Spontaneous Intracerebral Hemorrhage_ Treatment and Prognosis

8/9/2019 Spontaneous Intracerebral Hemorrhage_ Treatment and Prognosis

1/22

Official reprint from UpToDate

www.uptodate.com ©2014 UpToDate

Authors

Guy Rordorf, MD

Colin McDonald, MD

Section Editor

Scott E Kasner, MD

Deputy Editor

Janet L Wilterdink, MD

Spontaneous intracerebral hemorrhage: Treatment and prognosis

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 suchlimitations 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]:

Reversal of anticoagulation — For patients who develop an ICH, all anticoagulant and antiplatelet drugs should be

®

®

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 suggestinsulin 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 inpatients with acute stroke includes initial nulla per os (NPO) status until swallowing function is evaluated. Some

experts suggest that patients with a GCS


2/22


3/22

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 agraded approach to the management of elevated ICP, beginning with simple measures that include the following [1]:

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


4/22


5/22

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:

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 andsystematic 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]:

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

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 thehemorrhage

●

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'.)

●

22


6/22

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


7/22


8/22

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.

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:

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 patient’s 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

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].

•

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].

●

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


9/22


10/22

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

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.

1.

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.

2.

Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral3.

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 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 keepcerebral 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.)

●

f 22


11/22

hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke

Association. Stroke 2010; 41:2108.

Maas MB, Rosenberg NF, Kosteva AR, et al. Surveillance neuroimaging and neurologic examinations affect care for

intracerebral hemorrhage. Neurology 2013; 81:107.

4.

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.

5.

Ciccone A, Celani MG, Chiaramonte R, et al. Continuous versus intermittent physiological monitoring for acute

stroke. Cochrane Database Syst Rev 2013; 5:CD008444.

6.

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.

7.

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.

8.

Balami JS, Buchan AM. Complications of intracerebral haemorrhage. Lancet Neurol 2012; 11:101.9.

Manno EM. Update on intracerebral hemorrhage. Continuum (Minneap Minn) 2012; 18:598.10.

Andrews CM, Jauch EC, Hemphill JC 3rd, et al. Emergency neurological life support: intracerebral hemorrhage.

Neurocrit Care 2012; 17 Suppl 1:S37.

11.

Martin M, Conlon LW. Does platelet transfusion improve outcomes in patients with spontaneous or traumatic

intracerebral hemorrhage? Ann Emerg Med 2013; 61:58.

12.

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.

13.

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.

14.

Menon RS, Burgess RE, Wing JJ, et al. Predictors of highly prevalent brain ischemia in intracerebral hemorrhage.

Ann Neurol 2012; 71:199.

15.

Garg RK, Liebling SM, Maas MB, et al. Blood pressure reduction, decreased diffusion on MRI, and outcomes after

intracerebral hemorrhage. Stroke 2012; 43:67.

16.

Qureshi AI. Significance of lesions with decreased diffusion on MRI in patients with intracerebral hemorrhage. Stroke

2012; 43:6.

17.

Butcher KS, Jeerakathil T, Hill M, et al. The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial.

Stroke 2013; 44:620.

18.

Gould B, McCourt R, Asdaghi N, et al. Autoregulation of cerebral blood flow is preserved in primary intracerebral

hemorrhage. Stroke 2013; 44:1726.

19.

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.

20.

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.

21.

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.

22.

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.

23.

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.

24.

Naidech AM, Garg RK, Liebling S, et al. Anticonvulsant use and outcomes after intracerebral hemorrhage. Stroke

2009; 40:3810.

25.

Messé SR, Sansing LH, Cucchiara BL, et al. Prophylactic antiepileptic drug use is associated with poor outcome

following ICH. Neurocrit Care 2009; 11:38.

26.

Poungvarin N, Bhoopat W, Viriyavejakul A, et al. Effects of dexamethasone in primary supratentorial intracerebral


27.

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.

28.

f 22


12/22

Dorman HR, Sondheimer JH, Cadnapaphornchai P. Mannitol-induced acute renal failure. Medicine (Baltimore) 1990;

69:153.

29.

Schwab S, Spranger M, Schwarz S, Hacke W. Barbiturate coma in severe hemispheric stroke: useful or obsolete?

Neurology 1997; 48:1608.

30.

Neurological and Neurosurgical Intensive Care. Ropper, AH (Ed), Raven Press, New York 1993.31.

Ott KH, Kase CS, Ojemann RG, Mohr JP. Cerebellar hemorrhage: diagnosis and treatment. A review of 56 cases.

Arch Neurol 1974; 31:160.

32.

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.

33.

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.

34.

Morgenstern LB, Demchuk AM, Kim DH, et al. Rebleeding leads to poor outcome in ultra-early craniotomy for


35.

Minematsu K. Evacuation of intracerebral hematoma is likely to be beneficial. Stroke 2003; 34:1567.36.

Hankey GJ. Evacuation of intracerebral hematoma is likely to be beneficial--against. Stroke 2003; 34:1568.37.

Donnan GA, Davis SM. Surgery for intracerebral hemorrhage: an evidence-poor zone. Stroke 2003; 34:1569.38.

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.

39.

Nakano T, Ohkuma H. Surgery versus conservative treatment for intracerebral haemorrhage--is there an end to the

long controversy? Lancet 2005; 365:361.

40.

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.

41.

Gautschi OP, Schaller K. Surgery or conservative therapy for cerebral haemorrhage? Lancet 2013; 382:377.42.

Prasad K, Mendelow AD, Gregson B. Surgery for primary supratentorial intracerebral haemorrhage. Cochrane

Database Syst Rev 2008; :CD000200.

43.

Brown DL, Morgenstern LB. Stopping the bleeding in intracerebral hemorrhage. N Engl J Med 2005; 352:828.44.

Broderick JP. The STICH trial: what does it tell us and where do we go from here? Stroke 2005; 36:1619.45.

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.

46.

Cruz-Flores S. Early surgery and initial conservative therapy did not differ for outcomes in lobar intracerebral

hematomas. Ann Intern Med 2013; 159:JC11.

47.

Al-Shahi Salman R. Haemostatic drug therapies for acute spontaneous intracerebral haemorrhage. Cochrane

Database Syst Rev 2009; :CD005951.

48.

O'Connell KA, Wood JJ, Wise RP, et al. Thromboembolic adverse events after use of recombinant human

coagulation factor VIIa. JAMA 2006; 295:293.

49.

Mayer SA, Brun NC, Broderick J, et al. Safety and feasibility of recombinant factor VIIa for acute intracerebral


50.

Mayer SA, Brun NC, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl JMed 2005; 352:777.

51.

Mayer SA, Brun NC, Begtrup K, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral


52.

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.

53.

Sugg RM, Gonzales NR, Matherne DE, et al. Myocardial injury in patients with intracerebral hemorrhage treated with

recombinant factor VIIa. Neurology 2006; 67:1053.

54.

Subramaniam S, Demchuk AM, Watson T, et al. Unexpected posthemorrhagic hydrocephalus in patients treated with

rFVIIa. Neurology 2006; 67:1096.

55.

He J, Whelton PK, Vu B, Klag MJ. Aspirin and risk of hemorrhagic stroke: a meta-analysis of randomized controlledtrials. JAMA 1998; 280:1930.

56.

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.

57.

Biffi A, Halpin A, Towfighi A, et al. Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy.

Neurology 2010; 75:693.

58.

f 22


13/22

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.

59.

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.

60.

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.

61.

Kase CS, Kurth T. Prevention of intracerebral hemorrhage recurrence. Continuum (Minneap Minn) 2011; 17:1304.62.

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.

63.

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.

64.

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.

65.

González-Duarte A, Cantú C, Ruíz-Sandoval JL, Barinagarrementeria F. Recurrent primary cerebral hemorrhage:

frequency, mechanisms, and prognosis. Stroke 1998; 29:1802.

66.

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.

67.

Yano K, Reed DM, MacLean CJ. Serum cholesterol and hemorrhagic stroke in the Honolulu Heart Program. Stroke

1989; 20:1460.

68.

Shinkawa A, Ueda K, Hasuo Y, et al. Seasonal variation in stroke incidence in Hisayama, Japan. Stroke 1990;

21:1262.

69.

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.

70.

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.

71.

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.

72.

Amarenco P, Labreuche J, Lavallée P, Touboul PJ. Statins in stroke prevention and carotid atherosclerosis:

systematic review and up-to-date meta-analysis. Stroke 2004; 35:2902.

73.

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.

74.

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.

75.

Hackam DG, Austin PC, Huang A, et al. Statins and intracerebral hemorrhage: a retrospective cohort study. Arch

Neurol 2012; 69:39.

76.

Hackam DG, Woodward M, Newby LK, et al. Statins and intracerebral hemorrhage: collaborative systematic review

and meta-analysis. Circulation 2011; 124:2233.

77.

McKinney JS, Kostis WJ. Statin therapy and the risk of intracerebral hemorrhage: a meta-analysis of 31 randomized

controlled trials. Stroke 2012; 43:2149.

78.

Westover MB, Bianchi MT, Eckman MH, Greenberg SM. Statin use following intracerebral hemorrhage: a decision

analysis. Arch Neurol 2011; 68:573.

79.

Goldstein LB. Statins after intracerebral hemorrhage: to treat or not to treat. Arch Neurol 2011; 68:565.80.

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.

81.

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.

82.

Counsell C, Boonyakarnukul S, Dennis M, et al. Primary intracerebral hemorrhage in the Oxford-shire communityStroke Project. Cerebrovasc Dis 1995; 5:26.

83.

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.

84.

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.

85.

f 22


14/22

Flaherty ML, Haverbusch M, Sekar P, et al. Long-term mortality after intracerebral hemorrhage. Neurology 2006;

66:1182.

86.

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.

87.

Zia E, Engström G, Svensson PJ, et al. Three-year survival and stroke recurrence rates in patients with primary

intracerebral hemorrhage. Stroke 2009; 40:3567.

88.

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.

89.

González-Pérez A, Gaist D, Wallander MA, et al. Mortality after hemorrhagic stroke: data from general practice (The

Health Improvement Network). Neurology 2013; 81:559.

90.

Franke CL, van Swieten JC, Algra A, van Gijn J. Prognostic factors in patients with intracerebral haematoma. J

Neurol Neurosurg Psychiatry 1992; 55:653.

91.

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.

92.

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.

93.

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.

94.

van Beijnum J, Lovelock CE, Cordonnier C, et al. Outcome after spontaneous and arteriovenous malformation-

related intracerebral haemorrhage: population-based studies. Brain 2009; 132:537.

95.

Beslow LA, Licht DJ, Smith SE, et al. Predictors of outcome in childhood intracerebral hemorrhage: a prospective

consecutive cohort study. Stroke 2010; 41:313.

96.

Lo WD, Hajek C, Pappa C, et al. Outcomes in children with hemorrhagic stroke. JAMA Neurol 2013; 70:66.97.

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.

98.

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.

99.

Jordan LC, Kleinman JT, Hillis AE. Intracerebral hemorrhage volume predicts poor neurologic outcome in children.Stroke 2009; 40:1666.

100.

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.

101.

Rodriguez-Luna D, Rubiera M, Ribo M, et al. Ultraearly hematoma growth predicts poor outcome after acute


102.

Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after


103.

Dowlatshahi D, Demchuk AM, Flaherty ML, et al. Defining hematoma expansion in intracerebral hemorrhage:

relationship with patient outcomes. Neurology 2011; 76:1238.

104.

Portenoy RK, Lipton RB, Berger AR, et al. Intracerebral haemorrhage: a model for the prediction of outcome. JNeurol Neurosurg Psychiatry 1987; 50:976.

105.

Young WB, Lee KP, Pessin MS, et al. Prognostic significance of ventricular blood in supratentorial hemorrhage: a

volumetric study. Neurology 1990; 40:616.

106.

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.

107.

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.

108.

Hallevi H, Albright KC, Aronowski J, et al. Intraventricular hemorrhage: Anatomic relationships and clinical

implications. Neurology 2008; 70:848.

109.

Staykov D, Volbers B, Wagner I, et al. Prognostic significance of third ventricle blood volume in intracerebralhaemorrhage with severe ventricular involvement. J Neurol Neurosurg Psychiatry 2011; 82:1260.

110.

Maas MB, Nemeth AJ, Rosenberg NF, et al. Subarachnoid extension of primary intracerebral hemorrhage is

associated with poor outcomes. Stroke 2013; 44:653.

111.

Mayer SA, Sacco RL, Shi T, Mohr JP. Neurologic deterioration in noncomatose patients with supratentorial


112.

f 22


15/22

Leira R, Dávalos A, Silva Y, et al. Early neurologic deterioration in intracerebral hemorrhage: predictors and

associated factors. Neurology 2004; 63:461.

113.

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.

114.

Flemming KD, Wijdicks EF, St Louis EK, Li H. Predicting deterioration in patients with lobar haemorrhages. J Neurol

Neurosurg Psychiatry 1999; 66:600.

115.

Arima H, Wang JG, Huang Y, et al. Significance of perihematomal edema in acute intracerebral hemorrhage: the

INTERACT trial. Neurology 2009; 73:1963.

116.

Cucchiara B, Messe S, Sansing L, et al. Hematoma growth in oral anticoagulant related intracerebral hemorrhage.

Stroke 2008; 39:2993.

117.

Falcone GJ, Biffi A, Brouwers HB, et al. Predictors of hematoma volume in deep and lobar supratentorial

intracerebral hemorrhage. JAMA Neurol 2013; 70:988.

118.

Hart RG, Boop BS, Anderson DC. Oral anticoagulants and intracranial hemorrhage. Facts and hypotheses. Stroke

1995; 26:1471.

119.

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.

120.

Dowlatshahi D, Butcher KS, Asdaghi N, et al. Poor prognosis in warfarin-associated intracranial hemorrhage despite

anticoagulation reversal. Stroke 2012; 43:1812.

121.

Toyoda K, Okada Y, Minematsu K, et al. Antiplatelet therapy contributes to acute deterioration of intracerebral

hemorrhage. Neurology 2005; 65:1000.

122.

Naidech AM, Bernstein RA, Levasseur K, et al. Platelet activity and outcome after intracerebral hemorrhage. Ann

Neurol 2009; 65:352.

123.

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.

124.

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.

125.

Nilsson OG, Lindgren A, Brandt L, Säveland H. Prediction of death in patients with primary intracerebral

hemorrhage: a prospective study of a defined population. J Neurosurg 2002; 97:531.

126.

Flibotte JJ, Hagan N, O'Donnell J, et al. Warfarin, hematoma expansion, and outcome of intracerebral hemorrhage.

Neurology 2004; 63:1059.

127.

Brott T, Broderick J, Kothari R, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke

1997; 28:1.

128.

Sansing LH, Messe SR, Cucchiara BL, et al. Prior antiplatelet use does not affect hemorrhage growth or outcome

after ICH. Neurology 2009; 72:1397.

129.

Thompson BB, Béjot Y, Caso V, et al. Prior antiplatelet therapy and outcome following intracerebral hemorrhage: a

systematic review. Neurology 2010; 75:1333.

130.

Hemphill JC 3rd, Bonovich DC, Besmertis L, et al. The ICH score: a simple, reliable grading scale for intracerebral


131.

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.

132.

Godoy DA, Piñero G, Di Napoli M. Predicting mortality in spontaneous intracerebral hemorrhage: can modification to

original score improve the prediction? Stroke 2006; 37:1038.

133.

Hemphill JC 3rd, Farrant M, Neill TA Jr. Prospective validation of the ICH Score for 12-month functional outcome.

Neurology 2009; 73:1088.

134.

Muir KW, Weir CJ, Murray GD, et al. Comparison of neurological scales and scoring systems for acute stroke

prognosis. Stroke 1996; 27:1817.

135.

Bar B, Hemphill JC 3rd. Charlson comorbidity index adjustment in intracerebral hemorrhage. Stroke 2011; 42:2944.136.

Becker KJ, Baxter AB, Cohen WA, et al. Withdrawal of support in intracerebral hemorrhage may lead to self-fulfilling

prophecies. Neurology 2001; 56:766.

137.

Zahuranec DB, Brown DL, Lisabeth LD, et al. Early care limitations independently predict mortality after intracerebral

hemorrhage. Neurology 2007; 68:1651.

138.

Zahuranec DB, Morgenstern LB, Sánchez BN, et al. Do-not-resuscitate orders and predictive models after


139.

Creutzfeldt CJ, Becker KJ, Weinstein JR, et al. Do-not-attempt-resuscitation orders and prognostic models for 140.

f 22


16/22


17/22

GRAPHICS

Glasgow coma scale

Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

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

f 22


18/22

Modified Rankin scale

Score Description

0 No symptoms at all

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

2 Slight disability; unable to carry out all previous activities, but able to look after own affairs

without assistance

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

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

bodily needs without assistance

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

6 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.


f 22


19/22

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 Scale definition Score

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.

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

month and his/her age. The answer must be

correct - there is no partial credit for being

close. Aphasic and stuporous patients who do

not comprehend the questions will score 2.

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.

0 = Answers both questions correctly.

1 = Answers one question correctly.

2 = Answers neither question correctly.

_____

1c. LOC commands: The patient is asked to

open and close the eyes and then to grip and

release the non-paretic hand. Substitute

another one step command if the hands cannot

be used. Credit is given if an unequivocal

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.

0 = Performs both tasks correctly.

1 = Performs one task correctly.

2 = Performs neither task correctly.

_____

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),

0 = Normal.

1 = Partial gaze palsy; gaze is abnormal inone 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.

_____

f 22


20/22

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

quadrants) are tested by confrontation, using

finger counting or visual threat, as

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,

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. Doublesimultaneous stimulation is performed at this

point. If there is extinction, patient receives a

1, and the results are used to respond to item

11.

0 = No visual loss.

1 = Partial hemianopia.

2 = Complete hemianopia.

3 = Bilateral hemianopia (blind including

cortical blindness).

_____

4. Facial palsy: Ask - or use pantomime to

encourage - the patient to show teeth or raise

eyebrows and close eyes. Score symmetry of

grimace in response to noxious stimuli in the

poorly responsive or non-comprehending

patient. If facial trauma/bandages, orotrachealtube, tape or other physical barriers obscure

the face, these should be removed to the

extent possible.

0 = Normal symmetrical movements.

1 = Minor paralysis (flattened nasolabial

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

appropriate position: extend the arms (palms

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

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.

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

for full 10 seconds.

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

_____

6. Motor leg: The limb is placed in the

appropriate position: hold the leg at 30

degrees (always tested supine). Drift is scored

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

full 5 seconds. _____

f 22


21/22

if the leg falls before 5 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 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

explanation for this choice.

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

period but does not hit bed.

2 = Some effort against gravity; leg falls to

bed by 5 seconds, but has some effort against

gravity.

3 = No effort against gravity; leg falls to

bed immediately.

4 = No movement.


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

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.

0 = Absent.

1 = Present in one limb.

2 = Present in two limbs.


explain:________________

_____

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

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.

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.

_____

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 recedin eneral

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,

_____

f 22


22/22

neurological exam. If visual loss interferes with

the tests, ask the patient to identify objects

placed in the hand, repeat, and produce

speech. The intubated patient should be asked

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.

in conversation about provided materials,

examiner can identify picture or naming card

content from patient's response.

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 physicalbarriers 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

neglect): Sufficient information to identify

neglect may be obtained during the prior

testing. If the patient has a severe visual loss

preventing visual double simultaneousstimulation, 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 may also

be taken as evidence of abnormality. Since the

abnormality is scored only if present, the item

is never untestable.

0 = No abnormality.

1 = Visual, tactile, auditory, spatial, or

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.

_____

_____

Adapted from: Goldstein LB, Samsa GP, Stroke 1997; 28:307.


Documents

Spontaneous Intracerebral Hemorrhage_ Treatment and Prognosis