Parkinsonism

Clinical assessment

Diagnosis is primarily clinical, based on presence of bradykinesia PLUS at least one of tremor or rigidity. Unilateral onset and good response to levodopa strongly support Parkinson's Disease. Careful history needed to identify potential secondary causes (drugs, toxins, infections, stroke). Examination assesses for cardinal features, gait, balance, and non-motor symptoms. Look for features atypical for PD (e.g., early falls, symmetry, poor levodopa response, prominent autonomic failure or dementia early) which might suggest secondary cause or Parkinson-Plus syndrome.

Investigations

• Usually no specific diagnostic test for Parkinson's Disease.
• Response to Levodopa trial can be diagnostic for PD.
• Neuroimaging (MRI Brain): Usually normal in PD, but helpful to exclude secondary causes (stroke, tumor, hydrocephalus).
• Blood tests: To rule out mimics or secondary causes (e.g., thyroid function, copper studies for Wilson's disease - rare).
• Consider DaTscan (SPECT imaging) in specialist centers to assess dopamine transporter levels (can help differentiate PD from essential tremor, but not PD from Parkinson-Plus syndromes).

Diagnostic criteria

UK Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria commonly used: Step 1 (Parkinsonism): Bradykinesia + (Rigidity or Resting Tremor). Step 2 (Exclusion criteria for PD). Step 3 (Supportive criteria for PD - e.g., unilateral onset, persistent asymmetry, excellent levodopa response).

Non-pharmacological management

• Patient and family education and support.
• Physiotherapy: Crucial for gait training, balance exercises, stretching, improving mobility and preventing falls.
• Occupational Therapy: Strategies for adapting daily activities, home safety assessment.
• Speech Therapy: For hypophonia (voice exercises) and dysphagia.
• Exercise: Regular physical activity is highly beneficial.
• Nutritional advice (manage constipation, ensure adequate intake).
• Psychosocial support, management of depression/anxiety.

Pharmacological treatment

• Symptomatic Treatment (Primarily replaces/mimics dopamine):
• - Levodopa (usually combined with a peripheral decarboxylase inhibitor like Carbidopa or Benserazide): Most effective drug for motor symptoms of PD. Start low, titrate slowly based on response and side effects. Example: Levodopa/Carbidopa 100/10mg or 100/25mg, start ½ or 1 tab TID, increase gradually. Side effects: Nausea, vomiting, orthostatic hypotension, confusion, hallucinations, motor fluctuations (wearing-off, dyskinesias) with long-term use. (H/RR level initiation).
• - Dopamine Agonists (e.g., Pramipexole, Ropinirole): Can be used as initial therapy (esp. younger patients) or adjunct to levodopa. Less potent motor effect than levodopa, higher risk of non-motor side effects (somnolence, impulse control disorders, hallucinations).
• - MAO-B Inhibitors (e.g., Selegiline, Rasagiline): Mild symptomatic effect, may delay need for levodopa or reduce levodopa dose.
• - COMT Inhibitors (e.g., Entacapone): Used with levodopa to reduce 'wearing-off' time.
• - Amantadine: Mild benefit for tremor, bradykinesia, rigidity; also helps levodopa-induced dyskinesias.
• Management of Drug-Induced Parkinsonism:
• - Stop or reduce dose of offending drug if possible.
• - Anticholinergic drugs: Benzhexol (Trihexyphenidyl) 2-15 mg daily in divided doses (start 1mg/day, increase slowly). Primarily helps tremor and rigidity. Side effects limit use, especially in elderly (confusion, dry mouth, constipation, urinary retention, blurred vision). Use cautiously, monitor closely.
• Follow specific Ugandan treatment algorithms/guidelines.

Monitoring

Monitor motor symptoms (UPDRS scale if possible), functional status, non-motor symptoms. Monitor response to medication and side effects (nausea, hypotension, dyskinesias, hallucinations, impulse control issues). Assess for falls risk. Monitor caregiver burden.