neuro 2

Broca and Wernikes are associated with the left side of the brain 

the right side of the brain is more involved in the nuances of speech like tone, rhythm, the way things were said NOT so much what was said.. "THE RIGHT WAY TO SAY SOMETHING"

may know what you want to say after hearing and seeing something but then cannot say it. 

Broca's area can also be unchecked and will cause a fluent aphasia because the wernikes area cannot moderate what you are saying

• Primary auditory to Wernike's area (association area)
• Primary visual cortex to Angular gyrus (association area) to Wernikes area

From Wernike's area (arcuate fasciculus) to the broca's area

Broca's NONFLUENT aphasia: produce few words, either written or spoken, use stock phrases repeatedly (e.g., “OK,” “Oh boy!”); words are produced with great difficulty, leave out all but the most meaningful words in a sentence and to speak or write in a telegraphic manner.

Wernikes FLUENT Aphasia: substitutions of one letter or word for another, insertion of new and meaningless words, or stringing together of words and phrases in an order that conveys little or no meaning. patients have difficulty comprehending whether their own speech makes sense

• Motor cortex--that enables vocal muscles to move 
• Brocas 
• Wernikes area

interpretation defects--spatial orientation impaired

irritative- causes hallucinations and random visions that may not be present 

destructive: contralateral defects in the visual field--you will only be able to see half the image (homonymous hemianopsia)

the fovea does

The central regions like the fovea are located in the back of the parietal lobe. 

The peripheral regions are located more anteriorly

some components of the central and posterior are common to both eyes but the more left you go peripherally that stuff is only gonna show on the left periphery

Primary visual cortex is associated with area 17 IN THE CALCARINE FISSURE 


and association areas are located in 18 and 19-- they start in the occipital lobe but expand into the temporal lobe as well

is located in the temporal lobe with the hippocampus.. it is associated with olfaction but does not cross the thalamus

damage--you will not be able to make new memories after the damage occurs...prior to the damage all the memories you made will be intact

granular-densely packed with cells and each region is able to detect a different sound intensity

Area 41 transverse temporal gyrus

Does not cause deafness because you are receiving input from both ears-- you may have decreased sensitivity or decreased ability to localize the stimuli in the CONTRALATERAL SIDE

bilateral damage=deafness

Irritative lesions-- will cause overstimulation of sensation-- tingling, burning in the CONTRALATERAL side effected. 

destructive lesions: will cause impaired ability to localize or measure the intensity of the painful stimuli. (because of the way the cortex is organized you can determine location and intensity--homonculus)

visual agnosia: you can see everything but you cannot recognize or name things by looking at it. 

Jeff: can see everything in his vanity--but to get the toothpaste he can't just look at the toothpaste and grab it-- he has to touch feel smell etc everything to be able to recognize what the toothpaste is-- because visual association cortex is not working.

too many items around can confuse him

Agnosia--the inability to recognize things

multimodal-- it requires input from many different parts of the brain

Wisconsin Card Sorting test 

requires attention, visual processing, and working memory

There are two parts the dorsolateral that is more associated with working memory, attention, focus, and solving higher order thinking tasks-- connections to the parietal, somatosensory, visual, and auditory regions

• Ventromedial: connections to limbic system 
• impulse, and inappropriate behavior suppression

• Area 4: motor cortex-- causes flaccid paralysis 
• Area 6: premotor cortex--causes spastic paralysis

will cause hyper-movements--abnormal movements--more likely to start as a twitch in the finger or the lip and move its way throughout the homunculus  (Jacksonian March)

due to ectopic foci--increased amount of sodium gated channels

it is an association cortex that is found in area 6 of the frontal cortex-- it can be stimulated to induce muscle movements but it will require a greater input as it has a higher threshold. Movements will be slower and will involve larger groups of muscles 

found in the motor cortex and the premotor cortex-- they are not closely packed together 

the motor cortex is additionally associated with betz cells that are long pyramidal cells that have long axons that extend down into the spine and initiate voluntary movement

• primary motor cortex--area 4
• premotor cortex--association region located in area 6

The multimodal area here is associated with assembling sensory movements to plan movement-- apraxia-- coping a behavior will be impaired

damage to the right side of the parietal lobe-associated with spatial attention...

multimodal defect

you will draw and recognize things on the right side only because left side info comes into the right side but the right side is damaged

Dorsal motor of vagus nerve

inferior vestibular nucleus

medial vestibular nucleus

trigeminal nucleus and fiber

inferior olivary nucleus

medial lemniscus

17. raphe nucleus

pyramid

hypoglossal

14. inner arcuate fibers

vagus nerve fibers

anterolateral pathway

nucleus ambiguus

posterior spinocerebellar and anterior spinocerebellar tracts

9. inner cerebellar penduncle

lateral cuneate nucleus

cuneate nucleus

• solitary tract 
• solitary nucleus

3. hypoglossal nucleus

2. medial longitudinal fasciculus

fourth ventricle

central canal

solitary nucleus

vagus nerve fiber

19. arcuate fiber

hypoglossal fibers

hypoglossal nucleus

medial longitudinal fasciculus

medial lemniscus

Ralphe nucleus--seratonin production

pyramid

Inferior olivary nucleus

nucleus ambigus

Anterior-lateral tract (corticospinal tract)

• Posterior spinocerebellar tract 
• Anterior spinocerebellar tract

trigeminal nuclei and tract

lateral cuneate nucleus

fasciculus cuneatus

nucleus cuneatus

grascilis nucleus

Dorsal motor nucleus of vagus

carries information from the ansa lenticularis and the lenticular fasiculus to the thalamus

carry fibers from the Gpe

carries Gi around the medial edge

• third ventricle 
• Pineal gland 
• superior colliculi 

red: medial geniculate (usually in very close proximity to the thalamic structures)

• Pink: fornix 
• Hypothalamic sulcus

• underneath the pineal gland is the posterior commissure 
• and under that is the cerebral aqueduct and under that is the fourth ventricle 
• between the red nuclei is the VTA
• under the LG is the optic tract 

Lamina terminalis-osmoreceptors outside the blood brain barrier that detect the Na+ concentration

• a. third ventricle
• b. fornix 
• c. lateral ventricle 
• d. thalamus 
• e. putamen 
• f.
• g. hippocampus 
• h.
• i. pons
• j. cerebral peduncle 
• k. substansia nigra 
• l. hypothalamus 
• m. caudate tail 
• n. middle cerebellum peduncle

motion

usually due to a lacunar stroke and this damages the thalamus-- symptoms will be contralateral loss of sensation in the arms, face, and legs. Eventually after a while they will feel constant pain here upon stimuli like touch (still on the contralateral side)

sheath of neurons that are located in the lateral region and they receive incoming and outgoing information and regulate their activity by releasing GABA

recieves information from cranial nerve 2 and sends information to the visual cortex which is located in the calcarine sulcus

receives information from the inferior colliculi and the superior olive and Sends information to the auditory cortex in the traverse temporal gyrus

gets sensory information from the trigeminal and gustatory nerves and sends it out to the somatosensory cortex 

will be able to interpret information relating to facial sensation and taste

fine touch conscious, proprioception, vibration

• receives info from the spinothalamic tract, dorsal trigeminal tract, and the post column medial lemniscus
• sends it to the somatosensory tract

how you interpret pain, temperature, conscious proprioception

thalamic nuclei

receive input from the ansa leticularis and the lenticularis fasiculis and the cerebellum (via the superior cerebellar peduncle) and send information to the motor cortex

thalamic nucle

Hippocampus, amygdala, septal area(basal forebrain), cingulate gyrus, uncus

Connects the neocortex and the hypothalamus together

ELABS 

• Emotion 
• Long term memory 
• Autonomic nervous sytem function 
• Behavior modification 
• Smell

--Most common cause: alcohol (thiamine B1 deficiency) 

Wernike: more reversible condition.. associated with visual disturbance, gait ataxia, and acute confusion 

• Korshakoff: severe memory loss (old and new) 
• they will make things up to fill in the gaps (confabulation)

tumor of the Rathke pouch (anterior pituitary) that can put pressure on the optic nerve and also on the hypothalamus causing hypothalamic syndrome

optic chiasm can be affected too

bitemporal hemianopsia--loss of vision in the outer fields..so inner fields are intact 

tells you that you are full and not hungry-- triggers satiety and inhibits hunger

adenohypohyis (rathke pouch)

neruohypohypsis

Supraoptic hypothalamic nuclei

Paraventricular hypothalamic nuclei

• Sexual behavior 
• these nuclei are larger in men-- heterosexual 

if they are smaller in men-- Homosexual

RECALL of Aversive and pleasurable stimuli 

not like amygdala which is more processing the aversive stimuli and denoting it as bad

dopamine inhibition of prolactin (damage to this will cause too much prolactin to be formed)

There is a system here that was found to be targeted for hot flashes in women

• ventromedial: satiety center 
• dorsomedial: olfactory and fear rage aggression and aversion

Promotes hunger and sleep wake cycle. Oxrexins are released to stimulate hunger

• stimulation: feeding 
• lesion: anorexia

Thyroid releasing hormone--controls metabolism by regulating how much of this hormone is released

• releases histamine 
• -involved with being awake and alert (attentive)

-when you have benadryl (antihistamine) you feel drowsy

Involved in cooling-- vasodilate and sweating helps cool temperature down 

Involved in heating.. also involved in fear aggression, analgesia (why my head burns up when I am scared)

releases VIP GRP and ADH 

circadian rhythms-- feeding and thirst behaviors

they typically affect more than one nucleus so you are more likely to have a lot of different types of symptoms

Posterior Pituitary: made from neuro-ectoderm. hypothalamic neurons make vasopressin and oxytocin which are stored in the synaptic terminals (in the posterior pituitary) and then released in the blood stream for secretion by the pituitary gland 

Anterior Pituitary: Ectoderm derivative--there are hypothalamic releasing factors that get released into the TUBEROINFUNDIBULAR TRACT and then stimulate the pituitary gland to release whatever hormone

it gathers information from external and internal stimuli and then responds by means of hormonal, autonomic, and COGNITIVE mechanism to maintain a level of homeostasis 

drive related behaviors-- physiological discomfort we feel when we are not in homeostasis-- reproduction, growth, stress, and energy. Sleep, reward, pain, food intake

• 16. nucleus accumbens 
• 17.septal nuclei

above 17= septal pellucidum

mammilothalamic tract

Habenulointerpenduncular tract

temporal lobes especially where the amygdala are located

Kluver bucy: amygdala are destroyed and you get extreme sexual tendencies, oral fixation, absence of fear and VISUAL AGNOSIA

VTA to nucleus accumbens is a main pathway

• includes the basal forebrain and the nucleus accumbens 
• anhedonia--lack of pleasure 

Cholinergic pathway (basal forebrain): cognition  

1. tamed attitude/placid--you are undisturbed, quiet, you are not provoked , you do not get angry, lack of motivation to do things (apathy) 

2. you would not be able to discriminate aversive vs not..inappropriate response to threat

• Recognizes aversive situation 
• threat in sounds and faces
• fear anger

Deals with putting short term memory into long term and specifically also deals with declarative memory (recall for certain facts and stories) 

Focal epilepsy-- it typically affects one side of the brain so symptoms are apparent only on the one side of the brain

Site of adult neurogenesis

• affects the striatum-- you get random unwanted movements because the inhibitory effects are suppressed 
• but you can also get depression and memory issues 

LATERAL NUCLEUS IS ALSO AFFECTED

Hypothalamic dysfunction that causes you to be fat and eat a lot--issues with the ventromedial nucleus probably

delayed or absent puberty because of migration defect of GNrh from site of release in the hypothalamus to the pituitary

• damage to the mammilary bodies--which are associated with recall of pleasure and aversive memories 
• Short term memory is affected first and then long term memory is affected

• Dad has to have a faulty gene for this to be passed down 
• --causes hypothalamic dysfunction where they will gain weight and eat a lot (never feel satiated-- can be issues with the ventromedial section)

A dye is given and it usually stays within the brain blood vessels. But if there is necrosis or abnormal vascular proliferation from growth factors released by the tumor the dye can be released and enhance the lesion. 

If enhanced (it appears white) indicative of a high grade tumor

because they do not have lymph nodes, they typically spread within the CNS and not outside it, the way they move you cannot completely resect the tumor

• Cytoplasmic inclusion-- Rabies 
• found in the saliva of animals 

• Have trouble swallowing 
• Affect PNS first and then make their way to the CNS (cerebellum and brainstem are more commonly affected)

Intranuclear inclusion-- HSV infection

Hemorrhagic-- especially in temporal lobes caused by HSV

typically associated with COWDRY bodies which are intranuclear inclusions

Central Pontine Myelinolysis (osmotic) 

Any sort of hyponatremia (usually seen in alcoholics, malnutrtional cases, electrolyte instability)-- correcting to fast can cause demyelination commonly in the pons 

(myelin stains blue)

• mammillary bodies 
• hypothalamus
• and periaqeuductal area

involved in preventing apoptosis 

mutations of this can lead to ALS

ALS-- caused by a destruction of anterior horn nuclei and can also be caused by damage to the corticospinal tract. 

weakness and fasiculations 

• can be genetic WERDNIG HOFFMAN.. SMN1 gene mutation
• or viral (polio--virus can access the motor receptors)

Silver stain syphillus

Lymohocytosis seen with viral infections

• Syphiliis-- loss of the posterior column of the spinal cord--loss of conscious proprioception, vibration, pressure, and fine touch 
• "tabes dorsalis" 

obliterative endarteritis--- concentric endothelial and fibroblastic proliferative thickening that causes occlusion of the artery

Central pontine myelinolysis

JC virus causes death of oligodendrocytes and astrocyte enlargement and proliferation 

mainly in the white matter 

Progressive Multifocal Leukoencephalopathy (white dots everywhere within the cortex)

Angioma--congenital disorder often associated with (polycystic kidney disorder, ehler's danlos, and aorta narrowing diseases)

when blood passes through it causes this protrusion 

and if it ruptures it can cause a a subarachnoid bleed

found in branch points of vessels

Spongey encephalopathy on a histology slide 

Amyloid build up of prions--beta folded. can cause normal proteins to become mis-folded

can be transmitted from one individual to another

Kuru (eat brain) and cretyzfeld Jacob

Cryptococcus-- soap like lesions on imaging 

india stain of CSF

commonly found in pigeon poop and you inhale it and can cause meningitis--often affects immunocompromised people

Meningitis--- you can see many inflammatory cells within the meninges. If bacterial they will mostly be neutrophils if viral they will be lymphocytes

Purulent--think bacterial meningitis (accompanied by lower sugar and higher protein levels in the CSF)

viral meningitis would probably appear with lymphocytosis

laminar infarct-- around the cortical layer-- occurs more in a linear pattern than a wedge like appearance

wedge shaped things are usually infarcts due to ischemic injury or perfusion defect

• ambigus gets information from the heart
• and dorsal from the thorax and the abdomen

VPM nucleus receive nociceptive information from the face, while neurons in the VPL nucleus receive nociceptive information from the rest of the body.

extends from lateral geniculate to the calcarine fissure

the tract that is coming out of the lateral geniculate (napolean's hat)

Doll's eye: the eyes will move in the direction opposite to the way the head was tilt 

Cold water to the tympanic membrane--the eyes will turn in the direction of the cold--if asymmetric or this does not occur-- abnormal

coordination of eye and head movements--it allows you to keep your eyes on a target despite your head moving around

• a. vestibuspinal neck, trunck, head, and eyes 
• b. tectospinal: superior colliculus--controls vertical gaze

P and N type channels--these are targeted in epileptic patients to decrease the amount of neurotransmitter released (predominant on the presynaptic) 

T type-- to reduce the amount of calcium that can flow through and cause the spikes (more predominant on the post synaptic)

• one MONOgenic cause of epilepsy where a single gene is sufficient to cause epilepsy... 
• usually polygenic causes of epilepsy 

mutation in voltage gated channel

Focal seizure that is progressing to the other hemisphere

generalized seizure because abnormality is present in every lead

• Normal 
• eye movements can cause artifact 
• 8-12 hz

• is a glutamate agonist which causes motor cell death in ALS
• superoxide dimuatase which normally protects against against oxidative stress-if mutated can cause cell death as well

Dopamine binds to D2 and decreases the release of Acetylcholine. BUT in parkinson's disease-- there is no dopamine so there is more ACH released 

to fix this imbalance-- muscurinic antagonists (scolpamine, atropine, ipra)

it is seen in parkinsons when the Ldopa has good effect for some time and after some time it doesnt but then after some time it has an effect again 

• this is unusual bc parkinson is a progressive disease and gets worse as more neurons die 
• eventually there shouldn't be terminals left to pick up the dopa and convert it to dopamine

• Lethargy 
• Euphoria 
• Vomit (other GI disturbances) 
• Orthostatic hypotension and hypertensive crisis especially when used with MAO inhibitors
• Delusions
• On and off phenomena 
• Priapism 
• Athetosis

• usually occurs in front of an audience 
• history of drug use, psychotic 

• resist eye opening 
• waxing and waning 
• pelvic thrusting 
• asynchronous head movements 

No response to AEDs

Levetiracetam and Lamotrigine

Valproate, PB

porphyria

inhibits VMAT... monamine reuptake so dopamine is in the cleft for longer and has greater potential for being degraded.... 

in huntingtons (caudate is affected) gaba production is decreased and dopamine increases 

in parkinsons- the substansia nigra is affected.. dopamine is decreased and Ach is increased

hepatic injury

Parkinsons-- blocks NMDA receptors

Alzhemiers medication targeted at NMDA receptors (decreased glutamate activity)

• Benz 
• Trihex 

• (Benz symbol has 3 triangles) 
• "Dont sleep if you want a mercedes"

capone 

tolcapone is able to cross the BBB and inhibit COMT from degrading dopamine

left often used for Parkinsons because it can cause vascular damage 

• Bro nonselective 
• Roti nonselective
• Apo --nonselective 
• Prami...D2 agonist
• Ropi..D2 agonist 

D2 binding typically causes decreased Ach release

sedation

inhibits gaba T enzyme so gaba is not degraded 

also prevents glutamate receptors (AMPA and Kainate from functioning)

"clona" "pams" : benzos: gaba A agonist cause influx of chlorine causing inhibition of the neuron 

barbituates: do the same thing

binds to L Calcium receptor  prevents the release of gabpentin 

side effect: sedation

• leveacetams
• and brigacetams

Sodium and T-type calcium channel blocker; GABA-T inhibitor; HDAC inhibitor

Carb: Ca T receptor inhibitor and Na channel blocker

Lacoamide: carbonic anhydrase inhibtior and Na channel blocker

• they are both sodium channel blockers and also can block glutamate receptors
• first one blocks AMPA and kainate 
• second one does NMDA

"Topi fel..oh No"

Rufiamdie Zoniasmide Phenytoin Lamotrigine

• SIADH, low Na
• SJS

zeitgebers--light, social, temperature

endogenous-- the timing of hormones and certain physiological changes occur every 24 hours 

internal clocks can operate independently, but are influenced by external cues (entrainment-allows the internal clocks to adjust their timing to match changes in the external environment, such as shifts in the light-dark cycle. However, even in the absence of entraining cues, the internal clocks continue to generate rhythmic signals.

• a. obstructive--nrem or rem
•     muscle weakness-- contraction of upper respiratory muscles and diaphragm does not occur which causes collapse of the oralpharynx-- causing snoring and hypoxia--this usually induces wake 

B. central--damage to the brainstem

Iron deficiency associated with dopamine synthesis--can cause discomfort in legs that causes the urge to move them and can cause disruption in sleep

• you start appearing as if awake 
• rapid eye movements 
• some more sympathetic tone 
• ATONIA 

ERECTION DURING NIGHT-- if this is not happening seek cardiology support there may be a narrowing of artery 

Cortisol and Thyroid stimulating hormone decrease during sleep, rise upon awakening

Growth hormone, prolactin and LH secretion increases at night/sleep

Melatonin increases at night/sleep and is produced until sunlight cues its decrease

night terrors where they are in significant danger and to save themselves they will hurt themselves because there is NO ATONIA

• Nightmares
• Sleep paralysis 
• and REM behavior disorder

Bed wetting-- has to do with genetic malformations in the innervation of the bladder 

Somnamulism-- sleep walking 

Night terrors: wake up screaming and crying and are inconsolable and have no memory of doing this

• irresistible urge to fall asleep 
• defect in orexin/hypocretin 

Cataplexy (REM)/atonia-- narcolepsy 

atonia here is aware

cannot sleep-- but they do not just randomly fall asleep everywhere like in narcolepsy 

primary: no direct link to a medical condition--many psychotic people have this because they are always so stressed

secondary: there is a medical link

• dorsal: inspiration
• ventral: inspiration and expiration

Measures brain activity of the superior cortical region (mainly the pyramidal cells cause they are usually the outer most cell.)

Conductance-- the ions will also be released from an action potential, repel , and disperse 

when they disperse= the difference in voltage that is measured 


Normal EEG does not mean no abnormalities because it is dependent on a specific time

• odd numbers: left 
• even numbers: right 
• the read is organized with one hemisphere on the top and the other hemisphere at the bottom

When the patient is placed on two medications, but still has convulsing activity 

surgery if the location allows for it (temporal lobe, corpus collusm) 

if in motor, then you may have to consider neruostimulation  devices

• electrodes for each eye
• muscles to see the contraction scalp to measure electrical activity of the brain

• Theories: significant amount of waste/toxins build up in the brain during the day 
• when we sleep there is increased CSF flow to remove these waste products

short term to long term memory occurs in our sleep

olfactory bulb

typical absence seizure presentation--spike wave and like about 3 of them in a second

a eeg where all the channels look the same is NOT normal it should be different

Following an ischemic injury to the brain, liquefactive necrosis is more common--will be accompanied by inflammation--messy death of cells.

• reactive Gliosis after CNS injury like stroke (infarction)
• astrocytes and other glial cells go to the site of injury and proliferate and release material to form a glial cell. This scar prevents regeneration of function in the area now-- afunctional

Right hemisphere stroke: SECONDARY TO ATHEROSCLEROSIS 

embolic strokes are more hemorrhagic-- they are smaller breaks that usually go and settle in multi-flow regions or in the veins (appear red) as opposed to blanch or white (thrombolic)

dementia because of the neuronal loss 

obliterative endarteritis: blood vessels are occluded with a lot of WBC in and around the vessel especially PLASMA CELLS 

There is inflammation of the dorsal nerve roots that eventually cause degradation of the posterior column

N. meningititis especially will release toxins that cause damage to the blood vessels and can cause adrenal glands to bleed out (shock--hypotension and tachycardia)

N meningitis--gram negative diplococci 

affects the subarachnoid

Shock--decreased blood pressure, heart rate is increased 

going to affect all the arteries (watershed areas will be more commonly affected because two blood supplies)

• hippocampus 
• purkinje cells 
• cortical neurons (3 and 5)

"Water purk where there are 3-5 hippos"

mrna

superior cerebellar peduncle

vestibulocerebellar tract

• 28. superior vestibular nucleus 
• 26. lateral vestibular nucleus

anterior spinocerebellar tract

• facial nerve 7-- expressions 
• and facial nerve tract thick round part=genu

tegmental tract

anterolateral (spinothalamic) tract

lateral lemniscus

trigeminal nucleus and tract

solitary nucleus-- visceral (7, 9, 10)

inferior cerebellar peduncle

middle cerebellum peduncle

Cranial nerve 6: abducens nuclei and tract

vermis of cerebellum

fourth ventricle

MLF

ralphe nuclei

medial lemniscus

trapezoid body

pontocerebellar tract

pontine nuclei

corticospinal tract

IDH and ATXR are mutated in Atrocytomas... IDH mutated has a better prognosis 

in glioblastomas IDH is normal and TERT is mutated causing the abnormal telomere lengthening

very similar to pilocystic-- rosenthal fibers are more circular rather than rod like 

associated with seizures (temporal lobe affected)

medulloblastoma

common sites of cancer for pilocytic and medulloblastoma

• cancer of cells in the cerebellum 
• can spread downwards
• rosette--small blue cells around the pink space

marker that is positive in medulloblastoma

oligodendroglioma-- notice the "O" cells: there is a lot of white space around the nucleus... 

cell affected is not oligodendrocytes

mitotic figure--chromatin spreading apart

mitotic figures--close together and look very similar

is more common in young adult females and imaging will show a mass hanging off the dura but it will not invade the cortex

choroid plexus benign cancer-- they are still finely lined

choroid plexus carcinoma--because the cells are stacking up on top of each other and they are supposed to be single layer 

this can cause blockage and lead to hydrocephalus

• Neurofibroma 2 
• and radiation typically from prior cancer removal (LICE removal) 

these tumors grow faster around progesterone but can grow without it as well

associated with syncytial meningioma

Transitional/mixed meningioma-a very slow growing arachnoidal cell cancer. Commonly associated with whorl bodies and psomma 

there is another type--syncytial (mengiothelial) cancer: these are more commonly associated with pseudonuclear inclusions--they have white spots within their nucleus

whorl bodies--commonly seen in transitional/mixed meningioma

Pssoma bodies--calcium deposits commonly seen in meningioma transitional type

• TDP
• but eye movements and sphincters are spared

• Riluzole--antiglutmate
• Radicava--oxygen radical scavenging 
• Relyvrio--protection against mitochondria and er dysfx

Certain viruses can cause the plaques to accumulate faster (HSV)

microglial activation can be impaired so they don't clear up the plaques but the increased inflammation can cause greater production of and greater neuronal death

Gold standard: biopsy and you will see spongey encephalopathy 

EEG will show sharp waves and MRI will show basal ganglia hyperdensity 

thats why the disease is associated with ataxia

• used in Alzheimers disease-- correlated with edema and brain bleeds so must have MRI prior to infusion
• (1st infusion, 5th, 7th, and 14th)

Done, Gala, stigmine--AchE antagonist 

• Glutamate antagonist 
• Levanemab and Donanemab

hyperlipidemia and smoking

DM and then HTN

causes SJS and gingival thickening and bone sx

ciliary body of the eye muscles that produce the aqueous fluid for the chamers 

and pas plana has the zonules

it has an endothelial cell that transports fluid out via active transport

it is coated by a thin lipid layer (slows evaporation), thick aqueous layer (antibacterial, supplies o2, and washes away the debris), and the mucin layer-- decreases surface tension 

lacrimal gland produces the tears and removed by the lacrimal sac and duct near the nose (there is a punctum (hole that allows the fluid to be drained)

sympathetically innervated--controls the upper eyelid

oil glands

mucous

tears

The orbitcularis has two parts-- orbit (forceful voluntary contraction-- when there is bright light something gets stuck in your eye etc)....involves both the upper and lower eyelid 

palpebral: gentle closing.. voluntary and involuntary closing


the levator--originating in the apex will cause the eyes to open

• goes up and in 
• originates in the maxillary muscle

down and in  (opposite of what you would expect).. superior rectus goes up and out 

it originates from the sphenoid

zinn

• eye socket made up of 7 bones 
• sphenoid- strongest 
• ethmoid-weakest (paper thin)

• not a diffuse 
• perivascular rosette

• visual and verbal
• mood, motor, behavior, circadian rythtm

• Picks--frontal lobe 
• PSP--supranuclear upgaze palsy
• CDB

example of contralateral neglect: had to cross out all the circles that had gaps in them... he is able to accurately do that if the gap is on the right side but not if its on the left side