DBS, Parkinson's Disease, and Suicide

To the Editor: I read with interest Dr. Mahgoub's and Dr. Kotbi's case report, “Acute depression and suicidal attempt following lowering the frequency of deep brain stimulation.”¹ The authors report the case of a 66-year-old patient treated with deep brain stimulation (DBS) of the subthalamic nucleus (STN) for Parkinson's disease (PD) of 20 years' duration, who suffered an acute depressive episode associated with a suicide attempt after the modification of his DBS stimulation parameters.

In this patient, a reduction of the frequency of the stimulation from 185 Hz to 60 Hz was noted with the induction of an acute suicidal state. By increasing the frequency, the depressive state improved, and the suicidal ideations subsided. Dr. Mahgoub and Dr. Kotbi write that “Our case demonstrates the risk of suicide when lowering the frequency of the stimulation… Patients at high risk for suicide should be excluded from deep brain stimulation surgery.”

Some differentiations and specifications here might be needed: The patient reported by the authors was treated with DBS of the subthalamic nucleus (STN). Although DBS STN for PD is known to be associated with a plethora of neuropsychiatric adverse effects, such as confusion, psychosis, depression, mania, and suicidal ideation,² noteworthy within this context is that psychosis, depression, and suicidal ideation are known also in patients with PD not undergoing DBS treatment.³

The authors write that DBS “has now also been extended to other neuropsychiatric conditions and has shown some promising results in patients suffering from profound depression.” It is advisable though to differentiate that while the main target for DBS for PD is the STN, DBS applied to treat depression has different targets, such as the nucleus accumbens, the subgenual cingulate (Cg25), and the ventral capsule and ventral striatum (VC/VS).⁴

The relationship between stimulation settings of the DBS device and neuropsychiatric adverse effects is known; however it is important to note that the literature shows considerable contrasting findings in this matter.²

Some authors reported that stimulation induced limbic effects, whereas termination of stimulation led to a resolution of the limbic symptoms;⁵ in contrast to the case reported by Dr. Mahgoub and Dr. Kotbi. Still other authors specified that limbic side effects were not affected by changing the stimulation parameters, but required the changing of the localization of the stimulating contacts or subsided solely after pharmacological treatment.²

Although Dr. Mahgoub and Dr. Kotbi's report is important, the statement that “our case demonstrates the risk of suicide when lowering the frequency of the stimulation” cannot be made with such implicitness. The plethora of contrasting reports on this subject matter² does not allow for generalization of findings, especially if they are based on a single case report. More research is yet needed to elucidate the polyhedral relation between STN DBS, PD, and suicide.