánchez Gil-Hernández Urtiz A. Study of the effectiveness of the liberatory manoeuvre in Lindsay-Hemenway syndrome. Rev Med Hosp Gen Méx. 2016; 94: 1-6.

8. Hemenway WG, Lindsay JR. Postural vertigo due to unilateral sudden partial loss of vestibular function. Ann Otolaryngol. 1956; 65: 692- 706.

9. Mandalà M, Santoro GP, Awrey J, Nuti D. Vestibular neuritis: recurrence and incidence of secondary benign paroxysmal positional vertigo. Acta Otolaryngol. 2010; 130: 565-567.

10. Pardal Refoyo JL, Pérez Plasencia D, Beltrán Mateos LD. Isquemia de la arteria vestibular anterior (síndrome de Lindsay-Hemenway) Revisión y comentarios. Acta Otorrino-laringol Esp. 1998; 49: 599- 602.

11. Harada K, Oda M, Yamamoto M, Nomura T, Ohbayashi S, Kitsuda C. A clinical observation of benign paroxysmal positional vertigo (BPPV) after vestibular neuronitis (VN). Acta Otolaryngol. 1993; 503: 61-63.

12. Boffi A. Positional nystagmus and vertigo in vestibular neuronitis. The Laryngoscope. 1965; 75: 484-489.

13. Korres S, Gkoritsa E, Giannakakou-Razelou D, Yiotakis I, Riga M, Nikolpoulos TP. Vestibular evoked myogenic potentials in patients with BPPV. Med Sci Monit. 2011; 17: 42-47.

Gkoritsa EZ (2016) The Lyndsay-Hemenway Syndrome: Two Case Reports. Review and Comments. J Ear Nose Throat Disord 1(1): 1014

Received : 04 Aug 2016
Accepted : 06 Oct 2016
Published : 08 Oct 2016
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