Drug-induced movement disorders (DIMDs) form an important subgroup of secondary movement disorders, which despite conferring a significant iatrogenic burden, tend to be under-recognized and inappropriately managed.

We aimed to look into phenomenology, predictors of reversibility, and its impact on the quality of life of DIMD patients.

We conducted the study in the Department of Neurology at a tertiary-care centre in India. The institutional ethics-committee approved the study. We assessed 55-consecutive DIMD patients at presentation to our movement disorder clinic. Subsequently, they followed up to evaluate improvement in severity-scales (UPDRS, UDRS, BARS, AIMS) and quality of life (EuroQol-5D-5L). Wilcoxan-signed-rank test compared the scales at presentation and follow-up. Binary-logistic-regrerssion revealed the independent predictors of reversibility.

Fourteen patients (25.45%) had acute-subacute DIMD and 41 (74.55%) had tardive DIMD. Tardive-DIMD occurred more commonly in the elderly (age 50.73±16.92 years, p<0.001). Drug-induced-Parkinsonism (DIP) was the most common MD, followed by tardivedyskinesia. Risperidone and levosulpiride were the commonest culprit drugs. Patients in both the groups showed a statistically significant response to drug-dose reduction /withdrawal based on follow-up assessment on clinical-rating-scales and quality of life scores (EQ-5D-5L). DIMD was reversible in 71.42% of acute-subacute DIMD and 24.40% of patients with chronic DIMD (p=0.001). Binary-logistic-regression analysis showed acute-subacute DIMDs and DIP as independent predictors of reversibility.

DIP is the commonest and often reversible drug-induced movement disorder. Levosulpiride is notorious for causing DIMD in the elderly, requiring strict pharmacovigilance.

We investigated the influence of oral cannabidiol (CBD) on vacuous chewing movements (VCM) and oxidative stress parameters induced by short- and long-term administration of haloperidol in a rat model of tardive dyskinesia (TD).

Haloperidol was administered either sub-chronically via the intraperitoneal (IP) route or chronically via the intramuscular (IM) route to six experimental groups only or in combination with CBD. VCM and oxidative stress parameters were assessed at different time points after the last dose of medication.

Oral CBD (5 mg/kg) attenuated the VCM produced by sub-chronic administration of haloperidol (5 mg/kg) but had minimal effects on the VCM produced by chronic administration of haloperidol (50 mg/kg). In both sub-chronic and chronic haloperidol groups, there were significant changes in brain antioxidant parameters compared with CBD only and the control groups. The sub-chronic haloperidol-only group had lower glutathione activity compared with sub-chronic haloperidol before CBD and the control groups; also, superoxide dismutase, catalase, and 2,2-diphenyl-1-picrylhydrazyl activities were increased in the sub-chronic (IP) haloperidol only group compared with the CBD only and control groups. Nitric oxide activity was increased in sub-chronic haloperidol-only group compared to the other groups; however, the chronic haloperidol group had increased malondialdehyde activity compared to the other groups.

Our findings indicate that CBD ameliorated VCM in the sub-chronic haloperidol group before CBD, but marginally in the chronic haloperidol group before CBD. There was increased antioxidant activity in the sub-chronic group compared to the chronic group.

Facial covering and mask use is generally considered a preventive measure in reducing spread of infectious respiratory illnesses. With the COVID-19 pandemic, covering of the face, except the eyes, has become the norm for the first time for most people. Social interactions and clinical observation rely heavily on non-verbal communication of which facial expression is of utmost importance. While clinicians, especially in mental health settings, are acutely aware of the loss of information transmitted through the lower half of the face, signs of tardive dyskinesia may be forgotten in the list of potentially missed information.

To reflect on possible failure to detect orobuccolingual movements of tardive dyskinesia due to use of facial masks.

Reflection on a clinical case of a patient with a treatment refractory psychosis who presents to an outpatient appointment with a facial mask. After the appointment, a family member transmitted having observed what appeared to be involuntary masticatory movements in the patient.

Facial masks and coverings occult signs that may be visible on the lower half of the face.

Facial masks and coverings are essential in preventing COVID-19 contagion. Clinicians must keep in mind loss of information when part of the face is not visible. Tardive dyskinesia with orobuccolingual movements may be missed behind a mask. Family or other people who cohabit with the patient are essential information providers.

Individuals with tardive dyskinesia (TD) who completed a long-term study (KINECT 3 or KINECT 4) of valbenazine (40 or 80 mg/day, once-daily for up to 48 weeks followed by 4-week washout) were enrolled in a subsequent study (NCT02736955) that was primarily designed to further evaluate the long-term safety of valbenazine.

Participants were initiated at 40 mg/day (following prior valbenazine washout). At week 4, dosing was escalated to 80 mg/day based on tolerability and clinical assessment of TD; reduction to 40 mg/day was allowed for tolerability. The study was planned for 72 weeks or until termination due to commercial availability of valbenazine. Assessments included the Clinical Global Impression of Severity-TD (CGIS-TD), Patient Satisfaction Questionnaire (PSQ), and treatment-emergent adverse events (TEAEs).

At study termination, 85.7% (138/161) of participants were still active. Four participants had reached week 60, and none reached week 72. The percentage of participants with a CGIS-TD score ≤2 (normal/not ill or borderline ill) increased from study baseline (14.5% [23/159]) to week 48 (64.3% [36/56]). At baseline, 98.8% (158/160) of participants rated their prior valbenazine experience with a PSQ score ≤2 (very satisfied or somewhat satisfied). At week 48, 98.2% (55/56) remained satisfied. Before week 4 (dose escalation), 9.4% of participants had ≥1 TEAE. After week 4, the TEAE incidence was 49.0%. No TEAE occurred in ≥5% of participants during treatment (before or after week 4).

Valbenazine was well-tolerated and persistent improvements in TD were found in adults who received once-daily treatment for >1 year.

Lack of awareness of tardive dyskinesia (TD) and poor insight into mental illness are common in schizophrenia, raising the possibility that these phenomena are manifestations of a common underlying dysfunction.

We investigated relationships between low awareness of TD and poor insight into mental illness in 130 patients with schizophrenia and TD. We also examined selected demographic and clinical correlates of these two phenomena.

Sixty-six (51%) patients had no or low awareness of TD and 94 (72%) had at least mild impairment of insight into their mental illness. Low awareness of TD was not significantly correlated with greater impairment of insight into mental illness. Regression analyses indicated that the Positive and Negative Syndrome Scale (PANSS) disorganised factor (β = 0.72, t = 11.88, p < 0.01) accounted for 52% of the variance in insight into mental illness (adjusted R2 = 0.55) (F[2, 127] = 81.00, p < 0.01) and the Extrapyramidal Symptom Rating Scale (ESRS) dyskinesia subscale score (β = 0.47, t = 6.80, p < 0.01), PANSS disorganised factor (β = −0.26, t = −3.73, p < 0.01), and ESRS parkinsonism subscale score (β = 0.31, t = 4.55, p < 0.01) together accounted for 37% of the variance in awareness of TD (adjusted R2 = 0.37) (F[3, 126] = 26.87, p < 0.01).

The two phenomena appear to be dissociated, and may be domain-specific.

Tardive dyskinesia (TD) is a movement disorder observed after chronic neuroleptic treatment. Smoking is presumed to increase the prevalence of TD. The question of a cause-effect-relationship between smoking and TD, however, remains to be answered. Purpose of this study was to examine the correlation between the degree of smoking and the severity of TD with respect to differences caused by medication.

We examined 60 patients suffering from schizophrenia and TD. We compared a clozapine-treated group with a group treated with typical neuroleptics. Movement disorders were assessed using the Abnormal-Involuntary-Movement-Scale and the technical device digital image processing, providing rater independent information on perioral movements.

We found a strong correlation (.80 < r < .90, always p < .0001) between the degree of smoking and severity of TD. Repeated measurements revealed a positive correlation between changes in cigarette consumption and changes of the severity of TD (p < .0001). Analyses of covariance indicated a significant group-effect with a lower severity of TD in the clozapine-group compared to the typical-neuroleptics-group (p = .010). Interaction-analyses indicated a higher impact of smoking on the severity of TD in the typical-neuroleptics-group compared to the clozapine-group (p = .033).

Concerning a possible cause-effect-relationship between smoking and TD, smoking is more of a general health hazard than neuroleptic exposure in terms of TD.

The pathophysiology of tardive dyskinesia (TD) is not completely understood.

To assess the relationship of TD with 5-HT2A receptor gene, serotonin transporter gene (5 HTT), and catechol-o-methyltransferase (COMT) gene polymorphisms.

Our study comprised 111 unrelated subjects who strictly met DSM-IV criteria for schizophrenia and 32 TD, and 79 healthy unrelated controls; all the subjects were of Turkish origin. The analyses of 5-HT2A receptor gene, 5 HTT gene, and COMT gene polymorphisms were performed using polymerase chain reaction (PCR) technique.

The polymorphisms of these genes were not significantly different between the schizophrenic patients, TD and control subjects.

Our findings indicated that 5-HT2A receptor gene, 5 HTT gene, and COMT gene polymorphisms were similar in schizophrenia with non-TD, schizophrenia with TD, and healthy controls. These polymorphisms, though, do not help to evaluate the susceptibility to TD.