CLINICAL AND MRI CORRELATES IN 27 PATIENTS WITH ACQUIRED PENDULAR NYSTAGMUS

Citation
Li. Lopez et al., CLINICAL AND MRI CORRELATES IN 27 PATIENTS WITH ACQUIRED PENDULAR NYSTAGMUS, Brain, 119, 1996, pp. 465-472
Citations number
41
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
119
Year of publication
1996
Part
2
Pages
465 - 472
Database
ISI
SICI code
0006-8950(1996)119:<465:CAMCI2>2.0.ZU;2-J
Abstract
Clinical and MRI investigations were carried our on 27 patients with a cquired pendular nystagmus in an attempt to delineate possible sites o f lesions responsible for pendular nystagmus and mechanisms underlying the frequent ocular disconjugacy of this nystagmus. The aetiologies w ere multiple sclerosis (n=21), brainstem stroke (n=3) and other neurol ogical conditions. In at feast 59% of the patients, pendular nystagmus appeared >1 year after the first symptom of the disease. Patients' MR Is were characterized by multiple areas of abnormal signal and were an alysed statistically to identify areas where lesions overlapped signif icantly between patients. Statistically significant overlap occurred i n areas containing the red nucleus, the central tegmental tract the me dial vestibular nucleus and the inferior olive. Patients with horizont al pendular nystagmus showed predominantly pontine lesions whereas pat ients with torsional pendular nystagmus showed predominantly medullary involvement. The nystagmus was conjugate in 15 patients and disconjug ate in amplitude or direction in 12. Internuclear ophthalmoplegia or a symmetrical visual acuity occurred in similar proportions in both grou ps. Patients with conjugate pendular nystagmus had a higher incidence of symmetrical, 'mirror image' lesions on MRI than patients with disco njugate nystagmus. The abundance of abnormal MRI signals in our sample suggests that large or multiple structural lesions may be required to elicit pendular nystagmus, predominantly in the pens but also in the midbrain and medulla. The involvement of structures projecting to the inferior olive supports the hypothesis that oscillatory properties of olivary neurons causes the rhythm of pendular nystagmus. The delay obs erved between the onset of the underlying disease and the pendular nys tagmus supports a mechanism operating via neural deafferentation. Disc onjugancies in pendular nystagmus cannot be explained on the basis of the associated internuclear ophthalmoplegias nor on the basis of asymm etrical visual acuity. The association between symmetrical MRI lesions and conjugate nystagmus suggests that asymmetrical damage to brainste m structures concerned with binocular alignment may underlie disconjug ate pendular nystagmus.