Article Link
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6283785
Ward KM, Citrome L.Neurol Ther. 2018 Dec;7(2):233-248. doi: 10.1007/s40120-018-0105-0. Epub 2018 Jul 19.PMID: 30027457 Free PMC article. Review.
Abstract
Introduction: Drug-induced parkinsonism (DIP) and tardive dyskinesia (TD) are stigmatizing movement disorders associated with exposure to dopamine receptor blocking agents such as antipsychotics, but they differ in their pathophysiology and clinical management. Treatment for one may worsen the other, and there are important diagnostic clues that assist in making an accurate assessment and instituting a rational treatment plan.
Methods: A literature review was executed to identify articles relating to the presentation, pathophysiology, epidemiology, and management of DIP and TD.
Results: DIP and TD prevalence estimates range from approximately 20 to 35% among antipsychotic users, but may be higher in select populations. DIP often presents as bradykinesia and rigidity, as well as rhythmic tremor, and the majority of cases appear within hours to weeks of initiation of therapy with an antipsychotic, or if dosage of the antipsychotic is increased. TD onset is delayed, typically appearing after at least 3 months or longer of treatment, and patients will commonly present with involuntary, abnormal facial movements such as lip smacking, puckering, chewing, or tongue protrusion. DIP often resolves with discontinuation of the causative agent, but TD may be permanent. Broadly, proposed mechanisms underlying these adverse events include decreased dopamine concentrations in the nigrostriatal pathway of the striatum and dopamine hypersensitivity, for DIP and TD, respectively. Pharmacologic treatment approaches for DIP have commonly included anticholinergic agents such as benztropine; however, anticholinergic medications can make TD worse. Switching the antipsychotic medication to one with lower propensity for DIP is an option for some patients. Amantadine, a non-anticholinergic agent used for the treatment of DIP, may be preferred in patients with comorbid DIP and TD. In TD, treatment options include the new reversible vesicular monoamine 2 transporter inhibitors, valbenazine and deutetrabenazine.
Conclusions: It is important for clinicians to be able to recognize DIP and TD in patients using antipsychotics so that they can minimize the impact of these adverse events on their patients’ quality of life. Accurate diagnosis will drive the selection of the correct treatment. Plain language summary available for this article.
Summary
My selected article is about how to distinguish between (and manage) drug-induced parkinsonism and tardive dyskinesia. According to Ward and Citrome, symptoms of drug-induced parkinsonism manifest days to months after antipsychotic initiation whereas tardive dyskinesia may develop months or years later. Drug induced parkinsonism often presents as bradykinesia, rigidity, and rhythmic tremor, similar to the TRAP symptoms seen in primary Parkinson’s Disease. Patients with tardive dyskinesia, however, presents with “involuntary, abnormal facial movements such as lip smacking, puckering, chewing, or tongue protrusion”. I selected this article because a common medication given in my unit was benztropine. Benztropine (Cogentin) is an anticholinergic agent that selectively inhibits dopamine transporters but also presents affinity for histamine and muscarinic receptors. It is typically used to alleviate symptoms of drug-induced parkinsonism but if administered in patients with tardive dyskinesia, benztropine can precipitate worsening symptoms. Similarly, medications used for the management of TD may worsen symptoms of drug-induced parkinsonism. Tetrabenazine, a (vesicular monoamine transporter 2) VMAT2 inhibitor “treats tardive dyskinesia but also potentially contributes to drug-induced parkinsonism risk”. Therefore, proper identification of these antipsychotic induced side effects is imperative. Although literature describes distinct presentations to help differentiate drug induced parkinsonism from tardive dyskinesia, overlapping symptoms make it difficult to tell the difference between the two. For instance, both drug induced parkinsonism and tardive dyskinesia may present with bradykinesia, rigidity, and unstable gait. Monitoring for EPS effects weekly during initial treatment is recommended by the American Psychiatric Association to help identify drug-induced parkinsonism vs tardive dyskinesia. Management of drug-induced parkinsonism includes discontinuation of the offending antipsychotic and switching to another antipsychotic. For tardive dyskinesia, discontinuation of anticholinergic agents is necessary to prevent worsening of symptoms. Treatment with newer VMAT-2 inhibitors (valbenazine and deutetrabenazine) is then indicated. Overall, medications such as amantadine can be used to treat both drug induced parkinsonism and tardive dyskinesia.
