Introduction
Tardive dyskinesia (TD) assumed to be related with the hypersensitivity or upregulation of the dopamine receptor, but the precise mechanism remains unclear and therefore, no definite treatment option is established. With the occurrence, dose-reduction or discontinuation of the medication is considered for the main managing strategy. In the mid-2000s, there were some cases reporting TD in patients with long-term administration with 8mg of risperidone (RSP), an atypical antipsychotics, but no cases of TD have been reported with 2mg low dose medication. In the present case, TD occurred even with low dose of RSP, an atypical antipsychotics. Even the symptoms were relived with medication adjustment by a neurologist, the gait disturbance persisted and afterwards, improvements in gait disturbance were observed with gait rehabilitation.
Case presentation
An 80-year-old women who maintained medication on bipolar disorder for 20 years with no any other abnormal findings, started taking RSP since June 2017. The patient had dizziness and hang over symptoms after taking RSP. The medication was discontinued from December 31, 2018 and for symptom control, the patient started to take anticholinergics, Trihexine. Intra-oral involuntary movement began since March 2019 and the patient was admitted to the neurology department on March 22, 2019. To identify the presence of brain lesion, brain imaging were performed. No specific findings other than global brain atrophy and calcified atherosclerosis were found. With suspicion of RSP-induced TD, the patient was discharged after medication treatment. The symptoms persisted after discharge and the patient was admitted to the neurology department on June 10, 2019 with symptoms of whole body tremor worsened from May 2019.
After adjusting medication, systemic involuntary movements seemed to improve, but the patient was referred to the rehabilitation department due to persistent gait disturbance. Gait rehabilitation through lower limb muscle strength exercise and balance training were performed. There found no enhancement to the L/Ex Fair on MMT, but improvements in coordination and balance were found leading to standing static balance enhancements, from Fair to Good. The patient was discharged after monocane gait in Walker gait 20m was found to be possible.
Conclusion
The present patient with TD had improvements in symptoms with medication adjustment, but gait disturbance persisted. With balance training pushfully carried out aiming to independent gait, the patient was recovered to condition in which monocane gait was possible. The findings from the present case suggest that medication adjustment is important in patients with TD, better outcomes can be expected when accompanied with active rehabilitation in early stages of the disorder.
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