Binocular Visual Loss Caused by Acute Cardioembolic Stroke(2)

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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 2 — CLINICAL MASTERCLASS & ADVANCED IMAGING INTERPRETATION

Binocular Visual Loss Caused by Acute Cardioembolic Stroke

SECTION 10 — CLINICAL PRESENTATION: NEURO-OPHTHALMOLOGIC MASTERCLASS

10.1 Clinical Spectrum of Acute Binocular Visual Loss

Acute binocular visual loss represents one of the most catastrophic neurological symptoms, indicating bilateral involvement of central visual processing structures. Unlike monocular vision loss, which frequently reflects ocular or anterior optic pathway pathology, binocular visual loss almost always implies post-chiasmal or cortical dysfunction, most commonly due to ischemic stroke.

The clinical spectrum includes:

  • Complete cortical blindness
  • Partial bilateral visual field deficits
  • Altitudinal visual loss
  • Visual agnosia
  • Simultanagnosia
  • Visual hallucinations

The clinical presentation is often dramatic, abrupt, and associated with profound psychological distress.

10.2 Cortical Blindness: Clinical Characteristics

Cortical blindness is defined as the loss of visual perception with intact pupillary reflexes and structurally normal eyes.

Core Diagnostic Features:

Feature

Description

Visual acuity

   Profound reduction or no light perception

Pupillary reflex

   Preserved

Fundus exam

   Normal

Optic disc

   Normal

Ocular motility

   Intact

Blink to threat

   Absent

Awareness 

   The patient may deny blindness (Anton syndrome)

10.3 Anton Syndrome: Visual Anosognosia

Some patients demonstrate anosognosia for blindness, termed Anton syndrome, characterized by:

  • Denial of blindness
  • Confabulation of visual experiences
  • Lack of insight into deficits

This phenomenon occurs due to bilateral occipital plus parietal lobe involvement, disrupting both visual perception and awareness networks.

SECTION 11 — NEURO-ANATOMICAL CORRELATION OF VISUAL DEFICITS

11.1 Visual Cortex Functional Mapping

Cortical Region

Function

V1 (Calcarine cortex)

  Primary visual perception

V2–V3

  Visual association

V4

  Color perception

V5 (MT area)

  Motion perception

Inferotemporal cortex

  Object recognition

Posterior parietal cortex

  Spatial integration

Bilateral involvement of V1 → complete cortical blindness
Partial involvement → specific visual deficits.

11.2 Lesion Localization and Clinical Correlation

Lesion Location

Clinical Syndrome

Bilateral calcarine cortex

Complete blindness

Occipitotemporal junction

Visual agnosia

Bilateral V5

Akinetopsia

Occipitoparietal cortex

Balint syndrome

SECTION 12 — ADVANCED IMAGING INTERPRETATION

12.1 Imaging Modalities Overview

Modality

Diagnostic Role

Noncontrast CT

Hemorrhage exclusion

CT angiography

Vessel occlusion

CT perfusion

Penumbra evaluation

MRI DWI

Infarct core

MR perfusion

Tissue viability

DSA

Gold standard + treatment

12.2 DSA: Gold Standard for Posterior Circulation Stroke

Digital subtraction angiography (DSA) provides:

  • Real-time dynamic flow assessment
  • Collateral circulation visualization
  • Distal branch occlusion detection
  • Endovascular treatment guidance

In this case, DSA demonstrated:

  • Bilateral posterior cerebral artery embolism
  • Distal calcarine branch occlusion
  • Reduced cortical blush

12.3 Figure 1 — Detailed Interpretation


Figure 1. Digital Subtraction Angiography demonstrating acute embolic occlusion of bilateral posterior cerebral arteries at the distal P2–P3 segments.

Imaging Analysis:

  • Abrupt vessel cutoff
  • Absent distal opacification
  • Delayed collateral filling
  • Poor parenchymal blush

Clinical Correlation:

  • Direct explanation for sudden binocular visual loss
  • Suggests cardioembolic source

12.4 Figure 2 — Coronal DSA Projection


Figure 2. Coronal DSA projection revealing symmetrical perfusion defects in bilateral occipital lobes.

Imaging Analysis:

  • Bilateral symmetrical hypoperfusion
  • No cortical capillary phase
  • Marked flow delay

Interpretation:

Strong radiologic signature of bilateral occipital infarction, confirming cortical blindness etiology.

12.5 Figure 3 — Post-Treatment Angiography

Figure 3. Post-thrombolysis cerebral angiography showing partial recanalization of distal PCA branches.

Imaging Analysis:

  • Partial restoration of antegrade flow
  • Improved parenchymal blush
  • Residual distal emboli

Clinical Correlation:

Partial reperfusion → potential for visual recovery depending on ischemic duration.

SECTION 13 — ADVANCED STROKE IMAGING BIOMARKERS

13.1 CT Perfusion Parameters

Parameter

Clinical Meaning

CBF (Cerebral Blood Flow)

Tissue perfusion

CBV (Cerebral Blood Volume)

Viable tissue

MTT (Mean Transit Time)

Hemodynamic delay

Tmax

Penumbra indicator

Bilateral occipital hypoperfusion with preserved CBV indicates salvageable penumbra.

13.2 MRI Diffusion-Perfusion Mismatch

Diffusion restriction + perfusion deficit mismatch identifies a therapeutic window for reperfusion.

SECTION 14 — DIFFERENTIAL DIAGNOSIS OF ACUTE BINOCULAR VISUAL LOSS

14.1 Major Differential Diagnoses

Etiology

Key Features

Posterior circulation stroke

Sudden onset, DSA occlusion

Migraine aura

Reversible, headache

Occipital seizure

EEG abnormality

Posterior reversible encephalopathy syndrome (PRES)

Hypertension, MRI edema

Bilateral optic neuritis

Painful vision loss

Pituitary apoplexy

Endocrine signs

Toxic-metabolic encephalopathy

Altered sensorium

14.2 Stroke vs Migraine Visual Loss

Feature

Stroke

Migraine

Onset

Sudden

Gradual

Duration

Persistent

Transient

Pain

Absent

Severe

DSA

Occlusion

Normal

SECTION 15 — CLINICAL DIAGNOSTIC ALGORITHM

Step 1: Rapid Neurologic Assessment

Step 2: Noncontrast CT

Step 3: CTA + CTP

Step 4: MRI DWI + PWI

Step 5: Emergency DSA

Step 6: Endovascular intervention

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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