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CORE: Neuro > Intro > Flashcards

Intro Flashcards

1
Q

Describe ventricular anatomy

A

lateral ventricles (frontal, temporal, occipital horns; body, atrium/trigone) => 3rd ventricle => cerebral aqueduct => 4th ventricle => foramen of Luschka/lateral or foramen of Magendie (midline) ==> obex/opening to spinal canal

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2
Q

parts of the third ventricle

A

chiasmatic/supraoptic recess, infundibular recess, suprapineal recess, pineal recess, cerebral aqueduct, and massa intermedia

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3
Q

massa intermedia

A

interthalamic adhesion

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4
Q

CSF is produced by?

A

choroid plexus – located in body/temporal horn of lateral ventricles, roof of 3rd/4th

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5
Q

CSF volume

  • ventricle
  • subarachnoid space
A

150: 25 + 125 mL

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6
Q

CSF production in a day

A

~500 mL/day

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7
Q

CSF absorption

A

arachnoid granulations and lesser extent by lymphatic system/cerebral veins

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8
Q

cytotoxic edema

A

cell swelling by damaged Na K ATPase ion pumps

most commonly due to infarct, restricted diffusion

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9
Q

vasogenic dema

A

interstitial edema, increased capillary permeability

common with neoplasm, infection, infarct

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10
Q

interstitial edema

A

imbalances in CSF flow, commonly due to obstructive hydrocephalus

transependymal flow of CSF, periventricular

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11
Q

subfalcine herniation

A

cingulate gyrus slides under falx; compression ACA

contralateral hydrocephalus from foramen of monro obstruction

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12
Q

transtentorial herniation

A

DOWNWARD:
medial temporal lobe slides under tentorium

ipsilateral CN3 paresis, compression PCA, duret hemorrhages, compression contralateral cerebral peduncle

UPWARD: superior transtentorial herniation of vermis due to posterior fossa mass effect

obstructive hydrocephalus from aqueductal compression

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13
Q

cerebellar tonsillar herniation

A

displaced through foramen magnum, compression of medulla

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14
Q

communicating hydrocephalus

A

venticular enlargement, no obstructing lesion

subarachnoid hemorrhage or normal pressure hydrocephalus

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15
Q

noncommunicating hydrocephalus

A

obstructive lesion

3rd ventricle colloid cyst
posterior fossa mass obstructing 4th ventricle

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16
Q

intra vs extra-axial:
beneath pia
meninges/subarachnoid

A

intra-axial

extra-axial

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17
Q

perimesencephalic cisterns/basal cisterns

A

suprasellar, prepontine, interpeduncular, ambient, quadrigeminal

surround midbrain/pons

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18
Q

T1 shortening signal

T2 shortening signal

A

bright

dark

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19
Q

brain lesions demonstrate pathologic prolongation of longitudinal recovery

A

T1 dark, T2 bright

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20
Q

causes of T1 hyperintensity

A

gadolinium, fat, protein

melanin, mineralization, slow-flow blood, calcium, paramagnetic stages of blood (intra/extracellular methemoglobin)

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21
Q

causes of T1 hypointensity

A

paramagetic states of blood (except hyperacute blood, extracellular methemoglobin), calcification, fibrous lesion, highly cellular tumors, vascular flow voids, muscin

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22
Q

FLAIR

A

T2 weighted signal with suppresion of water based on T1 characteristics

white matter darker than gray matter

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23
Q

PD sequence

A

conventional spin echo proton density

highest signal to noise ratio

useful to evaluate MS, demyelinating plaques in posterior fossa

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24
Q

diffusion weighted images

A

DWI/ADC

brownian motion of water; signal lost with increases (pathologic processes)

CSF is dark

25
Q

differential for restricted diffusion

A

acute stroke, bacterial abcess, cellular tumors (lymphoma, medulloblastoma), epideroid cyst, herpes encephalitis, CJD cruetzfelt jakob disease

26
Q

DWI vs ADC signal with reduced diffusion

A

DWI bright, ADC dark

DWI: reduced diffusion will be hyperintense (less Brownian motion, less loss of signal)

27
Q

T2 shine through

A

DWI images are T2 weighted so T2 hyperintense signals will shine through on DWI

28
Q

b-value in MRI

A

higher b-value -> more contrast, detects reduced diffusivity

29
Q

GRE/T2*

A

susceptible to signal loss from magnetic field inhomogeneities

180 degree rephasing pulse is omitted

30
Q

blooming artifact

A

hemosiderin, calcium produce inhomogeneities in magnetic field; makes small lesion conspicuous

31
Q

differential diagnosis of multiple dark spots

A

hypertensive microbleeds, cerebral amyloid angiopathy, familial cerebral cavernous malformations, axonal shear injury, multiple hemorrhgic metastases

32
Q

MR spectroscopy

A

chemical composition of brain

may help determine radiation necrosis vs recurrent tumor, glioblastoma v metastasis

33
Q

MR spectroscopy: glioblastoma vs mets

A

glioblastoma: gradual transition abnormal to normal
metastasis: abrupt transition

34
Q

ratios of specific compounds

A

NAA decreases and choline increases with tumors

order: Cho, Cr, NAA

35
Q

canavan disease MR spectroscopy

A

elevated NAA

36
Q

lactate doublet MR spectroscopy

A

high grade tumors (anaerobic metabolism)

37
Q

Hunters angle

A

line connecting tallest peaks should point up; normal spectrum

38
Q

perfusion MR

A

brain imaged repeatedly with gadolinium injection

gadolinium causes magnetic field distrubance which transiently decreases image intensity

T2* images

useful for stroke and tumors

39
Q

what causes parenchymal enhancement

A

disruption of BBB

infection, inflammation, neoplasm, trauma, vascular etiologies

40
Q

BBB is formed from?

A

astrocytic foot processes of brain capillary endothelial cells

41
Q

what parts of the brain do not have BBB

A

choroid plexus, pituitary gland, pineal gland, tuber cinerium (inferior hypothalamus, controls circadian), area postrema (inferior of 4th ventricle, controls vomiting)

42
Q

vascular enhancement in brain

A

localized increased blood flow

vasodilation, hyperemia, neovascularity, AV shunting

43
Q

sources of extra-axial enhancement

A

dura (pachymeninges)

arachnoid (leptomeninges)

44
Q

ddx for periventricular enhancement

A

CNS lymphoma, infectious ependymitis (CMV), primary glial tumor, MS

45
Q

CNS lymphoma on imaging

A

hyperattenuating on CT
restricted diffusion due to cellularity
low T2 signal

centrally necrotic in immunocompromised patients

46
Q

ddx gyriform enhancement

A

herpes encephalitis, meningitis, subacute infarct, posterior reversible encephalopathy syndrome

47
Q

nodular intra-axial enhancement

A

metastatic disease

48
Q

subcortical gray white junction enhancement with edema

A

hematogenously disseminated mets

49
Q

posterior fossa disease: mets

A

venous dissemination of mets via retroclival venous plexus

50
Q

ddx rim enhancing lesion

A

MAGIC DR

mets, abscess, glioma, infact, contusion, demyelinating, radiation

51
Q

pachymeningeal/dural enhancement

A

falx, tentorium, cavernous sinuses covered by dura

dural enhancement on MRI is indication of dural edema, not BBB breakdown

52
Q

ddx of pachymeningeal enhancement

A

intracranial hypotennsion, postoperative, post lumbar puncture, meningeal neoplasm (meningioma), granulomatous disease (sarcoid, TB, fungal disease)

53
Q

ddx leptomeningeal enhancement

A

meningitis, leptomeningeal carcinomatosis, viral enchephalitis, slow vascular flow

54
Q

fine linear vs thick nodular enhancement in meningitis

A

fine/linear: bacterial or viral

nodular: fungal

55
Q

leptomeningeal carcinomatosis neoplasms

A

MOCLEGG

medulloblastoma, oligodendroglioma, choroid plexus tumor, lymphoma, ependymoma, glioblastoma, germinoma

56
Q

mets that cause leptomeningeal carcinomatosis

A

lymphoma, breast

57
Q

ddx of FLAIR hyperintensity

A

meningitis/leptomeningeal carcinomatosis

subarachnoid hemorrhage

pt on oxygen or propofol; increased subarachnoid FLAIR

58
Q

slow flow of peripheral vessels

A

moya moya

CORE: Neuro (21 decks)

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