Vertigo is a type of dizziness felt as a shift in a person's relationship to the normal environment (a feeling that the room is spinning is common) or a sense of movement in space. As patients age, vertigo becomes an increasingly common presenting complaint.
True vertigo, from the Latin "vertere," to turn, is a distinct, often severe form of dizziness that is a movement hallucination.
There are four major types of dizziness :
- disequilibrium, and
Most patients with true vertigo have a peripheral vestibular disorder, such as benign positional vertigo. This is usually associated with tinnitus and hearing loss.
Central disorders, such as brain stem or cerebellar lesions, tend to be more chronic but less intense than peripheral disorders and are not associated with hearing loss. Central disorders account for only 15 percent of patients with vertigo.
Another very common cause of vertigo that worsens with a change in position is dehydration. Dehydration often follows vomiting or diarrhea. Vertigo often causes nausea and vomiting, so it may be hard to distinguish inner ear problems from dehydration. Victims of vertigo that gets worse with changes in position should be seen by a physician. Untreated, inner ear problems can lead to a loss of hearing and dehydration can lead to shock.
Any condition that affects the brain can cause vertigo. One of the easiest ways to remember other causes of vertigo is to use the mnemonic AEIOU TIPS :
- A - alcohol
- E - epilepsy or exposure
- I - insulin
- O - overdose or oxygen deficiency
- U - uremia
- T - trauma
- I - infection
- P - psychosis or poisoning
- S – stroke
Diagnosis of Vertigo
Because vertigo can have multiple concurrent causes (especially in older patients), a specific diagnosis can be elusive. The duration of vertiginous episodes and the presence or absence of auditory symptoms can help narrow the differential diagnosis (Table 1). Psychiatric disorders, motion sickness, serous otitis media, cerumen impaction, herpes zoster, and seizure disorders also can present with dizziness.
The physical examination should include measurements of orthostatic vital signs and an otoscopic examination. The neurologic examination should include the Dix-Hallpike maneuver to differentiate peripheral from central vertigo (Figure 1 ).
Differential Diagnosis of Vertigo
- Benign paroxysmal positional vertigo
- Perilymphatic fistula (head trauma, barotrauma)
- Vascular ischemia: transient ischemic attack
- Ménière's disease
- Vertiginous migraine
- Labyrinthine concussion
- Vascular ischemia: stroke
- Vestibular neuronitis
- Anxiety disorder
- Acoustic neuroma
- Cerebellar degeneration
- Cerebellar tumor
- Multiple sclerosis
- Vestibular ototoxicity
Figure 1. Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient's head 45 degrees to the right (A). The physician supports the patient's head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient's head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.
Drug Treatment of Vertigo
There are at least four major neurotransmitters of the vestibular system involved in the "three neuron arc" between the vestibular hair cells and oculomotor nuclei that drives the vestibulocular reflex. There are also a host of other neurotransmitters which modulate function. Glutamate is the major excitatory neurotransmitter (Serafin et al, 1992). Acetylcholine (ACH) is both a peripheral and central agonist affecting muscarinic receptors. Receptors found in the pons and medulla, presumably those involved with dizziness, are almost exclusively of the M2 subtype (Barton et al, 1994). Gamma-aminobutyric acid (GABA) and glycine are inhibitory neurotransmitters found in connections between second order vestibular neurons and onto oculomotor neurons (Spencer et al, 1992). Stimulation of the two types of GABA receptors, GABA-A and GABA-B, have similar effects on vestibular pathways (Neerven et al, 1989), but specific GABA-B agonists, such as baclofen, decrease the duration of vestibular responses in animal models (Cohen et al, 1987).
The circuitry by which several other neurotransmitters affect vestibular responses is less well understood. Histamine is found diffusely in central vestibular structures and centrally acting antihistamines modulate symptoms of motion sickness (Takeda et al, 1989). Both the H1 and H2 subtypes of histamine receptors affect vestibular responses (Serafin et al, 1992). Norepinephrine is involved centrally in modulating the intensity of reactions to vestibular stimulation (Wood, 1979) and also affects adaptation. Dopamine affects vestibular compensation, and serotonin is involved with nausea.
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