‘ Ecstasy’-induced subarachnoid haemorrhage

5. Kaido T, Hoshida T, Uranishi R, Akita N, Kotani A, Nishi N,
Sakaki T. Radiosurgery-induced brain tumor. J Neurosurg 2001; 95:
710–713.

‘Ecstasy’-induced
subarachnoid haemorrhage:
an under-reported
neurological complication?
Gabriel Yin Foo Lee MBBS (HONS) MS,
Grace Wooi Kee Gong MBBS,
Nikitas Vrodos FRACS, Brian Patrick Brophy FRACS
Department of Neurosurgery, Royal Adelaide Hospital, Adelaide, Australia

Summary In the face of escalating recreational use of ‘Ecstasy’
(3,4-methylenedioxymethamphetamine, MDMA), physicians need to
be aware of its possible adverse effects. We report two young patients who suffered subarachnoid haemorrhage following ingestion of
‘Ecstasy’ tablets. Angiographic studies demonstrated features consistent with vasculitis in both cases. Recognition of this association is
important and highlights the significance of eliciting a careful drug
history, particularly in cases of ‘angiogram negative’ subarachnoid
haemorrhage.
ª 2003 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2003) 10(6), 705–707
0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved.
doi:10.1016/S0967-5868(03)00151-6

Keywords: ecstasy, MDMA, subarachnoid haemorrhage, vasculitis
Received 13 November 2002
Accepted 6 December 2002
Correspondence to: Dr Gabriel Lee, Department of Neurosurgery, Sir Charles
Gairdner Hospital, Hospital Avenue, Nedland, Western Australia.
Tel.: +61-8-93463333; Fax: +61-8-93463824;
E-mail: gabriellee@ozemail.com.au

INTRODUCTION
It is increasingly well recognised that recreational use of Ecstasy
(MDMA) can lead to life threatening consequences. While neurological complications are uncommon, this may represent an
under-reported phenomenon. We present two young patients in
whom Ecstasy use was associated with non-aneurysmal subarachnoid haemorrhage.
CASE 1
A 29-year-old woman experienced a sudden onset of severe occipital headache which was associated with nausea and vomiting 5
days prior to presentation to the Royal Adelaide Hospital. The
patient complained of severe photophobia. On clinical examination, the patient was alert and orientated. There was marked nuchal rigidity. Neurological examination did not reveal any focal
deficit. CT head scan was normal. Subsequent lumbar puncture
revealed blood stained CSF with photospectrometric evidence of
xanthochromia. The patient underwent conventional four vesselcerebral angiography which demonstrated evidence of ‘beading’
ª 2003 Elsevier Ltd. All rights reserved.

705

of vessels within the posterior circulation. The angiographic appearances were most marked on the (L) superior cerebellar artery
(Fig. 1). Further investigation with MRI/MRA revealed no significant abnormality. Serum testing revealed an erythrocyte sedimentation rate (ESR) of 11 and C-reactive protein (CRP) of 4.
Antinuclear antigen (ANA) was negative.
Following the patient’s admission, her friends subsequently
volunteered information of illicit drug use by the patient. On repeated questioning, the patient admitted that she had used
‘Ecstasy’ on the day of ictus. She denied having previously used
‘Ecstasy’ or any other recreational drugs.
The patient was observed without neurological deterioration.
She was discharged at Day 13 of her admission. The delay was
due to persistent headaches. Follow-up cerebral angiography 2
months later showed that the abnormalities had completely resolved.
CASE 2
A 24-year-old man smoked marijuana and subsequently consumed
one and a half ‘Ecstasy’ tablets while at a party. Several hours
later, he experienced a sudden severe retro-orbital headache and
felt unwell. Soon after arriving home, he suffered a witnessed
episode of generalised tonic-clonic seizure lasting approximately
1 min. This was followed by a brief period of post-ictal confusion.
On arrival at the emergency department, he was alert and orientated. Neurological examination was otherwise unremarkable. He
had a further generalised seizure in the emergency department
which was aborted by intravenous midazolam.
The patient underwent a CT head scan. This revealed the
presence of subarachnoid haemorrhage which was mainly localised to several parasagittal sulci towards the vertex (Fig. 2). Cerebral angiography demonstrated evidence of focal ‘beading’ of
peripheral branches to the (R) anterior cerebral cortex consistent
with angiographic arteritis. MRI/MRA head scan confirmed the
presence of subarachnoid haemorrhage but no other abnormalities.
The patient remained well subsequently with resolution of his
headaches and no further seizures. He was discharged at Day 4
following his admission.
DISCUSSION
MDMA, also known as ‘Ecstasy’, is a three ring-substituted,
methoxylated analogue of methamphetamine. It was first synthesized in Germany in 1914 and used initially as an appetite suppressant.1;2 During the late 1970s and 1980s, it found a secondary
use in the United States as an adjunct to psychotherapy.1;2 The
current widespread recreational use of MDMA by teenagers can
primarily be traced back to the British dance hall phenomenon
called ‘raves’.3 The use of MDMA was reported by 8% of 15- and
16-year-old British students surveyed in 1994.4 A more recent
survey at three dance events in Edinburgh, Scotland demonstrated
that over 80% of participants had previously used Ecstasy and
amphetamines. Furthermore, 35% stated that they used Ecstasy on
a weekly basis.5 Its use has since spread across to other continents.3;6 A random survey of illicit drug use by American undergraduate students revealed that 24% of those surveyed reported
use of MDMA, exceeding use of lysergic acid diethylamide (LSD)
and cocaine.3 Furthermore, MDMA has also become a popular
choice for University students and attendees at rave parties in
major coastal American cities.3 Studies from Australia 7 and
Germany 6 have similarly demonstrated a high rate of MDMA
usage. A 1999 survey of drug use in Norwegian adolescents further showed that MDMA was used by adolescents who also used
other legal and illegal substances in a polydrug-use pattern.8
Journal of Clinical Neuroscience (2003) 10(6)

706 Lee et al.

Fig. 1

(A,B) Conventional cerebral angiogram demonstrating focal narrowings (‘beading’) in multiple vessels within the posterior circulation.

Fig. 2 Non-contrast enhanced CT head scan demonstrating subtle
subarachnoid haemorrhage within several parasagittal sulci on the left.

MDMA induces a feeling of euphoria and ecstasy.1 This is said
to contribute to the pleasure of dancing at raves and discos.9 The
drug can also lead to transcendental experiences and other ‘desired’
perceptual changes.1 Its use, however, has been associated with a
number of adverse effects. These may include anorexia, trismus,
bruxism, nausea, muscle aches, stiffness, gait ataxia, sweating,
restlessness, brooding, insomnia and fatigue.3;10;11 More serious adverse effects include hyperthermia, convulsions, cardiac
tachyarrthymias, aortic dissection, rhabdomyolysis, disseminated
intravascular coagulation, renal failure, hyponatraemia, hepatotoxicity and aplastic anaemia. Reported neurological complications
include cerebral infarction, cerebral haemorrhage, cerebral venous
sinus thrombosis and seizures.1;9;12–16
MDMA is believed to principally affect the serotonergic system. It selectively destroys serotonin nerve terminals in rats and
Journal of Clinical Neuroscience (2003) 10(6)

primates.17;18 Serotonin plays a major role in thermoregulation and
interference with this mechanism is believed to be the cause of the
hyperthermia which arises as a complication of MDMA misuse. It
also acts on the noradrenergic pathway which probably contributes to hyperthermia.9 Hyperthermia was postulated to account for
many of the changes seen in deaths associated with the misuse of
amphetamine derivatives. Postmortem examination typically reveals pathological changes in the liver, brain and heart which are
similar to those found in heat stroke.9 Milroy et al.9 concluded that
that the deaths associated with MDMA use in their study resulted
from hyperthermia, disseminated intravascular coagulopathy and
shock.
Cocaine and amphetamine misuse are both well recognized
causes of intracerebral and subarachnoid haemorrhage.1;19–23 Administration of either drug can lead to a hypertensive crisis. This
may trigger a haemorrhage from a pre-existing vascular abnormality.1 Cocaine can further induce vasospasm by a direct smooth
muscle effect as well as augmenting the physiological effects of
catecholamines.1 This leads to cerebral ischaemia which may be
further aggravated by increased thromboxane production and enhanced platelet aggregation.1;24 In contrast, cerebral angiitis has
been reported to occur more frequently with amphetamine misuse.1;25 In these cases, angiography has demonstrated pronounced
irregularity and ‘beading’ in the middle and anterior cerebral arterial branches.
In contrast, the effect of MDMA on cerebral vasculature is not
known. To date, there has only been one publication alluding to
the possible association of subarachnoid haemorrhage with
MDMA abuse. Gledhill et al.26 described a 25-year-old patient
who presented with a ruptured posterior communicating artery
aneurysm 6 h following Ecstasy ingestion. The authors suggest
that an ‘acute sympathetically mediated surge in blood pressure’
may have triggered aneurysmal rupture. They further hypothesized that repeated use causes recurrent surges in systemic blood
pressure which may also lead to a progressive weakening of the
vessel wall, thus predisposing to aneurysmal formation.22;26 On
the other hand, McEvoy et al.22 reason that MDMA ‘probably
causes a degree of vasculitis’ on the basis of its chemical derivation
from amphetamines. The current report provides circumstantial
ª 2003 Elsevier Ltd. All rights reserved.

Management of massive calcified transdural thoracic disk herniation

evidence that MDMA can lead to subarachnoid haemorrhage in the
absence of a vascular malformation. In both cases, there were angiographic features typical of vasculitis.
The current report highlights several points. Firstly, an accurate and truthful history of drug intake is required from any young
patient who presents with spontaneous subarachnoid haemorrhage, particularly in ‘angiogram negative’ cases. Secondly, it is
difficult to ‘prove’ that an adverse neurological event is related to
a drug particularly when there are no previous reports of such an
association.22 Causation can only be established as clinicians and
researchers begin to recognise such a possibility. Thirdly, the
precise incidence of MDMA-induced non-aneurysmal subarachnoid haemorrhage is unknown. To the best of our knowledge,
there are no previous case reports of such a neurological complication. Whether this represents a rare phenomenon or significant under-reporting from lack of awareness remains to be
determined.

707

23. Neiman J, Haapaniemi HM, Hillbom M. Neurological complications of drug
abuse: pathophysiological mechanisms. Eur J Neurol 2000; 7(6):
595–606.
24. Togna G, Tempesta E, Togna AR, Dolci N, Cebo B, Caprino L. Platelet
responsiveness and biosynthesis of thromboxane and prostacyclin in
response to in vitro cocaine treatment. Haemostasis 1985; 15:
100–107.
25. Margolis MT, Newton TH. Methamphetamine (“speed”) arteritis.
Neuroradiology 1971; 2: 179–182.
26. Gledhill JA, Moore DF, Bell D, Henry JA. Subarachnoid haemorrhage
associated with MDMA abuse. J Neurol Neurosurg Psychiatry 1993; 56(9):
1036–1037.

Management of massive
calcified transdural thoracic
disk herniation

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ª 2003 Elsevier Ltd. All rights reserved.

Mohammed Al-Barbarawi MB BS CHAM,
Lali H.S. Sekhon MB BS (HONS) PHD (SYD) FRACS
Department of Neurosurgery, Royal North Shore Hospital and the
University of Sydney, Sydney, Australia

Summary Thoracic disc herniation is a not uncommon pathology
faced by the spinal surgeon. The management of massive intradural thoracic disc herniation with ventral cord compression is
problematic both in terms of obtaining adequate decompression
and ensuring no subsequent leakage of cerebrospinal fluid. A 54year-old woman presented with a 10 year history of back pain and
left leg pain. Over the past 6 months she experienced a progressive spastic paraparesis in both legs with recent urinary incontinence. A left anterolateral thoracotomy for excision of T8/9 thoracic
disc protrusion was affected. A transdural decompression was
performed with resection of the calcified dura and performance of a
Gore-Tex duraplasty and pleuroplasty. A free muscle graft was
placed in the intervening space and the chest drains were placed
on non-suction. A spinal drain was maintained for 5 days. She
made an excellent neurological recovery. Avoidance of cerebrospinal leakage is paramount when performing transthoracic approaches as negative intrapleural pressure can lead to persistence
of leakage. This report documents a safe and reliable way to deal
with massive intradural thoracic disc rupture with avoidance of
subsequent spinal fluid leak.
ª 2003 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2003) 10(6), 707–710
0967-5868/$ - see front matter ª 2003 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jocn.2003.02.001

Keywords: calcified disc, cerebrospinal fluid, dural tear, subarachnoid-pleural fistula, thoracic disc herniation
Received 2 December 2002
Accepted 14 February 2003
Correspondence to: A/Prof. Lali Sekhon, Department of Neurosurgery,
Level 7, Royal North Shore Hospital, St. Leonards, NSW 2065, Australia.
Tel.: +61-2-99268703; Fax: +61-2-94375172;
E-mail: surgeon@spinalneurosurgery.com

INTRODUCTION
Thoracic disc herniation (TDH) is a common MR imaging
finding, but clinically significant TDH is rare, occurring with an
Journal of Clinical Neuroscience (2003) 10(6)