Nondisabling stroke is where Emergency Medicine earns its keep. The threats are quieter, the windows are wider, and the misses—especially in younger and female patients—are more common. In this Part 2 or our 2-part podcast update on ED stroke management with Dr. Katie Lin and Dr. Walter Himmel we explore non-disabling strokes, where symptoms are mild enough that patients can continue daily activities if deficits persist. Yet, non-disabling does not mean benign. Nondisabling strokes occupy the same ischemic continuum as high risk TIAs and carry a substantial risk of early recurrent disabling stroke. In this EM Cases podcast we answer questions such as: Which patients with non-disabling stroke can safely be discharged from the ED with prompt follow-up and which require urgent investigation or admission? Which stroke mimics do we need to be on the look out for and how do we identify them at the bedside? How dangerous is thrombolysis in a patient with presumed stroke who turns out to be a stroke mimic? What are the key distinguishing features between a stroke and functional neurologic disorder? What are the most common causes of stroke in young people that we commonly miss? How does stroke etiology dictate the management pathway? What are the indications for carotid endarterectomy in patients with nondisabling stroke and what is the ideal timing of the endarterectomy? When is dual antiplatelet therapy vs single antiplatelet therapy vs anticoagulant therapy indicated? What is the best medication strategy for the patient on a DOAC for atrial fibrillation who presents to the ED with a nondisabling stroke? For patients not on a DOAC for atrial fibrillation who come in with a stroke, when is it safe to start anticoagulation? and many more…

Podcast production, sound design & editing by Anton Helman; Voice editing by Braedon Paul

Written Summary and blog post by Anton Helman, edited by Katie Lin, November, 2025

Cite this podcast as: Helman, A. Himmel, W. Lin, K. Nondisabling Strokes Recognition and Management. Emergency Medicine Cases. November, 2025. https://emergencymedicinecases.com/nondisabling-strokes-recognition-management. Accessed November 15, 2025

Nondisabling stroke accounts for a substantial proportion of ED cerebrovascular presentations. Although clinical deficits are mild, the 30-day risk of neurologic deterioration or disabling stroke is about 4-5%. ED priorities include precise phenotyping, urgent vascular imaging when indicated, early secondary prevention, and reliable short-interval follow-up. The key operational pivot is from “major/minor” toward disabling vs nondisabling—a distinction that determines whether to activate reperfusion pathways or pursue prevention-first pathways. Nondisabling stroke is where quiet presentations carry big stakes. Deficits may be subtle, windows feel wider, and the risk of being lulled into false reassurance is real—especially in younger patients and women.

Pitfall: a common pitfall is getting lulled into a false sense of reassurance for expedited workup when a patient presents with a nondisabling stroke. While nondisabling strokes do not require as rapid workup and treatment as disabling strokes, urgent workup and management should still be a priority.

As discussed in Part 1, The very first decision is whether the symptoms are disabling vs nondisabling, not whether the presentation is consistent with a “major vs minor” stroke. Disabling means the deficit(s)—if persisted—would compromise independence: language that prevents functional communication, dominant-hand motor weakness that prevents ADLs or work, gait failure, major visual field loss, or depressed consciousness. Nondisabling implies that, even if the deficit remained, independent living would still be possible (e.g., mild facial droop, subtle sensory change, small visual field cut that doesn’t affect reading/driving, mild dysarthria without aphasia). The classification determines tempo: disabling strokes get immediate CT and stroke-protocol CTA to consider reperfusion; nondisabling strokes still demand urgent prevention—non-contrast CT now to screen for intracranial hemorrahge, CTA soon thereafter—but the pathway is focused on stopping the next event.

Source: Dr. Katie Lin’s SYNAPSE: EM Neuro Essentials Course (www.SynapseCourse.com)

Emergency physicians miss approximately 1 in 10 strokes. Short term morbidity and mortality are 8 fold higher in missed strokes. Conversely, a similar proportion of “strokes” turn out to be mimics. Recognizing the difference is critical for avoiding both under- and overtreatment.

Functional presentations can mimic stroke. The key is inconsistency and distractibility.

Pitfall: Functional ≠ feigned. Up to 60% of patients with functional presentations have underlying organic disease—always rule out stroke first. Avoid diagnosing a “functional condition” in a patient without prior objective testing and/or neurologic consultation. Err on the side of stroke until proven otherwise. FND features do not exclude stroke.

Data show very low rates of hemorrhage (0–1%) when thrombolytics are given to stroke mimics as compared to the 3–5% seen in true strokes.
Thus, for disabling presentations, it’s safer to err on the side of treating as a potential true stroke when in doubt, including shared decision-making, informed consent when possible, and timely specialist consultation.

Strokes in the young are rare but can be devastating when missed. Approximately 13–18% of all strokes in North America occur in individuals under the age of 50. This proportion has increased over the past two decades. Younger patients are more likely to be labeled migraine, anxiety, or “functional”—particularly women—despite a vascular event. Etiologies also differ: dissection, PFO-related emboli, hypercoagulable states, and intracranial disease figure more prominently, yet we often default to “too young for stroke.”

Bottom line: Any sudden focal neurological deficit in a young person should be treated as a stroke until proven otherwise.

Non-disabling strokes and TIAs share pathophysiology, prognosis and treatments. The DOUBT study found that 13% of TIA presentations as short as 5 minutes in duration are subsequently found to have evidence of stroke lesions on MRI. 2-17% of patients with TIA or minor stroke suffer a subsequent disabling stroke within 90 days, most within 48 hours.

The ABCD2 score lacks sufficient sensitivity and specificity to reliably stratify short-term stroke risk after TIA, particularly for identifying patients at very low or very high risk. The score does not account for critical high-risk features such as ipsilateral large artery stenosis, atrial fibrillation, recurrent or crescendo TIAs, or imaging evidence of acute infarction, all of which substantially increase early stroke risk independent of ABCD2 score. As a result, patients with low ABCD2 scores may still harbor significant vascular pathology and face substantial risk, undermining the score’s utility for disposition or management decisions. Instead, current best practice focuses on clinical features to risk stratify patients. These are the features that predict a subsequent disabling stroke and mandate urgent imaging and treatment:

Persistent nondisabling deficits and resolved high-risk features share the same message: active cerebrovascular pathology with high risk for early subsequent stroke. A persistent deficit—even when “mild”—raises the pretest probability of a treatable lesion such as symptomatic carotid stenosis, intracranial atherosclerosis, or cervical artery dissection, and the opportunity for secondary prevention. Resolved high-risk features—true motor weakness (often described as heaviness), speech or language disturbance, major visual field loss, or depressed consciousness—suggest potentially high risk vascular territory at risk for susequent stroke from ongoing vascular pathology. Either scenario should trigger urgent head CT to exclude hemorrhage, early CTA head and neck to define the vasculature, and immediate antithrombotic decisions. The goal is to prevent the next stroke event, which is at highest risk within the first 48 hours to one week.

~¼ Large-artery atherosclerosis (carotid/intracranial):

~¼ Lacunar/small-vessel:

~¼ Other/cryptogenic (dissection, thrombophilia, hyperviscosity; higher in young):

Etiology is not an academic afterthought—it determines secondary prevention timelines, including both medications and interventional procedures. Large-artery atherosclerosis (carotid or intracranial) may require a surgical approach when symptomatic ICA stenosis is present; pre-op therapy is typically single antiplatelet, and the procedural window is early (after the first 48 hours, but ideally within the first couple of weeks). Lacunar or small-vessel disease typically requires an antiplatelet-based prevention strategy with aggressive risk-factor control; thrombolysis is reserved for disabling presentations within the treatment window. Cardioembolic sources (most commonly atrial fibrillation, but also structural heart disease) shift the plan toward oral anticoagulation once it is safe, so an ECG at the time of presentation and arrangements for rhythm monitoring and echocardiography matter even in nondisabling stroke or high risk TIA cases. Cervical artery dissection and other “cryptogenic/other” mechanisms are proportionally more common in younger patients; they necessitate CTA head/neck to confirm the diagnosis and typically lead to a short course of dual antiplatelets for TIA/nondisabling stroke presentations while awaiting confirmatory testing for underlying stroke etiology.

The appropriate acute imaging study in suspected ischemic stroke is a stroke-protocol CTA performed immediately, not a delayed “carotid stenosis” CTA intended for elective surgical planning. The stroke-protocol CTA provides time-sensitive information essential to emergency management: identifying the site of occlusion, assessing collateral circulation, and detecting stenosis or dissection that may alter acute therapeutic decisions.

A normal early CT or CTA does not exclude ischemic stroke. Lacunar infarcts, distal vessel occlusions, and small ischemic cores can be radiographically occult in the hyperacute phase. Clinicians should treat the clinical syndrome, and when imaging findings appear discordant with the patient’s presentation, pursue specialist advice rather than prematurely excluding the diagnosis.

Carotid and vertebral Doppler ultrasonography remain useful for secondary prevention and pre-operative assessment, but they do not substitute for CTA when available to inform real-time decisions in the ED.

Carotid endarterectomy remains one of the few surgical interventions in stroke care that meaningfully alters outcomes. Patients with symptomatic internal carotid artery stenosis of 70–99% derive the greatest absolute risk reduction in recurrent stroke with early CEA. Selected patients with 50–69% stenosis may also benefit, depending on plaque/composition/stability, comorbidities, and symptoms.

Timing is critical: CEA is typically deferred for the first 48 hours following ischemic stroke to avoid reperfusion injury in the “hot brain” phase, then performed as soon as safely feasible—ideally within 7–14 days of the index event. The benefit declines substantially with delay beyond two weeks.

Emergency clinician priorities:

Once intracranial hemorrhage is ruled out:

High-risk TIA and nondisabling stroke live on the same continuum and should be managed with the same urgency. Load antiplatelets in the ED and tailor the regimen to mechanism. Most patients without endarterectomy plans or atrial fibrillation benefit from a short course of dual antiplatelet therapy (DAPT)—typically  21 days—then de-escalation to monotherapy. Pragmatically, aspirin 160–325 mg loading then 81 mg daily combined with clopidogrel 300 mg loading then 75 mg daily is common; aspirin with ticagrelor 180 mg loading then 90 mg twice daily is a reasonable alternative. Benefit is front-loaded in the first three weeks; bleeding risk rises after, which is why DAPT is not continued indefinitely as a standard. Use single antiplatelet therapy if carotid surgery is anticipated, extend dual antiplatelet therapy when intracranial atherosclerosis is the culprit per local protocol, and/or transition to anticoagulation when cardioembolic sources such as atrial fibrillation are identified and it is safe to do so. For symptomatic cervical artery dissection with TIA or nondisabling stroke, treatment typically involves a short course of DAPT, while asymptomatic dissection commonly receives single-agent therapy for months in coordination with the stroke team.

Single antiplatelet medication options:

DAPT (short course ~21–28 days):

Etiology-specific nuances:

Cardioembolic sources (e.g., AF): oral anticoagulation for secondary prevention; initiation/timing individualized (consider infarct size, hemorrhagic risk, and neurology guidance) but typically within 4 days; the trend as of 2025 is to start a DOAC as soon as 24 hrs after the stroke initiation for smaller infarcts with low hemorrhagic transformation risk.

Smoking cessation, diabetes optimization, physical activity, and diet counselling—all should begin in the ED discharge summary or follow-up instructions.

Disposition decisions for patients presenting with acute nondisabling stroke should be individualized, guided by risk stratification and institutional resources. Admission to a specialized stroke unit is associated with improved outcomes even in nondisabling presentations and should be prioritized when high-risk features are present or reliable outpatient follow-up cannot be assured.

Hospital admission or observation is recommended for patients with any of the following:

Selected patients with nondisabling stroke can be discharged safely from the ED when all of the following are satisfied:

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