Vestibular evoked blood flow response in the basilar artery.

OBJECTIVE

Monitoring of the basilar artery (BA) is difficult and has been sparsely performed. The aim of this study was to present physiological data of functional transcranial Doppler sonography (TCD) of the BA during caloric vestibular stimulation in healthy volunteers.

METHODS

TCD of the BA was performed in 26 healthy volunteers (14 women, 12 men, age 25.1+/-3 years) during caloric vestibular stimulation. Vertigo was documented using electronystagmography (ENG) and a subjective vertigo scale ranging from 0 to 10 points. Simultaneously, capnogpraphy was performed.

RESULTS

All subjects experienced vertigo, nausea and oszillopsia during vestibular irrigation. The average subjective vertigo was for a period of 106 s (+/-65.4); the average subjective estimated degree of vertigo was 6.7 points (+/-1.5). In all subjects, ENG demonstrated horizontal nystagm to the left non-irrigated side. In 14 subjects the subjective vertigo was rated by the individuals as extreme (point score > or =7) and in 12 subjects as low (point score <7). Mean flow velocity (MFV) in the BA increased significantly during vestibular irrigation, being more prominent in the initial irrigation and vertigo phase (5.8+/-5.9%, P<0.05) than in the second vertigo phase (2.2+/-8.8%, P<0.05). The calculated pulsatility index (PI), which indicates the condition of the small resistance vessels, decreased significantly (-4.9+/-8.1%; 4.3+/-8.9%, P<0.05) during both phases of vestibular activation. End tidal pCO2 did not change significantly (constant 5.4+/-0.4 Vol%), but respiration frequency was significantly increased during vestibular stimulation (12.3+/-3.8 min(-1) to 16.4+/-5.3 min(-1) and 16.3+/-4.8 min(-1), P<0.05) probably as a vegetative sign of vertigo. The observed MFV- and PI-changes were more prominent, although not quite significant, in the subgroup of subjects who experienced extreme subjective vertigo than in the subgroup who experienced low subjective vertigo.

CONCLUSIONS

These observations indicate that MFV increase in the posterior circulation is due to activation of the vestibulocerebellum. In addition, it is possible that the previously elaborated MFV increase in the MCA might contribute to MFV increase in the BA via the posterior communicating artery. The difference in the 2 subgroups (extreme vertigo vs. low vertigo) may reflect the great variety of anatomical and physiological conditions of the peripheral vestibular organ, the brainstem anatomy and the corresponding blood supply. For clinical purposes this TCD-test may contribute to the investigation of the vasomotor reserve of the posterior circulation, e.g. in patients with vertebrobasilar ischemia, bilateral vestibular loss or local neurodegenerative disease.