Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A growing amount of evidence suggests that a disturbance of immunological function is of importance in the pathogenesis of multiple sclerosis. This is reflected in the drugs used to slow progression and to treat relapses. Immunosuppressive drugs such as azathioprine, cyclophosphamide and cyclosporin might have some potential to slow down progression of multiple sclerosis, but their use is limited by potentially serious adverse effects. Recently, it was shown that interferon-beta-1b can diminish the exacerbation rate in multiple sclerosis without leading to unacceptable adverse effects. Nevertheless, symptomatic treatment remains of crucial importance in the management of multiple sclerosis patients. Spasticity, depression, fatigue and urinary, paroxysmal and sensory symptoms can all be alleviated to some extent with pharmacological interventions, although rehabilitation procedures and psychosocial consultations are no less important. Further therapeutic approaches to multiple sclerosis will be directed at either the specificity of the immune response or the grade of activation of the immune response. Magnetic resonance imaging techniques will play an important role in the evaluation of efficacy of new therapeutic agents.
 ...
PMID:Multiple sclerosis therapy. A practical guide. 772 28

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.
 ...
PMID:Medical rehabilitation of chronic progressive disseminated encephalomyelitis (MS). 1087 9

While pain is a common problem in patients with multiple sclerosis (MS), it is not frequently mentioned by patients and a more direct approach is required in order to obtain information about pain from patients. Many patients with MS experience more than one pain syndrome; combinations of dysaesthesia, headaches and/or back or muscle and joint pain are frequent. For each pain syndrome a clear diagnosis and therapeutic concept needs to be established. Pain in MS can be classified into four diagnostically and therapeutically relevant categories: (i) neuropathic pain due to MS (pain directly related to MS); (ii) pain indirectly related to MS; (iii) MS treatment-related pain; and (iv) pain unrelated to MS. Painful paroxysmal symptoms such as trigeminal neuralgia (TN), or painful tonic spasms are treated with antiepileptics as first choice, e.g. carbamazepine, oxcarbazepine, lamotrigine, gabapentin, pregabalin, etc. Painful 'burning' dysaesthesias, the most frequent chronic pain syndrome, are treated with TCAs such as amitriptyline, or antiepileptics such as gabapentin, pregabalin, lamotrigine, etc. Combinations of drugs with different modes of action can be particularly useful for reducing adverse effects. While escalation therapy may require opioids, there are encouraging results from studies regarding cannabinoids, but their future role in the treatment of MS-related pain has still to be determined. Pain related to spasticity often improves with adequate physiotherapy. Drug treatment includes antispastic agents such as baclofen or tizanidine and in patients with phasic spasticity, gabapentin or levetiracetam are administered. In patients with severe spasticity, botulinum toxin injections or intrathecal baclofen merit consideration. While physiotherapy may ameliorate malposition-induced joint and muscle pain, additional drug treatment with paracetamol (acetaminophen) or NSAIDs may be useful. Moreover, painful pressure lesions should be avoided by using optimally adjusted aids. Treatment-related pain associated with MS can occur with subcutaneous injections of interferon-beta or glatiramer acetate, and may be reduced by optimizing the injection technique and by local cooling. Systemic (particularly 'flu-like') adverse effects of interferons, e.g. myalgias, can be reduced by administering paracetamol, ibuprofen or naproxen. A potential increase in the frequency of pre-existing headaches after starting treatment with interferons may require optimization of headache attack therapy or even prophylactic treatment. Pain unrelated to MS, such as back pain or headache, is common in patients with MS and may deteriorate as a result of the disease. In summary, a careful analysis of each pain syndrome will allow the design of the appropriate treatment plan using various medical and nonmedical options (multimodal therapy), and will thus help to improve the quality of life (QOL) of the patients.
 ...
PMID:Current management of pain associated with multiple sclerosis. 1833 59

Disease-modifying treatments (DMTs), which are the foundation of multiple sclerosis (MS) care, reduce clinical exacerbations (relapses) and slow disease progression; however, improving quality of life (QOL) is an unmet need for many individuals with MS. DMTs, including interferon-beta, glatiramer acetate, natalizumab, mitoxantrone, and fingolimod, reduce the rate and severity of relapses, the accumulation of brain and spinal cord lesions as shown on magnetic resonance imaging (MRI), and disability progression. Many studies link diminished QOL with specific MS symptoms (fatigue, impaired mobility, spasticity, etc). Even in patients already receiving DMTs, symptoms and QOL may improve with additional agents that treat specific symptoms, thereby improving patient function and ability to perform activities of daily living (ADLs). Patients have reported that mobility impairment is one of the worst aspects of MS. Almost half of patients treated with DMTs reported no improvement in mobility. However, blocking the voltage-dependent potassium channels on the surface of demyelinated nerve fibers may improve signal conduction. Dalfampridine, a potassium channel blocker, received Food and Drug Administration (FDA) approval for all forms of MS specifically to improve walking, which was demonstrated by increased walking speed. By improving walking in some patients with MS, the effects of dalfampridine may complement those of DMTs and address the stated priorities of many patients.
 ...
PMID:Functional improvement and symptom management in multiple sclerosis: clinical efficacy of current therapies. 2176 53

Neuromyelitis optica (NMO) or Devic's disease is an inflammatory neurologic disease characterized by severe optic neuritis and transverse myelitis. Other features of NMO include female preponderance, higher onset age, severe functional disability, longitudinally extensive spinal cord lesions (longer than 3 vertebral segments), and oligoclonal IgG bands negativity. Brain lesions are not uncommon in NMO. The relation between NMO and multiple sclerosis (MS) has long been a matter of controversy, but since the discovery of anti-aquaporin 4 (AQP4) antibody (NMO-IgG), an NMO-specific autoantibody, the clinical, MRI, and laboratory features that distinguish NMO from MS have been clarified. Anti-AQP4 antibody binds to the extracellular domain of AQP4, which is highly expressed in endfeet of astrocytes. Recent neuropathological studies, analysis of CSF-GFAP levels during relapse and experimental studies strongly suggest that NMO is an anti-AQP4 antibody-mediated astrocytopathic disease and that T cell-mediated CNS inflammation is necessary to develop NMO. Also, IL-6 is remarkably elevated in the CSF and appears to regulate plasmablasts to produce anti-AQP4 antibody. Therefore, from the therapeutic point of view, depletion of anti-AQP4 antibody, suppression of T cell response to trigger relapse and anti-IL-6 therapy seem to be pivotal. High-dose intravenous methylprednisolone is the first-line therapy for acute exacerbations of NMO. But plasma exchange should be started soon if corticosteroid is not efficacious. If untreated, AQP4 antibody-positive patients are highly likely to experience relapses within a year. Thus, immunosuppressive therapy (corticosteroids, immunosuppressants, rituximab) should be initiated without delay. Preliminary results suggest that eculizumab, an anti-C5 monoclonal antibody, can also prevent relapse in NMO, Meanwhile, interferon-beta, a first-line disease modifying drug of MS, is not effective in NMO. Symptomatic therapy for pain, paresthesia, spasticity, dysuria and constipation which commonly occur in the chronic stage of NMO is also important to improve patients' quality of life.
 ...
PMID:[Treatment of neuromyelitis optica]. 2257 70

Neruomyelitis optica (NMO) is an inflammatory disease of the central nervous system characterized by severe optic neuritis and transverse myelitis, usually with a relapsing course. It is crucial that treatment is started as early as possible to avoid new relapses and further disability. Treatment of NMO spectrum disorders is divided into two objectives: one is to control the inflammatory damage in acute attacks and the other one is a maintenance treatment to avoid relapses. The former is based on high-dose intravenous corticosteroids and plasmapheresis, the latter is based on low-dose corticosteroids and immunosuppressants. High-dose intravenous methylprednisolone is the first-line therapy for acute exacerbations of NMO spectrum disorders. Plasmapheresis should be started soon if corticosteroid is not efficacious. Maintenance therapy is based on low-dose oral corticosteroids and non-specific immunosuppressant drugs, like azathioprine, tacrolimus, mycophenolate mofetil and mitoxantrone. New therapy strategies using monoclonal antibodies like rituximab; an anti-CD20 monoclonal antibody, and eculizumab; an anti-C5 monoclonal antibody, can also prevent relapse in NMO. On the other hand, interferon-beta, natalizumab and fingolimod, a first-line disease modifying drug of multiple sclerosis, is not effective in NMO spectrum disorders. Treatment of the symptom for spasticity, pain, dysuria may significantly improve the quality of life of the NMO patient.
 ...
PMID:[Treatment of neuromyelitis optica]. 2377 90