Does the National Institutes of Health Stroke Scale Favor
Left Hemisphere Strokes?
Daniel Woo, MD; Joseph P. Broderick, MD; Rashmi U. Kothari, MD; Mei Lu, PhD;
Thomas Brott, MD; Patrick D. Lyden, MD; John R. Marler, MD; James C. Grotta, MD;
for the NINDS t-PA Stroke Study Group
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Background and Purpose—The National Institutes of Health Stroke Scale (NIHSS) is a valid, reproducible scale that
measures neurological deficit. Of 42 possible points, 7 points are directly related to measurement of language compared
with only 2 points related to neglect.
Methods—We examined the placebo arm of the NINDS t-PA stroke trial to test the hypothesis that the total volume of
cerebral infarction in patients with right hemisphere strokes would be greater than the volume of cerebral infarction in
patients with left hemisphere strokes who have similar NIHSS scores. The volume of stroke was determined by
computerized image analysis of CT films and CT images stored on computer tape and optical disks. Cube-root
transformation of lesion volume was performed for each CT. Transformed lesion volume was analyzed in a logistic
regression model to predict volume of stroke by NIHSS score for each hemisphere. Spearman rank correlation was used
to determine the relation between the NIHSS score and lesion volume.
Results—The volume for right hemisphere stroke was statistically greater than the volume for left hemisphere strokes,
adjusting for the baseline NIHSS (P,0.001). For each 5-point category of the NIHSS score ,20, the median volume
of right hemisphere strokes was approximately double the median volume of left hemisphere strokes. For example, for
patients with a left hemisphere stroke and a 24-hour NIHSS score of 16 to 20, the median volume of cerebral infarction
was 48 mL (interquartile range 14 to 111 mL) as compared with 133 mL (interquartile range 81 to 208 mL) for patients
with a right hemisphere stroke (P,0.001). The median volume of a right hemisphere stroke was roughly equal to the
median volume of a left hemisphere stroke in the next highest 5-point category of the NIHSS. The Spearman rank
correlation between the 24-hour NIHSS score and 3-month lesion volume was 0.72 for patients with left hemisphere
stroke and 0.71 for patients with right hemisphere stroke.
Conclusions—For a given NIHSS score, the median volume of right hemisphere strokes is consistently larger than the
median volume of left hemisphere strokes. The clinical implications of our finding need further exploration. (Stroke.
1999;30:2355-2359.)
Key Words: dominance, cerebral n cerebral infarction n tomography, x-ray computed n infarction volume
T
60% of left-handed persons,7,8 the NIHSS may measure the
severity and size of strokes in the right hemisphere differently
than strokes in the left hemisphere. In a recently published
report, Krieger et al9 reported that the minimum baseline
NIHSS score for fatal brain swelling in left hemisphere
strokes was 20 compared with a minimum baseline NIHSS
score of 15 for right hemisphere strokes.
We examined the placebo arm of the NINDS t-PA Stroke
Trial to test the hypothesis that the median size of cerebral
infarction in patients with right hemisphere strokes would be
greater than the median size of infarction in patients with left
hemisphere strokes who have similar NIHSS scores.
he National Institutes of Health Stroke Scale (NIHSS) is a
valid, reproducible scale that measures neurological deficit1–3 and is one of the most frequently used scales in stroke
intervention trials.4 – 6 In addition, the NIHSS is increasingly
used clinically by physicians and nurses to evaluate stroke
patients in emergency departments and hospital settings.
Of the 42 possible points on the NIHSS score, 7 points are
directly related to measurement of language (orientation
questions, 2; commands, 2; aphasia, 3) and only 2 points are
related to neglect.1 Because the left hemisphere is the
language-dominant hemisphere in 99% of right-handed persons (which represents 90% to 95% of the population) and
Received August 18, 1999; final revision received August 18, 1999; accepted August 18, 1999.
From the Departments of Neurology (D.W., J.P.B.) and Emergency Medicine (R.U.K.), University of Cincinnati, Cincinnati, Ohio; Biostatistics and
Research Epidemiology, Henry Ford Health System, Detroit Mich (M.L.); the Department of Neurology, Mayo Clinic, Jacksonville, Fla (T.B.); the
Department of Neurology, University of California–San Diego, San Diego, Calif (P.D.L.); the Division of Stroke and Trauma, NINDS, Bethesda, Md
(J.R.M.); and the Department of Neurology, University of Texas Medical School, Houston, Tex (J.C.G.).
Correspondence to Daniel Woo, MD, University of Cincinnati College of Medicine, Department of Neurology, 231 Bethesda Ave, ML 0525,
Cincinnati, OH 45220. E-mail [email protected].
© 1999 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
2355
2356
Stroke
November 1999
Subjects and Methods
For the 624 patients in the NINDS rt-PA Stroke Trial, 312 were
treated with tissue plasminogen activator (TPA) and 312 were treated
with placebo. In this report, we used only placebo-treated patients
because it was expected that TPA would have a confounding effect
on lesion volume. Methods for calculation of CT lesion volumes are
provided in Appendix I.
Statistical Methods
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We excluded all patients with brain stem strokes. Tests of association
between lesion volume, stroke hemisphere, baseline, and 24-hour
NIHSS score were performed on the basis of a cube-root transformation of the lesion volume.10,11 This approach transforms a
3-dimensional volume into a 1-dimensional measure that stabilizes
the variance. After the transformation, the variance was close to the
mean and a logistic regression analysis was performed to compute
the test statistics with generalized estimating equations.12 A value of
P,0.05 indicated significant associations between the lesion volume
and stroke location or NIHSS score.
Because the lesion volume was significantly different between left
and right hemisphere strokes after controlling for the NIHSS score at
baseline, exploratory analyses were performed. Patients were stratified according to 5-point categories on the NIHSS (0 to 5, 6 to 10,
11 to 15, 16 to 20, 21 to 25, and .25) and then by hemisphere of
stroke. The rationale for the use of these categories has been reported
previously.3 To summarize, 45 variables constructed from 35 baseline measures were selected to test for linearity in the log odds. On
the basis of this analysis, the NIHSS score was divided into 5-point
categories.
The transformed lesion volumes for these smaller subgroups were
then compared with the use of a logistic regression model by NIHSS
score and location of stroke by hemisphere. In addition, Spearman
correlation coefficients were calculated and tested for a zero correlation between NIHSS score and location of stroke by hemisphere. A
Wilcoxon rank sum test was used to compare the scores for
individual items of the NIHSS for right and left hemisphere strokes.
Because the range of scores for each item was small, we used the
mean score to describe the data.
Results
For the 290 patients with hemispheric stroke enrolled in the
placebo arm of the NINDS rt-PA Stroke Trial, 216 (75%)
patients had a CT scan performed at 3 months or later than 3
months. CT scans were performed after 18 hours but ,3
months in 71 (24%) patients, which was then used as the
extrapolated 3-month lesion volume. A total of 287 (99%)
patients had a CT scan performed at .18 hours. There was a
total of 151 patients with left hemisphere strokes and 139
patients with right hemisphere strokes. The baseline NIHSS
was associated with stroke location (right or left hemisphere,
P50.01) and 3-month lesion volume (P#0.001). After adjusting for baseline NIHSS score, the lesion volumes for
patients with right hemisphere stroke were greater than the
lesion volumes for patients with left hemisphere stroke
(Figure, P#0.001).
The median volume of stroke in placebo-treated patients by
5-point strata of baseline and 24-hour NIHSS scores is
presented in Table 1. The median volume of right hemisphere
stroke was greater than the median volume of left hemisphere
stroke for all NIHSS categories at baseline and at 24 hours.
For each 5-point category of the NIHSS score ,20, the
median volume of right hemisphere strokes was more than
double the median volume of left hemisphere strokes. The
difference in volume for these small subgroups reached
statistical significance for baseline NIHSS scores of 16 to 20
Cube-root lesion volume for right and left hemisphere strokes
compared with baseline NIHSS score. Shaded areas represent
95% confidence intervals.
and $26 and for 24-hour NIHSS scores of 11 to 15 and 16 to
20. There was a trend toward a larger volume in right
hemisphere strokes for 24-hour NIHSS scores of 0 to 5
(P50.06) and 6 to 10 (P50.06). The difference in significance values reflects the smaller power of the subgroup
analysis compared with that in the Figure, which used data
from the entire placebo arm of the NINDS rt-PA Stroke Trial.
The median volume of right hemisphere strokes was
approximately equal to the median volume of left hemisphere
strokes in the next highest 5-point category (Table 1). For
example, the median volume of infarction for a 24-hour
NIHSS score of 16 to 20 in patients with a right hemisphere
stroke was 133 mL (interquartile range 81 to 209 mL) as
compared with a median volume of infarction of 102 mL
(interquartile range 28 to 158 mL) for patients with a left
hemisphere stroke with a 24-hour NIHSS score of 21 to 25.
At the baseline NIHSS examinations, 36% of left hemisphere strokes had an NIHSS score .20 compared with 13%
of right hemisphere strokes (P#0.001). At 24 hours, 28% of
left hemisphere strokes had an NIHSS score .20 compared
with only 13% of right hemisphere strokes (P,0.01).
The Spearman correlation coefficient (r) of the NIHSS
scores with 3-month lesion volume by stroke hemisphere is
shown in Table 2. The correlation between the NIHSS score
at 24 hours and CT lesion volume was very good regardless
of location (right hemisphere r50.72, P#0.0001; left hemisphere r50.71, P#0.0001; and all strokes including brain
stem r50.68).
The mean score of each NIHSS item for patients with left
and right hemisphere strokes is shown in Table 3. The only
items that did not show hemispheric preference were level of
consciousness (item 1a), visual fields (item 3), and limb
ataxia (item 7). Level of consciousness questions (item 1b)
and commands (item 1c), right arm motor (item 5b), right leg
motor (item 6b), and dysarthria (item 9) were significantly
greater in patients with left hemisphere stroke than patients
with right hemisphere stroke. Best gaze (item 2), facial palsy
(item 4), left arm motor (item 5a), left leg motor (item 6a),
and sensory change (item 8) were found to be statistically
Woo et al
TABLE 1. Median 3-Month Lesion Volume by Location and
NIHSS Strata
Location
n
Lesion Volume
(Interquartile Range)
L hemisphere
9
1.5 (0.5–9.4)
R hemisphere
6
3.5 (0.0–27)
6–10
L hemisphere
33
3.0 (0.5–18)
R hemisphere
43
7.5 (2.1–32)
11–15
L hemisphere
27
11 (1.7–28)
R hemisphere
34
33 (10–76)
L hemisphere
27
24 (5.6–70)
R hemisphere
36
80 (24–124)
L hemisphere
35
102 (29–151)
R hemisphere
15
137 (121–189)
L hemisphere
20
75 (15–225)
R hemisphere
2
205 (170–240)
0–5
L hemisphere
27
1.4 (0.0–9.4)
R hemisphere
36
4.7 (1.0–13)
6–10
L hemisphere
26
6.4 (1.7–19)
R hemisphere
28
20 (5.7–37)
L hemisphere
29
11 (1.5–37)
R hemisphere
33
50 (15–93)
L hemisphere
26
48 (13–111)
R hemisphere
22
133 (81–209)
L hemisphere
27
102 (28–158)
R hemisphere
11
121 (80–170)
L hemisphere
12
180 (68–277)
R hemisphere
4
215 (95–270)
TABLE 3.
P
0.99
16–20
21–25
.26
0.18
0.15
0.005
0.18
0.01
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NIHSS at 24 h
11–15
16–20
21–25
.26
0.06
0.06
0.04
0.001
0.24
0.16
*Values were calculated on the basis of the transformed lesion scale to
compare lesion volume for patients with right and left hemisphere strokes.
significantly greater in right hemisphere strokes compared
with left hemisphere strokes. Because of the large number of
items compared, the probability value should be considered
descriptive.
Discussion
Our study demonstrates that for a given NIHSS score, the
total lesion volume for patients with right (usually nondominant for language) hemisphere strokes is statistically larger
than the lesion volume for patients with left (usually domiTABLE 2. Correlation of Lesion Volume With Baseline and
24-Hour NIHSS Scores
n
Baseline
NIHSSS*
24-h
NIHSSS*
P†
L hemisphere
151
0.56
0.72
#0.0001
R hemisphere
139
0.61
0.71
#0.0001
All patients
287
0.54
0.68
#0.0001
*Spearman correlation coefficient.
†Value testing for zero correlation between NIHSSS and 3-month lesion
volume.
2357
Mean Item Score for Right vs Left Hemisphere
NIHSS Item
NIHSS at baseline
0 –5
Does NIHSS Favor Left Hemisphere Strokes?
n
Left
n
Right
P
1a. Level of consciousness (LOC)
151
0.37
136
0.27
0.38
1b. LOC questions
151
1.51
136
0.34
#0.0001
1c. LOC commands
151
0.82
136
0.11
#0.0001
2. Best gaze
151
0.60
136
0.83
#0.0001
3. Visual fields
151
1.07
136
1.18
0.35
4. Facial palsy
151
1.51
136
1.71
#0.0001
5a. L arm weakness
151
0.15
135
2.72
#0.0001
5b. R arm weakness
151
2.61
136
0.12
#0.0001
6a. L leg weakness
151
0.42
135
2.33
#0.0001
6b. R leg weakness
151
2.34
136
0.29
#0.0001
7. Limb ataxia
151
0.09
136
0.12
0.49
8. Sensory
151
0.93
136
1.14
0.02
9. Language
151
2.05
136
0.23
#0.0001
10. Dysarthria
149
1.46
136
0.98
#0.0001
11. Extinction/neglect
151
0.79
136
1.28
#0.0001
*Probability value scores were compared by use of the Wilcoxon rank sum
test.
nant for language) hemisphere strokes. This difference reflects the weighting of the NIHSS with regard to language
function, which is localized to the dominant and usually the
left hemisphere as compared with hemineglect, which is more
prominently related with nondominant hemisphere strokes.
Measurement of language accounts for 7 of 42 possible points
in the NIHSS as compared with only 2 points associated with
neglect.
Our findings may have implications for clinical trials as
well as clinical practice. The baseline NIHSS score has been
associated with the volume of infarct at 3 months, the clinical
severity of stroke at 3 months, the risk of intracerebral
hemorrhage in the setting of thrombolytic therapy,13,14 and
the likelihood of arterial clot on conventional cerebral angiogram (written communication from Thomas J. Tomsick,
University of Cincinnati, 1999). The NIHSS is frequently
used as an exclusion criteria for acute stroke trials,4 – 6 both for
patients with very mild strokes and low NIHSS scores and
patients with very severe strokes and high NIHSS scores.6
Persons with nondominant or right hemisphere strokes with a
mild deficit as measured by the NIHSS may be less likely to
be enrolled in clinical trials or be treated with TPA in clinical
practice than patients with mild dominant left hemisphere
strokes. In the placebo group of the NINDS t-PA Stroke Trial,
151 patients had a left hemisphere stroke and 139 patients had
a right hemisphere stroke. Similarly, among TPA-treated
patients in the NINDS t-PA Stroke Trial, 160 patients had a
left hemisphere stroke and 135 patients had a right hemisphere stroke.
When the NIHSS was initially developed and reported, it
was found to have a high interrater reliability (k50.69) and
correlated with both lesion volume and outcome.1 Brott et al1
reported that the Spearman correlation of the NIHSS score at
1 week to lesion volume at 1 week was 0.74 (1.0 representing
perfect correlation and zero representing no correlation) and
that this was true for both left hemisphere (0.72) and right
2358
Stroke
November 1999
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hemisphere (0.74) strokes. It was also found that the correlation between baseline NIHSS score and 7- to 10-day CT
lesion volume had a strong correlation (r50.74, P#0.0001)
that occurred regardless of which cerebral hemisphere was
involved (r50.72 for left hemisphere, r50.74 for right
hemisphere).2 Our results are consistent with the original
analysis of Brott et al.
The high degree of correlation between the NIHSS score
and lesion volume for both hemispheres may seem counterintuitive to the idea that the NIHSS is “more sensitive” to the
size of left hemisphere strokes. Yet, a high correlation simply
refers to the amount of change in the score compared with a
change in lesion volume. In the Figure, the total lesion
volume correlated well with the baseline NIHSS score for
both right and left hemisphere strokes. It is clear that the slope
of the regression line is the same for both right and left
hemisphere lesions but that the intercepts are different. Thus
the NIHSS accurately reflects underlying lesion volume over
a range of volumes, with an offset between the 2 hemispheres
reflecting the overrepresentation of the left hemisphere in the
NIHSS items.
A limitation of this study is that it represents the findings
of a single database within a highly selected patient population. Our findings need to be verified in other data sets11 in
which the volume of cerebral infarction is carefully measured. Patients in the NINDS t-PA Stroke Trial were examined serially by investigators certified to use the NIHSS and
who underwent rigorous retraining every 6 months.3 Therefore it is likely that our results would be replicated in a future
study.
The NIHSS reliably and accurately predicts the volume of
infarction but does so differently, depending on stroke location. A multivariate model of outcome that includes location
of stroke as well as other relevant items such as the NIHSS
score may be required to more accurately predict clinical
outcomes. Such a model may provide clinicians and investigators with better estimates of hemorrhage risk, long-term
outcome, and the likelihood of intra-arterial clot in patients
with stroke. The clinical implications of these findings need
further investigation.
Appendix I
Calculation of CT Lesion Volume
CT images were obtained and processed at baseline, 24 hours, 7 to
10 days, and 3 months after stroke onset. All of the CT scans were
performed on third- or fourth-generation CT scanners. Technical
factors included 120 kV, 170 mA, matrix size of 5123512, and
scanning time of 3 seconds per slice for posterior cranial fossa and
2 seconds per slice for the supratentorial compartment. All slices
were contiguous without interruption with a display field of view of
20 cm. All the CT scans were to be performed from the level of the
foramen magnum to high vertex region.
All of the CT scan images were sent to the Coordinating Center for
central review. CT scan data were archived on either magnetic tape
or optical disk for a lesion volume calculation in 75% of Part 1
patients and optical disk archiving in multiple formats thereafter. For
CT scans that did not have available magnetic tape or optical disk,
the lesion volume was calculated on the basis of the CT film.
Two different methods were used for evaluating the size of the
lesion volume. To measure CT lesion volume, a CT technologist
trained by the Central Coordinating Neuroradiologist manually
traced the lesion on the digitized image on a computer screen for
each slice of the CT scan. The volume of the lesion size was
calculated from the number of slices in which the lesion was visible
on the CT scan. The Central Coordinating Neuroradiologist then
analyzed the entire CT scan and inspected the lesion outlined by the
CT technologist and manually made appropriate corrections. The
final corrected lesion volume outlined by the Central Coordinating
Neuroradiologist was entered into the CT scan database.
The second method of lesion volume calculation was CT scan
review by the physicist trained by the Central Coordinating Neuroradiologist. Proprietary software developed at Henry Ford Hospital15
was used to automatically segment normal and abnormal tissue.
Preset threshold CT units were used to segment lesion volume.
Segmented lesion volumes were calculated by computer. Segmentation was done from the histogram of the CT image. In addition, a
nonlinear edge-preserving filter was used to suppress noise.16,17
After automated segmentation, manual correction to the lesion
segmentation was performed by the physicist. Finally, the Central
Coordinating Neuroradiologist reviewed the entire CT scan, and
appropriate corrections were carried out manually on each slice of
the CT scan before final data entry. The hard copies of films that did
not have a copy on magnetic tape or optical disk were sent to the
University of Virginia for lesion measurements. The hard copies
were digitized with the use of a Lumisys model 150 digital scanner
set at 100-mm spot size or a Vidar scanner at 8 bits per pixel and 150
dots per inch. These images were transferred to a Hewlett-Packard
Apollo 9000 series computer for linear and volume measurements.
Lesion volume was calculated with segmentation performed on each
slice. The operator manually outlined the lesion on each slice
multiplied by the slice thickness. The lesion was identified on all the
slices, which were then added for the calculation of the final volume
of the lesion. Quality control checks were performed to ensure that
all images were properly scanned and available for lesion measurements. Slice thickness and the measurement scale were taken into
account for calculations of each lesion volume.
For our analyses, we included only those patients who had a
measured lesion volume on a CT performed after 18 hours of
symptom onset. The volume of any hemorrhagic component (symptomatic or asymptomatic) was included in the lesion volume. CT
lesion volume at 3 months or later was used when available. For
patients without a 3-month or later lesion volume, we used the lesion
volume of the latest CT scan performed after 18 hours of symptom
onset.
Appendix II
The following persons and institutions participated in the NINDS
rt-PA Stroke Trial: Clinical Centers: University of Cincinnati (150
patients), Principal Investigator: T. Brott; Co-investigators: J.
Broderick, R. Kothari; M. O’Donoghue, W. Barsan, T. Tomsick;
Study Coordinators: J. Spilker, R. Miller, L. Sauerbeck; Affiliated
Sites: St. Elizabeth (South), J. Farrell, J. Kelly, T. Perkins, R. Miller;
University Hospital, T. McDonald, Bethesda North Hospital, M.
Rorick, C. Hickey; St. Luke (East), J. Armitage, C. Perry, Providence, K. Thalinger, R. Rhude, The Christ Hospital, J. Armitage, J.
Schill, St. Luke (West), P.S. Becker, R.S. Heath, D. Adams; Good
Samaritan Hospital, R. Reed, M. Klei; St. Francis/St. George, A.
Hughes, R. Rhude, Bethesda Oak, J. Anthony, D. Baudendistel, St.
Elizabeth (North), C. Zadicoff, R. Miller; St. Luke-Kansas City, M.
Rymer, I. Bettinger, P. Laubinger; Jewish Hospital, M. Schmerler, G.
Meiros; University of California, San Diego (146), Principal Investigator: P. Lyden; Co-investigators: J. Dunford, J. Zivin; Study
Coordinators: K. Rapp, T. Babcock, P. Daum, D. Persona; Affiliated
Sites: UCSD, M. Brody, C. Jackson, S. Lewis, J. Liss, Z. Mahdavi,
J. Rothrock, T. Tom, R. Zweifler; Sharp Memorial, R. Kobayashi, J.
Kunin, J. Licht, R. Rowen, D. Stein; Mercy Hospital, J. Grisolia, F.
Martin; Scripps Memorial, E. Chaplin, N. Kaplitz, J. Nelson, A.
Neuren, D. Silver; Tri-City Medical Center, T. Chippendale, E.
Diamond, M. Lobatz, D. Murphy, D. Rosenberg, T. Ruel, M. Sadoff,
J. Schim, J. Schleimer; Mercy General, Sacramento, R. Atkinson, D.
Wentworth, R. Cummings, R. Frink, P. Heublein; University of
Texas Medical School, Houston (104). Principal Investigator: J.C.
Grotta, Co-investigators: T. DeGraba, M. Fisher, A. Ramirez, S.
Woo et al
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Hanson, L. Morgenstern, C. Sills, W. Pasteur, F. Yatsu, K. Andrews,
C. Villar-Cordova, P. Pepe; Study Coordinators: P. Bratina, L.
Greenberg, S. Rozek, K. Simmons; Affiliated Sites: Hermann
Hospital, St. Lukes Episcopal Hospital, Lyndon Baines Johnson
General Hospital, Memorial Northwest Hospital, Memorial Southwest Hospital, Heights Hospital, Park Plaza Hospital, Twelve Oaks
Hospital; Long Island Jewish Medical Center (72), Principal Investigators: T.G. Kwiatkowski (6/92-), S.H. Horowitz (12/90 –5/92);
Co-investigators: R. Libman, R. Kanner, R. Silverman, J. LaMantia,
C. Mealie, R. Duarte; Study Coordinators: R. Donnarumma, M.
Okola, V. Cullin, E. Mitchell; Henry Ford Hospital (62), Principal
Investigator: S.R. Levine; Co-investigators: C.A. Lewandowski, G.
Tokarski, N.M. Ramadan, P. Mitsias, M. Gorman, B. Zarowitz, J.
Kokkinos, J. Dayno, P. Verro, C. Gymnopoulos, R. Dafer, L.
D’Olhaberriague; Study Coordinators: K. Sawaya, S. Daley, M.
Mitchell; Emory University School of Medicine (39), Principal
Investigator: M. Frankel (7/92–10/95), B. Mackay (11/90 – 6/92);
Co-investigators: J. Weissman, J. Washington, B. Nguyen, A. Cook,
H. Karp, M. Williams, T. Williamson; Study Coordinators: C. Barch,
J. Braimah, B. Faherty, J. MacDonald, S. Sailor; Affiliated sites:
Grady Memorial Hospital, Crawford Long Hospital, Emory University Hospital, South Fulton Hospital: M. Kozinn, L. Hellwick;
University of Virginia Health Sciences Center (37), Principal Investigator: E.C. Haley, Jr; Co-investigators: T.P. Bleck, W.S. Cail, G.H.
Lindbeck, M.A. Granner, S.S. Wolf, M.W. Gwynn, R.W. Mettetal,
Jr, C.W.J. Chang, N.J. Solenski, D.G. Brock, G.F. Ford; Study
Coordinators: G.L. Kongable, K.N. Parks, S.S. Wilkinson, M.K.
Davis; Affiliated Sites: Winchester Medical Center, G.L. Sheppard,
D.W. Zontine, K.H. Gustin, N.M. Crowe, S.L. Massey; University of
Tennessee (14), Principal Investigator: M. Meyer (2/93-), K. Gaines
(11/90 –1/93); Study Coordinators: A. Payne, C. Bales, J. Malcolm,
R. Barlow, M. Wilson; Affiliated Sites: Baptist Memorial Hospital,
C. Cape; Methodist Hospital Central, T. Bertorini; Jackson Madison
County General Hospital, K. Misulis; University of Tennessee
Medical Center, W. Paulsen, D. Shepard; Coordinating Center:
Henry Ford Health Sciences Center, Principal Investigator: B.C.
Tilley; Co-investigators: K.M.A. Welch, S.C. Fagan, M. Lu, S. Patel,
E. Masha, J. Verter; Study Coordinators: J. Boura, J. Main, L.
Gordon; Programmers: N. Maddy, T. Chociemski; CT Reading
Centers: Part A, Henry Ford Health Sciences Center, J. Windham, H.
Soltanian Zadeh; Part B, University of Virginia Medical Center, W.
Alves, M.F. Keller, J.R. Wenzel; Central Laboratory: Henry Ford
Hospital; N. Raman, L. Cantwell; Drug Distribution Center: A.
Warren, K. Smith, E. Bailey; National Institute of Neurological
Disorders and Stroke, Project Officer: J.R. Marler. Data and Safety
Monitoring Committee: J.D. Easton, J. F. Hallenbeck, G. Lan, J. D.
Marsh, MD Walker; Genentech Participants: Juergen Froelich, MD,
Judy Breed, Fong Wang-Chow.
Acknowledgments
This study was supported by contracts from the National Institutes of
Neurological Disorders and Stroke (N-01-NS-02382, N01-NS-
Does NIHSS Favor Left Hemisphere Strokes?
2359
02374, N01-NS-02377, N01-NS-02381, N01-NS-02379, N01-NS02373, N01-NS-02378, N01-NS-02376, and N01-NS-02380).
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Does the National Institutes of Health Stroke Scale Favor Left Hemisphere Strokes?
Daniel Woo, Joseph P. Broderick, Rashmi U. Kothari, Mei Lu, Thomas Brott, Patrick D. Lyden,
John R. Marler and James C. Grotta
for the NINDS t-PA Stroke Study Group
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Stroke. 1999;30:2355-2359
doi: 10.1161/01.STR.30.11.2355
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