Brain, Vol. 115, No. 5, 1303-1321, 1992
© 1992 Guarantors of Brain
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NEUROLOGY OF LATENT NYSTAGMUS
1MRC Human Movement and Balance Unit, National Hospital for Neurology and Neurosurgery London 2Department of Ophthalmology, The Hospital for Sick Children London 3Moorfields Eye Hospital London 4The Radcliffe Infirmary Oxford, UK
Correspondence to:
Correspondence to Michael A. Gresty, MRC Human Movement and Balance Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
We report eye movement findings in 30 patients with latent nystagmus and who were found to have a variety of associated oculomotor disorders.
Latent nystagmus is defined clinically as nystagmus which appears on covering one eye and beats towards the uncovered eye. Recordings showed that the latent nystagmus in 28 patients had slow phases with linear or exponentially decreasing velocity. This nystagmus is termed ‘LN’ In 13 of these patients certain manoeuvres (e. g. pursuit) provoked nystagmus with exponentially increasing slow phase velocities characteristic of the congenital form of nystagmus termed ‘CN’ and we propose that this is a forme fruste of CN. In two patients the nystagmus provoked by cover was latent CN.
Twenty-nine patients had a history of strabismus and one had a marked phoria. Some patients had amblyopia whilst others had normal vision in each eye Although binocular vision was usually absent, six patients had varying degrees of stereopsis.
A temporonasal predominance of monocularly elicited optokinetic response previously associated with LN, was present only in a minority of patients. Some responses were bidirectionally absent or of low velocity, possibly the result of a cortical impairment of visual motion detection. The most deranged responses had slow phases which were in the opposite direction to the stimulus as described in CN. The presence of ‘forme fruste’ CN in many of these patients suggests that some of the derangements of optokinetic responses are due to CN. The findings indicate a greater overlap between the incidences of LN and CN than previously estimated.
Thirty percent of patients had large saccadic ‘square wave’ intrusions These were not present when there was marked amblyopia They are attributed to a competitive incongruence of visual fields and eye positions.
Dissociations found between the presence and severity of strabismus, stereopsis, amblyopia and optokinetic abnormalities point to these features being relatively independent although associated in typical clusterings This is evidence against the theory that strabismus and LN are directly caused by nasotemporal optokinetic imbalance which persists because of failure to develop binocular vision. The variability of findings favours the view that LN and CN arise from a genetic or acquired embryological disorder with various degrees and directions of expression.
Received February 12, 1992. Revised March 20, 1992. Accepted April 15, 1992.
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