Vestibulocochlear derangements have been studied in three groups of patients: 200 unselected patients with migraine (Series I), 80 migrainous patients referred because of their symptoms for full neuro-otological examination (Series II), and 116 patients with tension headache who served as controls (Series III). Significant differences were established between tension headache and migraine in respect of incidence and severity of symptoms and their time of onset in relation to the headache. In migraine, vestibulocochlear disturbances can occur as an aura, accompanying the headache or during headache-free periods, the highest incidence occurring during the headache. In Series I, 59 per cent reported vestibular and/or cochlear symptoms and these were of disabling severity in 5 per cent. Significantly, 50 per cent had a history of motion sickness and 81 per cent experienced phonophobia during the headache, the probable mechanism of which is discussed. Persisting vestibulocochlear derangements were found in 77.5 per cent of Series II, largely vestibular and of both central and peripheral origin. Involvement of the vertebrobasilar vascular system appears to be the most likely explanation. Possible links between Ménière's disease, benign paroxysmal vertigo and migraine are discussed.

Mechanosensitive ion channels may play a key role in transducing vascular smooth muscle (VSM) stretch into active force development. To test this hypothesis, we recorded single-channel and macroscopic currents during mechanical stimulation of enzymatically dispersed vascular smooth muscle cells. Patch pipette suction activated a nonselective cation channel that was permeable to K+, Na+, and Ca2+. Whole cell stretch was accomplished using two patch-type micropipettes attached to the cell ends with suction. Stretch elicited a sustained depolarization with a magnitude similar to that observed in pressurized arteries. Under whole cell voltage clamp, stretch activated an inward current with a reversal potential near -15 mV. In another series of experiments, whole cell stretch failed to modify the current-voltage relationship for voltage-gated calcium currents. Thus, in VSM, both single-channel and whole cell data are consistent with activation of a nonselective cation channel by stretch. This mechanism may, in part, account for pressure-induced activation of intact blood vessels.

The role of vision in the control of balance in patients with Parkinson's disease (PD) and cerebellar disease (CD) was studied by measuring body sway with eyes open, closed, and in response to visual stimuli generated by discrete lateral displacements of a moveable room which enclosed the subjects. In response to room movement, normal subjects swayed by an amount intermediate between sway with eyes open and eyes closed and their response attenuated on repetition of the movement, a process depending on shifting from predominantly visual to proprioceptive control. CD patients swayed more than controls with eyes open or closed and as shown by high 'Romberg quotients' (eyes closed/eyes open sway ratio) were able to use visual information to control much of their unsteadiness. CD patients had a normal attenuation of response to repetition of the room movement. PD patients had normal sway with eyes open or closed but their responses to room movement were abnormal, being proportionately larger and failing to attenuate during successive stimuli. The results indicate that cerebellar lesions seem largely to spare the visuopostural loop and also spare the ability to shift from a visual to a proprioceptive control of postural sway. In contrast, the findings in PD suggest that the visuopostural loop is hyperactive and that its influence cannot easily be de-emphasized when visual information is misleading. The latter finding suggests that basal ganglia participation in posture is concerned with the reweighting of the various sensorimotor loops controlling posture in the process of adapting to novel situations.