Your next evaluation walks in the door with a diagnosis of “Vertigo”. They state that they woke up one morning feeling “spinny” or “dizzy” and “very nauseous”. They may have tried to get out of their bed and realized that they weren’t even able to stand! Well, you hear the words “I got dizzy when I got out of bed one morning” and your mind immediately flashes to one diagnosis in particular: BPPV. Classic. Vertigo originating from a positional change that resolves within 1 minute or less. Easy peasy. Except for one thing: your patient just let you know that their vertigo lasted for 2 days straight with no relief. Changes in position don’t seem to affect their symptoms one way or another. Well that doesn’t sound like BPPV. What do you do now?
Vestibular neuritis (also called vestibular neuronitis in some literature), and the similar condition labyrinthitis, often result from a viral insult to the vestibular portion of cranial nerve VIII (Rizk) or the vestibular labyrinth, respectively. Behind BPPV, they are the second and third most common causes of peripheral vertigo (Strupp 2013), so they are very common conditions that outpatient PTs should be familiar with! They are usually preceded by an upper respiratory infection or gastrointestinal infection within the previous 2 weeks (Herdman, 2014), which triggers the inflammation of this nerve. The most common presentations include the following criteria, but are not necessarily limited to these:
- Acute onset of unrelenting moderate to severe vertigo, often lasting several days
- Vertigo that is relatively unaffected by positional changes but can be exacerbated by head movements
- Moderate to severe nausea and vomiting
- Postural imbalance
- Unilateral hearing loss, fullness or pressure in affected ear (labyrinthitis only)
The severity of these symptoms usually subsides within a few days of initial onset, but can last for up to a week (Herdman, 2014). After this acute period is over, patients usually are left with symptoms that are milder but often still impact quality of life, including:
- Generalized “dizziness”, “lightheadedness”, “rocking”, “fogginess”
- Mental and physical fatigue
- Difficulty with quick head movements
- Oscillopsia (gaze instability with head movement)
Let’s take a look at what is actually happening when a patient experiences these conditions.
The semicircular canals and otolith organs send input to the central nervous system via the vestibular portion of the vestibulocochlear nerve (CN VIII) (Shupert 2020). Head movements to the right result in increased firing of the semicircular canals in the right inner ear and inhibited firing of the left semicircular canals and vice versa. Their respective vestibular nerves send this signal to our CNS to give us the sense of angular and rotational head movement, as well as general positioning information of our head and neck (Shupert 2020). Our otolith organs, the utricle and saccule, send a similar signal via our vestibular nerve to give our CNS the input of linear horizontal and vertical head movement respectively (Shupert 2020). The vestibular nerve is a vital proponent in how our brain interprets our head movements at any given time.
As stated earlier, vestibular neuritis occurs when the superior branch of the vestibular nerve becomes inflamed, and labyrinthitis occurs when the entire labyrinth becomes inflamed, resulting in associated hearing loss as the cochlea is also affected. They most often occur after an upper respiratory infection, GI infection, or an infection from Herpes Simplex Virus (HSV) (Shupert 2020). COVID has been a particularly potent culprit of these conditions (Pazdro-Zastawny 2022). When this happens, the signal that the affected nerve is giving our CNS is altered, delayed, or in severe cases, absent. This acute disruption of the peripheral vestibular system gives our CNS “mismatching” signals about our head position and head movement, hence, the feeling of vertigo (Shupert 2020). Often very severe and unrelenting vertigo. This usually continues to occur until the inflammation settles and the cerebellum suppresses the function of the unaffected ear to undo this mismatched information the CNS is receiving. After this takes place, the vertigo has subsided but the patient is often left with what we call a vestibular hypofunction, meaning the affected peripheral vestibular system is functioning at a lower capacity than the unaffected side. Some people may completely recover from the acute phase and become symptom free. Some people suffering from a hypofunction generally experience the milder symptoms listed above, such as general dizziness with head movement and a feeling of “fogginess”, that may persist until they receive specialized treatment (Shupert 2020). Now that we know what is going on physiologically when vestibular neuritis or labyrinthitis occurs, let’s discuss how to assess a patient for this condition!
Vestibular neuritis or labyrinthitis primarily affects the peripheral vestibular system, therefore patients will present with peripheral signs in the objective assessment. There are several tests that can be performed in clinic to assess the peripheral vestibular system, including but not limited to:
- Head thrust (or head impulse) test: patient will not be able to keep eyes fixed on a set midline point when their head is quickly thrust to their affected side (Schubert 2004)
- Dynamic visual Acuity test: patient will have a greater than 2 line difference when reading words on a word chart with their head moving compared to when it is still (Hain 2022)
- Gaze evoked nystagmus: patient may display increased horizontal beating nystagmus that beats away from the affected ear. The nystagmus may be stronger when the patient’s gaze is looking toward the beating of the nystagmus. (Leigh RJ 2006)
Central signs such as smooth pursuits, saccades, convergence, and skew eye deviation tests should all within normal limits, since the central vestibular has not been affected.
It is also important to assess a patient’s balance following a viral insult to the inner ear, especially in the acute or sub-acute phases, as our hip strategies are heavily influenced by our otolith organs in the inner ear and often become compromised to some degree following the infection. Patients may display some or all of the following deficits or deviations:
- Wide base of support when walking
- Decreased cadence
- Difficulty with head turns when walking or standing
- Difficulty with balance involving eyes closed
- Difficulty with single leg stance or tandem stance (Herdman, 373)
Okay, so you’ve assessed a patient and determined through your subjective and objective findings that they may have experienced a vestibular neuritis or labyrinthitis. Where do we go from here?
Once the acute onset has begun, it is recommended to begin steroid use (specifically methlyprednisone) as quickly as possible to reduce inflammation and spare as much function of the vestibular nerve as possible (Sjogren 2019). Vestibular suppressants, such as Meclizine or Antivert, will often be prescribed to the patient for symptom relief, however long term uses of these medications are generally not recommended as they may delay recovery (Peppard 1986). Use of these medications in tandem with bed rest are beneficial for the first 2-3 days; after this, it is recommended to decrease use of vestibular suppressants to allow for central compensation (Herdman 2014). In this phase, we can begin vestibular adaptation exercises as they have shown to speed recovery to initiate them as tolerated as early as possible (Hall 2021). Gaze stabilization exercises are a great way to introduce this to a patient, however the degree of which a patient tolerates these exercises will greatly vary. Slow introduction to these exercises is best, as well as modification of patient’s day to day activities to allow for plenty of rest while their inner ear recovers.
Some patients do not completely compensate and may continue to feel symptoms of dizziness and imbalance after the initial inflammation has passed (Rizk). This is likely due to lasting, and often permanent, damage to the inner ear from the infection, resulting in that hypofunction we discussed earlier. Now, even though function to the inner ear may never return, through the magic of appropriately prescribed and dosed vestibular adaptation exercises, the cerebellum picks up the slack and allows for vestibular compensation!
If you have assessed your patient and have determined that they have oscillopsia (blurred vision with head movement), you likely have a patient with gaze instability on your hands. What is the best exercise for them? Gaze stability exercises, or what we also call VOR (vestibulo-ocular reflex) retraining. This involves the patient stabilizing their gaze on a non-moving (VOR x 1) or moving (VOR x 2) target while they move their head at a speed of ~2 Hz in a 60 degree range of motion. The most updated clinical practice guidelines for vestibular hypofunction recommend to begin with VOR x 1 and to have the patient perform this 3-5 times per day for a total of 12-20 minutes per day for 4-6 weeks (Hall 2021). This is one of the simplest yet most effective exercise interventions you can prescribe for them and has been shown to be more effective than non-vestibular specific interventions in reducing a patient’s continued symptoms of dizziness. Progressions to this exercise can involve:
- Increasing duration of time spent performing each set
- Having the patient stand and perform as opposed to sitting
- Narrowing their base of support or having them stand on compliant surface
- Performing while walking (and properly guarded for safety)
Combine these exercises with dynamic balance interventions of your choosing based on their specific deficits, and you have yourself a great plan of care! Patients should be taught the value of pacing and recovery techniques as well so as to manage symptoms as they arise. Educating your patient on what is happening to them, the prognosis of their condition, and steps they can take to improve their symptoms will go such a long way on their road to feeling themselves again.
- Rizk, H. G., & Shaw, S. (n.d.). Labyrinthitis and vestibular neuritis. Vestibular Disorders Association. Retrieved February 27, 2023, from https://vestibular.org/article/diagnosis-treatment/types-of-vestibular-disorders/labyrinthitis-and-vestibular-neuritis/
- Strupp M, Dieterich M, Brandt T. The treatment and natural course of peripheral and central vertigo. Dtsch Arztebl Int 2013; 110:505–515.
- Herdman, Susan, and Richard Cledaniel. Vestibular Rehabilitation. 4th ed. Philadelphia: F.A. Davis, 2014
- Shupert, C., & Kulick, B. (2020, May 06). Labyrinthitis and Vestibular Neuritis. Retrieved February 24, 2022
- Pazdro-Zastawny K, Dorobisz K, Misiak P, Kruk-Krzemień A, Zatoński T. Vestibular disorders in patients after COVID-19 infection. Front Neurol. 2022 Sep 20;13:956515. doi: 10.3389/fneur.2022.956515. PMID: 36203969; PMCID: PMC9531925.
- Michael C Schubert, Ronald J Tusa, Lawrence E Grine, Susan J Herdman, Optimizing the Sensitivity of the Head Thrust Test for Identifying Vestibular Hypofunction, Physical Therapy, Volume 84, Issue 2, 1 February 2004, Pages 151–158, https://doi.org/10.1093/ptj/84.2.151
- Leigh RJ, Zee DS. “The Neurology of Eye Movements, 4th ed.” New York: Oxford University Press; 2006
- Sjögren, J., Magnusson, M., Tjernström, F., & Karlberg, M. (2019, March). Steroids for Acute Vestibular Neuronitis-the Earlier the… : Otology & Neurotology. Retrieved February 24, 2022
- Peppard SB. Effect of drug therapy on compensation from vestibular injury. Laryngoscope 1986; 96:878.
- Hall CD, et al. Vestibular Rehabilitation for Peripheral Vestibular Hypofunction: An Updated Clinical Practice Guideline. JNPT. 2021