E Eryaman1, I D Oz, B Y Ozker, S Erbek, S S Erbek. 1. Department of Otolaryngology, Baskent University Faculty of Medicine, Ankara, Turkey. esraer@superonline.com
Abstract
OBJECTIVE: Recent studies show that benign paroxysmal positional vertigo (BPPV) may also affect the macula of the saccule. We investigated vestibular evoked myogenic potential (VEMP) results in patients with BPPV. MATERIALS AND METHODS: The study group included 31 patients (31 ears) diagnosed with posterior canal BPPV and the control group included 23 healthy volunteers (46 ears) with no neurotologic symptoms. After VEMP recordings were performed, mean latency values for p13 of the study and control groups were compared. RESULTS: VEMP responses were elicited in all controls (46 ears). In the study group, responses were normal in 19, delayed in 5, and absent in 7 ears. There was a significant difference between abnormal VEMP rates for patients versus controls (p < 0.001). Although VEMP responses were elicited in all non-affected ears of patients, there was a delayed response in 6 (19%) non-affected ears. This was statistically significant when compared with controls (p = 0.002). There was no correlation between abnormal VEMPs and the number of canalith reposition maneuvers required (p = 0.392). CONCLUSION: Our findings suggest the prolongation of mean latency values for p13 of VEMP in patients with BPPV might signify neuronal degeneration in the macula of the saccule, and the absence of VEMP waves might represent the extent of damage. Also, high latency values for p13 in non-affected ears of patients might indicate bilateral neural degeneration in BPPV.
OBJECTIVE: Recent studies show that benign paroxysmal positional vertigo (BPPV) may also affect the macula of the saccule. We investigated vestibular evoked myogenic potential (VEMP) results in patients with BPPV. MATERIALS AND METHODS: The study group included 31 patients (31 ears) diagnosed with posterior canal BPPV and the control group included 23 healthy volunteers (46 ears) with no neurotologic symptoms. After VEMP recordings were performed, mean latency values for p13 of the study and control groups were compared. RESULTS: VEMP responses were elicited in all controls (46 ears). In the study group, responses were normal in 19, delayed in 5, and absent in 7 ears. There was a significant difference between abnormal VEMP rates for patients versus controls (p < 0.001). Although VEMP responses were elicited in all non-affected ears of patients, there was a delayed response in 6 (19%) non-affected ears. This was statistically significant when compared with controls (p = 0.002). There was no correlation between abnormal VEMPs and the number of canalith reposition maneuvers required (p = 0.392). CONCLUSION: Our findings suggest the prolongation of mean latency values for p13 of VEMP in patients with BPPV might signify neuronal degeneration in the macula of the saccule, and the absence of VEMP waves might represent the extent of damage. Also, high latency values for p13 in non-affected ears of patients might indicate bilateral neural degeneration in BPPV.