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OBJECTIVE To optimize the technique of implanting laminotomy plate electrodes for spinal cord stimulation and to minimize the discomfort of the patients during surgery. This operation is often performed while the patient is under local anesthesia, which is very stressful for the patient, or under general anesthesia, which precludes the use of test stimulation. An alternative approach is to perform the implantation with a spinal anesthetic and to examine whether stimulation-induced paresthesiae can still be evoked to guide the positioning of the electrode. METHODS Spinal anesthesia was induced by bupivacaine (12.5–20 mg), which produced complete motor block and anesthesia up to a midthoracic level. After a single-level laminotomy (thoracic vertebrae 9–11) a four-pole plate electrode was inserted into the epidural space. Stimulation was applied with commonly used parameters, and the electrode was positioned so that the paresthesiae covered the painful region. RESULTS In 19 patients (20 procedures) with different forms of neuropathic pain, implantation of laminotomy plate electrodes could be performed under spinal anesthesia without problems. In all patients, it was possible to evoke paresthesiae, the distribution of which could be reproduced postoperatively. The paresthesia thresholds during surgery were only moderately higher than those recorded after implantation (mean, 3.1 versus 2.1 V, respectively). During an interview after the intervention, no patient reported that he or she had experienced surgery as painful or uncomfortable. CONCLUSION Implantation of laminotomy electrodes can be performed conveniently with spinal anesthesia because it minimizes discomfort for the patient and enables the use of intraoperative test stimulation to guide the positioning of the electrode. In spite of the total motor block and anesthesia, paresthesiae representing the activation of the dorsal columns can be evoked and are well perceived, and the thresholds are not abnormally high. This observation supports the notion that the subarachnoidal anesthetic agent acts predominantly on the spinal rootlets rather than on the spinal afferent pathways.

OBJECTIVE The aim of the present study is to monitor the extracellular gamma-aminobutyric acid (GABA) levels in the lumbar dorsal horn of allodynic rats, which respond to spinal cord stimulation (SCS) with a normalization of the tactile withdrawal threshold. In addition, we monitored the GABA levels in nonresponding and sham-stimulated rats. METHODS Partial constriction injury of the sciatic nerve was performed, and a permanent electrode for SCS was inserted into the spinal canal. The response to SCS was assessed with von Frey hairs in awake animals. Later, microdialysis was performed in the dorsal horn of the spinal cord under halothane anesthesia. The concentration of GABA in the microdialysate was assessed by high-performance liquid chromatography. RESULTS Extracellular GABA levels in rats with sciatic nerve lesions and allodynia (2.3 +/- 0.5 nmol/L) were significantly lower (P < 0.001) than in control rats with intact sciatic nerves (8.1 +/- 1.0 nmol/L), whereas only slightly decreased GABA levels (5.7 +/- 1.1 nmol/L) were detected in nonallodynic rats with sciatic nerve lesions. In the allodynic rats, which respond to SCS by a normalization of the tactile withdrawal threshold, significantly (P < 0.001) increased GABA levels (6.7 +/- 2.3 nmol/L) were detected after SCS. In contrast, neither the allodynic rats, which did not respond to SCS, nor the sham-stimulated allodynic rats displayed increased GABA levels in response to stimulation. CONCLUSION Our results indicate that the development of allodynia, a common symptom in neuropathic pain states, may be linked to a decreased spinal release of GABA. We suggest that an SCS-induced release of GABA could be important for the suppression of allodynia observed in rats after SCS. Similar mechanisms could also be involved in the SCS-induced alleviation of pain in patients with peripheral neuropathy.

Spinal cord stimulation (SCS) has been increasingly used in the treatment of ischemia caused by obliterative diseases in the extremities and in the cardiac circulation. The most promising effects have been obtained when physicians suspect that a major vasospastic component underlies the ischemic symptoms (e.g., as in Raynaud's disease). Despite the clinical success of this treatment method, little is known about the mechanisms underlying the pain relief it produces and its anti-ischemic effects. Most earlier experimental studies have used normal animals or animals with cerebral vasospasm induced by injection of autologal blood into the cerebrospinal fluid space. In the present study, we applied SCS in a rat model via implanted electrodes to study the effect of preemptive stimulation on the ischemia caused by vasospasm in a neurovascular flap in the groin; the vasospasm was induced by mechanical pressure applied to the feeding artery. In rats treated with SCS, delivered with parameters similar to those used clinically, the percentage of flaps recovering normal microcirculation after the spasm was significantly higher than in the untreated control group (100 and 28%, respectively; P < 0.05), and the maximal blood flow after the ischemic episode was significantly higher in the SCS group than in the control group (127 and 51 arbitrary units, respectively; P < 0.05). The percentage of animals regaining the premanipulation circulation after the provocation of a second spasm was also greater in the SCS-treated group than in the control animals (50 and 14%, respectively; P < 0.05). Pilot studies showed that this protective effect was specific to SCS given before spasm induction, an observation corroborated by clinical experiences.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric spinal cord stimulation (SCS) is widely used as a treatment modality for ischemic pain in peripheral arterial insufficiency. The background for the therapeutic effect may be a temporary inhibition of sympathetically maintained peripheral vasoconstriction. In this series of experiments, the involvement of different types of cholinergic and adrenergic receptor subclasses in the vasodilatory effect was explored in anesthetized rats. The microcirculation in hindlimb skin and hamstring muscle was studied by the laser Doppler technique. The ganglionic blocker hexamethonium as well as the nicotinic receptor antagonist chlorisondamine abolished the effect in both vascular beds, whereas the muscarinic receptor antagonists pirenzepine and atropine were ineffective. Among the adrenergic receptor active compounds, phentolamine, prazosine (an alpha 1-receptor antagonist), and clonidine in high doses suppressed the SCS-induced vasodilation. Yohimbine (an alpha 2-receptor antagonist) did not alter the effect. The beta-adrenergic compounds had a differential effect on muscle and skin perfusion. Atenolol, a beta 1-receptor antagonist, inhibited SCS-induced vasodilation only in the skin, whereas the beta 2-receptor antagonist butoxamine selectively depressed the muscle response. The vasodilatory effect of SCS in the animal model used here seems to a large extent to be mediated by an inhibitory effect on peripheral vasoconstriction maintained via efferent sympathetic activity involving nicotinic transmission in the ganglia and the postganglionic alpha 1-adrenoreceptors. The involvement of beta-receptors seems to be different in skin and muscle, beta 1 being more important for the changes in the skin and beta 2 being more important for those in muscle. The high-intensity antidromic response, earlier believed to explain how SCS exerted its vasodilatory effect, was resistant to cholinergic and adrenergic manipulations and seems to depend on entirely different mechanisms.

The mechanism underlying the beneficial effect of electrical stimulation of the posterior surface of the spinal cord in chronic pain states are unknown. The prolonged pain relief following a short stimulation period is believed to imply the activation of long-lasting neurochemical processes, mainly in the spinal cord, but possibly also involving other parts of the central nervous system. Previous studies have demonstrated that substance P and serotonin are released in the cat dorsal horn during spinal cord stimulation (SCS) with electrical parameters similar to those used in the clinic. However, gamma-aminobutyric acid (GABA) has also been hypothesized to play a role in the effect of SCS, but there have been no studies of the possible effects of SCS on GABA release. The authors applied SCS to anesthetized rats and monitored the extracellular concentration of GABA in the lumbar dorsal horns by microdialysis and a sensitive reverse-phase high-performance liquid chromatography technique. After 30 minutes of SCS, the GABA level increased significantly (by almost 270%) in comparison with the basal level recorded before stimulation, from 3.6 +/- 1.0 nmol/L to 13.1 +/- 2.2 nmol/L (mean +/- the standard error of the mean; P < 0.05). The peak release was delayed and appeared in the 30-minute fraction collected after stimulation. Also, perfusion of the dialysis probes with potassium (100 mmol/L) induced an increase of the GABA level. In control experiments without electrical stimulation, slowly decreasing GABA levels were observed throughout the experiments. The present results may suggest an involvement of GABA in the mechanism of SCS-induced pain relief.(ABSTRACT TRUNCATED AT 250 WORDS)

Background Percutaneous balloon compression is an effective, low-cost, simple therapeutic modality with the special advantage of being the only percutaneous technique that can be simply performed with the patient under general anesthesia for the treatment of trigeminal neuralgia. Objective To identify surgical and individual parameters that could influence outcome in patients with trigeminal neuralgia treated with percutaneous balloon compression. Methods Within a 5-year period, 66 consecutive percutaneous balloon compressions were performed in 47 patients. The medical and surgical records of all patients were retrospectively reviewed and analyzed for a possible correlation between the following parameters and outcome: balloon shape, balloon volume, compression time, age, sex, type of pain, duration of disease, previous procedures, and trigeminal division affected. Univariate and multivariate analyses were used to test for statistical significance. Results The initial success rate was 85%, and 36% of the responders are still pain free with a mean follow-up of approximately 20 months, whereas in 33 patients, trigeminal pain recurred after a mean of approximately 17 months. Of the investigated parameters, significant correlations were obtained between balloon shape and all aspects of outcome, previous operations and complication rate, pain type and complication rate, and compression time and postoperative numbness. Conclusion The balloon shape is a parameter with a very strong impact on outcome, and balloon volume should be adjusted to this parameter. Persistent elliptical balloon shapes should raise consideration of aborting the procedure. There were no differences in outcomes between 60 seconds and longer compression times. The number of previous operations did not correlate with pain relief, but seemed to increase the risk of complications. Patients with multiple sclerosis seemed to obtain similar benefit from the procedure as do patients with classic trigeminal neuralgia.

OBJECTIVE: Spinal cord stimulation (SCS) is a well-established treatment for neuropathic pain; nevertheless, 40% of patients fail to obtain satisfactory pain relief and in many patients, the effect tends to diminish with time. Based on animal experiments, intrathecal baclofen was previously introduced clinically to enhance suboptimal SCS effects. Later animal experiments demonstrated similar data for clonidine. The aim of this study was to elucidate whether intrathecal clonidine or baclofen enhances the effect of SCS in neuropathic pain patients in whom the pain relieving-effect of SCS is inadequate. METHODS: A randomized, double-blind, placebo-controlled clinical trial was conducted with 10 patients experiencing neuropathic pain with insufficient pain relief with SCS alone. Clonidine, baclofen, and saline (control) were intrathecally administered by bolus injections in combination with SCS. RESULTS: Seven of 10 patients reported significant pain reduction when SCS was combined with active drugs. The mean visual analog scale ratings were reduced by more than 50% with either drug combined with SCS. Four patients previously treated with SCS alone later underwent implantation of a pump for long-term administration of clonidine or baclofen. In the 2 patients with clonidine pumps with a mean follow-up of 15 months, the combined therapy produced pain reduction of 55% and 45%, respectively. The corresponding effect with baclofen was 32% and 82%, respectively, at 7 months follow-up. CONCLUSION: A trial with clonidine and baclofen combined with SCS may be warranted in patients who do not obtain satisfactory pain relief with SCS alone or experienced a decreasing therapeutic effect.

Electric stimulation of the dorsal spinal cord (DCS) in the treatment of pain in peripheral vascular disease is known to enhance peripheral circulation, but the mechanisms are still obscure. An earlier study has provided indirect evidence that the vasodilator effect is dependent upon alteration of sympathetic vasomotor activity. In the present study, surgical interruption of sympathetic pathways was performed to define the role of the sympathetic system for the stimulation-induced vasodilation. Three groups of normal rats were used: one group subjected to lumbar sympathectomy, one group sham-operated about 1 week before performing spinal cord stimulation, and a third group, without pretreatment, serving as a second control. Stimulation was applied to one dorsal column at the thoracolumbar junction, and peripheral microcirculation was recorded in hind limb skin and muscle by laser Doppler technique. The stimulation parameters were chosen to correspond with those used clinically in man. A cold test with monitoring of cold-induced changes in peripheral blood flow was used to assess the completeness of the sympathectomy. The preoperative cold test induced a reciprocal response, vasoconstriction in the skin and vasodilation in muscle. DCS with clinical parameters did not produce this reciprocity in the control and sham-operated rats, but induced a vasodilation in both skin and muscle. After complete sympathectomy, defined as postoperative disappearance of the vasomotor responses to cold, the vasodilation in skin and muscle in response to DCS was abolished; however, the vasodilatory response to high-intensity stimulation (approximately 10 times the motor threshold) was not affected. Incomplete sympathetic denervation in some animals resulted in partial preservation of a vasodilatory response to DCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Spinal cord stimulation has been reported to relieve ischemic pain and to enhance peripheral circulation. To elucidate the still unknown mechanisms behind these effects, changes in the peripheral blood flow in the skin of the hind paw after stimulation applied to the dorsal column was studied in the normal rat. A substantial flow increase, monitored by laser Doppler technique, was observed in response to stimulation with an intensity comparable to that used clinically in man, recruiting only low-threshold neuronal elements. The response remained after transection of the dorsal roots, as well as after spinal cord section rostrally to the stimulating electrode. Furthermore, monitoring of antidromic compound action potentials in a peripheral nerve indicated that the stimulus intensity applied to dorsal columns recruited solely low-threshold, large-diameter fibers. Stimulation failed to produce an increase in blood flow in addition to that produced by guanethidine and hexamethonium, but high-intensity dorsal column or dorsal root stimulation still was effective. The results indicate that spinal mechanisms are essential and that antidromic activation of primary afferent fibers is unlikely to account for the peripheral vasodilatation induced by low-intensity spinal cord stimulation. Our observations suggest a transitory inhibition of sympathetic vasoconstriction as the principal underlying mechanism.

Balloon compression of the rootlets behind the trigeminal ganglion for the treatment of trigeminal neuralgia has become an increasingly popular method among neurosurgeons. However, the method has recognized complications, including double vision. Although occurring infrequently, diplopia may cause the patient significant disability. To minimize the risk for this complication, we analyzed our patients with respect to the surgical technique.We reviewed our joint consecutive series of 193 patients with trigeminal neuralgia treated with balloon compression. The medical records and the intraoperative x-ray images were analyzed.We identified six patients with double vision postoperatively. In analyzing these occurrences, we found that the balloon was inflated outside Meckel's cave in four patients, the balloon was initially inflated too deeply in one patient, and the anatomy of Meckel's cave was probably aberrant in one patient. In five of the six patients, the symptoms resolved within 5 months.By meticulous surgical technique with close attention to the anatomic position and the shape of the inflated balloon, most cases of postcompression diplopia should be avoided.

The mechanism underlying the beneficial effect of electrical stimulation of the posterior surface of the spinal cord in chronic pain states are unknown. The prolonged pain relief following a short stimulation period is believed to imply the activation of long-lasting neurochemical processes, mainly in the spinal cord, but possibly also involving other parts of the central nervous system. Previous studies have demonstrated that substance P and serotonin are released in the cat dorsal horn during spinal cord stimulation (SCS) with electrical parameters similar to those used in the clinic. However, gamma-aminobutyric acid (GABA) has also been hypothesized to play a role in the effect of SCS, but there have been no studies of the possible effects of SCS on GABA release. The authors applied SCS to anesthetized rats and monitored the extracellular concentration of GABA in the lumbar dorsal horns by microdialysis and a sensitive reverse-phase high-performance liquid chromatography technique. After 30 minutes of SCS, the GABA level increased significantly (by almost 270%) in comparison with the basal level recorded before stimulation, from 3.6 +/- 1.0 nmol/L to 13.1 +/- 2.2 nmol/L (mean +/- the standard error of the mean; P0.05). The peak release was delayed and appeared in the 30-minute fraction collected after stimulation. Also, perfusion of the dialysis probes with potassium (100 mmol/L) induced an increase of the GABA level. In control experiments without electrical stimulation, slowly decreasing GABA levels were observed throughout the experiments. The present results may suggest an involvement of GABA in the mechanism of SCS-induced pain relief.(ABSTRACT TRUNCATED AT 250 WORDS)

The neurohumoral mechanisms behind the pain-suppressing effect of dorsal column stimulation (DCS) still remain obscure. Experimental observations have indicated an inhibitory role for serotonin and, under certain conditions, also for substance P (SP), on nociceptive transmission in the spinal cord. Furthermore, some observations suggest that these substances might be involved in the effect of DCS. The present series of experiments was undertaken to investigate whether serotonin and SP are released in the dorsal horn by DCS. Twenty-one adult cats, in some experiments anesthetized, in others decerebrated at the midcollicular level, were used. Microdialysis probes were implanted bilaterally in lumbar dorsal horns (L5-L7) and perfused with Krebs' solution. Dialysates were analyzed for serotonin by high-performance liquid chromatography or for SP by radioimmunoassay. DCS was applied at the thoracolumbar junction with current parameters similar to those used clinically in humans. DCS induced a significant release of serotonin in the dorsal horn of decerebrated animals (173 +/- 83% increase; mean +/- standard error; n = 4; P less than 0.01), whereas the levels of the metabolite 5-hydroxyindoleacetic acid were not significantly influenced. In contrast, no release of SP could be recorded in response to DCS in the decerebrated preparation, although peripheral nociceptive stimulation (pinch) and noxious electric dorsal root stimulation induced an elevation of the SP levels. However, in intact animals DCS provoked a marked SP release in the dorsal horn (190 +/- 92% increase; n = 7; P less than 0.01). The release of serotonin and SP after DCS may indicate that these substances participate in the mediation of the pain alleviating effect of DCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous bedside monitoring of regional cerebrocortical blood flow was carried out using laser Doppler flowmetry (LDF) in four comatose patients. Newly designed thin and flexible optical probes that were easily implanted into the cortex were employed. When the patients were in a deep comatose state, the recordings revealed a conspicuous relationship to intracranial pressure. As the patients improved, the flux values gradually increased, and the recordings showed characteristic changes in the wave pattern, presumably related to the restoration of an impaired cerebral autoregulation. Changes in regional cerebrocortical blood flow were also observed during routine nursing procedures, the use of medications, and voluntary activities, as demonstrated by one patient after a complete recovery. Although the volume of tissue scanned with LDF was limited, and the flux values did not directly express regionalf cerebrocortical blood flow in terms of milliliters per unit volume, changes in cerebral circulation were portrayed clearly in the flow recordings. Thus. LDF, which is simple to use. permits continuous bedside monitoring of the cerebral microcirculation. Its use should improve the management of comatose patients and also open avenues for a better understanding of the cerebral circulation in pathological states.