Psychophysiological dizziness …

Douglas J Lanska MD MS MSPH

Neuro-Ophthalmology & Neuro-Otology

Updated 05.20.2024
Released 10.22.2003
Expires For CME 05.20.2027

Psychophysiological dizziness

Author: Douglas J Lanska MD MS MSPH

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Psychophysiological dizziness

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Introduction

Overview

The author explains the clinical presentation, pathophysiology, diagnostic work-up, and management of psychogenic vertigo. A close association between anxiety and dizziness or vertigo has been recognized since antiquity, but recognition and management of this problem continue to be difficult for many clinicians. Anxiety may result from various forms of dizziness because of the sudden, dramatic, and unpleasant associated sensations and from fear of falling, injury, or death. The main concern with differential diagnosis is whether the apparent psychiatric manifestations are a consequence of an underlying organic vestibular or other disorder or whether the condition is primarily psychiatric.

Key points

	• Anxiety and depression are strongly associated with dizziness.
	• Patients and their spouses tend to have a high degree of concordance for the patient's self-reported dizziness severity and dizziness handicap, although spouses tend to overestimate the severity of dizziness.
	• Psychophysiological (psychogenic) dizziness is generally characterized as a vague giddiness or dissociated sensation due to impaired central integration of sensory and motor signals in patients with acute and chronic anxiety. The dizzy sensation is typically persistent (ie, duration is frequently of months or longer), protracted (ie, lasting hours) 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.
	• 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. Anxiety and depression are particularly frequent concomitants of the neurologic manifestations of Meniere disease and vestibular migraine, compared with patients with vestibular neuritis of benign paroxysmal positioning vertigo.
	• Psychophysiological (psychogenic) dizziness is thought to be due to impaired central integration of sensory and motor signals, particularly in patients with acute and chronic anxiety.
	• The main concern with differential diagnosis is whether the apparent psychiatric manifestations are a consequence of an underlying organic vestibular or other disorder or whether the condition is primarily psychiatric.
	• Psychophysiological dizziness may be alleviated by treatment with antidepressants, anxiolytic medications, and cognitive behavioral modification techniques with desensitization for situational anxiety.

Historical note and terminology

Recognition of a close association between anxiety and dizziness or vertigo has been an integral component of the medical literature since antiquity (69; 05). A close association between anxiety and dizziness was emphasized by Sigmund Freud in an early paper on anxiety neurosis, an important component in the psychodynamic formulation of psychogenic dizziness (42; 81; 05). There has been an increased recognition of the situational specificity of certain symptoms, and behavioral therapeutic measures have been instituted to address this (05).

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 (16; 122; 121; 129; 148; 112; 141; 123).

Beginning in 1986, Brandt and Dieterich, defined “phobic postural vertigo” as a clinical syndrome of postural dizziness and unsteadiness, with a chronic fluctuating or waxing-and-waning course and momentary flares, variously precipitated by vestibular syndromes, medical illness, or psychological distress, and accompanied by anxiety, depression, and obsessive-compulsive personality traits (19; 16; 64; 65; 36). Postural vertigo was thought to arise from an anxiety-related focus on transient discrepancies between anticipated and actual movements (ie, an “efferent-afferent mismatch”) that occur with normal voluntary motion (16).

Beginning in 1989, Jacob and colleagues characterized the symptom of “space-motion discomfort” as an uneasiness about spatial orientation and an increased awareness of motion stimuli (72; 75; 74). They found that, among patients with anxiety, those with greater space-motion discomfort had greater “somatosensory dependence,” meaning that they relied more strongly on somatosensory information for controlling posture.

In 1995, Bronstein described “visual vertigo” as a sensation of unsteadiness or dizziness on exposure to complex or moving visual stimuli among patients after acute peripheral or central vestibulopathies (20; 21). There were obvious similarities between phenomena labelled as space-motion discomfort and visual vertigo, including the situational triggers. One proposed explanation was that visual vertigo was caused by a “visual-vestibular mismatch,” meaning a discordance between visual and vestibular inputs after a vestibular injury (93), but Bronstein’s group later emphasized increased vigilance concerning vestibular sensations and higher-than-normal reliance on visual cues for spatial orientation (which was labelled “visual dependence”) (25; 26). The term “visual vertigo” was renamed “visually induced dizziness” when it was adopted by the Bárány Society into its International Classification of Vestibular Disorders (13).

Beginning in 2004, Staab and colleagues described the clinical syndrome of “chronic subjective dizziness” (128; 127), which resembled Brandt and Dieterich’s phobic postural vertigo, but focused more on physical than psychological symptoms. Chronic subjective dizziness was considered to be a syndrome of persistent non-vertiginous dizziness or unsteadiness with heightened sensitivity to motion of self or objects in the environment, and difficulty performing tasks that require precise visual focus (128; 129; 127).

In 2006, the Bárány Society charged a working group to standardize nomenclature for vestibular diseases and disorders, resulting in formation of the Committee for Classification Vestibular Disorders of the Bárány Society to oversee development of the International Classification of Vestibular Disorders (ICVD). Deliberations of the committee from 2010 to 2012 produced a consensus that phobic postural vertigo, space motion discomfort, visual vertigo, and chronic subjective dizziness all, in effect, were 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” (129).

Clinical manifestations

Presentation and course

	• Anxiety and depression are strongly associated with dizziness.
	• Overall, about half of the patients evaluated with vertigo or dizziness suffer from a psychiatric comorbidity.
	• Psychophysiological (psychogenic) dizziness is generally characterized as a vague giddiness or dissociated sensation due to impaired central integration of sensory and motor signals in patients with acute and chronic anxiety.
	• The dizzy sensation is typically persistent, 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 often poorly (imprecisely) described, but some patients may report a turning “inside the head” or “rocking sensations” while walking, rather than a sense of spinning of the head or of the world spinning around the head.
	• The concept of persistent postural-perceptual dizziness has emerged as a unifying framework for many aspects of psychophysiological dizziness with diagnostic criteria developed by the Committee for the Classification of Vestibular Disorders of the Bárány Society.
	• Patients with postural-perceptual dizziness may develop anxiety, avoidance behaviors, secondary functional gait disorders, and severe disability.

Anxiety and depression are strongly associated with dizziness (94; 62; 63; 86; 107; 132; 79). In a specialized treatment population, nonorganic dizziness and vertigo represents about 10% to 20% of the treatment problem, and more than 40% of patients with organic vertigo or dizziness have concomitant psychiatric comorbidity, so that overall, about half of the patients evaluated with vertigo or dizziness suffer from a psychiatric comorbidity (86; 29). Although a history of anxiety or depression are risk factors for psychiatric symptomatology in the setting of dizziness, many patients with dizziness and associated anxiety or depression symptoms have no prior history of such symptoms nor current pharmacological treatment for these disorders (94). A longer duration of dizziness symptoms before diagnosis is associated with higher anxiety levels, and on the other hand those with higher anxiety levels have an increased risk of residual dizziness (133).

Patient and spouse perceptions of dizziness severity and dizziness handicap often have a high degree of congruence, although spouses tend to overestimate dizziness severity (109). Patients and spouses also have a high degree of concordance for anxiety and depression: anxious patients tend to be married to anxious spouses, and depressed patients tend to be married to depressed spouses. However, healthcare providers significantly underestimate patient anxiety and symptoms of autonomic system activation (77).

Psychophysiological (psychogenic) dizziness is generally characterized as a vague giddiness or dissociated sensation due to impaired central integration of sensory and motor signals in patients with acute and chronic anxiety (31; 02; 08; 15; 07; 22; 06; 87; 92). The dizzy sensation is typically persistent (ie, duration frequently of months or longer), protracted (ie, lasting hours) or continuous, with periodic exacerbations, often punctuated by episodes of hyperventilation-induced presyncope (eg, with breathlessness, hyperpnea, acral or perioral paresthesias, and even carpopedal spasms) (139; 87; 127). Specific provocative factors may be identified, such as the presence of crowds, driving, or being in confined places (eg, elevators). Episodes are often poorly (imprecisely) described, but some patients may report a turning “inside the head” or “rocking sensations” while walking, rather than a sense of spinning of the head or of the world spinning around the head (58; 103; 139; 69). They may be accompanied by apparent manifestations of anxiety, including apprehension, dread, nervousness, tension, restlessness, and autonomic manifestations (eg, papillary dilation, tachycardia, hypertension, and coolness of the extremities) without a clearly identifiable appropriate stimulus. There may be chronic hypersensitivity to one’s own motion (without directional specificity), to the movement of objects in the environment, and to settings with complex visual stimuli (eg, grocery stores) (127; 104). They are not associated with facial pallor or vomiting, and they are not relieved with recumbency.

Agoraphobia is an irrational fear or anxiety of leaving the familiar setting of home or of being in places or situations from which escape might be difficult or embarrassing, or where help may not be readily available (03). The anxiety leads to avoidance of specific situations, such as being home alone; being outside of the home alone; being in crowds; traveling in a car, bus, or airplane; being on a bridge; or being in an elevator. As a result, affected patients avoid or dread such situations and may require the presence of a companion to confront the feared situation. Almost all individuals who present with agoraphobia also have (or have a history of) panic disorder. Agoraphobia must be distinguished from social and specific phobias and from separation anxiety disorder, all of which are also characterized by avoidance behavior.

Panic attacks may cause or contribute to episodic sensations of dizziness (123). A panic attack is a brief episode of intense fear or discomfort with at least four of the following symptoms developing abruptly and peaking within 10 minutes: (1) dizziness, lightheadedness, unsteadiness, or faintness; (2) palpitations or tachycardia; (3) chills or hot flashes; (4) diaphoresis; (5) tremulousness; (6) paresthesias; (7) dyspnea or a “smothering” sensation; (8) a sensation of choking; (9) nausea; (10) chest pain; (11) feelings of unreality or being detached from oneself; (12) fear of losing control or “going crazy”; and (13) fear of dying (03). Dizziness, lightheadedness, unsteadiness, and faintness are among the typical manifestations of panic attacks (90). In some cases, the dizziness, lightheadedness, faintness, diaphoresis, paresthesias, dyspnea or “smothering” sensation, and fear of dying may be components of a hyperventilation attack.

Panic disorder is characterized by extreme and unreasoning anxiety and fear and recurrent, unexpected panic attacks with at least a 1-month period of concern about repeated attacks and the consequences of such attacks as well as a significant change in behavior (eg, avoidance) (03). Such panic attacks cannot be a result of another medical condition (eg, vertigo, hyperthyroidism, asthma, chronic obstructive pulmonary disease, or cardiac arrhythmia), or medication or drug use (eg, caffeine, amphetamines, or cocaine). Panic disorder may occur with or without agoraphobia.

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 “gray out,” and, depending on the cause, palpitations, acral and perioral paresthesias, and carpopedal spasms. Presyncope may occur with cerebral vasoconstriction and generalized cerebral ischemia associated with anxiety-induced hyperventilation. True syncope is rare with hyperventilation. Episodes of presyncope are generally relieved with recumbence.

Phobic postural vertigo is a specific form of psychogenic dizziness that has been defined by Brandt and colleagues (64; 16; 17; 18; 81; 84; 28; 111) as follows:

	(1) Dizziness is experienced while upright and during gait, despite normal clinical balance and routine otoneurologic tests.
	(2) Patients describe nonrotational dizziness, with fluctuating unsteadiness, and postural and gait instability, often in the form of brief attacks (ie, lasting seconds to minutes), or the perception of transient illusory body perturbations for, at most, seconds.
	(3) Attacks occur spontaneously or with specific perceptual stimuli or social situations (eg, bridges, staircases, empty rooms, store aisles, streets, meetings, or when driving a car).
	(4) Anxiety and distressing vegetative symptoms often (but not always) accompany the attacks of dizziness, and there is a tendency for generalization and dependent or avoidance behavior to develop.
	(5) Patients often have psychiatric comorbidities, including obsessive-compulsive type personalities, hypochondriasis, generalized anxiety disorders, panic disorder with or without agoraphobia, and (reactive) depression (40).
	(6) Onset typically occurs following an illness (usually a vestibular disorder that has subsequently resolved) or an important psychosocial stress or conflict.

The concept of persistent postural-perceptual dizziness has emerged as a unifying framework for many aspects of psychophysiological dizziness (121; 129; 148; 112; 141; 123). The Committee for the Classification of Vestibular Disorders of the Bárány Society has proposed diagnostic criteria for persistent postural-perceptual dizziness (Table 1). Patients with postural-perceptual dizziness may develop anxiety, avoidance behaviors, secondary functional gait disorders, and severe disability (112). Patients with postural-perceptual dizziness have difficulties with postural control across multiple sensory challenges (121). Short episodes of momentary worsening dizziness constitute a distinctive feature of persistent postural-perceptual dizziness that helps differentiate persistent postural-perceptual dizziness from other types of psychogenic dizziness (68).

Table 1. Bárány Society Diagnostic Criteria for Persistent Postural-Perceptual Dizziness

A. Symptoms of dizziness, unsteadiness, or “non-spinning vertigo” on most days for at least 3 months. Symptoms persist for prolonged (hours-long) periods but may wax and wane in severity, and do not need to be present continuously throughout the day.

B. Persistent symptoms occur without specific provocation, but are exacerbated by upright posture, active or passive motion without regard to direction or position, and exposure to moving visual stimuli or complex visual patterns.

C. The disorder is triggered by events that cause vertigo, unsteadiness, dizziness, or problems with balance, including acute, episodic, or chronic vestibular syndromes; other neurologic or medical illnesses; and psychological distress. When triggered by acute or episodic dizziness or vertigo, symptoms may occur intermittently at first, and then consolidate into a persistent pattern. When triggered by chronic dizziness or vertigo, symptoms may develop slowly at first and worsen gradually.

D. Symptoms cause significant distress or functional impairment.

E. Symptoms are not better accounted for by another disease or disorder.

Generalized anxiety and depression may contribute to chronic dizziness complaints (123). Anxiety and depression symptoms may also result from (ie, be caused by) other forms of dizziness because of the sudden, dramatic, and unpleasant associated sensations and from fear of falling, injury, or death (33; 43; 70; 23; 44; 110; 125; 46; 34; 40; 49; 63; 78; 154; 107; 137; 04). Patients with a positive history of psychiatric disorders have significantly more emotional distress, regardless of the specific phenomenology or diagnostic category of dizziness, including those with benign positional vertigo, vestibular migraine, vestibular neuritis, or Meniere disease (11). A subgroup of dizziness patients with comorbid anxiety is characterized by an increased subjective impairment and health care utilization due to their dizziness (146). They also have significant handicaps and an elevated risk of depression, anxiety, and migraines (04; 136).

People with vertigo and dizziness are at a higher risk of various psychiatric disorders, particularly anxiety, depression, and panic disorder (10). Nevertheless, anxiety and depression are more common in some types of vertigo than others, possibly as a function of ability of patients to exert control over recurrent or persistent symptoms (34; 154). In particular, anxiety and depression are more common in patients with Meniere disease and migrainous vertigo than in those with benign paroxysmal positioning vertigo or vestibular neuritis (34; 154). Persistence of dizziness following an episode of benign positional vertigo is correlated with mental stress that is affected by the duration and recurrence of benign positioning vertigo, age, and gender (39).

Patients with previous, episodic, chronic, or progressive dizziness or vestibular dysfunction may develop a fear of falling, which causes or contributes to anxiety and depression, and itself causes considerable functional impairment (123). In a comparison of patients with persistent postural-perceptual dizziness and other forms of dizziness, most of the patients in both groups experienced mild anxiety; those with a pathological degree of anxiety were more likely to have persistent postural-perceptual dizziness, whereas those with depression were more likely to be in the group of other dizziness (97).

Thus, clinicians should not be too eager to make a diagnosis of psychophysiological (psychogenic) dizziness, as there is a real risk of missing a clinically important underlying disorder (43; 70). Indeed, some advocate considering dizziness “psychiatric” only if it is part of a recognized psychiatric symptom complex and cannot be explained by a vestibular disorder (70).

Prognosis and complications

Patients with vertigo or dizziness commonly suffer from psychiatric comorbidity, and those with psychiatric comorbidity have more severe psychosocial impairment than patients with vertigo or dizziness who do not have psychiatric disorders; the most severe vertigo or dizziness-related handicaps occur in those with nonorganic vertigo or dizziness and psychiatric comorbidity (86). Anxiety is an indicator for dizziness-related impairment (32; 86), but no well-controlled studies exist regarding prognosis for psychophysiological dizziness. Available case series report wide ranges of results, from gloomy to optimistic, with various therapies. Brandt reported that most patients with phobic postural vertigo had a favorable course, with three fourths showing improvement and a quarter being symptom free, even though there was a “considerable rate of psychic disability” at follow-up (16). Dependent, avoidant, anxious, or obsessive-compulsive personality characteristics, hypochondriasis, fainting, and psychosocial stressors were predictive of a more protracted course and more disability from psychogenic dizziness (81; 70).

Patients with persistent postural perceptual dizziness have a higher burden of dizziness and a lower physical health-related quality of life compared to other dizzy patients, even after adjusting for anxiety and depression (130).

Biological basis

	• Patients with vestibular pathology have a high frequency of abnormalities on psychometric tests, and vestibular pathology may precipitate psychiatric illness in susceptible people, particularly to the development of agoraphobia and other disabling phobic avoidance behavior.
	• Some individuals may be predisposed to visually induced dizziness because of atypical visuo-vestibular processing, which is then exacerbated and becomes clinically manifest if a vestibular insult (or more generalized insult) occurs.

Anatomic localization

The vestibular system may be interlinked with the emotion processing systems because patients with psychiatric disorders often experience subjective unsteadiness, dizziness, or vertigo, and because patients with vestibular vertigo syndromes often suffer from anxiety and depression (11). A functional MRI study suggested that spontaneous functional activity of the cuneus and precuneus are altered in patients with persistent postural-perceptual dizziness (91).

Patients with vestibular pathology have a high frequency of abnormalities on psychometric tests, and vestibular pathology may precipitate psychiatric illness in susceptible people, particularly to the development of agoraphobia and other disabling phobic avoidance behavior (73; 71; 69; 33; 16; 99; 23; 35; 44; 55; 110; 125; 127; 24; 100; 116; 147). Vertigo and accompanying impaired spatial orientation, illusions of movement, impaired postural control, and nausea and vomiting, may be extremely disabling and stressful and not easily controlled, leading to anxiety, avoidance behavior, and depression (69; 16; 99; 107; 147). In some patients, precipitating dizziness or vertigo events trigger anxiety-related changes in postural strategies associated with increased attention to head and body motion and co-contraction of leg muscles (29; 01). Once a pattern of symptoms (eg, phobic postural vertigo) is established, continued manifestations may be largely independent of continued symptomatic vestibular dysfunction (69); in fact, continued clinically evident manifestations of vestibular dysfunction are uncommon in such patients (151). The extent to which mild vertigo or dizziness becomes a chronic clinical problem depends heavily on the patient’s psychological makeup and reaction to symptoms (151; 48; 47; 96). Mild dizziness or vestibular symptoms are common, but they become contributing factors for psychiatric dysfunction, chronic dependent illness behavior, avoidance behavior, and persisting handicap and disability in only a small minority of patients with predisposing personality traits, excessive autonomic system reactivity, secondary gain, etc. (151; 80; 29). Certainly, the combination of vestibular and psychiatric pathology seems to cause more persistent symptoms and more disability than either would in isolation (18; 48; 80; 118). The presence of comorbid disease may also increase the magnitude of disequilibrium, anxiety, and distress (24).

In patients with postural-perceptual dizziness, areas involved in multisensory vestibular processing show progressive gray matter volume decrease over time, which might be caused by or contribute to maladaptive mechanisms within the course of disease (148). Multiple studies of such patients have described changes in gray matter volume, cortical folding, blood flow, and connectivity in different brain regions involved in vestibular, visual, emotional, and motor processing, which have been interpreted as demonstrating significant alterations in multiple networks involved in maintaining balance (135). However, the problem with such studies is the lack of consistency between them. No consistent and coherent set of structural or functional abnormalities has emerged to help explain the clinical findings.

Some individuals may be predisposed to visually induced dizziness because of atypical visuo-vestibular processing; this is exacerbated and becomes clinically manifest if a vestibular insult (or more generalized insult) occurs (113).

Pathophysiology

Psychophysiological (psychogenic) dizziness is thought to be due to impaired central integration of sensory and motor signals, particularly in patients with acute and chronic anxiety (16). Anxiety affects the integration of visual, vestibular, and somatosensory inputs in the maintenance of postural balance, and it particularly affects postural perturbations in the antero-posterior axis (51).

In one study of subclinical agoraphobia, compared with controls, functional connectivity was lower in brain networks that integrate visual vestibular and emotional response to guide movement in space (67).

With phobic postural vertigo the subjective sense of postural stability is apparently dissociated from objectively maintained balance capabilities (147). Affected individuals have an accentuated internal focus on balance control with increased attention to postural adjustments even during undemanding balance situations. This promotes inappropriate postural adjustments, with increased muscle co-contractions and body sway, and an oversensitivity to external stimuli (29; 147).

Early pathophysiologic models of persistent postural-perceptual dizziness emphasized the adverse effects of anxiety on postural control and spatial orientation, whereas more recent models incorporated alterations in the predictive processing of sensory inputs and alterations in motion perception, as well as prioritization of postural stability over fluid locomotion to explain symptoms, physiologic and neuroimaging data, and effects of current treatments (124).

Patients with persistent postural-perceptual dizziness do not display a global worsening of passive self-motion perception as quantified by vestibular perceptual thresholds, but displayed elevated thresholds for only roll tilt and z-translation thresholds, which are both reliant on accurate gravity perception (83); this suggests that patients with persistent postural-perceptual dizziness may exhibit impaired processing of graviceptive cues.

Epidemiology

	• Psychophysiological (psychogenic) dizziness is common and generally represents between 10% and 25% of patients presenting to neurologic offices with complaints of dizziness or vertigo.
	• Psychiatric comorbidity in patients with nonfunctional vestibular syndromes affects nearly 50% of affected individuals, with particularly high rates in patients with vestibular migraine and Ménière disease.

Psychophysiological (psychogenic) dizziness is common and generally represents between 10% and 25% of patients presenting to neurologic offices with complaints of dizziness or vertigo (29); it represents an even higher proportion of patients presenting to neuro-otologists (98) or among those presenting with dizziness following a large-scale traumatic event, such as an earthquake (138). The prevalence of psychiatric dysfunction among patients with balance dysfunction is much higher than in the general population, and the prevalence of balance system dysfunction is similarly high in patients with panic disorder or agoraphobia (150; 151). Reliable figures are not available regarding the population prevalence of such disorders, although surveys found over 10% of a working-age sample to have dizziness concurrent with anxiety or avoidance behavior (151; 153).

Psychogenic dizziness may also occur in children and adolescents (37; 54; 89; 142) and is one of the most common etiologies of dizziness among children and adolescents evaluated in tertiary neuro-otology clinics (54); consequently, children and adolescents with recurrent episodic vertigo or other types of persistent dizziness should be screened for possible associated psychological symptoms (89).

The proportion of psychogenic cases among diagnoses for dizziness and vertigo varies by specialty and over time (106). In a systematic review, psychogenic cases represented proportions of cases by specialty: otolaryngology 15%, emergency medicine 3%, general practice 2%, neurology 8%, and physical therapy 3% (106). Among intractable dizziness cases seen in departments of otolaryngology, 70% were diagnosed with psychiatric conditions by psychiatrists, the most common psychiatric diagnosis being unspecified depressive disorder (52). It is not clear, though, whether the psychiatric dysfunction (or its medication treatment) is a cause of the reported dizziness, or whether the intractable dizziness led to psychiatric dysfunction.

Psychiatric comorbidity in patients with nonfunctional vestibular syndromes affects nearly 50% of affected individuals, with particularly high rates in patients with vestibular migraine and Ménière disease (29).

Diagnostic workup

	• It is important to adopt an approach to the assessment of dizziness and vertigo that does not simply address structural factors but rather one that assesses structural, functional, and psychiatric elements.
	• Standardized measures can be administered that quantify patient self-reports of dizziness, vertigo, anxiety, and autonomic system arousal.
	• Diagnostic studies that may be helpful in selected patients with dizziness include audiometry, electronystagmography, bithermal caloric testing, brainstem auditory evoked potentials, and cranial imaging. These should be ordered selectively, depending on the type of dizziness and suspected underlying etiologies.

Recognizing the high prevalence of comorbid psychiatric disease with nonfunctional (“structural”) vertiginous syndromes, as well as the common occurrence of psychophysiological dizziness, it is important to adopt an assessment approach to the assessment of dizziness and vertigo that does not simply address structural factors, but rather one that assesses structural, functional, and psychiatric elements (29). Correct and early diagnosis of “functional dizziness,” occurring either as the primary condition or as a secondary disorder resulting from an underling “structural” vestibular syndrome, is essential to enable adequate treatment and thereby prevent or limit behaviors that could reinforce chronic functional dizziness (29).

To assist providers in obtaining information pertinent to the role of anxiety and autonomic system activation in patient complaints of dizziness, standardized measures can be administered that quantify patient self-reports of dizziness, vertigo, anxiety, and autonomic system arousal (77). Such instruments can include the Dizziness Handicap Inventory (76; 82). The Dizziness Handicap Inventory is a reliable, comprehensively validated, and clinically useful tool to measure self-perceived handicap associated with the symptom of dizziness. Although the utility of the original subscale structure of the Dizziness Handicap Inventory has been questioned (131; 85), patterns of response by patients on these measures can enable providers to correctly diagnose dizziness disorders associated with clinically significant anxiety whether related or unrelated to a history of vestibular system impairment (77). Other instruments can include the Vertigo Symptom Scale (152), which has a stable two-factor structure related to vertigo-balance and autonomic-anxiety (145), and the Beck Anxiety Inventory (09; 105).

In all patients with dizziness or vestibular complaints, careful examination of the eyes, ears, cardiovascular system, nervous system, and vestibular system is indicated, whether or not a psychogenic basis is suspected. Vestibular imbalance is indicated by nystagmus, past-pointing, and postural and gait abnormalities. Clinical disturbances of the vestibulospinal pathways are assessed with several tests including past-pointing, stance, the Romberg test (88), and tandem gait with eyes closed.

Hyperventilation produces presyncope with perioral and acral paresthesias, and potentially carpopedal spasms (119; 53; 95; 27; 45; 102; 38). To produce these sensations in the office, the patient is asked to breathe deeply and quickly for 3 minutes though 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. Some patients with organic forms of dizziness will have reproduction of their symptoms with hyperventilation; hyperventilation can increase the sensitivity of the vestibular system, and some patients will develop nystagmus as a result of hyperventilation-induced “unmasking” of a vestibular disorder, so appropriate caution is necessary in interpreting the results of such testing (69; 70).

In some cases, additional diagnostic tests will be required. These should be ordered selectively, depending on the type of dizziness and suspected underlying etiologies (87). Diagnostic studies that may be helpful in selected patients with dizziness include audiometry, electronystagmography, bithermal caloric testing, brainstem auditory evoked potentials, and cranial imaging (50; 06; 12; 41; 56). In particular, a high percentage of patients with normal examinations and nonspecific vertigo suffer from peripheral vestibular dysfunction that can be documented with electronystagmography and rotatory-chair testing (69; 50; 12; 41). In many patients, though, diagnostic tests and cranial imaging are unrevealing.

Patients with psychogenic dizziness or panic disorder may have abnormalities on audiograms, electronystagmography, or other vestibular tests (73; 71; 69; 120; 60). In some cases, such abnormalities may precipitate a psychiatric decompensation or make manifest a latent psychiatric problem. In others, some vestibular or related abnormalities (eg, oscillopsia) may produce a visual-vestibular mismatch and lead to bodily symptoms, anxiety, and avoidance behavior. A high proportion of patients suffering from panic attacks with dizziness have abnormal audiometric and vestibular function testing, particularly those with moderate or severe agoraphobia (73; 71). Close attention to vestibular and postural abnormalities is indicated in such patients.

Posturography may show abnormalities in patients with psychogenic dizziness (150; 151; 84; 28; 70; 108). For example, posturography may show a significant increase in sway activity in patients with phobic postural vertigo, particularly across the frequency range of 3.5 to 8 Hz, which does not impair objective postural stability (84; 28). The increased sway activity may represent a change in postural strategy, rather than a form of sensorimotor dysfunction. In particular, there may be increased coactivation of antagonistic muscles, as occurs when learning a new motor task, when unpredictable environmental perturbations may be encountered, and when uncertainty exists about the required task (28). Objective balance skills in these patients were not impaired during demanding balance tests at the limits of postural control; in fact, patients with phobic postural vertigo performed better with more difficult tasks than with easier tasks (28), but postural instability was strongly related to agoraphobia (150). Body sway velocity and length were higher in panic patients (108). Abnormal posturography scores with eyes open were related to high anticipatory anxiety, whereas abnormal scores with eyes closed were related to phobic avoidance (108). The postural sway patterns in patients with phobic postural vertigo or panic disorder are different from the patterns in hyperventilation patients (who typically have a concentration of lower frequency sway) and from that in malingerers (who typically show larger sway amplitudes without falls) (84).

Management

	• An optimal multidisciplinary treatment approach incorporates patient education and tailored treatment strategies, including vestibular rehabilitation, cognitive and behavioral therapies, and medications to reduce morbidity.
	• Some patients may benefit from brief vestibular rehabilitation training.
	• If underlying vestibular disorders are identified, appropriate therapy directed at these is indicated, even if there is significant psychiatric or “psychogenic” overlay.

The overall treatment approach for psychophysiological dizziness should be multidisciplinary (30). In general, treatment may incorporate patient education and tailored treatment strategies, including vestibular rehabilitation, cognitive and behavioral therapies, and medications to reduce morbidity (29; 30; 112).

Available low-quality evidence suggests that psychophysiological dizziness may be alleviated by treatment with antidepressants, anxiolytic medications, cognitive behavioral modification techniques with desensitization for situational anxiety, and psychotherapy (57; 73; 59; 114; 14; 118; 126; 101; 117; 140). Patients with nonspecific dizziness report more sleep disruption and depressive symptoms than controls, and patients with sleep disruption are more likely to respond to antidepressant medication (14). Selective serotonin reuptake inhibitors may be helpful in relieving anxiety and the impairment due to psychophysiological dizziness (118; 126). In patients with chronic dizziness and secondary anxiety, targeting pharmacologic treatment for comorbid anxiety is beneficial for subjective symptoms of chronic dizziness (115; 140). There is no evidence from placebo-controlled randomized trials regarding pharmacological treatments (specifically SSRIs and SNRIs) for persistent postural-perceptual dizziness (143).

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) and instructing the patient in relaxation exercises and other techniques (eg, breathing into a paper bag while attempting to slow the respiratory rate); presyncope can be further alleviated by use of antidepressant, anxiolytic, and beta-blocker medications (57; 59; 114; 14).

Phobic postural vertigo can be treated by relieving patients of their fear of a severe underlying organic disease, assuring them that the nature of their condition is known, and providing detailed explanations of the mechanisms involved in causing and precipitating attacks. Additional treatment includes selective administration of antidepressants, short-term psychotherapy, self-controlled desensitization (ie, by repeated exposure to precipitating situations within the context of behavioral therapy), and advocacy of regular but not overly strenuous physical activity (16; 137). Cognitive behavioral therapy has only a limited long-term benefit for phobic postural vertigo (61).

Some patients may benefit from brief vestibular rehabilitation training (149; 70; 61; 101; 134). Vestibular rehabilitation training of patients with persistent postural perceptual dizziness is likely to be helpful in individuals with anxiety and depression (66). Interdisciplinary treatment, including utilization of psychiatric and psychology professionals, may be helpful in patients with psychophysiologic dizziness (62; 101; 117).

Further work is necessary to determine whether any nonpharmacological interventions may be effective for the treatment of persistent postural-perceptual dizziness (144).

If underlying vestibular disorders are identified, appropriate therapy directed at these is indicated, even if there is significant psychiatric or “psychogenic” overlay (43). The management of such patients can be difficult, as many do not accept consideration of a non-organic component to their illness (70).

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Psychophysiological dizziness

Differential Diagnosis

dizziness
vertigo
organic vestibular disorder
psychiatric disorders
generalized anxiety disorder
- panic attacks with or without agoraphobia
- hyperventilation syndrome
- conversion reaction
- neurosis
- depression
- mania

Also Relevant

Benign paroxysmal positional vertigo
Benign paroxysmal vertigo
Dizziness
Positional vertigo

Clinical Categories

Neuro-Ophthalmology & Neuro-Otology

Web References

Guidelines

AAN: Therapies for benign paroxysmal positional vertigo

Psychophysiological dizziness …

Psychophysiological dizziness

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Bárány Society Diagnostic Criteria for Persistent Postural-Perceptual Dizziness

Prognosis and complications

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Patient Profile

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Also in This Category

Toxic and nutritional deficiency optic neuropathies

Nystagmus

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Von Hippel-Lindau disease

Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

Psychophysiological dizziness

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Bárány Society Diagnostic Criteria for Persistent Postural-Perceptual Dizziness

Prognosis and complications

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Patient Profile

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Toxic and nutritional deficiency optic neuropathies

Nystagmus

Third nerve palsy

Von Hippel-Lindau disease

Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

This is an article preview.
Start a Free Account
to access the full version.