Professionals' Q&A: Management of the stages of Parkinson's
Dr Nin
Bajaj joined us in May 2011 to answer questions from healthcare
professionals on the stages of Parkinson's and implications for professionals
working with people with the condition.
Nin is clinical director of the National Parkinson
Foundation Centre of Excellence in Derby.
The answers below are Nin's professional opinion.
Question categories:
Diagnosis stage
Aurora, occupational therapist: Many of my patients
develop stiff and painful shoulders very early on in the condition.
What causes this and what should I do to help regain/maintain
function?
Nin: Frozen shoulder appears to be a common early feature in
Parkinson's and often results in Parkinson's patients being
referred first to orthopaedic surgeons. Often maximising the
dopaminergic control is the key to ameliorating this.
Maintenance stage
Tracey, Speech Therapist: My question is about saliva
management. Do you ever prescribe glycopyrronium [an antimuscarinic
agent] tablets to patients in earlier stages of Parkinson's (ie not
palliative) to manage excess saliva and is it more effective than
hyoscine patches? Any contraindications with Parkinson's meds?
Dosage?
Nin: If drooling is mild I often use low dose amitriptyline,
which has reasonable anticholinergic effects and is less inducing
of confusion in the elderly than say benzhexol.
For moderate to severe drooling, I always refer for salivary
gland Botox which generally works well. Hyoscine and atropine based
patches frequently cause confusion in elderly patients.
Complex stage
James, Parkinson's nurse: Patient bed bound
with Parkinson's and dementia, parkinsonism well controlled
but clasp knife type rigidity in upper limbs, contracted fingers
causing pressure sores to tips of fingers and maceration. Any drug
therapies likely to help? Benzodiazepine caused excessive sedation,
is baclofen contraindicated/unlikely to help, what about
dantrolene? Any advice very gratefully received.
Nin: This is a difficult issue. The finger contractions may be
secondary to a non-erosive arthropathy which can occur in
Parkinson's or alternatively secondary to dystonic contracture.
Either case might respond to Botox injections into the forearm
flexors as the treatment of choice.
Lesley, Nurse Manager: How can one differentiate between
symptoms of poorly controlled Parkinson's, anxiety attacks and/or
side effects of Parkinson's drugs all of which are expressed with
similar symptoms? How does one unravel the mystery in an elderly
Parkinson's sufferer with moderate dementia?
Nin: The best way to unravel complex patients is a trick the
late Professor Marsden taught me in the early 90s. He used to draw
out a time chart with the drugs and timings noted. He would then
shade in the symptoms either as 'on' or 'off' phenomena. The link
between symptoms and drug timings would then become very obvious
and the solution to these issues would also be logical, eg if
anxiety appeared on the time chart 30 minutes before each levodopa
dose was due, it could be classified as an 'off' symptom and the
solution would include any of the continuous dopaminergic
stimulation (CDS) approaches listed above.
Sarah, Parkinson's nurse: What is your opinion on the use of PEG
feeding in advanced/end stage Parkinson's? We sometimes support
people with Progressive Supranuclear Palsy (PSP) to have an
elective PEG. I tend to assess each Parkinson's case individually.
Ethical dilemma!
Nin: I have no problem with use of PEG in advanced Parkinson's.
If patients can't take oral intake safely, despite liquidisation,
then PEG is the best way forward as we expect them to have a
reasonable life span even when they reach that phase of
Parkinson's.
Zahid, Consultant: How do you manage advanced Parkinson's
in patients who are post op and are on parenteral nutrition with
nasogastric (NG) feeding as it interferes with dopamine
absorption?
Nin: In this scenario, you could consider replacing some or all
of their dopamine with a rotigotine patch. Being transdermal,
rotigotine gets round the GI absorption problems.
Rotigotine may not be suitable for older Parkinson's patients at
risk of dopamine agonist side effects, eg confusion,
hallucinations. In these folks, you will have to adjust the
dopamine to compensate for absorption issues, eg try and give it
when the parenteral feed is not running, adjust the protein content
of the parenteral feed to minimise amino acid competition with
dopamine, increase the dopamine dose or give more
frequently.
Length of stages
Luis, Parkinson's UK Helpline Adviser: On the helpline we are regularly asked 'how long
someone has' before Parkinson's becomes very problematic, how long
before they reach the 'advanced' stages of Parkinson's. Our answer
is generally that it is different from person to person, so very
hard to answer. What would your answer be?
Nin: It is very different from patient to patient and varies
with the kind of Parkinson's (benign tremulous versus akinetic
rigid where people fall a lot), the age of onset (younger onset can
be both worse, if idiopathic, or more benign if secondary to
certain genes, eg PINK1) and whether patients get dementia
early.
I generally say we give most patients a very good 5 years, a
more variable 5 to 10 years, and after 10 years it all depends on
whether they are unfortunate enough to develop dementia or not.
End of life
Alison, Parkinson's nurse: When is it appropriate to
open discussion on end of life planning?
Nin: In my view, patients with Parkinson's can be improved with
appropriate drug management until they have severe dementia. In
this scenario, it is hard to improve the motor state without
aggravating the confusion and hallucinations, although the latter
can be managed with acetylcholinesterase inhibitors such as
rivastigmine.
I would only consider discussion of palliation in
Parkinson's disease dementia where there were recurrent infections
and poor life quality despite the best medical management.
George, Professor of Health Research: I am interested in the fourth
stage and have a question about the role of hospice and specialist
palliative care in Parkinson's. Do you think this type of care is
appropriate or should specialists in Parkinson's hold the reigns
'until the end of life'?
Nin: I think there is a role for a specialist in Parkinson's to
manage patients until they develop moderate to severe dementia.
After this, when little can be done to improve the motor state
without worsening the mental state, the patient would best be
managed by a palliative care specialist with input from a
Parkinson's specialist as required.
Tim, Parkinson's UK Advisory Services Manager: We often
hear the phrase that people die 'with' Parkinson's not 'from' it.
How true do you think this is? Is there a better way that we can
respond to people's real fears about the development of the
condition?
Nin: I'm afraid that most studies show that Parkinson's takes
about 10 years off your life expectancy if you develop it before
the age of 65. Older Parkinson's patients fare much better, losing
only 2 to 3 years on their normal counterparts.
Drug therapy
Parkinson's UK: For information about any of the Parkinson's
drugs mentioned below, please take a look at our pages on drug treatments for Parkinson's.
Gina, Parkinson's nurse: If a patient has a history of Lewy body
dementia and is unable to swallow usual levodopa therapy, we
usually start them on rotigotine patch. What do you think the
initial dose should be and to what dose do you think it's safe to
titrate to considering potential side effects and risk of
exacerbating symptoms of Lewy body dementia?
Nin: Dopamine agonists are poorly tolerated in patients with
Lewy body dementia or Parkinson's disease dementia complex. Caution
therefore has to be exercised in using rotigotine in those nil by
mouth. You might get away with a very small dose starting at 2mg od
and if tolerated going to 4mg.
A safer bet would be madopar dispersible either orally or down
an NG tube if the dysphagia is acute.
Daiga, Parkinson's UK National Education Adviser: Is it best to
start patients on levodopa as a monotherapy?
Nin: This depends on the age and other medical illnesses. If a
Parkinson's patient is under 70 years old, you will probably get
away with a dopamine agonist as monotherapy. You might get away
with a dopamine agonist in older patients as long as they
don't have other medical illnesses, otherwise dopamine agonists
have more short-term side effects limiting tolerability such as
sleepiness and hypotension.
In patients above 70, I usually consider levodopa as first line
therapy. But even then, I try and introduce low dose dopamine
agonists, eg rotigotine up to to 8mg, as second line agents.
Sheena, Parkinson's nurse: Is it appropriate to adjust dopaminergic
medication when patients present with severely increased anxiety
prior to each dose but without significant motor function
disruption?
Nin: Anxiety can be related to changes in dopaminergic levels or
can be independent of this. Generally when it is related to
dopamine, it is in the context of a motor 'off' state. Increasing
dopamine levels in this context can reduce the anxiety.
Anxiety can also be secondary to reductions in brain monoamines
as part of the parkinsonian process per se as cell types other than
dopamine neurones also die. This may be treated with a tricyclic
such as nortriptyline. Anxiety secondary to the psychological
adjustment of having a Parkinson's diagnosis is best handled by
targeted cognitive behavioural therapy.
Liz, Parkinson's nurse: I've read that 24 hour continuous
apomorphine infusions lead to the dopamine receptors becoming
desensitised. Is there a danger that this could happen with
other 24 hour continuous dopamine receptor agonists such as
rotigotine and the long acting versions of ropinirole and
pramipexole?
Nin: This appears true for apomorphine, although not in all
patients, and some groups, especially Italians, are great believers
in 24 hour apomorphine. Personally I rarely believe apomorphine
beyond the waking hours is useful.
This does not appear to be an issue with the other long acting
agonists and may reflect differential binding to the dopamine
receptors and/or affinity for certain receptor subtypes
(apomorphine is predominately D1 whilst the other agonists are
mainly D2).
Mike, Parkinson's nurse: Are there any reliable ways of dealing
with biphasic dyskinesias?
Nin: Biphasic dyskinesia or dystonia is due to peak/trough drug
fluctuations and the key is to smooth out drug delivery with
continuous dopaminergic approaches. You are now spoilt for choice
with a range of long acting dopamine agonists.
Other approaches include fractionation of levodopa, use of
entacapone +/-, a monoamine oxidase B inhibitor, to incease
levodopa half-life.
Rachel, Parkinson's nurse: I see a few Parkinson's patients
with biphasic dystonia on levodopa (mainly abdomen, foot and neck
regions). I find this symptom very difficult to manage and wondered
if you had any suggestions of how to manage this.
Nin: Biphasic dystonia is often secondary to levodopa
fluctuation. A variety of continuous dopaminergic approaches may
help, including addition of long-acting dopaminergic agonists (eg
rotigotine, ropinirole XL or pramipexole MR), addition of
entacapone to each levodopa dose and also the use of
monoamine-oxidase B inhibitors, such as rasagiline or
selegiline.
Rosemary, Pharmacist: I have a patient who is taking co-careldopa 5
times daily, and now on ReQuip XL at top dose taken in the morning.
Also on Azilect (if I remember correctly). He finds that the
effects are wearing off by about midday. What else can I recommend
at this stage? He has tried staggering the dose by having one a bit
later on, which does help. Overall though the slow-release product
has really helped. He is an active gentleman and it's very
important to him to be able to carry on working.
Nin: You can add in entacapone to each of the levodopa doses and
if that suits switch the levodopa to Stalevo.
Medhat, Consultant: What's your view on whether starting treatment
at diagnosis/early is more beneficial? Do you treat your patients
early?
Nin: I am a great believer in treating patients both early and
optimally. Most patients presenting to their doctor with
parkinsonian motor features have had an extensive loss in
dopaminergic neurones. If you carry out an FP-CIT scan on such
patients, the deficit is often marked (type 2 abnormalities tend to
predominate).
This means it takes a lot of dopa/dopamine agonist treatment in
the initial stages to get them back to near normal dopamine levels.
I therefore use fairly high dose treatment early on in the disease
course and having done so often find that I do not have to do
anything more than tweak drugs in subsequent years.
I also think that normalising dopamine levels early allows
patients to maintain high levels of phsyical function and once they
lose this functionality it is very hard to salvage it. I must
stress that this is a personal view and no trial has directly
addressed this issue, although trials such
as ADAGIO show some supportive data in this direction.
Jayesh, Primary Care Pharmacist: Cost of medicines is high in the
NHS. With 3 Parkinson's products coming off patent in the near
future, what is your opinion of generic substitution of brand
medication in Parkinson's? Is the debate similar in generic versus
brand antiepileptic medication and if so is there evidence either
way?
Nin: The cost of Parkinson's meds will come down and with the
recent price reduction of ReQuip have already come down even before
the generics hit the market.
I have no problems with generic formulations but 2 rules need
obeying:
- I would resist changing a patient on established therapies onto
generic versions as there can be profound changes in
pharmacokinetics leading to substantial changes in effect.
- If the generic does not appear to be working, it should be
changed to a more conventional and proven
brand.
Impulse control disorder
Liz, Consultant Physician Geriatrics: Do you have a view
on use of naltrexone in Parkinson's?
Nin: I have no experience of using the opiate naltrexone for
Parkinson's although patients on blogs report improvements in
cognition, pain and general wellbeing. I note that the
Michael J. Fox Foundation has funded a clinical trial in the use of
naltrexone to counteract the symptoms of impulse control
disorders in Parkinson's patients on dopamine agonists.
Mel, Parkinson's nurse: Have you any recommendations for treatment
and management of symptoms such as apathy and loss of motivation
for social activities? I have a gentleman who spends long hours on
the computer, mainly on chat forums. Agonists in the past have led
to financial problems so he's only on a minimal amount of Madopar.
We are thinking about trying antidepressants as the patient is fed
up with his behaviour but can't seem to motivate himself to change.
His motor symptoms are reasonably stable and
controlled.
Nin: This behaviour is known as punding and is suggestive of
impulse control disorder (ICD). ICD has an incidence of up to 17%
in patients on dopamine agonists, although all current data is on
ropinerole and pramipexole.
Approaches include reducing or stopping dopamine agnoists
altogether and using levodopa instead (the incidence of ICD with
levodopa is substantially less, around 8% in some studies).
Sometimes we resort to using atypical antipsychotics, eg quetiapine
and clozapine although their effectiveness is purely anecdotal.
There is an ongoing trial of naltrexone in ICD and we await the
results with interest.
Research
Emily, neurology research nurse: Hi there, I am
interested to find out about the recent research that is being or
due to be carried out in Parkinson's.
Parkinson's UK: Hi Emily, please take a look at our list of
current Parkinson's research projects
around the UK which may be looking for participants. We update
this list regularly as we hear of new studies.
And our current research pages
give information about the research we fund.
Gail, Parkinson's UK education and training officer: As
part of a cure are we looking into finding a way to change the
structure of the dopamine receptors in the basal ganglia so that
they stop dying or even so that they reproduce themselves? Or is
this impossible?
Nin: Various teams have been exploring ways to stop dopaminergic
neurones from dying, eg using viral vectors to carry neurotrophic
growth factors into the basal ganglia part of the brain. Others
have looked at stem cell approaches to replace the dead
neurones.
There is an ongoing study using the patient's own bone marrow as
a source of stem cells to inject into the bloodstream and hope that
these migrate into the brain. None of these approaches has yet
worked but we live in hope.
Information for professionals
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