Phobic Postural Vertigo

Psychogenic vertigo, particularly phobic postural vertigo (PPV), ^[1,2] is common. Of 768 consecutive neurologic patients presenting at our dizziness unit in Munich between 1989 and 1992 Table 1, 158 (21%) had benign paroxysmal positioning vertigo and 129 (17%) had PPV, whereas less than 10% had other well-known disorders such as Meniere's disease and vestibular neuritis. The frequency of psychogenic vertigo and the diagnostic uncertainties prompt this review.

Patients with somatization symptoms consult specialists for their symptom of primary concern; with vertigo, it is the neurologist or otolaryngologist. I will discuss the interrelationship between psychiatric disorders and vestibular function and different forms of psychogenic vertigo before defining the clinical entity of PPV.

Vestibular dysfunction secondary to psychiatric disorders and psychiatric disorders secondary to vestibular dysfunction.

Attempts to define a neurophysiologic link between psychiatric disorders and somatic symptoms have concentrated on vertigo for centuries, ^[3-5] even before the remarkable group of 19th century scientists discovered the functions of the labyrinths and laid the foundation of modern vestibular and ocular motor research. ^[6-7] The vestibular-psychiatric interrelationships include the following: (1) schizophrenic patients often have abnormal responses in vestibular testing; ^[8] (2) patients with anxiety neurosis exhibit greater sensitivity and directional preponderance in vestibular testing; ^[9] (3) psychiatric, in particular schizophrenic, patients are more susceptible to motion sickness; ^[10] (4) patients with vestibular symptoms, particularly Meniere's disease, have a high frequency of abnormalities on psychometric tests; ^[11-13] (5) feeling dizzy or unsteady are among the 13 cardinal symptoms of panic attacks as defined in DSM-IV, ^[14] and the dizziness may even be present between attacks; ^[15] (6) psychiatric morbidity is high in unselected patients with vestibular disorders and remains high on strictly selected patients with documented organic vestibular dysfunction; ^[16] and (7) organic vestibular disease may precipitate as sequelae--panic attacks, with or without agoraphobia, ^[17,18] and forms of psychogenic vertigo such as motorist's disorientation syndrome, ^[19] space phobia, ^[20] and PPV. ^[21]

Schilder ^[22] argued that the importance of the vestibular apparatus and body acceleration for the internal representation of our body image accounted for the secondary psychiatric symptomology in patients with primary vestibular disorders. Although such a psychoanalytic conceptualization cannot be verified empirically, the vestibular-psychiatric interrelationship is inescapable.

Different forms of psychogenic vertigo.

Dizziness is one of the 13 cardinal symptoms of panic attacks, but dizziness and vertigo may be somatic symptoms in a number of psychiatric conditions Table 2, including schizophrenia and mood, somatoform, and dissociative disorders. However, except in somatoform disorders in which the dizziness/vertigo may be the most prominent manifestation, the other conditions rarely occasion neurologic evaluation when there is an obvious primary psychiatric diagnosis.

The two major psychiatric conditions manifesting as psychogenic vertigo are panic disorder and agoraphobia, conditions that can exist separately or together. Diagnosis of panic disorder requires one or more unexpected panic attacks with at least 4 of 13 symptoms, 1 of which is dizziness. Agoraphobia is fear of being in places or situations from which escape may be difficult or embarrassing or help might not be available in the event of sudden development of an incapacitating or embarrassing symptom, including dizziness or falling. Although an association of PPV with anxiety disorders is evident, not all patients present with symptoms of anxiety or panic during attacks of vertigo. However, most patients develop a disabling phobic/avoidance pattern. ^[23] PPV as typology retains great clinical utility. These patients first and foremost seek contact to neurologists and not psychiatrists or psychotherapists since their prevailing complaint is distressing postural imbalance and vertigo.

Phobic postural vertigo.

PPV occurs primarily in patients with an obsessive-compulsive personality and is often misdiagnosed as organic vertigo. The diagnosis is based primarily on six characteristic features: ^[24]

(1) Dizziness and subjective disturbance of balance while standing or walking despite normal clinical balance tests such as Romberg, tandem walking, balancing on one foot, and routine posturography.

(2) Fluctuating unsteadiness in episodes lasting seconds to minutes or momentary perceptions of illusory body perturbations.

(3) Although the attacks can occur spontaneously, there is usually a perceptual stimulus (bridge, staircase, empty room, street) or social situation (department store, restaurant, concert, crowd) from which the patients have difficulty withdrawing and they recognize as a provoking factor. There is a tendency for rapid conditioning, generalization, and avoidance behavior to develop.

(4) Anxiety (57%) and distressing vegetative symptoms occur during or after vertigo. Most patients have attacks both with and without anxiety.

(5) Obsessive-compulsive type personality, labile affect, mild depression.

(6) Onset of the condition frequently follows a period of particular emotional stress, after a serious illness, or following an organic vestibular disorder.

Huppert et al. ^[21] performed a retrospective study on 154 patients diagnosed with PPV. The age distribution ranged from 17 to 70 years, with a clear peak in the fourth and fifth decade (mean age, 41.5 years) and with both sexes affected equally Figure 1. In 32 patients (21%), PPV followed an acute vestibular disorder, particularly benign paroxysmal vertigo (14 patients) and vestibular neuritis (10 patients). There was a transition from organic vertigo to PPV without a symptom-free interval. In view of this, the 21% may seem unexpectedly low, but the percentage increases if we include patients in whom the condition was initiated by head or whiplash trauma. Since post-traumatic dizziness symptoms often resemble those of otolith dysfunction, one might speculate that otoconia are dislodged, resulting in unequal loads on the macular bed and a tonus imbalance between the two otoliths--otolithic vertigo. ^[2,25,26] The symptoms of otolithic vertigo (which is centrally compensated within weeks) are similar to those of PPV, suggesting that the latter evolved from an initial otolith dysfunction.

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Figure 1. Distribution of age and sex (female, white columns; male, black columns) of 154 patients with phobic postural vertigo. ^[21]

Hypothetical mechanism: a disturbance of space constancy caused by decoupling of the efference copy signal.

We are not aware of the subtle self-generated bodily fluctuations or involuntary head movements that occur at upright stance. The environment also appears stationary during active movements, although relative movements between head and surroundings cause shifts of the retinal image. Space constancy seems to be maintained as follows: The voluntary impulse for initiation of a movement is simultaneously accompanied by an appropriate efference copy signal to make identification possible. Von Holst and Mittelstaedt ^[27] suggested that the efference copy is used to readjust the perceptual systems (based on previous experience) to interpret incoming sensory information such as results from movement of the observer relative to a stationary environment rather than vice versa. A decoupling would cause the sensory effects of normal postural adjustments (of which we are usually unaware) to be interpreted as arising from either external body perturbations or motion of the surroundings. If there is no efference copy for body motion, e.g., if we move our eyeball by placing the finger on the eyelid, we see illusory movements of the environments, oscillopsia. The description of the sensation of vertigo in phobic patients (involving involuntary bodily fluctuations and the occasional perception of individual head movements as disturbing external acceleration) can be explained by a transient uncoupling of efference and efference copy, leading to a mismatch between anticipated and actual motion. ^[1,2] Healthy people can experience mild sensations of vertigo of that kind without simultaneous anxiety if they are in a state of exhaustion, when the difference between voluntary head movements and involuntary fluctuations becomes blurred. In the phobic patient, this partial uncoupling Figure 2 could be caused by being preoccupied with constant anxious controlling and checking of balance regulation. This leads to the perception of sensorimotor adjustments that would otherwise occur unconsciously by means of learned and automatically released muscle activation programs to maintain the upright posture.

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Figure 2. Schematic diagram of the sensorimotor derangement, or the neural mismatch concept, of phobic postural vertigo as caused by decoupling of the efference copy signal. An active movement leads to sensory stimulation, the messages of which are compared with a multisensory pattern of expectation calibrated by early experience of motions (central store). The pattern of expectation is either prepared by the efference copy signal, which is emitted parallel to and simultaneously with the motion impulse, or by vestibular excitation during passive vehicular transportation. If concurrent sensory stimulation and the pattern of expectation are in agreement, self-motion is perceived while space constancy is maintained. If the efference copy signal (corollary discharge) is inappropriate, there is a sensorimotor mismatch, and a self-generated head motion or body sway may be erroneously perceived as external perturbations, causing the subjective postural vertigo. ^[2]

Phobic postural vertigo, a panic disorder?

One is tempted to label PPV as a subtype of panic disorder in which vertigo is the major complaint. ^[28,29] A psychiatric evaluation of 42 patients, ^[23] however, revealed that PPV is a clinical entity that should not be confused with panic disorder or agoraphobia. Diagnostic classification by structured clinical interview techniques (SCID) according to DSM-III-R criteria revealed the high rate of psychopathologic co-morbidity in PPV Table 3. However, in the largest subgroup of the patients (43%), vertigo manifested without anxiety or panic attacks. Thus, PPV occurs with or without anxiety; the key to diagnosis is the monosymptomatic subjective postural imbalance without falls rather than anxiety. This makes the nosologic differentiation from panic disorders with agoraphobia necessary.

The two described conditions that most resemble PPV are space phobia ^[20] and mal de debarquement syndrome. ^[30,31] Space phobia, a pseudo-agoraphobic syndrome, describes a fear of absent visuo-spatial support (open spaces) and of falling, unlike the fear of public places found in agoraphobia. The average age of onset is 55 (agoraphobia 24), ^[20] and the condition shows a poor response to psychotherapy. This is a special form of late-onset phobia that is often induced by an illness or fall and is characterized by a constant uncertainty rather than by vertigo attacks. Mal de debarquement syndrome refers to the sensation of rocking and swaying that is commonly experienced with sea travel and persists in some individuals on return to land for weeks to years. Here the period of motion exposure, inducing after effects (such as seamen's legs), acts as the inducing stimulus for a persistent sensorimotor derangement, a development that resembles PPV initiated by an organic vestibular dysfunction.

Clinical course.

We asked 78 patients with PPV to evaluate their condition 6 months to 5.5 years after their original referral. ^[24] Two results seem most important: (1) We had not misdiagnosed anyone with PPV. (2) A favorable course with a 72% improvement rate (22% of patients becoming symptom free). The majority of patients with PPV experienced complete remission or considerable improvement, even if their condition had lasted between 1 and 20 years prior to diagnosis. Despite the encouraging rate of improvement of PPV in the long run, there was still a considerable rate of psychic disability at follow-up. ^[23]

The first therapeutic session must follow the diagnostic work-up. For patients to believe a psychogenic diagnosis, they must have a neurologic examination, vestibular testing, and possibly brain imaging. Our therapeutic regimen consists mainly of relieving the patients of their fear of a severe organic disease by providing them with a detailed explanation of the mechanism that causes, and the factors that provoke, PPV attacks. Such therapy is usually achieved in two to three sessions. We do not subject the patients to long-term psychotherapy. We attempt to guide the patients by suggestion, assuring them that the nature of the disease is known and that self-controlled therapy is possible. We discourage the patients from being preoccupied with their symptoms (decoupling of catastrophic thoughts), provided the obsessional symptoms are not too severe. With severe obsession, we administer antidepressant agents such as imipramine in addition to psychotherapy, and we recommend a self-controlled desensitization, within the context of behavioral therapy, by repeated exposure to situations that evoke the vertigo. We advocate regular but not overly strenuous physical activity to improve the sense of diminished fitness.

The desire of patients with PPV to learn about the psychogenic mechanism and their willingness to engage actively in treatment are encouraging experiences for physicians. Having studied and treated PPV for more than 10 years, we find this syndrome to be a distinct clinical entity based upon its typical features, the reliability of the diagnosis, and the favorable response to short-term suggestive and behavioral therapy.

Acknowledgments

The author would like to thank Michele Seiche for her critical reading of the manuscript.