Vestibular dysfunction in Gulf War syndrome

Citation
Ps. Roland et al., Vestibular dysfunction in Gulf War syndrome, OTO H N SUR, 122(3), 2000, pp. 319-329
Citations number
35
Categorie Soggetti
Otolaryngology
Journal title
OTOLARYNGOLOGY-HEAD AND NECK SURGERY
ISSN journal
01945998 → ACNP
Volume
122
Issue
3
Year of publication
2000
Pages
319 - 329
Database
ISI
SICI code
0194-5998(200003)122:3<319:VDIGWS>2.0.ZU;2-F
Abstract
METHODS: Vestibular complaints of Gulf War veterans were characterized by a nested case-control study of 23 veterans with 3 different Gulf War syndrom es and 20 matched control subjects. All subjects completed a standardized s ymptom questionnaire and underwent standard audiovestibular tests administe red by audiologists blinded to group identities. RESULTS: The prevalence of reported dizzy spells was higher in veterans wit h Gulf War syndromes 1 (100%), 2 (85%), and 3 (100%) than in controls (25%, P < 0.0001). Dizzy spells were more frequent, lasted longer, and involved a wider variety of accompanying symptoms in veterans with syndrome 2 than i n those with syndromes 1 and 3. Audiovestibular testing showed greater inte rocular asymmetry of nystagmic velocity on sinusoidal harmonic acceleration in syndromes 1 (P = 0.015) and 2 (P = 0.002), greater asymmetry of saccadi c velocity in syndrome 2 (P = 0.4), diminished nystagmic velocity after cal oric stimulation bilaterally in syndrome 3 (P = 0.02 to 0.04), more subject s with pathologic nystagmus (P = 0.09), and greater interside asymmetry of wave I to III interpeak latency on auditory brain stem response in syndrome s 1 (P = 0.005) and 2 (P = 0.07). Asymmetry of gain on sinusoidal harmonic acceleration and pathologic nystagmus were most strongly associated with sy mptoms of paroxysmal vertigo (P = 0.002 and 0.07, respectively); asymmetry of saccadic velocity, with the severity of vertigo (P = 0.004); and abnorma l caloric response, with chronic dysequilibrium (P = 0.006). CONCLUSIONS: The findings are compatible with a subtle neurologic injury fr om organophosphate-induced delayed neurotoxicity.