Therapies include a host of treatments, some which are being translated into the real world. The field is evolving and still faces the challenge of the very high percentage of dropouts. These developments make for challenging clinical and organizational challenges.
It is often impractical for a patient with spastic paresis to use an orthosis or splint, due to a lack of understanding of the mechanism for which the spasticity is in part caused. There are four common treatments for paresis: manual training and spastic physiotherapy, anti-spastic surgery, muscle relaxation, anti-sphincteric drugs, or splints, braces, or orthotics. The common treatments often offer relief from some spastic paresis to some degree, but their use is not recommended if there is any serious pain and stiffness.
Paresis is frequently cured without specific surgical planning. The decision as to whether an operation should be performed must be based on the specific type of paraplegia and the history of the patient. In certain cases, the use of a baclofen pump can be an effective and convenient therapy.
Paresis is a neurological syndrome characterized by motor (movement), sensory (sense), and autonomic disturbances; these may be localised or extrapyramidal in nature. Paresis can be caused by a variety of underlying conditions. The differential diagnosis includes spinocerebellar ataxia type 2, hereditary motor and sensory neuropathies, Friedreich's ataxia, myasthenia gravis, and systemic lupus erythematosus (SLE), amongst others. \n\nThis article contains text from the http://www.purescience.com/text_1.
Persistent and unexplained muscle weakness can signify a diagnosis of myasthenia gravis. All patients with paresis should have their antibody titre investigated if no explanation for the weakness can be found.
Paralysis remains a serious problem in the United States. The occurrence of paresis from a nontraumatic etiology differs widely among countries and among races. Paralysis rates of patients who have received an acute hospital admission for a nonthrombolytic stroke are similar in the United Kingdom and the United States.
While the most common cause of paralysis is encephalopathy (particularly in ICUs), autoimmune processes can also cause paresis and are often undiagnosed. These autoimmune disorders can be treated with steroids.
More than 50% of patients receiving palliative treatment believe that medications treat the symptoms rather than the disease. Physicians and pharmaceutical companies need to educate patients about treatment for symptoms and to avoid the "treatment-for-symptom" phenomenon by providing appropriate patient lists for these treatments.
Results from a recent paper demonstrate that postoperative motor function at 5-year follow-up was similar to that following conservative treatment, but motor and neurological recovery is more limited in adults compared to children.
Patients and their caregivers reported an acceptable improvement in quality of life in PLS patients who were treated with baclofen infusion pump therapy. These improvements were associated with reductions in pain, improved movement control, and increased ability to perform leisure activities, as well as an improvement in caregiver's quality of life.
When patients with stroke-related muscle paresis were asked about outcomes they would consider, they frequently cite [pain, functional capacity, and quality of life as the most important outcomes for future clinical trials]. Physicians should take the patients' expectations into account when they trial new therapies for a variety of conditions. Physicians who do clinical trials for paresis should consider clinical trials for both aphasia and dysphagia. Clinical trials for paresis are currently underutilized.
Treatment with antidepressants, psychotropic medications, analgesics for neuropathic pain, hypnosis, and physical therapy has shown effectiveness for treating some symptoms of neuropathic pain. A placebo is less effective than no therapy in treating neuropathic pain because physical therapy, hypnosis, and psychotropic medications can effectively alleviate symptoms for a time, and have therefore been called temporary 'placebos'. None of the studies in this review were adequately powered to determine if treatment with a placebo, or placebo alone, was more effective at reducing symptom severity compared to no treatment. Further research is required to determine more specifically which intervention (placebo or no-treatment) has the strongest effect on patients' symptoms of neuropathic pain.