Lightheadedness and vertigo pathophysiology
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Differentiating Lightheadedness and Vertigo from Other Symptoms |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Pathophysiology
- Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the brain, or with the nerve connections between these two organs.
- The most common cause of vertigo is benign paroxysmal positional vertigo, or BPPV. Vertigo can be a symptom of an inner ear infection. Vertigo can be a symptom of an underlying harmless cause, such as in BPPV or it can suggest more serious problems. These include drug toxicities (specifically gentamicin), strokes or tumors(though these are much less common than BPPV), syphilis.
- Vertigo can also be brought on suddenly through various actions or incidents, such as skull fractures or brain trauma, sudden changes of blood pressure, or as a symptom of motion sickness while sailing, riding amusement rides, airplanes or in a motor vehicle. Vertigo can also be caused by Carbon Monoxide poisoning. It is also one of the more common symptoms of superior canal dehiscence 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 virus. If conventional therapies fail, consult with a neuro-oncologist familiar with PNS.
Neurochemistry of vertigo
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 ofemesis but has little influence on vertigo and motion sickness.