DOI: 10.5137/1019-5149.JTN.9237-13.0

Case Report

Cerebral Infarction Caused by Pituitary Apoplexy:
Case Report and Review of Literature
Pitüiter Apopleksiye Bağlı Beyin İnfarktüsü: Olgu Sunumu ve
Literatürün Gözden Geçirilmesi
Chenxi Zhang1, Feng Feng2, Yicheng Zhu3, Renzhi Wang1, Bing Xıng1
1Peking Union Medical College Hospital, Departments of Neurosurgery, Beijing, China
2Chinese Academy of Medical Sciences, Departments of Radiology, Beijing, China
3Peking Union Medical College, Departments of Neurology, Beijing, China

Corresponding Author: Bing Xıng / E-mail: [email-masked]

ABSTRACT
Pituitary apoplexy followed by cerebral infarction is rare. In this report, we present a 42-year-old man who had been diagnosed of pituitary
adenoma presented with a sudden onset of unconsciousness, left hemiplegia and right ptosis. Investigations revealed the development of
pituitary apoplexy. The extension of tumor mass compressed the supraclinoid portion of the right internal carotid artery, resulting in the
cerebral infarction in the right anterior and middle cerebral artery territory. Left anterior cerebral artery territory infarction was also found,
which could be caused by vasospasm provoked by pituitary apoplexy. The patient underwent decompression surgery via transsphenoidal
approach after four weeks’ conservative treatment, and pathological examination revealed hemorrhage and necrosis of the pituitary adenoma.
His symptoms improved within five months’ follow-up. Since pituitary apoplexy producing cerebral infarction is rare, clinicians should be alert
to that possibility, and delayed transsphenoidal surgery following conservative management with steroids is the appropriate management of
such an occurrence.
Keywords: Cerebral infarction, Compression, Internal carotid artery, Pituitary apoplexy, Vasospasm

ÖZ
Pitüiter apopleksi sonrasında beyin infarktüsü nadirdir. Burada, ani başlangıçlı bilinç kaybı, sol hemipleji ve sağ pitozis ile başvuran ve hipofiz
adenomu tanısı alan 42 yaşındaki bir erkek hasta sunulmuştur. İncelemeler pitüiter apopleksi gelişimini ortaya koydu. Tümör kitlesinin uzantısı
sağ anterior ve orta serebral arter bölgesinde serebral infarktüs ile sonuçlanacak şekilde sağ internal karotid arter supraklinoid kısmını
sıkıştırmış idi. Pitüiter apopleksi tarafından tetiklenen vazospazmın neden olmuş olabileceği sol anterior serebral arter bölgesi infarktüsü de
bulundu. Dört haftalık tutucu tedavi sonrasında transsfenoidal yaklaşım ile dekompresyon ameliyatı yapıldı ve patolojik muayenede hipofiz
adenomu nekrozu ve kanama saptandı. Hastanın belirtileri beş aylık takip ile düzeldi. Serebral infarktüse neden olan pitüiter apopleksi nadir
olduğundan klinisyenler bu olasılık açısından dikkatli olmalıdır. Böyle bir durumda uygun tedavi ve steroidler ile tutucu tedavi sonrasında
geciktirilmiş transsfenoidal cerrahidir.
ANAHTAR SÖZCÜKLER: Serebral infarktüs, Kompresyon, İnternal karotid arter, Pitüiter apopleksi, Vazospazm

Introduction
Pituitary apoplexy is an acute clinical syndrome typically
characterized by a sudden headache, visual impairment,
altered consciousness and ocular palsy. Hemorrhage and/or
infarction of pituitary adenomas are the most common causes.
Pituitary apoplexy occurs in 0.6-10% of patients with pituitary
adenomas (5). However, pituitary apoplexy complicated by
cerebral infarction is rare. Here, a case of pituitary apoplexy
followed by cerebral infarction is reported.
Case report
A 42-year-old man presented with an acute high fever
(40°C). Several hours later, he developed a sudden onset
of unconsciousness after urinating and admitted to our
hospital. He had just been clinically diagnosed of pituitary

782

adenoma 2 weeks ago after suffering from headache for 8
months (Figure 1). On admission, his score of GCS (Glascow
Coma Scale) was 4/15(E2V1M1). His body temperature was
38.7°C. Physical examination revealed anisocoria (right>left),
right ptosis and impaired light reflex. His neck was stiff and
Babinski sign on the left side was positive. Computerized
tomography (CT) scans of the brain showed cerebral ischemia
in the bilateral anterior and right middle cerebral artery
territory (Figure 2). Transcranial Doppler ultrasound (TCD)
detected decreased blood flow velocity within the bilateral
anterior and right middle cerebral arteries. T1-weighted nonenhanced Magnetic resonance imaging (MRI) demonstrated
intratumoral hemorrhage in the hypophysial fossa invading
the cavernous sinus (Figure 3A). And T2-weighted MRI showed
the infarction of bilateral anterior and right middle cerebral
artery territory (Figure 3B). Magnetic resonance angiography
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Zhang C. et al: Pituitary Apoplexy and Cerebral Infarction

(MRA) confirmed narrowing of the supraclinoid segment of the
right internal carotid artery (Figure 4A). Serum examination
revealed a slight decrease in free triiodothyronine and free
thyroxine while corticoid and growth hormone levels were
normal.

The patient was initially treated with mannitol and steroids
for massive cerebral infarction and levothyroxine sodium for
hypopituitarism. His temperature decreased to 37.4°C and
his consciousness improved that his GCS score reached nine
(E2V1M6) during the next week. The muscle strength of his
right limbs was in grade V, while the left was still in paralysis.
His symptoms of cranial nerve palsy persisted. Four weeks after
the onset, transsphenoidal surgery was performed to remove
the tumor for decompression. Pathological examination
revealed hemorrhage and necrosis of the pituitary adenoma.

Figure 1: Coronal T1-weighted non-enhanced MRI showing a
pituitary mass with isointensity before the acute attack.

A

B

Figure 2: Computerized tomography scan showing massive low
density area in the bilateral anterior and right middle cerebral
artery territory (arrow) with a heterogeneous density lesion
occupying the suprasellar cistern (arrowhead).
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Figure 3: Coronal T1-weighted non-enhanced MRI showing
focal high signal intensity around the cavernous portion of right
internal carotid artery (A, arrow), while Coronal T2-weighted MRI
showing high signal intensity in the bilateral anterior and right
middle cerebral artery territory (B, arrow).

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Zhang C. et al: Pituitary Apoplexy and Cerebral Infarction

Immunohistochemical staining results demonstrated it
negative for all the anterior pituitary hormone.
Postoperatively, his right ptosis and light reflex improved
rapidly. One week after the operation, MRA was carried out,
confirming the decompression of the narrowed internal
carotid artery (Figure 4B). The motor power of his left lower
limb recovered to grade V- within five months after the
operation, and that of the left upper to grade II.
Discussion
Sudden onset of headache, vomiting, visual impairment
and decreased consciousness are common complications
of pituitary apoplexy, while cerebral infarction secondary
to pituitary apoplexy is rare. To our best knowledge, only
14 cases have been reported since 1952 (3, 4, 6, 7, 9-13, 15-

18, 20). The clinical features of these cases are summarized
in Table I, II. All the cases reported before were male, with
ages ranging from 15 to 77 years. This demographic feature
was in consistent with epidemiological studies on pituitary
apoplexy, which showed men were more commonly affected
with ages reported between 15 and 90 years (14, 19). Motor
symptoms were found in almost all the cases except the one
reported by Pozzati et al. (15), where the patient instead
developed central facial weakness. Consciousness alteration
and cranial nerve palsy were also common complications. As
to the affected vessels, the cavernous portion or supraclinoid
portion of internal carotid artery, anterior cerebral artery and
middle cerebral artery were most likely to be involved.
In our case, the patient, a middle-aged male, lost consciousness
and developed left hemiplegia and right cranial III nerve palsy

Table I: Reported Cases of Cerebral Infarction Caused by Vasospasm Secondary to Pituitary Apoplexy

Reference

Age/Sex

Symptoms

Vessels Involved

Treatment

Outcome

Bilateral ICA

Conservative
care

Improvement

Pozzati et al., 1987 (15)

15/M

Reduced consciousness,
right cranial III/VI nerve
palsy, left central facial
weakness

Itoyama et al., 1990 (9)

45/M

Reduced consciousness,
right hemiparesis, visual
disturbances

Left ACA and left MCA

Delayed TSA

Improvement

Rodier et al., 2003 (16)

35/M

Left hemiplegia, frontal
syndrome with apathy,
unconsciousness

right and left ACA,
right MCA

Decompression
surgery#

Improvement

Akutsu et al., 2004 (3)

29/M

Reduced consciousness,
Left ACA and MCA
transient right hemiplegia

Early TSA

Improvement

Present case, 2012

42/M

Left hemiplegia,
unconsciousness, right
cranial III nerve palsy

Delayed TSA

Improvement

Right ICA
(supraclinoid portion)
Left ACA

ICA: internal carotid artery, ACA: anterior cerebral artery, MCA: middle cerebral artery, TSA: transsphenoidal approach, #: the operation method was not
described.

A

B

Figure 4: MRA showing the stenosis of the supraclinoid segment of right internal carotid artery compressed by the hemorrhagic
pituitary mass (A, arrow), and postoperative MRA illustrating decompression and restoration of the right internal carotid artery
(B, arrow).

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Zhang C. et al: Pituitary Apoplexy and Cerebral Infarction

during the course of the illness. The right internal carotid
artery and left middle cerebral artery were confirmed to
be involved in this case, which was in accordance with the
clinical features mentioned above.
Furthermore, there are two possible mechanisms of
cerebral infarction caused by pituitary apoplexy that have
been suggested: vasospasm and mechanical compression.
Vasospasm may be caused by subarachnoid hemorrhage, the
release of vasoactive substances from a pituitary adenoma
or hypothalamic damage (2). Four cases attributed to

vasospasm are listed in Table I. Bilateral cerebral arteries are
theoretically speculated to be involved in cases of vasospasm,
and angiography can verify the existence of vasospasm (3, 9).
Mechanical compression is caused by the extension of the
tumor mass. In patients with pituitary apoplexy, intrasellar
pressure will be markedly elevated to a mean value of 47
mmHg, high enough for the lesion to invade the cavernous
sinus and cause narrowing or occlusion of internal carotid
artery (21). What’s more, the bony structure surrounding
the cavernous sinus spares no compensatory space for the

Table II: Reported Cases of Cerebral Infarction Caused by Mechanical Compression of Major Vessels Secondary to Pituitary Apoplexy

Reference

Age/
Sex

Symptom

Vessels
Involved

Treatment

Outcome

Schnitker and Lehnert,
1952 (18)

65/M

Left hemiplegia,
reduced consciousness

Right MCA

Conservative
care

Death

Rosenbaum et al.,
1977 (17)

77/M

Left hemiparesis,
unconsciousness

Right ICA
(supraclinoid
portion)

Early craniotomy Death

Majchrzak et al.,
1983 (13)

29/M

Left hemiparesis,
unconsciousness

Right ACA

Delayed
craniotomy

Improvement

Bernstein et al.,
1984 (4)

48/M

Left hemiparesis,
Reduced consciousness

Bilateral ICA
(cavernous
portion)

Early TSA

Improvement

Clark et al.,
1987 (7)

40/M

Right hemiplegia, dysphagia,
right facial palsy

Left ICA
(supraclinoid
portion)

Conservative
care

Extensive
infarct

Lath and Rajshekhar,
2001 (11)

40/M

Left hemiplegia, reduced
consciousness, left facial palsy,
vision loss

Right ACA

Early TSA

Death

Rodier et al.,
2003 (16)

35/M

Left hemiplegia, frontal
syndrome with apathy,
unconsciousness

Bilateral ACA,
Right MCA

Decompression
surgery#

Improvement

Kurschel et al.,
2005 (10)

61/M

Unconsciousness

Bilateral ICA

Conservative
care

Death

Yang et al.,
2008 (20)

43/M

Left hemiplegia, visual
disturbances

Right
ICA(cavernous
portion)

Early TSA

Improvement

Lill et al.,
2009 (12)

59/M

Left hemiparesis,
unconsciousness, right cranial
III and IV nerves palsy

Bilateral ICA

Conservative
care

Death

Chokyu et al.,
2011 (6)

50/M

Right
Left hemiparesis, right cranial III
ICA(cavernous
nerve palsy
portion)

Delayed TSA

Improvement

42/M

Left hemiplegia,
unconsciousness, right cranial
III nerve palsy

Right ICA
(supraclinoid
portion)
Left ACA

Delayed TSA

Improvement

Present case, 2012

ICA: internal carotid artery, ACA: anterior cerebral artery, MCA: middle cerebral artery, TSA: transsphenoidal approach, #: the operation method was not
described.
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Zhang C. et al: Pituitary Apoplexy and Cerebral Infarction

compressed vessels, which further exacerbate compression
(20). Eleven cases due to mechanic compression are displayed
in Table II, one of which actually shares both mechanisms.
In the present case, MRI demonstrated intratumoral
hemorrhage intruding the cavernous sinus and MRA
revealed the result of invasion, narrowing of the supraclinoid
segment of the right internal carotid artery, which led to
the development of cerebral infarction causing hemiplegia.
Therefore, mechanical compression played the main role in
the right cerebral infarction. However, as to the infarction
of left anterior cerebral artery territory, little evidence
of compression was found in MRI or MRA images. We
speculated that it could be caused by transient vasospasm
that was relieved before performing MRA, leaving no signs of
vasospasm in the angiography.

edema was considered as the common cause of mortality in
early decompression surgery (20). As Clark et al. suggested,
the early removal of pituitary tumor increased the risk of
hemorrhagic transformation following recanalization of
the obstructed arteries, which might result in hemorrhagic
infarction (7). Therefore, delayed decompression following
conservative therapy with steroids can be a better choice.
Even though our patient developed severe conscious
disturbances, he became stable and even improved to some
extent after the initial conservative therapy. In account of
the risk of hemorrhage infarction, we decided to perform a
delayed surgical decompression through the transsphenoidal
route, which resulted in the immediate improvement of the
patient’s oculomotor palsy and delayed recovery of his motor
weakness.

Because of the rarity of cerebral infarction following pituitary
apoplexy, clinicians should pay much attention to the
differential diagnosis and early management. There is a high
risk of misdiagnosing these cases as a common ischemic
stroke that is often caused by thrombosis or embolism. The
recommended early management for this kind of ischemic
stroke includes antiplatelet therapy and sometimes even
thrombolysis therapy (1). However, if the ischemic stroke is
caused by hemorrhagic pituitary apoplexy, such treatment
will promote further hemorrhage into the damaged tissue
and the patient’s condition will deteriorate. To avoid such
tragedy, emergent cranial MRI is needed. Cranial MRI has a
better capability of identifying pituitary apoplexy than cranial
CT. In our case, the initial cranial CT did not show definite
hemorrhage or infarction in the pituitary. Only after the
performance of emergent cranial MRI were we able to confirm
the existence of pituitary apoplexy and find the relationship
between pituitary apoplexy and cerebral infarction. When
patients with a history or symptoms of pituitary adenoma
develop ischemic stroke, emergent cranial MRI should be
performed to rule out pituitary apoplexy, which has a great
impact on the formulation of the treatment plan.

In conclusion, pituitary apoplexy producing cerebral infarction
is rare. Mechanical compression and vasospasm are proposed
as two main mechanisms leading to this complication. Both
seem to have played a role in the present case. Emergent
cranial MRI is suggested in patients with pituitary adenoma
who present with signs of cerebral infarction. Delayed
decompression surgery through the transsphenoidal
approach following conservative management with steroids
is appropriate as our case demonstrates.

The primary goal of treatment is to reduce the intratumoral
pressure (20). Of the five who received conservative care in
the literature, four died or developed extensive infarction and
only one improved. Nine of the fourteen patients mentioned
above were operated upon, two via a transcranial approach,
six via a transsphenoidal approach and one via an undefined
decompression approach. Seven of these had good outcome
while two died. Compared to conservative management
alone, surgical decompression is more advisable when
patients develop severe visual or mental impairment or
deteriorate progressively with focal ischemic deficit. However,
the optimal timing for the surgical treatment is controversial
(6). Early decompression surgery is often advocated in
pituitary apoplexy, since it may reverse visual compromise
and restore ICA blood flow (8). Of the five who received
surgical decompression in the acute stage, two patients died,
while all the three delayed decompression cases had a good
outcome. The combined effect of the infarct and the brain

2. Ahmed SK, Semple PL: Cerebral ischaemia in pituitary
apoplexy. Acta Neurochir(Wien) 150(11): 1193-1196, 2008

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