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6.2 Electrode-Tissue Interface in Deep Brain
Stimulation
6.2.1 Electrode Implantation
Since the 1990s, deep brain stimulation (DBS) has become an increasingly
acceptable technology. It represents the current approach for treating debili-
tation clinical conditions such as movement disorders related to Parkinson's
disease, essential tremor, dystonia and epilepsy, all of which cannot be solved
with less invasive methods. Implantable neurostimulation has been previously
applied as spinal cord stimulation for pain management and hearing
augmentation in cochlear implants, as discussed above. Since an unexpected
positive side effect of this treatment is the improvement in the patient's mood,
the method has been adapted to treat severe cases of depression where the
individual does not respond to medication, psychotherapy or electroconvulsive
treatment. It has also been used to treat Tourette's syndrome, phantom
limb pain and obsessive-compulsive disorders, although it is not clear if the
long-term benefits outweigh the risks in these particular cases. Exciting results
have, however, been obtained in post-traumatic coma cases, when minimally
conscious patients regained some ability to speak, move and be fed without
depending on a gastrostomy tube. 11-13
There is a limited understanding of the mechanisms by which DBS achieves
such beneficial effects. In neurological conditions such as Parkinson's disease,
brain function is severely impaired by synchronization processes. The resting
tremor happens with a frequency dictated by neurons in the thalamus and the
basal ganglia, which fire in a synchronized and periodically manner. In normal
conditions these neurons fire incoherently when activating premotor areas and
the motor cortex. At the present time, when patients with advanced Parkinson's
no longer respond to drug therapy, electrodes are surgically implanted in target
areas of the brain and electrical deep brain stimulation is applied with a
frequency above 100 Hz. The technique was developed empirically and mimics
the effects of tissue lesioning by suppressing neuronal firing, which in turn
suppresses the peripheral tremor. DBS causes nearby astrocytes to release
adenosine triphosphate (ATP), a precursor to adenosine, through a catabolic
process. In turn, adenosine A1 receptor activation depresses excitatory trans-
mission in the thalamus, this causing an inhibitory effect that imitates ablation
or lesioning. In contrast with thermocoagulation, the procedure is reversible
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