Clinical Pharmacist

December 2011

Vol 3

There is no definitive first-line treatment for managing the motor symptoms of Parkinsons disease.
Treatment choice should take into account factors such as patient age, adverse effects and comorbidities

Parkinsons disease
management
By David Kearney, DipPharmPrac, and
Louise Dunsmure, DipClinPharm, MRPharmS

anagement of Parkinsons disease (PD) should be

tailored to the needs of individual patients and
the aim of treatment is to relieve motor and nonmotor symptoms (see Box 1, p369, for the management of
non-motor symptoms). Available therapies provide
symptomatic relief only currently there is no way to
restore function, halt deterioration or cure PD.
Management is guided by recommendations from the
National Institute for Health and Clinical Excellence and
the Scottish Intercollegiate Guidelines Network.1, 9

SUMMARY
There is no cure for Parkinsons disease (PD). Management focuses on
relieving the motor and non-motor symptoms of the condition. Most
treatments for the motor symptoms (for example levodopa, dopamine
agonists and monoamine-oxidase-B inhibitors) work by increasing
dopamine in the central nervous system.
Generally, selective serotonin reuptake inhibitors are used to manage
depression for patients with PD. Psychosis is usually managed using
atypical antipsychotics. Rivastigmine is used first line for the treatment of
PD-related dementia.

choice of medicine is guided by predominant symptoms,

concomitant conditions, age and whether symptomatic
relief or avoidance of adverse effects is more important to
the patient (see Box 3, p372).

Motor symptoms
A firm diagnosis of PD is essential before starting
treatment (see accompanying article, p361).
Most medicines used to manage the motor symptoms of
PD enhance the activity of dopamine in the basal ganglia,
either through direct replacement, agonism of dopamine
receptors, or prevention of the breakdown or reuptake of
dopamine. However, there is no recognised, unequivocal
first-line treatment and initial choice should take into
account: a patients clinical symptoms; the relative
importance of symptom control versus motor
complications; a desire to avoid specific adverse effects;
and concomitant medical conditions.
Treatment decisions will also depend on the stage of a
patients disease: either early disease (those with functional
disability requiring symptomatic therapy) or later disease
(those who have developed motor symptoms following
treatment with levodopa). When to start treatment is
discussed in Box 2 (p370).

Early disease
Motor symptoms in early PD are managed with either
levodopa, a dopamine agonist or a monoamine-oxidase-B
(MAO-B) inhibitor. If a MAO-B inhibitor is used initially,
then levodopa would normally be added when further
symptom control is required (see Figure 1, p371). The

David Kearney is senior neurology pharmacist at

University Hospitals of Leicester NHS Trust and
Louise Dunsmure is advanced pharmacist for
neurosciences at Leeds Teaching Hospitals NHS
Trust.
E: david.kearney@uhl-tr.nhs.uk

Levodopa Levodopa has been the gold standard treatment

for PD since its introduction in the 1960s. It is still
considered the most efficacious medicine for PD, despite
the introduction of newer medicines.
After starting levodopa treatment, patients experience
rapid improvement in their symptoms and quality of life.
However, this period is followed by decreased efficacy and
levodopa-related motor disturbances, known as
dyskinesias. The time this takes to occur can vary from
months to years about half of all patients experience

AVAILABLE
THERAPIES
PROVIDE
SYMPTOMATIC
RELIEF ONLY
CURRENTLY
THERE IS NO WAY
TO RESTORE
FUNCTION, HALT
DETERIORATION OR
CURE PARKINSONS
DISEASE

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Clinical Pharmacist

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Patients with Parkinsons disease (PD) can develop non-motor

symptoms as the disease progresses. The non-motor features of PD
include depression, psychosis, dementia, sleep disturbances and
autonomic dysfunction.1

Depression Depression has been reported to affect 4050% of

patients with PD. However, this may be an underestimate because
diagnosing mild depression in patients with PD is complicated by
the fact that many of the clinical features of mild depression are
also motor features of PD.1
Managing depression in patients with PD requires a combination
of psychotherapy and pharmacotherapy where possible. Although
monoamine-oxidase-B (MAO-B) inhibitors and the dopamine
agonists pramipexole and ropinirole have some antidepressant
effects, PD-related depression is generally managed using selective
serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants
(TCAs). The choice of treatment is dependent on patient
characteristics and other medicines that the patient is using
(eg, SSRIs can be used for patients receiving rasagiline but TCAs
should be avoided).
The role of SSRIs for the management of patients with PD and
depression has been debated for many years. Before 2001 there
were some reports that these medicines worsened the motor
symptoms of PD and increased the incidence of extrapyramidal
side effects. However, DellAgnello and colleagues demonstrated
that SSRIs do not significantly worsen extrapyramidal symptoms.2
Mood swings, anxiety and feelings of dread are possible symptoms
of the off state of PD. On-off fluctuations should be monitored in
these patients and the control of motor symptoms reviewed.

Psychosis Around a third of patients with PD develop psychosis

secondary to PD and its management presents a challenge.3
Psychosis can be triggered by the introduction of new medicines
or by changes in the doses of existing anti-Parkinsonian medicines.
Therefore, PD therapy should be reviewed for all patients who
develop psychosis and the doses reduced where possible. Many
patients are unable to tolerate dose reductions and in such cases
the use of medicines to manage patients with moderate-to-severe
psychotic symptoms is appropriate. Mild psychotic symptoms in
people with PD may not need to be actively treated if they are
tolerated by the patient and carer.1
Treatment should be with atypical antipsychotic medicines.
Typical antipsychotic drugs (eg, phenothiazines and haloperidol)
must not be used because they exacerbate the motor features of
PD. Clozapine is the only atypical antipsychotic that is licensed in
the UK for the management of psychosis in PD. However, its use is
limited due to adverse effects and the monitoring that is required.
Quetiapine, olanzapine, risperidone or aripiprazole are often used
but are not licensed for this indication.
The place of quetiapine in the management of psychosis in PD
has been evaluated in both open-label studies and randomised
trials. Eight open-label studies, including 191 patients who
received quetiapine, demonstrated an improvement in symptoms of
psychosis for 152 patients (80%). Studies comparing quetiapine
with clozapine for this indication have had mixed results.4, 5 Despite
the conflicting evidence, quetiapine remains a first-line treatment
for the management of psychosis in patients with PD.
Dementia PD-related dementia (PDD) affects 2040% of patients
with PD6 and the incidence increases by 13.7% each year for
patients aged 7079 years.

Many patients with Parkinsons disease experience sleep disturbances

PDD is associated with a reduction in cholinergic functioning
within the brain and therefore management can include the use of
cholinesterase inhibitors. Rivastigmine is used first line oral
administration appears to improve cognition and activities of daily
living for patients with PDD. A clinically meaningful benefit occurs
in about 15% of cases. The oral preparation of rivastigmine is the
only cholinesterase inhibitor licensed for the management of PDD.
Rivastigmine patches are not licensed for this indication but can
be used when a patient develops nausea and vomiting as an
adverse effect with the oral preparation.
Donepezil and galantamine have demonstrated some limited
efficacy for the management of PDD.
The role for memantine in the management of PDD is currently
being explored following the positive results of a 24-week
randomised controlled trial in 75 patients with PDD or Lewy body
dementia. There was a significant difference in clinical global
impression of change score at week 24 for patients who received
memantine compared with placebo.7

Sleep disturbances Some 6090% of patients with PD

experience sleep disturbances. These can include daytime
sleepiness or an inability to sleep at night due to nocturia, tremor
or dyskinesias. Depression can also aggravate existing sleep
disturbances.
Treatment requires accurate identification of the cause and
interventions to address the underlying issue (eg, adjusting levodopa
dose to reduce dyskinesia). Modafinil may provide a therapeutic
option for patients with daytime sleepiness.1 Hogl and colleagues
conducted a double-blind, randomised, placebo-controlled
crossover study involving 15 patients and results suggested that
sleepiness (measured using the Epworth sleepiness scale) was
significantly improved with modafinil therapy.8 Although the
European Medicines Agency recommends that modafinil should be
used only for the treatment of sleepiness associated with
narcolepsy, it is prescribed off-label, under the supervision of sleep
specialists, for some patients with PD and daytime sleepiness.

Autonomic dysfunction Patients who develop autonomic

dysfunction, such as postural hypotension, urinary dysfunction or
constipation, should receive symptomatic support.

CLINICAL FOCUS

Box 1: Managing non-motor symptoms of Parkinsons disease

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dyskinesias after five years of levodopa treatment, and it is

suspected that this effect occurs more rapidly in younger
patients. Because of this effect, and the availability of other
proven first-line options, many clinicians reserve levodopa
for later in the course of the disease.
Levodopa is a precursor of dopamine and is
administered in combination with a peripheral dopadecarboxylase inhibitor (with carbidopa as co-careldopa,
or with benserazide as co-beneldopa) to limit peripheral
metabolism of levodopa to dopamine. Levodopa readily
crosses the blood brain barrier and is then converted to
dopamine. Reducing peripheral metabolism allows lower
doses to be administered and reduces adverse effects such
as nausea and postural hypotension.
Levodopa is started at low doses (eg, 50mg one to three
times a day) and titrated according to effect and
tolerability. Taking levodopa with food can limit
gastrointestinal effects but dietary protein can affect
absorption and therefore, in advanced disease, it may be
beneficial to take the medicine on an empty stomach.
Somnolence and psychiatric adverse effects, such as
hallucinations, psychosis and impulse control disorders,
are rare but warrant close observation.
Modified-release preparations of levodopa were
developed in an effort to provide more stable plasma
levels, thereby reducing motor complications. However,
variable absorption means that these advantages have not
been realised. Despite this, modified-release preparations
have been useful in simplifying drug regimens and
providing relief for patients with night-time symptoms.

OVER TIME A
PATIENTS
RESPONSE TO
INITIAL TREATMENTS
WILL DECLINE.
WHEN THIS
OCCURS, PATIENTS
EXPERIENCE
SWITCHING OFF

Dopamine agonists Dopamine agonists are commonly

used as initial therapy when levodopa therapy is delayed
(especially for younger patients) and as adjuvants to
levodopa in later PD. They act on post-synaptic dopamine
receptors and have been in use since the 1970s.
Ergot-derived dopamine agonists, such as pergolide and
cabergoline, are associated with cardiac valve and
pulmonary fibrotic effects and have been largely
superseded by the non-ergot-derived dopamine agonists
pramipexole, ropinirole and rotigotine. Dopamine agonists

Box 2: When to start treatment

Consensus about when to start
treatment is lacking. For many
years after the discovery of
levodopa it was usual practice to
start treatment at the time of
diagnosis due to the rapid
improvement in quality of life once
treatment had started.
There was also a belief that early
treatment could be neuroprotective
for functioning dopaminergic
neurons and may normalise the
function of neurons in the basal
ganglia (and therefore delay disease
progression).10 However, by the
1990s concerns over levodopainduced motor complications and

are less effective than levodopa at controlling motor

symptoms but are considerably less likely to cause
dyskinesia.
Modified-release and topical preparations of dopamine
agonists offer the convenience of once-daily dosing to
patients who are often on complex drug regimens.12
Adverse effects of dopamine agonists are similar to
those of levodopa, but impulse control disorder and
somnolence are more common. Impulse control disorders,
such as pathological gambling, binge eating and
hypersexuality, are thought to be more common in young
males and those with a previous history of mood disorders,
alcohol abuse and obsessive compulsive disorder. Patients
and their carers should be adequately counselled regarding
these effects and the causative medicine tapered and
discontinued if they occur.

MAO-B inhibitors Rasagiline and selegiline are MAO-B

inhibitors. They increase the amount of dopamine at
receptors in the striatum by preventing its metabolism.
They are used as initial therapy, especially if dopamine
agonists should be avoided, or as levodopa-sparing
medicines in later disease. Rasagiline is more commonly
used because selegiline is associated with hallucinations,
insomnia and confusion (caused by amphetamine-like
metabolites). Both medicines have the potential to interact
with many medicines due to their inhibition of monoamine
oxidase, which may not be fully selective for MAO-B.

Later-stage disease

the availability of other drugs led to

a change in strategy.
Current guidance recommends
starting therapy once motor
symptoms affect a patients ability
to function.1, 9
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Over time a patients response to initial treatments will

decline. When this occurs, patients experience switching
off , also referred to as wearing off or off time, as
plasma drug concentrations reach a trough (this manifests
as akinesia and rigidity). In addition, motor complications,
such as dyskinesia and dystonia, occur at peak serum
levels. Patients can fluctuate rapidly or erratically between
these two states this is known as the on-off
phenomenon.
Wearing off can be countered by increasing the dose of
a patients medicines or shortening the interval between
doses. However, increasing the dose can induce or worsen
motor complications, especially with levodopa. If
amendments to dosing regimens fail to correct the
problems, combinations of drugs will be necessary (see
Figure 1, p371).

Catechol-O-methyltransferase

inhibitors The
catechol-O-methyltransferase (COMT) inhibitors,
entacapone and tolcapone, increase the amount of
levodopa that can cross the blood brain barrier by
preventing its metabolism to 3-O-methyldopa. They
mainly act peripherally, although tolcapone might also
have some central action.
COMT inhibitors increase the half-life of levodopa
and are useful in reducing off time for patients with
fluctuating motor symptoms, especially when these occur
at the end of a dose interval. The dose of levodopa may
need to be reduced when a COMT inhibitor is added
because increased levodopa levels can worsen dyskinesia.
COMT inhibitors are rarely used with levodopa as initial
therapy because the combination has been shown to

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Clinical Pharmacist

Confirmed diagnosis of Parkinsons disease (PD)

Troublesome symptoms?

Yes

No

Treatment not
yet required

Elderly patient

Young patient

Monitor disease
and progression
Symptoms are
troublesome
but not severe

Commence
treatment with
dopamine
agonist or
MAO-B*
inhibitor

Satisfactory
control
monitor
disease and
progression

Satisfactory
control
monitor
disease and
progression

Severe
symptoms

Commence
treatment with
levodopa

Unsatisfactory control
Unsatisfactory
control

Combination treatment
with dopamine agonist
plus levodopa (with or
without MAO-B* inhibitor)

Unsatisfactory control
or side effects

Satisfactory
control
monitor
disease and
progression

Satisfactory
control
monitor
disease and
progression

Troublesome
drug-induced
dyskinesia

End-of-dose wearing off

and/or on-off
fluctuations

Start
amantadine or
antimuscarinic

Optimise dose and

frequency of
administration

Unsatisfactory
control

Unsatisfactory control

Consider adding COMT

inhibitor or MAO-B* inhibitor
(if not already used)
Consider apomorphine, levodopa
intestinal gel or neurosurgery

Unsatisfactory control

Satisfactory
control
monitor
disease and
progression

Satisfactory
control
monitor
disease and
progression

Key: *monoamine-oxidase-B; catechol-O-methyltransferase

shorten the time to onset of dyskinesia.13 COMT inhibitors

can worsen dyskinesia, cause abdominal discomfort and
colour the urine.
Tolcapone is a more potent COMT inhibitor than
entacapone but, due to hepatotoxicty, is reserved for
patients with an inadequate response to entacapone.
Entacapone is available in a combination product with
levodopa and carbidopa (Stalevo). The use of this product
may improve adherence and the range of strengths
available enables small adjustments of levodopa dose.

Antimuscarinics Antimuscarinics were the first available

medicines for PD, but their use has been superseded by
drugs that are more efficacious and better tolerated
(troublesome adverse effects include urinary retention,
constipation and confusion).
Generally, the use of these drugs is now limited to
younger patients with severe tremor and dystonia in their
feet, and patients with later-stage disease and dyskinesia
(for these patients it is useful because the mode of action
does not involve dopaminergic stimulation).

CLINICAL FOCUS

Figure 1: Parkinsons disease treatment algorithm, adapted from Parkinsons Disease in Focus11

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Low doses of tricyclic antidepressants are also

occasionally used for nocturnal akinesia, impaired sleep,
and for patients with early morning symptoms (due to
their long half-life).

Amantadine Amantadine has been used for the

management of PD since 1968 and works by preventing
the reuptake of dopamine at synapses. It is now used only
for the management of levodopa-induced dyskinesias.14
However, increasing doses are often required to overcome
tachyphylaxis and eventually for many patients the drug
will need to be stopped.

Last-line treatment
Despite optimal management some patients disease
progresses such that dyskinesia and off periods become
unmanageable and conventional treatment is ineffective.
For such patients, management options are apomorphine,
co-careldopa intestinal gel (Duodopa) or nonpharmacological options.

DESPITE OPTIMAL
MANAGEMENT SOME
PATIENTS DISEASE
PROGRESSES SUCH
THAT DYSKINESIA
AND OFF PERIODS
BECOME
UNMANAGEABLE
AND CONVENTIONAL
TREATMENT IS
INEFFECTIVE

Apomorphine Apomorphine is a potent dopamine

receptor agonist. It is administered subcutaneously to
avoid extensive first-pass metabolism. Apomorphine has a
rapid onset of action and a short duration of action (up to
100 minutes). Intermittent bolus doses are used for rapid
termination of off periods and continuous subcutaneous
infusions are used for patients with advanced motor
symptoms.
Treatment with apomorphine is started by specialists
after a trial (using bolus administration of escalating
doses) to assess response and tolerability. The medicine
can be highly emetic so patients are given domperidone,
20mg three times a day, for two to three days before
starting treatment. Apomorphine is associated with fewer
psychiatric effects than other dopamine agonists.

into the duodenum via a percutaneous gastrostomy tube.

Because of its expense and the invasive route of
administration, the use of Duodopa is limited to those
with severe motor fluctuations that are not managed by
other drug therapies.

Non-pharmacological options Patients with

idiopathic PD associated with severe motor complications
that are unresponsive to oral, topical and invasive
pharmacological treatments may be considered for deep
brain stimulation (DBS). DBS is a neurosurgical
procedure that involves implanting electrodes into either
the ventro-intermediate nucleus of the thalamus, the
globus pallidus internum or the subthalamic nucleus. The
electrodes are connected to a pulse generator, which is
implanted subcutaneously on the anterior chest wall.
Once the electrode is activated the electrical stimulation
causes a depolarising block within the pathway between
the specific nucleus and the substantia nigra and aims to
interfere with the abnormal electrical impulses that cause
PD symptoms.
DBS is associated with psychiatric adverse effects,
dysphagia and gait problems.15
DBS has been recommended by NICE since 2003 but,
before this, ablative surgical procedures were used as lastline options for the symptoms of PD. The ablative
surgeries (subthalamotomy, pallidotomy or thalamotomy)
used electrical current to destroy tissue within areas of the
brain where inappropriate activity can cause the
symptoms of PD. These procedures are associated with
seizures and facial weakness.

Interrupting therapy
Drug holidays were previously used to decrease or
delay the onset of dyskinesias for patients with later-stage
disease. This strategy is no longer recommended due to
the risk of inducing neuroleptic malignant syndrome
through the rapid withdrawal of dopamine stimulation.1 In
addition, patients experience worsening of their motor

Levodopa intestinal gel Duodopa is a soluble gel form

of levodopa plus carbidopa that is administered directly

Box 3: Medicines used for the treatment of Parkinsons disease1

MEDICINE

PLACE IN THERAPY

DEGREE OF SYMPTOM
CONTROL

MOTOR COMPLICATIONS

UK PRODUCTS

Levodopa

First-line or adjuvant therapy

+++

Yes

Co-beneldopa, co-careldopa

Dopamine agonists

First-line or adjuvant therapy

++

No

Bromocriptine, cabergoline, pergolide,

pramipexole, ropinirole, rotigotine

MAO-B inhibitors

First-line or adjuvant therapy

++

No

Rasagiline, selegiline

COMT inhibitors

Adjuvant to levodopa

++

No

Entacapone, tolcapone

Amantadine

Reduction of dyskinesia

Lack of evidence

No

Amantadine

Antimuscarinics

Young patients with early PD and

severe tremor, adjuvant in dyskinesia

Lack of evidence

No

Orphenadrine, procyclidine,
trihexyphenidyl

Modified-release
levodopa

Used to improve adherence and to

provide symptom control overnight
and on waking

+++ (initial therapy) Yes

++ (adjuvant)

Co-beneldopa MR, co-careldopa MR

Apomorphine

Severe motor complications and

off-time with other therapy

No

Apomorphine

+++

Yes

Co-careldopa (Duodopa)

Levodopa intestinal gel Severe motor complications and

off-time with other therapy

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Clinical Pharmacist

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Deep brain stimulation can be considered for some patients with late-stage
idiopathic Parkinsons disease

Future treatments
Neuroprotection (therapeutic strategies intended to slow
or halt the progression of loss of dopaminergic neurones)
and neurorestoration (replacing the missing or damaged
dopaminergic cells) are believed to be the future of PD
management .

Neuroprotection Although it has been proposed that

antioxidants, such as ubidecarenone (co-enzyme Q10) or
vitamin E, could offer neuroprotection by scavenging
harmful free radicals, there is little evidence to support
their use in PD.
A small study conducted in 2002 reported that
ubidecarenone at doses of 1,200mg per day provided a
significant change in total unified Parkinsons disease
rating scale from baseline compared with placebo after
16 months.17 There have been no other large-scale studies
that support or refute the use of ubidecarenone.
Other products could offer neuroprotection and
require further investigation, including those with antiapoptotic or pro-mitochondrial properties. It is believed
that rasagiline may be anti-apoptotic and research into
this is under way.

Neurorestoration The role of neurorestoration for the

management of patients with PD is being explored.
Studies investigating the place of gene therapy (eg, the
growth factor neurturin) and tissue transplantation
(human and animal) are under way currently, and it is
hoped that new therapeutic options will be made available
in the future.

10
11
12

13

14

References
1

National Institute for Health and Clinical Excellence. Parkinsons

disease: national clinical guideline for diagnosis and management in
primary and secondary care. June 2006. www.nice.nhs.uk/cg035
(accessed 31 October 2011).
DellAgnello G, Ceravolo R, Nuti A, et al. SSRIs do not worsen
Parkinson's disease: evidence from an open-label, prospective study.
Clinical Neuropharmacology 2001;24:2217.
Naimark D, Jackson E, Rockwell E, et al. Psychotic symptoms in
Parkinsons disease patients with dementia. Journal of the American
Geriatric Society 1996;44:2969.
Kurlan R, Cummings J, Raman R, et al. Quetiapine for agitation or
psychosis in patients with dementia and parkinsonism. Neurology
2007;68135663.
Morgante L, Epifanio A, Spina E, et al. Quetiapine and clozapine in
parkinsonian patients with dopaminergic psychosis. Clinical
Neuropharmacology 2004;27:1536.
Weintraub D, Koester J, Potenza MN, et al. Impulse control disorders in
Parkinson disease: a cross-sectional study of 3,090 patients. Archives of
Neurology 2010;67:58995.
Aarsland D, Ballard C, Walker Z, et al. Memantine in patients with
Parkinsons disease dementia or dementia with Lewy bodies: a double

15

16
17

blind, placebo-controlled, multicentre trial. Lancet Neurology

2009;8:6138.
Hogl B, Saletu M, Brandauer E, et al. Modafinil for the treatment of
daytime sleepiness in Parkinsons disease: a double-blind, randomised,
crossover, placebo-controlled polygraphic trial. Sleep 2002;25:9059.
Scottish Intercollegiate Guidelines Network. Diagnosis and
pharmacological management of Parkinsons disease. January 2010.
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Tugwell C. Parkinsons Disease in Focus. London: Pharmaceutical Press;
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Olanow CW, Obeso JA, Stocchi F. Continuous dopamine-receptor
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Stocchi F, Rascol O, Kieburtz K, et al. Initiating levodopa/carbidopa
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STRIDE-PD study. Annals of Neurology 2010;68:1827.
Thomas A, Iacono D, Luciano AL, et al. Duration of amantadine benefit
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Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early
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symptoms, which is often more troublesome than the

dyskinesia itself.
Therapy interruptions are sometimes unavoidable (eg,
for patients undergoing surgery, especially gastrointestinal
surgery) and can occur if patients become unable to take
their usual oral treatments. The consequences of missing
doses varies from minor loss of control to neuroleptic
malignant syndrome. Patients with PD undergoing
surgery are more likely to experience post-operative
complications and this may, in part, be due to omitted
doses. If enteral administration is not possible then
alternative methods of drug administration should be
used, such as topical rotigotine or subcutaneous
apomorphine.16

December 2011