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Neuro Flashcards

1
Q

cells of the brain

A

neural tube is finished by day 19 -21 (FA), 28-29 days (Goljan)
- point first 2-3 weeks

CNS:
neurons - Nissl bodies in dendrites and cell bodies
-injury –> Wallerian degeneration - axon degenerates distally, retracts proximally
-regeneration occurs in PNS
- chromatolysis aka axonal reaction - reaction of neuronal cell body in response to axonal injury –> increased protein synthesis, displacement of nucleus to periphery, dispersion of Nissl bodies, round cellular swelling

Peripheral NS:

  • Schwann cells sense axonal degeneration and quickly being to degrade myelin and secrete cytokines that recruit macrophages –> myelin debris is cleared quickly
  • in CNS - BBB means that microglia are recruited more slowly –> extremely slow removal of myelin debris, years!
    - axonal growth is suppressed via myelin-associated inhibitory factors and astrocyte produced glial scar (ahead of where the neuron could regenerate)

astrocytes - extracellular K+ buffer, remove excess neurotransmitter, BBB, glycogen fuel reserve, reactive gliosis

  • neuroectoderm
  • GFAP

mesoderm –> microglia ~ macrophages

  • not readily discernible by Nissl stain
  • HIV-infected microglia fuse –> multinucleated giant cells

Schwann cells - 1 neuron, GBS
oligodendrocytes - many neurons, neuroectoderm (so fried-egg appearance on histology)
-injured in MS, PML, and the leukodystrophies
-but in MS - antibodies against myelin sheath
-in PML - oligodendrocyte is damaged

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2
Q

spina bifida occulta

A

dura is intact

associated with tuft of hair/skin dimple

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3
Q

holoprosencephaly

A

failure of hemispheres to separate
- sonic hedgehog pathway mutations, trisomy 13, and fetal alcohol syndrome

cleft lip/palate
cyclopia

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4
Q

posterior fossa malformations

A

Chiari 1 - ectopic cerebellar tonsils

  • asymptomatic kid, adults with headaches and cerebellar symptoms
  • associated with syringomyelia
  • syringomyelia - can extend into anterior horns and further –> host of symptoms including DCML affected, UMNs affected, scoliosis due to paresis of paravertebral muscles

Chari 2

  • herniation of vermis and tonsils
  • aqueductal stenosis
  • associated with meningomyelocele

Dandy-Walker - failure of cerebellar vermis to form –> absent cerebellum

  • cystic enlargement of 4th ventricle, non-communicating hydrocephalus
    - congenital aqueductal stenosis – hydrocephalus because the sutures havent fused
    - in an adult - ventricles would dilate and you would have normal pressure hydrocephalus
  • associated with spina bifida
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5
Q

polio

A

fecal-oral transmission
damages anterior motor horn (LMN damage) –> asymmetric flaccid paralysis, hyporeflexia

v.s. Werdnig-Hoffmann disease - AR, inherited degeneration of anterior motor horn –> floppy baby

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6
Q

ALS

A

UMN and LMN disorder
-LCST and anterior horn affected

Zn-Cu SOD mutations associated with familial cases

fatal, treat with riluzole (decreases glutamate excitotoxicity)

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7
Q

Friedreich ataxia

A

AR, GAA repeat in frataxin gene

  • controls Fe regulation in mitochondria –> increased free radical damage
  • cerebellum and multiple spinal cord tracts are damaged

staggering gait, frequent falls, kyphoscoliosis, HCM (cause of death)

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8
Q

meningitis bugs

A

neonates - GBS (can also cause sepsis in newborn, premature rupture of membranes –> chorioamnionitis –> fetal sepsis), E coli, Listeria (pregnant women should NOT eat soft cheeses, tumbling motility)

  • Listeria is a gram positive rod
  • Trichomonas also has tumbling motility

kids/teens - N. meningitidis, enters through nasopharynx

adults/elderly - S. pneumo (gram pos diplococci)
- S. pneumo - alcoholics, asplenics

non-vaccinated infants - H. flu (gram negative coccobacilli)
- vax against capsule

Coxsackie virus - most common viral cause
-photophobia esp with viral etiology

fungi in immunocompromised
-CSF - lymphocytes and low CSF glucose

S aureus following neurosurg

treat with antibiotics and steroids (prevents scar tissue formation and obstructive hydrocephalus)
- sensory deafness is a common complication of meningitis

(v.s. encephalitis - MSE changes, sleepy)

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9
Q

watershed areas

A

areas between ACA/MCA and MCA/PCA

damage occurs due to severe hypotension

upper leg/upper arm weakness and defects in higher order visual processing

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10
Q

global cerebral ischemia

A

mild - insulinoma (hypoglycemia), transient confusion with quick recovery

moderate - infarcts (shock, hypotension, anemia) in watershed areas

  • damage to pyramidal neurons of cortex (layers 3, 5, 6) –> cortical laminar necrosis
  • pyramidal neurons of hippocampus, vulnerable hippos
  • Purkinje layer of cerebellum

severe - diffuse necrosis of brain –> vegetative/death

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11
Q

focal ischemia

A

thrombotic - pale, wedge (occurs at branch points of arteries), periphery of cortex

emboli - hemorrhagic infarct, periphery of cortex, usu involves MCA

hypoxic - common during CV surgeries, affects watershed areas

lacunar - secondary to hyaline arteriolosclerosis

  • tiny infarcts, which are reabsorbed –> lacuna
  • lenticulostriate vessels (off MCA) are most affected
  • depending on the part of the brain - you can have pure sensory (thalamus) or pure motor infarcts (internal capsule)

ischemia –> pale infarct –> liquefactive necrosis

1) 12-24 hrs - red neurons, pyknotic nuclei
2) 1d-1w - neutrophils, microglia
3) 1w-1mo - reactive gliosis + vascular proliferation
4) cyst lined by astrocytes = glial scar

ischemic stroke can cause vascular dementia - encephalomalacia

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12
Q

intracerebral hemorrhage

A

most commonly due to Charcot-Bouchard microaneurysms - complication of HTN
basal ganglia
- not visible on angiography
- hemorrhage would appear as a hyperdensity on CT

aneurysmal rupture –> blood clot

sympatholytics - methyldopa and clonidine stimulate a2 receptors
- can be use intracranial hemorrhages caused by HTN

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13
Q

SAH

A

rupture of berry/sacular aneurysm - lacks media layer at the branch point

  • most commonly located in anterior circle of Willis
  • will see bleed on the bottom of the brain
  • usually at branch of ACA –> will compress optic chiasm
  • if PCA is involved –> oculomotor nerve compression
  • seen in Ehlers-Danlos, ADPKD

remember - Struge-Weber has port-wine stain and AV malformation on that same side of the brain

  • interestingly - only 10% SAH is due to AVM
  • AVMs cause intraparenchymal bleeding

4-10 days after hemorrhage –> vasospasm (due to blood clot breakdown or rebleed) –> ischemic infarct
-use nimodipine

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14
Q

epidural hematoma

A

talk-and-die syndrome
- uncal herniation - CN3 palsy

subdural hematoma - bridging vein rupture, waxing/waning consciousness (?)

CT to visualize blood (MRI is no good)

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15
Q

herniation

A

tonsilar herniation - compresses brainstem –> cardiopulmonary arrest

subfalcine herniation - ACA compression, infarct

uncal herniation - CN3 compression –> eyes down and out, pupils dilated (PSNS tone is lost)
-can compress PCA - infarction of occipital lobe
(-pulls paramedian artery - duret hemorrhages on brain stem) Pathoma
- (FA) compresses contralateral crus cerebri at Kernohan notch —> ipsilateral paresis

transtentorial –> caudal displacement of brain stem –> Duret hemorrhages, fatal

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16
Q

strokes by artery

A

MCA - contralateral hemiparesis and hemisensory loss of face and upper limb

  • lower limbs are spared/minimally affected
  • Wernicke’s + right superior quadrant visual field defect
  • Brocas - aphasia (left), hemineglect (right)
  • can have gaze and visual field disturbances

ACA - contralateral hemiplegia lower limb
- bilateral ACA occlusion –> behavior symptoms, primitive reflexes, urinary incontinence

lenticulostriate artery - contralateral paralysis and sensory loss of face and body

cerebellar arteries: ipsilateral horner and decreased pain and temp from face
-decreased pain and temp from contralateral body

posterior inferior cerebellar - lateral medulla
-dysphagia, hoarseness, and decreased gag reflex

anterior inferior cerebellar - lateral pons and facial nucleus

  • ipsilateral facial paralysis - facial nucleus
  • ipsilateral pain and temp loss of face (trigeminal nucleus) and contralateral loss of pain/temp in extremities (ALT)
  • ipsilateral hearing loss
  • cerebellar dysfunction

basilar - damage to base of the pons (corticobulbar and corticospinal tracts, paramedian tegmentum)
- locked in syndrome (but also loss of horizontal eye movements)

PCA - occipital lobe, contralateral hemianopia with macular sparing

if there is no hemorrhage - pt is a candidate for tPA

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17
Q

leukodystrophies

A

lysosomal storage, etc. disorders

metachromatic leukodystrophy - arylsulfatase, myelin cant be degraded and accumulates in lysosomes
-central and peripheral demyelination

Krabbe disease - galactocerebroside acc in macrophages –> destruction of myelin sheath
-peripheral neuropathy, developmental delay, optic atrophy

adrenoleukodystrophy - impaired metabolism of FAs –> FAs acc in adrenals, white matter, and testes

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18
Q

MS

A

HLA-DR2

T cells abnormally react to myelin –> release IFNy –> call in other WBCs

optic neuritis = monocular vision loss, pain on eye movement, Marcus Gunn pupil
Lhermitte phenomen
symptoms exacerbate with increased body temp

treat

  • high dose IV steroids during acute attack
  • INFb slows disease progression, can use glatiramer, natalizumab

treat symptoms

  • neurogenic bladder - catheterization, antimuscarinic antagonists
  • spasticity - baclofen, GABA-B receptor agonists
  • pain - TCAs, anticonvulsants
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19
Q

Progressive multifocal leukoencephalopathy

A

latent JC virus reactivation –> destruction of oligodendrocytes
rapidly progressive neuro signs –> death

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20
Q

osmotic demyelination

A

central pontine demyelination

= locked in syndrome (anything with the pons will lead to locked-in syndrome)

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21
Q

Picks disease

A

frontotemporal dementia

  • behavioral variant or primary progressive dementia variant
  • may have associated movement disorders

round aggregates intracytoplasmic inclusions of tau protein - seen on silver stain

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22
Q

Parkinson’s

A

normally: cortex –> BG –> cortex
- D1 receptors on striatum increase stimulation of cortex
- D2 receptors on striatum decrease inhibition of cortex
- Parkinsons - loss of dopamine, excess cholinergic activity

features

  • contain Lewy bodies - a-synuclein, eosinophilic
  • later onset dementia
  • MPTP - contaminant in illegal drugs can cause parkinsonian symptoms
    • why? - because MPTP is metabolized into a toxic metabolite by MAO-B
  • defects in ubiquitin-proteasome system have also been implicated in parkinsons

drugs = BALSA
- dopamine agonists - bromocriptine (ergot), *pramipexole, *ropinirole

  • increases dopamine availability - amantidine (increases released, decreases uptake) –> tox - anticholinergic effects, ataxia, livedo reticularis (lace-like mottled skin)
  • increases L-dopa availability -levidopa/carbidopa (carbidopa inhibits DOPA decarboxylase, peripheral dopamine causes N&V)
    - levidopa - absorbed in SI by neutral-AA transporter
    - levidopa adverse effects - arrhythmias (due to increased peripheral catecholamines), on-off (dyskinesia-akinesia) will long-term use
    - why do you get on-off symptoms - as PD progresses, therapeutic window for levidopa narrows (possibly due to nigrostriatal degeneration). Small changes in serum drug levels (as occurs between doses) leads to motor fluctuations
  • pergolide - D2 agonist
    - entacapone, tolcapone - prevent peripheral L-DOPA degradation, inhibit peripheral COMT
    - can add entacapone for pts who are experiencing wearing-off periods in between doses
  • prevent dopamine breakdown - selegine (MAO-B inhibitor), tolcapone (inhibits central COMT)
  • curb excess cholingeric activity - benztroptine, trihexyphenidyl

clinical note: many neurologists use selegiline, anticholinergics, and amantadine
- levidopa/carbidopa are secondary option

VS Lewy body dementia - where dementia is early onset (dementia and hallucinations) –> then progresses to parkinsonian features

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23
Q

Huntington’s

A

gain-of-function mutation - mutated huntingtin gene –> increased histone deacetylation –> histone and DNA interact more tightly –> unable to transcribe neutrophic factors

degeneration of GABAergic neurons in CAUDATE nucleus and Ach neurons

increased dopamine in brain

tetrabenazine and reserpine - inhibit VMAT (vesicle monoamine transporter) –> decreased dopamine vesicle packaging and release

haloperidol - D2 antagonist

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24
Q

normal pressure hydrocephalus

A

wet, wacky, wobbly

  • magnetic gait
  • frontal lobe - inhibits bladder contractions

due to decreased CSF resorption
- idiopathic, secondary to brain trauma or SAH

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25
Q

Childhood CNS tumors

A

kids - BELOW tentorium

*pilocytic astrocytoma - benign, cerebellum, astrocytes with thick eosinophilic processes (Rosenthal fibers), GFAP pos

ependymoma - malignant, perivascular pseudo-rosettes, rod shaped bodies found near nucleus
- most commonly in 4th ventricle

medulloblastoma - neuroectoderm (granular cells of cerebellum), malignant

  • small, round blue cells + homer-Wright rosettes
  • mets via CSF, drop mets on SC

craniopharyngioma - epithelial remnants of Rathke’s pouch

  • nests of squamous epithelium with wet keratin in the center
  • supratentorial
  • optic chiasm compression
  • recurrent
  • calcifications on imaging

pinealoma - Parinaud syndrome

1) vertical gaze palsy - compression of tectum
2) obstructive hydrocephalus
3) precocious puberty - bHCG production

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26
Q

adult CNS tumors

A

Glioblastoma multiforme - grade 4 astrocytoma

  • cerebral hemispheres, crosses corpus callosum
  • GFAP pos
  • pseudopalisading necrosis - necrosis surrounded by an edge of viable cells

oligodendroglioma

  • calcified, fried-egg cells, chicken-wire capillaries
  • frontal lobe - may present with seizures

meningioma - benign, females (tumor expresses estrogen receptor), arachnoid cell origin

  • found in cerebral convexities, dural tail
  • whorled cells –> which can calcify to form psammoma bodies
  • seizures

schwannoma - CN8, internal acoustic meatus, CPA

  • bilateral in NF2
  • S100 positive
  • cells arranged around eosinophilic cores

hem-angio-blastoma

  • hemangio +retinal angioma = VHL
  • can produce EPO
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27
Q

conjunctivitis

A

most commonly due to adenovirus

swollen periauricular node

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28
Q

refractive errors + glasses

A

hyperopia - farsighted, eye too short –> light focuses behind retina, correct with convex/converging lens
v.s. myopia

astigmatism - abnormal curvature of cornea

presbyopia - impaired accomodation

constantly having to change glasses - sorbitol is accumulating in lens and changing the refractive index of the lens

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29
Q

cataracts

A

acquired: …alcoholic, smoker, prolonged corticosteroid use
congenital: … trisomies, TORCHeS, Marfan, Alport, NF2, myotonic dystrophy

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30
Q

aqueous humor pathway

A 
trabecular outflow (90%) --> episcleral vasculature
-increased with M3 agonist

uveoscleral outflow - increased with PG agonist

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31
Q

glaucoma

A

optic disc atrophy with thinning of outer rim of optic nerve head (aka cupping) - white/bright part of the optic disc looks larger

open-angle - increased age, AA, FH

  • painless
  • primary or secondary (blocked tracbecular meshwork due to WBCs from uveitis, RBCs form vitreous hemorrhage, retinal elements from retinal detachment)

closed-angle aka narrow = problems in iris lead to downstream problems

  • primary - forward movement of lens against iris –> obstruction of aq humor flow through pupil –> fluid builds up behind iris –> pushes peripheral iris against cornea –> blocking flow through trabecular meshwork
  • secondary - hypoxia from retinal disease –> vasoproliferation in iris
  • chronic closure - asymptomatic but damage to optic nerve and peripheral vision
  • acute closure - EMERGENCY, increased IOP pressures iris fwd… –> very painful, red eye. Sudden vision loss, halos around lights, frontal headache, fixed + mid-dilated pupil. DONT give epi because it dilates pupil.

Drugs:
a agonists - epi (a1), brimonidine (a2) - decreases aq humor synthesis
- foreign body sensation, redness

b-blockers - decrease aq humor synthesis, no vision changes

diuretics - acetazolamide (decreased humor synthesis), no vision changes

cholinomimetics (M3) - pilocarpine, carbachol, physostigmine, echothiophate - increased outflow via contraction of ciliary muscle and opening of trabecular meshwork

bimatoprost, latanoprost (PGF2) - increased outflow through uveoscleral pathway
- darkens color of iris and increases eyelash growth

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32
Q

uveitis

A

all layers of eye include the choroid, ciliary body, and iris (past the cornea)

associated with systemic inflammatory disorders

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33
Q

age-related macular degeneration

A

dry (80%) -deposition of yellowish material with gradual decrease in vision (Drusen)
- subretinal inflammation and abnormal ECM proliferation –> hypoxia (–> stimulates local VEGF)
-prevent with multivitamin and antioxidant supplements (disease is due to chronic oxidative damage), stop smoking
= GRADUAL

wet (exudative) - RAPID loss of vision due to bleeding (after neovascularization of choroid)
-pt will have metamorphopsia - distortion of straight lines
-anti-VEGF injections -
ranibizumab

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34
Q

diabetic retinopathy

A

nonproliferative - damaged capillaries leak blood –> hemorrhages and macular edema
-treat with blood sugar control

proliferative - chronic hypoxia –> vessel proliferation –> traction on retina
-treat with peripheral retinal photocoagulation, surgery, anti-VEGF

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35
Q

retinal detachment

A

retina separates from pigmented epithelium –> degeneration of photoreceptors –> vision loss

breaks are more common in pts with high myopia and/or history of head trauma

often preceded by posterior vitreous detachment –> retinal detachment –> monocular vision loss

surgical emergency

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36
Q

central retinal artery occlusion

A

retinal artery

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37
Q

retinitis

A

retinitis
CMV, HSV, VZV, etc.
- retinal edema and necrosis

v. s. retinitis pigmentosa
- inherited retinal degeneration
- painless, progressive vision loss - starts with night
- blindness (rods are affected first)
- bone spicule-shaped deposits around macula - black dots

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38
Q

Horner syndrome

A 
PAM is horny
associated with lesion of SC above T1 
-Brown-Sequard syndrome
-synringomyelia
-Pancoast tumor aka superior sulcus tumor- stellate ganglion alongside SC

thalamus –> synapse in lateral horn –> superior cervical ganglion (C2) –> sweat glands, smooth muscle of eyelid, pupillary dilator

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39
Q

CN4

A

innervates SO

CN6 - LR
CN3- rest
- PSNS fibers are on the periphery of CN3 - compression is more likely to cause mydriasis as opposed to ischemia (ex DM)

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40
Q

BBB

A

astrocyte foot processes - BM - tight junctions between capillary endothelium

area postrema
OVLT - osmotic sensing
neurohypophysis

vasogenic edema if endothelial tight junctions are destroyed

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41
Q

CSF

A

glucose can be consumed by cancer cells too

Cl- higher in CSF - 120
Mg is also higher

scenario: orbital fracture –> fluid drip
- what fluid is dripping out? - check Cl-

aqueductal stenosis - most common cause of hydrocephalus in kids

valsalva –> venous –> dural sinuses –> CSF –> will flow easily out of needle during LP = tells if entire subarachnoid space is patent
- dont hold your breath during exercise - disk will herniate due to pressure of CSF

hydrocephalus - meningitis due to TB at base of brain –> scar tissue –> blocked foramens of L and M

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42
Q

battle sign

A

basilar skull fracture, posterior fossa

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43
Q

dementia

A

1) neurodegeneration
2) cognitive deficit
3) loss of function

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44
Q

PB poisoning

A

papilledema - due to increased vessel permeability

due to ….acid (?)

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45
Q

essential tremor

A

most commonly diagnosed movement disorder - AD

worsens when holding object (v.s. Parkinsons - these folks have a resting tremor)

symptoms improve with alcohol consumption

treat with propanolol - b1/b2 blocker has CNS effects

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46
Q

tuberous sclerosis

A

AD - late manifestations

hamartomas

  • tubercles/hamartomas that bulge into ventricles - hamartomas of astrocytes
  • angiomyolipomas
  • cardiac tumors - rhabdomyomas

mental retardation

Shagreens patches - hypopigmented patches that are hard to see, use Wood’s light

47
Q

NF

A

AD - late manifestations

cafe au lait spot, axillary freckling, acoustic neuroma, meningioma, *optic glioma (benign)

plexiform neurofibromas - benign tumor of peripheral nerve

pheochromocytoma - pt presents with HT

48
Q

CMV

A

most common congenital infection - culture fetal urine

periventricular calcifications

49
Q

pig herder

A

taenia, cysticercosis –> seizures

50
Q

barbiturates, benzos

A

barbs - GABA_A
- sedative, induction of anesthesia (thiopental)
INDUCES CYP450
- overdose treatment is supportive - assist respiration and maintain BP

benzos -pams, chlodiazepoxide, GABA_A

  • uses - obvious, night terrors, sleepwalking, general anesthetic, hypnotic
  • decrease REM sleep
  • ATOM are short-acting - have higher addictive potential
  • OTL metabolized outside the liver
  • antidote - flumazenil (competitive antagonist)

alcohol also binds to GABA receptor

51
Q

insomnia drugs

A

nonbenzo hypnotics:
ZZZ - zolpidem, zaleplon, esZopiclone
- act via BZ1 subtype of GABA receptor
- short duration - rapidly metabolized by liver
- decreased dependence risk
- sleep cycle less affected - compared to benzos
- antidote - flumazenil

suvorexant - orexin (hypocretin) receptor antagonist

  • orexin involved in wakefulness and appetite, deficiency leads to narcolepsy
  • no dependence
  • ADRs - abnormal dreams, URI, contraindicated with liver disease or CYP3A4 inhibitors

ramelteon - melatonin receptor antagonist (suprachiasmatic nucleus)
- no dependence

all insomnia drugs - adverse effects include headache, dizziness

52
Q

triptans

A

5-HT1b/d AGONIST –> induce vasoconstriction

  • inhibit trigeminal nerve firing
  • prevent VIP release

adverse effects - coronary vasospasm (so dont give to CAD pts), mild paresthesia, serotonin syndrome

53
Q

inhaled anesthetics

A

drugs with decreased blood solubility = rapid induction and recovery (induction based on how quickly you can equilibrate alveolar concentration with blood stream concentration, anesthetic acts when it is in the gas phase in blood)

  • higher solubility in blood means that more anesthetic must be absorbed before it can be transferred to other tissues
  • higher peripheral tissue solubility means more anesthetic is extracted from arterial blood –> AV gradient is greater –> blood saturation takes longer, so brain saturation takes longer

increased solubility in lipids = potent

-anes, N2O
N2O - fast induction, low potency
halothane is opp

myocardial depression, respiratory depression, N&V, increased cerebral blood flow (decreased cerebral metabolic demand)

hepatotox (halothane), nephrotox (methoxyflurane), enflurane (epileptogenic), expansion of trapped gas in body (N2O)

halothane hepatitis - metabolized by CYP450 –> metabolites lead to hepatocyte damage
- centrilobular hepatic necrosis - indistinguishable from viral hepatitis

malignant hyperthermia (AD) - also induced by sux

  • mutations in VS_RyR – > increased Ca2+ from SR
  • Ca-ATPase overworks to get Ca back into SR –> ATP depletion, heat generation –> rhabdomyolysis –> release of K, myoglobin, and creatine kinase into circulation
  • dantrolene - RyR antagonist, also used in neuroleptic malignant syndrome
54
Q

opioids

A

…loperamide, dextromethorphan, diphenoxylate, pentazocine

mu (endorphins), k (dynorphin), d (enkephalin)

open K+ channels, close Ca2+ –> decrease synaptic transmission –> inhibit release of Ach, NE, 5HT, glutamate, substance P

OD: miosis, bradycardia, hypotension (due to histamine release)

uses - …, acute pulmonary edema

adverse effects - N&V, miosis (except meperidine)

others:
- pentazocine - agonist/weak antagonist, used for analgesia, can cause withdrawal symptoms if pt is on opioid antagonist
- butorphanol - agonist/partial agonist, used in severe pain (labor, migraine), causes less respiratory depression but OD is not easily reverse with naloxone, can cause withdrawal symptoms if pt is on opioid antagonist
- tramadol - weak agonist, inhibits 5HT and NE reuptake
- involved with many NTs
- chronic pain, decreases seizure threshold, serotonin syndrome

55
Q

NM blockers

A

used in surgery, mechanical ventilation

depolarizing = sux - AchR AGONIST –> sustained depolarization –> prevents muscle contraction
phase 1) prolonged depolarziation, no antidote
2) repolarized but blocked - AchR available but desensitized, can be reversed with AchE inhibitors
- complications: hypercalcemia, hyperkalemia, mal hyperthermia

nondepolarizing - cur, competitive antagonists

  • can cause prolonged paralysis
  • reverse with: neostigmine + atropine, edrophonium, AchE inhibitors
56
Q

muscle relaxants

A

Baclofen - activates GABA_B at SC –> skeletal muscle relaxation
- used in MS, to relive muscle spasms

cyclobenzaprine - central acting skeletal muscle relaxant
- related to TCAs - similar anticholinergic effects

57
Q

Alzheimers

A

presentation - elderly with memory impairment and higher cortical dysfunction (aphasia, agnosia, apraxia)
- apraxia - inability to excute learned purposeful movements

senile plaques and NF tangles
- can have associated b-amyloid angiopathy
- amyloid in Alzheimers is red and turns yellow-green under birefringence
(vs amyloid deposition systemically - b-sheet, apple-green)

drugs:
memantine - NMDA_R antagonist, helps prevent excitotox (mediated by Ca2+)

donepezil, galantamine, rivastigmine, tacrine - AchE inhibitors

adverse effects - dizziness, confusion

58
Q

IV anesthesia

A

The Mighty King Proposes to Oprah

Thiopental (barb) - high potency, used for induction, rapidly redistributes into fat and tissue, DEcreases cerebral blood flow

Midazolam- endoscopy

Ketamine (arylcyclohexamines) - PCP analog, block NMDA receptors, increase cerebral blood flow, increases pulse and BP

Propofol - potentiates GABA_A, can cause hypotension (systemic vasodilation)

Opioids (morphine, fentanyl) - general anesthesia

59
Q

local anesthetics

A

esters and amIdes

in infected (acidic) tissue - alkaline anesthetics are charged (think NH2+) –> cant penetrate membrane –> need more anesthetic

order of nerve blockade - small-diameter fibers > large diameter, myelinated > unmyelinated, and size factor predominates
- loss: 1 pain, 2 temp, 3, touch, 4 pressure

ADRs: CNS excitation, bupivicaine (cardiotox), arrhythmias (cocaine), metHb (benzocaine)

60
Q

cavernous (ca-venous) sinus

A

cav sinus - pituitary - cav sinus
collects blood from eye + superficial cortex –> cavernous sinus –> IJ

optic chiasm (CN2) - then nerves descend in order, also have postG sympathetic pupillary fibers
CN6 runs with internal carotid

cavernous sinus syndrome - variable ophthalmoplegia, decreased corneal sensation, Horner syndrome, occasionally decreased maxillary sensation

  • CN6 is most susceptible to injury
  • CN6 palsy - eye is medially deviated

cavernous hemangioma = above tentorium cerebelli

  • located in brain parenchyma
  • clusters of dilated, thin-walled capillaries with little-no intervening nervous tissue
  • seizures
61
Q

vertigo

A

peripheral - inner ear (semicircular canal debris, vestibular nerve infection, Meniere disease, BPPV) –> delayed horizontal nystagmus with positional testing
- Meniere - vertigo, ringing, hearing problems unilaterally

central vertigo - brain stem, cerebellar lesion

  • directional or vertical nystagmus, skew deviation, diplopia, dysmetria
  • immediate nystagmus with positional testing
  • these pts will also be unable to perform tandem walking
62
Q

movement disorders

A

athetosis, chorea - BG lesion

dystonia - sustained, involuntary muscle contractions

hemiballismus - half-of-body ballistic, contralateral subthalamic nucleus (lacunar stroke)

intention tremor - cerebellar dysfunction

myoclonus - jerks, hiccups, metabolic abnormalities

63
Q

idiopathic intracranial HTN (pseudotumor)

A

factors - female, obese, vitamin A tox, tetracycline, danazol

headache, diplopia (CN6 palsy)

treat with weight loss, acetazolamide, topiramate, invasive procedures (shunt, optic nerve sheath fenestration)

64
Q

headaches

A

cluster - periorbital features

  • acutely used sumatriptan, 100% O2
  • prophylaxis - verapamil

tension - amitriptyline for chronic pain

migraine - 4-72hrs, due to irritation of CN5, meninges, or blood vessels

  • acute - NSAIDS, triptans, ergots
  • prophylaxis - lifestyle changes, b-blockers, CCB, amitriptyline, topiramate, valproate

v. s. trigeminal neuralgia - repetitive, unilateral, shooting pain down CN5 distribution, < 1 min
- treat with carbamazepine (same mechanism as phenytoin) = decreases Na current (by reducing the ability of Na channels to recover from inactivation)
- side effects - bone marrow suprression, SIADH, and P450 inducer

65
Q

brain lesions

A

frontal lobe - reemergence of primitive reflexes
amygdala - Kluver-Bucy syndrome - disinhibited behavior (hyperphagia, hypersexuality, hyperorality)
- HSV1 encephalitis

frontal eye field –> contralateral PPRF –> ipsilateral abducens nucleus….
frontal eye fields - eyes look towards lesion
paramedian pontine reticular formation - eyes look away from lesion
MLF in dorsal pons - …nystagmus of contralateral eye with abduction

dominant PARIETAL cortex - agraphia, acalculia, finger agnosia, LR disorientation

cerebellum

  • hemisphere - affects ipsilateral limbs, fall to side of lesion
  • vermis - central body ataxia, dysarthria, degeneration in chronic alcoholics

reticular activating system (midbrain) - coma

superior colliculus - stroke, hydrocephalus, pinealoma
- Parinaud syndrome - paralysis of conjugate vertical gaze, absent pupillary light reflex, impaired convergence

66
Q

primitive reflexes

A

disappear w/i first year of life - as frontal lobe matures and myelination of the CST is completed

Moro - hang on for life
Rooting - nipple seeking
Suckling
Palmar - baby holds finger
Plantar reflex - toes dorsiflex/spread (Babinski in adult)
Galant - stroking along spine causes flexion towards stimulated side

67
Q

clinical reflexes

A

Achilles - S1,2 buckle my shoe
Patellar - L3,4 kick the door
Biceps, brachioradialis - C5,6 pick up sticks
Triceps - C7, 8 lay them straight

Cremasteric - L1,2 make the testes move
Anal wink - S3,4 winks galore

conus medullaris syndrome = lesions at L2 - flaccid paralysis of bladder, rectum, impotence, saddle anesthesia

cauda equina syndrome

  • damage to S2-S4 - provide the sensory and motor innervation of LEs, pelvic floor, and sphincters
  • loss of anal wink reflex, loss of ankle-jerk reflex
  • low back pain, saddle anesthesia
  • S3-S5 damage –> bowel/bladder dysfunction
68
Q

vertebral disc herniation

A

C1-7 exit ABOVE vertebra, all else below

nerve below herniated disc is affected - nucleus pulposus herniates through outer ring

69
Q

cranial nerve reflexes

A

afferent - reflex - efferent

V1 (opthalmic branch) - corneal - 7 (temporal branch), processing in pons
- can be impaired by damage to superior orbital fissure (CN3-6)

V1 - lacrimation - V7
2 - pupillary - 3
9 - gag - 10
jaw jerk - V3
- 3 muscles close the jaw - Masseter, teMporalis, Medial pterygoid (Ms munch)
- 1 opens - lateral pterygoid (Lateral lowers)

70
Q

NTs and locations

A

Ach - Basal nucleus of meynert
- secrete decreased amts of Ach in Alzheimers

GABA - NAccumbens

NE - Locus ceruleus, increased in anxiety
- dorsal pons

Serotonin - raphe nucleus (located in brainstem)
- play a role in sleep-wake cycle, anxiety/mood, sexuality, eating, impulsivity

red nucleus - located in anterior midbrain
- neurons participate in motor coordination of UE

71
Q

sleep phys

A

circadian rhythm - suprachiasmatic nucleus (hypothal)
SCN –> NE –> pineal gland –> melatonin

alcohol, benzos, barbs associated with decreased REM sleep and delta wave sleep

  • NE associated with decreased REM sleep
  • benzos good for night terrors and sleepwalking (decrease REM and N3 stage)

oral desmopressin used for bedwetting

awake eyes open (better have your eyes open when you’re awake) - beta waves (high freq, low amplitude)
awake eyes closed - alpha

non-REM

  • N1 (5%) - theta, light sleep
  • N2 (45%) - sleep spindles + K complexes, deeper sleep, teeth grinding can occur
  • N3 (25%) - delta (lowest freq, highest amplitude), deepest non-REM, sleepwalking, night terrors, bedwetting (N3 is scary)

REM (25%), occurs every 90 min with progressively increasing duration - beta

  • loss of motor tone, brain uses inc O2, variable pulse and BP, increased Ach
  • dreams
  • sexual arousal
  • memory processing fx
  • depression decrease REM latency, increases total REM
  • extraocular movements due to PPRF

= BATS Drink Blood

elderly - decreased REM and slow-wave sleep, increased sleep onset latency, increased early awakenings

72
Q

aphasia

A

Repetition IMPAIRED:
Broca - expressive, frontal lobe
- Brocas aphasia - may say a few small words
- cant repeat

Wernicke - comprehension, temporal lobe

  • may make up new words, speak in sentences that have no meaning
  • repetition is poor

Conduction - fluent, comprehension is intact, damage to arcuate fasciculus
- pt unable to repeat words

Global

Repetition INTACT

  • transcortical motor - like Brocas, but can repeat words (brocas area spared)
  • transcortical sensory - like Wernickes but can repeat words
  • transcortical mixed - nonfluent, impaired
73
Q

seizures

A

partial: originate in medial temporal lobe, often preceded by aura
simple - no LOC, complex - impaired consciousness

generalized
absence - 3Hz spike
myoclonic, tonic-clonic, tonic, atonic (drop seizures, mistaken for fainting)

74
Q

cranial nerves

A

10/12 nerves arise in brainstem

1-2-3-4 above the pons
- 4 arises dorsal (side that is stuck to the cerebellum) and immediately decussates
in the pons: 5(lateral)....6-7-8
in medulla: 9-10-11
between pyramid and olive: 12
75
Q

dorsal features of brain stem

A

side that is stuck to the cerebellum

pineal gland
superior colliculi - conjugate vertical gaze center
inferior colliculi - auditory center

76
Q

substantia nigra

A

midbrain

77
Q

spinal tracts

A

DCML:
somatosensory receptor –> first order neuron, cell body in DRG –> ascend ipsilaterally in dorsal column –> synapse 1 in nucleus gracilis and nucleus cuneatus in ipsilateral medulla –>

spinothalamic/anterolateral:

78
Q

PKU v.s tyrosinemia

A

PKU - *intellectual disability, growth retardation, *seizures, hypopigmentation and eczema (excess phe inhibits tyrosinase), musty body odor

tyrosinemia - due to deficient fumarylacetoacetate hydrolase

  • signs and symptoms due to intermediates of tyrosine metabolism
  • liver involvement, Fanconi syndrome, growth failure, rickets
  • treat with nitisone –> otherwise can have neurologic crises (MSE changes, peripheral neuropathy) and death
79
Q

dopamine hydroxylase deficiency

A

dopamine –> NE

deficiency - dysautonomia
- ptosis, orthostatic hypotension, hypoglycemia, and hypothermia

80
Q

HIV-associated dementia

A

pts with CD4 <200

SUBcortical dementia - attention/working memory (recall) problems, executive dysfunction, slow information processing
- HIV affects subcortical/deep gray matter structures

inflammatory activation of microglial cells

1) HIV-infected monocytes enter brain
2) activated macrophages and microglia form microglial nodules around area of necrosis
2) neuronal damage from cytokines and direct toxic effects of HIV-derived proteins

81
Q

viruses in the brain

A

HSV - intranuclear acidophilic inclusions

CMV - intranuclear basophilic inclusions

82
Q

sciatic nerve

A

( L4-S3) sciatic nerve –> tibial nerve and common peroneal (swings anterior)

  • sciatic nerve innervates hamstrings (posterior thigh muscles)
  • damage to tibial nerve will affect plantar flexion and sensation of plantar foot
    - injury to popliteal fossa = weakness on foot plantar flexion (tibial nerve innervates gastroc, soleus, plantaris), can also see weakness on inversion and toe flexion
    - tibial nerve injury at tarsal tunnel - sensory loss over sole BUT plantflexion and inversion remain intact (these branches are earlier)
  • pos straight leg raise test - sciatic nerve root irritation

common peroneal –> deep peroneal (medial) and superficial peroneal (lateral)

  • common peroneal nerve contacts lateral neck of fibula, susceptible to compression injury
  • damage to deep peroneal = foot drop - cant dorsiflex or extend toes
  • superficial peroneal –> eversion and sensation over dorsolateral foot
83
Q

femoral nerve

A

from L2,3,4

  • knee extension - quads
  • hip flexion - iliopsoas
  • forms saphenous nerve (anterior lower leg) - sensation for arch of foot, medial foot, shin, and anteromedial thigh

femoral block at inguinal crease - anesthetizes skin and muscles of anterior thigh, femur, and knee

  • also anesthetizes saphenous nerve
  • femoral block for torn quad

femoral canal only contains lymphatics

84
Q

Cryptococcus

A

yeast form only

pigeon droppings and soil - enters through respiratory tract

predilection for CNS - CSF doesnt contain alternative complement pathway

85
Q

pudendal nerve

A

S2-4

ischial spine is the landmark for the pudenal nerve block - used in vaginal and perineum surgeries

86
Q

obturator nerve

A

innervates thigh adductor muscles and medial skin of thigh

87
Q

anti-epileptics

A

lamotrigine - blocks VS-Na channels

  • pts can develop benign rash or a life-threatening rash (SJS-TEN)
  • SJS involves < 10% of body, TEN involves >30% of body
  • characterized by flu-like symptoms, mucocutaneous lesions, epidermal necrosis
  • rash means you HAVE to discontinue lamotrigine

others with SJS/TEN - carbamazepine, phenobarbital, phenytoin

88
Q

phrenic nerve

A

C3-C5 = phrenic nerve

irritation can occur with lung tumors –> dyspnea, hiccups, referred pain to shoulder

other effects of lung tumors

  • pancoast tumor can cause Horner syndrome, brachial plexus (C5-T1) and shoulder pain, upper extremity edema, and SC compression/paraplegia if tumor extends into intervertebral foramina
  • centrally located tumor - SVC syndrome
89
Q

Rabies

A

ssRNA, bullet-shaped capule

  • glycoprotein spikes that bind to NAchR
  • retrograde travel to CNS

starts with flu-like prodome

progresses to fever, agitation, disorientation, pharyngospasm, photophobia –> flaccid paralysis coma and death

pharyngospasm –> avoidance of food and water
- dysphagia + hypersalivation = foaming

90
Q

CJD

A

rapidly progressive demnentia and myoclonic jerks of extremities

91
Q

pseudodementia

A

cognitive impairment associated with depression

92
Q

diabetic neuropathy

A

decrease in vibratory sensation, proprioception, and temperature sensation

diminished reflexes, motor weakness

93
Q

Guillan-Barre

A

Campy then GB

antibodies against pathogen cross-react with ganglioside components of myelin
- segmental demyelination and endoneural inflammatory infiltrate

ascending paralysis

  • hits respiratory muscles
  • Bell’s palsy - CN7
  • areflexia
94
Q

Beriberi

A

can cause demyelination of peripheral nerves - NO inflammation
- classically distal LE is involved

95
Q

subthalamic nucleus

A

below thalamus, above substantia nigra, medial to internal capsule

damage to subthalamic nucleus - decreases the excitation of the globus pallidus internus –> reduces inhibition of thalamus

  • thalamus is MORE excited –> contralateral hemiballism
  • damage is most commonly due to a lacunar stroke
96
Q

internal capsule

A

damage will have contralateral pure motor or combined sensorimotor deficits

97
Q

Wilson’s disease

A

atrophy of lentiform nucleus (globus pallidus and putamen)

98
Q

VPLN or VPMN

A

nuclei in thalamus

damage results in complete contralateral sensory loss

damage to thalamus - thalamic syndrome, contralateral burning or stabbing

99
Q

pts with longstanding HTN

A

AV nicking on fundoscopic exam

100
Q

synaptophysin

A

neurons, neuroectoderm, neuroendocrine cells

101
Q

GFAP

A

glial cell tumors

= astrocytomas, oligodendrogliomas, ependymomas

102
Q

mammillary body

A

Papez circuit of limbic system - involved in cortical control of emotion and memory

fornix –> projects to mammillary bodies

103
Q

corpus callosum

A

splenium or damage of tail - alexia without agraphi

104
Q

NAch receptors

A

upon binding 2 molecules of Ach –> Na and Ca influx and K outflux –> end-plate potential is generated

105
Q

febrile seizures

A

supportive care, antipyretics - though antipyretics will no reduce the risk of further febrile seizures (due to the presence of circulating inflammatory mediates that lower the seizure threshold)

v. s. heat stroke in kids
- oxidative P stops at 108F –> end organ damage

106
Q

neurosyphilis

A

tabes dorsalis - sensory ataxia and Argyll Robertson pupils (small irregularly shaped pupils that dont respond to light)
- areflexia, neurogenic bladder (overflow incontinence)

progressive dementia and generalized paralysis

107
Q

NMDA receptor blockers

A

ketamine, felbamate, memantine

108
Q

ear

A

stapedius nerve stapedius oscillates more widely –> hyperacusis
- ipsilateral hyperacusis is seen in Bell’s palsy

tensor tympani - innervated by mandibular branch of V3

109
Q

orbital floor fracture

A

infraorbital nerve

110
Q

facial nerve

A

motor of the face

impaired by temporal bone or zygomatic orbit fractures

111
Q

hypothalamic nuclei

A

ventromedial - satiety –> destruction leads to hyperphagia
lateral - hunger

anterior - heat dissipation
posterior - heat conservation

arcuate - secretes dopamine, GnRH, and GHRH

paraventricular - ADH, CRH, oxytocin, TRH
supraoptic - ADH, oxytocin

suprachiasmatic - circadian, pineal gland function

in kids - hypothalamic lesions are most likely gliomas
- adults - mets

112
Q

antiseizure drugs

A

phenytoin, carbamazepine - blocks Na+ channels

valproate - blocks Na+ channels and increases GABA levels

levetiracetam - modulates GABA and glutamate release

ethosux - blocks thalamic T-type Ca2+ channels

vigabatrin - irreversible inhibitor of GABA transaminase, so GABA is not degraded
- can be used in treatment-resistant epilepsy

status epilepticus - lorazepam _ phenytoin (long-acting anti-convulsant)

113
Q

brain injury and edema

A

ischemic injury:

  • cytotoxic edema - due to impaired Na/K ATPase
  • vasogenic edema - increased vasc permeability due to pro-inflammatory cytokines

side note - neutrophils do infiltrate the brain during the first 48 hrs

114
Q

sensory receptors

A

phasic receptors - Pacinian corpuscles (subQ and IM), Meissner corpuscle (fingertis), hair follicles

tonic receptors - Merkels, Ruffini, tactile disks (hairy skin)
- rate of APs encodes stimulus intensity

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