Vertigo and Dizziness

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Musculoskeletal medicine doctors will sometimes be asked to assess patients with vertigo as to whether it is related to their neck. Or patients may ask their GP whether the vertigo is coming from their neck. The aim of this article is not to provide a comprehensive outline on the assessment and treatment of all forms of dizziness, for that please see the external resources section below. The aim is rather to provide a basic framework of assessment and detail conditions that may be associated with musculoskeletal disorders such as vestibular migraine and cervical vertigo. BPPV can be associated with head trauma but again is best learned about from the external resources. The most important thing for the Musculoskeletal doctor to know is that all causes of vertigo, particularly in their chronic forms, very commonly in themselves cause neck pain.

The Vestibular System

The vestibular system controls your stability: the stability of your visual world, the stability of your posture and gait, and your subjective equilibrium. Everyone understands hearing, but few understand what vestibular function does and how disastrous it is to lose it.

The vestibular system controls stability by detecting head movement and generating corrective responses. Eye movements cancel out head movements and give you clear vision. Postural responses keep you stable to protect you from falling. You feel sensations in your body so you know you are turning.

The otoliths are the sensory regions for linear acceleration: the utricle and saccule. The semicircular canals are the sensory regions for angular head rotation: posterior, horizontal, and anterior. Each labyrinth we therefore have five sensory regions, so ten in total. EVERY head movement has both angular and linear components. So BOTH canals and otoliths are activated. There has been massive sea-change in the last 10 years, now all 10 bilateral structures can be tested in specialised labs.

Complete bilateral loss of vestibular function causes oscillopsia "bouncing vision." The head moves and the eyes don't compensate, the image on the retina smears.

The image on the retina must be stable for clear vision. There are basically two kinds of eye movements. Saccades – very rapid “ballistic” movements, where the vision jumps from target to target. E.g. during reading. Vision is switched “off” during the saccade so there is no blur on the retina. Smooth slow eye movements – for example smooth pursuit of moving targets, like following your finger. Saccades eliminate smear. The vestibular sensors detect head movement and move the eyes to correct for it.

Assessment Principles

Practice Point
Focus on the timing and triggers rather than the quality of the dizziness.

Put little diagnostic weight onto the "quality of dizziness" (spinning, unbalanced etc). This question is invalid and unreliable; patient descriptions are normally vague and circular and it is normally not possible to make an accurate diagnosis by starting with this question. For example when tested 6 minutes later, ~50% of patients pick different answers. It creates false confessions and patient descriptors are normally vague and circular. Chest pain diagnostic algorithms do not start with the quality of pain, as it is understood that pain descriptions are not useful. The same can be said for dizziness, and so the clinician should focus on timing and triggers. Timing and trigger reports are clear, consistent and reliable. [1]

You will be less confused if you emphasise timing, triggers, and associated symptoms.

Timing means continuous vs intermittent, frequency, and duration. It leads to three main symptom complexes: Acute Vestibular Syndrome (AVS), Episodic Vestibular Syndrome (EVS), and Chronic Vestibular Syndrome (CVS). You can get overlap and/or evolution, e.g. AVS to CVS (e.g. VN to PPPD)

Triggers means is there anything that brings it on. Turning over in bed as a trigger is highly specific for BPPV.[2] Other potential triggers: Positional changes of head or body, standing up, Rapid head movements, Walking in dark room, Loud noises, Coughing, nose blowing, sneezing, straining, Underwater diving, elevators, airplane travel, Exercise, Shopping malls, narrow or wide-open spaces, grocery stores, Diet, fasting, alcohol, Menstrual periods, Boat or car travel, Anxiety or stress.

ASSOCIATED SYMPTOMS can also help Dx. Palpations, Anxiety, Migraine headache, Autophany (can hear eye movement, hear chewing, etc), Auditory symptoms (deafness, tinnitus, aural fullness), Vegetative symptoms (N + V)

Acute Vestibular Syndrome

These patients have persistent continuous vertigo for hours or days. They have spontaneous and/or gaze evoked nystagmus and present with nausea and vomiting as well as difficulty with gait. Important to remember is that head movements make all causes of vertigo worse, including in AVS. If the AVS is unprovoked then your main differential is vestibular neuritis vs posterior circulation stroke. These can be differentiated using the HINTS plus examination.[3] The ABCD2 score can also be used. If the score is 4 or less with normal standard neuro exam and gait then stroke is very unlikely (<1% chance)[4] If you're not sure and admission not suitable, refer OPD and prescribe aspirin for 6-12 weeks (highest risk period for subsequent stroke).

Peter Johns advocates to remove the famous central versus peripheral vertigo table as it is mostly incorrect, with the only correct part being that central vertigo will usually have other neurological features[5] One should always consider red flag conditions when there is significant headache or neck pain or the patient is unable to stand unaided. The presence of the following neurological symptoms or deficits also warrant concern: focal weakness of face or limbs, dysarthria, diplopia, dysphagia, dysmetria, dysphonia, spontaneous vertical nystagmus (not during Dix-Hallpike test).[6]

Red Flags
  • Unable to stand unaided
  • Significant headache or neck pain
  • Focal weakness of face or limbs
  • Diplopia, dysphagia, dysmetria, dysphonia
  • Spontaneous vertical nystagmus (normal to have vertical nystagmus during Dix-Hallpike)

As part of the assessment, one should ask about associated symptoms. Important associated symptoms include nausea, hearing loss, tinnitus, aural fullness, ear pain, discharge, ataxia, and fever. Important in the musculoskeletal setting is obtaining a neck pain history, in particular with regards to previous whiplash. A general medical assessment may be indicated for evaluation of medical causes: infection, metabolic, cardiac, and medications, etc.

The examination should also include gait, Romberg, and Tandem Romberg tests with eyes closed. If these tests are normal then a full cerebellar examination is not required. The tympanic membranes should be visualised. Blood pressure, orthostasis, pulse, and arrhythmia may need to be assessed.

Episodic Vestibular Syndrome

Vestibular Migraine

Vestibular migraine is vastly under-diagnosed, being the most common cause of central vertigo, and the second most common cause of vertigo overall. It is more common in woman, average age 40. Almost half episodes can be vertigo only, 30% never get a headache. Vestibular migraine is a “Committee Diagnosis” like Meniere’s and chronic subjective vertigo. Treatment similar to normal migraine

There is no bedside diagnostic examination. The clinician should rule out other causes especially CVA. Nystagmus is rarely seen unless remove fixation, and tends to be sustained (cf BPPV), low velocity, and often vertical. There is also no diagnostic investigation, but consider neuroimaging if available (very low yield if normal neuro exam). Audiograms can look like Meniere’s with fluctuating low tone sensorineural hearing loss.

A simplified approach to diagnosis is as follows[7]

  1. Episodes
    • At least 5 episodes of vestibular symptoms of moderate to severe intensity
    • lasting 5 min–72 h
  2. Migraine history
    • Current or previous history of migraine +/ aura
    • According to the International Classification of Headache Disorders (ICHD).
  3. Migraine features
    • One or more migraine features++ with at least 50% of the vestibular episodes.
  4. Consider other causes
    • Not better accounted for by another vestibular or ICHD diagnosis.

Considering the differential diagnosis, when compared to BPPV, vestibular migraine relapses shorter interval and shorter duration and nystagmus doesn’t fatigue and isn’t torsional-vertical. With vestibular neuritis, vestibular migraine may have a positive head thrust test. With posterior circulation CVA or TIA it is unusual to have repeated episodes. When considering Meniere's it is important to remember that vestibular migraine is ten times more common, and 50% of Meniere's patients have migraine, too.

Treatment is as per normal migraine treatment.


There are many great resources online for assessing and treating BPPV. The Barany article is the gold standard, linked at the bottom of this article. The important point to know is that if it remains untreated, most patients will develop secondary neck pain and sometimes get referred to MSK physicians for "cervical vertigo." Detecting and treating their BPPV cures their neck pain.

Chronic Vestibular Syndrome

PPPD and vestibulopathy are the main differentials.

PPPD is the cardinal functional disorder of the vestibular system. Often after some kind of insult has resolved – vestibular neuritis, BPPV, vestibular migraine – but the brain isn’t interpreting signals properly. Classic is middle aged woman, says they’re overwhelmed at the supermarket, very functionally debilitated. Treatment is reassurance and exposure and vestibular rehabilitation

"Cervical Vertigo"

Maintain cautious regarding neck pain as a cause of vertigo, especially in chronic vertigo.

Neck pain is common in all causes of vertigo: Neck pain and stiffness is a common finding of most causes of dizziness, particularly chronic forms. For example most patients with untreated chronic BPPV ( >6 months) eventually develop neck pain (87%) and headache (75%), and the pain significantly improves or resolves after treatment of BPPV. In patients with unilateral vestibular loss prevalence of neck pain rises from 21% initially to 51% after 5 years.[8] Another good example is pain is more common than nausea amongst migraineurs.

Worsening with neck movement isn't specific: Most neurovestibular causes of vertigo are worsened with head movement

So be very careful about diagnosing “cervical vertigo” before ruling out neurovestibular causes

Vestibular dysfunction leads to abnormal head positioning, unable to maintain good horizontal positioning. Head extension needed to extend visual field to help compensate, but also need to flex more frequently to look at the ground and feet. Patients with bilateral loss have a nose down posture, may reflect decreased muscle tone from loss of vestibular input. The otoliths help to maintain good tonic postural activity of the neck!!

Cervical Vertigo, also known as cervicogenic vertigo or cervicogenic dizziness is a controversial entity. There is evidence that it is a distinct disorder but there is no agreed upon pathophysiology, reliable test, or diagnostic criteria. Reliable and well established tests support an alternative diagnosis in almost all patients with vertigo. [9] In centres with advanced capabilities for assessing vertigo, cervical vertigo is rare. However in settings of neck trauma, dizziness is common.

All clinical studies on the condition have three major weak points: inability to confirm the diagnosis, no specific laboratory test, and unexplained discrepancy between those with severe neck pain with no vertigo and those with moderate neck pain with severe vertigo.[9]


There are multiple models that attempt to explain cervical dizziness, and they are discussed in the sections below.

Abnormal Sensory Input

The Vestibulospinal reflex is a system for maintaining balance, posture, and, stability. When you close your eyes, the to and fro swaying is the vestibulospinal system righting the body. Some authors further subdivide the terminology and say that the vestibulospinal reflex is for muscles below the neck, and the vestibulochollic reflex if for the neck muscles. There is no objective test for detecting deficient or excessive vestibulospinal activity.

Vestibulospinal reflex.png

Cervical facet joints are densely innervated, 50% of all cervical proprioceptors in joint capsules C1-C3. There are dense mechanoreceptors in the gamma-muscle spindles of deep segmental upper cervical muscles. Mechanoreceptor function can be altered by pain, trauma, fatigue, degeneration. There are direct connections to the vestibular and visual systems.[9]

The vestibulospinal tract is a descending motor pathway (extrapyramidal) that gives motor commands that control posture. The medial tract is for neck muscles, head stabilisation / coordination, and eye movement. The lateral tract is for antigravity muscles, the leg extensors for upright posture.

Vestibulospinal tract.png

There are multiple sources of indirect evidence for abnormal sensory inputs in cervical dizziness.

  • Noxious stimulation of posterior neck muscles (such as vibration) can cause dizziness
  • Local anaesthetic injections to upper cervical nerves or muscles can cause dizziness.
  • Whiplash leads to deficits in neck position sense.
  • There may be relief of vertigo with a medial branch block in whiplash.[10]
  • Manual therapy seems to be effective.[11]
  • There is often a disturbance in vestibulospinal control of optokinetic pursuit: Eye pursuit normal with static head, abnormal with head rotation.

Cervical vertigo may result from a sensory mismatch between vestibular and cervical inputs where the cervical input is dominant due to altered input from the upper cervical proprioceptors to the vestibular nuclei.[9] In whiplash cervical input may be dominant over vestibular with neck activation when there is pain or stiffness.[12]

The neural mismatch model describes a mismatch between centrally expected and actual neck movement. For example head movement may be smaller than intended due to stiffness, which the brain perceives as external pertubation, with the result being that the individual experiences motion sickness. [13]

Cervical Cord Compression

Cervical cord compression or abutment, such as occurring following whiplash, can cause dizziness with or without pain. It is theorised that there is compression of the ascending or descending tracts that interact with the vestibular and cerebellar systems.[14]

Rotational Vertebral Artery Occlusion

Also known as bow-hunters syndrome, this condition is rare and very difficult to diagnose. There is reversible vascular insufficiency from compression at the C1/2 junction with contraversive head movement. The dizziness may only come on after many seconds. Dissection, spasm, and stenosis of a vertebral artery can also cause dizziness.[15]

Sympathetic Dysfunction

The so-called Barré – Liéou lesion describes impingement or stimulation of the cervical sympathetic plexus causing reflex vasoconstriction of the vertebrobasilar system. Symptoms include vertigo, tinnitus, headache, blurred vision, dilated pupils, nausea. This is a controversial diagnosis, that is not supported by experimental evidence.[14]

Migraine Associated Cervicogenic Vertigo

Cervical vertigo patients overlap considerably with migraine. Neck pain is more common than nausea amongst migraineurs. It is thought that neck pain can stimulate migraine, and thereby lead to dizziness. Vestibular migraine is the second most common cause of vertigo after BPPV. Migraine could be a link between cervical pain and vertigo through reciprocal connections between the vestibular and trigeminal nuclei.[9][14]

Spontaneous Intracranial Hypotension

See also: Cerebrospinal Fluid Leak

There is classically a daily orthostatic headache. The headache worsens with upright positioning, and improves when supine. It often starts abruptly. The pain may be felt in the entire head, or more localised in the bifrontal, occipital, or upper cervical regions. A significant minority of patients do not have an orthostatic headache. Associated symptoms include tinnitus, photophobia, phonophobia, dizziness, nausea and vomiting, and difficulty hearing. The condition is sometimes described in association with migraine, POTS, and Ehlers-Danlos syndrome. [16]

There are three subtypes making up three quarters of causes[16]. The remaining one quarter are indeterminate. The three types are

  • Dural tear often from a ventral osteophyte that leads to an extradural CSF collection
  • Nerve root diverticulum that leaks causing extradural fluid collection
  • Fistula connecting the CSF to the venous system without extradural fluid collection.

As part of the assessment one should check for hypermobility using the Beighton scoring system. Measure the opening pressure, but only 34% with confirmed spinal CSF leaks were found to have a CSF pressure of ≤60 mm H2O. MRI imaging of the brain will show findings in most cases, but may be normal in chronic leaks.[16]

The epidural blood patch is the mainstay of treatment.[16]


There is no validated method of assessment or diagnosis


  • History of neck injury
  • Pain in back of neck, radiates temporo-parietally, may only be present with palpation
  • Symptoms worse with neck pain and neck movement
  • Symptoms better with interventions that relieve neck pain
  • Vertigo lasts minutes to hours


  • Reproducible vertigo with neck movement, making sure to keep the vestibular canals stationary. i.e. move the torso with respect to the head, rather than the head with respect to the torso. For example the examiner holds the patient's neck still with their hands while the patient: slowly rotates their torso for rotation testing, and slowly brings their torso backwards and forwards for flexion and extension testing.
  • +/- weak nystagmus that does not change with gravity, but rather with head on neck position (wait 30 seconds)
  • Tender suboccipitally, C1 and C2 transverse processes
  • Tender C2 and C3 spinous processes
  • Tender myofascial structures
  • Restricted upper C-spine range of motion


There is no agreed criteria for diagnosis of cervical vertigo. My take on diagnosis is as follows, considering the following factors.

  1. Neck Pain
    • Correlation of vertigo with neck pain
    • But requiring neck pain doesn’t account for all models (e.g. RVAS)
    • Temporal proximity – onset of dizziness after injury to the neck
  2. Examination Features
    • No proven test
    • Provocation of dizziness with neck movement without vestibular apparatus movement.
    • Nystagmus on head turning that doesn’t change with gravity
    • Severe stiffness of the neck
  3. Imaging
    • Cervical osteoarthritis and/or IVDD
    • Disc abutting cervical cord
    • High cervical disease on MRI
  4. Exclude Other Causes
    • Almost all cases of vertigo can be accounted for by other conditions
    • Especially vestibular diseases and migraine


Both Mulligan and Maitland mobilisations appear to be beneficial. A Mulligan approach involves a sustained natural apophyseal glide (SNAG) to the left C1 transverse process into left rotation as the SNAG is sustained. A self-SNAG can be done; the patient performs an anterior glide to the C2 spinous process using a strap into extension with the pressure maintained until neutral. The Maitland technique has the patient prone, and the therapist performs posterior-anterior passive joint mobilisation to C2.[11]


Barany BPPV.pdf
Barany PPPD.pdf

All Barany documents

The following are very helpful free resources for learning about vertigo and dizziness.


  1. Newman-Toker, David E.; Cannon, Lisa M.; Stofferahn, Matthew E.; Rothman, Richard E.; Hsieh, Yu-Hsiang; Zee, David S. (2007-11). "Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting". Mayo Clinic Proceedings. 82 (11): 1329–1340. doi:10.4065/82.11.1329. ISSN 0025-6196. PMID 17976352. Check date values in: |date= (help)
  2. Lindell, Ellen; Finizia, Caterina; Johansson, Mia; Karlsson, Therese; Nilson, Jerker; Magnusson, Måns (2018). "Asking about dizziness when turning in bed predicts examination findings for benign paroxysmal positional vertigo". Journal of Vestibular Research: Equilibrium & Orientation. 28 (3–4): 339–347. doi:10.3233/VES-180637. ISSN 1878-6464. PMID 30149484.
  3. Peter Johns. The Big 3 of Vertigo.
  4. Kerber, Kevin A. (2020-02). "Acute Vestibular Syndrome". Seminars in Neurology. 40 (1): 59–66. doi:10.1055/s-0039-3402739. ISSN 1098-9021. PMID 31994145. Check date values in: |date= (help)
  5. Peter Johns Vertigo myth: Central vs peripheral tables help you make the diagnosis in vertigo
  6. Tintinalli, Judith E., et al. Tintinalli's emergency medicine : a comprehensive study guide. Chapter 170: Vertigo. New York: McGraw-Hill Education, 2018.
  7. Peter Johns. Vestibular Migraine- A very common but rarely diagnosed cause of vertigo. Youtube.
  8. Wilhelmsen, Kjersti; Ljunggren, Anne Elisabeth; Goplen, Frederik; Eide, Geir Egil; Nordahl, Stein Helge G. (2009-05-16). "Long-term symptoms in dizzy patients examined in a university clinic". BMC ear, nose, and throat disorders. 9: 2. doi:10.1186/1472-6815-9-2. ISSN 1472-6815. PMC 2693507. PMID 19445693.
  9. 9.0 9.1 9.2 9.3 9.4 Li & Peng. Pathogenesis, Diagnosis, and Treatment of Cervical Vertigo. Pain physician 2015. 18:E583-95. PMID: 26218949.
  10. Hahn et al.. Response to Cervical Medial Branch Blocks In Patients with Cervicogenic Vertigo. Pain physician 2018. 21:285-294. PMID: 29871373.
  11. 11.0 11.1 Li & Peng. Pathogenesis, Diagnosis, and Treatment of Cervical Vertigo. Pain physician 2015. 18:E583-95. PMID: 26218949.
  12. Magnusen 2006
  13. Brandt & Huppert. A new type of cervical vertigo: Head motion-induced spells in acute neck pain. Neurology 2016. 86:974-5. PMID: 26826207. DOI.
  14. 14.0 14.1 14.2
  15. Choi et al.. Rotational vertebral artery occlusion: mechanisms and long-term outcome. Stroke 2013. 44:1817-24. PMID: 23696552. DOI.
  16. 16.0 16.1 16.2 16.3 Grief et al. Spontaneous intracranial hypotension. Practical Neurology. May 2020. Full Text