Brief Report

Aura attacks from acute convexity
subarachnoid haemorrhage not due to
cerebral amyloid angiopathy

Cephalalgia
31(3) 368–371
! International Headache Society 2010
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DOI: 10.1177/0333102410384885
cep.sagepub.com

DK Field1 and TJ Kleinig2
Abstract
Background and purpose: Convexity subarachnoid haemorrhage (cSAH) has recently been recognised as a cause of
recurrent aura-like symptoms, mimicking transient ischaemic attacks (TIAs). Subarachnoid haemorrhage and recurrent
aura-like episodes can occur in patients with cerebral amyloid angiopathy (CAA), which has been the presumed cause in
the majority of reported cases. However, this syndrome can occur following cSAH secondary to other conditions, and it
is important for clinicians to investigate and manage such patients appropriately.
Method: Case series.
Results: We describe two patients who presented with recurrent stereotyped transient neurological symptoms in the
setting of acute cSAH identified on MRI. In one patient, SAH occurred secondary to cerebral venous sinus thrombosis. In
the other, SAH was due to extension of a traumatic subdural haematoma.
Conclusions: Conditions other than CAA can cause the clinicoradiological syndrome of cSAH with recurrent TIA-like
events. Gradient echo or susceptibility-weighted imaging should be included in the diagnostic work-up of patients
presenting with such events. When cSAH is detected, the full differential diagnosis for this should be considered.
Aetiologies other than CAA can cause this syndrome and management can vary greatly depending on the underlying
cause.
Keywords
Aura, subarachnoid haemorrhage, cortical spreading depression, TIA mimic, cerebral amyloid angiopathy
Date received: 20 April 2010; revised: 25 July 2010; accepted: 21 August 2010

Introduction
Transient ischaemic attack (TIA) mimics are important
to identify, as misdiagnosis can lead to inappropriate
management. An important TIA-mimic syndrome has
recently been recognised in which convexity subarachnoid haemorrhage (cSAH) causes flurries of transient
aura-like sensory or sensorimotor deficits (1,2). This
syndrome may be a relatively common cause of ‘‘late
life migraine accompaniments’’ (3,4), as well as transient neurological symptoms in patients with cerebral
amyloid angiopathy (CAA) (5), a condition which has
been associated with atraumatic cSAH (6,7), particularly in those aged over 60 years (7).
However, there are many possible causes of cSAH
(8), and CAA should not be assumed as the cause of
TIA-mimic syndrome in the elderly. We describe two
patients over the age of 60 years who presented with the
clinicoradiological syndrome of cSAH with recurrent

TIA-like events, not due to CAA. In one case, the cause
of cSAH was cerebral venous sinus thrombosis
(CVST); in the other, a traumatic subdural haematoma
had extended to the subarachnoid space.

Patient 1
An 81-year-old woman with preceding hypertension,
dyslipidaemia and breast cancer presented with recurrent transient episodes of right-sided numbness and

1
2

Flinders Medical Centre, Australia.
Royal Adelaide Hospital, Australia.

Corresponding author:
Deborah K. Field, Department of Neurology, Flinders Medical Centre,
Bedford Park, South Australia
Email: dkfield79@gmail.com

Field and Kleinig
weakness. She had tripped and fallen two weeks previously, sustaining a right orbital floor fracture with associated retrobulbar haemorrhage, orbital compartment
syndrome and altitudinal field loss.
She presented to the hospital after repeated episodes
of numbness which spread gradually over minutes to
involve the right shoulder, arm and then leg. There was
associated mild-moderate right-sided weakness.
Symptoms resolved in 10–20 minutes. She experienced
four episodes over as many days and had another event
shortly after admission to the hospital. Neurological
examination was unremarkable except for the preexisting altitudinal field loss. Computed tomography
(CT) scan of the head demonstrated a left fronto-parietal subdural haematoma, which was not present on
the scan from two weeks prior. MRI confirmed the
subdural haematoma, but also demonstrated extension
into the subarachnoid space around the central sulcus
(Figure 1). Electroencephalogram showed focal slowing
in the left temporal region but no epileptiform activity.
The patient was initially loaded with phenytoin, and
then commenced on sodium valproate. Episodes did
not subsequently recur.

369
recurrent transient episodes of left-sided weakness.
A fronto-temporal headache had occurred three
weeks previously, lasting for three days. Two weeks
after the initial headache, he experienced an episode
of left facial and arm weakness, and slurred speech,
which resolved after 15 minutes. The following day
he had a similar episode which lasted 10 minutes.
Approximately one week later, he had the third episode, which consisted of left facial droop with tingling
sensation spreading from the left arm to the left leg over
10 minutes. This latter episode lasted for 30 minutes,

Patient 2
A 70-year-old man with hypertension, dyslipidaemia
and type II diabetes mellitus presented with

Figure 1. Fluid attenuated inversion recovery (FLAIR) image
showing left subdural haematoma and left central sulcus subarachnoid haemorrhage.

Figure 2. (A) Magnetic resonance venogram showing sagittal
sinus thrombosis, (B) FLAIR image showing right central sulcus
subarachnoid haemorrhage.

370
was associated with a mild occipital headache and precipitated his presentation to the hospital.
Neurological examination was unremarkable. CT head
scan showed cSAH in the right central sulcus, as well as a
positive Delta sign, suggestive of sagittal sinus thrombosis.
MRI of the brain confirmed the sagittal sinus thrombosis
(Figure 2A), as well as the right central sulcus SAH (Figure
2B). Thrombophilia and autoimmune screens were negative. The patient was started on heparin and warfarin.
During hospital admission he developed three further transient episodes of left facial and arm weakness, which
resolved within 10 minutes and were associated with occipital headache. Following commencement of sodium
valproate he experienced no further episodes.

Discussion
We present two cases of cSAH-associated recurrent
transient aura attacks secondary to a traumatic subdural haematoma and CVST, respectively. Although
it has long been known that CAA can cause recurrent
TIA-like symptoms (5), it has only recently been appreciated that cSAH is a common (and perhaps invariable)
concomitant (1). CT scanning, while effective at detecting large and hyperacute SAH, becomes less sensitive
with time and lesser degrees of haemorrhage; MRI is
far superior in these settings (9), especially when fluidattenuated inversion recovery (FLAIR), gradient echo
and susceptibility-weighted imaging sequences are used
(8). Because recurrent episodes can occur long after the
initial CT signature hyperdensity has resolved, it is only
recently, as newer imaging sequences are routinely
employed, that the link to cSAH has been appreciated.
Several cSAH cases of unknown aetiology with similar recurrent neurological symptoms can be found in
the literature (10), and it has been proposed that cases
not meeting diagnostic criteria for CAA (11) may represent a ‘‘forme fruste’’. This suggestion is not unreasonable, as CAA was the probable cause of every case
of convexity superficial siderosis discovered incidentally
in a recent community-based MRI study (6).
However, CAA is not the only cause of cSAH (8),
and it is important to consider other aetiologies, particularly in the absence of convexity cerebral microbleeds. Acute cSAH can occur following trauma,
cerebral venous thrombosis, Moya Moya disease, primary CNS angiitis, arteriovenous malformations and
fistulas, severe atherosclerotic carotid stenoses and
drug- and pregnancy-related vasculopathies. Although
‘‘TIA-like’’ episodes have been occasionally reported in
association with cerebral venous thrombosis (12,13), no
reports have previously associated this with both cSAH
and recurrent transient neurological symptoms.
A recent retrospective study (7) of 29 patients with
atraumatic cSAH found that the majority of such

Cephalalgia 31(3)
patients over the age of 60 years had evidence of
CAA on imaging, whereas those 60 years or younger
tended to have imaging findings of reversible cerebral
vasoconstriction syndrome (RCVS). Our two patients,
both well over the age of 60, demonstrate the importance of considering causes of cSAH other than CAA.
Patient 1, in particular, illustrates the necessity of
taking a history regarding recent trauma, as she did
not develop symptoms from her haemorrhage until
almost two weeks post-fall. Kumar et al.’s study (7)
also noted that severe headache was a prominent clinical feature in those 60 years or younger, but was rare in
those over this age, whereas transient sensory or motor
symptoms tended to occur in those greater than 60 (7 of
the 8 patients with these symptoms were over 60 years
old). In keeping with these findings, severe headache
was not a feature in our two patients (although patient
2 had mild headache), and both presented with recurrent transient neurological symptoms. The cause for
this apparent age-related difference in clinical presentation remains unclear, and requires further study, but
could possibly reflect altered cerebral vascular reactivity with age (14,15).
It has been previously recognised that cSAHassociated transient neurological episodes evolve in a
fashion more consistent with migrainous aura than
with epilepsy or ischaemia (1). Coupled with recent studies which have demonstrated cortical spreading depression (CSD) in both experimental (16) and human SAH
(17), it is probable that CSD induced by subarachnoid
blood products is the pathophysiological mechanism
and that the reported efficacy of anticonvulsants in this
setting is probably from suppression of CSD. Our current report demonstrates that CAA should not be
assumed as the cause when this syndrome is encountered
in clinical practice. The full differential diagnosis of
cSAH should be considered, as treatment aimed at the
underlying cause may vary significantly, from (for
instance) anticoagulation for cortical vein thrombosis,
to immunosuppression for cerebral vasculitis, or embolisation for a dural arteriovenous fistula.
In summary, aetiologies other than CAA can cause
the clinicoradiological syndrome of convexity SAH
with recurrent TIA-like events. Not only should gradient echo or susceptibility-weighted imaging be performed in all patients presenting with recurrent
TIA-like events; for patients in whom cSAH is detected,
the full range of underlying diagnostic possibilities
should be considered.

References
1. Kleinig TJ, Kiley M and Thompson PD. Acute convexity
subarachnoid haemorrhage: a cause of aura-like symptoms
in the elderly. Cephalalgia 2008; 28: 658–663.

Field and Kleinig
2. Izenberg A, Aviv RI, Demaerschalk BM, et al. Crescendo
transient aura attacks: a transient ischaemic attack mimic
caused by focal subarachnoid haemorrhage. Stroke 2009;
40: 3725–3729.
3. Fisher CM. Late-life migraine accompaniments as a
cause of unexplained transient ischaemic attacks. Can
J Neurol Sci 1980; 7: 9–17.
4. Fisher CM. Late-life migraine accompaniments-further
experience. Stroke 1986; 17: 1033–1042.
5. Greenberg SM, Vonsattel JP, Stakes JW, Gruber M and
Finklestein SP. The clinical spectrum of cerebral amyloid
angiopathy: presentations without lobar haemorrhage.
Neurology 1993; 43: 2073–2079.
6. Vernooij MW, Ikram MA, Hofman A, Krestin GP,
Breteler MM and Van Der Lugt A. Superficial
siderosis in the general population. Neurology 2009; 73:
202–205.
7. Kumar S, Goddeau RP, Selim MH, et al. Atraumatic
convexal subarachnoid haemorrhage: Clinical presentation, imaging patterns and etiologies. Neurology 2010;
74: 893–899.
8. Cuvinciuc V, Viguier A, Calviere L, et al. Isolated acute
nontraumatic cortical subarachnoid haemorrhage. Am
J Neuroradiol 2010; 00: 1–8.
9. Mitchell P, Wilkinson ID, Hoggard N, et al. Detection of
subarachnoid haemorrhage with magnetic resonance
imaging. J Neurol Neurosurg Psychiatry 2001; 70:
205–211.
10. Patel KC and Finelli PF. Nonaneurysmal convexity
subarachnoid haemorrhage. Neurocrit Care 2006; 4:
229–233.

371
11. Knudsen KA, Rosand J, Karluk D and Greenberg SM.
Clinical diagnosis of cerebral amyloid angiopathy:
validation of the Boston criteria. Neurology 2001; 56:
537–539.
12. Bousser MG, Chiras J, Bories J and Castaigne P.
Cerebral venous thrombosis-a review of 38 cases. Stroke
1985; 16: 199–213.
13. Chang DI, Yoon SS and Chung KC. Superior sagittal
sinus thrombosis and transient ischaemic attacks: possible mechanism. J Korean Med Sci 1998; 13: 566–568.
14. Rogers RL, Meyer JS, Mortel KF, Mahurin RK and
Thornby J. Age-related reductions in cerebral vasomotor
reactivity and the law of initial value: a 4-year prospective
longitudinal study. J Cereb Blood Flow Metab 1985; 5(1):
79–85.
15. Riecker A, Grodd W, Klose U, et al. Relation between
regional functional MRI activation and vascular reactivity to carbon dioxide during normal aging. J Cereb Blood
Flow Metab 2003; 23(5): 565–573.
16. Dreier JP, Ebert N, Priller J, et al. Products of haemolysis
in the subarachnoid space inducing spreading ischaemia
in the cortex and focal necrosis in rats: a model for
delayed ischaemic neurological deficits after subarachnoid haemorrhage? J Neurosurg 2000; 93: 658–666.
17. Dreier JP, Woitzik J, Fabricius M, et al. Delayed ischaemic neurological deficits after subarachnoid haemorrhage
are associated with clusters of spreading depolarisations.
Brain 2006; 129: 3224–3237.