HEADACHE CURRENTS
Headache Currents
Headaches Attributed to Ischemic Stroke and Transient Ischemic Attack
Felipe Araujo Andrade Oliveira, MD; Pedro Augusto Sampaio Rocha-Filho, MD, PhD
Introduction.—Although headaches attributed to
ischemic strokes and transient ischemic attack occur
frequently, they are often overlooked and underdiagnosed as
manifestations of cerebrovascular disease.
Method.—This is a narrative review.
Results.—The prevalence of headache attributed to
ischemic stroke varies between 7.4% and 34% of cases and of
headache attributed to transient ischemic attack, from 26% to
36%. Headache attributed to ischemic stroke is more frequent
in younger patients, in migraineurs, in those who have
suffered a larger stroke, a posterior circulation infarction, or a
cortical infarction, and is less frequent in lacunar infarctions.
The most common pattern of headache attributed to ischemic
stroke is a mild to moderate bilateral pain, not associated with
nausea, vomiting, photophobia, or phonophobia. This
headache usually has a concomitant onset with focal
neurologic deficit and improves over time. The few studies
that have assessed the value of headache for a prognosis of
ischemic strokes have demonstrated conflicting results. There
are no clinical trials on pain management or prophylactic
treatment of persistent headache attributed to ischemic stroke.
Conclusion.—Headache attributed to ischemic stroke is
frequent and usually has a tension-type headache pattern. Its
frequency varies according to the stroke’s etiology. Further
studies are required on pain management, prophylactic
treatment, and characteristics of this headache.
Key words: headache, headache disorders, secondary, vascular
headaches, stroke, transient ischemic attack
Abbreviations: CSD cortical spreading depression, ICHD
International Classification of Headache Disorders, TIA transient
ischemic attack
INTRODUCTION
Cerebrovascular diseases are among the leading causes of
death and disability in most countries and worldwide account
for 16.8% of deaths and 10.2% of disability-adjusted life-years
From the Postgraduate Program in Neuropsychiatry and Behavioral Sciences,
Universidade Federal de Pernambuco (UFPE), Recife, Pernambuco, Brazil (F.A.A.
Oliveira); Department of Neuropsychiatry, Universidade Federal de Pernambuco (UFPE),
Recife, Pernambuco, Brazil (P.A. Sampaio Rocha-Filho); Headache Clinic, Hospital
Universitario Oswaldo Cruz, Universidade de Pernambuco, (UPE), Recife, Pernambuco
Brazil (P.A. Sampaio Rocha-Filho).
Address all correspondence to P.A. Sampaio Rocha-Filho, Rua General Joaquim Inácio,
830, Sala 1412 – Edf The Plaza Business Center, Recife, Pernambuco – CEP: 50070-270,
Brazil, email: pedroasampaio@gmail.com
Accepted for publication December 12, 2018.
Headache
© 2019 American Headache Society
1
(DALYs). This is particularly relevant in low- and middle-
income countries where, over the last 20 years, there has been
an increase in incidence and disability caused by cerebrovascu-
lar diseases.1,2
The clinical presentation of ischemic strokes is dominated
by focal neurologic deficits secondary to the ischemic event.
Headaches related to ischemic strokes are often overlooked by
both patients and clinicians, despite their high prevalence.3
Headaches related to ischemic stroke and transient isch-
emic attack (TIA) are classified by the International
Classification of Headache Disorders, 3rd Edition (ICHD3)
in the section referring to secondary headaches in Chapter
6, Headache a­ttributed to cervical or cranial vascular dis-
orders. The diagnosis of headache attributed to ischemic
strokes is determined by the close temporal relationship
between the onset of headache and the development of
signs and symptoms of an ischemic stroke or when head-
ache leads to a diagnosis of an ischemic stroke. An im-
provement in the headache attributed to ischemic stroke
follows the clinical improvement of the ischemic stroke.4
The headache attributed to TIA normally begins simultane-
ously with the clinical signs of TIA and must resolve alongside
the clinical improvement of TIA or within 24 hours. In neither
of these cases are the clinical features of headache taken into
account for diagnosis.4
The objective of this article is to review the epidemiology,
the pathophysiology, and the clinical features of headaches
­attributed to ischemic stroke and TIA. We also review whether
the presence of headache is related to the prognosis of stroke.
METHODS
This is a narrative review. We conducted a literature review
in the PubMed database with the following terms: (1) head-
ache; (2) stroke; (3) cerebrovascular disease; and (4) transient
ischemic attack. All articles in English considered relevant were
included. There was no limitation on the date of publication.
EPIDEMIOLOGY
Table 1 summarizes the observational studies performed in pa-
tients with ischemic stroke, in which the prevalence of headache
attributed to ischemic stroke was between 7.4% and 34%.5-20
With the exception of 3 studies,9,17,21 it was not possible to
Conflict of Interest: None.
Funding: This research received no specific grant from any funding agency in the public,
commercial, or non-for-profit sectors.
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Headache Currents

Table 1.—The Reported Prevalence of Headache Attributed to Ischemic Stroke and Transient Ischemic Attack

Diagnostic
Criteria of the Definition of Headache Related to
Study Study Design Data Collection N ICHD Stroke or TIA Prevalence of Headache
Portenoy, Observational; Prospective; 165 No Not reported 17% of lacunar infarctions
1984 case series 2 hospitals 29% of non-lacunar
infarctions
36% in TIAs
Loeb, 1985 Observational; Retrospective 90 No Not reported 30% of TIAs
case series
Koudstall, Observational; Prospective, 3126 No Not reported 18% of ischemic strokes
1991 case series multicentric
Vestergaard, Observational; Prospective; 214 No Headache complaints appearing 26% of ischemic strokes
1993 case series 1 hospital 3 days before to 3 days after onset
of stroke symptoms
Arboix, 1994 Observational; Prospective; 195 No Not reported 41% of non-lacunar
case series 1 hospital infarctions
23% of lacunar
infarctions
26% of TIA
Kumral, 1994 Observational; Prospective; 2255 No Cephalic pain appearing just before 16% of ischemic strokes
case series 1 primary care or after other stroke symptoms
center
Ferro, 1995 Observational; Prospective; 182 No Headache from 48 hours before plus 34% of ischemic strokes
case series 1 hospital 24 hours after stroke onset 5% of lacunar infarctions
Ferro,1995 Observational; Prospective; 205 No Headache from 48 hours before plus 29% of TIA
case series 1 hospital 24 hours after stroke onset
Salgado, 1995 Observational; Prospective; 145 No Headache from 48 hours before plus 10% of lacunar
case series 1 hospital 24 hours after stroke onset infarctions
Leira, 2002 Observational; Prospective 241 No Not reported 30.6% of ischemic strokes
prospective
cohort
Rathore, 2002 Observational; Retrospective 474 No Not reported 22.4% of ischemic strokes
prospective
cohort
Verdelho, Observational; Prospective; 668 Yes Present during hospitalization for 31% of strokes (including
2007 prospective 1 hospital stroke with a duration of at least hemorrhagic stroke)
cohort 24 hours
Tentschert, Observational; Prospective; 2196 No Headache at stroke symptom onset. 27% of ischemic strokes
2005 case series 1 hospital and TIA
Mitsias, 2005 Observational; Prospective; 375 No Headache that occurred between 24 31.5% of ischemic strokes
case series 1 hospital hours before the ischemic stroke
and the following 24 hours
Arboix, 2005 Observational; Prospective; 484 No Present during 72 hours prior to the 9.3% of lacunar
case series 1 hospital ischemic stroke initiating infarctions
Hansen, 2012 Observational; Prospective; 299 No Not reported 33.5% of strokes
prospective 1 hospital (including hemorrhagic
cohort stroke)
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Headache Currents

Table 1.—Continued

Diagnostic
Criteria of the Definition of Headache Related to
Study Study Design Data Collection N ICHD Stroke or TIA Prevalence of Headache
Kropp, 2013 Observational; Prospective, 4431 No Not reported 31.5% of ischemic strokes
cross-sectional multicentric (aged 18 and TIAs
to 55)
Chen, 2013 Observational; Prospective, 11523 Yes ICHD 7.4% of ischemic strokes
retrospective multicentric
cohort
Maino, 2013 Observational; Prospective, 2473 No Headache occurring simultaneously 17% of ischemic strokes
prospective multicentric with ischemic stroke or TIA and TIAs (analyzed
cohort together)
Abadie, 2014 Observational; Prospective 1185 No Headache initiates immediately 13.5% of ischemic strokes
retrospective before or immediately after
cohort ischemic stroke signs begin
Aghangar, Observational; Prospective, 263 Yes ICHD (only considered headache 18.6% of ischemic
2015 case series multicentric that lasted more than 24 hours) strokes
Pollak, 2015 Observational; Prospective, 2001 No Present on admission or during the 8.4% of ischemic strokes
case series multicentric first day in hospital 28% of TIAs
ICHD = International Classification of Headache Disorder; TIA = transient ischemic attack.

determine from the methodology whether the definition of
headache attributed to ischemic stroke was in accordance with
ICHD criteria. It is likely that the frequency of headache at-
tributed to ischemic stroke was underestimated, since patients
with a lower level of consciousness and/or aphasia are usually
excluded from studies.3 For headaches attributed to TIA, there
was a prevalence ranging from 26% to 36%.6,12,22,23
Headaches with ischemic stroke are significantly more frequent
in younger patients.7,16 Abadie et al. analyzing data from 1185
ischemic stroke patients included in the Dijon Stroke Registry in
France, found a lower average age among those who had head-
ache (67.1 ± 19.6 vs 77.0 ± 13.9 years; P < .001).7 Tentschert et al.
analyzing data from 2196 ischemic stroke patients included in
the Vienna Stroke Registry, found a lower age among those who
had headache (median: 65 vs 70; P < .001). Age remained signif-
icant after controlling for confounding variables.16
A single study demonstrated a significantly higher occurrence
of headache in female gender (OR: 1.3, 95% CI: 1.1-1.6).16
However, other studies revealed an equal involvement of both
sexes.5,7,15 Only 2 of these studies performed a multivariate anal-
ysis to see which characteristics were related to headache, and
they found divergent results. One group of investigators found
an association between occurrence of headache and female sex
with a small effect of gender (OR: 1.3; 1.1-1.6). The other study
included a smaller number of patients (182 vs 2196) and could
not have detected this difference.15,16 The association between
female gender, lower age group, and headache was reported
when only patients with lacunar infarctions were assessed.13
Patients with a prior history of migraine were more likely to
present with headache attributed to ischemic stroke in 2 studies.
In these studies, migraine remained a risk factor in multivari-
ate analysis (OR: 6.7, 95% CI: 1.4-31.2);15 and (OR: 1.7, 95%
CI: 1.3-2.2).16 In 1 study, the presence of prior medical history of
angina and myocardial infarction were also associated with the
presence of headache attributed to ischemic stroke with an OR
1.56 (95% CI: 1.17-2.10) and 1.42 (CI 95%: 1.06-1.90), respec-
tively.5 This association was not reported by another study.15
A prior diagnosis of systemic arterial hypertension was sig-
nificantly associated with a lower incidence of headache at-
tributed to ischemic stroke in 2 studies.5,14 One of these studies
included 3126 patients from the Dutch TIA Trial. There was a
question about headache in this trial. However, the definition
of headache attributed to stroke is not provided in the method-
ology.5 The other study, performed by Mitsias et al. included
546 patients from a single center.14 These r­ esults were not con-
firmed by Tentschert et al. (paper previously described in this
section).16 All these studies performed multivariate analysis. We
consider the study performed by Mitsias et al. the “better evi-
dence,” because this study provided a clear definition of “head-
ache attributed to stroke” in the methodology.
4 | Headache | Month 2019
Some characteristics of a stroke are associated with head-
ache. Headache is significantly more frequent in larger isch-
emic lesions (OR: 2.62 for infarctions that affect more than
half a lobe),10 in ischemic stroke of the vertebrobasilar sys-
tem,10,12,15,17 and in ischemic stroke with cortical versus subcor-
tical involvement.5,12
The frequency of headache in small vessel cerebrovascular dis-
ease (lacunar infarction) ranges from 5% to 23%.5,11,13,15,17,24-26
This kind of stroke has a lower frequency of headache when
compared with other etiologies.5,11,15,17 There was no difference
in frequency of headache between cardioembolic and athero-
thrombotic large vessel infarctions.15,17
In studies in which only lacunar infarctions were analyzed,
infarctions accompanied by headache were significantly
more frequent in the deep gray matter or in the brainstem,
mainly in the midbrain, than in infarctions in the supra-
tentorial white matter. The vertebrobasilar system is more
densely innervated by trigeminovascular system than the ca-
rotid system, and this may contribute to this difference of
frequency.13,24
PATHOPHYSIOLOGY
The pathophysiology of headache attributed to ischemic
stroke and TIA has not as yet been well established. The ath-
erosclerotic process is painless, and the cerebral parenchyma
and intraparenchymal blood vessels are insensitive to painful
stimuli.27 In extensive cerebral infarctions with mass effect and
structural herniation, the displacement and compression of
pain-sensitive structures such as the meninges and the proxi-
mal segment of the intracranial arteries may cause headache.
However, this does not apply to most cases, especially when
consciousness is preserved, and other pathophysiological expla-
nations are necessary.
One of the main hypotheses suggests a pathophysiology
involving cortical spreading depression (CSD) triggered by
cerebral ischemia, with the consequent activation of the trigem-
inovascular system. Spreading depolarization has already been
detected in patients with malignant ischemic stroke28 and with
delayed ischemic stroke after aneurismal subarachnoid hemor-
rhage.29 The fact that migraineurs, those with larger ischemic
strokes, and those with cortical strokes are more likely to pres-
ent headache attributed to ischemic stroke suggests CSD par-
ticipation in the pathophysiology of this headache. However,
headache often occurs in very close temporal relation with the
stroke onset. It would have been expected that there would
be a delay between CSD and headache. It is also difficult to
­explain with this model those headaches secondary to lacunar
Headache Currents
infarction and the fact that headache is significantly more
frequent in vertebrobasilar strokes.
Trigeminovascular innervation is denser in the posterior
circulation. This could contribute to the higher prevalence of
headache in ischemic stroke in this topography.30-33
The release of prothrombotic, inflammatory, and excito-
toxic substances during the acute phase of an ischemic stroke
may cause headache. Serotonin and prostaglandins are released
during the process of platelet aggregation.8 A positive correla-
tion between the cerebrospinal fluid levels of glutamate, nitric
oxide, and interleukin-6, and the presence of headache and
neurological deterioration in the acute phase of ischemic stroke
has been demonstrated. The levels of these substances would
be markers of severity, and the presence of headache could be
secondary to the presence of these substances.8,30
The ischemia of structures associated with physiological
pain processing and involved in the generation of clinical
pain conditions may also be important in the pathophysi-
ology of headache. A study comparing a group of ischemic
stroke patients with and without headache by mapping the
topography of the lesion with magnetic resonance imaging
(MRI) demonstrated a higher probability of headache in the
ischemic lesions in the insular cortex, particularly in the an-
terior region.34 The insular cortex is involved in the process-
ing of painful and as non-painful somatosensory inputs,35,36
and its anterior part seems to participate in the emotional
and attentional processing of pain.37,38 An association was
also reported between headache and ischemic lesions in the
somatosensory cortex and in the cerebellum.34 Insula and
somatosensory cortex also participate of pathophysiology
­
of migraine.39 The authors suggest that headache in stroke
might be centrally driven.34
In an MRI voxel-base mapping study, Seifert et al demon-
strated an association between the location of the infarction and
the characteristics of the headache, such as intensity (posterior
insular cortex, cerebellum, and temporal operculum), nausea
(middle and superior occipital lobe, lateral thalamus, and cere-
bellum), cranial autonomic symptoms (middle temporal cortex,
superior parietal lobe, and postcentral gyrus), and phonophobia
(cerebellum).40
Headache may persist for more than 3 months after ischemic
stroke. When this occurs, the diagnosis is “Persistent Headache
attributed to past ischemic stroke.”4 The pathophysiology for
this phenomenon is not well understood. Nociceptor inputs
after stroke may lead to a process of central sensitization and
may consequently favor persistence of the pain.41 We speculate
that, as a consequence of the organization of the infarction, there
may be structural changes that causes stretching of pain sensitive
5 | Headache | Month 2019
Headache Currents

Table 2.—Characteristics of Headaches Attributed to Strokes (Including Studies With Ischemic and Hemorragic Strokes)

Temporal
Speed of Relation With Characteristics Duration of Location of
Study N Development Focal Signs of Headache Intensity Headache Headache
Portenoy, 1984 215 (including 50 50% sudden† 60% before† 50% — — 50% unilateral†
hemorrhagic throbbing†
stroke)
50% gradual 25% together 28% bifrontal
15% after
Vestergaard, 238 (including 24 — 43% before† 63% pressure- 38% severe† — 41% bifrontal†
1993 hemorrhagic like†
stroke)
30% together 15% throbbing 25% moderate 36% unilateral
(70% ipsilateral to
stroke)
27% after 8% stabbing 18% mild
†
Arboix, 1994 240 (including 45 — 10% before 65.5% Incapacitating in 29.5 hs in —
hemorrhagic throbbing† 26% of ischemic cardioembolic
stroke) strokes‡ strokes‡
14.5% 26.5 hs in
pressure-like thrombotic
strokes
17 hs in TIAs
19.5 hs in
lacunar
infarctions
Tentschert, 2196 — — 66% pressure- — — 61% bilateral‡
2005 like‡
20% stabbing 39% unilateral
(65% ipsilateral
for ischemic
strokes)
8% throbbing
4% burning
2% circular
Verdelho, 2007 124 (including 48 21% sudden† 26% before† 53% pressure- 45% severe† 3.8 days† 55% bilateral†
hemorrhagic like†
stroke)
19% gradual 30% together 24% throbbing 39% moderate 42% unilateral
60% don’t 27% after 5% stabbing 13% mild
remember
10% others 3% unknown
8% unknown
Arboix, 2005 484 (only lacunar — 7% before‡ 80% pressure- — — —
infarctions) 93% together like‡
6 | Headache | Month 2019
Table 2.—Continued
Temporal
Speed of Relation With Characteristics
Study N Development Focal Signs
Seifert, 2016 41
TIA = transient ischemic attack; VAS = visual analog scale.
†
Including ischemic and hemorrhagic strokes.
‡
Only ischemic strokes.
structures and may also disrupt central pain pathways localized
in brainstem, insula, or somatosensory cortex. Comorbid de-
pression, fatigue, and sleep apnea may also play a role.42
CLINICAL CHARACTERISTICS OF HEADACHE
ATTRIBUTED TO ISCHEMIC STROKE
Table 2 summarizes the main clinical features of headache
attributed to ischemic stroke. Some of the papers cited in this
table contain mixed series (hemorrhagic and ischemic strokes).
Few studies have described the characteristics of headache
attributed to stroke. The pain was described as pressure-like in
14.5% to 66% and as throbbing in 8% to 80% of cases.12,16,34
Mild to moderate pain intensity is more frequent, but can be
incapacitating in 26% of cases with ischemic stroke. Headache
is more severe with posterior circulation ischemic strokes.12,21
Nausea was reported in 28%,34,40 and vomiting in 6.5% of
­patients with headache.12 Photophobia and phonophobia were
found in 24% of cases.34 Headache was unilateral in 39% of
patients, being ipsilateral to cerebral infarction in 65% of these
cases.16 Occipital headache has a sensitivity of 15% and specificity
of 88% for posterior circulation stroke.15 In lacunar infarctions,
the headache was described by most patients as having started at
the same time as the focal neurologic deficit, and was described as
mild, poorly localized, and with a pressure-like pain.13,24
THE TEMPORAL DEVELOPMENT OF
HEADACHE ATTRIBUTED TO STROKES
The mean duration of pain was 19.5 hours in lacunar in-
farctions, 29.5 hours in cardioembolic ischemic stroke, and
26.5 hours in infarctions secondary to large artery atheroscle-
rosis12 One study prospectively evaluated 124 stroke patients
Headache Currents
Duration of Location of
of Headache Intensity Headache Headache
80% pressure- 4.9 (±2.5) mean pain 67% frontal‡
like; intensity on VAS‡
16% throbbing 63% temporal
10% stabbing 53% occipital
31% nuchal
69% diffuse
(including 39% of hemorrhagic strokes) for 8 days. The mean
duration of headache was 3.8 days. The onset of headache on
the day the stroke initiated occurred in 87% of the patients, and
in the remaining patients, onset occurred between days 2 and 5.
The headache mostly behaved in a continuous manner, but de-
creased in frequency and intensity over the days.21
Few studies evaluated persistent headache attributed to a
prior ischemic stroke. One study that followed 275 patients for
6 months after the stroke (90.5% had ischemic stroke) reported
persistent headache attributed to stroke in 23% of patients after
3 months and in 23.4% after 6 months. Headache was consid-
ered a new pain by 15.3% of patients at 3 months and by 13.1%
of patients at 6 months.20 This new headache was characterized
predominantly as a pressure-like headache (44.4% on admis-
sion, 43% at 3 months, and 58.6% at 6 months). The headache
did not worsen with movement in 73.8% and 66.7% at 3 and
6 months, respectively.20
About 216 of these patients were contacted 3 years after their
stroke and 7.2% still reported a persistent headache. In 18.8%
of these patients, the headache occurred daily.43 There are no
clinical trials on the pain management or prophylactic treat-
ment of persistent headache attributed to ischemic stroke.
HEADACHE RELATED TO ISCHEMIC STROKE
AS A MARKER OF SEVERITY
In a retrospective cohort study conducted in Taiwan with
11,523 adults who had suffered an ischemic stroke, the presence
of headache was associated with a better prognosis. Those with
headache had a lower frequency of in-hospital deterioration (5.5
vs 8.4%, adjusted RR 0.62, 95% CI 0.52-0.78, P < .001), of
neurological worsening (4.5 vs 6.7%, adjusted RR 0.64, 95%
7 | Headache | Month 2019
CI: 0.52-0.79, P < .001) and of medical complications (0.4 vs
0.9%, adjusted RR 0. 13, 95% CI: 0.08-0.21, P < .001), as well
as a better neurological recovery as measured by the National
Institutes of Health Stroke Scale (0.08 vs 0.2; P = .02). The
prognosis was also measured by the modified Rankin Scale, in
which the proportion of patients presenting with values from
0 to 2 (better prognosis) was higher in patients with headache
in the first month after ischemic stroke (adjusted RR 0.85, 95%
CI 0.72-0.95, P < .05). Such an association was not maintained
at 3 and 6 months after the event.17
Another study also reported an improved prognosis in ­patients
with headache during ischemic stroke or TIA. This prospective
cohort with 2473 patients monitored over a median period of
14.1 years observed a lower chance of vascular death in these
­patients (adjusted HR 0.73; 95% CI 0.68-0.91). However, in
this same study, the chance of a cerebrovascular event and myo-
cardial infarction reoccurring was similar between the groups
with and without headache.44 This cohort study was not orig-
inally designed to assess headache as a prognostic factor. In
addition, only minor ischemic strokes were included, which
compromises its generalizability. Another retrospective cohort
of 1185 stroke patients reported no association between the
presence of headache attributed to ischemic stroke and mortal-
ity at 30 days (RR: 1.01; 95% CI 0.53-1.92; P = .97).7
One prospective study linked headache with a poorer prog-
nosis. A Spanish cohort of 241 stroke patients was prospectively
assessed using the Canadian Stroke Scale, during the first 48
hours of hospital admission. The presence of headache was
significantly associated with an early neurologic deterioration
(OR 16.01, 95% CI 5.40-47.48; P < .001, logistic regression).8
Because of its design, this study is the best evidence that head-
ache is associated with a worse prognosis of stroke.
All studies described in this review may have methodologi-
cally been limited by selection bias, as more severe patients who
have altered levels of consciousness or those with aphasia could
not provide information on the presence of headache. Thus,
patients with poor prognosis were not included. These studies
did not control for any effect of migraine on the prognosis of
stroke. Studies on ischemic depolarization suggested that mi-
graineurs could have an accelerated loss of viable tissue in the
area at risk for infarction.45 Also, different follow-up periods
and endpoints used make it difficult to compare the studies.
KEY CONCLUSIONS
1. Headache attributed to ischemic stroke is frequent (7.4%–34%)
and has a greater chance of occurring in younger patients,
in migraineurs, in larger ischemic lesions, in vertebrobasilar
strokes, and in ischemic stroke with cortical involvement.
Headache Currents
2. The most common pattern of headache attributed to stroke
is mild to moderate bilateral pain, not associated with nau-
sea, vomiting, photophobia, or phonophobia. This headache
usually improves over time, but around one-fifth of patients
develop a persistent headache attributed to stroke.
3. There are no clinical trials on pain management or prophy-
lactic treatment of persistent headache attributed to ischemic
stroke, requiring further studies on the subject.
4. There are conflicting data on headache as a predictor for
prognosis in the acute phase of the stroke, requiring further
studies on the subject.
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