week 14 Flashcards
ADHD onset and 2 symptms
< 12 years old
▪ Diminished sustained attention
▪ Increased impulsivity or hyperactivity
3 presentations of ADHD
▪ Predominantly inattentive presentation (6+ symptoms of inattention and a few of hyperactivity/impulsivity)
▪ Predominantly hyperactive/impulsive presentation
▪ Combined presentation
kids vs adult ADHD diagnosis
adults only need 5 of the criteria not 6
in adults think they just masked it as kids
substance use disorder is a
Chronic, relapsing disorder characterized by
▪ Compulsive drug-seeking and drug-taking disorders
▪ Loss of control over drug intake
▪ Negative affect when access to the drug is withheld
3 stages of addiction
- acute reinforcement and drug use (brain areas for motivation)
–>hijack reward system
- escalation of drug use/dependence (change brain areas in executive function and inhibitory control)
–>dorsal stratum forms habits (cues, goals)
–> impaire PFC
3.late stage- withdrawal/ incubation/ relapse (changes to reward network and executive function)
–> VTA (all stages)
–>relapse with PFC and nucleus accumbens
–> limbic (amygdala and hippocampus) = cue related and stress (CRH or cortisol)
key brain areas in substance abuse
VTA- dopamine
nucleus accubens- GABA and acetylcholine
amygdala, hippocampus, dorsal straitum, PFC
neuro in ADHD
inhibit motor, executive function, dorsal striatum thalamus
inhibit attention
inhibit timing and perception via parietal and cerebllum
reward anticipation- VTA
excessive activity of default mode network
D1 receptors and alpha adenoreceptors via stimulant medication
conjunctiva=
mucous over inner eye (palpebral) and anterior aspect of sclera (bulbar conjunctiva)
palpebrae
skin on outer, conjunctiva on inner
cilia on lid margin (eyelashes) with sebaceous glands (glands of Zeis and glands of moll)
orbicularis oculi and elevator palpebral muscles
tears via meibomian glands (sebaceous gland)
tear film consists of
tears, lipids, mucous
orbital septum
separates eyelid from orbit- barrier to infection
lacrimal glands innervation
CN VII and SNS
where do lacrimal glands drain
to lacrimal sac then inferior meatus
common bacterial and viral causes of conjunctivitis
▪ Bacterial
* Staph aureus, s. pneumonia
[[[-, H. influenzae, M.
catarrhalis
- Chlamydial and gonococcal]]]]]
▪ Viral (usually adenovirus)
is viral or bacterial conjunctivitis more common
viral
are viral and bacterial conjunctivitis self limiting
yes
bacterial vs viral conjunctivitis
▪ Bacterial conjunctivitis tends to have more purulent discharge and last for less time than a viral conjunctivitis
gornnorheal and chlamydial conjunctivitis
treat urgently bc can scar and ulcer the cornea
trachoma (ulcer, abrasion, scar cornea and conjunctiva) –> blindness (chlamydia)
blepharitis
inflamed eyelid
cause of blepharitis (inflamed eyelid)
hordeolum (stye)
seborrheic dermatitis
drugs, allergy
sjogren syndrome (autoimmune)
what causes a stye (hordeolum)
staph aureus
infects sebaceous or suderiferous gland
chalazion
granulomatous inflammation of the eye
via lipid products breakdown of bacteria or block sebaceous glands
keratitis
HSV 1 or HSV2 cause corneal damage –> ulceration
after HSV “resolution”, lives latent in trgieminal ganglion and is reactivated (ie. stress, sun, hormones)
HSV3 (herpes) causes dermatitis of CN V1 dermatome (Hutchinson’s sign if tip of nose involved)
lateral inhibition of the retina
helps to enhance the contrast between light and dark and able to do fine discrimination of edges and patterns
rod bipolar cells vs cone bipolar cells
rod- scotopic (low light) and have on centers
cone- photooptic (bright/colour) and have on centre and off centers
on center
activated when light hits the center of their receptive field, and the center is brighter than the surround.
which has on and off center in bipolar cells
rod= on
cone= on and off
oppositional regulation: on and off have opposite response to same stimuli to help contrast and edge detect –> visual acuity
one is inhibited while other stimulate
what needs to be regenerated in the dark after activation so cell can respond again
rhodopsin (in rods)
how to regenerate rodopsin
trans retinal seperates from opsin (GPCR)
opsin is bleached and inactive
trans retina goes back to cis retinal ( in pigment layer)
cis retinal combines with opsin
ready to respond to light again
in dark pupils vs light
dilate in dark
constrict in light
rods in the light are
bleached / saturated - cant respond to light
bipolar cells are for
patterns of light at retina (on and off center)
horizontal cells in retina for
sharpening contrast
amacrine cells in retina for
detecting changes in vision (i.e. movement, light on/offf)
graded vs action potential in visual processing
photoreceptor (graded receptor potential) –> bipolar cell –> ganglion cell (action potential) –> brain
more light intensity = more AP
optic nerve is formed by axons of ____,. it also forms the _______—
formed by ganglion cell axons
creates optic disc (blindspot)
optic tract forms when
optic nerve fibers cross over at optic chiasm
where does optic tract synapse
and optic radiations synapse in
thalamus
visual cortex
scotoma
area with vision loss in an otherwise normal visual field
brain areas involved in vision
primary visual cortex (registers shape and colour of stove)
secondary visual cortex (recongize shape and colour of stove)
primary somatosensory cortex (registers finger is hot)
secondary somatosensory cortex (recognize how hot)
Pareto-occipito-temporal association cortex (combine visual and tactile info)
amyblyopia
lazy eye
lesion in primary visual cortex can cause
cortical blindness
lesions in secondary visual cortex can cause
movement agnosia (i.e. movement not noted)
visual agnosia (i.e. cant copy drawings, or identify common objects)
colour agnosia (i.e. grey scale)
medial rectus
lateral rectus
inferior rectus
superior rectus
inferior oblique
superior oblique
levator palpeerde superioris
ciliary muscle
pupillary sphincter
medial rectus: adduct eye (to nose)
lateral rectus: abduct eye (to ears)
inferior rectus: down, extorsion
superior rectus: up, intorsion
inferior oblique: elevate and abduct
superior oblique: down and abduct
levator palpebrae superioris: elevate upper eyelid
ciliary muscle: contract; increase lens convexity (accomodation- near vision)
pupillary sphincter: miosis; pupillary constriction
where are the cranial nerves located
I - olfactory bulb
II- retina
III and IV- midbrain (3+4)
V- midbrain, pons and medulla
VI, VII, VIII- pons (6-8)
IX, X, XI, XII- medulla (9-12)
what is the somatic and visceral motor neurons of ocultomotor CN III
somatic motor- oculomotor motor nucleus
visceral motor- dinger westphal nucleus (EDW)
Oculomotor motor nucleus in CN III for what eye movements
all eye movements/ muscles except
superior oblique (down and abduct)
lateral rectus (abduct)
dinger westphal nucleus (EDW) of CN III for what innervations
PNS
-pupillary spincter (miosis)
-cillary muscle (accomodation- near visioN)
if the oculomotor motor nucleus (somatic) of CN III had external opthalamoplegia (weak eye muscles) what would happen
eye would be down and abducted
if visceral (EDW) of CN III was damaged what would it cause
lose accomodation
pupil dilate (Mydriasis)
accomodation reflex via which CN
I and III
in the accomodation reflex (close object) which muscle and CN III nucleus is used
convergence of eyes (adduct) via medial rectus and motor nucleu
increased convexity of lens via ciliary muscle snd EDW
constrict pupils via sphincter pupillae and EDW
pupillary reflex (CNI and CNIII) light in one eye causes constriction of both pupils`
CNIII EDW nucleus
pupillary reflex (CN III EDW) in which area of midbrain
pretectal area
the accomodation reflex is not in this area
CN IV trochlear nerve innervates which muscle
contralateral superior oblique muscle
(eye down and abduct + intorsion)
PS the CN III innervated the inferior oblique muscle for extorsion
why is intorsion and intorsion important
when move head helps maintain visual stability
diplopia (double vision) if
CN IV damaged and cant do intorsion… then extoersion dominates
muscle and CN
CN III all except the following
CN IV - superior oblique (abduct and down)
CN VI- lateral rectus (abduct)
which muscle does CN VI innervate
lateral rectus (abduction)
how are CN III, VI, and VI connected
by a tract
▪ = Medial Longitudinal Fasciculus (MLF)
vestibulo-ocular reflex via
CN III, IV, VI to stabilize gaze during head mvoemnts
Medial Longitudinal Fasciculus (MLF) tract helps
if want to look to left which muscles are used
Left eye use lateral rectus (VI) (abduct)
right eye use medial rectus (CN III) (adduct)
if damaged can cause diplopia
cataracts
opacity of the lens
type of cataract
cortical (spoke like)
nuclear sclerosis (yellow brown)
posterior subscapsular
most common cataracts
nuclear sclerosis and usually from aging
cataracts symptoms
vision get worse but can become more myopic (near sighted)
uveitis types
inflammation of choroid layer
iris (iriditis)
iris + ciliary body (iridocyclitis)
posterior compartment (posterior uveitis)
most common type of uveitis
anterior uveitis (anterior chamber) (includes Iritis/iridocyclitis/anterior cyclitis)
what can cause anterior uveitis
IBD, lupus, aids, herpees , idiopathic
glaucoma
elevated intraocular pressure
optic nerve damage
impaired drainage of aqeuous humour
leading cause of blindness
2 types of glaucoma
- open angle: aqueous humor accesses trabecular meshwork and increases pressure via resistance of outflow of aqueous humour (block trabecular meshwork)
- closed angle: iris adheres to trabecular meshwork and physically impedes aquesous drainage (close angle btw iris and cornea)
most common glaucoma
primary open angle
what is secondary angle closure glaucoma associated with
diabetes
retinal detachment
Separation of the neurosensory retina from the retinal pigment epithelium
full thickness tear (rhegmatogenous)- most common (vitreous humor seeps under retina) (fluid accumulate under retina)
no break (non-rhegmatogenous):
retinal vascular disease- diabetes mellitus
hyperglycemia effect lens (cataracts, glaucoma from neovascuarization) and rentina too
2 types
▪ Background (preproliferative) diabetic retinopathy
▪ Proliferative diabetic retinopathy
▪ Background (preproliferative) diabetic retinopathy
▪ Proliferative diabetic retinopathy
▪ Background (preproliferative) diabetic retinopathy
–> microvascular changes but no neovascularization
▪ Proliferative diabetic retinopathy
–> from neovascualrization
cotton wool spots
buildup of axoplasmic debris in retinal nerve fiber layer
form cystoid bodies (mitochondria accumulate in damaged axons)
macular degeneration
macula for central vision and fine details
early stages: drusen (lesions beneath retina)
macular degeneration types
atrophic (dry) or exudative (wet)
dry- slow (infalm, drusen)
wet-rapid, develop neovascular membrane with disordered blood vessels, can leak
