Multiple system atrophy

HEALTH INFORMATION

Understanding why and how MSA occurs

WHAT WE KNOW

Multiple system atrophy (MSA) is a progressive degenerative neurological disorder that affects adult men and women, usually in their 50s or 60s. It is caused by degeneration or atrophy of nerve cells in specific areas of the brain. It is still unclear as to why cells become damaged in people with MSA and further research needs to be conducted into why and how this happens.

The shrinking of the cells can cause problems with movement, balance and autonomic functions of the body such as bladder and blood pressure control.

Symptoms may include fainting spells and problems with heart rate, erectile dysfunction, and bladder control. Motor impairments (ie, loss of or limited muscle control or movement, or limited mobility) may include tremor, rigidity, and/or loss of muscle coordination as well as difficulties with speech and gait (the way a person walks).

The clinical features of MSA overlap with those of Parkinson’s disease, and for this reason, early cases of MSA are often misdiagnosed as Parkinson’s disease. We now know that the feature that definitively identifies MSA pathology is the buildup of a protein called alpha-synuclein in oligodendrocytes, the support cells of the brain.

These cells are responsible for producing myelin, which is the specialised membrane that encases the nerve fibres in the brain. The alpha-synuclein protein buildups in the brain of people with MSA mean that the oligodendrocytes cannot properly make myelin, and without myelin the neurons will degenerate and eventually die.

The cause of MSA is unknown, no specific risk factors have been identified, and there is no cure or effective treatment. Treatment for MSA includes medications and lifestyle changes to help manage symptoms. The condition progresses gradually and eventually leads to death.

What else is happening in Multiple system atrophy research at NeuRA?

FEEL THE BUZZ IN THE AIR? US TOO.

Brain and Knee Muscle Weakness Study

Why Does Quadriceps Weakness Persist after Total Knee Replacement? An Exploration of Neurophysiological Mechanisms Total knee replacement is a commonly performed surgery for treating end-staged knee osteoarthritis. Although most people recover well after surgery, weakness of the quadriceps muscles (the front thigh muscles) persists long after the surgery (at least for 12 months), despite intensive physiotherapy and exercise. Quadriceps muscle weakness is known to be associated with more severe pain and greatly affect daily activities. This study aims to investigate the mechanisms underlying weakness of the quadriceps muscles in people with knee osteoarthritis and total knee replacement. We hope to better understand the relationship between the changes of the brain and a loss of quadriceps muscle strength after total knee replacement. The study might be a good fit for you if you: Scheduled to undergo a total knee replacement; The surgery is scheduled within the next 4 weeks; Do not have a previous knee joint replacement in the same knee; Do not have high tibial osteotomy; Do not have neurological disorders, epilepsy, psychiatric conditions, other chronic pain conditions; Do not have metal implants in the skull; Do not have a loss of sensation in the limbs. If you decide to take part you would: Be contacted by the researcher to determine your eligibility for the study Be scheduled for testing if you are eligible and willing to take part in the study Sign the Consent Form when you attend the first testing session Attend 3 testing sessions (approximately 2 hours per session): 1) before total knee replacement, 2) 3 months and 3) 6 months after total knee replacement. The testing will include several non-invasive measures of brain representations of the quadriceps muscles, central pain mechanisms, and motor function and questionnaires. Will I be paid to take part in the research study? You will be reimbursed ($50.00 per session) for travel and parking expenses associated with the research study visits. If you would like more information or are interested in being part of the study, please contact: Name: Dr Wei-Ju Chang Email: w.chang@neura.edu.au Phone: 02 9399 1260 This research is being funded by the Physiotherapy Research Foundation.  
PROJECT