Monitoring pain response with deep brain stimulation

Monitoring pain response with deep brain stimulation

Abstract

The following is a review on monitoring pain response with deep brain stimulation.  Deep brain stimulation (DBS) has been clinically proven to be successful for various forms of chronic pain however further research is required since specific mechanisms of actions are not understood. Techniques such as beamforming and artefact rejection can be used to understand the whole brain activity and newer techniques such as null beamforming easily outscores normal beamforming since it works even in presence of artefacts such as DBs electrodes. Also, long term effects of DBs can also be observed and these have helped to better understand the brain activity as well help surgeons get specific targets for surgery.

Introduction

The most common neurodegenerative disorder after Alzheimer’s is Parkinson’s disease (PD), which is increasing its social and economic burden on society as the general population ages (LM & MM, 2006). According to some recent surveys the incidence of PD especially in industrialized countries is about 0.3% for the entire general population, 1% in people who are over 60 and increasing to 4% in people above 80 years (CA, 2008).

In PD, the substantia nigra pars compacta is mainly affected which leads to an inadequate formation of dopamine, which in turn affects the normal transmission of impulses originating from the basal ganglia (BG) (J, 2008). The basal ganglia are the main area responsible for conducting various cortical functions through the limbic and occulomotor loops (BG-thalamo-cortical loops) (AP et al., 2005). Mainly in the motor as well as occulomotor circuits the BG is deemed responsible for selecting which initiated actions will be carry forwarded and allowed to be expressed that act through the brain stem motor networks as well as thalamo cortical networks (J, 2008). Motor dysfunctions are one of the main One of the main indicators of PD and form a big part of its clinical diagnosis.

Background

Deep brain stimulation (DBs)

In the early 1990’s usage of deep brain stimulation (DBs) for Parkinson’s disease started being widely accepted by the general population with the popularity increasing exponentially. The teams of scientists and doctors form Grenoble (Benabid et al., 1987) and Lille (Benabid et al., 1991). Blond and Siegfried (1991) published data and findings which was the main reason for reigniting an interest in this technique especially after various earlier publications (IS et al., 1982) had failed to generate any interest or acceptance for using DB for PD. The main appealing thing about this reinvented technique was creating a beneficial effect on the affected tissue without destroying it. Prior to this technique neurosurgeons would only be partly or not successful whilst destroying the tissue in the process. Also, the early experiences (before 1960) with this technique were burdened with mortality and morbidity (Benabid et al., 2009). Recent advances in neuroimaging etc. have aided this technique further. It has been documented that during thalamotomy there is macrostimulation of the Vim i.e., ventral intermediate. The stimulation is a relatively high frequency (100 Hz) that helps block the contralateral tremors whereas it was noted that a low frequency (50hz) actually drove tremor (Benabid et al., 2009).  Permanently implanting the electrode to the area that chronically stimulates Vim at high frequency was a proposition put forth to suppress the tremors that also avoids any complications that may arise from a thalamotomy. On increasing the stimulation voltage beneficial effects were observed including blocked tremors whereas adverse effects were also avoided on reducing the voltage.

Reviewing the potential risks involved in DBs forms an essential and big part of patient’s preoperative assessment. Still the mechanisms by which DBs exerts its effects is still controversial (R et al., 2007). On comparison with high frequency DBs in thalamus that gave promising results for lesions it was assumed that DBs works by inhibiting neuron firing. This was one of the main reasons supporting the surgeon’s decision to target the STN, which has been known to be extremely reactive in primate models of PD (Benabid et al., 2009). But recent studies have proven that more complex mechanisms might be involved (Benabid et al., 2009). One theory is that it may be working by desynchronizing pathological rhythms located in the basal ganglia (Wilson et al., 2011). Deep brain stimulation also brings a host of problems concerned with the management of PD. For e.g., there are various complication arising out of brain surgery (infection, hemorrhage), neuropsychiatric issues arising due to stimulation are also present, hence intensive follow-up sessions are required to monitor and adjust the