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Introduction

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For more than 150 years, the medical literature has contained descriptions of patients with chronic dizziness and motion sensitivity, accompanied by varying degrees of anxiety and phobic behaviors. In 1871, Karl Westphal, a German neurologist, coined the term agoraphobia to describe a syndrome of dizziness, spatial disorientation, and anxiety experienced by individuals in the busy open marketplaces of 19th century European villages.1 Westphal considered postural control, spatial orientation, and threat assessment to be fully integrated components of locomotion, a view that was lost as clinical neuro-otologic and psychiatric practice diverged through the 20th century. The term agoraphobia was linked to panic attacks as a primary psychiatric diagnosis. In the 1980s and 1990s, neuro-otologists and psychiatrists renewed their interest in interactions among vestibular and anxiety disorders. Brandt and Dieterich described phobic postural vertigo (PPV) in the German medical literature in 19862 and in the English medical literature a decade later.3 They defined PPV as a syndrome of postural dizziness and fluctuating unsteadiness provoked by environmental or social stimuli (e.g., crossing bridges; descending staircases; traveling on busy streets or through crowds). They reported that PPV could be triggered by vestibular disorders, medical illnesses, or psychological stress.4 They included two behavioral criteria in their original definition of PPV: (1) obsessive-compulsive personality traits, labile affect, and mild depression; and (2) anxiety and vegetative disturbance.2 Brandt, Dieterich, and colleagues found PPV to be the second most common cause of vestibular symptoms in their university-based neuro-otology practice, behind only benign paroxysmal positional vertigo (BPPV).3 Diagnostic studies differentiated PPV from panic disorder, agoraphobia as currently defined in modern psychiatric nomenclature, and other psychiatric disorders, suggesting that it is a primary neuro-otologic condition with behavioral elements.3 Huppert and colleagues5 found that PPV could be diagnosed quite reliably. They contacted 105 patients who were diagnosed with PPV 5 to 16 years earlier (average 8.5 years) and reaffirmed the diagnosis in all patients. No patients had been misdiagnosed, and none had developed other neurological or vestibular conditions. Two other studies showed that the long-term course of PPV was marked by chronic dizziness and unsteadiness that waxed and waned over time. Symptoms tended to decrease gradually, but rarely resolved.5 Curiously, Westphal reported this same pattern in his reports in the 1870s.1 Behavioral outcomes of PPV were not as good. Two-thirds of patients developed clinically significant anxiety or depression.3 Finally, recent studies found that behavioral factors may affect the natural course of PPV and outcomes of treatment.6,7

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In the early 2000s, Staab and Ruckenstein defined chronic subjective dizziness (CSD),7,8 which had three features: (1) persistent nonvertiginous dizziness lasting 3 months or more; (2) hypersensitivity to motion stimuli, including a patient's own movement and motion of objects in the visual surround; and (3) difficulty with precision visual tasks such as reading or using a computer. The definition of CSD was influenced not only by the ...

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