B6W7 - Eye And Visual Pathways

Front 1

What is the embryological origin of the eye?

Back 1

Retina - Prosencephalon (forebrain)
Other parts (cornea, lens) - nearby ectoderm and endoderm

Front 2

Label the following eye diagram.

Back 2

.

Front 3

Where can you find anterior and posterior chambers? How are they different from compartments?
What type of fluid can you find inside?

Back 3

Compartments - anterior and posterior are separated by the lens and ciliary muscles. Posterior compartment is filled with vitreous humors and the anterior is filled with aqueous humor.
Chambers - part of the anterior compartment, anterior and posterior are separated by pupil and iris.

Front 4

What are the functions of Sclera? Cornea? Is the cornea vascularised?

Back 4

Sclera:
- site of attachments of ocular muscles
- protective and supportive role

Cornea:
- Allows entry of light
- Principle mechanism for focusing image on the retina.

Cornea is not vascularised. Metabolic needs supplied by aqueous humor and environmental oxygen.

Front 5

What are the 5 layers of the cornea?

Back 5

From inner to outer:
- Endothelium
- Descemet's membrane (DM)
- Stroma
- Bowman's membrane
- Epithelium

Front 6

What are the functions of choroid? Is it vascularised? Other than blood vessels, what other type of cells can be found in this layer?

Back 6

Function:
- Supplies nutrients and oxygen to all layers of the eye
- Absorbs light to prevent light scattering within the eye

It is heavily vascularised.

Other types of cells: melanocytes (also melanin pigments)

Front 7

What are the functions of ciliary processes?

Back 7

Ciliary processes are extensions of the ciliary body.

- Anchors the lens in place
- Forms aqueous humour that fills the anterior compartment

Front 8

What emerge from the cilary processes and insert into the capsule of the lens?

Back 8

Zonule fibres.

Front 9

Describe the flow of the vitreous humor?

Back 9

Vitreous humor fills the anterior compartment, both anterior and posterior chambers.
It is produced in the posterior chamber by ciliary processes -> through pupil -> anterior chamber -> absorbed by the Schlemm's canal.

Front 10

What is glaucoma?
Describe open and close angle glaucoma?
Which one is more common?

Back 10

Glaucoma => a spectrum of related disorders characterized by progressive loss of ganglion cells (GC) and their axons (optic nerve). It is strongly associated with increase intraocular pressure (IOP).

Open angle glaucoma
- Sites of resistance to aqueous flow lie within the drainage (Schlemm's canal)

Closed angle glaucoma
- Anatomically closed angle of the iris with the Schlemm's canal - anatomically disrupts drainage.

Open angle (60%) > closed angle (0.5%)

Front 11

What are the 3 histological layers of the lens?

Back 11

1. Capsule
- thick basement membrane + collagen IV; carbohydrate rich.

2. Subcapsular epithelium - only at the anterior surface.
- Single layer of cuboidal epithelium.

3. Lens fibres.
- Highly differentiated subcapsular epithelial cells.
- Contains protein - crystallins.

Front 12

What are the risk factors for cataract?

Back 12

- Aging of the lens
- Diabetes
- Steroid therapy
- Poor nutrition
- Smoking
- Irradiation

Front 13

Describe the process of accommodation.

Back 13

Accommodation - the ability of the lens to focus on an object, far or distant.

This is achieved by the ciliary muscles and the elastic property of the lens.
Close object: ciliary muscles contract -> forward displacement of the choroid and ciliary body -> relieves the tension of the zonules -> lens bulges due to its innate elastic property.
Pupil also dilates.

The opposite for distant object.

Front 14

What are the 2 muscles of the iris? What are they innervated by?

Back 14

1. Dilator pupillae
- Radially oriented
- Extending from the ciliary body.
- Sympathetic innervation

2. Constrictor pupillae
- Circularly oriented
- Parasympathetic innervation

Front 15

What are the 10 layers of the retina?

Back 15

From outer to inner (PSsN PN PGN L):
1. Pigment epithelium
2. Outer segments
3. Inner segments
4. Outer nuclear layer
5. Outer plexiform layer
6. Inner nuclear layer
7. Inner plexiform layer
8. Ganglion cell layer
9. Nerve fibre layer
10. Inner limiting membrane

Front 16

What are the cells you can find in the retina? In what layer can you find them?

Back 16

.

Front 17

In response to increased light, do photoreceptor increases or decreases its glutamate release?

Back 17

PR decreases its release of glutamate in response to light.

Front 18

What type of bipolar cells (b/p) is activated in response to increase light?
What receptors are expressed in this cell?

Back 18

'ON' bipolar cells.
It expresses metabotropic glutamate receptors.

Front 19

What type of bipolar cells (b/p) is activated in response to increase light?
What receptors are expressed in this cell?

Back 19

'OFF' bipolar cells.
It expresses ionotropic glutamate receptors.

Front 20

2mm lesion centered on the fovea resulted in how much % loss of ganglion cells input to the brain?

Back 20

25%
GC is highly condensed at the foveal rim.

Front 21

What ganglion cells contribute to the magnocellular pathway?
What is the magnocellular pathhway important for? Where is it most commonly located?

Back 21

Parasol ganglion cell.
Magnocellular pathway is important in detecting form and motion.

Parasol GC are most common in peripheral retina.

Front 22

What ganglion cells contribute to the parvocellularpathway?
What is the magnocellular pathhway important for? Where is it most commonly located?

Back 22

Midget ganglion cells. It relays information from individual L and M cones, carrying info about form, position and colour.

Parvocellular pathway is important for:
- to provide information with high spatial resolution
- To relay colour coded information from medium to long wavelength.

Front 23

Name the 4 locations of the brain where ganglion cells project

Back 23

1. Nucleus of the optic tract.
2. Pretectal area - pupillary reflex.
3. Superior colliculus - visual/auditory/somatosensory coordination.
4. Dorsal lateral geniculate nucleus (dLGN)

Front 24

What are the 3 types of ganglion cells? And what are their functions?

Back 24

1. Parasol cells - detecting movement and are sensitive to contrast.
2. Midget GC - mediate high acuity and red/green colour vision.
3. Small bistratified - sensitive to blue light and mediate blue/yellow colour vision.

They are projected to different layers of the dLGN.

Front 25

Through what pathway does the visual information from the dLGN transmitted to V1?

Back 25

Meyer's loop (part of geniculocalcarine tract)

Front 26

Lesions in the visual pathways.

Back 26

.

Front 27

Describe the pathway for pupillary reflex.

Back 27

Optic nerve (CN II) -> optic chiasm -> optic tract -> Pretectal area -> bilateral innervation to Edinger Westpal nucleus (parasympathetic nuclei of CN III) -> ipsilateral innervation of ciliary ganglion -> CN III -> ciliary muscles.

Front 28

Describe the accommodation reflex pathway.

Back 28

CN II -> occipital lobe -> accommodation centre (peristriate area 19) -> edinger westphal nucleus -> CN III -> ciliary muscles + medial rectus muscle + sphincter pupillae muscle

Front 29

What is the nerve innervation of:
- the cornea?
- sphincter pupillae muscle (or circular muscle)?
- dilator pupillae muscle (or radial muscle)?

Back 29

Cornea - Opthalmic nerve, V1.
Sphincter pupillae muscle - parasympathetic fibres (CN III)
Dilator pupillae m - sympathetic fibre; long ciliary branches of V1.

Front 30

Where in the retina can you find high concentration of vitamin A?
What is the function of vit A?

Back 30

Vit A (or xantophyll pigments) is in high concentration in the macula.

It functions to filter damaging short wavelength light.

Front 31

What type of photoreceptors can be found in the fovea?

Back 31

Red and green cones.

Fovea does not contain alot of rods and blue cones.

Front 32

Label the extraocular muscles below. What are the nerves innervation?

Back 32

SO4 LR6 Rest 3

Front 33

What is the main sensory nerve of the eye?

Back 33

Opthalmic nerve (V1). It carries the sympathetic fibres which dilate the pupil.

Front 34

What is Age-related Macular Degeneration (AMD)?

Back 34

AMD - vision loss due to degeneration of the photoreceptors, possibly caused by degeneration of pigmented epithelium and/or neovascularisation of the outer retina.

Front 35

What is the early signs of AMD?

Back 35

- Drusen (white spots)
- Area of cell loss, centered on the macula

Front 36

What are the 2 types of AMD? How can they be differentiated?

Back 36

1. Dry AMD
- due to degeneration of pigmented epithelial layer -> loss of photoreceptors

2. Wet AMD
- due to abnormal blood vessels growth leading to blood and protein leakage below the macula.

Differentiated by red (blood) spot in wet AMD.

Front 37

What are the risk factors of AMD?

Back 37

- Age
- Smoking
- Family history
- Risky Complement Factor H (CFH) gene.
- High cholesterol
- Eating fish 1/week decreases risk of early AMD by 40%
- Hypertension
- Race (high in Caucasian than African)

Front 38

What muscles are responsible for the movements of the eye?

Back 38

.

Front 39

How is glaucoma diagnosed?

Back 39

- Initial diagnosis is based on assessment of the optic disc (OD)
- Assessment of intraocular pressure (IOP) - however 50% of diagnosed glaucoma occurs in the absence of increased IOP.

Front 40

What are the risk factors for glaucoma?

Back 40

- Increase IOP
- family history - first degree relative is associated with 4x increased risk.

Front 41

Autoimmune disorders of the NS

How is MS diagnosed?

Back 41

Diagnosis of MS – by McDonald criteria:

o A clinical diagnosis, at least 1 clinical episode. Episodes separated by time and space
o Tests to use: MRI, CSF, evoked potentials (visual, somatosensory, brainstem)

Front 42

Autoimmune disorders of the NS

What are the risk factors for MS?

Back 42

Risk factors for MS:
o Female gender
o Young age ~ 20s. (>40s rare)
o Family history of MS
o Distance from equator – vitamin D
o Increased risk with increased distance from the equator  less vit D which is involved in Tc autoregulation.
o Race (northern Europe descend highest. Asian, African and Native American has the lowest risk)
o Epstein-Barr virus infection

Front 43

Autoimmune disorders of the NS

What is damaged in MS? Describe the pathophysiology.

Back 43

MS is an autoimmune disease attacking the oligodendrocytes of the CNS.

Pathophysiology:
Autoreactive Tc normally controlled by Treg cells
↓
Failure of regulation when autoreactive Tc stimulated by Ags (EBV, unknown)
↓
Tc express adhesion molecules to BBB and penetrate (by expression of degrading enzyme; Matrix Metalloprotease (MMP))
↓
Activated Tc re-encounter myelin (or stimulated Ag) and activates microglia (an APC)
↓
Microglia expresses MHC II which promotes Tc differentiation to Th1 and Th2 and microglia activation.
↓
• Th1 activates macrophages which causes cellular damage to myelin
• CD8 Tc upregulated by IFN-gamma, released by macrophages, causes damage to oligodendrocytes
• Th2 stimulates Bc to release Abs which can cause: antibody mediated injury and/or antibody mediated remyelination

Front 44

Autoimmune disorders of the NS

Why are there intermittent MS episodes?

Back 44

Intermittent episodes because of remyelination processes (may be triggered antibody)

Front 45

Autoimmune disorders of the NS

What are the common presentations of MS?

Back 45

Common clinical presentations of MS:
o Optic neuritis
o Sensory symptoms
o Motor deficit
o Cerebellar symptoms
o Brainstem (esp. diplopia)
o Transverse myelitis (motor, sensory or bladder)
o Fatigue

Front 46

Autoimmune disorders of the NS

What are the possible clinical courses of MS?

Back 46

.

Front 47

Autoimmune disorders of the NS

What are the managements for MS acutely, disease modifying treatment, long-term?

Back 47

o Acute attack: corticosteroids (IV – methylprednisone)
o Disease modifying treatment – INF-beta, alpha, autoimmune cytotoxic drugs: galtiramer, natalizumab, mitoxantrone)
o Long-term: rehab, education, lifestyle changes, etc.

Front 48

Autoimmune disorders of the NS

What is ADEM (acute disseminated encephalomyelitis)?

Back 48

ADEM => a monophasic autoimmune disease of the CNS which involved demyelination normally affecting children, and normally occur following infection of vaccination (rabies, small pox). It responses better to corticosteroids (high dose methylprednisolone) and usually no relapses.

Front 49

Autoimmune disorders of the NS

What is Devic’s (Neuromyelitis optica) syndrome? Where does it attack?

What is it pathogenesis? (Name the attacker, and the attackee)
Should we give steroids in acute attacks?

Back 49

Monophasic or recurrent demyelinating condition which attacks the optic nerve or spinal cord ( More severe than MS)

NMO – IgG and attacks the Aquaporin 4 on the membrane of astrocytes. Still unclear how this leads to demyelination

No, plasmapharesis appears to help though

Front 50

Autoimmune disorders of the NS

What is Guillain-Barre Syndrome (GBS)? What are the most common clinical presentations?

Back 50

GBS is an autoimmune demyelination disorder of the PNS. Tc mediated and triggered by post infection/vaccination, surgery or idiopathic. MOST commonly viral infections (similar to ADEM but for PNS)

Common clinical presentation: ascending paralysis (legs -> arms -> face)

Front 51

Autoimmune disorders of the NS

What are the common organisms associated with GBS?

Back 51

campylobacter jejuni, cytomegalovirus, EBV, mycoplasma pneumonia. CMV gives bad prognosis, EBV better

Front 52

Autoimmune disorders of the NS

What is the management for GBS?

Back 52

o IVIG
o Treatment of complications:
 DVT prophylaxis, ICU, pressure care, pain management, rehabilitation.
 Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) -> inflammatory neuropathy. Progressing at least 2 months. Treatment: prednisolone, cyclophosphamide, cyclosporine, IVIG, plasmapheresis.

Front 53

Neurotransmitter system

Explain why L-dopa can cross the BBB and dopamine cannot.

Back 53

Dopamine is charged and charged molecules cannot cross BBB.

Front 54

Neurotransmitter system

What part of the cathecolamine pathway is missing in people who have albinism? (it is also the reason for lack of pigment)

Back 54

Tyrosine hydroxylase.

Front 55

Neurotransmitter system

Where is dopamine released? (2 pathways)

Name some of the functions that dopamine is involved in and 2 diseases that are thought to be associated with abnormal levels of dopamine.

Back 55

Dopaminergic system starts in the midbrain from 2 nuclei:
- Nisogastrial pathway - Substantia nigra, projects to striatum (caudate putamen)
Involves in: motor coordination
- Mesolimbic pathway - Ventral tegmentum area, projects to pre-frontal cortex.
Involves in: planning, decision making, executive function.

Dopamine plays an important role in movement, mood and memory (mmm) (also has a role in sleep, dream and other things like reward system).

Associated diseases: Parkinson’s disease, schizophrenia.

Front 56

Neurotransmitter system

Why is it that oral amphetamine increases the levels of alertness of the CNS but IV injection of adrenal does not?

Back 56

Adrenal cannot cross BBB but amphetamine simply upregulates the production of cathecolamines in the CNS.

Front 57

Neurotransmitter system

Serotonin – where is it produced? Where can it be found?

Back 57

The precursor of serotonin is tryptophan (fom milk) and it requires vit B6 for production.
Serotonin production occurs in the raphe nuclei (rostral), it has very extensive innervation especially to the limbic areas of the brain. That pharmacologically involved in migraine control and LSD.

Front 58

Neurotransmitter system

What are the functions of serotonin?

Back 58

SAADD

Sleep wake cycle
Anxiety
Aggression
Descending pain pathway
Depression (lack)

Front 59

Neurotransmitter junction

What is the primary function of Ach? How is it broken down?
What disorder is associated with reduced Ach?

Back 59

Ach - main NT at the NMJ
Functions in CNS:
- learning and memory
- Arousal and sleep wake cycle
Break down - cholinesterase (synaptic cleft)

Decrease Ach is associated with Alzheimer's.

Front 60

Neurotransmitter system.

What are the sites of Ach production?

Back 60

Ach production:
- tegmental complex
- Pontomesencephalon
- basal forebrain complex

Front 61

Neurotransmitter system

Where is the site of orexin production?
What is its functions?

Back 61

Hypothalamic nuclei.

Functions:
- Hunger pathway
- Interphase between CNS and PNS
- Promote wakefulness.

Front 62

What are the actions of the superior oblique muscle?

Back 62

On primary position:
depression, intorsion and abduction.

On adducted eye:
depression.

SO-LID (lateral rotation, intorsion, depression)

Front 63

What are the signs for:
III nerve palsy?

Back 63

1. Complete ptosis (levator palpebrae muscle - control eyelid)
2. Loss of pupillary reflex - dilated iris.
3. Failure of elevation and adduction (SR, IO, MR)
4. Failure of depression (IR)
5. Eye down and out on primary position (uncompensated IR and LR on primary position)

Failure to adduct, down movement.

Front 64

There are 2 divisions of III nerve: superior and inferior. What muscles do they control?

Back 64

Superior division:
- superior rectus muscle
- levator palpebrae muscle

Inferior division:
- Inferior rectus muscle
- Inferior oblique muscle
- Medial rectus muscle
- pupil/ciliary body

Front 65

What are the signs for:
IV nerve palsy?

Back 65

Failure to depress on abducted position.

Front 66

What special test you can do to test CN IV palsy?

Back 66

Bielschowsky head tilt test.

Eye elevates with head tilt to that side.

Front 67

What are the signs for VI nerve palsy?

Back 67

Eye fails to abduct on lateral gaze.

Thyroid eye disease may mimic VI nerve palsy.

Front 68

Describe the horizontal gaze pathways.

Back 68

Contralateral -> Lateral gaze centre -> VI nuclei -> MLF -> III nucleus.

Hint 68

Muscles include: LR (CN VI) and MR (CN III)

Front 69

Describe what happens in gaze palsy.

Back 69

Lesion at the CN VI nuclei -> neither eye (AFFECT BOTH EYE) will move towards the lesion side.

Front 70

Describe what happens in internuclear opthalmoplegia.

Back 70

Lesion at the medial longitudinal fasciculus (MLF) - connection between CN VI nuclei and CN III nuclei.

Failure of the contralateral eye (ONLY ONE EYE) to the VI nucleus to adduct.

Front 71

Describe what happens in 'one-and-a-half' syndrome. What are the symptoms?

Back 71

Lesions at CN VI nucleus + Medial Longitudinal Fasciculus (MSF) - between CN VI and CN III nuclei.
Symptoms: failure of both eye to look towards the lesion side + failure of the contralateral eye to the VI nucleus to adduct??

Front 72

Describe the 5 types of normal eye movements.

Back 72

1. Vestibular - normal eye movement according to the vestibular system.
2. Optokinetic - eye movements to follow objects at high speed and return to the starting position (e.g. looking at trees from a moving car)
3. Saccadic - fast movement
4. Smooth pursuit - movement to smoothly follow a moving object.
5. Convergence - simultaneous inward movement of both eyes.

Front 73

Differentiate between cerebellar with vestibular nystagmus.

Back 73

Cerebellar nystagmus is damage to gaze holding ability. It is gaze evoked, fast phase in direction of gaze, slow phase exponentially decreasing.

Vestibular nystagmus - slow phase linear.??