663

Clinical-CT Correlations in TIA, RIND, and Strokes

with Minimum Residuum
L. CALANDRE, M . D . , S. GOMARA, M . D . , F. BERMEJO, M . D . , J. M. MILLAN, M.D.,

AND G. DEL POZO, M . D .

SUMMARY An approach to the controversy of the physiopathology and classification of ischemic stroke
is attempted in this study. The computed tomographies (CT) of 88 patients with transient ischemic attacks
(TIA), 46 with reversible ischemic neurologic deficits (RIND) and 70 with ischemic strokes with minimum
residuum (SMR) are analysed. The incidence of focal ischemic lesions on CT is 25% in TIA and RIND and
35% in SMR, when the study was performed after the first 24 hours. The incidence of cerebral infarction
was much lower when the CT was performed within the first 24 hours after the clinical event. No significant
differences in size or location of the infarction were found between the different groups. Deep infarctions
were smaller than superficial ones. TIA duration correlated neither with the incidence of CT abnormalities
nor with the size of the lesions. No correlation was found between doppler or oculoplethysmography
abnormalities, clinical groups and CT findings. In reference to the structural lesions that underlie the
clinical syndromes, TIA, RIND and SMR should not be considered as different groups.
Stroke Vol 15, No 4, 1984
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THE CLINICAL CONCEPT of transient ischemic at-
tack (TIA) is based mainly on the supposition that it is
provoked by focal cerebral ischemia without infarc-
tion. This idea has been supported by studies in which
no infarctions are found on computed tomographies
(CT) performed in TIA cases.1"3 But there are other
reports that contrariwise show a significant incidence
of infarctions on CT of patients with transient neuro-
logical deficits.4"6 Although TIAs and completed
strokes are usually managed as different conditions,
clinical experience shows that completed strokes with
minimum residuum are in many aspects similar to long
lasting TIAs or to reversible ischemic neurological
deficits (RINDs). In order to study the differences and
correlations between these groups we analysed the fea-
tures of CT performed in patients diagnosed of TIA,
RIND and completed ischemic stroke with minimum
residuum (SMR). The results obtained can be useful in
order to achieve a practical classification for the man-
agement and study of focal cerebral ischemia.
Material and Methods
Two hundred and four patients with the diagnosis of
focal cerebral ischemia have been analysed. All were
studied in the Neurology Department within a month
after the stroke. The diagnosis was based upon clinical
and CT findings. Patients with a history of previous
completed strokes were excluded. In all the patients at
least one CT was performed after the current neuro-
logical event. Depending on clinical symptoms the
ischemia was considered to occur either in the carotid
system or in the vertebrobasilar system. The differ-
ences in clinical evolution permitted classification in
three groups: 1: TIAs. When focal neurological symp-
toms lasted less than 24 hours. 2: RINDs. When neuro-
logical symptoms or signs lasted more than 24 hours
but cleared completely before one month. 3: SMR.
From the Department of Neurology and Section of Neuroradiology,
"1 de Octubre" University Hospital, Madrid, Spain.
Address correspondence to: Dr. L. Calandre, Servicio de Neuro-
logica, Hospital "I de Octubre," Ctra. de Andalucia, Madrid, Spain.
Received October 13, 1983; revision # 1 accepted January 17, 1984.
When after one month mild neurological signs persist-
ed which did not hamper the basic daily activities of
the patient. CTs were performed in a 160 x 160 ma-
trix. Focal ischemic lesions included parenchymatous
low-density areas and focal areas of dilatation of a
ventricle or a cistern. The area of the low-density le-
sion was measured in the slice in which the width of the
lesion was greatest, giving the results in real brain
dimensions. Depending on their location the lesions
were considered as superficial (frontal, parietal tempo-
ral and occipital lobes), deep (thalamus, caudate, in-
ternal capsule, putamen and corona radiata) and cere-
bellar. Diffuse cerebral atrophy was not taken into
consideration. Contrast-enhancement studies are not
mentioned because they were rarely performed.
In several cases directional doppler sonography and/
or oculopneumoplethysmography were performed.
Quoted as pathologic are only those cases with evi-
dence of severe stenosis or occlusion of the ipsilateral
internal carotid artery. Angiographic studies were per-
formed in few cases so it seemed not useful to analyse
them. The statistical significance of differences was
studied by means of Student's / test (for means) and
Chi-square test, with Yates correction (for propor-
tions).
Results
Out of 204 cases, 88 were diagnosed as TIAs, 46 as
RINDs and 70 as SMR. In the TIA group 67 cases were
in the carotid system (amaurosis fugax cases were not
included in this series) and 21 in vertebrobasilar sys-
tem. In the RIND group 41 cases were in the carotid
system and 5 in the vertebrobasilar system. In the SMR
group 61 cases were in the carotid system and 9 in the
vertebrobasilar system. Fifty cases had only one CT
performed, in each case during the 24 hours that fol-
lowed the neurologic event. Two of them showed focal
lesions (both SMR). In 154 patients at least one CT
was performed after the first 24 hours (with a mean
period between the stroke and performance of the CT
of 50 days — standard deviation of 55 days —; all the
patients being treated during this period by a neurolo-
gist). The incidence of CT abnormalities in the differ-
 664
TABLE 1 Incidence and Size of C7 Lesions
Low-density lesion
area (cm2)
Normal Abnormal
CT(%) CT(%) Mean Range
TIA cases 47 (75) 16 (25) 0.58 0.09-1.32
RIND 30 (75) 10 (25) 1.54 0.11-11.1
SMR 33 (65) 18 (35) 1.03 0.06-1.18
All these CT were performed after 24 hours.
ent groups is set out in table 1. In each case the CT
lesion side correlated with neurological focality side,
although in one case two infarctions were found, one
in each cerebral hemisphere. In 30 patients two CTs
were performed: in 5 the same lesion appeared in both
CTs, in 7 the first CT was normal and the infarction
appeared in the second CT, and in 18 patients both CTs
were normal. The mean values of low-density areas are
set out in table 1. Although the low-density areas in
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TIAs seem to be smaller than in the other groups the
difference is not statistically significant. Among the
CT lesions five were areas of ventricle or cistern focal
dilatation (4 TIA and one RIND case). The location of
low-density areas was the following: frontal lobe, 4;
parietal, 13, temporal, 7; occipital, 4; thalamus/inter-
nal capsule, 7; putamen/caudate/corona radiata, 4 and
cerebellum, 2. The mean area of deep lesions was
significantly smaller than the area of superficial lesions
(p < 0.05). In all the groups the incidence of superfi-
cial lesions was higher than the incidence of deep le-
sions. Out of 35 vertebrobasilar system cases 7 showed
a focal lesion while of 169 carotid system cases a CT
lesion was found in 34. The correlation between the
length of the TIA and the area of CT lesions is set out in
table 2. No significant differences are found among the
different groups. Thirty seven TIA patients suffered
several ischemic events. Ten of these cases showed a
lesion on CT. Although that figure seems to be higher
than that of single TIAs the difference is not signifi-
cant.
Doppler and oculoplethysmography tests were ab-
normal in 12 out of 48 TIA cases, 7 of 18 RIND cases
and 6 of 18 SMR cases (without significant differ-
ences). Of 23 cases with abnormal CT in which a
doppler or oculoplethysmography were performed, 5
were abnormal. Of 86 cases with normal CT the tests
were abnormal in 20 (without significant difference).
Discussion
In the management of focal ischemic cerebral dis-
ease it has been considered that TIAs constitute a well
differentiated group when compared with completed
strokes (those with persistent neurological deficit). In
the last years an intermediate group, that of RINDs,
has been described.7 In some series,8"19 strokes with
minimum residuum have been considered in the same
group of TIAs. In fact, there are qualified authors who
state that TIAs, RINDs and SMR should be considered
as similar;" others consider that they are different
groups;12 others suggest that new studies are needed to
identify the groups13 and, finally, an author states that a
STROKE VOL 15, No 4, JULY-AUGUST 1984
new approach to this problem should be attempted.14
An important question is that it has not yet been possi-
ble to establish a physiopathological difference be-
tween TIAs and completed strokes. Nevertheless,
when the many experimental studies on this subject are
reviewed the following conclusions can be pointed out:
Transient arterial occlusions (of carotid or middle cere-
bral arteries) can lead to a cerebral ischemia and per-
manent occlusions can provoke only transient cerebral
ischemia. Whether infarction develops or not depends
mainly on two factors: "~18 the severity of local cerebral
blood flow (CBF) decrease (the focal CBF has to be
lower than 10 cc/100 gr/min. to produce infarction);
and the time hypoperfusion lasts (at least 15 minutes to
produce infarction). A little higher CBF (12-18 cc/100
gr/min.) can provoke a reversible failure of neuronal
activity (which duration is not still well determined),
without infarction. Permanent occlusion can lead to
various types of neurological deficit depending mainly
on the function of collateral circulation.l9 Not always a
greater extent of the infarction correlates with a more
severe clinical deficit.20 There is not a direct correla-
tion between infarction site and clinical disability, ex-
cept for infarctions located in the internal capsule
which correlate with a severe hemiparesia.21
CBF studies in patients with TIAs show that it is not
unusual to find hypoperfusion areas persisting longer
than the neurological symptoms, even in cases without
evidence of infarction on CT. 2223 Only slight differ-
ences are found between TIAs and RINDs.22 Angio-
graphical studies do not show remarkable differences
between TIA, RIND and SMR groups, abnormalities
of extracranial vessels appearing with quite similar
features and incidence in the three groups.24"26
CT studies have provided a new viewpoint regard-
ing the identification of focal cerebral ischemia
groups. Some authors found that no infarction oc-
curred in TIA cases.1"3 Other reports show that CT
evidence of infarction is not rare, with an incidence
about 14 to 2 0 % . ^ 21~N Such incidence is clearly high-
er than the 6% we found in 60 patients (mean age: 60
years) without any symptoms of cerebral ischemia
studied in our Department. In any case, it is well
known that CT abnormalities are much less frequent in
TIA than in completed stroke cases.28 Also, the timing
of performance of the CT greatly influences the detec-
tion of the infarction. The correlation between CT and
autopsy findings decreases with the size of the infarc-
tion.30 That clinical-CT correlation is not as good as
TABLE 2 TIAs Duration and CT Features
Low-density
Number Number of area
of abnormal (mean size)
Duration cases CTs (cm2)
Less than 15 minutes 36 5 0.43
15 to 30 min. 9 3 0.55
30 min. to 6 hours 25 1 0.31
6 to 12 hours 5 1 0.70
12 to 24 hours 17 2 1.08
 COMPUTED TOMOGRAPHY IN TIA, RIND AND STROKES/Calandre el al
one would expect is shown by a recent report in which
infarction volume is measured in different types of
focal cerebral ischemia.31 One of the conclusions is
that neither by the clinical signs nor by prognosis can
be found any difference between patients with normal
and abnormal CT in cases of cerebral ischemia with
slight clinical deficit.
There is not definite evidence for considering TIAs,
RINDs and SMR as well differentiated groups. We do
not know if a TIA is provoked by transient ischemia
without infarction or it is secondary to an infarction,
the mild symptoms being due to a particular location or
size. In attempting to study some of these questions we
analysed 204 patients with the diagnosis of focal cere-
bral ischemia studied with CT. Eighty eight were
TIAs, 46 RINDs and 70 SMR. It surprised us the
difficulty in establishing a neat difference among these
groups, because of the subjective and mild symptoma-
tology. The moment of performance of the CT was
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important: out of 50 cases in which the CT was per-
formed in the first 24 hours only 2 showed a focal
lesion, while of 154 cases studied after 24 hours 44 had
an abnormal CT. The fact that in several cases a first
and a second CT were both normal (even in SMR
cases) probably reflects the low resolution of our CT
scanner. TIA, RIND and SMR groups did not show
any significant difference in the incidence of CT le-
sions or in the location of these lesions. The frequency
of CT abnormalities seemed to be higher in multiple
TIAs than in single TIA. No correlation was found
between CT lesions and doppler or oculoplethysmo-
graphy abnormalities. Deep infarctions were signifi-
cantly smaller than superficial ones. Some of the for-
mer could be considered as lacunes. In fact there are
reports in which lacunar infarctions are found fre-
quently in patients with TIAs. 30 In series of lacunar
infarctions, cases with transient neurological deficits
are not rare,32 this finding being in accordance with the
current concepts that are held regarding lacunes.33 M
Our principal conclusion is that a clear cut difference
in frequency or features of cerebral infarction as visu-
alized on CT in TIAs, RINDs and SMR has not been
found. Although some cases of TIA or RIND are prob-
ably secondary to a cerebral ischemia without paren-
chymatous lesion, other cases are provoked by a cere-
bral infarction which, either because of its small size or
its location in areas of low clinical significance is mini-
mized in its neurological symptoms (by mechanisms,
not yet completely understood.)35
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Failure of Flunarizine to Improve Cerebral Blood

Flow or Neurologic Recovery in a Canine Model of
Complete Cerebral Ischemia
Downloaded from http://stroke.ahajournals.org/ by guest on January 30, 2018

LESLIE A. NEWBERG, M . D . * PETTER A. STEEN, M . D . , P H . D . I JAMES H. MILDE,

AND JOHN D. MICHENFELDER, M.D.I

SUMMARY Ten minutes of cerebra] ischemia was produced in 12 dogs by temporary ligation of the venae
cavae and aorta. After reperfusion the dogs received the calcium entry blocker, flunarizine, 6 fig/kg infused
over a ten minute period. Cerebral blood flow (CBF) and metabolism (CMROx) were measured pre-
ischemia and for 2 h post-ischemia in 6 dogs. At the end of the study brain biopsies were analyzed for
cerebral metabolites. Neurologic recovery was evaluated for up to 48 h post-ischemia in an additional 6
dogs. The results of each study were compared to those previously obtained in untreated animals. The
cerebral blood flows (when expressed as a percent of the pre-ischemic control value) of the flunarizine-
treated and untreated groups were similar throughout the post-ischemlc period. Following an initial
hyperemia, the CBF fell to significantly less than the pre-ischemic control values, and remained approxi-
mately 26% of control during the final 90 min in both groups. The CMRO2 was also the same for both
groups. Cerebral metabolites were similar although abnormal in both groups. Flunarizine produced
pulmonary edema in 5 of 6 dogs studied for neurologic recovery. Four of these dogs died within 12 h and
another dog demonstrated severe neurologic damage. None of the untreated dogs developed pulmonary
edema, but 6 of 7 dogs evidenced severe neurologic damage or were dead at 48 h. Thus, flunarizine failed to
improve either cerebral blood flow or neurologic outcome when given after complete cerebral ischemia in
the dog. A cardiodepressive effect of flunarizine might have contributed to the poor neurologic outcome.
These results are compared to those obtained following treatment with another calcium entry blocker,
nimodipine, in the same animal model.
Stroke Vol 15, No 4, 1984

REPERFUSION of the brain following complete cere-
bral ischemia is characterized by a prolonged hypoper-
fusion state M at a time when neurons may be capable
of complete functional recovery.5 Increases in cerebro-
vascular resistance occur independently of intracranial
pressure6 and may limit cerebral recovery.7 According-
ly, an effective cerebral vasodilator might have a sig-
nificant impact upon the neurologic outcome follow-
From the Department of Anesthesiology, Mayo Medical School and
Mayo Clinic, Rochester, Minnesota 55905.
Assistant Professor in Anesthesiology, Mayo Medical School,* Vis-
iting Scientist from Ulleval Hospital, Oslo, Norway, Research Associ-
ate, Mayo Clinic,t and Professor in Anesthesiology, Mayo Medical
School.! This work was supported in part by NIH Grant NS-7507 from
the National Institute of Health, United States Public Health Service,
and Dr. Steen by a grant from the Laerdal Foundation for Acute Medi-
cine. Address correspondence to: Leslie A. Newberg, M.D., Depart-
ment of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905.
Received October 12, 1983; revision # 1 accepted January 5, 1984.
ing a period of complete cerebral ischemia.
Nimodipine, a calcium entry blocker, has been report-
ed to inhibit vasoconstriction in potassium depolarized
vascular smooth muscle;8 to moderately improve cere-
bral blood flow (CBF) following a period of complete
global ischemia in dogs9"10 and to improve neurologic
outcome.9 Another calcium entry blocker, flunarizine,
has been reported to be a potent cerebral vasodilator,"
to dramatically improve CBF after complete cerebral
ischemia in dogs maintained on cardiopulmonary
bypass,12 and to protect the brain of mice and rats
against cerebral hypoxia-anoxia.13 We therefore stud-
ied the effects of flunarizine on CBF, cerebral metabo-
lism of oxygen (CMRO 2 ), and neurologic recovery in
an established intact canine model of complete cere-
bral ischemia and compared the results to those ob-
tained from untreated groups4-14 and from pre-treated9
and post-treated10 nimodipine groups using the same
model.
 Clinical-CT correlations in TIA, RIND, and strokes with minimum residuum.
L Calandre, S Gomara, F Bermejo, J M Millan and G del Pozo

Stroke. 1984;15:663-666
doi: 10.1161/01.STR.15.4.663
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1984 American Heart Association, Inc. All rights reserved.
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Print ISSN: 0039-2499. Online ISSN: 1524-4628

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