Extrapyramidal Side Effects

EXTRAPYRAMIDAL SIDE EFFECTS

• Caused by antipsychotics.
• • More common with high-potency typical antipsychotics (compared to atypical antipsychotics).
• Various movement disorders caused are collectively referred to as “extrapyramidal symptoms/extrapyramidal side effects”.

Mechanism:

• Due to dopamine receptor blockade in nigrostriatal tract (neural pathway from substantia nigra to striatum).

TYPES OF MOVEMENT DISORDERS:

• Acute dystonia.
• Acute akathisia
• Drug-induced parkinsonism
• Tardive dyskinesia
• Neuroleptic malignant syndrome

1. Acute dystonia:

• Earliest side effect.
• Occurs within minutes (more with injectable antipsychotic).

Features:

• Characterized by sudden contraction of muscle group –
• Symptoms like torticollis, trismus (contraction of jaw muscles), eyeballs deviation (oculogyric crisis due to extraocular muscle contraction) & laryngospasm.

Management:

• Immediate administration of parenteral anticholinergicsa (benztropine, promethazine or diphenhydraminea).
• Prevent prophylactic use of oral anticholinergics during typical antipsychotics prescription.

2. Acute akathisia:

• Commonest side effect of antipsychotics.

Features:

• Characterized by an inner sense of restlessness along with objective.
• Observable movements (fidgeting of legs, pacing around, inability to sit or stand in one place for a long time).

Management:

• Beta-blockers (propranolol DOC)
• Anticholinergics
• Benzodiazepines.
• Prevented by changing to 2nd generation or low potency 1st-generation antipsychotics (lesser incidence of akathisia).

3. Drug induced parkinsonism:

Features:

• Characterized by triad – Rigidity, bradykinesia & resting tremors.

Management:

• Anticholinergics.
• Changing to 2nd gen. antipsychotics or low-potency 1st gen. antipsychotics.
• Dose reduction can be tried.
• Prevented by prophylactic anticholinergic use.

4. Tardive dyskinesia:

5. Neuroleptic malignant syndrome: 

• Fatal side effect of antipsychotics.

Features: 

• Characterized by,
• • Muscle rigidity.
  • Elevated temperature (greater than 38°C). Increased CPK (creatine phosphokinase) levels.

Other symptoms: 

• Diaphoresis, tremors, confusion, autonomic disturbances, liver enzyme elevation & leukocytosis.

Mechanism: 

• D2 antagonism at various levels.
• D2 receptors blockade in corpus striatum→ Causes muscle contraction & rigidity → Initiating heat generation.
• Continuing muscle damage→ Result in myoglobinuria & renal failure.
• D2 receptors blockade in hypothalamus interferes with heat regulation.
• D2 receptors blockade of spinal neurons causes autonomic disturbances.
  • Increased CPK indicates muscle injury.

Management:

• Early recognition of symptoms & prompt withdrawal is paramount importance.

Treatment:

• Skeletal muscle relaxants (dantrolene).
• Dopamine agonists (amantadine & bromocriptine).

Supportive measures:

• Adequate hydration.
• During antipsychotics treatment is restarted – 2nd gen. antipsychotics should be used.

NOTE: ALL EXTRAPYRAMIDAL SIDE EFFECTS ARE ALSO CAUSES BY ATYPICAL ANTI-PSYCHOTICS BUT WITH LESSER INCIDENCE.

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