Digital movement analysis, a new objective method of measuring tardive dyskinesia and drug-induced parkinsonian tremor: acceptability, reliability and validity

1996 ◽  
Vol 246 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Flemming M. Nilsson ◽  
Birgitte L. Hansen ◽  
Christian Büchel ◽  
Wagner F. Gattaz ◽  
Jes Gerlach
CNS Spectrums ◽  
2020 ◽  
pp. 1-10
Author(s):  
Robert A. Hauser ◽  
Jonathan M. Meyer ◽  
Stewart A. Factor ◽  
Cynthia L. Comella ◽  
Caroline M. Tanner ◽  
...  

Abstract Accurate diagnosis and appropriate treatment of tardive dyskinesia (TD) are imperative, as its symptoms can be highly disruptive to both patients and their caregivers. Misdiagnosis can lead to incorrect interventions with suboptimal or even deleterious results. To aid in the identification and differentiation of TD in the psychiatric practice setting, we review its clinical features and movement phenomenology, as well as those of other antipsychotic-induced movement disorders, with accompanying links to illustrative videos. Exposure to dopamine receptor blocking agents (DRBAs) such as antipsychotics or antiemetics is associated with a spectrum of movement disorders including TD. The differential diagnosis of TD is based on history of DRBA exposure, recent discontinuation or dose reduction of a DRBA, and movement phenomenology. Common diagnostic challenges are the abnormal behaviors and dyskinesias associated with advanced age or chronic mental illness, and other movement disorders associated with DRBA therapy, such as akathisia, parkinsonian tremor, and tremor related to use of mood stabilizing agents (eg, lithium, divalproex). Duration of exposure may help rule out acute drug-induced syndromes such as acute dystonia or acute/subacute akathisia. Another important consideration is the potential for TD to present together with other drug-induced movement disorders (eg, parkinsonism, parkinsonian tremor, and postural tremor from mood stabilizers) in the same patient, which can complicate both diagnosis and management. After documentation of the phenomenology, severity, and distribution of TD movements, treatment options should be reviewed with the patient and caregivers.


2017 ◽  
Vol 49 (5S) ◽  
pp. 313-314
Author(s):  
Samantha E. Scarneo ◽  
Julie P. Burland ◽  
Alex M. Wafer ◽  
Gabrielle EW Giersch ◽  
Ryan M. Curtis ◽  
...  

1996 ◽  
Vol 6 ◽  
pp. 131-132
Author(s):  
G. Gardos ◽  
D.E. Casey ◽  
A. Perenyi ◽  
J.D. Cole ◽  
E. Kocsis ◽  
...  

Author(s):  
Susan H. Fox

Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.


1991 ◽  
Vol 159 (3) ◽  
pp. 399-403 ◽  
Author(s):  
Keith W. Brown ◽  
Thomas White

The effect of drug-induced Parkinsonism and of the topography of the dyskinetic movements on the psychological consequences of tardive dyskinesia was assessed in 20 schizophrenic subjects and 20 non-dyskinetic schizophrenic controls matched for age, sex, the presence of anticholinergic medication, and the presence and severity of drug-induced Parkinsonism. Limb–truncal subscale scores but not orofacial scores had a significant correlation with cognitive impairment and with negative symptoms. Drug-induced Parkinsonism was found to be a powerful confounding variable.


1992 ◽  
Vol 14 (5) ◽  
pp. 340-344 ◽  
Author(s):  
Thomas E. Hansen ◽  
William L. Brown ◽  
Ronald M. Weigel ◽  
Daniel E. Casey

1997 ◽  
Vol 2 (3) ◽  
pp. E4 ◽  
Author(s):  
Jamal M. Taha ◽  
Jacques Favre ◽  
Thomas K. Baumann ◽  
Kim J. Burchiel

The goals of this study were to analyze the effect of pallidotomy on parkinsonian tremor and to ascertain whether an association exists between microrecording findings and tremor outcome. Forty-four patients with Parkinson's disease (PD) who had drug-induced dyskinesia, bradykinesia, rigidity, and tremor underwent posteroventral pallidotomy. Using a 1-μ-tip tungsten electrode, microrecordings were obtained through one to three tracts, starting 10 mm above the pallidal base. Tremor severity was measured on a patient-rated, 100-mm Visual Analog Scale (VAS), both preoperatively and 3 to 9 months (mean 6 months) postoperatively. Preoperatively, tremor was rated as 50 mm or greater in 24 patients (55%) and as less than 25 mm in 13 patients (30%). Postoperatively, tremor was rated as 50 mm or greater in five patients (11%) and less than 25 mm in 29 patients (66%). The difference was significant (p = 0.0001). Four patients (9%) had no postoperative tremor. Tremor improved by at least 50% in eight (80%) of 10 patients in whom tremor-synchronous cells were recorded (Group A) and in 12 (35%) of 34 patients in whom tremor-synchronous cells were not recorded (Group B). This difference was significant (p = 0.03). Tremor improved by at least 50 mm in all (100%) of the seven Group A patients with severe (>= 50 mm) preoperative tremor and in nine (53%) of 17 Group B patients with severe preoperative tremor. This difference was also significant (p = 0.05). The authors proffer two conclusions: 1) after pallidotomy, tremor improves by at least 50% in two-thirds of patients with PD who have severe (>= 50 mm on the VAS) preoperative tremor; and 2) better tremor control is obtained when tremor-synchronous cells are included in the lesion.


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