Official reprint from UpToDate

www.uptodate.com 2014 UpToDate

Spontaneous intracerebral hemorrhage: Treatment and prognosis
Authors
Guy Rordorf, MD
Colin McDonald, MD

Section Editor
Scott E Kasner, MD

Deputy Editor
Janet L Wilterdink, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2014. | This topic last updated: May 21, 2014.
INTRODUCTION Intracerebral hemorrhage (ICH) is the second most common cause of stroke, following ischemic
stroke. Mortality and morbidity is high. Initial goals of treatment include preventing hemorrhage extension, as well as the
prevention and management of elevated intracranial pressure along with other neurologic and medical complications.
The treatment and prognosis of spontaneous intracerebral hemorrhage will be reviewed here. Other aspects of ICH are
discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)
INITIAL TREATMENT Management of intracerebral hemorrhage (ICH) includes both medical and surgical interventions
[1,2].
General management issues Guidelines from the American Heart Association/American Stroke Association
(AHA/ASA) recommend that patients with ICH receive monitoring and management in an intensive care unit [1,3]. This
recommendation is based upon the frequent association of ICH with elevations in intracranial pressure and blood
pressure, the need for intubation and mechanical ventilation, and multiple medical issues and complications. Many
neurologic as well as medical complications that require urgent intervention occur subsequent to the initial evaluation [4].
Ideally, acute neurosurgical care should be available at the hospital in which patients are cared for [5]. In addition, there is
some evidence that intensive monitoring and stroke unit care is associated with improved outcomes in patients with acute
stroke [6,7].
Early DNR orders or limitations to care are not always inappropriate after ICH; the difficulty lies in deciding when such
limitations are indeed the most appropriate approach [8]. Because prognostication for individual patients with acute ICH is
an uncertain science, current guidelines suggest careful consideration of aggressive, full care during the first 24 hours after
ICH onset and postponement of new DNR orders during that time [1,3]. This recommendation does not apply to patients
with preexisting DNR orders. (See 'Prognosis' below.)
Specific recommended interventions for patients with ICH include [1,9]:
Sources of fever should be treated, and current guidelines suggest the use of antipyretic medications to lower body
temperature to normothermia in febrile patients with stroke [1,3]. (See "Initial assessment and management of acute
stroke", section on 'Fever'.)
Hyperglycemia in the first 24 hours after stroke is associated with adverse outcomes, and current guidelines suggest
insulin treatment to target serum glucose level between 140 to 180 mg/dL (>7.8 to 10 mmol/L) [1,3]. Hypoglycemia
should be avoided. (See "Initial assessment and management of acute stroke", section on 'Hyperglycemia' and
"Initial assessment and management of acute stroke", section on 'Hypoglycemia'.)
Intermittent pneumatic compression is the mainstay for prevention of venous thromboembolism in patients with acute
ICH. (See "The use of antithrombotic therapy in patients with an acute or prior intracerebral hemorrhage".)
Normal saline initially should be used for maintenance and replacement fluids; hypotonic fluids are contraindicated as
they may exacerbate cerebral edema and intracranial pressure. Hypervolemia should be avoided as it may worsen
cerebral edema [10]. (See 'Intracranial pressure' below.)
Dysphagia is common and is a major risk factor for developing aspiration pneumonia. Prevention of aspiration in
patients with acute stroke includes initial nulla per os (NPO) status until swallowing function is evaluated. Some
experts suggest that patients with a GCS <8 be intubated to decrease the risk of aspiration [10,11]. (See "Medical
complications of stroke", section on 'Dysphagia and aspiration'.)
Reversal of anticoagulation For patients who develop an ICH, all anticoagulant and antiplatelet drugs should be
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discontinued acutely after the onset of hemorrhage, and anticoagulant effect should be reversed immediately with
appropriate agents [1,3].
Aggressive use of intravenous vitamin K, unactivated prothrombin complex concentrate (also called factor IX complex),
and other factors may be necessary in patients who suffer an ICH while taking warfarin. Reversal of anticoagulation in this
setting is discussed in detail separately. (See "Reversal of anticoagulation in warfarin-associated intracerebral
hemorrhage", section on 'Reversal agents'.)
Newer oral anticoagulants are increasing used as alternatives to warfarin therapy. While there is less clinical experience
with their reversal in the setting of ICH, a number of measures have been suggested to guide treatment in the setting of
hemorrhagic complications. These are discussed separately. (See "Management of bleeding in patients receiving targetspecific oral anticoagulants".)
Protamine sulfate is recommended for urgent treatment of patients with heparin-associated ICH [1,3]. Protamine sulfate
can be administered by slow intravenous infusion (not greater than 20 mg/min and no more than 50 mg over any
10-minute period). The appropriate dose of protamine sulfate is dependent upon the dose of heparin given and the time
elapsed since that dose. (See "Therapeutic use of heparin and low molecular weight heparin", section on 'Heparin reversal
with protamine'.)
Patients with severe coagulation factor deficiency or thrombocytopenia should receive appropriate factor replacement or
platelet transfusion [3].
For patients on antiplatelet therapy, the limited available data suggests that platelet transfusions do not improve outcomes
[12]. (See "Clinical and laboratory aspects of platelet transfusion therapy", section on 'Indications for platelet transfusion'.)
Blood pressure The mean arterial pressure (MAP) is often elevated in patients with ICH. Management of hypertension
is complicated by competing risks and potential benefits:
Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding, causing
hemorrhage expansion and potentially worse outcomes [13,14]. (See "Spontaneous intracerebral hemorrhage:
Pathogenesis, clinical features, and diagnosis", section on 'Hemorrhage enlargement'.)
However, an increased MAP may be necessary to maintain cerebral perfusion in some patients, and lowering the
arterial pressure (eg, to a systolic blood pressure [SBP] below 130 mmHg) may cause ischemia and worsen
neurologic injury. Two observational studies have found that greater acute BP reductions are associated with
increased incidence of areas of decreased diffusion on MRI scan [15-17], however, other studies have not found that
BP lowering affects regional CBF [18,19], and the implication of these findings for prognosis is as yet undefined .
There are limited clinical trial data to inform decision making. Outcomes of death and severe disability were found to be
similar among patients groups in the INTERACT2 trial, which randomly assigned 2839 patients with acute (within 6 hours)
ICH and elevated blood pressure to either intensive blood pressure lowering (target systolic blood pressure (sBP) <140
mm Hg within one hour) versus traditional management (target SBP <180 mm Hg) [20]. Intensive blood pressure lowering
was associated with improved measures of disability according to modified Rankin scores, a secondary outcome measure.
Adverse events were similar in the patient groups. The smaller INTERACT study and other nonrandomized studies have
suggested that more aggressive BP lowering is associated with reduced hematoma growth [1,21-23]. Another larger trial
(ATACH II) is in progress [17].
Guidelines for treatment Current guidelines for managing elevated blood pressure in acute spontaneous ICH are
as follows [1,3]:
For patients with SBP >200 mmHg or MAP >150 mmHg, consider aggressive reduction of blood pressure with
continuous intravenous infusion of medication accompanied by frequent (every five minutes) blood pressure
monitoring
For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, consider
monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral
perfusion pressure in the range of 61 to 80 mmHg
For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a
modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using
intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes
These guidelines as well as the results of INTERACT2 also concluded that in patients presenting with a SBP of 150 to 200
mm Hg, acute lowering of SBP to 140 mm Hg is probably safe [3]. Labetalol, nicardipine, esmolol, enalapril, hydralazine,
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nitroprusside, and nitroglycerin are useful intravenous agents for controlling blood pressure [1].
Seizure prophylaxis and treatment The reported risk of seizures in patients with acute spontaneous ICH ranges from
4.2 to 29 percent [1,10]. Seizures are more common in lobar as compared to deep hemorrhage [24]. The frequency
depends in part on the extent of monitoring, as seizures associated with ICH are often nonconvulsive [1]. (See
"Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Clinical presentation'
and "Nonconvulsive status epilepticus".)
If a seizure occurs, appropriate intravenous antiepileptic drug (AED) treatment should be administered to prevent recurrent
seizures [3]. The choice of the initial antiepileptic agent depends upon individual circumstances and contraindications.
Current guidelines suggest the use of intravenous fosphenytoin or phenytoin in this setting [1]. (See "Initial treatment of
epilepsy in adults" and "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis".)
While some experts suggest a brief period of AED prophylaxis soon after ICH onset as a potential means of reducing the
risk for early seizures in patients with lobar hemorrhages [1], 2010 guidelines recommend against prophylactic use of
AEDs [3] This strategy has not been tested prospectively in clinical trials. While two case series have found that
prophylactic treatment with AEDs was associated with poorer outcomes (a concern that has also been raised for
subarachnoid hemorrhage patients), these were nonrandomized, observational studies, and sample size did not allow for
examination of a differential effect from different AEDs [25,26].
Intracranial pressure Increased intracranial pressure (ICP) due to ICH can result from the hematoma itself and from
surrounding edema, and may contribute to brain injury and neurologic deterioration. Current guidelines recommend a
graded approach to the management of elevated ICP, beginning with simple measures that include the following [1]:
Elevate the head of the bed to 30 degrees, once hypovolemia is excluded.
Analgesia and sedation, particularly in unstable, intubated patients
Sedation should be titrated to control pain and minimize ICP elevation, while still permitting clinical evaluation of the
patient's neurologic status [1]. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam.
Suggested agents for analgesia and antitussive effect are morphine or alfentanil. (See "Sedative-analgesic
medications in critically ill adults: Selection, initiation, maintenance, and withdrawal".)
Normal saline initially should be used for maintenance and replacement fluids; hypotonic fluids are contraindicated.
Mild hypernatremia should be tolerated.
Glucocorticoids should NOT be used to lower the ICP in most patients with ICH. A randomized trial found that
dexamethasone did not improve outcome but did increase complication rates, primarily infection [27].
Invasive monitoring and treatment of ICP should be considered for patients with GCS <8 (table 1), those with clinical
evidence of transtentorial herniation, or those with significant IVH or hydrocephalus [3]. Measuring ICP directly allows
directed treatment of ICP and blood pressure with a goal of maintaining a cerebral perfusion pressure (CPP) of 50 to 70
mmHg. More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol and hypertonic saline
solution), ventricular catheter drainage of cerebrospinal fluid, and neuromuscular blockade [1,3].

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Intravenous mannitol is the treatment of choice to lower increased intracranial pressure, quickly and effectively
lowering ICP [28]. It is administered as an initial bolus of 1 g/kg, followed by infusions of 0.25 to 0.5 g/kg every six
hours. The goal of therapy is to achieve plasma hyperosmolality (300 to 310 mosmol/kg) while maintaining an
adequate plasma volume; major side effects include hypovolemia and a hyperosmotic state [1]. (See "Evaluation and
management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis'.)
Marked hyperosmolality should be avoided to prevent precipitation of acute renal failure [29]. (See "Complications of
mannitol therapy" and "Serum osmolal gap".)
Barbiturate anesthesia can be used if mannitol fails to lower ICP to an acceptable range. Barbiturate coma acts by
reducing cerebral metabolism, which results in a lowering of cerebral blood flow and thus decreases ICP [1]. It is of
variable benefit for the treatment of elevated ICP from a variety of causes and is associated with a high rate of severe
side effects, especially arterial hypotension [30]. Continuous electroencephalogram monitoring is suggested during
high-dose barbiturate treatment, with the dose titrated to a burst-suppression pattern of electrical activity [1]. (See
"Evaluation and management of elevated intracranial pressure in adults", section on 'Barbiturates'.)
Hyperventilation to a PaCO2 of 25 to 30 mmHg causes dramatic and rapid lowering of ICP. However, the effect only
lasts for minutes to a few hours. Thus, we reserve hyperventilation until the above therapies have been maximized

[31]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Hyperventilation'.)
Neuromuscular blockade is sometimes employed to reduce ICP in patients who are not responsive to analgesia and
sedation alone, as muscle activity can contribute to increased ICP by raising intrathoracic pressure, thereby reducing
cerebral venous outflow [1].
Drawbacks of neuromuscular blockade include an increased risk of pneumonia and sepsis. In addition, the ability to
evaluate the neurologic status is lost once the patient is paralyzed. (See "Use of neuromuscular blocking medications
in critically ill patients".)
Cerebrospinal fluid drainage by intraventricular catheter placement (ventriculostomy) is an effective means of
lowering ICP [1]. Ventriculostomy also allows direct monitoring of ICP. However, there are no prospective studies
evaluating its effect on outcomes in patients with ICH.
Ventriculostomy is often used in the setting of obstructive hydrocephalus, which is a common complication of
thalamic hemorrhage with third ventricle compression, and of cerebellar hemorrhage with fourth ventricle
compression. Ventriculostomy is also frequently used in the setting of intraventricular hemorrhage with
hydrocephalus. (See "Intraventricular hemorrhage", section on 'External ventricular drain'.)
Surgery The indications for surgery in patients with ICH vary with the site of the bleed.
Cerebellar hemorrhage Surgical removal of hemorrhage with cerebellar decompression should be performed for
patients with cerebellar hemorrhages greater than 3 cm in diameter who are deteriorating, or who have brainstem
compression and/or hydrocephalus due to ventricular obstruction [1,3,32]. Surgery decreases the risk of brainstem
compression and obstructive hydrocephalus. External drainage alone, without posterior fossa decompression, may create
the theoretical opportunity for upward herniation of the cerebellar mass and is not recommended.
Supratentorial hemorrhage Surgical hematoma evacuation for supratentorial ICH is controversial; some patients
may benefit, but indications for surgical treatment have not been conclusively defined [1,3,33-41].
We reserve surgical therapy for patients with life-threatening mass effect from supratentorial ICH, individualizing treatment
decisions based on assessments of prognosis with and without surgical therapy. Current guidelines suggest consideration
of standard craniotomy only for those who have lobar clots >30 mL within 1 cm of the surface [1,3]. No other patient group
is recommended for surgery, and no surgical method other than standard craniotomy is supported. The routine evacuation
of supratentorial ICH in the first 96 hours is not recommended.
Open craniotomy is the most widely studied surgical techniques in patients with supratentorial ICH [1]. Other methods
include endoscopic hemorrhage aspiration, use of fibrinolytic therapy to dissolve the clot followed by aspiration, and
CT-guided stereotactic aspiration. Studies of these less invasive techniques are in progress [42].
A 2008 meta-analysis reviewed 10 randomized trials including 2059 patients [43]. Surgery was associated with a reduced
risk of death and dependency (OR 0.71; 95% CI 0.61 to 0.91). However, the benefit was not robust, and there was
significant heterogeneity for death as an outcome.
The largest trial in the meta-analysis was the STICH trial. In this study, the 503 patients assigned to early (median time to
surgery was 30 hours after hemorrhage onset) surgical hematoma evacuation were slightly more likely to have a favorable
outcome at six months compared to those managed with initial conservative treatment, but the trend did not reach
statistical significance [39]. Benefit from those assigned to early surgery was nonsignificantly more likely in patients who
had craniotomy as opposed to alternate techniques, and in those with hematoma located 1 cm or less from the cortical
surface. The fact that 26 percent of patients initially assigned to conservative medical management underwent surgical
evacuation may limit the ability of the study to show a benefit from surgery [40,44,45].
Subsequently, the STITCH II trial found that rates of unfavorable outcomes at six months were similar in the 307 conscious
patients treated with early (within 48 hours of onset) surgical hematoma evacuation versus the 294 patients treated
conservatively (59 versus 62 percent) [46]. Limitations in interpreting the results of this study include the selected nature of
the patients treated, (conscious, without intraventricular extension), as well as a high crossover rate; 21 percent of patients
assigned to conservative therapy did undergo surgery [47].
When STITCH II data were combined with individual patient data from 14 other trials, a survival benefit for surgery was
suggested for subgroups of patients, including those with poorer prognosis on presentation, those who deteriorated after
presentation, and those with superficial ICH and no intraventricular extension [42,46]. Further studies are required to
conclusively determine which patients should receive surgical therapy.
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Because of the questionable efficacy of surgery, it should only be considered as a life saving procedure to treat refractory
increases in ICP; even in these instances, decisions should be addressed on a per patient basis:
Surgery should not be considered for patients who are either fully alert or deeply comatose. Patients with
intermediate levels of arousal (obtundation-stupor) are more appropriate candidates.
Features that support performing surgery include a recent onset of hemorrhage, ongoing clinical deterioration,
involvement of the nondominant hemisphere, and location of the hematoma near the cortical surface.
Features in favor of less aggressive therapy include serious concomitant medical problems, advanced age, stable
clinical condition, remote onset of hemorrhage, involvement of the dominant hemisphere, and inaccessibility of the
hemorrhage
Intraventricular hemorrhage Patients with intraventricular extension of the ICH are at risk for hydrocephalus,
especially if the third and fourth ventricles are involved. Such patients should be closely monitored. When neurologic
deterioration occurs, an emergent CT scan should be done to exclude the development of hydrocephalus. Patients with
neurologic deterioration in the setting of ventricular enlargement may be candidates for ventriculostomy and external
ventricular drainage.
The management of intraventricular hemorrhage is discussed in detail separately. (See "Intraventricular hemorrhage".)
Hemostatic therapy While hemostatic therapy offers the potential to improve outcomes by stopping ongoing
hemorrhage and preventing hemorrhage enlargement, clinical trials have had mixed results. Current guidelines and
systematic reviews have concluded that recombinant factor VIIa treatment for acute ICH that is not associated with
warfarin use is investigational and should not be used for treatment of ICH outside the context of a clinical trial [1,3,48].
The use of factor VIIa for warfarin-associated ICH is discussed in detail separately. (See "Reversal of anticoagulation in
warfarin-associated intracerebral hemorrhage".)
The agent that has been most studied for use in ICH is activated recombinant factor VIIa (rFVIIa), which promotes
hemostasis at sites of vascular injury [49]. (See "Therapeutic uses of recombinant coagulation factor VIIa in
non-hemophiliacs", section on 'Mechanism of action'.)
While preliminary studies suggested that treatment with rFVIIa was safe and effective for ICH [50,51], results from the
multicenter double-blind phase 3 clinical trial showed no benefit for primary clinical outcomes [52]. The trial randomly
assigned 841 patients with spontaneous ICH to receive either rFVIIa (20 or 80 mcg/kg) or placebo within four hours of
symptom onset. Compared with placebo, treatment with rFVIIa was associated with a significant reduction in hematoma
growth but did not result in improvement in the primary outcome measures, death or severe disability at day 90. In
contrast, the earlier multicenter phase 2B study evaluated 399 patients with spontaneous ICH and found that treatment
significantly reduced the risk of severe disability or death compared with placebo at 90 days (absolute risk reduction of 16
percent) [51].
Recombinant factor VIIa has a potential risk of serious side effects from activation of the coagulation system or thrombosis
[49]:
In the phase 3 trial, the overall frequency of thromboembolic serious adverse events was similar among treatment
groups, but the rate of arterial thromboembolic serious adverse events (myocardial infarction or cerebral infarction)
was significantly higher in the group assigned to 80 mcg/kg when compared with placebo (8 versus 4 percent) [52].
Similar findings were noted in an analysis of pooled data from three earlier randomized controlled trials of rFVIIa for
spontaneous ICH, in which the rate of arterial thromboembolic serious adverse events was significantly increased in
those assigned to high-dose rFVIIa (120 to 160 mcg/kg) compared with placebo (5.4 versus 1.7 percent) [53].
Small open-label studies suggest that rFVIIa treatment for ICH is associated with increased rates of troponin
elevation and myocardial infarction [54] and higher than expected rates of posthemorrhagic hydrocephalus [55]. (See
"Therapeutic uses of recombinant coagulation factor VIIa in non-hemophiliacs", section on 'Safety issues'.)
SECONDARY TREATMENT ISSUES Early mobilization and rehabilitation are suggested in patients with ICH who are
clinically stable [1,3].
Resumption of antiplatelet therapy Our experience with the use of aspirin suggests that it is probably safe to resume
therapy after the acute phase of ICH provided that blood pressure is well controlled and that the indication for antiplatelet
treatment is sufficiently strong that the potential benefit outweighs the increase in risk of recurrent ICH. (See 'Timing and
dose' below.)
There are limited data that specifically address this issue. Therefore, most decisions must be made by extrapolating from
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the limited data regarding antiplatelet therapy and the risk of primary ICH. Meta-analyses of randomized controlled trials
suggest that aspirin use is associated with an approximately 40 percent relative increase in the risk of initial ICH, which
translates into a very small absolute increase in risk [56,57]. In the setting of cerebral amyloid angiopathy, aspirin use may
be associated with a greater risk of recurrent ICH [58]. (See "The use of antithrombotic therapy in patients with an acute or
prior intracerebral hemorrhage", section on 'Risk associated with antithrombotic therapy' and "Cerebral amyloid
angiopathy", section on 'Avoiding anticoagulants and antiplatelet agents'.)
Although aspirin reduces the risk of ischemic stroke by 25 percent, this benefit is largely negated by the associated
increased risk of recurrent ICH, which typically causes more disability than ischemic stroke. Therefore, we do not
recommend aspirin or antiplatelets for those patients with only an "average" risk of recurrent ischemic stroke. What exactly
constitutes "average" or "above average" risk is not certain, but we consider hypertension, diabetes, hypercholesterolemia,
and the absence of heart disease to be markers of average risk. Atrial fibrillation, cardiomyopathy, large vessel extracranial
and intracranial stenoses, and malignancy can be considered as markers for those with "above average" risk who may
benefit from long-term antiplatelet therapy after ICH.
We also suggest not resuming aspirin or antiplatelet therapy for primary prevention of cardiovascular disease. In the few
existing primary prevention studies, patients with any prior ICH were excluded. Such patients should avoid aspirin unless a
compelling indication for aspirin use develops later on.
Timing and dose The timing of antiplatelet use after ICH is largely empiric. There is risk of rebleeding and
hematoma expansion in the first several hours. At 10 days, rebleeding is unlikely. The AHA/ASA guidelines of 2006 state
that antiplatelets should be discontinued for at least one to two weeks [59].
Some experts have argued that aspirin can be used safely as soon as 48 hours after ICH in those who require prophylaxis
for venous thromboembolism. We agree, provided neuroimaging has demonstrated a stable ICH. (See "The use of
antithrombotic therapy in patients with an acute or prior intracerebral hemorrhage", section on 'Prevention'.)
If aspirin is used after ICH, we agree with others that a lower dose (30 to 160 mg daily) is both effective and safer than
higher doses. (See "The use of antithrombotic therapy in patients with an acute or prior intracerebral hemorrhage".)
Resumption of anticoagulation The question of when to restart anticoagulation in patients at high risk for embolic
events who have suffered an ICH has not been definitively answered [60]. For patients who require anticoagulation soon
after a cerebral hemorrhage, the AHA/ASA guidelines conclude that intravenous heparin may be safer than oral
anticoagulation [60]. In addition, the guidelines suggest that oral anticoagulants may be resumed three to four weeks after
onset of the hemorrhage with rigorous monitoring and maintenance of INRs in the lower end of the therapeutic range. It is
reasonable to consider risk factors for recurrent ICH when making risk/benefit decisions regarding resumption of oral
anticoagulation. (See 'Recurrence' below.)
Resumption of anticoagulation is discussed in greater detail separately. (See "The use of antithrombotic therapy in patients
with an acute or prior intracerebral hemorrhage".)
Secondary prevention Efforts to control blood pressure over the long term are likely to significantly reduce the risk of
recurrent ICH. Guidelines published in 2010 suggest a goal blood pressure of <140/90 [3]. In the PROGRESS trial, among
over 6000 patients with prior cerebrovascular events and a mean baseline blood pressure of 147/86, a modest reduction in
blood pressure of 9/4 mmHg decreased the rate of ICH by 50 percent (95% CI 26%-67%) [61]. In the subgroup of 611
patients with prior ICH, there was a similar 49 percent risk reduction (95% CI 18%-68%) for recurrent ICH.
While treating hypertension is the most important step to reduce the risk of ICH, and probably recurrent ICH, stopping
smoking, heavy alcohol use, and cocaine use are also recommended [1,62].
There are insufficient data to recommend general restrictions on the use of statin agents [3]. While a number of studies
have found an inverse relationship between total and LDL-cholesterol and the risk of ICH [63-71], treatment with statins
does not appear to increase the risk of primary ICH or to negatively impact prognosis according to a number of studies and
meta-analyses [72-78]. Given the conflicting data, it seems to be reasonable to weigh the benefits and possible risks of
statin therapy in individual patients who are otherwise at risk for ICH recurrence [79-81]. (See 'Recurrence' below.)
PROGNOSIS
Mortality and functional outcome The 30-day mortality from ICH ranges from 35 to 52 percent [82-90]; one-half of
these deaths occur within the first two days [84,88,91]. A systematic review estimated that between 12 and 39 percent of
patients achieve independent function [89].
The prognosis after ICH depends upon the location of hemorrhage (supra versus infratentorial location), size of the
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hematoma, level of consciousness, patient age, and overall medical health and condition [1,84,85,87,90-93]. In addition,
preceding oral anticoagulation therapy, and possibly antiplatelet therapy, appears to be associated with worse outcomes
after ICH [91,94]. One study found that hemorrhage from a cerebral arteriovenous malformation were associated with a
lower case-fatality rate, despite a similar hemorrhage volume and a higher admission Glasgow coma scale compared with
spontaneous ICH [95]. Other studies also suggest that hemorrhage due to vascular malformations is associated with lower
mortality than other causes of ICH [96,97].
Long-term survival after primary ICH also appears to be decreased compared with controls from the general population
matched for age and sex [85,87,90,98,99]. A retrospective cohort study identified 411 patients with first ever ICH and
found that the annual risk of dying compared with controls was increased 4.5-fold during the first year after ICH and
2.2-fold during years two to six [85]. A subsequent longitudinal prospective cohort study evaluated patients who had
survived the first three months after ICH and observed that the mortality at seven years was significantly higher than
controls (32.9 versus 19.4 percent) [98]. In a population-based cohort of patients hospitalized after ICH in the Greater
Cincinnati/Northern Kentucky area, the ten-year survival was 18 percent [86]. Major causes of mortality appear to be
stroke and ischemic heart disease [99].
Risk factors for poor outcomes
Initial ICH volume and level of consciousness The ICH volume on initial head CT scan and level of
consciousness on admission may be particularly important prognostic indicators [84,97,100]. This point is illustrated by a
study of 188 patients with ICH that analyzed predictors of 30-day mortality [84]; the following observations were made:
An ICH volume of 60 cm3 or greater on initial CT and a Glasgow coma scale score (table 1) of eight or less predicted
a 30-day mortality of 91 percent.
An ICH volume less than 30 cm3 and a Glasgow coma scale score of nine or more predicted a 30-day mortality of 19
percent.
The method for calculating ICH volume from head CT is discussed separately. (See "Spontaneous intracerebral
hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Head CT'.)
Other studies have also found that GCS is a useful predictor of outcome [101].

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Hematoma growth and clinical deterioration

Hematoma growth, particularly within the first 24 hours, is also an independent predictor of mortality and poor
outcome [102]. In a meta-analysis of 218 patients with spontaneous ICH who had a head CT scan within three hours
of onset and follow-up head CT within 24 hours, each 10 percent increase in ICH growth was associated with
increased mortality (hazard ratio 1.05, 95% CI 1.03-1.08) and worse outcome as measured by the modified Rankin
scale (odds ratio 0.84, 95% CI 0.75-0.92) [103]. That is, for each 10 percent increase in hematoma volume, patients
were 5 percent more likely to die and 16 percent more likely to increase one point on the modified Rankin scale (table
2). A subsequently published analysis found that while all measures of hematoma growth are robust predictors of
worse outcomes, absolute increases in hemorrhage volume have higher predictive values compared with relative
increases [104].
Risk factors for hematoma enlargement (contrast extravasation or spot sign on CTA, blood pressure, antithrombotic
therapy) are also associated with worse outcomes and discussed separately. (See "Spontaneous intracerebral
hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Hemorrhage enlargement'.)
Intraventricular and subarachnoid extension of ICH may be present on initial evaluation or occur subsequently.
Data from a number of studies suggest that extension of blood into the ventricles and/or subarachnoid space is an
independent predictor of poor outcome in patients with spontaneous ICH [97,105-111]. One of the largest of these
reports evaluated 406 patients with ICH, 45 percent of whom had intraventricular extension of hemorrhage [109].
After controlling for age and ICH volume, a poor outcome at discharge (defined as a modified Rankin scale score of 4
to 6 (table 2)) was significantly more likely in patients with intraventricular hemorrhage than in those without
intraventricular hemorrhage (odds ratio 2.25, 95% CI 1.40-3.64). Intraventricular hemorrhage is discussed in detail
separately. (See "Intraventricular hemorrhage".)
Early neurologic deterioration within 48 hours after ICH onset is not infrequent and is associated with a poor
prognosis. Potential mechanisms include hemorrhage enlargement, development of hydrocephalus, and perilesional
edema [102,112]. The inflammatory response to the hemorrhage may also play a role.
In a cohort study of 266 patients with ICH admitted within 12 hours of stroke onset, early neurologic

deterioration occurred in 61 (23 percent) and was associated with an eight-fold increase in the probability of a
poor outcome (95% CI 2.7-25.5) [113]. Independent predictors of early neurologic deterioration on admission
included elevations in body temperature, neutrophil count, and serum fibrinogen level (odds ratios 24.5, 2.1,
and 5.6, respectively), all of which could be interpreted as markers of an inflammatory response. Factors
measured at 48 hours that were associated with early neurologic deterioration included ICH growth on repeat
head CT, intraventricular bleeding, and high systolic blood pressure.
In many [91,112,114,115] but not all [113] reports, the initial ICH volume on CT is an independent predictor of
early deterioration. The degree and subsequent expansion of perilesional edema is strongly related to the size
of the initial ICH volume, and at least in one study, did not appear have an independent effect in predicting
outcome [116].
Preceding antithrombotic use In the setting of an acute ICH, patients with preceding use of anticoagulants or
antiplatelet agents appear to have larger initial hematoma volumes or greater hemorrhage enlargement leading to worse
outcomes [117,118]. However, the available evidence associating antithrombotic use with poor outcomes is mainly
observational.
Oral anticoagulants Patients on oral anticoagulant therapy have a mortality rate of 52 to 73 percent after ICH
[94,117,119,120]. In nonrandomized comparisons, these rates appear to be higher than those not on anticoagulation
therapy with reported relative risks ranging from 3 to 4 [94,117]. This increased risk may be mitigated, but not
eliminated by rapid reversal of anticoagulation [121].
Antiplatelets The evidence regarding preceding antiplatelet use with prognosis after ICH is not as clear, with
some [94,118,122-124] but not all [120,125-129] studies reporting worse prognosis or greater hematoma
enlargement with ICH. A systematic review of 25 cohort studies concluded that prior antiplatelet use was associated
with increased mortality (OR = 1.3), but not poor functional outcome after ICH [130].
ICH score A simple six-point clinical grading scale called the ICH score has been devised to predict mortality after
ICH [131]. This scale incorporates several clinical components that may be independent predictors of outcome.
The ICH score is determined by adding the score from each component as follows:
Glasgow Coma Scale (GCS) score 3 to 4 (= 2 points); GCS 5 to 12 (= 1 point) and GCS 13 to 15 (= 0 points) (table
1)
ICH volume 30 cm3 (= 1 point), ICH volume <30 cm3 (= 0 points)
Intraventricular extension of hemorrhage present (= 1 point); absent (= 0 points)
Infratentorial origin yes (= 1 point); no (= 0 points)
Age 80 (= 1 point); <80 (= 0 points)
Thirty-day mortality rates increased steadily with ICH score; mortality rates for ICH scores of 1, 2, 3, 4, and 5 were 13, 26,
72, 97, and 100 percent, respectively. No patient with an ICH score of 0 died, and none had a score of 6 in the cohort.
The ICH score has been validated by retrospective [132] and prospective [133,134] analysis. A modified ICH score [132]
using the National Institutes of Health Stroke Scale (NIHSS) score [135] (table 3) in place of the GCS score may be a
better predictor of good outcome than the original ICH score.
Other factors Patient age and overall medical health and condition have an important role in the patients survival
and morbidity after ICH [136].
Accumulating data suggest that the early use of do not resuscitate (DNR) orders, along with decisions to limit aggressive
treatments and/or withdraw medical care may negatively influence outcome in patients with ICH, and may even invalidate
some prognostic models that do not control for this variable [8,137-140].
A number of reports have noted that elevated admission blood glucose after ICH is a poor prognostic indicator
[9,85,91,141-144]. However, it is unclear if elevated glucose directly contributes to poor outcome, or if it alternatively is
present secondarily as part of the stress response to severe ICH.
Low total and LDL cholesterol have been linked to a risk of ICH. (See "Spontaneous intracerebral hemorrhage:
Pathogenesis, clinical features, and diagnosis", section on 'Risk factors'.) In one study of 108 patients with ICH, lower
serum LDL-cholesterol predicted early hematoma growth, neurologic deterioration, and three-month mortality [145].
At least two studies have found that extensive white matter lesions on CT or MRI is associated with worse outcomes
8 of 22

[146,147]. Another study found that elevated C-reactive protein levels were an independent predictor of mortality after ICH
[148].
A number of studies have found that a significant number of patients with ICH have acute ischemic lesions on diffusionweighted MRI imaging that are not contiguous to the hematoma [15]. The implication for these findings for prognosis are
as yet undefined, although one study found that the presence of these lesions were associated with increased odds of
death and disability [16]. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis",
section on 'Mechanisms of brain injury'.)
Recurrence Recurrent hypertensive ICH occurs in as many as 5 percent of patients [88,149-151]. Recurrence is most
common within two years of the first hemorrhage [150]. In one study with a three-year follow-up, the risk for subsequent
cerebral infarction was similar to the risk of recurrent hemorrhage [88].
Uncontrolled hypertension appears to be the most important risk factor for recurrent hemorrhage [149]. Other risk factors
variably identified as associated with recurrent ICH include [3,62,152]:
Uncontrolled hypertension
Lobar location of initial ICH
Older age
Male gender
Ongoing anticoagulation
Apolipoprotein E epsilon 2 or epsilon 4 alleles
Greater number of microbleeds on MRI
Ischemic stroke history
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond
the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and
they answer the four or five key questions a patient might have about a given condition. These articles are best for patients
who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces
are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are
best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to
your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the
keyword(s) of interest.)
Basics topics (see "Patient information: Hemorrhagic stroke (The Basics)")
Beyond the Basics topics (see "Patient information: Hemorrhagic stroke treatment (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS

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Patients with acute ICH should be managed in an intensive care unit. General management issues include:
Discontinuation of all anticoagulant and antiplatelet drugs, and immediate reversal of anticoagulant effects with
the appropriate agents. (See "Reversal of anticoagulation in warfarin-associated intracerebral hemorrhage".)
Maintenance of normothermia and evaluation and treatment of fever source. (See "Initial assessment and
management of acute stroke", section on 'Fever'.)
Normal saline initially should be used for maintenance and replacement fluids. (See 'General management
issues' above.)
Treating hyperglycemia (elevated serum glucose >185 mg/dL (>10.3 mmol/L) with insulin; hypoglycemia should
be avoided. (See "Initial assessment and management of acute stroke", section on 'Hyperglycemia'.)
Prevention of aspiration in patients with acute stroke includes initial nulla per os (NPO) status until swallowing
function is evaluated. (See "Initial assessment and management of acute stroke", section on 'Swallowing
assessment'.)
Current guidelines suggest consideration of aggressive full care during the first 24 hours after intracerebral
hemorrhage (ICH) onset and postponement of new do not resuscitate (DNR) orders during that time. (See
'General management issues' above.)

10 of 22

Prevention of deep venous thrombosis and venous thromboembolism. (See "The use of antithrombotic therapy
in patients with an acute or prior intracerebral hemorrhage".)
Initial management of elevated intracranial pressure (ICP) includes elevating the head of the bed to 30 degrees and
use of analgesia and sedation. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam.
Suggested agents for analgesia and antitussive effect are morphine or alfentanil.
Invasive monitoring and treatment of ICP should be considered for patients with GCS <8 (table 1), those with clinical
evidence of transtentorial herniation, or those with significant IVH or hydrocephalus. More aggressive therapies for
reducing elevated ICP include osmotic diuretics (eg, mannitol), ventricular catheter drainage of cerebrospinal fluid,
and neuromuscular blockade (See 'Intracranial pressure' above.)
Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding. Labetalol,
nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful intravenous agents for
controlling blood pressure. (See 'Blood pressure' above.)
For patients with systolic blood pressure (SBP) >200 mmHg or mean arterial pressure (MAP) >150 mmHg, we
suggest aggressive reduction of blood pressure with continuous intravenous infusion of medication
accompanied by blood pressure monitoring every five minutes (Grade 2C).
For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, we suggest
monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep
cerebral perfusion pressure in the range of 61 to 80 mmHg (Grade 2C).
For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, we
suggest a modest reduction of blood pressure to a target MAP of 110 mmHg or target blood pressure of 160/90
mmHg using intermittent or continuous intravenous medication accompanied by reexamination of the patient
every 15 minutes (Grade 2C).
Appropriate intravenous antiepileptic treatment should be used to quickly control seizures for patients with ICH and
clinical seizures. (See 'Seizure prophylaxis and treatment' above.)
For patients with cerebellar hemorrhages >3 cm in diameter who are deteriorating or who have brainstem
compression and/or hydrocephalus due to ventricular obstruction, we recommend surgical removal of hemorrhage
(Grade 1B).
Surgery for supratentorial ICH is controversial, and current guidelines suggest consideration of standard craniotomy
only for those with life-threatening mass effect who have lobar clots within 1 cm of the surface. The routine
evacuation of supratentorial ICH is not recommended. (See 'Surgery' above.)
Recombinant factor VIIa treatment for acute ICH is investigational and should not be used for the treatment of ICH
outside the context of a clinical trial. (See 'Hemostatic therapy' above.)
The 30-day mortality from intracerebral hemorrhage ICH ranges from 35 to 52 percent. Among survivors, the
prognosis for functional recovery depends upon the location of hemorrhage, size of the hematoma, level of
consciousness, patient age, and overall medical health and condition. (See 'Prognosis' above.)
Treating hypertension is the most important step to reduce the risk of ICH, and probably recurrent ICH. Stopping
smoking, heavy alcohol use, and cocaine use are also recommended. (See 'Secondary prevention' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral
hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association
Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research
Interdisciplinary Working Group. Stroke 2007; 38:2001.
2. Manno EM, Atkinson JL, Fulgham JR, Wijdicks EF. Emerging medical and surgical management strategies in the
evaluation and treatment of intracerebral hemorrhage. Mayo Clin Proc 2005; 80:420.
3. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral

11 of 22

hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke 2010; 41:2108.
4. Maas MB, Rosenberg NF, Kosteva AR, et al. Surveillance neuroimaging and neurologic examinations affect care for
intracerebral hemorrhage. Neurology 2013; 81:107.
5. Abid KA, Vail A, Patel HC, et al. Which factors influence decisions to transfer and treat patients with acute
intracerebral haemorrhage and which are associated with prognosis? A retrospective cohort study. BMJ Open 2013;
3:e003684.
6. Ciccone A, Celani MG, Chiaramonte R, et al. Continuous versus intermittent physiological monitoring for acute
stroke. Cochrane Database Syst Rev 2013; 5:CD008444.
7. Langhorne P, Fearon P, Ronning OM, et al. Stroke unit care benefits patients with intracerebral hemorrhage:
systematic review and meta-analysis. Stroke 2013; 44:3044.
8. Hemphill JC 3rd, Newman J, Zhao S, Johnston SC. Hospital usage of early do-not-resuscitate orders and outcome
after intracerebral hemorrhage. Stroke 2004; 35:1130.
9. Balami JS, Buchan AM. Complications of intracerebral haemorrhage. Lancet Neurol 2012; 11:101.
10. Manno EM. Update on intracerebral hemorrhage. Continuum (Minneap Minn) 2012; 18:598.
11. Andrews CM, Jauch EC, Hemphill JC 3rd, et al. Emergency neurological life support: intracerebral hemorrhage.
Neurocrit Care 2012; 17 Suppl 1:S37.
12. Martin M, Conlon LW. Does platelet transfusion improve outcomes in patients with spontaneous or traumatic
intracerebral hemorrhage? Ann Emerg Med 2013; 61:58.
13. Ohwaki K, Yano E, Nagashima H, et al. Blood pressure management in acute intracerebral hemorrhage: relationship
between elevated blood pressure and hematoma enlargement. Stroke 2004; 35:1364.
14. Sakamoto Y, Koga M, Yamagami H, et al. Systolic blood pressure after intravenous antihypertensive treatment and
clinical outcomes in hyperacute intracerebral hemorrhage: the stroke acute management with urgent risk-factor
assessment and improvement-intracerebral hemorrhage study. Stroke 2013; 44:1846.
15. Menon RS, Burgess RE, Wing JJ, et al. Predictors of highly prevalent brain ischemia in intracerebral hemorrhage.
Ann Neurol 2012; 71:199.
16. Garg RK, Liebling SM, Maas MB, et al. Blood pressure reduction, decreased diffusion on MRI, and outcomes after
intracerebral hemorrhage. Stroke 2012; 43:67.
17. Qureshi AI. Significance of lesions with decreased diffusion on MRI in patients with intracerebral hemorrhage. Stroke
2012; 43:6.
18. Butcher KS, Jeerakathil T, Hill M, et al. The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial.
Stroke 2013; 44:620.
19. Gould B, McCourt R, Asdaghi N, et al. Autoregulation of cerebral blood flow is preserved in primary intracerebral
hemorrhage. Stroke 2013; 44:1726.
20. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral
hemorrhage. N Engl J Med 2013; 368:2355.
21. Anderson CS, Huang Y, Arima H, et al. Effects of early intensive blood pressure-lowering treatment on the growth of
hematoma and perihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in
Acute Cerebral Haemorrhage Trial (INTERACT). Stroke 2010; 41:307.
22. Qureshi AI, Mohammad YM, Yahia AM, et al. A prospective multicenter study to evaluate the feasibility and safety of
aggressive antihypertensive treatment in patients with acute intracerebral hemorrhage. J Intensive Care Med 2005;
20:34.
23. Qureshi AI, Palesch YY, Martin R, et al. Effect of systolic blood pressure reduction on hematoma expansion,
perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the
antihypertensive treatment of acute cerebral hemorrhage study. Arch Neurol 2010; 67:570.
24. Kuramatsu JB, Sauer R, Mauer C, et al. Correlation of age and haematoma volume in patients with spontaneous
lobar intracerebral haemorrhage. J Neurol Neurosurg Psychiatry 2011; 82:144.
25. Naidech AM, Garg RK, Liebling S, et al. Anticonvulsant use and outcomes after intracerebral hemorrhage. Stroke
2009; 40:3810.
26. Mess SR, Sansing LH, Cucchiara BL, et al. Prophylactic antiepileptic drug use is associated with poor outcome
following ICH. Neurocrit Care 2009; 11:38.
27. Poungvarin N, Bhoopat W, Viriyavejakul A, et al. Effects of dexamethasone in primary supratentorial intracerebral
hemorrhage. N Engl J Med 1987; 316:1229.
28. Helbok R, Kurtz P, Schmidt JM, et al. Effect of mannitol on brain metabolism and tissue oxygenation in severe
haemorrhagic stroke. J Neurol Neurosurg Psychiatry 2011; 82:378.

12 of 22

29. Dorman HR, Sondheimer JH, Cadnapaphornchai P. Mannitol-induced acute renal failure. Medicine (Baltimore) 1990;
69:153.
30. Schwab S, Spranger M, Schwarz S, Hacke W. Barbiturate coma in severe hemispheric stroke: useful or obsolete?
Neurology 1997; 48:1608.
31. Neurological and Neurosurgical Intensive Care. Ropper, AH (Ed), Raven Press, New York 1993.
32. Ott KH, Kase CS, Ojemann RG, Mohr JP. Cerebellar hemorrhage: diagnosis and treatment. A review of 56 cases.
Arch Neurol 1974; 31:160.
33. Hankey GJ, Hon C. Surgery for primary intracerebral hemorrhage: is it safe and effective? A systematic review of
case series and randomized trials. Stroke 1997; 28:2126.
34. Batjer HH, Reisch JS, Allen BC, et al. Failure of surgery to improve outcome in hypertensive putaminal hemorrhage.
A prospective randomized trial. Arch Neurol 1990; 47:1103.
35. Morgenstern LB, Demchuk AM, Kim DH, et al. Rebleeding leads to poor outcome in ultra-early craniotomy for
intracerebral hemorrhage. Neurology 2001; 56:1294.
36. Minematsu K. Evacuation of intracerebral hematoma is likely to be beneficial. Stroke 2003; 34:1567.
37. Hankey GJ. Evacuation of intracerebral hematoma is likely to be beneficial--against. Stroke 2003; 34:1568.
38. Donnan GA, Davis SM. Surgery for intracerebral hemorrhage: an evidence-poor zone. Stroke 2003; 34:1569.
39. Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with
spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral
Haemorrhage (STICH): a randomised trial. Lancet 2005; 365:387.
40. Nakano T, Ohkuma H. Surgery versus conservative treatment for intracerebral haemorrhage--is there an end to the
long controversy? Lancet 2005; 365:361.
41. Gregson BA, Broderick JP, Auer LM, et al. Individual patient data subgroup meta-analysis of surgery for
spontaneous supratentorial intracerebral hemorrhage. Stroke 2012; 43:1496.
42. Gautschi OP, Schaller K. Surgery or conservative therapy for cerebral haemorrhage? Lancet 2013; 382:377.
43. Prasad K, Mendelow AD, Gregson B. Surgery for primary supratentorial intracerebral haemorrhage. Cochrane
Database Syst Rev 2008; :CD000200.
44. Brown DL, Morgenstern LB. Stopping the bleeding in intracerebral hemorrhage. N Engl J Med 2005; 352:828.
45. Broderick JP. The STICH trial: what does it tell us and where do we go from here? Stroke 2005; 36:1619.
46. Mendelow AD, Gregson BA, Rowan EN, et al. Early surgery versus initial conservative treatment in patients with
spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet 2013; 382:397.
47. Cruz-Flores S. Early surgery and initial conservative therapy did not differ for outcomes in lobar intracerebral
hematomas. Ann Intern Med 2013; 159:JC11.
48. Al-Shahi Salman R. Haemostatic drug therapies for acute spontaneous intracerebral haemorrhage. Cochrane
Database Syst Rev 2009; :CD005951.
49. O'Connell KA, Wood JJ, Wise RP, et al. Thromboembolic adverse events after use of recombinant human
coagulation factor VIIa. JAMA 2006; 295:293.
50. Mayer SA, Brun NC, Broderick J, et al. Safety and feasibility of recombinant factor VIIa for acute intracerebral
hemorrhage. Stroke 2005; 36:74.
51. Mayer SA, Brun NC, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J
Med 2005; 352:777.
52. Mayer SA, Brun NC, Begtrup K, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral
hemorrhage. N Engl J Med 2008; 358:2127.
53. Diringer MN, Skolnick BE, Mayer SA, et al. Risk of thromboembolic events in controlled trials of rFVIIa in
spontaneous intracerebral hemorrhage. Stroke 2008; 39:850.
54. Sugg RM, Gonzales NR, Matherne DE, et al. Myocardial injury in patients with intracerebral hemorrhage treated with
recombinant factor VIIa. Neurology 2006; 67:1053.
55. Subramaniam S, Demchuk AM, Watson T, et al. Unexpected posthemorrhagic hydrocephalus in patients treated with
rFVIIa. Neurology 2006; 67:1096.
56. He J, Whelton PK, Vu B, Klag MJ. Aspirin and risk of hemorrhagic stroke: a meta-analysis of randomized controlled
trials. JAMA 1998; 280:1930.
57. Hart RG, Halperin JL, McBride R, et al. Aspirin for the primary prevention of stroke and other major vascular events:
meta-analysis and hypotheses. Arch Neurol 2000; 57:326.
58. Biffi A, Halpin A, Towfighi A, et al. Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy.
Neurology 2010; 75:693.

13 of 22

59. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient
ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke
Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the
American Academy of Neurology affirms the value of this guideline. Stroke 2006; 37:577.
60. Furie KL, Kasner SE, Adams RJ, et al. Guidelines for the prevention of stroke in patients with stroke or transient
ischemic attack: a guideline for healthcare professionals from the american heart association/american stroke
association. Stroke 2011; 42:227.
61. Chapman N, Huxley R, Anderson C, et al. Effects of a perindopril-based blood pressure-lowering regimen on the risk
of recurrent stroke according to stroke subtype and medical history: the PROGRESS Trial. Stroke 2004; 35:116.
62. Kase CS, Kurth T. Prevention of intracerebral hemorrhage recurrence. Continuum (Minneap Minn) 2011; 17:1304.
63. Thrift AG, McNeil JJ, Forbes A, Donnan GA. Risk factors for cerebral hemorrhage in the era of well-controlled
hypertension. Melbourne Risk Factor Study (MERFS) Group. Stroke 1996; 27:2020.
64. Giroud M, Creisson E, Fayolle H, et al. Risk factors for primary cerebral hemorrhage: a population-based study--the
Stroke Registry of Dijon. Neuroepidemiology 1995; 14:20.
65. Iribarren C, Jacobs DR, Sadler M, et al. Low total serum cholesterol and intracerebral hemorrhagic stroke: is the
association confined to elderly men? The Kaiser Permanente Medical Care Program. Stroke 1996; 27:1993.
66. Gonzlez-Duarte A, Cant C, Ruz-Sandoval JL, Barinagarrementeria F. Recurrent primary cerebral hemorrhage:
frequency, mechanisms, and prognosis. Stroke 1998; 29:1802.
67. Segal AZ, Chiu RI, Eggleston-Sexton PM, et al. Low cholesterol as a risk factor for primary intracerebral
hemorrhage: A case-control study. Neuroepidemiology 1999; 18:185.
68. Yano K, Reed DM, MacLean CJ. Serum cholesterol and hemorrhagic stroke in the Honolulu Heart Program. Stroke
1989; 20:1460.
69. Shinkawa A, Ueda K, Hasuo Y, et al. Seasonal variation in stroke incidence in Hisayama, Japan. Stroke 1990;
21:1262.
70. Noda H, Iso H, Irie F, et al. Low-density lipoprotein cholesterol concentrations and death due to intraparenchymal
hemorrhage: the Ibaraki Prefectural Health Study. Circulation 2009; 119:2136.
71. Wang X, Dong Y, Qi X, et al. Cholesterol levels and risk of hemorrhagic stroke: a systematic review and
meta-analysis. Stroke 2013; 44:1833.
72. Woo D, Kissela BM, Khoury JC, et al. Hypercholesterolemia, HMG-CoA reductase inhibitors, and risk of intracerebral
hemorrhage: a case-control study. Stroke 2004; 35:1360.
73. Amarenco P, Labreuche J, Lavalle P, Touboul PJ. Statins in stroke prevention and carotid atherosclerosis:
systematic review and up-to-date meta-analysis. Stroke 2004; 35:2902.
74. Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective
meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366:1267.
75. Leker RR, Khoury ST, Rafaeli G, et al. Prior use of statins improves outcome in patients with intracerebral
hemorrhage: prospective data from the National Acute Stroke Israeli Surveys (NASIS). Stroke 2009; 40:2581.
76. Hackam DG, Austin PC, Huang A, et al. Statins and intracerebral hemorrhage: a retrospective cohort study. Arch
Neurol 2012; 69:39.
77. Hackam DG, Woodward M, Newby LK, et al. Statins and intracerebral hemorrhage: collaborative systematic review
and meta-analysis. Circulation 2011; 124:2233.
78. McKinney JS, Kostis WJ. Statin therapy and the risk of intracerebral hemorrhage: a meta-analysis of 31 randomized
controlled trials. Stroke 2012; 43:2149.
79. Westover MB, Bianchi MT, Eckman MH, Greenberg SM. Statin use following intracerebral hemorrhage: a decision
analysis. Arch Neurol 2011; 68:573.
80. Goldstein LB. Statins after intracerebral hemorrhage: to treat or not to treat. Arch Neurol 2011; 68:565.
81. Amarenco P, Labreuche J. Lipid management in the prevention of stroke: review and updated meta-analysis of
statins for stroke prevention. Lancet Neurol 2009; 8:453.
82. Anderson CS, Chakera TM, Stewart-Wynne EG, Jamrozik KD. Spectrum of primary intracerebral haemorrhage in
Perth, Western Australia, 1989-90: incidence and outcome. J Neurol Neurosurg Psychiatry 1994; 57:936.
83. Counsell C, Boonyakarnukul S, Dennis M, et al. Primary intracerebral hemorrhage in the Oxford-shire community
Stroke Project. Cerebrovasc Dis 1995; 5:26.
84. Broderick JP, Brott TG, Duldner JE, et al. Volume of intracerebral hemorrhage. A powerful and easy-to-use predictor
of 30-day mortality. Stroke 1993; 24:987.
85. Fogelholm R, Murros K, Rissanen A, Avikainen S. Long term survival after primary intracerebral haemorrhage: a
retrospective population based study. J Neurol Neurosurg Psychiatry 2005; 76:1534.

86. Flaherty ML, Haverbusch M, Sekar P, et al. Long-term mortality after intracerebral hemorrhage. Neurology 2006;
66:1182.
87. Sacco S, Marini C, Toni D, et al. Incidence and 10-year survival of intracerebral hemorrhage in a population-based
registry. Stroke 2009; 40:394.
88. Zia E, Engstrm G, Svensson PJ, et al. Three-year survival and stroke recurrence rates in patients with primary
intracerebral hemorrhage. Stroke 2009; 40:3567.
89. van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of intracerebral
haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet
Neurol 2010; 9:167.
90. Gonzlez-Prez A, Gaist D, Wallander MA, et al. Mortality after hemorrhagic stroke: data from general practice (The
Health Improvement Network). Neurology 2013; 81:559.
91. Franke CL, van Swieten JC, Algra A, van Gijn J. Prognostic factors in patients with intracerebral haematoma. J
Neurol Neurosurg Psychiatry 1992; 55:653.
92. Tuhrim S, Dambrosia JM, Price TR, et al. Intracerebral hemorrhage: external validation and extension of a model for
prediction of 30-day survival. Ann Neurol 1991; 29:658.
93. Stein M, Misselwitz B, Hamann GF, et al. Intracerebral hemorrhage in the very old: future demographic trends of an
aging population. Stroke 2012; 43:1126.
94. Saloheimo P, Ahonen M, Juvela S, et al. Regular aspirin-use preceding the onset of primary intracerebral
hemorrhage is an independent predictor for death. Stroke 2006; 37:129.
95. van Beijnum J, Lovelock CE, Cordonnier C, et al. Outcome after spontaneous and arteriovenous malformationrelated intracerebral haemorrhage: population-based studies. Brain 2009; 132:537.
96. Beslow LA, Licht DJ, Smith SE, et al. Predictors of outcome in childhood intracerebral hemorrhage: a prospective
consecutive cohort study. Stroke 2010; 41:313.
97. Lo WD, Hajek C, Pappa C, et al. Outcomes in children with hemorrhagic stroke. JAMA Neurol 2013; 70:66.
98. Saloheimo P, Lapp TM, Juvela S, Hillbom M. The impact of functional status at three months on long-term survival
after spontaneous intracerebral hemorrhage. Stroke 2006; 37:487.
99. Hansen BM, Nilsson OG, Anderson H, et al. Long term (13 years) prognosis after primary intracerebral
haemorrhage: a prospective population based study of long term mortality, prognostic factors and causes of death. J
Neurol Neurosurg Psychiatry 2013; 84:1150.
100. Jordan LC, Kleinman JT, Hillis AE. Intracerebral hemorrhage volume predicts poor neurologic outcome in children.
Stroke 2009; 40:1666.
101. Parry-Jones AR, Abid KA, Di Napoli M, et al. Accuracy and clinical usefulness of intracerebral hemorrhage grading
scores: a direct comparison in a UK population. Stroke 2013; 44:1840.
102. Rodriguez-Luna D, Rubiera M, Ribo M, et al. Ultraearly hematoma growth predicts poor outcome after acute
intracerebral hemorrhage. Neurology 2011; 77:1599.
103. Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after
intracerebral hemorrhage. Neurology 2006; 66:1175.
104. Dowlatshahi D, Demchuk AM, Flaherty ML, et al. Defining hematoma expansion in intracerebral hemorrhage:
relationship with patient outcomes. Neurology 2011; 76:1238.
105. Portenoy RK, Lipton RB, Berger AR, et al. Intracerebral haemorrhage: a model for the prediction of outcome. J
Neurol Neurosurg Psychiatry 1987; 50:976.
106. Young WB, Lee KP, Pessin MS, et al. Prognostic significance of ventricular blood in supratentorial hemorrhage: a
volumetric study. Neurology 1990; 40:616.
107. Lisk DR, Pasteur W, Rhoades H, et al. Early presentation of hemispheric intracerebral hemorrhage: prediction of
outcome and guidelines for treatment allocation. Neurology 1994; 44:133.
108. Tuhrim S, Horowitz DR, Sacher M, Godbold JH. Volume of ventricular blood is an important determinant of outcome
in supratentorial intracerebral hemorrhage. Crit Care Med 1999; 27:617.
109. Hallevi H, Albright KC, Aronowski J, et al. Intraventricular hemorrhage: Anatomic relationships and clinical
implications. Neurology 2008; 70:848.
110. Staykov D, Volbers B, Wagner I, et al. Prognostic significance of third ventricle blood volume in intracerebral
haemorrhage with severe ventricular involvement. J Neurol Neurosurg Psychiatry 2011; 82:1260.
111. Maas MB, Nemeth AJ, Rosenberg NF, et al. Subarachnoid extension of primary intracerebral hemorrhage is
associated with poor outcomes. Stroke 2013; 44:653.
112. Mayer SA, Sacco RL, Shi T, Mohr JP. Neurologic deterioration in noncomatose patients with supratentorial
intracerebral hemorrhage. Neurology 1994; 44:1379.
14 of 22

113. Leira R, Dvalos A, Silva Y, et al. Early neurologic deterioration in intracerebral hemorrhage: predictors and
associated factors. Neurology 2004; 63:461.
114. Qureshi AI, Safdar K, Weil J, et al. Predictors of early deterioration and mortality in black Americans with
spontaneous intracerebral hemorrhage. Stroke 1995; 26:1764.
115. Flemming KD, Wijdicks EF, St Louis EK, Li H. Predicting deterioration in patients with lobar haemorrhages. J Neurol
Neurosurg Psychiatry 1999; 66:600.
116. Arima H, Wang JG, Huang Y, et al. Significance of perihematomal edema in acute intracerebral hemorrhage: the
INTERACT trial. Neurology 2009; 73:1963.
117. Cucchiara B, Messe S, Sansing L, et al. Hematoma growth in oral anticoagulant related intracerebral hemorrhage.
Stroke 2008; 39:2993.
118. Falcone GJ, Biffi A, Brouwers HB, et al. Predictors of hematoma volume in deep and lobar supratentorial
intracerebral hemorrhage. JAMA Neurol 2013; 70:988.
119. Hart RG, Boop BS, Anderson DC. Oral anticoagulants and intracranial hemorrhage. Facts and hypotheses. Stroke
1995; 26:1471.
120. Rosand J, Eckman MH, Knudsen KA, et al. The effect of warfarin and intensity of anticoagulation on outcome of
intracerebral hemorrhage. Arch Intern Med 2004; 164:880.
121. Dowlatshahi D, Butcher KS, Asdaghi N, et al. Poor prognosis in warfarin-associated intracranial hemorrhage despite
anticoagulation reversal. Stroke 2012; 43:1812.
122. Toyoda K, Okada Y, Minematsu K, et al. Antiplatelet therapy contributes to acute deterioration of intracerebral
hemorrhage. Neurology 2005; 65:1000.
123. Naidech AM, Bernstein RA, Levasseur K, et al. Platelet activity and outcome after intracerebral hemorrhage. Ann
Neurol 2009; 65:352.
124. Naidech AM, Jovanovic B, Liebling S, et al. Reduced platelet activity is associated with early clot growth and worse
3-month outcome after intracerebral hemorrhage. Stroke 2009; 40:2398.
125. Foerch C, Sitzer M, Steinmetz H, Neumann-Haefelin T. Pretreatment with antiplatelet agents is not independently
associated with unfavorable outcome in intracerebral hemorrhage. Stroke 2006; 37:2165.
126. Nilsson OG, Lindgren A, Brandt L, Sveland H. Prediction of death in patients with primary intracerebral
hemorrhage: a prospective study of a defined population. J Neurosurg 2002; 97:531.
127. Flibotte JJ, Hagan N, O'Donnell J, et al. Warfarin, hematoma expansion, and outcome of intracerebral hemorrhage.
Neurology 2004; 63:1059.
128. Brott T, Broderick J, Kothari R, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke
1997; 28:1.
129. Sansing LH, Messe SR, Cucchiara BL, et al. Prior antiplatelet use does not affect hemorrhage growth or outcome
after ICH. Neurology 2009; 72:1397.
130. Thompson BB, Bjot Y, Caso V, et al. Prior antiplatelet therapy and outcome following intracerebral hemorrhage: a
systematic review. Neurology 2010; 75:1333.
131. Hemphill JC 3rd, Bonovich DC, Besmertis L, et al. The ICH score: a simple, reliable grading scale for intracerebral
hemorrhage. Stroke 2001; 32:891.
132. Cheung RT, Zou LY. Use of the original, modified, or new intracerebral hemorrhage score to predict mortality and
morbidity after intracerebral hemorrhage. Stroke 2003; 34:1717.
133. Godoy DA, Piero G, Di Napoli M. Predicting mortality in spontaneous intracerebral hemorrhage: can modification to
original score improve the prediction? Stroke 2006; 37:1038.
134. Hemphill JC 3rd, Farrant M, Neill TA Jr. Prospective validation of the ICH Score for 12-month functional outcome.
Neurology 2009; 73:1088.
135. Muir KW, Weir CJ, Murray GD, et al. Comparison of neurological scales and scoring systems for acute stroke
prognosis. Stroke 1996; 27:1817.
136. Bar B, Hemphill JC 3rd. Charlson comorbidity index adjustment in intracerebral hemorrhage. Stroke 2011; 42:2944.
137. Becker KJ, Baxter AB, Cohen WA, et al. Withdrawal of support in intracerebral hemorrhage may lead to self-fulfilling
prophecies. Neurology 2001; 56:766.
138. Zahuranec DB, Brown DL, Lisabeth LD, et al. Early care limitations independently predict mortality after intracerebral
hemorrhage. Neurology 2007; 68:1651.
139. Zahuranec DB, Morgenstern LB, Snchez BN, et al. Do-not-resuscitate orders and predictive models after
intracerebral hemorrhage. Neurology 2010; 75:626.
140. Creutzfeldt CJ, Becker KJ, Weinstein JR, et al. Do-not-attempt-resuscitation orders and prognostic models for
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intraparenchymal hemorrhage. Crit Care Med 2011; 39:158.

141. Passero S, Ciacci G, Ulivelli M. The influence of diabetes and hyperglycemia on clinical course after intracerebral
hemorrhage. Neurology 2003; 61:1351.
142. Fogelholm R, Murros K, Rissanen A, Avikainen S. Admission blood glucose and short term survival in primary
intracerebral haemorrhage: a population based study. J Neurol Neurosurg Psychiatry 2005; 76:349.
143. Appelboom G, Piazza MA, Hwang BY, et al. Severity of intraventricular extension correlates with level of admission
glucose after intracerebral hemorrhage. Stroke 2011; 42:1883.
144. Bjot Y, Aboa-Eboul C, Hervieu M, et al. The deleterious effect of admission hyperglycemia on survival and
functional outcome in patients with intracerebral hemorrhage. Stroke 2012; 43:243.
145. Rodriguez-Luna D, Rubiera M, Ribo M, et al. Serum low-density lipoprotein cholesterol level predicts hematoma
growth and clinical outcome after acute intracerebral hemorrhage. Stroke 2011; 42:2447.
146. Lee SH, Kim BJ, Ryu WS, et al. White matter lesions and poor outcome after intracerebral hemorrhage: a nationwide
cohort study. Neurology 2010; 74:1502.
147. Caprio FZ, Maas MB, Rosenberg NF, et al. Leukoaraiosis on magnetic resonance imaging correlates with worse
outcomes after spontaneous intracerebral hemorrhage. Stroke 2013; 44:642.
148. Di Napoli M, Godoy DA, Campi V, et al. C-reactive protein level measurement improves mortality prediction when
added to the spontaneous intracerebral hemorrhage score. Stroke 2011; 42:1230.
149. Chen ST, Chiang CY, Hsu CY, et al. Recurrent hypertensive intracerebral hemorrhage. Acta Neurol Scand 1995;
91:128.
150. Bae H, Jeong D, Doh J, et al. Recurrence of bleeding in patients with hypertensive intracerebral hemorrhage.
Cerebrovasc Dis 1999; 9:102.
151. Hanger HC, Wilkinson TJ, Fayez-Iskander N, Sainsbury R. The risk of recurrent stroke after intracerebral
haemorrhage. J Neurol Neurosurg Psychiatry 2007; 78:836.
152. Huhtakangas J, Lppnen P, Tetri S, et al. Predictors for recurrent primary intracerebral hemorrhage: a retrospective
population-based study. Stroke 2013; 44:585.
Topic 1084 Version 20.0

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GRAPHICS
Glasgow coma scale
Score
Eye opening
Spontaneous

Response to verbal command

Response to pain

No eye opening

Best verbal response

Oriented

Confused

Inappropriate words

Incomprehensible sounds

No verbal response

Best motor response

Obeys commands

Localizing response to pain

Withdrawal response to pain

Flexion to pain

Extension to pain

No motor response

Total

The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three
parameters: best eye response (E), best verbal response (V), and best motor response (M). The
components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS score of 9.
A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate
injury; and a score of 8 or less represents severe brain injury.
Graphic 81854 Version 2.0

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18 of 22

Modified Rankin scale

Score

Description

No symptoms at all

No significant disability despite symptoms; able to carry out all usual duties and activities

Slight disability; unable to carry out all previous activities, but able to look after own affairs
without assistance

Moderate disability; requiring some help, but able to walk without assistance

Moderately severe disability; unable to walk without assistance and unable to attend to own
bodily needs without assistance

Severe disability; bedridden, incontinent and requiring constant nursing care and attention

Dead

Reproduced with permission from: Van Swieten JC, Koudstaa PJ, Visser MC, et al. Interobserver agreement for
the assessment of handicap in stroke patients. Stroke 1988; 19:604. Copyright 1988 Lippincott Williams &
Wilkins.
Graphic 75411 Version 10.0

National Institutes of Health Stroke Scale (NIHSS)

Administer stroke scale items in the order listed. Record performance in each category after each subscale
exam. Do not go back and change scores. Follow directions provided for each exam technique. Scores
should reflect what the patient does, not what the clinician thinks the patient can do. The clinician should
record answers while administering the exam and work quickly. Except where indicated, the patient should
not be coached (ie, repeated requests to patient to make a special effort).

Instructions
1a. Level of consciousness: The investigator
must choose a response if a full evaluation is
prevented by such obstacles as an
endotracheal tube, language barrier,
orotracheal trauma/bandages. A 3 is scored
only if the patient makes no movement (other
than reflexive posturing) in response to
noxious stimulation.

Scale definition

Score

0 = Alert; keenly responsive.

1 = Not alert; but arousable by minor
stimulation to obey, answer, or respond.
2 = Not alert; requires repeated stimulation
to attend, or is obtunded and requires strong
or painful stimulation to make movements (not

_____

stereotyped).
3 = Responds only with reflex motor or
autonomic effects or totally unresponsive,
flaccid, and areflexic.

1b. LOC questions: The patient is asked the

0 = Answers both questions correctly.

month and his/her age. The answer must be

correct - there is no partial credit for being

1 = Answers one question correctly.

close. Aphasic and stuporous patients who do

not comprehend the questions will score 2.

2 = Answers neither question correctly.

Patients unable to speak because of

endotracheal intubation, orotracheal trauma,

_____

severe dysarthria from any cause, language

barrier, or any other problem not secondary to
aphasia are given a 1. It is important that only
the initial answer be graded and that the
examiner not "help" the patient with verbal or
non-verbal cues.
1c. LOC commands: The patient is asked to

0 = Performs both tasks correctly.

open and close the eyes and then to grip and

release the non-paretic hand. Substitute

1 = Performs one task correctly.

another one step command if the hands cannot

be used. Credit is given if an unequivocal

2 = Performs neither task correctly.

attempt is made but not completed due to

weakness. If the patient does not respond to

_____

command, the task should be demonstrated to

him or her (pantomime), and the result scored
(ie, follows none, one or two commands).
Patients with trauma, amputation, or other
physical impediments should be given suitable
one-step commands. Only the first attempt is
scored.
2. Best gaze: Only horizontal eye movements
will be tested. Voluntary or reflexive
(oculocephalic) eye movements will be scored,
but caloric testing is not done. If the patient
has a conjugate deviation of the eyes that can
be overcome by voluntary or reflexive activity,
the score will be 1. If a patient has an isolated
peripheral nerve paresis (CN III, IV or VI),

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0 = Normal.
1 = Partial gaze palsy; gaze is abnormal in
one or both eyes, but forced deviation or total
gaze paresis is not present.
2 = Forced deviation, or total gaze paresis
not overcome by the oculocephalic maneuver.

_____

score a 1. Gaze is testable in all aphasic

patients. Patients with ocular trauma,
bandages, pre-existing blindness, or other
disorder of visual acuity or fields should be
tested with reflexive movements, and a choice
made by the investigator. Establishing eye
contact and then moving about the patient
from side to side will occasionally clarify the
presence of a partial gaze palsy.
3. Visual: Visual fields (upper and lower

0 = No visual loss.

quadrants) are tested by confrontation, using

finger counting or visual threat, as

1 = Partial hemianopia.

appropriate. Patients may be encouraged, but

if they look at the side of the moving fingers
appropriately, this can be scored as normal. If
there is unilateral blindness or enucleation,

2 = Complete hemianopia.
3 = Bilateral hemianopia (blind including
cortical blindness).
_____

visual fields in the remaining eye are scored.

Score 1 only if a clear-cut asymmetry,
including quadrantanopia, is found. If patient
is blind from any cause, score 3. Double
simultaneous stimulation is performed at this
point. If there is extinction, patient receives a
1, and the results are used to respond to item
11.
4. Facial palsy: Ask - or use pantomime to

0 = Normal symmetrical movements.

encourage - the patient to show teeth or raise

eyebrows and close eyes. Score symmetry of

1 = Minor paralysis (flattened nasolabial

grimace in response to noxious stimuli in the

poorly responsive or non-comprehending
patient. If facial trauma/bandages, orotracheal
tube, tape or other physical barriers obscure
the face, these should be removed to the
extent possible.

fold, asymmetry on smiling).

2 = Partial paralysis (total or near-total
paralysis of lower face).
3 = Complete paralysis of one or both sides
(absence of facial movement in the upper and
lower face).

5. Motor arm: The limb is placed in the

0 = No drift; limb holds 90 (or 45) degrees

appropriate position: extend the arms (palms

down) 90 degrees (if sitting) or 45 degrees (if

for full 10 seconds.

supine). Drift is scored if the arm falls before

10 seconds. The aphasic patient is encouraged
using urgency in the voice and pantomime, but
not noxious stimulation. Each limb is tested in
turn, beginning with the non-paretic arm. Only
in the case of amputation or joint fusion at the
shoulder, the examiner should record the score
as untestable (UN), and clearly write the
explanation for this choice.

_____

1 = Drift; limb holds 90 (or 45) degrees, but

drifts down before full 10 seconds; does not hit
bed or other support.
2 = Some effort against gravity; limb
cannot get to or maintain (if cued) 90 (or 45)
degrees, drifts down to bed, but has some
effort against gravity.

_____

3 = No effort against gravity; limb falls.

4 = No movement.
UN = Amputation or joint fusion,
explain:________________
5a. Left arm
5b. Right arm

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6. Motor leg: The limb is placed in the

0 = No drift; leg holds 30-degree position for

appropriate position: hold the leg at 30

degrees (always tested supine). Drift is scored

full 5 seconds.

_____

21 of 22

if the leg falls before 5 seconds. The aphasic

patient is encouraged using urgency in the

1 = Drift; leg falls by the end of the 5-second

period but does not hit bed.

voice and pantomime, but not noxious

stimulation. Each limb is tested in turn,

2 = Some effort against gravity; leg falls to

beginning with the non-paretic leg. Only in the

case of amputation or joint fusion at the hip,
the examiner should record the score as
untestable (UN), and clearly write the

bed by 5 seconds, but has some effort against

gravity.
3 = No effort against gravity; leg falls to
bed immediately.

explanation for this choice.

4 = No movement.
UN = Amputation or joint fusion,
explain:________________
6a. Left leg
6b. Right leg
7. Limb ataxia: This item is aimed at finding
evidence of a unilateral cerebellar lesion. Test
with eyes open. In case of visual defect,
ensure testing is done in intact visual field. The
finger-nose-finger and heel-shin tests are
performed on both sides, and ataxia is scored
only if present out of proportion to weakness.
Ataxia is absent in the patient who cannot

0 = Absent.
1 = Present in one limb.
2 = Present in two limbs.
UN = Amputation or joint fusion,
explain:________________
_____

understand or is paralyzed. Only in the case of

amputation or joint fusion, the examiner
should record the score as untestable (UN),
and clearly write the explanation for this
choice. In case of blindness, test by having the
patient touch nose from extended arm
position.
8. Sensory: Sensation or grimace to pinprick
when tested, or withdrawal from noxious
stimulus in the obtunded or aphasic patient.
Only sensory loss attributed to stroke is scored
as abnormal and the examiner should test as
many body areas (arms [not hands], legs,
trunk, face) as needed to accurately check for
hemisensory loss. A score of 2, "severe or total
sensory loss," should only be given when a
severe or total loss of sensation can be clearly

0 = Normal; no sensory loss.

1 = Mild-to-moderate sensory loss; patient
feels pinprick is less sharp or is dull on the
affected side; or there is a loss of superficial
pain with pinprick, but patient is aware of
being touched.
2 = Severe to total sensory loss; patient is
not aware of being touched in the face, arm,

_____

and leg.

demonstrated. Stuporous and aphasic patients

will, therefore, probably score 1 or 0. The
patient with brainstem stroke who has bilateral
loss of sensation is scored 2. If the patient
does not respond and is quadriplegic, score 2.
Patients in a coma (item 1a=3) are
automatically given a 2 on this item.
9. Best language: A great deal of information
about comprehension will be obtained during
the preceding sections of the examination. For
this scale item, the patient is asked to describe
what is happening in the attached picture, to
name the items on the attached naming sheet
and to read from the attached list of
sentences. Comprehension is judged from
responses here, as well as to all of the
commands in the preceding general

0 = No aphasia; normal.
1 = Mild-to-moderate aphasia; some
obvious loss of fluency or facility of
comprehension, without significant limitation
on ideas expressed or form of expression.
Reduction of speech and/or comprehension,
however, makes conversation about provided
materials difficult or impossible. For example,

_____

neurological exam. If visual loss interferes with

the tests, ask the patient to identify objects

in conversation about provided materials,

examiner can identify picture or naming card

placed in the hand, repeat, and produce

speech. The intubated patient should be asked

content from patient's response.

to write. The patient in a coma (item 1a=3)

will automatically score 3 on this item. The
examiner must choose a score for the patient
with stupor or limited cooperation, but a score
of 3 should be used only if the patient is mute
and follows no one-step commands.

2 = Severe aphasia; all communication is

through fragmentary expression; great need
for inference, questioning, and guessing by the
listener. Range of information that can be
exchanged is limited; listener carries burden of
communication. Examiner cannot identify
materials provided from patient response.
3 = Mute, global aphasia; no usable speech
or auditory comprehension.

10. Dysarthria: If patient is thought to be

normal, an adequate sample of speech must
be obtained by asking patient to read or repeat
words from the attached list. If the patient has
severe aphasia, the clarity of articulation of
spontaneous speech can be rated. Only if the
patient is intubated or has other physical
barriers to producing speech, the examiner
should record the score as untestable (UN),
and clearly write an explanation for this choice.
Do not tell the patient why he or she is being
tested.

0 = Normal.
1 = Mild-to-moderate dysarthria; patient
slurs at least some words and, at worst, can
be understood with some difficulty.
2 = Severe dysarthria; patient's speech is so
slurred as to be unintelligible in the absence of
or out of proportion to any dysphasia, or is
mute/anarthric.
UN = Intubated or other physical barrier,
explain:________________

11. Extinction and inattention (formerly

0 = No abnormality.

neglect): Sufficient information to identify

neglect may be obtained during the prior

1 = Visual, tactile, auditory, spatial, or

testing. If the patient has a severe visual loss

preventing visual double simultaneous
stimulation, and the cutaneous stimuli are
normal, the score is normal. If the patient has
aphasia but does appear to attend to both
sides, the score is normal. The presence of
visual spatial neglect or anosognosia may also
be taken as evidence of abnormality. Since the

_____

personal inattention or extinction to bilateral

simultaneous stimulation in one of the sensory
modalities.
2 = Profound hemi-inattention or
extinction to more than one modality;

_____

does not recognize own hand or orients to only

one side of space.

abnormality is scored only if present, the item

is never untestable.
_____
Adapted from: Goldstein LB, Samsa GP, Stroke 1997; 28:307.
Graphic 61698 Version 4.0

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