The vestibular system functions to detect the position and movement of our head in space. This allows for the coordination of eye movements, posture, and equilibrium. The vestibular apparatus found in the inner ear helps to accomplish this task by sending afferent nerve signals from its individual components. The utricle and the saccule are responsible for sensing linear acceleration, gravitational forces, and tilting of the head. The neuroepithelium found in the utricle and saccule is the macula which provides neural feedback about horizontal motion from the utricle and vertical motion from the saccule. Embedded within the otolithic membrane of the macula are small calcium carbonate crystals known as otoliths that assist in hair cell response to the inertial drag of endolymph. Angular acceleration and rotation of the head in various planes are sensed by the three semicircular ducts that are oriented at right angles to one another. Each of the semicircular ducts contains a dilation near the opening to the utricle. This dilation is called the ampulla which contains a neuroepithelial structure called the "crista ampullaris." The crista ampullaris is coated by a gelatinous protein-polysaccharide substance known as the cupula which holds the hair cells in place. Unlike the macula, the crista ampullaris does not contain otoliths. In addition to the functions associated with the peripheral vestibular system, the central vestibular system allows for processing and interpretation of afferent signals and the output of efferent signals. Efferent signals include the vestibulo-ocular reflex, which allows the eyes to remain fixed on an object while the head is moving. This is accomplished by coordinating movement between both eyes involving the parapontine reticular formation and output to various extraocular eye muscles involving the oculomotor and abducens nerves. The vestibulospinal reflex maintains balance and posture through the coordination of spinal musculature with head movement. Cognitive functions that involve the central vestibular system are based on established neural pathways, although many pathways are still unknown. The known central vestibular connections include the vestibulo-thalamo-cortical tract, dorsal tegmental nucleus to entorhinal cortex tract, and nucleus reticularis pontis oralis to hippocampus tract. These tracts form a series of complex connections that play a functional role in self-motion perception, spatial navigation, spatial memory, and object recognition memory.[3][2][6][1]

The mechanism involved with the function of the peripheral vestibular system involves the acceleration of endolymph within the various structures of the vestibular apparatus. Head movement in various directions is responsible for this acceleration that results in the stimulation of the stereocilia of hair cells. When the head stops accelerating, hair cells return to their baseline position which allows them to respond to further changes in endolymph acceleration. Depending on the direction of acceleration, the inertial drag of the endolymph will push the stereocilia either towards or away from the fixed kinocilium. Movement towards the kinocilium causes tip links to pull open cation channels resulting in depolarization of the hair cell via potassium ion influx. Movement away from the kinocilium results in closure of the cation channels and hyperpolarization and reduction in afferent firing rates. Depolarization results in the opening of calcium channels. Calcium channel opening results in neurotransmitter release across the synaptic cleft, leading to nerve transmission to the vestibular ganglion. Nerve signals pass through the 20,000 bipolar neurons in the vestibular ganglion and leave along the vestibular nerve. The vestibular nerve joins the cochlear nerve and enters the brainstem at the pontomedullary junction. The primary processor of vestibular signals is the vestibular nucleus complex that extends from the rostral medulla to the caudal pons. Many signals are sent from the vestibular nucleus to either the thalamus, cortex, or cerebellum that help to process and adjust efferent signals to postural or ocular muscles. Of note, the hippocampus plays an important role in spatial memory, including the functions of navigation and orientation.[6][1][7]

Many tests can help determine if the vestibular system is functioning properly. The oculocephalic reflex is a simple test used to determine if the brainstem of a comatose patient is intact using the reflexes of the vestibular system. The test involves rotating a patient’s head horizontally, which should activate the vestibular system on the ipsilateral side of rotation. This results in the patient’s eyes slowly deviating to the side opposite of head movement if the brainstem is intact. If the brainstem is not intact, the eyes will follow the movement of the head to the ipsilateral side.

Caloric testing is a test that uses differences in temperature to diagnose damage to the acoustic nerve. A small amount of cold water or air is gently delivered into one of your ears. Your eyes should show an involuntary movement called nystagmus. Then they should turn away from that ear and slowly back. If water is used, it is allowed to drain out of the ear canal. Next, a small amount of warm water or air is gently delivered into the same ear. Again, your eyes should show nystagmus. Then they should turn toward that ear and slowly back. [10]

More specific tests for components of vestibular function includes videonystagometry, the most common vestibular function test. The test is divided into three parts including ocular motor, positional testing, and caloric testing. Other diagnostic modalities include rotation tests and video head impulse testing (VHIT). Both of these tests use devices to monitor eye movements when the head is rotated in various directions to test the integrity of the vestibulo-ocular reflex.[3][11]

Dysfunction of the vestibular system can manifest symptomatically as vertigo, nausea, vomiting, visual disturbance, hearing changes, and various cognitive deficits. The relationship of the vestibular system to cognition is not well understood, but many patients with vestibular dysfunction exhibit impairment of spatial navigation, learning, memory, and object recognition. The pathophysiology of vertigo can be defined as peripheral or central. Peripheral vertigo is more common than central vertigo, and three of the most common etiologies include benign paroxysmal positional vertigo, Meniere disease, and viral labyrinthitis.

Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo and lasts for seconds to minutes. Most cases are idiopathic but the pathophysiology is believed to be due to displaced otoconia in the posterior semicircular canal that causes an inappropriate sensation of movement. BPPV is diagnosed based on a thorough history and use of the Dix-Hallpike test with associated reproduction of vertigo symptoms and nystagmus. There are many movement techniques used to treat BPPV; however, the Epley maneuver is often cited as being one of the most effective. The technique involves rotating and tilting the head and body in various ways to reposition displaced otoconia in the inner ear. For acute, severe exacerbations of BPPV, anti-vertigo medications are indicated to help with symptom control.

Meniere disease is another cause of peripheral vertigo that can last for hours and also manifest with symptoms of hearing loss and tinnitus. The pathophysiology of Meniere disease is the expansion of endolymph volume within the membranous labyrinth. This volume expansion impacts both the vestibular apparatus and cochlea that are both filled with endolymph. Expansion of endolymph within the cochlear duct results in defects in hearing that differentiate it from BPPV. Meniere disease is diagnosed based on clinical criteria, and currently, no curative treatments exist. Symptoms are managed with anti-vertigo medications, low-salt diet, and surgical decompression of the endolymphatic sac as a last option.

Viral labyrinthitis, also known as "vestibular neuritis," is another cause of peripheral vertigo that can be attributed to inflammation of the vestibular nerve, secondary to a viral infection. Symptoms include a simultaneous loss of hearing and balance function in the affected ear that can last from days to weeks. Treatment involves symptom control with anti-vertigo medications, and symptoms will typically resolve in one to three weeks. In addition to the pathologies listed, vestibular function in the elderly has been well studied as a contributing factor to dizziness and imbalance leading to falls. This is due to the significant loss of both Type 1 and Type 2 hair cells that occurs most prominently between the ages of 65 and 70.[3][12][7][13]

Salicylate (aspirin) can reversibly eliminate outer hair cell electromotility to induce hearing loss. Salicylate competitively binds to the motor protein reversibly inhibiting electromotility. Other symptoms of aspirin toxicity include nausea, vomiting, tinnitus, hyperpnea, and disorientation. Other common ototoxic agents include aminoglycosides, furosemide, cisplatin, and quinines.[14]