Introduction Drug-induced parkinsonism (DIP) is a form of parkinsonism caused by medications that block dopamine receptors or deplete dopamine levels in the brain. Unlike idiopathic Parkinson’s disease, drug-induced parkinsonism is often reversible once the offending medication is identified and discontinued. However, early recognition is crucial to prevent long-term complications.

Causes of Drug-Induced Parkinsonism

Certain medications, particularly those that interfere with dopamine pathways, can lead to drug-induced parkinsonism. The most common culprits include:

1. Antipsychotic Medications (Neuroleptics) – Dopamine D2 Blockers

• Typical Antipsychotics: Haloperidol, Chlorpromazine, Fluphenazine
• Atypical Antipsychotics (in high doses): Risperidone, Olanzapine, Aripiprazole

2. Anti-Nausea and Gastrointestinal Drugs

• Metoclopramide (commonly prescribed for nausea and vomiting)
• Prochlorperazine (used for vertigo and dizziness)

3. Calcium Channel Blockers

• Flunarizine and Cinnarizine are known to induce parkinsonism, especially in elderly individuals.

4. Mood Stabilizers and Antiepileptic Drugs

• Lithium, Valproate (rare but reported).

5. Other Drugs

• Amiodarone (cardiac medication)
• Certain antidepressants, particularly older tricyclics.

Risk Factors

Individuals at higher risk of developing DIP include:

• Elderly patients
• Those with a family history of Parkinson’s disease
• Individuals taking high doses or prolonged courses of dopamine-blocking medications
• Women are more susceptible than men

Symptoms of Drug-Induced Parkinsonism

DIP symptoms closely mimic those of idiopathic Parkinson’s disease and typically emerge weeks to months after initiating the offending medication. Common symptoms include:

• Bradykinesia (slowness of movement)
• Rigidity (muscle stiffness)
• Resting Tremors (less common in DIP compared to Parkinson’s disease)
• Postural Instability
• Facial Masking (reduced facial expression)
• Shuffling Gait

Unlike idiopathic Parkinson’s disease, drug-induced parkinsonism is often symmetrical (affecting both sides of the body equally).

Diagnostic Approach

• Clinical History: Identifying recent medication changes is crucial in diagnosing DIP.
• Drug Withdrawal Test: Improvement of symptoms after stopping the suspected medication helps confirm the diagnosis.
• Dopamine Transporter (DaT) Scan: A normal DaT scan differentiates DIP from true Parkinson’s disease, where dopamine transporter loss is evident.

Management of Drug-Induced Parkinsonism

1. Medication Discontinuation:
   • Gradually tapering or discontinuing the offending drug often results in symptom reversal.
2. Switching Medications:
   • Substituting the problematic drug with a safer alternative that has minimal dopamine-blocking effects.
3. Symptomatic Treatment:
   • Levodopa or dopamine agonists are generally avoided unless symptoms persist after discontinuing the offending drug.
4. Physical Therapy:
   • Exercises to improve gait, balance, and muscle strength can accelerate recovery.
5. Monitoring and Follow-up:
   • Regular follow-up is essential, as symptoms may take weeks to months to fully resolve.

Prognosis

• In most cases, DIP symptoms improve within 1 to 6 months after stopping the causative drug.
• However, some individuals, particularly older adults or those with underlying neurological vulnerabilities, may develop persistent parkinsonism.

Prevention Strategies

• Avoiding unnecessary use of dopamine-blocking drugs.
• Prescribing the lowest effective dose for the shortest duration possible.
• Regularly monitoring high-risk individuals for early symptoms of DIP.

Conclusion

Drug-induced parkinsonism is a potentially reversible condition that mimics Parkinson’s disease. Prompt recognition and withdrawal of the offending medication are key to successful recovery. Healthcare providers should remain vigilant in monitoring patients on dopamine-blocking medications, particularly older adults and those with risk factors, to ensure timely intervention and improved outcomes.