What can be done to manage augmentation?

Augmentation, or worsening of restless legs syndrome (RLS) symptoms with treatment with dopamine agonists, occurs commonly, in around 8% of people on dopamine agonists for RLS. There are steps that can be taken to minimise the risk of developing augmentation and manage it if and when it occurs. Dr David Cunnington (sleep physician) discusses an approach to diagnosing and managing augmentation.

Video timeline:

  • 00:00 – 00:53 What is augmentation?
  • 00:53 – 01:56 What are the clinical features of augmentation?
  • 01:56 – 03:22 Minimising the risk of augmentation
  • 03:22 – 05:00 Managing augmentation
  • 05:00 – 06:04 Summary

Related posts and links:

Transcript:

Augmentation in restless leg syndrome can be difficult to manage and actually occurs relatively commonly. So I hope to be able to explain to you an approach that can be used to both minimise the risk of augmentation and help manage symptoms when they occur.

So augmentation is when people who run long term treatment with dopaminergic agonists develop a worsening in their restless leg symptoms.

It was first described in 1996 and at that point was felt that about 75 percent of people on levodopa or other short term dopamine agonists would go on to develop augmentation.

In the year since when it has been more systematically studied, it appears that around eight percent of people on long term dopamine agonists develop augmentation.

The common symptoms that people describe, which actually characterise augmentation is not just a worsening or greater intensity of symptoms. It’s finding that symptoms occur earlier in the day, so that can be two to four hours earlier than they were previously coming on.

It takes shorter for symptoms to come on after sitting down or beginning to rest. Symptoms occur in other parts of the body, so spread up the legs, into the arms, into the trunk and drugs seem to have a shorter duration of effect and aren’t as effective for as long a period.

Based on that, the International Restless Leg Syndrome Study Groups developed some questions that can be used in a clinical sense to screen for augmentation, that go along the lines of the common symptoms that people describe.

So these are four clinical questions that can be used and again asking about, “Do the symptoms appear earlier? Are higher doses of the drug now needed? Has the intensity of symptoms worsened? Have symptoms spread to other parts of the body?”

So when we’re starting people on treatment for restless leg syndrome, that’s really the time to think about minimising the future risk of augmentation.

So it’s important to look at non-drug strategies in managing restless leg symptoms before using any prescription medication, so making sure iron stores are adequate, looking at strategies such as massage or pacing or movement as a way of managing people’s symptoms.

In the US, there’s an FDA-approved device that actually massages the calves and does produce symptomatic improvement in restless leg symptoms. But that’s not available in Australia.

If people do need a medication, then it’s thinking about not necessarily starting them on a dopamine agonist, but looking at other families of medications, such as the alpha-2-delta ligands, like gabapentin, pregabalin or enacarbil that’s available in other markets.

If people do need a dopamine agonist, because they don’t respond to for example alpha-2-delta ligands, I then try to minimise the dose and duration of exposure to dopamine agonists.

There’s some thought but not great evidence that using a long-acting dopamine agonist lowers the risk and the evidence for this or the thoughts around this is that levodopa seems to have the highest risk of augmentation and the longest acting of the dopamine agonists rotigotine seems to have the lowest risk of augmentation. That sort of leads this thinking in that regard.

If someone has already got augmentation and it has developed, then my approach is generally to ensure that people’s iron stores are adequate. Sometimes augmentation can develop in people who are actually stable on dopamine agonists but get low iron stores which exacerbates their restless leg symptoms.

If augmentation is relatively mild, I won’t necessarily switch people off dopamine agonists. I might even temporarily increase the dose, really get a sense that if they’re beginning to develop augmentation, I’m going to have to switch them off the drug at some point.

But if they’re really difficult to control and they’re actually not doing too badly, temporarily increasing the dose at least buys more time before they have to switch off the drug.

Another alternative is splitting the dose of the dopamine agonist, so that they’re a lower dose at two time points or getting them to take the dopamine agonist a little earlier.

If people don’t respond to that strategy or have got more severe symptoms, they do need to switch from the dopamine agonist to something else.

The aim is to really get people off dopamine agonists but it’s not always possible. So they will end up reducing the dose of dopamine agonists, if I can’t switch them completely to something else and will sometimes actually switch to a different dopamine agonist but really the only one I would switch to is rotigotine because of its longer duration of action and therefore reduce propensity or at least thought reduced propensity for developing augmentation.

This is also a group where I will consider a high potency opioid as a bridge so that people might be on an opioid for a couple of months while they’re off the dopamine agonist, letting things settle and eventually rotating back to going on to a dopamine agonist again.

So augmentation is the worst thing of symptoms that comes about as a consequence of long term treatment with dopamine agonists. So to minimise augmentation, it’s important to use the minimum effective dose and duration of treatment with dopamine agonists that we can possibly manage.

If augmentation does develop, eventually you are going to need to switch the patient to something else, such as one of the alpha-2-delta ligands along our acting dopamine agonist such as rotigotine or a high potency opioid or even I often find in severe patients a combination of two or even three of these agents.

Just because someone develops augmentation doesn’t mean they can’t ever go back onto dopamine agonists and often it’s a case of just giving them a break from the dopamine agonist for a period of time as they try for a couple of months. Then they find they can usually get back to the dopamine agonist and again be successfully treated with it for quite a long period.

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