Saturday 8 December 2012

Vertigo ("Dizzy, lightheaded")

1.11 Vertigo ("Dizzy, lightheaded")

Presentation
This may be a nonspecific complaint which must be refined further into either an altered somatic sensation (giddiness, wooziness); orthostatic blood pressure changes (lightheadedness, 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, but 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 dys- rhythmias 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 underlying medical problems and adjustment of their medications.



If there is light-headedness that is unrelated to changes in position and posture and there is no evidence of disease found on physical examination and laboratory evaluation, 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 horizontal, 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 provocative 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, cerebellopontine 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 symptomatic, are more likely self-limiting.



In the emergency department, treat moderate to severe symptoms of vertigo with intravenous diazepam (Valium) 10 mg or diphenhydramine (Benadryl) 50mg. Add promethazine (Phenergan) 25mg iv for nausea. If there are no contra- indications (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, promethazine (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 if 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 perilymph, and consider otolaryngologic referral for further evaluation and positional Central etiologies include multiple sclerosis, temporal lobe epilepsy, basilar migraine and hemorrhage in the posterior fossa. A slow-growing acoustic neuroma in the cerebellopontine 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 pateints 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 disconjugate, 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 supressed 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.


No comments:

Post a Comment