As this year is nearing the end, PW recaps some of the research presented tardive dyskinesia in 2024.
Drug-Induced Movement Disorders
Antipsychotics, despite their effectiveness, pose significant risks, especially as cumulative doses and drug combinations increase, explain Nora Vanegas-Arroyave and colleagues. A major concern is drug-induced movement disorders (DIMDs), caused by dopamine receptor blockers, affecting those on antipsychotics or dopamine antagonists for gastrointestinal issues. DIMDs can vary in onset, symptoms, and treatment response, making precise diagnosis critical. Though anticholinergics can treat some DIMDs like drug-induced parkinsonism (DIP) and acute dystonic reactions, they are ineffective for tardive dyskinesia (TD), akathisia, or neuroleptic malignant syndrome (NMS). Misuse of anticholinergics, especially in older adults, can elevate cognitive and peripheral side effects, as many anticholinergic medications contribute to cognitive dysfunction and increase risks of anticholinergic toxicity.1
The motor dysfunction seen in DIMDs results from the blockade of D2 receptors, which reduces dopamine signaling, causing abnormal movement patterns in patients with DIP. For hyperkinetic conditions like TD, prolonged D2 receptor blockage leads to receptor hypersensitivity, worsening dopamine imbalance. Research shows that anticholinergics may worsen TD by further disrupting dopamine-acetylcholine balance, underscoring the lack of clinical support for their use in TD treatment.1
Anticholinergic medications are linked to a wide array of adverse effects, particularly concerning in older adults who are more vulnerable to cognitive impairments. Recent studies associate high anticholinergic usage with memory loss, cognitive decline, and physical impairments. Over 600 medications with anticholinergic properties complicate patient regimens, often adding to anticholinergic burden, which is linked to increased risk of falls, delirium, and dementia. Experts emphasize cautious tapering when discontinuing anticholinergics to prevent cholinergic rebound symptoms.1
Given these challenges, individualized approaches to antipsychotic and anticholinergic management are recommended. Guidelines urge clinicians to assess DIMD risk in patients on antipsychotics regularly. Medications like valbenazine and deutetrabenazine, approved for TD, are preferred for treating DIMDs without anticholinergic side effects. Anticholinergic tapering, monitored carefully, improves cognition and quality of life for many patients, highlighting the importance of a tailored, evidence-based approach to medication management.1
TD Measurement Scales
According to Robert H Farber and colleagues, TD has traditionally been evaluated using the Abnormal Involuntary Movement Scale (AIMS), a clinician-rated tool considered the standard for assessing treatment efficacy in TD. However, AIMS lacks insight into how these uncontrolled movements affect patients’ lives and can be challenging to administer. To address this, the Tardive Dyskinesia Impact Scale (TDIS) was developed as a patient-reported outcome measure specifically designed to capture the unique impacts of TD. This study aimed to assess whether TDIS could reliably measure the impact of TD.2
Utilizing data from qualitative research and two phase 3 trials of a VMAT2 inhibitor, the study assessed the TDIS’s psychometric validity. Patient interviews confirmed the TDIS accurately captured TD impacts, organized into two main domains: physical and socioemotional. Quantitative analysis demonstrated that TDIS scores correlated weakly with AIMS, showing it captures distinct information. TDIS also proved responsive to treatment, with scores reflecting patient improvements over time. The TDIS, alongside AIMS, offers a comprehensive evaluation of TD’s impact, providing insights that are valuable for tracking TD-related changes in patients’ lives over time.2
Transcranial Stimulation in TD
Xiaoli Lyu and colleagues investigated the efficacy and safety of transcranial direct current stimulation (tDCS) for treating TD in long-term hospitalized schizophrenia patients. Sixty-four inpatients diagnosed with schizophrenia and TD were randomly assigned to either an active tDCS group (N=35) or a sham group (N=29). The treatment consisted of 15 sessions, each lasting 30 minutes with a 2 mA intensity, targeting the left dorsolateral prefrontal cortex with an anode and the right supraorbital region with a cathode. The primary outcome measure was the change in Abnormal Involuntary Movements Scale (AIMS) score, while secondary outcomes were assessed using the Positive and Negative Syndrome Scale (PANSS) and the Scale for the Assessment of Negative Symptoms (SANS).3
Results showed that 81.25% of participants completed the study. The active tDCS group experienced significant improvements in overall AIMS scores and facial-oral motor subscores compared to the sham group (P<0.05). Notably, 50% of the active group saw at least a 30% reduction in AIMS scores, versus only 8.3% in the sham group (P<0.01). While there were no significant differences in PANSS or SANS scores between groups, a tingling sensation was reported more frequently in the active group (P<0.05). 3
In conclusion, tDCS appears to be a promising, safe option for reducing facial-oral symptoms of TD in chronically hospitalized schizophrenia patients, though further studies are warranted to confirm its benefits across broader symptom measures.3
