The cause of vestibular migraines is currently unclear; however, one hypothesized cause is that the stimulation of the trigeminal nerve leads to nystagmus in individuals with migraines. Approximately 40% of all migraine patients will have an accompanying vestibular syndrome, such as vertigo, dizziness, or disruption of the balance system.Other suggested causes of vestibular migraines include the following: unilateral neuronal instability of the vestibular nerve, idiopathic asymmetric activation of the vestibular nuclei in the brainstem, and vasospasm of the blood vessels supplying the labyrinth or central vestibular pathways resulting in ischemia to these structures. Vestibular migraines are estimated to affect 1–3% of the general population and may affect 10% of people with migraine . Additionally, vestibular migraines tend to occur more often in women and rarely affect individuals after the sixth decade of life. Motion sickness
Motion sickness is common and is related to vestibular migraine. It is nausea and vomiting in response to motion and is typically worse if the journey is on a winding road or involves many stops and starts, or if the person is reading in a moving car. It is caused by a mismatch between visual input and vestibular sensation. For example, the person is reading a book that is stationary in relation to the body, but the vestibular system senses that the car, and thus the body, is moving. Alternobaric vertigo
Alternobaric vertigo is caused by a pressure difference between the middle ear cavities, usually due to blockage or partial blockage of one eustachian tube, usually when flying or diving underwater.
Persistent onset is commonly paired with central vertigo signs and symptoms.The characteristics of an episodic onset vertigo are indicated by symptoms lasting for a smaller, more memorable amount of time, typically lasting for only seconds to minutes. Pathophysiology
The neurochemistry of vertigo includes six primary neurotransmitters that have been identified between the three-neuron arc that drives the vestibulo-ocular reflex (VOR). Glutamate maintains the resting discharge of the central vestibular neurons and may modulate synaptic transmission in all three neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. Gamma-Aminobutyric acid (GABA) is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections among the cerebellar Purkinje cells, the lateral vestibular nucleus, and the vertical VOR. Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. Dopamine, histamine, serotonin, and acetylcholine are neurotransmitters thought to produce vomiting. It is known that centrally acting antihistamines modulate the symptoms of acute symptomatic vertigo. Diagnosis
Tests for vertigo often attempt to elicit nystagmus and to differentiate vertigo from other causes of dizziness such as presyncope, hyperventilation syndrome, disequilibrium, or psychiatric causes of lightheadedness.