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Irish Institute of Clinical Neuroscience 14th Annual Neurology Update Meeting

Young- and late-onset Parkinson’s disease (PD) have different mechanisms and behaviours, the recent IICN Annual Neurology Update Meeting heard.

Prof Tim Lynch, Consultant Neurologist, Mater Hospital, Dublin, gave a comprehensive presentation asking ‘Are young- and late-onset Parkinson’s disease different diseases?’ He acknowledged that while it was a difficult topic, especially as age is one of the biggest risk factors in PD, it was a clinically important question to ask. For a person with young-onset PD presenting with bradykinesia and tremor, the diagnosis, a process that can take up to 18 months to two years, can be very difficult to accept. However, once that is overcome, the patient’s bradykinesia and tremor can be managed, if possible. However, he added he is reluctant to use levodopa in young patients, using it either sparingly or with a low dose and he avoids going rapidly to the high dose.

For an older PD patient with a risk of falling and breaking a hip, levodopa would be prescribed from an early stage. In both young and old, physicians should expect rest tremors. Gait-freezing, Prof Lynch added, is also a complex problem.

“It is sometimes responsive to levodopa but is not necessarily dopamine responsive; it may not be a dopamine deficiency at all.”

Motor symptoms also vary and PD has diverse variable features and diverse pathology. Furthermore, non-motor symptoms vary and can include hallucinations, which can be visual, olfactory and auditory. This is more common in older-onset patients but can be observed in younger patients too.

Other symptoms can include:



Sleep disorders.

According to the Brain Research Trust, earlier disease onset (EDO) is defined as the patient being below the age of 55 years at disease onset. ‘Tremor dominant’ is defined as patients aged 55 or over at onset. The rest tremor is the sole initial symptom or has sustained dominance over bradykinesia and rigidity.

Non-tremor dominant patients are categorised as being aged 55 years or over at onset. They have predominantly bradykinetic motor features with no or mild rest tremor. Rapid disease progression sees death within 10 years of the first symptom, irrespective of age. There is no dementia but it progresses to advanced motor disability.

“The tremor-dominant patient does not have much other trouble and does better but there are some that dement rapidly and progress rapidly,” said Prof Lynch. He added that there is overlap between the four above categories.

In young-onset PD, a doctor will find family history of the disease in 20 per cent of cases and these patients will survive longer. However, dyskinesia and dystonia are more common in younger patients.

He described the conditions of young- and old-onset PD as linked, having different mechanisms and behaving differently.

When asked by a delegate from the floor, Prof Lynch said he believed that 100 per cent of PD patients aged under 50 years have a strongly genetic form of the disease. Regarding overcoming freezing, he said that aerobic exercise on a treadmill leads to temporary benefit.

However, it has recently been found that a physical, cognitive and emotional challenge could be more successful. Studied Irish patients have been given a maze-type problem to solve on the Nintendo Wii and experienced improvements eight weeks later.

“The brain needs novelty,” Prof Lynch said. “Being goal-directed was not enough.”

In an answer to another question, he said that if someone is not levodopa-responsive and has an abnormal DaTscan, an atypical form of PD might be present.

Regarding the difference between maladaptive networks and neural plasticity, Dr Conor Fearon, who designed the Wii task, was asked to field the question by Prof Lynch.

“There is definitely some imaging evidence to say that patients with a freezing gait develop either functional or structural changes that are probably maladaptive,” he said. “If they lose habitual control of movement and over time they probably develop plastic changes that compensate for those things, they connect with other locomotive areas of the brain; the cerebellum, the brain stem.”

He added that it is not clear whether it is maladaptive or the best compensation that they can do.

“As regards reversing those changes, I think it’s difficult to say that we’re causing any plastic change in late-stage disease. But if we treat those things early on, we can prevent those maladaptive changes.”

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