A RARE CASE REPORT OF AMISULPRIDE INDUCED URINARY RETENTION

Amisulpride is an atypical antipsychotic with the preferential action on D2/D3 receptors. Its common adverse effects are extrapyramidal symptoms, insomnia, hyperkinesia, anxiety, weight gain, agitation, hyperprolactinemia. We have witnessed a adverse effect of urinary retention induced by amisulpride at minimal dosage and would like to present the same.

18F-APN-1607 Tau PET in Progressive Supranuclear Palsy-Like Symptoms Caused by TBK1 Mutations

Background Pathogenic mutations in the TANK-binding kinase 1 (TBK1) gene have been associated with progressive supranuclear palsy (PSP)-like extrapyramidal symptoms, amyotrophic lateral sclerosis (ALS), as well as cognitive and behavioral alterations. However, the question as to whether TBK1 mutations may be associated with tau burden remains unanswered. Methods To investigate whether patients presenting with PSP-like extrapyramidal symptoms caused by TBK1 mutations have evidence of tau deposition as reflected by positive 18F-APN-1607 tau PET imaging findings. Four patients who showed PSP-like extrapyramidal symptoms, ALS, and cognitive/behavioral alterations were consecutively enrolled between August 2019 and August 2020. Patients underwent TBK1 gene sequencing and 18F-APN-1607 tau PET imaging. All PET images were interpreted in a blinded fashion with respect to genetic results. Brain structural changes were investigated with MRI, whereas 11C-CFT or 18F-DTBZ PET imaging was performed to identify dopaminergic degeneration. Results Pathogenic TBK1 mutations were identified in three of the four study patients. The three mutation carriers – but not the case without – showed positive 18F-APN-1607 binding in PSP-related regions, suggesting the presence of tau pathology. Mesencephalic atrophy (hummingbird sign) was observed in all TBK1 mutation carriers, and two of them also had evidence of frontotemporal atrophy. Dopaminergic degeneration was evident in all cases, regardless of TBK1 mutations. Conclusions Pathogenic TBK1 mutations in patients with PSP-like extrapyramidal symptoms are associated with positive 18F-APN-1607 tau PET imaging findings. Our data should prompt additional investigations on the potential role of tau accumulation in the pathogenesis of disease conditions associated with TBK1 mutations.

Role of COMT V158M Polymorphism in the Development of Dystonia after Administration of Antipsychotic Drugs

Antipsychotics (APDs) represent the main pharmacological strategy in the treatment of schizophrenia; however, their administration often may result in severe adverse effects, such as extrapyramidal symptoms. Typically, dystonic movements are considered the result of impaired function and/or abnormalities of dopaminergic neurotransmission/signaling in the basal ganglia. The catechol O-methyltransferase (COMT) gene is located within the 22q11.2 region, and its product is an enzyme involved in transferring a methyl group from S-adenosylmethionine to catecholamines, including dopamine. Studies showed that COMT Val158Met polymorphism modifies enzymatic activity and, consequently, synaptic dopamine concentration in specific brain areas. We identified a patient with 22q11.2 deletion syndrome presenting with cervical and trunk dystonia after paliperidone administration, which persisted even after drug discontinuation. Given the patient’s genetic condition, we hypothesized that the dopaminergic dysfunction had been aggravated by COMT involvement, thus causing dystonia. In line with this hypothesis, we carried out a study on psychiatric patients in chronic treatment with APD to evaluate the distribution of the COMT Val158Met polymorphism and its role in the onset of adverse extrapyramidal symptoms. The study included four patients with dystonia after administration of APDs compared to 17 patients who never presented adverse drug reactions. Our data suggest that the Val/Val and Met/Met polymorphisms of the COMT gene are associated with a protective effect for the development of collateral extrapyramidal symptoms in patients treated with APDs, while the Val/Met genotype could be considered a risk factor for the development of dystonia after APDs administration.

Antipsychotic treatment effects and structural MRI brain changes in schizophrenia

Background Progressive brain structural MRI changes are described in schizophrenia and have been ascribed to both illness progression and antipsychotic treatment. We investigated treatment effects, in terms of total cumulative antipsychotic dose, efficacy and tolerability, on brain structural changes over the first 24 months of treatment in schizophrenia. Methods A prospective, 24-month, single-site cohort study in 99 minimally treated patients with first-episode schizophrenia, schizophreniform and schizoaffective disorder, and 98 matched healthy controls. We treated the patients according to a fixed protocol with flupenthixol decanoate, a long-acting injectable antipsychotic. We assessed psychopathology, cognition, extrapyramidal symptoms and BMI, and acquired MRI scans at months 0, 12 and 24. We selected global cortical thickness, white matter volume and basal ganglia volume as the regions of interest. Results The only significant group × time interaction was for basal ganglia volumes. However, patients, but not controls, displayed cortical thickness reductions and increases in white matter and basal ganglia volumes. Cortical thickness reductions were unrelated to treatment. White matter volume increases were associated with lower cumulative antipsychotic dose, greater improvements in psychopathology and cognition, and more extrapyramidal symptoms. Basal ganglia volume increases were associated with greater improvements in psychopathology, greater increases in BMI and more extrapyramidal symptoms. Conclusions We provide evidence for plasticity in white matter and basal ganglia associated with antipsychotic treatment in schizophrenia, most likely linked to the dopamine blocking actions of these agents. Cortical changes may be more closely related to the neurodevelopmental, non-dopaminergic aspects of the illness.

The Therapeutic Effect of Edible Horticultural Therapy on Extrapyramidal Symptoms in Patients with Schizophrenia

Extrapyramidal symptoms (EPSs) are common adverse reactions to antipsychotics in patients with schizophrenia. The purpose of this study was to investigate the effects of edible horticultural therapy (EHT) on EPSs in schizophrenic patients. This study assessed the changes in psychopathological symptoms and extrapyramidal symptoms in patients with schizophrenia before and after participating in a six-session EHT. Forty schizophrenic patients, recruited from Wuhan Wudong Hospital, were randomly assigned to the EHT group (average age: 45.40 ± 13.960 years) or the control group (average age: 49.30 ± 12.516 years). The EHT program held weekly sessions from May 2020 to June 2020. A psychiatrist assessed the psychopathological symptoms and extrapyramidal symptoms of schizophrenic patients in both groups with the Chinese version of the Positive and Negative Syndromes Scale (PANSS) and the Rating Scale for Extrapyramidal Side Effects (RSESE). After six courses of horticultural therapy, the terms of positive, negative, and general symptoms on the PANSS significantly improved in the EHT group. Moreover, the EPSs were also significantly improved in the EHT group. However, there was no change in the PANSS and RSESE scores in the control group. This study shows that EHT has the potential to improve not only psychopathological symptoms but also EPSs in psychiatric patients. This adds new evidence for EHT as an adjunct to treatment for schizophrenia.

ASYMPTOMATIC TRANSIENT SA-NODE CONDUCTION BLOCK IN A PATIENT WITH ACUTE RISPERIDONE+TRIHEXYPHENYDYL TABLET POISONING

BACKGROUND: a case report of 17year old male with acute risperidone + trihexyphenidyl poisoning with transient sinoatrial block without any CNS or neuromuscular complications. CONCLUSION: Risperidone does possess cardiotoxicity as of cardiac conduction abnormalities mainly affecting SA 1 and AV nodes rather than prolongation of QT interval without causing hypotension or myocardial injury . Such a nonlethal conduction aberrancy was observed at a dose of 75mg risperidone was only transient and reversed physiologically without any additional treatment. Further protection from extrapyramidal symptoms was offered by combined drug trihexyphenidyl at cost of sedation.

Exercise and Worsening of Extrapyramidal Symptoms during Treatment with Long-Acting Injectable Antipsychotics

Second-generation antipsychotic medications are used to treat schizophrenia and a range of other psychotic disorders, although adverse effects, including cardiovascular and metabolic abnormalities and extrapyramidal symptoms, are often inevitable. Studies have shown that exercise, as an adjunct therapy, can be effective in reducing the core symptoms of schizophrenia as well as ameliorating intrinsic and antipsychotic-induced cardiometabolic abnormalities. However, it is noteworthy that exercise may need to be implemented with caution in some individuals receiving certain antipsychotic treatment regimens. We report here two cases of exercise-associated worsening of extrapyramidal symptoms in two individuals with schizoaffective disorder treated with a long-acting injectable antipsychotic medication over the course of a 12-week exercise program. This worsening of extrapyramidal symptoms can be attributed to an increase in blood flow to the site of injection during exercise, accelerating the rate of absorption and bioavailability of the antipsychotic medication and subsequently increasing dopamine D2 receptor blockade. When monitoring drug therapy for patients receiving long-acting injectable antipsychotic medications, pharmacists and other healthcare professionals need to consider exercise as a contributing factor for the emergence of extrapyramidal symptoms.

Successful Combination Therapy of Trazodone and Fluvoxamine for Pica in Alzheimer's Disease: A Case Report

Pica in Alzheimer's disease (AD) makes it difficult for caregivers to provide care. However, few effective medications have been reported for pica in AD. We report a case of AD with pica that was successfully improved by trazodone and fluvoxamine. An 80-year-old woman with AD was admitted to our hospital due to aggravated pica, including eating weeds in the facility's garden and eating a dishwashing sponge. Her pica was accompanied by oral tendency, prosopagnosia, and placidity. She took rivastigmine and memantine, but these were ineffective for her pica. She was given olanzapine and perospirone, but both were discontinued due to over-sedation and severe extrapyramidal symptoms, respectively. We then administered trazodone and fluvoxamine, both of which have demonstrated effectiveness for pica in frontotemporal dementia (FTD). Her pica behaviors then disappeared without daytime sleepiness. In this case, pica with oral tendency, which was accompanied by prosopagnosia and placidity, may be interpreted as a partial symptom of Klüver–Bucy syndrome (KBS). KBS is often seen in FTD, but also occurs in late-stage AD. Our case together with previous reports showing that trazodone and fluvoxamine were effective for pica in FTD suggest that the same common drug therapy may be successful in pica with oral tendency, regardless of the subtype of dementia.