Visual variant of vertigo
Visual vertigo is characterized by having vertigo symptoms that are triggered by visual stimuli. These symptoms can develop in individuals with a vestibular disorder (i.e. vestibular neuritis, Meniere disease. Benign paroxysmal positional l vertigo (BPPV), migraine).
Visual vertigo was first described in the late 1970s (2, 3). It can be referred to as visuo-vestibular mismatch (6), and Space and Motion disorder (7) as well. Visual vertigo does not demonstrate a preference for race or gender. Patients with decreased vestibular function (5, 8), decreased proprioceptive function (9), and certain CNS insults (10) are more visually-invoked into an episode of vertigo. However, visual vertigo does not occur in every patient with vestibular or proprioceptive dysfunction, and, ultimately, what causes some patients with vestibular disorders to develop visual dependence, and therefore increased likelihood of visually-invoked vertigo, is unknown. Anxiety and depression are often observed in these patients, but they have not been shown to play a role in the development of visual vertigo (4).
The etiology of visual vertigo’s origin is the triggering of a visual stimuli causing vestibular symptoms. This is due to a vestibular insult the impairs the patient’s ability to spatially and physically orient themselves using primarily their vestibular system. By consequence, patients with visual vertigo exhibit increased visual dependence to spatially orient (4). They are also found to have postural balance hypersensitivity to moving or tilted visual stimuli (4, 5). Visual dependence has its limitations and patients with visual vertigo is triggered by busier, more disorienting, visual fields.
Common causes of vestibular insults are the main risk factors for visual vertigo. This includes benign paroxysmal positional vertigo (BPPV), migraines, and vestibular neuritis. Insults to regions affecting the ability of the vestibular system or proprioceptive system to appropriately spatially and posturally orient sometimes exhibit increased visual dependence for orientation. This hypersensitivity can manifest itself as a tilted or moving object, or a busy visual field, evoking vertigo.
The pathophysiology of visual vertigo is not fully understood. It occurs in patients with previous or current vestibular insults. A normal individual is primarily using vestibular or proprioceptive input over visual input for spatial orientation and postural control. However, in visual vertigo, a patient has increased visual input dependence because the vestibular system is unable to fully compensate for a disorienting visual field (1, 2, 3). Therefore, patients with decreased vestibular function (5, 8), decreased proprioceptive function (9), and certain CNS insults (10) are more visually-invoked into an episode of vertigo. However, visual vertigo does not occur in every patient with vestibular or proprioceptive dysfunction, and, ultimately, what causes some patients with vestibular disorders to develop visual dependence, and therefore increased likelihood of visually-invoked vertigo, is unknown.
The differential diagnosis includes many of the common causes of vertigo, including BPPV, Meniere disease, vestibular neuritis, migraine, and brainstem or cerebellar stroke.
Make sure to distinguish oscillopsia from visual vertigo. Oscillopsia is the movement of the visual field while visual vertigo is triggered by a visual stimulus but maintains vestibular symptoms. Asking a thorough history is essential to differentiate between oscillopsia and visual vertigo.
Visual vertigo arises in patients with a present or previous vestibular insult. Therefore, it is important to learn about the different types of vestibular insults and their potential treatments so that the therapy may be tailored depending on the origin of the patient’s symptoms. However, it is important to note that the original vestibular insult is often in the patient’s past, so they are less able to accurately recall the original symptoms, not allowing for confirmation of the insult’s etiology.
A typical patient is one that suffers from an acute vestibular insult, like vestibular neuritis, causing vertigo symptoms. Then, weeks after the episode is resolved, the patient reports continued vertigo that is triggered visually.
The visual variant of vertigo is accompanied by the same classic vertigo symptoms: dizziness, swaying and tilting, disorientation, unsteadiness, spinning, and a possible pull to one direction. Other symptoms that may present with visual vertigo is headache, sweating, nystagmus, nausea and vomiting, and tinnitus. It is important to remember that visual vertigo’s uniqueness stems from it being a visual stimulus that produces vestibular symptoms.
Visual vertigo is a clinical diagnosis, and the physician can utilize a variety of visual stimuli to try and elicit an episode of vertigo. If the patient’s vertigo is brought on by visual stimuli, the diagnosis is highly suspected.
Patients with visual vertigo have hypersensitivity to moving or tilted visual stimuli (4, 5). A physician can test patients with moving or tilted visual stimuli to evoke an episode of vertigo.
Before treatment, it is important for the physician to try and identify the cause of the original vestibular insult (i.e. vestibular neuritis, Meniere disease, BPPV, migraine). However, often the patient’s original vestibular insult was in the past and history is therefore often unable to be confirmed. If one is identifiable, treat the underlying disease when possible.
In addition, vestibular rehabilitation should also be offered to these patients. These training regimens consist of progressive visual and postural movements (twisting, turning) along with walking exercises (11, 12). The Cawthorne-Cooksey approach was one of the original methods and can still be used today but the approach is now commonly individualized to fit the patient’s needs (13).
In additional to conventional vestibular rehabilitation, approaches taken to reduce hypersensitivity to visual stimuli are also recommended. These are gradually progressive and repetitive exercises that promote desensitization and increase tolerance to visual stimuli. The visual stimuli are largely introduced by the form of optokinetic stimuli (16)
Until recently, no pharmacotherapy has been shown to be effective for the treatment of visual vertigo. However, a comparative case series was conducted from 1992 to 2015 that showed a marked improvement in visual vertigo symptoms among patients taking acetazolamide (94.7%) versus patients taking placebo (66.7%) (14).
Research has indicated that the therapeutic exercises mentioned above are effective in reducing dizziness symptoms and the associated psychological sequalae (15). No data has been collected on how effective adjunctive pharmacotherapy in conjunction with therapeutic exercises is compared to either treatment alone.
1. Bronstein AM (2002) Underrated neuro-otological symptoms: Hofffman and Brookler 1978 revistied. Br Med Bull 63:213:221.
2. Hood JD (1980) Unsteadiness of cerebellar origin: an investigation into its cause. J Laryngol Otol 94:865-876.
3. Hoffman RA, Brookler KH (1978) Underrated neurotologic symptoms. Laryngoscope 88:1127-1138.
4. Guerraaz M, Yardley L, Bertholon P, Pollak L, Rudge P, Gresty MA, Bronstein AM (2001) Visual vertigo: symptom assessment, spatial orientation and postural control. Brain 124:1646-1656.
5. Bronstein AM (1995) Visual vertigo syndrome:clinical and posturography findings. J Neurol Neurosurg Psychiatry 59:472-476.
6. Longridge NS, Mallinson AI, Denton A (2002) Visual vestibular mismatch in patients treated with intrtympanic gentamicin for Ménière’s disease. J Otolaryngol 31:5-8.
7. Jacob RG (1988) Panic disorder and the vestibular system, Psychiatr Cli n North Am 11:361-374.
8. Peterka RJ, Benolken MS (1995) Role of somatosensory and vestibular cues in attenuating visually induced human posturai sway. Exp Brain Res 105:101-110.
9. Bronstein AM (1986) Suppression of visually evoked postural responses. Exp Brain Res 63:655-658.
10. Bronstein AM, Hood JD, Gretsy MA, Panagi C (1990) Visual control of balance in cerebellar and parkinsonian syndromes. Brain 113:767-779.
11. Black FO, Pesznecker SC (2003) Vestibular adaptation and rehabilitation. Curr Opin Otolaryngol Head Neck Surg 11:355-360.
12. Pavlou M, Shummway-Cook A, Horak F, Yardley L, Bronstein AM (2004) Rehabilitation of balance disorders in the patient with vestibular pathology. In ‘Clinical disorders of balance, posture and gait’ by Bronstein AM, Brandt T, Wllacott M, Nutt J (Eds). Edward Arnold Publishers, London 2004.
13. Cawthorne T (1952) The rationale of physiotherapy in vertigo and facial palsy. Physiotherapy 38:237-241.
14. Sluch I, Elliott M, Dvorak J, Ding K, Farris B (2017). Acetazolamide: A New Treatment for Visual Vertigo. Neuro-Ophthalmology (Aeolus Press) 41 (6):315–20.
15. Pavlou M, Lingeswaran A, Davies RA, Gresty MA, Bronstein AM (2004) Simulator based rehabilitation in refractory dizziness, J Neurol.
16. Vitte E, Semont A, Berthoz A (1994) Repeated optokinetic stimulation in conditions of active standing facilitates recovery from vestibular deficits. Exp Brain Res 102L141-148.