Habituation deficit of the nociceptive R2 blink reflex: functional changes in patients with phobic postural vertigo (PPV)

Aims: Studies have shown that patients exposed to repeated stimuli perceive further stimulation as being less intense. This is termed habituation and is intended to prevent the organism from overstimulation and enables it to concentrate better on new incoming stimulation that may be more important. Habituation deficit is generally considered to reflect cortical overexcitability or central sensitization and was described in several chronic pain conditions such as migraine or tension-type headache. Phobic postural vertigo (PPV) is often followed by organic vertigo disease such as vestibular neuritis, benign paroxysmal positional vertigo, vestibular migraine, Menière‘s disease and it was hypothesized that hypersensitivity to movement perception is one important mechanism leading to PPV. Verification of insufficient blink reflex habituation in PPV patients would confirm cortical overexcitability and may hint at central sensitization as one pathophysiological mechanism for the development of this disease. Methods: We investigated 60 patients with PPV and compared them to age- and sex-matched healthy volunteers. The habituation pattern was examined using the nociceptive blink reflex (nBR). The R2 response of the nBR was analyzed by specific stimulation of Aδ- fibers in the area of V1 on both sides. To investigate the habituation, we chose a block design (10 blocks each 6 pain stimuli). Habituation was defined as a decrease in R2 response of the sequence blocks compared to block 1. Results: Patients with PPV reported a decreased subjective pain threshold. The preliminary analysis of the nBR showed a lack of habituation in patients with PPV compared with 20 healthy controls in terms of a decreased slope of the area under the curve. We could not identify differences in regard to latency. Conclusion: Our analysis indicates habituation deficits in patients with PPV, which could be a part of the pathophysiological basis of this disease.