Psychophysiological dizziness

Douglas J Lanska MD FAAN MS MSPH (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

)
Originally released October 22, 2003; last updated November 23, 2019; expires November 23, 2022

This article includes discussion of psychophysiological dizziness, chronic subjective dizziness, phobic postural vertigo, psychiatric dizziness, psychic dizziness, psychogenic dizziness, psychogenic vertigo, and psychophysiological vertigo. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

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 (Jacob 1988; Balaban and Jacob 2001). 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 (Freud 1895; Kapfhammer et al 1997; Balaban and Jacob 2001). There has been an increased recognition of the situational specificity of certain symptoms, and behavioral therapeutic measures have been instituted to address this (Balaban and Jacob 2001).

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 (Brandt 1996; Staab 2006; Söhsten et al 2016; Staab et al 2017; Wurthmann et al 2017; Popkirov et al 2018; Trinidade and Goebel 2018; Staab 2019).

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 (Brandt and Dieterich 1986; Brandt 1996; Huppert et 1995; Huppert et 2005). Phobic 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 (Brandt 1996).

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 (Jacob et al 1989; Jacob et al 1993; Jacob et al 2009). 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 (Bronstein 1995a; Bronstein 1995b). 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 (Longridge et al 2002), 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”) (Cousins et al 2014; Cousins et al 2017). The term “visual vertigo” was renamed “visually induced dizziness” when it was adopted by the Bárány Society into its International Classification of Vestibular Disorders (Bisdorff et al 2009).

Beginning in 2004, Staab and colleagues described the clinical syndrome of “chronic subjective dizziness” (Staab et al 2004; Staab et al 2007), 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 (Staab et al 2004; Staab et al 2007; Staab et al 2017).

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” (Staab et al 2017).

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