Detection, Prevention, and Management of Extrapyramidal Symptoms

Tamra Jean Courey,MSN

Disclosures

Journal for Nurse Practitioners. 2007;3(7):464-469. 

In This Article

Pathophysiology

EPSs are commonly attributed to the sensitive connection between the APM, also known as the neuroleptic, and the dopamine D2 receptor-blocking properties.[2] The term neuroleptic implies holding the neuron, designating the seriousness of the side effects produced from the APM.[1] It is theorized that administering APMs, which are D2 antagonists, initiates blockage of dopamine receptors in the basal ganglia, thus creating a reduction of dopamine responses to the brain.[1,4] This reduction can generate alteration in a person's movement and functioning, thus resulting in EPSs. Although there are significant pathophysiologic changes in dopaminergic activity, fluctuations in other neurotransmitters such as serotonin, norepinephrine, and acetylcholine may also contribute to the symptoms.[4] Two classifications of APMs are involved in blockage of dopamine transmission, the first and second generation.

Traditional first-generation APMs ( Table 1 ), were first introduced in the 1950s to help regulate the activity of dopamine and to reduce the symptoms of many psychiatric illnesses, including schizophrenia.[5,6] These medications diminish the florid psychotic symptoms of schizophrenia, while reestablishing normalcy of thought, mood, and behavior. The main deterrent for adherence to these medications is their potential to induce a range of damaging side effects, including anticholinergic symptoms, cardiovascular effects, neuroleptic malignant syndrome, and EPSs.

Troublesome side effects from the APMs led to pursuit of improved treatment profiles that included discovery of the second-generation, novel, or atypical antipsychotic medications (AAPMs) ( Table 2 ).[5,6] AAPMs are newer serotonin-dopamine antagonist agents that are often chosen as first-line therapy in addressing psychotic symptoms. These drugs are chosen over the first-generation APMs primarily because the incidence of EPSs is minimal to nonexistent and their side effect profiles are atypical for antipsychotic medications.[7] In addition, AAPMs have superior efficacy for therapeutically treating the other symptoms of schizophrenia such as alogia, anergia, avolition, apathy, and affect flattening, whereas the first-generation agents lacked this quality. Even though the AAPMs have a positive side effect profile, there is still a need for caution when prescribing these medications. Some of these medications can instigate EPSs especially at elevated dosages.[5,7,8] From the drugs listed in Table 2 , clozapine (Clozaril) initiates EPSs the least and risperidone (Risperdal) the most frequently.[5,6]

In addition to APMs inducing EPSs, there are other commonly used medications that can also put a client at risk of developing EPSs. Some cold medications (decongestants), anticonvulsants, antihistamines, and selective serotonin reuptake inhibitor antidepressants may increase the risk of EPSs.[3,7]

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