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Four patients with extensive occlusive disease of the extracranial arteries are described. All suffered attacks of visual loss due to transient retinal ischaemia and all developed the haemorrhagic changes of low-flow retinopathy. Resting cerebral blood flow was within normal limits in all patients. The attacks were provoked by falls in systemic blood pressure or, in one patient, by facial heating. The probable mechanism in this last case is thought to be diversion of blood to a dilated external carotid vascular bed. Temporary cerebral and brachial symptoms occurred but no permanent changes developed. Successful surgical reconstruction was achieved in two patients with relief of symptoms.

SUMMARY Five patients with optic neuropathy, four vascular and one demyelinating, are described who each complained of an unusual symptom. Bright flashes of light (phosphenes) occurred in the affected eyes and were evoked by sudden unexpected sounds. Movement of the eye alone did not reproduce the symptom. In all patients the phenomenon was sufficiently prominent to interfere with sleep and was the main complaint of one patient. An anticonvulsant (phenytoin) greatly reduced the frequency and intensity of the phosphene in one patient.Phosphenes are visual sensations perceived in the absence of visual (luminous) stimuli and may occur in optic nerve disease, but are unusual. Eye movement phosphenes in optic neuritis are now well recognised1 and phosphenes induced by sound have been described in three patients with different ocular conditions.2 Other positive visual phenomena may also be seen in optic nerve disease. Chromatopsia may be a feature of Leber's optic neuropathy and tabetic optic atrophy and may occur in druginduced toxic optic neuropathy.3 We have observed central visual loss in Leber's optic neuropathy due to scotomata described as "dense clouds of brilliant coloured lights". We describe five patients with anterior optic nerve disease with sound or auditory evoked phosphenes and discuss the possible mechanism for this. All the patients presented with rapid unilateral visual loss, optic disc swelling and large sectorial visual field defects. Examination at this time did not reveal any abnormalities other than in the right eye. Visual acuity in the right eye was 6/60, N24 and no Ishihara colour plates could be identified. He had a right relative afferent pupil defect. Ocular movements and slit lamp examination were normal. The optic disc was swollen in the superonasal quadrant and the arteries were attenuated. Visual field charting showed an inferonasal sector defect to all isoptres on the Goldmann Chart (fig 1)

A 48-year-old man presented with a vertical gaze palsy associated with secondary syphilis. It is suggested that the eye movement disorder is due to syphilitic endarteritis in the mesodiencephalic region.

Patients with neurological disease were examined for dissociations between the performance capabilities of pursuit, immediate onset passive and active optokinetic responses to determine whether these functions are subserved by separate mechanisms. We found a patient in whom pursuit was intact in the presence of severely impaired optokinetic responses and another in whom optokinetic responses were intact in the presence of severely deranged pursuit. These dissociations suggest that pursuit and immediate onset optokinetic responses are mediated, to some extent, by separate mechanisms as the results are not explicable in terms of a continuum of performance ability related to target size. Another patient, who had virtually no pursuit or passive optokinetic responses, produced high slow phase velocities of active optokinetic response, which demonstrates that the active form of optokinetic response can be more than a linear addition of pursuit and passive optokinetic responses.

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