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PubMed1985

Evidence for substance P-immunoreactive spinal afferents that mediate bronchoconstriction.

The origin and functional role of capsaicin-sensitive substance P-(SP-) immunoreactive (IR) nerve fibres in the lower airways were studied in the guinea-pig. Stellatectomy caused a significant reduction of SP-IR in the lung and pulmonary artery. Immunohistochemical analysis, however, did not reveal any clear-cut change in the number and distribution of SP-IR fibres in the lung of these animals. After combined stellatectomy plus local capsaicin treatment of the vagal nerves, most SP-IR nerves disappeared in the lower airways. The bronchoconstriction induced by capsaicin was significantly reduced after stellatectomy and abolished after stellatectomy plus capsaicin pretreatment of the vagal nerves. Ether inhalation caused bronchoconstriction, which was not influenced by stellatectomy but markedly reduced by combined capsaicin treatment of vagal nerves and stellatectomy. Stellate ganglion stimulation in animals that had been chemically sympathectomized by 6-OH-dopamine caused bronchoconstriction, which was resistant to cholinergic or adrenergic receptor blockade. This response was absent after systemic capsaicin pretreatment, suggesting that it was due to antidromic stimulation of afferent fibres traversing the stellate ganglion. In conclusion, the present data suggest that the lower airways receive SP-IR capsaicin-sensitive C-fibre afferents of both vagal and spinal origin. These sensory fibres seem to have branches both within the bronchial smooth muscle and around blood vessels.

Afferent Pathways↗
PubMed1996

Cardiac neurones of autonomic ganglia.

The properties of the postganglionic sympathetic neurones supplying the heart and arising in the stellate and adjacent paravertebral ganglia of various species are discussed with respect to their location, morphology, synaptic input and membrane characteristics. Results from our laboratory on the morphology of rat stellate neurones projecting to the heart were obtained either by intracellular injection of hexammine cobaltic (III) chloride or by retrograde labelling of cells using cobalt-lysine complex. Intracellular recordings were made from cells using electrodes filled either with potassium chloride plus hexammine cobaltic chloride or potassium acetate. Neurones which projected axons into cardiac nerve branches arising from the stellate ganglion were termed putative cardiac neurones, because of the possibility that some supply pulmonary targets. Putative cardiac neurones had unbranched axons and were ovoid or polygonal in shape, but showed considerable variation in soma size and in the complexity of dendritic trees. The mean two-dimensional surface area was 463 microns2 and the mean number of primary dendrites was seven. Other studies have found that the morphology of rat stellate ganglion neurones is similar to that of superior cervical ganglion cells. However, in strains of rat displaying spontaneous hypertension, dendritic length may be increased. Histochemical studies do not, as yet, seem to have demonstrated a distinctive neurochemical profile for stellate cardiac neurones, but various types of peptide-containing intraganglionic nerve fibres have been identified in the guinea pig. In our electrophysiological studies, putative cardiac neurones were found to receive a complex presynaptic input arising from the caudal sympathetic trunk and from T1 and T2 thoracic rami. In addition, 16% of cardiac neurones received a synaptic input from the cardiac nerve. The properties of postganglionic parasympathetic neurones distributed in the cardiac plexus and termed intrinsic cardiac neurones are discussed, including the results of studies on cultures of these neurones.

Animals↗
PubMedDate not supplied

Sympathetic neurogenic control of blood flow in human nasal mucosa.

Nasal mucosal blood flow was investigated in patients undergoing a stellate ganglion blockade. Elimination of the sympathetic neurogenic control did not affect the resting blood flow in the mucosa, as registered with the 133Xe washout technique. This indicates that the basal sympathetic vasoconstrictor activity is low in the mucosal vessels that regulate blood flow. With laser doppler flowmetry, the normal pattern of spontaneous oscillations in blood flow was seen to be altered following stellate ganglion blockade. This suggests that vasomotion in the mucosa is partly dependent on sympathetic neurogenic activity. Furthermore, the decrease in blood flow normally induced by a peripheral cold provocation could not be elicited after the ganglion blockade, which means that the decrease is mediated by sympathetic vasoconstrictor fibres.

Adult↗
PubMed1986

Autonomic nervous system regulation of epicardial coronary vein systolic and diastolic blood velocity as measured by a laser Doppler velocimeter.

The velocity of blood in a major epicardial coronary vein accompanying the left anterior descending coronary artery of dogs was measured by means of a 140-micron fiber optic probe connected to a laser Doppler velocimeter. Right atrial pressure, left ventricular intramyocardial and cavity pressures, aortic pressure, as well as peripheral and central coronary venous pressures were compared with the velocity of blood measured in the epicardial coronary vein midway between the sites of the catheters measuring proximal and distal coronary vein pressures. During control conditions, coronary vein velocity was 14-18 cm/s during systole and 1.0-2.1 cm/s during diastole. Right stellate ganglion stimulation, norepinephrine or isoproterenol increased diastolic coronary vein velocity significantly, whereas left stellate ganglion stimulation did not. Average peak systolic velocity was not affected by these interventions. During these positive inotropic interventions, the peak coronary vein velocity usually occurred later in the cardiac cycle than during control conditions. Positive inotropic interventions appeared to decrease coronary vein velocity during systole and increase it during diastole. Left vagosympathetic trunk stimulation decreased diastolic but not systolic coronary vein velocity and usually caused peak coronary vein velocity to occur earlier in the cardiac cycle than during control states. Changes induced by vagosympathetic trunk stimulation usually occurred within one cardiac cycle. It is concluded that coronary vein blood velocity can be influenced by the autonomic nervous system.

Animals↗
PubMed1996

Postnatal development of the putative neuropeptide-Y-mediated sympathetic--parasympathetic autonomic interaction.

OBJECTIVE: Intense stellate ganglion stimulation causes a long-lasting inhibition of cardiac vagal responses in adult dogs. This inhibition is thought to result from the release of neuropeptide Y from sympathetic nerve terminals, which, in turn, blocks the release of acetylcholine from parasympathetic neurons. The purpose of this study was to characterize the developmental expression of this autonomic interaction in the dog. METHODS: We studied and compared the effects of 5-min trains of right stellate ganglion stimulation on cardiac chronotropic responses to supramaximal vagal stimulation trains in 10 neonatal dogs, 8 one-month-old puppies, 8 two-month-old puppies and 8 adult dogs. RESULTS: In the adult group, after 5 min of stellate stimulation, inhibition of the vagal chronotropic response was observed in 7 of 8 (87.5%). Inhibition was observed in 100% of the one-month-olds and in 87.5% of the two-month-olds. In contrast, in the neonates, inhibition was observed in only 4 of 10 (40%) (P < 0.05). The maximum percent inhibition of the cardiac vagal response was significantly less in the neonates than in the older puppies (P < 0.001) and adults (P < 0.01), and the summated inhibition also tended to be less in the neonates (P < 0.05 compared to one- and two-month-old puppies). Finally, in 60% of the neonates and 37.5% of all other animals vagal responses after stellate stimulation were facilitated, i.e. at least 20% greater than the pre-stellate stimulation values. CONCLUSION: The putative neuropeptide-Y-mediated, sympathetic-parasympathetic interaction is not fully expressed in the canine neonate. It appears to develop quite rapidly postnatally, being fully expressed by 1 month of age. We hypothesize that this developmental change is likely the result of maturation of sympathetic nervous system function after birth. The facilitation of the vagal chronotropic response, observed in some animals after stellate stimulation, is a new finding, and may represent yet another type of autonomic interaction.

Animals↗
PubMedDate not supplied

Quinine amblyopia: is current management appropriate?

Thirty-one patients blind from overdoses of quinine are reported. One died from cardiotoxicity. Of the survivors, thirteen received bilateral stellate ganglion block, seven unilateral block, five a variety of other treatments aimed at increasing retinal blood flow, and five no specific treatment. Nine patients recovered vision completely but twenty were left with varying degrees of visual field constriction and one was blind at last follow-up. No treatment for oculotoxicity was of benefit. Since experimental and clinical observations show that the primary toxic effect of quinine is on photoreceptor cells, stellate ganglion block and other vasodilator treatments have no rational basis and should no longer be recommended.

Amblyopia↗
PubMed1975

Prolonged sympathetic activation and pulmonary surfactant: absence of effect in anesthetized cats.

Cats were anesthetized with either sodium pentobarbital or ketamine hydrochloride, paralyzed, and artifically ventilated. The stellate ganglion was electrically stimulated for one hour (10 V, frequency = 10 per sec, and 0.5 to 1.0 msec pulse duration), alternating periods of stimulation and rest of 20 sec each, while control animals were sham operated. After stimulation, static deflation pressure-volume relationships of the excised lungs were compared. Regardless of the anesthetic used, no change in static lung compliance was found between experimental and control groups, and one hour of stellate stimulation did not produce significant changes in lung volumes at maximum distending pressures, in lung weight/body weight ratios, or in minimum surface tension measurements of lung extracts. We concluded that prolonged intermittent stimulation of the stellate ganglion does not alter significantly the function of alveolar surfactant.

Anesthesia, General↗
PubMedDate not supplied

Effects of stellate ganglionectomy on the cat cardiovascular function.

The effects of stellate ganglionectomy on cardiovascular function were assessed in pentobarbital-anesthetized cats. A right stellectomy produced much more profound bradycardiac effects than a left stellectomy. This finding demonstrated that the stellate ganglion exerted a lateralized influence on heart beat in the cat. The cardiovascular response of intact cats to phase 4 (overshoot) of the Valsalva-like maneuver (VM) was reflex bradycardia. In response to VM, however, reflex bradycardia was completely abolished by a right or bilateral stellectomy, or by pretreatment with propranolol, but not by a left stellectomy alone or with phentolamine. The data indicated that the right stellate ganglion in cats makes a major contribution to cardiovascular control, especially over reflex bradycardia mechanisms.

Animals↗
PubMed1992

[Stellectomy in the treatment of patients with long QT syndrome].

The authors present the surgical technique of stellate ganglion excision as a therapeutic method in patients with the long QT syndrome. The operations were performed through an anterior supraclavicular approach. Discussing the anatomic considerations, the possibilities of complications and side effects, both temporary and permanent, including Horner's syndrome are reviewed. On the base of the review of present literature and the postoperative results in patients treated in the Otolaryngological Department of the Medical Academy in Bydgoszcz, the authors confirm that the results of stellate ganglion excision in patients with the long QT syndrome are encouraging, but the possibilities of complications, including sudden death after stellectomy, must be taken into consideration.

Adult↗
PubMed2000

Transthoracic endoscopic sympathectomy for craniofacial hyperhidrosis: analysis of 46 cases.

BACKGROUND AND PURPOSE: Craniofacial hyperhidrosis may result in social phobia and has a strong negative impact on the quality of life. The traditional therapeutic options are psychotherapy and pharmacologic treatment, but these often fail. We wished to investigate whether transthoracic endoscopic sympathectomy (TES) of the lower part of the stellate ganglion is efficient and safe in the treatment of craniofacial hyperhidrosis. PATIENTS AND METHODS: Between July 1995 and September 1999, a total of 21 men and 25 women with a mean age of 41.2 years (range 22-58 years) underwent TES for craniofacial hyperhidrosis. All patients were placed in a semisitting position under single-lumen intubated anesthesia. We ablated the lower part of the stellate ganglion at the second rib using a storz 8-mm 0 degrees thoracoscope via one 0.8-cm incision just below each axilla. Questionnaires were sent to all patients postoperatively. RESULTS: Among these 46 patients, 92 sympathectomies were performed. Usually, TES was accomplished within 15 minutes (range 7-20 minutes). The surgical complications were minimal: one segmental atelectasis of the lung (2%). There was no surgical mortality. With a mean postoperative follow-up of 32.1 months (range 3-51 months), the results of TES were highly satisfactory in most patients although 37 (80%) developed compensatory sweating of the trunk and lower limbs, the distribution being the axillae in 15 (33%), back in 36 (78%), lower chest and abdomen in 22 (48%), lower limbs in 34 (74%) and sole in 1. The recurrence rates of craniofacial hyperhidrosis were 0 in the first and the second years and 2% each in the third and fourth years. CONCLUSION: Transthoracic endoscopic sympathectomy is a safe and effective method for treating craniofacial hyperhidrosis.

Adult↗
PubMedDate not supplied

Thermal grill illusion and complex regional pain syndrome type I (reflex sympathetic dystrophy).

BACKGROUND AND OBJECTIVES: In normal humans, placing a hand on a thermal grill containing warm elements separated by cool ones produces a burning sensation. In this case report, responses to a thermal grill in a patient with neuropathic pain were examined. METHODS: The responses of a 31-year-old woman with complex regional pain syndrome type I (reflex sympathetic dystrophy) to a thermal grill were evaluated before and after stellate ganglion block. RESULTS: The patient experienced a burning sensation when the unaffected hand was placed on the grill and could distinguish which element was warm and which was cool. An intolerable burning sensation caused the patient to quickly (within 4 seconds) withdraw the affected hand when it was placed on the grill. Touching cool elements with the affected hand produced an intense burning sensation (cold allodynia), whereas touching warm elements produced a pleasant warm sensation. Stellate ganglion block with phenol, local anesthetic, and steroid resulted in long-lasting absence of cold allodynia. CONCLUSION: The thermal grill may be a useful a tool to help understand the pathophysiology of complex regional pain syndrome type I.

Adult↗
PubMed1983

Lung injury edema in dogs. Influence of sympathetic ablation.

Increased vascular permeability characterizes lung injury pulmonary edema and renders fluid balance in the injured lung especially sensitive to changes in hydrostatic pressure. Pulmonary edema is often associated with increased sympathetic nervous system activity which can lead to pulmonary venoconstriction. This postcapillary venoconstriction could raise microvascular pressure and might therefore increase edema in the injured lung. We produced lung injury edema in dogs with oleic acid and directly measured small (less than 2 mm) pulmonary vein pressure. We found that the small pulmonary vein pressure was increased from 9.8 +/- 0.5 mmHg to 12.6 +/- 0.5 mmHg (n = 10) by oleic acid injury edema. The increase was not due to a rise in left atrial pressure since the small pulmonary vein-left atrial pressure gradient also increased. To test if this increase in the postcapillary pressure gradient was sympathetically mediated, we either unilaterally ablated the stellate ganglion or produced unilateral alpha adrenergic blockade with phenoxybenzamine before giving oleic acid. Both of these "antisympathetic" interventions prevented the increase in pulmonary vein pressure caused by oleic acid edema in the protected lung but not in the intact contralateral lung. These interventions produced a 30 +/- 6.8% reduction in the amount of edema caused by oleic acid. Restoring the increase in small vein pressure by inflating a balloon in the left atrium of dogs with bilateral stellate ganglion ablations abolished the reduction in edema produced by antisympathetic treatment. However, the decrease in edema was not significantly correlated with the reduction in pulmonary vein pressure. Thus, the mechanism of the effects of these antisympathetic interventions remains unclear. We conclude that lung injury edema causes sympathetically mediated pulmonary venoconstriction and that antisympathetic interventions significantly reduce lung injury edema and microvascular pressure.

Animals↗
PubMed1997

Mechanisms whereby propofol mediates peripheral vasodilation in humans. Sympathoinhibition or direct vascular relaxation?

BACKGROUND: Anesthetic induction and maintenance with propofol are associated with decreased blood pressure that is, in part, due to decreased peripheral resistance. Several possible mechanisms whereby propofol could reduce peripheral resistance include a direct action of propofol on vascular smooth muscle, an inhibition of sympathetic activity to the vasculature, or both. This study examined these two possibilities in humans by measuring the forearm vascular responses to infusions of propofol into the brachial artery (study 1) and by determining the forearm arterial and venous responses to systemic (intravenous) infusions of propofol after sympathetic denervation of the forearm by stellate blockade (study 2). METHODS: Bilateral forearm venous occlusion plethysmography was used to examine forearm vascular resistance (FVR) and forearm vein compliance (FVC). Study 1 used infusion of intralipid (time control) and propofol at rates between 83 and 664 micrograms/min into the brachial artery of 11 conscious persons and compared responses to arterial infusions of sodium nitroprusside (SNP) at 0.3, 3.0, and 10 micrograms/min. Venous blood from the infusion arm was assayed for plasma propofol concentrations. In study 2, after left stellate block (12 ml 0.25% bupivacaine + 1% lidocaine), six participants were anesthetized and maintained with propofol infusions of 125 and 200 micrograms.kg-1.min-1. Simultaneous right forearm (unblocked) blood flow dynamics served as the time control. In three additional conscious participants, intrabrachial artery infusions of SNP and nitroglycerin, both at 10 micrograms/min, were performed before and after stellate blockade of the left forearm to determine whether the sympathetically denervated forearm vessels could dilate beyond the level produced by denervation alone. RESULTS: In study 1, infusion of intralipid or propofol into the brachial artery did not change FVR or FVC. Sodium nitroprusside significantly decreased FVR in a dose-dependent manner by 22 +/- 5%, 65 +/- 3%, and 78 +/- 2% (mean +/- SEM) but did not change FVC. During the incremental propofol infusions, plasma propofol concentrations increased from 0.2 to 10.1 micrograms/ml and averaged 7.4 +/- 1.1 micrograms/ml during the highest infusion rate. In study 2, stellate ganglion blockade decreased FVR by 50 +/- 6% and increased FVC by 58 +/- 10%. Propofol anesthesia at 125 and 200 micrograms.kg-1.min-1 progressively reduced mean arterial pressure. In the arm with sympathetic denervation, FVR and FVC showed no further changes during propofol anesthesia, whereas in the control arm FVR significantly decreased by 41 +/- 9% and 42 +/- 7%, and FVC increased significantly by 89 +/- 27% and 85 +/- 32% during 125 and 200 micrograms.kg-1.min-1 infusions of propofol, respectively. In the three additional conscious participants, intraarterial infusion of SNP and nitroglycerin (TNG) after the stellate blockade resulted in a further decrease of FVR and a further increase of FVC. CONCLUSIONS: In contrast to SNP infusions, propofol infusions into the brachial artery of conscious persons caused no significant vascular responses, despite the presence of therapeutic plasma concentrations of propofol within the forearm. The effects of propofol anesthesia on FVR and FVC are similar to the effects of sympathetic denervation by stellate ganglion blockade. Thus the peripheral vascular actions of propofol appear to be due primarily to an inhibition of sympathetic vasoconstrictor nerve activity.

Adult↗
PubMed2003

Single CNS neurons link both central motor and cardiosympathetic systems: a double-virus tracing study.

Two anatomical experiments were performed to test the hypothesis that single CNS neurons link the central areas that regulate the somatomotor and sympathetic systems. First, the retrograde neuronal tracer cholera toxin beta-subunit was injected into the lateral parafascicular thalamic nucleus, a region that projects to both the motor cortex and striatum. Several days later, a second injection of the retrograde transneuronal tracer, pseudorabies virus (PRV), was made in the same rats in the stellate ganglion, which provides the main sympathetic supply to the heart. Using immunohistochemical methods, we demonstrate that the cholinergic neurons of the pedunculopontine tegmental nucleus (PPN) are connected to both systems. The second experiment used two isogenic strains of Bartha PRV as double transneuronal tracers. One virus contained the unique gene for green fluorescent protein (GFP) and the other had the unique gene for beta-galactosidase (beta-gal). GFP-PRV was injected in the stellate ganglion and beta-gal-PRV was injected into the primary motor cortex. Double-labeled neurons were found in the lateral hypothalamic area (50% contained orexin) and PPN (approximately 95% were cholinergic). Other double-labeled neurons were identified in the deep temporal lobe (viz., amygdalohippocampal zone and lateral entorhinal cortex), posterior hypothalamus, ventral tuberomammillary nucleus, locus coeruleus, laterodorsal tegmental nucleus, periaqueductal gray matter, dorsal raphe nucleus, and nucleus tractus solitarius. These results suggest these putative command neurons integrate the somatomotor and cardiosympathetic functions and may affect different behaviors (viz., arousal, sleep, and/or locomotion).

Animals↗
PubMed2005

The effects of therapeutic ultrasound on heart rate variability: a placebo controlled trial.

The effect of therapeutic ultrasound (US) on nervous system is controversial and the effect on autonomic nervous system is not clear. Therefore, the present placebo-controlled trial was planned to investigate the effects of therapeutic US application on right-side stellate ganglion, by using analysis of heart rate variability (HRV). A total 12 healthy volunteers were included in the study. RR intervals were recorded for 5 min before and after the US application, in supine and sitting positions. All procedures were repeated in all participants with sham US one week later. The heart rate (HR) was obtained by time-domain analysis and low frequency (LF) power (%), high frequency (HF) power (%) and LF/HF ratio values were obtained by frequency-domain (power spectral density) analysis. After the US application, there was a decrease in the HR (p = 0.002) and the HF power (%) component (p = 0.015) in supine position and a decrease in HR (p = 0.002) and LF/HF ratio (p = 0.028) in sitting position. There was no significant difference after the sham US application. In conclusion, we observed that therapeutic US application on stellate ganglion causes alterations on HRV parameters.

Adult↗
PubMed1990

Effects of increasing heart rate induced by efferent sympathetic neuronal stimulation, isoproterenol or cardiac pacing on myocardial function and oxygen utilization.

The effects of increasing heart rate by six different methods on cardiac function were investigated in 17 open-chest anesthetized dogs. Heart rate was increased approximately 30% by (1) right interganglionic nerve stimulation, (2) atrial pacing, (3) ventricular pacing, (4) atrioventricular sequential pacing, (5) right stellate ganglion stimulation, and (6) isoproterenol administration. During heart rate increases induced by atrial pacing left ventricular intramyocardial pressure, coronary blood flow, oxygen delivery per unit of myocardial oxygen consumption, and myocardial efficiency were unchanged. Ventricular pacing reduced left ventricular cavity and septal intramyocardial pressure, while circumflex coronary flow increased, resulting in reduced oxygen delivery relative to myocardial oxygen consumption. Similarly, atrioventricular sequential pacing increased circumflex coronary artery flow and myocardial oxygen consumption, and decreased septal intramyocardial pressure and oxygen delivery per unit of myocardial oxygen consumption. Right stellate ganglion stimulation and isoproterenol increased left anterior descending and circumflex coronary artery blood flow, intramyocardial pressure, and myocardial oxygen consumption. Estimated myocardial efficiency (left ventricle) was decreased by ventricular pacing and isoproterenol, and was unchanged by atrial pacing and right interganglionic nerve stimulation. Increases in heart rate induced by right interganglionic nerve stimulation did not alter myocardial oxygen consumption, or the index of cardiac efficiency. It is concluded that augmentation of heart rate by either ventricular or atrioventricular pacing impairs myocardial function so that there is a decrease of left ventricular efficiency and isoproterenol augments chronotropism and myocardial force relative to cardiac external work so there is a reduction in cardiac efficiency. In contrast, atrial pacing or right interganglionic nerve stimulation augments chronotropism such that myocardial oxygen consumption and efficiency are unchanged.

Animals↗
PubMedDate not supplied

Autonomic influences on regional cardiac [14C]2-deoxyglucose uptake in paced dog heart.

Sixteen dogs were anesthetized with pentobarbital sodium and placed on positive pressure ventilation. Twelve animals were cardiac paced and four animals were non-paced controls. In four of the paced animals, the left cut peripheral end of the cervical vagus was stimulated electrically. In another four animals, the decentralized left stellate ganglion was stimulated efferently. The four remaining paced animals were controls. The animals were injected i.v. with a single bolus of [14C]2-deoxyglucose, 100 microCi/kg. After 45 minutes of periodic stimulation, the hearts were removed, sectioned and prepared for autoradiography. Cardiac pacing significantly (p less than 0.02) decreased systolic blood pressure, and significantly increased (p less than 0.05) glucose utilization by all regions of the heart, with the exception of the left ventricular endocardium and the left ventricular papillary muscles. Vagal efferent stimulation elicited significant (p less than 0.05) decreases in glucose utilization in both the right atrium and right ventricle. Conversely, efferent stellate ganglion stimulation had no effect on the glucose utilization of any regions of the myocardium studied. This study demonstrates that both cardiac pacing and cardiac vagal efferent neuronal stimulation can produce distinct changes in regional myocardial glucose utilization.

Animals↗
PubMed2003

[Two cases of severe vertigo occasioned by neck rotation and its correlation with the direction of vertebral artery at its origin].

We report two cases of severe vertigo with neck rotation. The first case is that of a 54-year-old woman. She suffered from severe vertigo during neck rotation to the right. Angiography demonstrated that the origin of the left vertebral artery (VA) became kinked when she turned her head to the right. The second case is that of a 59-year-old man. He suffered from severe vertigo during neck rotation to the left. Angiography demonstrated that the kink in the right VA at its origin became worse with the patient's turning his head to the left. We resected nerve fibers from the stellate ganglion at the origin of the respective vertebral arteries and corrected the kink in the arteries at their origin. Both patients were relieved of vertigo after the operation the fact that there was vertigo occasioned by neck rotation. The direction of neck rotation was identical with that of a kink in the VA at its origin in both patients. Therefore, the direction of neck rotation is useful information for the diagnosis of vertigo induced by neck rotation. In terms of the treatment, though vascular reconstruction such as vein graft bypass between the VA and the carotid artery or transposition of the VA onto the subclavian artery has been established for VA stenosis and occlusion, the resection of nerve fiber from the stellate ganglion at the origin of VA is also effective and safe, especially when a kink in the VA at its origin accompanies with neck rotation.

Female↗