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A patient suffering from an acute myocardial infarction presented on the seventh and eighth days of hospitalization recurrent episodes of ventricular fibrillation refractory to antiarrhythmic treatment. The life-threatening ventricular fibrillation was suppressed by percutaneous pharmacological block of the left stellate ganglion.
Patients suffering from the long QT syndrome (LQTS) are threatened by sudden arrhythmic cardiac death. This case report describes a new therapeutic approach to ventricular tachyarrhythmias refractory to oral pharmacological treatment (propranolol + phenytoin) using a drug-reservoir-pump system for the pharmacologic blockage of the left stellate ganglion.
PURPOSE: There are cases when ocular pain persists long after ocular surgery and can not be reduced by anti-inflammatory drugs. Our purpose was to evaluate the effect of stellate ganglion block(SGB) on such prolonged post-operative ocular pain. METHOD: The subjects were 35 patients. Divided into two groups. One we called the nociceptive pain group, containing 29 cases in which the trigeminal nerve in the orbit or passing through it was intact. The other we called the neuropathic pain group, containing 6 cases in which pain accompanied paralysis of the trigeminal nerve. SGB was performed two times per week. SGB was deemed effective when pain was reduced markedly and the administration of anti-inflammatory drugs became almost unnecessary. RESULTS: SGB was 96.6% effective in the nociceptive pain cases with the SGB performed an average of 5.9 times. On the other hand, in the neuropathic pain group, even though SGB was performed an average of 52.6 times it was only 66.7% effective. CONCLUSIONS: SGB may be useful for the treatment of prolonged post-operative ocular pain, but the elimination of neuropathic pain is more difficult than the elimination of nociceptive pain.
This study was designed to see whether during ischemia a metabolic advantage results with left-sided ablation of the stellate ganglion (SGA), an available clinical technique. Its effects on hemodynamics and regional metabolism during myocardial ischemia were compared with those of electrical stimulation of the left vagus nerve (VS), a nonclinical technique, and those of a control condition (ischemia without intervention). The left anterior descending coronary artery (LADa) of 30 dogs was constricted to reduce blood flow by 50% and then 75% from that before constriction and after autonomic intervention (baseline). Electrocardiogram, left-ventricular (LV) first-time derivative (dP/dt), and systemic, LADa, and LV end-diastolic pressures were continuously recorded. Before and during each constriction, cardiac output and regional myocardial blood flow (by microspheres), blood gas tensions, pH, hemoglobin O2 saturation, lactate, glucose, sodium, and potassium concentrations were measured. During ischemia, SGA and VS each decreased heart rate, myocardial contractility (dP/dt), and filling pressures, the decrease in each variable being greater with VS. Also during ischemia, myocardial O2 delivery and consumption decreased to the same extent in the ischemic zone with VS, but the O2 delivery/consumption ratio was higher only with SGA. In addition, ischemic lactate production was lower with SGA and VS than with no autonomic intervention. It is concluded that left-sided SGA or VS to a heart rate of 80 to 90 beats per minute similarly mitigated metabolic impairment during myocardial ischemia. Although the study was only designed to compare modification of ischemia by two different techniques, the results suggest that ischemic zone O2 delivery/consumption ratio and hemodynamic stability were better with SGA.
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Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and alpha-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p less than 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.
A triple-labelling immunofluorescence technique was used to study the patterns of coexistence of calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY), and tyrosine hydroxylase (TH) in the guinea-pig stellate ganglion. CGRP-immunoreactive postganglionic neurons, which all were of the non-catecholaminergic type, could be divided into NPY-positive and NPY-negative populations. Sweat glands, which are a known target of CGRP-immunoreactive sympathetic neurons, exhibited exclusively fibers of the CGRP+/NPY- phenotype. Lack of coexistence of CGRP- and NPY-immunoreactivity was also observed in nerves within skeletal muscle, brown adipose tissue and hairy skin. The findings document a previously unknown diversity of CGRP-immunoreactive postganglionic sympathetic neurons, and indicate the existence of an addition, presently unidentified target of non-catecholaminergic, CGRP-immunoreactive sympathetic neurons.
Ninety-one patients suffering from idiopathic sudden hearing loss are presented. Twenty-two patients were given medical treatment (vasodilators, steroid hormones and vitamins) alone (group 1). Forty-nine patients were treated with stellate ganglion block (SGB) plus oxygen hyperbaric therapy (OHP) (group 2) and 20 patients were treated with SGB plus OHP along with medical treatment (group 3). The SGB plus OHP treated patients were given bupivacaine, which induced Moor's anterior approach of SGB and then exposed to oxygen at a pressure of 2.4 ATA for 90 min. In group 1, 69% of the patients treated within one week after onset exhibited over 10 dB pure tone average improvement, with only 33% patients treated one to two weeks after onset experiencing over 10 dB. However, 74% of the patients in group 2 and 100% of the patients in group 3 who were treated within two weeks after onset exhibited over 10 dB improvement. More significantly, of the patients which experienced complete loss of hearing, 83% in group 2 and 100% in group 3, exhibited over 10 dB improvement, compared to only 33% in group 1. Moreover, 8 (40%) patients in group 3 recovered to within 20 dB of their normal hearing levels. In group 2, 17 patients were treated two to six weeks after onset and 12 (71%) patients had over 10 dB improvement. SGB plus OHP therapy was shown effective in the treatment of sudden idiopathic hearing loss even when patients were treated more than two weeks after onset.
The effect of peripheral sympathetic block on the autonomic nerve function of the heart was studied using the head-up tilt test (HUTT) and right stellate ganglion block (RSGB). Blood pressure (BP), heart rate (HR) and the parameters of power spectral analysis of HR variability recorded during the HUTT were measured in 8 patients with chronic pain syndrome before and after RSGB. In the control state, the mean HR and the LF/HF component recorded during HUTT significantly increased whereas the HF component markedly decreased. Conversely, the mean HR and LF/HF and HF components during HUTT did not significantly alter after the RSGB procedure. There were no significant differences between the BP values before and after RSGB. These results suggest that RSGB suppresses cardiac sympathetic function without significantly affecting BP and thus may be a safe and effective therapy for the chronic pain syndrome.
We present the case of a patient who experienced residual ischemic symptoms and invalidating chronic pain after an injury where three fingers of his left hand were sliced off by a chain saw. He underwent 5 stellate ganglion RF neurolysis over a two year period, followed by progressive and complete pain relief. We will underscore the value of CT guidance during needle placement and the efficacy of RF neurolysis.
Plasma epinephrine (E) and norepinephrine (NE) concentrations were measured (radioenzymatic assay) in blood samples simultaneously withdrawn from the aorta (Ao) and coronary sinus (CS) on 10 anesthetized dogs immediately before and during a 1-min period of electrical stimulation of the left stellate ganglion (4 V, 4 ms, 10 Hz). Heart rate and systolic blood pressure significantly increased in response to electrical stimulation (152 +/- 8 to 180 +/- 15 beats/min and 128 +/- 12 to 149 +/- 12 mmHg, mean +/- SE; P less than 0.05). Plasma NE concentrations were not significantly different in the Ao and the CS (432 +/- 110 and 319 +/- 67 pg/ml) before the stimulation, whereas a net removal of E was present across the myocardium (Ao, 172 +/- 61; CS, 71 +/- 22 pg/ml). A large NE spillover in the CS was observed during the stimulation (Ao, 1,555 +/- 513; CS, 10,583 +/- 3,753 pg/ml). A significant output of E from the myocardium was also present (Ao, 165 +/- 42; CS, 291 +/- 74 pg/ml) during the stimulation. Determination of NE and E concentrations by high-performance liquid chromatography in five of the dogs confirmed the observation made with the radioenzymatic assay, i.e., a significant uptake (66%) of blood-borne E was present across the myocardium in the control situation (Ao, 320 +/- 97; CS, 110 +/- 23 pg/ml), whereas plasma E concentrations in the CS (280 +/- 61 pg/ml) were 1.5 times the values found in Ao (184 +/- 56 pg/ml) under electrical stimulation. These observations give further support to the hypothesis that endogenous tissue E can act as a cotransmitter of sympathetic fibers.
Ischemic optic neuropathy (ION) is a common disease that can cause a loss of visual acuity in the elderly. We treated ION patients with stellate ganglion block (SGB) and investigated its effects on picture visual evoked potential (P-VEP) and blood flow in the ophthalmic artery (OA) and internal carotid artery (ICA). Twelve ischemic eyes in 12 patients diagnosed by the same ophthalmologist were investigated in this study. All patients were treated with daily SGB on the affected side with 2-3 mL of 2% lidocaine for a treatment period of 10-15 days. In ION eyes before SGB, compared with healthy eyes, the latency of P-VEP P(100) was delayed (123 +/- 14 ms versus 98 +/- 3 ms; P < 0.05), and the amplitude was reduced (4.24 +/- 1.76 microV versus 10.26 +/- 4.09 microV; P < 0.05). After SGB, the latency and amplitude returned to normal (103 +/- 6 ms versus 98 +/- 3 ms; 10.43 +/- 4.88 microV versus 10.26 +/- 4.09 microV; P > 0.05). Before treatment, the blood flow velocities of the OA and the ICA on the ischemic side were slow and the resistance indexes were high, but SGB reduced these changes. SGB did not affect the OA and the ICA on the healthy side. We conclude that SGB improves P-VEP and OA and ICA blood flow in ION eyes. Further studies are needed to confirm that this is an effective method for the treatment of ION.
Neuropeptides are known to modulate the excitability of mammalian sympathetic neurons by their actions on various types of K+ and Ca2+ channels. We used whole cell patch-clamp recording methods to study the actions of substance P (SP) on dissociated adult guinea pig stellate ganglion (SG) neurons. Under current-clamp conditions, SG neurons exhibited overshooting action potentials followed by afterhyperpolarizations (AHP). The K+ channel blocker tetraethylammonium (1 mM), the Ca2+ channel blocker Cd2+ (0.1-0.2 mM), and SP (500 nM) depolarized SG neurons, decreased the AHP amplitude, and increased the action potential duration. In the presence of Cd2+, the effect of SP on membrane potential and AHP was reduced. Under voltage-clamp conditions, several different K+ currents were observed, including a transient outward K+ conductance and a delayed rectifier outward K+ current (IK) consisting of Ca(2+)-sensitive [IK(Ca)] and Ca(2+)-insensitive components. SP (500 nM) inhibited IK. Pretreatment with Cd2+ (20-200 microM) or the high-voltage-activated Ca2+ channel blocker omega-conotoxin (10 microM) blocked SP's inhibitory effects on IK. This suggests that SP reduces IK primarily through the inhibition of IK(Ca) and that this may occur, in part, via a reduction of Ca2+ influx through voltage-dependent Ca2+ channels. SP's actions on IK were mediated by a pertussis toxin-insensitive G protein(s) coupled to NK1 tachykinin receptors. Furthermore, we have confirmed that 500 nM SP reduced an inward Cd(2+)- and omega-conotoxin-sensitive Ba2+ current in SG neurons. Thus the actions of SP on IK(Ca) may be due in part to a reduction in Ca2+ influx occurring via N-type Ca2+ channels. This study presents the first description of ionic currents in mammalian SG neurons and demonstrates that SP may modulate excitability in SG neurons via inhibitory actions on K+ and Ca2+ currents.
OBJECTIVE: Radio-cephalic arteriovenous fistulas (AVFs) have high early failure ratio. Increased sympathetic activity and spasm of radial artery during the surgery may responsible for early occlusion rate. DESIGN: Fifty patients were randomized to two groups (each containing 25 patients). Stellate Ganglion Blockade (SGB) was performed in Group 1. Another group was considered as control group (Group 2) to make statistical comparisons. All AVFs were performed under local anesthesia in both groups. RESULTS: Average fistula flow was 201.4+/-40.4 ml/min in Group 1 and 155.6+/-27.4 ml/min in Group 2 (p < 0.001). While average peak velocity of radial artery was 167.1+/-31.3 cm/sec in Group 1, it was 107.8+/-15.8 cm/sec in Group 2 (p < 0.001). Thrill was found in all Group 1 patients, but there was thrill only 13 of the Group 2 patients (p < 0.001). Mean maturation time was 41.4+/-6.8 days after surgery in Group 1 and 77.1+/-10.5 days in Group 2 (p < 0.001). Adequate vascular access was obtained 19 patients in Group 1 and 12 patients in Group 2 (p = 0.041). CONCLUSION: AVF occlusion rate is much more common in early postoperative period. Diminished sympathetic tonus by preemptive SGB not only increases early patency rate but also increases fistula maturation rate.
1. The effect of burst patterned preganglionic stimulation on the efficacy of transmission at the cat stellate ganglion in vivo was studied to determine whether the increase in acetylcholine (ACh) release that occurs at preganglionic terminals with similar stimulation is synaptically active.2. Stimulation of the whole or a portion of the thoracic sympathetic trunk between rami T4 and T5 with recording of evoked compound action potentials in the inferior cardiac nerve yielded a preparation with a subliminal fringe with a mean value 2.5 times the size of the discharge zone.3. Preganglionic stimulation with 0.5 s bursts at 10, 20 and 40 Hz with 10 s interburst intervals caused an increase with time in the area of the compound action potential evoked by a single interburst test stimulus. The increase reached 70-75% of the final value after the first burst, 75-90% after 5 bursts and was virtually complete after 5 min. It was then maintained without attenuation as stimulation was continued.4. On cessation of burst patterned stimulation test compound action potentials returned to control levels with a half-time of 5 min.5. The increase in area of test compound action potentials with 40 Hz intraburst frequency was always as great as the increase following tetanization of the pathway. The increases with 20 and 10 Hz bursts were less.6. There was no increase in area of compound action potentials when equally spaced pulses at 2 Hz or less were applied preganglionically, nor was there any increase when 40 Hz burst patterns were delivered directly to the inferior cardiac nerve.7. It is concluded that burst patterned preganglionic activity at frequencies similar to those observed in vivo can recruit rapidly into the discharge zone all of the ganglionic neurones that were originally in the subliminal fringe. It is proposed that this effect is related directly to the increase in ACh release at ganglionic synapses that such activity has been shown to induce.
After injection of wheat germ agglutinin conjugated horseradish peroxidase (WGA-HRP) or choleragenoid conjugated HRP (B-HRP) into lower cervical and upper thoracic dorsal root ganglia (DRG), HRP reaction product was observed in peripheral fibers of spinal afferents and in postganglionic cell bodies of the stellate ganglion (SG) in the guinea pig. After WGA-HRP injection into C8-T3 or T5 DRG, HRP-labelled cells were observed to cluster at the rami within the SG, with peak labelling observed 36 h after injection. SG cell labelling occurred with B-HRP as well, but not with native HRP after injection into thoracic DRG. Injection of this tracer in C8 DRG gave rise to a small number of labelled cells. In contrast to the labelling pattern following thoracic or C8 DRG injections, injection of WGA-HRP or native HRP into C6 DRG, led to random SG cell labelling. We conclude that the anterograde transsynaptic transport, following injection of WGA-HRP into thoracic DRG, provides a method to selectively label a population of postganglionic sympathetic neurons within the SG. A combination of transsynaptic and retrograde transport appears to be responsible for labelling after injection into C8 DRG, whereas labelling after C6 DRG injections seems to be due primarily to retrograde transport.