06:04

By Dr David Cunnington In Health Professionals, Restless legs syndrome, Videos

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
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 05:00 – 06:04 Summary

Related posts and links:

What is restless legs syndrome?
Treatment for restless legs syndrome
Brochure on augmentation from Willis-Ekbom (RLS) Foundation

Transcript:
Augmentation in restless leg syndrome can be di!cult 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 "rst 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
"nding 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
e#ect and aren’t as e#ective 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.
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 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 o#

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 o# the drug at some point.

But if they’re really di!cult to control and they’re actually not doing too
badly, temporarily increasing the dose at least buys more time before they
have to switch o# 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 o# 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 di#erent 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
o# 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 e#ective 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 "nd 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 "nd 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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