The effect of antipsychotic-induced extrapyramidal disorders on patient’s compliance with schizophrenia (a clinical case)

Extrapyramidal disorders are common adverse events in antipsychotic therapy. However, their diagnosis is difficult due to broad differential diagnosis, and often their specific clinical variant is not recognized, and timely intervention is not performed, which leads to severe patient suffering. This affects the quality of life of patients with schizophrenia and leads to their refusal to receive therapy, which aggravates the course of the disease. The article presents a clinical case of a 33-year-old patient at a psychiatric hospital with schizophrenia combined with such rare severe extrapyramidal disorders as antipsychotic-induced tardive dyskinesia and tardive dystonia.The diagnosis was carried out in accordance with the criteria of the International Classification of Diseases, Tenth Revision (ICD-10). The intensity of clinical manifestations was assessed using the Positive and Negative Syndrome Scale (PANSS), the Abnormal Involuntary Movement Scale (AIMS), and the Barnes Akathisia Rating Scale (BARS). Compliance was assessed using the Method for Measuring Medication Adherence in Psychiatry. Detailed differential diagnosis of tardive dyskinesia and tardive dystonia with akathisia and Huntington’s disease was presented. Substantiated treatment strategy and positive clinical dynamics with increased compliance were described.

Late-Onset Dystonia With Low-Dose Olanzapine in an Older Person: A Case Report

Drug-induced dystonias are rare but can occur with second-generation antipsychotics. They are usually dose-related and occur soon after dose initiation. This case describes the development of dystonia after two years of olanzapine 5 mg daily in an older person with Alzheimer’s dementia. The dystonia resolved after diphenhydramine treatment on day two of hospitalization, but then the patient became delirious, which was treated with lorazepam on day three. Six days after admission, she developed tremors and rigidity that self-resolved. Her dystonia resolved after 11 days. The recurrence of symptoms during the hospitalization may have been a result of the progression of her dementia. This is the first known case of a patient developing dystonia after chronic use of low-dose olanzapine. This was not characterized as tardive dystonia because the dystonia was resolved with anticholinergic medication. This case illustrates the difficulty of using anticholinergics to treat dystonias in older people, which can precipitate delirium. Choosing an alternative antipsychotic with less extrapyramidal symptom risk is challenging as she had previous trials with quetiapine and risperidone. Clozapine was deemed an unfavorable alternative, as laboratory monitoring would be burdensome. Olanzapine-induced dystonias can develop anytime during therapy. Families must balance the desire for mood stabilization with antipsychotics side effects.

Long-Term Follow-Up of 12 Patients Treated with Bilateral Pallidal Stimulation for Tardive Dystonia

Tardive dystonia (TD) is a side effect of prolonged dopamine receptor antagonist intake. TD can be a chronic disabling movement disorder despite medical treatment. We previously demonstrated successful outcomes in six patients with TD using deep brain stimulation (DBS); however, more patients are needed to better understand the efficacy of DBS for treating TD. We assessed the outcomes of 12 patients with TD who underwent globus pallidus internus (GPi) DBS by extending the follow-up period of previously reported patients and enrolling six additional patients. All patients were refractory to pharmacotherapy and were referred for surgical intervention by movement disorder neurologists. In all patients, DBS electrodes were implanted bilaterally within the GPi under general anesthesia. The mean ages at TD onset and surgery were 39.2 ± 12.3 years and 44.6 ± 12.3 years, respectively. The Burke–Fahn–Marsden Dystonia Rating Scale (BFMDRS) performed the preoperative and postoperative evaluations. The average BFMDRS improvement rate at 1 month postoperatively was 75.6 ± 27.6% (p < 0.001). Ten patients were assessed in the long term (78.0 ± 50.4 months after surgery), and the long-term BFMDRS improvement was 78.0 ± 20.4%. Two patients responded poorly to DBS. Both had a longer duration from TD onset to surgery and older age at surgery. A cognitive and psychiatric decline was observed in the oldest patients, while no such decline ware observed in the younger patients. In most patients with TD, GPi-DBS could be a beneficial therapeutic option for long-term relief of TD.

Chronic form of Pisa syndrome after prolonged exposure to low-dose amisulpride treatment

Pisa syndrome is a movement problem defined by tonic, sustained lateral flexion with a slight posterior rotation of the trunk. It seems to be a side effect of antipsychotic medicine in most cases. The clinical duration of Pisa syndrome can be acute, chronic, or recurrent. As far as we know, no reports are available in the literature on the chronic form of Pisa syndrome caused by low-dose amisulpride. A case of refractory tardive dystonia form of Pisa syndrome during treatment with stable low-dose amisulpride is presented in this report. Long-term, low-dosage amisulpride therapy may induce tardive dystonia even in patients with no other risk factors for dystonia.

Antipsychotic Drug Induced Tardive Dyskinesia

A typical antipsychotics are at a lower risk of developing extra-pyramidal symptoms (EPS). But now, atypical antipsychotics are increasingly being associated with neurological side effects such as tardive dyskinesia, tardive dystonia, akinesia, parkinsonism, akathisia, bradykinesia, tremor etc. in which one of the major cases reported is Olanzapine induced tardive dyskinesia (TD). Schooler and Kane criteria is used for diagnosing tardive dyskinesia. Many cases have been published on this particular drug-induced side effect. In many instances tardive dyskinesia is misdiagnosed as tardive dystonia. Here we report the case of tardive dyskinesia associated with the use of antipsychotic drugs in a 50-year-old adult male suffering from persistent delusional disorder in a tertiary health care centre in India. The patient was on Olanzapine therapy for more than 2 years. Upon recurrent episodes of somatic delusions, Olanzapine dose was increased. When the patient developed symptoms of TD, the dose of Olanzapine was de-escalated. Even though the drug dose was reduced, the symptoms persisted which lead to the diagnosis of olanzapine induced TD. Based on this, Olanzapine was stopped and Clozapine treatment was initiated. On follow up, the patient was found to be relieved of the symptoms and complete recovery was achieved after 2 months of clozapine treatment.

Tardive Dystonia and Dyskinesia Responsive to Deep Brain Stimulation

Tardive disorders encompass phenomenologically diverse delayed-onset persistent involuntary motor symptoms associated with exposure to dopamine receptor blocking agents. Two common tardive disorders encountered in the clinical setting include tardive dyskinesia and tardive dystonia. This chapter presents a patient with severe refractory tardive dyskinesia and also tardive dystonia, manifesting as frequent and disabling retropulsion. He initially underwent bilateral globus pallidus interna (GPi) deep brain stimulation (DBS) but was found to have lead migration secondary to his severe hyperkinetic movements. He had persistent symptoms despite lead revision and ultimately required bilateral subthalamic nucleus (STN) rescue DBS implantation. The rescue procedure was synergistic with the initial GPi DBS and markedly improved his symptoms. Severe tardive dyskinesia and dystonia may respond to bilateral GPi DBS, and if necessary, rescue STN DBS can be added.