17. PARKINSONISM

Parkinsonism is a clinical syndrome defined by bradykinesia (slowness of movement) plus at least one of the following: tremor, rigidity or postural instability. All patients with Parkinson’s disease have parkinsonism, but not all parkinsonism cases are Parkinson’s disease.

Classification

1. Primary Parkinsonism

Also known as idiopathic Parkinson’s disease or paralysis agitans. It is a degenerative disorder without a known external cause.

2. Secondary (Symptomatic) Parkinsonism

Occurs due to an identifiable cause:

  • Post-encephalitic states
  • Toxins: MPTP, manganese, carbon monoxide
  • Drugs: reserpine, metoclopramide, phenothiazines, haloperidol, methyldopa
  • Vascular parkinsonism
  • Tumours in basal ganglia
  • Punch-drunk syndrome (in boxers)
  • Infections like HIV or influenza

3. Parkinsonism-Plus Syndromes

These are degenerative disorders that show extra neurological features beyond typical parkinsonism:

  • Progressive supranuclear palsy
  • Multiple system atrophy (MSA) – includes MSA-P, Shy–Drager syndrome, and MSA-C
  • Diffuse Lewy body disease
  • Wilson’s disease
  • Huntington’s disease (in children)

Pathology of Primary Parkinsonism

Parkinson’s disease occurs due to:

  • Loss of pigmented neurons in substantia nigra and locus coeruleus
  • Presence of Lewy bodies in affected neurons
  • Degeneration of the nigrostriatal dopamine pathway

The major chemical problem is depletion of dopamine in the striatum. Non-dopaminergic neurons also degenerate later, causing non-motor symptoms.

Clinical Features

General

  • More common after age 50–60
  • Early features: tiredness, muscle aches, unilateral slowness, depression

Tremors

  • Typical resting tremor (“pill-rolling”)
  • Decreases with voluntary movement
  • Often starts unilaterally
  • Can involve hands, jaw, head or legs

Rigidity

  • Increased muscle tone (lead-pipe rigidity)
  • With tremor, it becomes cogwheel rigidity

Hypokinesia / Akinesia

Difficulty starting movements, slowness, and reduced automatic movements.

Bradykinesia

  • Slowness in voluntary movements
  • Reduced arm swing while walking
  • Expressionless “mask-like” face
  • Handwriting becomes small (micrographia)

Postural Instability

  • Appears later, usually after 5 years
  • Stooped posture, tendency to fall
  • Shuffling gait and difficulty turning

Non-Motor Symptoms

  • Urinary urgency or retention
  • Constipation
  • Erectile dysfunction in males
  • Depression, sleep problems
  • Cognitive decline in later stages

Diagnosis

Diagnosis is clinical; no definitive test confirms Parkinson’s disease.

The acronym TRAP helps recall the four main features:

  • Tremor at rest
  • Rigidity
  • Akinesia / bradykinesia
  • Postural instability

Additional tests are used if symptoms are atypical:

  • Blood tests for Wilson’s disease (serum copper, ceruloplasmin)
  • CT or MRI for other causes
  • PET or SPECT in complex cases

Management

Treatment aims to control symptoms and improve quality of life.

General Measures

  • Stop any offending drug causing symptoms
  • Physiotherapy and occupational therapy
  • Home adjustments to reduce falls

Drug Therapy

1. Anticholinergics

Trihexyphenidyl, benzhexol, orphenadrine.

  • Useful mainly for tremors
  • Not preferred in elderly
  • Side effects: urinary retention, glaucoma, confusion

2. Amantadine

Mild antiparkinsonian effect; helps early in disease or combined with L-dopa.

Side effects: psychosis, edema, mottled skin (livedo reticularis).

3. Levodopa (L-dopa)

  • Most effective for bradykinesia and rigidity
  • Combined with carbidopa or benserazide to prevent peripheral breakdown
  • Started at low doses and increased slowly
  • High doses may cause dyskinesias and hallucinations

Long-term issues include:

  • Wearing-off effect
  • Peak-dose dyskinesia
  • On–off phenomenon

4. Dopamine Agonists

Ergot-derived: bromocriptine, pergolide.
Non-ergot: pramipexole, ropinirole, rotigotine, apomorphine.

  • Prefer non-ergot agents due to fewer serious side effects
  • Can cause impulse-control disorders (gambling, overeating) and sleepiness

5. MAO-B Inhibitors

Selegiline, rasagiline.

  • Reduce dopamine breakdown
  • May slow neuronal degeneration
  • Used early in disease

6. COMT Inhibitors

Tolcapone, entacapone.

  • Increase levodopa availability
  • Useful in fluctuation phases

7. Rivastigmine

Used in patients with dementia.

Surgical Treatment

  • Deep brain stimulation (subthalamic nucleus or globus pallidus) is used in severe cases.
  • Thalamotomy is rarely used today due to drug effectiveness.

Detailed Notes:

For PDF style full-color notes, open the complete study material below:

Share your love