| Vertigo Classification and external resources |
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| ICD-9 | 438.85 |
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| eMedicine | neuro/ |
Vertigo (from the Latin vertigin-, vertigo, "dizziness," originally "a whirling or spinning movement," from vertere "to turn"[1]) is a specific type of dizziness, a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is actually stationary with respect to the surroundings.
There are two types of vertigo: subjective and objective. There is a subjective vertigo when a person has a false sensation of movement. In the case of objective vertigo, the surroundings appear to move past a person's field of vision.
The effects of vertigo may be slight. It can cause nausea and vomiting and, in severe cases, it may give rise to difficulties with standing and walking.
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Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the syndrome and Meniere's disease.
Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or viruses.
Vertigo is typically classified into one of two categories depending on the location of the damag vestibular pathway. These are peripheral or central vertigo. Each category has a distinct set of characteristics and associated findings.
Vertigo can also occur after long flights or boat journeys where the mind gets used to turbulence, resulting in a person's feeling as if he is moving up and down. This usually subsides after a few days.
Vertigo can also occur when exposed to high levels of sound pressure rattling the inner ear in which throwing off ones balance and others.
The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles.
Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA.
Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and 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. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.
The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholine, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.
Tests of vestibular system (balance) function include electronystagmography (ENG), rotation tests, Caloric reflex test,[2] and Computerized Dynamic Posturography (CDP).
Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER).
Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT or CT).
Treatment is specific for underlying disorder of vertigo:
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