Photo Credit: Veronika Oliinyk
Recent research published in 2024 examined various tardive dyskinesia (TD) topics. They included the following:
- Transcranial direct current stimulation;
- A new clinical tool for documenting and rating TD; and
- Schizophrenia-associated genetic markers in the HLA region as risk factors for tardive dyskinesia.
Transcranial Stimulation
One study evaluated the efficacy and safety of transcranial direct current stimulation (tDCS) in treating TD in chronically hospitalized patients with schizophrenia. Sixty-four inpatients diagnosed with schizophrenia and TD were randomly divided into two groups: 35 received active tDCS treatment, while 29 underwent a sham procedure. The treatment involved 15 sessions, each lasting 30 minutes, with a current intensity of 2 mA applied to specific brain regions. The primary outcome was measured by changes in the Abnormal Involuntary Movements Scale (AIMS), while secondary outcomes were assessed using the Positive and Negative Syndrome Scale (PANSS) and the Scale for the Assessment of Negative Symptoms (SANS).
Results showed that 52 patients (81.25%) completed the study. The active group experienced a significant reduction in both total AIMS scores and facial-oral subscores compared to the sham group. In the active group, 50% of patients showed a 30% or greater improvement in AIMS scores, compared to only 8.3% in the sham group. However, there were no significant differences between the groups regarding PANSS and SANS scores. A notable difference was found in the occurrence of tingling sensations, an adverse effect reported more frequently in the active group.
Overall, tDCS appears to be a promising and safe option for reducing facial-oral motor symptoms in patients with TD and schizophrenia.
The Clinician’s Tardive Inventory
Another study aimed to develop and test the reliability of the Clinician’s Tardive Inventory (CTI), a new tool designed to assess TD symptoms and their functional impact. Traditional TD scales have not fully captured the range of clinical signs and functional impairments, prompting the need for this integrated instrument. The CTI was created by a movement disorder neurologist, revised by a Steering Committee of five neurologists and two psychiatrists, and assesses abnormal movements across various body areas (eyes, face, tongue, mouth, jaw, limbs) along with complex movements and vocalizations. Symptom frequency is rated from 0 (absent) to 3 (constant), and functional impairments, including daily activities, social impact, distress, and physical harm, are also rated on a 0–3 scale.
The CTI underwent reliability testing through video/vignette assessments reviewed by movement disorder specialists. Four clinicians rated each video, and interrater reliability was analyzed using intraclass correlation (ICC), while test-retest reliability was assessed via the Kendall tau-b. The most common movements were observed in the tongue/mouth (77.8%) and jaw (55.6%). The CTI demonstrated strong reliability, with ICCs for movement frequency ranging from 0.76 to 0.92, and for functional impairments from 0.82 to 0.92. Test-retest reliability correlations ranged from 0.66 to 0.87, confirming the CTI’s consistency.
In conclusion, the CTI is a reliable new instrument for evaluating TD symptoms and functional impacts, though further validation studies are recommended.
Genetic Markers in TD
One final study aimed to investigate the genetic factors involved in the pathology of TD. Building on previous research suggesting a possible link between TD and the Complement Component C4 gene in the HLA region, the team explored two schizophrenia-associated single-nucleotide polymorphisms (SNPs) within the HLA region: rs13194504 and rs210133.
A sample of 172 patients with schizophrenia from three clinical sites in Canada and the USA was analyzed to assess the relationship between these SNPs and TD occurrence and severity. TD severity was measured using the Abnormal Involuntary Movement Scale (AIMS).
Results showed that the rs13194504 AA genotype was associated with reduced TD severity, as reflected by lower AIMS scores (P=0.047), although it was not linked to TD occurrence. In contrast, the SNP rs210133 was not significantly associated with either the occurrence of TD or AIMS scores.
In conclusion, the findings suggest that the rs13194504 AA genotype may influence the severity of TD in schizophrenia patients, while SNP rs210133 does not appear to play a significant role in either the occurrence or severity of TD. Further research is needed to better understand the genetic factors contributing to TD.
