Parkinson's Disease

DefinitionEtiologyEpidemiologyPathophysiologyClinical Presentation
WorkupGoalsMed ChoicesClinical TrialsPipeline AgentsResourcesRefs

Idiopathic progressive, neurodegenerative disorder characterized by resting Tremor, Rigidity, Akinesia/bradykinesia, and Postural instability ('TRAP'). Symptoms usually manifests when ~80% of dopamine producing cells within substantia nigra (SN) becomes non-functional resulting in dopamine depletion.


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Proposed Classification Scheme for Parkinsonism

Ref: Galpern WR, Lang, AE Ann Neurol 2006; 59:449-458.

Classical Parkinsonism

  • Sporadic
    • Idiopathic Parkinson's disease
  • Genetic
    • LRRK2 mutations
    • SNCA mutations, duplications
    • Parkin mutations
    • PINK1 mutations
    • DJ-1 mutations
    • Others (e.g. SCA2)

Atypical parkinsonism

  • Sporadic
    • Dementia with Lewy bodies
    • Multiple system atrophy
    • Progressive supranuclear palsy
    • Corticobasal degeneration
    • Others
  • Genetic
    • Frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17)
    • Others
      • Wilsons disease
      • Huntington's disease

Secondary Parkinsonism

  • Drug induced
  • Toxin induced
  • Vascular/infection

Environmental risk factors for idiopathic PD

  • Unknown, but the following have been suggested as associated with increased risk:
    • Environmental toxins
    • Pesticides/herbicides
    • Head trauma
  • Environmental factors that have been suggested to have a protective effect
    • Smoking
    • Caffeine
    • Elevated urates
    • Use of non-steroidal anti-inflammatory drugs


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  • Prevalence: Approx. 160 per 100,000
  • Incidence: 10 to 20/100,000/year

Both prevalence and incidence increase with age

  • 85% diagnosed are above the age 65 years
    • Approx. 100,000 Canadians affected
    • Approx. 6.3 million worldwide


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  • Loss of dopaminergic neurons in the substantia nigra leads to dopamine depletion within the basal ganglia. Multiple neurotransmitter abnormalities occur in the basal ganglia circuitry resulting in motor symptoms of PD
  • Non motor symptoms of PD, such as neuropsychiatric, autonomic, sleep and pain likely result from degeneration of cortical and other brainstem regions
  • Exact mechanisms of neurodegeneration are unknown, likely involves genetic and environmental factors

Light Box-1a-Parkinson Disease-Pathophysiology Alogrithm


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Clinical Presentation:

1. Motor symptoms


"Pill-rolling", resting tremor

  • Usually begins unilaterally in the hand, less often the leg. May spread over several years
  • Tremor can also involve the legs, lips, jaw, and tongue, Rarely involves the head
  • Anxiety, emotional excitement, or stressful situations exacerbate the tremors
  • Not all patients with PD develop tremor

Light Box-1-Parkinson Disease-Clinical Presentation-Essential vs Parkinson Tremor


  • May begin unilaterally and spread to involve contralateral side
  • Cog wheel rigidity due to overlay of tremor
  • Lead pipe rigidity is increased tone that is present throughout the range of movement
  • Will increase with activation (ask subject to open and close opposite hand)

Akinesia / Bradykinesia

  • Slow movements
  • Masked facies (expressionless), decreased blink
  • Speech may be hypophonic, stuttering or dysarthria
  • Ability to initiate voluntary movement is decreased
  • Affects routine tasks (buttoning, writing (micrographia), typing, tying knots, difficulty rising from seated position)

Postural instability and gait dysfunction

  • Usually appears later in the disease course, but may occur early in some
  • Tendency to fall forward (propulsion) or backward (retropulsion)
  • Loss of postural reflexes
  • Stooped posture
  • Difficulty in starting to walk, turning, and stopping
  • Shuffling gait with short, quick steps (festinating gait)
  • Decreased arm swing
  • Freezing may occur which is sudden inhibition of movements



Motor fluctuations

  • On/Off phenomenon:
    • May occur with advancing disease due to disease progression and chronic levodopa treatment
    • Periods of satisfactory or good control (on effect) is followed by periods of near immobility (off effect)
    • Symptoms of wearing off are apparent when the duration of levodopa effect subsides
  • Dyskinesia:
    • Over time many patients with PD may develop medication-induced dyskinesia some of which can be disabling
    • Many PD patients may be either unaware of dyskinesia or not have any functional disability with the involuntary movements

Musculoskeletal problems

  • Camptocormia (bent-spine)
  • Head drop (less common)
  • Kyphosis


2. Non-Motor symptoms


  • Dementia can occur later in the course of disease in 10-15% patients
  • Short-term memory and visuoperceptual functions may be affected


  • Sense of presence: Well formed visual and less commonly auditory and tactile hallucinations
  • Paranoid delusions: May be associated with cognitive impairment; Can be triggered by dopaminergic drugs; always rule out other causes of delirium e.g. infection

Mood disorders

  • Depression
  • Anxiety
  • Apathy
  • All very common in PD. May be 'premotor' features i.e. occur years before onset of PD

Sleep disorders

  • Excessive daytime sleepiness
  • Insomnia
  • REM sleep behaviour disorder (may be a 'premotor' feature)
  • Sleep disorders are very common and are often drug-induced

Autonomic dysfunction

  • Urinary frequency and nocturia
  • Constipation
  • Postural hypotension


  • Can be multifactorial due to rigidity or dystonia or 'central'
  • Sensory symptoms-Numbness/tingling


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Investigation and Workup:

Diagnosis of PD is based upon clinical evaluation

  • Thorough history of presenting complaints
  • Family and occupational history
  • Neurological exam
  • Response to dopaminergic therapy
  • Neuroimaging-CT/ MRI brain: Rule out structural abnormalities such as hydrocephalus, tumour, or lacunar infarcts


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Treatment Goals:
  • To understand challenges associated with the diagnosis
  • To ensure the choice of initial drug therapy, and the timing of treatment initiation leads to best outcome
  • To minimize or delay onset of motor complication such as "wearing off", "on/off fluctuations", etc.
  • To ensure patient management is individualized, based on the severity, level of disability, cost, patient preference and age
  • To minimize acute and long-term side effects of medications, by effective communication
  • To manage non-motor symptoms


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Therapeutic Choices:

No known cure and treatment is therefore largely symptomatic:

  • Dopaminergic
  • Non-dopaminergic agents
  • Non-pharmacologic interventions
  • Surgical



  • Interference with work, activities of daily living (ADL), or social and leisure function
  • Gait disturbance; falls
  • Patient's preferences-control of non-disabling but socially embarrassing condition such a tremor


Medication options/strategies:

There are a few options available for the treatment of Parkinson's. Of these, levodopa, may be the most efficacious, but the potential for developing disabling dyskinesias, often leads to trial of other agents, particularly in younger individuals. Consequently, there is no standardized approach with a "first line" treatment as such, and treatment is often individualized.



  • Dopamine replacement: Levodopa (highly effective and usual agent of choice for most)
  • Dopamine receptor agonist: Pramipexole, ropinirole
  • COMT inhibitors: Entacapone; extends the duration of action of levodopa
  • MAO-B inhibitors: Rasagiline, selegiline; for early monotherapy and as add-on to extend duration of action of levodopa



  • Anticholinergics: Benztropine; trihexyphenidyl-rarely used but may help tremor-dominant conditions
  • Antiglutaminergic: Amantadine (most helpful as treatment for dyskinesia but can have mild antiparkinsonian effects)


Other agents for non-motor symptoms:

  • Low dose atypical neuroleptic: (serotonin/dopamine antagonist): Quetiapine and clozapine (with CBC monitoring) for visual hallucinations and psychosis

NOTE: Typical neuroleptics e.g. haloperidol should not be used in PD due to risk of worsening motor function, atypical neuroleptics e.g. olanzapine and risperidone should be used cautiously.

  • Clonazepam/lorazepam-may be useful in associated sleep disorders e.g. REM sleep behaviour disorder (RBD), and anxiety
  • Antidepressants: Tricyclics and SSRI, for anxiety and depression
  • Melatonin-for insomnia, and RBD
  • Anticholinergics e.g. oxybutynin-for overactive bladder syndrome
  • Stool softeners and laxatives-for constipation
  • Analagesic use as required for musculoskeletal discomfort
  • Ipratropium spray, sublingual atropine drops-administered topically for drooling saliva


  • Rehabilitation with physical and occupational therapy to help improve functional outcomes in subjects with specific gait and balance problems
  • Emotional and psychological support of patient and family
  • Speech therapy for dysarthria
  • Adaptive strategies → adjustments in their homes to reduce the risk of falls and assist mobility; use of cane or walker when required
  • Providing resources about support groups, counsellors, societies


Deep brain stimulation (DBS)

  • Usually <70 years old; must be levodopa responsive and have no cognitive problems
  • Procedure is reversible
  • Adjustable for optimal benefit vs side-effects
  • Potential (infrequent) complications of DBS
    • Hemorrhage, ischemia, seizures, death in 1%
    • Dysarthria
    • Cognitive decline
    • Mood disturbances



Dopamine precursor/Dopamine decarboxylase inhibitor

  • Levodopa/Carbidopa
  • Levodopa/Benserazide
  • Levodopa/Carbidopa/Entacapone



  • Dopamine replacement therapy
  • Carbidopa and Benserazide inhibit peripheral breakdown of Levodopa (L-Dopa) by inhibiting decarboxylation, thereby increasing availability of L-Dopa to cross the blood brain barrier (BBB)
  • Within the basal ganglia L-Dopa is then converted to dopamine




Immediate Release (100/10; 100/25; 250/25)

  • Start 100/10 mg or 100/ 25 mg PO ½-1 tab TID; Adjust dose according to response, increase 100/25 mg (1 tablet) PO every 7 days or 250/25 mg (1/2-1 tablet) PO every 7 days
  • Most will get benefit with 400-600 mg levodopa. No maximum dose but unusual to require >2 g/d

Extended release (100/25; 200/50)

  • Can use instead of IR however no real advantage as slower, less predictable time of onset. Maybe useful at bedtime for nocturnal akinesia
  • Start 200/50 mg PO BID, then adjust dose according to response, increase dose by 0.5-1 tab/day every 3 days giving dose interval of at least 4-8 hours during the waking day; Max. 600 mg/2400 mg/day

Levodopa/Benserazide (50-12.5; 100-25; 200-50)

  • 100/25 mg PO once daily or BID; May increase every 3-4 days until optimal effect is achieved; optimal dosage 400/100 mg to 800/200 mg/day divided into 4-6 doses
  • Note:
  • May use 200/50 mg form for maintenance therapy once the optimal dosage has been determined
  • May use 50-12.5 mg form when frequent dosing is required to minimize adverse effects

Caveat: Simultaneous ingestion of L-dopa with high protein meals could decrease absorption and may impact on efficacy

Anti-Parkinson's agent/COMT inhibitor

  • Entacapone



  • Reversible and selective inhibitor of peripheral catechol-O-methyltransferase (COMT)
  • When administered with Levodopa, it decreases the peripheral degradation of Levodopa via the COMT mediated pathways, leading to more sustained Levodopa serum levels
  • Enhanced serum concentrations of L-Dopa increases availability for traversing the blood-brain barrier




  • 200 mg PO with each dose of Levodopa/Carbidopa or Levodopa/Benserazide, Maximum up to 8 times/day (1600 mg/day)
  • Note: May require an average decrease of 25% in the daily Levodopa dose if patient is taking Levodopa ≥800 mg/day or had moderate-to-severe dyskinesias before beginning therapy


Combination Therapy:

Anti-Parkinsonian dopaminergic agent

  • Levodopa/Carbidopa/Entacapone



  • Dopamine replacement therapy/Catechol-O-methyltransferase (COMT)



Caribodopa/Levodopa/Entacapone (Stalevo)

  • Therapy should be individualized and adjusted according to the desired therapeutic response
  • The combination is supplied as tablets in 6 different strengths

Light box-4-Parkinson Disease-Medication-Stalevo Dosage Forms


Anti-Parkinson's agent/Monoamine oxidase (MAO) B inhibitor

  • Selegiline
  • Rasagiline



  • Selective irreversible Monoamine Oxidase B (MAO-B) Inhibitors
  • Inhibition of MAO-B prevent breakdown of dopamine
  • May also increase dopaminergic activity by interfering with dopamine reuptake at the synapse




  • Starting dose 2.5 mg PO BID, then 5 mg PO BID daily with meals. Maintenance dose 5 mg PO BID


  • Oral 1 mg once daily; may have to reduce levodopa dose if taken concurrently


Anti-Parkinson's agent, Dopamine agonist

  • Pramipexole
  • Ropinirole



  • Activates postsynaptic dopamine receptors in the striatum and substantia nigra
  • Longer duration of action compared to levodopa
  • No effect of food on absorption via GI tract




Immediate release form

  • Initial 0.125 PO TID; may increase dose gradually every 5-7 days; usual range 1.5-4.5 mg/day divided TID; Max. 4.5 mg/day
  • Renal impairment
    • Clcr 35-59 mL/minute: Initial: 0.125 mg BID; Max 1.5 mg BID
    • Clcr 15-34 mL/minute: Initial: 0.125 mg once daily; Max.1.5 mg once daily

Extended release form-(USA)

  • Initial: 0.375 mg PO once daily; increase gradually to 0.75 mg once daily; Max. 4.5 mg once daily
  • Renal impairment:
    • Clcr >50 mL/min no dose adjustment required
    • Clcr 30-50 mL/min: Initial: 0.375 mg every other day; may increase to 0.375 mg/dose after 1 week and every week as required; Max: 2.25 mg once daily


Immediate release form

  • 0.25 mg PO (TID); increase by 0.25 mg/dose every 7 days; daily dose may be increased by 0.5 to 1.0 mg/dose after a month until a desired response is achieved; Max. 24 mg/day


Anti-Parkinson's agent/NMDA receptor inhibitor

  • Amantadine



Possibly enhances dopamine action by:

  • Blocking the reuptake of dopamine into presynaptic neurons or by increasing dopamine release from presynaptic fibers
  • Reduces levodopa-induced dyskinesia by antagonism of NMDA glutamate receptors




  • Usual dose 100 mg PO BID; Max. 400 mg/day in divided dose
    • Note: Start 100 mg/day once daily in Patients taking another anti-Parkinson drug or debilitated; may increase dose to 100 mg twice daily after 1-2 weeks, if needed
  • Renal impairment:
    • Clcr 30-50 mL/min: 200 mg on day 1, then 100 mg PO once daily
    • Clcr 15-29 mL/min: 200 mg on day 1, then 100 mg PO every other day
    • Clcr <15 mL/min: 200 mg every week

Anti-Parkinson's agent/Anticholinergic agent

  • Benztropine
  • Trihexyphenidyl



  • Possesses both anticholinergic and antihistaminic effects
  • May also inhibit reuptake and storage of dopamine, thereby prolonging the synaptic action of dopamine




  • 0.5-1 mg PO/IM/IV once daily at night; increase dose every 5-6 days; usual dose 1-2 mg/day in two divided doses; Max. 6 mg/da


  • 1 mg PO QID on first day; then increase by 2 mg every 3-5 days; usual dose 6-10 mg/day in divided doses; Max. 15 mg/day


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Clinical Trials:
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Pipeline Agents:
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Pharmacist Resources:

Disease has a slow and chronic course. A Pharmacist will have frequent encounters the patients and/or their caregiver(s)

1. Tips for patient care


  • Encourage patients to:
    • Exercise and adopt a healthy life style
    • Keep follow-up appointments with their neurologist
    • Maintain regular activity but avoid overwork and fatigue
    • Remain mentally active (intellectual games-crosswords, sudoko etc.)
  • Patients with PD who have sudden onset of sleep (usually medication induced) should be cautioned about driving


  • Compliance is necessary to achieve treatment benefit, it is essential to consider patient, families and caregivers expectation because side effects are the main reason for non-adherence to medications
  • Most drug therapy is required when symptoms interfere with everyday life
  • Evaluate cost and affordability and insurance coverage for patients
  • Consider lower starting doses in elderly patients and debilitated patients
  • Vigilance about medication interactions is important
  • Encourage patients to establish prescribed routine for pill-taking
  • Ensure dosing changes are gradual rather than abrupt
  • Enquire about swallowing difficulties and offer alternatives when patients begin to have difficulty with oral medications
  • Advise patients to use medications as prescribed and to ask before crushing prescription medications
  • Psychosis is usually drug induced in patients with Parkinson's disease; remember to consider reversible causes such as intercurrent infections etc.
  • Be aware of dopamine agonist adverse effects, such as obsessions relating to hypersexuality, pathological gambling etc
  • Child proof closures and blister packs may present challenges for the PD patient, this issue should promptly resolved by the pharmacist
  • With prescribed therapy, consider concurrent risk factors and disease states

Unlabelled/Alternate uses include but are not limited to

  • Selegiline
    • Attention-deficit/hyperactivity disorder (ADHD)
  • Levodopa /Caribodopa
    • Restless leg syndrome
    • Dopamine agonists-Restless leg syndrome (RLS)


  • Ensure patient, family and/or care givers are well informed about disease and its management
  • Include family or social support in lifestyle modification
  • Physical and occupational therapy should be available for people with PD
  • Patient and family should be made aware of local support groups as well as online information, eg from :
    • Canadian Parkinson's Society
    • National Parkinson's Foundation
    • National Institute of Neurologic Disorders and Stroke
    • The Michael J. Fox Foundation for Parkinson's Research
  • Families and caregivers should be made aware of the potential for patients impulsive behaviour which could be partly due to denial/ or embarrassment, and/or medication side effects
  • Depression, psychosis and dementia are common in PD patients, should be discussed with the family or the caregivers
  • Some patients experience GI problems, cognitive impairment, sleep disturbances-these issues should be discussed with the patient, and advise accordingly


As the disease progresses patients and families need to be aware of:

  • Fall risk-encourage the use of canes and walkers where appropriate
    • Remove rugs and avoid uneven floors
  • Near end stage PD be aware of
    • Aspiration risk and ensuing pneumonia
    • Bedsores (due to immobility)
    • Hypotension, autonomic dysfunction-investigate and treat
  • Medications should be instituted if symptoms are interfering with daily activities
  • Be aware of impulse control disorder (abnormal behaviours, such as hypersexuality, pathological gambling, compulsive eating (usually sweets) that can occur in up to 15% of patients treated with a dopamine agonist
    • - People at risk are younger, male, often with preexisting or family history of addiction.


  • Assess adherence at each visit
  • Treatment should be titrated slowly to avoid unnecessary side effects
  • Speech therapy may be helpful in those with dysarthria
  • Treatment of anxiety, depression and sleep disturbances with appropriate medications may be beneficial

Expected outcome

  • Highly variable and unpredictable


2. Scales and Tables:


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Core Resources:

  • Brust JCM (2007) Current Diagnosis and Treatment (Neurology) (2nd ed.) New York: McGraw Hill
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al (eds). Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Grimes D, Gordon J, Snelgrove B. et al. Canadian Guidelines on Parkinson's Disease. Can J Neurol Sci. 2012;39: S1-S30
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Rowland LP et al. (2010) Merritt's Neurology (9th ed.) Philadelphia: Lippincoot Williams and Wilkins
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011
  • National Collaborating Centre for Chronic Conditions. Parkinson's disease: national clinical guideline for diagnosis and management in primary and secondary care. London: Royal College of Physicians, 2006


Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates


Journals/Clinical Trials:

  • Block, G, Liss, C, Reines, S, et al. Comparison of immediate-release and controlled-release carbidopa/levodopa in Parkinson's disease: A multicenter 5-year study. Eur Neurol 1997; 37:23
  • Emre M, Aarsland D,Albanese A, Rivastigmine for Dementia Associated with Parkinson's Disease N Engl J Med 2004; 351:2509-2518
  • Fahn, S, Bressman, SB.Should levodopa therapy for Parkinsonism be started early or late? Evidence against early treatment. Can J Neurol Sci 1984; 11:200
  • Galpern WR, Lang, AE Interface between tauopathies and synucleinopathies: A tale of two proteins. Ann Neurol 2006; 59:449-458
  • Hauser RA, Cantillon M, Pourcher E et al. Preladenant in patients with Parkinson's disease and motor fluctuations The Lancet Neurology 2011; 10: 221-229
  • Hauser, RA, McDermott, MP, Messing, S. Factors associated with the development of motor fluctuations and dyskinesias in Parkinson disease. Arch Neurol 2006; 63:1756
  • Kumar, N, Van Gerpen, JA, Bower, JH, Ahlskog, JE. Levodopa-dyskinesia incidence by age of Parkinson's disease onset. Mov Disord 2005; 20:342
  • Marks MJ, Bartus RT, Siffert J et al. Gene delivery of AAV2-neurturin for Parkinson's disease The Lancet Neurology 2010; 9: 1164-1172
  • Mizuno Y, Hasegawa K, Kondo T et al. Clinical efficacy of istradefylline (KW-6002) in Parkinson's disease Mov Disord. 2010; 25:1437-43
  • Olanow C W, Rascol O, Hauser R, et al, A Double-Blind, Delayed-Start Trial of Rasagiline in Parkinson's Disease ADAGIO Study Investigators N Engl J Med 2009; 361:1268-1278
  • Postuma, RB, Lang, AE. Homocysteine and levodopa: should Parkinson disease patients receive preventative therapy? Neurology 2004; 63:886
  • Rascol O, Brooks DJ, Korczyn AD, et al, A Five-Year Study of the Incidence of Dyskinesia in Patients with Early Parkinson's Disease Who Were Treated with Ropinirole or Levodopa. 056 Study Group.N Engl J Med 2000; 342:1484-1491
  • Shrivastava A The hot cross bun sign Radiology 2007, 245: 606-607
  • The Parkinson Study Group CALM Cohort Investigators. Long-term effect of initiating pramipexole vs levodopa in early Parkinson disease Arch Neurol 2009; 66:563-70
  • The Parkinson Study Group. Levodopa and the Progression of Parkinson's Disease N Engl J Med 2004; 351:2498-2508
  • The Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson's disease in DATATOP patients requiring levodopa. Ann Neurol 1996; 39:37-45
  • Williams A, Gill S, Varma T, et al, for the PD SURG Collaborative Group Deep brain stimulation plus best medical therapy versus best medical therapy alone for advanced Parkinson's disease (PD SURG trial) The Lancet Neurology 2010; 9:581-591


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Susan Fox, MB ChB, MRCP (UK), PhD, Associate Professor of Neurology, University Health Network, Toronto Western Hospital, University of Toronto
.......................................... PHARMACY REVIEWER:
Tejal Patel, B.Sc.(Pharm), Pharm.D., Clinical Assistant Professor, School of Pharmacy, University of Waterloo, ON Canada

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