Their hypothesis was that in ALS the primary motor cortex can’t communicate with the rest of the brain properly and that this is likely due to underlying problems with either the structure or neurochemistry of the upper motor neurons. They also used two other tests to measure neurochemicals in the primary motor cortex and monitor the deterioration of white matter in the same area. Having established a loss of motor function among the ALS patients, the researchers then used functional MRI scans to measure how well the primary motor cortex was communicating with the rest of the brain. Of the 52 patients, 48 also showed overly responsive tendon reflexes, 21 showed spasticity, a condition in which there is an an abnormal increase in muscle tone or stiffness of muscle, and 15 exhibited the Babinski sign, a foot reflex in which the big toe flexes up instead of down when the foot is stroked or scratched - a normal reflex in children up to two years old but not in older people. Foot tapping frequency was recorded for each patient and was significantly reduced in ALS patients. Together the five sites recruited 52 patients with ALS and 52 healthy controls. “Having five different centres can capture a wider population with a more varied disease pattern.” “One of the things that impedes research in single-centre studies is that we only have a very small sample,” says Dey. The researchers analyzed data collected from five Canadian university hospitals, all part of CALSNIC: the U of A, University of Calgary, McGill University, University of Toronto and University of British Columbia. He’s also director of the Comprehensive Analysis Platform to Understand, Remedy, and Eliminate ALS ( CAPTURE ALS) and the Canadian ALS Neuroimaging Consortium (CALSNIC), which played an important role in the new study. Toupin Chair in Neurological Sciences and a member of the Neuroscience and Mental Health Institute. Kalra is a neurologist and professor in the Division of Neurology, the Henri M. “And if it does, by how much? Because right now riluzole has been shown to increase survival of patients by three to six months on average, but we don’t know exactly how it does that,” she notes. “We’d like to know in future studies if improving neurochemistry with medication will improve functional connectivity,” he says.Īvyarthana Dey, a PhD student in the Faculty of Medicine & Dentistry and the Neuroscience and Mental Health Institute and lead author of the study, says she also wants to know whether the increased NAA levels seen with riluzole will correlate with improved survival. ![]() Now Kalra wonders whether the reverse is true. NAA is the same neurochemical that Sanjay Kalra and his team have identified as an ALS marker. Studies have shown that the drug riluzole can improve patients’ life expectancy, and also that levels of N-acetylaspartate (NAA), a neurochemical associated with healthy neurons, increase with use of the drug. ![]() Eventually the brain loses the ability to communicate with muscles essential to our survival. As motor neurons fail, the primary motor cortex loses the ability to communicate with muscles - and as it turns out, the rest of the brain - resulting in muscle stiffness and weakness. Knowing this, they’re now aiming to find out whether the marker might also offer a test to evaluate new treatments to improve brain function.Īmyotrophic lateral sclerosis, or Lou Gehrig’s disease, is a terminal neurological disease. ![]() University of Alberta researchers have identified a neurochemical marker related to the loss of motor function and communication breakdown between the primary motor cortex - the part of the brain that controls our muscles - and the rest of the brain in ALS patients.
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