NEUROSURGERY
Management of stroke
C
atia Gradil
Manuel Cunha e Sa
Abstract
Stroke continues to be associated with high mortality and disability rates,
posing a great burden on society.
Recognition and modulation of stroke risk factors have allowed its
management to evolve from rehabilitation to prevention.
Maximizing the benefit of acute thrombolysis imposes a more efficient
practice. Multiple studies have addressed the role of decompressive cra-
niectomy, revascularization, recanalization, carotid stenosis treatment,
haematoma evacuation, the role of intraventricular thrombolysis and
the use of minimally invasive techniques in stroke treatment. Although
some techniques have been proven beneficial, others are still in need
of properly designed trials to assess their impact in stroke outcomes.
Keywords Craniectomy; endarterectomy; haemorrhagic; ischaemic; stroke
Introduction
Incidence and burden
Cardiovascular disease continues to rank highest in population-
based mortality indicators on the impact on society of any spe-
cific disease. Performances such as years of life lost measured in
the UK in 2010, where stroke ranked third only to ischaemic
heart disease and lung cancer, reflect the magnitude of the
burden of this preventable disease.1
The Global Burden of Diseases, Injuries and Risk Factors Study
2010 found stroke to be the world’s second most common cause of
death. From 1990 to 2010, the age-standardized incidence of stroke
significantly decreased by 12% in high-income countries and ap-
pears to have shown an increasing trend in low-income countries.
In 2010, the absolute number of people with a first stroke (16.9
million), stroke survivors (33 million), stroke-related deaths (5.9
million) and disability adjusted life-years lost (102 million) had
significantly increased since 1990, with most of the burden origi-
nating from low-income and middle-income countries.2
Stroke units
‘Time Is Brain’:
“Compared with the normal rate of neuron loss in the ageing
brain, the ischemic brain ages 3.6 years each hour without
treatment.”3
Multidisciplinary care within dedicated stroke units is known
to reduce mortality and disability independently of age, sex and
stroke severity.
tia Gradil MD is an SpR in Neurosurgery at the The National Hospital
Ca
for Neurology and Neurosurgery, London, UK. Conflict of interest: none
declared.
Manuel Cunha e Sa  MD is Head of the Department of Neurosurgery at
Hospital Garcia de Orta, Almada, Portugal. Conflict of interest: none
declared.
SURGERY 33:8
With the introduction of reperfusion therapy, stroke man-
agement has evolved from rehabilitation to emergent, posing
greater attention on shortening pre-hospital delay. Accurate
clinical recognition reinforcing public awareness and medical
staff training, rapid means of transport to designated stroke
centres and bridging therapies initiated on site with a mobile
stroke unit concept could significantly increase the dismaying
only 8% of patients who are currently eligible for intravenous
thrombolytic treatment.
A New York state-wide large observational study comparing
mortality for patients admitted with acute ischaemic stroke at
designated stroke centres and non-designated hospitals, found
the former carried lower 30-day all-cause mortality, reduced 1-
day and 1-year follow-up stroke-specific mortality and allowed
for a higher rate of thrombolytic therapy.4
In 2010, a metropolitan, centralized model with a small
number of high-volume specialist centres for acute stroke man-
agement capable of providing hyper-acute care in the first 72
hours was introduced in London. This concept appears to have
increased the rate of intravenous thrombolysis treatment from
5% to 12% of all stroke patients, reduced fatality while
decreasing the 90-day cost per patient, predominantly as a result
of shorter length of hospital stay.5
Primary prevention
Modifiable risk factors
Ischaemic stroke is a known preventable cause of disability and
death.
Realizing that three-quarters of all strokes are first-time
events, understanding the natural history of such devastating
disease and appreciating the entailed individual and global public
health burden reinforce primary prevention with modulation of
risk factors. Risk factor assessment tools predictive of stroke
have been developed, and although consensually helpful, none
are without inherent limitations in predicting the multivariate
influence of contributors. Ageing, black ethnicity and genetic
influence are accountable for non-modifiable factors contributing
to cerebrovascular events. Transient ischaemic attack is widely
regarded as a sign of impending stroke; as such, its occurrence
must be regarded as an opportunity for stroke prevention.
On the other hand, lifestyle modification with physical activity
and a healthy diet have acknowledged direct benefit and are
recommended to all individuals; weight reduction is indicated
when body mass index (BMI) is above 25 kg/m2.
In 2010, the two leading risk factors for global disease burden
were high blood pressure and tobacco smoking. In hypertensive
patients medication should target blood pressure values to under
140/90 mmHg, an aim which holds true amongst diabetics.
Smoking should be strongly discouraged and alcohol consump-
tion should be eliminated or reduced; drug abuse, particularly
cocaine and amphetamines, should be ceased and its addiction
treated accordingly.
Asymptomatic stenosis
The prevalence of severe asymptomatic carotid stenosis may be
as high as 3%.6
Multiple studies have established the relationship between
atherosclerotic disease of the extracranial internal carotid,
400 Ó 2015 Published by Elsevier Ltd.
 NEUROSURGERY

carotid bulb and vertebral arteries and both transient cerebro- to CAS, although in certain younger patient subgroups might be
vascular ischaemia and stroke. equivalent.
Not forgetful of the protective roles of intracranial collateral
circulation through a fully developed circle of Willis and the Types of stroke and their management
presence of leptomeningeal supply, contributive mechanisms of
Cerebral
carotid atherosclerotic disease to ischaemic events include:
Ischaemic: stroke should be considered in the presence of an
artery-to-artery embolism of thrombus originated within the
acute neurologic deficit or altered level of consciousness. Com-
plaque; plaque rupture with acute occlusion; atheroembolism of
mon clinical presentation may course with nausea, vomiting or
crystals; and the recognition of a degree of stenosis beyond
headache and include abrupt onset of facial, mono- or hemi-
which there is a pressure drop, a flow reduction, or both, with
paresis, hemisensory deficit, mono- or bi-nocular visual loss,
resulting reduced cerebral perfusion; stenosis 60% or higher are
visual field defect, aphasia or dysarthria.
estimated to carry such haemodynamic burden.
Physical examination aims to: detect extracranial causes of
Currently there is no indication to screen the general popu-
stroke symptoms; distinguish stroke from stroke mimics (found
lation. There are even those who argue against identifying ca-
in 19e30%); document degree of deficit for adequate follow-up
rotid stenosis in those with no prior history of anterior territory
commonly using the National Institutes of Health Stroke Scale
transient attack or stroke.
(NIHSS); establish a topographic diagnosis; identify comorbid-
ities such as polycythaemia rubra vera, thrombotic thrombocy-
Management
topenic purpura, coagulopathies, heavy protein diseases, and
any conditions that may influence treatment decisions.
Carotid endarterectomy: although preceded by many retro-
In 1991, the Oxfordshire Community Stroke Project (OCSP) pro-
spective and observational studies, the existing guidelines on
posed a classification into four subtypes of cerebral infarction
management of asymptomatic carotid artery stenosis arose
capable of predicting prognosis, based solely on presenting signs
originally from the Asymptomatic Carotid Atherosclerosis Study
and symptoms.13 The Trial of Org 10172 in Acute Stroke Treatment
(ACAS) published in 1995. This controlled clinical trial randomly
(TOAST) method was develop to classify ischaemic stroke into
assigned patients with asymptomatic carotid stenosis of 60% or
specific subtypes based on the mechanism of infarction14 e Table 1.
higher (NASCET method) to either the association of aspirin (the
Emergent non-contrast CT scan is essential when considering the
role of newer antiplatelet drugs was not yet proven) and risk
diagnosis of stroke and to rule out the presence of haemorrhage.
factor control (limited to blood pressure and diabetes) or the
Ischaemic stroke courses with focal cerebral hypoperfusion of
above in association with carotid endarterectomy (CEA). The end
the affected vascular territory. Most importantly, perfusion pa-
points were perioperative stroke or death and ipsilateral
rameters can be used to differentiate irreversible, infarct core
ischaemia thereafter. The trial ended before completion with an
from ischaemic penumbra, an area with enough hypoperfusion
advantage of the CEA group, yielding an aggregate risk over 5
to cause neuronal dysfunction but still salvageable if blood
years for ipsilateral stroke and any perioperative stroke or death,
supply is promptly restored with targeted treatment. Currently,
estimated in 5.1% in the surgical versus 11% in the medically
CT perfusion (CTP) and MR perfusion (MRP) are two perfusion
only treated group (RR reduction of 53%). The calculated
approaches with good application, with the former holding the
perioperative stroke morbidity and overall mortality was 2.3%.7
advantage of rapidity and accessibility in the emergency setting.
Published in 2004, the Medical Research Council of Great
Perfusion-weighted image (PWI) was thought to represent
Britain Asymptomatic Carotid Surgery Trial (ACST) randomized
ischaemic penumbra, whereas DWI-lesions identified the
asymptomatic patients with carotid artery stenosis of 70% or
ischaemic core, with the resulting PWI/DWI mismatch repre-
higher to immediate CEA versus indefinite deferral of the pro-
senting salvageable tissue. There are now sufficient data to
cedure. Primary outcomes were perioperative stroke, myocardial
support paradigm shift with insights that the mismatch does not
infarct or death and non-perioperative stroke. Perioperative
optimally define penumbra and visible zone of perfusion ab-
stroke or death in either group was 3.1%. The 5-year risk was
normality overestimates penumbra by including regions of
calculated in 6.4% for the immediate surgery group and almost
benign oligaemia.
doubled (11.8%) in the deferred CEA group for any stroke or
Technological advances have allowed for determination of
peri-operative death.8
cerebral blood flow (CBF) with Xe-CT, infrared spectroscopy MRI
Interestingly, although the ACST overall supported the ACAS
in response to acetazolamide challenge test or positron emission
results despite its more inclusive end points, neither study was
tomography scan to measure oxygen extraction fraction.15
able to show an increase in surgical benefit with greater degrees
of stenosis within the range of 60e99%. Management

Carotid stenting: the meta-analysis of short-term and long-term

outcomes of carotid artery stenting (CAS) versus CEA published
in 2011 pooled outcomes of several randomized trials in
asymptomatic and symptomatic carotid disease. The inclusion of
SPACE,9 CREST,10 CAVATAS11 and EVA-3S12 showed signifi-
cantly less frequent long-term stroke events after CEA. Although
confirming a higher risk for peri-procedural cranial nerve injury
and myocardial infarction, the outcomes of CEA seemed superior
Medical
‘Time Is Brain’:
“The typical patient loses 1.9 million neurons each minute in
which stroke is untreated.”3
Salvage of penumbra is known to significantly reduce fatality
rates and proportion of dependants at 3e6 months after stroke.
Intravenous thrombolytic therapy with recombinant tissue

SURGERY 33:8 401 Ó 2015 Published by Elsevier Ltd.

 NEUROSURGERY
Stroke subtype classifications
Classification Mechanism of brain infarction
OCSP Topographic Clinical Pattern
I. Lacunar infarcts (LACI) Acute stroke including one of the
major recognized lacunar
syndromes: pure motor, pure
sensory, sensorimotor, ataxic
hemiparesis, dysarthria (clumsy
hand syndrome)
II. Total anterior circulation Ischaemia in both the deep and
infarcts (TACI) superficial territories of MCA with
higher cerebral dysfunction such
as dysphasia, dyscalculia,
visuospatial disorder;
homonymous field defect;
ipsilateral motor and/or sensory
deficit involving two areas of the
face, arm and leg
III. Partial anterior circulation Presence of two of the three
infarcts (PACI) components of TACI syndrome
with higher cerebral dysfunction
alone, or with more restricted
sensorimotor deficit than those
classified as LACI
IV. Posterior circulation infarcts Syndrome including ipsilateral
(POCI) cranial nerve palsy with
contralateral motor and/or sensory
deficit; bilateral motor and/or
sensory deficit; disorder of
conjugate eye movement;
cerebellar dysfunction without
long-tract deficit; isolated
homonymous visual field defect
TOAST Aetiology
1 Large vessel disease
2 Small vessel disease
3 Cardioembolism
4 Other aetiology
5 Undetermined/multiple possible
etiologies
OCSP: Oxfordshire Community Stroke Project; TOAST: Trial of Org 10172 in
Acute Stroke Treatment.
Table 1
plasminogen activator (rtPA) is the standard treatment and
licensed for use within 4.5 hours of stroke onset, although the
risk of symptomatic intracerebral hemorrhage (SICH) e its most
feared complication e is non-negligible. Older age, higher stroke
severity assessed by NIHSS, hyperglycaemia, antiplatelet use,
atrial fibrillation, congestive heart failure, renal impairment and
early ischaemic changes on pretreatment brain imaging are
known to be associated with SICH.16 Up to one-third of patients
who suffer delayed deterioration following a hemispheric
ischaemic stroke do so from brain oedema. Several factors have
SURGERY 33:8
been recognized to influence its manifestation from clinically
silent to fatal. Usually resulting from occlusion of the internal
carotid artery (ICA) or proximal MCA, life-threatening oedema
courses with pupillary abnormalities and a decrease in the level
of consciousness reflecting brainstem compression.
The role of stroke units cannot be overemphasized. Patients
warrant intensive medical care with airway management and
mechanical ventilation, blood pressure control, fluid management
and glucose and temperature control. Unlike its role in traumatic
brain injury, continuous intracranial pressure monitoring in
ischaemic stroke does not appear to usefully correlate with
neurological deterioration, better assessed by modern techniques
of brain physiology monitoring, clinical and radiological signs.
Validation from results of the DEFUSE study showed age,
NIHSS, infarct volume, admission white blood cell count and
hyperglycaemia to be independent determinants of neurological
progression, occurring as early as within the first 24 hours and as
late as more than a week after stroke onset.17
Decompressive craniectomy: Systematic reviews and retro-
spective studies addressing the role of hemicraniectomy for
massive MCA infarct showed that factors such as timing of sur-
gery, dominant versus non-dominant infarction, presence of
signs of herniation before surgery and concomitant vascular
territories have questionable effect on outcome.18
The first few prospective, randomized studies which
addressed survival and functional outcomes associated with
medical treatment versus medical and decompressive craniec-
tomy (DC) treatments following malignant MCA infarct were the
DESTINY, HAMLET and DECIMAL trials. Independently
designed, their data contributed to a pooled analysis of 93 pa-
tients where DC performed within 48 hours was found to reduce
mortality. In light of the inclusion criteria used in the pooled
analysis, the Massachusetts General Hospital created the STATE
acronym as a guide to neurosurgical consultation: the National
Institutes of Health Stroke Score >15 with a decreased level of
consciousness 1 on the item 1a of the NIHSS; Time of inclusion
within 45 hours of symptom onset; Age: 18e60 years; Head CT
scan showing involvement >50% of the MCA Territory without
or with ACA or PCA involvement or DW MRI showing >145 cm3
infarct volume; Expectations regarding both survival and
disability explained and written informed consent signed by pa-
tient or legal responsible.19
Revascularization: previous studies have shown that
extracranialeintracranial (EC–IC) bypass surgery has no pre-
ventive effect on future ipsilateral ischaemic stroke in the pres-
ence of symptomatic atherosclerotic carotid occlusion and
haemodynamic ischaemia.
The North American Carotid Occlusion Surgery Study Trial, a
multicentre, randomized trial published in 2011 questioned the
benefit of STA-MCA bypass against antithrombotic treatment and
risk factor modification alone in patients with symptomatic ICA
occlusion and haemodynamic cerebral ischaemia. The results
showed the EC-IC bypass plus medical therapy did not reduce the
risk of recurrent ipsilateral ischaemic stroke at 2 years and was
terminated early.20 As more is learned on cerebral physiology
there may be a role for revascularization in certain subgroups.
402 Ó 2015 Published by Elsevier Ltd.
 NEUROSURGERY
Recanalization: intravenous thrombolysis, intra-arterial
thrombolysis trials or their combination, newer devices to
mechanically disrupt and remove clot from intracranial arteries,
balloon angioplasty with stent placement and other multimodal
strategies are still being explored to increase ischaemic stroke
patient eligibility beyond 4.5 hours and maximize arterial
recanalization.21 Mechanical thrombectomy has emerged as an
adjuvant or stand-alone treatment modality allowing for the
expansion of the therapeutic window, being proved to be safely
administered within an 8-hour window in large-vessel intra-
cranial obstruction.
Addressing symptomatic carotid stenosis: similarly to the sur-
gical benefit found in the asymptomatic carotid population,
surgical plus medical treatment compared with medical treat-
ment alone found superiority of outcome in the former. In two
large-scale prospective, randomized trials, NASCET and ECST,
endarterectomy was found to be of some benefit for 50e69%
symptomatic stenosis and highly beneficial for 70e99% stenosis
without near-occlusion. A pooled analysis of ECST, NASCET and
VACSP found endarterectomy to be associated with significant
benefit for any stroke or operative death and ipsilateral carotid
ischaemic stroke and operative stroke or death in patients har-
bouring 50e69% stenosis. In higher stenosis a highly statistically
significant reduction in the risks of each of the main outcomes
was found in the surgical arm. Furthermore, three consistent,
clinically significant subgroups were found across the 50e69%
and 70e99% stenosis groups: surgical benefit (if operative risk is
below 6%) was greater in men, amongst the elderly and its su-
periority decreased with time since the latest symptom onset.22
Post-thrombolytic patients suffering from carotid occlusion
might benefit from early CEA but additional data are still
required to confirm its safety.
Haemorrhagic: haemorrhagic stroke accounts for about 10
e20% of all strokes but is responsible for 30e50% overall 30-day
stroke-related mortality and disability amongst survivors. Pri-
mary intracranial hemorrhage (ICH), the most frequent form
(about 80% of all cases), occurs in the absence of an underlying
structural lesion such as aneurysms, vascular malformations,
tumours or as consequence of traumatic injury.
The frequency of spontaneous rupture of small penetrating
vessels damaged by longstanding and poorly controlled hyper-
tension or amyloid angiopathy is highest in the basal ganglia, the
majority of which arise in the putamen, followed by lobar,
thalamic, pontine and cerebellar hemorrhages.
The incidence of ICH increases significantly after age 55 and
doubles with each decade of age until 80. It predominately affects
men, and favours Blacks and Japanese. Hypertension and high
alcohol intake have also been found to be contributive risk factors.
Depending on its location, clinical presentation may vary with
frontal lobe ICH coursing with headache and contralateral hem-
iparesis; temporal lobe bleed may be asymptomatic or associate
itself with fluent dysphasia; parietal ICH causes mostly a
contralateral hemisensory deficit and occipital lobe presents with
contralateral homonymous hemianopsia with some sparing of
the superior quadrant.
In the presence of ICH, treatable, underlying vascular abnor-
malities should be sought with CTA, MRA or DSA.
SURGERY 33:8
Management
Medical
In a stroke unit setting, medical measures include hyper-
glycaemic control, osmotic agents, prophylactic anti-epileptic
medication (in lobar ICH) and hypothermic measures aiming to
decrease intracranial pressure and protect the surrounding pen-
umbra tissue. The rate of re-haemorrhage in the first 24 hours is
non-negligible, with some reporting it occurring in up to 26% of
ICH cases, supporting the benefit of blood pressure control and
replacement haemostatic therapy.
Haematoma evacuation: volumes of intraparenchymal and
intraventricular hemorrhage (IVH), and presence of IVH alone, are
believed to be predictors of poor prognosis independently of age,
neurologic status and clot anatomy. The resulting destruction and
compression on the surrounding brain affecting perfusion and
venous drainage, in parallel to the neurotoxicity of blood break-
down products, has led researchers to pursue the benefit in sur-
gical evacuation by decreasing the load of mass effect and toxicity.
Following its predecessor, STICH II addressed the early sur-
gical benefit over initial conservative treatment of alert patients
with supratentorial, lobar, superficial (less than 1 cm from
cortical surface) intraparenchymal haemorrhage. Its results
demonstrated that early surgery did not increase mortality or
disability at 6 months and might have a clinically relevant sur-
vival advantage in that subgroup.23 In both trials almost all pa-
tients were treated with craniotomy with haematoma evacuation.
With image-guided techniques and modern stereotactic
neurosurgery allowing for minimally invasive procedures, the
MISTIE and MISTIE II trials attempted treating ICH with local
delivery of rtPA through minimally invasive technique. The latter
evaluated safety, efficacy and dose escalation of rtPA. Patients
with ICH volumes above 20 ml and stable for 6 hours were
treated with either 0.3 mg or 1 mg of rtPA every 8 hours to either
final volumes of less than 10 ml or reaching 72 hours. This
resulted in safe and feasible intraparenchymal clot removal, with
efficacy found to relate to the positioning of the ventricular
catheter.24
EVD with rtPA: spontaneous intraparenchymal haemorrhage
carries a 45% frequency of ventricular extension, particularly
when of large volumes originating from the basal ganglia or
thalamus. Decompression of the haematoma into the ventricle
has proven not to be beneficial with decompression ranges for
each anatomical location identified. Clinically, there is often a
decrease in consciousness level at time of rupture and clot
mediated inflammation, fibrosis, hydrocephalus, herniation and
ischaemia carry an associated mortality of 50e80%.
The CLEAR IVH trial enrolled patients aged 18e75 years with
spontaneous ICH less than 30 ml with massive ventricular
extension and external ventricular drain in place for obstructive
hydrocephalus. Patients were randomized to either receive 12
hourly 3 mg of rtPA or 3 ml saline through the ventricular drain
until resolution of the clot was confirmed. The rtPA-treated
group had a higher rate of clot resolution (18%/day versus 8%/
day in the placebo-treated group). The 30-day fatality rate was
17% and a 50% good functional outcome was found at 180 days,
suggesting clot removal is beneficial in patients with IVH.25
403 Ó 2015 Published by Elsevier Ltd.
 NEUROSURGERY
CLEAR III is a multicentre, randomized controlled trial
designed with a primary outcome to measure mRS at 180 day and
is expected to reach completion in 2015.
Neuroendoscopy: neuroendoscopic surgery has been suggested
as a valid alternative to placement of external ventricular
drainage alone or with intraventricular fibrinolysis for IVH.
Cerebellar
Ischaemic: cerebellar ischaemia accounts for 3.4% of all strokes
and is about two-thirds as common as cerebellar haemorrhage.
Most commonly, it results from atherosclerosis of the intra-
cranial or extracranial vertebral artery. The PICA territory is most
often involved, followed by the SCA and the AICA, with multiple
involvement occuring in as many as 15%. Other culprits are
cardiac and artery-to-artery embolizations and traumatic dissec-
tion of vertebral arteries, but hypercoagulable states, venous
thrombosis and cocaine use may also be responsible.
Given its unspecific presentation, cerebellar stroke must be
kept in mind when considering the differential diagnosis of
poorly lateralizing symptoms with as dizziness, vertigo and
vomiting, unsteadiness of gait and headache.
Modulation of the motor function occurs through uncrossed
or doubly crossed pathways to and from the hemispheres
explaining the ipsilateral limb coordination deficit found with
hemispheric lesions, while lesions affecting the vermis result in
truncal ataxia and dysarthria.
Posterior circulation infarction often involve both cerebellar
hemispheres and the brainstem with its associated stroke syn-
dromes in combination with cerebellar dysfunction.
Misdiagnosis can be further coupled by low diagnostic sensitivity
of the widely available brain CT scan, often rendering a diagnosis
when the feared complications such as cytotoxic oedema and its
mass effect restricted to the confinements of the posterior fossa
result in obstruction of the fourth ventricle, acute hydrocephalus,
basal cistern compression, midbrain and pons deformities and often
fatal transtentorial and/or transforaminal herniations.
Management: acute cerebellar stroke presenting without initial
hydrocephalus or mass effect must be admitted for tight neuro-
logic observation and serial imaging.
The incidence of patients who develop oedema following
cerebellar infarction is unknown, and so is the frequency of life-
threatening swelling. Maximum degree of swelling has been
determined to take place between 48 and 96 hours.
In addition to medical management, and although lacking
prospective controlled trials, surgical decompression can reduce
mortality and improve long-term recovery in patients with ma-
lignant acute cerebellar oedema and is thus recommended by
current stroke guidelines to prevent and treat herniation and
brainstem compression.
The most appropriate neurosurgical approach has not been
established and varies amongst ventriculostomy alone or in
combination with craniectomy with opening of the foramen
magnum with or without resection of the posterior arch of C1,
durotomy and stroketectomy or tonsillar resection if decom-
pression alone renders insufficient. Although fatal, ascending
transtentorial herniation rarely complicates EVD placement in
patients with a full posterior fossa.
SURGERY 33:8
Although radiologic features which may herald deterioration
such as hydrocephalus, brainstem deformity and basal cistern
compression have been suggested, similarly to hemispheric
strokes, the decision to proceed with surgical decompression still
relies on clinical progression; surgery is believed to be best
tackled before neurological deterioration rather than performed
in the emergency setting. Neugebauer et al. have suggested a
cerebellar stroke treatment algorithm which bases surgical indi-
cation upon Glasgow Coma Scale (GCS) score, BAEP/SEP and
neuroradiological parameters.
Both hydrocephalus and brainstem compression course with
decreased level of consciousness. Associated focal neurological
signs found with the latter, such as ipsilateral VI nerve palsy,
facial paresis, hemiparesis and cardiac dysrhythmias or irregular
breathing patterns, may help determine whether ventriculostomy
or suboccipital craniectomy would be more beneficial.
Preoperative level of consciousness, lack of cranial nerve
impairment and reduced mass effect predict favourable neuro-
logic outcomes. On the contrary, older age and associated
brainstem infarct appear to carry higher mortality rates, with
deterioration being more dependent on initial infarct volume
rather than the specific vascular territory.
Haemorrhagic: spontaneous cerebellar haemorrhage accounts
for about 5e10% of all intracranial hemorrhages and 10e20% of
all cerebellar strokes. The vast majority of patients are hyper-
tensive, although similarly to supratentorial haemorrhages
structural lesions, coagulopathies or trauma may play a role.
Spontaneous haemorrhage has been described to most
frequently involve the AICA and the SCA in the deep cerebellar
nuclei extending through the ipsilateral and/or contralateral
hemisphere. It can also extend in to the cerebellar peduncles,
aqueduct or fourth ventricle, further contributing to acute
obstructive hydrocephalus. Clinical deterioration results from
expanding oedema or further bleed.
Management: as in case of ischaemic stroke, cerebellar hae-
morrhage warrants appropriate medical care.
In presence of cerebellar hemorrhage, surgical procedures
may vary along the spectrum of temporary to permanent CSF
diversion with or without haematoma evacuation, or decom-
pressive suboccipital craniectomy with or without removal of the
posterior arch of C1, performed in one or separate surgical stages
pending on the efficacy of the first in alleviating signs of brain-
stem compression.
Alternative management options to cerebellar bleed such as
endoscopic burr hole evacuation, stereotactic aspiration or lysis
with thrombolytic agents are still awaiting to be properly
addressed with well-designed studies.
In the absence of controlled randomized trials, controversy also
persists on the surgical indication being derived from radiological
features or clinical status alone or in combination. As such, factors
such as mass effect with signs of cisternal effacement or brainstem
compression, dimensions of the haematoma regardless of neuro-
logical status and level of consciousness regardless of imaging
findings are used by different centres. Some advocate the
following rationale: patients with GCS 15e14 and haemorrhages
smaller than 4 cm should receive conservative treatment alone;
surgical treatment should be reserved for those with admission
404 Ó 2015 Published by Elsevier Ltd.
 NEUROSURGERY
GCS less than 13 or with haematoma greater than 4 cm, regardless
of their neurological status.
Many have shown that postoperative outcome correlates with
preoperative status. Others have found cerebellar hemorrhages
more forgiving, reporting cases where patients with fatal space
occupying strokes recover fully, doubting if a point of no return
actually exists.
Decreased level of consciousness, a vermian haematoma and
acute hydrocephalus seem to contribute independently to a
higher risk for neurologic deterioration.
Conclusion
Recognition and modulation of stroke risk factors have allowed
its management to evolve from rehabilitation to prevention.
Maximizing the benefit of acute thrombolysis imposes a more
efficient practice with increased public and medical awareness,
as do development of pre-hospital bridging treatments, perhaps
individually designed and creation of metropolitan models with
less but highly specialized centres with multidisciplinary stroke
medical care. Although certain surgical techniques are associated
with improved outcome, others are still in need of properly
designed clinical trials. A
REFERENCES
1 Murray CJ, et al. UK health performance: findings of the Global
Burden of Disease Study 2010. Lancet 2013; 381: 997e1020.
2 Feigin VL, et al. Global and regional burden of stroke during 1990
e2010: findings from the Global Burden of Disease Study 2010.
Lancet 2014; 383: 245e54.
3 Saver JL. Time is brain-quantified. Stroke 2006; 37: 263e6.
4 Xian Y, Holloway RG, Chan PS, et al. Association between stroke
center hospitalization for acute ischemic stroke and mortality. J Am
Med Assoc 2011; 305: 373e80.
5 Hunter RM, et al. Impact on clinical and cost outcomes of a
centralized approach to acute stroke care in London: a comparative
effectiveness before and after model. PLoS One 2013; 8: e70420.
6 de Weerd M, et al. Prevalence of asymptomatic carotid artery ste-
nosis in the general population: an individual participant data meta-
analysis. Stroke 2010; 41: 1294e7.
7 Executive Committee for the Asymptomatic Carotid Atherosclerosis
Study. Endarterectomy for asymptomatic carotid artery stenosis. J Am
Med Assoc 1995; 273: 1421e8.
8 Halliday A, Mansfield A, Marro J, et al. MRC Asymptomatic Carotid
Surgery Trial (ACST) Collaborative Group. Prevention of disabling and
fatal strokes by successful carotid endarterectomy in patients
without recent neurological symptoms: randomised controlled trial.
Lancet 2004; 363: 1491e502.
9 Eckstein HH, Ringleb P, Allenberg JR, et al. Results of the Stent-
Protected Angioplasty versus Carotid Endarterectomy (SPACE) study
to treat symptomatic stenoses at 2 years: a multinational, prospec-
tive, randomised trial. Lancet Neurol 2008; 7: 893e902.
10 Paraskevas KI, Mikhailidis DP, Liapis CD, Veith FJ. Critique of the
Carotid Revascularization Endarterectomy versus Stenting Trial
(CREST): flaws in CREST and its interpretation. Eur J Vasc Endovasc
Surg 2013; 45: 539e45.
SURGERY 33:8
11 Ederle J, Bonati LH, Dobson J, et al. CAVATAS Investigators. Endo-
vascular treatment with angioplasty or stenting versus endarterec-
tomy in patients with carotid artery stenosis in the Carotid and
Vertebral Artery Transluminal Angioplasty Study (CAVATAS): long-term
follow-up of a randomised trial. Lancet Neurol 2009; 8: 898e907.
12 Mas JL, et al. EVA-3S investigators. Endarterectomy versus Angio-
plasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S)
trial: results up to 4 years from a randomised, multicentre trial.
Lancet Neurol 2008; 7: 885e92.
13 Sung SF, Chen SC, Lin HJ, et al. Oxfordshire Community Stroke Project
classification improves prediction of post-thrombolysis symptomatic
intracerebral hemorrhage. BMC Neurol 2014; 14: 39.
14 Adams Jr HP, Bendixen BH, Kappelle LJ, et al. Classification of sub-
type of acute ischemic stroke. Definitions for use in a multicenter
clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment.
Stroke 1993; 24: 35e41.
15 Garrett MC, Komotar RJ, Merkow MB, Starke RM, Otten ML,
Connolly ES. The extracranial-intracranial bypass trial: implications
for future investigations. Neurosurg Focus 2008; 24: E4.
16 Adams Jr HP, et al. Guidelines for the early management of adults
with ischemic stroke: a guideline from the American Heart Associa-
tion/American Stroke Association Stroke Council, Clinical Cardiology
Council, Cardiovascular Radiology and Intervention Council, and the
Atherosclerotic Peripheral Vascular Disease and Quality of Care Out-
comes in Research Interdisciplinary Working Groups: the American
Academy of Neurology affirms the value of this guideline as an
educational tool for neurologists. Stroke 2007; 38: 1655e711.
17 Vora NA, Shook SJ, Schumacher HC, et al. A 5-item scale to predict
stroke outcome after cortical middle cerebral artery territory infarc-
tion: validation from results of the Diffusion and Perfusion Imaging
Evaluation for Understanding Stroke Evolution (DEFUSE) Study.
Stroke 2011; 42: 645e9.
18 Gupta R, Connolly ES, Mayer S, Elkind MS. Hemicraniectomy for
massive middle cerebral artery territory infarction: a systematic re-
view. Stroke 2004; 35: 539e43.
19 Agarwalla PK, Stapleton CJ, Ogilvy CS. Craniectomy in acute ischemic
stroke. Neurosurgery 2014; 74(suppl 1): S151e62.
20 Powers WJ, Clarke WR, Grubb Jr RL, Videen TO, Adams Jr HP, Derdeyn CP,
COSS Investigators. Extracranial-intracranial bypass surgery for stroke
prevention in hemodynamic cerebral ischemia: the Carotid Occlusion
Surgery Study randomized trial. J Am Med Assoc 2011; 306: 1983e92.
21 Tsivgoulis G, Katsanos AH, Alexandrov AV. Reperfusion therapies of
acute ischemic stroke: potentials and failures. Front Neurol 2014; 5: 215.
22 Rerkasem K, Rothwell PM. Carotid endarterectomy for symptomatic
carotid stenosis. Cochrane Database Syst Rev 2011 Apr 13. Issue 4.
Art. No.:CD001081.
23 Mendelow AD, Gregson BA, Rowan EN, et al. Early surgery versus
initial conservative treatment in patients with spontaneous supra-
tentorial lobar intracerebral haematomas (STICH II): a randomised
trial. Lancet 2013; 382: 397e408.
24 Dey M, Stadnik A, Awad IA. Spontaneous intracerebral and intra-
ventricular hemorrhage: advances in minimally invasive surgery and
thrombolytic evacuation, and lessons learned in recent trials.
Neurosurgery 2014; 74(suppl 1): S142e50.
25 Akhtar A, Kamal AK. CLEAR: the intraventricular haemorrhage
thrombolysis trial. J Pak Med Assoc 2013; 63: 928.
405 Ó 2015 Published by Elsevier Ltd.