Neuro Flashcards
What are the four recesses of the third ventricle?
Chiasmatic (supraoptic) recess
Infundibular Recess
Suprapineal Recess
Pineal Recess
What is the massa intermedia of the third ventricle?
Interthalamic adhesion - gray and white matter structure that passes through the third ventricle to connect the bilateral thalami.
What connects the third and fourth ventricles?
Cerebral aqueduct (of Sylvius)
How does the fourth ventricle drain?
Continues inferiority as the central canal of the spinal cord. Into the subarachnoid space and basal cisterns via the paired foramina of Luschka (lateral) and single foramen of MAgendie (medial).
Where are the choroid plexi located?
Body and temporal horn of each lateral ventricle
Roof of third ventricle
Roof of fourth ventricle
No choroid plexus in the cerebral aqueduct or occipital or frontal horns of the lateral ventricles.
What are the volumes of the ventricles and subarachnoid space? How much CSF is produced per day?
Ventricular volume = 25 mL
Subarachnoid space = 125 mL
Total = 150
Produce about 500 ml/day
Replenish CSF 3-4 times per day.
Where is vasogenic edema primarily seen?
White matter - more interstitial space
Caused by increased capillary permeability.
What are the complications of subfalacine hernation?
Compression of the anterior cerebral artery (ACA) against the falx.
Contralateral hydrocephalus from foramen of Monro obstruction
What are the complications of transtentorial herniation?
Ipsilateral CN III (oculomotor nerve) compression - pupillary dilation and CN III palsy (down and out).
Compression of ipsilateral PCA and cause medial temporal/occipital infarct.
Upper brainstem Duret hemorrhages - shearing of perforating vessels due to downward force on the brainstem.
Compression of contralateral cerebral peduncle against Kernohan’s notch - hemiparesis ipsilateral to the herniated side.
What is communicating hydrocephalus and what are the causes?
Ventricular enlargement w/o obstructing lesion.
SAH - impeding arachnoid granulation reabsorption of CSF.
NPH- normal mean CSF pressure and clinical triad of dementia, ataxia, and incontinence.
What are the basal cisterns
CSF-filled spaces surrounding the midbrain and pons.
Suprasellar cistern Prepontine cistern Interpeduncular cistern Ambient cistern Quadrigeminal cistern
Causes of T1 shortening (hyperintensity)
Gadolinium Fat Proteinaceous substances Some paramagnetic stages of blood - intra- and extra-cellular methemoglobin Melanin Mineralization - copper, iron, manganese Slowly-flowing blood Calcium - rarely, if dispersed, not in bone.
Causes of T2 hypointensity
Most paramagnetic stages of blood - except hyperacute and extracellular methemoglobin
Calcification
Fibrous lesion
Highly cellular tumors (i.e. lymphoma and medulloblastoma)
Vascular flow-void
Mucin - desiccated mucin
How is Flair different from a T1 sequence?
T1: white matter is brighter than gray matter b/c fatty myelinated white matter has a shorter T1 time.
FLAIR: White matter is darker than gray matter.
What is the benefit of proton density images?
highest signal to noise ratio
Used for MS
What is the DDx for diffusion restriction?
Acute stroke Bacterial abscess Cellular tumors - such as lymphoma or medulloblastoma Epidermoid cyst Herpes encephalitis Creutzfeld-Jakob disease
What is a gradient recall echo (GRE) sequence?
Captures the T2* signal.
The 180-degree rephasing pulse is omitted, GRE images are susceptible to signal loss from magnetic field inhomogeneities.
Hemosiderin and calcium produce inhomogeneities- creates blooming artifacts on GRE.
DDx for dark spots on GRE sequences?
Hypertensive microbleeds - basal ganglia, thalami, cerebellum, and pons
Cerebral amyloid angiopathy - subcortical white matter, most commonly the parietal and occipital lobes
Familial cerebral cavernous malformation
Axon shear injury
Multiple hemorrhagic metastases
What are the things measured in magnetic resonance spectroscopy?
N-acetylaspartate - normal marker for neuronal viability - decreases in most abnormalities. In tumors NAA decrases and choline increases, but nonspecific.
Cr provides information about cellular energy stores
Measured in alphabetical order- Choline (cho), creatinine (cr), and NAA.
Hunter’s angle - connecting points - like plane taking off
What forms the blood brain barrier?
Astrocytic foot processes of brain capillary endothelial cells and prevents direct communication between the systemic capillaries and the protected extracellular fluid of the brain.
What CNS regions do not have a blood brain barrier?
No BBB = will enhance.
Choroid plexus
Pituitary and pineal glands
Tuber cinereum (controls circadian rhythm, located in inferior hypothalamus)
Area postrema (controls vomiting located at inferior aspect of 4th ventricle)
What is the tuber cinereum?
Located in inferior hypothalamus - controls circadian rhythm
What is the area postrema?
Located at inferior aspect of 4th ventricle - controls vomiting.
What are the causes of periventricular enhancement (intra-axial)?
Primary CNS lymphoma - can be periventricular enhancement, solitary brain mass, or multiple brain masses.
Infectious ependymitis - MC caused by cytomegalovirus. Usually features thin linear enhancement along the margins of the ventricles.
Primary Glial Tumor
MS
Causes of gyriform enhancement (intra-axial)?
Herpes encephalitis
Meningitis
Subacute infarct - 6 days to 6 weeks after ischemic event
PRES
What causes nodular subcortical enhancement (intra-axial)?
Hematogenously disseminated metastatic disease - arterial
Where are venous brain metastases found?
Posterior fossa through the retroclival venous plexus and Batson prevertebral venous plexus
Mnemonic for ring enhancing lesion?
MAGIC DR Metastasis Abscess Glioma Infarct Contusion Demyelination - C-shaped Radiation
DWI findings of an abscess
Diffusion restriction centrally due to high viscosity of central necrosis
Enhancement pattern of demyelinating disease?
Incomplete and “C” shaped. Lack of significant mass effect
What is pachymeningeal enhancement?
Dural enhancement.
No BBB in dura, but no water molecules in dura.
Dural enhancement on MRI is an indication of dural edema rather than BBB breakdown.
DDx of pachymeningeal enhancement?
Intracranial hypotension - vasogenic edema of dura
Postoperative
Post-lumbar puncture
Meningeal neoplasm - such as meningioma - can produce focal area of dural enhancement called dural tail, due to reactive changes in the dura.
Granulomatous disease - typically basal meninges (skull base)
Cancers that metastasize to the dura?
Breast and Prostate - irregular dural enhancement.
What is leptomeningeal enhancement?
Pia-arachnoid enhancement
DDx of leptomeningeal enhancement?
Meningitis
Leptomeningeal carcinomatosis - primary or metastatic disease
Viral encephalitis
Slow vascular flow
Mnemonic for primary CNS tumors that cause leptomeningeal enhancement
GEMCLOG
Glioblastoma Ependymoma Medulloblastoma Choroid plexus tumor Lymphoma Oligodendroglioma Germinoma
Causes of subarachnoid FLAIR hyperintensity
Meningitis and leptomeningeal carcinomatosis - with leptomeningeal enhancement
SAH - no enhancement - has susceptibility
Oxygen or propofol therapy.
What is the most common primary brain tumor to hemorrhage?
Glioblastoma
What intracranial metastases hemorrhage?
Melanoma, RCC, thyroid, and choriocarcinoma.
Lung and breast are less frequently hemorrhagic.
What brain tumors are hypointense on T2?
Metastases containing desiccated mucin - such as GI adenocarcinomas.
Hypercellular metastases - including lymphoma, germinoma, and some glioblastomas.
What brain tumors are hyperintense on T1?
Metastatic melanoma
Fat-containing tumors- such as dermoid or teratoma.
Hemorrhagic metastasis - RCC, thyroid, choriocarcinoma, and melanoma.
What types of intracranial lesions tend to have cysts?
Low-grade tumors
What is a glioma?
Primary CNS tumor arising from a glial cell - astrocytes, oligodendrocytes, ependymal cells, and choroid plexus cells.
What is an astrocyte?
Provide biochemical support to the endothelial cells that maintain the BBB, to maintain extracellular ion balance, and aid in repair after neuronal injury.
Throughout brain and spinal cord.
What is an oligodendrocyte?
Maintain myelin around CNS axons. Single can maintain myelin of dozens of axons. Throughout brain and spinal cord.
Counterpart is a schwann cell in a peripheral nerve.
What are ependymal cells?
Circulate CSF with its multiple cilia. Line ventricles and central canal of the spinal cord.
What is a Junvenile Pilocytic Astrocytoma (JPA)?
Pilocytic = “hair-like”
Benign, typically in the posterior fossa in children.
Well-circumscribed cystic mass with an enhancing nodule and relatively little edema.
May compress 4th ventricle if in posterior fossa. Can occur along the optic pathway with NF1. Posterior fossa JPA is not associated with NF1.
What does a low-grade astrocytoma look like?
Hyperintense mass on T2 without enhancement
What does an anaplastic astrocytoma look like?
Range of appearances from thickened cortex (similar to low-grade astrocytoma) to an irregularly enhancing mass that may appear identical to glioblastoma.
Will eventually progress to glioblastoma.
What is the DDx of a transcallosal mass?
GBM, lymphoma, or demyelinating disease.
What is Gliomatosis Cerebri and what does it look like?
Diffuse infiltrative mid-grade astrocytoma that affects multiple lobes.
Diagnostic criteria- involvement of at least two lobes plus extra-cortical involvement of structures such as the basal ganglia, corpus callosum, brainstem, or cerebellum.
Poor prognosis and may degenerate into GBM.
Exerts mass effect, but does not enhance.
What is an Oligodendoglioma and what does it look like?
Slow-growing cortical-based mass.
Young to middle aged patient with seizures.
Propensity to calcify (about 75%).
What is an ependymoma?
Tumor of ependymal cells that tends to occur in the posterior fossa in children and in the spinal cord in older adults.
What is a Lhermitte-Duclos tumor?
Dysplastic cerebellar gangliocytoma - part hamartoma and part neoplasm.
Associated with Cowden syndrome.
Corduroy or tiger-striped striated lesion in the cerebellar hemisphere. Enhancement is rare.
What are the embryonal/primitive neuroectodermal tumors (PNET)?
Atypical teratoid/rhabdoid tumor (ATRT)
Medulloblastoma
What is an Atypical Teratoid/Rhabdoid Tumor (ATRT)?
Agrgressive tumor that may appear similar to medulloblastoma, but occurs in slightly younger patients. Majority occur in posterior fossa.
Associated with malignant rhabdoid tumor of kidney.
What is a medulloblastoma?
Small-blue-cell origin tumor. One of the most common pediatric brain tumors.
MC occurs in midline cerebellar vermis. Slightly hyperattenuating on CT due to densly packed cells and is hypointense on T2 and has low ADC values. Avidly enhancing and may appear heterogeneous due to internal hemorrhage and calcification.
What are the most common childhood posterior fossa tumors?
Medulloblastoma, ependymoma, and pilocytic astrocytoma.
What are the brain tumors with a cyst and an enhancing nodule?
Juvenile Pilocytic Astrocytoma
Hemangioblastoma
Pleomorphic Xanthoastrocytoma
Ganglioglioma
What is a hemangioblastoma?
Cystic mass with enhancing mural nodule. Prominent vessels are often seen as tubular areas of flow void. Often associated with syrinx in spinal cord.
Highly vascular tumor associated with VHL
Most commonly in the cerebellum, medulla, or spinal cord.
30% of hemangioblastomas have VHL.
Hemangioblastoma in patient with VHL has a worse prognosis.
What is a Pleomorphic Xanthoastrocytoma?
Low grade astrocytoma variant.
Rare tumor of childhood and adolescents- typically with history of chronic epilepsy.
MC location is temporal lobe- supratentorial cortical cystic mass with an enhancing mural nodule. The overlying dura may be thickened and enhancing.
Main DDx is a ganglioglioma- however, ganglioglioma does not usually cause dural thickening.
What is the main imaging difference between a ganglioglioma and pleomorphic xanthoastrocytoma?
PXA causes dural thickening
What is a Ganglioglioma?
Rare, slow-growing neuroglial tumor- adolescent or young adult with medically refractory temporal lobe epilepsy.
Temporal lobe cyst and enhancing mural nodule, often with calcification. May cause calvarial remodeling and scalloping.
What tumors are associated with medically refractory temporal lobe epilepsy?
Pleomorphic Xanthoastrocytoma and Ganglioglioma
What are the intraventricular tumors?
Central neurocytoma Choroid Plexus Papilloma/carcinoma Intraventricular Meningioma Subependymal Giant Cell Asrocytoma (SEGA) Subependymoma
What is a central neurocytoma?
Low-grade tumor likely of neuronal origin that occurs in young adults.
Lobulated mass attached to the septum pellucidum with numerous intratumoral cystic areas. Calcification is common.
Lobulated mass attached to the septum pellucidum with numerous intratumoral cystic areas. Commonly with calcification.
Central Neurocytoma
What is a choroid plexus papilloma?
Rare intraventricular tumor. Arising from choroid plexus epithelial cells.
Lobulated, heterogeneous mass that avidly enhances. MC in the atrium of the lateral ventricle in children. In adults, the fourth ventricle is the most common.
Where are intraventricular meningiomas commonly found?
Trigone of the lateral ventricle.
What is a Subependymal Giant Cell Astrocytoma (SEGA)?
Low-grade astrocytoma variant that is associated with tuberous sclerosis.
Other findings of tuberous sclerosis - subependymal nodules and hamartomas (cortical and subcortical).
Classically- enhancing mass in the lateral ventricle near the foramen of Monro.
What is a Subependymoma?
Nonehancing low-grade tumor- thought to arise from subependymal astrocytes, ependymal cells lining the ventricles, or common precursor cells.
Tumor of middle age and older adults.
MC in obex of 4th ventricle (inferior 4th ventricle) or at formen of Monro in the lateral ventricle. Doesn’t enhance.
Nonenhancing mass arising from the inferior 4th ventricle?
Subependymoma
What type of lymphoma is primary CNS lymphoma?
Most commonly diffuse large B-cell lymphoma. Immature blast cells form lymphoid aggregates around small cerebral blood vessels in a periventricular location.
Brain does not contain native lymphoid tissue.
What is the appearance of primary CNS lymphoma in general?
Appearance of PCNSL depends on the immune status of the patient, but always periventricular location and high cellularity (hyperattenuating on CT, relatively hypointense on T2 and reduced diffusivity.
What is the appearance of primary CNS lymphoma in immunocompetent patients?
Enhancing periventricular mass in immunocompetent, often crossing the corpus callosum. Involvement of the frontal lobes and basal ganglia is most common.
What is the appearance of primary CNS lymphoma in immunocompromised patients?
Periventricular ring-enhancing lesion in the basal ganglia, due to central necrosis.
Difference between primary CNS lymphoma in immunocompetent and immunocompromised patients?
In immunocompromised- ring-enhancing due to central necrosis.
DDx of ring-enahncing basal ganglia mass in immunocompromised patient?
Lymphoma and toxoplasmosis
Ways to differentiate between lymphoma and toxoplasmosis for a ring-enhancing basal ganglia lesion in immunocompromised patient
Emperitcal anti-toxoplasmosis therapy and short-interval follow-up.
Thallium scanning- Lymphoma is thallium avid and toxo is not.
PET- lymphoma tends to be high grade and metabolically active. Toxo usually does not have avid FDG uptake.
Perfusion scanning- lymphoma has increased relative cerebral blood volume while toxo is hypovascular.
What does secondary CNS lymphoma look like?
Tends to involve the meninges and may cause leptomeningeal carcinomatosis or epidural cord compression. Less commonly may present as a parencymal mass.
MC primary tumors to cause CNS parencymal metastases
Lung, breast, and melanoma.
Where do meningiomas arise from?
Meningoepithelial cells called arachnoid “cap” cells.
What are multiple meningiomas associated with?
NF-2 or following radiation therapy.
MC tumors to metastasize to the dura
Breast (MC), lymphoma, small cell lung cancer, and melanoma.
Posterior fossa mass in a child that is hyperattenuating on CT with low ADC on MRI?
Medulloblastoma
Posterior fossa mass in child that is cystic with an enhancing mural nodule?
Juvenile Pilocystic Astrocytoma
Posterior fossa mass in a child that is intraventricular and pushes through fourth ventricular foramina?
Ependymoma
Posterior fossa mass in a child that is cystic with enhancing mural nodule and flow voids with history of VHL?
Hemangioblastoma
Posterior fossa mass in a child with slightly younger age that medulloblastoma, with similar imaging of an aggressive, heterogeneous mass? Renal mass present?
Atypical teratoid/rhabdoid tumor
Posterior fossa mass in an adult with history of primary malignancy? Enhancing mass with edema? Multiple lesions?
Metastasis
Posterior fossa mass in an adult that is cystic with enhancing mural nodule and flow voids? History of VHL?
Hemangioblastoma
Posterior fossa mass in an adult with minimal or little mural enhancement?
Astrocytoma
Posterior fossa mass in young adult, lateral location?
Medulloblastoma
What are the important structures of the CP angle?
CNV, CNVII, CNVIII, and AICA
What are the intracranial manifestations of VHL?
Hemangioblastoma - cerebellar hemisphere fluid-secreting tumor with a cyst and enhancing nodule. Prominent flow voids feeding the tumor.
Endolymphatic sac tumor - occurs along the posterior petrous ridge.
What is the only segment of the trigeminal nerve that does not traverse the cavernous sinus?
V3 - Exits inferiorly from Meckel’s cave through foramen ovale.
How does the abducens nerve (VI) enters the petrous portion of the temporal bone through what?
Dorello’s canal
What is the only nerve that travels in the medial venous sinusoids of the cavernous sinus?
VI
What is the only nerve in the cavernous sinus that does not exit the superior orbital fissure?
Maxillary nerve (V2) - exits the foramen rotundum.
What forms the pituitary gland?
Rathke’s pouch - superior invagination from the primitive oral cavity.
DDx of intrinsic pituitary mass
Pituitary adenoma, Rathke’s cleft cyst, and hypophysitis.
Craniopharyngioma may rarely occur in the sella, but essentially never occurs within the pituitary gland itself.
What is a pituitary microadenoma?
<10 mm in size
Usually symptoms due to hormone excess, not mass effect.
What is a pituitary macroadenoma?
> 10 mm in size. Usually present with mass effect (compression of optic chiasm) rather than endocrine dysfunction.
Usually encase the carotid, but tend not to narrow it. In contrast, meningiomas or metastases can narrow the carotid.
How to tell difference between macroadenoma and meningioma or metastases on imaging?
Macroadenoma usually encase the carotid, but tend not to narrow it. Meningiomas or metastases can narrow the carotid.
What is pituitary apoplexy?
Clinical syndrome of severe headache and endocrine dysfunction caused by hemorrhage into an otherwise normal pituitary.
What is lymphocytic hypophysitis?
Autoimmune inflammatory disorder usually seen in peripartum women that may affect the pituitary and infuncibulum. Present with DI, HA, visual impairment, and endocrine dysfunction.
Thickening and enhancment of the pituitary stalk.
What is granulomatous hypophysitis?
Granulomatous inflammation of the pituitary and infundibulum- can be secondary to sarcoid, Wegener granulomatosis, TB, and LCH.
MC suprasellar lesion in child vs adult?
Child- craniopharyngioma.
Adult- Pititary macroadenoma that has extended superiorly.
Mnemonic for extra-pituitary masses
SATCHMO
Sarcoidosis/Suprasellar extension of an adenoma
Aneurysm
Teratoma (dermoid cyst)/Tolosa Hunt
Craniopharyngiomia/Cleft cyst (Rathke’s)
Hypothalamic glioma (adults)/Hypothalamic hamartoma (children)
Meningioma/Metastasis
Optic nerve glioma
Second most common suprasellar mass in children?
Optic pathway astrocytoma.
Craniopharyngioma is MC.
Low-grade tumor in children. Aggressive tumor in adults.
What is the MC intracranial germ cell tumor?
Germinoma - 80% arise from the pineal region. 20% parasellar. Primarily seen in children and adolescents.
What is a Hypothalamic Hamartoma?
Ectopic hypothalamic neural tissue. Presents with precocious puberty and gelastic seizures (laughing spells).
Characteristically appears as a sessile mass between the pituitary stalk and the mammillary bodies. Does not enhance and is isointense to gray matter.
Suprasellar mass in child that is calcified, complex cystic mass, distinct from pituitary?
Craniopharyngioma
Suprasellar mass in child that is T2 hyperintense, enhancing mass with secondary signs of NF1?
Optic pathway glioma
Suprasellar mass in a child that avidly enhancing midline? Contains fat?
Germ cell tumor
Suprasellar mass in a child that is nonenhancing, gray-matter isointense mass? Presents with gelastic seizures and precocious puberty?
Hypothalamic hamartoma
Suprasellar mass in a child that is enhancing, enlarged pituitary stalk, with DI?
Langerhans Cell Histiocytosis Hypophysitis
Suprasellar mass in an adult that expands up from the sella with expansion of the sella?
Pituitary macroadenoma extension
Suprasellar mass in an adult with intense enhancement with a normal sella? Enhancing dural tail? Adjacent hyperostois? Narrows adjacent vasculature?
Meningioma
Suprasellar mass in an adult that is calcified, enhancing, complex cystic mass? Distinct from pituitary?
Craniopharyngioma
Suprasellar mass in an adult that is nonenhancing cystic mass without calcification?
Rathke’s cleft cyst
Suprasellar mass in an adult with enhancement equal to blood pool? Calcified rim (if thrombosed)?
Aneurysm
Suprasellar mass in an adult that is enhancing with enlarged pituitary stalk with DI?
Lymphocytic or granulomatous hypophysitis
Lymphocytic if peripartum; granulomatous if otherwise
What is the principal neuronal cell of the pineal gland? What is it’s function?
Pinealocyte - modified retinal neuronal cell that is innervated by the sympathetic plexus originating in the retina. Releases melatonin. Does not have a blood brain barrier.
What can a mass within the pineal gland cause?
Compression of the midbrain, compression of the cerebral aqueduct of Sylvius, or compression of the tectal plate - produces Parinaud syndrome- inability to look up, pupillary light dissociation, and nystagmus.
What is Parinaud Syndrome?
Upward gaze paralysis, pupillary light dissociation, and nystagmus.
Caused by compression of tectal plate - pineal gland lesion.
A mass of the pineal gland is intra or extra-axial?
Extra-axial
DDx of pineal masses?
Germ cell tumor, Pineal cyst, Pineocytoma, Pineaoblastoma, or metastases
What are the 2 most common pineal region tumors?
Germinoma and teratoma
What is a Pineocytoma?
Low-grade slow-growing pinealocyte tumor. Any solid component should enahnce. Pineocytoma may feature cystic change, however, which can make differentiation from a pineal cyst difficult.
What is a Pineoblastoma?
Highly malignant tumor of young children, of same primitive neuroectodermal tumor (PNET) type as medulloblastoma.
Trilateral retinoblastoma is used with bilateral retinoblastomas are also present (retina and pineal gland are light-sensing organs). The sella is additionally involved in quadrilateral retinoblastoma.
Presents with obstructive hydrocephalus. Poorly defined pineal mass that may invade into adjacent structures. High cellularity = restricted diffusion.
What is a trilateral retinoblastoma?
Bilateral retinoblastomas and a pineoblastoma.
When sella is involved = quadrilateral retinoblastoma.
What is the difference between a Pineocytoma and Pineoblastoma?
Pineocytoma - low-grade, slow-growing pinealocyte tumor.
Pineoblastoma - highly malignant tumor of young children.
Difference between a pineal germinoma and a pineaoblastoma?
Germinoma - engulfs and induces calcification of the pineal gland.
Pineoblastoma - peripherally calcifies in a pattern that looks like “exploded” calcifications.
What is a Vein of Galen Aneurysm?
Not a true aneurysm. Dilation of the vein of Galen due to an AVF between the anterior or posterior circulation and the venous plexus leading to the vein of Galen.
What is a quadrigeminal plate lipoma associated with?
Can be seen in isolation or associatd with agenesis or hypoplasia of the corpus callosum.
What is the MC cause of SAH?
Trauma
What is the grading of diffuse axonal injury?
Grade I - only the gray-white matter junctions
Grade II - involves the corpus callosum
Grade III - involves the dorsolateral midbrain
Sulcus that separates the motor strip from the sensory cortex?
Central sulcus.
Segments of the ICA?
Cervical (C1) Petrous (C2) Lacerum (C3) Cavernous (C4) Clinoid Segment (C5) Supraclinoid (C6-C7)
Branches of the cavernous (C4) segment of the ICA?
Meningohypophyseal trunk - supplies the pituitary tentorium, and dura of the clivus.
Inferolateral trunk - Supplies the 3rd, 4th, and 6th cranial nerves as well as the trigeminal ganglion.
Branches of the supraclinoid (C6-C7) segment of the ICA?
Opthalamic artery - just above carotid ring - can cause SAH, treated more aggressively.
Posterior Communicating Artery
Anterior Choroidal Artery - supplies the optic chiasm, hippocampus, and posterior limb of internal capsule.
Why are opthalmic artery aneurysms treated aggressively?
Just above superior carotid ring, can cause SAH.
What does the anterior choroidal artery supply?
Optic chiasm, hippocampus, and posterior limb of internal capsule.
Most distal branch of ICA before bifurcation into ACA and MCA.
Where does the recurrent artery of Heubner arise and what does it supply?
A1 segment - supplies the caudate head and anterior limb of the internal capsule.
Where do the medial lenticulostriate perforator vessels arise and what do they supply?
A1 segment - supply the medial basal ganglia.
Where do the lateral lenticulostriate perforator vessels arise and what do they supply?
MCA - supply the lateral basal ganglia including the lateral putamen, extrnal capsule, and the posterior limb of the internal capsule.
Where do the thalamoperforator vessels arise and what do they supply?
Posterior communicating artery and posterior cerebral artery - supplies the thalamus.
What symptom does a P-comm aneurysm cause?
CN III palsy.
What is the Artery of Percheron and where does it arise?
Variant where there is a dominant thalamic perforator supplying the ventromedial thalami bilaterally and the rostral midbrain. Arises from the P1 PCA segment.
Infarct will cause bilateral ventromedial thalamic infarction, with or without midbrain infarction.
What does a Artery of Percheron infarct look like?
Infarct of bilateral ventromedial thalami with or without midbrain infarction.
What circle of willis malformation is associated with aneurysms?
Double or plexiform A-comm
What circle of willis malformation is associated with holoprosencephaly?
azygos ACA - common ACA
What is the M1 segment of the MCA?
From the ICA terminus to the origin of the sylvian fissure
What is the M2 segment of the MCA?
Extends from the bottom to the top of the sylvian fissure
What is the M3 segment of the MCA?
Extends from the top of the sylvian fissure to the cortical surface
What is the M4 segment of the MCA?
Represents small cortical branches.
Where does the recurrent artery of Heubner arise?
MC from the A1 segment of the ACA, proximal to the AComm.
Supplies the head of the caudate and the anterior limb of the internal capsule.
What is the most common persistent carotid-basilar connection?
Persistent trigeminal artery - courses adjacent to the trigeminal nerve. Trident or tau sign on angio.
Associated with aneurysms.
What are the less common carotid to basilar connections?
Otic, hypoglossal, and proatlantal intersegmental arteries are rare.
Persistent trigenimal artery is most common.
What artery supplies the anterior limb of the internal capsule?
Recurrent artery of Heubner. Along with the head of the caudate.
What artery supplies the posterior limb of the internal capsule?
Anterior Choroidal artery. Along with the optic chiasm and hippocampus.
What is the goal of stroke imaging?
Who would benefit from therapy.
What is the only CT finding that absolutely precludes IV tPA within 3 hours of onset of stroke?
Hemorrhage.
Intra-arterial thrombolysis may be performed for an MCA thrombus within how may hours?
6 hours of stroke onset who are not candidates for IV tPA. No time frame for posterior circulation.
Additional exclusion criteria (besides hemorrhage) for tPA
Larger (>1/3 MCA territory)
Occlusion of distal ICA and proximal MCA and ACA (T-shaped occlusion).
Absence of penumbra of salvagable brain that represents at least 20% of the region of abnormal perfusion may preclude treatment with IV tPA.
What is the penumbra?
Does receive some perfusion, but reduced. <20 mL/100g tissue per minute compared to ~60mL/100g tissue per minute for normal gray matter.
What are the stages of evolution of an infarct?
Hyperacute (0-6 hours) Acute infarct (6-72 hours) Early subacute infarct (1.5 days - 5 days) Late subacute infarct (5 days - 2 weeks) Chronic
What happens in the hyperacute stage of infarction?
Na-K ATPase pump that maintains normal low intracellular Na fails. Sodium and water diffuse into cells - cell swelling and cytotoxic edema. Calcium diffuses into cells - triggers cascades that contribute to cell lysis.
DWI hyperintensity with ADC map hypointensity.
Why is diffusion restricted in hyperacute infarct?
0-6 hours
Shift from extracellular to intracellular water due to Na/K ATPase pump failure.
Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein.
What happens in the acute phase of an infarct?
6-72 hours
Characterized by increase in vasogenic edema and mass effect.
Damaged endovascular cells cause leakage of extracellular fluid and increase the risk of hemorrhage. Sulcal effacement and mass effect which peaks at 3-4 days - overlap between acute and early subacute phases.
Hyperintense on T2 of infarct core, best seen on FLAIR. Usually confined to the gray matter. DWI still positive. May see arterial enhancement via collateral flow.
What characterizes the acute phase of an infarct?
Increase in vasogenic edema and mass effect. Endothelial cell damage causes leakage of extracellualr fluid and increase risk of hemorrhage.
What happens in early subacute phase of infarct?
1.5 days to 5 days
Blood flow to affected brain is re-established by leptomeningeal collaterals and ingrowth of new vessels into the region of infarction. Have incomplete BBB = increase in vasogenic edema and mass effect, peaks 3-4 days.
Marked hyperintensity on T2 in both gray and white matter (early is just gray matter). ADC maps becomes less dark or even resolves, but DWI remains bright due to T2 shine through
In which phase does ADC normalize in an infarct?
Early subacute (1.5 -5 days).
DWI still positive due to T2 shine through.
What happens in Late subacute infarct?
5 days - 2 weeks
Resolution of vasogenic edema and reduction in mass effect.
Key imaging finding is gyriform enhancement - may be confused with neoplasm, but no mass effect. Enhancement can be seen from about 6 days to 6 weeks after initial infarct. “2-2-2 rule” - enhancement begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
DWI remains bright due to T2 shine through. ADC back to normal or show increased diffusivity.
What is the 2-2-2 rule of stroke?
Enhancment of subacute infarct begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
What happens in chronic infarct?
> 2 weeks
Cellular debris and dead brain tissue are removed by macrophages and replaced by cystic encephalomalacia and gliosis.
What is Wallerian Degeneration?
Atrophy of contralateral corticospinal tract due to cortical infarct.
What is cortical laminar necrosis?
Deposition of lipid-laden macrophages after ischemia - hyperintensity of T1 and T2 images.
Can be seen instead of encephalomalacia.
What are the high-flow vascular malformations?
AVM and dural AVF
What are the low-flow vascular malformations?
Cavernous malformation (cavernoma)
DVA (venous angioma)
Capillary telangiectasia
What is an arteriovenous malformation (AVM)?
Congenital high-flow vascular malformation. Directly connecting arteries and veins without capillary bed.
Present with seizures or bleeding
Spetzier-Martin scale helps evaluate surgical risk of AVM resection. Large draining to a deep vein in eloquent cortex is high risk.
AVM replaces rather than displaces brain - minimal mass effect.
What is the Spetzler-Martin scale?
Helps evaluate surgical risk for AVM resection.
Large AVM draining to a deep vein in eloquent cortex is high risk.
Small AVM draining into a superficial vein in non-eloquent cortex is low risk.
What does an AVM do to surrounding brain tissue?
Replaces rather than displaces brain. Minimal mass effect.
What is a Vein of Galen Malformation?
AVF from thalamoperforator branches into the deep venous system. The enlarged vein is actually an enlarged median prosencephalic vein.
MC cause of extracardiac high output cardiac failure. Can cause Parinaud syndrome due to mass effect in the pineal region.
What are Dural AVFs?
High-flow lesions characterized by AV shunts between the meningeal arterioles and dural venules.
Primary prognostic feature - presence and degree of cortical venous drainage.
Cognard classification.
Carotid-cavernous fistula (CCF) is subtype of dAVF - often caused by trauma with resultant fistula between cavernous carotid artery and the cavernous sinus. Enlargement of the superior orbital vein and shunting within the cavernous sinus can lead to eye symptoms such as proptosis and CN palsy.
What is the Cognard classification?
Prognostic indicator of dural AVFs. Shows increased risk of bleeding.
I: No cortical venous drainage. Lowest risk.
II: Reflus into dural sinus but not cortical veins.
IIB: Reflux into cortical veins: 10-20% hemorhage rate.
III: Direct cortical venous drainage: 40% hemorrhage rate
IV: Direct cortical venous drainage with venous ectasia: 66% hemorrhage rate
V: Spinal venous drainage. May cause myelopathy.
What is a Carotid-Cavernous fistula?
Subtype of dAVF often caused by trauma.
Fistula between cavernous carotid artery and the cavernous sinus. Enlargement of the superior orbital vein and shunting within the cavernous sinus can lead to eye symptoms such as proptosis and CN palsy.
What causes enlargement of the superior orbital vein and shunting within the cavernous sinus that can lead to eye symptoms such as proptosis and CN palsy?
CC fistula. Fistula between the cavernous carotid artery and the cavernous sinus.
What is a cavernous malformation?
AKA - cavernoma.
Vascular hamartoma with very small but definite bleeding risk. May cause seizures.
Often associated with adjacent developmental venous anomaly (DVA). Increased bleeding risk if DVA present, but DVA itself does not have any bleeding risk.
Multiple = familial cavernomatosis
Can be induced by radiation.
What is associated with multiple cavernomas?
Familial cavernomatosis
What is a Developmental Venous Anomaly (DVA)?
Abnormal vein that provides functional venous drainage to normal brain.
If resected, the patient will suffer a debilitating venous infarct.
What is a capillary telangectasia?
Astymptomatic vascular lesion of dilated capillaries with interspersed normal brain. Do not touch.
Faint, brush-stroke-like enhancing lesion in the brainstem or pons, without mass effect or surrounding edema. GRE may show blooming.
Angiographically occult, like cavernous malformation.
Overall, what is the MC cause of SAH?
Trauma.
Aneurysm rupture is by far the MC of non-traumatic SAH.
DDx of high attenuation material in the subarachnoid space
SAH (by far MC)
Meningitis
Leptomeningeal carcinomatosis
Intrathecal contrast administration
If clinical suspicion for SAH is high and CT is negative what is standard of care to do next?
LP for xanthochromia.
What can cause increased FLAIR signal in the subarachnoid space on MRI?
SAH, meningitis, leptomeningeal carcinomatosis, and residual contrast material.
Recent oxygen or propofol can also cause.
What are the MC sites of aneurysm?
AComm (33%)
PComm (33%)
MCA (20%)
Basilar tip (5%)
What is the Hunt and Hess score?
Clinical grading scale for aneurysmal SAH based solely on symptoms without imaging.
What is the Fisher Grade?
Classifies CT appearance of SAH. Grade 1 is negative on CT; grades 2 and 3 are <1 mm and >1mm thick respectively; grade 4 is diffuse SAH or intraventricular or parenchymal extension.
What is superficial siderosis?
Iron overload of pial membranes due to chronic repeated SAH.
Present with sensorineural deafness and ataxia.
Iron causes hypointensity on T2-weighted images outlining the affected sulci.
What is perimesencephalic SAH?
Type of nonaneurysmal SAH that is Dx of exclusion with much better prognosis than hemorrhage due to ruptured aneurysm.
Must be limited to cisterns directly anterior to the midbrain. Standard of care is to do perform catheter anigio twice, one week apart. Must be negative.
Unknown cause, but thought to represent angiographically occult venous bleeding.
What is reversible cerebral vasoconstriction syndrome (RCVS)?
Cause of nontraumatic, nonaneurysmal SAH and ischemia.
Presents with thunderclap HA and is characterized by prolonged (but reversible) vasoconstriction.
What are the inherited and non-inherited risk factors for the development of saccular aneurysms?
Inherited: Connective tissue diseases such as Marfan and Ehlers-Danlos, polycystic kidney disease, and NF 1.
Non-inherited: HTN and inflammatory vascular disease such as Takayasu or giant cell arteritis.
Fusiform aneurysms are usually due to atherosclerosis.
What is a fusiform aneurysm?
Segmental arterial dilation w/o a defined neck. Usually due to atherosclerosis, but may arise from chronic dissection
Do not occur at branch points. Vertebrobasilar system affected more commonly than anterior circulation.
Much less common than saccular
What is an Oncotic aneurysm?
Aneurysm caused by neoplasm.
Benign left atrial myxoma may peripherally embolize and cause a distal oncotic aneurysm.
Which transverse sinus is usually hypoplastic?
Left transverse sinus
What is the confluence of the superior sagittal sinus, transverse sinus, and the straight sinus called?
Torcular Herophili
What are the dural sinuses?
Superior sagittal sinus- drains the motor and sensory strips
Paired transverse sinuses
Sigmoid sinuses - connects to the jugular bulbs
Torcular Herophili is confluence.
What are the deep cerebral veins?
Paired internal cerebral veins, basal vein of Rosenthal, and Vein of Galen
Venous angle is intersection of the septal vein and the thalamostriate veins. Angiographic landmark for the foramen of Monro.
What is the Venous angle?
Intersection of the septal vein and the thalamostriate veins. Angiographic landmark for the foramen of Monro.
What is the angiographic langmark for the foramen of Monro?
Venous angle - intersection of the septal vein and the thalamostriate veins.
What are the superficial cerebral veins?
Vein of Troclard - connects superficial cortical veins to the superior sagittal sinus.
Vein of Labbe - drains the temporal convexity into the transverse or sigmoid sinus. Traction on during surgery can cause venous infarction and aphasia.
What is the Vein of Troclard?
Connects the superficial cortical veins to the superior sagittal sinus
What is the vein of Labbe?
Drains the temporal convexity into the transverse or sigmoid sinus.
What are the risk factors for venous thrombosis?
Pregnancy, oral contraceptives, thrombophilia, malignancy, and infection.
What does infarction of the parasagittal high convexity cortex suggest?
Superior sagittal sinus thrombosis
What does infarction of the bilateral thalami suggest?
Deep venous system thrombosis
What does infarction of the posterior temporal lobe suggest?
Transverse sinus thrombosis
What are the stages of iron in hemoglobin as it evolves?
Intracellular oxyhemoglobin –> deoxygenation –> Intracellular deoxyhemoglobin –> oxidation –> Intracellular methemoglobin –> cell lysis –> extracellular methemoglobin –> chelation –> Hemosiderin and ferritin
What stage of blood breakdown is bright on T1?
Methemoglobin stages - all others are dark on T1
Bright on both T1 and T2
What do the methemoglobin stages of blood break down look like?
Bright on T1 and T2, except for intracellular methemoglobin, which is dark on T2.
What are the stages of parenchymal hematoma on MR?
Hyperacute hematoma (0-6 hours) Acute hematoma (6-72 hours) Early subacute hematoma (3 days - 1 week) Late subacute (1 week - months) Chronic hematoma
What is a hyperacute parenchymal hematoma?
<6 hours
Intracellular oxyhemoglobin
Primarily intact RBCs containing oxygenated hemoglobin, which is diamagnetic
Center of the hematoma will be isointense on T1 and iso to slightly hyperintense on T2.
Key is peripheral rim of hypointensity on T2 due to deoxygenation of the most peripheral red cells.
What are the imaging findings of hyperacute parenchymal hematoma?
T1 isointense; T2 iso to hyperintense with dark rim.
What is an acute parenchymal hematoma?
6-72 hours
Intracellular deoxyhemoglobin
RBCs desaturate (lose oxygen), entire hematoma becomes hypointense on T2 and iso to mildly hypointense on T1
What is an early subacute parenchymal hematoma?
3 days to 1 week
Intracellular methemoglobin
Characterized by methemoglobin, which is paramagnetic and undergoes proton-electron dipole-dipole interactions (PEDDI) with water. PEDDI shortens T1 to cause hyperintensity on T1 images. Intracellular and extracellular methemoglobin and both hyperintense on T1.
In early subacute, blood remains hypointense on T2 images due to the paramgnetic effects of methemoglobin, which remains trapped in the red cells.
What is a late subacute parenchyaml hematoma?
1 week to months Extracellular methemoglobin (after RBC lysis)
Methemoglobin PEDDI effec persists are cell lysis- continued hyperintensity on T1.
Paramagnetic effects of methemoglobin lessens. Signal intensity on T2 images increases to that of CSF, due to RBC lysis and decrease in protein concentration.
May be peripheral enhancement of subacute to chronic infarct.
What are the T1 and T2 characteristics of blood in a hyperacute parenchymal hematoma on MR?
T2 isointense
T2 iso to hyperintense with dark rim.
What are the T1 and T2 characteristics of blood in a acute parenchymal hematoma on MR?
T1 iso or hypointense
T2 hypointense
What are the T1 and T2 characteristics of blood in a early subacute parenchymal hematoma on MR?
T1 hyperintense
T2 hypointense
What are the T1 and T2 characteristics of blood in a late subacute parenchymal hematoma on MR?
T1 hyperintense
T2 hyperintense
What are the T1 and T2 characteristics of blood in a chronic parenchymal hematoma on MR?
T1 iso or hypointense
T2 hypointense
How does chronic hypertension cause intraparenchymal hemorrhage?
Arteriolar smooth muscle hyperplasia, which eventually leads to smooth muscle death and replacement with collagen. The resultant vascular ectasia predisposes to hemorrhage.
What is the main clinical clue that hemorrhage is due to cerebral amyloid angiopathy?
Normotensive elderly adult
What is the primary imaging feature to suggest hemorrhage is due to cerebral amyloid angiopathy?
Location of hematoma - almost always lobar or cortical - usually in the parietal or occipital lobes.
MC primary brain tumor to cause hemorrhage?
Glioblastoma
Extracranial primary tumors to cause hemorrhagic metastases
Choriocarcinoma Melanoma Thyroid Carcinoma RCC Breast cancer - maybe
Patients on what drug may be at increased risk for hemorrhagic metastasis
Bevacizumab - Avastin, Genentech
Clues to the diagnosis of an underlying tumor causing hemorrhage
More than expected edema surrounding a hyperacute hematoma and heterogeneous blood product signal, suggesting varying breakdown stages of hemoglobin.
Presence of multiple enhancing masses.
If unclear- follow-up MRI once initial hemorrhage improves. May show a delay in the expected evolution of blood products, persistent edema, and enhancement of the underlying tumor.
What is a cavernoma?
Cavernous malformation - vascular hamartoma that consists of low-flow endothelial-lined blood vessels w/o intervening normal brain.
Angiographically occult.
What does vasculitis look like on MRI?
MC presentation is cerebral ischemia. Less commonly, may present with frank hemorrhage.
Multiple foci of T2 prolongation in the basal ganglia and subcortical white matter.
What is Moyamoya?
Non-atherosclerotic vasculopathy characterized by progresive stenosis of the intracranial ICA and their proximal branches, which leads to proliferation of fragile lenticulostriate collateral vessels.
Angio- enlarged basal perforating arteries gives a puff of smoke appearance.
Ivy Sign - FLAIR MRI shows tubular branching hyperintense structures within the sulci, representing cortical arterial branches that appear hyperintense due to slow collateral flow.
Susceptible to aneurysm, especially in the posterior circulation.
What is the Ivy Sign with Moyamoya?
FLAIR tubular branching hyperintense structures within the sulci, representing cortical arterial branches that appear hyperintense due to slow collateral flow.
What are people with Moyamoya susuceptible to?
Aneurysm formation, especially in the posterior circulation.
Intraparenchymal hemorrhage etiology in elderly adult with HTN? Hemorrhage in basal ganglia, cerebellum, or thalamus? Multiple basal ganglia microbleeds on T2*? Prior lacunes and periventricular WM disease?
Hypertensive hemorrhage
Intraparenchymal hemorrhage etiology in lobar or cortical hemorrhage? Elderly adult w/o HTN? Multiple parenchymal microbleeds on T2*?
Amyloid angiopathy
Intraparenchymal hemorrhage etiology with extensive subarachnoid blood? Aneurysm adjacent to hematoma?
Aneurysmal hemorrhage
Intraparenchymal hemorrhage etiology with parenchymal hemorrhage in a young patient? Enlarged feeding artery? Adjacent encephalomalacia?
AVM
Intraparenchymal hemorrhage etiology with hemorrhage adjacent to cavernous sinus or in posterior fossa? Enlarged meningeal artery or cortical vein?
dAVF
Intraparenchymal hemorrhage etiology with adjacent DVA on post-contrast images? Multiple dark spots on T2* (familial variant)?
Cavernous malformation
Intraparenchymal hemorrhage etiology with parasagittal or bilateral thalamic hemorrhage? Young patient, especially female? Increased density in cortical vein or dural sinus?
Venous thrombosis
Intraparenchymal hemorrhage etiology with more edema than expected? More heterogeneous signal than expected? Multiple enhancing lesions?
Hemorrhagic neoplasm
Intraparenchymal hemorrhage etiology with clinical history of infarct? History of thrombolytic therapy?
Hemorrhagic infarct
Intraparenchymal hemorrhage etiology with multifocal T2 prolongation in deep WM? History of systemic vasculitis? Multifocal stenosis/dilation on angiography?
CNS Vasculitis
Intraparenchymal hemorrhage etiology with occlusion of internal carotid arteries? Multiple collateral vessels?
Moyamoya
What is the key imaging finding of demyelinating disease?
Minimal mass effect relative to lesion size.
Enlarged Virchow-Robin spaces and a J-shaped sella can be seen in what?
Mucopolysaccharidoses.
