Key-words:
Artery of Percheron - endoscopic approach - pituitary - skull base - thalamic infarct
Introduction
The endoscopic endonasal approach to the skull base has become increasingly common
in recent years, with the consequent decrease in the microscopic transsphenoidal surgery.
Postoperative outcomes are good, and global morbidity and mortality rates are often
lower comparing to transsphenoidal surgery. Endonasal surgery allows for broader exposure
when an expanded approach is utilized, although some authors have reported a higher
rate of vascular complications when using an extended approach.[[1]],[[2]]
In their case series, Romero et al.[[3]] reported an arterial injury rate of 0.5% (0.125% for the internal carotid artery
[ICA]). Gardner et al.[[4]] found an ICA lesion rate of 0.3%. In the systematic review performed by Chin et
al.,[[2]] the ICA lesion rate with this technique range from 0.2% to 1%.
We describe the case of a patient who underwent endoscopic endonasal surgery (EES)
for an invasive pituitary adenoma, with unexpected damage to the artery of Percheron
(AOP) during the surgery, causing rostral midbrain and bilateral thalamic infarction.
This is a very rare complication, with only one previous case reported in the literature,
related to a second surgery.[[3]] Pathophysiology and associated clinical and radiological characteristics are discussed.
For this research, no funding was received.
All authors certify that they have no financial interest or nonfinancial interest
in the subject matter or materials discussed in this manuscript. An Institutional
Review Board (IRB) has approved the present study.
Case Report
A 52-year-old female patient presented to the emergency department complaining of
long-standing headache associated with diplopia. The patient presented the physical
features of acromegaly and left sixth cranial nerve palsy. Blood tests showed elevated
insulin-like growth factor-1 and prolactin levels.
Brain computed tomography (CT) scan showed a lesion with suprasellar extension and
also to the posterior fossa behind the dorsum sellae and posterior clinoid processes.
Pituitary magnetic resonance imaging (MRI) confirmed the sellar lesion with slight
homogeneous contrast enhancement. Suprasellar component produced chiasm and left optic
nerve distortion. The lesion also contacted with basilar artery and the P1 segments
of both posterior cerebral arteries (PCA), as well as the right cavernous sinus [[Figure 1]]a, [[Figure 1]]b, [[Figure 1]]c.
Figure 1: Axial (a), coronal (b), and sagittal (c) T1 with gadolinium magnetic resonance imaging,
showing the tumor with suprasellar and retroclival extension. Displacement and compression
of the chiasm and left optic nerve, as well as contact with basilar artery and P1
segments are observed
The patient underwent an expanded endoscopic endonasal approach with intraoperative
neurophysiological monitoring. The clivus, sella turcica, tuberculum sellae, and part
of the sphenoid planum were drilled. The sellar component and the suprasellar portion
were resected. Curved ring curettes were used to access and resect the retroclival
region and the area posterior to the dorsum sellae, although excision was probably
subtotal due to the lack of direct visualization. There were no incidents during the
surgery. Motor and somatosensory-evoked potentials remained stable at all times. Intraoperative
bleeding was minimal, and hemodynamic stability was maintained throughout the operation,
with systolic blood pressure between 90 and 120 mmHg during the surgery.
Nonreactive bilateral mydriasis was evidenced after the completion of surgery. Brain
CT scan revealed subarachnoid hemorrhage in perimesencephalic cisterns [[Figure 2]]. No hydrocephalus was observed. Sedation was slowly withdrawn. The patient presented
minimal left brachial flexion and preserved corneal reflexes with persistence of nonreactive
mydriasis. Given the patient's neurological status, we decided to maintain sedation
with intracranial pressure monitoring using a parenchymal sensor.
Figure 2: Axial computed tomography scan showing postoperative subarachnoid hemorrhage in the
basal and inter-peduncular cisterns
An MRI showed signal restriction in diffusion-weighted imaging (DWI)/apparent diffusion
coefficient sequences in rostral midbrain and paramedian thalami, suggesting acute
ischemia congruent with AOP infarction [[Figure 3]]a, [[Figure 3]]b, [[Figure 3]]c. MR angiography showed normal flow signal and normal morphology of circle of Willis
and main intracranial arteries. The right posterior communicating artery (PCOM) was
visible and prominent.
Figure 3: Postoperative axial diffusion-weighted imaging (a), fluid attenuated inversion recovery
(FLAIR) (b) and T2 (c) magnetic resonance imaging. Hypersignal is observed in the
bilateral medial thalamus and rostral midbrain, indicative of ischemia
After the withdrawal of sedation, the patient presented a Glasgow Coma Scale of 7
points, with bilateral third cranial nerve palsy. Tracheostomy and percutaneous gastrostomy
were performed, and the patient was transferred to an intensive rehabilitation center.
One year after surgery, the patient presented the following neurological sequelae:
third cranial nerve palsy requiring blepharoplasty, spastic tetraparesis, and neuropsychological
disorders with impulsivity and emotional lability.
Discussion
AOP is an unusual anatomical variant [[5]],[[6]] in which a single perforating artery of the P1 segment of the PCA supplies blood
to medial thalami and rostral midbrain bilaterally. It was first described by the
French neurologist Gerard Percheron in 1973. Thalamus and midbrain vascularization
is highly complex, with arterial afferents arising from the PCA and the PCOM through
perforating branches. Vascular supply to the thalami can be divided into four territories:
anterior, paramedian, inferolateral, and posterior. Thalamic paramedian arteries are
also responsible for vascularization to some regions of the brainstem, including interpeduncular
nucleus, decussation of the superior cerebellar peduncles, medial red nucleus, nuclei
of third and fourth cranial nerves, and the anterior periaqueductal gray matter. Given
this distribution, the involvement of AOP can cause bilateral paramedian thalamic
ischemia, with or without midbrain ischemia.
Clinical presentation of AOP occlusion [[7]],[[8]],[[9]],[[10]],[[11]],[[12]],[[13]],[[14]],[[15]],[[16]],[[17]],[[18]],[[19]] is variable due to interindividual differences in thalamus anatomy and function,
as well as to the variability in its vascularization. However, the presentation mainly
includes vertical oculomotor palsy, memory involvement, and alterations in the level
of consciousness. If the entire midbrain is affected, this leads to mesencephalothalamic
or thalamopeduncular syndrome, which can include other oculomotor disorders and the
involvement of long motor pathways.[[9]],[[11]],[[12]],[[13]]
AOP infarction can be diagnosed by brain MRI [[6]],[[14]],[[15]],[[20]] with visualization of the infarction at initial stages, showing hypersignal in
medial thalamus bilaterally, with or without mesencephalic involvement. The optimal
sequence for early detection is DWI. By contrast, the AOP is rarely visualized by
conventional arteriography due to its small size.
Based on a study of 37 patients, Lazzaro et al.[[6]] identified four ischemic patterns of AOP infarction. In their study, 43% of patients
presented bilateral paramedian thalamic involvement with midbrain, 38% presented bilateral
paramedian thalamic involvement without midbrain, 14% bilateral paramedian thalamic
with anterior thalamus and midbrain, and 5% showed bilateral paramedian thalamic involvement
with anterior thalamus without midbrain. Aryan et al.[[16]] reported the other case of AOP infarction after EES. Those authors described the
case of a patient who underwent a second surgery for pituitary adenoma with suprasellar
extension and chiasmatic compression. During the operation, they observed an episode
of hypertension and bradycardia that resolved spontaneously. They also observed minor
bleeding from the posterior part of the tumor capsule. The patient awoke with a low
level of consciousness and bilateral ptosis. On brain CT, they observed subarachnoid
hemorrhage in basal cisterns and the MRI showed thalamic infarction. Postoperatively,
the patient showed progressive improvement. At 6 weeks, she obeyed orders, but still
presented hemiparesis.
We agree with the mechanisms proposed by Aryan et al. to explain bilateral thalamic
infarction. We believe that AOP involvement may occur for two reasons in the context
of an endonasal endoscopic approach with expansion to the sellar region, as in our
case. The first and most likely cause is the involvement of the AOP in the region
of the basal cisterns during resection. In our case, visualization of the area without
resection of the sellar dorsum was limited. As a result, the use of ring curettes
without precise visual control could have resulted in inadvertent damage to the AOP.
However, due to the small size of this artery, the amount of bleeding in our patient
was unremarkable. In addition, in this case, intraoperative neurophysiological monitoring
did not warn us of the presence of a parenchymal lesion. The second potential cause
of the infarction could have been vascular irritation with vasospasm secondary to
postoperative subarachnoid hemorrhage. We papaverine during surgery and systolic blood
pressures were maintained throughout between 90 and 120 mmHg to ensure sufficient
irrigation.
Based on our experience, we believe that the following factors should be considered
when attempting to treat suprasellar and retrosellar lesion by the endonasal approach.
First, if the tumor cannot be adequately visualized, then resection should not be
attempted, even in the case of soft tumors that would otherwise be considered easily
resectable. Second, ring curettes may inadvertently damage small-caliber vessels.
Thus, these instruments should not be used without optimal visual control. Third,
in the case of retrosellar extension, dorsum sellae resection may be considered with
dislocation of the pituitary gland (if the gland is intact). Finally, intraoperative
neurophysiological monitoring may not detect thalamic lesions.
Conclusion
The present report describes a case of AOP infarction associated with extended EES.
Pituitary adenomas or other lesions with retrosellar extension may involve small perforating
arteries of the thalamus and brainstem; for this reason, every effort should be made
to try to preserve these vascular structures during surgery. Direct visualization
can prevent damage to small perforating arteries. However, it is important to keep
in mind that intraoperative neurophysiological monitoring of motor and sensory pathways
may not detect intraoperative damage to these small vessels.
Ethics approval
An IRB has approved the present study.
Patient consent
The patient has consented to the submission of the case report for submission to the
journal.
