Tardive dyskinesia responsive to deep brain stimulation

Tardive dyskinesia (TD) describes persistent, sometimes irreversible, abnormal involuntary movements appearing over the course of prolonged neuroleptic treatment, dose reduction or withdrawal of antipsychotics. Deep brain stimulation (DBS) involves continuous application of electrical stimulation pulses at high frequency to specific brain regions (Smith and Wichmann, 2008). The most likely mode of action so far suggests that network-wide modulatory effects of DBS mediate its clinical effects (Chen et al., 2013).

We describe a 40-year-old male, suffering from Bipolar I disorder (BPAD) for the last 24 years. The last relapse of major mood episode was in 2013 with mania with psychotic features. He stabilized on lithium SR 450 mg nocte, sodium valproate 200 mg BD and olanzapine 5 mg BD. Olanzapine was changed to asenapine 10 mg nocte prior to discharge.

He complained of hand tremors and muscle tension after a year of stability. Lithium was discontinued, and valproate was increased to 1200 mg daily. Lithium was restarted because of deterioration in mood. Asenapine was gradually increased to 20 mg. He complained of inner restlessness and perioral involuntary movements. Asenapine was weaned off. Involuntary movements worsened 1–2 months after stopping asenapine, involving neck, upper arm and truncal movements with involuntary muscle spasms. Lithium was discontinued.

He was then trialed sequentially on benztropine, tetrabenazine (four separate trials with severe akathisia as persistent issue), magnesium, melatonin, vitamin B6, lecithin, B3, zolpidem, benzhexol, clonidine and naltrexone with limited benefit. Clonazepam provided consistent short-term benefits. Clozapine was started and titrated up to 350 mg daily with marginal benefits. He also moderately benefited from periodic botulinum injections.

There was worsening of TD with psychosocial stress and improvement with sleep deprivation. The patient underwent bilateral globus pallidus internus (GPi) DBS. He reported more than 70% improvement in his TD on Abnormal Involuntary Movement Scale (AIMS) score over 6 months post-surgery. Clozapine was continued along with clonazepam PRN.

He remains psychologically stable with improvements in TD 9 months post-surgery. Interestingly, there was improvement in TD with sleep deprivation, possibly explained by sleep deprivation increasing dopamine and norepinephrine sensitivity, therefore increasing dopamine transmission (Salvadore et al., 2010).

As far as the authors are aware, this is the first reported case of treatment of TD by DBS in Australia. Bilateral DBS to GPi has been successful in treating severe TD in a young patient with significant functional impairment, similar to internationally reported results. DBS is a neuroinvasive procedure, but considering its safety and efficacy, it can be carefully considered in selected patients with severe TD after exhausting pharmacological options.