Asymptomatic visual loss in multiple sclerosis.
Visual disturbances are common in multiple sclerosis (MS) and often a result of acute demyelinating optic neuropathy. Careful examination of MS patients, who have never suffered optic neuritis, may also reveal asymptomatic visual loss. This type of silent disease activity was investigated by computerised resolution perimetry, which has the potential to reflect the percentage of functional retino-cortical neural channels. The time of onset and the evolution of asymptomatic visual loss was investigated. One approach was to retrospectively select patients who never had suffered acute optic neuritis from a closely monitored MS population and re-examine them again. Sixteen patients were identified and vision was evaluated during a period of 5.5-9 years of follow-up and compared with that in 14 healthy controls. The mean channel percentage of the MS group was 89 +/- 19 % (SD) on entry into the study, compared with 110 +/- 15% (SD) of controls (p < 0.003). At termination of the study the mean percentage was essentially unchanged both in MS patients (87 +/- 21%, SD) and controls (110 +/- 19%, SD). The second approach was to test a group of 7 patients with MS or strongly suspected MS, with the same method, in close connection with their first clinical exacerbation. All cases lacked visual symptoms and none had previously had acute visual loss. Again, virtually all performed subnormally in the vision tests, and to the same degree as in the first group of patients. Results were compared with those obtained from 25 MS patients who had experienced one or more attacks of optic neuritis. Compared with controls the loss of functional retino-cortical neural channels was 20% in patients without a previous history of optic neuritis and 30 % in patients who previously had experienced optic neuritis. We conclude that asymptomatic visual loss seems to be a universal feature of MS and has a substantial impact on the visual pathways, that it is present already at the time of clinical onset of the disease, and that any progression thereafter is slow enough to elude detection during several years of follow-up.
Lycke
J
J
Institute of Clinical Neuroscience, Department of Neurology, Göteborg University, Sahlgren's University Hospital, Sweden. jan.lycke@neuro.gu.se
Tollesson
P O
PO
Frisén
L
L
D000328:Adult; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000150:complications* / Q000473:pathology*; D009460:Neurologic Examination; D009902:Optic Neuritis / Q000473:pathology; D012160:Retina / Q000473:pathology / Q000502:physiology; D012189:Retrospective Studies; D014786:Vision Disorders / Q000209:etiology* / Q000473:pathology*; D014787:Vision Tests; D014792:Visual Acuity / Q000502:physiology; D014793:Visual Cortex / Q000473:pathology / Q000502:physiology; D014794:Visual Fields; D014795:Visual Pathways / Q000473:pathology*