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| CASE REPORT |
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| Year : 2013 | Volume
: 61
| Issue : 1 | Page : 73-75 |
A single microvascular decompression surgery cures a patient with trigeminal neuralgia, hemifacial spasm, tinnitus, hypertension, and paroxysmal supraventricular tachycardia caused by the compression of a vertebral artery
Yin Jia, Wang Wenhua, Zhang Quanbin
Department of Neurosurgery, Shanghai 10th People's Hospital, Tongji University School of Medicine, Shanghai 200072, China
| Date of Submission | 13-Dec-2012 |
| Date of Decision | 07-Dec-2012 |
| Date of Acceptance | 20-Jan-2013 |
| Date of Web Publication | 4-Mar-2013 |
Correspondence Address:
Zhang Quanbin
Department of Neurosurgery, Shanghai 10th People's Hospital, Tongji University School of Medicine, No. 301 Yanchangzhong Road, Shanghai 200072
China
 Source of Support: The current research was supported by grants
from the Foundation of Health Bureau of Shanghai (No. 2010133), Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.108016
This report presents a 72-year-old woman with posterior cranial fossa neurovascular compression syndrome that included paroxysmal supraventricular tachycardia. The patient underwent surgical exploration of the posterior cranial fossa, and a gross left vertebral artery was identified as the offending vessel. The neurovascular conflicts were associated with the cranial nerves V, VII, VIII, IX, and X. The patient experienced significant postoperative relief. Probably this is the first report of a single microvascular decompression, having cured such a high number of syndromes, including paroxysmal supraventricular tachycardia.
Keywords: Microvascular decompression, paroxysmal supraventricular tachycardia, vertebral artery
How to cite this article:
Jia Y, Wenhua W, Quanbin Z. A single microvascular decompression surgery cures a patient with trigeminal neuralgia, hemifacial spasm, tinnitus, hypertension, and paroxysmal supraventricular tachycardia caused by the compression of a vertebral artery. Neurol India 2013;61:73-5 |
How to cite this URL:
Jia Y, Wenhua W, Quanbin Z. A single microvascular decompression surgery cures a patient with trigeminal neuralgia, hemifacial spasm, tinnitus, hypertension, and paroxysmal supraventricular tachycardia caused by the compression of a vertebral artery. Neurol India [serial online] 2013 [cited 2023 Dec 7];61:73-5. Available from: https://www.neurologyindia.com/text.asp?2013/61/1/73/108016 |
| » Introduction | |  |
Since Dandy first reported the vascular compression of the trigeminal nerve, the concept of neurovascular compression syndrome as a cause of trigeminal neuralgia and hemifacial spasm has been accepted. Subsequent investigations have indicated that several other clinical syndromes, such as trigeminal neuralgia, deafness, tinnitus, vertigo, hemifacial spasm, glossopharyngeal neuralgia, and even neurogenic hypertension, can be due to the vascular compression of the trigeminal nerve, cochlear nerve, vestibular nerve, facial nerve, glossopharyngeal nerve, and vagus nerve, as well as the root entry zone (REZ) of these nerves. The clinical syndromes noted above may appear alone, but two or three can also occur together, [1] although four types of symptoms appearing together is rare. Moreover, paroxysmal supraventricular tachycardia (PSVT) caused by vascular compression had never been reported. The patient with five types of diseases mentioned above was cured successfully by a single microvascular decompression (MVD) surgery.
| » Case Report | | |
A 72-year-old woman presented with an 11-month history of hemifacial spasm and a 4-month history of a typical trigeminal neuralgia. The hemifacial spasm was limited to the area around the left eye, and the patient was experiencing paroxysms of electric shock-like pain that involved the third left trigeminal branch. This symptom was precipitated by eating. Additionally, she had experienced tinnitus in the left ear and paroxysmal palpitations for several months. Her blood pressure was 160/100 mmHg at admission. The data from 24 h Holter monitoring indicated PSVT, with a heart rate of 205 beats/min, presenting 18-24 times a day. Preoperative computed tomography angiography showed bilateral vertebral arteries (Vas), with the left artery, in particular, deflected to the left and flexed abnormally [Figure 1]a-c. Magnetic resonance imaging (MRI) showed a VA in the left side of the ventral brain stem [Figure 1]d-f. The patient underwent an MVD surgery in April 2012. During the MVD operation, after removing the arachnoid, the left VA was distended and flexed abnormally, and it compressed, from the left rostral ventrolateral medulla (RVLM) to the tentorium of the cerebellum, the VII, VIII, IX, and X cranial nerves and their REZ [Figure 2]a. The left trigeminal nerve was completely invisible [Figure 2]b. The surgery proceeded from the proximal part of the VA, and involved lifting the VA from the REZ of IX and X (the position of the left RVLM) and insertion of a Teflon pad [Figure 2]c. The offending vessel was also affixed to the dura mater of the petrosa with glue [Figure 2]d. Thus, the REZ of the facial nerve was completely decompressed, and the offending vessel was transposed [Figure 3]a. A Teflon pad was also spread between VA and VII, VIII cranial nerves on the cistern segment [Figure 3]b. Next, the trigeminal nerve was explored; because the strength of flexion of the vertebral arteries had squeezed this nerve to the tentorium tightly, the nerve had become only a thin sheet [Figure 3]c. The surgeons attempted to push the VA away, and a thick Teflon pad was inserted to shield the nerve [Figure 3]d (video clip). The symptoms, including neuralgia, spasm, tinnitus, and paroxysmal palpitations, disappeared immediately. The PSVT did not recur in the next 7 days of ECG monitoring. The patient recovered from mild postoperative facial paralysis of the left side, and her BP was 135/87 mmHg at the 8-month follow-up. At the same time, the data from 24 h of Holter monitoring indicated no PSVT at all. | Figure 1: Pre-operative computed tomography angiography (a-c) and MRI (d-f), The distended, tortuous VA is shown
Click here to view |
 | Figure 2: An intraoperative photograph of the relationship of cranial nerves VIII, IX, and X with the VA (a) Another intraoperative photograph of the relationship of the VA with cranial nerve VIII, the petrosal vein, and the invisible cranial nerve V (b) An intraoperative photograph showing how the offending vessel was displaced and the Teflon pad was inserted (c) An intraoperative photograph of the injection of glue between the VA and the dura mater of the petrosa (d)
Click here to view |
 | Figure 3: An intraoperative photograph shows the situation after the VA was affixed (a) An intraoperative photograph of a thin Teflon tap that was inserted between the VA and cranial nerves VII and VIII (b) An intraoperative photograph of the VA, the petrosal vein, cranial nerve VIII, and cranial nerve V, which can be found by displacing the distended, tortuous VA (c) An intraoperative photograph of the thick Teflon pad that was inserted between the distended, tortuous VA and cranial nerve V (d)
Click here to view |
| » Discussion | | |
When the offending vessel of neurovascular compression syndrome is the VA, MVD becomes more difficult than with other vessels. [2] For treating hemifacial spasm, interposition alone is insufficient. It is necessary that the offending vessel be displaced from the REZ of the facial nerve at the proximal region, as was performed in this case. Because the VA was gross and curved with high bending tension, the offending vessel may reset, causing recurrence. In this case, after decompression, the Teflon was affixed with glue to the dura mater of the petrosa, and the Teflon pad inserted into the neurovascular conflict was thick to diffuse the pressure.
After Annette and Gendell reported that a glossopharyngeal neuralgia patient with hypertension was cured by MVD surgery, [3] Morimoto subsequently confirmed that neurogenic hypertension may be caused by the compression of the posterior fossa vasculature in the left side of the RVLM. [4] This relationship is well known and popularly accepted. Whether neurovascular conflict can cause PSVT has never been reported. This case, in which PSVT was cured by MVD surgery, may be associated with the neurovascular compression of the nuclei of the cardiovascular center in the medulla or with effects on the excitation of the vagus nerve.
| » References | | |
| 1. | Kobata H, Kondo A, Iwasaki K, Nishioka T. Combined hyperactive dysfunction syndrome of the cranial nerves: Trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia: 11-year experience and review. Neurosurgery 1998;43:1351-61. 
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| 2. | Yang XS, Li ST, Zhong J, Zhu J, Du Q, Zhou QM, et al. Microvascular decompression on patients with trigeminal neuralgia caused by ectaticvertebrobasilar artery complex: Technique notes. Acta eurochir (Wien) 2012;154:793-7.
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| 3. | Annetta PJ, Gendell HM. Neurovascular compression associated with essential hypertension. Neurosugery 1978;2:165-73.
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| 4. | Morimoto S, Sasaki S, Miki S, Kawa T, Itoh H, Nakata T, et al. Pulsatile compression of the rostral ventrolateral medulla in hypertension. Hypertension 1997;29:514-8.
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[Figure 1], [Figure 2], [Figure 3]
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