Angiographical Analysis of Acute Cerebral Infarction
Followed by "Cascade"-Like Deterioration of Minor
Neurological Deficits. What is Progressing Stroke?
TADAYOSHI IRINO, M.D.,

MANABU WATANABE, M.D.,

MOTOKI GOTOH, M.D.,

MASATO NISHIDE,

AND TAKASHI TSUCHIYA,

M.D.,

M.D.

SUMMARY In order to understand the mechanism of clinical worsening in patients with cerebral
infarction, attention was focused on the changes in cerebral angiograms obtained repeatedly before and
after neurological deterioration. Among 212 stroke patients with minor neurological deficits, incomplete
hemiparesis progressed to complete hemiplegia in 15 patients several days after the beginning of symptoms.
On admission, 3 had internal carotid artery occlusion, 2 had stenosis of the internal carotid artery, 5 had
occlusion of the middle cerebral arterial trunk, 2 had occlusion of the middle cerebral arterial branch, and
3 had no angiographical ly visible occlusion. The changes between the first and the second angiograms were
of different varieties: another recurrent occlusion, progression of occlusion, new occlusion in the cerebral
arteries opacified through the collateral pathway, recanalization of the initially occluded artery, and no
change. Such different patterns of pathophysiological events show that the mechanism of neurological
worsening in infarcted patients is not uniform. Based on the results from the present study, several problems
which arose during the investigation and the somewhat vague definition of "progressing stroke" currently
in use are discussed.
Stroke, Vol 14, No. 3, 1983

VARIOUS KINDS OF TEMPORAL PROFILE exist
for the symptomatological patterns of cerebrovascular
disease. Transient ischemic attack, completed stroke,
reversible ischemic neurological deficit, and progressing stroke are the clinical categories generally accepted. Especially in the acute stage of stroke, except for
transient ischemic attack, clinical worsening of the
neurological symptoms can be observed not infrequently by repeated careful observations. Clinical
worsening of neurological symptoms in infarcted patients is generally caused by several intra- and/or extracranial pathological conditions. Recurrent attack also
must be taken into consideration. The mode of deterioration is either, abrupt, stepwise or linear slopelike. In
some cases, therefore, the definition between progressing stroke and other types of stroke followed by
deterioration is not easy. The reasons, we consider, are
that the definition of progressing stroke is obscure
when compared with transient ischemic attack and that
the pathophysiological aspects of progressing stroke
have not been as fully investigated as other types of
stroke.
In the present study, in order to understand the
mechanism of clinical worsening in infarcted patients,
attention was focused on the changes in neuroradiological examinations before and after clinical worsening
in patients who had minor neurological deficits at the
beginning of ischemic cerebrovascular disease. Results showed that the mechanism of clinical worsening
was not uniform but complicated with various alterations of cerebral arterial occlusion. This paper also
discusses several actual problems in the clinical study
of progressing stroke and the need for clarification of
the terminology.

510 stroke patients admitted to the Division of Cerebrovascular Diseases of Hanwa Hospital between
April 1978 and October 1980. All were diagnosed
following physical and neuroradiological examinations including computed tomographies and/or cerebral angiographies. Among them, 212 patients diagnosed as having ischemic cerebrovascular disease had
neither consciousness disorder nor complete hemiplegia; and 182 of them had incomplete hemiparesis, of
whom 15 progressed to same-sided complete hemiplegia within several days after onset. The time intervals
between onset and clinical worsening are summarized
in figure 1.
The clinical and angiographical findings of these 15
patients are summarized in table 1 and 2. Thirteen
were diagnosed as having ischemic stroke in the territory of the internal carotid artery, while the affected
area of the remaining 2 was in the vertebrobasilar artery territory. Three had internal carotid artery occlusion, 2 had stenosis of the internal carotid artery, and 5
had occlusion or stenosis of the middle cerebral arterial
branch. Angiographically visible occlusion of the cerebral arteries was not observed in 1 patient affected in
the internal carotid artery territory, and in 2 patients
affected in the vertebrobasilar artery territory.
For the 15 cases, additional cerebral angiographies
and computed tomographies were performed after neurological worsening in order to check what had happened in the process of neurological deterioration.
Angiographical changes observed before and after
neurological deterioration were compared with each
other to understand the pathophysiological developments participating in their neurological deterioration.
The judgment of neurological deterioration in the
present study was based on the progression from inMaterial and Methods
complete hemiparesis to same-sided complete hemiPatients selected for the present study were among
plegia, with or without development of consciousness
disorder.
The initial neurological deficits lasted at least
From the Division of Cerebrovascular Diseases, Hanwa Hospital, 11for more than 6 hours without symptomatological
11-7, Karita, Sumiyoshi, Osaka 558, Japan.
Downloaded from http://stroke.ahajournals.org/ by guest on June 24, 2016
Received December 3, 1981; revision accepted January 18, 1983.
worsening. Eight patients with an unstable neurologi-

364

STROKE

Intervals between Onset and Neurological
Deterioration in 15 Cases of Ischemic Stroke
Cases No.

2\
3
4
o—x.
5
X
6 0
7

o

admission

x

neurolgical deterioration

1983

TABLE 2 Angiographical Findings on Admission in 15 Patients
Followed by Apparent Neurological Deterioration
ICA: 13 cases
ICA occlusion

1

stenosis
MCA stem occlusion

3
2
4

stem stenosis

1

MCA branch occlusion

2

non-visible occlusion

1*

VA: 2 cases
non-visible occlusion

o—x

8"

VOL 14, No 3, MAY-JUNE

Total

9
10* o —
0-

15 cases

*Non-visible is applied for those who had no angiographically
visible occluded artery.

-X

11

2*

- X

graphical recanalization of the initially occluded artery. Here are some typical patients who showed neurological deterioration (see fig. 1):

12
13 • o —

-x

14
15

Case 1 (Case 7 in fig. 1)
1

2

3

4

5

6

7

8

9 10 11 12 13 14 15 16
Days after Onset

* : VB-stroke
* * : recurrent TIAs followed by completed stroke

FIGURE 1. Intervals between onset and neurological deterioration in 15 cases of ischemic stroke.

cal condition, within a few hours after onset, were
excluded from the present study. Those who developed motor dysfunction in the side contralateral to the
initially affected side were also excluded, because this
was assumed to be caused by another stroke, although
it cannot be denied completely that a same-sided deterioration was caused by recurrent stroke.
Results
The changes in the repeated angiograms are summarized in table 3. The changes seen were of different
varieties; i.e., recanalization, other occlusions, progression of the occlusion from the distal to the proximal portion, new occlusions in the cerebral arteries
opacified through the collateral pathway, and no
change. Computed tomography showed an increased
low density area in three patients, while one case
showed apparent hemorrhagic infarction after angioTABLE 1 Clinical Findings in 15 Patients Followed by Neurological Deterioration

A 46-year-old right-handed female was admitted 12
hours after the beginning of left-side hemiparesis with
mild numbness. She could move her left arm and leg
against gravity. Consciousness disturbance was not
observed. The Babinski reflex was positive for the left
side. Blood pressure on admission was 142/86 mm Hg
and EKG revealed atrial fibrillation. Auscultation of
the heart showed diastolic murmur typical of mitral
regurgitation. The right carotid angiogram on admission showed occlusion of the right middle cerebral
artery at its trifurcation, and the result of computed
tomography was judged as normal.
The degree of hemiparesis gradually progressed to
more on the second day of hospitalization. On the
morning of the third day, the patient was alert and
complained of complete left-sided hemiplegia. She
could not move her left arm and leg even against slight
gravity. At that time, additional angiography showed
recanalization of the initially occluded point and computed tomography showed an apparent high density
area suggesting the occurrence of hemorrhagic infarction (fig. 2).
Case 2 (Case 6 in fig. 1)

A 54-year-old right-handed male was admitted
within 24 hours after onset following repeated epiTABLE 3 Alterations of Cerebral Angiographies Before and After
Neurological Deterioration

Age

67 y.o. (average; 52-84)

Sex (M/F)

8/7

I. recanalization

AF( + )

5

II. progression of occlusion

HBP

6

a. propagation

3

3

b. stenosis to occlusion

3
2*

DM

c. non-visible occlusion to stenosis

p-stroke
S 1 year
> 1 year

3
5

HI. occlusion on collateral
IV. no change

2 cases

4
1

Total

AF: atrial fibrillation, DM: diabetes mellitus, HBP: hypertension, p-stroke: previous stroke.
•Basilar artery occlusion.
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15 cases

WHAT IS PROGRESSING STROKE?//nno et al.

FIGURE 2. Right carotid angiogram and
computed tomography in case 1 showing circulatory restoration and hemorrhagic infarction
after recanalization of initially occluded middle cerebral artery at its trifurcation.

\
f~

\

365

I

sodes of left-sided hemiparesis and numbness accompanying contralateral ocular nerve palsy. The deficits
lasted for two days and right brachial retrograde angiography showed no visible angiographical occlusion in
the territory of right carotid and vertebrobasilar artery.
The degree of hemiparesis progressed a little on the
next day. Two days later he developed consciousness
disorder and complete left-sided hemiplegia. The Babinski was positive for the right as well as the left. At
that time, transfemoral vertebral angiography was
done and occlusion of the basilar artery was diagnosed.
Computed tomography, repeatedly done, showed no
diagnostic abnormalities.
Case 3 (Case 11 in fig. 1)
A 62-year-old right-handed male was admitted three
days after the development of unilateral numbness. On
August 23 1980, he suddenly developed right-sided
hemiparesis and numbness with motor aphasia, but
disturbance of consciousness was not observed. Nearly 10 hours after the beginning of right-sided hemiparesis, left-sided carotid angiography showed occlusion
of the internal carotid artery and right carotid angiography clearly showed partial visualization of the middle cerebral arterial tree through the anterior communicating artery (fig. 3 (a)). On the following day, nearly
48 hours later, his hemiparesis progressed to complete
hemiplegia without consciousness disturbance. Angiography at the time of clinical worsening demonstrated
no change of the occluded internal carotid artery, but
showed the occlusion opacified through the collateral
pathway at its trifurcation (fig. 3 (b)).
Case 4 (Case 13 in fig. 1)
A 67-year-old right-handed female was admitted
suffering from sudden onset of left-sided incomplete
hemiparesis. Computed tomography on admission
gave normal results and cerebral angiography showed
occlusion of the right internal carotid artery with pretty
good opacification of anterior and middle cerebral arterial trees through pial anastomosis (fig. 4 (a)). The
Babinski reflex was positive on the left. Until the end
of the fifth day, the hemiparesis showed gradual deterioration. On the sixth day of hospitalization, the hemiparesis progressed to complete hemiplegia, and less

apparent opacification of the middle cerebral arterial
trees was diagnosed with the second angiography (fig.
4 (b)). Computed tomography, repeatedly performed,
showed a low density area typical of middle cerebral
arterial occlusion.
Case 5 (Case 9 in fig. 1)
A 63-year-old right-handed male was admitted following sudden onset of right-sided hemiparesis with
motor aphasia. He could handle his right arm and leg
against gravity. The Babinski was positive for the right
side. On admission, nearly 7 hours after onset, computed tomography gave normal results, while left cerebral angiography demonstrated occlusion of the middle cerebral artery at its trifurcation. The patient was
diagnosed as not having rheumatic heart disease even
by two-dimensional echocardiography. EKG showed
no atrial fibrillation. Hemiparesis showed slight progression on the third day. On the fourth day of hospitalization, the hemiparesis progressed to complete
hemiplegia with decreased patellar tendon reflex with
a positive Babinski sign. At the time, cerebral angiography showed occlusion of the middle cerebral artery
at its trunk.
Discussion
Even patients showing angiographically minimal or
nonvisible cerebral arterial occlusion frequently develop clinical worsening of neurological signs in careful
neurological follow-up. In some cases with unilateral
acute internal carotid arterial occlusion, consciousness
disturbance apparently progresses from mild to severe
in the acute stage1 in which advancing brain edema
might be considered to be responsible for the neurological deterioration.2 In addition to pathophysiological events in the brain secondary to primary cerebrovascular occlusion, (i.e., ischemia, brain edema, and
hemorrhagic infarction) recurrent stroke or visceral
complications (such as pneumonia or renal insufficiency) are considered to be crucial factors.3-4 Visceral
complications are mostly observed in patients suffering from severe brain damage with neurogenic influence on the visceral organs, while recurrence and intracerebral pathophysiological events may play roles in
clinical worsening in those with all degrees of severity.

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366

STROKE

{

The results of our study also suggest that patients with
minor neurological deficits at the beginning of their
symptoms are affected by varieties of vascular events,
most of which can be considered to have a causative
relationship with initial cerebrovascular occlusion. Although the definite conclusion cannot be obtained,
cases 2 and 3 might be due to recurrence, while the
other cases (cases 1, 2 and 5) might be caused by
sequalae following initial occlusion. Thus the clinical

VOL 14, No 3, MAY-JUNE 1983

FIGURE 3. (a) (b) Repeated angiograms in
case 3. Progression of occlusion of the middle
cerebral artery opacified through anterior
communicating artery can be seen.

profile of progressing stroke also seems to be caused
by different pathophysiological aspects, which might
be one of the reasons that clinical stages such as transient ischemic attack, completed stroke, or progressing stroke have been simply classified based on their
clinical features without these complicated pathological features being taken into consideration.5 However,
detailed grouping of the clinical stages is sometimes
necessary in order to perform specific treatment
against clinical worsening, because pathophysiological events participating in the neurological deterioration are quite different as the present study has shown,
as far as the changes of occlusive findings of cerebral
arteries are concerned. The mechanism of the recurrent
attack must be separated from other mechanism of
clinical worsening.
The intracranial pathophysiological events in patients with ischemic cerebrovascular disease can be
classified into two categories; occlusive changes in
cerebral arteries and ischemic changes in the brain.
These two are probably interrelated. The pathophysiological aspects for cerebral arterial occlusion can be
conceptionally divided into two categories; progression of occlusion and recanalization of the occluded

FIGURE 4. (a) (b) Repeated angiograms in case 4. Lessening of retrograde opacification of middle cerebral
arterial trees through pial anastomosis can be noted.
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367

WHAT IS PROGRESSING STROKE?//rmo et al.

artery. Lhermitte et al.6 reported that progression of the
occlusion can be further divided into antegrade and
retrograde thrombi. However, antegrade thrombus is
difficult to detect even by careful reading of angiographies, because the contrast medium cannot reach into
the distal portion beyond the arterial occlusion. Retrograde thrombus can often be recognized by repeated
angiographies as a progression of the occlusion point
from the distal to the proximal portion. However, we
must remember that a newly developed embolus arising from any extracranial embolic source like the carotid artery or the heart would also show similar angiographical features. Therefore, the progression of
occlusion seen in the present study might be due to an
antegrade thrombus or a new embolus. Occlusion of
the middle cerebral artery opacified through the anterior communicating artery in the internal carotid artery
occlusion, as seen in case 3, might be caused by a
newly developed embolic process either from an extracranial embolis source through a non-occluded internal
carotid artery of the opposite side or from an occluded
internal carotid arterial stump. The embolic process
originating from the carotid stump has been well explained by Barnett et al.7 as for that through the reversed ophthalmic artery. Combined occlusion of middle cerebral artery supplied by collateral pathway in
patients having internal carotid artery was reported by
Ring.8 Another phenomenon, referred to as spontaneous recanalization, must also be taken into consideration when considering the pathophysiological
changes of the infarcted brain. Some previous authors 9- " have also paid attention to the angiographical
circulatory restoration and found that this phenomenon
mostly does not contribute to neurological improvement but to clinical worsening accompanying hemorrhagic infarction as seen in case 1. Summarizing the
pathophysiological aspects for cerebrovascular occlusion shows that the mechanism participating in the
development of clinical worsening is not uniform.
These facts can be considered to explain controversies
surrounding the therapeutic effects against various
types of ischemic cerebrovascular disease including
progressing stroke.

of 1975,5 and thus it is not clear if the profile of progressing stroke in their paper is suitable for comparison
with current concepts. For example, they counted visceral complication as a cause of clinical worsening,
especially in patients with late or terminal worsening
with consciousness disorders; but this kind of deterioration process is seldom seen in patients with worsening of minor neurological deficits, as seen in the
present study. Whisnant,13 commenting on a paper
dealing with progressing stroke by Adams et al., said
that whether "progressing occlusion" or "thrombosis
with progressing ischemia" participate in neurological
deterioration would be investigated.
The Ad Hoc Committee in 19755 has defined progressing stroke as follows: "This category represents
the common circumstance where focal ischemia is
worsening and the process of infarction is beginning or
extending." A case example was given to explain the
clinical profile of progressing stroke. However, especially compared with TIA, the definition of progressing stroke is vague. This might be explained by the
small number of papers concerning progressing stroke,
because the nature, the degree, or the time duration of
the neurological symptoms have not been defined in
enough detail for a common working base for different
investigators. In addition, several problems which
have not yet been discussed, arise during the actual
observations or judgment of progressing stroke: 1) Is
the definition of progressing stroke clear-cut compared
with TIA? 2) How to distinguish progressing stroke
from natural course? 3) How to distinguish it from
recurrence? 4) How to continue clinical observation
even with interruption by patients' sleep period? In our
present study using repeated cerebral angiographies,
the clinical profile showing neurological worsening
might be due to angiographical side effects, although
the incidence of side effects in our institute has been
low. Based on the answers to these practical problems
and the present results obtained by neuroradiological
analyses of stroke patients showing neurological deterioration (which might be expressed as "cascade
stroke") the concept of the so-called "progressing
stroke" should be clearly defined as soon as possible.

Although little has been reported about progressing
stroke, a recent description of the treatment of progressing stroke by Millikan and McDowell12 has contributed to the rearrangement of some ideas on stroke
of this kind of clinical profile. A description has been
given by Adams et al.1 They retrospectively studied
and observed pathological findings and comparatively
observed clinical courses, then suggested that progression of occlusion of the cerebral arteries might occur in
progressing stroke, although they stressed that it was
very difficult to analyze the pathogenesis of progressing stroke using retrospective pathological study. Of
the 4 cases described in their paper, 3 were patients
having ischemic stroke in the territory of the vertebrobasilar artery and 1 in the internal carotid arterial territory. However, they did not give the details for the
definition of progressing stroke. Also, their paper was
published before the Ad Hoc Committee's definition

1. Adams RD, Torvik A, Fisher CM: Progressing stroke. Pathogenesis, In Millikan CH, Siekert RG, Whisnant JP (eds), Cerebral
vascular disease, Third Princeton Conference, Grune & Stratton,
New York, 1961, pp 133-150
2. Bruce DA, Hurtig HI: Incidence, course and significance of cerebral edema associated with cerebral infarction. In Price TR, Nelson
E (eds), Cerebrovascular disease, Eleventh Princeton Conference,
Raven Press, New York, 1979, pp 191-198
3. Meyer JS: Course, prognosis and medical management of patients
with acute stroke. In Meyer JS, Shaw T (eds). "Diagnosis and
management of stroke and TIAs". Addison-Wesley Publishing
Company Inc., USA, 1982, pp 155-172
4. Carter AB: Prognosis of cerebral embolism. Lancet 2: 514-519,
1965
5. Millikan CH, Bauer RB, Goldschmidt J, et al.: A classification and
outline of cerebrovascular disease. II. Stroke 6: 564-616, 1975
6. Lhermitte F, Gautier JC: Sites of cerebral arterial occlusion. In
Williams D (ed), Modern Trends in Neurology, Butterworths,
London, 1965, pp 123-140

References

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368

STROKE

7. Barnett HJM, Peerless SJ, Kaufmann JCE: "Stump" of internal
carotid artery. A source of further cerebral embolic ischemia.
Stroke 9: 448-456, 1978
8. Ring BA: Occlusio supra occlusionem. Intracranial occlusions following carotid thrombosis as diagnosedby cerebral angiography.
Stroke 2: 487^193, 1971
9. Bladin PF: A radiologic and pathologic study of embolism of the
internal carotid-middle cerebral arterial axis. Radiology 82: 615—

V O L 14,

No

3,

MAY-JUNE

1983

624, 1964
10. Dalai PM, Shah PM, Aiyar RR: Arteriographic study of cerebral
embolism. Lancet 1: 358-361, 1965
11. Irino T, Taneda M, Minami T: Sanguineous cerebrospinal fluid in
recanalized cerebral infarction. Stroke 8: 24-27, 1977
12. Millikan CH, McDowell FH: Progress in cerebrovascular disease.
Treatment of Progressing stroke. Stroke 12: 397^109, 1981
13. Whisnant JP: Discussion in Ref. (3)

Platelet Aggregability in Cerebral Thrombosis — Analyzed for
Vessel Stenosis
Yuzo OTSUKI, M.D.,* TOMOKO KONDO, M.D.,* HIDEO SHIO, M.D.,*
MASAKUNI KAMEYAMA, M.D.,* AND TSUNEMARO KOYAMA,

M.D.f

SUMMARY Platelet aggregation in the post-acute phase of 48 patients with cerebral thrombosis was
measured to see if any specific type of cerebral infarction is associated with enhanced platelet aggregation.
All patients were examined with cerebral angiography and computed tomography (CT). Stenotic lesions in
major cranial arteries were analyzed by measuring the apparent diameter. Severe stenosis was defined as 75
per cent constriction or more. Enhanced aggregation of platelets (secondary aggregation at 1 juM ADP or
less) was present in 5 of 25 patients (20%) who had severe vessel stenosis or occlusion. CT examination
frequently revealed both cortical and deep involvement. On the other hand, 13 of 23 patients (57%) with less
stenotic lesions showed enhanced aggregation and that was statistically significant (p < 0.05). Many
patients of this group had persistent hypertension and small deep infarctions. Platelet aggregation was also
measured in 20 hypertensive control subjects without stroke. Four of them (20%) showed enhanced
aggregation. Thesefindingssuggest that a combination of enhanced platelet aggregation and hypertension
increases the risk of small deep infarctions accompanied by mild stenotic changes of the major cranial
arteries.
Stroke, Vol 14, No 3, 1983

cranial artery abnormalities, e.g. the internal carotid,
M, portions of middle cerebral, the vertebral, the basilar, and proximal portions of the posterior cerebral
arteries. The severe stenotic group which showed 75
per cent or more constriction in some of these major
cranial arteries consisted of 25 patients (19 males, 6
females, mean age 50 years). The remaining 23 patients (15 males, 8 females, mean age 58 years) were
included in the less stenotic group: their angiograms
showed moderate constriction (less than 75 per cent) or
no stenosis.
Angiographic examination were usually performed
by the direct puncture method and selection of appropriate vessels was based upon clinical symptoms, e.g.
Patients and Methods
a left carotid angiogram was performed for a right
hemiparesis. Complete four vessels study was underThe diagnosis of cerebral thrombosis was based
taken in only a few patients. Diabetes mellitus was
upon the clinical histories, neurological evaluations,
found in three patients, 2 in the severe stenotic and one
CSF findings, and supported by above specialized exin the less stenotic group. All hypertensive patients in
aminations . Patients with myocardial infarction and/or
the less stenotic group received antihypertensive mediatrial fibrillation were excluded because of the wellcation. Despite this, labile hypertension persisted in
known association of embolism. A total of 48 patients
half of the patients and the remaining half were highly
were divided into two groups, according to their angioresistant to therapy. The majority of the severe stenotic
graphic findings. Angiograms were analyzed for major
group were almost normotensive and required no therapy for hypertension after their stroke.
From the *Department of Neurology and Geriatric Medicine, Faculty
of Medicine, Kyoto University, 54 Shogoin-Kawaracho, Sakyoku,
Platelet aggregation was examined by Born's turbiKyoto 606, Japan, and tthe Department of Neurosurgery, Ohtsu Mudometric method, in the post-acute period of cerebral
nicipal Hospital, 9-9 Motomiya, Ohtsu, Shiga, 520 Japan.
thrombosis (more than two weeks after onset). No
Address correspondence to: Yuzo Otsuki, M.D., 9-102 Kuze-Kasubject was taking drugs known to affect platelet funcmiohtani, Joyo, Kyoto 610-01,
Japan.
Downloaded from http://stroke.ahajournals.org/ by guest on June 24, 2016
tion within 7 days prior to examination. Blood was
Received July 28, 1981; second revision accepted October 27, 1982.
SINCE IT WAS OBSERVED that arterial thrombus is
initiated by white plugs of platelet, enhanced platelet
activity as a risk factor for cardio and cerebrovascular
diseases has been a matter of concern among many
investigators. Computed tomography (CT) provides a
useful tool to differentiate between cortical and deep
cerebral infarctions. Previously noted risk factors
should be re-evaluated with respect to each type of
cerebral infarction. We studied platelet aggregation in
patients with cerebral thrombosis who had CT and
angiographic evaluation to assess the correlation between enhanced platelet aggregation, degree of vessel
stenosis and type of cerebral infarction.

Angiographical analysis of acute cerebral infarction followed by "cascade"-like
deterioration of minor neurological deficits. What is progressing stroke?
T Irino, M Watanabe, M Nishide, M Gotoh and T Tsuchiya
Stroke. 1983;14:363-368
doi: 10.1161/01.STR.14.3.363
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1983 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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