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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.

What is the analgesic effect of EEG neurofeedback for people with chronic pain? A systematic review

Researchers: A/Prof Sylvia Gustin, Dr Negin Hesam-Shariati, Dr Wei-Ju Chang, A/Prof James McAuley, Dr Andrew Booth, A/Prof Toby Newton-John, Prof Chin-Teng Lin, A/Prof Zina Trost Chronic pain is a global health problem, affecting around one in five individuals in the general population. The understanding of the key role of functional brain alterations in the generation of chronic pain has led researchers to focus on pain treatments that target brain activity. Electroencephalographic (EEG) neurofeedback attempts to modulate the power of maladaptive EEG frequency powers to decrease chronic pain. Although several studies provide promising evidence, the effect of EEG neurofeedback on chronic pain is uncertain. This systematic review aims to synthesise the evidence from randomised controlled trials (RCTs) to evaluate the analgesic effect of EEG neurofeedback. The search strategy will be performed on five electronic databases (Cochrane Central, MEDLINE, Embase, PsycInfo, and CINAHL) for published studies and on clinical trial registries for completed unpublished studies. We will include studies that used EEG neurofeedback as an intervention for people with chronic pain. Risk of bias tools will be used to assess methodological quality of the included studies. RCTs will be included if they have compared EEG neurofeedback with any other intervention or placebo control. The data from RCTs will be aggregated to perform a meta-analysis for quantitative synthesis. In addition, non-randomised studies will be included for a narrative synthesis. The data from non-randomised studies will be extracted and summarised in a descriptive table. The primary outcome measure is pain intensity assessed by self-report scales. Secondary outcome measures include depressive symptoms, anxiety symptoms, and sleep quality measured by self-reported questionnaires. Further, we will investigate the non-randomised studies for additional outcomes addressing safety, feasibility, and resting-state EEG analysis.
PROJECT