Drug induced Parkinson’s: A comprehensive review of the issues and measures required to tackle the same

Abstract

Drug-inducedParkinsonism(DIP) closelyresemblesParkinson'sdisease(PD)inmotorsymptoms butiscausedbyspecificmedicationsdisruptingdopaminereceptorsandneurotransmitterbalance. PD involves a complex interplay of genetic, environmental, and biochemical factors resulting in the gradual degeneration of dopaminergic neurons. Environmental toxins and genetic mutations, such as LRRK2 and SNCA, contribute to the risk of developing PD. DIP primarily occurs due to the obstruction of dopamine receptors by certain drugs, notably antipsychotics and antiemetics, affecting dopamine transmission and causing Parkinsonian symptoms. Toxin-induced Parkinsonism(TIP)arisesfromexposuretosubstanceslikemanganese,herbicides,pesticides,and specific drugs, disrupting dopaminergic pathways and altering neurotransmission. This study examines various cases of DIP, emphasizing the significance of timely identification and intervention. A thorough understanding and proactive management of DIP are crucial for alleviatingsymptomsandimprovingpatientoutcomes.Healthcareprofessionalsneedtodiligently monitor patients using medications associated with DIP, adjust treatment plans, and educate patientsaboutpotentialsideeffects. Further researchisimperativetounravelthepathophysiology of DIP, considering genetic, environmental, and drug-related factors, to enhance clinical practices and optimize patient care. Addressing DIP requires a multifaceted approach, including early recognition, thoughtful management, and patient-centred care.