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DWI signal comes from what?
Restricted diffusion of water. Intracellular water can't move and is bright on DWI. CSF is freely mobile and dark on DWI.
Arachnoid Cyst appearance on DWI?
Epidermoid Cyst on DWI?
- Arachnoid contains CSF and is dark on DWI.
- Epidermoid Cyst is cellular and is bright on DWI.
What does ADC do?
Apparent Diffusion Coefficient. Separates water of different diffusion capacities. Freely diffusing water (CSF and extracellular) is bright. Intracellular is dark.
Tumor, trauma, infection can cause increase in both intracellular and extracellular water and make DWI equivocal.
ADC subtracts out T2 signal of intracellular edema, leaving CSF bright and areas of restricted diffusion dark.
Cerebral hematoma presenting as stroke is most likely...
hypertensive encephalopathy or amyloid angiopathy
Should you consider anything else if a patient has a SAH?
Search for AVM or aneurysm by MR or angiography.
Reversible causes of cerebral atrophy
Related to dehydration and starvation...
- Addison's dz
- Anorexia & bulimia
Intracranial mass lesion identified... 1st question...
Intra-axial or extra-axial.
Intra-axial are generally more dangerous and less easily treated.
MC intra-axial masses?
- Intracranial hemorrhage
- primary intracranial tumors (GBM)
MC extra-axial masses
- Subdural or Epidural Hematoma
- Dermoid or epidermoid cysts
Most reliable sign of an extra-axial mass in the posterior fossa?
widening of the ipsilateral subarachnoid space
In contrast, intra-axial masses will generally narrow the ipsilateral subarachnoid space.
Enhancement (Gd) pattern of extra-axial masses
Extra-axial masses typically show dural enhancement.
Extra-axial masses tend to enhance homogeneously (meningioma, neuroma) or not at all (cysts, extracerebral hematoma).
Enhancement (Gd) of intra-axial masses
generally ring-like enhancement with more surrounding edema
What is "gray matter pattern?"
When cytoxic edema results from cell death (MC infarct, trauma, encephalitis) causing white matter expansion with gray matter involvement and increased T2 signal or lucency on CT.
Cytotoxic edema involving the deep gray matter structures is likely...
Pure anoxia due to carbon monozide poisoning or respiratory arrest.
MC locations for HSV encephalitis involvement
Medial Temporal Lobes adjacent to the trigeminal ganglia.
Orbital frontal regions adjacent to the olfactory bulbs.
Colloquial ways to think about DWI and ADC
DWI - Diffuse White Infarct
ADC - Abnormally Dark Cerebrum/Cells
Causes of pediatric ischemic stroke
- Congenital heart dz
- Blood dyscrasias
- Arterial dissection
- Venous thrombosis
Causes of ischemic stroke in young adult
- Cardiac emboli
- Drug abuse
- Arterial dissection
- Venous thrombosis
Causes of ischemic stroke in elderly
- Cardiac emboli
- Venous Thrombosis
What is the "Insular Ribbon Sign?"
Subtle blurring of the gray-white layers of the insula caused by early edema. This can be seen within 6 hrs of MCA occlusion.
The most sensitive imaging sequence for brain ischemia?
DWI - diffuse white ischemia.
DWI can show evidence of ischemia within minutes of an ischemic event.
T2 hyperintensity may take 6-12 hours to appear.
Peak time for post-infarct hemorrhagic transformation?
What does it look like?
1-2 weeks post infarct.
Serpiginous line of petechial blood following the gyral contours of the infarcted cortex.
T1 no Gd: bright signal along affected gyrus from methemoglobin.
Petechial gyral pattern indicates...
post-infarct hemorrhagic transformation.
This is not seen in primary brain hemorrhage, and suggests underlying ischemic etiology.
Marked gyral enhancement T1 post Gd
hallmark of subacute infarct
MR intravascular enhancement is seen when and where?
Commonly seen during first week in the infarcted territory and is seen in both arteries and veins. This will resolve usually within 10 days of the acute event.
Things to look for on MR to indicate acute stroke (3)
- 1. Absent flow void
- 2. Increased signal on DWI (Diffuse White Ischemia)
- 3. Arterial enhancement
syncope, ataxia, CN abnormalities, homonymous visual field deficits and contralateral facial symptoms indicate a _____ stroke, involving the _____ vascular system.
visual changes, aphasia, sensorimotor deficits are caused by a __________ stroke, involving the _________ system.
What is amaurosis fugax?
What should be done?
Embolic occlusion of the ophthalmic branch of the ICA causing transient monocular blindness.
Evaluate the carotids for occlusive dz.
Majority of ischemic events of the ICA territory are due to ...
Atherosclerotic dz near the carotid bifurcation.
The ICA terminates into the ...
Anterior Cerebral Artery (ACA) and Middle Cerebral Artery (MCA)
What are the branches of the ACA?
What % of strokes involve the ACA?
1. Medial lenticulostriate (rostral portions of basal ganglia)
2. Pericallosal (corpus callosum)
3. Hemispheric (medial aspect of frontal and parietal lobes)
Where is the recurrent artery of Heubner?
It is the largest of the medial lenticulostriate branch vessels and supplies the head of the caudate and anterior internal capsule.
Stroke causing problems with speech production (motor aphasia), facial weakness, and disturbances in mood and judgement likely involves what vascular territory? What vessel?
Anterior-inferior aspect of the internal capsule, putamen, globus pallidus, caudate head.
Medial lenticulostriate branches.
What is the termination of the ACA?
It separates into upper callosomarginal and lower pericallosal branches which run parallel to corpus callosum from front to back and supply the medial cortex of the frontal and parietal lobes.
Stroke causing preferential leg weakness likely involves what vascular supply?
Contralateral ACA hemispheric occlusion.
Stroke causing incontinence and an awake but apathetic state known as akinetic mutism likely involves what vascular supply?
Bilateral ACA infarcts.
Which vessel supplies majority of blood flow to brain tissue and results in apx 2/3 of strokes?
Branches of the MCA?
- Lateral lenticulostriates
- Hemispheric branches
What supplies most of the basal ganglia? What is it a branch of?
- Lateral lenticulostriates.
- Branch of the MCA.
What supplies the lateral cerebral surface? It is a branch of what vessel?
- Hemispheric branches.
- Branch of the MCA.
What specific structures do the lateral lenticulostriate vessels supply?
- lateral globus pallidus
- superior half of internal capsule and...
- adjacent corona radiata
- majority of the caudate
What do isolated lesions to the globus pallidus or putamen cause?
MC they are asx, but may affect contralateral muscle tone and motor control.
Lesions of the internal capsule or corona radiata may cause what?
Pure or mixed sensory and motor deficits of the contralateral body.
What supplies the insula?
Hemispheric branches of the MCA.
What are some anterior branches of the MCA hemispheric arteries?
Anterior temporal artery: supplies anterolateral tip of temporal lobe
Operculofrontal arteries: supplies frontal lobe
Central sulcus arteries: supplies motor and sensory strips
What are some posterior branches of the MCA hemmispheric arteries?
Posterior parietal artery: supplies the parietal lobe behind the sensory strip.
Angular artery: supplies the posterolateral parietal and occipital lobes.
Posterior temporal artery: supplies the majority of the temporal lobe
What occlusion causes Broca's (motor) aphasia with intact comprehension?
Occlusion of the rostral MCA branches of the dominant hemisphere.
What occlusion causes receptive aphasia? What area is involved?
Occlusion of the posterior MCA branches of the dominant hemisphere with involvement of Wernicke area.
Stroke producing contralateral face, arm and leg weakness with face and arm affected more than leg.
Contralateral precentral (motor strip) gyrus MCA supply.
Stroke involving what distribution will commonly result in bizarre visualospatial deficits and sometimes left-sided neglect?
Posterior MCA infarct of the non-dominant right hemisphere.
Occlusion of the basilar artery usually causes...
Death secondary to infarction of the respiratory and cardiac centers in the medulla.
What % of infarcts occur in the PCA territories?
What do the PCAs arise from?
They are the termination of the Basilar artery.
What are branches of the PCA?
- Midbrain and thalamic perforating arteries.
- Posterior choroidal arteries.
- Cortical branches to the medial temporal and occipital lobes.
Stroke causing loss of the pupillary light reflex, impaired upgaze and somnolence. What territory? What anatomic areas?
Proximal segments of PCA causing midbrain infarct damaging the quadrigeminal plate, third cranial nerve nuclei, and reticular activating formation, respectively.
What is the MC symptom from thalamic infarct? What vascular territory?
- Contralateral sensory loss.
- PCA territory.
Headache, vertigo, nausea, vomitting, and ataxia are hallmarks of a __________ stroke. The vast majority of these are of this type.
85% are ischemic, 15% are hemorrhagic.
What is the order of cerebellar branches (bottom to top)? Which most commonly infarcts?
- PICA-Posterior Inferior Cerebellar Arteries
- AICA-Anterior Inferior Cerebellar Arteries
- SCA-Superior Cerebellar Arteries
The PICA. It is the first branch and is easily affected by vertebral artery dissection.
What is Wallenberg Syndrome?
Ataxia, facial numbness, Horner syndrome, dysphagia, and dysarthria from involvement of the medulla from a PICA infarct.
What are typical triggers of watershed infarcts?
- Cardiac arrest
- Massive hemorrhage
- Surgery under general anesthesia
What is "Rosary Bead Sign?"
What does it indicate?
What are common symptoms?
string of small deep white matter lesions indicating a watershed infarct.
Sx: weakness isolated to upper arms ("Man in a barrel syndrome"), cortical blindness, and memory loss.
Typical locations of lacunes from small vessel infarcts?
- Lenticular nucleus (37%)
- Pons (16%)
- Thalamus (14%)
- Caudate (10%)
- Internal Capsule/Corona Radiata (10%).
MC from long-standing HTN.
Infarct of which portion of the internal capsule is clinically most important? why?
The posterior limb.
Corticospinal tracts are in the posterior limb, with infarcts causing severe sensory, motor, or mixed deficits.
What are Virchow-Robin spaces? What is their clinical significance?
Where are they commonly seen?
Enlarged perivascular spaces.
No clinical relevance.
Should follow CSF signal on all sequences and follow along the path of penetrating vessel.
Common in the medial temporal lobes and inferior 1/3 of putamen and thalamus.
Primary consideration of patchy infarcts across multiple vascular territories? common triggers?
Common triggers: autoimmune d/o, drug use, polyarteritis nodosa, idiopathic (Giant cell arteritis).
Younger patient with headache, sudden focal deficits, and often seizures is a characteristic presentation for _______.
MC locations for venous occlusion?
- Transverse sinus
- Superior sagittal sinus
- Cavernous sinus
What is "empty delta sign?"
When is it seen?
Filling defect of the superior sagittal sinus on CECT.
Usually present 1-4 weeks after occlusion but may not be seen in the more acute or more chronic phases.
What is the sequence of hemoglobin degradation?
- Oxygenated Hb (<1 day)
- Deoxy Hb (1-2 days)
- Met Hb (1-3 weeks)
- Hemosiderin (1+ months)
Which space surrounds the blood vessels and communicates with the ventricular system?
Subarachnoid Hemorrhage is MC d/t ...?
What if SAH is seen in conjunction with parenchymal or subdural bleed (non-traumatic)?
Consider vascular malformation of brain, spinal cord, or dura.
Classical presentations of 3 common brain aneurysms?
1. Posterior communicating artery aneurysm - unilateral third nerve palsy.
2. Internal carotid artery/parasellar aneurysm - cavernous sinus syndrome.
3. Anterior communicating artery aneurysm - optic chiasmal syndrome (bitemporal field defect).
Conditions assoc with intracranial aneurysm?
- Systemic infection
- Polycystic Kidney Dz
What % of people with SAH with have multiple aneurysms?
DDx for intraparenchymal hemorrhage?
- Hypertensive hemorrhage
- Vascular malformation
- Drug effects
- Amyloid angiopathy
- Hemorrhagic neoplasm
Where are the MC locations for hypertensive hemorrhage?
- 1. Putamen 35-50%
- 2. Subcortical WM 30%
- 3. Cerebellum 15-20%
- 4. Thalamus 10-15%
- 5. Pons 5-10%.
Intracranial vascular malformation subtypes?
- Cavernous malformation
- Venous malformation
MC location for AVM? Bleeding risk?
2-3% annual risk of bleeding, but risk increases to 5-10% in the first year after initial bleed.
Where do adult brain tumors occur MC?
Where do pediatric brain tumors occur MC?
Adults - 70% Supratentorial
Pediatric - 70% Posterior fossa
What % of adult brain neoplasms are metastatic?
WHO Classification scheme for brain neoplasms recognizes how many major categories? What are they? Intra-axial or extra-axial?
7 Major categories based on cell of origin.
Glial cell MC Intraxial
1. Glial Cells (40-50% of all PRIMARY brain neoplasms - MC Astrocytoma... MC Astrocytoma is GBM)
- NON-GLIAL MC extra-axial
- 2. Nerve sheath
- 3. Mesenchymal
- 4. Lymphocytic/Leukocytic
- 5. Germ cells
- 6. Other neuroepithelial
- 7. Endo/Meso/Ectodermal
Types of Gliomas
- Astrocytoma (MC is GBM)
- Choroid plexus tumors
Nerve sheath tumors
- Neurofibroma (arises from fibroblasts/Schwann cells)
Mesenchymal Cell Tumors
meninges, blood vessels, bone
- Osteocartilaginous tumors, sarcoma
Germ cell tumors
- Teratomatous types (embryonal carcinoma, yolk sac tumor, teratoma, choriocarcinoma)
WHO classification "Other neuroepithelial cell" neoplasms
- Rathke's cleft cyst
What is the MC type of intracranial herniation? What anatomic structures are involved?
The cingulate gyrus is displaced under the margin of the interhemispheric falx.
What is the classic clinical triad for hydrocephalus?
- Papilledema (d/t partial obstruction of venous outflow from the optic nerve).
What are 3 basic questions that should be asked when evaluating an intracranial abnormality?
Is it a MASS?
Intra-axial or Extra-axial?
Where is the tumor margin?
What is "white matter buckling?"
Extra-axial neoplasms will push on the gray matter and indent ("buckle") the underlying white matter.
Intra-axial neoplasms will tend to expand the white matter and compress the overlying gray matter.
What is the general T1 and T2 appearance of brain neoplasms?
What are some hemorrhagic brain neoplasms?
Choriocarcinoma, melanoma, thyroid carcinoma, renal carcinoma.
Two substances that will be T1 bright in brain tumors?
What neoplasms are hyperdense on CT? What do they tend to look like on T2?
Those with high cellular density...
- Lung Ca
- Colon Ca
- Breast Ca
These tend to be hypointense on T2 given less free water.
When should postoperative brain MR for new baseline be performed? Why?
Within 72 hrs of surgery secondary to development of enhancing granulation tissue after this time. Any enhancement within 72 hours of surgery can be presumed to be residual tumor.
Brain tumors found more commonly in females?
- Pituitary tumor
Brain tumors more commonly in males?
- Pineal germinoma 10:1.
- Pineal parenchymal tumor 5:1
- Medulloblastoma 3:1
- Choroid plexus papilloma
- CNS lymphoma
- Hamartoma of tuber cinereum
What is the MC type of glioma?
What is the most malignant type?
What is the peak incidence for GBM?
MC location of GBM?
Deep white matter of the frontal lobe (the largest lobe of the brain)... then temporal lobe.... then basal ganglia.
Classic appearance for GBM?
expansile mass with central necrosis, ring enhancement, and a large area of surrounding vasogenic edema.
MC hemorrhagic brain neoplasms?
What is the 3yr survival for GBM?
- Demyelinating Dz
- Resolving hematoma/Radiation necrosis
What is a "butterfly glioma?" What is included in DDx?
GBM which has bihemispheric spread through the corpus callosum with involvement on both frontal lobes and having a butterfly appearance.
Lymphoma is the other CNS tumor that can spread this way and be bihemispheric.
What does increased T2 signal in the corpus callosum represent in a patient with GBM?
It is not edema but rather tumoral spread through the corpus callosum.
What are the primary low grade astrocytomas?
- Fibrillary astrocytoma
- Pilocytic astrocytoma
- Subependymal giant cell astrocytoma
- Gemistocytic astrocytoma
- Protoplasmic astrocytoma
- Pleomorphic xanthoastrocytoma
What % of low grade astrocytomas will degenerate into higher grade (III or IV) astrocytomas?
What % of higher grade vs lower grade tumors enhance?
90% of GBMs enhance, while on 50% of lower grade tumors will show any enhancement.
What neoplastic disease process is the result of widespread infiltration of neoplastic cells in varying degrees of differentiation, involving at least three lobes of the brain?
MC location of oligodendroglioma?
What is a characteristic feature?
- 85% supratentorial
- 50-65% in frontal lobe.
- 100% show calcification on microscopy.
- 70% have gross calcifications on CT.
Despite this a calcified neoplasm is still more likely to be an Astrocytoma given that astrocytomas are so much more common.
Heterogeneous calcified mass within the periphery of a frontal lobe with calvarial erosion and relative absence of edema in an adult should suggest what dx?
Calcified Glial tumors
Old Elephants Age Gracefully
What is the MC subtype of brain lymphoma?
Almost always Non-Hodgkins B-Cell Lymphoma.
Four MC primary CNS neoplasms?
- Low-grade Astrocytoma
MC tumor seen in pts with chronic temporal lobe epilepsy?
MC location of a gangliocytoma?
Floor of the third ventricle
MC congenital brain tumors in infants <60 days old?
- Teratoma (MC) 2/3 are supratentorial
- S-PNET (Supratentorial Primitive Neuroectodermal Tumor)
- Choroid plexus papilloma
MC extra-axial mets?
Leptomeningeal spread is characterized by...?
Basilar cistern involvement.
Pts commonly present with cranial nerve palsies
For pachymeningeal involvement consider
- dural metastases including lymphoma
- Erdheim-Chester disease
- idiopathic hypertrophic cranial pachymeningitis
For leptomeningeal involvement consider
- tuberculous leptomeningitis
- lymphoma / leukemia infiltration leptomeningeal metastases
For pituitary and hypothalamic involvement consider
- Langerhan's cell histiocytosis pituicytoma
- ectopic posterior pituitary (intrinsic high T1 signal)
- lymphocytic hypophysitis metastasis local masses: (meningioma, optic nerve glioma, hypothalamic astrocytoma)
For cranial nerve involvement consider
- tuberculous leptomeningitis
- lymphoma / leukemia infiltration leptomeningeal metastases
- optic neuritis
- optic nerve glioma
- optic nerve meningioma
For parenchymal involvement consider
- multiple sclerosis / ADEM
- chronic deep white matter ischaemic change (in asymptomatic cases it is often not possible to distinguish between these and neurosarcoidosis lesions)
- when enhancing, consider...
- cerebral metastases
- tumefactive demyelination
- acute demyelination
- primary brain tumours
MC finding of Neurosarcoidosis?
Parenchymal involvement is the most common finding and can be in a number of forms:
1. extension of leptomeningeal disease up perivascular spaces
2. periventricular high T2 white matter lesions (often indistinguishable from MS or chronic small vessel ischaemic change)
may have low T2 components (without haemorrhage) due to high cellularity
3. enhancing masses / nodules