Myelin Basic Protein (MBP) or a fragment thereof may enter CerebroSpinal Fluid (CSF) and other body fluids in an Etiologically nonspecific fashion to provide information about the status of Central Nervous System (CNS) Myelin damage.

MBP ImmunoChemically detected is referred to as MBP-like material (MBPLM). The clinical utility of the assay for MBPLM in CSF is to document the presence, continuation, or resolution of CNS Myelin injury.

The analysis of CSF for MBPLM is subject to many variables, among which are the AntiSera and the form of the assay utilized.

The dominant Epitope of CSF MBPLM is in the decapeptide of 80-89 from the intact MBP molecule of 170 residues. Normally, CSF has no detected MBPLM.

Following an acute relapse of MS, MBPLM rises quickly in the range of ng/ml and rapidly declines and disappears.

The presence of MBPLM in CSF in Chronic and Progressive phases of the disease is unusual, but it may sometimes be detected in low levels, depending on the assay used for detection.

The level of CSF MBPLM is related to both the mass of CNS Myelin damage and how recently it occurred.

The level of CSF MBPLM rarely is elevated in Optic Neuritis. The level of CSF MBPLM is unrelated to CSF protein level, level of IgG, presence of OligoClonal Bands or pleocytosis.

CSF MBPLM has the potential of serving as a marker of therapeutic effectiveness in MS and does have predictive value for response to GlucoCorticoids given for worsening of disease.

The detection of MBPLM in body fluids other than CSF would be of great value because of the resulting improved feasibility for objectively monitoring the natural history of MS and response to therapy.

Studies on Blood have yet to produce a valid assay of MBPLM. Urinary MBPLM, though different in its features from that in CSF, may provide a correlate, not with acute DeMyelination in MS as is the case for CSF, but with progression of disease.

Background
An important controversy on the development of Multiple Sclerosis (MS) after an isolated episode of Optic Neuritis (ON) exists.

Magnetic Resonance Imaging (MRI) is the method of election in order to detect DeMyelinated Lesions in MS.

The current study was designed to determine the prevalence of Brain abnormalities on MRI and to asses the further development of MS after an isolated Idiopathic ON in our population.

Patients And Methods
From 1991 to 1995, 60 patients with decrease of Visual Acuity were studied, 35 (28 women, half age 31 +/- 10 years) completed criteria of Idiopathic ON.

A Brain MRI was performed in all patients after the diagnosis of Idiopathic ON and they subsequently were followed in the outpatient clinic from our center for a mean time of 29 +/- 16 months.

24 out of the 35 patients were treated with CorticoSteroids in different ways.

Results
It has been found 43% of the patients with idiopathic ON to have Brain Lesions by MRI.

During the follow-up 14% of the patients developed a Clinically Definite MS; all of them had a pathological Brain MRI at the basal evaluation (p = 0.009).

None of the patients that were treated with high-dose of intravenously CorticoSteroids developed MS.

Conclusions
The prevalence of silent Cerebral Lesions in the MRI after an Idiopathic ON is elevated in our population although further development of MS is lower possibly due to the short follow-up carried out.

The presence of Lesions in the MRI confers a high risk for developing MS after an Idiopathic ON.

• Comment in: Med Clin (Barc) 1998 May 9;110(16):638

We have monitored the cell surface phenotypic changes occurring in T, B and NK Cells of Chronic/Progressive Multiple Sclerosis (MS) patients after total Lymphoid Irradiation (TLI) plus Low-Dose Prednisone (TLI-LDP) therapy in comparison to sham TLI-LDP.

TLI-LDP resulted in a marked reduction in the relative and absolute number of total CD3⁺ T-Cells: (CD4⁺ Helper T-Cells, CD4⁺ CD45RA⁺ naive T-Cells) and CD19⁺ B-Cells for at least 1 year after treatment.

No change occurred in the percent CD8⁺ T-Cells although the number of these cells declined after RadioTherapy.

The CD4⁺/CD8⁺ T-Cell ratio was also decreased.

The relative percent of CD16⁺ NK Cells increased steadily after TLI-LDP while the number of NK Cells transiently declined but returned to baseline values 1 year later.

An increase in the percent of CD2⁺ CD3⁺- cells and a decrease in their number after therapy was also observed.

In contrast, no significant changes in the number of T, B or NK Cells were seen in the MS patients receiving sham TLI-LDP.

These results provide further evidence that RadioTherapy causes a reduction of ImmunoCompetent T & B-Cells and that a population of possibly NK Cells and/or Immature T-Cells appears to be repopulating the circulation after TLI.

In addition, a correlation was observed between alterations in Lymphocyte populations and the presence or absence of contrast enhancing or new T₂ Lesions on Brain Magnetic Resonance Imaging (MRI) in the TLI-LDP treated MS patients.

Patients devoid of contrast enhancing or new T₂ Lesions had a decreased percentage of CD3⁺ and CD4⁺ T-Cells prior to therapy and at six months following TLI-LDP, compared to patients with such Lesions.

An association was also observed between stability in disease activity as determined on the Expanded Disability Status Scale and relative values of CD3⁺ T-Cells.

In a double-blind prospective randomized trial, we assessed the efficacy and safety of modified Total Lymphoid Irradiation (TLI).

Plus, Low Dose Prednisone (TLI-LDP) as compared to sham TLI plus identical Prednisone therapy (sham TLI-LDP) in 46 patients with Progressive forms of Multiple Sclerosis (MS).

No significant difference existed between groups at study entry in patient age, sex, duration of MS, or disability status.

However, following treatment, significantly fewer TLI patients showed a sustained one point decline in the Expanded Disability Status Scale, the primary study endpoint.

As compared to the sham TLI group using the Kaplan-Meier Product-limit survival analysis, (P<0.005).

Risk for relapse requiring treatment with intravenous MethylPrednisolone was reduced by 54% in the TLI-treated group (P<0.05).

Significantly fewer TLI-LDP patients had Gadolinium enhancing plus new T₂-weighted lesions (P=0.018) when compared to the sham group post-treatment.

There was also a substantial and significant decrease in Blood Lymphocytes in the TLI-LDP group when compared to either pretreatment values or to sham TLI-LDP through at least 12 months post-therapy.

Side-effects secondary to TLI were generally mild and well-tolerated.

These results further support the hypothesis that TLI and systemic ImmunoSuppression have a beneficial effect in Progressive forms of MS.