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Non-convulsive status epilepticus
6 Breadmore R, Desmond P, Opeskin K. Intracranial
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rupture of internal carotid artery. Austral Radiol
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8 Haran RP, Chandy MJ. Intracranial aspergillus granuloma. Br J Neurosurg 1993;7:383± 8.
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1988.
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1983;13:306± 9.
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ZAB, Al-Sohaibani MO, Aziz SA. Cranial and intracranial aspergillosis of sino-nasal origin. Report of nine
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and cerebral aspergillosis: cure with medical therapy.
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141

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Non-convulsive status epilepticus: a treatable cause of confusion in
pituitary apoplexy
J. J. CRAIG & J. M. GIBSON
Department of Neurology, RoyalVictoria Hospital, Belfast, Northern Ireland, UK

Abstract
Confusion occurring in pituitary apoplexy is well described. We describe a case of pituitary apoplexy associated with confusion, occurring as a result of non-convulsive status epilepticus. Electroencephalography should be performed in pituitary
apoplexy associated with confusion if this treatable and potentially serious complication is not to be missed.
Key words: Confusion, non-convulsive status epilepticus, pituitary apoplexy.

Introduction

Case report

Non-convulsive status epilepticus is a rare cause of a
confusional state and is probably unfamiliar to many
neurosurgeons. We describe a case of pituitary
apoplexy in which this occurred. The confusion
cleared with appropriate treatment, prior to surgical
removal of the pituitary.

A 60-year-old woman, with a 5-year history of chronic
frontal headache, presented with increasingly severe
generalized headache associated with vomiting for 6
days, and drowsiness for 2 days. On admission she
was dehydrated, with a low grade fever (37.9Ê C) and
tachycardia (12 min), but was normotensive (120/

Correspondence: Dr J. M. Gibson, Department of Neurology,Ward 21, Royal Victoria Hospital, Belfast, BT12 6BA, UK.Tel: 01232 240503
Ext. 4325. Fax: 01232 235258. E-mail
Received for publication 25 June 1998. Accepted 25 October 1998.

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142

J. J. Craig & J. M. Gibson

60 mmHg). Glasgow coma scale (GCS) was 7/15
(M=5, V=1, E=1) and marked neck stiffness was
present. All re¯ exes were pathologically brisk and the
plantar responses were extensor. Otherwise examination was unremarkable. Intermittently, for up to half
an hour, the GCS was noted to fall to 4/15. During
these episodes continuous repetitive stereotyped
`plucking’ movements of the hands, and occasional
lip-smacking movements were observed.
Laboratory studies showed a mild peripheral leucocytosis and no other abnormalities.The serum sodium
was 143 mmol/l on admission to hospital and remained
normal throughout. Brain CT was normal apart from
slight enlargement of the sella. Lumbar puncture
revealed clear cerebrospinal ¯ uid (CSF) at an opening
pressure of 70 mm of CSF with 9 3 106/l lymphocytes,
49 3 106/l erythrocytes, a protein concentration of
0.63 g/l, a glucose concentration of 3.6 mmol/l (serum
glucose 8.3 mmol/l) and no organisms on direct microscopy or culture. An electroencephalogram (EEG)
demonstrated continuous high amplitude, repetitive,
single sharp waves, consistent with status epilepticus
(Fig. 1), which diminished with the administration of
intravenous diazemuls.
The initial diagnosis was non-convulsive status
epilepticus (NCSE), due to presumed infective meningoencephalitis and treatment was commenced with
intravenous chlormethiazole and benzylpenicillin,
cefotaxime, acyclovir and dexamethasone. She
continued to be obtunded, however, EEG remaining

unchanged. Intravenous clonazepam was substituted
in place of chlormethiazole.Within hours she became
fully orientated, but had a right-sided third nerve
palsy. Visual acuity and ® elds to confrontation were
normal. EEG at this stage did not demonstrate any
epileptic activity. MRI showed a large mass arising
from the pituitary fossa on T1 weighted images with
well de® ned peripheral enhancement (Fig. 2). This
extended superiorly to the optic chiasm and inferiorly into the sphenoid sinus. It was composed centrally
almost entirely of low signal on T1 weighted images
and high signal on T2 weighted images, indicating
the presence of ¯ uid within the lesion, in keeping
with pituitary apoplexy.
The tumour was approached trans-sphenoidally
and proved to be a null cell adenoma, which contained
areas of necrotic, bloody material. Postoperatively
the third nerve palsy resolved. The patient remains
on hydrocortisone and thyroxine replacement therapy.
No further seizures have occurred.

FIG. 1. EEG on admission showing continuous, highamplitude, single sharp waves, maximal anteriorly, consistent
with status epilepticus.

FIG. 2. Gadolinium-enhanced MRI showing pituitary
tumour enhancing peripherally with contrast, with inferior
hypodensity suggestive of tumour necrosis.

Discussion
Pituitary apoplexy occurs in approximately 2% of
patients with pituitary tumours,1,2 because of haemorrhagic infarction or necrosis of the tumour. The
diagnosis of the condition can be difficult and is
often delayed, as in our case, because in addition to
its relative rarity, the presenting symptoms and signs
can suggest more common conditions and the existence of an adenoma is usually unsuspected at the
time of the ictus.3 The features of the syndrome
include headache of acute onset, vomiting,
meningism, visual impairment, ophthalmoplegia and
deterioration in the level of consciousness.2 Alteration in the level of consciousness, attributed to such
diverse causes as brain-stem or hypothalamic dysfunction, vasospasm and metabolic derangement is not
uncommon.3,4 However, its occurrence because of

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Petrous Ewing’s sarcoma
seizure activity is poorly documented, despite the
recognized occurrence of epilepsy secondary to local
mass effects from pituitary adenomata.5
The case presented illustrates the usefulness of
EEG in de® ning NCSE as the cause of stupor in
our patient. Although EEG changes including
diffuse slowing have previously been reported in
pituitary crises,6,7 EEG is rarely performed in this
setting. We therefore predict that if the initial
working diagnosis had been pituitary apoplexy,
rather than meningo-encephalitis we would not have
performed an EEG and NCSE would not have been
identi® ed, which might have been to the detriment
of the patient.
NCSE accounts for up to 20% of all cases of
status epilepticus 8 (the remaining 80% having
convulsive status epilepticus) and is frequently
missed.9 This is because, despite the usual presence
of continuous epileptic activity on EEG, NCSE is
essentially behavioural in presentation without
prominent or any motor manifestations. 1 0
Although considered by some to be a relatively
benign condition, 1 1 certain types have been
shown to be associated with serious morbidity
and mortality.12 Treatment is often effective.1 0 We
would suggest that EEG should be performed in
pituitary apoplexy associated with confusion to avoid
missing this treatable and potentially serious
complication.

143

References
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Primary petrous bone Ewing’s sarcoma
K. DESAI, A. GOEL & T. D. NADKARNI
Department of Neurosurgery, King Edward Memorial Hospital and Seth G. S. Medical College, Parel, Mumbai, India

Abstract
A case of primary Ewing’s sarcoma involving a large portion of the petrous temporal bone in an eighteen month old child is
reported. The lesion was treated by radical surgery and adjuvant chemotherapy and radiotherapy. An extremely rare age of
presentation, an unusual location and an excellent response to treatment are the highlights of this case.
Key words: Chemotherapy, Ewing’s sarcoma, petrous bone, skull base surgery.

Introduction
Primary Ewing’s sarcoma arising from the skull base in
general and petrous bone in particular are extremely
uncommon.1± 4 On our literature survey we located

three cases of primary Ewing’s sarcoma involving the
petrous bone arising either primarily within it or by
virtue of secondary extension.1,2 An additional case of
Ewing’s sarcoma involving the petrous temporal bone
is reported and the literature of the subject is reviewed.

Correspondence: Dr Atul Goel, Department of Neurosurgery, K. E. M. Hospital, Parel, Mumbai, India. Tel: 4129884, Fax: 91± 22±
4143435, E-mail
Received for publication 30 September 1998. Accepted 20 November 1998.