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Vertigo
ICD-10 A881, H81, R42, T752
ICD-9 078.81, 386, 780.4
OMIM [1]
DiseasesDB 29286
MedlinePlus [2]
eMedicine /
MeSH {{{MeshNumber}}}

Vertigo, a specific type of dizziness, is a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is stationary with respect to the earth or surroundings. There are two types of vertigo: subjective and objective. Subjective vertigo is when a person feels a false sensation of movement. Objective vertigo is when the surroundings will appear to move past a person's field of vision.

The effects of vertigo may be slight. It can cause nausea and vomiting and, if severe, may give rise to difficulty with standing and walking.

The word "vertigo" comes from the Latin "vertere", to turn + the suffix "-igo", a condition = a condition of turning about.[1]

Causes of vertigoEdit

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).

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.

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.

Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway. These are peripheral or central vertigo. Each category has a distinct set of characteristics and associated findings.

Vertigo in context with the cervical spineEdit

According to chiropractors, ligamental injuries of the upper cervical spine can result in head-neck-joint instabilities which can cause vertigo.[How to reference and link to summary or text] In this view, instabilities of the head neck joint are affected by rupture or overstretching of the alar ligaments and/or capsule structures mostly caused by whiplash or similar biomechanical movements.

Symptoms during damaged alar ligaments besides vertigo often are

  • dizziness
  • reduced vigilance, such as somnolence
  • seeing problems, such as seeing "stars", tunnel views or double contures.
  • Some patients tell about unreal feelings that stands in correlation with:
  • depersonalization and attentual alterations

Medical doctors (MDs) do not endorse this explanation to vertigo due to a lack of any data to support it, from an anatomical or physiological standpoint. Often the patients who have an odyssey of medical consultations without any clear diagnosis and are sent to a psychiatrist because doctors think about depression or hypochondria. Standard imaging technologies such as CT Scan or MRI are not capable of finding instabilities without taking functional poses.[How to reference and link to summary or text]

Neurochemistry of vertigoEdit

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. Acetylcholinc, 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.

Diagnostic testingEdit

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).

TreatmentEdit

Treatment is specific for underlying disorder of vertigo.

See alsoEdit

ReferencesEdit

External linksEdit


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