Mackenzie Vestibular cheat sheet

Semicircular canals sense angular acceleration; the two horizontal canals lie roughly 30 degrees off horizontal, so they are best excited by yaw rotation about a slightly tilted axis.

Semicircular canal afferents fire tonically at rest (~70-100 spikes/s in primates); ampullopetal flow excites horizontal canal hair cells while ampullofugal flow inhibits them; vertical canals show the opposite polarity.

Otolith organs: utricle is roughly horizontal and senses horizontal linear acceleration and head tilt; saccule is roughly vertical and senses vertical linear acceleration including gravity.

Ewald's laws: response to ampullopetal stimulation exceeds ampullofugal response in the horizontal canal, and excitation is the more effective direction for vertical canals.

Vestibulo-ocular reflex latency is short (~5-7 ms) with three-neuron arc from Scarpa's ganglion to vestibular nuclei to abducens/oculomotor nuclei.

VOR gain is normally near 1.0 for high-acceleration head turns; gain falls with age and with unilateral or bilateral vestibular loss.

Vestibulospinal pathways: lateral vestibulospinal tract from lateral vestibular nucleus facilitates ipsilateral extensor tone; medial vestibulospinal tract coordinates head and neck posture.

Velocity storage prolongs the horizontal VOR time constant (to roughly 15-20 s) and is responsible for the slow phase of caloric nystagmus persisting beyond the stimulus.

Duration is the strongest triage rule: seconds suggests BPPV, minutes to hours suggests vestibular migraine or Meniere disease, and days suggests vestibular neuritis, stroke, or concussion.

Trigger pattern: position change triggers BPPV; spontaneous episodes without trigger suggest migraine or Meniere; constant unsteadiness suggests bilateral loss or central disease.

Meniere disease: recurrent spontaneous vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency hearing loss, tinnitus, and aural fullness; low-frequency SNHL on audiogram supports it.

Vestibular neuritis: acute prolonged vertigo with positive head impulse test, no focal neurologic signs, no new hearing loss; superior division involvement is most common.

Vestibular migraine criteria include at least five episodes of vestibular symptoms lasting 5 minutes to 72 hours with a personal or family history of migraine, per Bárány Society criteria.

HINTS exam for acute vestibular syndrome: normal head impulse plus direction-changing nystagmus plus skew deviation suggests central lesion; all three peripheral-pattern findings favor peripheral cause.

Presyncope, orthostatic symptoms, and palpitations suggest cardiovascular cause; bilateral symptoms with oscillopsia point to bilateral vestibulopathy or central disease.

Red flags for central cause: new headache or neck pain, diplopia, dysarthria, dysphagia, hemianesthesia, truncal ataxia, vertical or direction-changing nystagmus, and inability to stand unassisted.

Head impulse test: grasp head, ask patient to fixate a target, deliver quick 10-20 degree low-amplitude thrusts unpredictably; corrective saccade indicates reduced VOR gain on that side.

Nystagmus: note direction, whether it is spontaneous or gaze-evoked, and whether it suppresses with fixation; peripheral nystagmus is horizontal with a torsional component and unidirectional.

Dix-Hallpike maneuver tests posterior canal: head turned 45 degrees toward tested ear, patient moved rapidly from sitting to supine with neck extended 20 degrees; upbeating torsional nystagmus with latency and fatigue is positive.

Supine roll test tests horizontal canal: head turned 90 degrees to each side while supine; geotropic nystagmus is more intense on the affected side, apogeotropic on the unaffected side.

Skew deviation: alternate cover test in primary gaze; vertical corrective movement indicates skew and suggests central lesion.

Head-shaking nystagmus: 20 seconds of horizontal head shaking at about 2 Hz; a single direction of nystagmus suggests peripheral asymmetry, and direction reversal suggests central lesion.

Dynamic visual acuity: compare visual acuity with head still versus during passive head oscillation at about 2 Hz; a drop of two lines or more suggests VOR deficit.

Romberg and Fukuda stepping tests: increased sway with eyes closed and feet together suggests vestibular or proprioceptive loss; Fukuda rotation of more than 45 degrees suggests asymmetric tone.

Caloric testing uses bithermal water or air at 30 and 44 degrees C; COWS mnemonic: cold-opposite, warm-same for the slow phase direction; reduced response is calculated with Jongkees formula.

Jongkees formula: unilateral weakness = ((right warm + right cool) minus (left warm + left cool)) divided by total of all four responses, times 100; 25 percent or more is generally abnormal.

vHIT measures VOR gain at high head velocities (roughly 150-250 degrees/s); gain below about 0.8 with corrective saccades suggests hypofunction; it can miss partial deficits.

cVEMP: loud clicks or tone bursts (500 Hz) recorded from sternocleidomastoid; tests saccule and inferior vestibular nerve; response is reduced in inferior vestibular neuritis.

oVEMP: recorded below the eyes with upward gaze; tests utricle and superior vestibular nerve; absent responses suggest superior division involvement.

Rotary chair sinusoidal testing quantifies VOR gain, phase, and symmetry; it can test low frequencies and is useful in bilateral vestibulopathy and suspected central disease.

VNG oculomotor subtests include saccades, smooth pursuit, optokinetic nystagmus, and gaze holding; abnormalities suggest central rather than peripheral disease.

Test timing and medication matter: suppressant drugs and acute symptoms can alter caloric and rotational results; document medications and time since symptom onset.

Posterior canal BPPV is most common (roughly 60-90 percent), then horizontal canal, then anterior canal; posterior canal is diagnosed with Dix-Hallpike.

Epley canalith repositioning: starting from Dix-Hallpike position, rotate head 90 degrees to opposite side, then roll patient to side and prone, then sit up; each position held until nystagmus settles.

Semont liberatory maneuver: rapid swing from affected side to opposite side through sitting; useful for posterior canal with persistent symptoms.

Horizontal canal geotropic nystagmus: use Lempert (barbecue) 360-degree roll or Gufoni maneuver; apogeotropic variant uses Gufoni or forced prolonged positioning.

Post-maneuver instructions commonly include avoiding lying flat and avoiding rapid head movements for 24-48 hours, though evidence for restriction is limited.

Treatment response is assessed by repeat Dix-Hallpike or supine roll; if negative and symptoms resolve, no further maneuver is needed.

Persistent nystagmus lasting more than about one minute or atypical direction should prompt reconsideration of central cause or canal conversion.

Canal conversion can occur after repositioning, most often to horizontal canal; re-test with supine roll if new rotational vertigo appears.

Vestibular rehabilitation is built on habituation, adaptation of the VOR, and substitution with visual, somatosensory, and motor strategies.

Gaze stabilization exercises use small-amplitude head rotations while fixating a target; they drive VOR adaptation and are dosed by symptom provocation and duration.

Unilateral hypofunction: early mobilization and vestibular rehabilitation improve compensation; static positional avoidance can delay recovery.

Bilateral vestibulopathy: focus on substitution, balance training, and fall prevention; oscillopsia and unsteadiness in the dark are typical.

Static and dynamic balance training should progress from firm to compliant surfaces and from eyes open to eyes closed, with safety guarding.

Symptom exacerbation during exercises is expected and should be brief; prolonged nausea or vomiting suggests the dose is too high.

Outcome measures include Dizziness Handicap Inventory, Dynamic Gait Index, Timed Up and Go, and computerized posturography.

Home exercise programs require documented instruction, frequency, and a follow-up plan; adherence and fall risk should be reviewed at each visit.

Central patterns: direction-changing or vertical nystagmus, impaired smooth pursuit, saccadic dysmetria, abnormal optokinetic responses, and normal head impulse with acute vertigo.

Cerebellar lesions can produce downbeat nystagmus; vestibular nucleus lesions can produce upbeat or torsional nystagmus; these patterns warrant neuroimaging.

Vertebrobasilar insufficiency can cause vertigo with diplopia, dysarthria, dysphagia, ataxia, or drop attacks; symptoms are often abrupt and may be positional.

Concussion-related dizziness often combines vestibular, ocular-motor, cervicogenic, and autonomic components; screen for headache, photophobia, and exertion intolerance.

VOMS assessment includes smooth pursuit, saccades, convergence, VOR, and visual motion sensitivity; symptom provocation of 2 or more points is considered positive.

Cervicogenic dizziness is diagnosed clinically after ruling out other causes; it is associated with neck pain and improves with cervical proprioceptive training.

Persistent postural-perceptual dizziness is a functional disorder with persistent unsteadiness and visual motion sensitivity lasting 3 months or more; treatment is rehabilitation and cognitive behavioral therapy.

Return-to-activity progression after concussion should be gradual and symptom-limited, with medical clearance for high-risk or contact activity.

Informed consent for vestibular testing should cover the nature of testing, expected dizziness or nausea, fall risk, and alternatives.

Fall precautions during caloric, rotary chair, and repositioning procedures include a clear path, seated recovery, and assistance for patients with balance deficits.

Document test parameters, patient position, symptom report, nystagmus characteristics, and interpretation separately from the raw findings.

Record medications that affect vestibular function, including suppressants, and note time since last dose.

Follow infection control and equipment cleaning protocols for goggles, electrodes, and chair surfaces between patients.

Scope of practice varies by jurisdiction; technicians may perform testing but interpretation and diagnosis remain with the licensed clinician.

Report critical findings, such as suspected central lesion or sudden hearing loss, to the referring provider promptly and document the communication.

Reimbursement documentation should link the diagnosis, the test performed, and the medical necessity; avoid vague phrases without objective findings.