• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/83

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

83 Cards in this Set

  • Front
  • Back
intracranial hemorrhage that:
-does not cross suture lines.
-can cross falx, tentorium

rupture of?
epidural hematoma

*rupture of middle meningeal a, can cause transtentorial herniation and CNIII palsy.
crescent shaped hemorrhage that crosses suture lines. gyri is preserved since pressure is distributed equally.

cannot cross falx, tentorium

rupture of?
subdural hematoma = rupture of bridging veins.

*delayed onset of symptoms

-seen in elderly, alcoholics, blunt trauma, shaken baby, whiplash
risk after subarachnoid hemorrhage
1-3 days after- risk of vasspasm due to blood breakdown products.

rx: nimlodipine (calcium channel blockers)

*the vasospasm can cause focal neuro deficits and doesn't show up on CT
lobar strokes all over the brain - usally in basal ganglia and internal capsule.

cause?
parenchymal hematoma: caused by hypertension, amyloid angiopathy.
recurrent lobar hemorrhages, associated with advanced age, in cerebral hemispheres
cerebral amyloid angiopathy

smaller and less severe compared to hypertensive hemorrhage
focal neuro deficits + small amounts of bleeding in basal ganglia, internal capsule, pons
charcot bouchard psuedoaneurysms

pathogenesis: long standing HTN --> hyaline arteriolosclerosis --> dilation (pseduoaneurysm) --> small amounts of bleeding

*it does have blood in the subarachnoid space but it does not have the "worst headache" symptoms like saccular hematoma.
how long does it take for irreversible damage in the brain?
5 minutes
what are the findings in the brain after ischemia for:
1/2 day - 2 days:
day 2 - 3:
day 3 - 5:
week 1 - 2:
> 2 weeks:
1/2 day - 2 days: red neurons (sign of irreversible injury)
day 2 - 3: necrosis and neutrophils
day 3 - 5: macrophages
week 1 - 2: reactive gliosis + vascular proliferation (see liquefactive necrosis)
> 2 weeks: glial scar
How does a stroke appear on:
MRI:
Noncontrast CT:
How does a stroke appear on:
MRI: bright within 3-30 mins
Noncontrast CT: bright on noncontrast in ~24 hrs

*bright indicates hemorrhage - so tPA is contraindicated
When do you use tPA in ischemic brain disease?
Use tPA in an ischemic stroke- when emboli block large vessels (can be secondary to a fib, endocarditis, PFO)

Also used in lacunar infarcts (HTN --> block small vessels of basal ganglia, pons, internal vapsule)

DO NOT use if there is hemorrhage (aka bright areas on noncontrast CT)
microscopic findings in an ischemic neuron:
shrinking of neuronal body
deep eosinophilia of cytoplasm
pyknosis of nucleus (shrinking)
loss of Nissl substance
How would a neuron appear, microscopically, after the axon is severed?
round, swollen nucleus 1-2 days post cut
peripherally located nuclei
granular Nissl substance
Lateral ventricle --> 3rd ventricle via ____.
3rd ventricle --> 4th ventricle via ___.
4th ventricle --> subarachnoid space via (3)
foramen of monro
cerebral aqueduct
foramina of luschka - 2- (lateral), magendie (medial)
dementia, ataxia, urinary incontinence
normal pressure hydrocephalus - expansion of ventricles distorts fibers of corona radiata, but NO increase in subarachnoid space volume.

*a reversible cause of dementia in elderly
decreased CSF absorption in arachnoid villi
communicating hydrocephalus - leads to increase intracranial pressure, papilledema, and hernation
hydrocephalus ex vacuo
ventricular enlargement occurs secondary to atrophy of the brain (alzheimers, HIV, Pick's)

Intracranial pressure is normal; triad is not seen.
where does spinal cord end?

where does subarachnoid space end?

What is the region between these two points?
spinal cord ends @ L2

subarachnoid space ends @ S2

L3-L5 = region to perform a lumbar puncture

*to do epidural (saddle block) you go under S2 (no subarachnoid)
In the dorsal columns, where are the arms and legs represented?
arms = lateral, legs = medial (just as you are oriented)
In the corticospinal tract and spinothalamic tract, where are the arms and legs represented?
legs= lateral in Lateral corticospinal tract and spinothalamic tract

arms = medial
floppy baby + tonge fasciculations

median age of death = 7 mo
Werdnig-Hoffman disease - presents as "floppy baby"

degeneration of anterior horns- LMN involvement only.
pathogenesis of amytropic lateral sclerosis

Rx?
defect in superoxide dismutase 1 --> free radical injury of neurons

Rx = riluzole which decreases presynaptic glutamate release (excitatory neurotransmitter)

*starts distal --> proximal, no sensory/cognitive loss
5 major symptoms of tabes dorsalis
1. impaired proprioception + locomotor ataxia
2. shooting lightening pain "Charcot's joints"
3. no DTRs
4. positive romberg
5. eyes accomodate but do not react to light
10 yo presents with:
-ataxia of all 4 limbs
-skeletal abnormalitis: pes cavus, hammer toes, kyphoscoliosis
-hypertrophic cardiomyopathy

What are the 3 CNS regions degenerated?
Friedreich's ataxia

degeneration of:
- spinocerebellar degeneration
- dorsal column
- sensory cells of dorsal root ganglia
5 symptoms of Brown Sequard syndrome
1. ipsilateral UMN signs below lesion
2. ipsilateral proprioception signs below lesion
3. contralateral pain/temp signs below lesion
4. ipsilateral loss of all sensation at level
5. LMN signs at level of lesion
Landmark dermatomes:
C2, C3, C4
C2 = posterior half of skull cap
C3 = high turtleneck shirt
C4 = low-collar shirt
What dermatomes are
- at the nipple
- at the umbilicus
- at the inguinal ligament
- along the knee caps
- penis and anal zones
What dermatomes are
- at the nipple: T4
- at the umbilicus: T10
- at the inguinal ligament: L1
- along the knee caps: L4
- penis and anal zones: S2,3,4
What nerve roots are being tested with the following reflexes:
-Biceps
-Triceps
-Patella
-Achilles
What nerve roots are being tested with the following reflexes:
-Biceps: C5
-Triceps: C7
-Patella: L4
-Achilles: S1
Which CNs lie medially at the brainstem?
CN 3 (oculomotor), 6 (abducens), 12 (hypoglossal)
what does the superior and inferior colliculi responsible for?
superior = conjugate vertical gaze center
inferior = auditory
parinaud syndrome

4 characteristics
paralysis of conjugate vertical gaze due to lesion in superior colliculi (pinealoma - possibly germinoma which secretes hormones)

-upward gaze palsy
-absent pupillary light reflex
-failure of convergence
-wide based gait
what is the only CN without thalamic relay to cortex?
olfactory CN I
what are the functions of V1, V2, V3 trigeminal nerves
V1 = opthalmic - sensory
V2 = maxillary - sensory
V3 = mandibular - sensory (tongue, tensor tympani, external ear) and motor (mastication) - V3 does BOTH motor and sensory
what CN opens eyelid, which closes eyelid
opens = CN3 (levator palpebrae)
close = CN7 (orbicularis oculi)
Tongue innervation:
anterior 2/3: taste, sensation

Posterior 1/3 taste, sensation

Tongue root/pharynx = taste, sensation
anterior 2/3: taste = CNVII, sensation = CNV3 mandibular

Posterior 1/3 taste, sensation = CNIX

Tongue root/pharynx = taste + sensation = CNX
Ear innervation:

external ear: (2)
middle ear muscles: stapedius, tympanic membrane
inner ear: tensor tympani
external ear: CNX (posterior), CNV3

middle ear muscles: CNVII stapedius, CNIX tympanic membrane

inner ear: CNV3 - tensor tympani
6 functions of facial nerve (CNVII)
1. facial movement - saying "ma"
2. taste from anterior 2/3 tongue
3. lacrimation
4. salivation (submandibular, sublingual)
5. eyelid closing (orbicularis oculi)
5. stapedius muscle in ear - damage causes hyperaccusis
6 functions of glossopharyngeal nerve (CNIX)
1. taste and sensory from posterior 1/3 of tongue.
2. swallowing
3. salivation (parotid glands)
4. carotid receptors
5. stylopharyngeus (elevates larynx, pharynx) + gag reflex
6. tympanic membrane sensation
8 functions of Vagus n (CNX)
1. sensation and taste from epiglottic region
2. swallowing
3. palate elevation
4. midline uvula
5. talking
6. coughing
7. thoracoabdominal viscera
8. aortic arches
what cranial nerves are in the:
midbrain
pons
medulla
midbrain: 3,4
pons 5-8
medulla 9-12
what 3 things exit the optic canal

*part of the middle cranial fossa- through sphenoid bone
CNII, opthalmic artery, central retinal vein

*opthalmic vein exits via the superior orbital fissure
what exits the superior orbital fissure (6 things)
CN III, IV, V1, VI (all the eye movers)
opthalmic vein
sympathetic fibers
what exits the:
foramen rotundum
foramen ovale
foramen spinosum
foramen rotundum - CN V2 (maxillary)
foramen ovale - CN V3 (mandibular)
foramen spinosum - middle meningeal artery
Posterior cranial fossa goes through temporal or occipital bone:

what goes through:
internal auditory meatus:
jugular foramen:
hypoglossal canal:
foramen magnum:
Posterior cranial fossa goes through temporal or occipital bone:

what goes through:
internal auditory meatus: CN VII(stapedius), VIII
jugular foramen: IX, X, XI jugular vein
hypoglossal canal: CN XII
foramen magnumL spinal roots of CN XI, brain stem, vertebral arteries
cavernous sinus syndrome
opthalmoplegia, opthalamic and maxillary sensory loss
what 5 CNs travel through cavernous sinus?
CN III, IV, V1, V2, VI

plus blood from the eye and superficial cortex --> cavernous sinus --> internal jugular vein

*all the muscles of the eye + sensory of the eye (V1) and maxilla (V2)
CN XII lesion
tongue deviates toward side of lesion

(tongue on injured side is atrophic)
CN V lesion
jaw deviates toward side of lesion (lesion side is weak, muscle contracts toward that side)
CN X lesion
uvula deviates away from side of lesion, weak side collapses and uvula points away.
CN XI lesion
weakness turning head to contralateral side of lesion (SCM). shoulder droop on side of lesion (trapezius)
Facial UMN lesion
contralateral paralysis of lower face only
facial LMN lesion
ipsilateral paralysis of upper and lower face
Bell's palsy (4 potential complications)
complete destruction of facial nerve with inability to close eye on involved side
-also can get hyperacusis (no stapedius innervation), decrease in salivation (submandibular, sublingual), loss of taste on ant 2/3 tongue
6 causes of Bell's palsy
AIDS
Lyme disease
Herpes simplex
sarcoidosis
tumors
diabetes
Kuh
La
Mi
Kuh = CN X (palate elevation)
La = CN XII (tongue)
Mi = CN VII (facial)
what 3 muscles close jaw
what muscle opens jaw
3 closers: masseter, temporalis, medial pterygoid

1 open: lateral pterygoid

*all innervated by CN V3
damage to R. Meyer's loop (temporal lobe - MCA) will cause what visual field defect?
left upper quadrantic anopia

*meyer's loop loops around the inferior horn of the lateral ventricle
damage to R. dorsal optic radiation (parietal lobe - MCA) will cause what visual field defect?
left lower quadrantic anopia
damage to upper section of the calcarine fissure - PCA - will cause what visual field defect?
left hemianopia with macular sparing
Patient with MS has right MLF damage.

how would the right and left eye appear when trying to look LEFT.
Right eye = doesn't move, medial rectus palsy- cannot adduct (look left)

Left eye = right-beating nystagmus

*essentially you have: medial rectus palsy on side affected, and nystagmus in (ajacent) abducting eye.

Remember, the MLF connects one CN VI nuclei to the adjacent eye's CN III so that when you adduct one eye, the other one will abduct.
What are the 3 genes for early onset alzheimers?

what is the gene for late onset alzheimers?
Early onset:
APP (21)
presenilin-1 (14)
presenilin-2 (1)

Late onset = Apo E4 (19)

Bad "4" you

*APP, presenilin are thought to promote production of AB-amyloid
what is the protective gene for alzheimers
ApoE2 (19) is protective

you're going "2" be fine
3 gross path findings in alzheimers?
1. widespread cortical atrophy - esp. hippocampus/nucleus basalis (where ACh is made)

2. senile plaques (AB-amyloid) --> may cause amyloid angiopathy --> intracranial hemorrhage (sudden death), recurrent lobar hemorrhage

3. neurofibrillary tangles (intracellular abnormally phopshorylated tau protein) = insoluble cytoskeletal elements. tangles correlate with degree of dementia.
dementia, aphasia, parkinsonian aspects, change in personality.
Pick's disease (frontotemporal dementia)

*see pick bodies = intracellular, aggregated tau protein
Parkinsonism + dementia + hallucination = ?

what histological finding is key?
Lewy Body Dementia

Lewy body = alpha synuclein defect
Rapidly progressive (weeks - months) dementia with myoclonus = ?
Creutzfeldt Jakob disease
spongiform cortex (bubbles and holes in neurons of gray matter)
Creutzfeldt Jakob disease
5 clinical syndromes of multiple sclerosis
1. optic neuritis - visual disturbances, central scotoma (macular damage), painful eye movements.

2. internuclear opthalmoplegia: MLF is demylinated and damaged --> adduction (medial rectus) paralysis + other eye has abduction nystagmus

3. Cerebellar dysfunction - tremor, ataxia, nystagmus

4. motor sensory symptoms: incontinence, hemiparesis, fatigue (most common symptom), scanning speech (sound drunk)
Patient presents with scanning speech, intention tremor, and nystagmus.

Rx?
Multiple sclerosis rx = beta-interferon (chronic), prednisone (for acute relapses)
endoneural inflammatory infiltrate with lymphocytes and macrophages.

how does the weakness present?
what is treatment?
Guillan Barre: autoimmune attack of peripheral myelin (segmental demyelination of LMNs) due to molecular mimicry (c. jejuni, herpes)

Rx: respiratory support (can cause autonomic dysfunction- cardiac irregularities, hypotension), plasma pharesis, IV immunoglobulins

*almost all patients survive in weeks-months
Progressive multifocal leukoencephalopathy
destruction of oligodendocyres --> demyelination of CNS.

Associated with JC virus reactivation. In AIDS, usually fatal.
Acute disseminated (postinfectious) encephalomyelitis
inflammation + demyelination after chickenpox (HSV-3), measles or rabies/small pox vaccine

*SSPE = abormal measles (rubeola) virus that persists in CNS --> dementia, spasticity, seizures.
Charcot Marie Tooth disease
defective production of proteins used in peripheral nerves or myelin --> motor + sensory neuropathy.

*see weakness of foot dorsiflexion from involvement of perineal nerve
Patient with verigo has positional testing and shows DELAYED horizontal nystagmus.

where is the etiology located?
peripheral vertigo = inner ear etiology (semicircular canal debris, vestibular n infection, Meniere's disease)
Patient with verigo has positional testing and shows IMMEDIATE horizontal nystagmus.

where is the etiology located?
central vertigo = brain stem or cerebellar lesion (vestibular NUCLEI, posterior fossa tumor)
triad for sturge-weber
1. port wine stain
2. ipsilateral leptomeningeal angiomas
3. pheochromocytomas
patient with mental retardation, seizures, ash leaf spots and sebacious adenoma.

what 4 types of TUMORS are they at risk for?
1. hamartomas in CNS, skin, organs.

2. cardiac rhabdomyoma

3. renal angiomyolipoma

4. subependymal giant cell astrocytoma
4 tumors in von hippel lindau
1. cavernous hemangiomas in skin, mucosa, organs

2. bilateral renal cell carcinoma

3. hemangioblastoma in retina, brain stem, cerebellum

4. pheochromocytoma
3 most common primary brain tumors in adults
1. glioblastoma multiforme
2. meningioma - arises from arachnoid cells, resectable.
3. schwannoma- often CNVIII, resectable, @ cerebellopontine angle; S-100 positive.
pathologic findings of pilocytic (low grade) astrocytoma (most common pediatric brain tumor- benign good prognosis)
rosenthal fibers - esopinophilic, corkscrew fibers.

gross - cystic and solid.

foudn in posterior fossa but may be supratentorial.
highly malignant cerebellar tumor with rosettes and perivascular psuedorosettes.
medulloblastoma - histo see small blue cells (this is a PNET tumor =primitive neuroectodermal tumor)

radiosensitive.

*since its located in the cerebellum, it can compress the 4th ventricle --> hydrocephalus
childhood tumor found INSIDE the 4th ventricle

see what 2 findings histologically?
ependymoma - poor prognosis.

see perivascular psuedorosettes and rod-shaped blepharoplasts near nucleus.
craniopharyngioma
-presentation
-histology
childhood equivalent of prolactinoma- often calcified and filled with thick brown fluid rich with cholesterol crystals
4 signs of uncal hernation
1. ipsilateral dilated pupil/ptosis - stretching of CNIII

2. contralateral homonymous hemianopia - compression of ipsilateral posterior cerebral artery

3. ipsilateral paresis - compression of contralateral crus cerebri

4. paramedian artery rupture from caudal displacement of brainstem.