Neuro IX Flashcards
Central retinal artery occlusion presentation
acute, painless monocular vision loss.
central retinal artery occlusion findings
1) Retina cloudy with attenuated vessels.
2) “cherry-red” spot at fovea (center of macula)
central retinal artery occlusion management
Evaluate for embolic source.
Embolic sources of central retinal artery occlusion
1) carotid artery atherosclerosis
2) cardiac vegetations
3) PFO
retinitis pigmentosa presentation
Painless, progressive vision loss beginning with night blindness (rods affected first)
retinitis pigmentosa etiology
inherited retinal degeneration.
retinitis pigmentosa findings
1) Bone spicule-shaped deposits around macula.
retinitis pathophys
retinal edema and necrosis leading to scarring.
retinitis causes
1) often viral (CMV, HSV, VZV)
2) bacterial
3) parasitic
retinitis association
immunosuppression
papilledema pathophys
Optic disc swelling (usually bilateral) due to increased ICP.
papilledema fundoscopy findings
Enlarged blind spot + elevated optic disc with blurred margins.
Miosis pathway
1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III.
2nd neuron: short ciliary nerves to pupillary sphincter muscles.
pupillary light reflex pathway
Light in either retina sends a signal via CN II to pretectal nuclei in midbrain that activates bilateral Edinger-Westphal nuclei; pupils contract bilaterally.
Mydriasis pathway
1st neuron: hypothalamus to ciliospinal center of Budge (C8-T2)
2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face.
marcus gunn etiology
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 pathophys
lesion of spinal cord above T1 leads to sympathetic denervation.
Horner syndrome pathway
1st order neuron from hypothalamus to synapse in lateral horn
2nd order neuron from lateral horn to superior cervical ganglion
3rd order neuron from superior cervical ganglion to various sympathetic innervations.
***look at all landmarks
horner syndrome associations
1) pan coast tumor
2) Brown-Sequard
3) late-stage syringomyelia.
Superior oblique functions
Abducts, introits, and depresses while adducted
ocular motility diagram
FA 488
How do you test for SO function?
Have patient look down.
How do you test for IO function?
Have patient look up.
Pathophys of CN III motor dysfunction
Due primarily to vascular disease (DM: glucose –> sorbitol) due to decreased diffusion of oxygen and nutrients to the interior fibers from compromised vasculature residing on outside of nerve.
Pathophys of CN III PS dysfunction
Fibers on periphery are first affected by compression.
Causes of CN III PS dysfunction
1) posterior communicating artery aneurysm
2) uncle herniation
CN IV palsy presentation
1) eyes move upward, particularly with contralateral gaze
2) head tilt toward side of lesions (problems going down stairs, may present with compensatory head tilt in opposite direction).
CN VI palsy presentation
Medially directed eye that can’t abduct
Meyer loop
Inferior retina; loops around inferior horn of lateral ventricle.
dorsal optic radiation
Superior retina; takes shortest path via internal capsule.
MLF function
crosstalk between CN VI and CN III, allowing eyes to move in same horizontal direction.
MLF characteristics
highly myelinated.
Most common cause of dementia in elderly?
AD
ApoE2 and alzhheimers
Decreases risk of sporadic form
ApoE4 and alzheimers
increased risk of sporadic form
familial forms of AD
1) APP
2) presenilin-1
3) presenilin-2
gross findings in AD
1) widespread cortical atrophy
2) narrowing of gyro
3) widening of sulci
neurofibrillary tangles
intracellular hyperphosphyrlated tau protein = insoluble cytoskeletal elements.
what correlates with degree of dementia in AD?
number of neurofibrillary tangles.
FTD association
can also have movement disorders + progressive aphasia.
FTD pathology
1) hyperphosphorylated tau inclusions
2) ubiquitinated TDP-43
lewy bodies found…
primarily in cortex.
2nd most common cause of dementia in elderly?
vascular dementia
Imaging findings in vascular dementia
MRI or CT shows multiple cortical and/or subcortical infarcts.
myoclonus type associated with JCD
“startle myoclonus”
prions in CJD transform to…
Beta pleated sheet (resistant to proteases)
Other causes of dementia
1) syphilis
2) HIV
3) *hypothyroidism
4) B1 deficiency
5) B3 deficiency
6) B12 deficiency
7) Wilson disease
8) NPH
what happens if you correct hypernatremia too quickly?
cerebral edema/herniation (from high to low, your brain will blow)
osmotic demyelination presentation
1) paralysis
2) dysarthria
3) dysphagia
4) diplopia
5) loss of consciousness
other common presentation of MS
1) hemiparesis
2) hemisensory symptoms
Charcot triad of MS
SIN
Scanning speech
Intention tremor (also incontinence, and INO)
Nystagmus
CSF findings in mS
1) increased IgG
2) elevated myelin basic protein
gold standard for MS diagnosis
MRI
Disease modifying therapies for mS
1) beta-interferon
2) glatiramer
3) natalizumab
management of acute MS flares
IV steroids
treatment for neurogenic bladder in MS
1) catheterization
2) muscarinic antagonists
treatment for spasticity in MS?
1) baclofen
2) GABA-B receptor agonists
acute inflammatory demyelinating polyradiculopathy pathophys
Most common subtype of GBS. Destroys Schwann cells leading to inflammation and demyelination of peripheral nerves and motor fibers.
Other findings in acute inflammatory demyelinating polyradiculopathy
1) facial paralysis (up to 50%)
2) ANS dysregulation –> cardiac irregularities, HTN, hypotension
3) sensory abnormalities
acute inflammatory demyelinating polyradiculopathy prognosis
Almost all patients survive. Majority recover completely after weeks to months.
CSF findings in GBS/acute inflammatory demyelinating polyradiculopathy
Increased CSF protein with normal cell count.
Term for CSF findings in GBS
albuminocytologic dissociation
potential sequela of GBS
increased protein may cause papilledema
GBS pathophys
molecular mimicry. *no definitive link to pathogens though.
GBS management
1) Plasmapheresis
2) IVIG
Acute disseminated (post infectious) encephalomyelitis pathophys
Multifocal periventricular inflammation and demyelination after infection or vaccination.
Acute disseminated (post infectious) encephalomyelitis presentation
Rapidly progressive multifocal neurologic symptoms + altered mental status
Other name for CMT…
Hereditary motor and sensory neuropathy.
CMT pathophys
Defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath.
pes cavus
high arch
CMT presentation
1) pes Casus
2) lower extremity weakness
3) sensory deficits
