Anda di halaman 1dari 11

Review Article

Diagnosis and
Address correspondence to
Dr Shelagh Coutts, Foothills
Medical Centre, 1403 29th St
NW, C1242, Calgary, AB,
Canada T2N 2T9,
scoutts@ucalgary.ca.
Relationship Disclosure:
Management
Dr Coutts receives
research/grant support from
the Canadian Institutes
of Transient
of Health Research
(CRH-112319), the Heart
and Stroke Foundation of
Canada (G-16-00012585),
Ischemic Attack
and Genome Canada Shelagh B. Coutts, MD, MSc, FRCPC
(143TIA-Penn).
Unlabeled Use of
Products/Investigational
Use Disclosure: ABSTRACT
Dr Coutts reports no disclosure. Purpose of Review: This article reviews the diagnosis, investigation, and recom-
* 2017 American Academy mended management after a transient ischemic attack (TIA) and discusses how to
of Neurology.
make an accurate diagnosis, including the diagnosis of mimics of TIAs.
Recent Findings: Up to a 10% risk of recurrent stroke exists after a TIA, and up to
80% of this risk is preventable with urgent assessment and treatment. Imaging of
the brain and intracranial and extracranial blood vessels using CT, CT angiography,
carotid Doppler ultrasound, and MRI is an important part of the diagnostic assess-
ment. Treatment options include anticoagulation for atrial fibrillation, carotid revas-
cularization for symptomatic carotid artery stenosis, antiplatelet therapy, and vascular
risk factor reduction strategies.
Summary: TIA offers the greatest opportunity to prevent stroke that physicians
encounter. A TIA should be treated as a medical emergency, as up to 80% of strokes
after TIA are preventable.

Continuum (Minneap Minn) 2017;23(1):8292.

INTRODUCTION rologic signs or symptoms referable


Transient ischemic attack (TIA) and to known cerebral arterial distributions
minor ischemic stroke are associated without direct measurement of blood
with brain dysfunction in a circum- flow or cerebral infarction. It is impor-
scribed area caused by a regional re- tant to note that TIA and stroke repre-
duction in blood flow (ie, ischemia), sent different ends of an ischemic
resulting in either transient or minor continuum from the physiologic per-
observable clinical symptoms. Identi- spective, but clinical management is
fication of ischemia is important as similar. The historical time-based defi-
20% of patients with ischemic stroke nition of TIA was based on full resolu-
present with a TIA in the hours to days tion of all symptoms within 24 hours
preceding the stroke.1,2 Up to 80% of of onset. The time-based definition has
strokes after TIA are preventable; thus, been debated in light of diffusion-
early diagnosis and treatment are key. weighted MRI demonstrating relevant
ischemic lesions in 30% to 50% of
DEFINITION AND CLINICAL patients fulfilling the time-based defi-
DIAGNOSIS nition of TIA (Case 4-1).3,4 It is also
The clinical definitions of TIA and is- relevant that the diagnoses of TIA
chemic stroke are based on focal neu- and minor stroke are commonly used

82 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


KEY POINT

Case 4-1 h Minor ischemic stroke


and transient ischemic
A 57-year-old man presented with
attack should be
a 2-minute episode of left hand
managed similarly.
weakness. During the episode, his
left hand became unusable and he
could not pick anything up; he was
able to lift his arm, although it felt
weak. He was able to walk and talk
normally throughout the episode.
On presentation to the emergency
department, he was completely
back to normal. Head CT and CT
angiogram were normal. However,
the diffusion-weighted MRI
showed a small lesion in the right
hemisphere consistent with his
symptoms (Figure 4-1).
Comment. This case illustrates
that transient neurologic symptoms FIGURE 4-1 Diffusion-weighted MRI
can be associated with evidence of showing restricted
diffusion in the
ischemia on diffusion-weighted right hemisphere.
brain MRI sequences. As many
as 50% of patients clinically
diagnosed with a transient ischemic attack using a time-based definition
have evidence of restricted diffusion on an acute MRI scan.

interchangeably and recorded as such nitions of stroke and TIA is that they
in medical records. Although this article rely on the presumed cause of the symp-
focuses primarily on TIA, a significant toms: ischemia. Symptoms are attrib-
difference in the outcome of TIA com- uted to ischemia based mainly on the
pared to minor ischemic stroke has not time course of the deficits (an acute
been demonstrated by compelling evi- deficit is more consistent with ische-
dence. Treatment to prevent ischemic mia), the distribution of the deficits,
stroke following TIA and treatment to and background risk factors for ische-
prevent recurrent stroke following mia in the patient. Because patients
minor ischemic stroke are also similar. vary in reliability in reporting the events
Very early assessment of these patients they have experienced, even an astute
also makes the distinction between TIA physician may find it challenging to
and minor ischemic stroke difficult. make a certain diagnosis based on the
The diagnosis of TIA depends on history and physical examination alone.
the quality and quantity of information Even experts do not agree about which
available and the time of assessment. clinical events are in fact TIAs.5Y7
The main criteria used are the clinical One of the problems with assessment
history or objective findings on neuro- is that half of all patients presenting to
logic examination consistent with focal emergency departments and physicians
neurologic dysfunction at some point offices in North America with transient
of the evaluation and imaging of the or mild neurologic deficits have symp-
brain. A limitation of the clinical defi- toms with an uncertain diagnosis or

Continuum (Minneap Minn) 2017;23(1):8292 ContinuumJournal.com 83

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


Transient Ischemic Attack

KEY POINT
h Making the correct prognosis. Some have, indeed, had an Although the proportion of patients
diagnosis of transient ischemic event, but others have had with true ischemia is lower in those
ischemic attack is key, symptoms related to a stroke or TIA without motor or speech symptoms,
as 50% of patients mimic, such as migraine, epilepsy, multi- it is important not to miss patients
assessed for possible ple sclerosis, or peripheral nerve en- with true TIAs and minor ischemic
transient ischemic trapment (Case 4-2). The prevalence strokes.10,11
attack will have an of these mimics is higher among clin-
alternative diagnosis ical presentations without motor and TAKING A HISTORY FROM A
(ie, are a mimic). speech symptoms. Motor and speech PATIENT WITH A POSSIBLE
symptoms may have a higher likeli- TRANSIENT ISCHEMIC ATTACK
hood of brain ischemia as the cause The diagnosis of TIA remains largely
of the symptoms because the differ- clinical and is based on taking an
ential diagnosis for such clinical pre- accurate history. This contributes to
sentations is much narrower, and the variability in the diagnosis of TIA,
patients who present with motor or with high rates of disagreement seen
speech symptoms are known to be at even between neurologists.5 As many
high risk for recurrent stroke.8 However, as 60% of patients referred to a TIA
patients who present with symptoms clinic will not have a final diagnosis
other than motor and speech symp- of TIA.12,13 Identification of possible
toms (eg, sensory symptoms or dizzi- TIA mimics is an important stage in
ness) have a more uncertain etiology.9 the assessment of patients with tran-
This is likely related to the higher sient neurologic symptoms. An accu-
probability of a nonischemic cause of rate diagnosis of a stroke mimic impacts
symptoms in these patients. Posterior treatment decisions and provides reas-
circulation ischemia can pose an ad- surance when the diagnosis is some-
ditional diagnostic challenge as symp- thing more benign than TIA.
toms are more variable than those that The clinical history is most accurate
occur with hemispheric ischemia.10 when taken close to the resolution of

Case 4-2
A 75-year-old man presented to the emergency department after
experiencing a 10-minute episode of right hand weakness 2 hours earlier,
after which he completely returned to normal. He had no significant
past medical history and was on no medications. Neurologic examination
was normal. Urgent brain CT showed a left-sided chronic subdural
hematoma. He was referred for neurosurgical assessment.
Comment. Many different mimics of transient ischemic attack exist, as in
this case. Hemorrhage is a rare, but important, cause of transient neurologic
symptoms. This case highlights the recommendation that all patients with
transient neurologic symptoms should have brain imaging not only to look
for ischemia but also to look for other causes of transient neurologic
symptoms. It also emphasizes the fact that clinically one cannot reliably
diagnose brain hemorrhage; brain imaging is necessary to differentiate
between ischemia and hemorrhage. Subdural hematomas are common in
the elderly and may occur spontaneously without a history of trauma. The
mechanism behind why subdural hematomas can present with transient
neurologic symptoms is not entirely clear, but theories include mechanical
compression of vessels, partial seizures, or spreading cortical depression.

84 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


KEY POINT
the event. Accuracy is also best when the exception of symptomatic large h Atrial fibrillation is a
the patient first reports symptoms com- vessel occlusive disease, recurrent ste- common cause of
pared to the history obtained after the reotyped events raise the possibility of transient ischemic attack
patient has provided multiple itera- an alternative diagnosis (eg, seizure). and ischemic stroke.
tions to medical personnel.
A TIA is a clinical syndrome charac- INVESTIGATIONS
terized by the sudden onset of a focal A full neurologic and cardiac exami-
neurologic deficit presumed to be on nation should be completed on all
a vascular basis. As the definition patients with suspected TIA. Blood
implies, key points of the history need pressure, pulse rate, and oxygen satu-
to be elicited from the patient. Imaging ration should be obtained, and an ECG
can support the diagnosis, but TIA is should be performed to evaluate for
primarily a clinical diagnosis. Descrip- atrial fibrillation. Many patients will also
tors such as numb, dead, heavy, require an echocardiogram and some
or weak may have different mean- form of extended cardiac monitoring
ings for different patients and require if no definitive cause is found for the
clarification, similar to the different TIA. For more information about as-
meanings patients may have for dizzy. sessment for a cardiac source of emboli,
The most important clinical determina- refer to the article Cardioembolic
tion is whether the neurologic symp- Stroke by Cumara B. OCarroll, MD,
toms are focal or nonfocal. Regional MPH, and Kevin M. Barrett, MD, MSc,14
cerebral ischemia causes focal symp- in this issue of Continuum.
toms. Focal neurologic symptoms usu- Routine blood work should also be
ally affect one side of the body (eg, completed on all patients, including:
weakness or sensory abnormality on & Complete blood count to measure
the right or left side). Nonfocal neuro- total hemoglobin and screen for
logic symptoms include generalized anemia or erythrocytosis as a cause
weakness, light-headedness, fainting, of TIA. Platelet count is relevant
blackouts, and bladder or bowel symp- as thrombocytosis is a potential
toms. Although patients with the cause of TIA.
nonfocal symptoms of syncope or & Coagulation screen (partial
presyncope are sometimes referred thromboplastin time, international
for assessment of possible TIA, loss of normalized ratio [INR]) as, rarely,
consciousness is only very rarely a disorders of coagulation can
symptom of stroke or TIA. present as a TIA. In specific clinical
After clarifying the patients symp- circumstances, more detailed
toms, the circumstances of the event screening bloodwork, including
should be determined. What was the a thrombophilia screen, may
patient doing at the time? Have the be advised.
symptoms occurred before? Was & Blood glucose, as hypoglycemia
the onset sudden or gradual? A vascu- and hyperglycemia are important
lar event usually has a sudden onset, potential mimics of a TIA.
with the deficit being maximal at the Hypoglycemia, in particular, needs
time of onset. A slow gradual migra- to be recognized and treated quickly.
tion of symptoms from one body part Fasting lipids and glucose need to
to another is frequently a symptom of be assessed as well, but these are often
a migrainous event. Whether or not obtained after the first visit. Although
the symptoms have happened before most patients will have a single diag-
is an important consideration. With nosis, diagnostic tests such as ECG and

Continuum (Minneap Minn) 2017;23(1):8292 ContinuumJournal.com 85

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


Transient Ischemic Attack

KEY POINT
h All patients with possible oxygen saturation can be useful to iden- rospectively recorded clinical features
transient ischemic attack tify the occasional patient who has of TIA associated with a higher risk of
require structural two concurrent diagnoses, such as TIA stroke are motor or speech symptoms
imaging of the brain to and pulmonary embolus or a myocar- and long duration. The total ABCD2
rule out mimics. dial infarction. score ranges from 0 to 7, with points
After basic investigations are com- given for five clinical factors: (1) age
pleted, brain imaging is key. In many 60 or older (1 point); (2) blood pres-
parts of the world, the first point of sure 140/90 mm Hg or higher (1 point);
assessment for patients with possible (3) clinical features of unilateral weak-
TIA is the emergency department; in ness (2 points) or speech impairment
this setting, a noncontrast CT scan of without weakness (1 point); (4) dura-
the brain is usually the first imaging tion of symptoms 60 minutes or more
study obtained. This is a key investi- (2 points) or 10 to 59 minutes (1 point);
gation as it rules out structural causes and (5) presence of diabetes mellitus
for the symptoms, such as subdural (1 point). The ABCD2 score was well
hematoma (Case 4-2), intracranial hem- validated on independent cohorts
orrhage, or brain tumor. with areas under the curve of 0.62 to
0.83 (0I5 = chance prediction and
PROGNOSIS 1I0 = perfect prediction). More im-
About 10% of patients presenting with portant, this score allowed stratifica-
TIAs or minor strokes will have a stroke tion of patients into high risk (score 6
within the next 90 days,8,15,16 with or 7, 8.1% 2-day risk of stroke), mod-
the highest risk period being the first erate risk (score 4 or 5, 4.1% 2-day risk
24 hours.17 Wide consensus exists that of stroke), and low risk (score 0 to 3, 1%
TIA and minor ischemic stroke are 2-day risk of stroke).
medical emergencies that necessitate The ABCD2 score has emphasized
immediate management.18 that taking a detailed history is impor-
tant, and it has raised awareness
Clinical/Event Features within the general medical community
and Scores that recognizing TIA is an important
Certain clinical features have been as- way of preventing stroke. However,
sociated with recurrent stroke after TIA. the problem with the ABCD2 score is
These include diabetes mellitus,8 hy- that patients in the low-risk category
pertension,19,20 symptom duration, and still have recurrent strokes.22 Also, in
weakness or speech disturbance.8,20 terms of absolute numbers, the majority
Using a combination of factors, clinical of recurrent strokes are in the moderate
risk stratification tools have been de- category. Some patients who are classi-
veloped to help identify patients at fied as having low risk on the ABCD2
high risk of recurrent events, includ- score may have important potentially
ing the California,8 ABCD (age, blood treatable TIA etiologies, such as symp-
pressure, clinical features, duration),20 tomatic carotid artery stenosis or atrial
and ABCD2 (which adds the presence fibrillation, that require urgent treat-
of diabetes mellitus to the factors mea- ment.23 These limitations have pre-
sured in ABCD)21 scores,with the aim vented widespread adoption of the
of determining the need for urgent ABCD2 score to triage patients with TIA.24
hospitalization and investigation. These The Rotterdam Study25 followed
scores were mostly developed with ret- patients with transient neurologic at-
rospective data. From these studies,8,20 tacks for 10 years and found an
it was determined that the major ret- increased risk of stroke not only in
86 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


KEY POINT
patients with focal symptoms (ie, pos- normal imaging being assessed as out- h Urgent imaging using
sible TIAs) but also in patients who had patients.29 Other modalities for imaging CT/CT angiography can
transient episodes of nonspecific cervicocephalic vessels, such as mag- identify patients at high
symptoms. It is likely that these pa- netic resonance angiography (MRA), risk for recurrent stroke.
tients represent a heterogeneous are also acceptable. Carotid duplex
group with variable risk of recurrent ultrasound is an additional noninva-
stroke. It is therefore timely for the sive modality commonly used to eval-
neurologic community to progress be- uate for hemodynamically significant
yond the ABCD2 score to improve our carotid occlusive disease at the bifur-
ability to define the clinical outcome of cation. Identification of high-grade
patients on an individual basis. Poste- stenosis in the carotid artery ipsilateral
rior circulation events, in particular, to retinal or hemispheric symptoms
can cause nonspecific symptoms.26 may be indicative of stroke mecha-
nism and near-term stroke risk. Carotid
Imaging and Prognosis ultrasound does not adequately evalu-
Evidence of an acute infarct on a ate the carotid circulation beyond the
noncontrast CT alone has been shown bifurcation (ie, distal cervical and in-
to be predictive of recurrent stroke in tracranial segments), and additional
patients with TIA (ie, patients whose vascular imaging modalities may be
symptoms had resolved), although the necessary when the index of clinical
proportion of patients with evidence suspicion is high for vertebrobasilar or
of acute infarcts was small (4%).27 Pa- intracranial occlusive disease.
tients with minor ischemic stroke and Brain imaging using MRI is a very
TIA who are at the highest risk of re- sensitive way of assessing for brain is-
current events and disability can be chemia. Diffusion-weighted imaging
identified using noninvasive CT angi- (DWI), which shows the abnormal dif-
ography (CTA).28 CTA is a quick and fusion of water in the setting of focal
easy addition to the noncontrast CT brain ischemia, is the most helpful se-
that is completed on most patients and quence. Up to 50% of patients clinically
provides much more information than diagnosed with a TIA using a time-
a noncontrast CT alone, with imaging of based definition have evidence of re-
the intracranial and extracranial vessels. stricted diffusion on an acute MRI scan.
The addition of better imaging tech- Most studies of recurrent stroke after
niques, such as multiphase CTA and TIA have shown an increased risk of
CT perfusion, provides the ability to short-term recurrent stroke in the pres-
identify more distal occlusions than ence of a lesion seen on DWI. How-
previously. Evidence of 50% or greater ever, the exact magnitude of the risk
stenosis or occlusion in a symptom- depends on the population studied.
relevant vessel in the intracranial or Whether the presence or absence of a
extracranial circulation puts a patient lesion on DWI changes the longer-term
at high risk of a recurrent stroke.28 (1- to 5-year) risk of stroke is less clear.
Understanding the pathophysiology of The lesion pattern on an MRI can
a TIA or minor ischemic stroke is par- change the vascular localization in up
amount to preventing recurrent stroke. to one-third of patients. Infarct topog-
Using CT/CTA to assess patients in the raphy can also be useful to inform
emergency department has allowed stroke mechanism (eg, involvement of
many patients to be safely triaged, with more than one vascular territory being
patients with abnormal CT/CTA admit- suspicious for a proximal embolic
ted for observation and those with source such as atrial fibrillation).
Continuum (Minneap Minn) 2017;23(1):8292 ContinuumJournal.com 87

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


Transient Ischemic Attack

KEY POINTS
h Although the presence Many stroke neurologists find MRI tients get the appropriate early assess-
of a lesion seen on particularly helpful in cases in which ment and treatment (Table 4-130).
diffusion-weighted the diagnosis is not 100% clear based
imaging can be helpful on the history. MRI results must TREATMENT
by proving that ischemia always be taken in the appropriate Recognition and management of TIA
occurred, the absence clinical context. Most stroke neurolo- offers the greatest opportunity to pre-
of a lesion does not rule gists would agree that patients who vent disabling stroke. Studies have
out ischemia. have a negative DWI but have truly shown up to an 80% reduction in the
h Finding out why a had TIAs clearly exist, and thus they risk of stroke after TIA with the early
transient ischemic will treat patients for TIA even with a implementation of secondary stroke
attack occurred is the negative DWI. There has been some prevention strategies,11,12 including
key to preventing a discussion over the past few years revascularization of patients with
recurrent stroke. about calling transient symptoms a symptomatic carotid artery stenosis,
h Recognition and clinical TIA, but calling symptoms in anticoagulation of patients with atrial
management of combination with a lesion seen on fibrillation, treatment with anti-
transient ischemic attack DWI a stroke. From a practical per- platelet agent(s), treatment with
offers the greatest spective, it does not matter what it is statins for most patients, manage-
opportunity to prevent called; what is important is that pa- ment of hypertension, and lifestyle
disabling stroke.

TABLE 4-1 Clinical and Imaging Features That Increase the Risk
of a Recurrent Stroke or Symptom Progression After
Transient Ischemic Attack or Minor Strokea

High Risk Low Risk


Feature
Timing Hours ago Weeks ago
Age (years) 960 G45
Blood pressure at presentation (mm Hg) 9140/90 G140/90
Diabetes mellitus Yes No
Symptoms Speech, weakness Dizziness,
numbness
Duration (minutes) 960 G10
Frequency of events One or few Many
Degree of clinical improvement Vanishing severe Improving
deficit mild deficit
Intracranial stenosis Severe None
Extracranial stenosis Present Absent
Intracranial occlusion Present Absent
Diffusion-weighted imaging lesion Multiple greater None
than single
Transcranial Doppler emboli detection 950 None
(microembolic signals/hour)
a
Modified with permission from Couillard P, et al, Expert Rev Cardiovasc Ther.30 B 2009 Taylor & Francis.
tandfonline.com/doi/full/10.1586/erc.09.105.

88 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


interventions, such as smoking ces- All patients with TIAs should be
sation or weight loss. on an antiplatelet agent, except for
Early carotid revascularization for pa- those who are being anticoagulated
tients with 50% or greater symptomatic for atrial fibrillation. For most pa-
carotid artery stenosis is an effective tients, it will be a single antiplatelet
form of stroke prevention when per- agent, usually aspirin monotherapy
formed within the first 2 weeks after (81 mg/d to 325 mg/d). Other op-
an event. If a patient is stable, surgery tions include 75 mg/d clopidogrel or
should be performed as soon as pos- a combination of 25 mg aspirin and
sible (Case 4-3). It is important to iden- 200 mg extended-release dipyridamole
tify carotid stenosis because, although 2 times a day.29
it causes only 10% of all TIAs, it causes Two randomized clinical trials have
50% of early recurrences. It is a treatable provided evidence for the short-term
condition, and it is tragic when a re- use of dual antiplatelet therapy after
current stroke occurs in someone wait- TIA and minor ischemic stroke. The Fast
ing for a carotid endarterectomy. Assessment of Stroke and Transient

Case 4-3
A 50-year-old man presented to the emergency department with an episode
of left hemiplegia that lasted 5 minutes. He smoked cigarettes but otherwise
had no significant past medical history. His examination was normal, with
blood pressure of 125/75 mm Hg and an ABCD2 (age, blood pressure, clinical
features, duration,
presence of diabetes
mellitus) score of 2.
Head CT was normal,
but CT angiography
showed a high-grade
stenosis of the right
internal carotid artery
(Figure 4-2). He was
started on 81 mg aspirin
and 40 mg of simvastatin
daily. The patient
underwent right carotid
endarterectomy the
next day without
complication.
Comment. This
patient had a transient
ischemic attack and was
at high risk of early FIGURE 4-2 CT angiogram demonstrating
recurrent stroke, although high-grade right internal carotid artery
stenosis (red arrow).
it was not identified as
such by the ABCD2 score.
Carotid artery stenosis is an important cause of a transient ischemic attack
with a high risk of recurrence. Early vascular imaging is required to
identify this treatable cause of stroke. Carotid revascularization should be
performed as soon as reasonably possible if the patient is medically stable.

Continuum (Minneap Minn) 2017;23(1):8292 ContinuumJournal.com 89

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


Transient Ischemic Attack

Ischemic Attack to Prevent Early Re- medical management alone. The study
currence (FASTER) trial compared the results showed aggressive medical man-
effectiveness of 3 months of treat- agement alone was superior to stent-
ment with 81 mg aspirin and 75 mg ing in the prevention of recurrent
clopidogrel commenced within 24 hours stroke. Medical management included
of onset versus aspirin alone in pa- 325 mg aspirin and 75 mg clopidogrel
tients with minor strokes/TIAs.31 This for 90 days, together with intensive
trial was small and ended early because medical management of modifiable
of slow recruitment; however, there was vascular risk factors. Medical manage-
a suggestion that the combination ther- ment was superior to stenting because
apy may reduce recurrent stroke events of a combination of higher than ex-
with a low risk of complications. The pected periprocedural risk and a lower
Clopidogrel in High-risk Patients With recurrence rate in the medical man-
Acute Non-disabling Cerebrovascular agement arm. Both arms received dual
Events (CHANCE) trial32 was performed antiplatelet therapy, so it is not known
in China and randomly assigned 5170 if the combination of aspirin and clo-
high-risk patients with TIA (defined pidogrel reduced the recurrent stroke
as an ABCD2 score of 4 or higher at risk; however, the National Institutes
assignment) and minor stroke to treat- of Health (NIH)-sponsored Platelet-
ment within 24 hours of onset with Oriented Inhibition in New TIA and
either combination therapy with clo- Minor Ischemic Stroke (POINT) trial34
pidogrel and aspirin (clopidogrel is examining this question and is cur-
at an initial dose of 300 mg, followed rently enrolling patients. It is hoped
by 75 mg/d for 90 days, plus aspirin at that this study will provide a definitive
a dose of 75 mg/d for the first 21 days) answer. For now, North American sec-
or placebo plus aspirin (75 mg/d for ondary stroke prevention guidelines
90 days). Recurrent stroke was seen do not recommend dual antiplatelet
in 8.2% of patients in the clopidogrel- agent therapy.29
aspirin group, as compared with 11.7%
of those in the aspirin-only group Outpatient Versus Inpatient
(hazard ratio, 0.68; 95% confidence Assessment
interval, 0.57Y0.81; PG.001). The risk For stroke prevention, the location of
of hemorrhage was not different in treatment matters less than the speed
the two groups. The CHANCE trial has of the assessment. However, in most
issues with generalizability, including parts of the world, assessing patients
the fact that it was a Chinese-only pop- and completing urgent (on the same
ulation, a high proportion of males were day, within a few hours) imaging is most
included, and the proportion of pa- easily done in the emergency depart-
tients treated with antihypertensive and ment given the easy access to imaging.
lipid-lowering medications was less In clinical settings that do not have
than typically seen in North American access to timely outpatient neuroimag-
populations. In the Stenting vs. Aggres- ing, patients are often admitted to the
sive Medical Management for Preven- hospital to complete TIA evaluation and
ting Recurrent Stroke in Intracranial expedite initiation of secondary pre-
Stenosis (SAMMPRIS) study,33 patients vention strategies. Some advantages
with recently symptomatic severe intra- of admitting the patient to the hospital
cranial stenosis were randomly assigned include close neurologic monitoring
to intracranial stenting plus aggressive and early completion of investigations
medical management or aggressive and appropriate treatment.
90 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


CONCLUSION attack fairly low among stroke-trained
neurologists. Stroke; 41(7):1367Y1370.
The assessment of TIA is all about doi:10.1161/STROKEAHA.109.577650.
making the correct diagnosis, and tak- 8. Johnston SC, Gress DR, Browner WS,
ing a good history is key. Once a TIA Sidney S. Short-term prognosis after
diagnosis has been made, cardiac and emergency department diagnosis of TIA.
JAMA 2000;284(22):2901Y2906. doi:10.1001/
neurovascular imaging can help inform jama.284.22.2901.
the potential etiology and guide initia-
9. Johnston SC, Sidney S, Bernstein AL, Gress DR.
tion of evidence-based secondary stroke A comparison of risk factors for recurrent TIA
preventative strategies. Ideally, obtain- and stroke in patients diagnosed with TIA.
ing the history, imaging, and identifying Neurology 2003;60(2):280Y285. doi:10.1212/
01.WNL.0000042780.64786.EF.
the etiology occur on the same day as
presentation to reduce the risk of re- 10. Rothwell PM, Giles MF, Chandratheva A,
et al. Effect of urgent treatment of transient
current cerebral ischemia. ischaemic attack and minor stroke on early
recurrent stroke (EXPRESS study): a prospective
REFERENCES population-based sequential comparison.
1. Hankey GJ, Warlow CP. Treatment and Lancet 2007;370(9596):1432Y1442.
secondary prevention of stroke: evidence, costs, doi:10.1016/S0140-6736(07)61448-2.
and effects on individuals and populations. 11. Lavallee PC, Meseguer E, Abboud H,
Lancet 1999;354(9188):1457Y1463. et al. A transient ischaemic attack clinic
doi:10.1016/S0140-6736(99)04407-4. with round-the-clock access (SOS-TIA):
2. Rothwell PM, Warlow CP. Timing of TIAs feasibility and effects. Lancet Neurol
preceding stroke: time window for prevention 2007;6(11):953Y960. doi:10.1016/
is very short. Neurology 2005;64(5):817Y820. S1474-4422(07)70248-X.
doi:10.1212/01.WNL.0000152985.32732.EE. 12. Prabhakaran S, Silver AJ, Warrior L, et al.
Misdiagnosis of transient ischemic attacks in
3. Easton JD, Saver JL, Albers GW, et al.
the emergency room. Cerebrovasc Dis
Definition and evaluation of transient
ischemic attack: a scientific statement for 2008;26(6):630Y635. doi:10.1159/000166839.
healthcare professionals from the American 13. Brazzelli M, Shuler K, Quayyum Z, et al.
Heart Association/American Stroke Association Clinical and imaging services for TIA and
Stroke Council; Council on Cardiovascular minor stroke: results of two surveys of
Surgery and Anesthesia; Council on practice across the UK. BMJ Open 2013;3(8).
Cardiovascular Radiology and Intervention; doi:10.1136/bmjopen-2013-003359.
Council on Cardiovascular Nursing; and the
Interdisciplinary Council on Peripheral Vascular 14. OCarroll CB, Barrett KM. Cardioembolic stroke.
Disease. The American Academy of Neurology Continuum (Minneap Minn) 2017;
affirms the value of this statement as an 23(1 Cerebrovascular Disease):111Y132.
educational tool for neurologists. Stroke 15. Wu CM, McLaughlin K, Lorenzetti DL, et al.
2009;40(6):2276Y2293. doi:10.1161/ Early risk of stroke after transient ischemic
STROKEAHA.108.192218. attack: a systematic review and meta-analysis.
Arch Intern Med 2007;167(22):2417Y2422.
4. Albers GW, Caplan LR, Easton JD, et al.
doi:10.1001/archinte.167.22.2417.
Transient ischemic attackVproposal for a new
definition. N Engl J Med 2002;347(21): 16. Giles MF, Rothwell PM. Risk of stroke early
1713Y1716. doi:10.1056/NEJMsb020987. after transient ischaemic attack: a systematic
review and meta-analysis. Lancet Neurol
5. Kraaijeveld CL, van Gijn J, Schouten HJ, Staal A. 2007;6(12):1063Y1072. doi:10.1016/
Interobserver agreement for the diagnosis
S1474-4422(07)70274-0.
of transient ischemic attacks. Stroke
1984;15(4):723Y725. doi:10.1161/ 17. Chandratheva A, Mehta Z, Geraghty OC, et al.
01.STR.15.4.723. Population-based study of risk and predictors
of stroke in the first few hours after a TIA.
6. Koudstaal PJ, Gerritsma JG, van Gijn J. Neurology 2009;72(22):1941Y1947.
Clinical disagreement on the diagnosis of doi:10.1212/WNL.0b013e3181a826ad.
transient ischemic attack: is the patient or
the doctor to blame? Stroke 1989;20(2): 18. Moreau F, Hill MD. Transient ischaemic
300Y301. doi:10.1161/01.STR.20.2.300. attack is an emergency: think about best
current stroke prevention options. Int J
7. Castle J, Mlynash M, Lee K, et al. Agreement Stroke 2008;3(4):251Y253. doi:10.1111/
regarding diagnosis of transient ischemic j.1747-4949.2008.00225.x.

Continuum (Minneap Minn) 2017;23(1):8292 ContinuumJournal.com 91

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


Transient Ischemic Attack

19. Hill MD, Yiannakoulias N, Jeerakathil T, et al. 27. Douglas VC, Johnston CM, Elkins J, et al.
The high risk of stroke immediately after Head computed tomography findings
transient ischemic attack: a population-based predict short-term stroke risk after
study. Neurology 2004;62(11):2015Y2020. transient ischemic attack. Stroke
doi:10.1212/01.WNL.0000129482.70315.2F. 2003;34(12):2894Y2898. doi:10.1161/
01.STR.0000102900.74360.D9.
20. Rothwell PM, Giles MF, Flossmann E,
et al. A simple score (ABCD) to identify 28. Coutts SB, Modi J, Patel SK, et al. CT/CT
individuals at high early risk of stroke angiography and MRI findings predict
after transient ischaemic attack. Lancet recurrent stroke after transient ischemic attack
2005;366(9479):29Y36. doi:10.1016/ and minor stroke: results of the prospective
S0140-6736(05)66702-5. CATCH study. Stroke 2012;43(4):1013Y1017.
doi:10.1161/STROKEAHA.111.637421.
21. Johnston SC, Rothwell PM, Nguyen-Huynh
MN, et al. Validation and refinement of 29. Olivot JM, Wolford C, Castle J, et al. Two
scores to predict very early stroke risk after aces: transient ischemic attack work-up as
transient ischaemic attack. Lancet outpatient assessment of clinical evaluation
2007;369(9558):283Y292. doi:10.1016/ and safety. Stroke 2011;42(7):1839Y1843.
S0140-6736(07)60150-0. doi:10.1161/STROKEAHA.110.608380.
22. Perry JJ, Sharma M, Sivilotti ML, et al. 30. Couillard P, Poppe AY, Coutts SB. Predicting
Prospective validation of the ABCD2 score recurrent stroke after minor stroke and
for patients in the emergency department transient ischemic attack. Expert Rev
with transient ischemic attack. CMAJ Cardiovasc Ther 2009;7(10):1273Y1281.
2011;183(10):1137Y1145. doi:10.1503/ doi:10.1586/erc.09.105.
cmaj.101668.
31. Kennedy J, Hill MD, Ryckborst KJ, et al. Fast
23. Wardlaw JM, Brazzelli M, Chappell FM, et al. assessment of stroke and transient ischaemic
ABCD2 score and secondary stroke prevention: attack to prevent early recurrence (FASTER):
meta-analysis and effect per 1,000 patients a randomised controlled pilot trial. Lancet
triaged. Neurology 2015;85(4):373Y380. Neurol 2007;6(11):961Y969. doi:10.1056/
doi:10.1212/WNL.0000000000001780. NEJMoa1215340.
24. Coutts SB, Wein TH, Lindsay MP, et al. Canadian 32. Wang Y, Wang Y, Zhao X, et al. Clopidogrel
Stroke Best Practice Recommendations: with aspirin in acute minor stroke or
secondary prevention of stroke guidelines, transient ischemic attack. N Engl J Med
update 2014. Int J Stroke 2015;10(3):282Y291. 2013;369(1):11Y19. doi:10.1056/
doi:10.1111/ijs.12439. NEJMoa1215340.
25. Bos MJ, van Rijn MJ, Witteman JC, et al. 33. Chimowitz MI, Lynn MJ, Derdeyn CP, et al.
Incidence and prognosis of transient Stenting versus aggressive medical therapy
neurological attacks. JAMA 2007;298(24): for intracranial arterial stenosis. N Engl J
2877Y2885. doi:10.1001/jama.298.24.2877. Med 2011;365(11):993Y1003. doi:10.1056/
NEJMoa1105335.
26. Paul NL, Simoni M, Rothwell PM, Oxford
Vascular Study. Transient isolated brainstem 34. Platelet-Oriented Inhibition in New TIA
symptoms preceding posterior circulation and Minor Ischemic Stroke (POINT) Trial
stroke: a population-based study. Lancet (POINT). clinicaltrials.gov/ct2/show/
Neurol 2013;12(1):65Y71. doi:10.1016/ NCT00991029. Updated July 18, 2016.
S1474-4422(12)70299-5. Accessed December 1, 2016.

92 ContinuumJournal.com February 2017

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Anda mungkin juga menyukai