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Table of Contents
Year : 2011  |  Volume : 27  |  Issue : 4  |  Page : 516-521

Stellate ganglion block for treatment of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage - A preliminary study

1 Department of Neuroanaesthesiology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication24-Oct-2011

Correspondence Address:
Hari H Dash
Department of Neuroanaesthesiology, Chief Neurosciences Centre, 6th Floor/Room No. 12, All India Institute of Medical Sciences, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-9185.86598

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Background : Stellate ganglion block improves cerebral perfusion by decreasing the cerebral vascular tone. Its effects on cerebral vasospasm to relieve neurological deficits have not been evaluated. This prospective observational study was carried out to evaluate the effect of stellate ganglion block on cerebral hemodynamics in patients with symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
Materials and Methods : Fifteen patients of either sex, aged 18-75 years, who underwent surgical clipping of aneurysm and developed refractory cerebral vasospasm were included. Stellate ganglion block was performed using 10 ml of bupivacaine 0.5% on the side with maximum cerebral blood flow velocity. Neurological status, cerebral blood flow velocity and pulsatility index were assessed before and 10 minutes, 30 minutes, 2 hours, 6 hours, 12 hours and 24 hours after stellate ganglion block.
Results : Improved Glasgow coma score was observed 30 minutes after stellate ganglion block. Neurological deficits reduced in 11 patients. Ipsilateral middle cerebral artery mean flow velocity decreased from 133.66 cm/sec before stellate ganglion block to 110.53 cm/sec at 6 hours (P<0.001) and 121.62 cm/sec at 24 hours (P<0.001) after stellate ganglion block. There was a decrease in ipsilateral anterior cerebral artery mean flow velocity after stellate ganglion block (P<0.001), which persisted for 12 hours. A decline in flow velocities was observed in contralateral middle cerebral artery (P=0.008) and anterior cerebral artery (P=0.041) for 12 hours.
Conclusion : This study suggests stellate ganglion block to be an effective modality of treatment for refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Keywords: Cerebral blood flow velocity, cerebral vasospasm, stellate ganglion block, subarachnoid hemorrhage, transcranial Doppler

How to cite this article:
Jain V, Rath GP, Dash HH, Bithal PK, Chouhan RS, Suri A. Stellate ganglion block for treatment of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage - A preliminary study. J Anaesthesiol Clin Pharmacol 2011;27:516-21

How to cite this URL:
Jain V, Rath GP, Dash HH, Bithal PK, Chouhan RS, Suri A. Stellate ganglion block for treatment of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage - A preliminary study. J Anaesthesiol Clin Pharmacol [serial online] 2011 [cited 2021 Feb 27];27:516-21. Available from:

   Introduction Top

Cerebral vasospasm is a recognized complication of subarachnoid hemorrhage (SAH). Angiographically detected vasospasm is more common, occurring in two third of patients, than symptomatic vasospasm (clinical evidence of cerebral ischemia). Symptomatic vasospasm may occur in 46% of patients. [1] Mortality is increased by 1.5-3 fold in the first 2 weeks after SAH due to cerebral vasospasm. [2] It is also a major cause of morbidity in aneurysmal SAH patients. [3] Management modality of vasospasm includes nimodipine, [4] hypervolemia, hypertension, hemodilution (HHH) therapy, [5] interventional neuro-radiological procedures like transluminal angioplasty [6] or intra-arterial administration of vasodilators. [7] These measures are associated with medical complications or may have procedural limitations. Newer options like magnesium, statins, endothelin antagonists, and fibrinolytic therapy are under investigation but large trials are awaited to prove their efficacy. [8] The effect of stellate ganglion block (SGB) on cerebral hemodynamics was recently assessed using transcranial Doppler (TCD). There was a significant increase in cerebral perfusion pressure due to decrease in cerebral vascular tone. [9] It is not yet known whether these effects of SGB would help relieve delayed ischemic neurological deficits in symptomatic cerebral vasospasm. A prospective study was carried out to evaluate the effect of SGB in surgically clipped aneurysmal SAH patients with symptomatic cerebral vasospasm. The primary aim was to assess any change in clinical status, and the secondary objective was to assess the changes of cerebral blood flow velocity (CBFV) by TCD.

   Materials and Methods Top

After institutional ethics committee approval and informed written consent from next of kin, patients of either sex, aged 18-75 years suffering from aneurysmal SAH, who underwent surgical clipping, and developed symptoms of cerebral vasospasm were studied over a period of 2 years. Symptom­atic vasospasm was defined as new onset of focal neuro­logical deficit or deterioration in the level of consciousness after excluding other possible causes such as re-bleed­ing, hydrocephalus, surgical complication, cerebral edema, electro­lyte disorder, infection and seizure. TCD confirmation of cerebral vasospasm (mean CBFV>120 cm/ sec) in any vessel, and clinical correlation was done before enrolling patients into the study. Exclusion criteria were asymptomatic patients with vasospasm, patients with more than one aneurysm, refusal of consent, history of allergy to local anesthetic agents, disturbed coagulation profile, and patients with pre-existing pupillary changes where assessment of effectiveness of SGB would be difficult.

All patients underwent surgical clipping of aneurysm and were treated in the postoperative period with a standard treatment protocol that included intensive care monitoring, maintaining normotension, fluid therapy to maintain normovolemia (positive fluid balance >500 ml/day), and spontaneous hemodilution to maintain a hematocrit of 30%. Normothermia (35.5°C-36.5°C) was maintained during the study period. All patients received oral nimodipine 60 mg every 4 hours. TCD study was performed daily by an experienced neuro-intensivist. On clinical suspicion of vasospasm, a diagnostic brain computed tomographic (CT) scan was done to rule out ventricular dilatation or focal brain lesion explaining the clinical symptoms. Then, HHH therapy was instituted. Hypervolemia was instituted with administration of colloids and crystalloids with volume infusion up to 3-4 L/day with a targeted central venous pressure of 10-12 mmHg. The systolic blood pressue was targeted to 160-200 mmHg. This was achieved with infusion of vasopressors (dopamine or noradrenaline). The lowest hematocrit allowed was 30%. If symptoms of cerebral vasospasm did not improve after 24 hours of HHH therapy, decision was taken to enroll the patient into the study.

Five-lead electrocardiogram, invasive arterial blood pressure, end-tidal carbon dioxide and arterial oxygen saturation were monitored continuously for 24 hours. Neurological status was assessed by an independent observer (neurosurgeon) who was unaware of the study. Middle cerebral artery (MCA) and anterior cerebral artery (ACA) on both sides were insonated through the temporal acoustic window using two 2 MHz transcranial Doppler ultrasound probes (Four-View™, Rimed Ltd, Israel) with separate TCD machines. The TCD probes were fixed at a constant angle using a headband, and a stable continuous tracing of waveform of blood flow velocities in vessels was established. Vessels were identified and confirmed using standard criteria. Baseline observations including neurological condition [Glasgow coma scale (GCS) score, motor deficits], hemodynamic parameters (heart rate, mean blood pressure), and TCD values [peak, mean, diastolic blood flow velocity, pulsatility index (PI)] in MCA and ACA on both sides were recorded. Under aseptic precaution, SGB was performed at C 6 level, using anterior paratracheal approach, on side showing maximum mean CBFV. Bupivacaine (0.5%) 10 ml was administered. After 10-15 minutes, onset of SGB was confirmed by the presence of an ipsilateral Horner's syndrome, ipsilateral increase in skin temperature. [10]

Baseline hemodynamic and TCD parameters were reassessed by the same observer at 10 minutes, 30 minutes, 2 hours, 6 hours, 12 hours and 24 hours after SGB. Simultaneously neurological status was assessed by the independent observer. Sedative medications were avoided during the study period. However, in mechanically ventilated patients, propofol 2-3 mg/ kg/hr was administered whenever deemed necessary. It was ensured that propofol administration discontinued at least 1-2 hr prior to the observation so that no residual sedative effects were observed. In mechanically ventilated patients, ventilator settings were not changed during the study period. A hematocrit of 30 ± 5% and temperature (35.5°C-36.5°C) was maintained throughout the study period.

Survivors were followed after discharge during their subsequent hospital visits. Outcome was assessed according to the Glasgow outcome scale (GOS) at 6 months after SAH. The proportions of patients achieving good recovery or moderate disability were considered having favorable outcome.

Data was analyzed using STATA 9.1 (College Station, Tx, USA). Results were expressed as mean (standard error). Generalized estimating equation (GEE) was applied to compare the difference in mean values over different time intervals since the observations were correlated. A P value <0.05 was considered statistically significant.

   Results Top

A total of 102 patients with diagnosis of aneurysmal SAH undergoing surgical clipping were admitted to our neuro-intensive care unit during the study period. Out of 38 patients with clinical suspicion of cerebral vasospasm, 23 did not meet the inclusion criteria. The remaining 15 patients with TCD-confirmed vasospasm were included in the study [Table 1]. The mean age was 45.5 ± 13.6 years, and mean weight was 60.5 ± 7.9 kg. SGB was successful in all patients. Signs of sympathetic blockade (Horner's syndrome, increase in ipsilateral skin temperature) were evident on the side of block after 11.2 ± 0.2 minutes of local anesthetic administration. The average duration of sympathetic block was 6.8 ± 5.0 hours. No change in heart rate and blood pressure were observed during the study period.
Table 1: Clinical details of the patients

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An improvement in GCS score was observed after 30 minutes of SGB (P=0.002) that persisted for 24 hours. There was a decrease in CBFV on ipsilateral side (P<0.001). The flow velocity in ipsilateral MCA decreased from 133.67(7.65) cm/sec prior to SGB to 110.53(5.78) cm/ sec at 6 hours after block (P<0.001). Though, a slight increase in CBFV, 121.62(5.91), was observed at 24 hours as compared to 6 hours after SGB, still the CBFV were significantly lower in comparison to the baseline value (P<0.001) prior to SGB. There was a decrease in ACA flow velocity from 106.07(6.42) before SGB to 95.76(4.81) 12 hours after SGB (P<0.001) [Table 2]. An increase in ipsilateral PI of MCA was observed after 30 minutes of SGB (P=0.001), which remained elevated for 24 hours [Table 2]. On the contralateral side of block, a significant decrease was observed in mean MCA (P=0.008) and ACA flow velocity (P=0.041) for 12 hours [Table 3]. No significant change was observed in PI of contralateral MCA and ACA except increase in PI of MCA at 24 hours [Table 3]. No complication was observed during study period.
Table 2: Observed transcranial Doppler parameters ipsilateral to Stellate Ganglion Block (Data are presented as mean ± standard error)

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Table 3: Observed transcranial Doppler parameters contralateral to Stellate Ganglion Block (Data are presented as mean ± standard error)

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Favorable outcome (GOS) at six months after SAH was seen in 11 (73%) patients. Three patients died and one remained vegetative. The cause of death in two patients was sepsis whereas another patient had severe vasospasm.

   Discussion Top

Our results demonstrate a temporal correlation between the effect of SGB and decrease in CBFV with concomitant improvement of neurological status. The use of SGB to improve cerebral blood flow for treatment of cerebrovascular events is not new. [11] In our study, using TCD, we have more objectively demonstrated the efficacy of SGB in increasing cerebral blood flow, as evident from the decrease in CBFV and clinical improvement in neurological status. Gupta et al. demonstrated that SGB produced a significant decrease in zero flow pressure, which is a surrogate marker of cerebral vascular tone, leading to improved cerebral perfusion pressure. [9] This is the logical explanation for clinical improvement in our patients. These findings also support the suggested use of superior cervical sympathetic block to relieve cerebral vasospasm in patients with SAH. Treggiari et al. demonstrated improved cerebral perfusion without change in vessel diameter at cerebral angiography. [12] The observations of our study are more significant as the patients studied had delayed ischemic neurologic deficits owing to refractory cerebral vasospasm. We have earlier demonstrated the efficacy of SGB in two patient's refractory to papaverine administration. [13]

Cervical sympathetic nerve activity blockade by SGB improves cerebral blood flow. The stellate ganglion contains the cell bodies of inferior cervical and first thoracic sympathetic ganglion. The cerebral vasculature receives a noradrenergic sympathetic nerve supply mainly through the fibers that originate in cervical ganglion, accompany the carotid artery, and project into ipsilateral cerebral hemisphere. [14],[15],[16] Cerebral vasculature, especially pial vessels, is densely innervated with noradrenergic sympathetic nerve fibers. Intracerebral vessels constrict in response to cervical sympathetic stimulation and dilate when these fibers are interrupted. [14],[16] Blockade of sympathetic nerve activity or reversal of over-activity may dilate intracerebral vessels improving cerebral blood flow.

There are conflicting reports on the changes in cerebral blood flow following SGB. [17],[18] Theoretically, there should be an ipsilateral increase in cerebral blood flow due to the effect of SGB, but in our study, a significant decrease in CBFV was noted on both sides. The decrease in flow velocity on the contralateral side may be due to improved global cerebral perfusion as a result of increased cerebral blood flow. Cerebral vasospasm, involves cerebral vasculature as a whole. A slight narrowing of all basal arteries takes place leading to increased flow velocities. [19] Moreover, the stellate ganglion may give projections to contralateral sympathetic pathways. [20] We chose to give SGB on the side of higher CBFV presuming the affected side to be more at risk of ischemic deficits than the other.

TCD is widely used as a monitoring tool to assess cerebral hemodynamics in patients with cerebral vasospasm. It is non-invasive and can be used repeatedly when required. It has been proved to be an ideal aid to monitor the effectiveness of various therapies instituted for vasospasm. Though cerebral angiography is gold standard for assessing cerebral vasospasm, it cannot be performed at frequent intervals as it is invasive and there is a need of a neuro-radiological suite. We used TCD as a modality for monitoring cerebral vasospasm. Physiological variables like hemodynamic parameters, carbon dioxide concentration, temperature and hematocrit may affect cerebral blood flow, thereby affecting TCD interpretation. All these parameters were maintained in the range recorded prior to SGB in all our patients.

In patients with neurological disorders, disturbances in cerebral vascular reactivity or cerebral autoregulation are associated with poor outcome. It is important that any intervention which is intended to use in patient with neurological disorders should not impair autoregulation. It has been demonstrated that SGB does not impair the cerebral vascular reactivity or cerebral autoregulation. [9] The present study shows that a drug induced chemical sympathectomy can improve cerebral perfusion in patients with symptomatic cerebral vasospasm. The potential benefits of cervical sympathectomy can be decreased morbidity and mortality attributed to vasospasm and decreased radiation exposure in an interventional neuro-radiology suite. It may help reduce the need for extreme hemodynamic end points in HHH therapy to obtain reversal of symptoms, which are of concern particularly in elderly patients. [12] Since the morbidity related to vasospasm may be associated with only mild symptoms, an effort should be made to correct even mild deficits with therapy of minimal adverse effects. The effect of chemical sympathectomy lasts much longer than the action of intra-arterial papaverine and it is thus helpful in dealing with distal and diffuse vasospasm. SGB can be used for the treatment of cerebral vasospasm as an adjunct to standard procedures, or when standard procedures are not applicable or have failed. It should ideally be carried out under fluoroscopic guidance or using ultrasound, to ensure correct placement of needle. The procedure needs to be performed by an expert in patients with compromised condition, as the margin of error is minimal. SGB offers an advantage over superior cervical block being technically relatively easier to administer and as a bedside procedure of low-cost, and familiarity with the technique among the pain physicians, intensivists and anesthesiologists. However, subjective nature of TCD is a limitation to this study.

To conclude, SGB seems to be a simple and minimally invasive technique, effective in improving cerebral perfusion by relieving symptomatic cerebral vasospasm. A large randomized controlled trial is needed to compare its efficacy with other treatment modalities for cerebral vasospasm and to evaluate the potential role of SGB as a single mode of therapy.

   References Top

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2.Biller J, Godersky JC, Adams HP Jr. Management of aneurysmal subarachnoid hemorrhage. Stroke 1988;19:1300-5.  Back to cited text no. 2
3.Carter BS, Buckley D, Ferraro R, Rordorf G, Ogilvy CS. Factors associated with reintegration to normal living after subarachnoid hemorrhage. Neurosurgery 2000;46:1326-34.  Back to cited text no. 3
4.Pickard JD, Murray GD, Illingworth R, Shaw MD, Teasdale GM, Foy PM, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid hemorrhage: British aneurysm nimodipine trial. Br Med J 1989;298:636-42.  Back to cited text no. 4
5.Origitano TC, Wascher TM, Reichman OH, Anderson DE. Sustained increased cerebral blood flow with prophylactic hypertensive hypervolemic hemodilution ("triple-H" therapy) after subarachnoid hemorrhage. Neurosurgery 1990;27:729-40.  Back to cited text no. 5
6.Newell DW, Eskridge JM, Mayberg MR, Grady MS, Winn HR. Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 1989;71:654-60.  Back to cited text no. 6
7.Kaku Y, Yonekawa Y, Tsukahara T, Kazekawa K. Super-selective intra-arterial infusion of papaverine for treatment of cerebral vasospasm after subarachnoid hemorrhage. J Neurosurg 1992;77:842-7.  Back to cited text no. 7
8.Weyer GW, Nolan CP, Macdonald RL. Evidence-based cerebral vasospasm management. Neurosurg Focus 2006;21:E8.   Back to cited text no. 8
9.Gupta MM, Bithal PK, Dash HH, Chaturvedi A, Mahajan RP. Effects of stellate ganglion block on cerebral haemodynamics as assessed by transcranial Doppler ultrasonography. Br J Anaesth 2005;95:669-73.   Back to cited text no. 9
10.Elias M. Cervical sympathetic and stellate ganglion blocks. Pain Physician 2000;3:294-304.  Back to cited text no. 10
11.Moore DC. Stellate ganglion block- therapy for cerebral vascular accidents. Br J Anaesth 2006;96:666-7.  Back to cited text no. 11
12.Treggiari MM, Romand JA, Martin JB, Reverdin A, Rufenacht DA, de Tribolet N. Cervical sympathetic block to reverse delayed ischemic neurologic deficits after aneurysmal subarachnoid hemorrhage. Stroke 2003;34:961-7.  Back to cited text no. 12
13.Prabhakar H, Jain V, Rath GP, Bithal PK, Dash HH. Stellate ganglion block as alternative to intrathecal papaverine in relieving vasospasm due to subarachnoid hemorrhage. Anesth Analg 2007;104:1311-2.  Back to cited text no. 13
14.Tuor UI. Local distribution of the effects of sympathetic stimulation on cerebral blood flow in the rat. Brain Res 1990;529:224-31.  Back to cited text no. 14
15.Umeyama T, Kugimiya T, Ogawa T, Kandori Y, Ishizuka A, Hanaoka K. Changes in cerebral blood flow estimated after stellate ganglion block by single photo emission computed tomography. J Auton Nerv Syst 1995;50:339-46.  Back to cited text no. 15
16.Edvinsson L. Neurogenic mechanisms in the cerebrovascular bed: Autonomic nerves, amine receptors and there effects on cerebral blood flow. Acta Physiol Scand Suppl 1975;427:1-35.  Back to cited text no. 16
17.Ono K, Kaneko T, Iwatsuki N, Tashima T, Hashimoto Y, Yamasuro M, et al. The effects of stellate ganglion block and oxygenation on head blood flow. Pain Clin 1989;10:211-6.  Back to cited text no. 17
18.Ohinata Y, Makimoto K, Kawakami M, Haginomori S, Araki M, Takahasi H. Blood flow in common carotid and vertebral arteries in patients with sudden deafness. Ann Otol Rhinol Laryngol 1997;106:27-32.  Back to cited text no. 18
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20.Kakuyama M, Toda H, Osawa M, Fukuda K. The bilateral effect of stellate ganglion block on the facial skin blood flow. Reg Anesth Pain Med 2000;25:389-92.  Back to cited text no. 20


  [Table 1], [Table 2], [Table 3]

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