What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Patient Print
0 Find synonyms

Find synonyms Find exact match

Ischemic stroke prognosis in adults
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Ischemic stroke prognosis in adults
View in Chinese
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: Jan 06, 2017.

INTRODUCTION — Stroke is the third most common cause of disability and second most common cause of death worldwide (see "Etiology, classification, and epidemiology of stroke", section on 'Epidemiology'). Clinicians are often asked to predict outcome after stroke by the patient, family, other healthcare workers, and insurance providers. A wide variety of factors influence stroke prognosis, including age, stroke severity, stroke mechanism, infarct location, comorbid conditions, clinical findings, and related complications. In addition, interventions such as thrombolysis, stroke unit care, and rehabilitation can play a major role in the outcome of ischemic stroke. Knowledge of the important factors that affect prognosis is necessary for the clinician to make a reasonable prediction for individual patients, to provide a rational approach to patient management, and to help patient and family understand the course of the disease.

This topic will review the factors that affect stroke prognosis, with a focus on the acute phase of ischemic stroke. The prognosis of intracerebral hemorrhage and subarachnoid hemorrhage is reviewed separately. (See "Treatment of aneurysmal subarachnoid hemorrhage", section on 'Prognosis' and "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section on 'Prognosis'.)

MAJOR PREDICTORS — In the acute phase of stroke, the strongest predictors of outcome are stroke severity and patient age. Stroke severity can be judged clinically, based upon the degree of neurologic impairment (eg, altered mentation, language, behavior, visual field deficit, motor deficit) and the size and location of the infarction on neuroimaging with MRI or CT. Other important influences on stroke outcome include ischemic stroke mechanism, comorbid conditions, epidemiologic factors, and complications of stroke.

Neurologic severity — The severity of stroke on neurologic exam is probably the most important factor affecting short- and long-term outcome [1-14]. As a general rule, large strokes with severe initial clinical deficits have poor outcomes compared with smaller strokes.

Neurologic impairment is measured quantitatively in many research studies, and increasingly in clinical practice, by use of the National Institutes of Health Stroke Scale (NIHSS), which measures neurologic impairment using a 15-item scale (table 1) or less often by use of the Canadian Neurological Scale (table 2). As an example, the combination of neurologic findings in patients with a large infarction involving the middle cerebral artery vascular territory typically includes forced gaze deviation, visual field deficit, hemiplegia, and aphasia or neglect, depending on the hemisphere involved, and yields a NIHSS score >15 for a right hemisphere infarction and >20 for a left hemisphere infarction.

Several studies have demonstrated that the NIHSS is a good predictor of stroke outcome [2,15-17]. One report analyzed NIHSS scores obtained within 24 hours of acute ischemic stroke symptom onset from over 1200 patients enrolled in a clinical trial [2]. Each additional point on the NIHSS decreased the odds of an excellent outcome at three months by 17 percent. At three months, the proportion of patients with excellent outcomes for NIHSS scores of 7 to 10 and 11 to 15 was approximately 46 and 23 percent, respectively. An NIHSS score of ≤6 predicted a good recovery (able to live independently, whether or not able to return to work or school), while a score ≥16 was associated with a high probability of death or severe disability. In many such studies, descriptors such as "good recovery" are based upon discharge location to home or independence in activities of daily living such as mobility. However, the NIHSS does not evaluate more complex goals such as return to prior level of employment, participation in leisure activities, or social participation. In general, recovery of these areas is less than those measured by the NIHSS.

The relationship of NIHSS score with final outcome varies according to the time elapsed from stroke onset [9,15], in part because early stroke-related deficits tend to be unstable, and because many patients experience gradual recovery. Thus, the NIHSS score associated with a specific disability outcome shifts to lower values over time [9]. One study found that the best predictor of poor prognosis at 24 hours was an NIHSS of >22, and the best predictor at 7 to 10 days was an NIHSS score of >16 [15]. In addition, the correlation of the NIHSS score with final disability outcome increases with time [9].

The Canadian Neurological Scale (CNS) is also useful for predicting outcome after acute ischemic stroke. A CNS score of <6.5 on admission is associated with increased 30-day mortality and a poor outcome at six months [17,18]. Although comparative data are limited, the results of one study suggest that the NIHSS is more accurate than the CNS for predicting outcome at three months [16].

An important limitation of both the NIHSS and the CNS scales is that they do not capture all stroke-related impairments. (See "Use and utility of stroke scales and grading systems", section on 'Stroke impairment scales'.)

Age — Advancing age has a major negative impact on stroke morbidity, mortality, and long-term outcome [1,5,7,10,12,19-23]. The influence of age in stroke outcome is seen in both minor and major strokes. Older adults (over 65 years) have increased chance of dying in two months after stroke and being discharged to the skilled nursing facility if they survive [24,25]. Advancing age is used in several predictive models. (See 'Global prognostic scales' below.)

Neuroimaging — Findings on neuroimaging including stroke size and location are an important adjunct to the neurologic exam when gauging prognosis. Early after stroke, the neurologic exam alone can suggest a falsely grim or favorable prognosis. For example, a patient may have a small stroke on neuroimaging and present with stupor or coma caused by seizure or metabolic derangement that is reversible. Conversely, a patient presenting with mild stroke and a low NIHSS score on examination may have large vessel occlusion and a large perfusion deficit on neuroimaging, suggesting the possibility of stroke progression and worse outcome.

Infarct volume — The volume of acute infarction on neuroimaging studies may be used to estimate stroke outcome [26]. In one small study, the volume of ischemic tissue determined by diffusion-weighted MRI within 36 hours of stroke onset combined with the NIHSS score and time from stroke onset to imaging predicted the functional outcome at three months better than any of the individual factors alone [11]. A much larger study analyzed data from over 1800 patients who had CT or MRI within 72 hours of ischemic stroke onset and found that initial infarct volume was an independent predictor of stroke outcome at 90 days, along with age and NIHSS score [8]. In these and most other reports [8,11,26], the vast majority of infarcts analyzed were supratentorial (eg, anterior circulation, middle cerebral artery territory) and the results may not apply to posterior circulation or infratentorial infarcts, in which an infarct of small volume can result in severe disability.

Infarct location — The prognosis for stroke recovery may vary by the affected vascular territory and site of ischemic brain injury.

Acute occlusion of the cervical internal carotid artery [27,28], basilar artery [29], or a large intracranial artery is associated with an increased risk of poor outcome [30-32]. It follows that involvement of total anterior circulation or posterior circulation also portends poor prognosis [18,33-35].

Strokes in the insular region (supplied by the insular branch of the middle cerebral artery) have been associated with increased mortality, which is often attributed to autonomic dysregulation [36,37]. However, this association may be confounded by infarct size [38]. Insular infarcts may undergo early expansion due to associated large vessel occlusion and progression of infarction in surrounding areas of initially viable but ischemic brain tissue [39].

Anterior choroidal artery infarctions may be more likely to progress in the first few days after stroke than other subtypes [40,41]. In a prospective study of over 1300 patients with acute ischemic stroke, anterior choroidal territory infarcts had intermediate long-term prognosis between lacunar infarcts and large artery territory hemispheric infarcts [40].

A retrospective report of 75 survivors of ischemic stroke in the middle cerebral artery territory found that strokes located in the internal capsule demonstrated a worse prognosis for recovery of hand motor function at one year than strokes in the corona radiata or motor cortex after controlling for infarct size [42].

There are limited and conflicting data regarding borderzone infarcts (ie, infarcts that occur along the boundaries of adjacent arterial territories, such as the middle cerebral and anterior cerebral artery territories) and outcome; some studies suggest a lower severity at onset and a good prognosis in most cases [43], while others describe severe impairment and poor recovery in a substantial proportion [44,45].

Other imaging findings — In addition to stroke volume and location, there are other features identifiable on neuroimaging that may suggest poor prognosis:

Diffusion-perfusion mismatch (ie, an ischemic brain lesion characterized by a core of infarcted tissue on MRI diffusion imaging that is embedded within a still viable but ischemic penumbral region on MRI perfusion imaging), which may be a risk factor for lesion enlargement (see "Neuroimaging of acute ischemic stroke", section on 'Identifying reversible ischemia')

Poor collateral blood flow [46,47]

Development of cerebral edema in nonlacunar ischemic stroke [48]

Ischemic stroke mechanism — The etiology or mechanism of ischemic stroke influences prognosis for recovery [49].

Patients with lacunar infarcts have a better prognosis up to one year after onset than those with infarcts due to other stroke mechanisms. However, the longer-term prognosis after lacunar stroke may not differ greatly from nonlacunar stroke. (See "Lacunar infarcts", section on 'Prognosis'.)

Compared with other ischemic stroke subtypes, cryptogenic stroke, where no mechanism of stroke is identified, tends to have a better prognosis up to one year following onset. (See "Cryptogenic stroke", section on 'Prognosis'.)

Patients with strokes of cardioembolic or large artery etiology tend to have worse prognosis for recovery compared with other ischemic stroke subtypes [49-52].

Comorbidities — A host of prestroke comorbid conditions are associated with an increased risk of poor outcome following ischemic stroke, including the following:

Anemia [53]

Atrial fibrillation [4,7,15,54,55]

Cancer [4,54]

Coronary artery disease [4]

Dementia [4,10,56]

Dependency [4,22,54]

Diabetes mellitus [14,57,58]

Hyperglycemia (eg, blood glucose >6.1 mmol/L [>110 mg/dL]) on admission [58,59]

Heart failure [4,54]

Myocardial infarction [60,61]

Periventricular white matter disease or leukoaraiosis [62-64]

Renal dysfunction or dialysis [4,65-69]

Poor nutritional status [70]

Low hemoglobin level [71]

The relationship between blood pressure in the acute phase of ischemic stroke and outcome is complex and is discussed separately. (See "Initial assessment and management of acute stroke", section on 'Blood pressure management'.)

Body mass index appears to be inversely related to stroke prognosis, such that patients who are underweight or normal weight have paradoxically higher mortality rates and worse functional outcomes than patients who are overweight or obese [72-74].

Finally, ischemic stroke that occurs in the postoperative period has a high short-term morbidity [75].

Epidemiologic factors — Differences in sex, race, and socioeconomic status may affect stroke recovery. There are conflicting data regarding sex differences and stroke outcome. While some studies found that men were more likely than women to have poor outcomes after ischemic stroke [4,71,76,77], others found that women had worse outcomes [6,78-84], and still others found no significant difference in outcomes according to gender [2,10].

There are racial and ethnic differences in outcome after stroke. In studies from the United States, black or nonwhite race is associated with a higher risk for poor outcome [62,81,85]. Lower levels of educational attainment [86,87], socioeconomic status [87-89], and lesser degrees of social support have been correlated with poor outcome following ischemic stroke, and a lower socioeconomic status has been associated with a worse health-related quality of life at five years [90,91]. However, it is unclear if these are independent prognostic factors, since lower socioeconomic status may also be associated with increased comorbidities and greater stroke severity [92,93].

Complications of stroke — Medical complications of acute ischemic stroke are common and influence outcome after ischemic stroke. The most frequent serious medical complications include pneumonia, the need for intubation and mechanical ventilation, gastrointestinal bleeding, congestive heart failure, cardiac arrest, deep vein thrombosis, pulmonary embolism, and urinary tract infection. (See "Medical complications of stroke" and "Stroke-related pulmonary complications and abnormal respiratory patterns" and "Cardiac complications of stroke".)

Early neurologic deterioration during the acute phase of ischemic stroke affects a significant minority and is associated with an increased risk of morbidity and mortality [94-99]. The mechanisms of early neurologic deterioration are heterogeneous and include extension of the infarct into surrounding areas of hypoperfused brain tissue, progressive edema, increased intracranial pressure, seizure, and hemorrhagic conversion of the infarct. Delirium, characterized by a disturbance of consciousness with decreased attention and disorganized thinking, is another potential complication of acute stroke.

Poststroke depression has a high prevalence and a negative impact on stroke outcome [56]. Stroke severity with subsequent disability and cognitive impairment are likely risk factors. (See "Medical complications of stroke", section on 'Depression'.)

PREDICTING RECOVERY — In the period from 12 hours to seven days after ischemic stroke onset, many patients who are without complications experience moderate but steady improvement in neurologic impairments [100].

The greatest proportion of recovery after stroke occurs in the first 3 to 6 months [3,6,101,102], though some patients experience further improvement up to 18 months [6]. In a prospective study that evaluated more than 1100 patients from Denmark with acute stroke, those who had mild disability tended to recover within two months and those who had moderate disability recovered within three months [3,102]. Patients with severe disability who recovered did so within four months, and those with the most severe disability within five months from onset (figure 1). Functional recovery was preceded by neurologic recovery by two weeks on average.

Accumulating data suggest that integrity of the ipsilesional corticospinal tract is necessary to allow for motor recovery, and that excessive corticospinal tract injury is a predictor of poor recovery [103-106]. The functional integrity of the corticospinal tract can be assessed by a variety of specialized techniques, including motor evoked potentials elicited by transcranial magnetic stimulation, and MRI methods such as diffusion-weighted imaging maps and diffusion tensor tractography. Despite the emerging importance of corticospinal tract integrity for motor recovery, none of these measures are in widespread clinical use.

Other data suggest that functional outcome at three months after stroke predicts survival at four years [62], and functional status at six months predicts long-term survival [107].

Specific neurologic deficits — Attempting to predict recovery from specific neurologic deficits is challenging and best provided by an experienced neurologist or physiatrist after careful clinical examination and review of pertinent neuroimaging. The time course and degree of improvement may vary for specific deficits, but as a general rule, mild deficits improve more rapidly and more completely than severe deficits [101].

Arm and hand weakness – An early study found that in patients with hemiplegic stroke, the first voluntary movements were observed between 6 to 33 days after onset [108]. In a prospective report of patients with arm disability, the maximum degree of functional recovery was reached within three weeks from stroke onset by 80 percent of patients, and within nine weeks by 95 percent [109]. Complete functional arm recovery was achieved by patients with initial mild and severe arm paresis in 79 and 18 percent, respectively.

The return of arm and hand function after stroke is particularly important to a good functional recovery. The flexor synergy seen after stroke limits the ability to isolate joint movements, so the ability to extend the fingers and release grasp is a significant component of a good motor outcome. Several studies have found that early active finger extension, grasp release, shoulder shrug, shoulder abduction, and active range of motion are associated with a favorable prognosis for arm and hand recovery at six months [110-113]. As an example, in a prospective cohort study of 188 patients with monoparesis or hemiparesis from anterior circulation ischemic stroke observed, patients with some voluntary finger extension and shoulder abduction of the hemiplegic limb on day 2 after stroke onset had a high probability (0.98) to regain some dexterity by six months [114]. In contrast, the probability for patients without these voluntary movements at two and nine days was 0.25 and 0.14, respectively.

Leg weakness and ambulation – In a study of 154 patients who were unable to walk after first ischemic stroke, multivariate modeling showed that patients who could maintain sitting balance for 30 seconds and perform muscle contraction (with or without actual limb movement) in the paretic leg within the first 72 hours after stroke had a probability for ambulating independently at six months of 98 percent [115]. For those who did not reach either functional level within 72 hours, the probability for ambulating independently at six months was only 27 percent.

Aphasia – Patients with poststroke aphasia are likely to experience some improvement from the initial impairment. Not surprisingly, the prognosis for full recovery is greatest when patients have milder degrees of aphasia at onset. The time course for recovery from aphasia is similar to that of motor function. One prospective study included over 300 patients with aphasia at admission; the time to maximal language recovery in 95 percent of patients with initially mild, moderate, and severe aphasia was 2, 6, and 10 weeks, respectively [116]. (See "Aphasia: Prognosis and treatment".)

Dysphagia – Early after stroke, approximately 50 percent of patients have difficulty swallowing, placing them at risk for aspiration [117]. Swallowing impairments commonly improve over time. A large multicenter trial found no benefit to early enteral feeding via a percutaneous endoscopic gastrostomy (PEG) tube compared with no tube feeding [118]. Risk factors for more longstanding dysphagia eventually requiring PEG tube placement include high National Institutes of Health Stroke Scale (NIHSS) score and bihemispheric infarcts [119,120]. In a retrospective cohort study of 563 patients admitted for stroke rehabilitation, feeding tubes were placed in 6 percent [121]. Of these, approximately one-third of feeding tubes were discontinued before patients were discharged from rehabilitation, and almost all of the rest were discontinued by one year. Persons with stroke lesions that were bilateral or in the posterior fossa were least likely to return to oral feeding. (See "Medical complications of stroke", section on 'Dysphagia and aspiration'.)

Sensory loss – Sensory impairment is found in 65 to 94 percent of stroke survivors; the reported incidence depends greatly on the method of assessment, with formal quantitative testing being the most sensitive [122]. Sensory loss is also common on the apparently unaffected side. Sensory impairment is associated with reduced mobility and less independence in activities of daily living [123]. However, there are currently no reliable predictors of recovery from sensory loss. Patients with infarcts involving the spinothalamic or trigeminothalamic pathways sometimes develop a debilitating central poststroke pain syndrome [124]. (See "Approach to the patient with sensory loss", section on 'Thalamic lesions'.)

Visuospatial neglect – Limited data suggest that full recovery from visuospatial neglect occurs in 70 to 80 percent of affected patients within three months of stroke onset [125,126].

Hemianopia – A study of 99 patients with acute stroke and homonymous hemianopia (HH) found that 17 percent of those with complete HH had full recovery at one month, whereas 72 percent with partial HH had full recovery [127]. It is important to counsel patients with hemianopia after stroke not to drive until they are cleared by an ophthalmologist or pass a formal driver rehabilitation program (offered at select rehabilitation centers). (See "Homonymous hemianopia", section on 'Driving'.)

Global prognostic scales — In stroke rehabilitation venues, the Orpington Prognostic Scale (OPS) [128,129] and the Reding three-factor approach [130] are in wide clinical use.

The OPS (table 3) includes assessments of arm motor function, proprioception, balance, and cognition, making it easier to perform than the NIHSS. The OPS is better at predicting return of function than NIHSS in those with mild to moderate stroke [128], possibly because balance is so critical to carrying out activities of daily living.

The Reding three-factor approach provides a useful way to gauge the speed and degree of recovery for an individual patient [130]. Patients are divided into one of three groups:

Motor deficit only

Motor deficit plus somatic sensory deficit

Motor deficit plus somatic sensory deficit plus homonymous visual field deficit

Once the group is determined for the individual patient, their recovery can be compared with a cohort of similar patients (figure 2) to estimate the probability of return to Barthel Index (table 4) score of ≥60. This level of function is a useful benchmark because most patients with a Barthel Index score ≥60 are able to walk with assistance and contribute to their activities of daily living; in addition, the likelihood of a supported discharge to the community rises substantially. With a Barthel Index score of 100, a discharge to the community at a level of independence becomes plausible, but requires adequate cognitive function.

A number of other prognostic models may be useful for predicting global outcome from acute ischemic stroke; however, none of the current models is established as generally valid, and none is widely used in clinical practice. These models include the ASTRAL score [131,132], DRAGON score [133], iScore [134,135], and PLAN score [54]. These stroke prognostic models are intended to be easy to calculate from data available on admission. However, they disregard information available from follow-up and testing, such as stroke etiology, treatment, and complications, that has an important impact on outcome [62,136]. The course of stroke often changes in the first days after onset, and assessment at later times (eg, from 1 to 10 days after stroke onset) is likely to provide a more reliable prognosis [9].

MORBIDITY AND MORTALITY — The estimated worldwide 30-day case fatality rate after first ischemic stroke ranges from 16 to 23 percent, though there is wide variation in reports from different countries [137,138]. Even minor ischemic strokes portend a diminished long-term prognosis. In a 10-year follow-up study of 322 patients with minor ischemic stroke, the cumulative mortality rate was 32 percent, almost twice that of the general population [139].

Intracerebral hemorrhage and subarachnoid hemorrhage are associated with higher morbidity and mortality than ischemic stroke [5,20,21,140-142]. (See "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section on 'Prognosis' and "Treatment of aneurysmal subarachnoid hemorrhage", section on 'Prognosis'.)

In a community-based study from the United States that evaluated 220 ischemic stroke survivors (age ≥65 years), the following neurologic deficits were observed at six months after stroke [143]:

Hemiparesis, 50 percent

Cognitive deficits, 46 percent

Hemianopia, 20 percent

Aphasia, 19 percent

Sensory deficits, 15 percent

Disability measures at six months after stroke were as follows [143]:

Depression symptoms, 35 percent

Unable to walk unassisted, 31 percent

Social disability, 30 percent

Institutionalization, 26 percent

Bladder incontinence, 22 percent

A systematic review from 2009 identified only three studies that specifically evaluated work status after stroke and used appropriate analytic methods [144]. In these reports, the proportion of patients at 6 to 12 months after stroke who had returned to paid employment was just over 50 percent [145-147]. A subsequent report evaluated a hospital-based cohort of 694 working-age (18 to 50 years) patients with transient ischemic attack (TIA), ischemic stroke, or hemorrhagic stroke and found that the risk of unemployment after eight years of follow-up was two- to threefold higher compared with the general population of vocational age [148].

Outcome from ischemic stroke can be assessed with the modified Rankin Scale and the Barthel Index. The modified Rankin Scale (table 5) measures functional independence on a seven grade scale. The Barthel Index (table 4) measures 10 basic aspects of self-care and physical dependency. These indices are reviewed in greater detail elsewhere. (See "Use and utility of stroke scales and grading systems", section on 'Modified Rankin Scale' and "Use and utility of stroke scales and grading systems", section on 'Barthel Index'.)

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 education: Recovery after stroke (The Basics)")


In the acute phase of stroke, the strongest predictors of outcome are stroke severity and patient age. Stroke severity can be judged clinically, based upon the degree of neurologic impairment (eg, altered mentation, language, behavior, visual field deficit, motor deficit), and the size and location of the infarction on neuroimaging with MRI or CT. Other important influences on stroke outcome include infarct location, ischemic stroke mechanism, comorbid conditions, epidemiologic factors, and complications of stroke. (See 'Major predictors' above.)

In the period from 12 hours to seven days after ischemic stroke onset, many patients who are without complications experience moderate but steady improvement in neurologic impairments. The greatest proportion of recovery occurs in the first three to six months after stroke, with lesser improvements thereafter. (See 'Predicting recovery' above.)

The return of arm and hand function after stroke is particularly important to a good functional recovery. Early active finger extension, grasp release, shoulder shrug, shoulder abduction, and active range of motion are associated with a favorable prognosis for arm and hand recovery at six months. (See 'Specific neurologic deficits' above.)

The estimated 30-day case fatality rate after first ischemic stroke ranges from 16 to 23 percent. Available data suggest that persistent neurologic deficits observed at six months after stroke include hemiparesis and cognitive deficits in 40 to 50 percent of patients, and hemianopia, aphasia, or sensory deficits in 15 to 20 percent. Disability outcomes at six months after stroke include depression, inability to walk unassisted, and social impairments in approximately 30 percent, and institutional care in approximately 25 percent. (See 'Morbidity and mortality' above.)

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


  1. Weimar C, König IR, Kraywinkel K, et al. Age and National Institutes of Health Stroke Scale Score within 6 hours after onset are accurate predictors of outcome after cerebral ischemia: development and external validation of prognostic models. Stroke 2004; 35:158.
  2. Adams HP Jr, Davis PH, Leira EC, et al. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology 1999; 53:126.
  3. Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS. Stroke. Neurologic and functional recovery the Copenhagen Stroke Study. Phys Med Rehabil Clin N Am 1999; 10:887.
  4. Saposnik G, Kapral MK, Liu Y, et al. IScore: a risk score to predict death early after hospitalization for an acute ischemic stroke. Circulation 2011; 123:739.
  5. Koennecke HC, Belz W, Berfelde D, et al. Factors influencing in-hospital mortality and morbidity in patients treated on a stroke unit. Neurology 2011; 77:965.
  6. Hankey GJ, Spiesser J, Hakimi Z, et al. Rate, degree, and predictors of recovery from disability following ischemic stroke. Neurology 2007; 68:1583.
  7. Andersen KK, Andersen ZJ, Olsen TS. Predictors of early and late case-fatality in a nationwide Danish study of 26,818 patients with first-ever ischemic stroke. Stroke 2011; 42:2806.
  8. Vogt G, Laage R, Shuaib A, et al. Initial lesion volume is an independent predictor of clinical stroke outcome at day 90: an analysis of the Virtual International Stroke Trials Archive (VISTA) database. Stroke 2012; 43:1266.
  9. Saver JL, Altman H. Relationship between neurologic deficit severity and final functional outcome shifts and strengthens during first hours after onset. Stroke 2012; 43:1537.
  10. Béjot Y, Troisgros O, Gremeaux V, et al. Poststroke disposition and associated factors in a population-based study: the Dijon Stroke Registry. Stroke 2012; 43:2071.
  11. Baird AE, Dambrosia J, Janket S, et al. A three-item scale for the early prediction of stroke recovery. Lancet 2001; 357:2095.
  12. König IR, Ziegler A, Bluhmki E, et al. Predicting long-term outcome after acute ischemic stroke: a simple index works in patients from controlled clinical trials. Stroke 2008; 39:1821.
  13. Robertson CE, Brown RD Jr, Wijdicks EF, Rabinstein AA. Recovery after spinal cord infarcts: long-term outcome in 115 patients. Neurology 2012; 78:114.
  14. Coutts SB, Modi J, Patel SK, et al. What causes disability after transient ischemic attack and minor stroke?: Results from the CT and MRI in the Triage of TIA and minor Cerebrovascular Events to Identify High Risk Patients (CATCH) Study. Stroke 2012; 43:3018.
  15. Frankel MR, Morgenstern LB, Kwiatkowski T, et al. Predicting prognosis after stroke: a placebo group analysis from the National Institute of Neurological Disorders and Stroke rt-PA Stroke Trial. Neurology 2000; 55:952.
  16. Muir KW, Weir CJ, Murray GD, et al. Comparison of neurological scales and scoring systems for acute stroke prognosis. Stroke 1996; 27:1817.
  17. Censori B, Camerlingo M, Casto L, et al. Prognostic factors in first-ever stroke in the carotid artery territory seen within 6 hours after onset. Stroke 1993; 24:532.
  18. Sumer MM, Ozdemir I, Tascilar N. Predictors of outcome after acute ischemic stroke. Acta Neurol Scand 2003; 107:276.
  19. Counsell C, Dennis M, McDowall M, Warlow C. Predicting outcome after acute and subacute stroke: development and validation of new prognostic models. Stroke 2002; 33:1041.
  20. Wong KS. Risk factors for early death in acute ischemic stroke and intracerebral hemorrhage: A prospective hospital-based study in Asia. Asian Acute Stroke Advisory Panel. Stroke 1999; 30:2326.
  21. Heuschmann PU, Wiedmann S, Wellwood I, et al. Three-month stroke outcome: the European Registers of Stroke (EROS) investigators. Neurology 2011; 76:159.
  22. Feigin VL, Barker-Collo S, Parag V, et al. Auckland Stroke Outcomes Study. Part 1: Gender, stroke types, ethnicity, and functional outcomes 5 years poststroke. Neurology 2010; 75:1597.
  23. Knoflach M, Matosevic B, Rücker M, et al. Functional recovery after ischemic stroke--a matter of age: data from the Austrian Stroke Unit Registry. Neurology 2012; 78:279.
  24. Steiner T, Mendoza G, De Georgia M, et al. Prognosis of stroke patients requiring mechanical ventilation in a neurological critical care unit. Stroke 1997; 28:711.
  25. Kammersgaard LP, Jørgensen HS, Reith J, et al. Short- and long-term prognosis for very old stroke patients. The Copenhagen Stroke Study. Age Ageing 2004; 33:149.
  26. Schiemanck SK, Kwakkel G, Post MW, Prevo AJ. Predictive value of ischemic lesion volume assessed with magnetic resonance imaging for neurological deficits and functional outcome poststroke: A critical review of the literature. Neurorehabil Neural Repair 2006; 20:492.
  27. Burke MJ, Vergouwen MD, Fang J, et al. Short-term outcomes after symptomatic internal carotid artery occlusion. Stroke 2011; 42:2419.
  28. Paciaroni M, Caso V, Venti M, et al. Outcome in patients with stroke associated with internal carotid artery occlusion. Cerebrovasc Dis 2005; 20:108.
  29. Weimar C, Goertler M, Harms L, Diener HC. Distribution and outcome of symptomatic stenoses and occlusions in patients with acute cerebral ischemia. Arch Neurol 2006; 63:1287.
  30. Smith WS, Tsao JW, Billings ME, et al. Prognostic significance of angiographically confirmed large vessel intracranial occlusion in patients presenting with acute brain ischemia. Neurocrit Care 2006; 4:14.
  31. Verro P, Tanenbaum LN, Borden NM, et al. CT angiography in acute ischemic stroke: preliminary results. Stroke 2002; 33:276.
  32. Lau AY, Wong KS, Lev M, et al. Burden of intracranial steno-occlusive lesions on initial computed tomography angiography predicts poor outcome in patients with acute stroke. Stroke 2013; 44:1310.
  33. Nedeltchev K, der Maur TA, Georgiadis D, et al. Ischaemic stroke in young adults: predictors of outcome and recurrence. J Neurol Neurosurg Psychiatry 2005; 76:191.
  34. Di Carlo A, Lamassa M, Baldereschi M, et al. Risk factors and outcome of subtypes of ischemic stroke. Data from a multicenter multinational hospital-based registry. The European Community Stroke Project. J Neurol Sci 2006; 244:143.
  35. Bogousslavsky J, Garazi S, Jeanrenaud X, et al. Stroke recurrence in patients with patent foramen ovale: the Lausanne Study. Lausanne Stroke with Paradoxal Embolism Study Group. Neurology 1996; 46:1301.
  36. Abboud H, Berroir S, Labreuche J, et al. Insular involvement in brain infarction increases risk for cardiac arrhythmia and death. Ann Neurol 2006; 59:691.
  37. Colivicchi F, Bassi A, Santini M, Caltagirone C. Prognostic implications of right-sided insular damage, cardiac autonomic derangement, and arrhythmias after acute ischemic stroke. Stroke 2005; 36:1710.
  38. Borsody M, Warner Gargano J, Reeves M, et al. Infarction involving the insula and risk of mortality after stroke. Cerebrovasc Dis 2009; 27:564.
  39. Ay H, Arsava EM, Koroshetz WJ, Sorensen AG. Middle cerebral artery infarcts encompassing the insula are more prone to growth. Stroke 2008; 39:373.
  40. Ois A, Cuadrado-Godia E, Solano A, et al. Acute ischemic stroke in anterior choroidal artery territory. J Neurol Sci 2009; 281:80.
  41. Derflinger S, Fiebach JB, Böttger S, et al. The progressive course of neurological symptoms in anterior choroidal artery infarcts. Int J Stroke 2015; 10:134.
  42. Schiemanck SK, Kwakkel G, Post MW, et al. Impact of internal capsule lesions on outcome of motor hand function at one year post-stroke. J Rehabil Med 2008; 40:96.
  43. Joinlambert C, Saliou G, Flamand-Roze C, et al. Cortical border-zone infarcts: clinical features, causes and outcome. J Neurol Neurosurg Psychiatry 2012; 83:771.
  44. Bang OY, Lee PH, Heo KG, et al. Specific DWI lesion patterns predict prognosis after acute ischaemic stroke within the MCA territory. J Neurol Neurosurg Psychiatry 2005; 76:1222.
  45. Bladin CF, Chambers BR. Clinical features, pathogenesis, and computed tomographic characteristics of internal watershed infarction. Stroke 1993; 24:1925.
  46. Kucinski T, Koch C, Eckert B, et al. Collateral circulation is an independent radiological predictor of outcome after thrombolysis in acute ischaemic stroke. Neuroradiology 2003; 45:11.
  47. Lima FO, Furie KL, Silva GS, et al. The pattern of leptomeningeal collaterals on CT angiography is a strong predictor of long-term functional outcome in stroke patients with large vessel intracranial occlusion. Stroke 2010; 41:2316.
  48. Battey TW, Karki M, Singhal AB, et al. Brain edema predicts outcome after nonlacunar ischemic stroke. Stroke 2014; 45:3643.
  49. Petty GW, Brown RD Jr, Whisnant JP, et al. Ischemic stroke subtypes : a population-based study of functional outcome, survival, and recurrence. Stroke 2000; 31:1062.
  50. Sprigg N, Gray LJ, Bath PM, et al. Early recovery and functional outcome are related with causal stroke subtype: data from the tinzaparin in acute ischemic stroke trial. J Stroke Cerebrovasc Dis 2007; 16:180.
  51. de Jong G, van Raak L, Kessels F, Lodder J. Stroke subtype and mortality. a follow-up study in 998 patients with a first cerebral infarct. J Clin Epidemiol 2003; 56:262.
  52. Lima FO, Furie KL, Silva GS, et al. Prognosis of untreated strokes due to anterior circulation proximal intracranial arterial occlusions detected by use of computed tomography angiography. JAMA Neurol 2014; 71:151.
  53. Barlas RS, Honney K, Loke YK, et al. Impact of Hemoglobin Levels and Anemia on Mortality in Acute Stroke: Analysis of UK Regional Registry Data, Systematic Review, and Meta-Analysis. J Am Heart Assoc 2016; 5.
  54. O'Donnell MJ, Fang J, D'Uva C, et al. The PLAN score: a bedside prediction rule for death and severe disability following acute ischemic stroke. Arch Intern Med 2012; 172:1548.
  55. McGrath ER, Kapral MK, Fang J, et al. Association of atrial fibrillation with mortality and disability after ischemic stroke. Neurology 2013; 81:825.
  56. Pohjasvaara T, Vataja R, Leppävuori A, et al. Cognitive functions and depression as predictors of poor outcome 15 months after stroke. Cerebrovasc Dis 2002; 14:228.
  57. Stöllberger C, Exner I, Finsterer J, et al. Stroke in diabetic and non-diabetic patients: course and prognostic value of admission serum glucose. Ann Med 2005; 37:357.
  58. Desilles JP, Meseguer E, Labreuche J, et al. Diabetes mellitus, admission glucose, and outcomes after stroke thrombolysis: a registry and systematic review. Stroke 2013; 44:1915.
  59. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke 2001; 32:2426.
  60. Szummer KE, Solomon SD, Velazquez EJ, et al. Heart failure on admission and the risk of stroke following acute myocardial infarction: the VALIANT registry. Eur Heart J 2005; 26:2114.
  61. Brammås A, Jakobsson S, Ulvenstam A, Mooe T. Mortality after ischemic stroke in patients with acute myocardial infarction: predictors and trends over time in Sweden. Stroke 2013; 44:3050.
  62. Kissela B, Lindsell CJ, Kleindorfer D, et al. Clinical prediction of functional outcome after ischemic stroke: the surprising importance of periventricular white matter disease and race. Stroke 2009; 40:530.
  63. Arsava EM, Rahman R, Rosand J, et al. Severity of leukoaraiosis correlates with clinical outcome after ischemic stroke. Neurology 2009; 72:1403.
  64. Ryu WS, Woo SH, Schellingerhout D, et al. Stroke outcomes are worse with larger leukoaraiosis volumes. Brain 2017; 140:158.
  65. Iseki K, Fukiyama K, Okawa Dialysis Study (OKIDS) Group. Clinical demographics and long-term prognosis after stroke in patients on chronic haemodialysis. The Okinawa Dialysis Study (OKIDS) Group. Nephrol Dial Transplant 2000; 15:1808.
  66. Kumai Y, Kamouchi M, Hata J, et al. Proteinuria and clinical outcomes after ischemic stroke. Neurology 2012; 78:1909.
  67. Yahalom G, Schwartz R, Schwammenthal Y, et al. Chronic kidney disease and clinical outcome in patients with acute stroke. Stroke 2009; 40:1296.
  68. Toyoda K, Fujii K, Fujimi S, et al. Stroke in patients on maintenance hemodialysis: a 22-year single-center study. Am J Kidney Dis 2005; 45:1058.
  69. Naganuma M, Koga M, Shiokawa Y, et al. Reduced estimated glomerular filtration rate is associated with stroke outcome after intravenous rt-PA: the Stroke Acute Management with Urgent Risk-Factor Assessment and Improvement (SAMURAI) rt-PA registry. Cerebrovasc Dis 2011; 31:123.
  70. FOOD Trial Collaboration. Poor nutritional status on admission predicts poor outcomes after stroke: observational data from the FOOD trial. Stroke 2003; 34:1450.
  71. Kimberly WT, Lima FO, O'Connor S, Furie KL. Sex differences and hemoglobin levels in relation to stroke outcomes. Neurology 2013; 80:719.
  72. Olsen TS, Dehlendorff C, Petersen HG, Andersen KK. Body mass index and poststroke mortality. Neuroepidemiology 2008; 30:93.
  73. Vemmos K, Ntaios G, Spengos K, et al. Association between obesity and mortality after acute first-ever stroke: the obesity-stroke paradox. Stroke 2011; 42:30.
  74. Doehner W, Schenkel J, Anker SD, et al. Overweight and obesity are associated with improved survival, functional outcome, and stroke recurrence after acute stroke or transient ischaemic attack: observations from the TEMPiS trial. Eur Heart J 2013; 34:268.
  75. Stamou SC, Hill PC, Dangas G, et al. Stroke after coronary artery bypass: incidence, predictors, and clinical outcome. Stroke 2001; 32:1508.
  76. Varona JF, Bermejo F, Guerra JM, Molina JA. Long-term prognosis of ischemic stroke in young adults. Study of 272 cases. J Neurol 2004; 251:1507.
  77. Chambers BR, Norris JW, Shurvell BL, Hachinski VC. Prognosis of acute stroke. Neurology 1987; 37:221.
  78. Niewada M, Kobayashi A, Sandercock PA, et al. Influence of gender on baseline features and clinical outcomes among 17,370 patients with confirmed ischaemic stroke in the international stroke trial. Neuroepidemiology 2005; 24:123.
  79. Petrea RE, Beiser AS, Seshadri S, et al. Gender differences in stroke incidence and poststroke disability in the Framingham heart study. Stroke 2009; 40:1032.
  80. Santalucia P, Pezzella FR, Sessa M, et al. Sex differences in clinical presentation, severity and outcome of stroke: results from a hospital-based registry. Eur J Intern Med 2013; 24:167.
  81. Roth DL, Haley WE, Clay OJ, et al. Race and gender differences in 1-year outcomes for community-dwelling stroke survivors with family caregivers. Stroke 2011; 42:626.
  82. Appelros P, Stegmayr B, Terént A. A review on sex differences in stroke treatment and outcome. Acta Neurol Scand 2010; 121:359.
  83. Gargano JW, Reeves MJ, Paul Coverdell National Acute Stroke Registry Michigan Prototype Investigators. Sex differences in stroke recovery and stroke-specific quality of life: results from a statewide stroke registry. Stroke 2007; 38:2541.
  84. Zhou G, Nie S, Dai L, et al. Sex differences in stroke case fatality: a meta-analysis. Acta Neurol Scand 2013; 128:1.
  85. Centers for Disease Control and Prevention (CDC). Differences in disability among black and white stroke survivors--United States, 2000-2001. MMWR Morb Mortal Wkly Rep 2005; 54:3.
  86. Grube MM, Koennecke HC, Walter G, et al. Association between socioeconomic status and functional impairment 3 months after ischemic stroke: the Berlin Stroke Register. Stroke 2012; 43:3325.
  87. Putman K, De Wit L, Schoonacker M, et al. Effect of socioeconomic status on functional and motor recovery after stroke: a European multicentre study. J Neurol Neurosurg Psychiatry 2007; 78:593.
  88. Jakovljević D, Sarti C, Sivenius J, et al. Socioeconomic status and ischemic stroke: The FINMONICA Stroke Register. Stroke 2001; 32:1492.
  89. van den Bos GA, Smits JP, Westert GP, van Straten A. Socioeconomic variations in the course of stroke: unequal health outcomes, equal care? J Epidemiol Community Health 2002; 56:943.
  90. Paul SL, Sturm JW, Dewey HM, et al. Long-term outcome in the North East Melbourne Stroke Incidence Study: predictors of quality of life at 5 years after stroke. Stroke 2005; 36:2082.
  91. Dhamoon MS, Moon YP, Paik MC, et al. Quality of life declines after first ischemic stroke. The Northern Manhattan Study. Neurology 2010; 75:328.
  92. Cox AM, McKevitt C, Rudd AG, Wolfe CD. Socioeconomic status and stroke. Lancet Neurol 2006; 5:181.
  93. Kerr GD, Higgins P, Walters M, et al. Socioeconomic status and transient ischaemic attack/stroke: a prospective observational study. Cerebrovasc Dis 2011; 31:130.
  94. Dávalos A, Toni D, Iweins F, et al. Neurological deterioration in acute ischemic stroke: potential predictors and associated factors in the European cooperative acute stroke study (ECASS) I. Stroke 1999; 30:2631.
  95. Tei H, Uchiyama S, Ohara K, et al. Deteriorating ischemic stroke in 4 clinical categories classified by the Oxfordshire Community Stroke Project. Stroke 2000; 31:2049.
  96. Toni D, Fiorelli M, Gentile M, et al. Progressing neurological deficit secondary to acute ischemic stroke. A study on predictability, pathogenesis, and prognosis. Arch Neurol 1995; 52:670.
  97. Ois A, Martinez-Rodriguez JE, Munteis E, et al. Steno-occlusive arterial disease and early neurological deterioration in acute ischemic stroke. Cerebrovasc Dis 2008; 25:151.
  98. Thanvi B, Treadwell S, Robinson T. Early neurological deterioration in acute ischaemic stroke: predictors, mechanisms and management. Postgrad Med J 2008; 84:412.
  99. Siegler JE, Martin-Schild S. Early Neurological Deterioration (END) after stroke: the END depends on the definition. Int J Stroke 2011; 6:211.
  100. Ward NS, Brown MM, Thompson AJ, Frackowiak RS. Neural correlates of motor recovery after stroke: a longitudinal fMRI study. Brain 2003; 126:2476.
  101. Cramer SC. Repairing the human brain after stroke: I. Mechanisms of spontaneous recovery. Ann Neurol 2008; 63:272.
  102. Jørgensen HS, Nakayama H, Raaschou HO, et al. Outcome and time course of recovery in stroke. Part II: Time course of recovery. The Copenhagen Stroke Study. Arch Phys Med Rehabil 1995; 76:406.
  103. DeVetten G, Coutts SB, Hill MD, et al. Acute corticospinal tract Wallerian degeneration is associated with stroke outcome. Stroke 2010; 41:751.
  104. Puig J, Pedraza S, Blasco G, et al. Acute damage to the posterior limb of the internal capsule on diffusion tensor tractography as an early imaging predictor of motor outcome after stroke. AJNR Am J Neuroradiol 2011; 32:857.
  105. Byblow WD, Stinear CM, Barber PA, et al. Proportional recovery after stroke depends on corticomotor integrity. Ann Neurol 2015; 78:848.
  106. Feng W, Wang J, Chhatbar PY, et al. Corticospinal tract lesion load: An imaging biomarker for stroke motor outcomes. Ann Neurol 2015; 78:860.
  107. Slot KB, Berge E, Dorman P, et al. Impact of functional status at six months on long term survival in patients with ischaemic stroke: prospective cohort studies. BMJ 2008; 336:376.
  108. TWITCHELL TE. The restoration of motor function following hemiplegia in man. Brain 1951; 74:443.
  109. Nakayama H, Jørgensen HS, Raaschou HO, Olsen TS. Recovery of upper extremity function in stroke patients: the Copenhagen Stroke Study. Arch Phys Med Rehabil 1994; 75:394.
  110. Fritz SL, Light KE, Patterson TS, et al. Active finger extension predicts outcomes after constraint-induced movement therapy for individuals with hemiparesis after stroke. Stroke 2005; 36:1172.
  111. Smania N, Paolucci S, Tinazzi M, et al. Active finger extension: a simple movement predicting recovery of arm function in patients with acute stroke. Stroke 2007; 38:1088.
  112. Katrak P, Bowring G, Conroy P, et al. Predicting upper limb recovery after stroke: the place of early shoulder and hand movement. Arch Phys Med Rehabil 1998; 79:758.
  113. Beebe JA, Lang CE. Active range of motion predicts upper extremity function 3 months after stroke. Stroke 2009; 40:1772.
  114. Nijland RH, van Wegen EE, Harmeling-van der Wel BC, et al. Presence of finger extension and shoulder abduction within 72 hours after stroke predicts functional recovery: early prediction of functional outcome after stroke: the EPOS cohort study. Stroke 2010; 41:745.
  115. Veerbeek JM, Van Wegen EE, Harmeling-Van der Wel BC, et al. Is accurate prediction of gait in nonambulatory stroke patients possible within 72 hours poststroke? The EPOS study. Neurorehabil Neural Repair 2011; 25:268.
  116. Pedersen PM, Jørgensen HS, Nakayama H, et al. Aphasia in acute stroke: incidence, determinants, and recovery. Ann Neurol 1995; 38:659.
  117. Smithard DG, O'Neill PA, England RE, et al. The natural history of dysphagia following a stroke. Dysphagia 1997; 12:188.
  118. Dennis MS, Lewis SC, Warlow C, FOOD Trial Collaboration. Effect of timing and method of enteral tube feeding for dysphagic stroke patients (FOOD): a multicentre randomised controlled trial. Lancet 2005; 365:764.
  119. Kumar S, Langmore S, Goddeau RP Jr, et al. Predictors of percutaneous endoscopic gastrostomy tube placement in patients with severe dysphagia from an acute-subacute hemispheric infarction. J Stroke Cerebrovasc Dis 2012; 21:114.
  120. Okubo PC, Fábio SR, Domenis DR, Takayanagui OM. Using the National Institute of Health Stroke Scale to predict dysphagia in acute ischemic stroke. Cerebrovasc Dis 2012; 33:501.
  121. Teasell R, Foley N, McRae M, Finestone H. Use of percutaneous gastrojejunostomy feeding tubes in the rehabilitation of stroke patients. Arch Phys Med Rehabil 2001; 82:1412.
  122. Doyle S, Bennett S, Fasoli SE, McKenna KT. Interventions for sensory impairment in the upper limb after stroke. Cochrane Database Syst Rev 2010; :CD006331.
  123. Tyson SF, Hanley M, Chillala J, et al. Sensory loss in hospital-admitted people with stroke: characteristics, associated factors, and relationship with function. Neurorehabil Neural Repair 2008; 22:166.
  124. Flaster M, Meresh E, Rao M, Biller J. Central poststroke pain: current diagnosis and treatment. Top Stroke Rehabil 2013; 20:116.
  125. Cassidy TP, Lewis S, Gray CS. Recovery from visuospatial neglect in stroke patients. J Neurol Neurosurg Psychiatry 1998; 64:555.
  126. Hier DB, Mondlock J, Caplan LR. Recovery of behavioral abnormalities after right hemisphere stroke. Neurology 1983; 33:345.
  127. Gray CS, French JM, Bates D, et al. Recovery of visual fields in acute stroke: homonymous hemianopia associated with adverse prognosis. Age Ageing 1989; 18:419.
  128. Lai SM, Duncan PW, Keighley J. Prediction of functional outcome after stroke: comparison of the Orpington Prognostic Scale and the NIH Stroke Scale. Stroke 1998; 29:1838.
  129. Kalra L, Crome P. The role of prognostic scores in targeting stroke rehabilitation in elderly patients. J Am Geriatr Soc 1993; 41:396.
  130. Reding MJ, Potes E. Rehabilitation outcome following initial unilateral hemispheric stroke. Life table analysis approach. Stroke 1988; 19:1354.
  131. Ntaios G, Faouzi M, Ferrari J, et al. An integer-based score to predict functional outcome in acute ischemic stroke: the ASTRAL score. Neurology 2012; 78:1916.
  132. Papavasileiou V, Milionis H, Michel P, et al. ASTRAL score predicts 5-year dependence and mortality in acute ischemic stroke. Stroke 2013; 44:1616.
  133. Strbian D, Meretoja A, Ahlhelm FJ, et al. Predicting outcome of IV thrombolysis-treated ischemic stroke patients: the DRAGON score. Neurology 2012; 78:427.
  134. Saposnik G, Raptis S, Kapral MK, et al. The iScore predicts poor functional outcomes early after hospitalization for an acute ischemic stroke. Stroke 2011; 42:3421.
  135. Saposnik G, Reeves MJ, Johnston SC, et al. Predicting clinical outcomes after thrombolysis using the iScore: results from the Virtual International Stroke Trials Archive. Stroke 2013; 44:2755.
  136. Caplan LR. Scores of scores. JAMA Neurol 2013; 70:252.
  137. Grysiewicz RA, Thomas K, Pandey DK. Epidemiology of ischemic and hemorrhagic stroke: incidence, prevalence, mortality, and risk factors. Neurol Clin 2008; 26:871.
  138. Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurol 2003; 2:43.
  139. Prencipe M, Culasso F, Rasura M, et al. Long-term prognosis after a minor stroke: 10-year mortality and major stroke recurrence rates in a hospital-based cohort. Stroke 1998; 29:126.
  140. Yoneda Y, Okuda S, Hamada R, et al. Hospital cost of ischemic stroke and intracerebral hemorrhage in Japanese stroke centers. Health Policy 2005; 73:202.
  141. Lee WC, Joshi AV, Wang Q, et al. Morbidity and mortality among elderly Americans with different stroke subtypes. Adv Ther 2007; 24:258.
  142. Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS. Intracerebral hemorrhage versus infarction: stroke severity, risk factors, and prognosis. Ann Neurol 1995; 38:45.
  143. Kelly-Hayes M, Beiser A, Kase CS, et al. The influence of gender and age on disability following ischemic stroke: the Framingham study. J Stroke Cerebrovasc Dis 2003; 12:119.
  144. Daniel K, Wolfe CD, Busch MA, McKevitt C. What are the social consequences of stroke for working-aged adults? A systematic review. Stroke 2009; 40:e431.
  145. Glozier N, Hackett ML, Parag V, et al. The influence of psychiatric morbidity on return to paid work after stroke in younger adults: the Auckland Regional Community Stroke (ARCOS) Study, 2002 to 2003. Stroke 2008; 39:1526.
  146. Wozniak MA, Kittner SJ, Price TR, et al. Stroke location is not associated with return to work after first ischemic stroke. Stroke 1999; 30:2568.
  147. Saeki S, Ogata H, Okubo T, et al. Return to work after stroke. A follow-up study. Stroke 1995; 26:399.
  148. Maaijwee NA, Rutten-Jacobs LC, Arntz RM, et al. Long-term increased risk of unemployment after young stroke: a long-term follow-up study. Neurology 2014; 83:1132.
Topic 14086 Version 16.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.