Implantable Components of the deep brain stimulator device
Placement and Programming of the Device
What are the General Therapeutic stimulation parameters for OCD?
Deep brain stimulation therapy results for OCD
Adverse Effects of DBS
What do the stimulating electrodes cause?
How DBS works?
Placement of the electrodes is performed in stereotactic conditions either under local or general anesthesia. One electrode with four contacts is placed on each side of the brain in the anterior limbs of the internal capsules, including the nucleus accumbens. These are the exact locations used in capsulotomy. Postoperatively, the accuracy of the electrode position is confirmed by computed tomography or magnetic resonance imaging (MRI). Stimulation parameters are optimized by the neurosurgeon, using an external programming unit, during the few weeks following surgery. This is achieved by using different combinations of the four electrode contacts, based on acute improvements in mood or anxiety or reduction in obsessive thoughts (9).
What are the General Therapeutic stimulation parameters for DBS?
The parameters controlled by programming the pacemaker are stimulation amplitudes, pulse durations, and frequencies. These parameters are derived primarily by trial and error. This method is easy for the treatment of Parkinson's because of the near immediate effects of DBS on tremor. On the other hand, the beneficial effects of deep brain stimulation for obsessive-compulsive disorder can take weeks to months to manifest. Thus, it is unclear what simulation amplitudes, pulse durations, and frequencies are most effective (7), making it more difficult to use deep brain stimulation to treat OCD.
The results are similar to those of ablation (lesioning) of the same region (7). However, deep brain stimulation is reversible, unlike ablation. The specific results vary from patient to patient ranging from complete absolution of obsessive thoughts to no discernable effects.
The major risks of device implantation include hemorrhage, infection, and seizure. However, the incidence of these risks is approximately 2 to 3% of implantation procedures. Device malfunction and battery depletion also occur, but battery depletion is not lethal. Simply, the effects of the stimulation will cease, and recurrence of obsessive thoughts will return (8).
The effects of the stimulation itself may cause paresthesia or other unusual or unpleasant sensory experiences; disequilibrium; weakness; difficulty in articulating words, caused by impairment of the muscles used in speech and changes in mood, memory, or cognition. These are the most common adverse effects (8).
What do the stimulating electrodes cause?
The electrode elicits both direct and indirect effects on local cells. The direct effects result from the depolarization and hyperpolarization of the neural membrane of the cells. However, the activity in the cell body is not representative of the spiking output generated in the axon. In essence, hyperpolarization of the cell body does not necessarily mean the axon will not generate an impulse. In fact, efferent output of cells within 2 mm of the electrode will generate stimulus at the same frequency as the therapeutic stimulation. In the case of OCD patients, this decreases the frequency of cell output in a hyper-activated region, causing a decrease in activity. The indirect effects occur as a result of activation of afferent inputs from the extracellular stimulus and their subsequent synaptic action on local cells (7).
It is common for the cell body to be directly hyperpolarized by the stimulus pulse, but the first few nodes of Ranvier are typically depolarized by the stimulus pulse because of the short internodal spacing of the axon when compared to the field of the electrode This depolarization initiates an impulse along the axon. Also, the threshold for activation of axonal terminals projecting into the region around the electrode is lower than the threshold for direct activation of local cells (7). This means that the impulse rate is largely determined by the electrode stimulation frequency.
Currently, scientists are not entirely certain how deep brain stimulation causes similar effects as lesions in the same region of the brain. Somehow the electrode stimulations override pathological activity patterns, but the patterns induced are not necessarily normal. Here are the four dominant theories:
1) Depolarization blockadeThrough stimulation induced alterations in voltage activation of the neural membrane, neural outputs near the stimulating electrode are blocked. Although this theory accounts for the results of DBS being similar to ablation, it doesn't take into account the possible independent activation of the efferent axon of projection neurons (7). Thus, it does not explain why impulses are still being generated around the area of the electrode.
2) Synaptic inhibition
Neurons can not generate electrical impulses when electrically stimulated due to activation of axon terminals near the stimulating electrode. However, for the same reason as the depolarization blockade theory, it looses credibility because it does not explain the ability of efferent axons to fire impulses (7).
3) Synaptic depression
Synaptic transmission failure of the efferent output of stimulated neurons as a result of transmitter depletion caused by excessive stimulation by the electrode. This theory is discredited because several in vivo experimental studies have shown increases in transmitter release and sustained changes in firing of neurons in efferent nuclei when repeatedly stimulated by an electrode (7).
4) Stimulation induced modulation of pathological network activity
This is the only general theory that is consistent with the current available data. It accounts for the continuing of firing of impulses by efferent axons located in the electrode region. The alteration in the neural network could have the same results as ablation therapy induces (7). Thus, both results are accounted for. However, this theory does not explain much. It simply states that the neural network is altered by the electrodes stimulations. We still are not sure how or why the network is altered.
