Things I struggle with Part 3 Flashcards
VPL nucelus
spinothalamic and dorsal columns/medial lemniscus- pain and termpature, pressure, touch, vibration, proprioception. first degress somatosensory
VPM nucelus
trigemenial and gustatosy- facial and taste sensation
LGN nucleus
CNII for ision
medial geniculate nucleus
superior olive and inferior colliculus of the tectum for hearing
ventral lateral nucelus
basal ganlgia and cerebellam for motor
limbic system- what are parts of it and function
hippocampus, amygdala, cingulate gyrus, and feeding, feeling, fighting, fleeing, fucking
mesocortical pathway
decreased activity leads to the negative symptoms of schizophrenia
mesolimbic pathway
increased activity leads to positive sympotms- target of anyipsychotic drugs
nigrostriatal patwhay
decreased activity leads to EPS symptoms-
tuboinfundibular pathway
decreased activity leads to increased prolactin
cerebeller lesion affects ipsi or contral
ipsilateral lesion=ipsi defect
the nuclei of the cerebellum from the lateral to mesail
dentate, emboliform, globose, fastigal
lateral cerebellar lesions do what
affect voluntary movement of extremities when injured there is propensity to fall towards the injured side
medial lesions of the cerebellum do waht
involvement of midline structures- tranquil ataxia, nystagmus, head tilting- bilateral axial defects
what does the basal ganglia do
it provides feed back to the cortex to modulate the movemetn
excitatory pathway of the basal ganglia
cortical inputs stimulate the striatum, stimulating the release of GABA which inhibits GABA release from the GPi disinhibiting the thalamus via GpI to increase motion
inhibitory pathway of the basal ganglia
cortical inputs stimulate the stiratum releasing GAB that disinhibits STN via GPe inhibition and STN stimulates GPi to inhibit the thalamus so decreased motion
dopamine in the basal ganglia
it binds D1 and this stimulates the excitatory pathway and D2 binds the inhibitory pathway to increase motion
athetosis
slow writhing movements especially with the fingers from the basal ganglia- writhing snake like movements
chorea
sudden jerky movemntts thatare purposeless from the basal ganglia
dystonia
sustains involuntar muscle contractions- like writers cramp and blepharspams eye lid twitch
essential tremor
high frequency tremor sustained with posture worsened with movement- contant tremor that tends to run in families-patients self medicate with alcohol- decreased tremor amplitude- beta blockers and primidone
hemibalsimus
sudden wild flailing of one arm and ipsilateral leg- contralaterla sub thalamic nucelus-
intention tremor
slow zigzag motion when posting extending toward a sudden target- tremor with movement from cerebellar dysfunction
myoclonus
sudden, brief uncontrolled muscle contraction- jerks, hiccupus, commong in metabolic abnormalities as enal and liver failure
resting tremor
uncontrolled moment of distal appendages- noticeble in hands and tremor is alleviated by movement
parkinson disease
degeneration of CNSs associtatd with Lewy bodies composed of alpha synuclein- intracellular eosinophilic inclusions and loss of dopaminergic neurons- depigmentation of substantial nigra- has tremor, rigidity, akinesia, postural instability, shuffling gait
Huntington disease
AD- CAG repear on the fourth chromosome- manifest between 30-50 and it is choreiform movements, aggression, depression, dementia- initially mistake for substance abust. increased dopamine, decreased GABA, neural death from NMDA-R binding and glutamate excitotoxicity. There is atrophy of the caudate and putamen with hydrocephalus ex vacuo.
what happens with the huntington gene
mediated gene causes transcriptional silencing and causes increased in histone deacetylation, which silence genees fro neuronal survival
confluent speech with intact comprehension but cannot repeat- what aphasia
brocaas area
fluent speech, impaired comprehension, impaired repetition- what aphasia
wenicke
fluent speech fluidity, intact comprehension cannot repeat- what aphasia
conduction aphasia- it is from damage to the arcuate fasiculus
nonfluent speech, impaired comprehension, impaired repetition- what aphasia
global- arcuate fasiculus, braca nad wernicke areas
nonfluent, intact comprehension, intact repetition- what aphasia
transcortical motor aphasia- affecting frontal lobe around broads are but broca is spared
fluent, impaired, intact- what aphasia
transcortical sensory- affects the temporal lobe around whence area but wenches area is spared
nonfluent, impaired comprehension, repetition intact- what aphasia
broca and wrench areas and arcuate fascicles remain intact surrounding watershed areas are affected
disinhibited behavior with hyperphagia, hyper sexuality, hyperorality associated with HSV1- where is the lesion
amygdala lesion-kluver bucy
hemispatial neglect syndrome- agnosia of the contralateral side of the world- where is the lesion
nondominant parietal cortex
agraphia, acalculia, finger agnosia, left and right orientation- where is the lesion
dominant parietal cortex
reduced levels of arousal and wakefullness- where is the lesion
reticular formation
confusion, opthalmoplegia, ataxia, memory loss (anterograde and retrograde), and confabulation and personality changes- where is the lesion
mamillary bodies
when B1 is given with glucose what is not fixed in wernicke korsakoff
the memory problems are not fixed
what enzyme is decreased with Werknicke B1 deficiency
eryhtrocyte transkelotase is decreased
tremor at rest, chorea, athetosis - where is the lesion
it is in the basal ganglia
intention tremor, limb ataia, loss of balance, damage to cerebellum fall towards lesion- where is the lesion
cerebellar hemisphere
what is degeneration of the cerebellum most commonly from
chronic alcohol
truncal ataxia and dysarthria- where is the lesion
cerebellar vermis which is central located because the middle parts are always affecting the middle
contralateral hemiballisums- where is the lesion
it is from sub thalamic nucelus
anterograde amnesia- inability to make new memories- where is the lesion
hippocampus bilaterally
eyes look away from the lesion- where is the lesion
it is paramedian pontoon reticular formation
eyes look away from the lesion- where is the lesion
frontal eye fields
what supplies the central sulcus of the brain
ACA
what supplies the outside of the brain
MCA
how do you treat increased intracranial pressure with ventialtion
if you hyperventilate the patients then there is vasoconsticrion and decreased blood flow and decreased intracranial pressure
watershed areas of the brain
between ACA and MCA and PCA
obstruction of the R brachiocephalic
impaired drainage of the right subclavlian and IJV so it drains to the right lymphatic drug and this leads right sided congestion and encouragement
contralateral paralysis and sensory loss of the face and upper limb, aphasia if dominant usually the left, and it is the left hemisphere. hemineglect if lesion is nondominat- what vessel is occluded
middle cerebral artery
contralateral paralysis and sensory loss of lower limb cam have some behavioral and urinary incontience- what vessel is occluded
anterior cerebral artery
contralateral paralysis and or sensory loss- face and body. absence of cortical signs like neglect, aphasia, visual field loss- what vessel is occluded
lenticulostriate artery
what does the lenticulostriate artery supply
the internal capsule and striatum
where do saccular aneurysms tend to be
bifurcatiosn at the circle of willis
wehere is the most common saccular aneurysm
it is at the ASA and ACA but and can cause subarachnoid hemorrhage
where is the aneurysm that squashes CNIII
from posterior communicating artery
charcot bouchard microanerusysm
associated with chronic hypertension affects small vessels in the basal ganglia and thalamic and not seen on agiogram. wit acute hypertesnive get intracerebral hemorrhage, and creates deep hemorrhage. The HTN leads to hyalinization and fibrosis of the vessel wall leads to bright sports on CT
what is the aneurysm causing- bitemporal hemianopia, and visual acuity defects- if ruptured it leads to contralateral lower extremity hemiparesis and sensory defects
ACA
what is the aneurysm causing- down and out and mydriasis, see ptosis and out
posterior communicating artery
what is the aneurysm causing- rupture leads to ischemia causing contralateral upper extremity and facial hemiparesis, sensory defits
middle cerebral artery
what causes- neuropathic pain and initial paresthesias followed by weeks to months of allodynia (painless stilmuli causes extreme pain, dyestheias
central post stroke pain syndrome of the thalamus
rupture of middle meningeal artery due to skull fracture, lucid itneraval and rapid expansion leading to transtentoral herniation and CNIII palsy- lens shaped lesion
epidural hematoma
rupture of riding brains from mild trauma, cerebral atrophy, elderly alcoholoism- crescent shaped crosses sutures
subdural hemtoma
rupture of aneurysm or AV malformation leading to rapid course and worse headache, bloody or yellow tinged spinal tap. 4-10 days after hemorrhage, vasospasm can occur leads to ischemic infarct
subarachnoid hemorahage
what do you give when there is a subarachnoid hemorrhage
nigedopine to prevent ischemic infarct
systemic HTN, and amyloid nagioathy recurrent locar hemorrahge storoke, vascultitis, neoplasm, reperfusion is from ischemic stroke, occurs in basal gnaglia, and internal capsule can be lobar or from lacuna strokes
intraparenchymal hemorrhage
what happens to the brain after 12-48 hours of ischmia
red neucons
24-48 hours of ischemia
necosis and neutrophils
3-5 days after ischemia
macrophages
1-2 weeks after ischemia
reactive gliosis, vacualr proliferation
more than 2 weeks after ischmia
glial scar and astocytes surround the cystic cavity
venous sinus thrombosis
increased intracranial pressure, and headache, seizures, focal neurologic deficits. May lead to venous hemorrhage associated with hyper coagulable states like pregnancy, OCP use ,factor V leiden
where are the arachnoid granulations located
superior saggittal sinus
what do you see if the cerebral aqueduct is blocked
the fourth ventricle is normal but the third and lateral ventricles are dilated
idiotpathic intracranial hypertension- pseudotumor cerebri
increased ICP with no apparent cause on impaging- increased with woman of child bearing age, vitamin A excess, danazol, tetracycline, obese- headache diplopia from Vi without change in mental status
why are their transient vision changes with pseudo tumor cerebri
transient vision changes from impaired axoplasmic flow in optic nerves that is worse with valsalva maneuvers
communicating hydrocephalus
decreased CSF absorption by arachnoid grannies from meningitis
normal pressure hydrocephalus
wacky, wobbley, wet- urinary incontinence, ataxia, cognitive dysfunction- elderly- increased CSF pressure but does not result in increased subarachnoid space volume. Expansion of centrical of the corona radiata
noncommunicating hydrocephalus
causes by structural blockage of CSF circulation in the ventricular system aka stenos of the aqueduct of selves like colloid cyst or forma on of monro
ex vacuo ventriculomegaly
appearance of CSF increase on imaging but actually due to decreased brain tissue and neuronal atrophy like advance HIV, AD, or Picks- ICP is normal
vertebral disc herniation
nucelus pulposis squirts out and it causes ocompression usually of s1 which causes absent ankle reflex
nerves C1-C7 it above the corresponding vertebrae. and the others exit below there.
In the c spine, the nerves sit on top and after C8 they exist below
where does the spinal cord end on adults
L1-L2
where is the lumbar puncture performed
L3-L4-5 or L4-L5
where in the dorsal columns are the arms and legs
arms are lateral legs are central
what is the lateral corticospinal tract
saracl and cervical
what is in the anterior corticospinal tract
voluntary motor
what does the anterior spinothalamic do
crude touch, pressure
what is the lateral spinothalamic doing
pain and temperature
dorsal columns: path and function
ascending pressure, vibration, fine touch, proprioception- sensory nerve ending-cell body in dorsal root ganglion- enters the ipsilateral DC- ispisalteral nucleus cuneatus or gracilis and decussated n the medulla and ascendds contra laterally in the medial lemmings then synapses at the VPL in the sensory cortex
spinothalamic: path and function
sensory ad and c fibers cell body in dorsal root ganglia, and enters the spinal cord and ipsilateral gray matter- decussate the anterior white commissure and ascends contralleraterlly VPL in the thalamus to the sensory cortexx- pain termapreue for lateral tract
anterior -crude touch and pressure
lateral coricospinal: path and function
decending is voluntary movement- UMN cell body in the motor cortex then internal capsule then pyramidal decussation and descends contralaterlly and cell body is in the anterior horn of the spinal cord
what are characteristics of LMN lesions
weak, atrphy, fasiculations, decreased reflexes, decreased tone, no babinski, flaccid paralysis
what are the characteristics of UMN lesions
hyperreflized, babinski, spastic paralysis, increased tone, no atrophy or fasiculations
clasp knife spasticity
can be caused by stroke to the internal capsule leading to pure motor weakness on contralateral side of arm, leg, face, and other UMN sides can be present
congential degeneration of anterior horns of spinal cord with LMN lesions only. Floppy baby syndrome with marked hypotonia and tongue fascinations. Influential type median death is around 7 months. It is autosomal recessive
Werdnig Hoffman syndrome
combined UMN and LMN deficits with no sensory or bowel/bladder dysfunction- due to loss of cortical and spinal cord motor neurons, can be caused by defect in superoxide dismutase 1, and commonly presents as asymetric limb weakness, fascinations, eventual atrophy
ALS
spares the dorsal columns and lesser tract in the upper throacic ASA territory is watershed area as the artery of Adamkiewisz supples the AS before T8
complete occlusion of the anterior spinal artery
degeneration and dymyleination of dorsal columns and roots progressive sensory ataxia and impaired proprioception- poor coordination. Associated with chariot joints, shooting pain, argyll robertson pupil
tertiary syphillus causing tabes dorsalis
syrinx expands and damages anterior white commissure of spinothalamic tract- bilateral loss of pain and temperature sensation in cpae like distribution seen with chair I malformation
syringomeyelia
subacute comobines degneration-demylination of spinocerebellat tracts lateral corticospinal tracts, dorsal collumns- ataxic gait an dimparied position and vibration sense
B12 deficiency
caused by poliovirus from fecal oral transmission. replicated in the oropharynx and small intestine spreading via bloodstream to CNS. Infection causes anterior horn destruction of spinal cord and LMN death- LMN lesion- weakness, hypotonia, flaccid paralysis, fascinations, hyporeflexia, muscle atrophy, increased WBC, increased slight of protein in the CSF and WBC in the CSF- virus is recovered from the stool or throat
poliomyelitis
AR recessive GAA repeat on chromosome 9 leading to gratin genre issues- degradation of multiple spinal tract and muscle weakness. Lose vibration sense, proprioception, staggering gait, frequent flailing, nystagmus, dysarthria, pets caves, hammer toes, diabetes, hyeprtrphic cardiomyopathy and kyphoscoliosis
friederich ataxia
what is the most common cause of death of friderich ataxia
it is from hypertrophic cardiomyopathy
what does the gene for friederich ataxia do
it is part of DNA replication and repair and leads to mitochondrial dysfunction
hemisection of the spinal cord so ipsilateral UMN sings below lesion level from corticospinal. Ipsilateral loss of tactile and vibration below lesion from dorsal column damage, contralateral pain and temperature loss below the level of the lesion from spinothalamic tract, ipsilateral loss of all sensation at the level of the lesion, ipsilateral LMN signs- if it is above T 1 then it could lead to hroner syndrome
Brown squared syndrome
rupture discleading to low back pain radiating to one or both of the legs ,saddle anesthesia, loss of anal wink, bowel and bladder dysfunction, loss of ankle jerk and plantar flexion
cauda equina
what is the anal wink level relfex
S4
compression at L2 leading to flaccid paralysis of the bladder and rectum leading to saddle anesthesia and impotence
conus medularis syndrome
what is the dermatome for the nipple
T4
what is the dermatome for the belly button
T10
what is the dermatome for the inguinal ligament
L1
what is the dermatome for knee caps down the leg
L4
what is the S,23,4, dermatomes
erection and sensation of penile and anal zones
what is the biceps reflex
C5,5
what is the triceps reflex
C7,8
what is the patella reflex
L3,4
what is the achilles reflex
S1,2
what is the anal wink reflex
S3,S4
moro reglex
hang on for life
rooting reflex
head moves toward one side if cheek is stroked
sucking reflex
sucking response on roof of mouth
palmar reflex
curling fingers in hang
plantar reflex
dorsiflexion of large toe and fanning of other toes with plantar stimulating. Babinski reflex is in the child but in adult it is from UMN lesion
galant reflex
smoking along one spine while newborn is in suspension
S1 radiculopathy
compression by disc herniation. posterior thigh and calf lateral foot and sensation. weakness of thigh extension, knee flexion, absent ankle jerk
L5 radiculopathy
- weakness of dorsiflexion, inversion and eversion of the foot and toe extension. No missing reflexes
what is parinaud sudnrome
paralysis of conjugate vertical gaze due to lesion of the superior colliculus- store, hydrocephalus, pinealoma
what does the interior colliculi do
it is from auditory
what does superior colliculus do
conjugate vertical gaze
what cranial nerve passes through the cribriform plate
CN I
what cranial nerve passes through the optic canal
CN II
what cranial nerve passes through the superior orbital fissure
V1, IV, III, VII
what cranial nerve passes through the foramen rotundum
v2
what cranial nerve passes through the foramen ovale
V3
what cranial nerve passes through the internal auditory meatus
VI, VIII
what cranial nerve passes through the jugular foramen
IX, X, XI,
what cranial nerve passes through the hypoglossal canaal
XII
what cranial nerve passes through the foramen magnus
XI
what does the nucleus solitarius do
visceral sesory information like taste, barorectoptions, and gut distention from VII, IX, X
what does the nucleus ambiguous do
motor innervation of pharynx, larynx, upper esophagus, swallowing palate elevation- aka swallow and speech
what odes the dorsal motor nucleus do
sends autonomic parasympathetic fibers to heart, lungs, upper GI
corneal reflex: afferent and efferent
afferent V1 and efferent is VII
lacrimation reflex: afferent and efferent
afferent V1 and efferent is VII
jaw jerk reflex: afferent and efferent
afferent V3 and efferent V3
pupillary reflex: afferent and efferent
afferent II and efferent is III
gag reflex: afferent and efferent
afferent Ix and efferent x
if the jaw is deviating is it towards or away from the lesion- and what is the nerve involved
it is jaw towards the lesion and it is from a CNV motor lesion
uvula deviates is it towards or away from the lesion- and what is the nerve involved
away from the lesion and it the vagus nerve for the lesion
the head is weak at turning and there is shoulder droop is it on the same side or way and what is the nerve
CN XI lesion and the head turns away from the lesion and shoulder droops on the side of the lesion
the tongue deviates is it towards or away from the lesion- and what is the nerve involved
the tongue deviates towards the side of the lesion and due to weakened tongue muscles on the side of the lesion
what are the muscles of mastication
masseter, temporalis, and medial pterygoid.
what innervates the muscles of mastication
V3
if the facial nerve lesion spares the forehead, where is the lesion
destruction of motor cortex or connection between motor cortex and facial nucleus in pons to contralateral paralysis of lower muscles of facial expression. Forehead is spared due to its bilateral UMN innervation
if the facial nerve lesion is full face, where is the lesion
it is a destruction of the facial nucleus or CN VI anywhere along the side of the course. Ipsiplateral paralysis of the upper and lower muscles of face. It also leads to hyperacusis
what causes hyperacusis
increased sound from paralysis of stapedius has high pitched sounds from facial nerve palsy
What can cause Bells Palsy
it can be from lyme disease, herpes simplex, herpes zoster, sarcoidosis, tumors, diabetes mellitus, treatment si acyclovir and corticosteroids
what are the signs of bells palsy
impaired eye closure, eyebrow sag, can’t smile, can’t frown, no nasolabial fold, decreased tearing, hyperacusis, decreased taste on the posterior part of the tongue
what CN are in the cavernous sinus
II, IV, V1, VI and V2
cavernous sinus syndrome
opthalmoplegia, decreased corneal sensation, orner syndrome, and occasional decreased maxillary sensation. can be secondary to pituitary tumor or mass effect carotid cavernous fistula cavernous sinus thrombosis related to primary infection.
which nerve in the cavernous sinus is most susceptible to injury
VI
what infections are most common in cavernous sinus
staph aureus, mucor, strep, rhizopus,
what are some of the symptoms of palsies with II, IV, VI
common with proptosis, conjunctival swelling, impaired ophthalmic draining
what order are they on the sides down the cavernous sinus
III, Iv, VI, V1, V2 down the sides and the trochlear is right next to the internal carotid artery
where is low frequency heard in the inner ear
low frequency heard at apex near helicotrema
where is high frequency heard in the inner ear
high frequency heard best at the base of the cochlea
conductive hearing loss
abnormal bone>air and localizes to the affected ear
sensorineural hearing loss
air>bone and localizes to the unaffected ear
the rinne test
it is to test for bone conduction
the weber test
it is the test for the midline of the fork and it localizes to one side or the other
what is a cholesteatoma and were dos it come from
it is a lesion of the tympanic membrane that can rupture the middle ear- it is an overgrowth of desquamated keratin debris within the middle ear that may erode the ossicles and the mastoid air cells- conductive hearing loss
what forms the superior of the orbit
thick orbital plate of the frontal bone
what forms the lateral side of the orbit
zygomatic bone and sphenoid wings form it
what forms the orbital floor
it is a think wall that separates from maxillary sinus- break common- the inferior rectus herniate into the maxillary sinus
what forms the medial wall of the orbit
ethmoid and lacrimal bones fracture and medial rectus gets trapped
what does the trabecular outflow do in the eye
it drains through the trabecular meshwork through the canal of scheme and episcleral vasculature and it can increase with M1 agonist
uveosceleral outflow
it drains into the uvea and sclera and increased prostaglandin agonist
aqueous hunmor production
produced by non pigmented epithelium on ciliary body- decreased by beta blockers, alpha 2 agonists, and accarbonic anhydrase inhibiotrs
hyperopia
eye too short for refractive power of cornea and lens- light focusses behind the retina
myopia
eye is too long, so it focusses in front of retina
astigmatism
abnormal curvature of the cornea and different refractive power at different axis
presbyopia
age related impaired accomindation focusing on near objects, and primarily die to decreased lens elasticity and often nessicitates reading glasses
cataract
painless often bilateral opacification of the lens. decreased vision. Acquired risk factors of increased age, smoking, excessive sunlight, prolonged corticosteroid use, diabetes, trauma, infection
what are the congenital risk factors for cataracts
galactosemia, galactokinase deficiency, trisomies, toche infections like rubella, marfan syndrome, alport syndrome, myotonic dystrophy, and NF2
open angle glaucoma
increased with age, race, family history, and painless and more common. Primary cause is unclear. secondary is blocked trabecular network from EBC or RBC can be from blocked retinal elements
closed angle glaucoma
primary is enlargement or forward movement of the lends against the central iris and obstruction of normal flow o fhumor through the pupil and flip builds up behind the virus pushing the peripheral iris against the cornea. it impedes frlow through the trabecular netwrk. Secondary is from hypoxia and retinal disease
chronic closure
asymptomatic with damage to optic nerve and peripheral vision
acute closure
true ophthalmic emergency. increased IOP pushes the iris forward and angle closes abruptly and very painful red eye, sudden vision loss, halos around lights, rock hard eye frontal headache
what do you not give with acute closure glaucoma
do not give epinephrone because of mydriatic effect
conjunctivitis
inflammation of conjunctiva and red eye .Allergic itchy eyes bilateral and could be from bacterial which treat and see pus. Viral is from adenovirus and sparse mucus discharge and swollen pre auricular node self-resolving
uveitis
inflammation of urea and it can have pus accumulated in the anterior chanmber of the ye and can be associated with system inflammatory disdeae
age related macular degeneration
degeneration of the macula and central area of the retina causes distorting and loss of central vision.
what is dry age related macular degeneration
deposition of yellowish extracellular material in and between bruch membrane and retninaly pigment epithelium with gradual vision loss and prevent progression with vitamins
what is wet age related macular degeneration
it is rapid loss of vision due to bleeding secondary to choroidal neovascularization treat with anti-vegf this is called ranibizumab
diabetic retinopathy and difference between non proliferative and proliferative
- retinal damage de to chronic hyperglycemia.
- nonproliferative- damaged capillaries leak bloos and lipids and fluid seep into retina causing hemorrhage and macular edema. Treat with blood sugar control
- proliferative- chronic hypoxia results in new blood vessel formation with resultatt traction on tretina
retinal vein occlusion
blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis and retinal hemorrhage and venous engorgement and edema in the affected area
retinal detachment
separation of the neurosensory layer of the retina from the outermost pigmented epithelium and degradation of photoreceptors and vision loss. May be secondary to retinal breaks, diabetic traction, inflammatory effusions. visualized on fundoscopy as crinkling of retinal issue and changes in vessel direction. Breaks are more common with high myopia or head trauma. Often proceed by flashes and floaters. It has eventual monocular loss of vision like a curtain draw down
central retinal artery occlusion
acute painless monocular vision loss, and retina is cloudy with attenuated vessels and cherry red spot at fovea- center of the macula- theres an embolic source from carotid artery atherosclerosis, vegetations, patent foramen ovale
what signs of reflex would you see on central retinal artery occlusion
no constriction of other eye with direct light because of destroyed retinal ganglial cells
retinitis pigmentosa
inherited retinal degneration. Painless progressive vision loss beginning with night blindness and rods are affected first- bone spicule shaped deposits around the macula
retinitis
retinal edama, necorsis, and leads to scar
what are the causes of retinitis
CMV, HSV, VZV and can be bacterial or parasitic or associated with immunosuppression
papiledema
optic disc swelling usually bilateral with increased ICP and it is engaged blind spot and elevated opt disc with blurred margins
miosis- what is the reflex
first neuron is the dinger wasteful nucleus to the chillily ganglia via CNIII and second neuron is short ciliary nerves to pupillary sphincter muscles
where is the origination of the Edinger westfall nucleus
it is in the midbrain
myadriasis
dilation it is from sympathetic.
marcus gunn pupil
afferent pupil light defect due to optic nerve damage or severe retinal injury. decreased bilateral pupillary constriction when light is shone in affected eye relative to unaffected eye.
horner syndrome
sympathetic denervation of the face- ptosis, anhidrosis, miosis- pan coast tumor, brown squared, late stage syringomyelia
what CN innervates the lateral rectus
CN VI
what CN innervates the superior oblique
CN IV
what CN innervates superior rectus, inferior rectus, , medial recturs, and inferior oblique
CN III
what motion does the superior oblique perform
it abducts, interest, and depresses while adducted
internuclear opthalmoplegia
when looking left, the left nucleus of the CNVI fires, which contacts the left lateral rectus and stimulates the contralateral right nucleus of the CNIII via the right MLF to contract the right medial rectus. Convergence stays normal
AD
most common cause of dementia in the elderly. Increased risk with ApoE2 decree and increased risk with APOE4. App, presenilin and have an increase risk. see widespread cortical atrophy, and narrowing of gyro and widening of the sulk. There is decreased ACh. Senile plaques are in the grey matter and extracellular beta amyloid core. May cause amyloid angiopathy and intracranial hemorrhage. AB synthesized by the cleavage of APP. Neurofibbrillary tangles are intracellular hyperphosphorylated tau proteins. Number of tangles determines how bad the disease is
why are people with downs at an increased risk of AD
they have an extra APP gene on chromosome 21
frontotemporal dementia
early changes in personality and behavior or aphasia. Aphasia is from primarily progressive aphasia. May have associated movement disorders. ALS like UMN/LMN degeneration. Previously called pick disease. Ave frontotemporal dementia and lobe degeneration. Inclusions of hyperphosphorylated taw protein and round eosinophilic lesions and TDP43 postiive
Lewy body dementia
initially dementia and visual hallucinations followed by parkinson like deatures- intracellular levy bodies with insoluble aggregates of alpha synuclein primarily in the cortex
vascular dementia
multiple arterial infarcts and or chronic ischemia. It is a step wise decline in cognitive function and impairment. It is theseoncd most common cause. Look at MRI which shows multiple cortical and subcortical infarcts
CJD
rapidly progressive dements with myoclonus. Spongiform cortex and protons from beta pleated sheet which is resistant to degradation
what are some other causes of dementia
HIV, hypothyroidism, vitamins B1, B3, or B12, wilson disease NPH
Central pontine myelinosis
acture paralysis, dysarthria, dysphaga, diplopia, loss of consciousness- caused locked in syndrome- massive axonal degeneration in pontine white matter. Secondary to osmotic changes. Commonly iatrogenic from rapid correction of hyponatremia.
what happens if hypernatremia is corrected too quickly
it causes edema and herniation
Charcot triad
scanning speech, intention tremor, incontinence, internuclear ophthalmoplegia, nystagmus
what is the CSF sign of MS
it is oligoclonal banding in the CSF.
what is seen on MS MRI
it is gold standard and there are periventricular plaques with destruction of cons. multiple white matter lesions.
pseudobulbar palsy
associated with MS. There is dysarthria, dysphagia, dysphonia, impaired tongue, facial movements
acute inflammatory demyelinating polyradiculopathy
GBS subtype that is an autoimmune condition attacking the schwann cells and inflation and demyelination of the peripheral nerve fibers. results in symmetric ascending muscle weakness/paralysis and beginning in lower extremtities. Can have some autonomic dysregulation. Increased CSF protein count. Associated with campylobacter jejuni and viral causes. Need respiratory support
acute disseminated post infectious encephalomyelitits
multifocal periventricular inflamtion and demyelination after infection or vaccination- rapidly progressive multifocal neurologic symptoms altered mental status
Charcot Marie Tooth
hereditay motor and sensory neuropath- progressive herditary nerve disorders related to defective production of proteins involved in the structure oand function of peripheral nerve or the myelin sheath. Typically autosomal dominant inherticane pattern associated with foot deformities, lower extremity weakness and sensory deficits
Krabbe disease
AR- lysosomal storage disorder due to degiceinct of galactocerebrosidase. buildup of glactocerebroside and pyochosine destroys myelin sheath. It is peripheral neuropathy, and developemental delay, optic atrophy and globoid cells
Metachromatic leukodystrophy
ar lysosomal strage disorder of arylsulfatase A deficiency. Buildup of sulfates impaired production and destruction of myelin sheath. Find central and peripheral demyelination with ataxia and dementia
PML
demyelination of the CNS due to destruction of oligodendrocytes and it is from reactivation of JC virus in MS or AIDs rapidly progressive and fatal from natalizumab and rituximab
adrenoleukodystrophy
X linked disorder of disrupted metabolism of long chain fatty acids and build up in nervous system, adrenal gland, testes- leads to long term coma death, and adrenal crisis
partial siezures
affect a single area of the brain and commonly originate from the temporal lobe often proceeded by an aura
simple partial
consciousness stays intact but it is only motor sensory and autonomic psychic
complex partial seizure
lose consciousness
epilepsy
a disorder of recurrent seizures fertile are not it
status epilepsy
continous or recurring siezures that may result in brain injury>5 min
causes of seizures by age: children adults, elderly
- children- genetic infection, febrile, trauma, congenital, metabolic
- adults-tumor, trauma, stroke, infection
- elderly- stroke ,tumor, trauma, metabolic infection
absence seizures
3hx frequency and no postictal confusion- treat with ethosuximide- staring spells
myoclonic seizures
repeated jerks
tonic clonic seizures
alternating stiffening and movement
tonic seizures
just tensing
atonic seizures
drop seizures where they fall to the floor
cluster headaches
unilateral in young male smokers, 15 minute 3 hour repetitive- repetitive brief headaches excruciating periorbiral pain with lacrimation and rhino rhea or Horners syndrome
treatment for cluster headahces
sumatriptan and O2
CNS tunmor that is in the cerebal hemispheres can cross the corpus collosum and its pseudopalisading pelomophic tumors cells with central areas of necrosis and hemorrhage and positive for GFAp
glioblastoma multiforme- grade IV astrocytoma
benign primary brina tumor. most often occurs near surfaces of brain and pasasagittal region arises from arachnoid cells it is extra acial- and may have a dural attachment often asmyptomati but can have focal neurological signs and seizures- see psammoma bodies which are calcifications
meningioma
cerebellla tumor associated with VHL and it is found with retinal angiomas- can produce erythropoetin like polycythmia- thin walled capillaries with minimal parenchyma
hemangioblastoma
cerebellopontine angle typically but can be from other peripheral nerves. vestibular is CNVVIII- bilateral vestibular are in NF2 are S100
these are schwannomas
rare slow growing tumors of fried egg cells, chicken wire capillaries and are in the frontal lobes
olidendroglioma
usually a prolactinoma with biemporal hemianopia with lactotrophy cells
piutiary adenoma
what brain lesion do AIDs patients tend to get
CNS lymphoma single ring enhancing lesion are high grade, poor prognosis and positive for EBV
pineal mass
germinoma with mass effect and cause obstruct hydrocephalus
well circumscribed in children found in posterior fossa like cerebellum- may be supratentorial and positive for GFAP= see rosenthal fibers- eosinophilic corkscrew fibers- cystic and solid
pilocytic astrocytoma
highly malignant cerebellar tumors a form of primitive neuroectodermal tumor can compress fourth ventricle causing noncommunicating hydrocephalus can send drop metastases to spinal cord- midline posterior fossa- increased intracranial pressure and cerebella dysfunction- homer wright rosettes and small blue cells
meduloblastoma
perivascular rosettes and rod shaped belpharoplasts- basal ciliary bodies found near the nucleus- can be in the 4th ventricle
ependymoma
childhood tumor with bitemporal heianopia- childhood supratentorial tumor- slow benign tumor of super cellar region with cyst and calcification and motor oil in the cells from ruthless pouch and have calcification and cholesterol crystals
craniopharyngioma
tumor of pineal gland causing compression of the tectum and vertical gaze palsy and obstructive hydrocephalus and compression of cerebral aqueduct and processors puberty and increased beta HCG- similar to seminoma
pinealoma
cingulate and subflacine herniation
flax cerebra can compress anterior cerebral artery
central herniation
downward transtentorial hernaition- durrette hemorrhage from basilar artery rupture- caudal displacement of the brainstem
uncal herniation
CNIII palsy with blow pupil, down and out
cerebellar tonsil herniation
coma and death and go through the foramen magnum
trigmeinal neuralgia
sudden pain in CN V stabbing and electric shock in short bursts from chewing, tooth brush ,temperature changes, carbamazepoins is first line and decrease NA channel recovery to decreased firing of neurons. CBC monitor for aplastic anemia
DRESS syndrome
2-8 weeks post drug exposure- fever, lymphadenopathy, facial edema, mobeliform skin rash and confluent erythema, actor I neurhoathy, cough, increased ALT and eosinophilia
what is the path of the ACL and what test do you use for ACL injury
it is from the lateral femoral tubercle to the anterior tibia- you should use the anterior drawer or Lachman test for it
what is the path of the PCL and what test do you use for PCL injury
PCL is from medial femoral condyle to the posterior tibia. Use the posterior drawer test
what is injured if the there is lateral force placed on the knee and it starts to bed that way from valgus force
it is an MCL tear
what is injured if there is varus force applied to the knoee and the lateral space widens
LCL
for the McMurray test, if there is external rotation applied and pain then its the
medial meniscus
for the McMurray test, if there is internal rotation applied and pain then its the
lateral meniscus
Osgood Schlatter: where is the injury, what should you feel on testing, and what is the repetitive stress from
there is an overuse injury to the secondary ossification centre of the apophysis f the tibial tubercle. Knee pain in adolescent and pain and swelling at the tibial tubercle and at the insertion of the patellar ligament which connects the tibia to the patella and quadriceps can avlse. This can lead to a callus formation at this tendon. It is from repetitive use of the quadriceps and from jumping
what is the function of the patella
it improves knee extension and provides nutrients to distal femur cartilage.
if the patella is broken, what movement cannot be performed
extension of the knee against gravity and there is a palpable gap in extension
what is injured in the unhappy triad and what causes this injury
ACL, MCL, medial meniscus- due to lateral force applied to a planted leg
what causes prepattellar bursitis and what is the inflammation
it is inflammation of the from and largest bursal sac of synovial fluid- it is from repeated trauma or pressure from excessive kneeling like gardening or housemaids
where is a Baker cyst and what is the common related condition
it is a popliteal collection in gastrocneumus-semimenbranous bursa and communciated with the synovial space and related to chronic joint disease
what are the muscles of the rotator cuff
supraspinatur, infraspinatus, subscapularis, teres minor
what motion does supraspinatus perform, when is it injured and what nerve innervates it
it does shoulder abduction and it is the most common injury should test the can test and its innervated by the supra scapular nerve
what motion does infraspinatus perform, when is it injured and what nerve innervates it
It is the lateral or external rotator of the shoulder and it is from a pitching injuryy and its innervated by the supra scapular nerve
what motion does theres minor perform, when is it injured and what nerve innervates it
it adducts and internally rotaties the arm/lateral rotation- it is from the axillary nerve
what motion does subscapularis perform, when is it injured and what nerve innervates it
it medially rates the arm so internal rotation and adduction- its from the sub scapular nerves
what is the repeated motion for medial epicondylitis
it is repeated flexion of the wrist
what is the repeated motion for lateral epicondylitis
repretitive extension so repetitive wrist extension
what is a scaphoid injury from and why
it is from the fall on the outstretched hand. It is in the anatomical snuff box, and it is retrograde blood supply. It sits on the radius and it is closest to the thumb