- Near-syncope secondary to decreased blood flow to the brain (such as orthostatic hypotension, cardiac pre-syncope)
- True vertigo
- Disequilibrium (a sensation of imbalance when standing or walking—often secondary to multiple sensory deficits)
- Vague lightheadedness other than vertigo, pre-syncope, or disequilibrium. Patients may complain of “heavyheadedness” or “wooziness.” This type of dizziness may occur with psychiatric disorders, hyperventilation syndrome, encephalopathies, and multisensory dizziness, as well as many other conditions not causing the first three types.9
The final common mechanism in near-syncopal dizziness is cerebral hypoperfusion. This may be due to a decrease in cardiac output, hypovolemia, or a failure of vasomotor tone.
Decreased cerebral perfusion leading to these symptoms can occur as the result of a number of underlying disorders, including impaired cardiac output due to arrhythmia or structural cardiovascular disease, vasovagal episodes, hypovolemia, or orthostatic hypotension. In studies of syncope, vasovagal or vasodepressor syncope accounts for about 40% of all cases.12-14
The differential diagnosis for dizziness due to cardiovascular causes is essentially the same as that for syncope. Often, patients will relate a history of syncopal or nearsyncopal events prior to the current episode. Although dizziness due to cardiac causes without syncope has not been extensively studied, true cardiac syncope is a serious entity whose one-year mortality rate has been estimated to be between 18% and 33%.12-14 In a recent meta-analysis of 12 studies, near-syncope was the cause of dizziness in 6% of patients.15 In one ED-based study, however, 16% of patients with dizziness were found to be near-syncopal.5 It should be noted that near-syncope is much more likely to be due to volume depletion rather than to a primary cardiac cause.
Of the cardiovascular etiologies for dizziness, impaired cardiac output due to arrhythmia is probably the most concerning and the most life-threatening. Both tachyarrhythmias and bradyarrhythmias can lead to significant cerebral hypoperfusion and symptoms of dizziness. In Stokes-Adams attacks, high-degree atrioventricular block is associated with either syncope or nearsyncope. If ventricular fibrillation is the cause, however, it is unlikely that dizziness will be the presenting complaint!
Structural cardiovascular disease, including valvular disease, cardiomyopathy, or other extracardiac vascular disease, can also lead to decrease in cardiac output and cerebral hypoperfusion.
Volume Depletion And Vasomotor Instability
Volume depletion is an important cause of dizziness secondary to near-syncope. It may be responsible for 75% of near-syncopal events.15 Occult gastrointestinal bleeding can go undetected for months before finally presenting with signs of volume depletion and significant anemia. Certain medications, particularly in the elderly, may lead to orthostatic hypotension, including antihypertensives, anti- Parkinsonian drugs, neuroleptics, and anticholinergics. Poor conditioning and autonomic insufficiency are other causes of orthostatic hypotension in the elderly. Also note that elderly patients may become dizzy with postural change without blood pressure changes.16,17 A recent study describes decreased cerebral oxygenation during postural change in the elderly.18
Vertiginous disorders are generally separated into peripheral (semicircular canals and vestibular nerve) and central (brainstem and cerebellum). Among the more common of these are benign paroxysmal positional vertigo, Ménière’s disease, and vestibular neuritis.19 Conflicting signals from the visual, proprioceptive, and vestibular systems result in the sensation of vertigo. Asymmetric input to the vestibular nuclei via afferent nerves from the otolith organs and the semicircular canals of the inner ear can also trigger symptoms.20
Peripheral causes of vertigo are the most common19— they account for up to 85% of patients with vertigo, with central causes being present only 15% of the time.21 In addition to a spinning-room sensation, patients with peripheral causes of vertigo often describe nausea, vomiting, and diaphoresis. Although these symptoms do not tend to be present in other causes of dizziness, rapid postural changes with associated orthostatic hypotension may elicit nausea, vomiting, and diaphoresis.22 A vertiginous component in the latter case, however, will be notably absent.
Benign Paroxysmal Positional Vertigo
Of the causes of peripheral vertigo, benign paroxysmal positional vertigo (BPPV) is the most common, accounting for 16% of patients with dizziness.15 The pathogenesis of this condition is thought to be due to the accumulation of freefloating particulate debris (specifically calcium carbonate crystals) within the endolymph of the posterior semicircular canal.23 Intraoperative observation of this phenomenon supports this conclusion. The exact nature of the relationship between this particulate matter and the onset of vertigo
is unclear. However, unilateral changes in endolymphatic pressure may be responsible, leading to asymmetric input to the vestibular nuclei.23 A history of prior head trauma is linked to the onset of BPPV, presumably due to dislodged endolymphatic debris. This condition appears to be more common in women than men by a 2:1 ratio, usually occurring between the ages of 60 and 70.20
This syndrome, which typically lasts less than 30 seconds, is characterized by a rapid onset of vertigo symptoms after a change in head position. Often, patients will complain of the acute onset of symptoms after rolling over in bed, gazing upwards, or bending forward.21 Torsional nystagmus, nausea, and/or vomiting are also prominent features.20,22,24 Patients may experience disequilibrium on standing and walking, and they will often obtain relief upon lying still with their eyes closed.
In addition to BPPV, peripheral vertigo may also be caused by other vestibular disorders, including Ménière’s disease and vestibular neuritis/labyrinthitis. Pathologic findings in Ménière’s disease include increased endolymph volume with distension of the endolymphatic system (endolymphatic hydrops). Presumably, the deleterious effects of this distension on hair cells lead to abnormal vestibular input with accompanying hearing loss.20 On formal audiometry, unilateral low-frequency hearing loss is the most common finding.
Ménière’s disease, like BPPV, may be associated with nausea, vomiting, and vertigo, but the duration of symptoms in Ménière’s disease tends to be hours rather than seconds, as in BPPV.25,26 It is significantly less common than BPPV, affecting just 5% of patients with dizziness in a recent critical review of the literature.15 Its onset is most frequently in the fifth decade of life. Ménière’s disease also differs from BPPV, as it is associated with a sensation of “fullness” in the affected ear, fluctuating sensorineural hearing loss, and tinnitus. Disequilibrium may also be present.
Vestibular neuritis is the most common term for an acute unilateral loss of peripheral vestibular function associated with vertigo, nausea, vomiting, spontaneous nystagmus, and disequilibrium.25,27 The time course of symptoms tends to be over a period of days, with symptoms generally peaking during the first day, then gradually improving over the next few days. In a recent review of acute vestibular syndromes, Hotson and Baloh state that in otherwise healthy patients, this constellation of symptoms is generally due to a viral infection.25 They concede, however, that fewer than half of affected patients have a preceding viral infection and that evidence for an inflammatory or infectious etiology to this syndrome is not compelling. The term “neurolabyrinthitis” is used when acute vestibular symptoms are accompanied by hearing loss.25 In their metaanalysis of 12 studies on dizziness, Kroenke et al report that vestibular neuritis or labyrinthitis affected 9% of patients presenting with dizziness.15
Post-traumatic Vestibular Syndromes
A rare cause of peripheral vertigo is perilymphatic fistula. This usually post-traumatic finding involves an abnormal connection between the middle and inner ear. It can be caused by a direct blow to the ear, a forceful Valsalva maneuver, or acute external pressure changes (as in scuba diving or descent in an airplane). Treatment consists of conservative therapy in the majority of patients, with surgical patching reserved for those with recurrent symptoms. Acute traumatic tympanic membrane rupture can produce immediate vertigo, nausea, and/or vomiting associated with hearing loss—a particularly disconcerting event when it occurs 100 feet below the surface. A similar constellation of symptoms is seen in patients with fractures through the petrous portion of the temporal bone.28
Central Vestibular Causes
Although peripheral causes of vertigo make up an estimated 85% of patients with vertigo, central causes include disorders with significant potential morbidity. These include vertebrobasilar insufficiency, basilar artery migraine, and infarcts or hemorrhage of the cerebellum and brainstem. Like patients with peripheral vertigo, patients with central vertigo tend to complain of severe imbalance. However, unlike their “peripheral” counterparts, they have little nausea. Rarely will they have any auditory symptoms.They have difficulty compensating for their vertigo, which is often accompanied by other neurologic complaints.29,30 Symptoms associated with brainstem ischemia include diplopia, ataxia, dysarthria, and facial weakness.31 The symptoms are often insidious in their progression.22
Infarction or hemorrhage in the inferior cerebellum may represent a neurosurgical emergency due to the potential for rapidly increasing mass effect in the posterior fossa. Blood supply to both the vestibular nuclei in the brainstem as well as to the cerebellum comes from the vertebrobasilar system. Insults to this area may present with prominent vertigo symptoms.32 (See Table 2.)
Other Neurologic Causes
In addition to vertebrobasilar insufficiency and cerebellar ischemia/hemorrhage, multiple sclerosis (MS), basilar artery migraine, and cerebellopontine angle (CPA) tumor are less frequent causes of vertigo. Vertigo is the initial manifestation of multiple sclerosis in 10% of patients and is present at some point in up to one-third of those with MS.33 Basilar artery migraine can produce severe occipital headache, vertigo, and temporal lobe seizures.31 Those with CPA tumors (usually acoustic neuromas) often complain of vertigo accompanied by hearing loss. In these patients, the slow hearing loss tends to be more prominent than vertigo, as the brain compensates for prolonged asymmetric vestibular input.25,31
Other Medical Causes Of Dizziness
In addition to cardiovascular, vestibular, and CNS causes of dizziness, several other clinical entities may require consideration. Among these are drug toxicity, hypoglycemia, anemia, and hypothyroidism.22 Aminoglycosides produce vertigo and disequilibrium through direct ototoxic effects on vestibular hair cells, as can cisplatin and certain other chemotherapeutic agents.29 Symptoms tend to be bilateral, often leading to disequilibrium rather than vertigo. Oscillopsia, the subjective sensation of oscillation of vision, occurs with bilateral vestibular dysfunction. It may be idiopathic or due to otologic or neurologic disease (such as cerebellar degeneration), autoimmune conditions, toxins, or neoplasms.34
Anticonvulsant toxicity, particularly involving phenytoin or carbamazepine, may cause CNS depression, nystagmus, and ataxia as well as dizziness. Phenytoin may also produce mild nystagmus at therapeutic concentrations. 35 Benzodiazepines, barbiturates, alcohol, and other CNS depressants may create a globally depressed mental status that may present as nonspecific dizziness.29
Symptomatic hypoglycemia may also result in nonspecific dizziness or lightheadedness associated with fatigue, palpitations, and nausea. More severe hypoglycemia can be associated with altered mental status, lethargy, seizures, and diaphoresis. In Kroenke et al’s meta-analysis of patients presenting with dizziness, 13% had dizziness thought to be metabolic in nature, including drug reactions, anemia, hypoglycemia, or thyroid disease.15
Disequilibrium is a feeling of imbalance when standing or walking and may be due to numerous causes. Sensory deficits may result in this condition even in the absence of vestibular dysfunction. Patients usually deny any abnormal head sensation and may refer to their condition as “dizziness in the feet.”9 Such patients may have impaired motor control. Physical examination may reveal decreased visual acuity, peripheral neuropathy (loss of proprioception), and abnormal vestibular function.
This category of dizziness provides the greatest diagnostic frustration to the physician. It may have medical or psychiatric etiologies. Psychiatric causes of dizziness, including anxiety and hyperventilation syndromes, may account for up to 16% of patients presenting with dizziness. 15 It may be more frequent in patients with major depression, anxiety, or somatization disorders. Hyperventilation may be associated with lightheadedness, perioral and peripheral numbness, tingling, and a sensation of intense anxiety. Patients with a history of similar episodes or previously diagnosed panic disorder may become hypervigilant to the onset of dizziness symptoms and precipitate recurrent attacks.31
Psychogenic dizziness is a diagnosis of exclusion. Take care to ascertain whether an underlying organic disorder is present, as patients with significant medical problems may also present with hyperventilation. Remember, psychiatric illness provides little protection against medical disease.