PMID- 29427000
OWN - NLM
STAT- MEDLINE
DCOM- 20190311
LR  - 20220331
IS  - 1179-1934 (Electronic)
IS  - 1172-7047 (Linking)
VI  - 32
IP  - 2
DP  - 2018 Feb
TI  - Tardive Dyskinesia Associated with Atypical Antipsychotics: Prevalence, 
      Mechanisms and Management Strategies.
PG  - 135-147
LID - 10.1007/s40263-018-0494-8 [doi]
AB  - All antipsychotics, including the atypical antipsychotics (AAPs), may cause 
      tardive dyskinesia (TD), a potentially irreversible movement disorder, the 
      pathophysiology of which is currently unknown. The prevention and treatment of TD 
      remain major challenges for clinicians. We conducted a PubMed search to review 
      the prevalence and etiology of and management strategies for TD associated with 
      AAPs. TD prevalence rates varied substantially between studies, with an estimated 
      prevalence of around 20% in patients using AAPs. The risk of TD is lower with 
      AAPs than with typical antipsychotics (TAPs) but remains a problem because AAPs 
      are increasingly being prescribed. Important risk factors associated with TD 
      include the duration of antipsychotic use, age, and ethnicity other than 
      Caucasian. Theories about the etiology of TD include supersensitivity of the 
      dopamine receptors and oxidative stress, but other neurotransmitters and factors 
      are probably involved. Studies concerning the management of TD have considerable 
      methodological limitations. Thus, recommendations for the management of TD are 
      based on a few trials and clinical experience, and no general guidelines for the 
      management of TD can be established. The best management strategy remains 
      prevention. Caution is required when prescribing antipsychotics, and regular 
      screening is needed for early detection of TD. Other strategies may include 
      reducing the AAP dosage, switching to clozapine, or administering vesicular 
      monoamine transporter (VMAT)-2 inhibitors. In severe cases, local injections of 
      botulinum toxin or deep brain stimulation may be considered. More clinical trials 
      in larger samples are needed to gather valid information on the effect of 
      interventions targeting TD.
FAU - Stegmayer, Katharina
AU  - Stegmayer K
AUID- ORCID: 0000-0002-4611-8966
AD  - University Hospital of Psychiatry, Bolligenstrasse 111, 3060, Bern, Switzerland. 
      katharina.stegmayer@upd.unibe.ch.
FAU - Walther, Sebastian
AU  - Walther S
AUID- ORCID: 0000-0003-4026-3561
AD  - University Hospital of Psychiatry, Bolligenstrasse 111, 3060, Bern, Switzerland.
FAU - van Harten, Peter
AU  - van Harten P
AD  - Psychiatric Centre GGz Centraal, Innova, Amersfoort, The Netherlands.
AD  - School for Mental Health and Neuroscience, Maastricht University, Maastricht, The 
      Netherlands.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - CNS Drugs
JT  - CNS drugs
JID - 9431220
RN  - 0 (Antipsychotic Agents)
SB  - IM
MH  - Antipsychotic Agents/*adverse effects
MH  - *Disease Management
MH  - Humans
MH  - Mental Disorders/drug therapy
MH  - PubMed/statistics & numerical data
MH  - *Tardive Dyskinesia/epidemiology/etiology/therapy
EDAT- 2018/02/11 06:00
MHDA- 2019/03/12 06:00
CRDT- 2018/02/11 06:00
PHST- 2018/02/11 06:00 [pubmed]
PHST- 2019/03/12 06:00 [medline]
PHST- 2018/02/11 06:00 [entrez]
AID - 10.1007/s40263-018-0494-8 [pii]
AID - 10.1007/s40263-018-0494-8 [doi]
PST - ppublish
SO  - CNS Drugs. 2018 Feb;32(2):135-147. doi: 10.1007/s40263-018-0494-8.