Patients will often return saying they are not obtaining good pain relief from deep brain stimulation. The problems fall into two major categories. First, there are changes in the patient that obviate good stimulation pain relief, and second there is a failure of the device.
When a patient reports good side effects, such as paresthesia from internal capsule stimulation, or obtains the usual side effects from periventricular stimulation when the voltage is turned up, this would indicate that the patient's electrode system is functioning properly, but that they have had something has changed in their own internal milieu that would prevent good analgesia. The main reasons for these patients not obtaining good pain relief from stimulation are as follows: First, the use of drugs that inhibit stimulation pain relief, such as a narcotic, would especially prevent good stimulation relief with periven-tricular stimulation and would require an increase in stimulation intensity for internal capsule and sensory nuclei stimulation. Second, depression may be a marker for depletion of serotonin and norepi-nephrine, which are necessary for the cascade effect of perivcentricular stimulation for pain relief. Thus, we usually continue our patients over the long term on a small amount of antidepressants, such as trazodone, 100 mg HS, or amitriptyline 50 mg HS, to help prevent tolerance to periventricular stimulation. Third, periods of high stress (anxiety, grief) tend to produce loss of pain relief for unknown reasons. The internal capsule stimulation patients are also maintained on antidepressants, because it has been our observation that patients who become depressed have a decreased response to all types of stimulation analgesia. These patients should first turn their stimulator off for approximately 2 weeks to reduce tolerance and stop medications that will interfere with stimulation of pain relief. A urine drug screen may help at times, and orally administered precursors of norepinephrin and serotonin such as L-dopa to enhance norepinephrine production or L-tryptophan for serotonin production, can be used to enhance analgesia.
Mechanical failure of the stimulation device can occur at several sites, which will be dealt with in order. Constant movement of the system, which is unavoidable, can produce failure of the insulation or electrical wiring, which produces a burning sensation over the wiring or connectors and indicates leakage of current through the insulation. This is usually followed, fairly quickly, by failure of the effective stimulation.
Skin erosion over the electrode burr hole locking device or extension connector to the electrode is a serious complication and requires removal of the hardware because of impending infection. We recommend waiting at least three months before replacing the system.
Fracture of the wiring and failure of electrical contact to the electrode is most commonly adjacent to a fixation point, usually at the locking plug under the scalp, requiring replacement of the electrode. In this situation, the wiring will sometimes show a break on radiography, but often does not, because the electrode and extension wire are multistranded and overlap on the radiographs.
Fracture of the electrode or extension wiring can cause sudden loss of stimulation, but at times can have a stuttering onset and is usually associated with trauma, such as a motor vehicle accident that produces snapping of the head and neck, which can also move the electrode. In this case, checking the impedance of the electrode, through the telemetry system, will usually show that the electrode impedance has increased, which indicates loss of continuity of the wiring.
Patients who have had stimulators for a long time may have battery depletion. This can usually be determined by telemetry, which either returns a response of battery depletion or no response at all, and is usually heralded by intermittent function of the stimulation system.
It is not unusual for patients who have failure of their stimulation system in the periventricular gray to report that their stimulator does not seem to be working but who do not have return of their pain and, therefore, feel that they do not need to have it repaired. This is usually followed in 10 days to 2 weeks by return of their pain to its original level, and they need their system replaced immediately. It is our observation that periventricular stimulation is cumulative and that this pain modulation system probably requires at least 10 days to return to its normal baseline levels, with return of the patient's pain to its prestimulation level.
Patients with VPL/VPM/IC electrodes are acutely aware when their batteries are depleted because of immediate loss of stimulation-induced paresthesias.
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