Transient Ischemic Attack

TOM SHEFI

NOV’ 5TH, 2018

https://www.youtube.com/watch?v=nngjxVc9QtQ
Every minute counts

 Occlusion of intracranial vessel

 No flow- death of brain tissue within 4-10 minutes

 Less than 16-18 ml/100g tissue- Hours
 Less than 20 ml/100g tissue- Hours-Days

 If blood flow is restored to tissue before significant infarction develops, the patient may
experience only transient symptoms and the clinical syndrome is called a transient
ischemic attack.
Pathophysiology

 necrotic pathway
 no glucose and O2-> not enough ATP->membrane ions stop functioning->neurons
depolarize -> Ca2+ influx->Glutamate release in excess -> neurotoxicity (also free
radicals formation)

 apoptotic pathway
 Lesser degrees of ischemia (penumbra) favor apoptotic death causing cells to die
days to weeks later.

 Fever and Hyperglycemia dramatically worsen brain injury during ischemia.

Pathophysiology

 Intrinsic to a vessel
 Remote
 Inadequate cerebral blood flow

 Rupture of a vessel in the subarachnoid space

Diagnosis?

 Diagnosis of TIA is Clinical and based upon a determination that the Sx are
more likely caused by brain ischemia than another cause.

 Problem? – Sx are transient, highly variable and often minor (as we’ll see
later )
Definition of TIA

 Old: Sudden onset of a focal neurologic symptom lasting less than 24

hours brought on by a transient decrease in blood flow, which renders the
brain ischemic in the area producing the symptom.

 New: Transient episode of neurologic dysfunction caused by focal

neurological symptom, without acute infarction.

 What's the difference? And Why ?

Epidemiology

 Overall prevalence of TIA among adults in the US is approximately 2%

Risk factors
Clinical manifestations and mechanisms

 Sx vary, dependent upon the pathophysiologic subtype

 Embolic
 Lacunar or small penetrating vessel
 Large Artery, Low Flow
Embolic

 Typically last hours rather than minutes (low flow TIA)

 When the source of the embolus is in a proximal vessel, recurrent emboli

can lodge in different branches of the vessel giving different symptoms

 Divided into anterior circulation (carotid, ACA, MCA) and posterior

(vertebrobasilar, PCA)- Sx depends upon the size of the emboli, size of the
artery occluded, the territory it supplies
 Complete MCA blockage will produce
contralateral hemiplegia, aphasia, in the
dominant hemisphere and anosognosia
or neglect in the nondominant
hemisphere

 Smaller emboli can result in a focal

symptom e.g. hand or arm weakness
and heaviness due to motor system
ischemia or as specific as a thumb
numbness due to ischemia in the sensory
strip
 transient ataxia, dizziness, diplopia,
dysarthria, quadrantanopsia,
hemianopsia, numbness crossed face
and body numbness and unilateral
hearing loss.

 Can produce a sudden overwhelming

stupor or coma due to bilateral medial
thalamic injury
 Lacunar stroke (small vessel TIA)

 Occasionally, recurrent
stereotyped TIA occur

Thought to be caused by
atherothrombotic obstructive
lesions at the origin of the
penetrating vessel. Or
lipohyalinosis

 Sx: Face, arm and leg

weakness or numbness due to
ischemia in the internal
capsule, pons or thalamus.

 Lacunar strokes may be

progressive rather than abrupt.
 Low Flow TIA anterior circulation

 Associated with atherosclerotic stenosis

lesion at the internal carotid artery
origin, when collateral flow from the
COW to the MCA\ACA is impaired

 Usually short lived (minutes) and often

recurrent. May occur as little as several
times per year, but typically more often
(once per week )

 Generally stereotyped, Sxs include

weakness, numbness of the hand arm
leg face tongue and or cheek, Aphasia
or neglect
Low flow TIA posterior circulation

 Recurrent Sx are NOT

stereotyped when the
lesion involves the
vertebrobasilar junction
 Why ?
Generalizations can be made
Typical

 Typical- Transient focal neurologic symptom that can be localized to a

single vascular territory.
Atypical

 Gradual buildup of symptoms (more than five minutes)

 March of symptoms from one body part to another
 Progression of symptoms from one type to another
 Isolated disturbance of vision on both eyes, characterized by the occurrence
of positive phenomena
 Isolated sensory symptoms with remarkably focal distribution such as in a
finger, chin or tongue
 Very brief spells (less than 30 sec)
 Identical spells occurring over a period of more than one year
 Isolated brainstem symptoms such as dysarthria diplopia or hearing loss
High Risk Lesions

 Internal carotid artery TIA

 Intracranial atherothrombotic disease
 Arterial, aortic or cardiac sources of emboli
 Dissection lesions
Internal carotid
artery TIA

 Atherothrombotic stenotic
lesion at the origin of the
internal carotid – site for
thrombus formation and
subsequent embolism. (Artery
to artery)

 Reduced blood flow with

further stenosis, when the COW
is compromised low flow TIA
ensues
 Intracranial atherothrombotic disease

 Can produce low flow or embolic TIA, most

commonly occurs at the posterior circulation.
(vertebral, vertebrobasilar, proximal basilar)

 Other important but less common sites- siphon

of the internal carotid and the MCA stem
 Arterial, Aortic or Cardiac sources of Emboli

 Cardioembolic stroke – 20% of all ischemic strokes.

 Occur suddenly with maximum neurologic deficit present at onset.
 Most often lodge in the intracranial internal carotid, the MCA the PCA or their branches. Less
frequently, ACA is involved.
 The most significant cause of cardioembolic stroke in the world is nonrheumatic atrial fibrillation ( non
valvular).
 Patients with a-fib have an average annual risk of stroke of 5%. Can be estimated by the
CHADVASCORE
 PFO, Paradoxical embolization or other atrial septal defect.
Transient…. Why
emergency ?

 TIA’s may herald strokes.

 Risk is 10-15% in the first
three months with most
events occurring in the first
2 days)

 ABCDD score
Diagnosis

 Based upon clinical features of the attack and neuroimaging findings.

 Typical vs Atypical ?
 How to diagnose ?
Problematic diagnosis

 Neurologic symptoms do not accurately reflect the presence or absence of

infarction, and the tempo of the Sx does not indicate the cause of the
ischemia.

 Some TIAs, such as those causing transient monocular blindness, diplopia, and
aphasia, are very specific for one vascular territory, while others, such as limb
weakness or numbness, are compatible with a number of different territories.

 This is a critical issue because Tx depends upon accurately identifying the

cause of the Sx and the nature, location and severity of causative cardiac
hematologic and cerebrovascular abnormalities
DD
DD

 Seizure- followed by postictal paralysis or loss of other functions

 Migraine aura- progressive neurologic deficit or disturbance with

subsequent complete recovery.
DD

 Focal or nonfocal nature of attacks

 Nature of Sx and their progression
 Progression and Course of Sx
 Associated Sx during and after the attacks
Nature of Sx

 Positive Sx indicate active discharge from CNS neurons (visual, auditory,

somatosensory or motor)
 Negative Sx indicate an absence or loss of function

 Seizures and migraine auras usually begin with positive symptoms while TIA’s
invariably are characterized by negative symptoms.
Progression and Course of Sx

 Migraine aura often progress slowly within one modality

 Bright objects move slowly across the visual field
 Paresthesia progress from one finger to all digits and up the arm etc.

 The progression occurs over minutes. After the positive Sx “migrate”, they are often followed by loss of
function
 Migranous aura typically progress from one modality to the other

 Seizures- consist of positive phenomena in one modality which progress very quickly during seconds.

 TIA Sx are negative; when more than one modality or function is involved, all are affected at about the
same time
Duration and Tempo

 Migraneous auras characteristically last 20-30 min’

 TIAs are usually fleeting, almost always lasting less than one hour
 Seizures last on average 30 sec to 3 min’
 Syncope is very brief (seconds)

 TIAS usually cluster during a finite period of time. Attacks that are
scattered over many years are almost always either faints, migraines or
seizures.
Precipitating factors

 Activation of seizures is well known to occur in some patients after

stroboscopic stimulation, hyperventilation, reading, cessation of
anticonvulsants, fever, and alcohol or drug withdrawal.
 TIAs can occur when blood pressure is reduced, or upon sudden standing
or bending.
 Dizziness and vertigo in patients with peripheral vestibulopathies are often
triggered by sudden movements and positional changes.
 Syncope commonly occurs when patients see blood, have or are about
to have phlebotomy or other medical procedures etc.

https://www.youtube.com/watch?v=rcbBWcOIZE4
Associated symptoms

 Headache is common after migraine aura and following a seizure.

Headache can also occur during a TIA, but rarely at the same time or
directly after neurologic symptoms.
 A bitten tongue, incontinence, and muscle aches are frequently
associated with seizure.
 Vomiting is common after migraine and occasionally follows syncope,
but is extremely rare after or during TIA.
 Nausea and a need to urinate or defecate often precede or follow
syncope; sweating and pallor are other common features of syncope.
Persistent neurologic deficits with abrupt
onset

 Intracerebral hemorrhages usually develop during minutes and cause

gradually increasing focal signs.
 Brain tumors can cause an abrupt onset or worsening of symptoms;
hemorrhage into a tumor is one mechanism for such a change. In
addition, some tumors which are outside the brain (eg, meningiomas)
reach a critical mass and can cause abrupt displacement of brain tissue
with the sudden onset of symptoms.
 Nonketotic hyperglycemic stupor is often associated with focal neurologic
signs; there may be a focal region of brain edema on brain imaging tests.
Persistent neurologic deficits with
abrupt onset

 MS attacks, can begin abruptly and may be have transient paroxysmal

pattern, Most often however, MS attacks develop over 5 to 21 days, a longer
period than strokes.

 Demyelination can occur around veins after various viral infections which
result in the abrupt onset of multifocal signs that develop over days. This
disorder is often called acute disseminated encephalomyelitis (ADEM). Other
viral infections, particularly cytomegalovirus, can cause focal brain lesions
associated with focal neurologic signs.

 Brain abscesses cause focal neurologic symptoms and signs which can begin
abruptly; fever, headache, and seizures are common accompanying signs.
Workup

 Brain imaging
 Neurovascular evaluation
 Cardiac evaluation
 Labs
 Brain Imaging

 MRI or CT is indicated in all

patients with suspected TIA
 dwMRI >MRI>CT
 DwMRI can confirm whether
only ischemia has occurred or
if there has also been an
element of infarction,
differentiating stroke from TIA.

 DWMRI can miss small infarcts,

lacunar TIA should be
followed up by MRI or CT
Neurovascular evaluation

 MRA
 CTA
 Carotid Duplex Ultrasonography
 Transcranial Doppler ultrasonography
Cardiac Evaluation

 ECG
 Holter\telemetry monitor for patients w/o clear etiology after initial brain
imaging and ECG.
 Ecocardiography, when no cause for TIA or stroke has been identified by
other aspects. (TEE or TTE)
Labs

 CBC
 PT\PTT
 Electrolytes & Creatinine
 Fasting glucose & lipids
 ESR
Okay… so you diagnosed a stroke…
Now what ?

 How severe is the stroke? How should we treat?

 NIHSS
 Level of consciousness
 Eye movement
 Visual field test
 Facial palsy
 Motor limbs
 Ataxia
 Sensory
 Language& speech
 Attention
https://www.mdcalc.com/nih-stroke-scale-score-nihss
TX- Primary

 Goal: prevent or reverse brain injury

 medical support

 IV Thrombolysis
 Endovascular revascularization
 Antithrombotic treatment
 Neuroprotection
 Stroke center and rehabilitation
IV Thrombolysis
Endovascular revascularization

 Large vessel occlusion often fail to open with IV rTPA alone.

 Endovascular revascularization has been studied as an alternative or

adjunctive tx of acute stroke in ptx who are ineligible for or have CI to
thrombolytics or in those who failed to ahciev vascular recanalization
Antithrombotic tx

 Aspirin is the only antiplatelet agent that hs been proven to beeffective

for the acute tx of ischemic stroke.

 (Anticoags did not demonstrate any bvenefit in the primary tx of

atherothrombotic cerebral ischemia and have also shown an increase in
the risk of brain and systemic hemorrhage.
Tx- medical support- HTN

 One the one hand… HTN doesn’t help…. On the other, we want to save
cerebral perfusion….. What do we do ?
It is preferable to reduce bp over hours or longer rather than minutes. Autoregulation of
CBF is impaired in Ischemic cerebral tissue, and higher AP may be required to maintain
CBF. So aggressive reductions of BP are to be avoided.

 Indication SBP>220 or DBP>130

 iF TPA is used, the goal is SPB<185 and DBP<110

 Goal of tx: reduce MAP by no more than 25% within min’to 2h. OR to 160/100-
110. (IV Nitroprusside, parentral labetalol or nicardipine also work)
Tx (secondary prevention) – by etiology- Large
artery disease

 Revascularization and intensive medical

therapy
 Antiplatelet, antihypertensive and statin for
multifactorial risk reduction
 Carotid stenting
 Endarterectomy (selected ptx with 50-99%
stenosis & life expectancy of 5 years + )

 Aspirin and clopidogrel was found to prevent

stroke following TIA better than aspirin alone
 thiazide and ACEi were found to be most
effective anti HTN therapy, in reducing stroke
burden
Tx- Small vessel disease

 Antiplatelet
 Anti HTN
 Statins
Tx- Cryptogenic TIA

 Anti HTN
 Antithrombotic
 Statin
 Lifestyle modification
Arterial\Cardiogenic TIA

 Lifelong Anticoagulants
Thank you!