Serial Visual Evoked Potentials In 90 Untreated Patients With Acute Optic Neuritis
Frederiksen JL, Petrera J
Surv Ophthalmol 1999 Oct;44 Suppl 1:S54-62
Univ of Copenhagen, Dept of Neurology, Glostrup, Denmark
PMID# 10548117; UI# 20014153
To establish the value of Visual Evoked Potentials (VEPs) for monitoring disease evolution, we undertook a population-based study of 90 untreated patients 12 to 57 years of age (median, 32 years) at the onset of Optic Neuritis (ON) and after 2, 4, 12, and 52 weeks.
Optic Neuritis was MonoSymptomatic (AMON) in 58 patients and part of the Clinically Definite Multiple Sclerosis (CD/MS) in 32 patients.
The VEP was abnormal in Eyes with acute ON in 69 (77%) of 90 patients at onset and in 80 (89%) of 90 patients at one or more of the follow-up sessions.
In eyes with acute ON, normalization of an initially abnormal VEP was observed during 1-year follow-up in 13 (19%) of 69 patients.
At onset of ON, VEP was abnormal in 35% of the clinically unaffected Eyes.
By parametric analysis of variance, the latencies (P = 0.0058), the amplitudes (P = 0.0298), and the combined VEP scores (P = 0.0345) in the eyes with acute ON were significantly associated with the time after onset.
The latencies were influenced by the presence of CD/MS (P = 0.0033), whereas the amplitudes were influenced by Visual Acuity (P = 0.0000).
When Visual Acuity was included in a multifactor model, the time after onset was, however, not significantly associated with the amplitude (P = 0.8826).
The mean latency of the VEPs in eyes with acute ON was significantly shorter in AMON than in ON as part of CD/MS.
This study provides evidence that VEP abnormality is often transitory, and that VEP often normalizes during follow-up.
The diagnostic yield is increased by repeating VEP in the spontaneous course of acute ON. Visual Evoked Potential is a sensitive tool for revealing SubClinical lesions.
Long-Term Follow-Up Of Isolated Optic Neuritis: The Risk Of Developing Multiple Sclerosis, Its Outcome, And The Prognostic Role Of Paraclinical Tests
Ghezzi A, Martinelli V, Torri V, Zaffaroni M, Rodegher M, Comi G, Zibetti A, Canal N
J Neurol 1999 Sep;246(9):770-5
Centro Studi Sclerosi Multipla, Via Pastori 4, I-21013 Gallarate, Italy
PMID# 10525973; UI# 99456937
We evaluated the risk of developing Clinically Definite Multiple Sclerosis (CD/MS) after an acute attack of isolated Optic Neuritis (ON) in 112 patients, in relation to demographic and paraclinical findings.
Patients were examined by Brain MRI, CSF analysis, and multiple Evoked Potentials (EPs); 10 were lost to follow-up, and the other 102 were enrolled in a prospective study (follow-up duration 6. 3 +/- 2.2 years).
Of these, 37 (36.3%) developed CD/MS after a mean interval of 2.3 +/- 1.6 years.
The risk of developing CD/MS was:
- 13% after 2 years
- 30% after 4 years
- 37% after 6 years
- 42% after 8 and 10 years
Gender, age, and season of ON onset did not affect the risk. MS occurred in 37 of 71 patients (52.1%) with one MRI lesion or more; no patient with a normal MRI developed the disease.
MS developed more frequently in patients with Intrathecal IgG synthesis than in those without (43% vs. 28%), but the difference was not statistically significant.
Multiple EPs showed a slight predictive value only including SomatoSensory EPs of the lower limb.
Multiple Sclerosis was mild in most cases (EDSS 2.2 +/- 1.9). The EDSS was less than 4 in 32 cases (86%), between 4 and 6 in 2 (5%), higher than 6.5 in 3 (8%).
Correlation Between Morphological And Functional Retinal Impairment In Multiple Sclerosis
Parisi V, Manni G, Spadaro M, Colacino G, Restuccia R, Marchi S, Bucci MG, Pierelli F
Invest Ophthalmol Vis Sci 1999 Oct;40(11):2520-7
Universita di Roma Tor Vergata, Cattedra di Clinica Oculistica, Roma, Italy
PMID# 10509645; UI# 99437344
To assess whether a correlation exists between Optic Nerve Fiber Layer (NFL) thickness and the Retinal or Visual pathway function in Multiple Sclerosis (MS) patients previously affected by Optic Neuritis.
Fourteen patients with a diagnosis of definite MS were examined. All had been affected by Optic Neuritis (MSON) with complete recovery of Visual Acuity (14 Eyes included in study).
These were compared with 14 Eyes from 14 age-matched control subjects. NFL thickness was measured by Optical Coherence Tomography (OCT).
Three different measurements in each quadrant (Superior, Inferior, Nasal, and Temporal) were taken and averaged.
The data in all quadrants (12 values averaged) were identified as NFL Overall, whereas the data obtained in the Temporal quadrant only (3 values averaged) were identified as NFL Temporal.
Retinal and Visual pathway function was assessed by simultaneously recording Pattern ElectroRetinoGrams (PERGs) and Visual Evoked Potentials (VEPs) using high-contrast (80%) checkerboard stimuli subtending 15 minutes and 60 minutes of the Visual arc (min arc) and reversed at the rate of two reversals per second.
In MSON Eyes there was a significant (P < 0.01) reduction in NFL thickness in both NFL Overall and NFL Temporal evaluations compared with the values observed in control Eyes.
PERG, (15-min arc checks) and VEP (15-min arc and 60-min arc checks), showed a significant (P < 0.01) delay in latency and reduction in amplitude.
NFL Overall and NFL Temporal values were significantly correlated (P < 0.01) to the PERG P50 latency and P50 to N95 amplitude recorded with 15-min arc checks.
No correlations (P > 0.01) between NFL values and the other ElectroPhysiological data (PERG recorded with 60-min arc checks and VEP recorded with 15-min arc and 60-min arc checks) were found.
There is a correlation between PERG changes and NFL thickness in MS patients previously affected by Optic Neuritis, but there is no correlation between VEP changes and NFL thickness.
Asymptomatic Visual Loss In Multiple Sclerosis
Lycke J, Tollesson PO, Frisen L
J Neurol 2001 Dec;248(12):1079-86
Institute of Clinical NeuroScience, Department of Neurology, Goteborg University, Sahlgren's University Hospital, Sweden
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 Computerized 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.
Optic Neuritis: Correlation Of Pain And Magnetic Resonance Imaging
Fazzone HE, Lefton DR, Kupersmith MJ
Ophthalmology 2003 Aug;110(8):1646-9
The Institute for Neurology and NeuroSurgery at Beth Israel North Medical Center, New York, New York 10128, USA
To demonstrate whether the Magnetic Resonance Imaging (MRI) localization of the abnormal enhancement of the Optic Nerve can be related to the Pain or pattern of Visual Field Loss associated with acute Optic Neuritis.
Retrospective observational series and MRI review from a referral Neuro-Ophthalmology service.
Seventy-three women and 23 men with Acute Optic Neuritis who had high resolution Gadolinium-enhanced fat-suppressed MRI within twenty days of the onset of Visual Loss.
he presence of Eye or other Fifth Cranial Nerve (V(1)) Pain, and Pain with Eye movement IpsiLateral to the affected Optic Nerve or no Eye Pain was recorded.
The NeuroRadiologist reviewed the MRI, masked to the affected Eye, and recorded the length and segment (Orbital, Canalicular, IntraCranial, or combination of segments) of abnormal Optic Nerve enhancement.
The presenting Visual Field defects were characterized as Diffuse, Central, Arcuate, Nasal or Temporal.
Main Outcome Measures
The types of Pain and patterns of Field Loss were correlated with the segments of Optic Nerve enhancement in the affected eye.
Five patients had nerves that did not enhance and were excluded from the outcome analysis.
In the 91 patients with abnormal enhancement, 70 experienced Eye/V(1) Pain, 67 had Pain with Eye movement and 17 patients had no Pain.
Enhancement of the orbital Optic Nerve occurred in 66 patients, 93.9% who had Eye/V(1) Pain and 92.4% who had Pain with Eye movement.
In the 25 patients with enhancement of the Canalicular, IntraCranial or both segments, without Orbital involvement, 32% had Eye/V(1) Pain and 24% had pain with Eye movement.
No pain occurred in 3% with enhancement of the Orbital segment and in 60% with enhancement of the other Optic Nerve segments.
The length of enhancement moderately correlated with Eye/V(1) Pain (r = 0.49, P = 0.01) and Pain with Eye movement (r = 0.37, P = 0.01).
Patients with enhancement longer than 10 mm had pain five times (P = 0.004) more frequent than did those with enhancement < or=10 mm.
There was no significant specific pattern of field loss associated with a particular location of enhancement, except Temporal field loss occurred in 25% of IntraCranial lesions (P = 0.04).
When Optic Neuritis involved the Orbital segment of the Optic Nerve, eye or other V(1) distribution Pain (94.3% vs. 32%) and Pain with Eye movement (91.4% vs. 24%) were significantly more frequent.
In contrast, pain was absent 20 times more often when the Orbital segment was not involved (60% vs. 3%).
Except for temporal field loss in eyes with IntraCranial nerve lesions, no pattern of Visual Field Loss appeared to correlate with the location or length of abnormal Optic Nerve enhancement.