When investigating the source of dizziness in a patient, it is useful to organize potential etiologies into four groups. The four major causes of dizziness and vertigo are peripheral vestibular, central vestibular, medical, and unlocalized. True vertigo, particularly rotatory vertigo, is often due to a peripheral vestibular (inner ear) disorder. Presyncope and loss of consciousness are not associated with vertigo of peripheral origin and should direct the examiner to investigate other, often cardiovascular or CNS causes. These are common clinical scenarios and illustrate the varied backgrounds from which a complaint of dizziness may arise, ranging from benign annoyance to signs of potentially life-threatening events.
Documentation of the impact of dizziness and vertigo on a patient’s quality of life is essential in formulating a treatment plan. Treatment options are driven by the severity of disease and limitation in activities of daily living. Disease impact will often differ between patients as what may be tolerable for a retired schoolteacher may not be tolerable for an airline pilot.
I. PERIPHERAL VESTIBULAR OR OTOLOGIC CAUSES OF VERTIGO
A. Benign paroxysmal positional vertigo.
1. Clinical features. Benign paroxysmal positional vertigo (BPPV) is characterized by brief vertigo associated with changes in head position. It is the most common cause of vertigo. It is typically the result of stimulation of the posterior semicircular canal by loose debris (calcium carbonate crystals) dislodged from the utricle. This dislodgement can result from trauma, labyrinthitis, or spontaneously. Typically the history is one of recurrent vertiginous episodes lasting not more than 1 minute and reproducible with repeated movement in the same direction. The Dix–Hallpike’s test (which is illustrated in Chapter 16) is commonly employed to diagnose BPPV and identify the affected labyrinth.
2. Treatment. Vestibular suppressant medications can lessen vertigo intensity but do not reduce the frequency of attacks. The mainstay of treatment is repositioning exercises to move the debris from the affected semicircular canal. Both office-based repositioning techniques and home exercises may be employed to accomplish this goal. Rarely, when positional vertigo is unresponsive to repositioning maneuvers, surgery may be considered.
a. Epley’s maneuver. It is a common technique used for canalith repositioning. It is most effectively used when the affected semicircular canal has been identified and can therefore be targeted (see Chapter 16).
Technique (Fig. 56.1).
(1) With the patient sitting upright, the head is turned 45˚ to the offending side, and the neck is extended 45˚.
(2) From this upright position with the head turned, the patient is reclined supine with the head hung over the edge of the exam table; this position is held for 10 to 15 seconds.
(3) The head is then slowly rotated away from the offending side, through midline, to 45˚ to the opposite side, keeping the neck extended throughout.
(4) The body and head are turned to face downward opposite to the offending side.
(5) After 10 to 15 seconds, the patient is slowly lifted to a seated upright position keeping the head turned away from the offending side.
(6) The head is then slowly returned to midline.
b. Modified Semont maneuver.
Technique (described for right-sided BPPV) (Fig. 56.1).
(1) The patient sits upright on the edge of the bed with the head turned 45˚to the left.
(2) The patient drops his/her head quickly to touch the right postauricular region to the bed and maintains this position for 30 seconds.
(3) The patient then rolls in a swift movement toward the left side, so that the trunk is lying supine and the head comes to rest on the left side of the forehead and maintains this position for 30 seconds.
(4) The patient sits up again.
This maneuver should be performed three times daily and repeated until symptom free for 24 hours.
FIGURE 56.1 Self-treatment of BPPV. (From Radtke A, von Brevern M, Tiel-Wilck K, et al. Self-treatment of benign paroxysmal positional vertigo: Semont maneuver vs Epley procedure. Neurology. 2004;63:150–152, with permission.)
c. Surgery. Very rarely, repositioning techniques are ineffective, and in severe cases of refractory BPPV surgery may be offered. Surgical options, which can be performed by a neurotologist, include semicircular canal plugging and vestibular neuronectomy.
3. Results. When applied to patients with BPPV, canalith repositioning is successful in relieving symptoms in up to 90% of patients. The techniques can be performed and taught by a wide range of clinicians. In those patients with recurrent symptoms, teaching the patient repositioning techniques will allow self-treatment and continued symptomatic relief.
4. Special circumstances. When BPPV is bilateral, treatment begins with the side that has a more robust nystagmus on Dix–Hallpike’s testing. Patients with severe disease may need pretreatment with 5 to 10 mg of diazepam 30 minutes prior to repositioning.
B. Vestibular neuronitis and labyrinthitis.
1. Clinical features. Vestibular neuronitis and labyrinthitis are often discussed together because of their similar presenting features. Both involve vertigo that can last for hours to days, often severe enough to induce nausea and vomiting. Labyrinthitis is associated with sensorineural hearing loss (SNHL), whereas vestibular neuronitis is not. These are typically self-limited conditions that are attributed to a viral infection. After the acute phase, vestibular equilibrium gradually returns over the course of several weeks in most patients.
2. Treatment. Using a combination of vestibular suppression, anti-inflammatory agents, antiemetics, and vestibular rehabilitation, treatment aims to reduce the severity and duration of acute symptomatology while allowing for vestibular recovery.
a. Vestibular suppression. Vestibular suppressants are generally grouped into three categories: benzodiazepines, antihistamines, and anticholinergics (Table 56.1). Benzodiazepines work via gamma–aminobutyric acid (GABA) potentiation and subsequent inhibition of vestibular stimulation. Anticholinergics and antihistamines work to suppress vestibular input. These medications are generally well-tolerated in low doses, although it is important to realize that a high level of vestibular suppression may reduce central compensation, and thus they are best used in a limited fashion. Antiemetics are a fourth category of pharmacotherapy, often used concurrently with vestibulosuppressants to target frequently associated nausea.
(1) Antihistamines. Antihistamines, notably those of the histamine-1 antagonist group, are commonly used in the management of peripheral vertigo. They are believed to exert a vestibulosuppressant effect via a central anticholinergic mechanism. Meclizine is most commonly used, starting at small doses (12.5 to 25 mg two to three times daily) and titrating to effect. Its effect is limited with adequate suppression typically lasting only 1 to 2 months. Promethazine is another antihistamine that also has antiemetic properties.
(2) Anticholinergics. Scopolamine is an anticholinergic medication commonly used in the prevention of motion sickness. It is not as valuable in the management of acquired vestibulopathy, but may be effective in the prophylaxis of motion sickness.
TABLE 56.1 Common Oral Medications for Treatment of Vertigo
(3) Benzodiazepines. They are a class of psychoactive drugs that work via central inhibitory GABA potentiation resulting in anxiolysis, sedation, and in some cases amnestic, anticonvulsant, and muscle relaxation effects. Lorazepam and diazepam are frequently used for their ability to prevent and mitigate attacks of dizziness and vertigo from a variety of etiologies. Diazepam at a low dose (5 to 10 mg) acts as a vestibulosuppressant and can be used for acute or chronic otologic dizziness. Care must be taken when utilizing benzodiazepines because of their increased potential for dependence and subsequent withdrawal symptoms on cessation of therapy.
(4) Antiemetics (Table 56.2). Antiemetics are used to relieve nausea and vomiting associated with vertigo. Prochlorperazine is a phenothiazine that exerts a strong antiemetic effect but also carries the risk of extra pyramidal side effects. Metoclopramide is a dopamine receptor antagonist and serotonin receptor antagonist/agonist with antiemetic and prokinetic properties. Ondansetron provides antiemesis via serotonin 5-HT3 receptor antagonism.
b. Corticosteroids/antivirals/antibiotics. Corticosteroids may be effective in treating associated hearing loss with labyrinthitis. Although most cases of labyrinthitis are believed to arise from viral infection, the addition of antiviral therapy to corticosteroids has not been shown to offer additional benefit. Antibiotics are of value in cases of bacterial or suppurative labyrinthitis; however, the decision to use antibiotics should be dictated by objective signs of infection.
c. Vestibular rehabilitation. It refers to physical therapy aimed at enhancing recovery from peripheral vestibulopathy. The exercises range from simple head-turning to increasingly more complex postural and ambulation challenges with and without head movement. Simple walking is a form of vestibular rehabilitation that can be recommended to patients with limited disequilibrium. The earlier vestibular rehabilitation takes place, the better the outcome, and patients should be titrated off vestibular suppressants to optimize vestibular challenge and recovery.
3. Results. Although there is some support for steroid use and vestibular rehabilitation enhancing vestibular recovery, randomized control trials are lacking. Fortunately, over 90% of patients with vestibular neuronitis or labyrinthitis will return to their presymptomatic baseline.
C. Méniere’s disease.
1. Clinical features. Méniere’s disease is characterized by the constellation of fluctuating SNHL, tinnitus, and vertigo. It is often associated with “aural fullness.” Episodes are recurrent and typically last 20 minutes or longer. Over time, the involved peripheral vestibular system experiences a reduction in responsiveness or “burns out.” It is a disease primarily of Caucasians with a slight female bias, and onset between 40 and 60 years of age. The histopathologic correlate is endolymphatic hydrops, the result of an overaccumulation of endolymph. The pathophysiologic mechanism is believed to be the result of membranous labyrinth microruptures allowing potassium-rich endolymph to mix with potassium-poor perilymph, thus disrupting biochemical gradients and neuronal conductivity.
2. Treatments. Treatment of Méniere’s disease is focused on vertiginous symptom control, as tinnitus and hearing loss are less amenable to intervention. Medical therapy is used at the outset of treatment with more invasive options reserved for symptoms refractory to conservative management.
a. Nonablative.
(1) Acute. As in labyrinthitis, antihistamines, anticholinergics, benzodiazepines, and antiemetics may be used to mitigate acute attacks of vertigo and nausea.
(2) Chronic. Salt restriction diet and diuretics are the mainstays of medical treatment. Their efficacy is believed to result from a reduction in endolymph. A combination of hydrochlorothiazide and triamterene is a commonly used regimen and can be titrated to effect. Also limiting alcohol, caffeine, and stress may be beneficial. Those patients with poor symptom control despite these measures may then be offered nonablative options such as intratympanic steroid injection or endolymphatic sac surgery (ESS). ESS is a hearing-preserving, nonvestibular-ablative endolymphatic sac decompressive procedure. The mechanisms by which it reduces vertigo are controversial.
TABLE 56.2 Common Oral Medications for Treatment of Nausea
|
Medication |
Dose |
|
Metoclopramide |
5–10 mg q6h |
|
Ondansetron |
8 mg t.i.d. |
|
Prochlorperazine |
5–10 mg t.i.d. to q.i.d. |
Abbreviations: t.i.d., three times a day; q.i.d., four times a day.
b. Ablative. For patients in whom conservative measures have failed, vestibular ablative options may be offered. Intratympanic gentamicin injection offers somewhat selective vestibular toxicity through a less invasive approach, but carries a significant risk of SNHL. Vestibular nerve section offers a high-rate of vertigo control with minimal risk to hearing. Labyrinthectomy is a complete vestibular-ablative procedure well-suited to patients with non-serviceable hearing.
3. Results. Diuretics have been shown to control vertigo and stabilize hearing in 50% to 70% of patients. In addition, the natural history of Méniere’s disease allows for spontaneous remission of episodic vertigo in 60% to 80% of patients. For those few with refractory vertigo, intratympanic steroid and endolymphatic sac decompression is effective at controlling vertigo in approximately 80% of patients, whereas ablative procedures such as intratympanic gentamicin, vestibular neuronectomy, and labyrinthectomy control vestibular symptoms in >90% of patients.
D. Perilymphatic fistula.
1. Clinical features. Perilymphatic fistula is a controversial clinical entity. Theoretically, it is characterized by the abnormal communication of perilymph between the labyrinth and the middle ear via the oval window, round window, or an aberrant pathway. It may result from barotrauma, penetrating middle ear trauma, stapedectomy, or occur spontaneously. The controversy in its diagnosis centers on the difficulty in identifying a microfistula intraoperatively and the lack of clear clinical criteria. It is described most often as vertigo with extreme pressure sensitivity that may be exacerbated by Valsalva’s maneuvers and pneumatic otoscopy. It may also be associated with sudden or gradual hearing loss and thus may mimic Méniere’s disease.
2. Treatments. Small fistulae may heal spontaneously with a short course of bed rest. In situations with stable hearing or when the clinical diagnosis is questioned, a trial of vestibular rehabilitation may be attempted. When there is a clear temporal relationship between a predisposing insult (e.g., scuba diving, ear surgery, or penetrating middle ear trauma), an exploratory tympanotomy may be undertaken by a neurotologist. The surgical goal is localization of a discrete fistula and patching with autogenous connective tissue. Postoperatively, a course of bed rest is undertaken to allow healing of the graft and efforts are made to minimize Valsalva coughing and straining.
3. Results. Bed rest is successful in many patients, and in cases where the fistula is evident, surgery can be very effective. Consideration of an alternate diagnosis such as superior semicircular canal dehiscence syndrome may be necessary in patients who undergo negative exploration.
E. Superior canal dehiscence syndrome.
1. Clinical features. Superior canal dehiscence syndrome (SCDS) is a sound- and pressure-induced vertigo caused by bony dehiscence of the superior semicircular canal. The characteristic torsional vertical nystagmus occurs in the plane of the affected canal with administration of sound and pressure changes. Patient complaints are variable and include autophony, sound-induced (Tullio’s phenomenon) or pressure-induced vertigo, conductive hearing loss and/or pulsatile tinnitus. Clinically, SCDS symptomatology overlaps with perilymphatic fistula and acquired horizontal canal dehiscence from cholesteatoma or chronic otitis media. However, history directs clinical suspicion and high-resolution CT demonstrating superior canal dehiscence is diagnostic.
2. Treatments. Surgical plugging of the affected superior canal can be beneficial in patients with debilitating symptoms due to this disorder.
3. Results. Success rates of surgical plugging of superior canal dehiscence are reported to range from 50% to 90%.
F. Ototoxicity.
1. Clinical features. Ototoxicity may be associated with a number of medications and manifests as hearing loss, tinnitus and/or dizziness, and vertigo. Clinically significant ototoxicity is commonly associated with aminoglycosides and other antibiotics, platinum-based antineoplastic agents, salicylates, quinine, and loop diuretics. Aminoglycoside gentamicin is notably vestibulotoxic, and this property is selectively utilized in vestibular ablation procedures as previously mentioned. Cessation of treatment will halt the continued insult, but recovery is variable and may be incomplete.
2. Treatments. Paramount to treatment is the avoidance of ototoxic medications whenever possible. Active treatment options are limited to vestibular rehabilitation and symptomatic supportive measures while central compensation and adaptation of the vestibulospinal and vestibulocervical reflexes occur.
3. Results. Although these compensatory mechanisms are of value, they are not typically sufficient in restoring complete function. Certainly prevention, if possible, is more effective than treatment in this condition.
G. Tumors involving the vestibulocochlear nerve.
1. Clinical features. Vestibular schwannoma is the most common lesion of the cerebellopontine angle (Fig. 56.2). These benign, slow-growing tumors can occupy the vestibular division of the eighth cranial nerve from the internal auditory canal to the cerebellopontine cistern. As the tumor enlarges, it can cause vestibulococholear nerve dysfunction both from local compression as well as disruption of blood supply. Tumor progression is typically gradual allowing for contralateral vestibular and central compensation to mask vestibular loss. More commonly, unilateral hearing loss and tinnitus prompt patients to seek care. Advanced tumors may show signs of vestibulopathy and result in life-threatening hydrocephalus and brainstem compression.
2. Treatments. The slow-growing nature of vestibular schwannoma and the inherent surgical risks require that treatment options be tailored to each patient. Patient age and documentation of tumor growth must be considered in the treatment planning because a certain percentage of tumors are quiescent. Young, healthy patients with active tumor growth may be encouraged to undergo surgery. Microsurgical resection offers a chance for complete tumor resection with a low rate of recurrence. Elderly patients who are poor surgical candidates may be better suited for observation in small quiescent tumors. Radiation therapy is another treatment modality that functions to arrest tumor growth and is often reserved for patients with demonstrated tumor growth who are poor surgical candidates.
FIGURE 56.2 Left-sided vestibular schwannoma on contrast-enhanced T1-weighted axial MRI.
3. Results. Success rates in the treatment of vestibular schwannoma must be weighed against the quiescent natural history of some tumors. Radiation therapy tumor control rates are reported >95% in some series, although it is unknown what percentage of these tumors were growing. Outcomes for microsurgical control of vestibular schwannomas are comparable to radiotherapy. Hearing preservation is not always possible with surgery and is dependent on tumor size and location. In addition, long-term data on radiotherapy also shows a high-rate of progressive SNHL in spite of tumor control.
II. CENTRAL NEUROLOGIC CAUSES OF VERTIGO
A. Ischemia or infarction.
1. Clinical features. Disruption of vertebrobasilar circulation to the brainstem, cerebellum, and peripheral vestibular system can cause dizziness and vertigo. The hallmark of this ischemia is the association of vertigo with other focal neurologic findings, particularly in a predictable anatomic distribution. Weakness, facial paresthesia, dysarthria, ataxia, diplopia, and visual disturbances are examples of symptoms that may also be present with transient ischemia or infarction of the brainstem. Because transient ischemia may be responsible for episodic vertigo, it is important to recognize it as such to prevent potential stroke.
2. Treatments. General supportive measures and the use of antiplatelet and anticoagulant medications remain the cornerstones of medical therapy for the management of acute ischemic stroke. More importantly for the clinician evaluating episodic dizziness in the outpatient center is the recognition of signs of transient ischemic attacks (TIAs). Preceding TIAs are a risk factor for atherothrombotic brain infarction and should prompt evaluation of other vascular risk factors such as hypertension, diabetes, obesity, hyperlipidemia, and smoking. Additionally, cardiac evaluation may be warranted in search of possible embolic sources depending on presenting signs. Further discussion on the treatment and prevention of ischemic cerebrovascular disease is discussed elsewhere in Chapter 36.
3. Results. Appropriate lifestyle modifications and the addition of antithrombotic (antiplatelets or oral anticoagulants when indicated) therapy are effective in reducing the incidence of stroke and permanent deficit after stroke in at-risk individuals. No therapy is 100% effective.
B. Basilar migraine and migrainous vertigo.
1. Clinical features. Classically described as a condition of adolescent females, basilar migraine (see ICHD-II) can affect males and females of any age though it does have a female preponderance. It is characterized by an aura causing hemianopic visual changes, vertigo, ataxia, numbness, or dysarthria followed by a throbbing occipital headache often associated with nausea. Symptoms are self-limited, with the aura lasting from a few minutes to an hour and a headache of variable duration. Basilar migraine is considered a distinct clinical entity from migrainous vertigo, which is characterized by episodic vertigo, but without related neurologic symptoms and in some cases, even without headache. Because it is more difficult to diagnose without the associated symptoms, some question migrainous vertigo as a clinical entity. Diagnosis of migrainous vertigo relies on indirect evidence in the form of relationship of symptoms to migrainous triggers and response to antimigraine medications. In both cases, and particularly with vertibrobasilar migraine, there is overlap between migrainous symptoms and those of more serious cerebrovascular derangement, and a thorough evaluation should rule out other causes of vertigo before the diagnosis of migraine is applied.
2. Treatments. Multiple treatment regimens exist for migraine. Abortive medical therapy is directed at resolving the symptoms shortly after onset. Medications such as ergotamine and the triptans fall into this category. Patients whose symptoms are more frequent may be candidates for preventive medical therapy in the form of ß-blocking agents, tricyclic antidepressants, antiepileptic drugs (AEDs), and calcium channel blockers. The treatment of migraine is discussed elsewhere in this text.
3. Results. With proper selection of medical therapy, the majority of migraine patients can achieve the goal of symptom prevention.
C. Seizures.
1. Clinical features. Seizures do not commonly cause vertigo in isolation. They are more often associated with accompanying features of complex partial seizures such as swallowing, lip-smacking, and alteration of consciousness. They may be the result of a CNS disorder such as tumor or brain injury or result from metabolic derangement. Evaluation of new-onset seizures with or without vertigo requires a thorough history and physical examination with ancillary testing directed at identifying potential underlying causes.
2. Treatments. AEDs are the primary therapy for seizures. In cases refractory to medication, surgical procedures exist to remove or isolate the epileptogenic focus. These treatments are discussed in detail in Chapters 38 and 39.
3. Results. The goal of therapy is to eliminate symptoms strictly with medication. Predicting the likelihood of effective treatment requires analysis of the underlying cause of seizure. Brain neoplasm and structural abnormalities may be more refractory to medical therapy than metabolic derangements.
D. Multiple sclerosis (MS).
1. Clinical features. MS is often diagnosed in young adults. Vertigo can be an associated symptom of CNS dysfunction and may be followed some time later with isolated weakness or visual disturbance. Clinical diagnosis is confirmed with MRI and/or CSF analysis.
2. Treatments. There are a number of immunomodulating agents used in the treatment of MS. These and other treatments are discussed in more detail elsewhere in Chapter 40.
3. Results. MS is a highly variable disease, and its effects on patients are myriad. Treatments are also varied with inconsistent results. The goal of appropriate therapy is to mitigate the severity of attacks while reducing their frequency.
E. Chiari’s malformations.
1. Clinical features. Symptoms suggestive of Chiari include headache, vertigo, ataxia, tinnitus, hearing loss, weakness, and numbness. Chiari’s malformations are often associated with downbeat nystagmus in the primary position.
2. Treatments. Conservative measures consisting of symptomatic control may be appropriate in certain patients. Those with progressive disease may require surgical decompression of the posterior fossa.
3. Results. Surgical decompression often relieves or at least halts the progression of brainstem compressive symptoms.
III. MEDICAL DIZZINESS
A. Postural hypotension.
1. Clinical features. Postural hypotension is a classic finding in elderly patients and may result from any number of causes. Symptomatically, it is described as lightheaded or presyncopal feeling when standing from sitting or lying. It can result from diminished cardiac output, antihypertensive medication with associated vasodilation or ß-blockade, dehydration, or autonomic insufficiency from underlying diabetic neuropathy, for example.
2. Treatments. Most important in the treatment of postural hypotension is to recognize it as such. With this in mind, a systematic hemodynamic review must be undertaken. Modification of a current medication regimen is straightforward. Exercise and improved hydration can improve underlying cardiac decompensation, and elastic stockings may be of benefit in optimizing cardiac return.
3. Results. Proper identification of hemodynamic insufficiency allows treatment modifications where able and is often successful at reducing the severity and frequency of postural hypotension.
B. Arrhythmia.
1. Clinical features. Symptoms of cardiac arrhythmia frequently include palpitations with or without chest pain. They may be associated with presyncope or even loss of consciousness but are not typically associated with true vertigo. Diagnostic workup includes cardiac monitoring, particularly during an episode, to secure the diagnosis.
2. Treatments. Cardiology referral is undertaken for evaluation and management of cardiac arrhythmia. Antiarrhythmic medications, pacemakers, and radiofrequency ablation of aberrant pathways of conduction may all be considered in treatment.
3. Results. Appropriate treatment can be very effective in managing most cardiac arrhythmias.
C. Hypoglycemia.
1. Clinical features. Metabolic derangements, such as insulin-dependent diabetic hypoglycemia, may be responsible for dysequilibrium but rarely true vertigo. Episodes of hypoglycemia and dysequilibrium may present acutely in patients who have used insulin for years.
2. Treatments. Treatment of hypoglycemia is acutely directed at increasing the serum blood glucose level and may require tailoring the diabetic regimen to prevent future episodes.
3. Results. Targeted treatment along with patient education is usually successful at resolving or decreasing the frequency of symptoms.
D. Medication-associated.
1. Clinical features. Medications that mediate CNS effects, such as AEDs, benzodiazepines, and psychogenics, may cause primary effects and side effects that create a sensation of dysequilibrium. This dysequilibrium is distinct from postural hypotension that may arise from antihypertensive medications as described above.
2. Treatments. Treatment is aimed at identifying, limiting, and/or removing the offending medication. Ideally, an alternative medication is found that offers a similar therapeutic profile.
3. Results. Removing the offending medication will remove the associated symptoms, but as with most medications, treatment effect must be weighed against side effect profile.
E. Infection.
1. Clinical features. Infectious labyrinthitis occurring due to a number of viral, bacterial, and fungal agents may cause vertigo. Patient exposures, vaccination history and associated signs and symptoms help to narrow the differential diagnosis.
2. Treatments. Identification of the causative infectious agent allows effective treatment with antibiotics, antivirals, or other supportive measures. Administration of mumps, rubella, rubeola, and varicella-zoster vaccines is the best method to prevent viral inner ear infections. Hearing aid and cochlear implantation are audiologic rehabilitation options as well.
3. Results. Results of treatment largely depend on the infectious etiology.
IV. UNLOCALIZED VERTIGO
A. Psychogenic. Anxiety, depression, and personality disorder are common codiagnoses in patients complaining of dizziness. It is a bidirectional relationship in that severe organic vertigo can cause symptoms of depression and anxiety given the potential unpredictability of attacks. In addition, patients with primary psychiatric diagnoses may also identify dizziness as a complaint, described as an out-of-body experience, a sense of floating or a racing sensation. It is important not to label a patient with a psychiatric diagnosis as having psychogenic dizziness until organic causes have been ruled out. Treatment should be directed at managing both organic and psychogenic factors simultaneously. SSRI medications and other antidepressants may be valuable in that role.
B. Malingering. Unfortunately, there are patients who misrepresent their symptoms for secondary gain. Objective testing, such as posturography, can be used to identify patients who may be falsely complaining of symptoms of dizziness.
C. Postconcussive. Concussions may be the result of mild-to-moderate traumatic brain injury (TBI) resulting in transient neurologic deficit with normal CT imaging of the brain. Nausea, vomiting, headache, and dizziness may present acutely. Focal neurologic deficits typically resolve over weeks to months following mild-to-moderate TBI, but cognitive, psychological, and emotional dysfunction may persist in more severe injuries. Supportive measures and vestibular rehabilitation are utilized to speed vestibular recovery.
D. Multifactorial. Because balance is a multifactorial process maintained through visual, proprioceptive, and vestibular input, decline in one component may be masked through central compensation mechanisms. In some patients, however, particularly the elderly multiply comorbid patient, a decline in balance input may not be met with adequate central compensation and equilibrium will be difficult to reestablish. Peripheral neuropathy, poor vision, and multiple vestibulosuppressant medications are examples of factors contributing to dysequilibrium that should be addressed. Continued walking, with assistance if necessary, is often recommended in an effort to prevent further decompensation.
E. Unknown. Although thorough history, physical examination, and judicious ancillary testing are effective in identifying the cause of dizziness in most patients, there remain those few whose symptoms arise from an unidentifiable source. This can be frustrating for both clinician and patient, and requires the clinician to counsel the patient regarding reasonable expectations in achieving a mutually acceptable outcome.
Recommended Readings
Amarenco P. The spectrum of cerebellar infarctions. Neurology. 1991;41:973–979.
Brandt TH. Phobic postural vertigo. Neurology. 1996;46:1515–1519.
Chawla N, Olshaker JS. Diagnosis and management of dizziness and vertigo. Med Clin North Am. 2006;96:291–304.
Derebery MJ. The diagnosis and treatment of dizziness. Med Clin North Am. 1999;83:163–177.
Hain TC, Yacovino D. Pharmacologic treatment of persons with dizziness. Neurol Clin. 2005;23:831–853.
International classification of headache disorders: 2nd edition. Cephalalgia. 2004;24(suppl 1):9–160.
Lynn S, Pool A, Rose D, et al. Randomized trial of the canalith repositioning procedure. Otolaryngol Head Neck Surg. 1995;113:712–720.
Minor LB. Superior canal dehiscence syndrome. Am J Otol. 2000;21:9.
Radtke A, von Brevern M, Tiel-Wilck K, et al. Self-treatment of benign paroxysmal positional vertigo: Semont maneuver vs Epley procedure. Neurology. 2004;63:150–152.
Solomon D. Distinguishing and treating causes of central vertigo. Otolaryngol Clin North Am. 2000;33(3):579–601.
Troost BT. Dizziness and vertigo. In: Bradley WG, Daroff RB, Fenichel GM, et al., eds. Neurology in Clinical Practice. 4th ed. Boston, MA: Butterworth-Heineman; 2004: chap 18.