Fig. 10.1
MRI in a patient harboring left vagoglossopharyngeal neuralgia together with apparent essential arterial hypertension. (a) Coronal view of T2 high-resolution sequence showing compression of the ventrolateral aspect of medulla by vertebral artery (VA) on left side (arrow). Axial T2 (b) and T1 with gadolinium (c) showing VA and posterior inferior cerebellar artery conflicting, in addition to the brainstem, the root entry/exit zone of the IXth and Xth cranial nerves on left side
Fig. 10.2
MRI with fusion of T2 and TOF-angio in a patient with apparent essential hypertension. Axial (a) and coronal (b) views of the vertebral artery compressing the ventrolateral aspect of the medulla on the right side
Fig. 10.3
MRI in a patient afflicted with left hemifacial spasm and apparent essential hypertension. Upper row: axial T2 (a) and TOF-angio (b) sequences showing megadolicho-vertebral artery (VA) and posterior inferior cerebellar artery (PICA) compressing the REZ of the VIIth cranial nerve (CN) on the left side. Lower row: axial T2 (c) and TOF-angio (d) sequences showing VA and PICA loops stretching and compressing the IXth and Xth CN on the left side
10.3 Surgical Technique
Installation and approach are approximately same as for HFS and VGPN MVD (Barker et al. 1995; Jianqing and Sindou 2015). The patient is placed in the contralateral decubitus position, the neck contralateral flexed to approach lower cranial nerves and VL medulla inferolaterally (Fig. 10.4).
Fig. 10.4
Access to the IX–Xth REZ and ventrolateral aspect of the medulla should be following an infrafloccular trajectory along the cerebellomedullary fissure. Main concern is to avoid hearing loss. The lesser the exposure of the cochleovestibular nerve complex, the better for preservation of hearing and vestibular function. The patient is placed in the contralateral decubitus position, the head in a three-pin holder, slightly flexed and rotated 15° toward the contralateral side. The neck is laterally flexed toward the contralateral side to expose the retromastoid-retrocondylar region without the view obstructed by the shoulder taking care not to stretch the brachial plexus especially in patients with a gracile neck. The ipsilateral shoulder is tapped and pulled caudally and posteriorly. Landmarks of skin incision and craniectomy are drawn posteriorly to the tip of the mastoid process. Keyhole (retromastoid, retrosigmoid, infrafloccular) approach for accessing IXth and Xth cranial nerves (CN) and the ventrolateral aspect of medulla on the right side. Landmarks of mastoid tip (M), transverse (T) and sigmoid (S) sinuses. Craniectomy for infrafloccular, access to IXth and Xth CN (dotted), and for comparison, craniectomy for infratentorial supracerebellar access to trigeminal CN (crosses)
A retromastoid craniectomy is performed posteriorly to the tip of the mastoid process with a semilunar shape of 2 cm in length and 1.5 cm in width, just posterior to the sigmoid sinus. The burr hole must not be turned too laterally onto the sigmoid sinus as this could endanger the external wall of the sinus, which is often reduced to a thin endothelial layer adhesive to the bone (Fig. 10.5). The use of a Doppler microprobe may help in detecting the posterior border of the sigmoid sinus. The dura is opened by making a small flap retracted along the sigmoid sinus. Then a self-retaining retractor, of the Yasargil type, mounted with a very thin blade of Sugita – Fukushima type – is placed on the inferolateral aspect of the cerebellum down to the cerebellomedullary fissure, to maintain the fissure opened (Sindou et al. 1992). The arachnoid is incised from XIth up to VIIIth nerves, and then the X–IXth root entry/exit zones are reached and the ventrolateral aspect of the medulla seen. The choroid plexus emerging from the lateral foramen of Luschka, which frequently covers the lower cranial nerves, is gently retracted to expose REZ and vessels at the brainstem (Fig. 10.6).
Fig. 10.5
Schematic views of IXth and Xth cranial nerves and ventrolateral (VL) aspect of the medulla on the right side. Upper view: superimposition of CT and MRI showing VL compression of brainstem by megadolicho-vertebrobasilar (VB) artery on the right side and retromastoid craniectomy to perform an inferolateral approach to the lower cranial nerves (CN). Lower view: superimposition of the lower part of the cerebellopontine angle to a drawing of the patient’s head in the lateral decubitus position
Fig. 10.6
Step-by-step technique for microvascular decompression of IXth and Xth root entry/exit zone and ventrolateral (VL) aspect of the medulla on the right side. (a) Inferolateral floccular trajectory to XIth and Xth–IXth cranial nerves, with REZ masked by choroid plexus (ch. pl.) REZ and VL medulla are compressed by a megadolicho-vertebrobasilar (VB) and posterior inferior cerebellar artery (PICA). (b) Access to the REZ after retraction of the choroid plexus. (c) Decompression after dissection of neural/vascular structures and translation of VB-PICA complex. (d) VB-PICA complex maintained apart after insertion of Teflon material
The compressive vessels most frequently found in the group of patients affected with HT were the posterior cerebellar artery (PICA) and the vertebrobasilar artery (VBA) and frequently the association of both as shown in Table 10.2. Compression was almost always ventral to the Xth–IXth rootlets. This implies that maneuvers on the conflicting vessels be done passing between the rootlets at the several interspaces. During mobilization of the compressive arteries, care should be taken to respect the tiny perforating collaterals and not to generate mechanical vasospasm. Throughout vascular manipulations, irrigation with warm saline and application of a few droplets of papaverine in solution (1 in 10 mL saline) are important measures to limit vasospastic reactions. Not too much of papaverine should be used because of its very acid PH.
After the compressive arteries have been identified and dislodged from their conflicting situation, often marked by engrooving the ventrolateral aspect of the medulla, the vessels have to be maintained apart in such a way not to return to the previous compressive location.
When an arterial loop has a sufficient laxity, it can be kept apart by means of slings approximately 3–4 cm in length and 2–3 mm in width, made of shredded fibers of Teflon felt. Slings are passed around the vessel to exert a pulling effect and are blocked to avoid recurrence of malposition.
When an arteriosclerotic/atheromatous megadolicho-artery (PICA or VBA or the complex of VBA + PICA, as seen in Fig. 10.3) is in cause, its rigidity makes transposition difficult if not somewhat dangerous. Dissection should start at the brainstem from caudal to rostral and the vessel maintained away by inserting a piece of semirigid prosthesis (Dacron or Teflon) and/or a cushion of Teflon fibers in between REZ/brainstem and the artery. Care must be taken not to exert a (too strong) “neurocompressive” effect.
Closure should be tight to avoid CSF fistula. For tightness, dural suturing may need additional patch of fascia lata and/or fatty tissue affixed onto the mastoid cells if opened.
10.4 Results
Few studies have directly addressed the clinical problem of HT as a consequence of a vascular conflict at the level of the IX–X REZ or ventrolateral medulla. Overall results, while promising, are still far from conclusive; yet no randomized controlled trial has been published on the issue. Studies published so far are case series, usually by one center and by a single surgeon. Table 10.4 summarizes the published series:
1.
First observations of an effect of MVD of the ventrolateral medulla were published by Jannetta in 1979 in a series of patients operated on for glossopharyngeal neuralgia (Jannetta and Gendell 1979). This was later followed by the largest series yet published, 53 patients, benefiting from MVD for various reasons (mostly trigeminal neuralgia and HSF) but also having hypertension at the time of decompression (Jannetta et al. 1985b). Out of the 53, in 42, decompression of the ventrolateral medulla (exclusively on the left side) was performed. The compressing vessel was either the VBA or PICA or a combination of both in a vast majority (see Table 10.2). After a follow-up of at least 6 months (maximum FU 7 years), 31 patients had normalized their BP. In the normalized group, 13 patients had no treatment at all at latest FU, 12 had decreased their treatment, and 6 had kept the same treatment as preoperatively.
The same group went on to publish in 1998 a series of patients in whom the indication for decompression was the refractory hypertension itself (Levy et al. 1998). In this retrospective series of 12 patients, all had only severe refractory HT with a major lability of BP values. All patients underwent preoperative MRI; however, existence of a conflict was determined at surgery. Vessels were found to contact the REZ of the IXth–Xth pair or the ventrolateral medulla in all patients. In 11 the compressive vessel was PICA, whereas in the remaining one it was the VBA (see Table 10.2). Successful decompression was achieved in all patients. After a mean FU of 51.7 months, 8 patients had improved their BP with a mean drop of the systolic of 42.3 mmHg (20 mmHg was considered a minimum for declaring improvement). One patient had worsening of his HT, and the others showed no change.
Table 10.1
WHO grading system for HTN
Grading | Systolic BP values | Diastolic BP values |
|---|---|---|
Normal | ≤140 | ≥90 |
Grade 1 | 140–159 | 90–99 |
Grade 2 | 160–179 | 100–109 |
Grade 3 | ≥180 | ≥110 |
2.
A number of papers, also directly addressing refractory HT due to vascular conflict at the ventrolateral medulla, has been published by the team of Erlangen in Germany under the coordination of Pr. Fahlbusch. In the initial publication in The Lancet in 1998, eight patients had been prospectively studied (Geiger et al. 1998). Patients were included if MRI showed a conflict at the level of the VL medulla or IXth–Xth REZ. In six the conflict was caused by PICA on the left side, in one by PICA bilaterally, and in the last one by PICA and the VBA. At 3 months seven patients had improved their HT to the point of normalization with a decrease in treatment. Only five patients were followed up to 1 year, and out of these, four had normal BP values. In none of the patients, it was possible to halt the antihypertensive treatment. The series was followed for another 36 months for a mean FU of 3.5 years (Frank et al. 2001). At the end of this period, three patients had normal BP with little or no medication, and two had the same status as preoperatively. In the remaining three, severe complications of uncontrolled HT occurred, with two deaths related to high BP values.
In a parallel publication, the same team attempted to provide mechanistic data by following the evolution of BP and sympathetic activity in parallel in 14 patients after MVD for severe refractory HT. The series was published in Stroke in 2009 (Frank et al. 2009). Mean FU was 26 months. At 1 year patients showed a significant decrease in blood pressure (monitored over 24 h) from 179 mmHg on average preoperatively to 139 mmHg. Furthermore sympathetic activity (monitored by peroneal microneurography) had a similar evolution. However, BP values returned to above normal at 2 years postoperatively (average 152) and the same held true for sympathetic activity. This led the authors to believe that neurogenic HT was mediated through sympathetic hyperactivity and that although their results were limited further investigations were warranted.
3.
Other small series and case studies were published by several authors with effects of HT being studied in patients undergoing MVD principally for other pathology (mostly HSF) (Morimoto et al. 1999; Van Ouwerkerk et al. 1989). These are detailed in Table 10.4.
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