Binocular Visual Loss Caused by Acute Cardioembolic Stroke(3)

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Binocular visual loss, acute visual loss, cardioembolic stroke, cerebral angiography, DSA, selective intraarterial thrombolysis, visual pathway infarction, posterior circulation stroke, occipital lobe infarction, cortical blindness, visual pathway ischemia, neuro-ophthalmology, emergency stroke imaging, interventional neuroradiology 


PART 3 — DIAGNOSTIC ALGORITHMS & DIFFERENTIAL DIAGNOSIS MASTER FRAMEWORK

Binocular Visual Loss Caused by Acute Cardioembolic Stroke

SECTION 17 — COMPREHENSIVE DIAGNOSTIC FRAMEWORK

Acute binocular visual loss represents a time-critical neurological emergency. Rapid differentiation between vascular, inflammatory, epileptic, metabolic, and functional etiologies is essential to prevent irreversible neuronal injury.

A structured, algorithmic diagnostic approach significantly improves:

  • Diagnostic accuracy
  • Therapeutic timing
  • Visual prognosis
  • Overall neurological outcome

17.1 Emergency Diagnostic Objectives

The primary objectives during emergency evaluation include:

  1. Rapid identification of life-threatening causes
  2. Immediate exclusion of intracranial hemorrhage
  3. Localization of the lesion along the visual pathway
  4. Identification of large vessel occlusion
  5. Determination of reperfusion therapy eligibility

17.2 Stepwise Diagnostic Algorithm for Acute Binocular Visual Loss

STEP 1 — Immediate Clinical Triage

Parameter

Key Assessment

Onset time

Sudden vs gradual

Pain

Presence or absence

Consciousness

Alert vs altered

Focal deficits

Hemiparesis, aphasia

Cardiovascular risk

AF, valve disease

Procedure history

Cardiac catheterization

Red Flags for Stroke:

  • Sudden onset
  • Complete bilateral blindness
  • Altered mental status
  • Recent invasive cardiac procedure

STEP 2 — Neurological Examination

Essential components:

  • Visual acuity
  • Pupillary light reflex
  • Funduscopic examination
  • Visual field testing
  • Gaze and eye movement
  • Cognitive status

Key Pattern:

Blindness + intact pupillary reflex + normal fundus → Cortical blindness

STEP 3 — Emergent Neuroimaging

Modality

Purpose

Noncontrast CT

Hemorrhage exclusion

CTA

Vessel occlusion

CT Perfusion

Penumbra

MRI DWI

Infarct confirmation

DSA

Gold standard

STEP 4 — Etiological Classification

Based on imaging and cardiac evaluation:

  • Cardioembolic
  • Large artery atherosclerosis
  • Small vessel occlusion
  • Dissection
  • Hypercoagulable state

SECTION 18 — ADVANCED DIFFERENTIAL DIAGNOSIS

Differentiating vascular from non-vascular causes of binocular visual loss is critical.

18.1 Vascular Causes

Etiology

Mechanism

Key Features

Cardioembolic stroke

Bilateral PCA emboli

Sudden blindness

Basilar artery occlusion

Brainstem ischemia

Coma + blindness

Vertebral artery dissection

Thromboembolism

Neck pain

Giant cell arteritis

Vasculitis

Headache, ESR↑

Hypotensive ischemia

Watershed infarcts

Shock

18.2 Neurological Non-Vascular Causes

Etiology

Hallmark

Occipital lobe seizures

Transient blindness

PRES

Vasogenic edema

Toxic encephalopathy

Global confusion

Hypoglycemia

Reversible loss

18.3 Ophthalmological Causes

Etiology

Key Feature

Bilateral optic neuritis

Pain, MS history

Acute angle-closure glaucoma

Severe eye pain

Bilateral retinal artery occlusion

Fundus whitening

18.4 Functional & Psychogenic Visual Loss

  • Normal imaging
  • Normal pupillary reflex
  • Inconsistent exam findings
  • Psychological stress history

SECTION 19 — DIAGNOSTIC DIFFERENTIATION MATRIX

Feature

Stroke

Migraine

Seizure

PRES

Psychogenic

Onset

Sudden

Gradual

Sudden

Gradual

Variable

Duration

Persistent

Transient

Seconds–minutes

Hours–days

Variable

Imaging

Infarct

Normal

Normal

Edema

Normal

EEG

Normal

Normal

Abnormal

Normal

Normal

BP

Normal

Normal

Normal

Severe HTN

Normal

SECTION 20 — ETIOLOGICAL WORKUP OF CARDIOEMBOLIC STROKE

Given that the patient underwent percutaneous mitral balloon valvuloplasty, the embolic risk was significantly elevated.

20.1 High-Risk Cardiac Sources

Condition

Embolic Risk

Mitral stenosis

Very high

Atrial fibrillation

Very high

Mechanical valves

Extremely high

LV thrombus

High

Recent MI

High

20.2 Cardiac Evaluation Protocol

  1. Transthoracic echocardiography (TTE)
  2. Transesophageal echocardiography (TEE)
  3. Continuous ECG monitoring
  4. Cardiac MRI (if needed)

SECTION 21 — ADVANCED NEURO-OPHTHALMOLOGY INTEGRATION

21.1 Key Clinical Bedside Tests

Test

Interpretation

Pupillary reflex

Preserved in cortical blindness

Blink-to-threat

Absent

Optokinetic nystagmus

Absent

Visual evoked potentials (VEP)

Absent cortical response

21.2 Visual Evoked Potential (VEP)

VEP is extremely valuable in:

  • Confirming cortical dysfunction
  • Differentiating optic neuropathy from cortical blindness
  • Prognostic stratification

SECTION 22 — STROKE MECHANISM MODEL IN THIS CASE

Mechanistic Sequence:

  1. Transseptal puncture
  2. Thrombus dislodgement
  3. Systemic embolization
  4. Bilateral PCA occlusion
  5. Cortical ischemia
  6. Acute binocular blindness

REFERENCES

  1. Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke. Stroke, 2019;50(12):e344–e418.
  2. Powers WJ, et al. 2018 Guidelines for the early management of acute ischemic stroke. Stroke, 2018;49:e46–e110.
  3. Saver JL. Time is brain—quantified. Stroke, 2006;37:263–266.
  4. Rizzo JF, Lessell S. Cortical blindness. Ophthalmology, 1994;101(10):1778–1783.
  5. Broderick JP, et al. Endovascular therapy after intravenous t-PA versus t-PA alone. N Engl J Med, 2013;368:893–903.
  6. Goyal M, et al. Endovascular thrombectomy after large-vessel ischemic stroke. Lancet, 2016;387:1723–1731.
  7. Biousse V, Newman NJ. Neuro-ophthalmology of stroke. Lancet Neurol, 2015;14:1168–1180. 
  8. Campbell BCV, et al. Imaging selection in ischemic stroke. N Engl J Med, 2015;372:1009–1018.

To be continued.

 

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