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
|