VERTIGO part 1

DEFINITION
Vertigo is a medical condition that characterized by a sense of dizziness and feeling motion when one is stationary or spinning movement.

PATHOGENESIS
Vertigo is not a desease, but a symptom. Spatia orientation is depend on three points, they are:

1. adequate sensation input (from sensoric organs: vision, balance and sensibility)
2. central integration
3. proper motor response

If information or sensor by eye (vision) is not match with information from labirin (ear), that makes vertigo.

ETIOLOGY

1. Vestibulum
2. Ear nerve
3. Reticulus from brain branch
4. Tabes dorsalis
5. Imagination
6. Generilized Illnes
7. Ophtalmic desease

CLASSIFICATION
Vertigo is classified into either peripheral or central depending on the location of the dysfunction of the vestibular pathway

A. Peripheral
Also called Otologic or Vestibular. Its mean that Vertigo which caused by problems with the inner ear or vestibular system. Motion sickness is sometimes classified as a cause of peripheral vertigo.

B. Central
If Vertigo arises arises from the balance centers of the brain. it is usually milder, and has accompanying neurologic deficits, such as slurred speech, double vision or pathologic nystagmus. Brain pathology can cause a sensation of disequilibrium which is an off-balance sensation


PATOPHYSIOLOGY
The neurochemistry of vertigo includes primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-occular reflex (VOR). many others play more minor roles.

Three neurotransmitters that work peripherally and centrally include:

1. Glutamate
2. Acetylcholine
3. GABA.

Three other neurotransmitters work centrally

1. Dopamine
2. Nor epinephrine
3. Histamine

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 an central synapses. GABA is thought to be inhibitory for commisures of the medial vestibular nucleus, and the vertical VOR.
Dopamine may accelerate vestibular compensation. Norepinrphrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamin is present only centrally, but its role is unclear. It is known that centrally acting antihistamins 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 an peripheral control of emesis but has little influence on vertigo and motion sickness