Parkinson's disease

Introduction
o Parkinson’s disease (PD) is a common neurodegenerative disorder with unknown cause.
o There is progressive loss of dopamine secreting cells of the pars compacta in the substantia nigra, a structure in the midbrain.
o These dopamine-producing cells in this midbrain structure project to the striatum of the basal ganglia forming neural circuits that regulate movement.
o Cell loss in thought to be due to neuronal cell inclusions called Lewy bodies.
o PD has a 1% worldwide prevalence and is associated with old age (mean age of onset is 65 years).
o
Presentation
o The triad of cardinal motor symptoms seen in PD is rigidity, bradykinesia and tremor. These worsen as the disease progresses.
o Motor signs and symptoms
• Triad
• Postural instability (characteristic shuffling gait with poor arm swing)
o Neuropsychiatric symptoms
• Depression
• Dementia
• Hallucinations
• Impulsive behaviours
o Autonomic symptoms
• Constipation
• Excess sweating
o Other signs and symptoms
• Fatigue
• Dysarthria
History
o Is there a family history of PD?
o Onset of symptoms? – rapid onset suggests an atypical parkinsonism
o Previous jobs (mining or wielding)? – chronic exposure to metals may cause a Parkinsonism syndrome.
o History of an inborn error of metabolism (e.g. Haemachromatosis) suggestive of a Parkinsonism syndrome.
o History of significant traumatic brain injury?
o History of encephalitis?
o History of strokes?
o Currently on neuroleptic treatment?
Examination
o Full neurological examination findings
• Increased tone
• Cogwheel rigidity
• Tremor (4-7hz)
• Micrographia
• Hypomimia
• Hypophonia
• Shuffling, festinating gait with stooped posture.
• Poor coordination
Radiological investigations
o The following are only performed if atypical features are present. The diagnosis of PD is based off the clinical history and examination.
o Magnetic Resonance Imaging (MRI) brain – normal in PD
o Functional imaging (123I-FP-CIT SPECT) – decreased basal ganglia (putaminal) pre-synaptic dopamine uptake
Management
o Patients with suspected to have PD should be referred to a neurologist quickly and untreated.
o If mild disease patients should be seen in 6 weeks, and in 2 weeks if complex and severe.
o Appropriate information should be given to patient and family, the patient should notify the DVLA of their condition.
o A multidisciplinary team comprising: a specialist nurse; physiotherapist; GP; occupational therapist; speech and language therapy; and neurologist should be involved in the care for the PD patients
o PD patients should be reviewed every 6-12 months by their neurologists.
o Physiotherapy should be available for PD patients to improve gait and movement and ultimately increase functional independence.
o Speech and language therapy for PD patients to improve the quality of speech and ensuring effective means of communication despite disease progression.
o The pharmacological treatment and dose is tailored to each PD patient.
o Similar medications are used in the early and late phase of the disease
o Early phase:
• Carbidopa/Levodopa – initially 50mg orally t.d.s. Then increase by 50-100mg/day increments every week till there is a response
• Dopamine agonists (non-ergot-derived agonist) – oral ropinirole 0.25mg t.d.s. Then increase by 0.25mg/dose for 3 weeks till response. After 3 week increase by 0.5mg/dose till 9mg/day dose. Finally increase by 1mg/dose at weekly intervals. Maximum dose is 24mg/day.
• Monoamine oxidase B inhibitors – oral rasagiline 1mg o.d.
• Beta-adrenergic antagonsists (beta-blockers)
• Amantadine – 100mg orally o.d. increase to 100mg b.d. (maximum 400mg/day)
• Anticholinergics
o Late phase (dose as per early phase):
• Modified-release levodopa – specialist guidance
• Dopamine agonists
• Monoamine oxidase B inhibitors
• Catechol-O-methyl transferase inhibitors – entacapone 200mg orally with each dose of carbidopa/levodopa (maximum 1600mg/day)
• Amantadine – 100mg orally o.d. for 1 week. Then increase to 100mg b.d. (maximum 400mg/day)
• Apomorphine – specialist guidance
o Surgical management in the form of bilateral subthalamic nucleus (STN) or globus pallidus interna (GPi) stimulation in indicated if:
• Motor complication are refractory
• No clinically significant mental health problems
• No comorbidities
• Levodopa responsive
o The need for palliative care should be assessed throughout all stages of the disease.
Complications
o Long term:
• Dementia
• Psychosis
• Depression
• Levodopa-induced dyskinesias
• Poor impulse control
• Motor fluctuations

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