Dizzy, fuzzy, lightheaded, spinning, off-balance, unsteady, rocky — patients use these and other words to describe clinical symptoms of vertigo, disequilibrium, and hypersensitivity to motion stimuli. Dizziness is a common complaint. Studies in the United States1–2 and United Kingdom3–5 found that the 1-month point prevalence of dizziness is about 20% in primary care settings. Most patients with dizziness have transient symptoms, but 1 in 3 have conditions that persist for 5 years or more,3 including 3% who are disabled by their symptoms.5 Most physicians think of vestibular dysfunction when patients complain of dizziness, but peripheral vestibular deficits and central neurotologic disorders cause only 50% to 60% of all cases of dizziness. Substantial numbers of dizzy patients have primary psychiatric (25% to 30%) or cardiopulmonary (2% to 40%) illnesses.6–8
Debates about the causes of dizziness date back to antiquity.9 The original descriptions of agoraphobia, which is translated literally as fear of the marketplace, included sensations of dizziness and disequilibrium in the open-air markets of historic villages. Otolaryngologic literature from the mid-1800s contained the first clear descriptions of panic attacks in people with dizziness.9 In more modern times, patients with medically unexplained dizziness frequently are diagnosed with “psychogenic dizziness,” a catch-all term that belies our understanding of the relationships between physical and psychological factors that initiate and sustain dizziness.10
Psychiatric disorders may cause dizziness directly, appear in the aftermath of medical causes of dizziness, or interact with physical illnesses in a combination of physical and psychiatric morbidity.12 Panic disorder with agoraphobia is the most common primary psychiatric cause of dizziness. Physical illnesses may trigger secondary panic attacks, phobic behaviors, generalized anxiety, depression, and somatization.13 These psychiatric symptoms may persist, even if the inciting medical conditions resolve.
Physical illnesses also may exacerbate pre-existing anxiety, producing a high level of co-existing physical and psychiatric symptoms.10 Finally, 15% to 25% of patients with chronic dizziness have symptoms that cannot be explained by identifiable, physical illnesses or psychiatric disorders.7,11,14 The core feature of this chronic subjective dizziness (CSD) is an acquired hypersensitivity to motion stimuli, including increased awareness of one's own movements and reduced tolerance for motion in the environment. This syndrome fits the definition of an undifferentiated somatoform disorder in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV),15 but its true cause is unknown.
Treatment research for patients with dizziness and psychiatric disorders is limited. Emerging data suggest that psychopharmacologic,11,16,17 psychotherapeutic,18 and behavioral19–22 interventions may be effective for both primary and secondary psychiatric disorders in patients with dizziness. Pilot data also indicate that serotonergic antidepressants and behavioral therapies may be effective for CSD, even in the absence of major psychiatric disorders.11,16
General Aspects of Dizziness
Overview of the Balance System
The balance system has three major functions: postural control, oculomotor control, and creation of internal spatial orientation maps. The balance system maintains control of posture through coordinated, reflexive actions on trunk and limb musculature. Deficits in postural control manifest as ataxia and falls. Vulnerable patients may develop a fear of falling. The balance system generates oculomotor commands through the vestibulo-ocular reflex (VOR). These signals compensate for head movements, allowing animals to keep visual targets in focus as they move about in their environments. Abnormalities in the VOR cause nystagmus, blurred vision, and oscillopsia (the perception of oscillations in the visual environment when patients move). As a result, patients may avoid activities with strong visual demands (eg, reading or working at a computer), producing considerable functional impairment.
Central balance pathways also create maps in the brain that represent spatial relationships between a person and objects in the environment. Inaccuracies in these internal spatial maps may cause disorientation and uneasiness in complex motion environments, such as busy shopping malls. These symptoms tend to be far more debilitating than fears of falling.
The balance system requires multiple sensory inputs to function properly. Visual, vestibular, and proprioceptive stimuli are the major sensory inputs in humans. Visual cues provide the bulk of information on the whereabouts and movements of objects in the environment. Visual inputs also contain strong orienting cues. Horizontal and vertical surfaces in the visual field provide potent inputs about the body's position in space. Vestibular end organs in the inner ear detect three-dimensional, angular, and linear movements of the head. Three semicircular canals in each inner ear detect angular accelerations, while two otoliths detect linear accelerations, including changes in the position of the head with respect to gravity. Proprioception provides critical information about the orientation of body and its physical contact with environment. In healthy people, these natural inputs reinforce one another. For example, when standing still, the eyes detect a constant relationship between oneself and static objects in the environment, vestibular end organs sense only the constant position of the head with respect to gravity, and proprioceptive receptors track the alignment of the body in a standing position.
Manmade conveyances challenge the balance system because they create situations in which balance inputs conflict with one another. Pilots are taught to fly by their instruments, not “the seat of their pants,” because their balance systems may misinterpret combinations of linear and angular accelerations in flight. Human responses to mismatched motion stimuli range from motion sickness to mild physiological arousal to intense panic. Amusement parks take full advantage of these reflexive responses with their funhouse illusions and myriad rides.
The complexity of the balance system makes it vulnerable to illnesses that affect several different organ systems. Neurotologic, cardiovascular, and psychiatric disorders are the principal causes of dizziness. Neurotologic conditions are divided into peripheral vestibular deficits and central vestibular disorders.3,4,7,8,12 Table 1 (see page 332) and Table 2 list the clinical characteristics of the most common peripheral and central vestibular disorders. Taken together, these illnesses are responsible for 50% to 60% of all cases of dizziness.
Common Peripheral Vestibular Deficits
Common Central Neurotologic Disorders
Cardiovascular causes of dizziness vary with age. From adolescence to middle adulthood, dysautonomias and dysrhythmias predominate. However, these conditions cause dizziness in only a small fraction (2% of 3%) of patients younger than 50. In contrast, coronary artery disease, congestive heart failure, and orthostatic intolerance cause dizziness in as many as 30% to 40% of older patients.8 Many older patients have multi-factorial dizziness. Combinations of chronic heart, lung, and metabolic diseases, impaired proprioception, and diminished visual acuity contribute to their symptoms. Side effects of prescribed and over-the-counter medications (eg, antihypertensives) may exacerbate these physical deficits.
Psychiatric disorders cause considerable morbidity in patients with chronic dizziness. Anxiety, depression, or somatization are present in 35% to 50% of tertiary care patients.23–25 Among all patients with chronic dizziness, 10% have primary psychiatric disorders, 10% have psychiatric disorders precipitated by transient medical illnesses, 10% have comorbid medical and psychiatric conditions in which the psychiatric disorders are the predominant features, and 5% to 20% have comorbid medical and psychiatric conditions in which medical illnesses are most problematic.23–25
The most effective tool for evaluating patients with dizziness is a detailed clinical history. The goal is to identify characteristic symptoms of physical and psychiatric disorders, keeping in mind that the presence of one does not exclude the other. Physical examinations, laboratory tests, and neuroimaging studies are used to confirm suspected diagnoses.
One of the biggest impediments to accurate diagnoses is ambiguous terminology. Patients and clinicians use words like vertigo, dizziness, and imbalance interchangeably. True vertigo refers to illusory movements of oneself or one's surroundings that typically are rotary in nature. Nausea and vomiting may accompany these symptoms. Vertigo is not subtle. Patients with true vertigo have little difficulty describing its illusory sensations. The duration of vertigo depends on its cause (Tables 1 and 2). Head movements usually aggravate vertigo, so patients may try to minimize their symptoms by remaining still.
The presence of vertigo, as described here, is almost always a symptom of physical illness. Other symptoms indicative of physical illnesses are ataxia, diplopia, and near syncope, especially when they are accompanied by relevant findings on physical examination (eg, nystagmus, dysconjugate gaze, orthostasis). These physical signs may be quite subtle, requiring special expertise, equipment, and testing to identify them.
Psychopathology and Dizziness
Psychiatric Causes of Dizziness
Psychiatric disorders are the sole cause of dizziness (a true psychogenic pattern of illness) in approximately 10% of patients referred to neurotologists. Almost all of these patients have panic disorder with or without agoraphobia.3,11–13,26 A much smaller number have somatoform disorders, usually conversion disorder or hypochondriasis.12,23
In cluster analyses that examined presentations of panic disorder, dizziness and lightheadedness were the second most common symptoms after chest pain and dyspnea.27 Patients with panic disorder have a history of panic attacks, with dizziness overshadowing cardiopulmonary symptoms and an absence of vertigo, syncope, or falls. Those with a chronic illness may have only limited symptom attacks of recurrent dizziness and mild autonomic arousal. They are more likely to report persistent hypersensitivity to motion cues. Many are impaired by agoraphobia and justify their phobic avoidance with catastrophic scenarios of becoming dizzy at inopportune moments.
Fewer than 1% of tertiary care patients with chronic dizziness have somatoform disorders.16,23–25 Those with conversion disorders complain of unsteadiness or imbalance and demonstrate an aphysiological gait on physical exam. The gait is typically wide-based, slow, and tentative, with a heavy reliance on physical support from others or the use of assistive devices. Conversion patients do not describe true vertigo, although they may report falls.
Patients with hypochondriasis are convinced that their dizziness is due to one or more specific physical illnesses, usually catastrophic diseases (eg, brain tumors) or conditions of dubious medical validity. They interpret all test results that are outside the normal range as clear evidence of disease. This is unfortunate in patients with dizziness because balance function tests frequently yield nondiagnostic abnormalities in those who are tense or anxious during testing.
Secondary Psychiatric Complications of Dizziness
Approximately 10% of patients referred for evaluation of chronic dizziness have histories of neurotologic illnesses but no evidence of active physical disease.10 Typical scenarios include patients with previous bouts of benign paroxysmal positional vertigo, vestibular neuronitis, or transient central nervous system events. Their histories indicate that the acute medical problems have resolved, leaving them with chronic sensations of dizziness, lightheadedness, or imbalance, accompanied by significant psychological distress. Patients may say, “When my dizziness first started it was like this, but now it's different.” This change in clinical course is extremely important, because treatments aimed at past medical illnesses provide little benefit for current psychiatric symptoms.
Such patients may acknowledge anxiety, depression, or preoccupation with their symptoms, but they blame their psychological morbidity on being chronically dizzy. In this regard, they are partially correct. The origins of their conditions lie in the medical events that produced their initial symptoms. However, psychosomatic mechanisms such as somatization and avoidance behaviors sustained their dizziness after the inciting events resolved. These psychiatric symptoms may give the false impression of psychogenesis.10
Acute vertigo is a provocative experience. Patients who experience acute vertigo have significantly more anxiety than those who develop acute nonvertiginous neurological deficits.28 As a result, they become hypervigilant about their own movements and environmental motion cues, which has two unfortunate consequences: they develop an anxious awareness of their own balance reflexes and become tentative about gait or position changes to the point that their caution overrides normal movements, and they become acutely aware of multiple motion stimuli and are more likely to feel overwhelmed in busy motion environments. This creates a vicious circle as anxiety promotes hypervigilance, hypervigilance interferes with normal balance reflexes, and seemingly abnormal balance function generates more anxiety. Patients then avoid situations in which they feel dizzy and anticipate these circumstances with trepidation. Phobic symptoms may be limited to dizziness-provoking situations (ie, a specific phobia of dizziness) or they may generalize to full-fledged agoraphobia and panic attacks. In one study, 60% of chronically dizzy patients had secondary anxiety limited to specific phobias, whereas 40% developed panic disorder with or without agoraphobia.10
Depression is a frequent secondary complication of chronic dizziness that strongly correlates with the intensity of anxiety. The number of patients who develop psychiatric symptoms after bouts of dizziness is not known, but epidemiological data suggest that 2% to 3% of primary care patients suffer from chronic dizziness complicated by psychiatric morbidity.23–26,28,29 In one prospective study,29 67 patients with vestibular neuronitis were followed for 6 months after hospitalization for their vestibular crisis. In most patients, dizziness resolved over several weeks. However, 13 patients (19.4%) had persistent dizziness. Almost all of them (11 of 13) had high levels of anxiety. Catastrophic thinking and dependent personality traits explained 35% of the variance in chronic dizziness.
Approximately 15% to 30% of tertiary care patients with chronic dizziness have comorbid physical and psychiatric illnesses that interact with each another.10,12,23–25 These patients can be divided into two groups — those in whom physical illnesses dominate the clinical picture, and those in whom psychiatric morbidity is most problematic. The first group (5% to 20% of tertiary care patients) have active physical illnesses that produce chronic or recurrent bouts of vertigo, ataxia, or near syncope. They suffer from chronic medical conditions that are complicated by secondary anxiety or depression. Several studies have shown psychological factors such as somatic anxiety, phobic avoidance, depression, dependent or avoidant personality traits, an external locus of control (ie, a sense that events are beyond one's control), and poor tolerance for physical deficits predict chronic disability to a greater extent than the severity of physical illness.19,20,30,31 Therefore, in addition to expert medical care, these patients require multifaceted psychiatric treatment that includes aggressive interventions for anxiety and depression as well as efforts to promote positive coping strategies and improve patients' sense of control. The need to rely on other people or assistive devices is a major challenge, but failure to accept reasonable assistance (eg, refusal to use a cane) may, paradoxically, decrease mobility. Patients with avoidant or dependent personality traits seem to have the most difficulty negotiating this reliance on others.
The second group of medical-psychiatric patients (about 10% of tertiary care patients) have a history of anxiety or a strong predisposition to anxiety predating the onset of dizziness. They have anxious temperaments, subclinical generalized anxiety, histories of psychosomatic responses to stressful situations, or strong family histories of anxiety disorders.10 When afflicted with physical causes of dizziness, they develop both chronic dizziness and persistent anxiety disorders. In contrast to patients with the otogenic pattern of illness, 60% of predisposed patients develop panic disorder, and nearly 40% manifest generalized anxiety disorder after they become dizzy. Only a small fraction have anxiety symptoms that stay limited to a specific phobia of dizziness.10 Thus, physical causes of dizziness, even transient ones, are capable of triggering serious anxiety disorders in predisposed patients. Secondary depressive symptoms may develop in proportion to the severity of anxiety.
This group may not need medical care beyond their initial evaluation if their physical illnesses are inactive. Psychiatric treatment is best directed at symptoms of anxiety and depression, with a full expectation that dizziness will decrease as the psychiatric disorders are brought under control. Interventions to help patients adapt to chronic dizziness have a secondary place in the treatment of this group, because a premature focus on adaptation detracts from the primary goal of eradicating symptoms.
Psychiatric evaluations of patients with chronic dizziness often yield comorbid diagnoses across the realms of anxiety, mood, and somatoform disorders. This multiplicity of diagnoses can be confusing to both patients and referring clinicians. We proposed a three-dimensional psychiatric profile for patients with chronic dizziness (Figure, see page 334) to provide a clearer snapshot of specific targets for psychiatric treatment.12 The three dimensions — fear response, mood state, and symptom focus — correspond to DSM-IV anxiety, depressive, and somatoform symptoms found in patients with dizziness. The profile is useful for patient education and treatment planning.
Chronic Subjective Dizziness
In rigorous diagnostic studies of patients with chronic dizziness, a significant number (up to 25%) have no identifiable medical or psychiatric illnesses.7,8,10,11,24,32 Typically, they report subjective sensations of dizziness, unsteadiness, and hypersensitivity to motion stimuli that occur on most days, often continuously throughout the day. Their symptoms are amplified in environments with complex visual cues (eg, grocery stores, shopping malls) or rapid motion stimuli (eg, fast-moving traffic). They have difficulties with tasks that require fine visual focus (eg, reading, using a computer). Patients with this clinical syndrome do not have vertigo, syncope, ataxia, major anxiety or depressive disorders, or the secondary gain found in patients with somatoform disorders, although long-term studies indicate that they are prone to secondary psychiatric illnesses.14,32
Several diagnostic terms have been applied to this clinical syndrome, including psychogenic dizziness, despite the absence of psychiatric symptoms (eg, panic attacks) that could be the genesis of the illness. The DSM-IV diagnosis is undifferentiated somatoform disorder. However, this diagnostic category implies psychiatric illness when none has been established. German investigators coined the term phobic postural vertigo (PPV),14,32 which also conveys a psychiatric quality that may not be warranted and uses vertigo in a broad, non-specific manner. We prefer the descriptive term chronic subjective dizziness (CSD).11
The cause of CSD is not known. In some cases, patients date the onset of their symptoms to a transient physical or psychiatric event that triggered dizziness; however, this is not a universal finding. Patients with CSD have an exquisite hypersensitivity to motion stimuli. They become conscious of small, natural perturbations in balance reflexes and respond with unnecessary corrective actions.
Motion hypersensitivity, once established, reinforces itself. In follow-up studies, CSD remitted spontaneously in less than one-half of cases.2,32 Motion hypersensitivity was demonstrated in an experiment in which patients with CSD and normal controls stood on a balance platform in front of a large, rotating visual field stimulus.33 This type of stimulus generates vection, an illusory sensation that one is tilting or rolling to the side. Normal people reflexively lean in the opposite direction. Patients with CSD leaned significantly less than controls and righted themselves more often, although they were never in danger of falling.
Two theories exist about the cause of CSD. One postulates the existence of subtle deficits in central vestibular pathways created by subthreshold neural insults or incomplete compensation for damage sustained during previous neurotologic illnesses.14 These deficits are thought to produce subtle errors in the internal spatial orientation maps, enough to generate constant sensations of imbalance, but not enough impair postural or oculomotor control.
The second theory uses the tenets of classical and operant conditioning to propose that individuals with CSD develop a conditioned hypersensitivity to normal motion stimuli leading to excessive attention to balance reflex activity. Physical and psychiatric illnesses, or normal events such as falls or momentary lightheadedness, are thought to provide the unconditioned stimuli. Then, the ubiquity of day-to-day motion cues reinforces the conditioned responses.
These theories are not mutually exclusive and may act in consort to initiate and sustain CSD. Neurophysiologic studies have demonstrated neural activity that could play a role in CSD. Repetitive vestibular inputs can entrain the firing patterns of central vestibular neurons, which retain the induced responses after the stimuli cease.34 Entrainment of abnormal stimuli from brief periods of illness could be a perpetual source of errors in internal spatial orientation maps. Neural pathways link the central vestibular system to fear centers in the limbic nuclei.13 A recent study demonstrated that exposure to recurrent motion stimuli induced fos expression (a marker of protein transcription) in the central nucleus of the amygdala before similar activity was detected in the vestibular nuclei.35 This suggests that provocative motion stimuli induce early responses in fear-related pathways.
No treatments have been developed specifically for patients with chronic dizziness and psychiatric illnesses. Interventions currently used in this patient population were adopted from established treatments for uncomplicated anxiety disorders or neurotologic illnesses. This may be a reasonable start, but refinements are needed to meet the challenges of chronic dizziness.
There are no controlled studies of any medications for patients with chronic dizziness and psychiatric disorders. Neurotologists often prescribe short courses of benzodiazepines because of their familiarity with using these medications to suppress dizziness during acute neurotologic illnesses. However, benzodiazepines might not be effective for patients with chronic dizziness. Their side effects mimic patients' symptoms, and tachyphylaxis is common.16
Three studies using selective serotonin reuptake inhibitors (SSRIs) to treat patients with chronic dizziness and psychiatric symptoms have been published.11,16,17 The first was a case series of 60 patients, two-thirds (n = 41) with major anxiety or depressive disorders.16 The others had CSD or subthreshold psychiatric symptoms. Thirty-two patients had physical neurotologic illnesses at some point in the course of their dizziness, but only 13 had active neurotologic conditions at the time they were treated with fluoxetine, sertraline, paroxetine, or citalopram. Thirty-eight (63%) patients in the intent to treat sample and 32 of 38 (84%) who were treated for at least 20 weeks had positive responses on the Clinical Global Impressions – Improvement Scale (CGI-I score less than 3). Response rates were equal for patients with and without major psychiatric disorders. One-quarter of the patients (n = 15) could not tolerate an SSRI.
The other two studies were open-label, prospective clinical trials.11,17 A US trial included 20 patients treated with 50 to 200 mg of sertraline daily for 16 weeks.11 None of the patients had active neurotologic illnesses at the time of treatment. Sixteen had major anxiety disorders, and four had CSD. Significant improvements were achieved at 8 weeks on measures of dizziness, functional impairment, anxiety and depression. Response rates were comparable in study completers with major anxiety disorders (8 of 11) and those with CSD (3 of 4). One-quarter of the patients (n = 5) could not tolerate sertraline.
In a Japanese study, 47 patients were grouped into four cells based on the presence or absence of active neurotologic illnesses and low or high scores on the Zung Depression Scale.17 All patients were treated with 20 mg of paroxetine daily. After 4 weeks, patients in both groups with high depression scores (ie, those with and without neurotologic illnesses) improved significantly. Physical vestibular dysfunction was not affected by paroxetine treatment. Patients with no identifiable physical illness and low depression scores (ie, those with CSD) did not benefit from paroxetine.
These uncontrolled data suggest that SSRIs are safe and effective for treating major anxiety and depressive disorders in patients with dizziness. SSRIs did not exacerbate dizziness, even in patients with active neurotologic conditions. Patients with CSD benefited from SSRIs in the case series and the US prospective trial, but not in the Japanese study. Differences in medication dosing and duration may explain this difference in outcomes. In the two studies with favorable results, patients with CSD needed at least 8 weeks to achieve a positive response. The 4-week duration of the Japanese study was probably too short, and the dose of paroxetine (20 mg per day) may have been too low for some patients. Controlled trials are required to verify these results, and additional studies will be needed to develop alternative therapies or augmentation strategies for patients who cannot tolerate SSRIs or fail to respond satisfactorily to SSRI therapy.
Vestibular and Balance Rehabilitation Therapy
Vestibular and balance rehabilitation therapy (VBRT) is a type of physical therapy that was developed to speed the process of central nervous system compensation for acute vestibular deficits. In conducting VBRT, physical therapists design exercises that expose patients to visual, vestibular, and proprioceptive stimuli in a graded fashion in order to improve their physical balance function.
Not surprisingly, VBRT may have positive psychological effects as patients lessen their sensitivity to motion stimuli, improve confidence in their balance, reduce beliefs about negative consequences of imbalance, and diminish avoidance behaviors that frequently develop during acute vestibular crises.19–22 From a psychological perspective, VBRT is a form of behavioral therapy. Researchers are just beginning to study the efficacy of VBRT for patients with dizziness-related psychiatric symptoms in the absence of active vestibular deficits.
Given the prevalence of anxiety disorders in patients with chronic dizziness, cognitive therapy would seem to be an ideal psychological treatment. Unfortunately, data are extremely sparse on its efficacy in dizzy patients with medical and psychiatric comorbidity. Even for patients with the psychogenic pattern of illness, there is little information about somatic outcomes. A pilot study combining cognitive therapy with VBRT in nine patients had a positive result.18
Chronic dizziness is a common problem in primary care settings, where approximately 7% of patients have symptoms that last for more than 5 years. One-third have clinically significant psychiatric symptoms, and 1 in 200 is disabled. In neurotology referral centers, 35% to 50% of patients have psychiatric morbidity, most of it undiagnosed and untreated.
Mental health professionals can reduce the burden of chronic dizziness by helping patients to understand its three-dimensional psychiatric profile: fear responses such as hypervigilance about motion cues, anticipatory anxiety, and phobic avoidance; changes in mood state ranging from demoralization to major depression; and an intense focus on physical symptoms. Psychiatric symptoms develop in one of three patterns of illness: a psychogenic pattern that is almost exclusively due to panic disorder, an otogenic pattern in which physical causes of dizziness trigger anxiety and depressive disorders, and an interactive pattern in which physical causes of dizziness exacerbate pre-existing anxiety, producing significant medical-psychiatric comorbidity.
Treatment research is limited and controlled studies are lacking, but emerging evidence suggests SSRIs may be safe and effective for chronic dizziness. Vestibular and balance rehabilitation therapy may reduce physical symptoms and improve psychiatric morbidity. Cognitive therapy may be a useful intervention, although it has not been tested in patients with chronic dizziness.
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Common Peripheral Vestibular Deficits
|Disorder||Type of Dizziness||Duration of Dizziness||Hearing Loss||Diagnostic Test||Treatment|
|Benign paroxysmal positional vertigo (BPPV)||Rotary vertigo or pitching sensations provoked by head movements in specific directions.||Acute symptoms last 20 to 30 seconds.
BPPV may be active for weeks to months.||No.||Dix-Hallpike test.||Canalith repositioning (Epley) maneuver.|
|Meniere's disease||Spontaneous and motion-provoked attacks of vertigo.||Acute attacks last days to weeks. Overall illness is episodic, with variable periods of remission.||Fluctuating low-frequency hearing loss; may become permanent.||Balance function tests and audiometery.||Salt restriction and diuretics for mild cases.
Gentamicin ablation of vestibular function for debilitating cases.|
|Vestibular neuronitis||Vertigo, ataxia, and motion sickness prompted by head movements in any direction.||Acute symptoms last for several days, and then fade over several weeks.||No.||MRI to rule out central lesions.||Vestibular suppressants and pulse steroids for acute symptoms.
|Trauma||Depends on type of injury.
May precipitate BPPV or acute vestibular loss with vertigo, ataxia, and motion sickness.||BPPV as above.
Symptoms of acute vestibular loss last for days, and then fade over several weeks.||Depends on type of injury.||Balance function tests.||BPPV as above. Vestibular suppressants for acute symptoms. Vestibular rehabilitation.|
|Ototoxicity||Vertigo, ataxia, oscillopsia.||May be temporary or permanent. Adaptation to permanent loss usually occurs.||Depends on extent of toxic exposure.||Determine history of exposure.
Balance function tests.||Minimize exposure to offending agent.
Common Central Neurotologic Disorders
|Disorder||Type of Dizziness||Duration of Dizziness||Hearing Loss||Diagnostic Test||Treatment|
|Vestibular migraine||Vertigo, ataxia, motion sensitivity.||Acute symptoms last hours to days. May occur before, during, or after headache.||No.||International Headache Society (IHS) criteria.||Migraine prophylactic and abortive agents.|
|Cerebrovascular accident (CVA)||Vertigo, ataxia, oscillopsia.||Acute onset. Gradual resolution may occur.
Possible adaptation to permanent loss.||Rare. Depends on site of stroke.||Evaluate for causes of stroke.||Reduce risk factors.
|Traumatic brain injury (TBI)||Vertigo, ataxia, chronic subjective dizziness (CSD).||Variable. Adaptation to vertigo is common.
CSD may be permanent.||Depends on type of injury.||Neuroimaging.
Balance function test battery.||Antidepressants.
|Cerebello- pontine angle tumors||Vertigo, ataxia, diplopia.||Progressive, although most tumors are benign and slow-growing.||Common.||MRI.||Observation. Surgical excision. Radiation therapy.|