This is the first direct evidence that DBS may eventually be able to treat cognitive impairment in Parkinson’s disease in addition to the movement related symptoms that it is presently used for. Their findings are published in the Journal of Neuroscience.
It is thought that around 1 in 500 people are affected by Parkinson’s disease, which means there are an estimated 127,000 people in the UK with the condition. According to the NHS, most people develop Parkinson's when they are over 50, although around 1 in 20 people with the condition first experience symptoms when they are under 40. Men are more likely to get Parkinson’s disease than women. The disease has many symptoms, which are classified as either ‘motor’ or ‘non-motor’. Typical motor symptoms are tremor, stiffness, and slowness of movement, while non-motor symptoms include disturbances of various parts of the autonomic nervous system, difficulties with speech, and cognitive impairment.
'Electrical stimulation of specific areas in the brain can effectively treat the motor symptoms of Parkinson’s, but exactly how this deep brain stimulation works is not fully understood,' said Dr James FitzGerald, a consultant neurosurgeon at NDS who co-authored the study with Dr Chrystalina Antoniades of NDCN, an expert in eye movements. 'Importantly, DBS is generally thought not to be effective for non-motor symptoms which patients often find very troubling.'
The researchers tested eye movements in Parkinson’s disease patients with DBS systems implanted in one of two locations in the brain: either the globus pallidus interna (GPi), or the subthalamic nucleus (STN), both of which are equally effective in treating motor symptoms. Like bodily movements, eye movements are known to be slowed down in PD, and stimulation at either of these locations improves the speed of simple reflexive eye movements such as looking towards a light when it goes on. The key finding in the study was that DBS could also improve performance in more complex tests that required input from higher cognitive centres, but only when the GPi was stimulated, not the STN.
Dr FitzGerald said: 'Part of the cause of Parkinsonian symptoms may be impairments in the way information flows from one circuit within the brain to another, as a result of overactivity of certain nerve cells in an area called the striatum. Our results suggest that one way that GPi DBS might be working is by calming down these overactive cells, thereby improving information flow between circuits. This appears to have benefits that go beyond simply controlling motor symptoms.'