1.11 Vertigo ("Dizzy, lightheaded")
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agk's Library of Common Simple Emergencies

Presentation
------------
This may be a nonspecific complaint which must 
be refined further into either an altered 
somatic sensation (giddiness, wooziness); 
orthostatic blood pressure changes (light- 
headedness, sensation of fainting); or the 
sensation of the environment (or patient) 
spinning (true vertigo). In inner ear disease, 
vertigo is virtually always accompanied by 
nystagmus, which is the ocular compensation for 
the unreal sensation of spinning; but the 
nystagmus may be extinguished when the eyes are 
open and fixed on some point (by the same 
token, vertigo is usually worse with the eyes 
closed). Nausea and vomiting are common 
accompanying symptoms. Less common (depending 
on the underlying cause) are hearing changes, 
tinnitus, cerebellar or adjacent cranial nerve 
impairment.

What to do: 
----------- 
- Have the patient tell you in his own words 
   what it feels like (without using the word 
   "dizzy"). Ask about any sensation of 
   spinning, factors which make it better or 
   worse, and associated symptoms. Ask about 
   drugs or toxins which could be responsible.
- Determine whether the patient is describing 
   vertigo (a feeling of movement of one's body 
   or surroundings) or a sensation of an 
   impending faint or a vague unsteady feeling.
- If the problem is near syncope or orthostatic 
   lightneadedness, then consider potentially 
   serious etiologies such as heart disease, 
   cardiac dysrhythmias or blood loss.
- With a sensation of dysequilibrium or an 
   elderly patient's feeling that he is going 
   to fall, look for peripheral neuropathy, 
   cervical spondylosis, stiff legs and 
   vasodilator medication. These patients 
   should be referred to their primary care 
   physicians for management of their under- 
   lying medical problems and adjustment of 
   their medications.
- If there is light-headedness that is un- 
   related to changes in position and posture 
   and there is no evidence of disease found on 
   physical examination and laboratory eval- 
   uation, then instruct the patient to 
   hyperventilate by breathing deeply in and 
   out fifteen times. If this reproduces the 
   symptoms, assess the patient's emotional 
   state as a possible cause of his symptoms.
- If the patient is having true vertigo, 
   examine for nystagmus, which can be horiz- 
   ontal, vertical or rotatory (pupils describe 
   arcs). Have the patient follow your finger 
   with his eyes as it moves a few degrees to 
   the left and right (not to extremes of gaze) 
   and watch whether there are more than the 
   normal 2 to 3 beats of nystagmus before the 
   eyes are still. You may detect nystagmus 
   when the eyes are closed by watching the 
   bulge of the cornea moving under the lid.
- If nystagmus is not clearly evident and the 
   patient can tolerate it, attempt a provo- 
   cative maneuver for positional nystagmus by 
   having the patient sit up and then lie back, 
   quickly hang his head over the stretcher 
   side and turn his head and eyes to one side. 
   Repeat to the other side. When this maneuver 
   produces positional nystagmus, it indicates 
   a benign inner ear dysfunction. A negative 
   test is not helpful.
- Examine ears for cerumen, foreign bodies, 
   otitis media, and hearing loss.
- Examine the cranial nerves. Test cerebellar 
   function (rapid alternating movement, 
   finger-nose, gait). Check the corneal blink 
   reflexes: if absent on one side in a patient 
   who does not wear contact lenses, consider 
   acoustic neuroma.
- Decide, on the basis of the above, whether 
   the etiology is central (brainstem, cereb- 
   ellopontine angle tumor, multiple sclerosis) 
   or peripheral (vestibular organs, eighth 
   nerve). Central lesions may require further 
   workup, otolaryngologic or neurologic 
   consultation, or hospital admission, while 
   peripheral lesions, although more symptom- 
   atic, are more likely self-limiting.
- In the emergency department, treat moderate 
   to severe symptoms of vertigo with intra- 
   venous diazepam (Valium) 10 mg or diphen- 
   hydramine (Benadryl) 50mg. Add promethazine 
   (Phenergan) 25mg iv for nausea. If there are 
   no contraindications (e.g. glaucoma) then a 
   patch of transdermal scopolamine can be worn 
   for three days. Some authors recommend 
   hydroxyzine (Vistaril, Atarax) while others 
   suggest corticosteroids (Solu-Medrol, 
   Prednisone). Nifedipine (Procardia) had been 
   used to alleviate notion sickness but is no 
   better than scopolamine patches, and should 
   not be used for patients with postural 
   hypotension or who take beta blockers. If 
   the patient does not respond, he may require 
   hospitalization for further parenteral 
   treatment.
- Treat vertigo symptoms in outpatients with 
   diazepam (Valium) 5-10mg qid, meclizine 
   (Antivert) 12.5-25mg qid, diphenhydramine 
   (Dramamine, Benadryl) 25-50mg qid, prometh- 
   azine (Phenergan) 25mg qid,or hydroxyzine 
   (Vistaril) 25mg qid, and bedrest as needed 
   until symptoms improve.
- Arrange for followup if there is no clear 
   improvement in 2 days or if there is any 
   suggestion of a central etiology.

What not to do:
---------------
- Do not attempt provocative maneuvers if the 
   patient is symptomatic with nystagmus.
- Do not give anti-vertigo drugs to elderly 
   patients with dysequilibrium. These 
   medications have sedative properties which 
   can make them worse.
- Do not make the diagnosis of Meniere's 
   disease (endolymphatic hydrops) without the 
   triad of paroxysmal vertigo, sensorineural 
   deafness, and tinnitus, along with a feeling 
   of pressure or fullness in the affected ear.

Discussion
----------

In general, the more violent and spinning the 
sensation of vertigo, the more likely the 
lesion is peripheral. Central lesions tend to 
cause less intense vertigo and more vague 
symptoms. 

Peripheral etiologies of vertigo or nystagmus 
include irritation of the ear (utricle, 
saccule, semi-circular canals) or the 
vestibular division of the eighth cranial 
(acoustic) nerve by toxins otitis, viral 
infection, or cerumen or a foreign body against 
the tympanic membrane. The term "labyrinthitis" 
should be reserved for vertigo with hearing 
changes, and "vestibular neuronitis" for the 
common short-lived vertigo without hearing 
changes usually associated with viral upper 
respiratory infections. Paroxysmal positional 
vertigo may be related to dislocated otoconia 
in the utricle and saccule. If it occurs 
following trauma, suspect a basal skull 
fracture with leakage of endolymph or peri- 
lymph, and consider otolaryngologic referral 
for further evaluation.

Central etiologies include multiple sclerosis, 
temporal lobe epilepsy, basilar migraine and 
hemorrhage in the posterior fossa. A slow- 
growing acoustic neuroma in the cerebello- 
pontine angle usually does not present with 
acute vertigo but rather a progressive 
unilateral hearing loss with or without 
tinnitus. The earliest sign is usually a 
gradual loss of auditory discrimination.

Vertebrobasilar arterial insufficiency can 
cause vertigo, usually with associated nausea, 
vomiting and cranial nerve or cerebellar signs. 
It is commonly diagnosed in dizzy patients who 
are older than 50, but more often than not the 
diagnosis is incorrect. The brainstem is a 
tightly-packed structure in which the 
vestibular nuclei are crowded in with the 
oculomotor nuclei, the medial longitudinal 
fasiculus, cerebellar, sensory and motor 
pathways. It would be unusual for ischmia to 
produce only vertigo without accompanying 
diplopia, ataxia, sensory or motor disturbance. 
Although vertigo may be the major symptom of an 
ischemic attack, careful questioning of the 
patient commonly uncovers symptoms implicating 
involvement of other brainstem structures. 
Objective neurologic signs should be present in 
frank infarction of the brainstem.

Either central or peripheral nystagmus can be 
due to toxins, most commonly alcohol, tobacco, 
aminoglycosides, minocycline, disopyramide, 
phencyclidine, phenytoin, benzodiazepines, 
quinine, quinidine, aspirin, salicylates, non- 
steroidal anti-inflammatories and carbon 
monoxide. Nystagmus occuring in central nervous 
system disease may be vertical and dis- 
conjugate, whereas inner ear nystagmus never 
is. Central nystagmus is gaze-directed (beats 
in the direction of gaze) whereas inner ear 
nystagmus is direction-fixed (beats in one 
direction regardless of the direction of gaze). 
Central nystagmus is brought out by visual 
fixation, which is supressed in inner ear 
nystagmus.

References:
-----------
- Herr RD, Zun L, Matthews JJ: A directed 
   approach to the dizzy patient. *Ann Emerg 
   Med* 1989;18:664-672.
- Froehling DA, Silverstein MD, Mohr DN et al: 
   Does this patient have a serious form of 
   vertigo? *J Am Med Assoc* 1994;271;385-388.
- Epley JM: Positional vertigo related to 
   semicircular canalithiasis. *Otolaryngol 
   Head Neck Surg* 1995;112:154-161.

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