Medical rehabilitation of chronic progressive disseminated encephalomyelitis (MS).

Eight years after diagnosis, 40% of MS patients develop a chronically progressive form. Annually we treat approximately 200 patients with progressive MS. Treatment consists of medication, i.e. agents that help to prevent future impairment, or interferon-beta injections, and intervals of mitoxantrone infusions (Novantrone(R)), and in some cases cyclic cyclophosphamide (Endoxan(R)) or nucleoside analogue cladribin (Leustatin(R)). Without clear scientific evidence, we recommend unsaturated fatty acids (thistle or sunflower oil), sufficient protein, and freshly prepared fruits and vegetables as a sound basis for remyelination. Remyelination profits from general prophylaxis in the use of ascorbic acid to help prevent urinary infections via acidification, autogenic training to reduce fatigue, improve ventilation of deeper airways, and stimulate vagotonic regeneration, and prevention of unnecessary immune stimulation caused by insects and some food. We recommend the use of sun hats and disencourage blood donation (Allain 1998). Physiotherapy can improve strength, reduce spasticity, and train the patient to compensate for dysbalance and ataxia; supported by beta blockers and good antispastics, tremor and gait disturbances can be positively influenced. Music and motion, speech therapy, realistic training of daily activities, and prudent psychotherapy complete the range of measurements to reconstitute as much as possible of the patient's individual freedom. In the individual, we eventually provide prudent technical aids and careful prognostic estimations. Cooperating with local and regional patient networks, we reinforce long-term disease management and spread up-to-date medical research results, and finally gather valuable contextual information and clinical data on an increasingly frequent idiopathic disease of the human central nervous system.

Improving medical approaches to primary CNS malignancies--retinoid therapy and more.

Successfully inducing differentiation in ectodermal diseases, retinoids harbour considerable therapeutic potential in the treatment of neuroectodermal-neuroepithelial malignancies. The principal tissue retinoid, retinoic acid, can be potently upregulated in vivo by a relatively specific catabolic inhibitor, R75251 (liarozole). Both substances have been given orally over 2 years in addition to standard treatment, and have been well tolerated. Corresponding closely to plasma retinoid levels, cutaneous side effects facilitate individual dosing. We evaluate this adjuvant retinoid approach and additional efforts to improve therapy of primary CNS malignancies, including the topical administration of retinoids in gamma linolenic acid.