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The first 25 slides, exactly as they appear. The full deck has 72 content slides.
Ophthalmology
Disorders of Higher Visual Functions Cortical Blindness ot
Built from Khurana — Neuro-Ophthalmology
What’s inside
10 sections · 72 slides
Overview
- What this topic is really about
How the Visual Brain Is Wired
The road from retina to the seeing cortex
- The signal's journey, in plain steps
- Three types of ganglion cell, three parallel channels
- Naming the seeing cortex: V1 to V6
- How the areas talk to each other
- Two great highways out of V1: 'what' vs 'where'
- Why the 'what/where' split matters clinically
When Specific Cortical Areas Fail
A syndrome for every damaged map
- The organising idea
- Higher visual syndromes mapped to their cortical area
- Area V1 — Anton syndrome (denial of blindness)
- Area V1 — blindsight and Riddoch phenomenon
- Area V1 — achromatopsia and visual ataxia
- Area V2 and V3 (extrastriate) disorders
- Area V5 disorders — akinetopsia and dyslexia
- The dorsal 'where' pathway — what it maps
- Balint's syndrome — the classic parietal triad
- More dorsal-pathway signs
- Distortions of space: allesthesia and rotation
- The ventral 'what' pathway — disorders of recognition
- Visual hallucinations: why the brain 'sees' things
- Charles Bonnet syndrome — hallucinations of the blind
- Charles Bonnet — recognition and treatment
- Telling the three hallucination types apart
- Drug-induced visual hallucinations
Cortical Blindness
When both occipital lobes go dark
- What cortical blindness is
- Causes of cortical blindness
- Clinical features — the recognisable pattern
- Management of cortical blindness
Other Visual Disorders
Night, day and sudden blindness
- Night blindness vs day blindness
- Amaurosis and amaurosis fugax
- Amaurosis fugax on examination, and uraemic amaurosis
Amblyopia — The 'Lazy Eye'
A healthy eye the brain never learned to use
- What amblyopia actually means
- Older classification 1 — functional vs organic
- Older classification 2 — arrest, extinction, congenital
- Present-day terms 1 — strabismic amblyopia
- Present-day terms 2 — stimulus deprivation amblyopia
- Present-day terms 3 — refractive amblyopias
- Present-day terms 4 — nystagmus and idiopathic
- Bringing the types together
- Which amblyogenic factors drive each type of amblyopia
Why Amblyopia Happens
Deprivation, competition and cortical inhibition
- The three amblyogenic mechanisms
- How normal binocular vision is built (Hubel & Wiesel)
- The X, Y and W systems — three retinal channels
- The X, Y and W retinal channels feeding the brain
- Monocular deprivation studies — the key experiment
- Binocular deprivation and experimental strabismus
- The retina's own role in amblyopia
- Active cortical inhibition
Recognising Amblyopia at the Bedside
The tell-tale clinical and laboratory signs
- Visual acuity — the defining feature
- Neutral-density filter and crowding
- Fixation pattern — where the amblyopic eye 'aims'
- Grades of eccentric fixation on the retina
- More on fixation — stability and paradox
- Other laboratory findings 1
- Other laboratory findings 2
Diagnosis and Management
Catch it early, clear the image, correct the dominance
- How the diagnosis is made
- Management — prevention, then treatment
Pulling It Together
The big ideas to keep
- Three ideas to carry away
- A patient is blind after bilateral occipital stroke but insists they can see and has NORMAL pupils. Why?
- References (1/2)
- References (2/2)
- Neuro-Ophthalmology