Approach
A thorough history will indicate the most likely system to be causing the balance disorder. Balance disorders should be distinguished from syncope or presyncope, in which degrees of loss of consciousness occur and which are likely to be due to cardiovascular or neurovascular causes, and require urgent evaluation.
The subsequent physical exam should focus on the system (vestibular, cerebellar/brainstem, extrapyramidal, spinal cord, or neuromuscular) suggested by the clinical history.
History
A detailed history should ascertain:
Pattern of dizziness
Constant versus episodic
Duration (seconds to minutes, hours, days)
Provoking factors: for example, spontaneous, head movement or positional change, visual flow sensitivity, or pressure-induced stimuli (e.g., coughing, sneezing, Valsalva)
Quality of dizziness
True vertigo versus lightheadedness versus disequilibrium
Accompanying symptoms
Hearing loss, tinnitus, or autophony
Headache or ear pain, pressure, discomfort
Other neurologic symptoms (vision loss, diplopia, visual auras, dysarthria, dysphagia, weakness, numbness, paresthesias)
Background medical history
Cardiovascular risk factors such as diabetes mellitus, hypertension and hyperlipidemia
Current drug use
Smoking status
Alcohol and caffeine intake
The following historical features are suggestive of specific causes:
Recent upper respiratory tract infection: viral vestibular neuritis or labyrinthitis.
Sudden onset of symptoms: vascular event affecting cerebellum or brainstem.
Vertigo or persisting auditory symptoms (hearing loss, tinnitus) and pain or blockage: inner ear disease and a vestibular cause of the balance difficulty.
True vertigo (the perception that the environment or that the person is spinning): very common in vestibular causes, such as benign paroxysmal positional vertigo (BPPV), but is not specific for this: for example, true vertigo instead of typical lightheadedness can result from cardiovascular disease.[39]
Oscillopsia (the perception that the person’s vision is oscillating): peripheral vestibular loss or cerebellar lesions.
Double-vision: brainstem dysfunction resulting in ophthalmoplegia. May be associated with dysarthria, dysphagia, and long tract (motor or sensory) symptoms (i.e., weakness, numbness, paresthesias involving the limbs).
Speech difficulties (in particular, slurring of speech): typical of cerebellar disease.
Sudden hearing loss: posterior cerebral circulation ischemia.
Fluctuating unilateral hearing loss: Meniere disease.
Fluctuating bilateral hearing loss: rarely bilateral simultaneous Meniere disease. Raises suspicion of autoimmune inner ear disease, a condition that requires emergency treatment to reduce the risk of permanent deafness and vestibulopathy.
Prior episode of acute vertigo from which there was recovery, followed by a more recent episode with persisting vestibular symptoms: sequential viral vestibular neuritis.
Chronic progressive imbalance accompanied by progressive bilateral sensorineural hearing loss in an older patient: degenerative inner ear disease.
Chronic imbalance in a younger person with bilateral peripheral vestibular loss: may be idiopathic (“idiopathic bilateral vestibular hypofunction”), in which case hearing is typically preserved.
Chronic imbalance with congenital hearing loss: congenital bilateral vestibular loss.
Difficulty walking: ataxia from a central cause (e.g., cerebellar ataxia), spinal cause (e.g., spastic paresis), or a peripheral neuropathy.
Difficulty initiating movement, difficulty turning while walking or getting up from a chair suggests extrapyramidal disease (parkinsonism).
Weakness and sensory loss: may be reported below the level of a spinal cord lesion.
Urinary or bowel dysfunction or erectile dysfunction: spinal cord lesions.
Focal back pain: structural lesions involving the spine.
History of head trauma: inner ear damage (i.e., vestibular concussion, canalithiasis, perilymphatic fistula) or central nervous system injury (postconcussion syndrome).
Coexisting symptoms of brainstem or cerebellar involvement: multifocal disease such as multiple sclerosis.
Physical exam
The physical exam should include:
General observation during history taking
Examination of the eye
Post-headshake nystagmus test
Dix-Hallpike maneuver (if no contraindication to cervical manipulation)
Vestibulo-ocular reflex (VOR) test
Cranial nerve examination
Speech examination
Coordination and gait assessment
Motor, sensory, and autonomic function examination
Cardiovascular examination.
General appearance:
Patients should be observed during the history taking, which may direct the physical exam further. For example, a patient who is seen by the examiner to have a wide-based gait and slurred speech should have an evaluation that focuses on cerebellar function, whereas a patient with a shuffling gait who speaks in a monotone and has a tremor should be assessed for other extrapyramidal signs.
Examination of the eye:
Horizontal jerk nystagmus beating away from the side of vestibular hypofunction is typically seen in unilateral peripheral vestibular disorders.
Pure vertical or pure torsional nystagmus indicates a central lesion.
Internuclear ophthalmoplegia (limited adduction of the ipsilesional eye with abducting nystagmus of the fellow eye) may be found with midline brainstem lesions.
Ipsilesional gaze palsy may result from lesions of the sixth nerve nucleus.
Ptosis and pupillary dilation may be seen on the side of third cranial nerve lesions.
Vertical misalignment of the eyes may be seen due to a skew deviation or fourth nerve palsy.
Ipsilateral Horner syndrome (miosis, pupillary dilation lag, and partial ptosis) occurs with central sympathetic pathway lesions.
Fundoscopy should be performed, to detect optic nerve abnormalities (e.g., optic atrophy may indicate prior optic neuritis and multiple sclerosis or be related to vitamin B12 deficiency) and retinal abnormalities (e.g., retinopathy with spinocerebellar ataxia). Small amplitude nystagmus may also only be apparent on fundoscopy (direction of the nystagmus is actually in the opposite direction to what is observed on fundoscopy as the posterior pole of the eye is being viewed).
Post-headshake nystagmus test:
This should be performed only if there is suspicion that the cause is vestibular.
As the spontaneous vestibular nystagmus, seen with acute peripheral vestibular loss, resolves within a few days, the post-headshake nystagmus test may be used to transiently bring out the vestibular nystagmus and help lateralize the vestibular deficit.
The patient's head is tilted 30º forward and then rapidly rotated from side-to-side for about 30 seconds. Transient vestibular (horizontal-torsional) nystagmus beating away from the weak side is then observed. Post-headshake nystagmus is most commonly seen following peripheral vestibular loss but may also occur with central vestibular lesions.
Positional testing (Dix-Hallpike maneuver):
Perform on all patients presenting with dizziness or balance difficulty provided there is no contraindication to cervical manipulation.
With the patient in the sitting position, turn the head 45º to the side being tested, and then rapidly bring the patient to a supine position with the neck extended and hanging down over the edge of the examining table.
Transient vertigo with torsional, vertical nystagmus (top of the eyes beating towards the dependent ear; geotropic nystagmus) after a latency of several seconds with fatiguing of the response (a positive result) confirms BPPV (canalithiasis) involving the posterior semicircular canal (90% of cases of BPPV) on the tested side.
If the result is negative perform the supine roll test to assess for lateral semicircular canal BPPV.[11]
Pure vertical or torsional nystagmus indicate a central vestibular disorder.
Dizziness without nystagmus provoked by positional testing is nonspecific but may still be due to BPPV.
Head-impulse test (Halmagyi maneuver):
If peripheral vestibular nystagmus is suspected, the head impulse test should be performed.[40] This tests vestibulo-ocular reflex function and demonstrates peripheral vestibular hypofunction.
The patient is instructed to maintain visual fixation on a target straight ahead. The patient's head is tilted forward in pitch by 30º. The patient's head is slowly turned to one side by 30º and then abruptly turned back to the forward position. The same is then done with the patient's head turned to the other side. If the vestibulo-ocular reflex is intact the patient's eyes remain fixed on the target. If peripheral vestibular loss is present the eyes will move with the head during abrupt movement toward the side of vestibular weakness. The eyes will then make a saccade (fast eye movement) back to fixate on the target.
Fistula test for superior canal dehiscence (SCD):
The fistula test can be performed using pneumatic otoscopy (exerting pressure on each ear canal with a rubber bulb) while recording the eye movements. Tragal compression can also be used to transmit pressure to the inner ear.
Valsalva maneuver can precipitate dizziness and nystagmus and can be a more sensitive test for SCD.
A positive fistula test provides support for doing a temporal bone CT.
Dynamic visual acuity test:
Should be performed only if vestibulopathy is suspected.
Vestibulo-ocular reflex function may be further assessed by testing visual acuity during continuous passive oscillation of the head at a frequency of 2 Hz (dynamic visual acuity). A decrease in visual acuity by more than 2 lines from baseline may indicate a deficient vestibulo-ocular reflex resulting from peripheral or central vestibulopathy.
Cranial nerve exam:
Examination of the remaining cranial nerves should be completed; deviation of the uvula or protruding tongue, and abnormal gag reflex are features of a lower cranial nerve palsy caused by a brainstem lesion.
Coordination, movement, and gait assessment:
Finger-to-nose testing is used to assess for upper extremity dysmetria (incoordination). Lesions of the cerebellar hemisphere result in contra-axial dysmetria of the ipsilateral arm. Heel-to-shin testing may be performed to assess for lower extremity dysmetria. Dysdiadochokinesis, an inability to perform rapid alternating movements, may be seen with cerebellar disease.
Patients are viewed while walking, then asked to walk in a straight line heel to toe (tandem walk). Cerebellar vermis lesions may cause an unsteady broad-based gait. In these cases tandem walk is also poor or cannot be performed.
Difficulty initiating movement, including turning while walking or getting up from a chair, and a shuffling gait suggests an extrapyramidal cause such as Parkinson disease. Spasticity causing a scissoring gait is seen in spinal cord lesions that result in upper motor neuron changes.
A positive Romberg test, where there is an inability to maintain posture with the feet together and the arms folded, indicates loss of proprioception from a peripheral neuropathy or a cerebellar lesion. Difficulty in sitting up without support (truncal ataxia) is commonly present in patients with cerebellar vermis lesions.
Motor, sensory, and autonomic nerve assessment:
The distribution of peripheral nerve involvement is important in generating a differential diagnosis: for example, multiple selected peripheral nerves involved (mononeuropathy multiplex from demyelinating neuropathy or vasculitis) versus a length-dependent sensory motor polyneuropathy (axonal dying back of fibers from toxic/metabolic damage).
Motor signs: hypertonia is an upper motor neuron sign and occurs in lesions of the cerebral white matter and corticospinal tract. Cogwheeling rigidity is a feature of extrapyramidal disease. Other signs associated with an upper motor neuron lesion include pyramidal distribution weakness, hyperreflexia, and an extensor plantar response. Lower motor neuron signs may occur with cervical or lumbar spine lesions. Lower motor neuron lesions cause muscle atrophy, muscle fasciculations, hyporeflexia, and muscle weakness.
Sensory signs: posterior column lesions result in loss of joint position sense. Spinothalamic tract lesions result in loss of temperature and pinprick sensation. A sensory level may be found over the trunk 2 to 3 dermatomes above the level of a spinal cord lesion. Small fiber loss results in loss of pinprick and temperature sensation. Large sensory fiber loss results in loss of joint position sense and vibration.
Abdominal reflexes may be lost with spinal cord lesions above T8. Beevor sign (movement of the umbilicus toward the neck with neck flexion) may result from lower abdominal weakness from a spinal lesion at the T10 level.
Autonomic: measure BP lying and then standing to examine for orthostatic hypotension. Schirmer test may be performed to confirm decreased tear production. Pupillary examination may show light-near dissociation.
Musculoskeletal abnormalities: pes cavus deformity or kyphoscoliosis may indicate a chronic or inherited disorder of the peripheral nerves: for example, Charcot-Marie-Tooth disease. Degenerative arthritis may occur as a complication of neuropathy (Charcot joints).
HINTS (Head-Impulse, Nystagmus, Test of Skew deviation):
Perform on patients with sudden-onset of symptoms and persistent vertigo over hours or days to help identify patients with central vertigo.[35]
3-step oculomotor exam. Results suggestive of central vertigo include negative head-impulse test (lack of corrective saccade), nystagmus with a vertical or rotatory element, bidirectional nystagmus, and abnormal movement (often with vertical diplopia) on test of skew.
HINTS Plus exams also include an auditory function assessment.
The HINTS and HINTS Plus exams appear to be more sensitive for stroke than early MRI.[36][37]
Vestibular findings on physical exam
Nystagmus:
Occurs with acute unilateral or asymmetric bilateral peripheral vestibular loss.
Characteristically mixed horizontal-torsional jerk form with the top of the eyes beating away from the side of vestibular weakness.
Becomes more severe with lateral gaze in the direction it is beating and dampens with gaze in the opposite direction and is suppressed by visual fixation.
Dizziness with vertical-torsional jerk nystagmus on Dix-Hallpike maneuver suggests BPPV.
Positive (head impulse test or Halmagyi maneuver) to the side of peripheral vestibular loss.[40]
Post-headshake nystagmus is most commonly seen following peripheral vestibular loss but may also occur with central vestibular lesions.[41]
A decrease in visual acuity on dynamic visual acuity testing may indicate a deficient vestibulo-ocular reflex caused by peripheral vestibulopathy.
Ataxia associated with oscillopsia in the absence of nystagmus is suggestive of bilateral peripheral vestibular loss.
Cerebellum findings on physical exam
Nystagmus:
Gaze-evoked nystagmus is seen as eyes beating toward the direction of gaze (vertical or horizontal) on attempted eccentric gaze. After the eyes are returned to primary position transient nystagmus beating in the opposite direction may occur (rebound nystagmus). Pure vertical or torsional nystagmus may also occur.
Pursuit eye movements may become saccadic (ratchety) with cerebellar lesions. This can be easily demonstrated by having the patient track a small horizontally or vertically moving target (e.g., following a pen top).
Saccadic eye movements may demonstrate overshoot dysmetria (eyes move on command from one target to another but overshoot the second target) and a refixation saccade is seen back toward the intended fixation target.
Speech may be affected resulting in slurring or staccato-type speech.
Impaired coordination:
Limb dysmetria: overshooting of limb on finger-to-nose or heel-to-shin testing.
Dysdiadochokinesis, an inability to perform rapid alternating movements, may also be seen with cerebellar disease.
Wide-based gait and truncal ataxia.
Sway is present with Romberg testing.
Brainstem findings on physical exam
Brainstem lesions can disrupt cerebellar pathways and cause the same physical signs as those for cerebellar lesions. The following are additional physical findings associated with a brainstem lesion.
Abnormalities in eye exam:
Back-to-back saccadic oscillations (ocular flutter) may be seen in patients with brainstem encephalitis.
Internuclear ophthalmoplegia (limited adduction of the ipsilesional eye with abducting nystagmus of the fellow eye) suggests a midline brainstem lesion.
Ipsilesional gaze palsy suggests lesions of the sixth nerve nucleus.
Ptosis and pupillary dilation may be seen on the side of third cranial nerve lesions.
Vertical misalignment of the eyes may be seen due to a skew deviation or fourth nerve palsy.
Deviation of the uvula or protruding tongue, and abnormal gag reflex, are features of a lower cranial nerve palsy.
Central sympathetic pathway lesions result in ipsilateral Horner syndrome, consisting of:
Miosis
Pupillary dilatational lag
Partial ptosis
Extrapyramidal findings on physical exam
Parkinsonism:
Lesions involving the basal ganglia result in bradykinesia; pill-rolling resting tremor of the hands; rigid muscle tone; hypophonia; loss of postural reflexes; postural instability.
Voice changes:
In progressive supranuclear palsy, the voice may take on an explosive or spastic quality and apraxia of speech may occur with corticobasal degeneration.
Myerson sign:
An inability to inhibit reflex blinking when repetitively tapped on the glabella.
Hypomimia:
The face may lack expression and appear mask-like.
Ocular motor abnormalities:
Hypometric saccades, irregular pursuit eye movements, and square wave jerks.
Vertical gaze palsy may occur with progressive supranuclear palsy.
Orthostatic hypotension:
Resulting from autonomic nervous system involvement; may be associated with parkinsonism in Shy-Drager syndrome.
Upper motor neuron signs:
Pyramidal weakness; hyperreflexia; extensor plantar responses.
Other:
Visual or sensory hemineglect or alien limb syndrome.
Spinal cord findings on physical exam
Upper motor neuron signs (corticospinal tract lesions):
Spastic muscle tone
Pyramidal distribution weakness
Hyperreflexia
Extensor plantar responses
Lower motor neuron signs (cervical or lumbar spine lesions):
Muscle atrophy
Muscle fasciculations
Hyporeflexia
Muscle weakness
Sensory signs:
Loss of joint position sense (posterior column lesions) may result in sway on Romberg testing
Loss of temperature and pinprick sensation (spinothalamic tract lesions)
A sensory level may be found over the trunk 2 to 3 dermatomes above the level of a spinal cord lesion
Reflexes:
Abdominal reflexes may be lost with spinal cord lesions above T8
Beevor sign (movement of the umbilicus toward the neck with neck flexion) may result from lower abdominal weakness from a spinal lesion at the T10 level
Neuromuscular findings on physical exam
Motor nerve denervation, which results in:
Muscle atrophy
Fasciculations
Weakness of the muscles affected
Loss or diminution of reflexes due to interruption of the reflex arc
Small sensory nerve loss, which results in:
Loss of pinprick sensation
Loss of temperature sensation
Large sensory fiber loss, which results in:
Loss of joint position sense
Loss of vibration sense
Autonomic nerve loss, which results in:
Orthostatic hypotension (on BP measurement)
Decreased tear production (confirm with Schirmer test)
Light-near dissociation on pupillary exam
The following musculoskeletal abnormalities may arise from peripheral neuropathies:
Pes cavus deformity
Kyphoscoliosis
Degenerative arthritis as a complication of neuropathy (Charcot joints)
Investigations
For all patients with possible vestibular disease the first-line tests include:
Caloric electronystagmography (ENG)
Rotary chair testing
Audiometry
Caloric ENG: water or air is used to stimulate the horizontal semicircular canal. The resulting nystagmus is measured. Responses to warm and cold stimuli are measured from each ear, and compared between ears. Reduced caloric responses are seen with peripheral vestibular hypofunction. Bilaterally increased responses may be observed in central vestibular diseases.[42][43]
Rotary chair testing: measures VOR gain, phase, symmetry, and time constant. Poorly compensated unilateral peripheral vestibular loss such as from viral vestibular neuritis results in reduced VOR gain, VOR phase lead, shortening of the VOR time constant, and rotational bias toward the side of vestibular hypofunction. With bilateral vestibular hypofunction such as resulting from exposure to ototoxic medication the VOR gain is very low and there is VOR phase lead with marked shortening of the VOR time constant. Central vestibular lesions can result in a prolonged VOR time constant.
Audiogram and auditory brainstem responses (ABRs): pattern of hearing loss may provide diagnostic information. Fluctuating low frequency sensorineural hearing loss is typically seen with Meniere disease. Unilateral sensorineural hearing loss may result from viral labyrinthitis, inner ear trauma, or retrocochlear pathology (e.g., vestibular schwannoma). Pseudo-conductive hearing loss may occur with SCD.
Other investigations to exclude specific diseases:[44][45]
MRI scan of the brain and temporal bones to exclude posterior fossa lesions including tumor, strokes, and demyelinating disease
CT of temporal bones if SCD is suspected. May also diagnose temporal bone fracture in post-traumatic vertigo, or reveal erosions in the bony labyrinth from inflammatory or iatrogenic causes
MRI of the spine when myelopathy is suspected
CT or MR angiography if vertebrobasilar insufficiency is suspected
Nerve conduction studies and electromyography when peripheral neuropathy is suspected (e.g., Guillain-Barre syndrome)
Vitamin B12 and methylmalonic acid level and blood film (subacute combined degeneration of the cord)
Serum antinuclear antibodies if lupus myelopathy is suspected
Serum thiamine level in suspected cases of Wernicke encephalopathy
Anti-GQ1b antibody titers in suspected cases of Miller Fisher syndrome
Cerebrospinal fluid (CSF) exam if meningitis is suspected
Neuromyelitis optica (NMO)-IgG titer in cases of suspected neuromyelitis optica
HIV testing if vacuolar myelopathy is suspected
Polymerase chain reaction for human T-lymphotropic virus (HTLV)-1 antigen, CSF/serum HTLV-1 antibody titer ratio for HTLV-1 associated myelopathy
Tuberculosis nucleic acid amplification test and chest x-ray in suspected cases of Pott disease
Venereal disease research laboratory (VDRL) test with serum fluorescent treponemal antibody absorption (FTA-ABS) if neurosyphilis is suspected, also CSF FTA-ABS
Anti-Yo, Ma, or Ri antibody titers in cases of suspected paraneoplastic cerebellar syndromes
Serum alpha-tocopherol if vitamin E deficiency is suspected
Serum immunoglobulin A-tissue transglutaminase titer if suspected celiac disease
Chest x-ray and mammograms to look for primary tumor in cases of metastatic disease
Serum prostate-specific antigen if prostate cancer is the suspected primary tumor
Use of this content is subject to our disclaimer