Keywords
microvascular decompression - ectatic atheromatous vertebrobasilar artery - intraoperative
hypertensive urgency
Introduction
As per the International Association for the Study of Pain (IASP), trigeminal neuralgia
(TGN) is defined as “a sudden and usually unilateral severe brief stabbing recurrent
pain in the distribution of one or more branches of the fifth cranial nerve.”[1]
It is usually an excruciating unilateral facial pain, lasting for < 2 minutes,[2] which occurs spontaneously or by a triggering factor such as gentle, innocuous stimuli
and segregated by a pain-free interval of varying duration. The region of transition
of central and peripheral myelination called the Obersteiner-Redlich zone or root
entry/exit zone (REZ) is vulnerable to pathophysiologic changes due to vascular compression
([Fig. 1]) that results in demyelination and altered transmission.[3]
[4]
Fig. 1 T2-weighted MRI showing ectatic basilar artery in a TGN patient.
The peripheral pathogenetic mechanism of TGN is induced by progressive dystrophy in
the peripheral branches of the trigeminal nerve, which can be evoked by the compression
syndrome ([Fig. 2]) (neurovascular compression due to neoplasms, narrowed bone canals, and others)
or allergic-immune reaction (mast cell degranulation and histamine release). This
predetermines long-lasting afferent impulsation and formation of a central pathogenetic
mechanism (a stable pathologic paroxysmal-type irritation focuses in the central nerve
system).[5] The pathologic substrate of this condition is mainly associated with demyelination
of the trigeminal root entry zone.[6]
Fig. 2 Intraoperative picture showing neurovascular conflict in trigeminal neuralgia.
In this regard, experimental evidence exists about ectopic impulse generation from
demyelinated axons.[7] Accordingly, the pulsatile compression would result in progressive demyelination
and subsequent ephaptic coupling, leading to aberrant impulse generation and spreading.[3]
Two cases of TGN developed intraoperative hypertensive urgency while undergoing microvascular
decompression (MVD), and both cases had ectatic vertebrobasilar artery (VBA) with
atheromatous plaques compressing the trigeminal nerve. It was managed and postoperative
period was uneventful. On long-term follow up, the blood pressure (BP) control was
found to be satisfactory in one of the cases, whereas in the other patient, it was
unchanged.
Patients and Methods
Fifty-four consecutive patients having medical refractory TGN who underwent MVD surgery
from January 2012 to January 2017 in two separate institutions were included in this
study.
Surgical Technique
Under general anesthesia, the patient laid in park bench position with affected side
facing up and head fixed in three-pin Mayfield head rest. Retromastoid suboccipital
craniotomy was done using craniotome. Dura was incised, followed by opening of subarachnoid
cistern to drain cerebrospinal fluid (CSF). Cerebellum retracted minimally to reach
the prepontine cistern. The neurovascular conflict was identified, and the thickened
arachnoid layer was dissected. The offending vessel was mobilized from the nerve,
and a thin Teflon patch was placed between them. Hemostasis was secured, dura sutured,
bone flap replaced, and wound closed in layers.
Perioperative Period and Follow-up
Two patients developed intraoperative hypertensive urgency with BP shooting up to
>180/120 mm Hg, and in both cases, the offending vessel was an ectatic atheromatous
VBA. In the event of occurrence of intraoperative hypertensive crisis in both the
cases, the hemodynamics was stabilized by immediate cessation of manipulation of the
vessel and temporary packing of the field, with anesthetic medications administering
inhalational sevoflurane at 1 MAC (minimum alveolar concentration) and propofol infusion
at 10 mg/min intravenously. Following normalization of BP, surgery proceeded at a
very slow pace with extreme extra caution and MVD was completed.
Immediate postoperative pain relief was achieved in all patients. Postoperative period
was uneventful. Patients were discharged after routine postoperative care and reviewed
in outpatient clinic after 1 and 6 months. Their clinical status were evaluated and
recorded.
Clinical Assessment
The offending vessel on the trigeminal nerve and perioperative hemodynamic status
of the patients were analyzed. BP and antihypertensive drug(s) dosage in the pre-,
peri-operative, and follow-up period was noted.
Drastic fluctuation in intraoperative BP was considered for analysis. Postoperative
BP status along with the requirement of antihypertensive medications for controlling
systemic hypertension was compared with the patient's preoperative status.
Statistical Analysis
The collected data were analyzed retrospectively. Quantitative variables were presented
as median (interquartile range) and non-normal distributions as mean. Standard deviation
(SD) for normal distributions was assessed. Categorical variables were presented as
absolute numbers and percentages. Pre- and postoperative BP comparisons were analyzed.
A p < 0.05 indicated statistical significance.
Results
Average age of patients at the time of surgery was 53.88 (± 7.50) years. Thirty-two
(59.26%) patients were male and 22 (40.74%) were female ([Fig. 3]). Average duration of pain symptom was 2.3 (± 0.77) years.
Fig. 3 Male and female distribution of TGN patients.
Twenty-five (46.30%) patients were hypertensive and compliant to antihypertensive
medications. As per Joint National Committee (JNC) 7 classification, 19 (76%) patients
were in JNC 7 stages 1 and 6 (24%) were in JNC 7 stage 2.
Hemifacial pain was distributed along the segment(s) of the trigeminal nerve and the
segment(s) involved were V2 in 13 (24.07%) patients, V3 in 9 (16.66%), V1V2 in 8 (14.81%),
and V2V3 in 24 (44.44%) patients.
The offending vessel was superior cerebellar artery (SCA) in 29 (53.70%) cases, anterior
inferior cerebellar artery (AICA) in 15 (27.77%), petrosal vein (PV) in 7 (12.96%),
and ectatic VBA in 3 (5.55%) cases ([Fig. 4]).
Fig. 4 Offending vessel compressing the trigeminal nerve and their numbers. AICA, anterior
inferior cerebellar artery; PV, petrosal vein; SCA, superior cerebral artery; VBA,
vertebrobasilar artery.
Intraoperative hypertensive urgency with BP > 180/120 mm Hg was noted in 2 (3.70%)
cases when mobilizing the offending vessel from the nerve. It was found that in both
the cases, the offending vessel was an ectatic atheromatous VBA. No drastic intraoperative
hemodynamic instability was encountered in 52 (96.30%) cases.
On follow-up of patients at 1 and 6 months after discharge, BP of 1 (4%) patient out
of the 25 hypertensive patients was found to be in good control. Preoperatively the
patient was in JNC 7 stage 2 on three-drug regimen and postoperatively in JNC 7 stage
1 on monotherapy drug regimen. This patient had an intraoperative hypertensive urgency.
The other patient who also had intraoperative hypertensive urgency was in JNC stage
1 preoperatively on a single antihypertensive drug, and it was unchanged in the follow-up
period too. BP status of all other hypertensive patients was unchanged in the follow-up
period. A Student t-test value of 0.848 signifies no correlation between MVD and postoperative long-term
BP control/normalization.
Discussion
Vertebrobasilar dolichoectasia is an extremely rare entity with an expected incidence
of 0.06–5.8%.[8] Direct compression by vertebrobasilar dolichoectasia is an uncommon cause for TGN.
The incidence, as estimated in previous reports, ranges from 0.9 to 5.7%. Piatt et
al reported 2 cases in a series of 105 patients.[9] Bederson et al reported 4 cases in a group of 256 operated cases. Klun et al reported
2 cases in a group of 220 operated patients.[9] Honey et al, in their series of 552 patients who underwent MVD for TGN, reported
13 (2.4%) patients with dolichoectatic vertebrobasilar compressions (10 males, 3 females)[10] ([Table 1]). The incidence of recurrence after MVD surgery for VBA compression has been reported
to range from 3 to 30%.[11] Mendoza and Illingworth reported that 90% of recurrences occurred within 2 years.[12]
Table 1
Reported cases of vertebrobasilar artery compression on trigeminal nerve causing trigeminal
neuralgia
|
Study
|
Vertebrobasilar artery cases
|
Total cases studied
|
Percentage of vertebrobasilar artery cases studied (%)
|
|
Piatt et al
|
2
|
105
|
1.90
|
|
Bederson et al
|
4
|
256
|
1.56
|
|
Klun et al
|
2
|
220
|
0.91
|
|
Honey et al
|
13
|
552
|
2.4
|
“Hypertensive urgency” is the term suggested for patients with severe hypertension
without acute end-organ damage, and “hypertensive crisis” is the term suggested for
patients with severe hypertension with end-organ damage.[13]
There are reports on intraoperative hypotension due to trigeminocardiac reflex[14]
[15] and even on long-term normalization/control of BP postoperatively after MVD.[16]
[17]
However, intraoperative hypertensive crisis during MVD in TGN is comparatively underreported.
Israelyan et al in their study reported intraoperative hypertension during trigeminal
nerve manipulation in 14.6 and 14.4% of patients in the semi-sitting position group
and semi-lateral position group, respectively.[18]
In this retrospective study, we came across two events of intraoperative hypertensive
urgency. In both the cases, the offending vessel was an atheromatous ectatic VBA (100%).
The rostral ventrolateral medulla (RVLM) regulates tonic sympathetic activity and
plays a critical role in baroreflex arcs. Current knowledge indicates that nerval
BP regulation is determined by the balance of powerful tonic excitatory and inhibitory
inputs.[19] Stimulation of the trigeminal nerve causes a vasopressor response by activating
the RVLM, an important brainstem vasomotor center.[20]
[21] Furthermore, TNS has been shown to decrease cerebrovascular resistance via the trigeminal-cerebrovascular
system.[22] When activated, these pathways, via RVLM and trigeminal-cerebrovascular system,
can lead to significant increase in cerebral perfusion, hence making the trigeminal
nerve a promising target in TBI management. Sympathetic nerve activity and BP are
temporary reduced by MVD in patients with severe hypertension with neurovascular compression.[23] TGN is associated with essential hypertension.[24]
There are animal and human studies that hypothesize the compression on rostral ventral
medulla (RVM) to be a cause of essential hypertension (neurogenic hypertension). MVD
of the lower cranial nerves and RVM has been performed to control or normalize BP
in essential hypertensive patients.[25]
Conclusion
Trigeminal neuralgia due to an ectatic atheromatous VBA is notorious for predisposing
to intraoperative hypertensive urgency, and postoperative long-term BP control in
hypertensive patients is not feasible after MVD.
