When properly managed, patients with movement disorders secondary to drugs can achieve full remission. Nevertheless, these disorders are often underrecognized in clinical practice, which could negatively impact the quality of life of patients and their caregivers for years [7]. Although they were primarily described with antipsychotic medications, several pharmacological substances were reported with movement disorders. Drug-induced movement disorders are a worldwide issue and usually occur while managing psychiatric and gastrointestinal motility disorders [8]. This is often the case because of the scarcity of medications that do not affect the nigrostriatal pathway. Acute antipsychotic-associated movement disorders, such as akathisia and parkinsonism, occur shortly after the initiation of the medication or titrations, and chronic antipsychotic-related movement disorders, such as tardive dyskinesia and tardive dystonia, usually occur after long-term exposure to antipsychotics [9]. Early identification and treatment increase the likelihood of mitigating adverse outcomes. Differential diagnosis between the idiopathic nature of the disorder and the secondary cause from a drug could be challenging in clinical practice. The most common approach to the occurrence of a side effect is the discontinuation of the offending drug, but sometimes the medication causing the adverse effect is essential for the management of the patient. Thus, the significance of studying side effects and how to best manage them with dose adjustment may be great for patients with difficult and uncontrolled primary disease and comorbidities. The differential diagnosis of drug-induced movement disorders should always include functional movement disorders, which can present with any type of abnormal movement [10]. It is noteworthy that the most common presentation of functional movement disorder overlaps with those secondary to drugs, in which tremor represents the most common clinical manifestation, followed by dystonia, myoclonus, and gait disorders [11]. The distinction between drug-induced movements and functional movement disorders is based on two main characteristics: inconsistency and incongruence [12]. Basal ganglia are a diversified array of linked nuclei that play a significant role in movement execution and signal relay. The classical paradigm suggests a direct (striatonigral) and indirect (striatopallidal) pathway inside the basal ganglia, including striatal projection neuron subpopulations, in which GABA plays an important role in the modulation of cortical impulses. Moreover, the cortical pathways can alter dopamine-dependent signaling, increasing or decreasing locomotor activity [13]. These pathways’ selective contributions have been demonstrated in mice with dopamine- and cAMP-regulated phosphoprotein Mr 32 kDa (DARP-32) deletion in nigrostriatal neurons in response to tropane alkaloids, such as cocaine [14]. Several neurotransmitter systems may be associated with the development of movement disorders. Any of these changes may result in impairments of the motor and cognitive systems. In this context, the dopaminergic system is distributed all across the cortical and subcortical regions. The D1 and D2 receptors are the most abundant in basal ganglia cells, with other receptor subtypes being less expressed. Dopamine-receptor-containing medium spiny neurons express specific receptor subtypes in their projections. The striatonigral circuit expresses D1 receptors selectively, whereas the striatopallidal pathway expresses D2 receptors. D1, D2, and D3 receptors are primarily responsible for locomotor control [15]. Serotonin regulates extrapyramidal motor activity via serotonin receptors in numerous cortical locations and the striatum. There are several subtypes of serotoninergic receptors, which have distinct distribution patterns. For example, 5HT1F and 5HT3A are absent in the caudate, substantia nigra, or globus pallidus. However, others have moderate or low expression levels in the same locations in marmoset brains [16]. The serotoninergic system more commonly regulates cognition to the detriment of motor functions than the dopaminergic system. Experimental animal models show that serotonin might influence dopaminergic motor performance in the nigrostriatal system. GABA is the primary inhibitory transmitter in the central nervous system and can modulate motor function by activating the GABAA receptor. More than sixteen receptor subunits of neurotransmitters, which play a significant role in motor control, have been found across the central nervous system ^[16][17][16,17].