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(Stroke. 2003;34:1450.)
© 2003 American Heart Association, Inc.

Original Contributions

Poor Nutritional Status on Admission Predicts Poor Outcomes After Stroke

Observational Data From the FOOD Trial

FOOD Trial Collaboration

Correspondence to Prof Martin Dennis, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, EH4 2XU, UK. E-mail msd{at}skull.dcn.ed.ac.uk

	Abstract

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Background and Purpose— Previous studies suggest that undernourished patients with acute stroke do badly. The data, however, are not robust. We aimed to reliably assess the importance of baseline nutritional status as an independent predictor of long-term outcome after stroke in a large prospective cohort enrolled in the Feed Or Ordinary Diet (FOOD) trial, a multicenter randomized trial evaluating various feeding policies.

Methods— Patients admitted to hospital with a recent stroke were enrolled in the FOOD trial. Data on nutritional status and other clinical predictors of outcome were collected at trial entry. At 6 months, the coordinating center collected data on survival and functional status (modified Rankin Scale). Outcome assessment was done by researchers blinded to baseline assessments and treatment allocation.

Results— Between November 1996 and November 2001, 3012 patients were enrolled, and 2955 (98%) were followed up. Of the 275 undernourished patients, 102 (37%) were dead by final follow-up compared with only 445 (20%) of 2194 patients of normal nutritional status (odds ratio [OR], 2.32; 95% CI, 1.78 to 3.02). After adjustment for age, prestroke functional state, and stroke severity, this relationship, although weakened, still held (OR, 1.82; 95% CI, 1.34 to 2.47). Undernourished patients were more likely to develop pneumonia, other infections, and gastrointestinal bleeding during their hospital admission than other patients.

Conclusions— These data provide reliable evidence that nutritional status early after stroke is independently associated with long-term outcome. It supports the rationale for the FOOD trial, which continues to recruit and aims to estimate the effect of different feeding regimes on outcome after stroke and thus determine whether the association observed in this study is likely to be causal.

Key Words: clinical trials • nutrition • prognosis • stroke outcome

	Introduction

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Malnutrition in hospital patients is a common and often unrecognized problem, especially in the elderly and those who remain in hospital for prolonged periods.¹ The reported frequency of malnutrition after stroke has varied from 8%² to 34%.³ This variation is probably due to patient selection, the definitions of malnutrition, and the method and timing of assessments. In general, these studies included only small numbers of patients (n=49⁴ to 201⁵), so the estimates of frequency were not only potentially biased but also imprecise. In routine clinical practice, it is not easy to assess stroke patients’ nutritional status for many reasons: A dietary and weight history may not be available if patients have communication problems; other sources of this information may not be available if, as is common, the patient lives alone; simple assessments of weight and height to estimate the body mass index (BMI) may be difficult or impossible in immobile stroke patients; specialized equipment such as weighing beds, hoists, or scales that accommodate wheelchairs may not be

See Editorial Comment, page 1455

available in the stroke unit; and because stroke patients often cannot stand, height cannot be directly measured but must be estimated from the patient’s demi-span or heel-knee length. Fortunately, simpler clinical assessments ("bedside" estimates of the patient size and fat distribution) have been shown to be practical and reliable and can be used to identify most patients with low BMI and abnormal anthropometry.⁶

Despite these difficulties in assessing nutrition after stroke, there is widespread belief that it may influence recovery. We aimed to establish whether nutritional status early in a patient’s hospital stay is associated with long-term survival and functional status in survivors. Here, we report an analysis of a prospective cohort comprising the first 3012 patients randomized in the Feed Or Ordinary Food (FOOD) trial. This is an international multicenter randomized trial to evaluate different feeding policies in hospitalized stroke patients, which will continue to recruit patients until at least 2004.⁷

	Methods

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The FOOD trial comprises a family of 3 randomized controlled trials that share the same randomization, data collection, and follow-up systems. These trials aim to compare the outcomes of hospitalized stroke patients managed with different feeding policies (Table 1). The trial has broad eligibility criteria. Any patient who is admitted to a participating hospital with a recent (within 7 days) stroke (first ever or recurrent) can be enrolled if the responsible clinician is uncertain of the best feeding policy and the patient or a relative consents to enrollment. Patients with subarachnoid hemorrhage are not included. Baseline data (Table 2) are collected during a phone call at trial entry. The randomizing clinician is asked to categorize patients as undernourished, normal, or overweight on the basis of their own bedside assessment or, when practical, from a fuller assessment that might include weight, height, dietary history, or blood tests. We have shown previously that the simple bedside categorization of nutritional status, performed by a range of healthcare professionals without explicit criteria or detailed training, accurately assesses BMI with reasonable interobserver reliability (unweighted =0.53 to 0.77).⁶ Six other baseline prognostic factors (Table 2) make up an outcome prediction model that can be collected in a variety of settings with good to excellent interrater reliability (unweighted =0.67 to 0.97) and that has been shown to accurately predict outcomes in several independent stroke cohorts.^8–11 When all the baseline data have been entered and checked, the computer gives a treatment allocation. Thus, baseline data are 100% complete.

View this table: [in this window] [in a new window]   TABLE 1. Possible Treatment Allocations in FOOD Trials 1, 2, and 3 and the Numbers of Patients Allocated to Each Treatment Group

View this table: [in this window] [in a new window]   TABLE 2. Baseline Characteristics

Randomization is stratified on the basis of the randomizing clinician’s judgment of the patient’s nutritional status (undernourished, normal or overweight). The protocol allows this assessment to be based on a full nutritional assessment if practical, but if not, it may rely on an informal assessment (see above). This flexible approach has been adopted because of the practical difficulties in adopting a standard methodology across all the centers with varying access to dietitians, weighing beds, etc, and because there is little agreement on how components of a comprehensive nutritional assessment should be summarized and a classification of overall nutritional status derived.

After hospital discharge or in-hospital death, the local coordinator completes a hospital discharge form and, from a review of the case notes, records any poststroke complications that occurred after randomization and before discharge or in-hospital death. This review was not explicitly performed by researchers blinded to baseline nutritional status or treatment allocation, nor was it audited centrally except to check for completeness and consistency of data.

The national coordinating centers collect follow-up information 6 months after enrollment by researchers blinded to the treatment allocation and baseline data by means of a postal questionnaire or structured telephone interview. If patients were unable to complete these, then the information was collected from a caregiver or proxy. The follow-up aims to establish patient vital status, place of residence, and functional ability on the modified Rankin Scale.

The FOOD trial has been approved by the multicenter research ethics committee in the United Kingdom and the local research committee at each center.

Statistical Analysis
We plotted Kaplan-Meier survival curves for patients in each baseline nutritional status category. The associations between baseline nutritional status, other baseline prognostic factors, survival, and functional status at final follow-up were explored. First, whether patients were alive at 6 months was used as the dependent variable in a logistic regression analysis, with nutritional status and other baseline prognostic factors as independent variables. Whether patients were alive and independent at 6 months was modeled similarly. Survival was also modeled with Cox proportional-hazards method, but the results are not shown for brevity. The normal weight group was used as the reference group for comparisons with the undernourished and overweight groups. Age was analyzed as a continuous variable. All other prognostic variables were analyzed as binary variables. No adjustments were made for multiple comparisons.

	Results

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Between November 1996 and February 28, 2001, 112 hospitals in 16 countries had enrolled 3012 patients; by November 2001, 6-month survival and modified Rankin scores were available for 2955 (98%). The patients’ baseline characteristics are shown in Table 2. Patients were enrolled a median of 5 days (interquartile range [IQR], 2 to 8 days) after stroke onset and 4 days (IQR, 2 to 7 days) after hospital admission. Of the 3012 patients, 279 (9%) were judged as undernourished and 495 (16%) as overweight. The undernourished patients were older and more often lived alone before the stroke than the other groups. The method of nutritional assessment was collected only after the first 664 patients had been enrolled in the pilot phase. It was available in 2295 of 3012 (76%). In total, 1388 patients (60%) had their nutritional status assessed informally (ie, based on simple observation), whereas the remainder had other assessments performed either individually or in combination: 448 (20%) were weighed or had their BMI calculated, 372 (16%) were assessed by a dietitian, 251 (11%) had blood indices, and 48 (2%) had anthropometry. Follow-up data were collected a median of 196 days (IQR, 177 to 224 days) after enrollment.

Table 3 shows the number and proportions of patients in each nutritional group who were reported to have developed a poststroke complication after randomization and before hospital discharge or in-hospital death. Interestingly, the undernourished patients had more pneumonia, other infections, and gastrointestinal bleeds than the others. Those of normal nutritional status were less likely to develop pressure sores than those who were undernourished or overweight.

View this table: [in this window] [in a new window]   TABLE 3. Number and Proportion of Patients Enrolled Who Were Reported as Having Developed a Poststroke Complication After Randomization and Before Hospital Discharge or In-Hospital Death

Of the 3012 patients enrolled, 632 (21%) died before their final follow-up. At final follow-up, 856 (37%) of 2323 survivors (28% of all patients) had a modified Rankin score of 0 to 2 (ie, independent in everyday activities), whereas the remainder were dependent. Of survivors, 1782 (77%; 59% of all patients) were living in their own or a relative’s home.

Figure 1 shows the Kaplan-Meier survival curves for patients in each of the 3 baseline nutritional categories. The patients who were undernourished at baseline appeared to have a poorer survival than those who were normal or overweight; the curves diverge early and continue to diverge throughout the follow-up period. The final outcomes of patients judged to be undernourished, normal, or overweight at baseline are shown in Figure 2. From the logistic regression (see Table 4), the undernourished patients were significantly more likely to die during follow-up than patients of normal weight (odds ratio [OR], 2.32; 95% CI, 1.78 to 3.02). Although adjusting for patient age, prestroke function, living conditions, and stroke severity (including ability to swallow) weakened this relationship (OR for undernourished compared with normal, 1.82; 95% CI, 1.34 to 2.47), it remained significant (P=0.0001). The overweight patients were not significantly different from the normal-weight patients (OR, 0.83; 95% CI, 0.65 to 1.08; adjusted OR, 0.87; 95% CI, 0.65 to 1.15). Results of the Cox proportional-hazards modeling were similar (results available on request).

View larger version (16K): [in this window] [in a new window]   Figure 1. Kaplan-Meier survival curves for patients who were undernourished, normal, or overweight at baseline in the FOOD trials.

View larger version (12K): [in this window] [in a new window]   Figure 2. Survival and functional status (top) and living circumstances (bottom) of patients at 6 months who were undernourished, normal, or overweight at baseline in the FOOD trials. Bar height corresponds to percentage of patients in each nutritional category with the outcome; actual numbers of patients with each outcome are superimposed on the bars.

View this table: [in this window] [in a new window]   TABLE 4. Results of Logistic Regression Showing Relationships Between Baseline Variables, Including Nutritional Status, and 6-Month Outcome

Undernourished patients were much more likely to be dead or dependent (ie, a modified Rankin score of 3 to 5) than those who were of normal weight (OR, 2.08; 95% CI, 1.50 to 2.88). Although adjusting for patient age, sex, prestroke function, living conditions, and stroke severity (including ability to swallow) weakened this relationship (OR, 1.52; 95% CI, 1.05 to 2.21), it remained statistically significant (P=0.03). Overweight patients were not significantly different from normal-weight patients (OR, 0.95; 95% CI, 0.77 to 1.18; adjusted OR, 0.91; 95% CI, 0.71 to 1.17). The association between being undernourished at baseline and being dead or dependent at final follow-up was similar in those in whom baseline nutritional status was measured informally and those whose status was formally measured, although even this large study did not have the power to establish whether any differences between these groups were statistically significant. Differences in survival and functional outcomes are reflected in the different living circumstances of patients who were undernourished at final follow-up compared with the rest of the patients (Figure 2b).

We investigated which of the other prognostic factors that we adjusted for were the main causes of the decreased strength of the association between being undernourished and outcome. The most important factor was the relationship between undernourishment and greater age. The second was the relationship between being undernourished and the inability to walk.

	Discussion

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We have shown that being undernourished immediately after stroke is associated with reduced survival, functional ability, and living circumstances 6 months later. The relationship, although weakened when adjusted for other prognostic factors, remains statistically significant and raises the possibility that the relationship is causal.

The strengths of this study include the large sample size; recruitment from a wide range of hospitals in many countries, which increases its generalizability; collection of other robust predictive factors, which have been shown to be valid and reliable in several independent cohorts; assessment of outcome by researchers blinded to baseline factors; and virtually complete follow-up at 6 months. Study weaknesses include an inability to establish a dose-response relationship between degree of undernutrition and outcome and lack of standardization of assessment of nutritional status. However, a simple clinical judgment of nutritional status may be both valid and reliable.⁶ Nevertheless, the bedside assessment of nutrition used to assess most patients in FOOD may have been influenced by some aspect of patient frailty or comorbidity (such as malignancy) rather than just their nutritional status. However, any such bias might be reduced because other factors that we took into account—ie, age and prestroke dependency—probably reflect patient frailty and comorbidity. In developing our predictive model, we tested whether inclusion of specific comorbidities (diabetes mellitus, ischemic heart disease, cardiac failure, known malignancy, renal impairment, anemia) significantly improved its accuracy; they did not.^8,9 Thus, one might conclude that our prediction model takes reasonable account of such comorbidities.

The association between baseline nutritional status and outcome that we have observed in this study may actually underestimate the importance of nutrition. First, if our simple classification of nutritional status leads to a proportion of patients being misclassified, then this would lead to an underestimation of the strength of the association between baseline nutritional status and outcome. Second, some of our patients may have become malnourished during hospital admission despite their allocated feeding regime and had poor outcomes. Our finding that inability to swallow was independently associated with poor outcomes (Table 4) would be consistent with this. Several studies have shown that stroke patients’ nutritional status may worsen during hospital admission despite reasonable efforts to provide adequate nutrition.^2,5,12,13 If we had serially measured nutritional status during admission, we may have found an even stronger relationship with outcome.

Previous studies of the association between baseline nutritional status after stroke and outcome have been hampered by small sample sizes, which limit their power to detect an association that is independent of other prognostic factors. Dávalos et al,¹² in a study of 104 patients, showed that malnutrition (serum albumin <35 g/L or triceps skin-fold thickness or mid-arm muscle circumference <10th percentile) was present in 16.3% on admission and 26.4% after 1 week. Malnutrition at 1 week was associated with poorer outcome (dead or Barthel Index score ≤50) at 1 month, more infections and pressure sores, and longer length of stay, but these associations were not statistically significant after adjustment for age, sex, swallowing ability, urinary cortisol, and stroke severity categorized with the Canadian Stroke Scale. Gariballa et al,⁵ in a cohort of 201 patients, investigated the association of age, sex, smoking history, modified Rankin score, previous illness, drug use, and serum albumin on admission with 3-month survival. They established that low serum albumin but not BMI, anthropometry, serum iron, and transferrin was significantly associated with decreased survival at 3 months (hazard ratio per 1 g/L, 0.91; 95% CI, 0.84 to 0.99). One can argue to what extent low albumin reflects a patients’ nutritional status rather than the presence of any comorbidity.

Our data showing that pneumonia, other infections, gastrointestinal hemorrhage, and pressure sores are more common in undernourished patients are consistent with previous work¹² and with our understanding of the effects of poor nutrition on the immune system and wound healing.¹⁴ The excess of gastrointestinal hemorrhage in undernourished patients might have several explanations: preexisting gastrointestinal disease (eg, peptic ulceration) that predisposes to undernutrition and hemorrhage, impaired healing of potential bleeding lesions, and adverse effects of enteral tubes inserted to improve nutrition. The excess of complications may help explain some of the observed difference in mortality at 6 months. However, these data on complications need to be interpreted with caution because of our lack of explicit blinding to baseline nutritional status and the lack of uniform definitions of complications with no central verification. The latter point might influence the absolute rates of complications but is less likely to influence the relative rates in different nutritional groups. In addition, the data are potentially confounded by variation in observation period arising from differential lengths of hospital stay, but because the differences in mean length of stay between nutritional groups are small, this is unlikely to be a major confounder.

Definitive evidence that any association between malnutrition and poor outcome is causal must come from randomized controlled trials that establish whether improving nutrition leads to better outcomes. Although a systematic review of randomized controlled trials evaluating nutritional supplementation^15,16 has suggested that its use may improve survival, there are very few trials in stroke patients.¹⁷ Additionally, the review comprised large numbers of very small single-center trials, many of which were of poor quality.^15,16 It is quite possible that any estimates of effect size were exaggerated by publication and other biases. One small randomized trial (n=42) has suggested that oral supplementation after stroke improves nutritional parameters, but it was far too small to demonstrate any effect on survival or functional status.¹⁸ Dávalos et al¹² argued for the need to establish in a randomized controlled trial whether early enteral feeding improves outcome after stroke, but no completed studies have been reported. Trial 2 of the FOOD family addresses this issue directly. A systematic review of randomized controlled trials comparing the outcomes of dysphagic stroke patients fed via nasogastric (NG) or percutaneous endoscopic gastrostomy (PEG) tube included only 2 completed trials.¹⁷ Eight of 26 PEG patients (31%) died compared with 14 of 23 control patients (61%). This review provided an implausibly large estimate of the effect of PEG tube feeding (OR for death, 0.28; 95% CI, 0.09 to 0.89; absolute difference, 30%).

The FOOD trial aims to establish whether more intensive feeding regimes (ie, oral supplements, earlier tube feeding, and greater use of PEG tube feeding) improve survival and functional outcomes after stroke. More than 4500 patients have been enrolled so far, but many more are required to show whether improving nutritional state after stroke actually improves patient outcomes and thus conclusively establish that the observed association between nutritional status and outcome is actually causal.

	Appendix

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FOOD Trial Coordinating Center
Prof M.S. Dennis (principal investigator and grant holder), G. Cranswick(trial coordinator), A. Fraser (Data Management Team), S. Grant (Data Management Team), A. Gunkel (interim trial coordinator), J. Hunter (Data Management Team), Dr S. Lewis (trial statistician), D. Perry (Information Technology manager), V. Soosay (computer programmer), A. Williamson (trial secretary), A. Young (Data Management Team).

Independent Data Monitoring Committee
Profs J. Bulpitt, A. Grant (chair), G. Murray, P. Sandercock.

National Coordinators
Drs N. Anderson (New Zealand), S. Bahar (Turkey), G. Hankey (Australia), S. Ricci (Italy).

Steering Committee
G. Bathgate, C. Chalmers, G. Cranswick, Prof M.S. Dennis, B. Farrell (grant holder), Prof J. Forbes (grant holder), Dr S. Ghosh, Prof P. Langhorne, Dr S. Lewis, J. MacIntyre, C.A. McAteer, Dr P. O’Neill, Dr J. Potter, Dr M. Roberts, Prof C. Warlow (grant holder).

Funders
Chest Heart & Stroke Scotland, the Chief Scientist Office, the NHS R&D HTA Program Grant, and the Stroke Association.

Writing Group
Prof M.S. Dennis (chair), Dr S. Lewis, Prof C. Warlow.

Members of the FOOD Trials Collaboration
Numbers in parentheses indicate the number of patients randomized by September 30, 2001, in that center.

Australia
Royal Perth Hospital, Perth (21): Dr G.J. Hankey, S. McDonald; Redcliffe Hospital, Redcliffe (18): T. Bennett, Dr J. Karrasch, C. Lowe; Royal North Shore Hospital, Sydney, New South Wales (15): E. O’Brien, F. Simpson; The Alfred Prahran (7): A. Bramley, Dr J. Frayne; New England Regional Hospital, Armidale (4): Dr G. Baker, Dr G. DeGabriele, J. Kennett, Dr J. Nevin; Princess Alexandra Hospital, Brisbane (4): Dr P.D. Aitken, K. Boch, Dr G. Hall.

Belgium
Algemeen Ziekenhuis, Sint-Jan Brugge (11): V. Schotte, C. Vandenbruaene, Dr G.T.O. Vanhooren, C. Vanmaele.

Brazil
Hospital Universitario Fraga Filho, Rio de Janeiro (23): Prof C. Andre, Dr M.A.S.D. Lima, Dr M.O. Py.

Canada
Saint John Regional Hospital, New Brunswick (11): S. Alward, Dr P. Bailey, P. Cook; Halfax Infirmary, Halifax, Nova Scotia (3): Dr S.J. Phillips, Y. Reidy.

Czech Republic
District Hospital, Pardubice (31): Drs E. Ehler, P. Geier, P. Vyhnalek; City Hospital, Ostrava (2): Drs C. Majvald, D. Skoloudik.

Denmark
H:S Hvidovre Hospital, Hvidovre (20): L. Bech, Dr D. Rizzi, Dr T. Soerensen; Bispebjerg Hospital, Kobenhavn, NV (1): Dr D. Rasmussen.

Hong Kong
Ruttonjee Hospital, Wanchai (21): Drs K.Y. Chan, E.S.L. Chow, C.K.L. Kng, C.P. Wong.

India
St John’s Medical College Hospital, Bangalore (167): Dr U. Devraj, Dr Manjari, Dr J.L. Pinheiro, Prof A.K. Roy; All India Institute of Medical Sciences, New Delhi (5): Drs S. Panda, K. Prasad, M. Tripathi.

Italy
Ospedale Beato Giacomo, Villa Citta Della Pieve, Perugia (50): L. Ambrosius, Dr G. Benemio, Dr M.G. Celani, B. Randolph, Dr S. Ricci, Ospedale Civile S Matteo Degli Infermi, Spoleto, Perugia (41): Dr E. Righetti, C. Ottaviani; Ospedale di Pistoia, Pistioa (25): Drs D. Sita, P. Vanni, G. Volpi; Ospedale "Sestilli," INRCA Ancona (22): Dr M. Del Gobbo, O. Scarpino; Morgagni, Pierantoni Hospital, Forli (21): Drs G. Benati, V. Pedone; Ospedale Niguarda, Milano (16): Drs A. Ciccone, I. Santilli, R. Sterzi; Ospedale Gubbio, Gubbio (15): Drs O. Cazzato, P. Parise; Hospital Civile S. Vito, Al Tagliamento (14): Dr A.G. Gregoris, M.L. Lorenzet, Dr M.T. Tonizzo; Ospedale Maggiore, Trieste (13): Drs L. Antonutti, F. Chiodo Grandi, N. Koscica, G. Nider; Castiglione del Lago Hospital, Perugia (11): Dr S. Cipolloni, N. Deboli, Dr C. Dembech, Dr M. Guerrieri, Dr S. Ricci, Dr E. Vignai; Ospedale Giovanni Ceccarini, Riccione (11): Drs M. Cornia, M.A. Passauiti; Universita di Sassari, Sassari (11): L. Bianco, P. Canu, E. Mereu, Dr A. Pirisi, Dr B. Zanda, Dr M. Zuddas; Ospedale Civile, Sassari (8): Dr G Casu; Ospedale di Todi, Todi, Perugia (6): Drs B. Biscottini, A. Boccali, P. Del Sindaco, T. Mazzoli; Ospedale Civile, Citta di Castello (6): Drs C.S. Cenciarelli, G.L. Girelli, G.M. Giuglietti; Ospedale "S. Maria delle Croci," Ravenna (4): Drs G. Bianchedi, G. Ciucci; Perugia University Hospital, Perugia (3): Drs G.A. Aisa, M.F. Fiueddio, P.M.C. Polidora, U. Senin; IRCCS C Mondino, Pavia (1): Drs A. Cavallini, S. Marcheselli, G. Micieli; Ospedale S Michele, Cagliari (1): Dr M. Melis; Ospedale Don Calabria, Verona (1): Drs B. Rimondi, P. Spagnolli; Hospital Abbadia San Salvatore, Abbadia San Salvatore (1): Dr G. Campanella, Dr R. Castro, M. Fiorella, Dr A.R. Gobbini, Dr G. Parisi, Dr G. Vedouini.

New Zealand
University of Auckland, Auckland (202): Dr N.E. Anderson, P. Bennett, Dr A.J. Charleston, Dr D.A. Spriggs; Hawkes Bay Hospital, Hastings (77): Dr T. Frendin, Dr J. Gommans, L. Wall; Tauranga Hospital, Tauranga (46): P. Blattmann, Dr A.M. Chancellor.

Poland
Teaching Hospital, Lublin (4): Prof Z. Stelmasiak; Hospital of a Province, Siedlce (3): Drs M. Lyczywek-Zwierz, A. Wlodek.

Portugal
Hospital Geral de Santo Antonio, Porto (17): Drs A. Bastosleite, M. Correia, C. Ferreira, M.G. Lopes; Centro Hospitalar Coimbra, Coimbra (14): Dr J.A. Grilo Goncalves; Hospital S. Joao, Porto (11): Drs P.M. Abren, M. Carvalho, R. Martins; Hospital de Santa Maria, Lisbon (7): Drs P. Canhao, Falcao, T. Pinho e Melo, A. Verdelho; Hospital Conde de Sao Bento, Santo Tirso (5): Dr C. Ferreira; Hospital Distrital de Oliveira de Azemeis, Oliveira de Azemeis (4): Drs E. Marques, F. Pais, M. Veloso.

Republic of Ireland
St Vincent’s Hospital, Dublin (2): Dr M. Crowe.

Singapore
Singapore General Hospital (46): C.F. Chan, Dr H.-M. Chang, Dr C.P.L.-H. Chen, H.P.A. Goh, Dr W. Luman, Dr M.C. Wong.

Turkey
Istanbul Medical School, Istanbul (53): Drs S. Bahar, O. Coban, M. Degirmencioglu, M.E. Gurol, Y. Krespi, B. Tugcu; Bakirkoy Inme Tedavi ve Arastirma Merkezi, Istanbul (32): Drs G. Bakac, D. Kirbas, D. Yandim Kuscu; Bakirkoy Ruh ve Sinir Hastaliklari, Istanbul (1): Drs H. Acar, S. Baybas, S. Kabey, E. Seakin, B. Yalginer.

United Kingdom
Western General Hospitals NHS Trust, Edinburgh (210): Prof M.S. Dennis, Dr R. Lindley, D. Shaw, P. Taylor; University Hospital Aintree, Liverpool (125): S. Evans, Dr A.K. Sharma; Ulster Hospital, Belfast (111): Drs J. Finnerty, M.J.P. Power; Scarborough Hospital, Scarborough (110): P. Davies, Dr J. Paterson; Christchurch Hospital NHS Trust, Christchurch (100): A. Graham, Dr A. Hanrahan, Dr D. Jenkinson, Dr J. Kwan, Dr S. Ragab; Brighton General Hospital, Brighton (99): Drs M.J. Bradshaw, M. Eddleston, S. Jamil; St Thomas’s Hospital, London (84): Dr A.G. Rudd, C. O’Conner; Poole Hospital, Poole (69): Drs M.T.A. Villar, A. Winson; Northwick Park Hospital, Harrow (68): K. Butchard, Dr D.L. Cohen; Falkirk & District Royal Infirmary, Falkirk (64): Dr S. Grant, N. Henderson, J. McCall; Barnsley District General Hospital, Barnsley (56): Drs M.K. Al-Bazzaz, A.I. Khan; Bishop Auckland General Hospital, Bishop Auckland (47): Drs K.V. Baliga, A.A. Mehrzad; Burnley General Hospital, Burnley (43): S. Davies, Dr M.N. Goorah, A. Joshi; Wishaw District General Hospital, Wishaw (40): Drs E. Forrest, A. Hendry; Leeds General Infirmary, Leeds (40): Dr P. Wanklyn; William Harvey Hospital, Willesborough, Ashford (38): Dr D.G. Smithard; Victoria Infirmary NHS Trust, Glasgow (37): Drs J. Potter, M. Roberts, A. Watt; Luton & Dunstable NHS Trust, Luton (34): E. Hutchins, Dr K. Mylvaganam; Northampton General Hospital, Northampton (33): Dr L. Brawn, J. Collier, Dr A. Gordon; Royal Victoria Hospital, Belfast (31): A. Hunter, Dr M. Watt, Dr I. Wiggam; North Bristol NHS Trust (Southmead), Bristol (31): Dr T. Allain, Dr P. Easton, A. Russ; St James’s University Hospital, Leeds (29): Dr J.M. Bamford, J. Hayes, E. Jackson, Dr T. Moorby; Salford Royal Hospitals Trust, Salford (24): A. Betteley, Dr P. Tyrrell; Royal Liverpool & Broadgreen University Hospital, Liverpool (24): H. Dickinson, H. Gardner, Dr C.I.A. Jack, K. Johnson; Peterborough District Hospital, Peterborough (23): C. Gerstner, Dr S. Guptha, Dr P. Owusu-Agyei; Stirling Royal Infirmary, Stirling (22): F.J. Dick, Dr D. Kennie; Stobhill NHS Trust, Glasgow (21): Dr C. McAlpine, J. Rodger; Hereford General Hospital, Hereford (17) Dr P.W. Overstall, M. Probert, Dr E. Wales; Princess Royal Hospital, Haywards Heath (15): M. Dormer, Dr M. Jones, R. Polley; Princess Margaret Hospital, Swindon (14): Drs B. Dewan, S. Kavsar, H. Newton, A. Paddon; King’s College Hospital, London (14): Dr I. Perez; Birmingham Heartlands Hospital, Birmingham (13): S. Bradley, Dr R. Shinton; Chesterfield & Nth Derbyshire Royal Hospital, Chesterfield (13): Drs M. Cooper, P. Metcalf; Perth Royal Infirmary, Perth (12): Drs B. Keegan, S. Johnston; Glasgow Royal Infirmary, Glasgow (10): Dr P. Langhorne, M. Shields; Queen Margaret Hospital NHS Trust, Dunferlime (10): Drs N. Chapman, S. Pound; Royal Devon & Exeter Hospital, Exeter (10): C. Fox, Dr M.A. James; St Thomas’s Hospital, Stockport (10): Drs Y. Adennala, M.L. Datta Chaudhuri; Glan Clwyd Hospital, Bodelwyddan (10): Dr B.K. Bhowmick, I. Evans; Kingston Hospital, Kingston On Thames (9): Drs C. Lee, C. Rodrigues; Lagan Valley Hospital, Lisburn, Belfast (9): Dr S.P. Gawley, K. Page; Bronllys Hospital, Brecon (8): Dr J. Buchan, Dr A. Dunn, Sister J. Hallam, Dr S. Manthri; Epsom General Hospital, Epsom (7): A.M. Daniels, Dr G. Lim; North Middlesex Hospital, London (7): Dr R.I. Luder; North Tyneside Health Care, North Shields (6): Dr R. Curless; Bronglais General Hospital, Ceredigion (6): L. Hudson, Dr P. Jones; Eastern General Hospital, Edinburgh (5): Dr L. Morrison; Aberdeen Royal Infirmary, Aberdeen (5): Drs R.S. Dijkhuizen, M.J. Maclean; Gloucestershire Royal Hospital NHS Trust, Gloucester (5): L.L. Bech, Dr D. Rizzi, Dr T. Sorensen; Royal Infirmary of Edinburgh, Edinburgh (4): M. Brogan, Dr G. Mead; Sandwell General Hospital NHS Trust, West Bromwich (3): Dr EM Smith; Dryburn Hospital, Durham (2): J. Clark, Dr P.M. Earnshaw, Dr M. Jain; Nottingham City Hospital, Nottingham (1): Dr D. Cohen;West Cumberland Hospital, Cumbria (1): Drs E.O. Orugun, N. Russell; Withington Hospital, Manchester (1): Prof P.A. O’Neill, S.J. Welsh; Singleton Hospital, Swansea (1): Dr W. Harris; Hairmyres Hospital, East Kilbride (1): Drs S. Marletta, J. Santamaria; Colchester General Hospital, Colchester (1): M.J. Keating, Dr T. Shawis.

	Acknowledgments

 
The FOOD Trial was supported by grants from the Health Technology Assessment Board of NHS Research and Development in UK; Stroke Association; Chief Scientist Office of the Scottish Executive; and Chest, Heart and Stroke Scotland.

	Footnotes

 
The Appendix, which can be found online at http://stroke.ahajournals.org, lists all individuals’ contributions.

The views expressed in this article are those of the authors and do not necessarily represent those of the funding bodies.

Received September 30, 2002; revision received November 26, 2002; accepted January 21, 2003.

	References

Top Abstract Introduction Methods Results Discussion Appendix References

 

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