Mackenzie Vestibular key terms

A swelling at one end of each semicircular canal that houses the cupula and hair cells. Angular head acceleration bends the cupula, changing afferent firing and driving the vestibulo-ocular reflex.

A gelatinous diaphragm spanning the ampulla of each semicircular canal. Endolymph flow deflects it, bending stereocilia and converting angular acceleration into neural signals.

The utricle and saccule, which detect linear acceleration and head tilt through otoconia-loaded maculae. They contribute to gravity-referenced posture and to vertical and torsional eye movements.

Tiny calcium carbonate crystals resting on the maculae of the utricle and saccule. When they dislodge into a canal, they cause canalithiasis, the usual mechanism of benign paroxysmal positional vertigo.

The potassium-rich fluid filling the membranous labyrinth. Its movement deflects the cupula and bends hair cell bundles, and its volume balance is central to Meniere disease.

A three-neuron reflex arc that moves the eyes opposite to head motion, stabilizing gaze. Its gain and latency are measured by head impulse testing and rotary chair, and it can be adapted through rehabilitation.

Descending pathways carrying vestibular signals to spinal motor neurons. They support postural tone and balance reactions, which is why vestibular loss produces sway and falls.

A central mechanism that prolongs and integrates vestibular signals beyond the peripheral time constant. It shapes nystagmus duration and is assessed with rotational and caloric testing.

Brief vertigo triggered by specific head position changes, caused by displaced otoconia in a semicircular canal. Diagnosis rests on positional testing showing characteristic nystagmus, and it resolves with canalith repositioning.

Free-floating otoconia within a semicircular canal, the most common mechanism of positional vertigo. It produces brief, fatigable nystagmus with a latency after the position change.

Otoconia adherent to the cupula rather than floating freely. It typically causes persistent positional nystagmus without latency, and it may respond less readily to standard repositioning maneuvers.

A positional test in which the seated patient's head is turned and lowered rapidly past the bed edge. A positive response is upbeating, torsional nystagmus with latency and reversal, indicating posterior canal involvement.

A canalith repositioning sequence of four timed head positions that walks posterior canal debris toward the utricle. It is the standard office treatment for posterior canal benign paroxysmal positional vertigo.

Positional vertigo arising from the lateral canal, diagnosed with the supine roll test. It shows direction-changing horizontal nystagmus, and treatment uses a barbecue roll or Gufoni maneuver.

The lateral canal positional test: the supine patient's head is turned quickly to each side. Geotropic or apogeotropic horizontal nystagmus identifies the affected ear and canalith location.

Horizontal nystagmus that beats toward the lower ear on lateral head turning. In the roll test it suggests free-floating debris in the horizontal canal.

Horizontal nystagmus beating away from the lower ear during lateral head turning. It often reflects debris adherent to or near the cupula of the horizontal canal.

Nystagmus present without provocative positioning or head movement. Its direction, waveform, and suppression by fixation help separate peripheral from central causes.

The observation that spontaneous peripheral nystagmus increases in intensity when gaze is directed toward the fast phase. It supports a peripheral rather than central localization.

A bedside maneuver in which the examiner delivers brief, unpredictable, high-acceleration head turns while the patient fixates. An overt or covert catch-up saccade indicates reduced vestibular function on that side.

A corrective eye movement that brings gaze back to target after a deficient vestibulo-ocular reflex. Overt saccades occur during the head turn; covert saccades occur after it and are seen best with recording.

A laboratory version of the head impulse maneuver that records eye velocity with high-speed video. It quantifies canal-specific vestibulo-ocular reflex gain and detects covert catch-up saccades.

Bithermal irrigation of each ear that induces endolymph convection and horizontal nystagmus. Comparing responses quantifies unilateral weakness and helps identify a reduced vestibular response.

A caloric calculation comparing the summed responses of the two ears. A significant asymmetry suggests reduced function on one side, though it does not by itself establish the cause.

A battery using infrared video goggles to record eye movements during oculomotor, positional, and caloric subtests. It documents nystagmus characteristics and quantifies caloric responses.

A test averaging surface electromyographic responses from the neck during loud sound or vibration. It assesses saccular and inferior vestibular nerve function and helps localize lesions.

A test recording brief extraocular muscle responses to loud sound or bone vibration. It reflects utricular and superior vestibular nerve function and complements cervical testing.

Controlled whole-body rotation that measures vestibulo-ocular reflex gain, phase, and symmetry across frequencies. It can identify bilateral loss and central adaptation abnormalities when other tests are inconclusive.

The normal dampening of nystagmus when the patient fixates on a target during caloric or rotational stimulation. Failure to suppress suggests a central vestibular disorder.

Reduced function of one labyrinth or vestibular nerve, producing vertigo, imbalance, and nystagmus acutely. Rehabilitation uses gaze stabilization and habituation to promote central compensation.

Loss of vestibular function in both ears, causing oscillopsia and unsteadiness that worsen in darkness or on uneven ground. Management emphasizes balance training and fall prevention rather than positional maneuvers.

The illusion that the environment bounces or blurs during head movement. It reflects a failing vestibulo-ocular reflex and is a hallmark of bilateral vestibular loss.

Rehabilitation in which the patient holds a target steady while rotating the head, progressively increasing speed and background complexity. It drives vestibular adaptation and reduces oscillopsia.

Repeated controlled exposure to movements that provoke symptoms, aiming to reduce the response over time. It is used for motion sensitivity and persistent postural-perceptual dizziness.

Mismatch among vestibular, visual, and somatosensory information about body motion. It underlies motion sickness and contributes to dizziness after concussion or vestibular loss.

Increased volume and pressure of endolymph within the inner ear. It is the presumed mechanism of Meniere disease, producing episodic vertigo, fluctuating hearing loss, tinnitus, and aural fullness.

A recurrent vestibular syndrome with episodic vertigo and migrainous features such as headache, photophobia, or aura. It is a common cause of episodic dizziness and is diagnosed clinically.

Chronic subjective dizziness lasting months, worsened by upright posture, motion, and visual complexity. It is a functional diagnosis managed with education, rehabilitation, and sometimes medication.

Findings such as limb ataxia, dysmetria, and gait instability that point to cerebellar involvement. In dizziness evaluation they raise concern for a central cause and warrant urgent workup.

A bedside triad of head impulse, nystagmus direction, and test of skew used in acute vestibular syndrome. A normal head impulse with direction-changing nystagmus or skew suggests stroke rather than vestibular neuritis.

Screening after head injury for dizziness, imbalance, and oculomotor or vestibular deficits. Findings guide graded return to activity and referral for targeted rehabilitation.