Spinal cord stimulation for nonspecific limb pain versus neuropathic pain and spontaneous versus evoked pain

OBJECTIVE: To compare the outcome of spinal cord stimulation (SCS) in patients with nonspecific limb pain versus patients with neuropathic pain syndromes and in patients with spontaneous versus evoked pain. METHODS: A retrospective review of 122 patients accepted for treatment with SCS between January 1990 and December 1998 was conducted. All patients first underwent a trial of SCS with a monopolar epidural electrode. Seventy-four patients had a successful trial and underwent permanent implantation of the monopolar electrode used for the trial (19 patients), or a quadripolar electrode (53 patients), or a Resume quadripolar electrode via laminotomy (2 patients). RESULTS: Of the 74 patients, 60.7% underwent implantation of a permanent device and were followed for an average of 3.9 years (range, 0.3-9 yr). Early failure (within 1 yr) occurred in 20.3% of patients, and late failure (after 1 yr) occurred in 33.8% of patients. Overall, 45.9% of patients were still receiving SCS at latest follow-up. Successful SCS (>50% reduction in pain for 1 yr) occurred in 83.3% of patients with nonspecific leg pain, 89.5% of patients with limb pain associated with root injury, and 73.9% of patients with nerve neuropathic pain. SCS was less effective for the control of allodynia or hyperpathia than for spontaneous pain associated with neuropathic pain syndromes. Third-party involvement did not influence outcome. There was a lesser incidence of surgical revisions when quadripolar leads were used than with monopolar electrodes. CONCLUSION: SCS is as effective for treating nonspecific limb pain as it is for treating neuropathic pain, including limb pain associated with root damage.     

脊髓电刺激治疗缺血性肢痛

背景 脊髓电刺激(spinal cord stimulation,SCS)在临床上已广泛用于治疗肢体缺血性疼痛,通过扩张外周血管、改善微循环、抑制痛觉传递等改善慢性缺血性静息痛、溃疡、坏疽等,但其扩张血管及镇痛的作用机制目前并不完全清楚. 目的 综述SCS治疗肢体缺血性疼痛的扩张血管及镇痛机制的研究进展及临床应用. 内容 阐述其诱导血管扩张及镇痛机制,包括通过交感神经系统调节机制、逆向激活感觉神经调节机制、抑制痛觉传递系统和激活镇痛物质的释放等,以及在临床应用中的适应证、疗效和并发症. 趋向 对不适合开放手术或血管介入手术的慢性肢体缺血疼痛患者,SCS治疗可作为一种合适的选择.     

Long term clinical outcome of peripheral nerve stimulation in patients with chronic peripheral neuropathic pain

BackgroundChronic neuropathic pain after injury to a peripheral nerve is known to be resistant to treatment. Peripheral nerve stimulation is one of the possible treatment options, which is, however, not performed frequently. In recent years we have witnessed a renewed interest for PNS. The aim of the present study was to evaluate the long-term clinical efficacy of PNS in a group of patients with peripheral neuropathic pain treated with PNS since the 1980s.MethodsOf an original series of 11 patients, 5 patients could be invited for clinical examination, detailed assessment of clinical pain and QST examination. The assessments were done both during habitual use of PNS and with the stimulator off.ResultsAverage pain intensity and pain unpleasantness ratings as assessed with visual analog and verbal rating scales showed significant beneficial effects of PNS. Quality of life measures (sleep and daily functioning) also showed positive effects. Quantitative Sensory Testing results did not show significant differences in cold pain and heat pain thresholds between the “ON” and “OFF” conditions.ConclusionIn selected patients with peripheral neuropathic pain PNS remains effective even after more than 20 years.     

Spinal cord stimulation in chronic pain management

As a general rule, even though it is always difficult to predict the efficacy of a method ina single patient, we consider SCS in every non-malignant chronic pain patient when other conservative treatments have failed. After three decades of clinical experience with SCS, we have learned a lot about its efficacy indifferent pain conditions and have made great technical progress with the materials and surgical procedures. Acceptance of the technique was slow at the beginning; however, we must be aware of the problems related to the application of a therapy that cannot be shamed, and thus the necessity of performing studies that include large numbers of patients. This is even more complicated when dealing with pain patients because of the well-known multifactoriality of pain. Nowadays, every algorithm for the treatment of different pain conditions includes SCS; consequently, every pain center should be able to offer this therapy in its treatment program. This article discusses what has been learned so far with regard to SCS, but there is a lot more to learn about this technique as well as about other types of neuromodulation procedures. As mentioned in the introduction of this article and discussed in the section on the effects of SCS, particularly in clinical applications like peripheral vascular disease and angina, the results of the interaction with the function of the nervous system can be observed in other systems in the body affecting pathologic conditions that are of interest to different specialists. Only the strict cooperation of different medical disciplines can provide substantial help in acquiring knowledge about the mechanisms put into play by SCS and the possible extension of its clinical applications. The complexity of the procedures of neuromodulation and the theoretic background needed for safe and proficient clinical use and for progress raise the issue for medical schools of offering courses in this new discipline.     

Spinal cord stimulation and cerebral blood flow in stroke: personal experience

Spinal cord stimulation (SCS) can increase cerebral blood flow (CBF) and improve stroke patients. In order to better understand the haemodynamic changes underlining the clinical improvement, we have studied with transcranial Doppler (TCD), SPECT and NIRS 18 patients harbouring a stroke. SPECT Group: An increase of regional CBF during SCS was measured far from the stroke areas in 9 patients, further decrease in CBF was found in 2, no changes in 1. TCD Group: An increase of CBF velocities during SCS was found in 4 patients, no changes in 6, a decrease in 1. NIRS Group: Data consistent with and increase in CBF were obtained during SCS in the only patient undergone such a study. In 6 patients studied with different techniques, data obtained fitted only in 2 patients. In 3 patients no changes in TCD faced with changes in SPECT. In one case an improvement in TCD was evident in the left while an improvement of SPECT was shown in the right site. SCS is a valid therapeutic tool in stroke patient even if, as matter of fact, parallelism between clinical and haemodynamic changes during SCS is not demonstrated in our patients, rising the question on the role of ischemic penumbra in mediating clinical improvement.     

Spinal cord blood flow change by intravenous midazolam during isoflurane anesthesia

We investigated the effects of IV midazolam on spinal cord blood flow in 32 cats anesthetized with isoflurane. Cats underwent laminectomy, and the lumbar spinal cord was exposed. A platinum electrode was inserted stereotaxically into the spinal cord to a depth of 1 mm-2 mm lateral to midline at L2. Arterial blood pressure, heart rate, and spinal cord blood flow (using the hydrogen clearance method) were measured before and at 5, 15, 30, 60, 90, and 120 min after an IV bolus of midazolam (0, 1, 2, or 4 mg/kg in saline 5 mL; n = 8 cats per dose). Arterial blood pressure was not affected by 0 or 1 mg/kg of midazolam but was decreased for 30 min by 2 or 4 mg/kg of midazolam. Heart rate did not change. Spinal cord blood flow was increased for 90 min by midazolam 1 mg/kg and for 15 min by midazolam 2 mg/kg but was not changed by midazolam 4 mg/kg. In conclusion, 1 mg/kg of midazolam increased feline spinal cord blood flow without changing arterial blood pressure. In contrast, a larger dose of midazolam (4 mg/kg) did not change spinal cord blood flow but substantially decreased arterial blood pressure during isoflurane anesthesia.     

Spinal cord stimulation for relief of abdominal pain in two patients with familial Mediterranean fever

Familial Mediterranean fever is a hereditary disease characterizedby recurrent attacks of fever and serosal inflammation thatcommonly presents as severe abdominal pain. Though colchicineremains the mainstay of treatment, a significant proportionof patients are partially responsive, unresponsive or intolerantto it. We present two such cases where spinal cord stimulation(SCS) was used to manage the paroxysmal abdominal pain associatedwith this disease. Abdominal visceral pain pathways and theapplication of SCS techniques in its management are discussed.     

Segmental neuropathic pain does not develop in male rats with complete spinal transections

In a previous study using male rats, a correlation was found between the development of "at-level" allodynia in T6-7 dermatomes following severe T8 spinal contusion injury and the sparing of some myelinated axons within the core of the lesion epicenter. To further test our hypothesis that this sparing is important for the expression of allodynia and the supraspinal plasticity that ensues, an injury that severs all axons (i.e., a complete spinal cord transection) was made in 15 male rats. Behavioral assessments were done at level throughout the 30-day recovery period followed by terminal electrophysiological recordings (urethane anesthesia) from single medullary reticular formation (MRF) neurons receiving convergent nociceptive inputs from receptive fields above, at, and below the lesion level. None of the rats developed signs of at-level allodynia (versus 18 of 26 male rats following severe contusion). However, the terminal recording (206 MRF neurons) data resembled those obtained previously post-contusion. That is, there was evidence of neuronal hyper-excitability (relative to previous data from intact controls) to high- and low-threshold mechanical stimulation for "at-level" (dorsal trunk) and "above-level" (eyelids and face) cutaneous territories. These results, when combined with prior data on intact controls and severe/moderate contusions, indicate that (1) an anatomically incomplete injury (some lesion epicenter axonal sparing) following severe contusion is likely important for the development of allodynia and (2) the neuronal hyper-excitability at the level of the medulla is likely involved in nociceptive processes that are not directly related to the conscious expression of pain-like avoidance behaviors that are being used as evidence of allodynia.     

Epidural clonidine does not decrease blood pressure or spinal cord blood flow in awake sheep

Preliminary data in animals and humans suggest that epidurally administered clonidine produces antinociception and is not neurotoxic. However, clonidine can produce vasoconstriction, and epidurally administered clonidine decreases spinal cord blood flow in anesthetized pigs. To examine the effect of epidurally administered clonidine on spinal cord blood flow in awake animals, the authors inserted lumbar epidural, femoral arterial and venous, pulmonary arterial, and left ventricular catheters in 13 adult sheep. Following a 24-h recovery, the authors injected saline (N = 6) or clonidine, 750 micrograms (17-25 micrograms/kg; N = 7) epidurally, and measured arterial blood gas tensions; temperature; heart rate; systemic and pulmonary arterial, right atrial, and pulmonary capillary wedge pressures; and spinal cord and renal blood flows (by radioactive microsphere injection) before and at 45 min and 4 h following injection. Epidural saline injection did not affect measured variables. Heart rate decreased from 112 +/- 9 to 86 +/- 4 beats/min (mean +/- SE; P = .003) and arterial PO2 decreased from 99 +/- 3 to 78 +/- 6 mmHg (P = .04) 45 min following clonidine injection. Temperature increased from 39.1 +/- .2 to 40.6 +/- 1 degree C (P = .0001) 4 h following clonidine injection. Epidural clonidine administration did not affect cardiac output, pulmonary and systemic pressures, or renal or spinal cord blood flows, except for an increase in mid-thoracic spinal cord blood flow 45 min following injection. The authors conclude that, in sheep, epidural clonidine does not produce dangerous cardiovascular depression or global spinal cord ischemia.     

Spinal cord anatomy,pain, and spinal cord stimulation mechanisms

The effectiveness and mechanisms of spinal cord stimulation described in literature rely on a proper understanding of spinal cord anatomy and pain theory. In this article we provide an overview of relevant spinal cord anatomy, pain mechanisms, and theories of pain perception. This includes the gate control theory that is the foundation for spinal cord stimulation as a treatment for chronic pain. Thereafter, we describe the different mechanisms of spinal cord stimulation. Specifically, there are considerations in anatomy, electrophysiology, neurochemistry, and neurophysiology of the central nervous system that play a role in how spinal cord stimulation modulates the pain “gate” system.     

Effect of electrical stimulation of peripheral nerves on neuropathic pain

STUDY DESIGN: Changes in the electrophysiologic response of spinal dorsal horn neurons elicited by peripheral electrical stimulation were examined. OBJECTIVE: To investigate whether the electrical stimulation of peripheral nerves causes an inhibition of pain at the spinal cord level. SUMMARY OF BACKGROUND DATA: The wide dynamic range neurons studied were known to be excited by primary afferent fibers, not only combined A (delta) and C nociceptive fibers, but also low-threshold mechanoreceptive A (beta) fibers and A (delta) fibers of down hairs. The wide dynamic range neurons are classified as nociceptive neurons. METHODS: Responses of wide dynamic range neurons in the lumbosacral dorsal horn to input from C fibers were studied in urethane chloralose-anesthetized cats. The posterior tibial nerve and sciatic nerve were stimulated simultaneously to examine the effect on the C fiber responses elicited by superficial peroneal nerve stimulation. RESULTS: Simultaneous stimulation of the posterior tibial nerve and sciatic nerve was performed with superficial peroneal nerve C fiber stimulation. CONCLUSIONS: This study demonstrated that electrical stimulation of peripheral nerves leads to inhibitory input to the pain pathways at the spinal cord level.     

Spinal cord blood flow following subarachnoid tetracaine

Spinal cord and spinal dural blood flow in the cervical, thoracic and lumbosacral regions were measured in dogs using the radioactive microsphere technique. Measurements were taken before and 20 and 40 minutes after lumbar subarachnoid injection of one of the following: physiologic saline; tetracaine 20 mg or tetracaine 20 mg with epinephrine 200 micrograms. No significant change in spinal cord or spinal dural blood flow occurred following subarachnoid physiologic saline or tetracaine with epinephrine. Dogs receiving subarachnoid tetracaine demonstrated a significant increase in lumbosacral spinal cord, and thoracic and lumbosacral dural blood flow at 20 and 40 minutes following injection. Cervical dural blood flow was significantly increased at 40 minutes after subarachnoid tetracaine. Lumbar subarachnoid tetracaine (20 mg) produces a regional spinal cord and generalized dural hyperemia which is prevented by the addition of epinephrine (200 micrograms).     

Spinal cord blood flow following sub-arachnoid lidocaine

Twelve mongrel dogs were randomized into two equal groups. Cervical, thoracic and lumbosacral spinal cord and spinal dural blood flows were measured using the radioactive microsphere technique. Blood flow determinations were made prior to and 20 and 40 minutes following lumbar subarachnoid injection of: two per cent lidocaine (100 mg) or two per cent lidocaine (100 mg) with 1/25,000 epinephrine (200 micrograms). Dogs receiving subarachnoid lidocaine demonstrated a decrease in mean arterial blood pressure of 23 per cent and 14 per cent (p less than 0.05), while dogs receiving lidocaine with epinephrine had a decrease of 38 and 34 per cent (p less than 0.05) at 20 and 40 minutes respectively. Cardiac index was not significantly changed in either group. Lumbar subarachnoid lidocaine (100 mg) produced a rapid regional dural hyperemia (observed at 20 minutes postinjection) and a delayed regional spinal cord hyperemia (observed at 40 minutes postinjection) which were not observed following the addition of epinephrine (200 micrograms).     

Spinal cord blood flow following subarachnoid lidocaine

Twelve mongrel dogs were randomized into two equal groups. Cervical, thoracic and lumbosacral spinal cord and spinal durai blood flows were measured using the radioactive microsphere technique. Blood flow determinations were made prior to and 20 and 40 minutes following lumbar subarachnoid injection of: (I) two per cent lidocaine (100 mg) or (2) two per cent lidocaine (100 mg) with 1/25,000 epinephrine (200 μg). Dogs receiving subarachnoid lidocaine demonstrated a decrease in mean arterial blood pressure of 23 per cent and 14 per cent (p < 0.05), while dogs receiving lidocaine with epinephrine had a decrease of 38 and 34 per cent (p < 0.05) at 20 and40 minutes respectively. Cardiac index was not significantly changed in either group. Lumbar subarachnoid lidocaine (100 mg) produced a rapid regional durai hyperemia (observed at 20 minutes postinjection) and a delayed regional spinal cord hyperemia (observed at 40 minutes postinjection) which were not observed following the addition of epinephrine (200 μg).