The Neuroradiology Journal 21: 661-665, 2008
www. centauro. it
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction A Case Report A. BEN-NAKHI, T.J.E. MUTTIKKAL, V.N.K. CHAVAN, A. YT AL-TURKOMANI, R. GUPTA Department of Radiology, Mubarak Al Kabeer Hospital; Farwaniya, Kuwait
Key words: pituitary apoplexy, cerebral infarction, vasospasm
SUMMARY – Pituitary apoplexy is usually the result of hemorrhagic infarction in pituitary adenoma. The clinical presentation of pituitary apoplexy varies widely and includes asymptomatic hemorrhage, classical pituitary apoplexy and even sudden death. Few cases of cerebral infarction associated with pituitary apoplexy have been reported in the literature. Pituitary apoplexy can cause narrowing of intracranial vessels by mechanical obstruction due to mass effect or by vasospasm resulting in cerebral ischemia. We report a case of pituitary apoplexy associated with cerebral infarction and the putative mechanisms.
Introduction Pituitary apoplexy usually results from hemorrhagic infarction in pituitary adenoma. The clinical presentation varies from asymptomatic hemorrhage, classical pituitary apoplexy to even sudden death. Only few cases of cerebral infarction associated with pituitary apoplexy have been reported in the literature. We report a case of pituitary apoplexy associated with cerebral infarction, and the pathogenesis based on the available literature. Case Report A 40-year-old man was brought to the emergency department with acute confusion. The patient had palpitation, followed by transient loss of consciousness. Subsequently he had an acute confusional state and transient rightsided hemiparesis. His medical history was unremarkable at the time of admission. Clinical examination revealed receptive dysphasia, with normal motor and sensory system including the plantar reflexes. CT scan (figure 1) on the day of admission showed acute infarct in the left parieto-occipital region extending to the external capsule and the claustrum. The
patient was treated as a case of cerebral infarction. Immunology screen, coagulation profile, lipid profile, hematological values, serum electrolytes and routine biochemical evaluation were normal. Doppler study of the carotids and the vertebral artery were normal. Apart from hypertension, the cardiovascular system work up including Holter monitoring was normal. MRI of brain done on the sixth day after admission showed left parieto-occipital infarction (figure 2A,B) and pituitary hemorrhage (figure 3). Dedicated study was done for the pituitary in the following week, showing adenoma encasing the left internal carotid artery and hemorrhage (figure 4A,B). The hormonal assay showed elevated prolactin level (4237 mIU/l) and very low cortisol level (13.59 nmol/l). The remaining evaluated hormonal levels were normal. On specific enquiry, the patient recalled past episodes of galactorrhoea. He did not have any history of loss of libido or erectile dysfunction. Low dose short synacthen test was positive with elevation of cortisol to normal levels confirming ACTH deficiency from the pituitary. Supplement steroid was given, in addition to bromocriptine which was given for suppression of hyperprolactinemia. The patient had significant improvement, but had residual dysphasia and was discharged for outpatient follow-up. 661
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction
A. Ben-Nakhi
Figure 1 CT scan on the day of admission showing acute infarct in the left parieto-occipital region extending to the external capsule and claustrum.
A
B
Figure 2 A) FLAIR image showing infarct in the left parieto-occipital region extending to the external capsule and claustrum. B) Diffusion weighted image showing infarct in the left parieto-occipital region extending to the external capsule and claustrum.
Discussion Pituitary apoplexy usually occurs with hemorrhagic infarction in pituitary adenoma 1. Pituitary apoplexy has been reported in previously 662
normal gland 2-5 and in pituitary gland with a non-neoplastic lesion 6. Pituitary apoplexy can occur due to severe intra-partum or post-partum shock 4,7. The clinical presentation of pituitary apoplexy may vary from asymptomatic
www. centauro. it
The Neuroradiology Journal 21: 661-665, 2008
Figure 3 Sagittal T1 weighted image showing pituitary hemorrhage.
A
B
Figure 4 A) Coronal T1-weighted image showing hyperintense pituitary hemorrhage and isointense adenoma encasing the left internal carotid artery. B) Coronal T1-weighted post contrast image showing enhancement of adenoma encasing the internal carotid artery.
hemorrhage 8, classical pituitary apoplexy characterized by sudden onset of headache, signs of meningeal irritation, visual impairment and altered level of consciousness 9 and even sudden death (8). However the pituitary apoplexy
following severe shock at or near the time of delivery, known as Sheehan syndrome usually presents with inability to lactate after delivery due to prolactin deficiency and amenorrhea due to gonadotrophin deficiency 7. In a large 663
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction
surgical series the incidence of asymptomatic hemorrhage within the pituitary adenoma was found to be 45.16 % 8. The exact mechanisms of pituitary apoplexy and its subsequent presentation remain unknown. In most instances pituitary apoplexy occurs spontaneously. The predisposing factors include diabetic ketoacidosis, postpartum hemorrhage, anticoagulant therapy, trauma, radiation therapy, bromocriptine administration and endocrine stimulation tests 10-13. An extensive literature search yielded 19 cases of cerebral infarction associated with pituitary apoplexy 2,9,12-28. Pituitary apoplexy can cause narrowing of the intracranial vessels by either mechanical obstruction due to mass effect or by vasospasm resulting in cerebral infarction. Ten cases of pituitary apoplexy resulting in direct compression of intracranial vessels causing cerebral infarction have been reported in the literature 13-22. In most of these cases the internal carotid artery was occluded by the mass effect resulting from apoplexy. In one case, the middle cerebral artery 18 and in another the anterior cerebral artery 19 was compressed. Vasospasm was the cause of infarct in six cases 9,12,23-26. Vasospasm was attributed to subarachnoid hemorrhage 12,24,25 and to the release of vasoactive agents from the pituitary tumour 9,23,24,29. Vasospasm and ischemia can occur on the same day after the pituitary apoplexy 23,24. In one of the case reports, the infarction was due to a combination of vascular obstruction due to mass effect and hypotension 27. The infarction was not immediate and occurred only after the patient developed severe arterial hypotension as a result of pituitary apoplexy. The infarction was due to the combined effect of hypotension and the internal carotid artery stenosis due to compression by the sellar mass on the carotid siphon along with ipsilateral atheromatous narrowing of the cervical portion of the internal carotid artery 27. Mukherjee et Al 28 reported a patient who had cerebral infarction and pituitary apoplexy, and hypothesized that ischemia due to internal carotid artery stenosis was the primary event which led to infarction in the pituitary macroadenoma. Muttikkal et Al reported a case of pituitary apoplexy along with cortical and deep grey matter infarcts due to global hypoxia. The apoplexy had occurred in a gland without any evidence
664
A. Ben-Nakhi
of pre-existing lesions, thus demonstrating the vulnerability of the normal pituitary gland for apoplexy in the event of global hypoxia 2. In our case, there was no evidence of fixed stenosis of the internal carotid or the major branches. The left internal carotid artery was encased by the pituitary adenoma. There was no imaging evidence of subarachnoid hemorrhage. The MRA which was done five days after the insult did not show any evidence of narrowing of the left internal carotid artery or middle cerebral artery. The inciting event in our case was the syncopy which occured after palpitation. The sudden hypotension thus ensued appears to have triggered the pituitary apoplexy. The occurrence of left middle cerebral artery territory infarct appears to be due to the combination of hypotension at the time of syncope along with the spasm of the artery which was encased by the adenoma, due to the release of vasoactive substances from the pituitary. Vasospasm and ischemia have been reported on the same day after the pituitary apoplexy 23,24. The infarction also affected the posterior watershed zone on the left suggesting significant hypotension at the time of insult. The sparing of left anterior cerebral artery territory was probably due to the support from the right anterior cerebral artery through the anterior communicating artery. Most authors have advocated early surgery for pituitary apoplexy, although even with early decompression the mortality may be high. Surgical decompression may or may not restore flow in the occluded vessel 17. Clark et Al 15 cautioned that decompression of the vessel might in fact be harmful in the presence of an established infarct on CT scan, by converting it into hemorrhagic infarct. Conservative management has been advocated for patients with isolated cranial nerve palsies but remains controversial 1. Considering the high incidence of asymptomatic hemorrhage in pituitary adenoma 8, the cases incidentally detected by MRI may be managed conservatively. In conclusion, cerebral infarction caused by occlusion of the internal carotid artery or arteries in the circle of Willis due to pituitary apoplexy is a rare event. Early surgical decompression offers overall better prognosis, however less severe cases may be managed conservatively as in our case.
www. centauro. it
The Neuroradiology Journal 21: 661-665, 2008
References 1 Semple PL, Webb MK, de Villiers JC et Al: Pituitary apoplexy. Neurosurgery 56: 65-72, 2005. 2 Eluvathingal Muttikkal TJ, Vattoth S, Keluth Chavan VN et Al: Perirolandic Sparing and Pituitary Apoplexy in Adult Brain with Global Hypoxia. The Neuroradiology Journal 20: 505-509, 2007. 3 Suh DC, Park JS, Park SK et Al: Pituitary hemorrhage as a complication of hantaviral disease. Am Journal Neuroradiol 16: 175-178, 1995. 4 Lavellee J, Morcos R, Palardy J et Al: MR of nonhemorrhagic postpartum pituitary apoplexy. Am Journal Neuroradiol 16: 1939-1941, 1995. 5 Reid RL, Quigley ME, Yen SS: Pituitary apoplexy. A review. Arch Neurol 42: 712-719, 1985. 6 Onesti ST, Wisniewski T, Post KD: Pituitary hemorrhage into a Rathke’s cleft cyst. Neurosurgery 27: 644646, 1990. 7 Vaphiades MS: Pituitary Apoplexy. http://www.emedicine.com/OPH/topic471.htm. Article Last Updated: 2007. 8 Wakai S, Fukushima T, Teramoto A et Al: Pituitary apoplexy: its incidence and clinical significance. J Neurosurg 55: 187-193, 1981. 9 Jeon BC, Park YS, Oh HS et Al: Pituitary apoplexy complicated by chemical meningitis and cerebral infarction. J Korean Med Sci 22: 1085-1089, 2007. 10 Thomas N, Simon R, Chacko G et Al: Regression of acromegaly following pituitary apoplexy. Neurol India 47: 161, 1999. 11 Matsuura I, Saeki N, Kubota M et Al: Infarction followed by hemorrhage in pituitary adenoma due to endocrine stimulation test. Endocr J. 48: 493-498, 2001. 12 Sanno N, Ishii Y, Sugiyama M et Al: Subarachnoid haemorrhage and vasospasm due to pituitary apoplexy after pituitary function test. Acta Neurochir 141: 10091010, 1999. 13 Bernstein M, Hegele RA, Gentili F et Al: Pituitary apoplexy associated with a triple bolus test. J Neurosurg 61: 586-590, 1984. 14 Sakalas R, David RB, Vines FS et Al: Pituitary apoplexy in a child. J Neurosurg 39: 519-522, 1973. 15 Clark JD, Freer CE, Wheatley T: Pituitary apoplexy: an unusual cause of stroke. Clin Radiol 38: 75-77, 1987. 16 Rosenbaum TJ, Houser OW, Laws ER: Pituitary apoplexy producing internal carotid artery occlusion. Case report. J Neurosurg 47: 599-604, 1977. 17 Lath R, Rajshekhar V: Massive cerebral infarction as a feature of pituitary apoplexy. Neurol India 49: 191-193, 2001. 18 Schnitker MT, Lehnert HB: Apoplexy in a pituitary chromophobe adenoma producing the syndrome of middle cerebral artery thrombosis. J Neurosurg 9: 210-213, 1952. 19 Majchrzak H, Wencel T, Dragan T et Al: Acute haemorrhage into pituitary adenoma with subarachnoid haemorrhage and anterior cerebral artery occlusion. J Neurosurg 58: 771-773, 1983. 20 Rodier G, Mootien Y, Battaglia F et Al: Bilateral stroke secondary to pituitary apoplexy. J Neurol 250: 494-495, 2003. 21 Dogan S, Kocaeli H, Abas F et Al: Pituitary apoplexy as a cause of internal carotid artery occlusion. J Clin Neurosci. 15: 480-483, 2008. 22 López N, Garcia A, Molto J et Al: Massive cerebral infarction secondary to apoplexy due to pituitary adenoma. Neurologia 2008 (Epub ahead of print).
23 Pozzati E, Frank G, Nasi MT et Al: Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. Neurosurgery 20: 56-59, 1987. 24 Akutsu H, Noguchi S, Tsunoda T et Al: Cerebral infarction following pituitary apoplexy. Neurol Med Chir 44: 479-483, 2004. 25 Bhansali A, Dutta P, Khandelwal N et Al: Pituitary apoplexy: an unusual cause of frontal lobe syndrome. Australas Radiol 49: 127-31, 2005. 26 Catenoix H, Nighoghossian N, Honnorat J et Al: Necrosis of a hypophyseal adenoma and ischemic cerebral vascular accident Rev Neurol 158: 734-736, 2002. 27 Lomban E, Bonneville F, Karachi C et Al: Massive stroke in a patient with pituitary apoplexy, cervical carotid artery stenosis and hypotension. Journal of Neuroradiology Source 33: 259-262, 2006. 28 Mukherjee S, Majumder A, Dattamunshi AK et Al: Ischaemic stroke leading to left hemiparesis and autohypophysectomy in a case of pituitary macroadenoma. J Assoc Physicians India 43: 801-802, 1995. 29 Nishi T, Oto T, Takeshima H et Al: Tissue factor expressed in pituitary adenomas cells contributes to the development of vascular events in pituitary adenomas. Cancer 86: 1354-1361, 1999.
Dr Abdelmohsen Ben-Nakhi Department of Radiology Mubarak Al Kabeer Hospital 1766 Farwaniya Kuwait 81028 Kuwait E-mail: [email protected]
665
www. centauro. it
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction A Case Report A. BEN-NAKHI, T.J.E. MUTTIKKAL, V.N.K. CHAVAN, A. YT AL-TURKOMANI, R. GUPTA Department of Radiology, Mubarak Al Kabeer Hospital; Farwaniya, Kuwait
Key words: pituitary apoplexy, cerebral infarction, vasospasm
SUMMARY – Pituitary apoplexy is usually the result of hemorrhagic infarction in pituitary adenoma. The clinical presentation of pituitary apoplexy varies widely and includes asymptomatic hemorrhage, classical pituitary apoplexy and even sudden death. Few cases of cerebral infarction associated with pituitary apoplexy have been reported in the literature. Pituitary apoplexy can cause narrowing of intracranial vessels by mechanical obstruction due to mass effect or by vasospasm resulting in cerebral ischemia. We report a case of pituitary apoplexy associated with cerebral infarction and the putative mechanisms.
Introduction Pituitary apoplexy usually results from hemorrhagic infarction in pituitary adenoma. The clinical presentation varies from asymptomatic hemorrhage, classical pituitary apoplexy to even sudden death. Only few cases of cerebral infarction associated with pituitary apoplexy have been reported in the literature. We report a case of pituitary apoplexy associated with cerebral infarction, and the pathogenesis based on the available literature. Case Report A 40-year-old man was brought to the emergency department with acute confusion. The patient had palpitation, followed by transient loss of consciousness. Subsequently he had an acute confusional state and transient rightsided hemiparesis. His medical history was unremarkable at the time of admission. Clinical examination revealed receptive dysphasia, with normal motor and sensory system including the plantar reflexes. CT scan (figure 1) on the day of admission showed acute infarct in the left parieto-occipital region extending to the external capsule and the claustrum. The
patient was treated as a case of cerebral infarction. Immunology screen, coagulation profile, lipid profile, hematological values, serum electrolytes and routine biochemical evaluation were normal. Doppler study of the carotids and the vertebral artery were normal. Apart from hypertension, the cardiovascular system work up including Holter monitoring was normal. MRI of brain done on the sixth day after admission showed left parieto-occipital infarction (figure 2A,B) and pituitary hemorrhage (figure 3). Dedicated study was done for the pituitary in the following week, showing adenoma encasing the left internal carotid artery and hemorrhage (figure 4A,B). The hormonal assay showed elevated prolactin level (4237 mIU/l) and very low cortisol level (13.59 nmol/l). The remaining evaluated hormonal levels were normal. On specific enquiry, the patient recalled past episodes of galactorrhoea. He did not have any history of loss of libido or erectile dysfunction. Low dose short synacthen test was positive with elevation of cortisol to normal levels confirming ACTH deficiency from the pituitary. Supplement steroid was given, in addition to bromocriptine which was given for suppression of hyperprolactinemia. The patient had significant improvement, but had residual dysphasia and was discharged for outpatient follow-up. 661
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction
A. Ben-Nakhi
Figure 1 CT scan on the day of admission showing acute infarct in the left parieto-occipital region extending to the external capsule and claustrum.
A
B
Figure 2 A) FLAIR image showing infarct in the left parieto-occipital region extending to the external capsule and claustrum. B) Diffusion weighted image showing infarct in the left parieto-occipital region extending to the external capsule and claustrum.
Discussion Pituitary apoplexy usually occurs with hemorrhagic infarction in pituitary adenoma 1. Pituitary apoplexy has been reported in previously 662
normal gland 2-5 and in pituitary gland with a non-neoplastic lesion 6. Pituitary apoplexy can occur due to severe intra-partum or post-partum shock 4,7. The clinical presentation of pituitary apoplexy may vary from asymptomatic
www. centauro. it
The Neuroradiology Journal 21: 661-665, 2008
Figure 3 Sagittal T1 weighted image showing pituitary hemorrhage.
A
B
Figure 4 A) Coronal T1-weighted image showing hyperintense pituitary hemorrhage and isointense adenoma encasing the left internal carotid artery. B) Coronal T1-weighted post contrast image showing enhancement of adenoma encasing the internal carotid artery.
hemorrhage 8, classical pituitary apoplexy characterized by sudden onset of headache, signs of meningeal irritation, visual impairment and altered level of consciousness 9 and even sudden death (8). However the pituitary apoplexy
following severe shock at or near the time of delivery, known as Sheehan syndrome usually presents with inability to lactate after delivery due to prolactin deficiency and amenorrhea due to gonadotrophin deficiency 7. In a large 663
Pituitary Apoplexy: a Rare Cause of Cerebral Infarction
surgical series the incidence of asymptomatic hemorrhage within the pituitary adenoma was found to be 45.16 % 8. The exact mechanisms of pituitary apoplexy and its subsequent presentation remain unknown. In most instances pituitary apoplexy occurs spontaneously. The predisposing factors include diabetic ketoacidosis, postpartum hemorrhage, anticoagulant therapy, trauma, radiation therapy, bromocriptine administration and endocrine stimulation tests 10-13. An extensive literature search yielded 19 cases of cerebral infarction associated with pituitary apoplexy 2,9,12-28. Pituitary apoplexy can cause narrowing of the intracranial vessels by either mechanical obstruction due to mass effect or by vasospasm resulting in cerebral infarction. Ten cases of pituitary apoplexy resulting in direct compression of intracranial vessels causing cerebral infarction have been reported in the literature 13-22. In most of these cases the internal carotid artery was occluded by the mass effect resulting from apoplexy. In one case, the middle cerebral artery 18 and in another the anterior cerebral artery 19 was compressed. Vasospasm was the cause of infarct in six cases 9,12,23-26. Vasospasm was attributed to subarachnoid hemorrhage 12,24,25 and to the release of vasoactive agents from the pituitary tumour 9,23,24,29. Vasospasm and ischemia can occur on the same day after the pituitary apoplexy 23,24. In one of the case reports, the infarction was due to a combination of vascular obstruction due to mass effect and hypotension 27. The infarction was not immediate and occurred only after the patient developed severe arterial hypotension as a result of pituitary apoplexy. The infarction was due to the combined effect of hypotension and the internal carotid artery stenosis due to compression by the sellar mass on the carotid siphon along with ipsilateral atheromatous narrowing of the cervical portion of the internal carotid artery 27. Mukherjee et Al 28 reported a patient who had cerebral infarction and pituitary apoplexy, and hypothesized that ischemia due to internal carotid artery stenosis was the primary event which led to infarction in the pituitary macroadenoma. Muttikkal et Al reported a case of pituitary apoplexy along with cortical and deep grey matter infarcts due to global hypoxia. The apoplexy had occurred in a gland without any evidence
664
A. Ben-Nakhi
of pre-existing lesions, thus demonstrating the vulnerability of the normal pituitary gland for apoplexy in the event of global hypoxia 2. In our case, there was no evidence of fixed stenosis of the internal carotid or the major branches. The left internal carotid artery was encased by the pituitary adenoma. There was no imaging evidence of subarachnoid hemorrhage. The MRA which was done five days after the insult did not show any evidence of narrowing of the left internal carotid artery or middle cerebral artery. The inciting event in our case was the syncopy which occured after palpitation. The sudden hypotension thus ensued appears to have triggered the pituitary apoplexy. The occurrence of left middle cerebral artery territory infarct appears to be due to the combination of hypotension at the time of syncope along with the spasm of the artery which was encased by the adenoma, due to the release of vasoactive substances from the pituitary. Vasospasm and ischemia have been reported on the same day after the pituitary apoplexy 23,24. The infarction also affected the posterior watershed zone on the left suggesting significant hypotension at the time of insult. The sparing of left anterior cerebral artery territory was probably due to the support from the right anterior cerebral artery through the anterior communicating artery. Most authors have advocated early surgery for pituitary apoplexy, although even with early decompression the mortality may be high. Surgical decompression may or may not restore flow in the occluded vessel 17. Clark et Al 15 cautioned that decompression of the vessel might in fact be harmful in the presence of an established infarct on CT scan, by converting it into hemorrhagic infarct. Conservative management has been advocated for patients with isolated cranial nerve palsies but remains controversial 1. Considering the high incidence of asymptomatic hemorrhage in pituitary adenoma 8, the cases incidentally detected by MRI may be managed conservatively. In conclusion, cerebral infarction caused by occlusion of the internal carotid artery or arteries in the circle of Willis due to pituitary apoplexy is a rare event. Early surgical decompression offers overall better prognosis, however less severe cases may be managed conservatively as in our case.
www. centauro. it
The Neuroradiology Journal 21: 661-665, 2008
References 1 Semple PL, Webb MK, de Villiers JC et Al: Pituitary apoplexy. Neurosurgery 56: 65-72, 2005. 2 Eluvathingal Muttikkal TJ, Vattoth S, Keluth Chavan VN et Al: Perirolandic Sparing and Pituitary Apoplexy in Adult Brain with Global Hypoxia. The Neuroradiology Journal 20: 505-509, 2007. 3 Suh DC, Park JS, Park SK et Al: Pituitary hemorrhage as a complication of hantaviral disease. Am Journal Neuroradiol 16: 175-178, 1995. 4 Lavellee J, Morcos R, Palardy J et Al: MR of nonhemorrhagic postpartum pituitary apoplexy. Am Journal Neuroradiol 16: 1939-1941, 1995. 5 Reid RL, Quigley ME, Yen SS: Pituitary apoplexy. A review. Arch Neurol 42: 712-719, 1985. 6 Onesti ST, Wisniewski T, Post KD: Pituitary hemorrhage into a Rathke’s cleft cyst. Neurosurgery 27: 644646, 1990. 7 Vaphiades MS: Pituitary Apoplexy. http://www.emedicine.com/OPH/topic471.htm. Article Last Updated: 2007. 8 Wakai S, Fukushima T, Teramoto A et Al: Pituitary apoplexy: its incidence and clinical significance. J Neurosurg 55: 187-193, 1981. 9 Jeon BC, Park YS, Oh HS et Al: Pituitary apoplexy complicated by chemical meningitis and cerebral infarction. J Korean Med Sci 22: 1085-1089, 2007. 10 Thomas N, Simon R, Chacko G et Al: Regression of acromegaly following pituitary apoplexy. Neurol India 47: 161, 1999. 11 Matsuura I, Saeki N, Kubota M et Al: Infarction followed by hemorrhage in pituitary adenoma due to endocrine stimulation test. Endocr J. 48: 493-498, 2001. 12 Sanno N, Ishii Y, Sugiyama M et Al: Subarachnoid haemorrhage and vasospasm due to pituitary apoplexy after pituitary function test. Acta Neurochir 141: 10091010, 1999. 13 Bernstein M, Hegele RA, Gentili F et Al: Pituitary apoplexy associated with a triple bolus test. J Neurosurg 61: 586-590, 1984. 14 Sakalas R, David RB, Vines FS et Al: Pituitary apoplexy in a child. J Neurosurg 39: 519-522, 1973. 15 Clark JD, Freer CE, Wheatley T: Pituitary apoplexy: an unusual cause of stroke. Clin Radiol 38: 75-77, 1987. 16 Rosenbaum TJ, Houser OW, Laws ER: Pituitary apoplexy producing internal carotid artery occlusion. Case report. J Neurosurg 47: 599-604, 1977. 17 Lath R, Rajshekhar V: Massive cerebral infarction as a feature of pituitary apoplexy. Neurol India 49: 191-193, 2001. 18 Schnitker MT, Lehnert HB: Apoplexy in a pituitary chromophobe adenoma producing the syndrome of middle cerebral artery thrombosis. J Neurosurg 9: 210-213, 1952. 19 Majchrzak H, Wencel T, Dragan T et Al: Acute haemorrhage into pituitary adenoma with subarachnoid haemorrhage and anterior cerebral artery occlusion. J Neurosurg 58: 771-773, 1983. 20 Rodier G, Mootien Y, Battaglia F et Al: Bilateral stroke secondary to pituitary apoplexy. J Neurol 250: 494-495, 2003. 21 Dogan S, Kocaeli H, Abas F et Al: Pituitary apoplexy as a cause of internal carotid artery occlusion. J Clin Neurosci. 15: 480-483, 2008. 22 López N, Garcia A, Molto J et Al: Massive cerebral infarction secondary to apoplexy due to pituitary adenoma. Neurologia 2008 (Epub ahead of print).
23 Pozzati E, Frank G, Nasi MT et Al: Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. Neurosurgery 20: 56-59, 1987. 24 Akutsu H, Noguchi S, Tsunoda T et Al: Cerebral infarction following pituitary apoplexy. Neurol Med Chir 44: 479-483, 2004. 25 Bhansali A, Dutta P, Khandelwal N et Al: Pituitary apoplexy: an unusual cause of frontal lobe syndrome. Australas Radiol 49: 127-31, 2005. 26 Catenoix H, Nighoghossian N, Honnorat J et Al: Necrosis of a hypophyseal adenoma and ischemic cerebral vascular accident Rev Neurol 158: 734-736, 2002. 27 Lomban E, Bonneville F, Karachi C et Al: Massive stroke in a patient with pituitary apoplexy, cervical carotid artery stenosis and hypotension. Journal of Neuroradiology Source 33: 259-262, 2006. 28 Mukherjee S, Majumder A, Dattamunshi AK et Al: Ischaemic stroke leading to left hemiparesis and autohypophysectomy in a case of pituitary macroadenoma. J Assoc Physicians India 43: 801-802, 1995. 29 Nishi T, Oto T, Takeshima H et Al: Tissue factor expressed in pituitary adenomas cells contributes to the development of vascular events in pituitary adenomas. Cancer 86: 1354-1361, 1999.
Dr Abdelmohsen Ben-Nakhi Department of Radiology Mubarak Al Kabeer Hospital 1766 Farwaniya Kuwait 81028 Kuwait E-mail: [email protected]
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