Wednesday, September 3, 2008

Dizziness and Vertigo

Dizziness and Vertigo

Avery Hayes - Kochar's Clinical Medicine for Students, 5th Edition. 2008

Dizziness is one of the most common complaints in clinical practice and affects approximately 20% to 30% of the general population. This symptom is responsible for numerous visits to emergency departments and outpatient clinics. Ongoing dizziness can lead to a loss of function, falls, and injuries. Balance-related falls account for more than one half of all accidental deaths in the elderly. Dizziness is a nonspecific symptom and may be used by the patient to describe a number of different experiences. Because the differential diagnosis is broad, the evaluation of the dizzy patient can be both overwhelming and time consuming.

Differential Diagnosis

Dizziness may be classified into four broad categories based on clinical characteristics, which will provide for more accurate diagnosis (Table 1):

· Vertigo (Table 2) is the illusory sensation of spinning or motion. The patient may feel as if their body or the environment is in motion. Vertigo may be peripheral in etiology, due to disorders of the vestibular end organs (semicircular canals and utricle), eighth cranial nerve, or the vestibular nuclei. Central causes of vertigo include ischemia or damage to brainstem structures, or the cerebellum.

· Presyncope is the sense of impending loss of consciousness due to impaired cerebral blood flow, or anoxia, which often implies an underlying cardiovascular, metabolic, or hematologic disorder.

· Disequilibrium is a sense that one is about to fall, often associated with motor or sensory dysfunction resulting in the inability to maintain balance and gait.

· Lightheadedness describes other nonspecific symptoms related to multiple sensory disturbances, psychiatric illness, and medication side effects that alter the sensorium.

Vertigo

A crucial aspect of the evaluation of vertigo is to differentiate peripheral from central causes (Table 3. The latter have more serious consequences and require emergent evaluation and treatment. The clinical presentation, nature of the nystagmus, and presence of associated neurologic signs and symptoms may help distinguish vertigo of peripheral and central etiologies. Peripheral causes of vertigo often present as abrupt, intense attacks, which last several seconds to minutes, and are accompanied by nausea and vomiting. Vertigo due to central causes may occur with a more gradual onset but have a prolonged duration of symptoms. The intensity of symptoms may be less severe with central causes but often the patient may be unable to stand or walk. Nystagmus associated with peripheral vertigo can be decreased with visual fixation and is typically unidirectional (horizontal with a rotary component). Nystagmus that is purely vertical is due to a central cause. During cases of prolonged vertigo, nystagmus from peripheral causes is diminished by compensation and generally does not last longer than 48 hours.


Table 1 Differential diagnosis of dizziness

Dizziness subtype

Type of sensation

Temporal characteristics

Differential diagnosis

Vertigo

Spinning or motion

Episodic or continuous

Benign paroxysmal positional vertigo
Meniere’s disease
Labyrinthitis
Vertebrobasilar ischemia
Cerebellar infarction or hemorrhage

Presyncope

Faint feeling, as though one were about to pass out

Episodic, may last seconds, may be relieved by recumbent position

Dehydration
Ischemic heart disease
Obstructive cardiac lesions
Cardiac arrhythmia
Neurocardiogenic syncope
Anemia
Hypoglycemia or hyperglycemia
Infection

Disequilibrium

A sense of unsteadiness of the lower extremities

Constant but may fluctuate in intensity

Multiple sensory deficits including peripheral neuropathy and vision loss

Lightheadedness

Nonspecific


Psychiatric conditions including anxiety, depression, panic attacks, and agoraphobia
Hyperventilation
Medications


Table 2 Differential diagnosis of vertigo

Peripheral vertigo

Central vertigo

Benign paroxysmal positional vertigo
Cerebellar hemorrhage or infarct
Acute vestibular neuritis
Labyrinthitis
Acoustic neuroma
Meniere’sdisease

Brainstem ischemia
Vertebrobasilar insufficiency


Table 3 Characteristics of peripheral and central vertigo

Characteristics

Peripheral

Central

Severity

Severe

Mild

Onset

Sudden

Gradual

Duration

Seconds to minutes

Weeks

Positional

Yes

No

Fatigable

Yes

No

Associated symptoms

Auditory

Neurological and visual

Nystagmus

Horizontal

Vertical

From Chawala N, Olshaker JS. Diagnosis and management of dizziness and vertigo. Med Clin North Am 2006;90:291-304, with permission.


Because brainstem structures subserve many neurologic functions, infarcts causing vertigo will also have neighborhood effects due to injury to other cranial nerve nuclei, long motor, or sensory tracts. Common presentations are summarized in Table 4. Lateral medullary infarcts cause vertigo by infarction of the vestibular nuclei. Associated symptoms and signs include Horner's syndrome, ipsilateral facial numbness, diplopia, dysphagia, or contralateral limb numbness. Patients with cerebellar infarcts have signs such as dysmetria, past-pointing, or dysdiadochokinesis. Vertigo associated with transient ischemic attack due to vertebrobasilar artery (VBA) insufficiency is associated with additional symptoms such as diplopia, transient blindness, drop attacks, or dysarthria. Stroke in the VBA distribution may have a wide range of findings depending on the branch affected and collateral blood supply. Symptoms include hearing loss, ophthalmoplegia, blindness, sensory loss, and ataxia. Other processes affecting the cerebellum such as hemorrhage may present with headache, severe gait ataxia, or depressed levels of consciousness. The cerebellum may also be involved in demyelinating disorders such as multiple sclerosis.

Peripheral causes of vertigo are more common than central etiologies. Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. This condition occurs when debris form the utricle forms a plug and circulates within the endolymph of the semicircular canals. This clot is thought to act as a plunger and induce a push-and-pull force on the cupula, creating asymmetric impulses between both ears that result in vertigo and nystagmus. Most patients describe episodes of vertigo that are triggered by changes in head position, such as looking up or rolling over in bed. Attacks are usually sudden in onset and generally last less than 60 seconds. BPPV is characterized by fatigability. The patient will develop tolerance to repeated head movements, causing a reduction in continued symptoms.


Table 4 Stroke syndromes associated with vertigo

Site (artery)

Clinical presentation

Labyrinth (internal auditory artery)
Lateral medullary infarct (vertebral artery, posterior inferior cerebellar artery)
Lateral pontomedullary infarction (anterior inferior cerebellar artery)
Cerebellum (posterior and anterior inferior cerebellar arteries, superior cerebellar artery)

Tinnitus, hearing loss
Horner's syndrome, cranial nerves V and VII, crossed sensory loss
Horner's syndrome, cranial nerves V and VII, crossed sensory loss, hearing loss
Limb dysmetria, ataxia

From Delaney K. Bedside diagnosis of vertigo: value of the history and neurologic examination. Acad Emerg Med 2003;10:1388-1395, with permission.


Labyrinthitis and vestibular neuritis are characterized by inflammation; either the canals of the inner ear, vestibular nerve, or nuclei can be affected. Both syndromes can follow a viral upper respiratory infection. Patients usually present with severe vertigo, nausea, and vomiting. Symptoms usually last from days to weeks. The vertigo gradually subsides as the inflammation resolves and central compensatory mechanisms evolve. Otitis media may cause a suppurative labyrinthitis due to bacterial spread form the middle ear through a ruptured membrane or perilymph fistula. These patients appear acutely ill and present with hearing loss and fever in addition to nausea, vomiting, and vertigo. Ramsay-Hunt syndrome is caused by Varicella zoster and is a variant of vestibular neuritis with involvement of the cranial nerves VII and VIII, causing facial paresis, tinnitus, hearing loss, and vertigo.

Meniere’s disease is due to an increase in the volume of endolymph, causing distention of the endolymphatic system. The classic triad is vertigo, tinnitus, and fluctuating sensorineuronal hearing loss. Attacks of vertigo are abrupt and may last from minutes to hours. Attacks also vary in intensity and may be associated with aural fullness or pain. Symptoms can be unilateral or bilateral.

Acoustic neuroma is a benign tumor composed of Schwann cells of the vestibular nerve. Patients often present with tinnitus and hearing loss. These tumors are slow growing and central compensation leads to less severe vertigo. Enlargement of the tumor within the cerebellopontine angle causes compression of the adjacent cranial nerves and brainstem, and may result in facial anesthesia and weakness.

Presyncope

As noted above, presyncope is the sensation that one is about to lose consciousness. Often, this is a milder manifestation of an event that ultimately could result in true syncope. The differential diagnosis and evaluation are the same as for syncope.

Disequilibrium

Dysequilibrium syndrome should be suspected when a patient feels unsteady, as though they are about to fall. This sensation is particularly prominent following a sudden change in position or with loss of visual cues, as when getting on or off an elevator. This phenomenon is triggered by loss of sensory inputs that cue the brain to position or the loss of musculoskeletal function interfering with the minor readjustments in position to maintain balance.

Disequilibrium can be seen in association with a number of disorders including peripheral neuropathy, visual impairment, severe arthritis, and Parkinson's disease. It is particularly common in patients with long-standing diabetes who may have several of these issues present simultaneously.

Lightheadedness

A substantial number of patients with dizziness describe relatively vague symptoms that are difficult to verbalize. Oftentimes these are characterized as a sensation of being lightheaded or floating. A majority of these patients have an underlying psychological issue including anxiety, depression, or increased stress. Physical examination is usually unremarkable. In some of these patients, subclinical hyperventilation may play a role.

Evaluation

Some patients may not be able to give an accurate history; therefore, the physical examination not only serves to differentiate peripheral from central causes of vertigo, but also helps to evaluate for causes of dizziness other than vertigo. Vital signs should be measured, including orthostatic blood pressure.

Physical examination should include a complete eye, ear, nose, and throat examination (looking for nystagmus, asymmetry, or defects in the pupillary reactivity and extraocular movements) and a funduscopic examination to check for papilledema. Inspection of the tympanic membranes should be performed to evaluate for scarring, fluid, or infection. If hearing loss is detected, the Weber and Rinne tuning fork examinations can differentiate between conductive and sensorineural hearing loss. Auscultation for carotid bruits and cardiac examination should be performed to evaluate for potential sources of emboli or obstructive cardiac lesions. A thorough neurological examination is important, including examination of motor strength and sensation, cranial nerves, cerebellar function, Rhomberg's test, and gait.

The Dix-Hallpike maneuver is used to diagnose BPPV (Fig. 1). The patient is seated upright on the examining table with the head held in the hands of the examiner for support. The patient's head is turned 45 degrees toward the side being tested. The patient is rapidly lowered to a supine position with the head hanging below the level of the examining table. The patient should be reminded to keep the eyes open because it is critical to see if vertigo occurs. After a short period of latency, a positive test is indicated by a burst of torsional-vertical nystagmus (the upper poles of the eyes beat torsionally toward the ground) associated with vertigo. The vertigo typically lasts between 20 to 40 seconds and is pathognomonic of the posterior canal variant of BPPV.


Figure 1 Dix-Hallpike maneuver. The patient is positioned with the head hanging 30 to 45 degrees over the table edge first in the midline, which is repeated with the head rotation to right and left. Frames one through four show the procedure in sequence.


If disequilibrium is suspected, it can be helpful to perform a finger touch test. The physician attempts to reproduce the symptom by having the patient turn or change position quickly. In the presence of the symptom, the patient is asked to touch the examiner's finger with their own. If the symptoms improve dramatically, it is very suggestive of disequilibrium.

If the complaint is lightheadedness, the patient should be asked to deliberately hyperventilate. If the symptoms are reproduced, this can help confirm the diagnosis and be used as a tool to reassure the patient.

Laboratory tests may not be helpful if the dizziness is caused by vertigo, but may indicate another cause. Complete blood counts, basic metabolic panel, and thyroid function tests may indicate the presence of anemia, electrolyte abnormalities, hypoglycemia, dehydration, or thyrotoxicosis causing symptoms. Electrocardiography may show signs of atrial fibrillation or ischemia.

Electronystagmography is an examination that records eye movements in response to vestibular, visual, cervical, caloric, rotational, and positional stimulation, and may be used to assess vestibular function. Audiologic evaluation can be performed if indicated to evaluate for patterns of hearing loss.

Patients with suspected central cause of vertigo require cranial imaging with either computed tomography (CT) or magnetic resonance imaging (MRI). CT will identify cerebellar hemorrhage or infarction and suggest the presence of tumor, but lacks the sensitivity to detect small infarcts in the brainstem. MRI has superior sensitivity and will identify small lesions including infarcts, tumors, and plaques. Magnetic resonance angiography will visualize the intracranial vasculature, including the vertebrobasilar system. Patients suspected of having an infarct should also be evaluated for a source of thromboembolism, including electrocardiogram to rule out atrial fibrillation and echocardiogram with a bubble study to evaluate for intracardiac shunt.

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