Extrapyramidal Symptoms (EPS) are a collection of movement-related side effects that can occur with certain medications, most frequently antipsychotic drugs. Prescribed for a range of psychiatric conditions, these drugs can cause symptoms that are not related to the brain’s pyramidal tracts, which control voluntary motor functions. Instead, they originate in the extrapyramidal system, which modulates movement.
The Neurological Basis of EPS
Antipsychotic medications function by interacting with neurotransmitters in the brain, with a focus on dopamine. Dopamine is a chemical messenger that helps regulate movement, acting like a traffic controller for nerve signals. The therapeutic effect of antipsychotics comes from their ability to reduce dopamine activity in specific brain pathways to manage psychosis.
This reduction is achieved through dopamine receptor blockade, where the medication occupies receptors on nerve cells, preventing dopamine from transmitting its signal. While beneficial for psychosis, this action is not perfectly targeted. The blockade can also occur in the nigrostriatal pathway, a part of the brain integral to the extrapyramidal system and motor function.
When dopamine signaling is dampened in this motor pathway, the regulation of movement is disrupted. The flow of information for smooth muscle function becomes irregular, leading to the involuntary movements recognized as EPS. The effects are dose-dependent, meaning the likelihood of experiencing them often increases with higher doses of the medication.
Classification of Extrapyramidal Symptoms
Extrapyramidal symptoms are categorized into several distinct types, each with a unique presentation.
- Acute dystonia involves sudden, involuntary, and sustained muscle contractions that can lead to abnormal postures or repetitive movements. It often affects the muscles of the neck, causing the head to twist to one side, the jaw, or the eyes, and typically appears within hours or days of initiating treatment.
- Akathisia is characterized by a profound inner feeling of restlessness and a compelling urge to be in constant motion. Individuals with akathisia may feel unable to sit still, constantly pacing, shifting their weight, or crossing and uncrossing their legs.
- Drug-induced parkinsonism mimics the symptoms of Parkinson’s disease. This includes a resting tremor, rigidity where muscles become stiff and resistant to movement, and bradykinesia, a noticeable slowness of movement.
- Tardive dyskinesia (TD) is a delayed-onset disorder that can appear after months or years of treatment. It is characterized by involuntary, repetitive movements, most commonly affecting the face, lips, and tongue, and can sometimes persist even after the medication is discontinued.
Medication Types and EPS Risk
The risk of developing EPS is not the same for all antipsychotics. These medications are divided into two main classes, first-generation and second-generation, with differing mechanisms that influence their side effect profiles.
First-generation antipsychotics (FGAs), also known as typical antipsychotics, include medications like haloperidol and chlorpromazine. They are potent blockers of the D2 dopamine receptor. This strong, non-selective blockade is effective for psychosis but also gives them a higher propensity to cause EPS.
Second-generation antipsychotics (SGAs), or atypical antipsychotics, include drugs such as risperidone and olanzapine. SGAs interact with dopamine receptors more loosely and also affect serotonin receptors. This dual action is why they carry a lower risk of causing most extrapyramidal symptoms compared to FGAs.
A lower risk does not mean no risk. While SGAs are less likely to cause dystonia and parkinsonism, some can still be associated with akathisia. They also carry their own set of potential side effects, such as metabolic changes leading to weight gain.
Managing and Treating EPS
When extrapyramidal symptoms occur, they are manageable through several clinical strategies. The approach is tailored to the specific type of symptom and the individual’s overall treatment plan.
A primary strategy is to adjust the medication regimen. This could involve lowering the dose of the antipsychotic. If symptoms persist, a clinician may switch from a high-risk medication, like an FGA, to an SGA with a lower EPS risk profile to alleviate side effects while maintaining psychiatric control.
In many cases, other medications are prescribed to counteract the EPS. For acute dystonia and parkinsonism, anticholinergic drugs like benztropine are frequently used to restore the balance between dopamine and acetylcholine. For akathisia, beta-blockers such as propranolol are often effective.
Continuous monitoring is a standard part of care for anyone taking antipsychotic medication. Regular check-ins allow doctors to screen for the early emergence of any abnormal movements. Patients should report any new or unusual physical symptoms to their doctor immediately for timely intervention.