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Timothy C. Hain,
MD 
Page last modified:
November 2, 2009
Psychological problems are related to vertigo in a complex way. They may both be a cause as well as a consequence of dizziness (Staab and Ruckenstein, 2003).
Psychological abnormalities are common in the general population, even more common in those who are ill, and are certainly also common in individuals with vertigo. In a recent study by Garcia et al in Portugal, out of 43 patients, a large number of psychological abnormalities were diagnosed by the SCL-90 (a standard psychological test) including:
| Somatization | 41.9% |
| Hostility | 20.9% |
| Interpersonal sensitivity | 18.6% |
| Anxiety | 23.3% |
| Phobic anxiety | 20.9% |
| OCD (obsessive compulsive disorder) | 53.5% |
| Depression | 30.2% |
| Paranoid traits | 11.6% |
| Psychotic traits | 2.3% |
This study suggests a remarkably large amount of psychological disability in persons with vertigo, especially in traits of somatization and obsessive compulsiveness. This varies from the author's clinical experience of the last 25 years. Other studies of patients with dizziness suggests that they mainly have reactive anxiety and depression (Savastano et al, 2007). A review of the prevalence of panic was published by Simon and others (1998). They document prevalance varying from 3 to 41%, in dizziness specialty clinic. Of this table, our experience matches best the findings of Clark et al (20%).
The Garcia study may simply be wrong -- it was not based on a large sample, it does not indicate the normal frequency of these disorders in a control population, and was also restricted to a particular area of the world.
However, we suspect that the Garcia study is more of a documentation of the general inadequacy of the psychological instruments used to diagnose psychological disorders in dizzy patients . The SCL-90, used here, is just a set of 90 questions that someone has administered to many people, developed some "norms", and which are sold as a standardized package to psychologists. Many "diagnoses" of psychologists (as documented in the DSM-4) include "dizziness" as a feature of psychological disease. This approach "begs the question" -- how can you diagnose a psychological disorder in persons with dizziness, as the criteria for the "diagnosis" include the very condition you are studying ?
It should be realized that psychological testing (unlike MRI scans, or even clinical examinations by neurologists) cannot diagnose "organic" disorders of the brain or neurochemistry. Questionnaires are subjective -- people can say whatever they please, irregardless of the state of their brain. Accordingly, in our opinion at least, these sorts of tests are not "diagnostic" of a disease, but rather are "descriptive" of a particular mental state, subscribed to at the time that the questionnaire was administered. Of course, the comments that we make about the SCL-90 would apply to any questionnaire based study, and nearly any research based completely on patient responses to written or oral questions.
In our opinion, shared by Savastino et al (2007), the most likely explanation for these sorts of lists are reactive psychological disturbances, rather than primary psychiatric problems. However, there are several ways to think about the "chicken-egg" question.
Simon and associates (1998) reviewed three explanatory models (hypotheses) regarding the known association between anxiety (panic) and dizziness.
At present there is no reliable method of consistently distinguishing among patients with dizziness caused by a psychiatric condition, nonlocalized dizziness, and the dizziness accompanied by a psychiatric condition. Thus, discussions of psychogenic dizziness are characterized by considerable opinion and a paucity of objective evidence. The biggest problem in evaluation of these patients is separating psychogenic from nonlocalized vertigo. Accordingly we will first discuss various types of nonlocalized vertigo, and then proceed to talk about psychogenic vertigo specifically.
We define nonlocalized dizziness vertigo as the situation where there is reasonable probability that the patient has a structural disorder of the brain or inner ear, but there no objective evidence to substantiate this hypothesis. Diagnoses often assigned to patients in acute care settings include: Unknown or nonspecific (acute) vertigo, Labyrinthitis, Post traumatic vertigo, "Vasovagal" syncope, and Hyperventilation syndrome. The "unknown or nonspecific" vertigo diagnosis is often appropriate in the acute setting. For example, one might see a patient in the ER (Emergency Room) with dizziness, note that routine ER labs (CBC, electrolytes, CT scan of head) are normal, and find no nystagmus, ataxia or otologic disturbance. One might reasonably in this case simply indicate that the diagnosis is unclear, coding the patient as "Vertigo", and either wait for the symptoms to remit spontaneously, or initiate a more detailed evaluation.
The labyrinthitis diagnosis as well as vestibular neuritis diagnosis is encountered mainly in emergency room settings, Strictly speaking, the diagnosis of labyrinthitis cannot be well substantiated in a non-localized patient as nystagmus and hearing complaints are required for a well-substantiated diagnosis. Patients typically present with dizziness, nausea and/or vomiting, and otherwise resemble patients with "unknown/nonspecific vertigo". Post traumatic vertigo is a nonlocalized vertigo that follows a significant head injury. Localizable diagnoses encountered in this setting, roughly in order of frequency, include benign paroxysmal positional vertigo, labyrinthine concussion, post-traumatic migraine, cervical vertigo, perilymph fistula, temporal bone fracture, and epileptic vertigo. Frequently these specific diagnoses are not made in the acute setting.
Vasovagal syncope is a diagnosis that is ordinarily based entirely on history, and in which there are no physical findings at the time of examination. Postural hypotension should be ruled out.
Hyperventilation syndrome requires more discussion and can be divided into three categories: 1) Persons with "normal" lightheadedness from hyperventilation, 2) Persons with structural ear or CNS disorders that are reactive to hyperventilation such as MS, and vestibular nerve injuries 3) Persons with panic/anxiety states who may hyperventilate inappropriately and are abnormally reactive to hyperventilation. In a classic study, Drachman and Hart (1972) evaluated 100 patients in a neurotology setting. Their protocol included two minutes of hyperventilation. In persons who had no physical findings, and became dizzy after this procedure, a diagnosis of "hyperventilation syndrome" was assigned. Roughly 30% of their patients were diagnosed as having hyperventilation syndrome. However, subsequent studies of large numbers of dizzy patients (e.g. Nedzelski, 1986), have failed to report such a large proportion of patients with hyperventilation syndrome. So, this issue is a controversial one. In our opinion, there are relatively few patients with hyperventilation syndrome. The two minute hyperventilation protocol of Drachman and Hart is overly sensitive, and instead we advocate one minute of hyperventilation. Hyperventilation sensitivity is nonspecific and a positive hyperventilation test does not exclude the presence of a vestibular or CNS lesions. Management consists of a combination of reassurance and small doses of benzodiazepines.
Summary: diagnosis of nonlocalized vertigo in the acute care situation is intrinsically difficult and often inaccurate.
Entities often assigned to patients in ambulatory settings are Unknown or nonspecific (chronic) vertigo, Disequilibrium of the elderly, Vertebrobasilar insufficiency, Vestibular Meniere's disease, and Unknown or Nonspecific Vertigo: These patients are generally those who have had intermittent or persistent dizziness or vertigo for several weeks or more, have a normal physical examination, and normal ENG, audiometry, and MRI. Many of these patients may have undocumented organic vestibular lesions. At present, we have no clinical tests that can identify lesions of the vertical semicircular canals or otolith organs or, for that matter, exclude lesions. For example, we encountered a case of a woman, presenting with vertigo, who had had a herpes zoster infection of the seventh and eighth nerve on one side, a year prior to examination. Caloric testing documented complete loss of lateral canal function on the side of lesion. Examination demonstrated a classic BPPV type nystagmus on the side of lesion, clearly documenting that posterior canal function remained in spite of a history and test pattern suggesting complete loss of function.
Disequilibrium of the Elderly: In elderly patients, it is unusual for the physician to say that he does not know what is causing dizziness. Instead, dizziness and/or ataxia without localizing signs are often designated as "disequilibrium of the elderly", and attributed to the ravages of age. For example, in a series of 740 patients with dizziness, Belal and Glorig (1986) reported that 79% were given the diagnosis of "presbyastasis," a term synonymous with disequilibrium of aging. According to the authors, this diagnosis was assigned to persons above the age of 65 in whom no specific cause of dizziness was identified. In a recent study, 116 elderly patients presenting to a highly subspecialized Neurotology setting were examined. After a thorough assessment, about 20% of patients were diagnosed as "Undetermined" and "vestibulopathy, undetermined"; about 10% were diagnosed as psychophysiologic (Baloh et al, 1989).
Should dizziness in elderly persons without a localizable lesion be attributed solely to aging? Most elderly do show some measurable sensory or central nervous system differences from younger people. However, a potential source of error is to attribute ataxia or dizziness to lesions that are not causally connected. For example, there are many patients with small infarction, minor sensory dysfunction, cataracts, etc., which by themselves would not be enough to cause ataxia, but which, possibly in combination, may be responsible for ataxia in the elderly. Moreover, how do we know that an arbitrary combination of sensory, central, and motor deficits is an adequate explanation for ataxia?
In the elderly, there is a special problem because of our unwillingness to subject patients to extensive diagnostic evaluations. For example, Fife and Baloh (1993) recently pointed out the high prevalence of bilateral vestibulopathy in elderly patients who had disequilibrium or dizziness of uncertain cause. This diagnosis usually requires rotatory chair testing, a test which is often difficult to obtain. The approach to the management of dizziness of nonlocalized cause in the elderly should be cautious and empirical. These patients usually need to be followed more closely than patients in whom a clear diagnosis is available. As in the younger population, empirical trials of medication, psychiatric consultation, and physical therapy may be helpful.
Vertebrobasilar TIA is a diagnosis that is often assigned to patients with nonlocalized vertigo who have multiple vascular risk factors (Grad and Baloh, 1989). When there are clear transient central nervous system symptoms and signs, the diagnosis can be made with confidence. However, in most instances, this is not the case and one must retain a healthy skepticism.
Vestibular Meniere's is a diagnosis mainly made by Otologists. It usually denotes episodic vertigo without otologic symptoms, with normal audiometry and MRI. This diagnosis should not be used to describe all vertigo of unknown cause. It should be used for patients whose symptoms suggest endolymphatic hydrops without hearing loss.
Overview: Diagnosis of nonlocalized vertigo in the ambulatory setting is ordinarily tentative and cautious.
The criteria for somatization syndrome requires between four and six unexplained symptoms, excluding dizziness. The problem is that otherwise unexplained nausea, headache, or fatigue might be caused by a vestibular imbalance, and accordingly studies reporting high incidence of somatization syndrome in dizzy patients must be looked upon with considerable suspicion. As such, in dizzy patients, somatization syndrome is usually a "wastebasket" diagnosis. Management is entirely psychiatric.
While modest symptoms of depression are more common in dizzy patients, patients will also point out that having an undiagnosed disabling illness can be accompanied by depression. In our experience, most depression is reactive rather than primary. The major exception occurs when dizziness symptoms are used by depressed patients who are attempting to make a contact with the medical system, hoping to obtain treatment without being labeled as having a socially stigmatizing psychiatric disorder. Of the antidepressants, tricyclics with a substantial anticholinergic component (e.g. amitriptyline) are best chosen for those patients in whom there is a suspicion of mixed organic/psychiatric disturbance or migraine. The SSRI family (Prozac, Zoloft, etc.), are reasonable choices where one thinks that depression is primary. Recall that the SSRI family often cause nausea as a side effect and also that Prozac has an inordinately long half life.
Dizziness is largely subjective and thus it can be simulated in an attempt to obtain compensation. Astute clinicians, armed with sufficient tools to detect nystagmus, can nearly always detect malingering of dizziness. There are also many laboratory methods of detecting malingering of dizziness or hearing.
In our opinion, patients who have spent perhaps a few hours on the web reading about dizziness, are very arrogant to think that they can successfuly fool a clinician who has several decades of experience with dizzy patients. A discussion concerning how one can detect malingering for one type of dizziness can be found here.
Many individuals with vestibular disorders complain of trouble thinking. Most commonly people say that they can't "multitask". Recent work has suggested that this difficult thinking is measurable and significant. Redfern and others recently documented that reaction times are longer in patients with unilateral vestibular loss than normal controls (2003). This effect increases when patients are attempting to balance. Normal subjects also exhibit longer reaction times when responding to postural perturbations. This appears to be due to a diversion of attention to postural demands, leaving less available for cognitive processing of other input (Redfern et al, 2002).
Sometimes stimulants are helpful. Of course, stimulants may make anxiety worse, and may be addictive too, so their use should be judicious.
It is well recognized that anxiety may accompany vertigo (Pollak et al, 2003). Anxiety could be a natural and logical consequence of a medical condition that is associated with unsteadiness and loss of control of bodily functions. Persons with Menieres' disease, for example, have reactive anxiety and depression (Savastino et al, 2007).
Having considerable anxiety provoked by a medical illness does not seem to us to be a disease, but rather a personality style. Nevertheless, the clinician seeking to improve the lot of his/her patients needs to be able to recognize reasonable and appropriate anxiety and separate it from unreasonable, counterproductive anxiety. All benzodiazepine medications (those in the "valium" family) reduce balance in otherwise normal persons. However, they may improve balance in persons with inner ear or central disturbances.
Similarly, depression is a natural reaction to loss. When depression becomes so severe that it impairs other aspects of ones life, then treatment for depression itself is reasonable. As all antidepressants impair balance to some extent, one should be cautious, and again, seek to take just the "right dose".
Brandt (1991) described a symptom complex that he terms "phobic postural vertigo" characterized by situationally triggered panic attacks, frequently including vertigo with unsteadiness. To us, this diagnosis seems quite difficult to distinguish from simple anxiety in someone who is dizzy.
Holberg et al suggested that persons with phobic postural vertigo might be more sensitive to proprioceptive disturbances than healthy subjects and also refrain from use of vision (2003). In essence then, they are suggesting that PPV might be a "somatosensory dependence" syndrome. As other authors suggest that phobic vertigo is typified by visual dependence, it seems that more research is needed.
Agoraphobia, dread of being in or crossing open places, is considered a "functional" cause of dizziness. Height phobia, or acrophobia often accompanies agoraphobia.
Agoraphobia and acrophobia, however, might be a logical reactions to dizziness rather than a cause, as agoraphobia is a reasonable adaptation to a condition that affects balance in an unpredictable way. Open places neither have surfaces that can be used for support nor close visual referents. Certainly, agoraphobia may also have psychic mechanisms. This determination as well as treatment are best made by a psychiatrically trained professional, after you have made a reasonable search for an organic disorder.
Space and Motion Discomfort (SMD)
This term has been used by the University of Pittsburgh group to describe individuals with agoraphobia, acrophobia, and visual vertigo. The term has not been adopted by most others who work with dizzy patients, and we see no particular reason to use it instead of the root terms themselves.
Some authors claim that exacerbation of dizziness and related symptoms by stimulating visual environments is typical of psychogenic vertigo (Staab and Ruckenstein, 2003. More can be found on this symptom under the heading of visual dependence. The difficulty of this assertion is that organic vertigo often results in sensitivity to visual environments. Another difficulty is that other authors claim the opposite, and that psychogenic vertigo is typified by increased dependence on somatosensory input (Holmberg et al, 2003).
In the author's opinion, these patterns reflect a sensory reweighting so that vestibular inputs are downweighted and replaced by greater dependence on anything else -- vision, somatosensory input, or internal estimates of bodily orientation and movement. They are not necessarily psychogenic, and in fact, usually are accompanied by an organic vestibular disturbance.
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