Table 1. Clinical data.
| before OCT examination | in further follow-up | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| MS | age at | therapy | relapses* | ON | age at | therapy was changed to | |||
| No | subtype | sex | onset | right | left | OCT/ MRI-MRS | |||
| 1 | RRMS | f | 34.5 | MITOX, GLAT, IFN(b), IFN(a) | 7 | 0 | 0 | 40.5 | natalizumab |
| 2 | RRMS | f | 18.5 | IFN(a), IFN(b) | 4 | 0 | 0 | 23.5 | natalizumab |
| 3 | RRMS | f | 36.0 | MITOX 1 , IFN(a) | 7 | 0 | 0 | 42.0 | natalizumab |
| 4 | RRMS | f | 31.5 | none | 3 | 0 | 0 | 38.0 | none |
| 5 | RRMS | m | 40.0 | IFN(a) | 3 | 0 | 0 | 45.5 | none |
| 6 | RRMS | f | 28.5 | IFN(b) | 3 | 0 | 0 | 39.0 | natalizumab |
| 7 | RRMS | f | 43.0 | GLAT, IFN(b), none 2 | 4 | 0 | 0 | 48.0 | natalizumab |
| 8 | RRMS | f | 40.0 | none | 2 | 0 | 0 | 42.25 | none |
| 9 | RRMS | m | 24.0 | none | 2 | 0 | 0 | 25.0 | none |
| 10 | RRMS | f | 18.0 | GLAT, none 3 | 2 | 0 | 0 | 19.75 | none |
| 11 | RRMS | f | 29.75 | IFN(a) 4 , none | 4 | 0 | 0 | 36.0 | none |
| 12 | RRMS | m | 31.0 | IFN(b) | 2 | 0 | 0 | 33.25 | IFN(b) |
| 13 | RRMS | m | 51.0 | IFN(b) | 2 | 0 | 0 | 52.0 | IFN(b) |
| 14 | RRMS | m | 27.5 | GLAT | 4 | 0 | 0 | 39.0 | GLAT |
| 15 | RRMS | f | 30.0 | IFN(b) 5 , none | 4 | 0 | 0 | 46.0 | none |
| 16 | RRMS | m | 39.0 | IFN(c) | 4 | 0 | 0 | 45.0 | IFN(c) |
| 17 | RRMS | f | 16.0 | GLAT | 4 | 0 | 0 | 61.0 | GLAT |
| 18 | RRMS | f | 26.0 | IFN(a), IFN(b), MITOX 6 , none | 9 | 1 | 1 | 32.0 | none |
| 19 | RRMS | f | 17.75 | IFN(a), IFN(b) | 6 | 1 | 3 | 19.75 | natalizumab |
| 20 | RRMS | f | 31.0 | IFN(a), IFN(b) | 4 | 1 | 0 | 36.0 | IFN(b) |
| 21 | RRMS | f | 20.0 | IFN(b) | 8 | 1 | 1 | 47.5 | IFN(b) |
| 22 | RRMS | m | 22.5 | GLAT, IFN(a), IFN(b), natalizumab | 10 | 0 | 1 | 42.5 | natalizumab |
| 23 | RRMS | f | 20.0 | IFN(a) | 3 | 0 | 4 | 41.0 | IFN(a) |
| 24 | SPMS | m | 40.0 | GLAT, MITOX 7 , none | 3 | 0 | 0 | 46.5 | none |
| 25 | SPMS | f | 13.0 | IFN(b), MITOX 8 , none | 5 | 0 | 0 | 27.0 | none |
| 26 | SPMS | m | 25.0 | IFN(c), GLAT, IFN(a), IFN(b) | 10 | 1 | 1 | 47.5 | IFN(b) |
| 27 | SPMS | m | 22.0 | IFN(b) | 5 | 1 | 0 | 30.5 | none |
| 28 | SPMS | f | 16.0 | IFN(a), MITOX 9 , none | 6 | 0 | 2 | 44.25 | none |
ON, optic neuritis;
*, relapses treated with high dose steroid pulse therapy; no included patient had an ON within 12 months prior to the beginning of the study;
GLAT, glatiramer-acetate 20mg subcutaneous once daily; MITOX, mitoxantrone; IFN(a), interferon beta 1a intramuscularly once per week; IFN(b), interferon beta 1a (44μg) subcutaneous trice per week; IFN(c), interferon beta 1b (250μg) subcutaneous alternate day. Most importantly, the disease activity remained high in further follow-up with a median observation period of 22 ± 0.5 months [33]. However, no significant reduction of either the RNFL or the TMV could be found in follow-up [33; 36].
1, discontinued (48mg mitoxantrone per m2 body surface); none, neither specific immunomodulatory or immunsuppressive therapy, drug holiday;
2, drug withdrawal 12 months before OCT examination;
3, drug withdrawal 6 months before OCT examination;
4, drug withdrawal 20 months before OCT examination;
5, high titres of anti-interferon autoantibodies, drug withdrawal 14 months before OCT examination;
6, mitoxantrone cumulative dose 96mg per m2 body surface, drug withdrawal 10 months before OCT examination;
7, mitoxantrone cumulative dose 92mg per m2 body surface, drug withdrawal 10 months before OCT examination;
8, mitoxantrone cumulative dose 92mg per m2 body surface, drug withdrawal 26 months before OCT examination;
9, mitoxantrone cumulative dose 108mg per m2 body surface, drug withdrawal 27 months before 1st OCT examination.