Vertigo and Dizziness
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.
Assessing Acute Dizziness
Do not put any 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. 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. 
Busting another myth is the dreaded central vs peripheral vertigo table. Peter Johns advocates to remove this useless table from your memory as it is mostly incorrect. The proper way of categorising vertigo is into acute vestibular syndrome, episodic vestibular syndrome, and their subtypes of triggered vs spontaneous. Peter Johns recommends a simpler approach. Seeing as the most important diagnoses in acute dizziness are BPPV, vestibular neuritis, and posterior circulation stroke, he divides vertigo into "short episodes" and "long episodes." For short episodes the main diagnosis to consider is BPPV. The test is the dix-hallpike test for posterior canal BPPV. If this is negative then the supine roll test should be performed for assessing horizontal canal BPPV. For long episodes, the most important diagnoses are vestibular neuritis and posterior circulation stroke. These can be differentiated using the HINTS plus examination. When thinking about triggers, it is important to keep in mind that head movements make all causes of dizziness worse. With vestibular neuritis and CVA, the vertigo is continuous, made worse by position change.
- 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)
Outside of the above, 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).
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, paulse, and arrythmia may need to be assessed.
- Vestibular neuritis and Labyrinthitis
- Meniere's disease
- Bilateral vestibular paresis or loss
- Superior semicircular canal dehiscence and perilymph fistula
- Tumours compressing the 8th cranial nerve
- Stroke and TIA in VB arterial dissection
- Multiple sclerosis
- Chiari malformation
- Cervical vertigo
- Postural hypotension
- Hypoglycaemia and diabetes mellitus
- Medication effects
- Viral syndrome
Unlocalised vertigo syndromes
- Anxiety and panic
- Posttraumatic vertigo
- Multisensory disequilibrium of the elderly
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
- At least 5 episodes of vestibular symptoms of moderate to severe intensity
- lasting 5 min–72 h
- Migraine history
- Current or previous history of migraine +/ aura
- According to the International Classification of Headache Disorders (ICHD).
- Migraine features
- One or more migraine features++ with at least 50% of the vestibular episodes.
- 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.
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.  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.
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.
Cervical facet joints 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.
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.
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.
- Manual therapy seems to be effective.
- 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. In whiplash cervical input may be dominant over vestibular with neck activation when there is pain or stiffness.
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. 
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 cereballar systems.
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.
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.
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.
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. 
There are three subtypes making up three quarters of causes. 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.
The epidural blood patch is the mainstay of treatment.
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.
- 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
- 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
- Cervical osteoarthritis and/or IVDD
- Disc abutting cervical cord
- High cervical disease on MRI
- 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.
The following are very helpful free resources for learning about vertigo and dizziness.
- Newman-Toker et al.. Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting. Mayo Clinic proceedings 2007. 82:1329-40. PMID: 17976352. DOI.
- Peter Johns Vertigo myth: Central vs peripheral tables help you make the diagnosis in vertigo https://www.youtube.com/watch?v=0FL377pUIlA
- Peter Johns. The Big 3 of Vertigo. https://www.youtube.com/watch?v=MwbqJvMDonU
- Tintinalli, Judith E., et al. Tintinalli's emergency medicine : a comprehensive study guide. Chapter 170: Vertigo. New York: McGraw-Hill Education, 2018.
- Peter Johns. Vestibular Migraine- A very common but rarely diagnosed cause of vertigo. Youtube. https://www.youtube.com/watch?v=XPIyXiv0UKg
- Li & Peng. Pathogenesis, Diagnosis, and Treatment of Cervical Vertigo. Pain physician 2015. 18:E583-95. PMID: 26218949.
- Hahn et al.. Response to Cervical Medial Branch Blocks In Patients with Cervicogenic Vertigo. Pain physician 2018. 21:285-294. PMID: 29871373.
- Li & Peng. Pathogenesis, Diagnosis, and Treatment of Cervical Vertigo. Pain physician 2015. 18:E583-95. PMID: 26218949.
- Magnusen 2006
- Brandt & Huppert. A new type of cervical vertigo: Head motion-induced spells in acute neck pain. Neurology 2016. 86:974-5. PMID: 26826207. DOI.
- Choi et al.. Rotational vertebral artery occlusion: mechanisms and long-term outcome. Stroke 2013. 44:1817-24. PMID: 23696552. DOI.
- Grief et al. Spontaneous intracranial hypotension. Practical Neurology. May 2020. Full Text