Neurostimulation is the application of precise targeted electrical stimulation on nociceptive pathways. Electric stimulation has a long history in medicine for treating various ailments. Beyond the application of electrodes on the skin such as in transcutaneous electrical nerve stimulation (TENS), electrodes have been applied directly to nociceptive pathways.
The nociceptive pathways are made up of tracts in the central and peripheral nervous systems. The central nervous system includes nociceptive pathways in the spinal cord and brain, specifically the dorsal roots, dorsal ganglion, spinothalamic tracts, and all ascending neural tracts to the cerebrum. The peripheral nervous system includes pathways outside the spinal cord, specifically various plexuses and peripheral nerves.
Components of the System
Spinal cord stimulation involves the placement of an electrical system to block nociception. The system comprises the surgical placement of epidural electrodes, cables, and radiofrequency transmitter or battery. Much of this method has evolved from cardiac pacemaker technology. The minimal invasiveness and trialing has led to the success of this approach. Neurostimulation can be placed during an outpatient procedure, with local anesthesia and sedation. The patient experiences minimal discomfort when the system is placed and during the postoperative period.
Before the system is placed, a simple trial of percutaneous lead placement can be performed. In this case, the patient goes home with the lead connected to a screener box. No incision is necessary and the procedure is performed using only local anesthesia. The purpose of the trial is to determine the effectiveness of the stimulation for relieving pain and improving the patient's quality of life. If this temporary method allows the patient to sleep better, use less pain medication, and sit and stand longer, then it becomes more convincing to place an internalized spinal cord stimulation system.
Mechanism of Action
The mechanism of action of spinal cord stimulation is based on the placement of epidural electrodes along the dorsal columns. Originally, spinal cord stimulation was called dorsal column stimulation. It is thought that spinal cord stimulation works through the gate-control theory of Wall and Melzack, which theorizes that stimulating large nerve fibers (A beta fibers) can inhibit or modulate smaller nerve fibers (A delta or C fibers), transmitting nociceptive input possibly at the dorsal root or horn of the spinal cord. Strategically placed epidural electrodes stimulate the dorsal columns (A beta fibers) to inhibit or modulate incoming nociceptive input through the A delta or C fibers. Ongoing research suggests that spinal cord stimulation may inhibit transmission in the spinothalamic tract, activation of central inhibitory mechanisms influencing sympathetic efferent neurons, and release of various inhibitory neurotransmitters.
Spinal cord stimulation can be applied to treat neuropathic pain conditions, including arachnoiditis, complex regional pain syndrome (formerly called reflex sympathetic dystrophy), neuropathies, brachial and lumbosacral plexopathies, radiculopathies, deafferentation syndromes, phantom limb pain, and postherpetic neuralgia. Clinical studies and 30 years of clinical experience have continued to show efficacy in these conditions. Visceral syndromes such as interstitial cystitis, chronic abdominal pain, and chronic pancreatitis have been treated with limited success.
Intractable pain caused by peripheral vascular disease and angina can be treated with spinal cord stimulation. Indeed, in Europe, the primary indication for spinal cord stimulation once was peripheral vascular disease. The success of stimulating the lower extremities may be based on microvascular blood flow changes via alterations in sympathetic outflow. It could also be that one is treating a concurrent ischemic neuropathy in the lower extremities.
Limited success of spinal cord stimulation may depend on the extent of peripheral vascular disease. Based on one study, spinal cord stimulation does not reduce the incidence of amputation in the lower extremities. The same rationale for using spinal cord stimulation for treating peripheral vascular disease is now being applied in clinical trials of patients with intractable angina, including those with patent coronary vessels who continue to have intractable angina and patients who are not candidates for coronary bypass and stent procedures. It is theorized that these patients have a neuropathic condition and microvascular blood flow deficiency.
Some painful conditions cannot be stimulated along the spinal cord and therefore are not responsive to spinal cord stimulation. Thus, peripheral nerve and plexus stimulation has evolved as a complementary neurostimulation approach. The mechanism of peripheral nerve and plexus stimulation is unclear since the electrodes are not stimulating the dorsal columns. Some postulate that a variation of the gate-control theory is involved at the peripheral nervous system level. Moreover, peripheral nerve stimulation may activate central structures leading to inhibition of various nociceptive pathways, similar to the way acupuncture results in somatosensory cortex activation.
Current clinical trials and experience have involved 3 different patient groups. First, intractable headaches caused by neuropathies of the trigeminal and occipital nerves may benefit from neurostimulation. Trigeminal neuralgia is a painful constant condition for which neurodestructive neurolysis may not work. Neurostimulation of the actual trigeminal ganglia has been performed. Stimulation of various branches of the trigeminal ganglia, such as supraorbital and auriculotemporal nerve, has been performed with limited success. Ongoing clinical research is under way on occipital nerve stimulation; electrodes are placed percutaneously and surgically along these nerves at the subcutaneous occiput level. The peripheral nerve stimulation system is placed in a manner similar to the spinal cord stimulation system.
Second, stimulation of the sacral nerves or lumbosacral plexuses can be beneficial for painful conditions resulting from chronic abdominal, pelvic, genital, and anal pain syndromes. Specific conditions that have been treated include interstitial cystitis, coccydynia, pyelonephritis, pancreatitis, rectal fugax, and vulvodynia. These perplexing syndromes are difficult to treat in significant part because we lack a complete understanding of what perpetuates them. Procedures allowing access to sacral and lumbosacral nerves include a retrograde epidural approach and a sacral transforaminal approach.
Third, some peripheral neuropathies, neuromas, and plexopathies are difficult to stimulate along the spinal cord and may not respond to spinal cord stimulation. Surgically or percutaneously placed electrodes along nociceptive pathways have been performed with success. The most common sites are along the ulnar, median, common peroneal, and saphenous nerves.
Neurostimulation of the central and peripheral nervous systems is playing a vital role in the treatment of various intractable pain conditions, including conditions for which we have limited pathophysiologic understanding, such as complex regional pain syndrome. Until we develop treatments that truly eliminate pain, neurostimulation can play a major role in improving the quality of life for pain patients. These systems do not damage neural pathways and could be removed when curative therapy becomes available.
As patients and their physicians become aware of the benefits of these techniques for managing intractable and difficult-to-treat pain syndromes, more people may be interested in undergoing this kind of treatment and will achieve improvements in the quality of their lives. The comedian Jerry Lewis lives with intractable low back pain and has attributed his spinal cord stimulation system with giving him his life back. Hopefully, he will continue to talk about his life and persuade others that they don't have "to live with it [pain]."
- Horsch S, Schulte S, Hess S. Spinal cord stimulation in the treatment of peripheral vascular disease: results of a single-center study of 258 patients. Angiology. 2004;55:111-118.
Albutaihi IA, Hautvast RW, DeJongste MJ, et al. Cardiac nociception in rats: neuronal pathways and the influence of dermal neurostimulation on conveyance to the central nervous system. J Mol Neurosci. 2003;20:43-52.
Augustinsson LE. Spinal cord stimulation in peripheral vascular disease and angina pectoris. J Neurosurg Sci. 2003;47(1 suppl 1):37-40.
Buschmann D, Oppel F. Peripheral nerve stimulation for pain relief in CRPS II and phantom-limb pain. Schmerz. 1999;13:113-120.
Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year literature review. J Neurosurg. 2004;100(3 suppl):254-267.
Erdek MA, Staats PS. Spinal cord stimulation for angina pectoris and peripheral vascular disease. Anesthesiol Clin North Am. 2003;21:797-804.
Jessurun GA, Hautvast RW, Tio RA, DeJongste MJ. Electrical neuromodulation improves myocardial perfusion and ameliorates refractory angina pectoris in patients with syndrome X: fad or future? Eur J Pain. 2003;7:507-512.
Murray S, Collins PD, James MA. Neurostimulation treatment for angina pectoris. Heart. 2000;83:217-220.
Rushton DN. Electrical stimulation in the treatment of pain. Disabil Rehabil. 2002;24:407-415.
Weiner RL. Peripheral nerve neurostimulation. Neurosurg Clin North Am. 2003;14:401-408.
Zamotrinsky AV, Kondratiev B, de Jong JW. Vagal neurostimulation in patients with coronary artery disease. Auton Neurosci. 2001;88:109-116.