Western Australian researchers have unravelled the mystery of why severely paralysed patients with certain types of muscle diseases still maintain normal eye movements - and the finding could aid the search for improved treatments, as well as help investigations into cardiovascular disease.

Professor Nigel Laing and his team at the Western Australian Institute for Medical Research (WAIMR) have discovered the reason why patients suffering from muscle diseases caused by mutations in the skeletal muscle actin gene (responsible for muscle contraction) are able to maintain normal eye movements, despite being severely paralysed.

Professor Laing said the specific line of research was sparked when one of the team's researchers - Dr Kristen Nowak - attended a patient convention and noticed that even patients who were otherwise severely paralysed, retained normal eye movement.

"We looked into this phenomenon and found that it had already been documented that eye muscles were not affected in patients with actin-based muscle diseases but, as there was no explanation as to why this occurred, we decided to conduct our own investigations," he said.

"We found that eye muscles have a similar actin composition to that of the heart - which have high levels of cardiac actin and some skeletal muscle actin - different from skeletal muscles which are mainly composed of skeletal muscle actin," he said.