Test 2: Visual CC Flashcards
**Presbyopia **
- Lens elasticity decreases with age= accomodation decreases= flatter lens.
- Near point recedes= people hold what they’re reading further and further away.
- One of the beauties of aging.
Glaucoma- Know what causes it, what glaucoma does to vision, and the symptoms
- Blocked outflow of fluid through canal of Schlemm. Pressure on the entire eyeball= damage to retina and optic nerve.
- Vision is BLURRED but not dimmed. Normal light gets to the retina but they have fewer photoreceptors= blurriness
- Peripheral vision is lost first and proceeds towards middle
Open angle glaucoma
- = angle between iris and cornea is normal and cause is unknown.
- accounts for 95% of cases.
Closed angle glaucoma
angle between iris and cornea is smaller and causes the blocked outflow
This amount of pressure will cause optic nerve damage
>20mm Hg
Pupillary light reflex
Light shined in one eye causes constriction of both pupils
**cataracts- know what it is and some possible causes. treatment? **
Proteins are constantly growing and being turned over in the lens. If the proteins aren’t turned over then the lens thickens and gets cloudy and opaque.
Causes: rubella (congenital), UV light, diabetes, radiation therapy, some drugs
Treatment: replace the lens
Uveitis
Inflammation of uvea (iris, ciliary body and choroid)= VASCULAR part of eye
Usually from eye injury
Retinal detachment
- What is it and how is treated
- chances of recovery
- boys vs girls
- things that can cause it?
- Neural retina tears away from pigment epithelium. Must be repaired surgically to avoid damage because neural retina will die without the blood supply (considered a medical emergency)
- RECOVERY IS DEPENDENT ON TIME (how quickly surgery is done) AND LOCATION (of detachemnt)
- males>females
- can be from trauma, surgery, genetics, etc.
Patient: recent trauma to the head, seeing flashes of light and specks floating.
DDx?
Detached retina from trauma. Fluid pulled apart the neural and pigmented epithelium. Must be treated ASAP.
- Is color blindness a real thing?
- Why is it more common in males?
- *Technically NO. *Loss of a cone color is “better thought of as color confusion”. The ability to **distinguish **colors is impaired.
- M-cone (absorbs green) and L-cone (red) are on the x-chromosome.
- Inability to detect RED
- Inability to detect **GREEN. **
- No red= PROTANOPIA
- No green=** DEUTERANOPIA**
**DEUTER= **two, green is the combination of two colors
PRO= professional, also “slang for prostitute”. I wasn’t allowed to wear red as a kid because it was too “prostitute like”.
What can blind people (striate cortical lesions) still detect? How?
Can have a puillary light refelx in the blind eye. **Normal circadian rhythm. **
Melanopsin-containing ganglion cells-Intrinsic light sensitivity- they will respond to light (even if rods and cones don’t) and send that info to the hypothalamus. They are also connected to the suprachiasmitic and pretectal nuclei.
Pathway of “blind sight”
Retina–> superior colliculus –> pulvinar –> posterior parietal cortex = tracking and orientation
Random shape floaty thing in your visual field.
What is it called? What causes it?
- Scotoma
- lesion of the retina or optic nerve.
- Causes: toxins, retinal hemorrhage, trauma, tumors.
Damage to right optic nerve. Which eyes have direct and consensual pupillary light reflexes?
Right eye (nerve damaged)= consensual light reflex
Left eye (normal)= direct light reflex (pretty sure it loses consensual because Rt eye cant process stuff?)
Hemifields
nasal and temporal
Monocular zone
crescent zone seen by only one eye
Papilledema
- **What is it? **
- **Sx? **
- **What is it usually a good sign for? **
- Block of axoplasmic flow (often from high ICP) causes swelling of the optic nerve head (= papilledema).
- Can cause partial/complete visual loss.
- increased ICP (intracranial pressure)
You’re playing catch with someone who sucks. They say they don’t see the ball moving
Akinetopsia= can’t see movement
Lesion to dorsal stream V5- involved in speed, motion and direction.
What’s involved in positioning of objects?
Parietal and occipital gyri.
Scotoma
- Randomly shaped region (bilateral or unilateral) of vision loss or reduction.
- It can be any shape
- LESION TO RETINA OR OPTIC NERVE from toxins, trauma hemorrhage
- Light in damaged eye: no consensual response in good eye, no direct response in bad eye
- light in good eye- normal response in both eyes
Congruous deficit
Visual field loss of one eye is the same as the other eye. More common when lesions are closer to visual cortex
Incongruous Lesion
More common in anterior lesions. Two eye visual fields are not the same.
Line of Gennarie
Myelinated fibers in layer 4b of Area 17= geniculocalacrine input
Macular sparing
Caudal visual cortex also supplied by MCA collaterals, so occlusion of calacrine from PCA won’t wipe it out
What can cause loss of **binocular vision? **
- LGN axons compete for parts area Area 17 during critical period of development. If visual input is weakened from one eye (congenital cataracts, strabismus or ambylopia) LGN from one eye fails
- Most of layer IV stellate cells get input from ONE eye only= loss of stereopsis (3Dness)
Achromotopsia
- Loss of color recognition without loss of object recognition due to **localized damage to certain part of association cortex. **
- NOT THE SAME AS COLOR BLINDNESS
Difficulty/inability to judge which object is closer.
Damage to magnocellular pathway especially in parietal association cortex. “where stream”
Apperceptive agnosia
inability to identify objects due to perceptual deficit
Associative Agnosia
Perception is fine, but interpretation (meaning) cannot by done
Object agnosia
Inability to recognize objects
Lesion in 18, 20, 21 of dominant (usually left) hemisphere.
Lesion to areas 18, 20, 21 on right vs left sides
Left (dominant)= object agnosia
Right (nondominant)= agnosia for drawing objects
I guess you might be my mom? Your face looks like everyone elses…
Prosopagnosia- bilateral lesion in 18, 20 and 21 (usually fusiform gyrus)
Balint Syndrome
- location of lesion
- Sx
- what isn’t affected?
- Bilateral lesion in parieto-occipital junction region= **medial superior temporal area (supramarginal gyrus according to his PP) **
- impaired saccades, optic ataxia (reaching for stuff), optic apraxia (can’t “fix” eyes), simultagnosia (can’t see whole picture instead of just one part/object)
- Reflex eye movement is spared
I wrote you a love poem, but I can’t read it. You sent me a letter back and I also can’t read it.. I’ll never know if it was a hate/love letter…..
alexia without agraphia- can write but not read
- Lesion of the splenium of the corpus collosum (carries visual information between cortices)
- +damage to adjacent occipatlal region (usually with homonymous hemianopia)
This is super common in MS.
- MLF syndrome. Ms’s want some–they get lonely.
- AKA internuclear ophathalmoplegia- damage to MLF = medial rectus palsy on attempted lateral gaze and monocular horizontal nystagmus when following moving object.
- **NORMAL CONVERGENCE. **
- **Unilateral= affects ipsilater medial rectus. **
One and a half syndrome
- lesion to abducens nucleus AND MLF (from other side abducens to ipsilateral medial rectus)
- Ipsilateral eye= no movement during horizontal gaze (adduction or abduction)
- Contralateral eye= only abducts
Argyll robertson pupil
Dissociation of pupillary light reflex and accomodation. Light reflex (direct and consensual) is messed up, but accomodation is fine.
Caused by: syphilis and diabetes.
Horner’s syndrome
transection of oculosympathetic pathway at any level. Miosis, ptsosis, hemianhydrosis, enophthalmos (opposite of exophthalmos–eyeball is too far in there)
Perinaud’s syndrome
- **Caused by? **
- Sx
- **Pineal gland **tumor compresses dorsal midrbain and pretectal areas
- impaired vertical gaze, large irregular pupils, eyelid abnormalities and impaired convergence.
Pneumonic I found online:
- *PERINAUD’S:**
- *P**seudo 6th nerve palsy/ Penial region
- *E**yelid Retraction (collier’s eyelid)
- *I**nternuclear ophthalmoplegia
- *N**ystagmus
- *A**ccomodation reflex present
- *U**pward gaze palsy
- *D**efective convergence/ Decerebrate rigidity
- *S**kew deviation
Primary Anopthalmos
Failure of optic vesicle to form= no eye development
Secondary Anopthalmos
development of forebrain is suppressed and eye problem is associated/from the forebrain issues
Microphthalmia
Mini-eye
arrested developmetn of the eye before the optic vesicle has formed. NO LENS
Coloboma
Key hold in retina (usually inferior to optic disk) due to defective closing of **retinal fissure **
Anophthalmia (general)
No eyeballs/eye tissue. Eyelids still form
(THANK GOD- THAT WOULD BE SOME TERRIFYING SHIT TO LOOK AT)
Cyclopia
Eyes fused into single media eye. Nose is above eye (proboscis)
Can be caused by holoprosencephaly (brain stuf is fused)
Central artery of the retina comes from?
Proximal hyaloid artery
Distal hyaloid artery?
Usually degenerates….if it doesnt then it looks like a worm sticking out of optic disc.
Congenital glaucoma
abnormal drainage mechanism through scleral venous sinus==> increased intraocular pressure
Good clincal sign (in the eye) indicating increased intracranial pressure?
**papilledema (edema of optic disc) **
Congenital ptosis
- failure of normal development of the levator palpebra superioris (trauma or dystrophy of superior division of occulomotor n)
- Failure of superior rectus
MYOPIA- what is it, how is it treated?
- Eyeball is too long (Anterior-post diameter)= rays **focus on vitreous humor **(don’t reach retina).
- Need CONCAVE lens
Hyperopia- anatomical issue, how is it fixed
- AP diameter is too short= parallel rays focus behind retina
- Needs CONVEX lens
Astigmia- what is it? Treatment?
- curvature of corneal surface isn’t uniform= light passage to cornea isn’t uniform
- cylindrical lens to equalize refraction
Blocking anterior choroidal artery
- what does it supply
- whats the deficit
- optic tract
- **contralateral homonymous hemaopsia **
Pituitary tumor usually….
- = lesion of optic chiasm
- bitemporal hemianopsia
- What if you squish the optic chaism laterally on one side (this is RARE)
- Both sides?
- ipsilateral NASAL hemianopsia
- binasal hemianopia = can be from calcified internal carotid arteries.
Uncal herniation
- ipsilateral hemiparesis (pressure on ALS in contralateral crus cerebri)
- Fixed dilated pupil, ptosis, down and out (pressure on ipsilateral occulomotor nerve)
- Contralateral homonymous Hemianopia- compression of PCA= ischemia of visual cortex. This probably is macular sparing?
Adie’s Syndrome
- **3 hallmarks: **large tonic pupil that reacts slowly to light, poor deep tendon reflexes, impaired sweating
- Damage to post ganglionic parasympathetic fibers leaving EDW nucleus.
- Seen in women with absent knee or ankle jerks.
Retinitis pigmentosa
- most common inherited cause of blindness.
- damaged retinal layer of rods and cones. No light recognition but pupillary light refelx may be spared.
- Circadian rhythm spared (melanopsin ganglion cells projecting to hypothalamus)
Most common cause of inherited blindness?
What is it? What are the two “pathways” this disease happens?
- **Retinitis pigmentosa= loss of photoreceptors **
- 25% from rhodopsin gene –> opsin accumulation –> degeneration of pigment layer
- Arrestin binding rhodopsiin defect–> constant stimulation –> degeneration
SX: loss of night vision followed by tunnel vision
retinitis pigmentosa.
the later the sx appear in life, the faster it progresses.
Acoomodation convergence (triple) reaction
Happens when you focus on a near object:
- Occular convergence- you focus on the near object by moving eyes together (medial rectus)
- Pupillary constriction = increased acuity
- thickening of lens from contraction of ciliary muscle
Input from visual association cortex (via superior brachium) –> superior colliculus
NO FRONTAL EYE FIELD INVOLVEMENT
A bear is coming at you: what happens to your pupils (pathway)
DILATION
Amygdala/Hypothalamus–> lateral horn (T1-T3)–> superior cervical ganglion –> post ganglionic fibers travel in carotid plexus to dilator pupillae muscle in iris
ALSO parasympathetics are inhibited.
Your lens is relaxed=
emmetropia- object at infinity is in sharp focus
Optic neuritis
(seen in MS)
Inflammation of optic nerve= **BLURRED **vision from loss/decreased fiber input.
Hemineglect- what is it? Where’s the lesion?
- Neglect of entire visual field
- Lesion in parietal cortex
The number 8 is ALWAYS red. What’s the issue?
Synesthesia- combination of two senses. Abnormality in fusiform area where overgrowth of one input encroaches on something else.
Macular degeneration is related to ___1____. Key sign is ____2__.
- AGE
- Drusens- yellow deposits in macula between retinal pigment epithelium and choroid.
Types of macular degeneration
- Dry- atrophy of pigment epithelial layer below retina. The vision loss is due to death of photoreceptors
- Wet- vision loss is from abnormal growth of blood vessels. Blood and proteins leak into the macula= irreversible photoreceptor damage.
Compare treatment and prognosis of wet vs dry macular degeneration
Wet= worse prognosis, treatments available (anti-VEGF, removal of blood before scarring= reversible)
Dry= better prognosis, no treatment.
I don’t care about you. I don’t care about people. I have NO EMOTIONS towards people.
Capgras Syndrome- disruption of visual info to amygdala= no emotional processing.
Mach band phenomenon
- what is it?
- what allows this to happen?
- At the boundry between two shades- the darker shade looks darker at the boundry and lighter shade looks lighter at the boundry
- Lateral inhibition
