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Syndrome Hages 440 Letters to the editor Stuttering pituitary apoplexy resem- and vomited. The following day he was a little MFT Yealand for us to report permitting J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.5.440 on 1 May 1990. Downloaded from bling meningitis better but three days later he became con- cases under their care. fused and complained of visual impairment. In the first clear description of pituitary He was admitted to a local hospital where he JB WINER, G PLANT apoplexy Brougham et al' suggested that the was found to have neck stiffness and a tem- National Hospitalfor Nervous Diseases, syndrome should be considered as the abrupt perature of40'C. A lumbar puncture revealed Queen Square, London development of headache, amblyopia, CSF which was xanthochromic and under 1 Brougham M, Heusner AP, Adams RD. Acute diplopia, drowsiness, confusion or coma. increased pressure with raised protein con- degenerative changes in adenomas of the These clinical features have now become pituitary body with special reference to well centration and a mixed pleocytosis. The foll- pituitary apoplexy. J Neurosurg 1955;7: established.23 However, Brougham et al men- owing day he developed peri-orbital and 421-39. tion one case of haemorrhage into a pituitary subconjunctival oedema and bilateral sixth 2 Reid RL, Quigley ME, Yen SSC. Pituitary tumour simulating rupture of an intracranial nerve palsies. His were apoplexy: a review. Arch Neurol 1985;42: deep tenden reflexes 712-9. aneurysm where ophthalmoplegia was absent and his conscious level began to 3 Wakai S, Fukushima T, Teratomoto A, Samo K. delayed several days.4 We have seen two cases deteriorate. He was transferred to a specialist Pituitary apoplexy: Its incidence and clinical where delay in diagnosis occurred as a result unit where he was found to be disoriented in significance. J Neurosurg 1981;55:187-93. of the subacute onset of symptoms. The time and place and pyrexial. Periorbital 4 Coxon RV. A case of haemorrhage into a pituitary tumour simulating rupture of an clinical picture was further confused by the oedema, bruising around the left eye and intracranial aneurysm. Guy's Hosp Rep finding ofa highly cellular cerebrospinal fluid marked neck stiffness were noted. Visual 1943;42:89-93. (CSF). acuity was 3/60 on the right and 6/18 on the 5 Bjerre P, Lindholm J. Pituitary apoplexy with sterile meningitis. Acta Neurol Scand The first case was a 50 year old warehouse left and he was unable to identify any of the 1986;74:304-7. attendant who had a five day history of Ishihara test plates. There was a temporal generalised headache and vomiting with two hemianopia to colour in the left eye and a days of double vision. His relatives had dense central scotoma on the right on con- noticed an intermittent droop of the right frontation. There was mild disc swelling with eyelid. He had previously been in good health absent venous pulsation. Lateral rectus weak- Intracranial haemorrhages occurring apart from the drainage ofa "cold abscess" in ness was complete and bilateral and upward in the idiopathic hypereosinophilic early childhood. He drank about 20 pints of movement of the right eye was limited. The syndrome beer each week. only other abnormal finding was total are- Examination revealed a slight pyrexia flexia. The hypereosinophilic syndrome (HES) can (37 5') with limitation of neck flexion but no The full blood count was normal as was the produce a range of neurological disorders. neck stiffness. He had a partial left third nerve urea although the serum sodium was low at Three major patterns of neurological palsy with a dilated but reactive left pupil and 126 mm/L. The CSF contained 1-2 G/L of involvement have been described: ence- a partial left ptosis. There was no field defect protein with a pressure of30 cms of CSF and phalopathy, sensory polyneuropathy, and and extra-ocular movements appeared full. a white cell count of 900 (106/L) of which central nervous system thrombo emboli. Power and tone was normal in the limbs. The 7900 were polymorphs and the rest lym- We describe an elderly woman with this biceps reflexes could be elicited on re- phocytes. There were 20 (106/L) red cells and syndrome who presented with right temporal inforcement but otherwise tendon reflexes a normal CSF glucose. Urine and serum lobe and left cerebellar hemisphere haemorr- were all absent. Plantar responses were flexor osmolarities suggested inappropriate secre- hages. and sensory testing was normal. An unen- tion of ADH. A plain skull radiograph An Indian woman aged 72 years first hanced CT scan was performed to exclude an showed an enlarged pituitary fossa and presented to our hospital in 1980 with general abscess. Lumbar puncture revealed opales- opacification of the sphenoid sinus. CT scan malaise and a nocturnal cough. Examination cent CSF under 19 cms pressure which con- revealed a suprasellar mass with lateral exten- at that time revealed a mild expiratory tained a concentration of 77 mg% of protein sion. Serum cortisol was low (60 mu/L) as wheeze. Her haemoglobin was normal but the with 52 white cells (5% polymorphs, 910% were levels of total thyroxine, TSH, prolac- white cell count was elevated at 46 000 x lymphocytes, 4% macrophages). No organ- tin, FSH and LH confirming pan- 10'/l (78% eosinophils and 15% neutrophils). isms were seen and the concentration ofsugar hypopituitarism. A random estimation of Her platelets, coagulation screen and auto was normal. An EEG showed an excess of growth hormone was slightly elevated antibodies were normal. A chest radiograph mainly posteriorly distribute slow waves. (16 6 mu/L). In view ofthe gradual evolution showed old calcified apical foci with some ill A provisional clinical diagnosis of a sub- of symptoms and the cellular CSF a prov- defined shadowing in the left mid zone. A http://jnnp.bmj.com/ acute meningoencephalitis was made and isional diagnosis of meningitis was made by bone marrow examination revealed eosino- treatment was started with intravenous the referring hospital. The CSF proved to be philia with both the red and white cell series Acyclovir and thiamine. Over the next three sterile and field defects and cranial nerve severely depressed. There was no excess of days there was a deterioration in his clinical signs resolved when antibiotics were with- blasts and no abnormal cells. state with a rising pyrexia to 39'C. He drawn and he was treated with intravenous A diagnosis of HES was made and she was developed bilateral ptosis with impaired steroids and thyroxine. started on a reducing dose of prednisolone. adduction and elevation of both eyes. Visual The presence of inflammatory changes in On discharge her white cell count was 10-7 x acuity in the right eye was reduced to count- the CSF in some cases ofpituitary apoplexy is 109/l with 100 eosinophils. Symptomatically ing fingers at one metre and a right altitudinal well documented in the literature. Bjerre and she had improved and her nocturnal cough on October 2, 2021 by guest. Protected copyright. field defect developed which extended below Lindholm' have recently emphasised the had disappeared. the horizontal meridian. occurrence of "sterile meningitis" as an She remained well on a small dose of A high resolution enhanced CT scan of the important feature of pituitary apoplexy and prednisolone and continued to have a normal orbits revealed a pituitary adenoma with report six cases where CSF examination eosinophil count over the next five years. She some suprasellar extension. Treatment with revealed an elevated leucocyte and or was lost to follow up in 1985 but according to Prednisolone was started immediately with polymorph count. Four further cases in the her general practitioner she continued to take rapid improvement ofvisual acuity to 6/7.5 in literature are cited. The presence of CSF prednisolone until 1987. She was admitted in the effected eye. Endocrine studies revealed a pleocytosis usually presents little diagnostic February 1989 after collapsing at home. normal prolactin (< 65 units) but low TSH concern in patients with a typical acute onset According to her son the event was sudden (0 2 uU/L) and free T4 (5 5 pm/L). He sub- where the diagnosis is confirmed by urgent and without warning. There was no history of sequently had an uneventful transphenoidal CT scanning. The subacute or stuttering head trauma or of a seizure. She was a non hypophysectomy and pathological examina- onset in our cases made diagnosis difficult smoker, non drinker and was not on any tion of the specimen was consistent with the and prompted this report. In the first case the medication. Systems enquiry, by proxy, was eventual diagnosis of infarction in a pituitary absence of a field defect on presentation normal. adenoma. compounded the difficulty in diagnosis. In On examination she was unconscious The second case was a 45 year old printer's the second case the lack of awareness of this (Glasgow coma scale Grade IV), apyrexial assistant who presented with symptoms ofthe mode of presentation of pituitary apoplexy but with no neck stiffness. General examina- carpal tunnel syndrome bilaterally. It was delayed establishing an accurate diagnosis tion was normal, BP 170/80. noted, a year later, that he had large hands despite the previous diagnosis of a pituitary On neurological examination, her pupils and other features of acromegaly. A pituitary tumour. were mid point and fixed. Fundoscopy was adenoma was confirmed on CT scan. Whilst normal and she had no obvious facial asym- awaiting a transphenoidal hypophysectomy metry. Her eye movements were difficult to he awoke with sudden onset frontal headache We thank Professor WI McDonald and Dr assess and she had a depressed gag reflex..
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