British Journal of Neurosurgery (1989) 3 , 225-228

SHORT REPORT

Acute Spontaneous Subdural Haematoma of Arterial Origin
GEORGE STEPHENSON 8i R. MYLES GIBSON
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Department of Neurosurgery, The General Infirmary, Leeds, United Kingdom

Abstract
Spontaneous arterial subdural haematoma is arguably a rare condition. We report on three patients who presented with
progressive neurological deficit or coma and who had been initially diagnosed as strokes. Explanations for the
development of this condition are reviewed and it is suggested that it is not as rare as previously thought.

Key words: Arterial origin, subdural haematoma, Sylvian jissure.

Introduction

Sudden alteration of consciousness or development of neurological deficit in a previously
healthy patient is commonly associated with a
cerebrovascular event. Acute subdural haematoma is well known in head injured patients in
association with traumatic laceration or contusion of the brain and tearing of bridging veins
in the subdural space. Less frequent but well
recognised is the acute subdural haematoma in
the presence of cerebral aneurysm, arteriovenous malformation or coagulopathy. Less appreciated is the spontaneous variety associated
with arterial rupture.
Here we add three further cases of spontaneous arterial subdural haematoma to the 20
cases so far reported in the literature.
Case 1

A previously well, 64-year-old male patient
developed sudden severe headache while waiting to be served at his local bank. He sat down
and subsequently collapsed on the floor. Witnesses thought he had a convulsion. He was
taken to the casualty department of his local

hospital where he was found to be cyanosed
and unresponsive to deep pain. His reflexes
were brisk and his plantars upgoing. There was
no external evidence of trauma to the head and
his BP was recorded as 145/100 mmHg. He
had no papilloedema or retinal haemorhages on
fundoscopy. He was admitted to the medical
unit with a diagnosis of subarachnoid haemorrhage. Routine blood investigations, coagulation screen, chest radiograph and ECG were all
reported as normal.
Three hours following admission he developed spontaneous extensor posturing and his
pupils became pin point and unreactive. A
computerised tomographic (CT) scan was
obtained which revealed a right sided subdural
haematoma with considerable midline shift
(Fig. 1). There were no associated brain
contusions or subarachnoid blood.
The patient was intubated and ventilated
without any paralysing agents being required
and transferred to the regional neurosurgical
unit.
At emergency craniotomy the dura was
found to be very adherent to bone. An
extensive subdural clot was evacuated to reveal

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George Stephenson & R. Myles Gibson
His condition deteriorated over the course of
the next 6 hours and he became unrousable. A
C T scan of the brain was obtained at this point
which showed a right sided subdural haematoma with midline shift but no other brain
injury.
He was transferred to the regional neurosurgical unit where an emergency craniotomy was
performed. The dura was very adherent to the
bone and the two were separated with the
utmost difficulty. A subdural clot was evacuated to reveal a small spurting artery in the
vicinity of the Sylvian fissure.
Postoperatively his hemiplegia rapidly resolved.
Case 3

A 66-year-old man, previously in good health,
was observed standing reading his paper in the
city railway station when he was seen to
collapse on the floor. He was taken to the local
FIG. 1. Case 1: CT scan showing R sided subdural Accident and Emergency department where he
haematoma with brain shift.
was found to be comatose with no response to
external stimuli and to have small fixed pupils.
a small bleeding cortical artery in the region of No evidence of head injury could be elicited
the Sylvian fissure. The rest of the brain and a skull radiograph revealed no fractures.
appeared normal and no contusions or vascular He was subsequently admitted to a general
malformations were noted.
medical ward with the diagnosis of a cerebroThe postoperative recovery was uneventful. vascular event. Three hours after admission his
The patient had a transient contralateral hemi- right pupil became fixed and dilated and a CT
paresis which resolved within days. Prior to scan was obtained. This showed an extensive
discharge 3 weeks later the patient underwent left parietal subdural haematoma with signififour vessel angiography which did not reveal cant midline shift. Despite the evacuation of
any abnormality.
this as well as postoperative ventilation on the
intensive care unit he succumbed 2 weeks
later. A necropsy was performed which showed
Case 2
the cause of his death to be a subdural
A 67-year-old male hospital inpatient awaiting haematoma which was arterial in origin. It was
myelography and suffering from polyarteritis assumed that this occured as a spontaneous
nodosa was found on the floor by his bed at 3 event as there was no associated brain laceraa.m. He was conscious and orientated but had tion or contusion suggestive of trauma and no
developed a left hemiparesis. He was not evidence of vascular malformation was found.
hypertensive and was taking prednisolone 10
mg per day. There was no sign of injury to his
Discussion
head and a skull radiograph did not show any
abnormality. It was thought that he had Most subdural haematomas are thought to be
suffered a stroke and neurological observations venous in origin, secondary to torn bridging
veins or venous sinuses. This view has been
were commenced.

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Spontaneous Subdural Haematoma

227

challenged by a number of authors who atheromatous plaque as a cause. There was no
propose that many acute and subacute trauma- history of trauma in any of our cases.
Vance" coined the phrase 'firehose rupture'
tic subdural haematomas are arterial in oriShenkid found 61.5% were of arterial after a series of post mortem examinations in
origin in his series of 39 traumatic subdural which he identified a cortical artery as the
haematomas.
source of bleeding. He postulated that these
Non-traumatic or spontaneous arterial sub- rents were found in surface cortical arteries
dural haematoma may result from aneurysmal where a twig came off at right angles which
or arteriovenous malformation rupture6,', may represented an area of potential weakness.
be secondary to turnours of the dura matere*gor O'Brien2 presented further histopathological
to Disseminated Intravascular Coagulation and evidence in support of the above hypothesis
showing microscopic deficiency in the wall of
other coagulopathies.
Spontaneous arterial subdural haematoma in the affected artery corresponding to the origin
the absence of the above conditions is a rarely in a small branch. Moreover he found no
reported event. Tokero et a l l o in a recent evidence of previous adhesions between the
paper have proposed certain criteria that dura and a cortical artery or of an arterial
should be fulfilled before this diagnosis can be knuckle of a surface artery protruding through
made. These are:
the arachnoid and adherent to the dura as
(a) there should be no history of head suggested by Drake.
Finally although hypertension was present
trauma;
in some of the reported cases it is thought not
(b) no damage to the underlying cortex;
(c) no aneurysm or arteriovenous malforma- to be an important predisposing factor12.
None of our cases was a known hypertensive
tion around the affected artery; and
(d) identification of a bleeding artery at but in Case 3 the post mortem examination
revealed changes in the heart consistent with
operation.
Thus, reviewing the reported cases in the chronic hypertension. In Cases 1 and 2 the
literature they concluded that only 20 could be dura was extremely adherent to the bone at
identified which satisfied these criteria. They craniotomy but no adhesions were noted bealso noted that there was a male preponderance tween the dura and cortical vessels.
The mortality from this condition as judged
(80%) and the average age was 56 years (range
37-80). Only eight of the 20 were known by the hitherto reported cases is around 50%.
hypertensives. Here we suggest a further three This closely approximates that of its traumatic
counterpart where the associated bruising and
cases for inclusion in the list.
All our patients were over 60 years old and laceration of the brain combined with the
all were male which is in keeping with resultant brain oedema soon lead to irreverpreviously published reports. In two cases an sible coma and tentorial herniation, whereas in
arterial source in the region of the Sylvian the spontaneous variety the absence of brain
fissure was found at operation and in our third oedema at the time of operation is a notable
case evidence of arterial bleeding was provided feature. One would expect the surgical treatby post mortem studies.
ment of spontaneous subdural haematoma
Several hypotheses have been put forward to from simple arterial rupture without associated
explain the development of these spontaneous brain injury to be more rewarding. The unexsubdural haematomas. Drake' in one of the pectedly high mortality must be in part attribuearlier reports argued that spontaneous arterial table to delay in recognition and prompt
rupture is impossible without some degree of surgical treatment, and in part to the well
trauma and suggests minor trauma that has recognised fact that the greatest surgical morgone unnoticed by the patient is responsible for tality in subdural haemorrhage occurs when
the haemorrhage. He also considered but the interval to coma is brief.
dismissed local arterial disease due to an
Talala & McKissock13 noted an ipsilateral

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228

George Stephenson Q R. Myles Gibson

hemiparesis in all eight patients in their series.
They attributed this to a supratentorial extraaxial mass causing compression of the contralateral pyramidal tracts against the tentorial
edge (Kernohan’s notch) in the absence of any
intra-axial mass effect. They concluded that
this constituted a clinical syndrome distinguishing the spontaneous subdural haematoma.
This has not been our experience with two of
our patients who had a hemiparesis.
The true incidence of non-traumatic subdural haematoma is not known at present. We
believe it is not as rare as the reports so far
have implied. We propose that this condition
be considered in the differential diagnosis of
the patient presenting with neurological deficit
of sudden onset in whom no signs of a vascular
aetiology such as previous hypertension, transient ischaemic attacks or myocardial infarction could be elicited. Features such as male
sex, age over 55 and neurological deterioration
should further alert one to the possibility of
this diagnosis and lead to early investigation by
computerised tomography scanning.

Address for correspondence: R. M. Gibson,
M.D., F.R.C.S., Consultant Neurosurgeon,
The General Infirmary at Leeds, Great George
Street, Leeds LS1 3EX, U.K.

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