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slurred speech. Pyrexia is absent.3 The cranial nerve symptoms are frequently, but not always, preceded by nausea,
vomiting and abdominal cramps, especially after ingestion
of contaminated foods. Incubation periods of between 3
hours and 54 days have been reported4 but 12–72 hours
is often quoted. The clinical diagnosis of botulism is
confirmed by injection of the patient’s serum into a
laboratory animal, which then shows signs of neurotoxicity.
Seven serotypes of the toxin are known, but only types
A, B and E have been consistently responsible for botulism
in man and trivalent antitoxin directed at these is the
treatment of choice. Prompt treatment is crucial since,
once the toxin has blocked neurotransmission at a synapse,
antitoxin will have no effect on that synapse. Even a
suspicion of botulism demands treatment with antitoxin,
without waiting for a laboratory test. Recovery from the
neurotoxic injury depends on the regeneration of
neuromuscular junctions, which may take many months
and is often incomplete. The implementation of ventilatory
support has reduced the mortality from 60–70% in the
early twentieth century to around 20% more recently.5
Even with the diagnosis of botulism, our patient’s progression within 45 minutes from an alert ambulatory state
to respiratory arrest is hard to explain. We suspect that his
earlier symptoms of weakness and somnolence reflected
increasing compromise of his tidal exchange, culminating in
the hypoxia/hypercardia that precipitated the arrest.
Previously unseen and unpredicted routes of infection
with botulinal toxin have emerged. Intravenous and nasal
routes from recreational drugs ‘cut’ with contaminated soil
particles and ‘inadvertent’ botulism in patients being
treated with botulinal toxin for dystonias and cosmetic
procedures8 have been reported. The possibility of the use
of C. botulinum and its toxin as a weapon for bio-terrorism is
considered both ‘real and frightening’.2,9
REFERENCES

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1 Davis LE. Botulism. Curr Treat Options Neurol 2003;5:23–31
2 Arnon SS, Schechter R, Inglesby TV, et al. Botulinum toxin as a
biological weapon: medical and public health management. JAMA
2001;285:1059–70
3 Gao QY, Huang YF, Wu JG, Liu HD, Xia HQ. A review of botulism in
China. Biomed Environ Sci 1990;3:326–36
4 Larson HE. In: Warrell DA, Cox TM, Firth JD, Benz EJ Jr, eds. Oxford
Textbook of Medicine, Vol. 1, 4th edn. 2003:551–3
5 Brett M. Botulism in the United Kingdom. Eurosurveillance 1999;4:9–11
6 Galazka A, Przybylska A. Surveillance of foodborne botulism in Poland:
1960–1998. Eurosurveillance 1999;4:60–72
7 Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States:
a clinical and epidemiologic review. Ann Intern Med 1998;129:221–8
8 Cherington M. Clinical spectrum of botulism. Muscle Nerve
1998;21:701–10
9 Whitby M, Street AC, Ruff TA, Fenner F. Biological agents as weapons
1: smallpox and botulism. Med J Aust 2002:176:431–3

Volume

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November 2003

An aneurysm is born
Kyo Niijima MD PhD
J R Soc Med 2003;96:550–551

When a de novo intracranial saccular aneurysm is detected at
a site where angiography was previously negative, the
interval between angiographies is usually a matter of
years1,2 rather than days.
CASE HISTORY

A woman of 76 with a history of hypertension developed
headache with mild disturbance of consciousness. There was
no personal or family history of inflammatory, collagen or
cerebrovascular disease. On neurological examination there
were no localizing features and laboratory data were all
within the normal range. Urgent cranial CT revealed diffuse
subarachnoid haemorrhage in the interpeduncular and
ambient cisterns, and a magnetic resonance angiogram
disclosed a single aneurysm, 12 mm in diameter, at the
bifurcation of the basilar artery (Figure 1). Eight days later,
the patient suddenly vomited and became comatose with
neck rigidity. 30 minutes after this, CT revealed a dense
subarachnoid haemorrhage localized in the left sylvian
fissure. Next day the basilar artery aneurysm, which was
then thought to be responsible for both vascular events, was
successfully occluded by endovascular coiling. At that time
a new aneurysm (Figure 2), 10 mm in diameter, was
observed at the bifurcation of the left middle cerebral
artery; the artery itself was not clearly visualized owing to
vasospasm. Because of the patient’s clinical state (semicomatose and dyspnoeic) the new aneurysm was left
untreated. 7 days later, magnetic resonance angiography
showed the left middle cerebral artery to be completely
occluded proximal to the aneurysm, which was no longer
visible (Figure 3). Thereafter the patient remained
stuporose with a right hemiplegia.
COMMENT

The shortest reported interval between an angiography and
the demonstration of a de novo aneurysm at further
angiography is 47 days.3 In the present case the interval
was 9 days. The arteriographic appearance was suggestive of
a true saccular aneurysm rather than a mycotic, dissecting
or arteriosclerotic aneurysm.
Department of Neurosurgery, Shiga National Hospital, 255 Gochi-cho, Yokaichi,
Shiga 527-8505, Japan

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second portion of the left middle cerebral artery are clearly
seen in the first magnetic resonance angiogram. Moreover,
on examination of the published work4–6 I could find no
report of false-negative magnetic resonance angiography for
an aneurysm greater than 10 mm in diameter. On this
evidence I conclude that this aneurysm did not exist at the
time of initial study 9 days earlier.
REFERENCES

Figure 1. Initial MR angiogram. A single aneurysm is seen at the
bifurcation of the basilar artery (arrow)

1 Matheus MG, Castillo M. Development of de novo aneurysm. Am J
Neuroradiol 2003;24:709–10
2 Tonn J, Hoffman O, Hoffmann E, et al. ‘‘De novo’’ formation of
intracranial aneurysms: who is at risk? Neuroradiology 1999;41:674–9
3 Yasuhara T, Tamiya T, Sugiu K, et al. De novo formation and rupture of
an aneurysm. Case report. J Neurosurg 2002;97:697–700
4 Schuierer G, Huk WJ, Laub G. Magnetic resonance angiography of
intracranial aneurysms: comparison with intra-arterial digital subtraction
angiography. Neuroradiology 1992;35:50–4
5 Okuhara M, Kiyosue H, Yamashita M, et al. Diagnostic accuracy of
magnetic resonance angiography for cerebral aneurysms in correlation
with 3D-digital subtraction angiographic images. A study of 133
aneurysms. Stroke 2002;33:1803–8
6 Jager HR, Mansmann U, Hausmann O, et al. MRA versus digital
subtraction angiography in acute subarachnoid haemorrhage: a blinded
multireader study of prospectively recruited patients. Neuroradiology
2000;42:313–26

Aortic root replacement in
pregnancy
Figure 2. Left internal carotid digital subtraction arteriogram 9
days later. A de novo saccular aneurysm is seen at the bifurcation of the
left middle cerebral artery (arrow)

Natasha Khan FRCS
James Clarke FRCA 2

Charles Pumphrey FRCP 1
Marjan Jahangiri FRCS

J R Soc Med 2003;96:551–552

When complex cardiac operations become necessary during
pregnancy, timing is crucial to survival of the fetus.
CASE HISTORY

Figure 3. MR angiogram 16 days after initial subarachnoid
haemorrhage. The left middle cerebral artery is completely occluded
proximal to the aneurysm, which is no longer visible

Could the middle cerebral artery aneurysm have been
missed at the original magnetic resonance angiography?
Digital subtraction arteriography is certainly more sensitive;
however, a basilar bifurcation aneurysm and the first and

A woman of 31, in the 10th week of her first pregnancy,
reported palpitations. She was tall, with fingers and toes
unusually long for her family, and had ‘double-jointed’
thumbs. She was also short-sighted and her hearing was
poor. There was no medical or family history of note. The
pregnancy had followed 3 years of infertility treatment.
Aortic regurgitation was diagnosed clinically, and she met
Departments of Cardiac Surgery, 1Cardiology, and 2Cardiovascular Anaesthesia,
St George’s Hospital NHS Trust, London SW17 0QT, UK
Correspondence to: Marjan Jahangiri FRCS, Department of Cardiac Surgery,
St George’s Hospital, Blackshaw Road, Tooting, London SW17 0QT, UK
E-mail: marjan.jahangiri@stgeorges.nhs.uk

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