Tardive sensory syndrome related to lurasidone:A case report

BACKGROUND Tardive sensory syndrome(TSS)is a subtype of tardive syndrome(TS),and its etiology is still uncertain.Lurasidone is an atypical antipsychotic that has high affinity for dopamine D2-and serotonergic 5HT2A-and 5-HT7-receptors.CASE SUMMARY A 52-year-old woman,previously diagnosed with schizophrenia,and with no history of movement disorders and no sensory paresthesia,had taken lurasidone,initiate dose 40 mg daily then up titration to 120 mg daily,since March 2021,and developed mandibular sensory(pain)paresthesia after 3 mo of administration.After switching from lurasidone to quetiapine,she reported obvious improvement in her mandibular pain.CONCLUSION It is noteworthy that TSS is a rare subtype of TS,and lurasidone,an atypical antipsychotic,usually has a lower risk of causing TS.In light of the temporal relationship,it is therefore concluded that use of lurasidone might have caused TSS in this patient.We reported this rare case as a reminder that clinicians should adopt a cautious approach when prescribing atypical antipsychotics,so as to prevent TS.

Multiple therapies relieve long-term tardive dyskinesia in a patient with chronic schizophrenia:A case report

BACKGROUND Tardive dyskinesia(TD)is a serious and disabling movement disorder;it impairs social function and quality of life and increases the mortality rate.TD is usually induced by the use of antipsychotic drugs;however,the underlying mechanism remains unclear.Pharmacotherapy of TD includes cholinergic drugs,benzodiazepines,ginkgo biloba extract(GBE),antioxidants,amantadine,propanolol,botulinum toxin,valbenazine,and deutetrabenazine,whereas the non-pharmacotherapy approach includes modified electroconvulsive therapy(MECT)and deep brain stimulation.We successfully treated a chronic schizophrenia patient with comorbid long-term severe TD using deutetrabenazine,clozapine,and MECT.CASE SUMMARY A 69-year-old woman who was diagnosed as having schizophrenia 16 years ago developed severe TD after 6-mo prescription of risperidone oral solution.Her TD symptoms did not resolve despite various treatments,such as GBE,vitamin E,trihexyphenidyl,promethazine,benzodiazepines,and switching to quetiapine and olanzapine.After admission,she was given deutetrabenazine 6 mg bid.Her buccal tremor was slightly resolved 3 d later;however,her tongue remained protruded and could not be retracted.Quetiapine was switched to clozapine on day 4,and the buccal tremor remarkably resolved,and the tongue could be retracted into the mouth from day 6 onward.After three sessions of MECT,the buccal tremor resolved further.Since then,she has been able to take a semifluid diet,and her quality of life improved remarkably during 6 mo of follow-up.CONCLUSION TD is a serious condition which could be caused by antipsychotic medications;however,the best strategy against TD is prevention and monitoring during using antipsychotics.For patients with TD caused by antipsychotic medication use,multiple measures should be considered like switching to clozapine,adjunction with deutetrabenazine,or even MECT.

Targeted to medication-induced dyskinesia and tardive dyskinesia:A role of 5-HT_(1A) receptor

Objective To outline the recent progress in drug discovery for medication-induced dyskinesia(Parkinson disease,PD)and tardive diskinesia(schizophrenia)with emphasizing the role of 5-HT1A receptor.Methods Development of extrapyramidal syndrome(EPS)followed either chronic L-DOPA administration in PD(L-DOPA-induced dyskinesia,LID)or antipsychotic treatment in schizophrenia(Tardive dyskinesia,TD)remains a challenge in the clinical practice and drug discovery.In addition to the abnormal dopamine activity in the nigrostrial area that contributes to the LID or TD,recent information indicates that 5-HT1A receptor also plays an important role which is merging as promising target in treatment of LID or TD.Results l-Stepholidine(l-SPD),isolated from the Chinese herb Stephania,is known as a dual dopamine receptor agent(D1 receptor agonistic and D2 antagonistic activity).In addition,we further demonstrated that l-SPD binds to 5-HT1A receptor and exhibits a partial agonistic activity.In LID rat model,l-SPD not only attenuated the development of L-DOPA-induced dyskinesia(LID),but also relived the established LID.The effect of l-SPD on LID was completely blocked by pretreatment of 5-HT1A receptor antagonist,indicating the role of 5-HT1A receptor.Furthermore,we designed and synthesis a dual dopamine/5-HT1A receptor agonist MCL-135,which also exhibits a significant relief on LID while elicits its antiparkinsonian action.Conclusions 5-HT1A receptor plys an important role in the development of LID,targeted to dual dopamine/5-HT receptor may represent a promising strategy for drug design and discovery in LID and TD treatment.

Tardive phenomenon presenting as isolated dysarthria: A rare entity mimicking stroke

Distinguishing stroke mimics constitutes a considerable challenge for clinicians in emergency department. Here, we illustrate an extremely rare patient presenting with acute onset isolated dysarthria, who finally received diagnosis of tardive phenomenon associated with betahistine. Through the presentation of this case, we point out tardive phenomenon as an alternative differential diagnosis of stroke. Furthermore, this case adds substantial data presenting an interesting manifestation of isolated dysarthria as a tardive phenomenon, occurring due to betahistine usage which is extremely rare in literature.

Deep brain stimulation in the treatment of tardive dystonia

Dystonia refers to a clinical syndrome in which sustained involuntary muscle contractions result in twisting and repetitive movements, or abnormal postures. Secondary dystonia is associated with acquired or exogenous causes, hereditary neurologic syndromes or neurodegenerative disorders. Tardive dystonia is a special type of secondary dystonia due to exposure to certain medicines such as neuroleptics, with a chronic and persistent extrapyramidal symptoms.

Therapeutic use of melatonin in schizophrenia:A systematic review

BACKGROUND Sleep dysfunction is a common problem in people with schizophrenia,and side effects of treatment often exacerbate metabolic and cardiovascular risk and may induce extrapyramidal side effects.Melatonin(N-acetyl-5-methoxytryptamine)is an endogenously produced hormone which has demonstrated direct and indirect antioxidant and neuroprotective effects.Previous studies have explored the use of exogenous melatonin in improving sleep outcomes in the general population,yet indications for use in schizophrenia are unclear.AIM To synthesize the evidence from clinical trials investigating prescribed melatonin as an adjunctive therapy in patients with schizophrenia.METHODS A systematic literature review of MEDLINE(Ovid),Embase,PsychINFO,and PubMed on the 27/08/20;and CINAHL and Cochrane Library databases,was conducted.Inclusion criteria were:a peer-reviewed clinical trial published in English;included a group of patients with schizophrenia;used melatonin as an adjunctive therapy;and reported any outcome of any duration.Exclusion criteria were:neurodegenerative diseases,primary sleep disorders,co-morbid substance use or animal studies.RESULTS Fifteen studies were included in the current review with the following primary outcomes:sleep(n=6),metabolic profile(n=3),tardive dyskinesia(n=3),cognitive function(n=2)and benzodiazepine discontinuation(n=1).CONCLUSION Adjunctive melatonin therapy has some positive outcomes for sleep,metabolic profile and tardive dyskinesia in patients with schizophrenia.No beneficial effect of melatonin was observed on outcomes of cognition or benzodiazepine discontinuation.Future studies utilizing larger samples and investigations specifically comparing the effect of melatonin as adjunctive therapy with different antipsychotics in patients with schizophrenia are required.

Therapeutic use of melatonin in schizophrenia-more than meets the eye!

Adjunctive melatonin use in schizophrenia, as supported by a modicum ofevidence, has multiple transcending chronobiotic actions, including fixingconcurrent sleep problems to bona fide augmentative antipsychotic actions,mitigating the risk of tardive dyskinesias, curbing the drastic metabolic syndromeand ultimately providing neuroprotective actions. Its use is rather an art thanscience!