Pituitary apoplexy presenting as aseptic meningitis without visual loss or ophthalmoplegia D. C. Reutens Neurology Registrar, Royal Perth Hospital, WA.
R. H. Edis Neurologist, Royal Perth Hospital, WA.
Abstract: Clinical and spinal fluid evidence of aseptic meningitis were the sole features at presentation in a patient with pituitary apoplexy. Visual impairment and bitemporal field defects developed later. Necrosis within a chromophobe adenoma was found at surgical decompression of the sella. (Aust NZ J Med 1990; 20: 590-59 1.) Key words: Meningitis, pituitary tumour, trans-sphenoidal surgery.
Pituitary apoplexy results from haemorrhage or infarction in a pituitary tumour and usually presents with acute headache, ophthalmoplegia, and visual disturbance.' Clinical and spinal fluid evidence of aseptic meningitis may occur, though not usually in isolation.' W e report a case of pituitary apoplexy presenting as aseptic meningitis without evidence of cranial nerve compression, alteration of conscious state or evidence of pituitary disease at presentation.
CASE REPORT In November 1988, a 39-year-old man with a two-week history of sore throat and rhinorrhea awoke with a severe bifrontal headache associated with vomiting, photophobia, chills and sweats. There had been no visual blurring, field disturbance or diplopia. He had not experienced symptoms of pituitary dysfunction in the past. Examination revealed an alert man whose temperature was 37.5 "C. Cardiovascular, respiratory and abdominal examination were normal. Signs of pituitary dysfunction, including testicular atrophy were absent and androgenisation was normal. Neck stiffness was noted but Kernig's sign was negative. Findings on neurological examination, in particular visual acuity, fields and ocular movements, were normal. Initial cerebrospinal fluid (CSF) examination revealed slightly turbid fluid at elevated pressure (240 mm), with elevated protein (0.72 g/l) and normal glucose concentrations. The CSF leucocyte count was 1,2OO/ul(86% polymorphs and 14% mononuclear cells). The CSF was sterile. Four days later, the headache became more severe and was associated with fever, visual blurring and deterioration of visual acuity to N 18 bilaterally, bitemporal field defects, vertical diplopia on downgaze and sensory loss over the left forehead and cheek. Enlargement of the pituitary fossa was seen on skull X-ray and a cranial CT Scan showed a ring enhancing pituitary mass containing
areas of hyperdensity (Figure 1). Apart from a decreased thyrotropin level (0.3 mull), there was no biochemical evidence of endocrine disease. Serum prolactin was not elevated. Persistence of the neurological deficit despite dexamethasone therapy led to trans-sphenoidal decompression of the sella ten days after presentation. Histological examination revealed some cells characteristic of a chromophobe adenoma with larger areas of haemorrhagic and necrotic tissue in which cellular details were obscured. Only a scanty leucocyte infiltrate was present and bacteria were not seen. One month later, the patient was neurologically normal and was taking thyroxine and cortisone at replacement doses.
DISCUSSION T h e clinical manifestations of pituitary apoplexy are highly variable and reflect tumour expansion, endocrinopathy and extrasellar leakage of blood or necrotic materiaL3 While meningism, sometimes a prominent feature at presentation, raises the possibility of aneurysmal subarachnoid haemorrhage or viral or bacterial meningitis, the physician may be alerted to the diagnosis b y neurological manifestations including severe retroorbital or periorbital headache, impaired conscious state, decreased visual acuity, visual field defects, ophthalmoplegia and trigeminal nerve dysfunction. Our case is unusual because aseptic meningitis was the sole presenting feature of pituitary apoplexy. It emphasises that infarction of a pituitary tumour may produce only mild or non specific symptoms. Wakai et aL4 noted that 45% of patients with haemorrhage in surgically verified pituitary adenomas had been asymptomatic and 14% had experienced minor symptoms such as headache, nausea, vomiting and ~
Correrpondence to: Dr D. C. Reutens, Neurology Department, Royal Perth Hospital, Box X2213, GPO, Perth, WA 6001, Australia.
590
Aust NZ J Med 1990; 20
REUTENS AND EDIS
to averting acute adrenal insufficiency, treatment with corticosteroids may improve visual function strikingly.' While a conservative approach may be successful, even in the presence of ophthalmoplegia," surgical decompression of the sella is indicated if impairment of vision or conscious state persists or progresses.',J This case emphasises that asep:ic meningitis may be the initial presentation of pituitary apoplexy. Early diagnosis, supportive therapy and sometimes neurosurgical decompression may be vital in preserving vision and sometimes even life. Acccptcd for publication: I7 November 1989
Acknowledgements T h e figures were prepared by the Department of Medical Illust ]-ationg, Royal Perth Hospital.
References
Figure 1: Cranial C T scan showing a ring enhancing pituitary mass.
vertigo. Clinically silent infarction may only be recognised when spontaneous resolution of pituitary hypersecretion occurs.' As in our case, expansion of the pituitary fossa on a skull X-ray suggests the correct diagnosis in the majority with pituitary apoplexy." However, causes of pituitary apoplexy with typical clinical features and normal skull X-rays have been reported.' In confirming and sometimes making the diagnosis, cranial C T scanning is essential. An abscess arising in a pituitary adenoma may also present with aseptic meningitis and resemble pituitary apoplexy in its radiological appearance.' In the present case, pituitary abscess was excluded on histological grounds. Beyond the initiation of appropriate hormone replacement and close monitoring of fluid and electrolyte balance, the optimum management of pituitary apoplexy is disputed. Dexaniethasone was used in our case because, in addition
ASEPTIC MENINGITIS IN PITUITARY APOPLEXY
1. Reid RI., Quigle) ME, Yen SSC. Pituitary apoplexy: a revicw. ilrch Ncurol 1985; 42: 712-9. 2. Bjerre P, 1,indholm J. Pituitary apoplexy with sterile meningitis. Acta Xeurol Scand 1986; 74: 304-7. 3. (hrdoro ER, Pcterson EW. Pituitary apoplexy: a review. Neurosurgery 1984; 14: 363-73. 1. Wakai S, Fukushima T, Teramoto A, Sario K. Pituitary apoplrxy: its incidence and clinical signifrcancc. J Neurosurg 1981; 55: 187-93. 5. Findling JW, Tyrrell JB, Aron DC, Fitzgerald PA, Wilson CB, Forshani PH. Silent pituirary apoplexy: subclinical infarction of an adrenocorticorrophin-producingpituitary adenoma. J Clin Endocriiiol Metabol 1981; 52: 95-7. 6. Fitz-Pdtrick D, Tolis G, iMcGarry EE, Taylor S. Pituitary d p n p k x y : the importance of skull roentgenograms and computtlrised tomography in diagnosis. JAM.4 1980; 214: 59-61. 7. Jeffcoate WJ,Birch C R . Apoplexy in small pituitary tumors. J Neurol Neurosurg Psychiatry 1986; 49: 1077-8. 8. Ford J, Torres LF, Cox T, Hayward R. Recurrent sterile ~iieiiiiigitiscaused by pituitary abscess. Postgrad Med J 1986; 62: 929-31. 9. Senelick RC, Van Dyk HJL. Chromophubt. adenoma masquerading as corticosteroid responsive optic neuritis. Am J Ophthalmol 1974) 78: 485-8. I0 Pelkonen R , Kuusisto A, Salmi J er a/. Pituitary function after pituitary dpoplexy. Am J Med 1978; 65: 773-8.
Aust NZ J Mcd 1990; 20
59 1
R. H. Edis Neurologist, Royal Perth Hospital, WA.
Abstract: Clinical and spinal fluid evidence of aseptic meningitis were the sole features at presentation in a patient with pituitary apoplexy. Visual impairment and bitemporal field defects developed later. Necrosis within a chromophobe adenoma was found at surgical decompression of the sella. (Aust NZ J Med 1990; 20: 590-59 1.) Key words: Meningitis, pituitary tumour, trans-sphenoidal surgery.
Pituitary apoplexy results from haemorrhage or infarction in a pituitary tumour and usually presents with acute headache, ophthalmoplegia, and visual disturbance.' Clinical and spinal fluid evidence of aseptic meningitis may occur, though not usually in isolation.' W e report a case of pituitary apoplexy presenting as aseptic meningitis without evidence of cranial nerve compression, alteration of conscious state or evidence of pituitary disease at presentation.
CASE REPORT In November 1988, a 39-year-old man with a two-week history of sore throat and rhinorrhea awoke with a severe bifrontal headache associated with vomiting, photophobia, chills and sweats. There had been no visual blurring, field disturbance or diplopia. He had not experienced symptoms of pituitary dysfunction in the past. Examination revealed an alert man whose temperature was 37.5 "C. Cardiovascular, respiratory and abdominal examination were normal. Signs of pituitary dysfunction, including testicular atrophy were absent and androgenisation was normal. Neck stiffness was noted but Kernig's sign was negative. Findings on neurological examination, in particular visual acuity, fields and ocular movements, were normal. Initial cerebrospinal fluid (CSF) examination revealed slightly turbid fluid at elevated pressure (240 mm), with elevated protein (0.72 g/l) and normal glucose concentrations. The CSF leucocyte count was 1,2OO/ul(86% polymorphs and 14% mononuclear cells). The CSF was sterile. Four days later, the headache became more severe and was associated with fever, visual blurring and deterioration of visual acuity to N 18 bilaterally, bitemporal field defects, vertical diplopia on downgaze and sensory loss over the left forehead and cheek. Enlargement of the pituitary fossa was seen on skull X-ray and a cranial CT Scan showed a ring enhancing pituitary mass containing
areas of hyperdensity (Figure 1). Apart from a decreased thyrotropin level (0.3 mull), there was no biochemical evidence of endocrine disease. Serum prolactin was not elevated. Persistence of the neurological deficit despite dexamethasone therapy led to trans-sphenoidal decompression of the sella ten days after presentation. Histological examination revealed some cells characteristic of a chromophobe adenoma with larger areas of haemorrhagic and necrotic tissue in which cellular details were obscured. Only a scanty leucocyte infiltrate was present and bacteria were not seen. One month later, the patient was neurologically normal and was taking thyroxine and cortisone at replacement doses.
DISCUSSION T h e clinical manifestations of pituitary apoplexy are highly variable and reflect tumour expansion, endocrinopathy and extrasellar leakage of blood or necrotic materiaL3 While meningism, sometimes a prominent feature at presentation, raises the possibility of aneurysmal subarachnoid haemorrhage or viral or bacterial meningitis, the physician may be alerted to the diagnosis b y neurological manifestations including severe retroorbital or periorbital headache, impaired conscious state, decreased visual acuity, visual field defects, ophthalmoplegia and trigeminal nerve dysfunction. Our case is unusual because aseptic meningitis was the sole presenting feature of pituitary apoplexy. It emphasises that infarction of a pituitary tumour may produce only mild or non specific symptoms. Wakai et aL4 noted that 45% of patients with haemorrhage in surgically verified pituitary adenomas had been asymptomatic and 14% had experienced minor symptoms such as headache, nausea, vomiting and ~
Correrpondence to: Dr D. C. Reutens, Neurology Department, Royal Perth Hospital, Box X2213, GPO, Perth, WA 6001, Australia.
590
Aust NZ J Med 1990; 20
REUTENS AND EDIS
to averting acute adrenal insufficiency, treatment with corticosteroids may improve visual function strikingly.' While a conservative approach may be successful, even in the presence of ophthalmoplegia," surgical decompression of the sella is indicated if impairment of vision or conscious state persists or progresses.',J This case emphasises that asep:ic meningitis may be the initial presentation of pituitary apoplexy. Early diagnosis, supportive therapy and sometimes neurosurgical decompression may be vital in preserving vision and sometimes even life. Acccptcd for publication: I7 November 1989
Acknowledgements T h e figures were prepared by the Department of Medical Illust ]-ationg, Royal Perth Hospital.
References
Figure 1: Cranial C T scan showing a ring enhancing pituitary mass.
vertigo. Clinically silent infarction may only be recognised when spontaneous resolution of pituitary hypersecretion occurs.' As in our case, expansion of the pituitary fossa on a skull X-ray suggests the correct diagnosis in the majority with pituitary apoplexy." However, causes of pituitary apoplexy with typical clinical features and normal skull X-rays have been reported.' In confirming and sometimes making the diagnosis, cranial C T scanning is essential. An abscess arising in a pituitary adenoma may also present with aseptic meningitis and resemble pituitary apoplexy in its radiological appearance.' In the present case, pituitary abscess was excluded on histological grounds. Beyond the initiation of appropriate hormone replacement and close monitoring of fluid and electrolyte balance, the optimum management of pituitary apoplexy is disputed. Dexaniethasone was used in our case because, in addition
ASEPTIC MENINGITIS IN PITUITARY APOPLEXY
1. Reid RI., Quigle) ME, Yen SSC. Pituitary apoplexy: a revicw. ilrch Ncurol 1985; 42: 712-9. 2. Bjerre P, 1,indholm J. Pituitary apoplexy with sterile meningitis. Acta Xeurol Scand 1986; 74: 304-7. 3. (hrdoro ER, Pcterson EW. Pituitary apoplexy: a review. Neurosurgery 1984; 14: 363-73. 1. Wakai S, Fukushima T, Teramoto A, Sario K. Pituitary apoplrxy: its incidence and clinical signifrcancc. J Neurosurg 1981; 55: 187-93. 5. Findling JW, Tyrrell JB, Aron DC, Fitzgerald PA, Wilson CB, Forshani PH. Silent pituirary apoplexy: subclinical infarction of an adrenocorticorrophin-producingpituitary adenoma. J Clin Endocriiiol Metabol 1981; 52: 95-7. 6. Fitz-Pdtrick D, Tolis G, iMcGarry EE, Taylor S. Pituitary d p n p k x y : the importance of skull roentgenograms and computtlrised tomography in diagnosis. JAM.4 1980; 214: 59-61. 7. Jeffcoate WJ,Birch C R . Apoplexy in small pituitary tumors. J Neurol Neurosurg Psychiatry 1986; 49: 1077-8. 8. Ford J, Torres LF, Cox T, Hayward R. Recurrent sterile ~iieiiiiigitiscaused by pituitary abscess. Postgrad Med J 1986; 62: 929-31. 9. Senelick RC, Van Dyk HJL. Chromophubt. adenoma masquerading as corticosteroid responsive optic neuritis. Am J Ophthalmol 1974) 78: 485-8. I0 Pelkonen R , Kuusisto A, Salmi J er a/. Pituitary function after pituitary dpoplexy. Am J Med 1978; 65: 773-8.
Aust NZ J Mcd 1990; 20
59 1
