VERTIGO part 3

TREATMENT

a. Medicamentosa

1. Anticholinergic : Scopolamin 0,2-0,4 mg; Atropin 0,2-0,4 mg
2. Antihistamin : Difenhidramin 50 mg 3dd; Dimenhidrinat 50 mg 3dd; Prometasin 25 mg 3 dd
   
3. Fenotiazin : Klorpromazin 25 mg 3dd
4. Butirofenon 1mg 3dd if antihistamin failed
   
5. Flunarizin (Ca blocker)

b. Fisiotherapy

1. Cooksey-cawthron
2. Brand

c. Diet
d. Psychoteraphy

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VERTIGO part 2

VERTIGO PHYSIOLOGIC
Vertigo physiologic is vertigo which caused by stimulations from environment, without vestibular, vision and somatosensoric dissorder.

1. Motion Sickness (induced by unfamilliar body accelerations or intersensory mismatch accentuated by fear or insecure)
2. Space Sickness (balance dissorder between semicircularis canal and otholit
3. Height Vertigo (subjectiv instability of postural balance and locomotoric induced by visual)
4. Optokinetic motion sickness (visual moving without vestibular or somatosensoric sign about move)
5. Arthrokinetic vertigo (ilussion that body is spinning if the extremities (pelvic and sholuder) rotated pasivly)
6. Auditori vertigo
7. Alternobarik vertigo (caused by eustachii tube closed/obstructed

VERTIGO PATHOLOGIC

1. Vestibulum
2. NC VIII
3. Brainstem reticulum
4. Tabes Dorsalis
5. Imagination
6. Generalized illness
7. Ophtalmic desease

Lets talk about vertigo pathlogic
1. Vestibulum

• Vestibular Neuritis (acut, nausea and vomit, 30-40 years old, without hearing loss, rotational vertigo, spontan nystagmus which ocular moving to contralateral from lession
• Viral labyrinthitis (like vestibular neuritis, 50% with hearing loss)
• Bacterial labyrinthitis
• Ramsay Hunt Syndrome (caused by herpes zoster oticus, nerve VII perifer paralised, pain in ear, and vesicel in meatus acusticus eksternus
• Menierre Syndrome
• Post traumatic vertigo
• BPPV

2. NC VIII, common is acoustic neurinoma
3. Brain stem reticulum (caused by vascular dissorder, vertigo, disartria, parestesi, hemiparese, tetraparese, pain in occipital lobus)
4. Tabes Dorsalis (defect on vertebra columna inmyelum which cause deep sensibility. patient often fall down in midnight.
5. Imagination (psychogenic)
6. Generalized illness (anemia, infection, uremia)
7. Ophtalmic desease (caused anomali refraction, astigmatism, post op catharact

TESTS

1. check heart rate
2. carotic pulse
3. auscultation aorta bruit
4. grasp and sucking refleks
5. Quix test
6. Romberg test
7. tandem walking

PROVOKATED TESTS

1. ortotastic hipotesion (measuring blood pressure while patient lying and 3 minutes after stand up)
2. Valsava manouver
3. Barany rotation
4. Caloric test
   

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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

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