Psychogenic dizziness
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Vendhan Ramanujam M.B.B.S [2]
Synonyms and keywords: Functional dizziness; hyperventilation syndrome; nonspecific dizziness; phobic postural vertigo; psychiatric dizziness; psychic dizziness; psychophysiologic dizziness; somatization
Overview
Psychogenic dizziness is a dizziness which is not characterized by true vertigo and it can be replicated by hyperventilation and psychiatric symptoms that usually precede its onset. It occurs in anxious or phobic individuals and do not include any specific symptoms[1][2][3]. A new proposal narrowly defines psychogenic dizziness as the dizziness which occurs exclusively in combination with other symptoms as part of a recognized psychiatric symptom cluster and this symptom cluster is not itself related to vestibular dysfunction[4][5]. Psychogenic dizziness should not be confused with the phenomenon of psychogenic overlay where the preexisting nucleus of nonpsychiatric dizziness is augmented by psychiatric factors that occur along with it. None of the DSM-IV Axis I1 psychiatric disorders (i.e., personality disorders) are characterized by dizziness or imbalance. Thus, in our view, the presence of a personality disorder does not alone justify a diagnosis of psychiatric dizziness. Partially overlapping the nosologic framework of vestibular diagnosis is the nosologic framework of Axis I and Axis I1 psychiatric disorders according to the DSMIV. 4
Classification
According to the newly proposed narrow definition, the following classification has been proposed[5]
- Psychiatric condition that entirely accounts for the patient’s dizziness like the panic disorder.
- A cluster of anxiety disorders where dizziness is a part of their symptom cluster like the generalized anxiety disorder.
- Psychiatric disorders where the psychiatric symptoms are vaguely described as having dizziness or imbalance by the patients like the description of poor concentration as swimming sensation in depressive disorders.
- Psychiatric disorders which present with neurologic symptoms including the symptom of imbalance which would fit in the narrow definition of psychiatric dizziness like the conversion disorder.
Pathophysiology
The following mechanisms mediate the relationship between anxiety disorders and vestibular disorders leading to the state of dizziness in psychiatric patients.
Psychological
- Somatopsychic: Patients may catastrophically interpret vestibular sensations as implying immediate danger and develop panic disorder which persists even after the resolution of the original vestibular disorder.
- Psychosomatic: occurrence of increased vestibular responses
Neuroanatomicol or Neurophysiologicol
Vestibular symptoms may induce panic attacks via somatopsychic mechanisms because This somatopsychic effect of abnormal vestibular sensations may be particularly likely in individuals already predisposed for developing panic disorder (e.g., those with family history of panic disorder). Once established, panic disorder can persist even after resolution of the original vestibular disorder. For example, through interoceptive conditioning, physical sensations other than vestibular sensations may acquire panictriggering ~apabi l i t ies .F~u~rt hermore, agoraphobic avoidance behaviors may persist because successful avoidance prevents the unlearning of avoidance behaviors, regardless of their original cause.48 The possibility of psychosomatic mechanisms is suggested by the occurrence of increased vestibular responses with increased arousal in normal subjects and p r ima t e ~ ~an~d- ~allt ered responses on rotational and positional testing with hyperventilati~n.~~,~~ Both increased arousal and hyperventilation are common in panic disorder with agoraphobia. Thus, patients might suffer from (reversible) vestibular dysfunction whenever they are anxious (i.e., during a large portion of their normal daily activities). It might be argued that the vestibular test abnormalities found in our agoraphobic were merely artifacts stemming from psychosomatic effects of hyperventilation or high arousal during the vestibular testing and therefore these patients belong in zone A. It is unlikely, however, that the vestibular laboratory abnormalities found can be explained by these mechanisms because vestibular laboratory abnormalities were unrelated to state anxiety during vestibular tests. The most specific electronystamographic abnormalities involved asymmetric responses on caloric tests consistent with peripheral vestibular dysfunction. Vestibulo-ocular reflex (VOR) gain was decreased rather than increased, and vestibular dysfunction was specifically related to questionnaire measures of space and motion discomfort and the occurrence of vestibular symptoms between panic attacks. Psychosomatic mechanisms might play a secondary role in individuals with a history of a vestibular disorder who have become asymptomatic as a result 1164 NEUROLOGY 48 May 1997 of central compensation. It is possible that increased arousal and hyperventilation might alter central vestibular compensatory processes, resulting in the reemergence of vestibular Recent evidence exists for a basis for a linkage between panic disorder and vestibular dysfunction. The principal current theories of the etiology of panic disorder include dysregulation of brainstem noradrenergic ~ y s t e m s , i~nv~o-lv~e~m ent of central serotonergic pathways,57a nd respiratory d y s ~ o n t r o l .R~e~la,t~io~nships between the vestibular system and structures of interest for panic disorder include connections between the locus coeruleus and the lateral vestibular nucleus and alterations in vestibular processing after iontophoretic administration of clonidine to the locus c o e r u l e u ~ , s~ig~n-if~ic~a nt vestibular input to the raphe serotonergic effects on vestibular p r o c e ~ s e s ,a~n~d ,v~e~st ibular-respiratory connect i o n ~ .A~ls~o,, ~th~e nucleus parabrachialis receives vestibular and visceral input and is connected with the limbic system, including the am~ g d a l aw, ~hi~ch coordinates autonomic and behavioral responses to emotional stimuli and is essential for the conditioning of fear response^.^^-^^
References
- ↑ Drachman, DA.; Hart, CW. (1972). "An approach to the dizzy patient". Neurology. 22 (4): 323–34. PMID 4401538. Unknown parameter
|month=ignored (help) - ↑ Nedzelski, JM.; Barber, HO.; McIlmoyl, L. (1986). "Diagnoses in a dizziness unit". J Otolaryngol. 15 (2): 101–4. PMID 3712537. Unknown parameter
|month=ignored (help) - ↑ MOORE, BE.; ATKINSON, M. (1958). "Psychogenic vertigo; the importance of its recognition". AMA Arch Otolaryngol. 67 (3): 347–53. PMID 13507801. Unknown parameter
|month=ignored (help) - ↑ Gresty, MA.; Bronstein, AM.; Brandt, T.; Dieterich, M. (1992). "Neurology of otolith function. Peripheral and central disorders". Brain. 115 ( Pt 3): 647–73. PMID 1628197. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Furman, JM.; Jacob, RG. (1997). "Psychiatric dizziness". Neurology. 48 (5): 1161–6. PMID 9153437. Unknown parameter
|month=ignored (help)