Stroke and TIA

By Gregory Eisinger, MD – one of our EM/IM residents

Read on for review of this week’s Conference on CVA and TIA. Greg organized his review to highlight each learning objective that we covered in

  1. Define CVA and TIA. Describe each disease process and the pathophysiology of each.

Per Rosen’s “Stroke can be defined as any vascular injury that reduces cerebral blood flow (CBF) to a specific region of the brain, causing neurologic impairment.” Strokes are most commonly ischemic (87%, 1/3 caused by thrombosis, 2/3 by embolism) but may also be hemorrhagic (13%). For the purposes of this review, we will focus on ischemic stroke (refer to small group session on ICH/SAH for hemorrhagic). Thrombotic stroke is caused by ulceration or rupture of intravascular plaques triggering platelet aggregation and clot formation. Embolic strokes are most often the result of mural thrombus formed in the left atrial appendage due to stasis caused by atrial fibrillation but may also orginate from other locations such as the carotid artery or LV. When cerebral blood flow is initially reduced, the affected tissue becomes electrically silent creating the characteristic symptoms. When flow is further decreased for a prolonged period of time, infarction occurs causing membrane rupture and cell death by coagulation necrosis. An ischemic penumbra of viable brain tissue surrounds the area of the infarct, sustained by tenuous flow through collateral vessels; salvaging this tissue is a major target of therapy. 

 TIA was classically defined as stroke symptoms which resolved in a period of less than 24 hours. However, this definition has recently become controversial and the current definition used by the AHA is: “a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.” TIA is a major risk factor for future stroke with ~10% incidence in the next 3 months and about half of hose occurring in the first 2 days.


Symptoms of stroke depend of the area of brain affected. Some common stroke syndromes include:

– Wallenberg (lateral medullary): PICA, dysphagia, dysarthria, ataxia, vertigo, nystagmus, diplopia, Horner’s, facial pain

            – Weber (medial midbrain): ipsilateral gaze palsy, contralateral weakness

            – Basilar: both medial and lateral Sx, locked in syndrome

            – MCA – sensory and motor loss to contralateral body and face, upper > lower extremity, plus aphasia (when dominant hemisphere is affected)

            – Posterior circulation: cranial nerve deficits, cerebellar Sx, altered LOC, “crossed brainstem syndromes (sensory loss on one side and motor on the other)

            – Thalamic: pure sensory, pure motor, ataxia-hemiparesis, thalamic pain syndrome, dysarthria-clumsy hand


The rule of 4’s is a helpful mnemonic for figuring out brainstem syndromes:


Diagnosis is often complicated by other conditions mimicking stroke such as: seizures with Todd’s paralysis, intoxication, metabolic derrangements (eg hypoglycemia), peripheral neuropathies, complex migraine, conversion disorder, aortic dissection, Wernicke encephalopathy, brain tumors or abscess, air embolism, Bell’s palsy, etc.


  1. Define the risk factors and incidence for CVA and TIA.

Risk factors for thrombotic stroke are similar to those for other forms of vascular disease and include diabetes, hypertension, hyperlipidemia, smoking, obesity, older age, male sex. Cardiac arrhythmias such as Afib and heart failure/MI predisposing to LV thrombus are major risk factors for embolic stroke. In younger patients stroke may be the result of a hypercoaguable state, trauma (eg BCVI, vascular dissections), vasculitis, pregnancy, use of OCPs, sickle cell disease, connective tissue disorders, fibromuscular dysplasia, or drug use (eg cocaine).  Stroke is very common with an incidence of almost 800,000 people per year in the US, averaging one stroke about every 40 seconds. In hospital mortality is about 5-10% for a stroke admission and only 10% of survivors regain full function.  

  1. Define the NIHSS. How do you use this to assess patients and what other scales are used to assess for stoke commonly used by EMS.

The NIH stroke scale is a quick bedside method for delineating the presence and severity of stroke symptoms. Scores have been shown to have high interrater reliability and correlation to the size of infarction. It has prognostic significance and helps to stratify Pt’s who would benefit from vs be at high risk for thrombolytic therapy. Other scales used by EMS which are under investigation include the Cinncinatti Prehospital Stroke Scale, the Los Angeles motor score, and the Rapid Arterial occlusion Scale. These scales allow field providers to make quick decisions about whether a presentation is concerning for stroke and route the Pt to a stroke center if indicated.

  1. Outline the basics steps in stroke management upon arrival to the ED. 

As with any condition, initial focus should be on the ABCs with particular attention to the airway. It is rare for stroke patients to become comatose and require intubation for reduced GCS in the absence of massive edema causing mass effect, increased ICP, midline shift, hemorrhagic stroke, or large brainstem strokes. However, stroke patients are at risk for aspiration, hypoxia, and hypercarbia and thus should have a low threshold for intubation prior to beginning imaging studies. However, use of paralytic and sedative agents compromises the ability to obtain a reliable neurologic exam which is important for assessment of stroke progression as well as the effects and complications of thrombolytic therapy.


Assuming stability or adequate control of the ABCs, attention then turns to characterizing the stroke and assessing candidacy for various interventions. The most crucial initial workup consists of noncontrasted CT of the head to rule out hemorrhage and screen for large ischemic infarct (though this is most often absent in the acute period), 12 lead EKG, and blood glucose level. Other CT findings of interest may include sucal effacement/loss of gray-white interface or collapsed ventricles suggesting increased ICP, and dense MCA sign. EKG should be examined for evidence of Afib or other arrhythmia as well as MI. Hypoglycemia should be treated and response assessed prior to administering tPA.


The next step in management is to consider indications and contraindications for thrombolytic therapy (eg tPA/alteplase). First step is assessment of last known well (LKW). IV tPA has been shown to be beneficial and reasonably safe if administered within the first 3 hours. However, exclusion criteria must be carefully considered and include: bleeding on head CT, minor or rapidly resolving Sx, active internal bleeding in past 21 days, use of anticoagulation with INR/PTT in therapeutic range, previous stroke, head trauma, or intracranial surgery in past 3 mo, any major surgery in past 2 wks, any Hx of ICH, intracerebral AVM or aneurysm, seizure at stroke onset, recent MI, persistent HTN >185/110. tPA can also be considered up to 4.5 hrs in patients without high-risk factors such as age >80, NIHSS >25, combination of DM AND prior stroke.  Dosing is 0.9 mg/kg (max 90 mg) with 10% as a bolus followed by 60 min infusion. If patient receives tPA, withhold aspirin for 24 hours to ensure no hemorrhagic conversion prior to administration. Intraarterial catheter-directed tPA can be considered in patients up to 6 hours. Various mechanical clot removal and recanalization devices have been shown to be safe and effective up to 8 hours. If heparinizing for embolic stroke, do not give a bolus and use the stroke sliding scale which has a lower goal PTT.


Further ED workup should include labs such as CBC, chemistry, coagulation studies, EtOH level, urine toxicology, hemoglobin A1c, and lipid profile. Depending on the results of the initial CT, a CT angiogram to assess the patency of the cerebral vasculature, CT perfusion study which can look for areas of ischemia and help distinguish reversible from irreversible ischemia, and MRI of the brain may be indicated. Further workup may include echocardiogram to search for source of cardioembolism (or paradoxical embolism), carotid doppler ultrasound to assess patency of extracranial vasculature, and ambulatory cardiac rhythm monitoring for silent Afib.


Targeted blood pressure control is a key component of the ED management of stroke. Though controversial due to a dearth of high quality evidence, most guidelines suggest permissive hypertension (treatment only for SBP >220 or DBP > 120) aimed at preserving cerebral perfusion in the setting of ischemic stroke unless the patient has received or is planned to received thrombolytics. Other contraindications to this approach include aortic dissection, acute MI, and severe pulmonary edema secondary to heart failure. If pharmacologic blood pressure control is needed, titratable agents such as nicardipine are preferred and care should be taken to avoid precipitous drop in BP (>20% in 1 hour) as this may worsen ischemia. Goal BP for Pts receiving tPA is typically cited as <180/105 in order to reduce risk of hemorrhagic conversion. Other goals include maintenance of normotension, normoglycemia, normonatremia, normoxia, normocarbia, and normothermia.


Ongoing assessment of vital signs and neurologic exam (ie serial NIHSS) and continuous cardiac monitoring should continue throughout the admission. Repeat head CT should be obtained for pt’s with any change in neurologic exam especially those receiving tPA. Hemorrhagic conversion occurs in approximately 7% of Pts receiving tPA. For these pts, consider administering TXA and/or cryoprecipitate.


Outside the safe range for the various interventions discussed above, stroke management focuses on reduction of risk for future strokes through lifestyle modification (eg diet, exercise, smoking cessation), use of ASA +/- clopidigrel and statin medications, and management of deficits including swallow assessment and use of enteral feeding tubes if necessary and participation in stroke rehab programs.


  1. Discuss the options for treatment and management of TIA

Emergency department workup and management of TIA is controversial and highly institution-specific. Though some argue that workup could be done either as an outpatient or inpatient depending on the stability of the patient and other factors, it is often done in the emergency department or observation unit. The goal of TIA workup is to identify the source of the ischemic event so that interventions aimed at reducing risk of stroke can be implemented. The primary sources which should be considered include focal stenosis in the anterior or posterior circulation (depending on the presenting symptoms) which can be accomplished with carotid doppler ultrasound or CTA/MRA, and assessment for cardioemoblic source such as atrial/ventricular thrombus or valvular vegetation using echocardiography. The ABCD2 score can be used to risk stratify and assist with planning disposition. Baby aspirin should be started if the pt is not already taking it and consideration should be given to escalating antiplatelet therapy (full strength ASA or clopidigrel) for Pts already on daily prophylactic ASA.