What Harm Does Pathological Synchronization in Parkinson's Disease Do?
Peter Brown, Institute of Neurology, London
Description: Like tuning in a station on the FM band of a radio, neuroscientists can detect the particular frequencies of our brains in action. And just as on the radio, a little noise and static is to be expected. In Parkinson's Disease (PD), as Peter Brown and colleagues are finding, too much of a certain type of frequency is a bad thing. Neurons in the basal ganglia produce a kind of overly synchronized beta frequency (in the 20 Hz range) that seems deeply implicated in some of the telltale symptoms of Parkinson's.
Brown's talk outlines efforts to record this "oscillatory synchrony" in PD, to figure out the physiological mechanisms behind it, and to connect beta synchrony directly to such key symptoms in PD patients as rigidity and bradykinesia (slowness in executing movements). Scientists can detect clusters of neurons in the subthalamic nucleus (a key component of the basal ganglia) "beating" at 20 Hz. Brown says the "exaggerated synchrony" of these neurons seems to have something to do with a chronic loss of the neurotransmitter dopamine. Ordinary subjects have a "fair amount of healthy beta activity," notes Brown, and when these subjects engage in voluntary movements, such as extending a forefinger, the beta activity is suppressed. But in PD patients, says Brown, uncontrolled beta activity seems to promote postural contraction "at the expense of voluntary movement."
Brown and others have recorded activity in the brains of PD patients undergoing two key treatments, Deep Brain Stimulation (where electrodes implanted in the brain try to break the pattern of normal neuronal firing) , and dopaminergic therapy. Both methods relieve the symptoms of slow movement and rigidity. Excessive beta oscillations are suppressed during these two treatments. This is "correlative evidence," says Brown, that beta activity is behind the symptoms. Scientists are trying to connect the dots, and find a causal link: After stimulating the neurons of the subthalamic nucleus to beat at 20 Hz, they observe a 20% slowing of movement. Brown is conducting additional studies that provide evidence in PD of a looping brain pathway involving not just the basal ganglia, but parts of the cortex, which has an "innate tendency for activity at 20 Hz," causing bradykinesia and rigidity, and which can be damped by the input of dopamine. In closing, Brown acknowledges he must bring "the beta story down to reality," since it doesn't seem to connect to other PD symptoms such as tremor, and "I've been a beta chauvinist here, and ignored other frequencies."
About the Speaker(s): Peter Brown obtained his medical degree from Cambridge University in 1984 and then joined the Medical Research Council Human Movement and Balance Unit before moving to the Institute of Neurology, London. He works as a neurologist at the affiliated National Hospital for Neurology and Neurosurgery, and within the Sobell Department of Movement Disorders and Motor Neurophysiology at the Institute of Neurology, where he leads the Clinical Motor Neurophysiology Group. The principal objective of this group's research program is to define how activity in large populations of neurons is coordinated in healthy movement and how such coordination may go awry in diseases, particularly those of the basal ganglia such as Parkinson's disease.
Host(s): School of Science, McGovern Institute for Brain Research at MIT
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