Pakistan Journal of

Neurological Sciences (PJNS)

Volume 10 | Issue 1 Article 14

3-2015

National guidelines for diagnosis and management

of Parkinson’s disease in Pakistan
Nadir A Syed
South City, Karachi

Farwa Ali
South City Hospital, Karachi

Khalid Sher
JPMC, Karachi

Amer Ikram
Doctors Hospital, Lahore

Bashir Soomro
Ziauddin, Karachi

See next page for additional authors

Follow this and additional works at: http://ecommons.aku.edu/pjns

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Recommended Citation
Syed, Nadir A; Ali, Farwa; Sher, Khalid; Ikram, Amer; Soomro, Bashir; Shahbaz, Naila; Sheerani, Mughis; Jamil, Sarwar; Numan,
Ahsan; Lakhair, Manzoor; Awan, Irshad; Barech, Saleem; and Basheer, Haroon (2015) "National guidelines for diagnosis and
management of Parkinson’s disease in Pakistan," Pakistan Journal of Neurological Sciences (PJNS): Vol. 10 : Iss. 1 , Article 14.
Available at: http://ecommons.aku.edu/pjns/vol10/iss1/14
National guidelines for diagnosis and management of Parkinson’s disease
in Pakistan
Authors
Nadir A Syed, Farwa Ali, Khalid Sher, Amer Ikram, Bashir Soomro, Naila Shahbaz, Mughis Sheerani, Sarwar
Jamil, Ahsan Numan, Manzoor Lakhair, Irshad Awan, Saleem Barech, and Haroon Basheer

This guidelines is available in Pakistan Journal of Neurological Sciences (PJNS): http://ecommons.aku.edu/pjns/vol10/iss1/14

 G U I D E L I N E S

NATIONAL GUIDELINES FOR DIAGNOSIS AND

MANAGEMENT OF PARKINSON’S DISEASE IN PAKISTAN

Nadir A Syed (South City,Karachi), Farwa Ali (South City Hospital, Karachi), Khalid Sher (JPMC, Karachi)
Amer Ikram (Doctors Hospital, Lahore), Bashir Soomro (Ziauddin, Karachi), Naila Shahbaz (DUHS, Karachi)
Mughis Sheerani (AKU, Karachi), Sarwar Jamil (AKU, Karachi), Ahsan Numan (services Hospital, Lahore)
Manzoor Lakhair (LUMS, Jamshoro), Irshad Awan (PIMS, Islamabad), Saleem Barech (BMC, Quetta)
Haroon Basheer (Pakistan Parkinson's Society)
ADVISOR’S:
Ronald Pfieffer (USA), Zeba Vanek (USA), Jawwad Bajwa (KSA), Mustafa Saad Siddiqui (USA), Daniel Truong (USA)

Correspondence to: Dr. Nadir A Syed, South City Hospital, Clifton, Karachi. Email: [email protected]
Date of Submission: December 28, 2014, Date of Revision: January 30, 2015, Date of Acceptance: February 1, 2015

INTRODUCTION TO PARKINSON’S DISEASE

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, after Alzheimer’s disease. Preva-
lence in people older than age 60 is approximately 1.4%.[1, 2] PD is characterized by many motor and non-motor symp-
toms. It presents with a range of motor symptoms usually consisting of asymmetric bradykinesia, resting tremor, and
rigidity; postural instability may develop later in the course of the disease.[3, 4] However 'pre-motor' PD-a range of non-
motor symptoms, particularly sleep disorders, mood disorders, impaired sense of smell, and constipation may occur up
to 20 years before the onset of motor symptoms.[5] The clinical paradigm has shifted from PD being considered a pure
motor or movement disorder to being recognized as a systemic synucleinopathy with many motor and non-motor symp-
toms and signs. The etiology of PD is largely unknown, but a combination of genetic and environmental factors is postu-
lated. Several genes have been associated with inherited and early onset form of PD (LRK1, PINK1, Parkin, and DJ-1)
but these represent only a small subset (10-15%) of all PD cases.[6] It is now known that PD can present with changes
in mood, sleep, behavior, cognition and autonomic function this can initiate referrals to psychiatric, general medicine,
geriatric, orthopedic and even rheumatology clinics, before neurological referral is considered. Etiology is multifactorial
and is thought to be related to multiple mechanisms. Factors associated with development or Parkinsonism include expo-
sure to oxidant toxins (e.g. pesticides, MPTP), head trauma, manganese exposure, head trauma.

General Approach to Parkinson’s disease

Diagnosis of Parkinson’s disease tion combined with clinicopathological correlation. In

subsequent studies it has been demonstrated to have up
The diagnosis of PD remains primarily clinical. In 1988, to 90 % accuracy in diagnosing PD when diagnosed by
Gibb and Lees developed the Queen Square Brain Bank an experienced neurologist. This is a three step recom-
(QSBB) criteria for PD, based on careful clinical observa- mended strategy for diagnosis of Parkinson’s disease.

PAKISTAN JOURNAL OF NEUROLOGICAL SCIENCES 40 VOL. 10 (1) JAN - MARCH 2015

UK Queen Square Brain Bank Criteria for the diag- palsy, cerebellar signs, early severe autonomic
nosis of Parkinson's disease[7] involvement, Babinski's sign, early severe dementia
with disturbance of language, memory or praxis
Step 1: Diagnosis of a Parkinsonian Syndrome • Exposure to Neurotoxin
• Presence of cerebral tumour or communicating
Bradykinesia (slow to initiate voluntary movement with hydrocephalus on neuroimaging
progressively reduced speed and amplitude of repetitive
actions) and at least one of the following: Step 3: Supportive Criteria for Parkinson's Disease
• Muscular rigidity
• Postural instability unrelated to primary visual, Three or more of the following are required for the
cerebellar, vestibular or proprioceptive dysfunction diagnosis of definite Parkinson's disease
• Resting tremor • Unilateral onset
• Rest tremor present
Step 2: Exclusion Criteria for Parkinson's Disease • Progressive disorder
• Persistent asymmetry primarily affecting the side
History of: of initial onset
• Repeated strokes with stepwise progression • Excellent response to levodopa (70%–100%)
• Repeated head injury • Severe levodopa-induced chorea
• Antipsychotics or dopamine-depleting drugs • Levodopa response for more than 5 years
• Definite encephalitis and/or oculogyric crisis on no • Clinical course of over 10 years
drug treatment
• More than one affected relative (Note: this exclusion Work up of Parkinsonism at Initial Presentation
criteria is usually ignored)
• Sustained Remission In patients with a clear clinical diagnosis and no atypical
• Negative response to large doses of levodopa (if signs the physician may decide not to order blood tests or
malabsorption excluded) neuroimaging studies. There is no definitive diagnostic
• Strictly unilateral features after 3 years test for PD. These tests are performed to diagnose other
• Other neurological features: supranuclear gaze conditions that may present like Parkinson’s disease.

[9-11]
Parkinson’s disease Mimics

Once structural, infectious, toxic and metabolic causes of Parkinsonism have been excluded, the evaluating physician
must consider features of the patient’s history and physical examination that may suggest an alternative cause for the
symptoms. A diagnosis of idiopathic PD should be assumed only after ruling out PD mimics such as other tremor disor-
ders, drug-induced Parkinsonism, vascular parkinsonism, normal pressure hydrocephalus and parkinsonism-plus condi-
tions. The following table outlines features that may help in the differential diagnosis of these conditions:[3]

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Parkinson’s disease more likely Alternative diagnosis more likely

Slow onset and progression of symptoms over months Sudden onset or rapid progression over days and weeks
and years should suggest an alternative diagnosis such as a
For example a 55 year old man presenting with slowly stroke, brain tumour or TB meningitis
progressive difficulty using left hand with a mild tremor
at rest over the past year

Unilateral disease or significant asymmetry on signs Symmetrical onset more commonly is associated with other
and symptoms in the beginning of the disease Parkinsoniansyndromes such as Diffuse Lewy Body disease,
Multisystem Atrophy, Progressive Supranuclear Palsy etc.

Tremor: Tremor:
Tremor usually involves extremities and, less commonly Enhanced physiologic tremor: Tremor related to anxiety
the jaw. Head tremor is almost never present in is present in outstretched hands and throughout the
idiopathic PD. 25% of Parkinson’s patients may never range of motion. Benign essential tremor is more
manifest a tremor. The classic tremor in Parkinson’s prominent when the patient stretches out his hands as
disease is a slow resting (low frequency) pill-rolling it is predominantly a postural tremor. Benign essential
tremor best seen when the hands are at rest or while tremor often involves the head causing a side-to-side or
the patient is walking.It decreases with activity and can up/down tremor (a 'no-no' or ‘yes-yes’ tremor). ). It can
be suppressed temporarily by the patient. Re-emergent affect the voice, is worsened with activity and is often
tremor: Tremor tends to diminish at least temporarily familial. Parkinson’s plus syndromes are less likely to
once the patient is asked to stretch out the arms and have a tremor at presentation.
may return as this becomes the new rest position.
Onset of tremor is generally unilateral and over time
may involve the other side

Responsive to Levodopa Lack of robust response to Levodopa

Autonomic symptoms include urinary urgency, orthostasis Early onset of multiple autonomic symptoms suggest
MSA

Bulbar involvement is possible Predominant early bulbar signs suggest a Parkinson’s

Plus syndrome like PSP

Falls occur late after significant rigidity or bradykinesia Frequent falls early in the course of disease suggests a
develop Parkinson’s Plus syndrome like PSP

Non motor symptoms may include constipation, anosmia,

insomnia and depression.

Lack of eye movement restriction except there may be some Vertical gaze palsy in which initial abnormality is impair-
impairment of conjugate upgaze and convergence ment of downgaze with intact oculocephalic maneuver
suggests PSP

Lack of early respiratory muscle compromise Stridor/strangulated dysarthria suggests MSA

Chronic history of neuroleptic use or antiemetic use

suggests a medication induced parkinsonism

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Table 1
Neuroimaging in Parkinson’s disease and Parkinson’s Plus Syndromes

In a patient with classic features of Parkinson’s disease, tant for the physician to partner with the patient and the
and absence of red flags for atypical Parkinsonism, family to treat PD. It is important that the patient under-
neuroimaging is not indicated initially. If the patient stands that the treatment will allow for many years of
subsequently develops any atypical features, then brain very adequate function but that the disease is progres-
MRI without contrast can be considered [10, 12] Treatment sive and incurable. Any patient with social or functional
of Motor Symptoms in Parkinson’s disease PD is the impairment should be initiated on treatment. Almost all
only common neurodegenerative condition in which patients that present to a physician require some form
effective long-term treatment is readily available. Spe- of treatment. The most obvious motor symptom for
cial care needs to be exercised in treating PD as both many patients is tremor, which is socially distressing;
under treatment and over treatment can worsen a however the tremor often does not impair function if it
patient's condition and may even accelerate the is not severe. Rigidity, bradykinesia and in later stages
progression to disability. The key is to treat the patient postural instability are frequently greater sources of
appropriately and not to under or over treat. This implies functional impairment. [13]
a level of treatment that relieves symptoms to the point
that the patient has a fairly good quality of life. The Overview of Pharmacologic Therapy for Motor
physician needs to explain to the patient early on that Symptoms in Parkinson’s disease [9, 13-17]
PD is an incurable but treatable disease that will require
a lifelong patient-physician partnership. The objectives Pharmacologic treatment options include: Carbidopa/
of optimal treatment should be clearly explained. The levodopa; sooner or later virtually all patients with PD
objectives should be to treatment to a point that the will require carbidopa/levodopa. Dopamine agonists
patient is adequately functional and has a good quality (although not as effective ascarbidopa/ levodopa, carry
of life. The first step in managing PD is to determine an advantage of delaying motor fluctuations and dyski-
whether treatment is needed or not. It is important for nesias, especially in younger patients) [35]. Monoamine
the physician to partner with the patient and the family oxidase type B inhibitors (symptomatic improvement is
to treat PD. The treatment usually results in many years modest with these); these are rasagiline and
of a productive and functional life. In many patients the selegiline)[36]. Anticholinergics (eg procyclidine and
disease does progress and the symptoms become trihexyphenidyl). These predominantly improve the
refractory to the treatments. Patients with social or tremor, drooling and urinary frequency. These are asso-
functional impairment should be initiated on treatment ciated with many adverse effects, which may be
and almost all patients that present to a physician particularly severe in the elderly and include urinary
require some form of treatment. The most obvious retention, constipation, blurred vision, dry mouth,
motor symptom for many patients is tremor, which is confusion, and orthostatic hypotension)[34,37]. Amanta-
socially distressing; however the tremor often does not dine [38] may reduce dyskinesias very effectively and can
impair function if it is not severe. Rigidity, bradykinesia also help tremor and fatigue. COMT inhibitors
and in later stages postural instability are frequently (entacapone, tolcapone)[39]; prolong the half-life of
greater sources of functional impairment. [30] The first carbidopa/levodopa and make it last longer and make it
step in managing a diagnosed case of PD is to deter- more effective.
mine whether treatment is needed or not. It is impor-

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Carbidopa/ levodop bromocriptine, are still used in Pakistan but should be
avoided due to the associated high frequency of cardiac
A variety of pharmacologic and non-pharmacologic valvular, peritoneal and pleural fibrosis. Common
treatments are effective in treating PD. The cheapest adverse effects of dopamine agonists include: Sedation
and the most effective medication is still (may be severe and cause sleep attacks that may be
carbidopa/levodopa. Common adverse effects include sudden and severe enough to cause car accidents).
nausea and light headedness. In the past there was Confusion, disorientation, hallucinations, delusions,
concern about potential neurotoxicity and acceleration psychosis and hallucinations. Postural hypotension and
of underlying disease associated with use of nausea. Impulse control disorder; this can consist of
carbidopa/levodopa but this concern has been laid to pathological gambling, hypersexuality, compulsive
rest. Recent studies reveal earlier use of eating, compulsive shopping, compulsive hobbying.
carbidopa/levodopa does not accelerate progression of
PD. Peak-dose dyskinesia (involuntary-dance like move- Response to Treatment as Parkinson’s disease
ments) may develop after several years of using Progresses
carbidopa/levodopa in younger patients and patients on
high doses. This is one reason why many neurologists As PD progresses the response to treatment varies.
would prefer to avoid carbidopa/levodopa as first line Early Parkinson's disease; The early stage of PD is also
treatment in the younger (<60 years age) patient and called the “honeymoon period” when symptoms
initiate treatment with a dopamine agonist and rasagil- respond well to a variety of treatments and there is a
ine instead. In individuals already on carbidopa/ sustained response to single doses of medications. [41]
levodopa, shortening the interdose interval and reduc- Late Parkinson's disease; As PD progresses, the
ing individual doses may reduce the severity and even response to dopamine therapy becomes less sustained,
postpone development of motor fluctuations and probably as a consequence of the loss of dopaminergic
complications [40]. In Pakistan the available formulation neurons. Motor fluctuations develop and the addition of
of levodopa contains 250 mg levodopa in combination MAO-B inhibitors or COMT-inhibitors may then be
with 25 mg of carbidopa. This may not be the optimal considered. These agents increase the potency of
formulation to be given in the earlier stages of PD. levodopa and prolong its effect by inhibiting the meta-
Using a 25 carbidopa/100 levodopa formulation bolic breakdown of levodopa and increasing its
(available as imported medicine) or quarter or half of bio-availability. If given in combination with Carbidopa/
the 25/250 pill may be better. levodopa they help to decrease off-time and prolong the
on-time. MAO-B inhibitors include selegiline and
Dopamine Agonists rasagiline. This class of drug produces modest sympto-
matic benefit but has not been shown to delay motor
Dihydroergocryptine, pergolide, pramipexole, ropinirole, complications. A rare adverse effect of selegiline but
piribedil, rotigotine, bromocriptine, cabergoline and not rasagiline is precipitation of a hypertensive crisis if
lisuride are the dopamine agonists used in PD. Ropin- consumed with tyramine containing foods. COMT-
irole is the most widely available and frequently used inhibitors includeentacapone and tolcapone. COMT-
dopamine agonist in Pakistan. There is no particular inhibitors produce moderate improvement in motor
difference in efficacy between different dopamine symptoms. Entacapone in combination with levodopa
agonists, so physicians should familiarize themselves shows minimal delay in onset of motor complications
with the dosage titration and potential adverse effect of (dyskinesia). Tolcapone comes with a black box warning
one of them. Ergot-based dopamine agonists, such as for fulminant liver failure, which may be fatal.

Treatment of Parkinson’s disease based on Patient’s Age

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In patients older than 60 years of age who present with dyskinesias that may occur with Carbidopa/levodopa
symptoms, consider starting with carbidopa/levodopa therapy, particularly in the young PD patients. Eventu-
as it is more effective and generally better tolerated. In ally even the younger patients may require Carbidopa/
younger patients (<60 years) it may be better to start levodopa as the disease progresses and a more potent
with one of the dopamine agonists in order to delay the medication is needed.
Table 1; Characteristics of commonly used medications for motor symptoms in PD [19]
Drug Class Indication Impact on Motor symptoms Important Adverse Effects
Levodopa First line therapy in patients over 60 years of age Excellent Motor fluctuations Dyskinesia
Dopamine Agonists First line therapy in younger patients Moderate Sedation/sleep attacks
or add on to carbidopa/levodopa Impulse control disorder
Pedal edema, Weight gain
MAO-B Inhibitors First line for mild disease with depression. Limited Serotonin syndrome and
Add on therapy for motor fluctuationsto carbidopa/levodopa hypertensive crises may rarely occur
Narrow therapeutic window
COMT inhibitors Add on therapy for motor fluctuations Improves wearing off of Carbidopa/levodopa Diarrhea
Anticholinergics Limited use. Only improves PD tremor Limited Confusion, Dry eyes/mouth
Urinary retention, Constipation
Amantadine Reduces dyskinesias and can improve Limited Confusion
wearing off symptoms Lividoreticularis
Pedal edema

Table 2 [3]
Relative Efficacy Profile

Factors affecting treatment choices Levodopa Dopamine Agonists MAO-B Inhibitors COMT Inhibitors
Efficacy on motor symptoms High Moderate Low Moderate
Ease of Use Low Moderate Moderate Low- Moderate
Risk of inducing motor complications High Low Low Low

Table 3 Relative Cost of Different Medications (as listed in Pharma guide 2014, electronic version)

Carbidopa/ Name of company Price in PKR /tablet Rasagiline 1 mg Name of company Price in PKR /tablet Ropinirole Name of Price in
levodopa 1 mg company PKR/tablet
25/250 mg
Aptidopa aptcure 8 Alzilo Searle 19.20 Propinol Shrooq 9.50
Dopasel kurative 8 Rasagin HiranisPharma 11.40 Reol Genome 16,66
Meddopa medera 8 Requip GSK 34.28
Neudopa Platinum 8 Amantadine 100 mg Name of company Price in PKR /tablet Ronirol Hilton 21.19
Sinedopa Valor/Al-Hameed 9 Amantin Gene-Tech 11.35 Ropinol Amarant 24,33
Sinemet OBS 14.61 PK-Merz Brookes 15.60 XMG Atco 12
Viofral Biocare 13.25

Table 4
Titration Template for Commonly Used Medications for Motor Symptoms in Parkinson’s disease [19, 20]

Medication Start of titration Weekly up-titration Maintenance dose Daily dose

Carbidopa/levodopa 50 mg AM 50 mg Q3day 3-4 x 100 mg 300-800 mg
Pramipexole 3x0.088 mg 2nd week 3x0.18mg
3rd week 3x0.35mg
Then weekly 3x0.18 mg 3x0.35-0.7 mg 1.05-3.3 mg
Pramipexole ER 0.25 mg AM 2nd week 0.52 mg 1x 1.05-2.1 mg 1.05-3.15 mg
3rd week 1.05 mg
4th week 2.1 mg
5th week 3.15 mg
Ropinirole 1 mg AM Weekly 1mg 3x 3-8 mg 6-24 mg
Ropinirole ER 2 mg AM 2 mg 6-24 mg 6-24 mg
Rotigotine Patch 2mg/24h 2mg/24 hr 4-8 mg/24h 8-16 mg/24h
Piribedil 50 mg HS 50 mg every 2 weeks 2-3 x 50 mg 150-250 mg
Selegiline 5-10 mg 5-10 mg
Rasagiline 1 mg 1 mg
Entacapone 50 mg AM 50 mg every 3 days 3-4 x 100 mg 600 mg
Tolcapone 100 mg AM 2-3 x 100 mg 600 mg
at 6-12 hour intervals
Amantadine 100 mg AM 100 mg q3days 1-3 x 100 mg 100-400 mg

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Deep Brain Stimulation in Parkinson’s disease [21]
dopamine or underlying anxiety/ depression. Nocturia
may disturb the normal sleep pattern and may be due
Deep brain stimulation of the sub thalamic nucleus or to an over active bladder or an underlying sub-clinical
globus pallidus internum is used in the treatment of motor urinary tract infection.. Dopaminergic drug-wearing-off
symptoms of PD. There are multiple theories to suggest may contribute to poor sleep and this may require a
the mechanism of action including a micro-lesioning bedtime dose of a long acting dopaminergic agent.
effect, resetting of aberrant pathways and circuits and Restless legs syndrome is commonly associated with
modulating excito-toxicity. Parkinson's disease and can be readily diagnosed and
treated. RLS presents with restlessness, pain, cramps
Deep brain stimulation of the subthalamic nucleus or globus or vague discomfort in the legs upon rest, particularly
pallidum may be considered in the following situations. after laying down to sleep at night. The symptoms
improve upon movement, such as moving the legs or
• Medication refractory disabling tremor. getting up and walking, but symptoms often return once
• Carbidopa/Levodopa responsive disease. the patient is recumbent again. RLS is associated with
• Motor fluctuations (on-off fluctuating motor symptoms involuntary leg movements as well, which can occur
that require high doses of medications that need to be during wakefulness or sleep. RLS symptoms should
given very frequently. trigger a search for underlying iron deficiency, which
• Disabling dyskinesias. should then be treated with iron replacement and
• Patient does not have dementia or severe depression. Vitamin C which may facilitate its absorption. If iron
deficiency is not present, RLS responds well to dopa-
Axial and autonomic symptoms and freezing of the gait minergic agonists such as ropinirole, typically adminis-
usually does not get better with this surgery. The surgery tered 2 hours before bedtime. Gabapentin, pregabalin
should only be done by high trained and experienced and tramadol also are effective REM sleep behavior
Parkinson’s disease surgeons and after the surgery the disorder includes a variety of presentations wherein
medications and the stimulator needs to be adjusted by patients may seem to be acting out dreams. Questioning
experienced Parkinson’s disease neurologists. It requires the family members may reveal the patient has been
life-long management by these teams and if not done and talking in their sleep or even thrashing around and
managed properly can often make the condition of the acting out physical fights while asleep (which may result
patient worse after the surgery. in injuries). Always screen for REM sleep behavior disorder
as it is a treatable condition.[22-25] It is usually responsive
Treatment of Non-Motor Symptoms in to a low dose of clonazepam.
Parkinson’s Disease
Depression And Anxiety:
Non-motor symptoms are a major contributor to impaired
quality of life of patients suffering from PD. [5] However, Mood disorders are common in Parkinson's disease and
these symptoms are often neglected during evaluation are frequently under-recognized and under-treated. PD
and treatment. Non-motor symptoms are often easily patients with depression may be difficult to motivate to
treatable, but lack of attention to them may make treat- engage in regular exercise and in rehabilitation
ment of motor symptoms more difficult.[12] Non-motor programs. They also are more likely to be noncompliant
symptoms include behavioral symptoms like depression, with treatment. Serotonin specific reuptake inhibitors
anxiety and psychosis, sleep disorders, dementia, dysau- (SSRI's) often are effective in usual doses and can
tonomia (dysphagia, drooling, constipation, urinary greatly improve the quality of life of the patients.
urgency and frequency, orthostatic hypotension) and Episodic shortness of breath and sweating are often
sensory symptoms (pain, Restless Legs Syndrome, numb- seen with advancing Parkinson's disease and may or
ness, joint stiffness in the limbs affected by the symp- may not respond to dopaminergic medication. These
toms, etc). Non-motor symptoms can precede motor resemble panic attacks.[17,18]. Anxiety can be a non-
symptoms by years. motor component of PD and although it perhaps most
often appears as a wearing off phenomenon, it also can
Sleep Disorders: present as a more pervasive sense of anxiety in some
patients. It can often be treated by giving the dopaminergic
These include rapid eye movement (REM) sleep behavi or medications more frequently at lower doses.
disorder (acting out dreams), insomnia, restless legs
syndrome (RLS), and poor sleep maintenance. Usually Dementia:
the history provides the diagnostic clues needed to
address sleep issues. Insomnia can be related to lack of PD dementia may develop in people after several years

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and correlates with the presence of subcortical and may be helpful. Speech therapy is important along with
cortical Lewy bodies. Environmental modifications are assessment of swallowing and advice regarding the
the best tolerated interventions. Try to minimize prevention of aspiration. Enteral feeding options
changes to routine, provide familiar things and memory (short-term nasogastric tube or percutaneous endo-
cues to minimize agitation. scopic gastrostomy) may be needed in advanced cases.
[24]
. Eating pureed and soft foods with the head slightly
Discontinue potential aggravators: bent may be better and extra care with thin fluids like
water and tough foods like meat that are more likely to
Anticholinergics, amantadine, tricyclic antidepressants, cause dysphagia is important. Pills can be also be
tolterodine and oxybutynin, benzodiazepines. If treatment crushed and administered with yogurt to facilitate
becomes necessary, the addition of a cholinesterase swallowing.
inhibitor, such as rivastigmine, donepezil or galantamine
may be considered. Memantine also may be tried.[26, 27] Orthostatic hypotension:

Psychosis: This is very important to recognize, prevent and treat as it

can cause dizziness, fainting spells and falls. This is
Symptoms of psychosis, such as hallucinations, aggravated by volume depletion, diuretics, antihyperten-
delusions, and illusions, are complications of therapy sive drugs, tricyclic antidepressants, nitrates and alpha-
and also may arise from the progression of the disease blockers used to treat prostatic hypertrophy. Dopaminer-
process. When they occur, it is important to first correct gic drugs also may induce orthostatic hypotension. It
any metabolic abnormalities or fluid imbalance and to improves with increased salt intake. Elevating the head-
treat any infection. It is important to minimize poly- end of the bed at night (30–40°) may be helpful, as may
pharmacy. Decreasing or stopping non-levodopa medi- wearing of waist-high elastic-pressure stockings and/or
cations and optimizing levodopa can improve psychosis. abdominal binders (if weather allows). Changing positions
Antipsychotics may be needed, but those that are slowly and exercises of the legs (leg crossing, toe raising,
potent dopamine depleting drugs can worsen Parkin- and thigh contraction) before sitting up and standing can
sonism, especially the typical antipsychotics. Quetia- help. If all of these are unsuccessful, medications, such
pine is a sedating antipsychotic that does not appear to as midodrine or fludrocortisone, may be necessary. [25,26].
worsen the motor symptoms of Parkinson's disease. Domperidone can block the peripheral effect of the dopa-
However as with other atypical antipsychotics, there minergic medications and can help as well.
may be a small risk of cardiac complications and therefore
its use requires considering the risks and benefits for Constipation:
each individual patient.
Constipation is a manifestation of general bradykinesia
Urinary Urgency, Frequency and Nocturia: and autonomic dysfunction in Parkinson’s disease. This
is a common problem aggravated by poor oral intake of
These are common autonomic symptoms in PD. Recog- water/fiber. Bowel dysfunction has two components
nizing and treating sub-clinical urinary tract infection is decreased bowel movement frequency and difficulty
very important. Initial treatment may involve reduced with the act of defecation. Decreased bowel movement
intake of fluids after 6 pm and no caffeinated drinks frequency results from slow colon transit and the
after 12 noon. If that is not sufficient, then anticholiner- difficulty with the act of defecation is due to impaired
gic medications may help. Anticholinergics that do not coordination and relaxation of the anorectal muscles.
cross the blood brain barrier are better, since these do Slow transit constipation often responds to increasing
not worsen cognition. Tolterodine (2 mg twice daily) can water intake, fiber (ispaghula husk) and regular use of
be considered for these symptoms. Botulinum toxin Milk of Magnesia or lactulose. Defecatory dysfunction
type A injected in the detrusor muscle can also help but usually does not respond to these interventions.
is a very expensive form of treatment that should be
given only by trained physicians.[22,23]. For patients who Drooling:
cannot tolerate medications, diapers and bedside
urinals should be available for patients. Drooling is another common and distressing symptom.
Drooling is typically due to impairment of the swallowing
Dysphagia: mechanism rather than overproduction of saliva and
may improve with chewing gum or sucking on honey or
Multiple factors contribute to dysphagia in PD. Optimization ice. Drooling may require use of anticholinergic agents
of motor control with dopamine replacement therapy or botulinum toxin injections into the salivary glands [19].

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However anticholinergics should generally be avoided in of motor and non-motor symptoms but also addressing
the elderly patients and those with cognitive impairment multiple areas of rehabilitation and improving the quality of
as they can result in confusion, hallucinations, blurring life of the individual as a whole. There is a significant role
of vision, constipation and urinary retention. for speech therapy, swallow evaluations, physical
therapy, exercise and gait training from the time of
Pain and Dystonia: diagnosis. Counseling patients and discussing possible
modifications to their life style and home set-up in
Patients with PD suffer from pain related to multiple anticipation of expected disease progressionalsoare
pathogenic mechanisms, including central and periph- important. There is increasing data to suggest that
erally mediated pain. Some of this may be related to exercise is neuroprotective for Parkinson’s disease, may
immobilization from bradykinesia or dystonia. Exercise, improve executive function and slow progression of
physical therapy, pain management and botulinum motor symptoms. SPARX trial and other smaller studies
toxin injections for dystonia may improve the quality of show that exercise improves motor scores in patients
life of the patient.[28-30] with Parkinson’s disease hence reducing falls and
improves quality of life.[31-44] Levodopa therapy is related
When to Refer to a Neurologist to increase homocystine due to its metabolism by COMT
enzyme. This theoretically increases the risk of stroke in
Primary care providers can diagnose and treat Parkinsons patients suffering from Parkinson’s treated with
however consider referring to a neurologist if diagnosis is not levodopa. It might be reasonable to treat prophylacti-
clear; difficulty in managing or complications with manage- cally with Vitamin B 12, folate, Vitamin B6.[45] Rehabili-
ment; suboptimal response with management options tation measures are focused towards improving mobility
and preventing fall-related morbidity. The team caring for
Importance of Multidisciplinary Care in the a PD patient should ideally be a combination of a physi-
Management of Parkinson’s disease cian, speech therapist, occupational therapist and
physical therapist.[13, 46, 47]
Effective management of PD not only includes management
Fall prevention in Parkinson’s Disease.

Gait Training: Take larger steps and make larger truns

Home modifications; - Imporve lighting. - Remove rugs and minimize clutter. - Avoid slippery surfaces

Careful selection of gait aid: Usually walker better than cane

Most Falls occur during Freezing: Use Laser pointers or visual cues to help re-initiate gait

Always consider an early referral to Physical medicine

Work closely with the family and care takers

[48, 49]
Resources and Support for Patients with Parkinson’s disease
There are many global patient education and advocacy forums where patients may be referred for information and
counseling.
Pakistan Parkinson's Society
American Parkinson’s Disease Association www.apdaparkinson.org
National Parkinson Foundation. www.parkinson.org
The Michael J. Fox Foundation for Parkinson's Research www.michaeljfox.org
World Parkinson Congress. www.pdf.org/world_parkinson_congress

PAKISTAN JOURNAL OF NEUROLOGICAL SCIENCES 48 VOL. 10 (1) JAN - MARCH 2015