Neuroimaging Flashcards
Ventricular Anatomy
Cerebral Edema
Edema within the brain can be caused by cell death, altered capillary permeability, or hemodynamic forces.
Cytotoxic Edema
Cytotoxic edema is cell swelling caused by damaged molecular sodium-potassium ATPase ion pumps. It can affect both gray and white matter.
Cytotoxic edema is caused by cell death, mot commonly due to infarct. Water ions trapped inside swollen cells feature reduced diffusivity.
Vasogenic Edema
Vasogenic edema is interstitial edema caused by increased capillary permeability. It is seen primarily in the white matter, as there is more interstitial space.
Vasogenic edema is caused most commonly by neoplasm, infection, or infarct.
Interstitial Edema
Interstitial edema is caused by imbalances in CSF flow, most commonly due to obstructive hydrocephalus.
Interstitial edema presents on imaging as periventricular fluid, often called “transependymal flow of CSF”, even though it is unlikely that the CSF actually flows across the ependymal cells lining the ventricles.
Herniation
The total volume in the skull is fixed. Increases in intracranial pressure may lead to herniation across a dural fold.
Herniation may be due to a mass lesion (such as a neoplasm or hematoma) or may be due to edema secondary to a large stroke. Because the volume of the posterior fossa is especially limited, cerebellar infarcts are prone to herniation.
Cerebellar tonsillar herniation
Downward displacement of the cerebellar tonsils through foramen magnum causes compression of the medulla.
Compression of medullary respiratory centers is often fatal.
Basal cisterns
The basal cisterns, also known as the perimesencephalic cisterns, are CSF–filled spaces surrouding the midbrain and pons.
Compression or effacement of the basal cisterns may be a sign of the impending or actual herniation.
Blood Brain Barrier (BBB) and enhancement
Micro or macro disruption of the blood brain barrier (BBB) produces parenchymal enhancement after contrast administration, which may be secondary to infection, inflammation, neoplasm, trauma, and vascular etiologies.
The BBB is formed by astrocytic foot processes of brain capillary endothelial cells and prevents direct communication between the systemic capillaries and the protected extracellular fluid of the brain.
Several CNS regions do not have a blood brain barrier, and therefore normally enhance: Choroid plexus, Pituitary and pineal glands, Tuber cinereum (controls circadian rhythm, located in the inferior hypothalamus). Area postrema (controls vomiting, located at inferior aspect of 4th ventricle).
The dura also lacks a blood brain barrier, but does not normally enhance. This phenomenon is subsequently explened in the section on pachymeningeal (dural) enhancement.
Vascular enhancement is due to a localized increase in blood flow, which may be secondary to vasodilation, hyperemia, neovascularity, or arteriovenous shunting. On CT, the arterial phase of contrast injection (for instance a CT angiogram) mostly shows intravascular enhancement. Parenchymal enhancement, including the dural folds of the falx and tentorium, is best seen several minutes after the initial contrast bolus.
On MRI, routine contrast-enhanced sequences are obtained in the parenchymal phase, several minutes after injection. Most intracranial vascular MRI imaging is performed with a noncontrast time of flight technique.
Intracranial enhancementmay be intra- or extra-axial. Extra-axial structures that may enhance in pathologic conditions include the dura (pachymeninges) and arachnoid (leptomeninges).
Perfusion
Perfusion MR is an advanced technique where the brain is imaged repeatedly as a bolus of gadolinium contrast is injected. The principle of perfusion MR is based on the theory that gadolinium causes a magnetic field disturbance, which (counterintuitively) transiently decreases the image intensity. Perfusion images are echo-planar T2* images, which can be acquired very quickly.
Perfusion MR may be used for evaluation of stroke and tumors.
Periventricular enhancement (intra-axial)
Enhancement of the subependymal surface can be either neoplastic, infectious, or demyelinating in etiology.
Primary CNS lymphoma is a malignant B-cell neoplasm that can have diverse presentations including periventricular enhancment, solitary brain mass, or multiple brain masses.
Primary CNS lymphoma is hyperattenuating on CT and demonstrates low ADC and low signal intensity on T2-weighted MRI due to hypercellularity.
Primary CNS lymphoma rarely involves the meninges. In contrast, the meninges (both pachymeninges and leptomeninges) are commonly involved when systemic lymphoma spreads to the brain.
CNS lymphoma tends to be centrally necrotic in immunocompromised patients, but usually enhances homogeneously in immunocompetent patients.
Infectious ependymitis is most commonly caused by cytomegalovirus. Infectious ependymitis usually features thin linear enhancment along the margins of the ventricles.
Primary glial tumor may cause periventricular enhancement.
Multiple sclerosis may affect the subependymal surface. Although the majority of demyelinating lesions do not enhance, an active plaque may demonstrate enhancement.
Gyriform enhancement (intra-axial)
Superficial enhancement of the cortical (gyral) surface of the brain can be due to either cerebral infection, inflammation, or ischemia.
Herpes encephalitis is a serious necrotizing infection of the brain parenchyma due to reactivation of latent HSV-1 infection within the trigeminal ganglion. The medial temporal lobes and cingulate gyrus are usually affected first and demonstrate gyral enhancement due to inflammation, petechial hemorrhage, and resultant BBB breakdown. The involved areas typically also demonstrate reduced diffusivity.
Meningitis may cause gyral enhancment in addition to the more typical leptomenigneal enhancement (subsequently discussed).
Subacute infarct can demonstrate gyriform enhancement lasting approximately 6 days to 6 weeks after the initial ischemic event.
In contrast to the gyriform enhancement of subacute infarct, an acute infarct may demnonstrate vascular enhancement due to reactive collateral vasodilation and resultant hyperemia.
Posterior reversible encephalopathy syndrome (PRES) is a syndrome of vasogenic white matter edema triggered by altered autoregulation that may demonstrate gyral enhancment. PRES may rarely exhibit restricted diffusion.
Nodular subcortical enhancment (intra-axial)
Nodular intra-axial enhancement is most commonly due to metastatic disease.
Hematogenously disseminated metastatic disease is commonly found at the subcortical gray-white junctions. Tumor emboli become “stuck” at the junction between the simple vasculature of the white matter and the highly branching vasculature of the gray matter.
Edema is almost always present with metastatic disease of the gray-white junction, although slightly more distal cortical metastases (e.g. pelvic malignancy spread via the Batson preverterbral venous plexus) leads to posterior fossa disease by transit through the retroclival venous plexus.
Ring enhancement (intra-axial)
Peripheral (ring) enhancment is a common presentation with a broad range of differential diagnoses. The two most common causes are high-grade neoplasm and cerebral abscess.
The mnemonic MAGIC DR (metastasis, abscess, glioma, infarct, contusion, demyelination, and radiation) may be helpful to remember the wide range of etiologies for ring enhancement, although it is usually possible to narrow the differential basedon the pattern of ring enhancement combined with additional MRI sequences and clinical history.
Metastasis: Hematogenous metastases are typically found at the subcortical gray-white junction. Metastases are often multiple, but smaller lesions may not be ring-enhancing.
Abscess: A pyogenic abscess is formed as a result of organization and sequestration of an infection, featuring a central region of viscous necrosis.
The key imaging findings of abscess are reduced diffusivity (bright on DWI and dark on ADC) caused by high viscosity of central necrosis and a characteristic smooth, hypointense rim on T2-weighted images.
Glioma: High grade tumors such as glioblastoma typically have a thick and irregular wall.
Multivoxel MRI spectroscopy will be abnormal outside the margin of an enhancing high grade glial neoplasm secondary to nonenhancing infiltrative tumor. This is in contrast to a demyelinating lesion, abscess, and metastasis, where the spectral pattern returns to normal at the margin of the lesion.
Perfusion MRI demonstrates elevated perfusion in a high grade glioma.
Infarct: Although subacute cortical infarcts often demonstrate gyral enhancment, ring enhancement can be seen in subacute basal ganglia infarcts.
In contrast to neoplasm and infection, a subacute infarct does not have significant mass effect.
Contusion: Both traumatic and nontraumatic intraparenchymal hemorrhage can show ring enhancement in the subacute to chronic stage.
Demyelinating disease: The key finding in ring-enhancing demyelinating disease is lack of significant mass effect. The “ring” of enhancement is often incomplete and “C” shaped.
Multiple sclerosis is the most common demyelinating disease. Enhancement suggests active disease.
Although the typical finding is an incomplete rim of enhancement, tumefactive demyelinating disease can look identical to a high-grade tumor.
Radiation necrosis may look identical to a high-grade tumor. On perfusion, cerebral blood volume is generally low in radiation necrosis and typically increased in a high grade glioma.
Pachymeningeal (dural) enhancement (extra-axial)
The pachymeninges (pachy means thick - a “thick-skinned” elephant is a pachyderm) refers to the dura mater, the thick and leather-like outermost covering of the brain.
In addition to surrounding the surface of the brain, the dura forms several reflections, including the falx, tentorium, and cavernous sinus.
The dura does not have a blood brain barrier. Although contrast molecules normally diffuse into the dura on enhanced CT or MRI, dural enhancement is never visualized on CT and is only viscualized on MRI in pathologic situations.
Dural enhancement is not seen on CT because both the skull and adjacent enhancing dura appear white.
Enhancement of normal dura is not visible on MRI because MRI visualization of enhancement requires both water protons and gadolinium. Although gadolinium is present in the dura, there are normally very few water protons. However, dural pathology often causes dural edema, which provides enough water protons to make the gadolinium visible. Therefore, dural enhancement on MRI is an indication of dural edema rather than BBB breakdown.
Differential diagnosis of pachymeningeal enhancement
Intracranial hypotension: Prolonged decrease in cerebrospinal fluid pressure can lead to vasogenic edema in the dura.
Intracranial hypotension clinically presents as a postural headache exacerbated by standing upright.
Intracranial hypotension may be idiopathic or secondary to CSF leak from surgery or lumbar puncture.
Imaging shows thick, linear dural enhancement, enlargement of the pituitary gland, and “sagging” of the cerebellar tonsils. There may also be subdural hemorrhage due to traction effect on the cerebral veins.
Postoperative: Dural enhancment may be seen postoperatively.
Post lumbar puncture: Diffuse dural enhancement is occasionally seen (<5% of the time) after routine lumbar puncture.
Meningeal neoplasm, such as meningioma, can produce a focal area of dural enhancement called a dural tail, due to reactive changes in the dura. Metastatic disease to the dura, most commonly breast cancer in a female and prostate cancer ina male, can cause irregular dural enhancement.
Granulomatous disease, including sarcoidosis, tuberculosis, and fungal disease, can produce dural enhancement, typically of the basal meninges (meninges of the skull base).
Leptomeningeal (pia-arachnoid) enhancement (extra-axial)
The leptomeninges (lepto means thin or narrow) include the pia and arachnoid.
Leptomeningeal enhancment follows the undulating contours of the sulci as it includes enhancement of both the subarachnoid space and the pial surface of the brain.
The differential diagnosis of FLAIR hyperintensity in the subarachnoid space overlaps with the differential for leptomeningeal enhancement. Subarachnoid FLAIR hyperintensity may be due to:
Meningitis and leptomeningeal carcinomatosis both have increased subarachnoid FLAIR signal and leptomeningeal enhancement
Subarachnoid hemorrhage manifests as increased subarachnoid FLAIR signal, without leptomeningeal enhancement. Blooming artifact on GRE and SWI from blood products will help differentiate subarachnoid hemorrhage from carcinomatosis.
Subarachnoid FLAIR signal is artifactually increased when the aptient is on oxygen or propofol therapy, without abnormal enhancement.
Differential diagnosis of leptomeningeal enhancment
Meningitis (either bacterial, viral, or fungal) is primary consideration when leptomeningeal enhancment is seen.
Leptomeningeal enhancment in meningitis is caused by BBB breakdown due to inflammation or infection.
Fine, linear enhancement suggests bacterial or viral meningitis.
Thicker, nodular enhancment suggests fungal meningitis.
Leptomeningeal carcinomatosis, also called carcinomatous meningitis, is spread of neoplasm into the subarachnoid space, which may be due to primary brain tumor or metastatic disease.
CNS neoplasms known to cause leptomeningeal carcinomatosis include medulloblastoma, oligodendroglioma, chroid plexus tumor, lymphoma, ependymoma, glioblastoma, and germinoma. Mnemonic MOCLEGG or GEMCLOG
Metastatic tumros known to cause carcinomatosis include lymphoma and breast cancer.
Viral encephalitis may produce cranial nerve enhancement within the subarachnoid space.
Slow vascular flow may mimic leptomeningeal enahcnement at first glance, but a careful examination shows the distinction. Slow flow appears as an intravascular distribution of FLAIR hyperintesity due to “unmasking” of the inherent high signal of blood, which remains int eh plane of imaging as the entire pulse sequence is obtained.
Slow flow of peripheral vessels in moyamoya disease causes the ivy sign.
Tumor-related complications
The three emergent complications of a brain tumor are the three H’s: Hemorrhage, Hydrocephalus, and Herniation. CT is a good screening method to evaluate for these complications.
Hemorrhage: Primary or metastatic brain tumors are often associated with neovascularity and tumoral vessels are more prone to hemorrhage than normal vasculature.
The most common primary brain tumor to hemorrhage is a glioblastoma.
Hemorrhagic metastases include melanoma, renal cell carcinoma, thyroid carcinoma, and choriocarcinoma. Although breast and lung cancer metastases are less frequently hemorrhagic on a case-by-case basis, these two malignancies are so common that they should also be considered in the differential of a hemorrhagic metastasis.
Mass intra- or extra-axial
After evaluation for emergent complications, the next step is to determine if the lesion in intra- or extra-axial. This distinction can sometimes be quite tricky.
Although metastases may be either intra- or extra-axial, the differential diagnosis for each space is otherwise completely different.
Findings of an extra-axial mass include a CSF cleft between the mass and the brain, buckling of gray matter, and gray matter interposed between the mass and white matter.
Findings of an intra-axial mass include absence of intervening gray matter between the mass and the white matter.
The presence of white matter edema is not specific to intra-axial masses. In particular, meningioma (an extra-axial dural neoplasm) is known to cause white matter edema of underlying brain.
Meningeal enhancement is seen more commonly in extra-axial masses (most commonly meningioma), but can also be seen in intra-axial masses.
Tumors hypointense on T2-weighted images include
Metastases containing desiccated mucin, such as some gastrointestinal adenocarcinomas. Not that mucinous metastases to the brain can have variable signal intensities on T2-weighted images, depending on the water content of the mucin. Hydrated mucin is hyperintense on T2-weighted images.
Hypercellular tumors, including lymphoma, medulloblastoma, germinoma, and some glioblastomas.
Tumors hyperintense on T1-weighted images include
Metastatic melanoma (melanin is hyperintense on T1-weighted images).
Fat-containing tumors, such as dermoid or teratoma.
Hemorrhagic metastasis (including renal cell, thyroid, choriocarcinoma, and melanoma).
Some tumors contain cystic compoments which are isointense to CSF on all sequences. (Note that cysts tend to be at the peripherey of enhancing low grade tumors. In contrast, although intra-tumoral necrosis of a high-grade tumor may also follow CSF signal, necrosis tends to be surrounded by enhancing tumor.
Glial Cells
A glioma is a primary CNS tumor that arises from a glial cell. Glial cells include astrocytes, oligodendrocytes, ependymal cells, and choroid plexus cells.
Glioma is not a synonym for a “brain tumor”. Only a tumor that arises from one of the aforementioned glial cells can accurately be called a glioma.
The normal functions of an astrocyte are to provide biochemical support to the endothelial cells that maintain the blood brain barrier, to maintain extracellular ion balance, and to aid in repair after a neurona injury.
Astrocytes are normally located throughout the entire brain (primarily in the white matter) and spinal cord.
The normal funnction of an oligodendrocyte is to maintain myelin around CNS axons. A single oligodendrocyte can maintain the myelin of dozens of axons. The counterpart in the peripheral nervous system is the Schwann cell, which maintains myelin around a single peripheral nerve. Unlike the oligodendrocyte, each Schwann cell is in charge of only a single axon.
Oligodendrocytes are normally located throughout the entire brain and spinal cord.
The normal function of an ependymal cell is to circulate CSF with its multiple cilia.
Ependydmal cells line the ventricles and central canal of the spinal cord.
The normal function of a choroid plexus cells is to produce CSF. A choroid plexus cell is a modified ependymal cell.
Choroid plexus cells are located intraventricularly, in the body and temporal horn of each lateral ventricle, roof of the third ventricle and roof of the fourth ventricle.
Grade I Astrocytoma
Juvenile pilocytic astrocytoma (JPA)
Juvenile pilocytic (hair-like) astroctyoma (JPA) is a benign World Health Organization (WHO) grade I tumor seen typically in the posterior fossa in children.
Imaging shows a well-circumscribed cystic mass with an enhancing nodule and relatively little edema. When in the posterior fossa, JPA may compress the fourth ventricle.
JPA can also occur along the optic pathway, with up to 1/3 of optic pathway JPA associated with neurofibromatosis type 1. Posterior fossa JPA is not associated with NF1.
Fibrillary Astrocytoma
Fibrillary astrocytomas are infiltrative tumors that include low-grade astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme (GBM).
Astrocytomas can occur in the brain or the spinal cord.
Low-grade astrocytoma is a WHO grade II tumor that typically presents as a hyperintense mass on T2-weighted images, without enhancement. Imaging findings may be subtle.
Anaplastic astrocytoma is a WHO grade III tumor. It features a range of appearances from thickened cortex (similar to low-grade astroctyoma) to an irregularly enhancing mass that may appear identical to glioblastoma. The natural history of the disease is eventual progression to glioblastoma.
Glioblastoma multiforme (GBM) is an aggressive WHO grade IV tumor of older adults. It is the most common primary CNS malignancy. GBM has a highly variable appearance (“multiforme”) but typically presents as a white matter mass with heterogenous enhancement and surrounding nonenhancing T2 prolongation. Most of the surrounding T2 prolongation is thought to represent infiltrative tumor.
GBM is an infiltrative disease that spreads through white matter tracts, through the CSF, and subependymally. Subependymal spread describes spread within the walls of the ventricles under the ependymal cells.
A GBM that crosses the midline via the corpus callosum is called a butterfly glioma. The differential diagnosis of a transcallosal mass includes glioblastoma, lymphoma, and demyelinating disease.
Other Gliomas
Gliomatosis cerebri is a diffuse infiltrative mid-grade (WHO II or III) astroctyoma that affects multiple lobes.
Diagnostic criteria include involvement of at least two lobes plus extra-cortical involvement of structures such as the basal ganglia, corpus callosum, brainstem, or cerebellum.
Gliomatosis has a poor prognosis and may degenerate into GBM.
The typical imaging appearance is diffuse T2 prolongation throughout the involved brain. Diffuse T2 prolongation can be seen in several entities, typically in immunocompromised patients, including lymphoma, progressive multifocal luekoencephalopathy (demyelination caused by JC virus), and AIDS encephalopathy.
Gliomatosis exerts mass effect but typically does not enhance.
Oligodendroglioma is a WHO grade II tumor that usually presents as a slow-growing cortical-based mass.
The typical patient is a young to middle-aged patient presenting with seizures.
Oligodendrogliomas have a propensity to calcify (approximately 75% calcify). Variants such as oligoastroctyoma and anaplastic oligodendroglioma are much more aggressive. Oligoastroctyoma is a mixed tumor with an astrocytic component. Although oligoastrocytoma can degenerate into GBM, typically prognosis is better than a pure GBM. Anaplastic oligodendroglioma is indistinguishable from GBM on imaging and has a poor prognosis.
Ependymoma is a tumor of ependymal cells that tends to occur in the posterior fossain children and in the spinal cord in older adults.
The pediatric posterior fossa ependymoma has been called the toothpaste tumor for its propensity to fill the fourth ventricle and squeeze through the foramina of Magendie or Luschka into the adjacent basal cisterns. Medulloblastoma, the most common pediatric brain tumor, also usually arises in the posterior fossa but does not typically squeeze through the foramina.
The adult spinal ependymoma can occur anywhere in the intramedullary spinal cord. The main differential diagnosis of an intramedullary spinal cord mass is an astrocytoma, which tends to occur in younger patients. It is not possible to reliably differentiate spinal cord ependymoma from astrocytoma on imaging.
Non-Glioma Primary Brin Tumors
Lhermitte-Duclos, also called dysplastic cerebellar gangliocytoma, is a WHO grade I cerebellar lesion that is part hamartoma and part neoplasm.
Lhermitte-Duclos is almost always seen in association with Cowden syndrome (multiple hamartomas and increased risk of several cancers).
The classical imaging finding is a corduroy or tiger-striped striated lesion in the cerebellar hemisphere. Enhancement is rare.
Embryonal Tumors
Embryonal Tumors represent a spectrum of WHO grade IV, aggressive childhood malignancies that are known as primitive neuroectodermal tumors (PNET). Intracranial PNET tumors are more commonly located in the posterior fossa but may occur supratentorially.
Atypical teratoid/rhabdoid tumor (ATRT) is a WHO IV, aggressive tumor that may appear similar to medulloblastoma, but occurs in slightly younger patients. The majority occur in the posterior fossa. ATRT is associated with malignant rhabdoid tumor of the kidney.
Medulloblastoma is a WHO grade IV tumor of small-blue-cell origin. It is one of the most common pediatric brain tumors.
Medulloblastoma most commonly occurs in the midline in the cerebellar vermis. It is slightly hyperattenuating on CT due to its densely packed cells and is accordingly hypointense on T2-weighted images and has low ADC values. The tumor is avidly enhancing and may appear heterogenous due to internal hemorrhage and calcification. The low ADC values can be a useful finding to differentiate medulloblastoma from ependymoma and pilocytic astroctyoma, the two other most common childhood posterior fossa tumors.
Leptomeningeal metastaic disease is present in up to 33% of patients. Sugar-coating (Zuckerguss) is icing-like enhancement over the brain surface. Imaging of the entire brain and spine should be performed prior to surgery.
When medulloblastoma occurs in a young adult (as opposed to a child), the tumor tends to arise eccentrically in the posterior fossa, from the cerebellar hemisphere.
Tumors with a cyst and an enhancing nodule
A few low-grade, fluid-secreting tumors present as a cyst with an enhancing mural nodule. (Juvenile pilocytic astrocytoma, Hemangioblastoma, Pleomorphic Xanthroastrocytoma (PXA), Ganglioglioma)
Hemangioblastoma is a highly vascular WHO grade I tumor associated with von Hippel-Lindau (VHL) syndrome that occurs most commonly in the cerebellum, medulla, or spinal cord. It only rarely occurs supratentorially.
Although associated with VHL, only 30% of patients with hemangioblastoma have VHL. Hemangioblastoma in a patient with VHL has a worse prognosis.
The classic appearance of hemagioblastoma is a cystic mass with an enhancing mural nodule. Prominent vessels are often seen as tubular areas of flow void. Less commonly, a hemangioblastoma may be solid or hemorrhagic.
When in the spinal cord, hemangioblastoma is often associated with a syrinx.
Pleomorphic Xanthroastroctyoma (PXA) is a low-grade WHO grade II astroctyoma variant.
PXA is a rare tumor of childhood and adolescents, typically with history of chronic epilepsy.
The most common location of PXA is the temporal lobe, where it typically presents as a supratentorial cortical cystic mass with an enhancing mural nodule. The overlying dura may be thickened and enhancing.
The main differential consideration, both by imaging and clinical presentation, is ganglioglioma; however, ganglioglioma does not usually cause dural thickening.
Ganglioglioma is a rare slow-growing neuroglial tumor that typically presents in an adolescent or young adult with medically refractory temporal lobe epilepsy.
Ganglioglioma characteristically appears as a temporal lobe cyst and enhancing mural nodule, often with calcification. Ganglioglioma may cause calvarial remodeling and scalloping.
Intraventricular Tumors
Central neurocytoma is a low-grade tumor likely of neuronal origin that occurs in young adults, from teenagers to young middle-aged patients. Prognosis is excellent.
Typical imaging appearance is a lobulated mass attached to the septum pellucidum, with numerous intratumoral cystic areas. Calcification is common.
Choroid plexus papilloma is rare intraventricular tumor. Choroid plexus papilloma is a low-grade (WHO I) neoplasm arising from choroid plexus epithelial cells. It is the most common brain tumor in babies < 1 year old, but may also occur in adults.
T2-weighted images show a lobulated, heterogenous or hyperintense mass that avidly enhances on T1-weighted MRI.
In children, the atrium of the lateral ventricle is the most common location.
In adults, the fourth ventricle is the most common location.
Less commonly, choroid plexus papilloma may arise from the third ventricle or cerebromedullary angle.
Choroid plexus papilloma and carcinoma (WHO grade III) are not reliably distinguishable.
Intraventricular meningioma appears as a solid mass, typically in the trigone of the lateral ventricle. It tends to ccur in older patients, similar to other meningiomas.
Intraventricular meniniomas are typically hypercellular and homogenously enhance, distinguishing them from other intraventricular neoplasms.
Subependymal giant cell astrocytoma (SEGA) is a low-grade (WHO I) astroctyoma variant that is associated with tuberous sclerosis. Other findings in tuberous sclerosis include subependymal nodules and hamartomas (cortical and subcortical). SEGA classically is an enhancing mass in the lateral ventricle near the foramen of Monro.
Subependymoma is a nonenhancing low-grade tumor of unclear origin thought to arise from subependymal astrocytes, ependymal cells lining the ventricles, or common precursor cells.
Subependymoma is a tumor of middle-aged and older adults. It is often found incidentally.
The most common locations are the obex of the 4th ventricle (inferior 4th ventricle) or at the foramen of Monro in the lateral ventricle. The tumor usually doesn’t enhance. Despite their similar names, subependymoma is not related to subependymal giant cell astroctyoma (discussed above, associated with tuberous sclerosis) or with ependymoma.
Primary CNS Lymphoma: Overview
Primary CNS lymphoma is lymphoma isolated to the CNS, most commonly diffuse large B-cell lymphoma. Immature blast cells form lymphoid aggregates around small cerebral blood vessels in a periventricular location. Note that the brain does not contain native lymphoid tissue.
PCNSL is known to “melt away” with chemoradiation but tends to recur aggressively.
The appearance of PCNSL depends on the immune status of the patient. Regardless of immune status, however, key imaging findings are a periventricular location and high cellularity (hyperattenuating on CT, relatively hypointense on T2-weighted images, and reduced diffusivity).
Primary CNS lymphoma: Immunocompetent patient
In an immunocompetent patient, PCNSL typically presents as an enhancing periventricular mass, often crossing the corpus callosum to involve both hemispheres. Involvement of the frontal lobes and basal ganglia is most common.
The differential diagnosis for a mass involving the corpus callosum includes lymphoma, glioblastoma multiforme, and demyelinating lesion.
PCNSL in an immunocompetent individual usually enhances homogenously, without central necrosis. This is in contrast to PCNSL in an immunocompromised patient, where central necrosis is typical.
Primary CNS lymphoma: Immunocompromised patient
In an immunocompromised patient, PCNSL typically presents as a periventricular ring-enhancing lesion in the basasl ganlgia. The ring enhancement is caused by central necrosis. The two primary differential considerations for a ring-enhancing basal ganglial mass in an immunocompromised patient are lymphoma and toxoplasmosis.
Several clinical and imaging options are available to differentiate between lymphoma and toxoplasmosis: Empirical anti-toxoplasmosis therapy and short-interval follow-up. Thallium scanning: CNS lymphoma is thallium avid and toxoplasmosis does not take up thallium. PET: CNS lymphoma tends to be high-grade and metabolically active. Toxoplasmosis usually does not have avid FDG uptake. Perfusion scanning: CNS lymphoma has increased relative cerebral blood volume while toxoplasmosis is hypovascular. Note that lymphoma and toxoplasmosis cannot be reliably differentiated by enhancement. Intra-axial enhancement is a measure of capillary leakage, not perfusion. Both will enhance.
Secondary CNS lymphoma
Secondary CNS lymphoma represents involvement of the CNS in a patient with known extra-cerebral lymphoma. Secondary CNS lymphoma tends to involve the meninges and may cause leptomeningeal carcinomatosis or epidural cord compression.
Less commonly, secondary CNS involvement of lymphoma may present as a parenchymal mass.
Metastatic disease to the brain
The most common primary tumors to cause parenchymal metastasis are lung, breast, and melanoma.
Most metastasis are hematogenous and arise at the gray-white junction, where there is a caliber change in the small arterioles.
Enhancement is universal, as capillaries produced by an extra-CNS primary tumor do not have a functioning blood brain barrier.
Larger metastases often feature marked edema, while small metastases may present as tiny enhancing foci apparent only on the post-contrast images.
Dural Neoplasms
Meningioma is by far the most common extra-axial tumor. It arises from meningoepithelial cells called arachnoid “cap” cells. Meningiomas typically occur in elderly adults with a female predominance and are most often asymptomatic.
The vast majority are benign, but 1-2% are anaplastic or malignant. Both benign and malignant meningiomas can metastasize, although this is uncommon.
Multiple meningiomas are seen in neurofibromatosis type 2 or following radiation therapy.
Meningiomas can occur anywhere in the neuraxis, but are most commoly supratentorial and parasagittal.
Meningiomas may also be intraventricular (in the trigone/atrium of the lateral ventricle) or intra-osseous. Intra-osseous meningioma may mimic fibrous dysplasia.
On noncontrast CT, meningiomas are usually hyperattunating relative to brain and approximately 25% calcificy.
On MRI, appearance can be variable with iso- or slightly hypointense signal on T1-weighted images and variable signal intensity on T2-weighted images. There is typically a broad-based attachment to the dura.
Meningiomas avidly enhance. An enhancing dural tail is thought to be due to vasoactive substances released by the meningioma rather than tumor spread to the dura.
Despite the extra-axial location of most meningiomas, there may be extensive white matter edema, thought to be due to vasoactive factors and a pial vascular supply. There is often a discordance between the size of meningioma and degree of white matter edema, with severe edema possible even with a very small tumor.
The most common tumors to metastasize to the dura are breast (most common), lymphoma, small cell lung cancer, and melanoma.
Posterior Fossa Masses: Differential Diagnosis
Overview and anatomy of the CPA
The cerebellopontine angle (CPA) is region between the pons and cerebellum and the posterior aspect of the petrous temporal bone. Important structures of the CPA include the 5th (trigeminal), 7th (facial), and 8th (vestibulocochlear) cranial nerves, and the anterior inferior cerebellar artery (AICA).
Most lesions of the CPA are extra-axial and lcoated in the CPA cistern itself, although some may arise in the internal adutory canal (IAC), temporal bone, or rarely intra-axially from teh pons or cerebellum. CPA masses are more common in adults.
Schwannoma
Schwannoma of the vestibulocochlear nerve, also known as a vestibular schwannoma, is by far the most common cerebellopontine angle mass, representing greater than 75% of all CPA masses.
Vestibular schwannoma is hyperintense on T2-weighted images and avidly enhances. The characteristic ice cream cone appearance describes the “cone” protruding through (and widening) the porous acoustics and the “ice cream” exerting mass effect on the cerebellar-pontine junction. Schwannoma may become cystic, especially when larger.
Schwannomas of other cranial nerves in the CPA, including the facial or trigeminal nerves, are less common. Trigeminal schwannoma may extend into Meckel’s cave.
Meningioma
Although meningioma is overall the most common extra-axial mass in adults, it is only the second most common mass of the CPA, representing approximately 10-15% of all CPA masses.
Meningiomas often feature a short segment of dural enhancement and may induce adjacent bony hyperostosis. Approximately 20% calcify, in contrast to schwannomas where calcification is rare.
In contrast to schwannoma, a CPA meningioma does not enlarge the porous acousticus.
Arachnoid cyst
An arachnoid cyst is a benign CSF-filled lesion that is usually congenital. Although most arachnoid cysts are supratentorial, the cerebellopontine angle is the most common infratentorial location.
An arachnoid cyst will follow CSF signal on all sequences, including complete suppression on FLAIR. Unlike an epidermoid cyst, an arachnoid cyst does not have restricted diffusion.
Aneurysm
Vertebrobasilar aneurysm (arising from the posterior inferior cerebellar artery, anterior inferior cerebellar artery, vertebral artery, or basilar artery) may appear as a well-defined, avidly enhancing CPA lesion and may be initially mistaken for a schwannoma or meningioma on contrast-enhanced CT.
On MRI, clues to a vascular etiology would be flow void and pulsation artifacts. MRA or CTA are diagnostic.
Epidermoid cyst
An epidermoid cyst is a congenital lesion arising from ectopic ectodermal epithelial tissue.
Epidermoids progressively enlarge from desquamation of keratinized epithelium lining the cyst. The mass characteristically insinuates in between structures, encasing cranial nerves and vessels. Gross pathology featrures a characteristic “cauliflower-like” surface.
On CT, epidermoid cyst may mimic arachnoid cyst and appear as a water-attenuation cystic structure. On MRI, an epidermoidcyst has similar signal characteristics to CSF on T1- and T2-weighted images. Unlike arachnoid cyst, an epidermoid does not usually suppress on FLAIR.
Diffusion sequences show very bright signal on diffusion-weighted images ( a combination of restricted diffusion and T2 shine through). Postsurgical DWI follow-up is critical to detect any residual focus, which will be DWI bright.
Rarely, epidermoids may exhibit signal hyperintensity on unenhanced T1-weighted imaging, also known as “white epidermoids”.
Intra-axial neoplasm
A posterior fossa intra-axial neoplasm may invade laterally into the CPA.
An exophytic brainstem glioma or metastasis may invade into the CPA.
Medulloblastoma tends to occur in the midline in children, though lateral involvement of the cerebellar hemipsheres can be seen in older children or young adults.
Ependymoma may extend into the CPA by squeezing through the lateral 4th ventricular foramina (of Luschka).
Hemangioblastoma, associated with von Hippel-Lindau (VHL) disease, typically presents in the cerebellar hemispheres as a fluid-secreting tumor with a cyst and enhancing nodule. There are often prominent flow voids feeding the tumor.
Overview and anatomy of the sella, suprasellar region, and cavernous sinus
The pituitary gland is formed from Rathke’s puch, which is superior invagination from the primitive oral cavity. The pituitary gland sits in the sella turcica, a cup-shaped depression of the basisphenoid bone. The pituitary is composed of an anterior and a posterior lobe. (Rathke’s pouch closes off to form a vesicle that involutes. Sometimes, the involution is incomplete and a cleft can be left behind, which may give rise to craniopharyngioma or Rathke’s cleft cyst.
The anterior lobe of the pituitary produces and secretes endocrine hormones, including growth hormone, ACTH, prolactin, TSH, FSH, and LH.
The posterior lobe of the pituitary is derived from neuroectoderm and is composed of axons from the hypothalums, through which vasopressin and oxytocin are transported.
The pituitray gland has a wide rage of normal morphology, depending on patient age, sex, and hormonal/pregnancy status. The gland may be convex superiorly in adolescent or pregnant females. The normal posterior pituitary is hyperintense on T1-weighted MRI and is called the “posterior pituitary bright spot”, best seen on sagittal images.
The empty sella is a normal variant when seen in isolation. An empty sella is partially filled with CSF, with the gland flattened against the floor of the sella. Empty sella is also a component of the constellation of findings in pseudotumor cerebri. Pseudotumor cerebri, also known as idiopathic inctranial hypertension, is a syndrome associated with elevated CSF pressure, visual changes, and headaches that is typically seen in obese black females. Imaging findings include empty sella, enlargement of Meckel’s cave, and optic disc protrusion into the posterior globes. The ventricles are normal in size or slightly reduced in caliber. The sigmoid or transverse sinus may be stenotic.
Approach to a sellar/parasellar mass
The first step in evaluation of a sellar region mass is to determine if the mass is intrinsic to the pituitary or if the mass represents an adjacent extra-pituitary lesion.
The differential for an intrinsic pituitary mass is rather limited and includes pituitary adenoma (by far the most common intrinsic pituitary mass), Rathke’s cleft cyst, and hypophysitis (inflammation of the pituitary). Craniopharyngioma may rarely occur in the sella, but essentially never occurs within the pituitary gland itself.
Intrinsic Pituitary Mass
A pituitary microadenoma is a pituitary adenoma <10 mm in size. Patients seek medical attention due to symptoms of hormone excess, not mass effect.
Most microadenomas are hypoenhancing relative to the pituitary, although ACTH-secreting adenomas may be hyperenhancing.
A macroadenoma is defined as an adenoma > 10 mm in size. Patients usually present with mass effect (e.g., compression of the optic chiasm) rather than endocrine dysfunction.
The bony sella is often enlarged. Macroadenomas may encase the carotid, but tend not to narrow it. In contrast, meningiomas or metastases can narrow the carotid. Pituitary macroadenoma may bleedafter medical treatment, producing a complex MRI appearance. Intrat-tumoral hemorrhage is distinct from pituitary apoplexy. Pituitary apoplexy is a clinical syndrome of severe headache and endocrine dysfunction caused by hemorrhage into an otherwise normal pituitary.
Lymphocytic hypophysitis is an autoimmune inflammatory disorder usually seen in peripartum women that may affect the pituitary and infundibulum. It presents with diabetes insipidus, headache, visualy impairment, and endocrine dysfunction.
MRI shows thickening and intense enhancement of the pituitary stalk,usually with enlargement of the pituitary gland that may appear similar to a macroadenoma.
Lymphocytic hypophysitis responds to steroid therapy.
Granulomatous inflammation of the pituitary and infundibulum can be secondary to sarcoidosis, Wegener granulomatosis, tuberculosis, and Langerhans cell histiocytosis (LCH). LCH hypophysitis is a dease of children. In all causes, imaging is dientical to lymphocytic hypohysitis.
Rathke’s cleft cyst may be limited to the pituitary gland but it is more commonly seen extrinsic to the pituitary.
Suprasellar Mass
The differntial diagnosis for an extra-pituitary lesion is broad, but the imaging findings together with clues about the patient’s age and clinical presentation can usually narrow the differential diagnosis to a few entities.
The most common suprasellar lesion in a child is craniopharyngioma, while the most common suprasellar lesion in an adult is a pituitary macroadenoma that has extended superiorly.
The SATCHMO mnemonic may be helpful to remember the spectrum of extra-pituitary masses; however, the order of the entities is NOT based on frequency of occurence. (Sarcoidosis/Suprasellar extension of an adenoma, Aneurysm, Teratoma (dermoid cyst)/Tolosa Hunt, Craniopharyngioma/Cleft cyst (Rathke’s), Hypothalamic glioma (adults)/Hypothalamic hamartoma (children), Optic nerve glioma)
Craniopharyngioma
Craniopharyngioma is themost common suprasellar lesion of childhood, arising from squamous epithelial remnants of Rathke’s pouch that produce keratin.
Craniopharyngioma occurs in a bimodal age distribution. The majority of cases are lesions of childhood, but craniopharyngioma may occur uncommonly in late middle age.
Most involve both the sella and suprasellar regions. Although craniopharyngioma may rarely involve only the sella, it is almost always separate from the pituitary gland.
Craniopharyngioma has potential for enamel production and almost always calcifies. The characteristic intracystic machine-oil seen on gross examination is composed of desquamated squamous epithelium, keratin, and cholesterol.
MRI shows a complex cystic mass containing protein or blood products (hyperintense on T1-weighted images).
There is avid enhancement of the solid elements and cyst walls.
In contrast to Rathke’s cleft cyst, craniopharyngioma almost always enhances, is almost always calcified, and is almost always separate from the pituitary.
Rathke’s cleft cyst
Similar to craniopharyngioma, Rathke’s cleft cyst is also a remnant of the embryologic Rathke’s pouch, the precursor of the anterior lobe of the pituitary gland. In contrast to craniopharyngioma, Rathke’s cleft cyst is made of simple columnar or cuboidal epithelium.
While craniopharyngioma is the most common suprasellar lesion of childhood, Rathke’s cleft cyst is typically seen in middle-aged adults, twice as commonly in females.
Rathke’s cleft cyst is reportedly very common in autopsy studes (up to 22% incidence), but clinically is usually asymptomatic or discovered incidentally.
Imaging appearance is dependent on the protein content of the cyst. The intra-cystic fluid may be isointense to CSF if low protein and hyperintense on T1-weighted images if high protein. High protein content may cause incomplete nulling of the intracystic fluid on FLAIR>
The claw sign represents enhancing pituitary tissue completely wrapped around the cyst.
It is usually possible to distinguish craniopharyngioma from Rathke’s cleft cyst. Unlike craniopharyngioma, Rathke’s cleft cyst does not enhance (although rim enhancement is often seen) and does not calcify. Rathke’s cleft cyst may occasionally be inseparable from the pituitary, but craniopharyngioma is nearly always distinct.
Meningioma (Suprasellar)
Meningioma is the second most common suprasellar tumor in adults. Most common in middle-aged females, it typically presents with visual loss due to optic pathway involvement. There are several dural reflections in the region of the sella from which a meningioma may arise, including the tuberculum sella, clinoid process, planum sphenoidale, and sphenoid wing.
Imaging shows a isointense signal on T1-weighted images, variable signal on T2-weighted images, and uniform, intense contrast enhancement. There is often an enhancing dural tail. Meningioma may cause adjacent hyperostosis due to vasoactive factors.
An important imaging finding of a parasellar meningioma is the tendency to encase and narrow the cavernous or supraclioid internal carotid artery.
In contrast to pituitary adenoma, the sella is usually normal and the pituitary can be identified separately.
Astrocytoma (optic pathway glioma)
An astrocytoma involving the visual pathway (optic nerve, optic chiasm, and optic tract) is the second most common suprasellar mass in children (craniopharyngioma is most common). A substantial minority of patients with optic pathway glioma have neurofibromatosis type 1. In contrast to the low-grade tumor of childhood, optic glioma is an aggressive tumor when it occurs in adults.
Tumors are isointense on T1-weighted images, hyperintense on T2-weighted images, and usually enhance.
Germinoma
The most common intracranial germ cell tumor is a germinoma, of which 80% arise in the pineal region and 20% arise in the parasellar region. Germinomas are primarily seen in children and adolescents.
Imaging shows a homogenous, intensely enhancing midline mass. The mass is hypointense on T2-weighted images and dark on ADC map due to hypercellularity.
Epidermoid and dermoid cysts
Epidermoid and dermoid cysts are congenital benign inclusion cysts.
Epidermoids occur most commonly in middle-aged adults in the cerebellopontine angle, but can be seen less commonly in the parasellar region. Epidermoids follow CSF signal on T1- and T2-weighted images. In contrast to a simple arachnoid cyst, epidermoid is hyperintense on FLAIR and diffusion sequences show restricted diffusion.
Dermoids are most common in young adult males in the posterior fossa, but may occasionally occur in the parasellar region. They may contain intracystic fat which can cause chemical meningitis or ventriculitis with rupture.
Hypothalamic Hamartoma
Hypothalamic hamartoma is not a true neoplasm, but represents ectopic hypothalamic neural tissue. It is a rare lesion of childhood that classically presents with precocious puberty and gleastic seizures (laughing spells)
Hypothalamic hamartoma characteristically appears as a sessile mass between the pituitary stalk and the mammillary bodies.
Hypothalamic hamartoma does not enhance and is isointese to gray matter.
Aneursym
A saccular supraclinoid internal carotid artery aneurysm may mimic a suprasellar tumor.
Although parasellar aneurysms are relatively uncommon, it is essential never to biopsy a mass that may represent an aneursym.
Pulsation artifact may be present on conventional MRI sequences. CTA or MRA would be diagnostic.
Metastasis (suprasellar) and Lymphoma
Breast cancer is by far the most common lesion to metastasize to the parasellar region.
Parasellar lymphoma is rare but may occur in older adults.
Differential Diagnosis of a suprasellar mass is highly dependent on age
Intrinsic Pineal Mass
The pineal gland is located in the midline at the level of the midbrain. It is situated between the thalami at the posterior aspect of the third ventricle. The internal cerebral veins and vein of Galen are located superior and posterior to the pineal gland, repsectively.
The principal neuronal cell of the pineal gland is the pinealocyte, which is a modified retinal neuronal cell that is innervated by the sympathetic plexus originating in the retina. The pineal gland releases melatonin, which modulates the sleep/wake cycle. The pineal gland does not have a blood brain barrier.
A mass lesion in the pineal region may cause compression of the midbrain, compression of the cerebral aqueduct of Sylvius, or compression of the tectal plate. Compression of the tectal plate produces Parinaud syndrome, which is the inability to look up (upward gaze paralysis), pupillary light dissociation, and nystagmus.
The first step in evaluating a pineal mass is to determine if the lesion is arising from the pineal gland itself or from an adjacent structure.
A mass of the pineal gland is extra-axial.
Tumors of pineal cell origin tend to lift the internal cerebral veins, while tentorial meningiomas tend to depress the internal cerebral veins. The relationship of any pineal region mass to the internal cerebral veins is key for surgical planning and approach.
Germ cell tumor
Extragonadal germ cell tumors can be found in the pineal gland as well as other intracranial and extracranial midline locations including the suprasellar region, mediastinum, and sacrococcygeal region. Extragonadal germ cell tumors are thought to be due to aberrant migration of totipotent germ cells during early embryogenesis.
Germinoma and teratoma are germ cell tumors, which are the most common and second most commmon pineal region tumors, respectively.
Germinoma (extra-gonadal seminoma) is the most commonn pineal region tumor and has a peak incidence in the second decade of life (age 10-19). Pineal germinoma is seen much more commonly in males, but suprasellar germinoa does not show a gender predilection. Germinoma is a highly cellular, avidly enhancing tumor that is slightly hyperdense on CT, isointense on T1- and T2-weighted images, and is dark on ADC map.
Germinoma characteristically “engulfs” the pineal gland and promotes its calcification, resulting in a central area of calcification.
Imaging of the entire neuraxis is recommended as leptomeningeal deposits can occur.
Treatment is readiotherapy, with excellent prognosis.
Pineal germinoma may present with a synchronous suprasellar germ cell tumor.
Teratoma is the second most common pineal region tumor and confers a worse prognosis than germinoma. Teratoma has a heterogenous imaging appearance. Intralesional fat is suggestive of teratoma. Teratoma is prone to hemorrhage and coarse calcification.
Pineal cyst
Pineal cysts are seen commonly on MRI and have a prevalence as high as 40% on autopsy series. They are more common in women. Most pineal cysts are less than 1 cm and asymptomatic, but may cause symptoms due to mass effect.
Very few pineal cysts grow and follow-up of small pineal cysts is not routinely recommended.
Pineal cysts are usually not entirely simple. Most cysts do not fully suppress on FLAIR. Most cysts do display some peripheral enhancement, and rim calcification can be seen about 25%of the time.
A differential consideration is a pineocytoma, which would demonstrate internal enhancement and may have cystic components. However, a truly cystic pineocytoma is considered very rare. A potential pitfall is that if imaging is delayed after contrast administration (by greater than 60 minutes), gadolinium may diffuse into the cyst, causing it to appear solid. In rare cases, it may not be possible to differentiate a hemorrhagic pineal cyst from a pineocytoma.
Pineocytoma
A pineocytoma is a low-grade (WHO grade I or II), slow-growing pinealocyte tumor.
Any solid component should enhance. Pineocytoma may feature cystic change, however, which can make differentiation from a pineal cyst difficult.
Pineoblastoma
Pineoblastoma is a highly malignant WHO grade IV tumor of young children, of the same primitive neuroectodermal tumor (PNET) type as medulloblastoma.
The term trilateral retinoblastoma is used when bilateral retinoblastomas are also present (both the retina and pineal gland are light-sensing organs). The sella is additionally involved in quadrilateral retinoblastoma.
Pineoblastoma often presents with obstructive hydrocephalus. Pineoblastoma characteristically appears as a poorly defined pineal mass that may invade into adjacent structures. High cellularity causes restricted diffusion.
In contrast to germinoma, which “engulfs” and induces calcification of the pineal gland, pineoblastoma peripherally calcifies in a pattern that has been likened to “exploded” calcification.
Pineoblastoma has a propensity for leptomeningeal metastasis and CSF seeding.
Pineal Metastases
Due to the lackof a blood brain barrier, metastasis to the pineal gland occur relatively commonly, but rarely in the absence of a known malignancy.
Leptomeningeal disease is present in two-thirds of patients with pineal metastasis.
Pineal region mass
Gliomas (most commonly astrocytomas) of varying grademay occur in adjacent intra-axial structure such as the tectum, midbrain, or splenium of the corpus callosum.
Despite the name, a vein of Galen “aneurysm” is not a true aneurysm. Instead, it represents dilation of the vein of Galen due to an arteriovenous fistula between the anterior or posterior circulationand the venous plexus leading to the vein of Galen.
The tentorial apex, adjacent to the pineal gland, is a characteristic location for meningioma.
As previously discussed, a tentorial meningioma tends to depress the internal cerebral veins, in contrast to a pineal-based mass, which typically elevates the internal cerebral veins.
A lipoma of the quadrigeminal plate is a rare lesion that can be seen in isolation or associated with agenesis or hypoplasia of the corpus callosum.
The quadrigeminal plate is another name for the tectum.
Extra-axial Hemorrhage
Acute extra-axial hemorrhage (subarachnoid, epidural, or subdural in location) is usually hyperattenuating when imaged by CT; however, blood must clot in order to be hyperattenuating. Hyperacute unclotted blood (and clotted blood in a patient with severe anemia) may be close towater attenuation on CT.
Subarachnoid hemorrhage (SAH)
Trauma is the most common cause of subarachnoid hemorrhage (SAH), while aneurysm rupture is the most common cause of non-traumatic SAH.
Traumatic SAH tends to occur contralateral to the side of direct impact, most often in the superficial cerebral sulci.
Epidural Hematoma
An arterial epidural hematoma is an extra-axial collection of blood external to the dura, classically caused by fracture of the squamous portion of the temporal bone and resultant tearing of the middle meningeal artery.
An arterial epidural hematoma has a lentiform shape and does not cross the cranial sutures, where the dura is tightly adherent to the cranium.
The swirl sign describes mixed high and low attenuation blood within the hematoma and suggests active bleeding. The low attenuation bloodis hyperacute unclotted blood while the high attenuation blood is already clotted.
A large epidural hematoma is a surgical emergency due to mass effect and risk of herniation, although small epidural hematomas can be conservatively managed with serial imaging.
Venous epidural hematomas are far less common than arterial epidurals and are due to laceration of the dural sinuses, usually occurring in the posterior fossa in children.
Subdural Hematoma
A subdural hematoma is a crescenteric extra-axial collection of blood located beneath the dura. Since it is underneath the dura, the hematoma can extend across the cranial sutures. Subdural hematomas often extend along the surfaces of the falx cerebri and tentorium cerebelli.
Subdural hematomas typically result from tearing of cerebral veins. Patients with atrophic involutional changes are at increased risk of subdural hematoma with even minor trauma, as the cerebral veins stretch to traverse the enlargd CSF spaces.
A particular danger is a subdural hematoma in a patient with a ventricular shunt because the shunted ventricular system does not function as a natural tamponade.
An isodense subdural hematoma is isoattenuating to gray matter. This occurs in the subacute phase approximately 1-3 weeks after the initial injury. Three important clues alerting to the presence of an isodense subdural are increased mass effect, white matter buckling, and an apparently thickened cortex.
Intraventricular hemorrhage
Intraventricular hemorrhage can occur due to tearing of the subependymal veins or from direct extension of subarachnoid or intraparenchymal hematoma.
Patients with intraventricular hemorrhage are at increased risk of developing noncommunicating hydrocephalus due to ependymal scarring, which may obstruct the cerebral aqueduct.
Intra-axial injury
The coup/contrecoup mechanism of brain trauma describes the propensity for brain to be injured both at the initial site of impact and 180° opposite the impact site, due to secondary impaction against the cranial vault.
Cortical contusion
A cortical contusion is caused by traumatic contact of the cortical surface of the brain against the rough inner table of the skull. Contusions affect the gyral crests and can occur in a coup or a contrecoup location.
A subacute cortical contusion may demonstrate ring enhancement and should be considered in the differential of a ring enhancing lesion if there is a history of trauma. Enhancement may continue into the chronic stage.
A chronic contusion appears as ecephalomalacia on CT. MRI is more specific, showing peripheral hemosiderin deposition as hypointense on T2-weighted images and blooming artifact on gradient echo sequences.
Intraperanchymal hematoma
Traumatic intraparenchymal hematoma can occur in various locatios, ranging from cortical contusion to basal ganlgia hemorrhage (due to shearing of lenticulostriate vessels).
Similar to a cortical contusion, a subacute intraparenchymal hematoma may show ring enhancement.
Diffuse axonal injury (DAI)/ Traumatic axonal injury (TAI)
Diffuse axonal injury (DAI) is the result of a shear-strain deformation of the brain.
The term traumatic axonal injury (TAI) has recently been introduced as this injury pattern is thought to be multifocal rather than diffuse; however, this text will use the term DAI, as that is the more common term.
DAI is caused by rotational deceleratin and subsequent reacceleration force that exceeds the limited elastic capacity of the axons.
The most common locations of DAI include the gray-white matter junction,the corpus callosum, and the dorsolateral midbrain. The higher the grade, the worse the prognosis. Grade I DAI involves only the gray-white matter junctions. Grade II DAI involves the corpus callosum. Grade III (most severe) DAI involves the dorsolateral midbrain.
CT is relatively insensitive for detection of DAI, although hemorrhagic DAI may show tiny foci of high attenuation in the affected regions.
MRI is much more sensitive to detect DAI, although detection relies on multiple sequences, including FLAIR, GRE, and DWI
GRE is extremely sensitive for hemorrhagic axonal injry; however, not all DAI is hemorrhagic. FLAIR is most sensitive for nonenhacing DAI. Diffusion sequences show restricted diffusion in acute DAI due to cytotoxic edema and cell swelling.
Zygomaticomaxillary complex fractures
Commonly but incorrectly know as the tripod fracture, a zygomaticomaxillary complex (ZMC) fracture causes a floating zygoma by disrupting all four of the zygomatic articulations.
The zygoma normally articulates with the frontal, maxillary, temporal, and sphenoid bones via the zygomaticofrontal, zygomaticomaxillary, zygomaticotemporal, and zygomaticosphenoid articulations.
A ZMC fracture causes disruption of the zygomatic articulations by fractures through the follow structures:
Lateral orbital rim fracture: Zygomaticofrontal disruption
Inferior orbital rim fracture: Zygomaticomaxillary disruption.
Zygomatic arch fracture: Zygomaticotemporal disruption.
Lateral orbital wall: Zygomaticosphenoid disruption.
Le Fort Fractures
The Le Fort classification describes a predictable pattern of midface fractures, all of which disrupt the pterygomaxillary buttress and cause detachment of the maxilla from the skull base. All Le Fort fractures are defined by fractures though the pterygoid plates.
Le Fort I (floating plate) detaches the maxillary alveolus from the skull base.
Le Fort II dissociates the central midface from the skull, causing the nose and hard palate to be moved as a single unit.
Le Fort III represents a complete midface dissocation.
Central sulcus
The central sulcus separates the motor strip (frontal lobe) from the sensory cortex (parietal lobe).
To find the central sulcus, follow the cingulate sulcus posteriorly on a slightly off-midline sagittal (left images above). The cingulate sulcus connects to the marginal ramus. Directly anterior to the marginal ramus is the paracentral lobule, which contains both the motor strip and the sensory cortex.
On an axial image, the central sulcus forms a characteristic upside down omega. The corresponding region of motor strip, just anterior to the omega, controls the hand.
Internal Carotid Artery
Cervical (C1): Doe not branch within the neck
Petrous (C2): Fixed to bone as the ICA enters the skull base, so a cervical carotid dissection is unlikely to extend intracranially.
Lacerum (C3): No branches.
Cavernous (C4): The meningohypophyseal trunk arises from the cavernous carotid to supply the pituitary, tentorium, and dura of the clivus. The inferolateral trunk also arises from C4 to supply the 3rd, 4th, and 6th cranial nerves, as well as the trigeminal ganglion.
Clinoid segment (C5): The carotid rings are two dural rings that mark the proximal and distal portions of the clinoid segment of the ICA. The carotid rings prevent an inferiorly located aneurysm from causing intracranial subarachnoid hemorrhage with rupture.
Supraclinoid (C6-C7): Gives off several key arteries:
The opthalmic artery supplies the optic nerve. It takes off just distal to the distal carotid ring in 90% of cases and can be used as a landmark for the distal ring. Aneursyms located superior to this ring can result in subarachnoid hemorrhage. Given this risk, these aneursyms are treated more aggressively than aneurysms located proximal to the distal dural ring, which are contained.
The posterior communicating artery (P-comm) is an anastomosis to the posterior circulation. A fetal posterior cerebral artery (PCA) is a variant supplied entirely by the ipsilateral ICA via an enlarged P-comm.
The anterior choroidal artery supplies several critical structures, despite its small size. It supplies the optic chiasm, hippocampus, and posterior limb of the internal capsule.
Circle of Willis
The A1 segment of the anterior cerebral artery (ACA) travels above the optic nerves and give off the recurrent artery of Huebner, which supplies the caudate head and anterior limb of the internal capsule. The A1 segment also gives rise to the medial lenticulostriate perforater vessels, which supply the medial basal ganglia.
Just outside the circle of Willis, the middle cerebral artery (MCA) gives rise to the lateral lenticulostriate perforator vessels to supply the lateral basal ganglia include the lateral putamen, external capsule, and the posterior limb of the internal capsule.
The posterior communicating artery (P-comm) travels between the optic tract and the 3rd cranial nerve, giving off anterior thalamoperforator vessels. A P-comm aneurysm may cause cranial nerve III palsy due to local mass effect.
The posterior cerebral artery (PCA) gives off thalamoperforators to supply the thalamus. Artery of Percheron is a variant where there is a dominant thalamic perforator supplying the ventromedial thalami bilaterally and the rostral midbrain, arising from a P1 PCA segment. An artery of Percheron infarct will result in bilateral ventromedial thalamic infarction, with or without midbrain infarction (the infarct may be V shaped if the midbrain is involved). Deep venous thrombosis may also result in bilateral thalamic infarcts.
The anterior choroidal artery is the most distal branch of the internal carotid artery. It supplies the optic chiasm, hippocampus, and posterior limb of the internal capsule.
Middle cerebral artery (MCA)
Although the transition form M1 to M2 is technically defined as the upward point of deflection into the sylvian fissure, in practical terms, the pre-bifurcation MCA is often called M1 and the post-bifurcation MCA is called M2.
Anterior Cerebral Artery (ACA)
The recurrent artery of Huebner arises most commonly from the A1 segment of the ACA, proximal to the anterior communicating artery. The recurrent artery of Heubner supplies the head of the caudate and the anterior limb of the internal capsule.
Persistent Carotid-Basilar Connections
A number of carotid to basilar connections are formed during embyrogenesis. These fetal anterior-posterior circulation connections normally regress before birth.
Occasionally, a fetal carotid-basilar connection may persist after birth. Each anomalous connection is named for the structures adjacent to its course in the head and neck.
A persistent trigeminal artery is the most common persistent carotid-basilar connection and has an association with aneurysms.
The persistent trigeminal artery courses adjacent to the trigeminal nerve. Angiography shows a charcteristic trident or tau sign on the laterla view due to the artery’s branching structure.
Saltzman type I connects to the basilar artery while Saltzman type II connects to the superior cerebellar artery.
The otic, hypoglossal, and proatlantal intersegmental arteries are rare persistent carotid-basilar connections.
Arterial Territories
Stroke Imaging and guidelines
The goal of stroke imaign is to determine who would benefit from therapy.
The goal of stroke therapy is to restore perfusion to the brain.
In the appropriate patients, intravenous or intra-arterial thrombolysis performed with tissue plasminogen activator (tPA) can have near-miraculous results. However, there is a grave risk of fatal hemorrhage if patients are inappropriately selected for therapy. The exact exclusion criteria for administration of thrombolytic therapy varies among institutions.
The American Heart Association (AHA) published guidelines for early management of adults with ischemic stroke (Stroke, 2007) and established recommendations for imaging and treatment of acute stroke.
Imaging of the brain is recommended before thrombolytic therapy is administered and the imaging study should be interpreted by a physician with expertise in reading brain studies. Initial imaging in suspected acute stroke is usually noncontrast CT, for the primary purpose of excluding hemorrhage. However, some authors assert that MRI is equally sensitive for detecting hemorrhage using GRE sequences.
Advanced imaging (with CT or MR) includes vascular imaging, diffuse-weighted imaging, and perfusion imaging. These advanced imaging studies may provide additional information, but are not required before the initiation of thrombolytic therapy. In fact, advanced imaging should not delay treatment.
Per AHA guidelines, the only CT finding that absolutely precludes intravenous tPA within 3 hours of onset of stroke is the presence of hemorrhage. Some authors advocate for extending the window for tPA administration to 4.5 hours from stroke onset, although this expanded window is not discussed in the AHA guidelines.
Intra-arterial thrombolysis may be performed for an MCA thrombus within 6 hours of stroke onset in patients who are not candidates for intravenous thrombolysis. Subsequent to the development of the AHA guidelines, some authors recommend extending the window for intra-arterial treatment of anterior circulation stroke to 8 hours. Similarly, many authors argue for no time limit for intraarterial tPA for posterior circulation infarction because these strokes can be catastrophic if untreated.
Some institutions add additional exclusion criteria for administration of intravenous tPA, although these additional criteria are not a part of the AHA guidelines:
Individuals with a large (greater than 1/3 MCA territory) infarct may be excuded from IV tPA.
Occlusion of the distal internal carotid artery and proximal MCA and ACA (a T-shaped occlusion) may preclude treatment with IV tPA.
Absence of a penumbra of salvageable brain that represents at least 20% of the region of abnormal perfusion may preclude treatment with IV tPA.
Perfusion stroke imaging
The role of perfusion CT or MRI in the management of acute stroke is evolving and remains controversial. The theoretical goal of perfusion imaging is to characterize the ischemic penumbra, which is the area of vulnerable brain adjacent to the infarct core that may also become infarcted without intervention. Currently, no clinical guidelines exist regarding the implementation of perfusion imaging.
The penumbra does receive some perfusion, but at a reduced rate compared to normal brain. Perfusion of the penumbra is < 20 mL/100 g tissue per minute in physiologic studies, compared to ~60 mL/100 g tissue per minute for normal gray matter. Such a low rate of perfusion causes cellular dysfunction and produces a neurologic defict, which may be restored with therapy.
The infarct core is usually dead tissue, which genrally cannot recover even after therapy.
Acute stroke: Noncontrast CT imaging
Noncontrast CT is the initial test of choice for evaluation of hyperacute infarct when the patient presents within the IV tPA time window (3 hours, or 4.5 hours at some institutions).
The main purpose of a noncontrast CT is to exclude patients who would be harmed by thrombolytic therapy as discussed above, most importantly to exclude those with hemorrhage.
Noncontrast CT in the hyperacute stage is relativley insensitive to detect early infarction compared to MRI. Sublte loss of gray-white differentiation in the insula or basal ganglia may be present on CT, thought to be due to decreased cerebral blood volume.
The insular ribbon sign describes the loss of gray-white differentiation in the insula. The gray-white junction becomes most conspicuous at very narrow stroke windows (window 30/level 30)
Obscuration of the lentiform nucleus (putamen and globus pallidus) is caused by loss of gray-white differentiation at the border of the lentiform nucleus and the posterior limb of the internal capsule.
The hyperdense artery sign describes direct visualization of the acute intravascular thrombus, most commonly seen in the MCA. The hyperdense artery sign is specific for ischemia when seen, but relatively insensitive (seen in approximately one third of cases). Some authors suggest that the prsence of the hyperdense artery sign portends a worse prognosis.
Acute stroke: MR Imaging
Detailed MRI imaging of the multiple temporal stages of stroke is discussed on the following pages. For the initial evaluation, diffusion sequences can detect acute infarction with high sensitivity within minutes of symptom onset. DWI is more sensitive than FLAIR in the detection of hyperacute stroke.
Evolution of Infarction
Hyperacute infarct (0-6 hours)
- Within minutes of critical ischemia, the sodium-potassium ATPase pump that maintains the normal low intracellular sodium concentration fails. Sodium and water diffuse into cells, laeding to cell swelling and cytotoxic edema.
- Calcium also diffuses into cells, which triggers cascades that contribue to cell lysis.
- By far the most sensitive imaging modality for detection of hyperacute infarct is MRI diffusion-weighted imaging (DWI). DWI hyperintensity and ADC map hypointensity reflect reduced diffusivity, which can be seen within minutes of the ictus.
- Diffusion is reduced in an acute infarct by two factors:
- 1) Shift from extracellular to intracellular water due to Na/K ATPase pump failure.
- 2) Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein.
- FLAIR may be normal. Subtle hyperintensity may be seen on FLAIR images in the hyperacute stage. These changes are seen less than two thirds of the time within the first six hours.
- Perfusion shows decreased cerebral blood volume of the infarct core, with or without a surrounding region of decreased cerebral blood flow, which represents the penumbra.
Acute infarct (6 hours - 72 hours)
- The acute infarct phase is characterized by increase in vasogenic edema and mass effect.
- Damaged vascular endothelial cells cause leakage of extracellular fluid and increase the risk of hemorrhage.
- On imaging, there is increased sulcal effacement and mass effect. The mass effect peaks at 3-4 days, which is an overlap time between the acute and early subacute phases.
- MRI shows hyperintenisty of the infarct coreon T2-weighted images, best seen on FLAIR. The FLAIR abnormality is usually confined to the gray matter. DWI continues to show restricted diffusion.
- There may be some arterial enhancement, due to increased collateral flow.
- Perfusion images most commonly show increase in size of the infarct core with resultant decrease in size of the penumbra.
Early subacute infarct (1.5 days - 5 days)
- In the early subacute phase, blood flow to the affected brain is re-established by leptomeningeal collaterals and ingrowth of new vessels into the region of infarction.
- The new vessels have an incomplete blood brain barrier, causing a continued increase in vasogenic edema and mass effect, which peaks at 3-4 days.
- MR imaging shows marked hyperintensity on T2-weighted images involving both gray and white matter (in contrast to the acute stage, which usually involves just the gray matter).
- The ADC map becomes less dark or even resolves if there is extensive edema; however, the DWI images typically remain bright due to underlying T2 shine through.
- Perfusion imaging shows continued expansion of the infarct core and further reduction in the ischemic penumbra.
Late subacute infarct (5 days - 2 weeks)
- The subacute phase is characterized by resolution of vasogenic edema and reduction in mass effect.
- A key imaging finding is gyriform enhancement, which may occasionally be confused for a neoplasm. Unlike a tumor, however, a subacute infarction will not typically demonstrate both mass effect and enhancement simultaneously. Enhancement can be seen from approximately 6 days to 6 weeks after the initial infarct. (The enhancement of a subacute infarct has also been described by the “2-2-2” rule, which states the enhancement begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
- DWI may remain bright due to T2 shine through, although the ADC map will either return to normal or show increased diffusivity.
Chronic Infarct
- In the chronic stage of infarction, cellular debris and dead brain tissue are removed by macrophages and replaced by cystic encephalomalacia and gliosis.
- Infarct involvement of the corticospinal tract may cause mass effect, mild hyperintensity on T2-weighted images, and eventual atrophy of the ipsilateral cerebral peduncle and ventral pons due to Wallerian degeneration. These changes can first be seen int eh subacute phase, with atrophy being the predominant feature in the chronic stage.
- DWI has usually returned to normal in the chronic stage.
- Occasionally cortical laminar necrosis is a histologic finding characterized by deposition of lipid-laden macrophages after ischemia that manifests on imaging as hyperintensity on both T1- and T2-weighted images.
Arteriovenous Malformation (AVM)
An arteriovenous malformation (AVM) is a congenital high-flow vascular malformation consisting of directly connecting arteris and veins without an intervening capillary bed. AVM occurs intra-axiallyand 85% are supratentorial. AVM usually presents with seizures or bleeding (usually parenchymal hemorrhage, rarely subarachnoid). Aneurysms of the feeding arteries or intra-nidal arteries are often seen, which predispose to bleeding.
The Spetzler-Martin scale helps to evaluate surgical risk for AVM resection. A large AVM draining to a deep vein in eloquent cortex is high risk, while a small AVM draining to a superficial vein in non eloquent cortex is low risk.
On imaging, AVM is characterized by a vascular nidues (“nest”) containing numerous serpentine vessels that appear as black flow-voids on MRI. There are usually adjacent changes to the adjacent brain including gliosis (T2 prolongation), dystrophic calcification, and blood products (blooming on T2* gradient imaging). The gliosis/encephalomalacia or mineralization seen in the adjacent brain is due to alteration in vascular flow from the AVM.
AVM replaces rather than displaces brain. It causes minimal mass effect.
Uncommonly, a bleeding AVM may be angiographically occult if the malformed vessels are compressed by the acute hematoma.
Factors that increase bleeding risk that are detectable by imaging include intra-nidal aneurysm, venous ectasia, venous stenosis, deep venous drainage, and posterior fossa location.
Treatment can be with embolization, stererotactic radiation, or surgical resection.
Vein of Galen malformation is a type of vascular malformation characterized by arteriovenous fistulae from the thalamoperforator branches into the deep venous system. The enlarged vein is actually an enlarged median prosencephalic vein. In childhood, a vein of Galen malformation is the most common extracardiac cause of high output cardiac failure. Vein of Galen malformation may also be seen in adults, but clinically would be either asymptomatic or may be the cause of Parinaud syndrome due to mass effect in the pineal region.
Dural arteriovenous fistula (dAVF)
Dural arteriovenous fistulas are a complex group of high-flow lesions characterized by arteriovenous shunts between the meningeal arterioles and dural venules.
The primary prognostic feature is the presence and degree of cortical venous drainage. The Cognard classification I through IV describes lesions with progressively increased risk of bleeding. Type V is reserved for spinal dAVFs.
Type I: No cortical venous drainage. Lowest risk of bleeding.
Type IIA: Reflux into dural sinus but not cortical veins.
Type IIB: Refulx into cortical veins: 10-20% hemorrhage rate.
Type III: Direct cortical venous drainage: 40% hemorrhage rate.
Type IV: Direct cortical venous drainage with venous ectasia: 66% hemorrhage rate.
Type V: Spinal venous drainage. May cause myelopathy.
Carotid-cavernous fistual (CCF) is a subtype of dAVF that is often caused by trauma with resultant fistual between the 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 cranial nerve palsy.
Cavernous Malformation (cavernoma)
A cavernous malformation (also called a cavernoma) is a vascular hamartoma with a very small but definite bleeding risk. The clinical course of a cavernous malformation is variable and the lesion may cause seizures even in the absence of significant hemorrhage.
Cavernous malformation is often associated with an adjacent developmental venous anomaly (DVA). There is increased risk of bleeding if a DVA is present. However, the DVA itself does not have any bleeding risk.
When multiple, cavernous malformations represent an inerited disorder called familial cavernomatosis.
Cavernous malformations can be induced by radiation treatment to the brain.
Noncontrast CT shows a well-circumscribed rounded hyperattenuating lesion. The hyperattenuation is due to microcalcification within the cavernoma.
MRI shows characteristic “popcorn-like” appearance of lobular mixed signal on T1- and T2-weighted images from blood products of various ages. There is a peripheral rim of hemosiderin which is dark on GRE and T2-weighted image. There is typically no enhancement, but intense enhancement may be seen with a long delay after contrast administration. Cavernous malformations may range in size from tiny (single focus of susceptibility artifact) to giant.
Cavernous malformations are usually occult by vascular imaging (CTA or angiography).
Developmental venous anomaly (DVA), also called venous angioma
A developmental venous anomaly (DVA) is an abnormal vein that provides functional venous drainage to normal brain.
DVA can usually only be seen on contrast-enhanced images, where it appears as a radially oriented vein with a characteristic caput medusa appearance.
A DVA is a Do Not Touch lesion. If resected, the patient will suffer a debilitating venous infarct. The DVA must be preserved if an adjacent cavernous malformation is resected.
Capillary telangiectasia
A capillary telangiectasia is an asymptomatic vascular lesion composed of dilated capillaries with interspersed normal brain. A capillary telangiectasia is another Do Not Touch lesion.
Post-contrast MRI shows a faint, brush-stroke-like enhancing lesion in the brainstem or pons, without mass effect or surrounding edema. GRE may show blooming due to susceptibility.
Similar to cavernous malformation, capillary telangiectasia is angiographically occult.
Subarachnoid Hemorrhage (SAH)
Overall, the most common cause of subarachnoid hemorrhage (SAH) is trauma. Aneurysm rupture is by far the most common cause of non-traumatic subarachnoid hemorrhage. No cause of the subarachnoid hemorrhage is identified in up to 22% of cases.
Clinically, non-traumatic subarachnoid hemorrhage presents with thunderclap headache and meningismus.
Noncontrast CT is the initial imaging modality in suspected subarachnoid hemorrhage. On CT, subarachnoid blood appears as high attenuation within the subarachnoid space. High attenuation material in the subarachnoid space may be due to SAH (by far the most common cause), meningitis, leptomeningeal carcinomatosis, or prior intrathecal contrast administration.
Noncontrast CT is >95% sensitive for detecting subarachnoid hemorrhage within the first six hours, with sensitivity slowly decreasing to 50% by day 5. If clinical suspicion for subarachnoid hemorrhage is high with a negative CT scan, the standard of care is to perform a lumbar puncture to look for xanthochromia.
If SAH is present on imaging or lumbar puncture shows xanthochromia, catheter angiography is the gold standard to evaluate for the presence of an aneurysm. Several recent studies have shown, however, that CT angiography is equivalent to catheter angiography inthe search for a culprit aneurysm in cases of SAH.
On MRI, acute subarachnoid hemorrhage appears hyperintense on FLAIR and demonstrates susceptibility artifact on gradient sequences. The differential diagnosis for increased FLAIR signal in the subarachnoid space is similar to the differential for high attenuation subarachnoid material seen on CT, including SAH, meningitis, leptomeningeal carcinomatosis, and residual contrast material. Note that meningitis and carcinomatosis will typically show leptomeningeal enhancement in addition to the abnormal FLAIR signal. Recent oxygen or propofol administration will also cause increased subarachnoid FLAIR signal.
Distribution of Subarachnoid hemorrhage
The pattern of subarachnoid hemorrhage may provide a clue to the location of the ruptured aneurysm. However, multiple aneurysms are seen in up to 20% of patients with SAH, and subarachnoid blood may redistribute if the patient was found down.
Hemorrhage in the anterior interhemispheric fissure suggests an anterior communicating artery aneurysm (33% of intracranial aneurysms).
Hemorrhage in the suprasellar cistern suggests a posterior communicating artery aneurysm (also 33% of intracranial aneurysms). Rarely, P-comm aneurysm rupture can result in isolated subdural hemorrhage.
Hemorrhage in the sylvian fissure suggests a middle cerebral artery aneurysm (20% of intracranial aneurysms).
Hemorrhage in the perimesencephalic cistern suggests either a basilar tip aneurysm (5% of intracranial aneurysms), which has a high morbidity, or the relatively benign nonaneurysmal perimesencephalic subarachnoid hemorrhage (subsequently discussed).
Grading of subarachnoid hemorrhage
The Hunt and Hess score is the clincal grading scale for aneursymal subarachnoid hemorrhage and is based soley on symptoms, without imaging. Grade I is the lowest grade, with only a mild headache. Grade V is the most severe, with coma or extensor posturing.
The Fisher grade calssifies the CT appearance of SAH. Grade 1 is negative on CT; grades 2 and 3 are < 1 mm thick and > 1 mm thick, respectively, and grade 4 is diffuse SAH or intraventricular or parenchymal extension.
Complications of subarachnoid hemorrhage
Vasospasm is the most common cause of morbidity and mortality in patients who survive the intial episode of subarachnoid hemorrhage. The peak incidence of vasospasm occurs approximately 7 days after the initial ictus. Vasospasm may lead to stroke or hemorrhage.
Approximately 20-30% of patients with subarachnoid hemorrhage will develop acute hydrocephalus, due to obstruction of arachnoid granulations. Treatment is ventriculostomy.
Superficial siderosis is a condition caused by iron overload of pial membranes due to chronic or repeated subarachnoid bleeding. Clinically, patients with superficial hypointensity on T2-weighted images outlining the affected sulci.
Imaging workup includes cranial and spinal imaging to evaluate for a source of bleeding.
Perimesencephalic subarachnoid hemorrhage
Perimesencephalic subarachnoid hemorrhage is a type of nonaneurysmal subarachnoid hemorrhage that is a diagnosis of exclusion with a much better prognosis than hemorrhage due to a ruptured aneurysm.
The hemorrhage must be limited to the cisterns directly anterior to the midbrain. The standard of care is to perform catheter angiography twice, one week apart. Both angiograms must be negative. Although the cause of the hemorrhage is unknown, it is thought to represent angiographically occult venous bleeding.
Although the clinical presentation of perimesencephalic subarachnoid hemorrhage is similar to aneursymal SAH (thunderclap headache), patients generally do well without residual neurological deficit. Some patients may experience mild to moderate vasospasm.
Reversible cerebral vasoconstruction syndrome (RCVS)
Reversible cerebral vasoconstriction syndrom (RCVS) is a cause of nontraumatic, nonaneurysmal subarachnoid hemorrhage and ischemia. RCVS presents with thunderclap headache and is characterized by prolonged (but reversible) vasoconstriction.
Saccular aneurysm
A saccular (also called berry) aneurysm is a focal outpouching of the arterial wall, most commonly arising at a branch point in the cricle of Willis. The aneurysm points in the direction of blood flow leading into the branch point. Saccular aneurysms are seen almost exclusively in adults, with a slight female predominance. Saccular aneursyms are caused by a combination of hemodynamic stress and acquired degeneration of the vessel wall.
Non-inherited risk factors for the development of saccular aneurysm include hypertension and inflammatory vascular disease such as Takayasu or giant cell arteritis.
Inherited diseases that predispose to anurysm formation include connective tissue diseases such as Marfan and Ehlers-Danlos, polycystic kidney disease, and neurofibromatosis type I.
The aneurysm neck is the opening that connects the aneurysm to the parent vessel and the anuerysm body is the aneurysm sac. The neck:body ratio affects treatment options. Aneurysms with relatively small necks are generally easier to treat endovascularly with coils.
Saccular aneurysms can be classified as small (<1 cm), medium (>1 cm and <2.5 cm), and giant (>2.5 cm). The larger the size, the greater the risk for rupture. Giant aneurysms often present with mass effect, causing cranial nerve palsy.
Fusiform Aneurysm
A fusiform aneurysm is segmental arterial dilation without a defined neck. Fusiform aneurysms are usually due to atherosclerosis, but may arise from chronic dissection.
In contrast to saccular aneurysms, fusiform aneurysms are more difficult to treat. Fusiform aneurysms of the vertebrobasilar system pose particular challenges, as critical perforating vessels may arise directly from the diseased artery.
Mycotic (infectious) aneurysm
Mycotic aneurysms account for only 2-4% of all intracranial aneurysms and are due to septic emboli. Bacterial endocarditis is the most common embolic source.
In contrast to saccular aneurysms, mycotic aneurysms form in the distal areterial circulation, beyond the circle of Willis. Mycotic aneurysms are fragile and have a high risk of rupture.
Oncotic aneurysm
An oncotic aneurysm is an aneurysm is an aneurysm caused by neoplasm.
A benign left atrial myscoma may peripherally embolize and cause a distal oncotic aneurysm.
Traumatic pseudoaneurysm
Aneurysms due to trauma are most commonly pseudoaneurysms, which don’t contain the typical three histologic layers of the vessel wall. Usually the vessel will exhibit abnormal luminal narrowing proximal to the aneurysm. Similar to mycotic aneurysms, traumatic pseudoaneurysms tend to occur distally.
Arteries close to bony structures (such as the basilar and vertebral artery) are prone to dissecting aneurysms.
Venous anatomy
Dural sinuses
The superior sagittal sinus (and its tributaries) drains the motor and sensory strips.
The paired transverse sinuses are usually asymmetric, with the left transverse sinus often hypoplastic.
The sigmoid sinus connects to the jugular bulb.
The torcular Herophili is the confluence of the superior sagittal sinus, the transverse sinus, and the straight sinus. The word torcular is from the Greek word for wine press, and Herophilus was a Greek anatomist. Technically, the term torcular Herophili refers to the depression on the inner table of the skull produced by the confluence of sinuses, but in general use, torcular Herophili refers to the actual confluence of sinuses.
Deep cerebral veins
The deep cerebral veins consist of the paired internal cerebral veins, the basal vein of Rosenthal, and the vein of Galen.
The venous angle (red dot in the diagram above) is the intersection of the septal vein and the thalamostriate veins. The venous angle is the angiographic landmark for the foramen of Monro.
Superficial cerebral veins
The vein of Trolard connects superficial cortical veins to the superior sagittal sinus.
The vein of Labbe drains the temporal convexity into the transverse or sigmoid sinus. Retraction injury to the vein of Labbe during surgery may lead to venous infarction and aphasia.
Venous thrombosis
Thrombosis of a cortical vein or a deep venous sinus is one of the more common causes of stroke in younger patients. Risk factors for venous thrombosis include pregnancy, oral contraceptives, thrombophilia, malignancy, and infection.
A clue to the diagnosis of venous thrombosis on noncontrast CT is increased density eithin the thrombosed sinus or cortical vein (the cord sign). On contrast-enhanced CT, the empty delta sign signifies a filling defect in the superior sagittal sinus.
MR venogram will show how lack of flow in the thrombosed vein or dural venous sinus.
Venous throbosis leads to venous hypertension, which may cause infarction and parenchymal hemorrhage. There are three characteristic patterns of venous infarction, dependent on the location of the thrombosed vein: Superior sagittal sinus thrombosis -> infarction of the parasagittal high convexity cortex. Deep venous system thrombosis -> infarction of the bilateral thalami. Transverse sinus thrombosis -> infarction of the posterior temporal lobe.
CT imaging of intraparenchymal hemorrhage
Noncontrast CT is usually the first imaging study performed in the emergency setting for a patient with a sudden neurologic deficit, headache, seizure, or altered level of consciousness.
CT is highly sensitive for detection of hyperacute/acut intracranial hemorrhage, which appears hyperattenuating relative to brain parenchyma and CSF. Acut hemorrhage may be nearly isoattenuating to water in severe anemia (hemoglobin <8 mg/dL).
MR imaging of hemorrhage
MR imaging of hemorrhage is complex. The characteristics of blood products change on T1- and T2-weighted sequences as the iron in hemoglobin eveloves through phsyiologic stages: Intracellular oxhyemoglobin -> deoxygenation -> intracellular deoxyhemoglobin -> oxidation -> intracellular methemoglobin -> cell lysis -> Extracellular methemoglobin -> chelation -> Hemosiderin and ferritin.
Each stage of this evolution adheres to a reasonably constant time course in the intraxial space and allows the radiologist to “date” the hemorrhage based on the unique characteristics on T1- and T2-weighted images for each stage.
In general, all stages of hemorrhage are isointense or slightly dark on T1-weighted images, except for the methemoglobin stages, which are bright.
Methemoglobin is bright on T1- and T2-weighted images, except for intracellular methemoglobin, which is dark on T2-weighted images.
In general, non hyperacute hemorrhage is dark on T2-weighted images, with the exception of extracellular methemoglobin, which is hyperintense on T2-weighted images. A hyperacute hematoma, containing primarly oxyhemoglobin, is slightly hyperintense on T2-weighted images but features a characteristic dark rim representing deoxygenation at the periphery of the clot.
The inherent slight hyperintensity of oxygenated blood on T2-weighted images becomes apparent in slow flow states, as seen in venous hypertension and moyamoya disease. Slowly flowing blood is not susceptible to the flow-void artifact and the resultant apparently “enhancing” vasculature really represents unmasking of the normal blood signal.
The expected evolution of blood products is highly dependent on macrophage elimination of blood breakdown products. These rules of thumb are not applicable to extra-axial blood and timing is generally not given for extra-axial blood, such as subdural hematoma.
Treatment of hemorrhage
In most cases, imaging is performed to evaluate for a treatable cause of hemorrhage, such as AVM or aneurysm. The mainstay of treatment of intraparenchymal hemorrhage is supportive, including blood pressure control and normalization of any coagulopathy.
Larger hemorrhage can be evacuated surgically if there is significant mass effect or risk of herniation. In particular, a hemorrhage >3 cm in the posterior fossa would generally be treated surgically as there is increased risk of brainstem compression or hydrocephalus from fourth ventricular obstruction.
Specific stages of parenchymal hematoma on MR
Hyperacute hematoma (<6 hours): Intracellular oxyhyemoglobin
- A few hours after red cell extravasation, a hyperacute hematoma is primarily composed of intact red cells containing oxygenated hemoglobin, which is diamagnetic.
- The center of the hematoma will be isointense on T1-weighted images and iso- to slightly hyperintense on T2-weighted images.
- The key finding of a hyperacute hematoma is a peripheral rim of hypointensity on T2-weighted images due to oxygenation of the most peripheral red cells. This peripheral dark rim is most conspicous on GRE sequences.
Acute hematoma (6-72 hours): intracellular deoxyhemoglobin
- After the red cellsdesaturate (lose oxygen), the entire hematoma becomes hypointense on T2-weighted images and iso- to mildy hypointense on T1-weighted images.
Early subacute hematoma (3 days to 1 week): Intracellular methemoglobin
- The subacute phase is characterized by methemoglobin, which is paramagnetic and undergoes proton-electron dipole-dipole interactions (PEDDI) with water. PEDDI shortens T1 to cause hyperintensity on T1-weighted images. Intracellular and extracellular methemoglobin are both hyperintense on T1-weighted images.
- In the early subacture phase, blood remains hypointense on T2-weighted images due to the paramagnetic effects of methemoglobin, which remains trapped in the red cells.
Late subacture hematoma (1 week to months): Extracellular methemoglobin (after RBC lysis)
- The methemoglobin PEDDI effect persists after cell lysis, causing continued hyperintensity on T1-weighted images.
- Paramagnetic effects of methemoglobin lessens. Signal intensity on T2-weighted images inccreases to that of CSF, due to RBC lysis and decreases in prtoein concentration.
- There may be peripheral enhancement of a subacute to chronic infarct.
Chronic sequela of hemorrhage: Hemosiderin and ferritin
- Salvaged iron atoms are deposited into hemosiderin and ferritin, which become permanently trapped in the brain parenchyma after the blood brain barrier is restored.
- Susceptibility effects of the stored iron produce characteristic hypointensity on T2-weighted and GRE images.
- Chronic hemorrhage may have peripheral enhancement.
Hypertensive Intraparenchyma Hemorrhage
Chronic hypertension is the most common cause of spontaneous adult intraparenchymal hemorrhage and is due to the secondary microangiopathic effects of chronic hypertension.
Chronic hypertension causes arteriolar smooth muscle hyperplasia, which eventually leads to smooth muscle death and replacement with collagen. The resultant vascular ectasia predisposes to hemorrhage.
Hypertensive hemorrhage occurs in characteristic locations in the basal ganglia, thalamus, and cerebellum.
In addition to location, imaging (MRI or CT) findings suggestive of a hypertensive bleed include additional stigmata of hypertensive microangiopathy, such as periventricular white matter disease and prior lacunar infarcts.
An additional MR-specific finding suggesting hypertensive hemorrhage is the presence of microhemorrhages on T2* (GRE or SWI) in the basal ganglia or brainstem.
Cerebral amyloid angiopathy (CAA) (Intraparenchymal hemorrage)
Cerebral amyloid angiopathy (CAA) is amyloid accumulated within the walls of small and medium arteris, ultimately causing vessel weakness and increased risk of hemorrhage.
While the spontaneous form of CAA occurs almost exclusively in elderly adults (in which population it is the second most common cause of nontraumatic hemorrhage), a hereditary variant has an earlier age of onset.
In addition to being a risk factor for hemorrhage, CAA can also occlude the lumens of small vessels and contribute to microangiopathy.
The main clinical clue that a hemorrhage is secondary to CAA is that the patient is a normotensive elderly adult.
The primary imaging feature to suggest CAA is the location of hematoma, which is almost always lobar or cortical, usually in the parietal or occipital lobes.
Aneurysmal hemorrhage
As discussed, aneurysmal hemorrhage is by far the most common cause of nontraumatic subarachnoid hemorrhage. If an intraparenchymal hematoma is due to an aneurysm, the hematoma is usually adjacent to the rupture aneurysm dome.
The pattern of subarachnoid blood may help to localize the aneurysm; however, if the patient was found down, then the blood will settle in the dependent portion of the brain, confounding a location.
CT angiography is the study of choice for further evaluation of nontraumatic subarachnoid hemorrhage.
Arteriovenus malformation (AVM)
An arteriovenous malformation is a congenital lesion consisting of abnormal high-flow arteriovenous connections without intervening normal brain.
In case of AVM rupture, the resultant hemtoma is usually parenchymal. In contrast to amyloid angiopathy, a hematoma from a bleeding AVM tends to affect younger patients.
Dural AV fistual (dAVF)
Dural AV fistulas are a group of high-flow vascular malformation characterized by a fistulous connection between a meningeal artery and a venous sinus or cortical vein. Cavernous sinus (cavernous-carotid fistula) and posterior fossa dAVFs are the most common types.
Imaging may show enlarged feeing arteries and enlarged or occluded dural sinuses, or enlarged cortical veins.
Venous thrombosis
Thrombosis of cortical veins or deep venous sinuses leads to venous hypertension, which may cause infarction and parenchymal hemorrhage.
Hemorrhagic neoplasm
Occasionally, the initial presentation of a brain tumor may be acute hemorrhage.
The most common primary brain tumor to cause hemorrhage is glioblastoma.
There are relatively limited number of extracranial primary tumors known to cause hemorrhagic metastases, including: (Choriocarcinoma, Melanoma, Thyroid carcinoma, Renal cell carcinoma, Although breast and lung cancer rarely cause hemorrhage on a per-case basis, they are such common cancers overall that they can always be considered when a hemorrhagic neoplasm is suspected.)
Patients treated with bevacizumab (trade name Avastin, Genetech) may be at increased risk for hemorrhagic metastasis.
Clues to the diagnosis of an underlying tumor causing hemorrhage include more-than-expected edema surrounding a hyperacute hematoma and heterogenous blood product signal, suggesting varying breakdown stages of hemoglobin.
The presence of multiple enhancing masses strongly suggests metastatic disease.
In cases where the diagnosis is unclear, a follow-up MRI should be performed oncethe initial hemorrhage improves. If tumor is present, the MRI may show a delay in the expected evolution of blood products, persistent edema, and enhancement of the underlying tumor.
Cavernous malformation
A cavernous malformation is a vascular hematoma that consists of low-flow endothelial-lined blood vessels without intervening normal brain.
Although non-hemorrhagic cavernomas have a characteristic MRI appearance (with “popcorn-like” lobular mixed/high signal on T1- and T2-weighted images and a dark peripheral hemosiderin rim), once bleeding occurs, the resultant hematoma has nonspecific imaging features. The presence of a developmental venous anomaly adjacent to a hematoma may suggest the diagnosis of a recently hemorrhaged cavernoma.
Angiography plays no role in the diagnosis. Cavernous malformations are angiographically occult.
Hemorrhagic transformation of infarct
In most cases, the clinical or imaging diagnosis of stroke is made before hemorrhagic transformation occurs; however, hemorrhage may occasionally be the presenting feature of an infarct.
More commonly, symptomatic hemorrhage occurs post-infarct in approximately 6-12% of patients receiving thrombolytic therapy.
Noncontrast CT can identify risk factors for hemorrhagic transformation after thrombolytic therapy, including a relatively large region of hypoattenuation and a dense artery sign. Note that per AHA guidelines, neither of these findings is an exclusion criterion for administration of IV tPA.
Vascultitis
Vasculitis affecting the CNS may be primary or secondary to systemic vasculitides.
The most common presentation of vasculitis is cerebral ischemia. Less commonly, vasculitis may present with frank hemorrhage.
Standard MRI imaging shows of vasculitis shows multiple foci of T2 prolongation in the basal ganglia and subcortical white matter.
Noninvasive vascular imaging (CTA or MRA) is relatively insensitive to small vessel involvement, but may show irregularity of involved large or medium vessels.
Angiography is the most sensitive test and shows multifocal areas of stenosis and dilation.
Moyamoya
Moyamoya is a non-atherosclerotic vasculopathy characterized by progressive stenosis of the intracranial internal carotid arteris and their proximal branches, which leads to proliferation of fragile lenticulostriate collateral vessles.
Angiography of the enlarged basal perforating arteries gives a puff of smoke appearance.
The ivy sign on FLAIR MRI represents tubular branching hyperintense structures within the sulci, representing cortical arterial branches that appear hyperintense due to slow collateral flow.
Patients with moyamoya disease are susceptible to aneurysm formation, especially in the posterior circulation. Perfusion studies show decreased flow in the affected vascular regions.
Summary of Hemorrhage Etiology
White Matter Overview
The typical MRI appearance of white matter injury is T2 prolongation of the affected white matter. Less commonly, tumefactive demyelination may be mass-like, enhance, and look very similar to a tumor.
The key imaging finding of demhelinating disease is minimal mass effect relative to the lesion size.
A frequent pattern of white matter disease consisting of scattered foci of T2 prolongation in the subcortical, deep, and periventricular white matter is seen very commonly, especially in older adults. In older patients, a similar pattern can be seen in chronic migraine headaches, as sequelae of prior infectious or inflammatory disease, and with demyelination.
Virchow-Robin spaces are tiny perivascular spaces that follow deep penetrating vessels into the subarachnoid space. Virchow-Robin spaces follow CSF signal on all sequences, including FLAIR. Enlarged Virchow-Robin spaces and a J-shaped sella can be seen in the mucopolysaccharidoses.
Ependymitis granularis represents frontal horn periventricular hyperintensity on T2-weighted images due to interstitial CSF backup. Despite the name (“-itis”), ependymitis granularis is not associated with inflammation.
Multiple Sclerosis
Multiple Sclerosis (MS) is idiopathic inflammatory destruciton of CNS axons in the brain and spinal cord. MS is likely autoimmunein etiology and may be associated with other autoimmune diseases such as Graves disease and myasthenia gravis.
MS is the most common chronic demyelinating disease. It often leads to severe disability.
MS is more common in middle-aged Caucasian females from northern latitudes.
There are two main clincial presentations of multiple sclerosis: 1) Relapsing-remitting (most common): Partial or complete resolution of each acute attack.
2) Progressive: No resolution or incomplete resolution between acute attacks. Primary progressive: Slow onset without discrete exacerbations. Secondary progressive: Similar to relapsing-remitting but with less complete resolution between attacks, leading to progressive disability.
Optic neuritis may represent the first sign of MS. The purpose of a brain MRI after optic neuritis is to look for other lesions, which may be clinically silent.
Histopathologically, destruction of myelin is caused by lymphocytes attacking oligodendrocytes (which makes CNS myelin).
Although MRI imaging is highly sensitive, there are no pathognomonic imaging findings. The McDonald criteria, last revised in 2010, describe strict imaging findings to diagnose MS. The McDonald criteria are most useful for clinically ambiguous cases.
In order to make the diagnosis of MS, there must be lesions separated in space (different areas of the CNS) and in time (new lesions across scans).
Suggestive imaging findings include periventricular ovoid foci of T2 prolongation that “point” towards the ventricles, called Dawson fingers. The corpus callosum is often affected, best seen on sagittal FLAIR.
In general an enhancing lesion is suggestive of active demyelination, as enhancement is thought to be due to inflammatory blood brain barrier breakdown.
Lesions that are dark on T1-weighted images are call “black holes” and are associated with more severe demyelination and axonal loss.
Chronic MS leads to cortical atrophy, thinning of the corpus callosum, and changes in MRI spectroscopy, with decrease in NAA, increase in choline, increase in lipids, and axonal loss.
Tumefactive MS describes the occasionally seen ring enhancement and mass-like appearance of an active MS plaque. In contrast to a brain tumor, the demyelinating lesion will not have any significant mass effect, and the ring of enhancement is usually incomplete.
MS involves the spinal cord in a substantial minority of patients and the spine is routinely evaluated in patients with MS. Spinal MS involvement is usually short-segment and unilateral. Isolated spinal cord involvement is seen in up to 20% of cases of MS.
Concentric (Balo) sclerosis
Concentric (Balo) sclerosis is a very rare variant of MS with pathognomonic alternating concentric bands of normal and abnomral myelin. It is seen more often in younger patients.
Marburg variant (acute multiple sclerosis)
Marburg variant of MS is a fulminant manifestation of MS, leading to death within months.
Devic Disease (neuromyelitis optica)
Devic diseaseis a demyelinating disease, distinct from MS, which involves both the optic nerves and spinal cord. Devic disease confers a worse prognosis compared to MS.
NMO-IgG, an antibody to aquaporin 4, is highly specific for Devic disease. NMO-IgG activates the complement cascade and induces demyelination.
Imaging shows MS-type lesions with involvement of the optic tracts and spinal cord. Brain lesions, if present, tend to be periventricular.
Osmotic Demyelination
Osmotic demylination is caused by a rapid change in extracellular osmolality, typically occuring after aggressive correction of hyponatremia. The quick osmotic gradient change causes endothelial damage, blood brain barrier breakdown, and release of extracellular toxins, which damage myelin.
Patients with poor nutritional status, including alcoholics, chronic lung disease patients, and liver transplant recipient, are the most susceptible to osmotic demyelination.
Osmotic demyelination is typically seen in the pons, but may occur elsewhere in the brainstem and deep gray nuclei. MRI features bilateral central T2 prolongation in the affected region. Signal abnormalities in the thalami and basal ganglia may also be present.
Marchiafava-Bignami
Marchiafava-Bignami is a fulminant demyelinating disease of the corpus callosum seen in male alcoholics.
Wernicke encephalopathy
Wernicke encephalopathy is an acute syndrome of ataxia, confusion, and oculomotor dysfunction, which may be caused either by alcoholism or generalized metabolic disturbances, such as bariatric surgery.
On imaging, there is T2 prolongation and possible enhancement within the mamillary bodies and medial thalamus. The non-alcoholic form may also affect the cortex.
Posterior Reversible Encephalopathy Syndrome
Posterior reversible encephalopathy syndrome (PRES) is a disorder of vasogenic edema with a posterior circulation predominance triggered by failed autoregulation and resultant hyperperfusion, most commonly caused by acute hypertension. In addition to hypertension, PRES is also associated with eclampsia, sepsis, autoimmune disorders, multidrug chemotherapy, and solid or stem cell transplantation.
In contrast to infarction, the edema is vasogenic in etiology, not cytotoxic. Diffusion may be normal, increased, or restricted.
Imaging shows symmetric regions of subcortical white matter abnormality (hypoattenuation on CT and T2 prolongation on MR), especially in the posterior circulation (occipital and parietal lobes are posterior fossa). Mild mass effect and enhancement can be seen.
Neck Anatomy
The retropharyngeal space is a potential space located posterior to the pharynx, separated from the pharynx by the pharyngobasilar fascia. The retropharyngeal space extends from the base of the skull to the upper mediastinum. Directly lateral to the retropharyngeal space are the carotid and parapharyngeal spaces.
The alar fascia is directly posterior to the retropharyngeal space. The alar fascia separates the retropharyngeal space from another postential space, the danger space, which acts as a trapdoor for infection to travel all the way from the neck to the diaphragm.
The preverterbral space (the anterior component of the perivertebral space in hte suprahyoid neck) is located just anterior to the vertebral body an dis bounded anteriorly by the prevertebral fascia.
The sublingual space is a potential space located at the base of the tongue,nestled between the genioglossus and geniohyoid muscles medially and the sling of the mylohyoid muscle inferiorly and laterally.
Directly inferior to the sublingual space is the U-shaped sumbandibular space. The sublingual space is separated from the submandibular space by the mylohyoid muscle anteriorly, although the sublingual space is contiguous with the submandibular space posteriorly.
Larynx anatomy
The layrnx is a fibrocartilaginous tube that extends from the skull base to the esophagus.
The cartilaginous components of the larynx include the epiglottis, thyroid cartiage, cricoid cartilage, and arytenoids. The cricoid cartilage is a complete ring that provides support for the larynx.
The supraglottic larynx extends from the epiglottis to the ventricle. The false vocal cords, the aryepiglottic folds, and the arytenoid cartilages are within the supraglottic larynx.
The glottis includes the true vocal cords and the thyroarytenoid muscle. The medial fibers of the thyroarytenoid muscle comprise the vocalis muscle. The true vocal cords are identified in the axial plane on CT or MRI by identifying the transition of paraglottic fat to muscle (thyroarytenoid muscle) within the wall of the larynx.
The subglottic larynx begins 1 cm inferior to the apex of the laryngeal ventricles and extends to the first tracheal ring.
Anatomy of the Paranasal Sinuses
The sinuses are lined with ciliary mucosa that propels secretions through the drainage pathways. Each pathway should be carefuly evaluated on a sinus CT.
The osteiomeatal unit (OMU) is teh common drainage pathway for the maxillary, frontal, and anterior ethmoid sinuses, which all drain into the middle meatus. Several air passages and a single bony structure (the uncinate process) make up the OMU, which is comprised of the maxillary sinus ostium, infundibulum, uncinate process, hiatus semilunaris, ethmoid bulla, and middle meatus. Some authors include the frontal recess as part of the OMU.
Isolated sinus disease of the maxillary sinus is most likely due to obstruction of the maxillary sinus ostium or infundibulum, while sinus disease affecting the maxillary, frontal, and anterior ethmoid sinuses is most likely due to obstruction of the hiatus semilunaris.
The maxillary sinus is the largest sinus and drains via ciliary action through the superiorly located maxillary sinus ostium.
The ethmoid sinus is comprised of multiple small air cells, diveded into anterior and posterior divisions. The basal lamella demarcates the boundary between the anterior and posterior ethmoids. The lateral wall of the ethmoid sinus is the lamina papyracea, a thin bone separating the ethmoid sinus from the orbit.
The anterior ethmoids drain via the frontal recess into the middle meatus (via the OMU). The posterior ethmoids drain via tiny ostia underneath the superior turbinate into the superior meatus.
The frontal sinus is absent at birth and represents an enlarged anterior ethmoid cell. The frontal sinus drains into the ethmoid infundibulum via the frontal recess.
The sphenoid sinus drains into the ethmoid cells via the sphenoethmoidal recess. Subsequently, the posterior ethmoid cells drain into the superior meatus via individual unamed ostia.
Anterior skull base and pterygopalatine fossa anatomy
The pterygopalatine fossa is the bridge between the face and the brain, and is an important potential pathway for the spread of tumor or infection.
The pterygopalatine fossa sits directly posterior to the maxillary sinus and inferior to the inferior orbital fissure. It can be thought of as a three-dimensional box with each of the six sides leading to important structures in the face.
The pterygopalatine fossa should contain symmetric fat and soft tissue. Asymmetry in the pterygopalatine fossa should raise concern for a mass, such as lymphoma or perineural spread of a salivary tumor (e.g., adenoid cystic carcinoma).
The contents of the pterygopalatine fossa are the pterygopalatine ganglion and branches of the internal maxillary artery.
The pterygomaxillary fissure is the lateral exit of the pterygopalatine fossa, which leads into the masticator space.
The sphenopalatine foramen is the medial exit of the pterygopalatine fossa. It leads into the nasopharynx via the superior meatus. The nasal margin of the sphenopalatine foramen is thought to be the site of origin of juvenile nasopharyngeal angiofibroma.
Foramen rotundum is the posterior opening to the middle cranial fossa. Cranial nerve V2 travels through foramen rotundum.
The inferior orbial fissure is the “roof” of the pterygopalatine fossa and opens anteriorly into the orbit. The infraorbital nerve and artery travel through the inferior orbital fissure.
The vidian canal is located directly below foramen rotundum. It contains the vidian nerve and vidian artery, also known as the nerve and artery of the pterygoid canal.
The pterygopalatine canal is the “floor” of the pterygopalatine fossa, which leads to the oral cavity via the greater and lesser palatine foramina. The pterygopalatien canal transmits the descending palatine nerve and artery.
The anterior skull base divides the anterior cranial fossa superiorly fromt eh paranasl sinuses and orbits inferiorly.
The cribiform plate of the ethmoid bone is the roof of the nasal cavity.
Overview of the temporal bone
The temporal bone can be anatomically and functionally divided into the external, middle, and inner ear. Although some pathologies can overlap, each division tends to be susceptible to unique pathologies.
This anatomic and functional division parallels the pathway of sound waves into the brain. Sound enters the head at the external ear, is amplified by the ossicles in the middle ear, and is finally converted into electrical impulses in the inner ear.
An additional functiona of the inner ear (not drawn above) is the balance and position sense provided by the vestibule and the semicircular canals. Together, the cochlea, vestibule, and semicircular canals make up the labyrinth.
The external auditory canal (EAC) is a fibrocartilaginous tube that sound passes through before reaching the middle ear.
Differential diagnosis of a petrous apex lesion
Overview of cervical lymph nodes
The cervical lymph nodes are divided into seven levels as recommended by the AJCC (American Joint Committee on Cancer), with consistent agreement between surgeons, oncologists, and radiologists. The lymph node levels are not defined by fascial planes, but instead are defined by anatomic landmarks and organized by patterns of lymphatic spread.
In an adult, 90% of head and neck cancers are squamous cell carcinoma: The role of the radiologist is not to provide a differential, but to stage the disease. The degree of lymph node involvement has a substantial prognostic value. For instance, a single metastatic lymph node decreases survival from a squamous cell carcinoma by 50% over an equivalent period.
Spine Tumors
The first step in evaluation of any spinal lesion is to determine its compartment of origin. Each compartment has its own differential considerations.
The three compartments are intramedullary (deep to the pia, usually within the substance of the cord itself), intradural-extramedullary (within the dura, but outside the pia), and extradural (external to the dura).
Disc bulges and herniations
The normal intervertebral disc is composed of a central gelatinous nucleus pulposus and a fibrous peripheral annulus fibrosus. A disc bulge, or heniation, occurs when the substance of the disc (nucleus pulposus, annulus fibrosus, or both) extends beyond the disc’s normal margins.
A broad-based disc bulge disc bulge is present when >180º of the disc circumference extends beyond the expected margins of the disc. Technically, the bulge must measure greater than 2 mm over greater than 180º of its circumference. In practice, the radiologist makes this diagnosis subjectively and exact measurements are typically unnecessary.
A herniation is a focal disc bulge. Technically, a herniation must involve less than 90º of the disc circumference. In practice, measurements are rarely performed.
The term “herniation” is a nonspecific, medicolegally charged umbressla term taht is generally avoided in dictations. The preferred description for herniation is either protrusion or extrusion, depending on the morphology. In this text “herniation” refers to both protrusions and extrusions.
A protrusion is a focal herniation where the diameter of the neck is greater than the diameter of the dome.
An extrusion is a focal herniation where the diameter of the neck is less than the diameter of the dome. This is analogous to a saccular aneurysm.
Disc herniation may contribute to nerve root impingement and spinal stenosis.
Both the medial-lateral position and the spinal level of herniation dictate which nerve root is impinged upon.
In the thoracic and lumbar spine, each nerve root exits below its corresponding vertebral body. For instance, the L4 nerve root exits below the L4 vertebral body at L4-L5.
In contrast, in the cervical spine, each root exits above its corresponding vertebral body. For instance, the C7 nerve root exits above the C7 vertebral body at C6-C7. At the cervicothoracic transition, the C8 nerve root exits below the C7 vertebral body and the T1 nerve root exits below the T1 vertebral body.
Four terms describe the medial-lateral position of herniation: Central, paracentral (adjacent to the subarticular facet join), foraminal, and far-lateral (extra-foraminal). A medial (central or paracentral) herniation will affect the descending nerve root corresponding to the level below the disc. For instance, central, or paracentral herniation of the L4-L5 disc will impinge the descending L5 root. In contrast, a lateral (foraminal or far-lateral) herniation will affect the exiting nerve root, which would be L4 at the L4-5 level.
Once protruded, disc material may separate from its parent disc to become a sequestered fragment, which may subsequently migrate inferioly or superiorly. The surgeon needs to know about a sequestered fragment because it may preclude a minimally invasive procedure.
