Keywords:
Neuroradiology brain, MR-Diffusion/Perfusion, MR, Physiological studies, Inflammation
Authors:
R. Dunne, P. Iyer, J. F. Meaney, A. Fagan, K. Curran, N. Colgan, K. Curran, G. Boyle, J. Redmond; Dublin/IE
DOI:
10.1594/ecr2011/C-1911
Conclusion
According to conventional description,
nystagmus originates from lesions in the neural integrator circuit involving the brainstem,
vestibular nuclei and cerebellum.
Studies have shown that infratentorial lesions are expected in up to 40% of patients with MS (9-11).
We expected to find higher numbers in our study group,
because we used 3T MRI which is more sensitive in identifying lesions.
If the traditional theory is true,
then we should have observed infra tentorial and brainstem lesions among all patients in the study group.
Instead we found brainstem lesions in only 12 patients and cerebellar lesions in only 8 patients.
Cortical lesions are expected in MS,
but we speculate that those occurring in the various eye fields in cortical areas do have a bearing on eye movements.
Given the fact that various cortical areas play a major role in the control of saccadic and pursuit functions and that any disruption in the cortical connections between these areas and neural integrator circuit in the brain stem could lead to nystagmus.
We conclude that disruption of white matter tracts in frontal,
temporal,
parietal and occipital visual cortical areas leading up to the brainstem could be the cause of nystagmus in patients with MS where no definite lesion is found in the neural integrator circuit.
In order to further elucidate this hypothesis a larger study would be required and also a study of the 3T MR findings in patients with nystagmus from causes other than MS.