• 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

1/60

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;

60 Cards in this Set

  • Front
  • Back
What is the DDX for density in the subarachnoid space
blood
cellular material : carcinomatosis disease, sarcoid
iodinated contrast
CSF hypotension
Anoxia
What pt tend to have contrast that leaks out of the meninges into the subarachnoid space
renal failure pt
Do pt with CSF hypotension and brain anoxia have fluid in the subarachnoid space
no, it just looks like it
global anoxia has dense venous stasis
CSF hypotension has crowded normal blood vessels
What is the white cerebellum sign
The density of the cerebellum and other infratentorial structures is preserved and shows a relatively hyperdense appearance that contrasts with the supratentorial structures
Do pts with CSF hypotension or brain anoxia have hydrocephalus
no
What happens to the venous sinuses in CSF hypotension
the size of the sinuses become more distinct and more easily seen
What are 3 signs of global anoxia
dense material in SA space, bright cerebellum, loss of grey white differenitation of the basal ganglia
If there is hydrocephalus and dense material in the subarachnoid space what is the ddx
blood
cellular material
iodinated contrast
What 2 pt tend to have iodinated material in the subarachnoid space
renal failure pts and pt with recent CT myelogram
What are the causes of cellular material in the SA space
carcinomatosis
Infection: Bacterial (pyogenic), TB, fungal
granulomatous: sarcoid
If a pt has diffuse SA would blood in the ventricles be expected
yes
Can coccidioidomycosis cause a pyogenic infection of the subarachnoid space
yes
What does coccidioidomyocosis typically affect first
lungs (it is an airborne infection)
Can coccidioidomyocosis go on to the disseminatedd form without the pt being immunocompromised
yes
What is- normal opening pressure of CSF
80-150mmhg
What is it called when opening pressure is elevated in an otherwise normal appearing brain on CT
idiopathic intracranial hypertension or pseudotumor cerebri
What are 2 clinical SS of IIH
headache and changes in visual acuity (papiledema)
What is a classic imaging feature of IIH on MR
focal narrowing of bilateral transverse sinuses
empty sella
flatened posterior globe
tortous and disended optic sheath
uncommonly slit like ventricles
What is the classic demographic of a pt with IIH
women , 3rd decade, obese
What are causes of intracranial htn besides IIH
3
mass, edema, DST
What are 4 general classifications for causes of stroke
cardiac (embolic)
prothrombic
inherited
aquired disorder
What are some cardiac causes of stroke 3
congenital heart disease (low output)
Valve disease (low output)
LA myxoma (embolic)
What are causes of prothrombic disorders which may lead to stroke 10
sickle cell
Protein S or C
antithrombin deficiency
factor 5 leiden
lupus anticoagulant
polycythemia
platelet disorder
leukemia
chemotherapy related
What is the ddx of inherited vascular disorders which may lead to stroke
2
neurocutaneous syndrome
CADASIL
What is the ddx of metabolic disorders which may lead to stroke
2
MELAS, homcystinuria
What are the acquired vascular disorders which may lead to stroke
dissection, moya-moya, systemic or CNS angiitis, migraines, birth control, methamphetamine
What are 4 causes of basal ganglia calcifications
fahrs syndrome
hypo/hyper parathyroidism
MELAS
HIV
What is MELAS
mitochondrial encephalopathy lactic acidosis
What is FAHRs syndrome
It is a rare degenerative neurological disorder characterized by calcifications and cell loss within the basal ganglia
What does CADASIL stand for?
(cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
What are the clinical SS of CADASIL
CADASIL may start with attacks of migraine with aura or subcortical transient ischemic attacks or strokes, or mood disorders between 35 to 55 years of age.
Where are the most common locations for MELAS to present
parietal and occipital lobes
What does MELAS look like on imaging
stroke-like cortical lesions that cross usual vascular territories
What lab/imaging technique can be used to determine if the pt has MELAS
spectroscopy, if it is put of the part of the brain that is not affected there will be a peak in the range of lactate
What does the S in MELAS stand for
stroke like episodes
When does MELAS typically present
2nd decade of life
What are the clinical signs and symptoms of MELAS
headache, hemianopsia, psychosis, aphasia
Does MELAS have basal ganglia calcification
yes
What causes the strokes associated with MELAS
proliferation of dysfunctional mitochondria in endothelial smooth muscles of small arteries
What are the MR findings of central pontine myelinolysis
4
pontine T2 hyperintensity
enlarged pons
Restricted diffusion
no abnormal enhancement
What does the T2 hyperintensity of CPM look like
symmetrical
bat wing contour
What is the DDX of T2 pontine hyperintensity
ischemia
infection
brainstem glioma
white matter pathology
If a pt has pontine hyperintensity on T2 and no enhancement what can be ruled out
infection (will usually have enhancement)
Besides the pontine area where else does CPM affect
3
basal ganglia, thalami, midbrain
What is the cause of CPM
rapid correction of sodium
Is it possible for CPM to not effect the pons and affect other areas of the brain
yes
How is CPM distinguished from MS or ADEM
CPM will have restricted diffusion whereas MS and ADEM will not
What does PRES stand for
posterior reveresible encephalopathy
What does PRES look like on MR
extensive hyperintensity of subcortical WM (T2) of the posteriror frontal parietal and occipital lobes
What does Press look like on CT
bilateral symmetric hypodensity of the posterior frontal, parietal and occipital lobe
Is there restricted diffusion in PRES syndrome
no, and therefore this is secondary to vasogenic edema
Does PRES have an acute onset
yes
What is the current favored theory for pathophysiology of PrES
vasoconstriction and hypoperfusion
What is PRES associated with
8
HTN
Eclampsia/preeclampsia
Acute GN
HUS
TTP
lupus
Sz
Drug toxicity
What are some examples of drugs which may cause PRES
4
tacrolimus FK 506
cyclosporine
erythropoietin
cisplatin
Can PRES involve the grey matter
yes, but is mostly subcortical white matter
Does PRES have restricted diffusion
yes, in the non-reversible areas
What is the 'posterior' in PRESS refer to
that the majority of the pathology is in the posterior circulation
What is the cause of the signal abnormality in PRES
vasogenic edema
If something is DWI positive (restricted diffusion) in PRES does that mean it is non reversible
yes, these areas are usually non-reversible