The following is a summary of “Role of Sensory Impairment in the Pathogenesis and Treatment of Psychosis and Tardive Dyskinesia,” published in the January 2023 issue of Psychiatry by O’Connell et al.
Tardive Dyskinesia is a medical condition that arises as a result of prolonged exposure to antipsychotic D2 Blockers. This exposure leads to the hypersensitization of the D2 dopamine receptors in the nigrostriatal pathway. The condition is characterized by choreiform movements that affect various body parts, including the oral, facial, buccolingual, truncal, and extremity regions. The onset of symptoms is gradual and may be exacerbated by coexisting medical conditions such as cognitive dysfunction and sensory deficits, which can impede prompt intervention. A male patient, aged 54, arrived at the emergency department in a wheelchair accompanied by his nursing aid. The patient reported worsening ataxia, neck extension, eye-rolling, and dysarthric speech. The individual presented with a medical background of developmental delay, a decade-long medical history of optic neuritis, and had undergone cochlear implantation for sensorineural hearing loss. In addition, the patient had been diagnosed with Major Depressive Disorder accompanied by Psychotic Features for four years. The treatment involved the use of atypical antipsychotics, and the patient had been switched to clozapine six months before seeking further treatment due to the exacerbation of auditory hallucinations. The patient exhibited physical manifestations of neck extension, eye-rolling, and dysarthric speech three months before the consultation. The initial course of treatment involved the administration of diphenhydramine by an outpatient psychiatrist to manage extrapyramidal symptoms.
The patient’s symptoms deteriorated, and three weeks before their current medical evaluation, clozapine was terminated due to the onset of ataxia. The patient’s hospitalization was complicated by visual and auditory disabilities, which restricted their ability to orient themselves and undergo evaluation. Incorporating staff education on the appropriate application of cochlear implant hearing aids has emerged as a crucial element of the treatment regimen. The patient exhibited a response to internal stimuli in the early morning hours before the placement and activation of cochlear implants. However, following the procedure, the patient was alert, oriented, and able to provide insightful descriptions of auditory hallucinations. The physical examination revealed abnormal involuntary movements characterized by choreiform movements in the lower extremities, buccolingual movements, and opisthotonos. The patient’s mental status examination revealed a reaction to internal stimuli, specifically a persecutory auditory hallucination that caused significant distress. The administration of Diphenhydramine was ceased owing to its anticholinergic properties that could lead to delirium and aggravation of tardive dyskinesia. In its place, a low dose of Olanzapine was initiated to manage auditory hallucinations and block hypersensitive D2 receptors.
The patient exhibited reduced auditory hallucinations and was released to an assisted living facility on the fifth day with physical therapy and fall precautionary supervision. In cases where tardive dyskinesia fails to show improvement, the recommended course of action is to consider using a vesicular monoamine transporter 2 (VMAT2) inhibitory agent. This particular case highlights the significance of the proficiency of the healthcare team in the execution of hearing aids and the difficulty of identifying and managing tardive dyskinesia in patients with hearing and visual impairments. Timely identification of tardive dyskinesia enables a gradual withdrawal of the causative agent to avoid the resurgence of sudden discontinuation symptoms. Non-responsive symptoms may necessitate the use of VMAT2-inhibiting agents.
