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Year : 2001  |  Volume : 49  |  Issue : 1  |  Page : 3-10

Acute subdural haematoma : a reappraisal.

Department of Neurosurgery, Neuroscience Centre, All India Institute of Medical Sciences, New Delhi - 110029, India.

Correspondence Address:
Department of Neurosurgery, Neuroscience Centre, All India Institute of Medical Sciences, New Delhi - 110029, India.

  »  Abstract

Acute subdural haematoma is a well-entrenched nosological entity implying subdural collection of blood following acute head injury. Pathologically, it is usually associated with or, for that matter, secondary to cerebral contusion and laceration. Based on cumulated experience, clinical and pathological studies it is proposed that, for too long the neurosurgeons have put emphasis on the clot rather than the totality of the pathological anatomy and that they have focused their therapeutic strategy on removal of the accumulated blood, unmindful of the associated parenchymatous lesion. Not surprisingly, such attempts have been associated with a very high mortality. On the basis of nearly four decades of personal experience and critical review of the literature, evidence has been provided that to reduce the mortality associated with this condition, it is necessary to evolve a strategy, not only to evacuate the blood but comprehensively deal with the associated parenchymatous lesions and the cascade of secondary insult to the underlying brain.

How to cite this article:
Tandon P N. Acute subdural haematoma : a reappraisal. Neurol India 2001;49:3-10

How to cite this URL:
Tandon P N. Acute subdural haematoma : a reappraisal. Neurol India [serial online] 2001 [cited 2023 Mar 25];49:3-10. Available from: https://www.neurologyindia.com/text.asp?2001/49/1/3/1309

'Words have crept into the medical vocabulary and
have often been retained long after the ideas for which
they stood have been refuted'. (Raymond Adams)
Nosologically a correct term, acute subdural
haematoma (ASDH), which is generally the tip of an
ice berg, has misled a generation of neurosurgeons in
evolving an appropriate management. Based on the
corollary of extradural haematoma, the 'logical'
treatment of this lesion was considered to be burr-hole
evacuation of the clot. If one uses the borrowed
expression from Adams, this label 'embalmed' a
fallacious theory.[1] It is not surprising therefore, that
Klun and Fettich[2] in a review of the largest series of
ASDH called it as one of the 'unsolved problems of
neurosurgery'. Much fatalistic nihilism developed
over this problem as mortality rates of 80 - 90 percent
were reported.[3],[4],[5],[6],[7],[8],[9] Many neurosurgeons doubted the
utility of surgery, specially within the first hours of
Pathophysiological Considerations :
ASDH and Cerebral Contusion
Following a review of approximately 3000 cases of
head injury, among which all fatal cases were
submitted to autopsy, Kristiansen and Tandon,12 in
1960 concluded that acute subdural haematoma is
seldom an isolated lesion. It was pointed out that, 'the
pathogenesis of subdural haemorrhage makes it nearly
inevitable that a small contusion in the pathological
sense is co-existent'. And further more, '.......there are
patients in whom the extensive associated contusion
and laceration may be the dominant feature, the SDH
only a relatively unimportant co-existent pathological
finding. In between these two grades are cases in
which the two lesions are independently significant
and add to the severity of each other'. This study had
also revealed that a thin layer of subdural blood was
consistently seen in association with traumatic
intracerebral haematoma which, from a pathological
stand point, was difficult to differentiate from cerebral
contusion with haemorrhage. Thus, in many patients
the cerebral contusion/laceration may, on one hand be
associated with a layer of subdural clot and on the
other, extend into the brain parenchyma to manifest as
an intracerebral haematoma. However, many
neurosurgeons at that time, (and even today) were
primarily concerned with removing the subdural clot
through multiple burr-holes and lamented about the
high fatality rates among these patients.
Mc Laurin and Tutor,[13] unaware of our observations
commented that, 'those patients in whom subdural
collections develop and who expire within first few
days, undoubtedly do so because of associated
cerebral damage.' They could not find any case at
autopsy 'which disclosed only venous rupture without
accompanying parenchymal injury'. They concluded
that, 'the neurological picture was primarily, if not
completely the result of associated direct brain
damage'. Courville and Blomquist,[14] in their autopsy
study on traumatic intracerebral haemorrhage had
already documented this. Jamieson and Yelland,[15] in a
study of 553 cases of traumatic SDH subdivided these
into simple SDH, SDH with contusion, and
complicated haematomas. The last category was
observed after severe acceleration-deceleration and
carried the highest mortality rates.
Richard and Hoff[16] described gross disruption of the
brain underlying the haematoma in 61% of the fatal
cases of ASDH. Britt and Hamilton[17] found massive
cerebral oedema or extensive contusion at necropsy in
the majority of their cases of ASDH. Adams et al,[18]
summarising their years of clinical and pathological
studies, concluded that 'the intradural haematomas
comprise 'pure' subdural haematomas caused by the
tearing of bridging veins in the subdural space, 'burst'
lobes (intracerebral and subdural haematomas in
continuity) and intracerebral haematomas (mainly in
the frontal and temporal lobes in relation to
contusion). Jennett and Teasdale[19] observed that the
relative contribution of the subdural and intracerebral
components vary, but there is a sizeable subdural
haematoma in most of the cases.
Based on aetiopathogenesis, Miller and Statham20
classified ASDH into three types: i) haematoma
associated with laceration of the brain, usually at
temporal pole, in which there is a mixture of
intracerebral contusion and haemorrhage and an acute
subdural haematoma, a condition known by some
neurosurgeons as 'burst temporal lobe'; ii) ASDH that
results from tearing of a bridging vein between the
surface of the brain and one of the main venous
sinuses; iii) haematoma due to bleeding from a small
artery on the surface of the brain that may have been
injured by an overlying fracture of the skull.
Amongst 5000 cases of head injury which included
209 cases of extradural haematoma, 257 cases of
temporal lobe lesions acting as expanding mass, there
were only 25 cases with ASDH without any detectable
parenchymatous lesion. The possibility of the
associated parenchymatous lesion, having been
overlooked at surgery cannot be ruled out, since many
patients in this series belonged to pre-CT era and not
all fatal cases had autopsy.[1] The significance of the
associated brain lesions in patients with ASDH is now
being generally recognized. The availability of CT
scan has been greatly responsible for establishing this
fact. In a series of 109 consecutive head injured
patients with the CT scan diagnosis of ASDH, there
were only 8 cases with pure ASDH, 49 patients had
contusion, while others had extradural haematoma,
intracerebral haematoma, subarachnoid haemorrhage
and brain swelling.[21] Wilberger et al[22] concluded that
the patho-physiological evidence supports the belief
that in ASDH 'the extent of primary underlying brain
injury is more important than the subdural clot itself,
in dictating the outcome'. Most other authors[23],[24],[25],[26]
found mortality and morbidity related to the extent of
underlying brain damage rather than the extent of the
subdural blood clot. Yet, till very recently, the surgical
attention was primarily directed to the removal of
compression due to the surface blood clot.
In view of the above, it could be safely concluded that
while a 'simple' ASDH due to tearing of the bridging
vein/veins without concomitant or associated cerebral
pathology, no doubt exists, it is a rarity than a rule.
Thus, in a vast majority of such cases, the
aetiopathogenesis, clinical picture and prognosis
cannot be explained simply on the basis of a surface
clot producing focal compression of the brain.
Acute subdural haematoma and
diffuse axonal injury
While cerebral contusion, laceration or intracerebral
haemorrhage are obvious on CT scans and to the
naked eye at operation or autopsy, diffuse axonal
injury (DAI), which may occasionally be suspected on
the basis of CT findings, can only be observed in
carefully conducted pathological studies. The
significance of this lesion in the clinical
manifestations and outcome of patients with ASDH
has, therefore, not received due attention. Considering
the biomechanism of both DAI and ASDH, both being
caused by rotational acceleration/deceleration, the coexistence
of the two is not unexpected. Infact, Adams
et al[18] and Gennarelli et al[27],[28] reported that 11% of
all patients with DAI have associated intracranial
haematomas. A detailed study of six fatal cases of
ASDH by Sahuquillo-Barris et al[29] revealed
widespread evidence of DAI in all. These authors
concluded that 'in some patients with a head injury,
acute SDH may be only an epiphenomenona of a
primary impact lesion of variable severity; that is a
diffuse axonal injury. In these cases, the final outcome
is fundamentally dependent on the severity of the
subjacent diffuse axonal injury'. It is, therefore,
understandable that the patients with ASDH who
remain unconscious from the moment of head injury,
as many do, clinically reflect the severity of this
primary damage rather than the compressive effect of
any associated subdural blood.
Acute subdural haematoma and
ischaemic neural damage
Ischaemic brain damage is the commonest
neuropathological abnormality found in patients, who
die of ASDH.[30] The pathological observations of
ischaemic brain damage in fatal head injury
patients,[31],[32],[33] angiographic evidence of cerebral
vasospasm in patients with severe head injury[34] and
post-traumatic temporal lobe lesions35 (generally
associated with overlying subdural blood), failed to
attract due attention of the neurotraumatologists. The
latter, in search for a cause for brain swelling, seem to
have been, preoccupied with the concept of 'luxury
perfusion'.[36],[37],[38],[39] More recently, studies on experimental
model of ASDH in rats have unequivocally
established the development of ischaemic brain
damage underlying the subdural blood.[40],[46] The
possibility of some 'species difference' in this
response has been pointed out by Shaver et al,[42] who
observed extensive areas of the white matter necrosis
under the haematoma in an infant piglet model of
ASDH. Zones of necrosis were also present in the
cortex though much less than in the rodent model.
While the precise mechanism by which ASDH causes
underlying brain ischaemia remains uncertain, there is
evidence to suggest that neither focal nor generalised
increased intracranial pressure could adequately
explain the condition. The possibility of direct effect
of some vasoactive substances released by the blood
clot, being responsible for the ischaemia, seems
attractive.[44] This finds confirmation in the
experimental studies by Chen et al.[30] Using
microdialysis techniques, they had demonstrated that
ASDH was associated with massive release of
glutamate, to six times the normal levels, for 20
minutes in the underlying cortex. They demonstrated
54 percent reduction in the ischaemic damage in
animals pretreated with a glutamate antagonist. This
was confirmed by Bullock et al[45] and Kuroda et al,[46]
who found profound increase in the levels of
extracellular excitatory aminoacids (EAA) within the
ischaemic zone under the SDH. They postulated that
the EAA induced increase in local cerebral glucose
utilization resulted in a breakdown of the metabolism
and cerebral blood flow coupling. Inglis et al[47] had
earlier demonstrated reduction of ischaemic brain
damage associated with tissue hypermetabolism in
ASDH following use of a glutamate antagonist.
It is important to note that Kuroda and Bullock[40]
failed to observe any significant effect on the
underlying area of cerebral ischaemia following
removal of the subdural blood in their rodent model of
ASDH. They hypothesised that clotted blood, in
contact with the cortical surface, initiates 'this focal
progression of ischaemia and oedema, which is not
reversed by removal of the haematoma...'. Duhaime et
al,[41] in a well planned experiment to elucidate the
relative role of increased pressure, vasoactive effects
or toxicity of the blood itself, concluded that blood in
prolonged contact with the cortical surface in the
absence of an increased pressure, ischaemia, or other
insults is insufficient to cause underlying infarction.
Schroder et al48 documented reversal of ischaemia
immediately after removal of an ASDH in two
patients. However, they believed that compression of
the microcirculation could be responsible for the
A more recent CT study on ASDH on 31 patients by
Domenicucci et al[49] provides an interesting angle to
this whole issue. Amongst these 31 patients, they
identified a group of 5, whose preoperative CT scans
showed intact subarachnoid space underlying the
haematoma and absence of blood in the cerebrospinal
fluid, though all of them had appreciable midline shift.
They classified these five cases as 'intradural'
haematoma and recorded a mortality of only 20% as
compared to the overall mortality of 68% for the
whole series. They considered the good result in these
patients with undamaged arachnoid barrier to be due
to the shielding of the cortex from the neurotoxic and
vasoactive substances preventing the 'ischaemic and
oedemigenic' response in the brain tissue.
It is known that such vasoactive and neurotoxic
substances are released not only by the subarachnoid
and subdural blood but also by the brain damaged by
an impact injury or ischaemia-induced by
hypoperfusion and hypotension occurring at the time
of injury. The relative contribution of each one of
these mechanisms in initiating and maintaining the
vicious cycle of increasing brain damage and oedema,
so commonly associated with ASDHS, is difficult to
Acute SDH and brain swelling
One of the least understood and most devastating
features of ASDH is the associated brain swelling
which frequently acquires malignant proportion
following evacuation of the haematoma. Among 178
patients with ASDH, Zumkeller et al,[50] recorded a
mortality of 50% when midline shift exceeded the
thickness of haematoma by 3 mm in the CT scan.
However, if the midline shift exceeded haematoma
thickness by 5 mm, the survival rate was only 25%. At
surgery itself, often quite unpredictably, the brain
herniates through the craniotomy following
evacuation of the clot, making dural closure
impossible. In some cases, a post-operative CT scan
shows cerebral hemispheric enlargement, with
persistent or even increased midline shift in absence
of any residual haematoma. The increased intracranial
pressure and the progressive downhill course,
unresponsive to the routine antioedema measures,
ends in a fatal outcome in nearly 70-80 percent of
such patients.[51] Britt and Hamilton17 found 'massive
cerebral oedema or extensive contusion' at necropsy
in the majority of their cases of ASDH. While this
phenomenon is not unknown following evacuation of
extradural haematomas, it is far more frequent in cases
of ASDH.[52],[53] Thus, Lanksch et al[54] found cerebral
oedema in 8% of 118 patients with extradural
haematoma as compared to 26% of 168 patients with
The long standing controversy regarding its
nomenclature - brain oedema versus brain swelling,
and its pathophysiology - vascular hyperperfusion
versus angiogenic or cytotoxic oedema, has not yet
been unambiguously resolved. Unilateral cerebral
swelling of an entire hemisphere, not specifically
attributable to contusion, intracerebral haematoma or
infarction was observed in 17 of 151 patients of
ASDH.[18] Its aetiopathogenesis continues to be illunderstood.
It is, therefore, not surprising that its
management remains a dismal chapter in
neurotraumatology. Considering the voluminous
amount of literature on the subject, no attempt will be
made to discuss it in any details. However, a brief
reference to some of the studies will justify the above
statements. In a series of experiments on ASDH,
which included measurements of brain tissue water,
blood-brain barrier studies with labelled sucrose and
electron microscopy observations, Gennarelli[55] failed
to find evidence of cerebral oedema in the swollen
brain. He attributed it to increased cerebral blood
volume as had already been suggested by Langfitt et
al[52] from their experimental studies and Bruce et al[38]
from the clinical data of patients with so-called
syndrome of 'malignant brain oedema'. On the other
hand, Tornheim and McLaurin,[56] in their
experimental studies, Galbraith et al[57] from
measurement of water content of white matter after
head injury in man and Yoshino et al,[58] following
dynamic CT studies in fatal head injury patients
concluded that acute oedema formation is a common
cause of brain swelling in cases of fatal head injury.
Kuroda and Bullock,[40] measured local cerebral blood
flow, before and after removal of ASDH in the rat led,
and conclude that focal ischaemic and oedema rather
than vascular engorgement or hyperaemia was the
major cause of hemispheric swelling, seen after
removal of haematoma.
It is true that cerebral circulatory disturbances are far
more common in patients with severe head injury than
is generally recognized. Earlier cerebral blood flow
(CBF) studies[36],[37],[38],[39] highlighted the incidence of
vasoparalysis leading to hyperaemia or 'luxury
perfusion' resulting in brain swelling. More recent
studies[40],[59],[60] established the high incidence of
impaired CBF, decoupling of CBF and metabolism,
failure of autoregulation, resulting in cerebral
ischaemia and infarction with consequent brain
oedema. The role of local pressure by the haematoma
and the release of vasoactive and cytotoxic substances
in this process, have already been described above.
Effects of compression by experimental intracranial
mass lesions on cerebral blood flow have been
elucidated by Jakobsson et al.[61],[62] A resolution of this
controversy is not just of an academic interest but has
direct bearing on the therapeutic management of these
patients. The currently recommended 'aggressive
treatment' of all severe head injury patients which
includes artificial respiration, high doses of
corticosteroids, intravenous mannitol, and even use of
barbiturates,63-66 not unexpectedly failed to reduce
the mortality drastically.[67],[68]
In more recent years, attention has been directed to
elucidate the molecular mechanisms underlying these
secondary 'autodestructive' processes. Excitotoxic
substances like glutamate and aspartate,[30[,[69],[70],[71] free
radicals,[72],[73] and platelet activating factor[74] have been
implicated. A cascade of events initiated by the
primary traumatic event is complicated by secondary
events of local and generalised increase in intracranial
pressure, abnormalities of cerebral perfusion and
ischaemia. These are undoubtedly overlapping events
as also self perpetuating vicious circles. Removal of
the subdural blood is, thus, only one and not
necessarily the most important component of any
therapeutic strategy aimed at reducing the currently
unacceptable mortality rates of ASDH, which remain
50 per cent or above.
Timing of surgery
A very high mortality associated with surgery for
ASDH, as mentioned earlier, prompted a number of
neurosurgeons to delay operations on such patients.
Futility of operating within 24 hours was a common
refrain till 1970s. A landmark paper by Seeling et al[75]
claimed a dramatic reduction in mortality to 30%, if
the subdural haematoma was evacuated within 4 hours
of injury, as compared to a mortality rate of 85%, if
the operation was delayed. Inspite of very concerted
efforts on the part of others, in achieving this 4 hour
target, there has been no clear confirmation of such
excellent results in the management of ASDH. Stone
et al[76] while claiming that direct admission to a
trauma centre yielded improved results, failed to find
any difference in mortality between patients operated
upon within 4 hours and those undergoing surgery
after 4 hours from injury. In a selected group of
patients of ASDH with admission GCS scores of 11 to
15, Croce et al[77] found no correlation between timing
of surgery and neurologic outcome. In contrast to this,
Dent et al[78] reported an unselected series of 211
patients of ASDH (GCS 3 to 15), 83 of whom were
managed with craniotomy (average GCS 7,8). Thirty
five percent of operated patients had their haematoma,
evacuated within 4 hours and 65% after 4 hours. Early
operated patients had a significantly lower incidence
of functional survival (early 24% v.s. delayed 51%).
Hatashita et al,[83] in their series of 60 patients with
ASDH observed a mortality of 62% for patients with
GCS scores of 4-6 operated within 4 hours, in contrast
to 33% for those operated upon from 4 to 10 hours. All
patients with GCS of 3 died while all patients with
GCS of 7 or more achieved functional recovery.
Wilberger et al[22] recorded a mortality rate of 59% for
patients operated on within 4 hours as compared to
69% for those operated on after 4 hours. However,
they observed that 'the results do not support the
crucial role of the timing of operative intervention
established by Seeling et al,[75] in 1981'.
While the debate regarding the benefits of early
surgery (within 4 hours) continues unabated, it is
generally agreed now that denial of operation during
the first 24 hours or delaying surgery in the hope of
improving the outcome has no basis at all. As
advocated by us earlier, we believe that surgery should
be performed as early as possible, specially in patients
with GCS of 8 or below, with more than five
millimeter shift of midline, without waiting for
deterioration in the clinical condition or rise of
intracranial pressure. Failure to observe progressive
improvement and not evidence of deterioration is in
itself an indication for surgery.[1]
Type of surgery
Believing the subdural clot to be the real culprit
responsible for the clinical condition of the patient,
the standard surgical procedure advocated in earlier
years was to deal with it through burr-hole evacuation.
This not only proved to be futile in majority of cases,
it also prevented the surgeon from appreciating the
associated brain lesions required to be attended to.
Classifying patients with ASDH with contusion as a
distinct entity already in 1960, we advocated, 'in the
management of these cases, attention must be paid to
both components of the lesion'. It was recommended
that 'severely damaged and lacerated tissue may be
sucked away and bleeding points cliped or
coagulated'. It was recognized that while burr-hole
evacuation was adequate for 'uncomplicated subdural
haematomas', larger opening was required to deal
with ASDH with contusion since there was a higher
frequency of clotted and mixed haematomas, which
are not easy to remove through a single burr-hole. In
addition, burr-holes did not permit adequate attention
to the underlying damaged brain.[12] Increasing
recognition of this problem made us abandon the
policy of using burr-hole evacuation for all cases of
ASDH (as also for patients with pulped
temporal/frontal lobes) and routinely use, either an
osteoplastic craniotomy or a large Scoville trephine.
This brought down our overall mortality for such
patients to 43%.[35] Following this practice, it was only
a rare occasion when we had to face the problem of
dural closure. This is now the generally accepted
policy, since several studies have confirmed improved
prognosis following craniotomy as compared to burrhole
The frequent occurrence of severe brain swelling, and
raised intracranial pressure unresponsive to standard
therapy prompted many surgeons to recommend
bifrontal or hemicranial removal of bone.[84],[85]
Phuenpatham et al[21] found removal of bone essential
in 28 out of 83 patients owing to brain bulging out
through the craniotomy opening, making the standard
closure impossible. Zumkeller et al[50] while favouring
craniotomy for evacuation of haematoma reserved
craniectomy for massive brain swelling. Rosenorn and
Gjerris[9] failed to find any difference in prognosis for
the different surgical treatments. Fell et al,[7] in their
series of 144 patients with ASDH, found no difference
in mortality between patients treated with multiple
burr-holes and subtemporal craniectomy (41 percent)
and large craniotomies (45 per cent).

   »   Conclusions Top

On the basis of the current knowledge, it is reasonable
to conclude the following
i) Isolated ASDH, acting as a compressive lesion, is
an uncommon clinicopathological entity.
ii) Majority of patients with ASDH have associated
focal (contusion / laceration / intracerebral
haematoma) or global (diffuse axonal injury,
subarachnoid haemorrhage) involvement of the
brain or both of these.
iii) In addition, ischaemia underlying the haematoma
and ipsilateral hemispherical brain swelling (?
hyperaemic, ? oedematous), which may be self
perpetuating, are consistent findings in most
patients with surgically significant haematoma.
iv) A combination of these factors, if not attended to
promptly, may lead to uncontrollable rise in
intracranial pressure with its adverse
consequences including foraminal herniations,
brainstem compression and haemorrhages.
v) The molecular basis underlying the cascades of
events, resulting in secondary damage, are now
better elucidated and understood.
vi) It is now established that even with successful
and early evacuation of the clot and the current
aggressive intensive care management, the
mortality still remains high, (50% or above).
Functional survival is even much lower. Some of
the routinely used ICU practices not only fail to
arrest or reverse the secondary changes, but may
aggravate the same.
vii) The future hope for further reduction in
morbidity and mortality lies in preventing,
arresting or reverting the molecular events
responsible for the secondary ischaemia and
cytotoxic oedema.
viii) It is obvious that the term ASDH does not reflect
the true pathology or pathogenesis of the lesion/s
determining the clinical picture or outcome.
ix) It is felt that this term has outlived its utility in
determining the appropriate therapeutic strategy.
However, realising the difficulty of abolishing a
long standing term, it is recommended that it
could be subclassified as SDH with or without
associated parenchymatous pathology which can
be established preoperatively with the current
diagnostic modalities. This would help to shift
the focus of attention from the haematoma to the
brain itself and permit better comparison of
different therapeutic modalities.

  »   References Top

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2.Klun B, Fettich M : Factors influencing the outcome in acute subdural haematoma. Acta Neurochirurg1984; 71 : 171-178.  Back to cited text no. 2    
3.Echlin FA, Sordillo SVR, Garvey TQ Jr : Acute, subacute and chronic subdural haematoma. J Amer Med Assoc 1956; 161: 1345-1350.  Back to cited text no. 3    
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5.McKissock W, Richardson A, Bloom WH : Subdural haematoma: A review of 389 cases. Lancet 1960; 1 : 1365-1369.  Back to cited text no. 5    
6.Ramamurthi B : Acute subdural haematoma. In : Handbook of clinical neurology : Injuries of the brain and skull. Vinken PJ, Bruyn GM (eds). North Holland Publishing Company Amsterdam. 1976; 275.  Back to cited text no. 6    
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9.Rosenorn J, Gjerris F : Long term review of patients with acute and subacute subdural haematomas. J Neurosurg 1978; 48 : 345-349.  Back to cited text no. 9    
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11.Vigouroux RP, Guillermain P : Post-traumatic hemisphere contusion and laceration. In : Progress in neurological surgery. Krayenbuhl H, Maspco PE, Sweet WH (eds). Vol. 10, Krager, Basel. 1981; 49-163.   Back to cited text no. 11    
12.Kristiansen K, Tandon PN : Diagnosis and surgical treatment of severe cranio cerebral injuries. J Oslo City Hosp (Supl.) 1960; 10 : 107-213.  Back to cited text no. 12    
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16.Richard T, Hoff J : Factors affecting survival from acute subdural haematoma. Surgery 1974; 75 : 253-258.  Back to cited text no. 16    
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18.Adams JH, Gennarelli TA, Graham DI : Brain damage in non missile head injury. Observations in man and subhuman primates. In : Recent advances in neuropathology. Smith WT, Cavanagh JB (eds). Churchill Livingstone Edinburgh. London, New York. 1982; 165-190.  Back to cited text no. 18    
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