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Fig. 7.29 Dental amalgam artifact (as shown by arrow in image)
Fig. 7.30 Total carotid occlusions: the ascending pharyngeal branch of the external carotid artery can be mistakenly interpreted as a hairline
open ICA
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Fig. 7.31 The lipid core appears as low-intensity TOF, variable signal in T1 and DP, and more often as intermediate signal in T2
7 Diagnostic Approach to Cerebrovascular Disease: CT and MRI
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Fig. 7.32 3D TOF-MRA with “angiographic-like” reconstructions and axial source image
Fig. 7.33 CE-MRA
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H. Muresian (ed.), Arterial Revascularization of the Head and Neck, DOI 10.1007/978-3-319-34193-4_8
Pharmacological Measures for the Treatment and Prevention of Stroke: The Choice of Initial Therapy
Sorin Tuta
In spite of progress in reducing the disease burden (especially in developed countries in the last decades), stroke still
represents the second leading cause of death and third leading contributor to disability-adjusted life-years all over the
world. Due to the aging of population and inherent limits of
therapies, even in developed industrialized countries, stroke
incidence had reached a plateau level. Correct and prompt
treatment in the acute stroke phase, as early as possible, and
adequate measures for secondary prevention together with
measures of population health strategies and specifi c primary prevention are the cornerstones for limiting fatalities
and disability related to this disease.
Compared with myocardial infarction, stroke has a more
complex and heterogeneous pathology; the two major categories of stroke, hemorrhagic and ischemic, are opposite
conditions regarding to treatment at least, but on the other
hand they could be connected through common lesions like
small vessel disease (cause of ischemic and hemorrhagic
stroke), common risk factors like arterial hypertension, or
treatment (cerebral hemorrhages induced by antithrombotic
treatments of ischemic stroke). Although much rare, subarachnoid hemorrhage and cerebral venous and sinus thrombosis are another two separate categories of stroke.
Pharmacological treatment of cerebral hemorrhage is
unfortunately limited compared to ischemic stroke, since trials like FAST [
1 ] (with recombinant activated factor VII)
and other hemostatic therapy failed to prove signifi cant benefi t, so the mainstream treatment is based on prompt decrease
of high blood pressure values (under 160 mmHg systolic values and if possible and tolerated to 140 mmHg for systolic
values in the fi rst 24 h from onset [ 2 ]) and general supportive
therapy and prevention of complications. Except the much
more rare situations of medical, non-aneurysmal cases of
subarachnoid hemorrhage, treatment of aneurysmal or malformative hemorrhages is surgical or endovascular (interventional). The opposite situation of a more complex
pharmacological treatment (and recently interventional,
endovascular) is currently available for ischemic stroke and
cerebral venous and sinus thrombosis, where the antithrombotic treatment is usually the fi rst-line therapy.
8.1 Acute Ischemic Stroke
The reduction of cerebral blood fl ow (CBF) under
10–12 ml/100 g cerebral tissue per minute produces irreversible necrosis in a few minutes in the core region of ischemia
(the region with the minimum fl ow within the hypoperfused
area), while in the surrounding penumbral area where CBF is
around 12–22 ml/100 g/min, the neuronal survival is variable, depending on metabolic factors and collateral fl ow, but
in majority of cases being up to 3–6 h from onset. The complete restoration of fl ow in this period of time could reverse
the neuronal and glial ischemic changes in the penumbral
area, with salvage of brain tissue at risk and improving or
reversing the neurologic defi cit quantifi ed by clinical scores
like NIHSS and modifi ed Rankin score.
From this point of view, the main priority of treatment of
the ischemic stroke is the rapid restoration of fl ow in the
obstructed artery followed by reperfusion of the ischemic
cerebral tissue.
After the successful 1995 NINDS trial [ 3 ], the recombi-
nant tissue plasminogen activator alteplase was approved for
intravenous (i.v.) therapy of acute ischemic stroke.
The analysis of the results [ 4 ] showed no signifi cant dif-
ference compared to placebo in the fi rst 24 h after administration, but at 3-month evaluation, the chances for
favorable results with active therapy were 1.7 times greater,
and the number needed to treat for a favorable outcome
(defi ned by a modifi ed Rankin scale of 0–1 ) was 11 (or
8
S. Tuta
Head of Stroke Unit , National Institute of Neurology and
Neurovascular Diseases, University of Medicine and
Pharmacy Carol Davila , Bucharest , Romania
e-mail:
sorin.tuta@gmail.com
Electronic supplementary material The online version of this chapter
(doi:
10.1007/978-3-319-34193-4_8 ) contains supplementary material,
which is available to authorized users.
192
only 3 if we consider 1 point decrease for any step in
Rankin score), with no differences in mortality, and a number needed to harm of 30.
The symptomatic intracerebral hemorrhage within 36 h
after the onset of stroke occurred in 6.4 % of patients given
t-PA, but the defi nition of the symptomatic hemorrhage in this
trial was very permissive – any new cerebral bleeding with
any increase of the neurologic defi cit scores and included
cases where a small hemorrhage was not the cause of decline
of neurological status score like NIHSS. The positive results
were obtained in all subtypes of ischemic stroke: large vessel
diseases, cardioembolism, or small vessel disease.
Since NINDS trial the dosage of alteplase is 0.9 mg/kg,
10 % being administered as i.v. bolus and the rest in continuous i.v. infusion during 1 h. The initiation of therapy should
have been done in the fi rst 3 h from onset [ 3 ].
The successful NINDS trial for i.v. alteplase used for
ischemic stroke in the fi rst 3 h from onset was doubled by the
ECASS III trial, which further prolonged the time window
for i.v. alteplase to 4.5 h from stroke onset. In this trial the
chance for good outcome was increased by 34 % (independency defi ned by an mRankin score 0–2), without additional
increasing of death rate [
5 ].
Other trials tried to explore longer time windows for
thrombolysis in acute ischemic stroke patients: IST3 up to
6 h [ 6 ] did not fi nd signifi cant differences for the group of
patients alive and independent at 6 months, and DIAS 3
using desmoteplase [ 7 ] and patients selected between 3 and
9 h from onset using the penumbra concept (with MRI or CT
scan proved mismatch) also failed to reveal improvement in
functional outcome compared to placebo.
The cerebral hemorrhage rate was higher than placebo,
like in the other trials with i.v. alteplase (2.4 % symptomatic
intracerebral hemorrhage (SICH), with 4 points increase in
NIHSS score), but was lower than before (7.9 % in NINDS
trial, 7 % in IST3 trial, 5.3 % in ECASS II). In-hospital mortality is signifi cantly higher in patients with symptomatic
cerebral hemorrhage after alteplase than in those without
(75.0 % vs 16.9 %) and represents one of the major predictive
factors for death [ 8 ]. Unfortunately treatment for correction
of coagulation in cerebral hemorrhages after i.v. alteplase did
not change the outcome.
Several prognostic scores have been developed to predict
the risk of symptomatic intracranial hemorrhage after ischemic stroke thrombolysis (the safe implementation of treatments in stroke (SITS)-SICH score, the SEDAN score (the
acronim SEDAN coming from main items used for the score:
S ugar -glucose level, E arly infarct signs, (hyper) D ense cere-
bral artery sign on admission computed tomography scan,
A ge and N IH Stroke Scale on admission), the hemorrhage
after thrombolysis (HAT) score, and the Multicentre Stroke
Survey score, but neither proved to be very reliable, ranging
in moderate level of predictive performance [ 9 ].
The SEDAN score performed a little better, its total sum
components ranging between 0 and 6 points. The component
parameters of the score are mentioned in Table
8.1 , as well as
the corresponding absolute risk of cerebral hemorrhage at
any score points [ 10 ].
Other scores (SITS-SICH score) took into account (beside
the mentioned parameters of SEDAN score) other factors
associated with an increased risk of cerebral hemorrhage like
the antiplatelet treatment before thrombolysis therapy, high
systolic blood pressure values, history of hypertension, a
longer than 180 min time from onset to treatment, and a
weight more than 95 kg [ 11 ]. A meta-analysis [ 12 ] of the
main randomized trials with alteplase for acute ischemic
stroke evaluated the results from 6756 patients included in
nine clinical trials. The i.v. thrombolytic treatment increased
the chances for a favorable outcome with functional independence (modifi ed Rankin score 0 and 1) especially for
those treated in the fi rst three hours (32.9 % of active-treated
patients compared with 23.1 % with placebo). In the 3–4.5 h
interval from stroke onset, the results were also positive, but
the magnitude of effect was lower (35.3 % vs 30.1 %), and a
nonsignifi cant therapeutic effect was noticed after 4.5 h from
onset. The benefi t was independent of age or lesion severity
(up to National Institutes of Health Stroke Scale (NIHSS)
score of 25, less than one-third of MCA territory, or CT
Alberta Stroke Program Early CT score (ASPECTS) above
6). As expected, the risk of symptomatic cerebral hemorrhage (at least 4 points increase of the NIHSS score due to
the hemorrhage) increased from 1.3 to 6.8 %, but in spite of
more death due to cerebral hemorrhage in the fi rst week, at
90 days from treatment, the death rate did not differ signifi cantly (17.5 % vs 16.5 %) because of delayed increase of
death rate in non- thrombolyzed large ischemic stroke. The
cerebral hemorrhage rate was independent of time from
onset, or the lesion extension within one-third MCA rule, for
the fi rst 3 h, but with an increasing rate after 3 h or large
cerebral lesions (more than one-third of MCA territory).
A Cochrane meta-analysis from 2014 included 27 trials,
and 10187 participants also demonstrated that the i.v. thrombolysis in the fi rst 3 h from onset of ischemic stroke was
more effi cient than standard treatment in reducing the combined risk of death and dependence [
13 ].
Because as time passes the central core of necrosis
expands in ischemic brain in the penumbral area, the effect
of recanalization of occluded artery will be better when time
from onset to treatment and reperfusion is shorter. The benefi t of treatment is visible decreasing with time; intravenous
alteplase initiated within 1.5 h of symptom onset was associated with an odd ratio of almost three times higher rates for
favorable outcome at 3 months compared with placebo,
while within 1.5–3 h was about 1.5 times higher compared
with 1.4 times within 3–4.5 h and not signifi cant effect anymore after 4.5 h [ 14 ]. The short therapeutic window of
S. Tuta
193
3–4.5 h from onset is one of the main limiting factors for the
proportion of patients possible to be treated; except of late
arrivers, another signifi cant part (15–25 % of patients) has an
unknown time from onset or a wake-up stroke. Imaging
strategies like the MRI DWI–FLAIR time mismatch are
studied in ongoing trials to confi rm the usefulness and safety
of this approach for time estimation of onset and to apply a
thrombolytic treatment for these patients [ 15 ].
Other trials with extended time window up to 6 h like
IST3 - which included more than 3000 patients - did not fi nd
signifi cant benefi t after 4.5 h, but due to a large number of
older than 80-year-old patients included it confi rmed that
these patients did not benefi t less than the younger ones,
although the benefi t is especially achived if they were treated
in the fi rst 3 h from onset [
6 ]. Other trials like DIAS 3 using
desmoteplase [
7 ] in a 3–9-h time window and multimodal
imaging (diffusion–perfusion MRI) for target mismatch
selection of patients having enough viable cerebral tissue
and a small necrotic core failed to prove a signifi cant benefi t
in this extended time window.
To date, the accepted time window for intravenous thrombolysis with alteplase is up to 4.5 h from the onset for
18–80-year-old patients and 3 h for those after 80 years old;
the most frequently used inclusion and exclusion criteria for
treatment are listed in Table
8.2 .
There are many predictive factors related to the possible
recanalization and reperfusion rate and also the chance for
functional independence rate at 3 months (defi ned by a modifi ed Rankin score between 0 and 2). Reperfusion in the fi rst
6 h was consistently superior to recanalization in predicting
tissue and clinical outcome. Reperfusion without recanalization was frequent and probably related to retrograde
Table 8.1 SEDAN score for predicting post i.v. thrombolysis cerebral symptomatic hemorrhage [ 10 ]
Parameter Allocated points for parameter Total obtained points Absolute risks ICH (%)
Blood glucose 145–216 mg/dl 1 point 0 1
Blood glucose >216 mg/dl 2 points 1 3.5
Early infarct signs on baseline CT 1 point 2 5.1
Hyperdense cerebral artery sign 1 point 3 9.2
Age >75 years 1 point 4 16.9
Baseline NIHSS score ≥10 1 point 5 27.8
Table 8.2 Indication and exclusion criteria for i.v thrombolysis of acute ischemic stroke
Indication criteria Exclusion criteria
Diagnosis of ischemic stroke causing a measurable
neurological defi cit
Signifi cant head trauma or prior stroke in previous 3 months
Symptoms suggest subarachnoid hemorrhage
Onset of symptoms <3–4.5 h before beginning treatment Arterial puncture at noncompressible site in previous 7 days
History of previous intracranial hemorrhage
Aged ≥18 years Intracranial neoplasm, arteriovenous malformation, or aneurysm
Recent intracranial or intraspinal surgery
Elevated blood pressure (systolic >185 mmHg or diastolic >110 mmHg)
Active internal bleeding
Acute bleeding diathesis, including but not limited to:
Platelet count <100,000/mm
3
Heparin received within 48 h, resulting in abnormally elevated aPTT greater than
the upper limit of normal
Current use of anticoagulant with INR >1.7 or PT >15 s
Current use of direct thrombin inhibitors or direct factor Xa inhibitors with
elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT; TT
or appropriate factor Xa activity assays)
Blood glucose concentration <50 mg/dl (2.7 mmol/L)
CT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)
Relative exclusion criteria
Only minor or rapidly improving stroke symptoms (clearing spontaneously)
Pregnancy
Seizure at onset with postictal residual neurological impairments
Major surgery or serious trauma within previous 14 days
Recent gastrointestinal or urinary tract hemorrhage (within previous 21 days)
Recent acute myocardial infarction (within previous 3 months)
Reproduced with permission from [
16 ]
8 Pharmacological Measures for the Treatment and Prevention of Stroke: The Choice of Initial Therapy