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A connection between balance system dysfunction and Agoraphobia (AG) in Panic Disorder (PD) has been found. Balance control of many patients with PD and AG rely mainly on visual cues (visual dependence) and moving visual stimuli in their peripheral visual field induce postural instability and anxiety. These features may maintain agoraphobic symptoms after standard treatments.
To study whether balance rehabilitation with moving peripheral visual stimuli would benefit patients with PD and AG not fully responders to standard treatments.
Six patients with PD and AG were included. Inclusion criteria: 1) panic-phobic symptoms despite adequate treatments (SSRIs for at least 3 months; cognitive behavioral therapy) and 2) balance dysfunction with instability during peripheral visual stimuli (posturography with and without peripheral visual stimulation).
The patients went through 10 sessions (3 sessions/week) of balance rehabilitation: static and dynamic exercises, with movements of eyes and head, during projection of peripheral visual stimuli (video-films, 32 times-accelerated, on large lateral screens). Descriptive and non-parametric analyses were applied.
After rehabilitation, the patients showed significant improvement both in panic-phobic symptoms (specific psychometric scale scores) (p < 0.05) and in balance performance (post-rehabilitation posturography with and without peripheral visual stimulation) (p < 0.05).
Balance rehabilitation with peripheral visual stimuli may increase the efficacy of standard treatments in patients with PD and AG and visual-balance dysfunction. Mechanisms of physical and emotional habituation to environmental destabilizing stimuli may be involved. Further larger and controlled studies are warranted.
This study sought to establish the prevalence of vestibular disorders, migraine and definite migrainous vertigo in patients with psychiatric disorders who were referred for treatment of dizziness, without a lifetime history of vertigo.
Out-patients in a university hospital.
Materials and methods:
Fifty-two dizzy patients with panic disorders and agoraphobia, 30 with panic disorders without agoraphobia, and 20 with depressive disorders underwent otoneurological screening with bithermal caloric stimulation. The prevalence of migraine and migrainous vertigo was assessed. The level of dizziness was evaluated using the Dizziness Handicap Inventory.
Dizzy patients with panic disorders and agoraphobia had a significantly p = 0.05 regarding the prevalence of peripheral vestibular abnormalities in the group of subjects with PD and agoraphobia and in those with depressive disorders. Migraine was equally represented in the three groups, but panic disorder patients had a higher prevalence of migrainous vertigo definite migrainous vertigo. Almost all patients with a peripheral vestibular disorder had a final diagnosis of definite migrainous vertigo according to Neuhauser criteria. These patients had higher Dizziness Handicap Inventory scores. The Dizziness Handicap Inventory total score was higher in the subgroup of patients with panic disorders with agoraphobia also presenting unilateral reduced caloric responses or definite migrainous vertigo, compared with the subgroup of remaining subjects with panic disorders with agoraphobia (p < 0.001).
Our data support the hypothesis that, in patients with panic disorders (and especially those with additional agoraphobia), dizziness may be linked to malfunction of the vestibular system. However, the data are not inconsistent with the hypothesis that migrainous vertigo is the most common pathophysiological mechanism for vestibular disorders.
To assess the efficacy of rehabilitation for dizzy patients after recent acute vestibular disturbance.
Forty patients recently hospitalised for an acute episode of rotational vertigo which lasted days were randomly divided into two groups. The first group (20 patients; group R) underwent active rehabilitation, while the second group (20 patients; group C) were told only to ‘perform their daily activities’. Group R subjects underwent a total of 10 sessions of rehabilitation, including exercises on a stabilometric platform, point de mire and a series of five exercises repeated five times daily. All patients performed static stabilometry (posturography), undertook the dynamic gait index test, and completed a dizziness handicap questionnaire and a visual analogue scale for anxiety, at baseline and on completion.
At 25 days, the rehabilitated patients obtained better results for all recorded outcomes, compared with the control group. The greatest difference in the rehabilitated subjects, compared with the control group, was for the dynamic gait index test; however, this difference was not statistically significant. The visual analogue scale anxiety score was statistically significantly more reduced in rehabilitated patients compared with control patients. Control patients maintained a higher visual dependence for postural control.
These results would appear to support the effectiveness of a supervised exercise programme for patients following acute onset of vestibular disturbance. A correlation was found in both groups between dynamic gait index results and anxiety. In our experience, a rehabilitation programme seems to reduce dependence on visual cues for postural control.
To investigate vestibular function in human immunodeficiency virus positive subjects.
We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness.
Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects.
In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).
We report a case of a 58-year-old man suffering from stiff-person syndrome and recurrent peripheral vertigo.
A case report and a review of the recent literature on stiff-person syndrome are presented.
The patient presented with recurrent episodes of vertigo with a pure peripheral pattern and with concomitant episodes of burning muscle pain, muscle twitching, weight gain and fatigue, worsening with tension or stress that also occurred in periods without vertigo. Cochlear examinations only showed presbyacusis-like hearing loss. The diagnosis of stiff-person syndrome was made with electromyographic examination and from findings in the blood and cerebrospinal fluid of high titres of anti-glutamic acid decarboxylase (GAD67) autoantibodies. In a two-year follow-up period, therapy for stiff-person syndrome abolished episodes of both stiffness and vertigo.
As far as we know, no other clinical case of acute vestibular damage with a possible correlation with anti-glutamic acid decarboxylase antibodies has been described. Peripheral vertigo possibly related to a lack of gamma aminobutyric acid underlines a possible role of gamma aminobutyric acid as a neurotransmitter in the peripheral vestibular system.
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