Key-words:
Artery of Percheron - endoscopic surgery - infarction - pituitary apoplexy
Introduction
Pituitary apoplexy is an acute emergency condition in neurosurgery. Urgent surgical
decompression is mandatory for decompression. Various complications reported after
pituitary apoplexy surgery such as vascular (infracts or bleed, direct vascular injury),
endocrinology (panhypopituitarism), and delayed surgery, resulting in nonimprovement
of visual symptoms or oculomotor deficits.[[1]] Various arterial territory can be involved either anterior circulation such as
small perforator of the internal carotid artery or middle/anterior cerebral artery
or posterior circulation such as the basilar top, posterior cerebral artery, or perforators.[[2]] Few cases of artery of Percheron (AOP) infarction reported in the English literature
after the endoscopic approach for pituitary adenoma.[[2]],[[3]],[[4]] AOP infarct following endoscopic transsphenoidal surgery for pituitary apoplexy
is not reported in the literature.
Case Report
A 55-year-old lady presented a sudden-onset headache followed by bilateral sudden
visual loss for 2 days. No prior history of visual loss or headache was noted. On
examination, she was drowsy, obeying, right eye perception of light (−), and left
eye-hand movement close to face without motor or sensory deficits. Computed tomography
(CT) scan shows a sellar-suprasellar lesion with hyperdensity within the lesion [[Figure 1]]a. Magnetic resonance imaging (MRI) shows sellar-suprasellar lesion size (3.5 ×
3 × 2.8) Cm, the lesion heterogeneously hyperintense in both T1W and T2W [[Figure 1]]b with areas of blooming on SWI [[Figure 1]]c. However, no evidence of infarction was found. Postcontrast images showed a thin
rim of peripheral contrast enhancement. Imaging was suggestive of pituitary apoplexy.
She underwent an endoscopic transnasal approach and decompression of tumor. Tumor
was soft, vascular, and subtotal decompression was performed. During surgery, there
was no notable cerebrospinal fluid (CSF) leak. In the postoperative period, the patient
was in altered sensorium with bilateral ptosis, and an immediate CT scan showed subtotal
decompression with blood in the interpeduncular cistern [[Figure 1]]d. Postoperative MRI showed (T2W and fluid-attenuated inversion recovery) [Figure
1e and f] hyperintense signal changes involving bilateral medial thalamus and rostral
midbrain. Diffusion imaging showed bilateral paramedian thalamic infarcts with rostral
midbrain infarct, suggestive of AOP infarct [[Figure 2]]a, [[Figure 2]]b, [[Figure 2]]c. The patient gradually improved in sensorium and was discharged after 10 days.
At 3 months of follow-up, the patient was obeying with partial ptosis in both eyes.
Figure 1: (a) Computed tomography (axial) showing mixed density suprasellar lesion. (b) Magnetic
resonance imaging (T2W, sagittal) showing seller-suprasellar solitary lesion with
multiple hyperintensity inside the tumor. (c) Magnetic resonance imaging (SWI, axial)
showing areas of blooming inside the tumor suggestive of bleed. (d) Postoperative
CT (axial) showing blood in interpeduncular cistern. (e) Postoperative magnetic resonance
imaging (axial) showing hyperintensity in bilateral paramedian thalamus. (f) Postoperative
magnetic resonance imaging (fluid-attenuated inversion recovery) showing rostral midbrain
signal changes. CT: Computed tomography, MRI: Magnetic resonance imaging
Figure 2: (a-c) Magnetic resonance imaging (diffusion-weighted imaging) showing diffuse restriction
involving bilateral paramedian thalamus and rostral midbrain suggestive of artery
of Percheron infarct. MRI: Magnetic resonance imaging
Discussion
AOP is a rare variant of perforator arising from the posterior cerebral artery (P1
segment).[[5]] It is an unpaired perforator arising from either side of the P1 segment, on average
8 mm lateral to basilar artery bifurcation, and supplying both paramedian thalamus
and rostral midbrain. The mean diameter was 2.1 mm, and it traverses on an average
of 1.5 cm before entering the brain.[[6]] Four patterns of infarct are commonly seen along with the midbrain “V” sign. The
infarct patterns are bilateral paramedian thalamus involvement with or without rostral
midbrain involvement and bilateral paramedian and anterior thalamus with or without
midbrain involvement.[[3]],[[7]] The occurrence of AOP infarct after pituitary surgery is rare. The infraction of
the AOP seen in primary pituitary adenoma, re-exploration cases of pituitary adenoma,
and postradiotherapy.[[2]],[[3]],[[5]] The cause of infarction could be the mechanical injury of the AOP, which was attached
to the cisternal surface of tumor capsule. The AOP usually is small in diameter. Therefore,
it seems that the amount of bleeding from it is not so much and controlled by itself.
This event could be met in the pituitary surgery with aggressive manipulation, especially
by curettage. The other probable cause of infraction could be vasospasm due to subarachnoid
hemorrhage (SAH) following surgery. The rare probability is hypotension during the
surgery, and it can happen due to hypopituitarism following apoplexy or hypercortisolism.[[2]] Meningitis in the postoperative period can also cause infarction of major vessels
as well as small perforators.[[8]]
Typical clinical features of the AOP infarct are unconsciousness after surgery with
or without cranial nerve involvement. MRI with diffusion-weighted imaging is the investigation
of choice and shows bilateral thalamus with paramedian midbrain infarct. In our case,
the probable cause was a breach of the posterior capsule, resulting in SAH. The SAH
leads to the vasospasm of the AOP. The underlying pituitary apoplexy caused the tumor
to firmer, as presented late. The acute blood may be converted into clot followed
by early fibrosis. Aryan et al.[[9]] reported a case AOP infarct following endoscopic transsphenoidal surgery for a
re-exploration case of pituitary adenoma. Intraoperatively, CSF leak was noted. Postoperative
CT scan showed diffuse SAH and MR showed AOP infract though managed with nimodipine
infusion. Patients recovered well with residual hemiparesis and ptosis. On the contrary,
our patient presented with apoplexy and underwent endoscopic transnasal surgery for
a primary tumor. We did not notice the CSF leak during surgery. In the postoperative
period, nimodipine was added and the patient slowly improved in sensorium. The pattern
of an infraction involving bilateral medial thalamus and rostral midbrain was suggestive
of the AOP infarction. The pattern of infarction is typical for AOP infarction. Hence,
if the postoperative images show the specific infarction pattern, medical treatment
should be initiated as early as possible. Preoperative diagnosis of AOP is challenging
as it is a small vessel, especially if a large adenoma distorting the surrounding
anatomy. However, MRI angiogram may help detect suspected cases of the presence of
AOP.
Management of this rare type of infarct is conservation.[[3]] Initial ventilator support if required followed by neurorehabilitation is the policy.
If the patient develops panhypopituitarism, then endocrinological support is mandatory.
The role of nimodipine to prevent vasospasm is not proven. The prognosis depends on
the pattern of infarct and the quality of supportive care.
Inform consent
Informed consent was taken from patient.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms.
In the form, the patient has given her consent for her images and other clinical information
to be reported in the journal. The patient understand that name and initial will not
be published and due efforts will be made to conceal identity, but anonymity cannot
be guaranteed.
