1,721,103 research outputs found
Therapy with Interferon beta-1b of a Patient with Childhood Multiple Sclerosis
No full textWe describe the case of a girl with paediatric multiple sclerosis (MS). The first attack occurred at the age of 5, the second attack occurred 4 years later. The number of attacks increased during puberty. Therapy with interferon beta-1b was initiated at the age of 13. Side effects are mild and the female patient has been relapse-free since the start of therapy
Paediatric Patient with Multiple Sclerosis and High Disease Activity
No full textWe describe a boy with first symptoms of childhood multiple sclerosis (MS) at the age of 11 years. The diagnosis MS was established after the second attack and a disease-modifying therapy was started with glatiramer acetate (Copaxone (R)). Due to high frequency of relapses and a progressing lesion load in cerebral MRI a conversion to interferon beta-1b (Betaferon (R)) was initiated and well tolerated. After a short stable period of disease further progression of MS has now occurred
Pediatric multiple sclerosis (encephalomyelitis disseminata)
No full textMultiple sclerosis (MS) is a chronic inflammatory demyelinating disorder of the central nervous system of unknown etiology normally affecting young adults. Approximately 3-5% of MS patients have onset before the age of 16 (pediatric MS). Neurological deficiencies can occur in multifocal localisations. McDonald's criteria include the dissemination in space and time of the disease activity. Symptoms include, for example, visual dysfunction and sensory or motor impairments. The most frequent clinical manifestation in the pediatric group is a relapsing-remitting disease course, with a milder course of disease and a lower rate of progression when compared to adult MS. Typical diagnostic findings are periventricular lesions of the white matter, oligoclonal bands in the cerebrospinal fluid and delayed evoked potentials. Relapses are treated with high-dose methylprednisolone. Prophylactic, immunomodulative therapies as suggested for adult MS patients are also used for children
MOLECULAR CHARACTERIZATION OF FOLATE RECEPTOR 1 MUTATIONS REVEAL PHENOTYPIC VARIATIONS OF CEREBRAL FOLATE TRANSPORT DEFICIENCY
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MOLECULAR CHARACTERIZATION OF FOLATE RECEPTOR 1 MUTATIONS REVEAL PHENOTYPIC VARIATIONS OF CEREBRAL FOLATE TRANSPORT DEFICIENCY
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Disease severity in multiple suleatase deficiency is determined by stability and residual activity of mutant formyl-glycine-generating enzyme
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