Anesth Analg 2005;100:1193-1196
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000144784.09919.2C
REGIONAL ANESTHESIA
The Effects of Stellate Ganglion Block on Visual Evoked Potential and Blood Flow of the Ophthalmic and Internal Carotid Arteries in Patients with Ischemic Optic Neuropathy
Feng Liu, PhD*,
Guozhong Xu, MB*,
Zheli Liu, PhD ,
Yan Zhao, MM ,
Xiaojun Lv, MM , and
Junke Wang, MM*
Departments of *Anesthesiology and Ophthalmology, The First Affiliated Hospital of China Medical University, Shenyang, China; and Departments of Stomach Surgery and Internal Medicine, LiaoNing Cancer Hospital, Shenyang, China
Address correspondence and reprint requests to Feng Liu, PhD, Department of Anesthesiology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China. Address e-mail to liufeng024{at}yahoo.com.cn.
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Abstract
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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 P100 was delayed (123 ± 14 ms versus 98 ± 3 ms; P < 0.05), and the amplitude was reduced (4.24 ± 1.76 µV versus 10.26 ± 4.09 µV; P < 0.05). After SGB, the latency and amplitude returned to normal (103 ± 6 ms versus 98 ± 3 ms; 10.43 ± 4.88 µV versus 10.26 ± 4.09 µV; 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.
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Introduction
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Ischemic optic neuropathy (ION) is an acute disease caused by obstructed blood flow to the optic disc. Stellate ganglion block (SGB) has been noted to have positive effects on ischemic eyes and constricted vessels (1). To evaluate the effects of SGB on ION, transcranial color Doppler imaging (TCDI) and electrophysiology techniques were used to measure the picture visual evoked potential (P-VEP) and the blood flow of the ophthalmic artery (OA) and internal carotid artery (ICA) in ION patients. These results were compared in the healthy side and the affected side before treatment.
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Methods
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This study had institutional ethics committee approval, and written informed consent was obtained from all patients. Twelve ION patients diagnosed by the same ophthalmologist were investigated in this study (Table 1).
Diagnostic criteria included 1) unexpected hypopsia not accompanied by eyeball rotation pain, the typical visual field defect is a horizontal or vertical hemianopsia, and there is no central defect; 2) cephalalgia and ophthalmalgia, especially caused by temporal arteritis; 3) optic disc appearing pale and swollen (1–3 diopters) with the edge obscured, usually a small amount of bleeding in the optic disc or retina nearby, with no change in the blood vessels of the retina; 4) fluorescence fundus angiography showing low fluorescent or slow filling in the optic disc in early stages, and the filling of the choroid is either slow or defective; 5) Raynaud syndrome in hands and feet; and 6) bulbar compression test showing significant decreased recovery rate of intraocular pressure. All patients with two of the above diagnostic criteria were investigated in this study.
SGB was performed as follows: patients were supine, with a small pillow placed under the shoulder, and the head was turned 30°–45° to the contralateral side. The point of puncture was at the level of C6: 2.5 cm above the sternoclavicular articulation and 1.5 cm lateral to the anterocervical median line (1–1.5 cm lateral to the cricoid cartilage). The common carotid artery was retracted, and a needle (7-gauge) was placed between the trachea and common carotid artery until it contacted bone, at which point it was withdrawn 1 mm. Lidocaine 2% (2–3 mL) was injected after negative aspiration for air, blood, and cerebrospinal fluid (1). Injection was performed daily on the ipsilateral side of the ischemic eye. Ten to 15 days was one period of treatment; all patients received treatment for three periods. The sign of successful injection was the appearance of ipsilateral Horner syndrome. Patients were kept on bed rest for 10–15 min after injection, and heart rate change was monitored at the same time.
The following variables were observed: the latency and amplitude of P-VEP P100 were measured with P-VEP (Neuropack II; Nihon Kohden, Japan). Peak systolic velocity, end-diastolic velocity, time-averaged maximum velocity, and resistance index (RI) were evaluated with TCDI (EMS; Anke Co., Shenzhen, China) in both the ischemic and healthy sides before and after treatment.
Data are expressed as mean ± sem. Statistical significance for variables was analyzed by repeated-measures analysis of variance followed by the Duncan test. One-way analysis of variance followed by the Scheffé/Dunnett t-test was used when appropriate. A P value <0.05 was considered statistically significant.
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Results
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When compared with healthy eyes, ION eyes displayed delayed latencies of P-VEP P100 (123 ± 14 ms versus 98 ± 3 ms; P < 0.05) and reduced amplitudes (4.24 ± 1.76 µV versus 10.26 ± 4.09 µV; P < 0.05). After SGB treatment, the latencies and amplitudes recovered to normal (compared with before treatment: 103 ± 6 ms versus 123 ± 14 ms; 10.43 ± 4.88 µV versus 4.24 ± 1.76 µV; P < 0.05; compared with the healthy eye: 103 ± 6 ms versus 98 ± 3 ms; 10.43 ± 4.88 µV versus 10.26 ± 4.09 µV; P > 0.05) (Table 2).
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Table 2. Changes of the Latencies and Amplitudes of Picture Visual Evoked Potential (P-VEP) P100 Both in Ischemic Eyes and in Healthy Eyes Before and After Treatment (n = 12)
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Compared with the healthy eye, the blood flow velocities of the OA and ICA of the affected side were slow, and the RIs were high (OA: 35.61 ± 8.03 cm/s versus 42.33 ± 6.70 cm/s; 8.95 ± 4.35 cm/s versus 13.82 ± 4.44 cm/s; 13.26 ± 4.87 cm/s versus 20.05 ± 7.25 cm/s; 1.77 ± 0.20 versus 1.25 ± 0.37; P < 0.05; ICA: 52.71 ± 8.82 cm/s versus 72.43 ± 8.15 cm/s; 25.82 ± 6.63 cm/s versus 34.00 ± 7.25 cm/s; 22.67 ± 5.45 cm/s versus 41.03 ± 6.82 cm/s; 2.26 ± 1.08 versus 1.53 ± 0.62; P < 0.05.). SGB reduced these changes (OA: 43.13 ± 7.96 cm/s; 12.98 ± 5.63 cm/s; 18.98 ± 6.15 cm/s; 1.17 ± 0.32; ICA: 74.33 ± 11.38 cm/s; 31.99 ± 4.83 cm/s; 40.25 ± 5.66 cm/s; 1.63 ± 0.45; P < 0.05 compared with before treatment; P < 0.05 compared with the healthy eye) but did not affect blood flow of the OA and ICA on the healthy side (Tables 3 and 4).
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Discussion
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In most published cases, ION was treated with steroids, hyperbaric oxygen, and optic neuropathy decompression, but the efficacy of these treatments is controversial (2–6). We treated ION patients with SGB and found that SGB is a clinically efficient method (7).
Blood supply to the optic nerve comes from two systems, the posterior ciliary artery and the central retinal artery, with the former being more important. The OA, a branch of the ICA, supplies blood to the postcilio artery and retinal artery.
Any general or ophthalmic disease, if accompanied by small blood supply to the optic disc and low or high intraocular pressure, may cause ION by affecting the balance between the perfusion pressure of small disc vessels and intraocular pressure. The high resistance changes of the OA and the ICA in the same side can also lead to ION by decreasing the perfusion pressure of the two systems, especially the ciliary circulation. Therefore, the occurrence and development of ION is the result of complex and multifactorial events.
P-VEP consists of a series of electric signals that are recorded in the cortex after the retina receives picture stimulation. It mainly reflects the function from ganglion cells to optic cortex. In our study, the latencies of P-VEP P100 in ION eyes were delayed slightly, and the amplitudes were reduced significantly. This result coincided with the findings of Cox et al. (8) and Xin et al. (9). ION is not an optic neuropathy, which primarily comes from the medulla, so it is easy to understand why the latencies were delayed slightly. Xin et al. (9) thought that the delayed latencies, which were different from the latencies recorded in retrobulbar neuritis, were related to the visual field defect. In retrobulbar neuritis patients, because of demyelination, the nervous pulse changes from a jumping conduction to a continual local electric current conduction, so the latencies of P-VEP P100 are delayed significantly. However, the reduced amplitudes of P-VEP P100 in ION eyes were the result of decreased optic systemic sensitivity and the necrosis of nerve fiber axons (9). In ION eyes whose visual acuities were seriously or moderately decreased, the amplitude of P-VEP P100 was also decreased. The amplitude of P-VEP P100, especially 15' P100, provides significant information for the diagnosis of ION.
The stellate ganglion is the junction of the infracervical sympathetic ganglion and the first thoracic sympathetic ganglion. Besides governing cerebral and cervical vessel tone, it ascends to the supracervical ganglion, branching and composing the ciliary ganglion. It then distributes into the ophthalmic vessels and pupillary muscles and governs their contraction and expansion. By distending the OA and ICA and dilating small convulsive vessels, SGB not only has the effect of increasing the local perfusion pressure of the ocular vessels and reducing their resistances, but also is useful to stabilize or reduce intraocular pressure by constricting the pupil of the ischemic eye. This improves the circulation to the retina and the choroids and therefore improves the optic ischemia and hypoxemia caused by the dysfunction of the autonomous nervous system. In addition, SGB can adjust the vasomotor function through the central nervous system and improve ocular microcirculation, including the blood supply for the optic nerve.
The constriction or obstruction of the carotid artery can cause a reduction in ocular blood supply, which may lead to the presentation of optic syndromes and diseases. The accuracy of TCDI checking the carotid artery is 95%–98% (10).
Some studies have shown that SGB can decrease the vascular resistance and increase the velocities, amounts, and diameters of the carotid, vertebral, and brachial arteries of the ipsilateral sides. The increase in binocular blood flow after bilateral SGB is larger than that after unilateral SGB. The reports about changes in contralateral blood flow are controversial. For example, some investigators have demonstrated that SGB increases contralateral blood flow. However, other investigators have shown contralateral blood flow to be reduced or unchanged. These variable findings have been attributed to differences in methods or experimental conditions (10–12). In this study, we found that when compared with the healthy eye side, the blood flow velocities of the OA and ICA in the ischemic side were slow and the RIs were high. SGB treatment can reduce these changes, but it did not affect the blood flow of the OA and ICA on the healthy eye side.
We did not have a control group without ION receiving SGB because of ethical concerns. On the other hand, it is difficult to enroll healthy volunteers. In future studies, we plan to have a control group in which we will treat ION patients with traditional treatment methods to compare the therapeutic effect with an SGB group.
In summary, our results indicate that SGB has significant effects on P-VEP and OA and ICA blood flow in ION eyes. Further study is needed to confirm that it is an effective method for treating ION. Further research is also needed to determine the mechanism behind the effect of SGB on P-VEP.
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Footnotes
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Accepted for publication August 27, 2004.
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References
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Abstract
Introduction
