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Movement disorders
Published in Henry J. Woodford, Essential Geriatrics, 2022
Tardive dyskinesia (TD) is a term for choreoathetoid movements that develop after a period of months to years on neuroleptic agents. The likelihood of its development appears to be related to cumulative exposure. Paradoxically, it is often precipitated or worsened by drug dose reductions or withdrawal. It is frequently permanent but may slowly improve once the causative agent has been discontinued. The most common manifestation is orofacial dyskinesia but athetosis or dystonia are possible. The risk of the development of TD with typical or atypical agents is controversial. A retrospective review of 21,835 older adults with dementia (mean age 83) who had been started on neuroleptic medication found that there were 5.24 cases of drug-induced movement disorders other than parkinsonism per 100 person-years with typical agents compared to 5.19 cases with atypical agents.123 This difference was not statistically significant (RR 0.99; 95% CI 0.86–1.15). All antipsychotic drugs should be discontinued in frail older people when possible. Anticholinergic drugs have been suggested to help with tardive dyskinesia but the evidence base is extremely weak.124 Given the known adverse effects, deprescribing such drugs should be strongly considered.
Prescribing for a first episode of schizophrenia-like psychosis
Published in Kathy J Aitchison, Karena Meehan, Robin M Murray, First Episode Psychosis, 2021
Kathy J Aitchison, Karena Meehan, Robin M Murray
Acute drug-induced dyskinesia refers to abnormal involuntary drug-induced movements, particularly orofacial. Of note is spontaneous or idiopathic orofacial dyskinesia, which is indistinguishable from drug-induced acute or tardive dyskinesia, seen in 5-15% of elderly individuals who have never received antipsychotic drugs.144
Examine the upper limbs
Published in Hani TS Benamer, Neurology for MRCP PACES, 2019
It is unlikely that you will be asked to see a patient with chorea (characterised by brief, abrupt and fidgety involuntary movements which flit randomly around the body). The most common cause of chorea in neurology clinics is dyskinesia due to levodopa in patients with Parkinson’s disease. Other causes include Huntington’s disease, Sydenham’s chorea, systemic lupus erythematosus, oral contraceptive pill, thyrotoxicosis, polycythaemia and neuro-acanthocytosis. Neuroleptics could also cause tardive dyskinesia, such as orofacial dyskinesia, including lip-smacking, chewing and grimacing.
Protective effect of hesperetin against haloperidol-induced orofacial dyskinesia and catalepsy in rats
Published in Nutritional Neuroscience, 2018
Dinesh Dhingra, Shikha Goswami, Nidhi Gahalain
The present study has revealed protective effect of hesperetin against haloperidol-induced increase in VCMs and catalepsy. Neuroleptics produce two main types of motor disturbances in humans–tardive dyskinesia and catalepsy, collectively called as extrapyramidal side effects, which result directly or indirectly from the blockade of dopamine D2 receptors. These effects constitute the main disadvantages for the therapeutic use of typical neuroleptics. Haloperidol treatment for 21 successive days significantly induced orofacial dyskinesia in rats, as indicated by significant increase in VCMs and tongue protrusion. This is also supported by the earlier study where haloperidol (1 mg/kg, ip) administered once daily in the morning for a period of 21 successive days produced orofacial movements such as VCMs and tongue protrusion in rats.14 It has been reported in the literature that chronic use of neuroleptics may lead to imbalance in the production and detoxification of free radicals. This contributes to the start of hyperkinetic movements in the orofacial region.42 In our study, hesperetin significantly reversed haloperidol-induced orofacial dyskinesia and this protective effect of hesperetin was equivalent to quercetin.
Anti-NMDA receptor encephalitis: still unknown and underdiagnosed by physicians and especially by psychiatrists?
Published in Acta Clinica Belgica, 2018
Tine Hermans, Patrick Santens, Celine Matton, Kristine Oostra, Gunter Heylens, Sarah Herremans, Gilbert M. D. Lemmens
However, the clinical presentation and its progression should have led sooner to the consideration of the diagnosis of an anti-NMDA receptor encephalitis. Firstly, the initial presentation with primarily psychiatric symptoms, even without major neurological complications or cognitive impairment, does not exclude the diagnosis of an anti-NMDA receptor encephalitis. A new onset psychosis is described in the literature as the most common initial diagnosis of anti-NMDA receptor encephalitis [4]. Secondly, there was a rapid progression over two to three weeks from a psychotic to a catatonic state, with only little to no response to psychopharmacological treatment (e.g. antipsychotics and benzodiazepines). Thirdly, the normal premorbid functioning and lack of any prodromal symptoms typical for the onset of schizophrenia, the absence of important personal and familial psychiatric history, and the absence of a significant effect of antipsychotics made the diagnosis of an underlying psychiatric disorder such as schizophrenia or bipolar disorder rather unlikely [7]. Negative urine drug screening and the absence of history of substance abuse excluded further a drug-induced psychotic state. Fourthly, the evolution to a stage of autonomic instability should have been explained by an underlying psycho-organic cause. Finally, the presence of orofacial dyskinesia (e.g. tongue movements) may have pointed to the diagnosis of an anti-NMDA receptor encephalitis. These were in our case seen as extrapyramidal side effects of the antipsychotic medication.