Clinical manifestations

Presentation and course

Dizziness is a nonspecific term that describes an unpleasant sensation of imbalance or altered orientation in space. The specific clinical manifestations of dizziness depend on which category or categories of dizziness exist: vertigo, disequilibrium, presyncope, or psychophysiological (psychogenic) dizziness (34; 36; 37; 82; 125; 100).

Vertigo is an illusion of movement due to an imbalance of tonic vestibular activity (82). It is usually rotatory, but sensations of body tilt or impulsion may also occur. Vertigo is commonly associated with nystagmus, oscillopsia, postural imbalance, and autonomic symptoms (eg, sweating, pallor, nausea, vomiting). Nystagmus is present in approximately 20% of emergency room visits for dizziness, but no further characteristics are recorded in at least a quarter of cases (70). In addition, documented descriptions usually conflict with the diagnosis when a peripheral vestibular disorder is diagnosed in the emergency room (70). As a result, documented details do not often allow a meaningful inference concerning the cause of the dizziness (70).

Disequilibrium is a state of nonvertiginous altered static (eg, standing) or dynamic (eg, walking) postural balance (63; 82). Patients with disequilibrium often complain of unsteadiness, imbalance, and falls (06). Sensory disequilibrium is caused by altered spatial orientation. Except in cases of visual-vestibular mismatch, patients with sensory disequilibrium generally do worse in the dark and frequently have a Romberg sign on examination (83). Motor disequilibrium is caused by impaired motor performance, possibly due to mechanical factors or to dysfunction of central and peripheral nervous system motor pathways. Motor disequilibrium, including that due to cerebellar dysfunction, is generally not exacerbated in the dark or by closing the eyes. Disequilibrium is significantly associated with increasing age, diabetes, arthritis, impaired vision, and decreased grip strength (152). Disequilibrium with poor postural balance is associated with increased fall risk after adjusting for subjective symptoms in older adults (01).

Presyncope is a syndrome characterized by a sensation of impending loss of consciousness and is commonly associated with generalized weakness, diaphoresis, nausea, and epigastric distress (116; 156; 119; 91; 73; 82). Other associated symptoms may include facial pallor or ashen-gray appearance, scotomata, visual dimming or grayout, and, depending on the cause, palpitations, acral and perioral paresthesias, and carpopedal spasms. Orthostatic hypotension is the most common cause, but arrhythmias, orthostatic intolerance (eg, postural orthostatic tachycardia syndrome), hyperventilation, panic attacks, and other conditions can produce presyncope. Symptoms, especially those due to orthostatic hypotension, may be exacerbated by exertion (especially postexertion), prolonged standing, increased ambient temperature, and eating (43). Episodes of presyncope are generally relieved with recumbency. True syncope is rare with hyperventilation, hypoglycemia, and postural orthostatic tachycardia syndrome (POTS).

Psychophysiological (psychogenic, functional) dizziness is a vague giddiness or dissociated sensation due to impaired central integration of sensory and motor signals in patients with acute and chronic anxiety (34; 82; 117; 33; 124; 136). Some anxious patients may use a counterproductive postural strategy of anxious anticipatory cocontraction of the antigravity muscles (12). This form of dizziness can also be seen in association with fear of heights and in patients with previous well-compensated vestibular lesions (117; 124; 136). Other terms employed for this category of dizziness include chronic subjective dizziness, phobic postural vertigo, space-motion phobia, and persistent postural-perceptual dizziness (146; 124; 136). The dizzy sensation is typically protracted or continuous, with periodic exacerbations, often punctuated by episodes of hyperventilation-induced presyncope. Specific provocative factors may be identified, such as the presence of crowds, driving, or being in confined places (eg, elevators). Episodes are not associated with facial pallor and are not relieved with recumbency. Women are more affected by chronic subjective dizziness than men (2:1) (117). It is important to emphasize, however, that anxiety and depression may be associated with, and may result from, other forms of dizziness because of the sudden, dramatic, and unpleasant associated sensations and from fear of falling, injury, or death (82; 81; 57). Consequently, the presence of anxiety or depression does not by itself indicate psychophysiological (psychogenic) dizziness. Nevertheless, patients’ emotional status can contribute to prolonged dizziness symptoms from the acute phase of dizziness or vertigo (128).

Epileptic vertigo/dizziness is primarily associated with temporal lobe seizures and rarely occurs as an isolated manifestation of seizures (154). Localized EEG abnormalities in such cases are most frequently temporal (80%) but may less commonly be parietal (12%) (154).

Depending on the cause, dizziness may be associated with various other symptoms including headache (14), daytime somnolence, and sleep apnea (145). To the extent possible, it is important to identify associated symptoms, recognizing that some associated symptoms may occur with more than one type of dizziness. Headache, for example, can occur with vertigo (eg, migraine, brainstem ischemia), motor dysequilibrium (eg, cerebellar infarct or hemorrhage), presyncope, and psychophysiologic dizziness (often associated with anxiety, sleep deprivation, and caffeine overuse/withdrawal).

It takes a careful approach to history-taking that seeks to clarify exactly what a patient means, sometimes rephrasing what they say to see if that is what they meant or giving examples (eg, “Like when you were a child and you turned around several times just to make yourself dizzy?”). The issues become even more complex in the elderly or those with multiple comorbid medical conditions because they often simultaneously have several different types of dizziness. For example, it is not uncommon for a diabetic patient to have presented with “dizziness” or “vertigo” after a fall and then to discover that he or she has fall-related benign paroxysmal positioning vertigo, plus symptomatic orthostatic hypotension and sensory disequilibrium (both from diabetic neuropathy, autonomic and large-fiber, with the orthostatic hypotension possibly aggravated by medications). The lack of a thorough history and careful clinical examination will typically result in only one of these factors being identified and the patient seeking consultation after consultation to address the forms of “dizziness” that haven’t been identified.

A major barrier to assessment of patients with dizziness is the common difference and perspective of patients and clinicians regarding this complaint. Although patients and providers both view dizziness as imbalance, patients more commonly describe dizziness in the context of lightheadedness, visual symptoms, and pain, whereas providers more frequently define dizziness according to motion sensitivity (144).

Problems of questionnaire-based research methods as a substitute for a medical history have confounded multiple studies in the literature that have naively dismissed traditional approaches to assessment of dizziness that categorize dizziness (eg, into vertigo, presyncope, disequilibrium, or chronic dizziness) in favor of those that advocate an emergency room-based categorization for all dizziness assessments.

Some articles consider all dizziness in one of three “vestibular disorder” categories: acute vestibular syndrome, spontaneous episodic vestibular syndrome, and triggered episodic vestibular syndrome (50). This latter approach is indeed useful in emergency settings to focus on recognizing the small subgroup of dangerous dizziness cases (eg, cerebral ischemia presenting with dizziness), but it has less utility elsewhere. The framework doesn’t really address dizziness that is not “vestibular” (eg, presyncope, disequilibrium), doesn’t address chronic dizziness (even if fluctuating), doesn’t address dizziness in younger individuals not at risk for cerebral ischemia, and doesn’t account well for the common situation of multifactorial dizziness, particularly in the elderly.

The prognostic implications of different categories of dizziness are very different, even if, in some cases, patients have difficulty clearly expressing the character of their dizzy sensations. For example, a cohort study of 1716 hypertensive patients recruited in the 1970s categorized patients as not dizzy, vertiginous, or nonvertiginous dizziness (32). The presence of dizziness had no impact on the risk for all-cause mortality, cardiovascular mortality, or stroke mortality. Only vertigo had a prognostic impact. The increased risk was particularly marked in stroke death with a hazard ratio of 2.4 (95% confidence interval 1.3-4.5) versus patients without dizziness and 2.2 (95% confidence interval 1.2-4.1) versus patients with dizziness excluding vertigo.

Another useful but limited categorization of dizziness adopts a 4-category scheme: (1) acute vestibular syndrome; (2) recurrent positional vertigo; (3) recurrent spontaneous vertigo; and (4) “chronic vestibular insufficiency (imbalance)” (164). Acute vestibular syndrome was defined as “a first-ever attack of acute, spontaneous, isolated vertigo” with two common causes noted to be vestibular neuritis (or labyrinthitis) and cerebellar infarction, but certainly a person may have more than one episode of acute vertigo without it being recurrent in the usual sense, brainstem infarction (without cerebellar infarction) may cause acute vertigo, and there are other peripheral causes of acute peripheral vestibulopathy that are not inflammatory. Recurrent positional vertigo was correctly noted to be most often caused by benign paroxysmal positioning vertigo and less commonly central in origin, but this ignores the very common problem of orthostatic dizziness and presyncope (eg, orthostatic hypotension, postural orthostatic tachycardia syndrome). Recurrent spontaneous vertigo has two common causes: Meniere disease and vestibular migraine. The final category of “chronic vestibular insufficiency (imbalance)” was stated to result from “bilateral, or severe unilateral, peripheral vestibular impairment” but leaves out chronic nonvestibular dizziness (eg, from nonvestibular or multifactorial disequilibrium, anxiety, fear of falling, persistent postural-perceptual dizziness, etc.). It would be more appropriate if these authors considered this a categorization of vertigo rather than the broader category of dizziness.

Prognosis and complications

Although prognosis and complications of dizziness are a function of the underlying causes, dizziness as a broad category is an important contributor to population-attributable disability, particularly among the aged, and is often associated with significant comorbidities and serious consequences, including falls, traumatic injuries, loss of autonomy, and institutionalization (126; 88; 103; 104; 04; 89). Dizziness is strongly associated with both an increased tendency to fall and increased injury rate from falls among adults (88; 04; 87). Dizziness among obese adults is associated with a higher rate of falling than among non-obese adults but is not associated with a significantly higher rate of fall-related injury (88). Some forms of dizziness present other subtype- or condition-specific risks, eg, orthostatic hypotension carries an additional risk of syncope (126).

Older individuals who report dizziness are more physically frail, have more chronic conditions and sensory impairments, and have poor self-perceptions of their own health than older persons without dizziness (47). In addition, older individuals with dizziness are less physically active, have worse lower extremity function, are more often fallers, and report lower self-rated health than persons without dizziness (77). Furthermore, dizziness causes great psychological distress and greater perceived disability (56), particularly in the elderly (35) and is more likely to persist or relapse (135).

Health-related quality of life is decreased in patients with dizziness compared with dizziness-free controls (112). Dizziness results in detrimental effects on work, travel, social life, and family life (22). Indicators for dizziness-related impairment include longer duration of dizziness (ie, onset 6 months or more ago), frequent dizziness (ie, at least once per day), the presence of anxiety or depression, use of sedative drugs, and impaired functional mobility (35). Risk factors for obtaining an occupational disability rating attributed to dizziness include older age and lower educational attainment (141).

In a systematic review, diving ability was negatively affected by dizziness or a vestibular disorder in most included studies, with a low risk of bias (159).

Clinical vignette

Case 1. A 51-year-old diabetic woman with end-stage renal disease was referred for evaluation of dizziness and falling. About 3 weeks previously, she developed episodes of weakness and dizziness and felt lightheaded, especially when standing. She had a loss of balance and sudden unexpected falls. She was given a walker, but this did not resolve her problems.

Her medical history was significant for complications of diabetes, including end-stage renal disease on peritoneal dialysis, retinopathy, amputation of a toe because of infection, hypertension, and multiple small vessel strokes. She was hospitalized for left face and arm weakness, which largely resolved over several days. She had been changed from enteric-coated aspirin therapy to warfarin therapy. She also had a history of major depression. Her medications included iron, multivitamins, enalapril 10 mg daily, warfarin sodium 5 mg daily, regular insulin 40 units in the morning, neutral protamine insulin 22 units in the evening, and amitriptyline 125 mg every evening for depression.

Other studies were reviewed. CT scan showed bihemispheric subcortical lacunar infarctions. Carotid ultrasound showed atherosclerotic disease without significant stenosis. Electrocardiogram, Holter monitor, and echocardiogram were normal. She was adequately anticoagulated with international normalized ratios between 2 and 3.

The patient discontinued the amitriptyline on her own 2 weeks prior to her initial neurology evaluation. She reported feeling much better and had no falls or dizziness after that. Her neurologic examination was significant for normal mentation, full visual fields, slight left facial weakness, no dysarthria, mild left hemiparesis with arm worse than leg, unsteadiness with turns, unsteadiness with tandem gait, inability to maintain stance with feet together and eyes open, diffusely depressed reflexes, graded distal sensory loss, and markedly decreased joint position sense in the toes.

Several factors probably contributed to the dizziness and falls in this case, including presyncope from orthostatic hypotension (as a result of the amitriptyline), motor disequilibrium related to her hemiparesis, and sensory disequilibrium related to her neuropathy and impaired proprioception. The most reversible factor was medication-induced orthostatic hypotension. Anticoagulation in the setting of dizziness and frequent falls was risky, particularly when the potential therapeutic benefit was questionable, as it was for prophylaxis of subcortical infarcts. In this case, management included the use of a quad cane, aggressive treatment of stroke risk factors, discontinuation of warfarin sodium, initiation of ticlopidine, and substitution of the selective-serotonin-reuptake inhibitor sertraline for the tricyclic antidepressant amitriptyline she had been taking.

Case 2. A 32-year-old man was referred for evaluation of dizziness. He was recovering from injuries sustained in a motor vehicle accident more than a year before. He fell asleep while driving, drove off the road, struck a fence, and was impaled by a portion of it, causing severe chest and abdominal injuries. He also mangled his right arm and injured nerves in his right leg.

He initially noted dizziness when he first tried to stand in the hospital 2 months after his accident. All of his subsequent episodes occurred with standing or with activity when standing. With some of these episodes, he lost consciousness. He had some warning, which he described as a pressure sensation bifrontally, followed by visual grayout and a sensation like he was going to faint. Associated spinning sensation, nausea, vomiting, diaphoresis, palpitations, carpopedal spasms, or acral or perioral paresthesias were not present. These episodes decreased markedly over several weeks, but he reported occasional similar episodes without loss of consciousness. They were precipitated by physical activity when standing but not by any specific head movement. He was on no medications.

On examination, his blood pressure supine was 116/78, with a pulse of 60. When standing, his blood pressure was 108/78, with a pulse of 80. He was not dizzy when standing in the office. A fistula test and Dix-Hallpike maneuvers were negative. He had difficulty using the right arm because of a posttraumatic mechanical restriction at the right elbow. His neurologic examination was normal except for a depressed right knee jerk and patchy sensory loss of the right index finger, the right anterior thigh, and the right medial lower leg.

Any category of dizziness can occur following trauma. For example, posttraumatic vertigo may result from a perilymphatic fistula, benign paroxysmal positioning vertigo, other labyrinthine or vestibular nerve injury, or central nervous system injury. Presyncope may result from blood loss, deconditioning following prolonged bed rest, medications, etc. Disequilibrium may result from musculoskeletal or neurologic injuries. Psychophysiological dizziness may be precipitated by trauma-induced anxiety. Although the patient did not have symptomatic orthostatic hypotension in the office, his dizziness was most consistent with presyncope due to orthostatic hypotension. His symptoms occurred only when standing and were associated with signs of cerebral hypoperfusion (including visual grayout, presyncope, and syncope). He had no vertigo and no signs or symptoms of anxiety or hyperventilation. Medications were not the cause of his problem. Most likely, his orthostatic hypotension was due to deconditioning following prolonged bed rest and possibly exacerbated by short gut syndrome and inability to retain adequate blood volume with much of his colon resected. Management of this problem should be directed at maintaining adequate blood pressure and blood volume. Initial measures in this patient could include a high salt diet, high fluid intake, a body stocking or thigh-high support stockings with an abdominal corset as needed, multiple small meals, caffeine or ibuprofen with meals, and use of various abortive maneuvers (eg, forcibly crossing legs, standing on toes, or contracting thighs) as needed with presyncopal symptoms to transiently increase blood pressure. Subsequent measures that could be considered, if necessary, would include use of fludrocortisone or midodrine.

Biological basis

Anatomic localization

Localization of dizziness depends on the specific type or types of dizziness, although in practice this can be difficult, especially because of poor reliability (consistency) of patient reports (113; 151; 66). This is even more of an issue if the history is obtained by questionnaire-based methods that do not work to actively clarify the patient’s meaning when he or she uses terms like “spinning” or “vertigo.”

Vertigo indicates dysfunction or imbalance within the central or peripheral vestibular pathways. Vertigo is usually rotatory, implying a disturbance of the semicircular canals or their central connections. Sensations of body tilt or impulsion indicate otolithic disturbances or dysfunction of central otolithic connections.

Sensory disequilibrium is caused by altered spatial orientation, possibly due to proprioceptive impairment, balanced bilateral or compensated unilateral vestibular dysfunction, visual-vestibular mismatch, or multisensory impairment.

Motor disequilibrium is caused by impaired motor performance, possibly due to mechanical factors or to dysfunction of central and peripheral nervous system motor pathways. The central motor pathways that may be affected in patients with motor disequilibrium include the pyramidal, extrapyramidal, and cerebellar systems, whereas the peripheral motor pathways include the peripheral nerves, neuromuscular junctions, and muscles.

Presyncope is due to diffuse and sudden impairment in cerebral metabolism, which may occur in isolation or as a precursor to loss of consciousness (ie, syncope). The sudden cerebral metabolic dysfunction occurs due to generalized cerebral ischemia or, less commonly, hypoglycemia or hypoxia.

Psychophysiological (psychogenic) dizziness is due to impaired central integration of sensory and motor signals in patients with acute and chronic anxiety. In the absence of a uniformly accepted nomenclature, many terms have been promulgated that are inconsistently used, including psychiatric dizziness, psychic dizziness, psychogenic dizziness or vertigo, psychophysiological dizziness or vertigo, phobic postural vertigo, visual vertigo (later called visually induced dizziness), chronic subjective dizziness, and most recently postural-perceptual dizziness. Under the auspices of the Bárány Society, a consensus emerged that phobic postural vertigo, space motion discomfort, visual vertigo, and chronic subjective dizziness are all, in effect, defining aspects of a distinct vestibular disorder. The disorder was named “persistent postural-perceptual dizziness” to reflect its main elements of persistent nonvertiginous dizziness, unsteadiness, or “non-spinning vertigo” that is “exacerbated by postural challenges and perceptual sensitivity to space-motion stimuli” (147).

Pathophysiology

Optimal balance requires continuous monitoring of body sway and other orientation information provided by the somatosensory, vestibular, and visual systems. The functional ranges of these systems partially overlap, allowing partial compensation for deficits and distortions (108; 109). For example, a normal subject can maintain an upright stance either with vision eliminated (eg, with eyes closed), with proprioception disrupted (eg, standing on a moving or tilting surface), or with vestibular function distorted (eg, as a result of rotationally induced vertigo). Loss or distortion of inputs from two or more systems is often associated with dizziness, loss of balance, and falls; thus, a patient with profound loss of proprioception and sensory disequilibrium, or with uncompensated unilateral vestibular dysfunction and vertigo, may fall if vision is eliminated (eg, if eyes are closed). This is the basis of the Romberg sign (83). The intensity of imbalance is a function of the mismatch between the sensory systems that results from deficient or distorted input from one or more components (18).

Hemispheric small vessel disease or demyelination can produce central nervous system disconnection—a decrease in connectivity between neural structures mediating balance and locomotion—that patients may report as dizziness. Loss of connectivity by age-related build-up of small vessel disease or demyelination may produce what patients report as “dizziness” through various mechanisms: eg, disconnection of cortical vestibular centers, disconnection between frontal gait centers and the basal ganglia, and disconnection between intended motor action (efference copy) and sensory reafference (62).

Epidemiology

Dizziness is a common clinical problem, affecting at least a third of the population in one form or another at some point during their lives (52; 79; 02; 153). Data from the 2001–2004 National Health and Nutrition Examination Surveys (cross-sectional surveys of U.S. adults) showed that 35.4% of U.S. adults aged 40 years and older (69 million Americans) suffer from dizziness or postural instability (02); subjects with dizziness had a 12-fold increase in risk of falling. Dysfunction increased significantly with age and is higher in those with diabetes or less than a high-school education. Similarly, the prevalence of self-reported faintness or dizziness in adults in the Oslo Health Study was 29%, reported more often by women than men and by those over the age of 60 (153), but even in children, dizziness is not uncommon (55). Participants with neck and shoulder pain or stiffness, mental disorders, fibromyalgia, chronic pain syndrome, ischemic stroke, cerebral hemorrhage, angina pectoris, or chronic bronchitis/emphysema as well as those who use certain medications (eg, tranquilizers or sedatives) were more likely to have symptomatic faintness or dizziness. An increasing number of reported diseases and an increasing number of medicines used gave an increasing likelihood of faintness or dizziness. The oldest participants did not have an increased likelihood of faintness or dizziness in a multivariate analysis controlling for sociodemographic variables, comorbid diseases, and use of medicines.

A systematic review of case series of dizziness and vertigo demonstrated significant differences in the proportions of particular diagnoses for patients presenting with dizziness or vertigo, depending on the specialty making the diagnosis (122). Otolaryngology diagnoses were dominated by benign paroxysmal positioning vertigo, psychogenic dizziness, and Meniere disease, whereas emergency room diagnoses were dominated by cardiac, neurologic, and “other” categories (122). Analysis over time revealed increasing temporal trends for some diagnoses such as benign paroxysmal positioning vertigo and vestibular migraine and a corresponding decreasing trend for diagnoses of Meniere disease (122). This undoubtedly reflects improved recognition of some forms of vertigo with episodic presentations (ie, benign paroxysmal positioning vertigo and vestibular migraine) that were frequently “lumped in” with Meniere disease. More work must be done before acute monophasic vertigo is correctly categorized, as it continues to be frequently labelled “vestibular neuritis” even when it is clearly not.

Dizziness and vertigo are associated with significantly increased utilization of healthcare resources and result in significantly more related costs for both primary and pertinent secondary care (161).

Older patients with dizziness. In a population-based cohort study of 1379 community-dwelling participants aged 60 and older, predictors of regular dizziness at 7-year follow-up included living alone, history of dizziness, history of osteoarthritis or rheumatoid arthritis, use of nitrates, presence of anxiety or depression, impaired vision, and impaired function of the lower extremities, whereas predictors of regular dizziness at 10-year follow-up included history of dizziness and impaired function of lower extremities (95).

In a study spanning multiple countries of persons aged 50 years or older, 12.4% of the participants were troubled by dizziness in the preceding 6 months. Prevalence ranged from 6.5% to 23.4% in different countries. Individual level predictors of dizziness included female gender, living alone, old age, poor education, lack of physical activities, and presence of comorbidities, depressive symptoms, or sensory problems (123).

In another study of a community in Poland, the prevalence of dizziness was 16%, with dizziness being more common in the elderly and in women (167). Among young people, dizziness was typically due to vertigo or presyncope, whereas among people aged 50 or older, dizziness was often due to disequilibrium. The most common precipitant of dizziness was postural change. Dizziness was more likely to occur among those suffering from high blood pressure, diabetes, hyperlipidemia, hypothyroidism, cardiac arrhythmia, and depression; some of these likely represent the effects of related disease processes or medications used to treat these and related conditions. Dizziness was more likely to occur among women using oral contraceptives or hormone replacement therapy and individuals taking antiepileptic drugs.

In the Cardiovascular Health Study of a community population of older adults (greater than or equal to 65 years) without dementia or stroke, dizziness on standing was associated with lower baseline cognition, incident dementia, incident stroke, and death (61). Similarly, dizziness over the past 2 weeks was associated with higher white matter grade, brain infarcts, lower baseline cognition, and death (61). In contrast, orthostatic hypotension at 3 minutes was modestly associated with death, but not with MRI findings, cognition, dementia, or stroke (61).

In a retrospective study of patients with balance-related complaints who underwent vestibular testing in a 1-year period from 2017 to 2018 in an academic balance center at a tertiary referral center, older patients (greater than or equal to 60 years of age) were more likely to have abnormal results in random saccades, positional, Dix-Hallpike testing, and posturography, with greater effect sizes in tests of central function (115). Although the causes of imbalance and vertigo were recognized as multifactorial, vestibular dysfunction was a major contributor to balance dysfunction in this elderly population.

In a cross-sectional study of dizziness and health-related quality of life among older adults in an urban population, dizziness was negatively associated with health-related quality of life, even after adjusting for comorbidities (90).

Dizziness is particularly common in vulnerable older people (76): in a prospective multicenter clinical trial of 779 persons aged 75 and older and at high risk of hospitalization, 63% experienced dizziness.

In a case series of patients hospitalized with the symptom of dizziness at a tertiary care neurologic department in China, vertigo and light-headedness were the most common types of dizziness (137); benign paroxysmal positioning vertigo and stroke or transient ischemic attack were among the leading final diagnoses (although those with benign paroxysmal positioning vertigo should not have necessitated admission).

Pediatric patients with dizziness. In the 2016 National Health Interview Survey for children ages 3 to 17 years, dizziness was reported in 2% (21). Evaluation by a health professional was reported for 42% of children with dizziness. The most common diagnoses reported for dizziness were depression or child psychiatric disorder (12%), side effects from medications (11%), head/neck injury or concussion (8%), and developmental motor coordination disorder (8%).

Very high self-reported rates of dizziness in German adolescents have also been documented (80), but the validity and significance of these data seem suspect. Almost three fourths of students (72%) in the 8th through 10th grades reported at least one episode of dizziness in the prior 3 months, more than half (52%) reported symptoms of orthostatic dizziness, 12% reported spinning vertigo, 12% reported swaying vertigo, and 15% reported unspecified dizziness (80). Most of these dizziness events were limited to less than 1 minute (80). In another study of adolescents, independent risk factors for dizziness included female gender, stress, muscular pain in the neck and shoulder region, sleep duration, and migraine; the population attributable risk explained by these risk factors was 26%, with muscular pain, stress, and migraine accounting for 11%, 4%, and 3%, respectively (41).

In a retrospective case series of 257 children aged 1 to 17 years (42% male, 58% female) with dizziness referred to a tertiary pediatric otorhinolaryngology center from 2015 to 2020, dizziness was classified as central in 19%, peripheral vestibular in 12%, hemodynamic in 11%, psychological/psychogenic in 6%, and unclassified in 44% (17). Of children with "central" vertigo, 41% had benign paroxysmal vertigo of childhood (7.8% of all children), and 8% had migraine-associated vertigo.

In a prospective cross-sectional, descriptive clinical study of pediatric vertigo in children under 18 years of age presenting to the Otolaryngology Clinic of a tertiary care hospital January 1, 2018, to April 30, 2019, 89 children presented with a primary complaint of dizziness among 10,950. Children were evaluated for various ENT ailments during the study period for a clinic-specific prevalence of 0.8% (53). The most common cause of dizziness in children younger than 6 years was benign paroxysmal vertigo of childhood; in older children, the most common cause was migraine-associated vertigo, which was also the most common overall diagnosis made (28%). This was followed by hemodynamic dizziness (eg, orthostatic hypotension and vasovagal syncope; 16%).

In a retrospective cohort study of 1021 children (age 21 years and younger; 61% female, 39% male) evaluated in a pediatric vestibular program between January 2012 and March 2019, the causes of dizziness and imbalance in the pediatric population were diverse, and many patients had multiple diagnoses that were interrelated (162). Common diagnoses included vestibular migraine (35%), benign paroxysmal positioning vertigo (22%), primary dysautonomia (16%), anxiety disorder (14%), and persistent postural perceptual dizziness (11%) (162). A high proportion of patients (44%) received multiple contributing diagnoses. Vestibular migraine was frequently diagnosed with benign paroxysmal positioning vertigo, persistent postural perceptual dizziness, or both.

Differential diagnosis

Confusing conditions

In most cases, careful history, provocative testing, and detailed examination will allow distinction of the major categories of dizziness and will often allow a specific etiologic diagnosis as well. Particularly in primary care, emergency room, and hospital settings, dizziness is most commonly of the lightheaded or presyncopal type and often associated with cardiovascular or other medical causes (114; 152; 94). Note, however, that particularly in the geriatric population patients may have multiple types of dizziness and multiple contributing causes, so a systematic clinical approach should be undertaken to evaluate each type of reported dizziness and to consider common contributing causes regardless of clinically reported dizziness type (94).

Vertigo is usually rotatory, and patients frequently describe it as "spinning," but patients may also describe sensations of body tilt or impulsion. Vertigo is commonly associated with nystagmus, oscillopsia, postural imbalance, nausea, and vomiting. Autonomic symptoms (eg, sweating, pallor, nausea, vomiting) are generally more severe with vertigo of peripheral origin than with vertigo of central origin. Common causes of vertigo in the elderly include benign paroxysmal positioning vertigo, neurolabyrinthitis, trauma, toxins, migraine, and posterior circulation or labyrinthine ischemia, particularly associated with posterior inferior cerebellar artery or anterior inferior cerebellar artery ischemia (85; 158). The proportion of elderly patients with cerebrovascular events among patients presenting with dizziness, vertigo, or imbalance is low (64), although a high index of suspicion is necessary, particularly to exclude a posterior circulation cause in the elderly. Common causes of vertigo in young adults include migraine, Meniere syndrome, viral neurolabyrinthitis, trauma, and toxins (86). Common causes of vertigo in children with normal ear drums (ie, children who did not show middle ear effusion or otitis media) are migraine and benign paroxysmal vertigo (26; 55; 58). Central nervous system causes of vertigo are uncommon in general clinical practice but are relatively selected for in neurologic practice (78). Compared with other causes of dizziness, vertigo more frequently results in medical consultation, sick leave, interruption of daily activities, and avoidance of leaving the house (112).

Patients with disequilibrium often complain of unsteadiness, imbalance, and falls. Sensory disequilibrium may be due to proprioceptive impairment (eg, from peripheral neuropathy or tabes dorsalis), balanced bilateral or compensated unilateral vestibular dysfunction (eg, due to aminoglycoside toxicity or the residua of viral neurolabyrinthitis), visual-vestibular mismatch (eg, due to impaired vision, ocular misalignment, or use of optic devices [ie, lens implants or new glasses]), or multisensory impairment. Except in cases of visual-vestibular mismatch, patients with sensory disequilibrium generally do worse in the dark and frequently have a Romberg sign on examination (83). Motor disequilibrium may be due either to mechanical factors (eg, severe arthritis or prosthetic limbs) or to dysfunction of central and peripheral nervous system motor pathways. The central motor pathways that may be affected in patients with motor disequilibrium include the pyramidal, extrapyramidal, and cerebellar systems, whereas the peripheral motor pathways include the peripheral nerves, neuromuscular junctions, and muscles. Motor disequilibrium, as from cerebellar dysfunction, is generally not exacerbated in the dark or with the eyes closed.

Presyncope is characterized by a sensation of impending loss of consciousness and is typically associated with weakness, diaphoresis, nausea, and epigastric distress. Other associated symptoms may include facial pallor or ashen-gray appearance, scotomata, visual dimming or grayout, neck pain, headache, cognitive slowing, leg buckling, angina, dyspnea, and, depending on the cause, palpitations, acral and perioral paresthesias, and carpopedal spasms (43). In some cases clinical recognition or significant orthostatic hypotension may require a high index of suspicion (especially if there are risk factors such as diabetes or use of commonly associated medications), because a third of the patients with even severe orthostatic hypotension (ie, a decrease in systolic blood pressure more than 60 mm Hg from baseline during a head-up tilt table test) are asymptomatic, and another quarter have atypical complaints (eg, headache, backache) that would not lead physicians toward the diagnosis of orthostatic hypotension (09). Presyncope occurs due to generalized cerebral ischemia or, less commonly, with hypoglycemia or hypoxia. Presyncope (and syncope) may occur with decreased cardiac output (eg, arrhythmias, obstructive cardiomyopathies, pulmonary emboli), inadequate peripheral vasoconstrictor mechanisms (eg, vasovagal response, sympatholytic drugs, primary autonomic insufficiency, central and peripheral nervous system diseases) causing orthostatic hypotension, postural orthostatic tachycardia syndrome (POTS) (127), cerebral vasoconstriction (eg, hyperventilation), hypovolemia, mechanical reduction in venous return (eg, cough, micturition), and alterations in the oxygen or nutrient content of the blood (eg, hypoxia, hypoglycemia). Independent risk factors for orthostatic hypotension include increasing age, prehypertension or hypertension, and diabetes (169). True syncope is rare with hyperventilation and hypoglycemia. Episodes of presyncope are generally relieved with recumbence. Some patients with supine hypertension and hypotensive reactions on head-up tilt may have nonspecific dizziness rather than clear presyncope (107).

Psychophysiological (psychogenic) dizziness is a vague giddiness or dissociated sensation due to impaired central integration of sensory and motor systems. The dizzy sensation is typically protracted or continuous, with periodic exacerbations, often punctuated by episodes of hyperventilation-induced presyncope. Specific provocative factors may be identified, such as the presence of crowds, driving, or being in confined places (eg, elevators). Episodes are not associated with facial pallor and are not relieved with recumbency (46). Other clinical evidence of coexistent acute and chronic anxiety is typically present, but it is important to recognize that anxiety may also result from other forms of dizziness, because of the sudden, dramatic, and unpleasant associated sensations, and from fear of falling, injury, or death (46).

Diagnostic workup

In the emergency room setting, three quarters of patients evaluated for dizziness are felt to have benign conditions, with the remainder felt to have serious conditions, but nearly half of emergency room diagnoses in such patients are corrected on review, with the diagnoses of stroke and vestibular neuritis most frequently requiring correction (129). Nevertheless, the risk of stroke after presumed nonstroke dizziness presentations to an emergency room is very low, supporting a nonstroke etiology for the overwhelming majority of such cases (72). In acute dizziness presentations, the combination of the ABCD(2) score, general neurologic examination, and a specialized oculomotor examination (nystagmus pattern, presence of skew deviation, head impulse test) can help assess the likelihood of an underlying acute stroke (68).

In all patients with dizziness or vestibular complaints, careful examination of the eyes, ears, cardiovascular system, nervous system, and vestibular system is indicated. Vestibular imbalance is indicated by nystagmus, past-pointing, and postural and gait abnormalities. Clinical disturbances of the vestibulo-ocular pathways are assessed by observing the nystagmus pattern (central vs. other), the presence of a skew deviation, and the head impulse test (68). Clinical disturbances of the vestibulospinal pathways are assessed with several tests, including past-pointing, stance, the Romberg test, and tandem gait with eyes closed (83).

Careful history and physical examination are frequently sufficient to classify the dizziness into one of the four major categories and, perhaps, even to suggest an etiologic diagnosis; however, sometimes patients' descriptions of dizzy sensations are confusing, particularly when the events are episodic. Therefore, provocative testing may help define the subjective sensation and the often-vague description of dizziness. Provocative testing can be used to produce physiologic sensations of vertigo or presyncope, which can then be compared and contrasted with the subjective sensations experienced by the patient.

The most common vestibular disorders can often be diagnosed based on history, examination, audiometry, and in some cases, basic vestibular function testing (164). Two common causes of a first-ever attack of acute, spontaneous, isolated vertigo (acute vestibular syndrome) are vestibular neuritis/labyrinthitis and cerebellar infarction. Recurrent positioning/positional vertigo is usually very brief (less than a minute, although patients may estimate a longer duration) and is caused by benign paroxysmal positioning/positional vertigo, but rarely it can have a central origin. Recurrent spontaneous vertigo that lasts for hours has two common causes: Ménière disease and vestibular migraine. Chronic vestibular insufficiency results from bilateral (or sometimes severe unilateral) peripheral vestibular impairment and may present as a form of dysequilibrium.

Physiologic vertigo can be induced in the office either by rotational or caloric testing. To perform rotational testing in the office, the patient can be seated in a rotary office chair with the head tilted 30 degrees forward, and then carefully rotated 10 times over 20 to 30 seconds. Tilting the head forward 30 degrees places both horizontal semicircular canals parallel to the floor and, therefore, perpendicular to the axis of rotation in the chair. As a result, both horizontal ducts are affected by rotational testing, with output from one duct stimulated, whereas output from the other canal is inhibited. The mismatch between the resulting vestibular imbalance and visual and somatosensory information produces physiologic vertigo, generally lasting less than 1 to 2 minutes. During this time, one can observe peripheral vestibular nystagmus and past-pointing. As a result of the risk of falls and injury, patients should not stand until the vertigo has resolved. Vertigo can also be produced with caloric testing (eg, by injecting cold or warm water into the patient’s external auditory canal); however, this is generally more uncomfortable for the patient than rotational testing as well as more time-consuming and messier for the examiner. Therefore, caloric testing is not recommended for provocative testing to determine the category of dizziness.

Hyperventilation produces presyncope with perioral and acral paresthesias and, potentially, carpopedal spasms, although the latter manifestation is rarely achieved with voluntary hyperventilation. To produce these sensations in the office, the patient is asked to breathe deeply and quickly for 3 minutes, through an open mouth with the lips not pursed. This is difficult to do even for cooperative patients, and considerable encouragement from the examiner is often required.

Clinical evaluation for autonomic dysfunction should be part of the comprehensive evaluation of a dizzy patient, involving assessment of orthostatic pulse and blood pressure (39). The patient's pulse and blood pressure both supine and standing must be assessed to diagnose presyncope due to orthostatic hypotension or orthostatic intolerance. Orthostatic hypotension is defined as a drop in systolic blood pressure of at least 20 mm Hg or a drop in diastolic blood pressure of at least 10 mm Hg within 3 minutes of standing or within 3 minutes of head-up tilt to at least 60° on a tilt table, regardless of whether the patient is symptomatic or asymptomatic (07; 44; 45); however, orthostatic decreases in systolic blood pressure up to 40 mm Hg correlate poorly with the presence of symptomatic postural dizziness (157). Variants of orthostatic hypotension are recognized. Initial orthostatic hypotension is a transient drop in systolic blood pressure of at least 40 mm Hg or in diastolic blood pressure of at least 20mm Hg within 15 seconds of standing. This may occur during active standing and less commonly with passive tilting. Initial orthostatic hypotension presumably results from transient mismatch between cardiac output and peripheral vascular resistance on standing. Orthostatic hypotension measurements performed within 1 minute of standing are the most strongly related to dizziness and individual adverse outcomes (60). In contrast, delayed orthostatic hypotension occurs after more than 3 minutes of standing or after more than 3 minutes of head-up tilt to at least 60° on a tilt table. This is typically detected by extending the period of orthostatic stress (standing or head-up tilt) in patients who present with symptoms consistent with orthostatic hypotension but without orthostatic hypotension during the 3-minute period of orthostatic stress used in routine clinical evaluation. Delayed orthostatic hypotension is thought to represent a mild or early form of sympathetic adrenergic failure.

A decrease in mean arterial blood pressure (ie, diastolic plus one third of pulse pressure) of at least 20% may be a better functional indicator of clinically significant orthostatic hypotension (157). In addition, some patients have “delayed” orthostatic hypotension, which occurs after 3 minutes of standing and which, therefore, is often overlooked in clinical settings (43). Patients with non-otologic dizziness and lightheadedness with a normal neuro-otological evaluation should be considered for head-upright tilt table testing, even with normal in-office clinical orthostatic blood pressure testing (39). In addition, some individuals, particularly those with Parkinson disease, may have orthostatic dizziness and cerebral hypoperfusion (as established with transcranial Doppler studies), even in the absence of drops in blood pressure sufficient to meet the diagnostic criteria for orthostatic hypotension (121).

Diagnostic criteria for “hemodynamic orthostatic dizziness/vertigo” (more simply, “orthostatic dizziness”) have been proposed, a label meant to encompass both orthostatic hypotension and postural orthostatic tachycardia syndrome (75). These diagnostic criteria were derived by expert consensus after review of research on hemodynamic orthostatic dizziness/vertigo, postural hypotension or tachycardia, and autonomic dizziness. Diagnosis of hemodynamic orthostatic dizziness/vertigo requires: (1) at least five episodes of dizziness, unsteadiness, or vertigo triggered by arising or present in the upright position, which subsides by sitting or lying down; (2) orthostatic hypotension, postural tachycardia syndrome, or syncope documented on standing or during a head-up tilt test; and (3) episodes are not better explained by another disease or disorder. Diagnosis of “probable” hemodynamic orthostatic dizziness/vertigo required: (1) at least five episodes of dizziness, unsteadiness or vertigo triggered by arising or present in the upright position, which subsides by sitting or lying down; (2) at least one of the following accompanying symptoms (ie, during episodes of dizziness): generalized weakness/tiredness, difficulty in thinking/concentrating, blurred vision, and tachycardia/palpitations; and (3) episodes are not better explained by another disease or disorder. The first more-definite category was not labeled as “definite,” but that is implied by the less-definite category being labelled as “probable.” Also, why five episodes are required and not some other number (eg, 3) is largely arbitrary. Finally, for the more-definite category, firmly establishing the diagnosis would require that criterion number 2 reproduced the symptoms; then, even one episode should be sufficient to make the diagnosis.

Diagnostic criteria for postural orthostatic tachycardia syndrome (POTS) include (1) a sustained heart rate increase of at least 30 beats per minute from supine to standing within 10 minutes of standing; (2) lack of orthostatic hypotension (ie, systolic blood pressure does not fall by more than 20 mm Hg and may increase with standing); (3) symptoms of orthostatic intolerance (eg, lightheadedness, weakness, palpitations, blurred vision, breathing difficulties, nausea, or headache) develop with standing and resolve with recumbency; (4) symptoms are present for at least 3 months; (5) absence of prolonged bed rest (deconditioning); (6) absence of medications that impair autonomic regulation (eg, vasodilators, diuretics, antidepressants, anxiolytic agents); and (7) absence of other conditions that might cause autonomic failure or orthostatic tachycardia (eg, active bleeding, anemia, dehydration, pregnancy) (127; 155). Plasma norepinephrine levels should be measured in both supine and standing positions (after at least 15 to 30 minutes in each position). Supine norepinephrine levels are often at the high end of the normal range in patients with POTS, whereas standing norepinephrine levels are usually elevated (often more than 600 pg/ml), reflecting an increased sympathetic neural tone while upright (127; 155).

Other provocative maneuvers that may be helpful in selected circumstances include a fistula test, Dix-Hallpike positioning maneuvers, assessment for positional nystagmus, carotid sinus massage, and the Valsalva maneuver (34; 82; 59). Some elderly patients with chronic dizziness are found to have weak, horizontal, direction-changing (usually apogeotropic) positional nystagmus, which can improve symptomatically with daily positional exercises, suggesting that mild persistent horizontal canal benign paroxysmal positioning vertigo is a cause of chronic otherwise idiopathic vertigo in the elderly (59).

In some cases, additional diagnostic tests will be required. These should be ordered selectively depending on the type of dizziness and suspected underlying etiologies; this approach will reduce the need for extensive laboratory testing, neuroimaging, and other low-yield tests (118). Unfortunately, studies have suggested that diagnostic testing is often indiscriminate and that the frequency of ordering multiple expensive tests is increasing, particularly in emergency rooms, where indiscriminate use of brain imaging is associated with a substantial increase in length of stay (69; 71; 08).

Most cases of persistent, recurrent, and isolated dizziness can be managed clinically without recourse to expensive CT or MRI studies (38; 29). Indeed, brain imaging for uncomplicated dizziness is unlikely to identify clinically significant imaging findings and is very unlikely to result in a change in clinical management (38). Diagnostic studies that may be helpful in selected patients with vertigo (not attributable to benign paroxysmal positioning vertigo) include audiometry, electronystagmography, bithermal caloric testing, brainstem auditory evoked potentials, and cranial neuroimaging (48; 13; 40; 28); these studies should not be ordered routinely (28; 38; 29).

The clinical value of neuroimaging for patients presenting to emergency rooms with dizziness is very low and appears to have declined over time (71; 08; 74; 03; 38; 130; 99; 05). Patients who are more likely to have abnormal findings on CT are those with severe headaches or some neurologic deficits (eg, gait abnormalities, limb ataxia, multiple neurologic deficits) in addition to dizziness, particularly among individuals over 60 years of age presenting with new-onset imbalance or disequilibrium or a history of recent head trauma, whereas those with isolated dizziness, lightheadedness, or monosymptomatic positional vertigo are very unlikely to have acute, life-threatening abnormalities (08; 25; 65; 110; 111; 133; 99; 05). With MRI, in particular, structural abnormalities of the brain and neck are common and nonspecific, and routine MRI is unlikely to identify specific etiologies for dizziness (28; 03).

Clinicians should, nevertheless, have a high index of suspicion in elderly patients for cerebrovascular disease involving the posterior circulation. Prompt cranial imaging should be carefully considered in patients with a first attack of acute persistent vertigo presenting to an emergency room, especially in association with central signs or age over 60 years, in order to exclude rare cases of cerebellar infarction (23; 102). When cranial neuroimaging is utilized, magnetic resonance imaging is superior to computed tomography for diagnosis of acute stroke in patients presenting with acute persistent vertigo to an emergency room (25) and should include diffusion-weighted imaging (102).

Diagnostic studies that may be helpful in patients with dysequilibrium vary greatly depending on the identified neurologic or mechanical deficits but may include electromyography and nerve conduction studies, cranial or spinal imaging, joint x-rays, and somatosensory evoked potentials. Diagnostic studies that may be helpful in selected patients with presyncope and syncope (not attributable to medications or vasovagal reactions) include electrocardiography, Holter monitoring, tilt table testing, glucose tolerance testing, and studies of autonomic and endocrine function.

Children may also have serious underlying disease when presenting with a history of frequent falls, dizziness, and imbalance (96). Assessment should include detailed clinical history as well as thorough physical and neurologic examinations while maintaining a low threshold for investigations, including radiological imaging. One case series of such pediatric presentations identified structural central nervous system abnormalities that accounted for the presenting symptoms: ie, frontal lobe arteriovenous malformation, exophytic brain stem glioma, and cerebellar-medullary angle arachnoid cyst with cerebellar tonsillar ectopia (96).

Although improvements in neuroimaging have identified evidence of injury in some cases following mild head trauma, clinicians must maintain a healthy level of suspicion to recognize possible exaggeration of symptoms and disability in patients with a financial incentive (165).

Clinicians should be aware that there may be multiple causes for dizziness in a single patient presentation. The frequency of patients receiving multiple diagnoses in a dizziness clinic is approximately 4% (171), but the frequency is much higher in a geriatric dizziness clinic population.

Management

Meta-analyses and systematic reviews are available for a few dizziness topics, such as benign paroxysmal positional vertigo and Meniere disease (67). There are no clinical practice guidelines that focus specifically on dizziness.

Drugs should be reviewed in all patients with dizziness. Drugs associated with dizziness include alcohol and other central nervous system depressant medications (eg, benzodiazepines, barbiturates, phenothiazines), aminoglycoside antibiotics, anticonvulsants, antidepressant medications, antihypertensive medications (eg, angiotensin-converting enzyme inhibitors), chemotherapeutic agents, loop diuretics (eg, furosemide), and salicylates (15). Abrupt withdrawal of selective serotonin reuptake inhibitors may cause a sudden drop in serotonin in the vestibular nucleus complex bilaterally, causing motor dysequilibrium without vertigo (142). The elderly are particularly susceptible to drug ototoxicity because (1) they are more likely to receive ototoxic drugs; (2) they have less reserve (due to age-associated vestibular end-organ changes, preexisting sensorineural hearing loss, and previous treatment with ototoxic drugs); and (3) they are more likely to have impaired renal function.

The treatment of dizziness varies by type and cause. In general, it is symptomatic and directed at the underlying cause. Vertigo (especially acute persistent vertigo) may be alleviated with vestibular sedatives, whereas these agents may exacerbate presyncope and disequilibrium (82). Some types of vertigo may also be amenable to specific curative therapies, most notably with canalith repositioning maneuvers for benign paroxysmal positioning vertigo (19; 84). The superior semicircular canal dehiscence syndrome is also amenable to canal plugging or canal resurfacing or “reproofing” surgical procedures (98; 101; 143; 97; 20; 120; 10). Vertigo associated with migraine may respond to abortive and prophylactic antimigraine treatments: one small randomized clinical trial found some benefit from the use of zolmitriptan for abortive treatment of vestibular migraine, and eight observational studies showed marginal improvement with migraine prophylactic medications such as nortriptyline, verapamil, or metoprolol (42). Other forms of episodic vertigo (such as Meniere syndrome) may benefit from pharmacological or surgical therapies (11; 82). Patients with acute persistent vertigo from peripheral vestibular lesions may benefit from vestibular exercises (24; 30; 166; 27; 31; 170; 82), though data are lacking on their efficacy in older patients (92); in general patients with presyncope, disequilibrium, and psychophysiological dizziness are unlikely to benefit from these exercises (82). In some older adults with dizziness but no documented vestibular deficit, addition of vestibular-specific gaze stability exercises to standard balance rehabilitation approaches has been reported to further reduce falls risk (51). Instrumental rehabilitation training on a moving platform can also be effective for treating vestibular balance disorders and can result in improved control of balance and greater independence in activities of daily living (31). Such treatment, however, is often not readily available.

Although treatment of presyncope varies depending on the underlying cause, in the common situation of orthostatic hypotension, medications should be carefully reviewed for potential contributions to the problem and, if necessary, the dosage should be changed or the suspect medications discontinued. Commonly implicated drugs include alcohol, calcium channel blockers, diuretics, insulin, monoamine oxidase inhibitors, nitrates, opiates, antiparkinsonian medications, phenothiazines, sympatholytics, and tricyclic antidepressants. Patients with orthostatic hypotension should also have assessment of blood volume status (eg, to exclude hypovolemia), hematocrit (eg, to identify anemia), cardiac function (eg, to identify conditions such as conduction block and aortic stenosis), and neurologic function (eg, to identify conditions such as peripheral neuropathies and parkinsonian syndromes).

Some patients with neurologic or other causes of orthostatic hypotension may respond to nonpharmacologic interventions, such as the following:

Physical counter-maneuvers for orthostatic hypotension-induced presyncope can include squatting, head flexion, leg crossing when standing, toe raises when standing, etc.; these maneuvers act by reducing venous pooling, secondarily increasing central blood volume, venous return, and cardiac output (160; 16; 43).

A minority of patients with neurogenic orthostatic hypotension require treatment with mineralocorticoids (eg, the synthetic mineralocorticoid fludrocortisone acetate), midodrine (a peripheral, selective, direct alpha1-adrenoreceptor antagonist) (93; 168), or other pharmacologic agents such as pyridostigmine (134; 139; 140; 131), erythropoietin, or the vasopressin analogue desmopressin acetate (49; 43). Fludrocortisone, 0.05 to 0.10 mg at bedtime, is helpful in expanding plasma volume and increasing peripheral vascular resistance; the long-term benefits appear to relate to an increase in peripheral vascular resistance, as the associated sodium retention and plasma volume expansion return to normal over time. For patients who do not respond successfully to nonpharmacological approaches plus fludrocortisone, midodrine may be helpful at an initial dose of 2.5 mg two or three times daily with gradual dose escalation to 10 mg three times daily as necessary and as tolerated, avoiding use in the 4-hour period before recumbency. Pyridostigmine can also significantly improve standing blood pressure in patients with neurogenic orthostatic hypotension without inducing or worsening supine hypertension apparently by acting to inhibit ganglionic acetylcholinesterase. Because ganglionic neural activity is minimal while one is supine, blocking acetylcholinesterase with pyridostigmine has little effect on supine blood pressure; in contrast, ganglionic neural activity can be facilitated with pyridostigmine during orthostatic stress, thus, augmenting the cholinergic efferent limb of the baroreceptor reflex and alleviating orthostatic hypotension. Although the effect of pyridostigmine is modest, it is clinically important and may alleviate symptoms in a significant percentage of patients with neurogenic orthostatic hypotension (131; 140). Little information is available on the optimal dosing regimen of pyridostigmine for such patients, but cautious dose titration may be helpful.

Presyncope due to postural orthostatic tachycardia syndrome (POTS) will often respond to some of the same measures employed for neurogenic orthostatic hypotension, with a focus on therapies directed at correction of the associated hypovolemia and the autonomic imbalance (127).

Presyncope due to anxiety-related hyperventilation can be alleviated by first helping patients to recognize the clinical manifestations of hyperventilation (with verbal education and intentional hyperventilation in the office), instructing the patient in relaxation exercises and other techniques (eg, breathing into a paper bag when attempting to slow the respiratory rate), and use of antidepressant and anxiolytic medications (particularly selective serotonin reuptake inhibitors).

Based on poor-quality data, and often only anecdotal reports, psychophysiological dizziness, including “persistent postural-perceptual dizziness,” may be alleviated by treatment with antidepressants, anxiolytic medications, cognitive behavioral modification techniques with desensitization for situational anxiety, and psychotherapy (150; 149; 148; 132); however, there is no evidence from placebo-controlled randomized trials regarding pharmacological treatments (specifically SSRIs and SNRIs) for persistent postural-perceptual dizziness (163). Anxiety associated with vestibular dysfunction may also be improved with selective serotonin reuptake inhibitors but will likely not improve objective measures of balance or vestibular function (138). Cognitive behavioral therapy has not been proven to have a significant long-term effect on phobic postural vertigo, persistent postural-perceptual dizziness, or other forms of psychophysiological dizziness (54), but it is still commonly advocated (124). Although psychophysiological dizziness is outside of the original spectrum of vestibular dysfunction for which vestibular rehabilitation was developed, vestibular rehabilitation can still be useful in the practical clinical management of patients with psychophysiological dizziness as it may reduce symptoms and improve quality of life (124; 105).

Vestibular rehabilitation therapy may improve perceived disability associated with complaints of dizziness post-concussion (106).