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Neuroimaging
CORE Radiology
| Question | Answer |
|---|---|
| Which structure connects the lateral ventricles to the third ventricle? | Foramen of Monro |
| Which structure connects the Third ventricle to the Fourth ventricle? | Cerebral Aqueduct (of Sylvius) |
| What structure drains the fourth ventricle into the subarachnoid space and basilar cisterns? | Foramina of Lushka (2 of them, located laterally) and Foramen of Magendie (single, located medially) |
| What structure(s) produces CSF? | Chorid plexus |
| In which structures is choroid plexus located? (3) | 1) body and temporal horns of the lateral ventricles, 2) roof of third ventricle, and 3) roof of 4th ventricle |
| Which structures absorb CSF? | Arachnoid granulations (leptomeningeal evaginations extending into the dural venous sinuses) and to a lesser extent, by the lymphatic system and cerebral veins |
| What is Cytotoxic edema and what causes it? Does it affect gray matter, white matter, or both? | Cell death (usually infarct) - causes cell swelling due to damaged Na-K ATPase pumps. It affects both gray and white matter. |
| What is Vasogenic edema and what causes it? Does it affect gray matter, white matter, or both? | Interstitial edema (neoplasm, infection, infarct) - caused by increased capillary permeability. It affects primarily white matter. |
| What is Interstitial edema and what causes it? Does it affect gray matter, white matter, or both? | Imbalances in CSF flow (obstructive hydrocephalus) - presents as periventricular fluid collections called "transependymal flow". Affects white matter. |
| What causes Subfalcine herniation and which structures are affected? | Cingulate gyrus slides under the falx cerebri. Can cause anterior cerebral artery compression against the falx causing infarction. |
| What are the two types of transtentorial herniation? | Downward and Upward. |
| What is another name for downward transtentorial herniation? | "Uncal" herniation |
| Describe Downward Transtentorial herniation. | Inferomedial displacement of the medial temporal lobe (uncus) through the tentorial notch, causing compression of the brainstem and adjacent structures (possibly death). |
| Describe Upward Transtentorial herniation. | Superior transtentorial herniation of the cerebellar vermis due to a mass in the posterior fossa. Causes obstructive hydrocephalus. |
| What causes (downward) cerebellar tonsillar herniation? | Downward displacement of the tonsils through the foramen of magnum which causing compression of the medulla (medulla contains respiratory centers so death may occur) |
| Describe Communicating Hydrocephalus and its causes. | Ventricular enlargement without an obstructing lesion which can be caused by subarachnoid hemorrhage which impedes arachnoid granulation absorption. |
| Describe Normal Pressure Hydrocephalus. Is it communicating or non-communicating in nature? | NPH is communicating hydrocephalus defined by normal intraventricular pressures. Creates triad: Wet, Wacky, Wobbly. |
| Describe Non-Communicating Hydrocephalus and its causes. | Ventricular enlargement and CSF buildup due to an obstructive lesion, usually a mass. |
| Describe intra-axial lesion location vs. extra-axial lesion location. | Intra-axial is within the brain parenchyma, under the pia mater. Extra-axial is outside, including the meninges and subarachnoid spaces. |
| List materials that are "T1" hyperintense. (7) | 1) Gadolinium, 2) Fat (and thus, myelin), 3) Proteinaceous material, 4) Early and Late subacute blood products, 5) Melanin, 6) Copper, Iron, or Manganese, 7) Calcium (when disperse, not in bone though it may be hypointense) |
| List materials that are "T2" hyperintense. | 1) Fluid, 2) Hyperacute Blood products, 3) Late Subacute Blood products |
| List materials that are "T2" hypointense. | 1) Acute blood products, 2) Early subacute blood products, 3) Chronic blood products, 4) Calcification, 5) Highly cellular tumors, 6) Vascular flow voids, 7) Dessicated mucin (hydrated/fresh mucin is T2-hyperintense) |
| What are the differential diagnoses for Restricted Diffusion on DWI? | 1) Acute stroke, 2) Bacterial Abscess, 3) Highly cellular tumors such as lymphoma and medulloblastoma, 4) Epidermoid Cyst, 5) Herpes Encephalitis, 6) Creutzfeld-Jakob Disease |
| What are the differential diagnoses for hypointensity on GRE (Gradient Echo recall) images? | 1) Hypertensive microbleeds, 2) Cerebral Amyloid Angiopathy, 3) Familial Cerebral Cavernous malformations, 4) Axonal shear injury, 5) Multiple hemorrhagic metastases |
| What is MR Spectroscopy? | A procedure which describes the chemical composition of a region in the brain. |
| What is the purpose of MR spectroscopy? | Distinguish between recurrent tumor vs. radiation necrosis or glioblastoma vs. metastases |
| What is the difference between glioblastoma and metastases on MR spectroscopy? | Glioblastoma: gradual transition between normal and abnormal spect due to its infiltrative nature. Mets have a more abrupt transition. |
| Which substances are observed on MR spectroscopy? | N-acetylaspartate (NAA), Choline (Cho), and Creatine (Cr) |
| Describe N-acetylaspartate (NAA). | NAA is a normal marker of neuronal viability that decreases in most abnormalities. |
| What happens to NAA vs. Cho on MR spectroscopy in most tumors? | NAA decreases, Cho increases |
| What information does Creatine provide for MR Spectroscopy? | Cr provides information about cellular energy stores |
| In which order do the peaks of NAA, Cho, and Cr occur on MR spectroscopy? | The peaks occurs in alphabetical order: 1) Cho, 2) Cr, 3) NAA |
| Give an example of a disorder where NAA is actually increased. | NAA increase is relatively rare but may be seen in Canavan Disease (a demyelinating disorder) |
| When might one see a lactate "doublet" on MR spectroscopy? What does a lactate doublet infer? | Lactate doublets may seen in high grade tumors, this indicates anaerobic metabolism |
| Describe "Hunter's angle" and it's significance. | Hunter's angle refers to the line connecting the tallest peaks of Cho, Cr, and NAA. If it increases steadily (like a plane taking off) this indicates a normal spectrum. Any other pattern is abnormal. |
| Disruption of which structure allows for brain parenchyma enhancement? | Blood brain barrier breakdown, which may be secondary to infection, inflammation, neoplasm, trauma, or vascular etiologies |
| Which regions of the central nervous system have no blood brain barrier and therefore, enhance normally? (5) | 1) Choroid plexus, 2) Pituitary gland, 3) Pineal gland, 4) Tuber cinereum, 5) Area postrema. The dura mater also lacks BBB but does not normally enhance. |
| What general causes vascular enhancement on MR of the brain? | Localized increase in blood flow which may be secondary to vasodilation, hyperemia, neovascularity, arteriovenous shunting, or contrast administration |
| Which extra-axial structure does not enhance normally, thus indicating pathology? | Dura mater (pachymeninges) and arachnoid mater (leptomeninges) |
| Which intra-axial structure does not enhance normally, thus indicating pathology? What does enhancement of this structure generally indicate? | The supependymal surface (periventricular regions). Enhancement at this location can indicate neoplasm, infection, or demyelination |
| What are the specific differential diagnoses of periventricular enhancement? (4) | 1) Primary CNS Lymphoma, 2) Infectious Ependymitis, 3) Primary Glial tumor, 4) Multiple Sclerosis (active plaques) |
| How does one differentiate between primary CNS Lymphoma and Lymphoma which has metastasized to the brain from another location? | Primary CNS lymphoma generally doesn't involve the meninges, but the meninges are commonly involved in metastatic Lymphoma from other locations |
| How does the appearance of Primary CNS Lymphoma vary between immunocompetent and immunocompromised patients? | CNS lymphoma will be centrally necrotic (ring-enhancing) in immunocompromised patients (in basal ganglia) while it generally enhances homogeneously in immunocompetent patients (basal ganglia, CC, or frontal lobes) |
| What is the most common infectious organism that causes Infectious Ependymitis? How does it characteeistically appear on MR? | Cytomegalovirus (CMV). Infectious ependymitis appears as very thin, linear enhancement along the margins of the ventricles |
| Is primary CNS Lymphoma hyperattenuating or hypoattenuating on CT? | Hyperattenuating |
| What are the signal characterisitics of Primary CNS Lymphoma on MR? | High DWI signal/Low ADC signal ("Restricted Diffusion") and Low T2 signal (all due to hypercellularity) |
| What are the general causes of superficial cortical (gyral) enhancement in the brain? | 1) Infection, 2) Inflammation, 3) Ischemia |
| What are the specific differential diagnoses of gyriform enhancement? | 1) Herpes Encephalitis, 2) Meningitis, 3) Subacute infarction, 4) Posterior reversible encephalopathy syndrome (PRES) |
| Describe Herpes Encephalitis and the locations of the brain where it often presents. | HSV encephalitis is a serious necrotizing infection due to reactivation of the HSV -1 virus within the trigeminal ganglion. Medial temporal lobes and cingular gyrus are usually the first locations affected. |
| Describe the pattern of DWI and ADC signal seen in HSV encephalitis? | Increased DWI signal , Reduced ADC signal ("Restricted Diffusion") |
| Describe Posterior Reversible Encephalopathy Syndrome (PRES). | Syndrome of vasogenic white matter edema triggered by altered vascular autoregulation due to Malignant hypertension or Eclampsia . Symptoms include headache, vision loss, seizures, and confusion. |
| What is another name for Posterior Reversible Encephalopathy Syndrome (PRES)? | Reversible Posterior Leukoencephalopathy Syndrome (RPLS) or more simply, Hypertensive Encephalopathy |
| Where within the brain parenchyma is arterial/hematogenously disseminated metastatic disease most often seen and why? | Gray-White junction (aka "subcortical area"), tumor emboli get stuck at this location after moving through the simple vasculature of the white matter (cant move through highly branching vasculature of the gray matter) |
| Where within the brain is venous/hematogenously disseminated metastatic disease most often seen and why? | Posterior fossa, due to transit via the retroclival venous plexus (i.e. - pelvic malignancy traveling up the spine via the valveless prevertebral venous plexus of Batson) |
| What are the differential diagnoses of "ring enhancement" within the brain parenchyma and what is the mnemonic to help you remember them? | MAGIC DR - (M) metastasis, (A) abscess, (G) glioma, (I) infarct, (C) contusion, (D) demyelination, (R) radiation therapy |
| What are the key imaging findings seen in brain abscess? | Restricted diffusion caused by high viscosity of central necrosis and a characteristically smooth, T2 hypointense rim |
| How does the rim enhancement of abscess vary from that of glioma? | Abscess: Thin, regular rim. Glioma: Thick, irregular rim. |
| Describe the typical location and age of infarcts that appear as a ring enhancing lesion? | Infarcts general appear as gyral enhancement but in the Basal ganglia they can appear as ring enhancement (in subacute phase). |
| How does one differentiate a ring-enhancing infarct or demyelinating process from a ring-enhancing neoplasm or abscess? | Infarct and Demyelination will not demonstrate mass effect while neoplasm and abscess generally will. |
| How does one distinguish between ring enhancing infarct and ring enhancing demyelinating process? | Infarct is generally a complete ring where demyelinating disease generally demonstrate an incomplete "C" shaped ring. |
| What does enhancement of multiple sclerosis plaques generally indicate? | Active disease |
| Which variant of multiple sclerosis can be indistinguishable from a high-grade tumor? | "Tumefactive" MS |
| How does one distinguish between radiation necrosis and a high-grade tumor? | MR Perfusion - cerebral blood volume will be low in an area of radiation necrosis and increased in a high-grade tumor |
| Which layer of the meninges does the term "pachymeninges" refer too? | Dura mater |
| Reflections of the dura mater create which 3 structures in the brain? | 1) Falx, 2) Tentorium, 3) Cavernous sinus |
| Is dural/pachymeningeal enhancement ever seen on CT? Why? | No, because of the close proximity of the highly attenuating skull. It makes these structure indistinguishable from one another. |
| Why doesn't normal dura enhance on MR even with administration of gadolinium? | Enhancement on MR requires both Gadolinium and protons. A small amount of gadolinium does diffuse into the dura but because normal dura contains very little water (and thus, few protons), enhancement will not occur |
| Describe the physiology that allows the dura to enhance on MR with administration of gadolinium. | Dural edema (due to dural pathology) increases the number of dura-contained water molecules and thus protons, allowing for better visualization of the gadolinium |
| What are the differential diagnoses that cause dural/pachymeningeal enhancement? (5) | 1) Intracranial hypotension, 2) Post-operative changes, 3) Post-lumbar puncture, 4) Meningeal neoplasm, 5 Granulomatous disease |
| Why does intracranial hypotension lead to dural/pachymeningeal enhancement? | Prolonged decreased CSF pressure can lead to vasogenic edema in the dura (thus, increase in water & its associated protons) |
| Describe the sings/symptoms, cause, and imaging findings of intracranial hypotension. | Posterior headache exacerbated by standing, may be idiopathic or due to CSF leak. Imaging shows linear dural enhancement, enlargement of the pituitary, sagging of the cerebellar tonsils, and possible subdural hemorrhage due to traction on cerebral veins. |
| What is a "dural tail"? What are the metastatic causes of a "dural tail" in a woman vs. man? | Dural tail = localized area of dural enhancement. Metastatic causes include Breast Ca in women and Prostate Ca in men |
| What are the 3 etiologies of "granulomatous" disease? | 1) Tuberculosis, 2) Sarcoidosis, 3) Fungal Disease |
| Which area of the meninges is typically affected by granulomatous disease? | Basal (skull base) dura/pachymeninges |
| What structures does the term "leptomeninges" refer to? | Arachnoid mater and pia mater |
| What are the differential diagnoses of leptomeningeal enhancement? (3) | 1) Meningitis (most common), 2) Leptomeningeal carcinomatosis, 3) Viral encephalitis. |
| Why do the leptomeninges enhance in meningitis? | Breakdown of the BBB |
| Describe the difference in appearance of leptomeningeal enhancement due to bacterial/viral meningitis vs. fungal meningitis. | Bacterial/viral meningitis appears as fine, linear leptomeningeal enhancement while fungal meningitis appears as thick, nodular leptomeningeal enhancement |
| Which primary CNS neoplasms are known to cause leptomeningeal enhancement? What is the mnemonic to remember these? | GEMCLOG: (G) Glioblastoma, (E) Ependymoma, (M) Medulloblastoma, (C) Choroid plexus tumor, (L) Lymphoma, (O) Oligodendroglioma, (G) Germinoma |
| Which process very closely mimics leptomeningeal enhancement? | Slow vascular flow (i.e. - Moyamoya disease) closely mimics leptomeningeal enhancement. It is defined by intravascular FLAIR hyperintensity along the internal border of the sulci. This is known as the "Ivy sign". |
| What are the differential diagnoses for FLAIR hyperintensity in the subarachnoid spaces? | They overlap somewhat with the DDDx for leptomeningeal enhancement: 1) Meningitis, 2) Leptomeningeal Carcinomatosis, 3) Subarachnoid hemorrhage, |
| Since both leptomeningeal carcinomatosis and subarachnoid hemorrhage demonstrate FLAIR hyperintensity in the subarachnoid space, how does one differentiate them? | Blooming artifact seen on GRE or SWI will be seen in subarachnoid hemorrhage. |
| What patient therapies may artifactually exaggerate subarachnoid FLAIR signal? (2) | Oxygen therapy or Propofol therapy |
| What are the 3 emergent complications of an intracranial neoplasm? | 1) Hemorrhage, 2) Hydrocephalus, and 3) Herniation |
| Which CNS neoplasms & metastases are prone to hemorrhage? | 1) Melanoma, 2) RCC, 3) Thyroid carcinoma, 4) Choriocarcinoma (Breast and Lung mets are less likely, but do occasionally demonstrate hemorrhage) |
| CNS neoplasm in which fossa are most likely to result in hydrocephalus? | Posterior fossa, due to effacement of the 4th ventricle |
| Which findings hint that a mass is extra-axial in location? | 1) CSF cleft between the mass and brain parenchyma, 2) buckling of gray matter, 3) gray matter interposed between the mass/white matter |
| Why do metastases always enhance? | Because of their vascularity which lacks BBB |
| Does the degree of enhancement seen in a CNS neoplasm correspond to the histological grade? | No |
| IF there is more than one CNS neoplastic lesion noted on a study, what is the most frequent diagnosis? | Metastases |
| CNS neoplasms are most often T2-bright and T1-dark so what is the differential if a lesion is hypointense on T2? (2) | 1) Metastases containing dessicated mucin (such as gastrointestinal adenocarcinomas) and 2) Hypercellular tumors (lymphoma, medulloblastoma, germinoma, and some glioblastomas) |
| CNS neoplasms are most often T2-bright and T1-dark so what is the differential if a lesion is hyperintense on T1? (3) | 1) Melanoma, 2) Fat containing tumors such as dermoid/teratoma, 3) hemorrhagic mets (RCC, thyroid carcinoma, choricarcinoma) |
| What is the definition of a glioma? List the types of glial cells (4) | Primary CNS tumor that arises from glial cells which include 1)astrocytes, 2) oligodendrocytes, 3) ependymal cells, and 4) choroid plexus cells |
| Describe the general characteristics and location of Juvenile Pilocytic Astrocytomas. | JPA's are benign (grade 1) tumors of the posterior fossa seen in children. Well defined cystic mass with a contained enhancing nodule and minimal edema. May cause hydrocephalus via compression of the 4th ventricle. |
| Other than the posterior fossa, where might JPA's been seen? What disorder is associated with JPA in this location? | JPA's may be seen along the optic pathway. When they are found in this location, they are often associated with Neurofibromatosis type 1 (Posterior fossa JPA is NOT associated with NF-1) |
| What are the 3 types of fibrillary astrocytomas? | 1) Low-grade astrocytoma, 2) Anaplastic (high-grade) astrocytoma, and 3) Glioblastoma multiforme |
| In what other location, other than the brain, can astrocytomas be found? | Spinal Cord |
| Describe the general characteristics and location of Low-grade Astrocytomas. | Grade II tumor that presents as a supratentorial or spinal cord T2-hyperintense, infiltrative/ill-defined mass that does NOT enhance with gadolinium. May be very subtle. |
| Is JPA a fibrillary-type astrocytoma? | No - it, by definition, is pilocytic in nature, not fibrillary |
| Describe the general characteristics and location of Anaplastic Astrocytomas. | Grade III tumor that presents as a supratentorial or spinal cord T2-hyperintense lesion that can vary in appearance from that of low-grade astrocytoma to that of glioblastoma |
| What type of tumor do Anaplastic Astrocytomas general progress to? | Glioblastoma |
| Describe the general characteristics and location of Glioblastomas. | Aggressive Grade IV tumor of older adults which can vary widely in appearance. Generally found in supratentorial white matter with heterogeneous enhancement and surrounding T2 hyperintensity. |
| What is the most common primary CNS malignancy in adults? | Glioblastoma multiforme |
| Is the T2 hyperintensity commonly seen surrounding Glioblastomas related to edema? | Most often not - it is usually indicative of surrounding infiltrative tumor extension. |
| What is the name given to a GBM that crosses the midline (trans-callosal extension) of the brain? | Butterfly Glioma |
| What are the differentials for lesions which cross the midline of the brain (exhibit trans-callosal spread)? (3) | 1) Butterfly glioma, 2) Lymphoma, 3) Demyelinating Disease |
| Describe the general characteristics and location of Gliomatosis cerebri. | Diffuse, infiltrative mid grade (III) astrocytoma that affects multiple lobes. |
| What are the diagnostic criteria and imaging characteristics of Gliomatosis cerebri? | Diagnostic criteria: Involvement of at least 2 lobes plus extra-cortical involvement (CC, BG, or cerebellum). Appears as T2-hyperintense, diffuse process. Exerts mass effect but doesn't enhance. |
| Describe the general characteristics and location of Oligodendroglioma. | Grade II that presents as a slow-growing cortical based mass. The typical patient is young to middle age, presenting with seizures. They have a propensity to calcify/contain calcifications (75%). Lack of edema b/c of slow growth. |
| Describe the general characteristics and location of Ependymomas. | Occurs in posterior fossa in kids or in the spinal cord of adults. Has tendency to fill the 4th ventricle and squeeze through the foramina of Lushka/Magendie into the basilar cisterns |
| What is the most common pediatric CNS neoplasm? | Medulloblastoma |
| Describe Lhermitte-Duclos tumor. | Benign Grade I non-glial primary CNS tumor which is part hamartoma and part neoplasm. ALWAYS seen in association with Cowden Syndrome. Classic finding is corduroy/tigroid striated lesion in the posterior fossa. Enhancement is rare. |
| What is another name for Lhermitte-Duclos tumor? | Dysplastic Cerebellar Gangliocytoma |
| Describe the general characteristics of Embryonal tumors. | Embryonal tumors are aggressive, grade IV childhood tumors which occur more often in the posterior fossa more frequently than the supratentorium. |
| What are the other names for Embryonal tumors? | Primitive neuroectodermal tumors (PNET) or "small blue cell tumors" |
| List the types of Embryonal tumors. | 1) Atypical Teratoid/Rhabdoid tumor (ATRT), 2) Medulloblastoma |
| Describe Atypical Teratoid/Rhabdoid tumor. | Aggressive Grade IV which is similar to medulloblastoma but occurs in slightly younger patients. Usually in posterior fossa. associated with malignant rhabdoid tumor of the kidney. |
| Describe the general characteristics of Medulloblastomas. | Aggressive Grade IV tumor that demonstrates hyperattenuation on CT due to cellularity. Hypointense on T2 and ADC. Avidly enhances. Appears heterogeneous because of internal hemorrhage and calcification. May metastasize to leptomeninges. |
| How does the location of medulloblastomas vary based on age? | Both occur in posterior fossa, but - Adults: arises at midline of cerebellar vermis, Kids: arises peripherally in cerebellar hemisphere. |
| Which tumors appear as a cystic structure with a contained enhancing nodule? | 1) Juvenile Pilocytic Astrocytoma, 2) Hemangioblastoma, 3) Pleomorphic Xanthoastrocystoma, 4) Ganglioglioma |
| Describe the general chaacteristics of Hemangioblastomas. | Highly vascular benign grade I tumor that commonly occurs in the cerebellum, medulla, or spinal cord. Cystic mass with enhancing mural nodule. |
| What disorder are Hemangioblastomas associated with? | Von Hippel Lindau (VHL) |
| When seen in the spine, what abnormality often accompanies a Hemangioblastoma? | Syrinx |
| Describe the general characteristics of Pleomorphic Xanthoastrocytoma (PXA). | Grade II astrocytoma variant found in the temporal lobe of kids. Cystic mass with enhancing mural nodule. Overlying dura may be thickened/enhancing. |
| What disorder is Pleomorphic Xanthoastrocytoma associated with? | Chronic epilepsy |
| Describe the general characteristics of Ganglioglioma. | Rare, slow growing neuroglial tumor in the temporal lobe of teens/young adults with medically refractory temporal lobe epilepsy. Cystic lesion with enhancing mural nodule. May cause cavarial scalloping. |
| What is the main imaging difference between PXA and Gangliglioma? | PXA will have dural thickening but ganglioglioma will not. |
| List the types of intraventricular tumors. (5) | 1) Central neurocytoma, 2) Choroid plexus papilloma/carcinoma, 3) Intraventricular meningioma, 4) Subependymal giant cell astrocytoma (SEGA), and 5) Subependymoma |
| Describe the general characteristics of Central Neurocytoma. | Low grade intraventricular tumor of neuronal origin in teens to middle aged adults. Appears as lobulated mass attached to the septum pellucidum with numerous microcysts/calcifications. |
| Describe the general characteristics of Choroid plexus papilloma/carcinoma. | Grade I (papilloma) or III (carcinoma) intraventricular lobulated, cauliflower-like, heterogeneous mass that avidly enhances on T1 images. The two forms are indistinguishable on imaging. |
| What is the most common brain tumor in babies under the age of 1 year. | Choroid Plexus papilloma |
| Where are Choroid plexus papilloma/carcinomas located in kids vs. adults? | Kids: Atrium of the lateral ventricle Adults: Fourth ventricle |
| Describe the general characteristics of Intraventricular Meningioma. | Solid mass, typically in the trigone of the lateral ventricle that occurs in older patients like most meningiomas. They are typically hypercellular and enhance avidly/homogeneously. |
| Describe the general characteristics of Subependymal Giant Cell Astrocytoma (SEGA). | Grade I astrocytoma-variant which is classically located at the Foramen of Monroe in the lateral ventricle. Enhances avidly. |
| Which systemic disorder is Subependymal Giant Cell Astrocytoma (SEGA) associated with? | Tuberous Sclerosis (which is also associated with subepndymal nodules and hamratomas (both cortical and subcortical) |
| Describe the general characteristics in Subependymoma. | Non-enhancing grade I tumor of unclear origin that affects middle aged to older adults. Often found incidentally. Found in 4th ventricle or at the foramen of Monroe in the lateral ventricle. |
| Since both Subependymal Giant Cell Astrocytoma and Subependymoma both occur at the foramen of Monroe, how can one distinguish between these two entities on imaging? | SEGA's will enhance. Subependymomas do not enhance. |
| Are Subependymomas related to SEGA or Ependymomas? | No - they are totally unrelated. |
| Where does primary CNS lymphoma typically occur within the brain? | Periventricular areas |
| What are the two main differentials for ring enhancing basal ganglia lesions in immunocompromised patients? | Primary CNS Lymphoma vs. Toxoplasmosis |
| What are the options for differentiating between Primary CNS Lymphoma and Toxoplasmosis when a ring enhancing basal ganglia lesion is found? | 1) Empirical anti-toxoplasma therapy, 2) Thallium scanning (lymphoma will be hot, toxo is not), 3) PET (avid uptake with lymphoma, no FDG activity with toxo), 4) Perfusion scanning (lymphoma = increased perfusion/blood volume, toxo = hypovacularity) |
| What are the most common tumors to cause parenchymal metastases to the brain? | 1) Lung, 2) Breast, 3) Melanoma |
| What is the most common extra-axial tumor? | Meningioma (arises from meningo-epithelial cells called "cap" cells) |
| Who typically gets Meningiomas? | Older patients, females > males (they are often benign and asymptomatic, only 1-2% demonstrate malignant conversion) |
| In which systemic disorder does one see multiple meningiomas? | Neurofibromatosis type 2 (or following radiation therapy) |
| When meningiomas are found to be intra-osseous, which other finding can they be confused for? | Fibrous Dysplasia |
| What are the imaging characteristics of Meningiomas? | CT: Hyperattenuating, often with internal calcifications MR: Iso- to hypointense on T1, variable signal intensity of T2 *They enhance avidly and often have a dural tail* |
| Do Meningiomas often cause edema? | Yes, and the edema is often out of proportion to the size of the meningioma (i.e. - small tumor, lots of edema) |
| What are the most common tumors to metastasize to the dura? | 1) Breast***, 2) Lymphoma, 3) Small cell lung cancer, and 4) Melanoma |
| What are the differential diagnoses for a posterior fossa mass in a child? (5) | 1) Medulloblastoma, 2) Juvenile Pilocytic Astrocytoma, 3) Ependymoma, 4) Hemangioblastoma, 5) Atypical Dermoid/rhabdoid tumor |
| What are the differential diagnoses for the posterior fossa mass in an adult? (4) | 1) Metastasis, 2) Hemangioblastoma, 3) Astrocytoma, 4) Medulloblastoma |
| What are the most common differential diagnoses for a tumor at the cerebellopontine angle? (5) | 1) Schwannoma, 2) Meningioma, 3) Arachnoid cyst, 4) Epidermoid cyst, 5) Aneurysm (of PICA, AICA, VA, or BA), 6) RARELY mets |
| What are the important structures which traverse the cerebellopontine angle? (4) | CN5, CN7, CN8, and the AICA |
| What is (by far) the most common mass found at the cerebellopontine angle? | Vestibular (CN8) Schwannoma - accounts for about 75% of the masses in this area - appears classically as "scoop of ice cream falling off the ice cream cone" |
| Into which structure do trigeminal Schwannomas often extend? | Meckel's Cave |
| Describe the general characteristics of Arachnoid cysts. | Benign CSF-filled lesion that is usually congenital. They are usually supratentorial in location but when found infratentorially, they are most frequently seen at the CPA |
| Describe the general characteristics of Epidermoid cysts. | Congenital lesion arising from ectopic ectodermal epithelial tissue. They progressively enlarge due to desquamation of their keratinized epithelial lining. Often have "cauliflower-like" surface and grow between/around nerves and vessels. |
| How does one distinguish between and epidermoid cyst and arachnoid cyst on CT? MR? | CT differentiation is impossible as they appear identical. One must perform MR: Epidermoid will show restricted diffusion while arachnoid will not. Arachnoid generally follows CSF characteristics. |
| Aside from Hemangioblastoma, what other intracranial neoplasm is associated with Von Hippel-Lindau? | Endolymphatic Sac Tumor, which occurs along the posterior petrous ridge |
| Pathology involving the anterior pituitary may interrupt secretion of which hormones? (6) | 1) GH, 2) ACTH, 3) Prolactin, 4) TSH, 5) FSH, 6) LH |
| Pathology involving the posterior pituitary may interrupt secretion of which hormones? (2) | 1) Vasopression (ADH) and 2) Oxytocin |
| What is the normal signal characterictic of the posterior pituitary on MR? | T1-hyperintense (aka - posterior pituitary bright spot) |
| Can an empty sella be a normal variant? | Yes - if seen in isolation (no other defects), CSF will fill the sella while the gland is flattened against the floor |
| When is an empty sella NOT a normal variant? | Pseudotumor Cerebri/Benign Intracranial Hypertension. |
| What are the *clinical* findings in Pseudotumor Cerebri/Benign Intracranial Hypertension? (3) | 1) elevated CSF pressure, 2) visual disturbances, 3) headaches (Most often seen in obese black females) |
| What are the *imaging* findings in Pseudotumor Cerebri/Benign Intracranial Hypertension? | 1) Empty sella, 2) enlargement of Meckel's cave, 3) Optic disc protrusion into the globes, 4) +/- mildly shrunken ventricles, 5) +/- Sigmoid/Transverse sinus stenosis |
| What are the differential diagnoses for a mass of the intrinsic pituitary (not necessarily the suprasellar region? | 1) Micro vs. Macro-adenoma, 2) Rathke's Cleft Cyst (although its more common for this to be extrinsic), 3) Lymphotcytic vs. Granulomatous Hypophisitis |
| What is the cut off for size of a pituitary "Micro" adenoma. | <1cm |
| How do the symptoms of Microadenoma vs. Macroadenoma differ? | Microadenoma is generally defined by symptoms of hormone excess (lactation due to excess Prolactin, etc). Macroadenoma is generally defined by symptoms of mass effect (headache, visual disturbance, etc) |
| Describe the signal characteristics of Pituitary Microadenomas? | Most are hypoenhancing compared to the surrounding pituitary parenchyma but if the microadenoma is ACTH secreting, it may be brighter than the surrounding pituitary parenchyma |
| Which type of patients get Lymphocytic hypohysitis vs. Granulomatous hypophysitis? | Lymphocytic = peripartum women Granulomatous = tuberculosis patients, Wegener's patients, kids with Langerhan's Cell Histiocytosis |
| What is the most common suprasellar (extrinsic pituitary) mass in a child? | Craniopharyngioma |
| What is the most common suprasellar mass in an adult? | Macroadenoma (that has extended superiorly out of the sella) |
| What is the mnemonic for remembering the causes of suprasellar mass? | SATCHMO: (S) Sarcoidosis/Suprasellar Adenoma, (A) Aneurysm, (T) Teratoma (dermoid cyst)/Tolosa Hunt, (C) Craniopharyngioma/Cleft (Rathke's) Cyst, (H) Hypothalamic glioma (adults)/Hamartoma (kids), (M) Meningioma/Mets, (O) Optic nerve glioma |
| Describe Tolosa-Hunt Syndrome . | Disorder characterized by severe unilateral headaches, extraocular palsies (with associated visual disturbance) and pain around the sides/back of the eye caused by idiopathic inflammation of the cavernous sinus or superior orbital fissure. |
| Describe the general characteristics of Craniopharyngioma. | Tumor arising from the squamous epithelial remnants of Rathke's pouch that produce keratin. May in volve the sella or suprasellar region but always separate from the pituitary. Has potential for enamel production and almost always calcifies. |
| What is the classic finding in gross specimens of Craniopharyngioma and what is this substance composed of? | Black "machine oil" type substance is usually contained in cystic regions on gross specimens - its made of keratin, desquamated squamous epithelium, and cholesterol. |
| Describe the imaging characteristics of Craniopharyngioma. | MR: Complex cystic mass containing blood or protein products which are hyperintense on T1. Avid enhance of the solid elements and cystic walls |
| Craniopharyngioma and Rathke's Cleft Cyst share a common developmental origin. How does one distinguish between these entities on imaging? | Cranipharyngioma enhances peripherally and centrally with contrast/gadolinium while Rathke's cleft cyst may only enhance peripherally if at all. Also, Rathke's cleft cyst does not calcify. |
| What is the shared embryonic origin of Rathke's Cleft Cyst and Craniopharyngioma? | Rathke's Pouch, a neuroectodermal outpouching of the primitive oral cavity with is the embryonic precursor of the anterior pituitary gland. |
| What is the age difference in patients with Craniopharyngioma vs. Rathke's cleft cyst? | Craniopharyngioma (kids, extremely rarely in middle aged adults) while Rathke's Cleft Cyst is typically seen in middle aged adults (2:1 Females:Males) |
| Describe the imaging characteristics of Rathke's Cleft Cyst. | Often isointense to CSF but may contain protein (high on T1) but only peripherally at rim |
| What are the symptoms associated with Rathke's Cleft Cyst? | Usually none, it is often an incidental finding. |
| What is the "Claw Sign"? | Enhancing pituitary tissue completely wrapped around a Rathke's Cleft Cyst |
| Describe the general characteristics of optic pathway gliomas. | Astrocytoma involving the optic nerve, optic chiasm, or optic tract. Low grade in kids, aggressive in adults. |
| Describe the imaging characteristics of optic pathway gliomas. | MR: Isointense on T1, Hyperintense on T2, usually enhancing |
| Describe the general characteristics of Germinomas. | 80% found in pineal region, 20% found in parasellar region. Usually seen in kids and adolescents. |
| Describe the imaging characteristics of Suprasellar Germinomas. | Homogeneous, intensely enhancing midline mass. Hypointense on T2, demonstrates Restricted Diffusion. |
| Describe the general characteristics of Dermoid cysts. | Congenital benign inclusion cyst which are most common in young males, usually seen in the posterior fossa but occasionally seen in the parasellar region. they contain intracystic fat. |
| What are the complications often experienced by patients with ruptured dermoid cysts? | Chemical meningitis or ventriculitis due to exposure of these structures to released fat |
| What type of aneurysm can mimic a suprasellar tumor? | Saccular Aneurysm of the supraclinoid portion of the internal carotid artery. A hint that a mass is an aneurysm is pulsation artifact on MR. |
| Describe the general characteristics of a hypothalamic hamartoma. | Hamartoma of the tuber cinereum which is not a true neoplasm, but rather, ectopic hypothalamic neural tissue. |
| What symptoms may a child with a hypothalamic harmartoma present with? | Precocious puberty and gelastic seizures (laughing spells) |
| What are the imaging characterisitics of Hypothalamic hamartoma? | Sessile mass between the pituitary stalk and mammillary bodies which appears isointense to gray matter |
| What are the differential diagnoses of a suprasellar mass in a child? (5) | 1) Craniopharyngioma, 2) Optic Pathway Glioma, 3) Germ Cell Tumor, 4) Hypothalamic hamartoma, 5) Langehan's Cell histiocytosis hypophysitis |
| What are the differential diagnoses of a suprasellar mass in an adult? (6) | 1) Pituitary macroadenoma extension, 2) Meningioma, 3) Cranipharyngioma (rarely), 4) Rathke's Cleft Cyst, 5) Aneurysm, 6) Lymphocytic or Granulomatous Hypophysitis |
| What are the differential diagnoses for an intrinsic pineal gland mass? (5) | 1) Germ cell tumor (Germinoma and teratoma), 2) Pineal cyst, 3) Pineocytoma, 4) Pineoblastoma 5) Metastases |
| Compression of the tectal plate by a pineal mass or pineal region mass can cause which two syndromes? | 1) Hydrocephalus (due to compression of the cerebral aqueduct) and 2) Parinaud's syndrome (paralysis of upward gaze due to compression of the superior colliculus |
| The relationship of a pineal mass to which vascular structure is critical for surgical planning? | Internal cerebral veins (they are often displaced upward by pineal gland/pineal region masses) |
| Describe the origin of extra-gonadal germ cell tumors. | Aberrant migration of totipotent germ cells during embryogenesis |
| What is another name for a Germinoma? | Extra-gonadal Seminoma |
| What are the differential diagnoses for an intrinsic pineal gland mass? (5) | 1) Germ cell tumor (Germinoma and teratoma), 2) Pineal cyst, 3) Pineocytoma, 4) Pineoblastoma 5) Metastases |
| Compression of the tectal plate by a pineal mass or pineal region mass can cause which two syndromes? | 1) Hydrocephalus (due to compression of the cerebral aqueduct) and 2) Parinaud's syndrome (paralysis of upward gaze due to compression of the superior colliculus |
| The relationship of a pineal mass to which vascular structure is critical for surgical planning? | Internal cerebral veins (they are often displaced upward by pineal gland/pineal region masses) |
| Describe the origin of extra-gonadal germ cell tumors. | Aberrant migration of totipotent germ cells during embryogenesis |
| What is another name for a Germinoma? | Extra-gonadal Seminoma |
| What is the most common tumor of the pineal region? | Germinoma |
| Describe the imaging characteristics of Pineal Germinoma. | Restricted diffusion, isointense on T1 and T2, avidly enhances. Often engulfs the pineal gland and promotes its calcification which creates a central nodule of calcification within the mass. |
| How does one distinguish between Pineal Germinoma and Pineal Teratoma on imaging? | Teratoma will contain fat, Germinoma will not |
| Describe the general characteristics of Pineal Cyst. | A generally stable cyst of the pineal gland which is more common in women. Follow up is not usually recommended unless new symptoms appear. They are generally <1cm and can be simple or multi-cystic. |
| In which imaging scenario is it difficult to differentiate between pineal cysts and solid tumors of the pineal? | If contrast is given to evaluate a pineal cyst and imaging is delayed by >1hr, contrast can diffuse into the cyst, causing it to appear solid |
| How does one differentiate pineal cyst from pineocytoma on MR? | Pineal cyst will only enhance peripherally and some have rim calcification. Pineocytoma often enhances internally as well. It can be difficult to differentiate between hemorrhagic pineal cyst and pineocytoma. |
| Describe the general characteristics of pineoblastoma. | Highly malignant grade IV tumor of young children which is derived from the same primitive neuroectodermal cells as medulloblastoma. |
| What is "Trilateral Retinoblastoma"? | Bilateral retinoblastomas and a pineoblastoma (termed because both the retina and pineal gland are light-sensing organs) |
| What is "Quadrilateral Retinoblastoma"? | Bilateral retinoblastoma, pineoblastoma, and a tumor of the sella (usually suprasellar retinoblastoma) |
| Describe the imaging characteristics of Pineoblastoma. | Poorly defined pineal mass which invades local structures and often presents as obstructive hydrocephalus. MR: Restricted diffusion. Has propensity for leptomeningeal metastasis and CSF seeding. |
| How does one differentiate between a Pineal Germinoma and a Pineoblastoma on imaging? | Pineal Germinoma tends to engulf the pineal gland, creating a central calcification. Pineoblastoma peripherally calcifies in a pattern likened to "exploded calcification" |
| What are differential diagnoses for (extrinsic) Pineal REGION tumor? | 1) Gliomas, 2) Vein of Galen Aneurysm, 3) Meningioma, 4) Quadrigeminal Plate Lipoma |
| Describe a Vein of Galen Aneurysm. | NOT a true aneurysm, rather, simply a dilated vein of Galen due to an arteriovenous fistula between the anterior or posterior circulation and the venous plexus leading to the vein of Galen. |
| Describe the variable effect of meningioma vs. pineal based mass on the internal cerebral veins? | Pineal based masses tend to elevate the internal cerebral veins while meningiomas tend to depress them. |
| What abnormalities can also be seen in the setting a quadrigeminal plate lipoma? | Hypoplasia or agenesis of the corpus callosum. |
| What is another name for the quadrigeminal plate? | Tectum |
| What finding should one consider if a ring enhancing cortical lesion is seen in a trauma victim? | Cortical contusion |
| How does chronic cortical contusion appear? | It appears as encephalomalacia. One may also see peripheral hemosiderin deposition on SWI on MR. |
| How does acute blood appear on CT? | Hyperattenuating (but only when clotted together, hyperacute unclotted blood as well as clotted blood in a patient with severe anemia may appear close to water attenuation on CT) |
| What is the most common cause of traumatic subarachnoid hemorrhage? | Head injury/trauma - tends to occur on the side of the head which is contralateral to the injury, often in the superficial cerebral sulci |
| What is the most common cause of non-traumatic subarachnoid hemorrhage? | Ruptured aneurysm |
| What is the most common cause of epidural hemorrhage? | Injury to the squamous portion of the temporal bone with resultant tearing of the middle meningeal artery |
| What shape does epidural hemorrhage appear as? | Lentiform, "lens-like" |
| Does epidural hemorrhage cross the midline/cranial sutures? | No |
| What is the "Swirl" sign seen in epidural hemorrhage refer to? What does this sign indicate? | Mised high and low attenuation blood within the hematoma - this indicates active bleeding |
| Can an epidural hemorrhage happen as the result of damage to cerebral veins? | Yes, but rarely when there is laceration of the dural sinuses (often seen in the posterior fossa in kids) |
| What is the most common cause of subdural hemorrhage? | Tearing of cerebral veins |
| Who is most prone to subdural hemorrhage? | Patients with parenchymal volume loss (atrophic involutional changes) because the cerebral veins are already stretched across the enlarged CSF spaces so even minor trauma can cause them to rupture. |
| Describe the appearance of a subdual hemorrhage. | Crescentic in appearance. Will cross midline/suture lines. |
| How does subacute subdural hemorrhage appear (approximately 1-3 weeks after the initial inciting event)? | Isoattenuating to grey matter - can be difficult to evaluate. 3 clues include: 1) mildly increased mass effect, 2) white matter buckling, and an apparently thickened cortex (which is not really thickened but appears so b/c of adjacent subacute blood) |
| What are the 3 main causes of intraventricular hemorrhage? | 1) Tearing of subependymal veins, 2) direct extension of subarachnoid hemorrhage, 3) direct extension of an intraparenchymal hemorrhage |
| What subacute-chronic complication must one worry about in a patient with intraventricular hemorrhage? | Obstructive/non-communicating hydrocephalus due to scarring of the ependymal surface which may block of the cerebral aqueduct as well as build up of degenerating blood products at the arachnoid granulations. |
| What causes diffuse axonal injury? | Rotational deceleration and subsequent re-acceleration force that exceeds the limited elastic capacity of axons |
| What are the most common locations of diffuse axonal injury? | Grey-white junction, corpus callosum, and dorsolateral midbrain (in increasing order of severity of presentation). |
| Describe the 3 grades of diffuse axonal injury. | Grade 1: involves only grey-white junction Grade 2: Corpus callosum Grade 3: Dorsolateral midbrain |
| How many points in the face must be fractured to create a "floating zygoma"? | Four - this type of fracture had previously been (incorrectly described as a tripod fracture but in fact 4 points must be fractured to create a floating zygoma) |
| What are the 4 bones/articulations in which fractures must occur to create a floating zygoma? | 1) Frontal (zygomaticofrontal), 2) Maxillary (zygomaticomaxillary), 3) Temporal (zygomaticotemporal) and 4) Sphenoid (zygomaticosphenoid) |
| What articulation does a "lateral orbital rim fracture" occur at? | Zygomaticofrontal |
| What articulation does a "inferior orbital rim fracture" occur at? | Zygomaticomaxillary |
| What articulation does a "zygomatic arch fracture" occur at? | Zygomaticotemporal |
| What articulation does a "lateral orbital wall fracture" occur at? | Zygomaticosphenoid |
| Describe a Le Fort type 1 fracture. | Horizontal fracture through all walls of the maxillary sinus which detaches the maxillary alveolus from the skull base and creates a floating/freely moving hard palate |
| Describe a Le Fort type 2 fracture. | Pyramidal fracture with sparing of the medial wall of the maxillary sinus that dissociates the midface from the skull allowing free movement of the nose and hard palate as a single unit |
| Describe a Le Fort type 3 fracture. | Complete midface dissociation due to fractures through the bilateral zygomatic arches which allows free movement of the entire midface |
| Which sulcus separates the motor strip of the frontal lobe from the sensory cortex in the parietal lobe? | Central sulcus |
| Which lobule contains both the motor strip and sensory cortex? | Paracentral lobule |
| What are the 7 segments of the internal carotid artery, in ascending order? | 1) Cervical (C1), 2) Petrous (C2), 3) Lacerum (C3), 4) Cavernous (C4), 5) Clinoid (C5), 6-7) Supraclinoid (C6-7) |
| What are the 3 main branches that take off from the supraclinoid segment of the internal carotid artery? | OPA! 1) Ophthalmic artery, 2) Posterior communication artery, 3) Anterior choroidal artery |
| What are the names of the 2 main trunks of the cavernous portion of the internal carotid artery? | 1) Meningohypophyseal trunk and 2) Inferolateral trunk |
| To which structures does the Meningohypophyseal trunk of the Internal Carotid Artery provide blood supply? (3) | Pituitary, Tentorium, Dura of the Clivus |
| To which structures does the Inferolateral trunk of the Internal Carotid Artery provide blood supply? (4) | CN3, CN4, CN6, and the Trigeminal ganglion |
| What vessel gives off the "Recurrent Artery of Heubner" and what structures does it supply? | The A1 segment of the ACA travels above the optic nerve and gives off the "recurrent artery of heubner" which supplies the caudate head and anterior limb of the internal capsule. |
| Which vessel gives off the "Lateral lenticulostriate perforator vessels" and what structures do they supply? | The MCA gives rise to the lenticulostriate perforator vessels which supply the lateral aspect of the basal ganglia including the lateral aspect of the putamen, external capsule, and the posterior limb of the internal capsule. |
| An aneurysm of which vessel may cause CN3 palsy due to localized mass effect? | Posterior communicating artery |
| Describe the "Artery of Percheron". What is it's significance? | a PCA P1 segment variant where there is a single dominant artery supplying the ventromedial thalami bilaterally as well as the rostral midbrain. An infarct would result in bilateral ventromedial thalamic infarction +/- V-shaped midbrain infarct |
| Which vessel supplies the thalamus? | PCA via thalamoperforator vessels |
| Which two entities may result in Bilateral Thalamic Infarction? | 1) Artery of Percheron Infarct or possibly 2) Deep venous thrombosis |
| What structures does the anterior choroidal artery supply? (3) | Optic chiasm, Hippocampus, and Posterior limb of the internal capsule |
| In what percentage of patients does "normal" circle of Willis anatomy occur? | Only 25% of patient have a "normal" circle of Willis while 75% have at least one variant vessel |
| Describe a "Persistent Trigeminal Artery". | A persistent carotid-basilar vascular connection that is normal during fetal development but should normally regress/involute. |
| What is the most common Carotid-Basilar Connection? What is it's significance? | Persistent Trigeminal Artery - it is prone to aneurysm |
| What sign might one see on angiography to denote a Persistent Trigeminal Artery? | "Trident" or "Tau" sign due to the artery's branching nature. |
| What are the two varieties of Persistent Trigeminal Artery? | Saltzman Type 1 - ICA to Basilar. Saltzman Type 2 - ICA to SCA |
| What are the names of the 3 persistent carotid-basilar connections which occur much more rarely than Persistent Trigeminal Artery? | 1) Otic artery, 2) Hypoglossal artery, 3) Proatlantal Intersegmental artery |
| Per AHA guidelines, what is the only CT finding that absolutely precludes the administration of tPA within 3 hours in the setting of acute stroke? | A finding of hemorrhage of any size |
| What is the theoretical goal of MR perfusion imaging in the setting of stroke? | Characterize an ischemic penumbra (the area of vulnerable brain adjacent to the infarct core which is dead tissue) which may also become infarcted without intervention. |
| Describe penumbra on MR perfusion imaging. | The penumbra receives some perfusion but at a reduced rate compared to the normal brain. Low perfusion causes cellular dysfunction which in turn, leads to neuro-deficit. |
| What are the exact values (ml/100g tissue per minute) in a penumbra vs. normal grey matter. | Penumbra perfusion is <20ml/100g tissue per minute (normal grey matter is ~60ml/100g tissue per minute). |
| What is the ideal initial test of choice when a patient presents with stroke symptoms within the 3 hour tPA window? | Noncontrast CT of the head (main purpose is to exclude hemorrhage, not to see the actual area of ischemic infarction) |
| If acute ischemic stroke is in fact visible on CT, how does it appear? | Region of low attenuation +/- insular ribbon sign |
| Describe the "Insular Ribbon" sign seen in the setting of acute stroke. | Loss of grey-white differentiation at the insula |
| Describe the "Hyperdense Artery" sign seen in the setting of acute stroke. | Direct visualization of the acute intravascular thrombus, most commonly seen in the MCA |
| What is the best MR sequence for determining the presence/absence of hyperacute stroke? | Diffusion (DWI) -- Acute stroke will be high signal intensity on DWI but low on ADC (aka "Restricted Diffusion"). |
| What 2 factors (at the cellular level) cause restricted diffusion to be seen on MR in hyperacute stroke? | 1) Shift from extracellular to intracellular water (cytotoxic edema) due to Na/K ATPase pump failure and 2) Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein. |
| What time frame denotes hyperacute stroke? | 0-6 hours after initial neuro-deficit onset. |
| How does acute stroke appear on FLAIR imaging in the hyperacute phase? | Often, no abnormality is seen on FLAIR in the hyperacute stage, but if it is, subtle hyperintensity may be seen |
| Name the two types of "high flow" vascular malformations. What does high flow imply? | 1) AVM (arteriovenous malformation) and 2) dAVF (dural arteriovenous fistula). A high flow state implies that shunting occurs. |
| Describe the general characteristics of an AVM. | Direct connection between an artery and vein with a capillary bed in between. 85% occur supratentorially. |
| What are the initial presenting symptoms in a patient with AVM? | Seizure or intracranial hemorrhage (parenchymal >SAH). Aneurysms of the feeding artery are often seen which predisposes these malformations to bleeding. |
| What is the name of the scale helped to evaluate surgical risk for AVM resection? | Spetzler-Martin scale (ie - large artery feeding into deep vein is high risk, small artery feeding into peripheral vein is lower risk) |
| Do AVM's cause significant mass effect? | No, because they tend to replace brain parenchyma rather than displace it |
| What are some imaging findings that suggest an AVM is more prone to bleeding? (5) | 1) Intra-nidal aneurysm, 2) venous ectasia, 3) venous stenosis, 4) deep venous drainage involvement, 5) posterior fossa location |
| What are the three potential treatment options for AVMs? | 1) Embolization, 2) stereotactic radiation, or 3) surgical resection |
| Which vein is actually enlarged in a "Vein of Galen malformation"? | It is not actually the vein of Galen, but rather an enlarged median prosencephalic vein, a thalamoperforator branch |
| What is the most common extra-cardiac cause of high output heart failure in a child? | Vein of Galen Malformation |
| What are the symptoms of vein of Galen malformation in adults? | They are either1) asymptomatic or 2) Parinaud's syndrome (paralysis of upward gaze due to compression of the superior colluiculus) |
| What vesseks are involved in a dural arteriovenous fistula (dAVF)? | Arteriovenous shunts between meningeal arterioles and dural venules |
| What is the primary prognostic feature of dAVFs? Which classification system stratifies the risk of bleeding in dAVF? | Presence and degree of cortical venous drainage. The Cognard Classification system describes progressive risk of bleeding in dAVF from class I to V. |
| List the classes (I-V) of the Cognard Classification system of dAVFs. | (I) No cortical venous drainage, lowest risk, (IIA) Reflux into dural sinus but not cortical veins, (IIB) Reflux into cortical veins, (III) Direct cortical venous drainage, (IV) Direct cortical venous drainage w/ venous ectasia, (V) Spinal venous drainage |
| What is the typical clinical presentation of a patient with Cognard type V dAVF bleed? | Myelopathy |
| Describe Cavernous Carotid Fistulas (CCFs). | Type of dAVF which is cause by trauma which results in a fistula between the cavernous portion of the carotid artery and the cavernous sinus (which is a venous drainage system) |
| What are the symptoms of Cavernous Carotid Fistulas? | Enlargement of the superior orbital vein and shunting within the cavernous sinus that causes eye symptoms like proptosis and cranial nerve palsy |
| List the Low-Flow vascular lesions (don't involve shunting) (3). | 1) Cavernous Malformation, 2) Developmental Venous Anomaly, 3) Capillary Telengiectasia |
| Describe Cavernous Malformations and their appearance on CTimaging. | AKA "Cavernoma" is a vascular hamartoma with a small but real bleeding risk. May also cause seizures. Appear as a well circumscribed hypoattenuating lesion with central hyperattenuation which represents calcification. |
| With which other vascular abnormality are Cavernoma's often associated with? | DVAs |
| What inherited syndrome is characterized by the presence of multiple cavernomas? | Familial Cavernomatosis |
| If not inherited or spontaneous, how might a cavernoma be acquired? | Radiation treatment to the brain |
| How does Cavernoma appear on MR imaging? | Popcorn-like appearance of lobular mixed signal on T1 and T2 due to blood products of varying ages. Hemosiderin may appear dark on GRE/SWI. No enhancement is typically seen. |
| Do Cavernomas typically show up on vascular imaging like CTA or angiography? | No |
| Describe the general characteristics of a developmental venous anomaly (DVA). | An abnormal vein that provides functional venous drainage to normal brain |
| How must one image a DVA? | Contrast enhanced imaging - it is the only way to see them. It will appear as a radially oriented vein with a characteristic "caput medusa" (outwardly radiating) appearance. |
| What would happen if one attempted to remove a DVA surgically? | The patient would suffer a debilitating venous infarct. DVA's are "Do Not Touch" lesions. If a cavernoma with adjacent DVA must be resected, care must taken to preserve the DVA. |
| Describe the general characteristics of a Capillary telangiectasia. | Asymptomatic vascular lesion composed of dilated capillaries with interspersed normal brain. |
| Are capillary telangiectasias resectable? | No - they, like DVAs- they are unresectable |
| Can capillary telangiectasia be seen on angiography? | No |
| How do capillary telangiectasias appear on post- contrast MR? | Faint, brush-stoke like enhancing lesion in the brainstem or pons without any evidence of mass effect or edema |
| If a noncontrast Ct is negative for subarachnoid hemorrhage but clinical suspicion is still high, what procedure should be performed? | Lumbar puncture to look for xanthochromia |
| What are the 6 differential diagnoses for increased FLAIR signal in the subarachnoid space? | 1) SAH, 2) meningitis, 3) Leptomeningeal carcinomatosis, 4) residual intrathecal contrast, 5) propofol therapy, 6) high flow oxygen therapy |
| Suprasellar cistern hemorrhage suggests a ruptured aneurysm in which vessel? | Posterior communicating artery |
| Sylvian fissure hemorrhage suggests a ruptured aneurysm on which vessel? | Middle Cerebral Artery |
| Perimesencephalic cistern hemorrhage suggests a ruptured aneurysm in which vessel? | The tip of the basilar artery |
| What is the name of the clinical grading system for aneurysmal SAH which is based soley on symptoms and not on imaging? | Hunt & Hess (Grade I = mild headache, Grade V = coma or extensor posturing) |
| What is the name of the imaging grading system for SAH based on CT findings? | Fisher Grade (Grade 1 = negative CT, Grade 2 is <1mm thick, Grade 3 is >1mm thick, Grade 4 is diffuse SAH with parenchymal or intraventricular extension) |
| What is the most common cause of morbidity and mortality in patients who survive SAH? | Vasospasm (occurs ~7 days post-SAH and can lead to stroke or additional hemorrhage) |
| What complication will 20-30% of patients with SAH experience? | Hydrocephalus due to blockage of the arachnoid granulation by broken down blood products. Treatment is ventriculostomy. |
| What is "Superficial Siderosis" and when is it seen? | Iron overload of the pial membrane due to chronic or repeated SAH. Will appear as T2 hypointensity outlining the affected sulci |
| What are the two main side effects of superficial siderosis? | Sensorineural deafness and ataxia |
| What is SAH called when it is limited to the cisterns directly anterior to the midbrain? What is it caused by? | Perimesenchephalic SAH which is NOT caused by ruptured aneurysm but rather, angiographically occult venous bleeding. It has a better prognosis than normal SAH. |
| Describe Reversible Cerebral Vasoconstriction Syndrome (RCVS). | Another cause of nontraumatic, nonaneurysmal SAH and ischemia. Caused (obviously) by prolonged but reversible vasospasm. |
| Describe a "saccular" aneurysm. | Focal outpunching of an arterial wall, usually at a branch point in the circle of willis. Caused by a combination of hemodynamic stress and acquired degeneration of the vessel wall. |
| What are the non-inherited causes of saccular aneurysm? (2) | Hypertension and Inflammatory Vascular Disease such as Takayasu or Giant Cell Arteritis |
| What are the inherited causes of saccular aneurysm? (4) | Connective tissue diseases like Marfan's syndrome, Ehlers-Danlos, Polycystic Kidney Disease, and NF1 |
| Describe saccular aneurysm by size. | Small: <1cm, Medium: 1-2.5cm, Giant: >2.5cm (Giant aneurysms can have mass effect and cause cranial nerve palsies |
| Describe a "fusiform" aneurysm. | Segmental arterial dilation without a defined neck. They are usually due to atherosclerosis but can be due to chronic dissection. In contrast to saccular aneurysms, they do not occur at branch points. Typically in posterior circulation (Vertebrobasilar). |
| Describe Mycotic (Infectious) aneurysms. | Very rare (only 2-4% of aneurysms), due to septic emboli, often from bacterial endocarditis. Form in distal arterial circulation beyond the circle of Willis. Fragile with high risk of rupture. |
| Describe Oncotic aneurysms. | Aneurysm caused by neoplasm. A benign left atrial myxoma may embolize peripherally and cause a distal aneurysm. |
| Describe Traumatic Pseudoaneurysm. | Due to trauma, don't contain all 3 vessel layers. Vessel will have narrowing proximal to the aneurysm. Happen distally. Arteries close to bony structures (basilar and vertebral arteries) are prone to dissecting pseudoaneurysms. |
| List one of the more common causes of stroke in young patients. | Venous thrombosis. |
| What are the risk factors for venous thrombosis? | 1) Pregnancy, 2) Oral contraceptives, 3) Thrombophilia, 4) Malignancy, 5) Infection |
| What sign may be seen on contrast CT that indicates venous thrombosis? | "Empty Delta" sign (fillisng defect in SSS) |
| What sign may be seen on non-contrast CT that indicates venous thrombosis? | "Cord" sign (increased density within the affected vein) |
| How does venous thrombosis cause infarction? | Venous hypertension |
| What region of the brain will become infarcted with thrombosis of the SSS? | Parasagittal high convexity |
| What region of the brain will become infarcted with thrombosis of the Deep venous system? | Bilateral thalami |
| What region of the brain will become infarcted with thrombosis of the transverse sinus? | Posterior aspect of the temporal lobe |
| Which form of hemoglobin defines the hyperacute phase of intra-axial hemorrhage? In what time frame is this seen? Describe its T1/T2 appearance. | Intracellular Oxyhemoglobin (T1 isointense, T2 iso to hyperintence). 0-6 hours. |
| Which form of hemoglobin defines the acute phase of intra-axial hemorrhage? In what time frame is this seen?Describe its T1/T2 appearance. | Intracellular deoxyhemoglobin (T1 iso to hypointense, T2 hypointense). 6-72 hours. |
| Which form of hemoglobin defines the early subacute phase of intra-axial hemorrhage? In what time frame is this seen?Describe its T1/T2 appearance. | Intracellular methemoglobin (T1 hyperintense, T2 hypointense). 3 days - 1 week. |
| Which form of hemoglobin defines the late subacute phase of intra-axial hemorrhage? In what time frame is this seen?Describe its T1/T2 appearance. | Extracellular methemoglobin (T1 hyperintense, T2 hyperintense). 1 week - 1 month. |
| Which form of hemoglobin defines the chronic phase of intra-axial hemorrhage? In what time frame is this seen? Describe its T1/T2 appearance. | Hemosiderin & Ferritin (T1 iso to hypointense, T2 hypointense). 1+ month. |
| What is the most common non-traumatic cause of intra-parenchymal brain hemorrhage in an adult? What is the mechanism? | Hypertension; via secondary microangiopathic effects of chronic hypertension (arteriolar smooth muscle hyperplasia ----> smooth muscle death and replacement with collagen which doesn't expand/contract appropriately. |
| Where within the brain does hypertensive hemorrhage characteristically occur? | Basal ganglia, thalamus, cerebellum (in addition to acute blood, one may see periventricular chronic microvascular change and old lacunar infarcts) |
| What is the second most common non-traumatic cause of intra-parenchymal brain hemorrhage in adults? | Cerebral amyloid angiopathy (CAA) - amyloid accumulates in small and medium vessel walls which causes weakening. Usually seen in the elderly but hereditary forms of amyloidosis may be seen in younger populations. |
| What is the biggest clinical clue that an intra-parenchymal hemorrhage is due to amyloid angiopathy? | Lack of hypertension |
| Where within the brain does amyloid-related hemorrhage characteristically occur? | Lobar/cortical areas within parietal/occipital lobes. |
| Which brain tumor is most often presents as intra-parenchymal hemorrhage? | Glioblastoma |
| Treatment with which specific chemotherapeutic monoclonal antibody are at increased risk of brain hemorrhage? | Avastin (Bevacizumab) |
| Describe Moyamoya disease and its appearance on Angiography. | Vasculopathy characterized by progressive stenosis of the intracranial portion of the ICA and their proximal branches which leads to proliferation of delicate/fragile lenticulostriate vessels. Angiography will opacify these vessels = "puff of smoke". |
| Describe the MRI findings of Moyamoya disease. | "Ivy Sign" which is hyperintensity along the affected sulci due to slow collateral flow through fragile lenticulostriate vessels. Mimics leptomeningeal enhancement. |
| When there is more edema than expected around an area of intra-parenchymal brain hemorrhage, what condition must one consider? | Hemorrhagic brain metastases. |
| Describe Virchow-Robin spaces within the brain. | Tiny perivascular spaces that follow deep penetrating vessels into the subarachnoid space. They will follow CSF signal intensity on all MR sequences. |
| Which disorder is associated with enlarged Virchow-Robin spaces? | Enlarged Virchow-Robin spaces along with a J-shaped sella are associated with Mucopolysaccharidoses. |
| What is "Ependymitis granularis" and how does it appear on imaging? | Back up of CSF flow which causes periventricular T2 hyperintensity at the frontal horns. Despite the "itis", it is NOT associated with inflammation. |
| What appearance on imaging would clue one in to the presence of demyelinating disease? | T2 hyperintensity with NO SURROUNDING MASS EFFECT |
| What is the most common demyelinating disease? | Multiple Sclerosis |
| Describe the two main clinical presentations of MS. | 1) Relapsing-Remitting (most common, partial to complete resolution follow each flare up) and 2) Progressive (incomplete to no resolution between flare ups) |
| Describe Primary Progressive MS vs. Secondary Progressive MS. | Primary Progressive MS has a slow onset without discrete episodes of exacerbation while Secondary Progressive MS is similar to Relapsing-Remitting with less complete resolution between acute flare ups. |
| What is the most common first-time presentation of MS? | Blindness known as optic neuritis. MR may show additional lesions which do not have corresponding clinical features. |
| Describe the histopathological basis of Multiple Sclerosis. | Lymphocytes attacking Oligodendrocytes and the myelin they create. |
| What is the name of the criteria used to characterize MS? | McDonald Criteria (last revised in 2010) |
| What is the characteristic imaging feature typically seen in MS? | "Dawson's Fingers" which are ovoid periventricular foci of T2/FLAIR hyperintensity which point towards the ventricles. |
| Which area of the brain is most often affected by the lesions of MS (and where Dawson's Finger's can often be seen)? | Corpus Callosum |
| What does enhancement of a demyelinating lesion indicate? | Acuity & Active demyelination due to active breakdown of the BBB. |
| Can ring enhancing lesions be seen in MS? | Yes, in tumefactive MS. The post-contrast T1-hypointense centers are called "black holes" and are associated with more severe demyelination and axonal loss. T1 post contrast hyperintense outer ring is typical (less severe) demyelination. |
| Describe the chronic changes seen on imaging which are associated with MS. | Cortical atrophy, thinning of the corpus callosum, and changes in MR SPECT (decreased NAA, increased Cho, increased lipids, and increased lactate) |
| What is "Tumefactive" MS? | The ring-enhancing lesions of MS and lesions which appear mass-like but exert little to no localized mass effect. |
| Can isolated spinal cord lesions be seen in MS? | Yes, but this is relative rare, seen in only up to 20% of cases. |
| Describe "Balo" Concentric Sclerosis. | Very rare variant of MS with pathognomonic alternating concentric bands of normal and abnormal myelin. Seen more frequently in younger patients. |
| Describe the Marburg-variant of multiple sclerosis. | An extremely acute, fulminant manifestation of MS leading to death within months of onset. |
| What is "Devic Disease"? | Also known as Neuromyelitis Optica. IT is a demyelinating disease distinct from MS (with worse prognosis) which involves both the optic nerves and spinal cord. Imaging will show MS type lesions in these areas. Brain lesions are rare. |
| Which antibody is specific for Neuromyelitis Optica/Devic Disease? | NMO-IgG against Aquaporin 4 channel. It activates the complement cascade, causing demyelination. |
| Describe Osmotic Demyelination. | Central Pontine Myelinolysis occurs with a rapid rise in extracellular osmolality, usually with aggressive correction of hyponatremia. The quick gradient change causes endothelial damage, BBB breakdown, and release of toxins leading to demyelination. |
| Aside from the pons, whereelse might osmotic demyelination occur? | Brainstem and deep grey nuclei. Will see T2 intensity centrally in the affected region. Signal abnormalities may also be present in the thalami and basal ganglia. |
| Which patients are at the greatest risk for osmotic demyelination? (4) | Patient with poor nutritional status, alcoholics, chronic lung disease patients, and liver transplant recipients. |
| Describe Marchiafava-Bignami Disease. | Fulminant demyelinating disease of the corpus callosum seen in male alcoholics. |
| Describe Wernicke Encephalopathy. | Acute syndrome of ataxia, confusion/confabulation, and oculomotor disturbance caused by alcoholism (classically) or in patients with metabolic disturbances such as bariatric surgery pts. |
| Describe the imaging findings of Wernicke Encephalopathy. | T2 intensity +/- gadolinium enhancement in the mammilary bodies and medial thalamus. The non-alcoholic form may also involve the cortex. |
| Describe PRES (Posterior Reversible Encephalopathy Syndrome) | Vasogenic edema with a posterior circulation predominance triggered by failed autoregulation and resultant hyperperfusion typically caused by acute hypertension. |
| Aside from hypertension, which other disorders are associated with PRES? (6) | Eclampsia, Sepsis, Autoimmune disorders, multidrug chemotherapy, solid organ transplant, and STEM cell transplant |
| What type of edema characterizes PRES? | Vasogenic edema (not cytotoxic as is seen in conjunction with infarction) |
| What are the imaging findings seen in PRES? | SYMMETRIC regions of subcortical white matter abnormality (hypoattenuation on CT or T2 intensity on MR) in the parietal lobe, occipital lobe, and posterior fossa. Mild mass effect and enhancement may be seen. |
| Describe CADASIL. | Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is an inherited disease characterized by recurrent stroke, migraine, subcortical dementia, and pseudobulbar palsy due to small vessel arteriopathy. |
| What is the hallmark clinical presentation of CADASIL? | Recurrent episodes of stroke or TIA which are always found in subcortical white matter or basal ganglia. Often, an associated migraine is present. May lead to dementia. |
| What are the imaging characteristics of CADASIL? | SYMMETRIC foci of T2 intensity in subcortical white matter which may become confluent as the disease progresses. Anterior temporal lobe or paramedian frontal lobe foci are sensitive and specific especially in conjunction with history of migraine. |
| While both present with symmetric subcortical white matterT2 intensity, what is the main difference in imaging findings between PRES and CADASIL? | PRES = posterior circulation while CADASIL = anterior circulation. |
| List the vasculitides that can affect cerebral circulation. (5) | 1) SLE, 2) Polyarteritis nodosa, 3) Giant cell arteritis, 4) and 5) Sjogren's dyndrome. |
| Which is the best imaging modality to evaluate cerebral vasculitis and what will be seen? | CT Angiography or Catheter Angiography are better than MRA. A "beaded" irregular appearance of the affect cerebral vessels will be seen. |
| In which area of the brain will microvascular ischemic changes never be seen? | Corpus Callosum. |
| What is Biswanger Disease? | Severe microvascular ischemic disease combined with dementia. |
| Describe Progressive Multifocal Leukoencephalopathy (PML). | Demyelinating disease caused by reactivation of JC virus in immunocompromised patients. There is progressive demyelination with lack of immune response. Occurs mostly in AIDS pts. Diagnosis is made via PCR of JC virus DNA from CSF. |
| Approximately 1 in 1,000 MS patients treated my the monoclonal antibody "Natalizumab" (Tysabri) will have superimposition of which disease on top of their MS? | Superimposed PML. This is extremely difficult to distinguish from MS itself. |
| Which imaging findings are associated with PML? | Asymmetric multifocal white matter lesions that may become confluent. There is almost never mass effect or enhancement. |
| Which white matter fibers are typically involved in PML? | Arcuate (subcortical "U") fibers (the myelinated tracts at the gray-white junction involved in conecting cortex to cortex. |
| What are the two primary differential diagnoses for white matter lesions in AIDS patients? | 1) PML (asymmetrical, no atrophy, subcortical areas affected) and 2) HIV encephalitis (bilateral, symmetrical, spares subcortical areas, and is associated with cerebral atrophy) |
| Describe Subacute Sclerosing Panencephalitis (SSPE). | SSPE is a demyelinating disease caused by reactivation of measles virus after a long, latent period. Will see white matter lesions with significant mass effect and edema (in contrast to most other white matter diseases). |
| Describe Acute Disseminated Encephalomyelitis (ADEM). | Monophasic demyelinating disorder seen primarily in kids after a viral infection or vaccination. Imaging findings are similar to MS (diagnosis may shift to MS if course becomes multiphasic) with lesions in brain, brainstem, or spinal cord. |
| Will you see optic neuritis in MS, ADEM, or both? | Can see Optic Neuritis in both MS and ADEM. |
| Describe the Hurst variant of ADEM? | An acute, fulminant form of ADEM that leads to death within days. Imaging findings are T2 intensity and white matter hemorrhage which may appear as confluent hematomas. |
| Describe the general sequelae of radiation induced white matter disease. | Small vessel arteritis and secondary ischemia |
| Describe the Acute phase radiation induced white matter injury. | Edema due to endothelial injury, though this is generally of little clinical consequence/significance. |
| Describe the Early Delayed phase of radiation induced white matter injury. | Occurs several weeks up to 6 months after treatment and presents due to demyelination. MR will show diffuse white matter T2 prolongation. |
| Describe the Late Delayed phase of radiation induced white matter injury. | Occurs from 6 months to many years after treatment, presents as white matter injury or focal radiation necrosis. Mass effect, edema, and enhancement are common. Radiation necrosis should be considered if ring-enhancing lesions are seen. |
| Aside from radiation-induced white matter injury, what are some example of radiation-related complications seen in the brain? (4) | Development of 1) Meningiomas, 2) Capillary telengiectasias, 3) Cavernous Malformations, and/or 4) Moya Moya disease |
| What are the 3 phases of radiation induced white matter injury? | 1) Acute, 2) Early Delayed, and 3) Late Delayed |
| True or False: Radiation-induced white matter disease can be potentiated by chemotherapy? | True |
| What are the three main mechanisms of development of intracranial pyogenic abscess? | 1) Hematogenous dissemination from other locations, 2) Direct spread from paranasal sinusitis/mastoiditis, or 3) Complication of bacterial meninigitis |
| What are the 4 stages of intracranial pyogenic abscess formation? | 1) Early cerebritis, 2) Late cerebritis, 3) Early abscess, 4) Late Abscess |
| From start to finish, how long does intracranial pyogenic abscess formation take? | ~ 2 weeks |
| After an intracranial pyogenic abscess becomes discrete, how does it appear on MR? | Ring-enhancing mass. T2 hyperintense core with T2 hypointense rim which is thin/smooth in nature. Restricted diffusion is common to to high cellularity. |
| How does the rim of a pyogenic abscess vary in appearance compared to the rim of a glioma or metastatic lesion? | Abscess is generally thin/smooth rimmed where it appears thickened/irregular in glioma/mets. |
| Describe the life threatening complication of abscess rupture into a ventricle? | Ventriculitis (has very high mortality) |
| Describe, in general, the intracranial phenomenon known as "Tuberculoma". | A localized tuberculous granuloma. |
| Which other intracranial entity is it difficult to differentiate from a Tuberculoma? How do you differentiate between the two? | Pyogenic Abscess. Tuberculoma will have T2 hypointense core while Pyogenic Abscess generally has T2 hyperintense core. |
| Describe the imaging characteristics of Tuberculomas. | Central hypointensity on T2, often with restricted diffusion |
| Which bug causes Lyme disease? Describe the intracranial appearance of CNS Lyme infection. | Borrelia burgdorferi. T2 hyperintensity in frontal subcortical white matter often with meningeal enhancement or enhancement of multiple cranial nerves. |
| What is the single most common CNS fungal infection in AIDS patients? | Cryptococcosis caused by Cryptococcus neoformans |
| At what CD4 count do AIDS patients typically become susceptible to Cryptococcus infection? | <100 cells/uL |
| What is the most common clinical presentation of intracranial Cryptococcal infection? | Chronic Basilar Meningitis. |
| What is the most common imaging finding seen in intracranial Cryptococcal infection? What are the more sensitive/specific findings? | Hydrocephalus (which is obviously extremely nonspecific) is the most common finding. Gelatinous pseudocysts which appear as rounded, water-signal lesions on T1/T2 along the basal ganglia perivascular spaces are far more specific but much less common. |
| Which specific location does Cryptococcus have a predilection for spread to? | Choroid Plexus. |
| What is a "Cryptococcoma" and how does it appear? | Foci of cryptococcal infection seen once the bug spreads to the choroid plexus and ventricles - appears as intraventricular ring-enhancing lesions. |
| What is the treatment for CNS Cryptococcus? | Fluconazole and Amphotericin B |
| What is the most common CNS infection seen in immunocompetent patients? | Neurocysticercosis caused by Taenia solium tapeworm parasite. |
| What are the 4 stages of Neurocysticercosis? | 1) Viable/Vesicular, 2) Colloidal, 3) Nodular/Granular, and 4) Calcified |
| Describe the imaging features of the Viable/Vesicular stage of Neurocysticercosis. | CSF-intensity cysts without enhancement. They may or may not have a central dot which represents a "scolex" |
| Describe the imaging features of the Colloidal stage of Neurocysticercosis. | This phase has the least specific imaging findings - the most common feature is ring-enhancing lesions with increased diffusivity. Edema is often seen. |
| Describe the imaging features of the Nodular/Granular stage of Neurocysticercosis. | Edema decreases as the cyst involutes and it's wall thickens. |
| Describe the imaging features of the Calcified stage of Neurocysticercosis. | Small intraparenchymal calcifications with small foci of susceptibility on SWI/GRE. |
| How does one differentiate Pyogenic abscess and the colloidal phase of neurocysticercosis? | Pyogenic abscess = core will demonstrate restricted diffusion, Colloidal Neurocysticercosis = core will demonstrate increased diffusivity |
| Can Neurocysticercosis be seen intraventricularly? | Yes - when seen, it is most often in the Aqueduct of Sylvius or 4th ventricle. As such, hydrocephalus may be a presenting symptom. The obstructing intraventricular cyst will best be seen on FLAIR (because the surrounding CSF is nulled in this sequence) |
| What is meant by the "Racemose" form of Neurocysticercosis? | Racemose describe the Viable/Vesicular phase cyst WITHOUT a scolex (because it has degenerated). |
| What is the treatment of Neurocysticercosis? | Albendazole, +/- steroids to reduce edema, +/- anti-seizure meds |
| What is the most common "mass lesion" in AIDS patients? | Toxoplasmosis caused by Toxoplasma gondii. |
| At what CD4 count do AIDS patients typically become susceptible to Toxoplasmosis infection? | < 100 cells/uL |
| What is the overall most common CNS infection seen in AIDS patients? | HIV encephalitis |
| What is the most typical imaging finding seen in Toxoplasmosis? | Single or multiple ring enhancing lesions in the basal ganglia. |
| What is the "Asymmetric Target" sign and what does it signify? | It is a sign which is not frequently seen but it relatively specific for Toxoplasma infection. It is an eccentric nodule of enhancementseen peripherally along the enhancing wall of a Toxoplasma ring lesion. |
| What is the primary differential for a ring enhancing basal ganglia lesion in an HIV patient. | CNS lymphoma. CNS lymphoma is more common in AIDS patients than Toxoplasma infection due to effectiveness of HAART therapy. |
| How does one differentiate CNS Lymphoma vs. Toxoplasmosis? | CNS lymphoma = restricted diffusion, increased relative cerebral blood volume on perfusion imaging, hypermetabolic on FDG-PET, and Thallium avid. Toxoplasma = increased diffusivity, no blood volume increase on perfusion, no FDG-PET or Thallium activity |
| Describe, in general, Herpes encephalitis. | Devastating necrotizing encephalitis caused by reactivation of latent HSV-1 virus within the trigeminal ganglion. |
| In what setting should you be most suspicious of Herpes encephalitis? | In any patient with fever, mesial temporal lobe signal abnormality, and acute altered mental status |
| When suspecting HSV encephalitis, which should be performed first... MRI or Lumbar puncture? | Lumbar puncture should come first as PCR for HSV from CSF is typically diagnostic |
| Describe MR image findings in HSV encephalitis. | Bilateral (but asymmetric) T2 intensity in the medial temporal lobs, insular cortex, cingulate gyrus, and inferior frontal lobes. Once it becomes hemorrhagic, foci of susceptibility can be seen. Gyral enhancement can be seen in the later stages. |
| If symptoms of HSV encephalitis occur in an immunocompromised patient, which other entity should be considered? | HSV-6 (as opposed to HSV-1), though enhancement and diffusion abnormalities may be absent |
| What are the differential diagnoses for medial temporal lobe lesions? (5) | 1) HSV encephalitis, 2) MCA infarction, 3) Infiltrating glioma, 4) Limbic encephalitis, 5) Seizure-related changes |
| What is the treatment for HSV encephalitis? | IV Acyclovir, as soon as possible |
| What causes HIV encephalitis? | Direct infection of CNS lymphocytes and microglial cells (CNS macrophages) by HIV virus |
| How does HIV encephalitis manifest? | Diffuse cerebral atrophy and symmetrical T2 intensity in the periventricular and deep white matter |
| At what CD4 count do AIDS patients typically become susceptible to CMV infection? | <50 cells/uL |
| What is the most common manifestation of intracranial CMV infection? | Ventriculitis or meningoencephalitis. Often characterized by subependymal FLAIR intensity and enhancement throughout the entire ventricular system. |
| How does CMV encephalitis appear in infants? | Atrophy, encephalomalacia, ventricular enlargement, and periventricular calcification |
| What is Creutzfeld-Jakob disease? | Neurodegenerative disease caused by Prions |
| Describe the typical MR appearance of Creutzfeld-Jakob disease. | "Cortical ribboning" which is FLAIR intensity and restricted diffusion along the cerebral cortex. The basal ganglia and thalami are often involved. The motor cortex will be spared. |
| What is the "Pulvinar Sign" and what does it signify? | DWI and FLAIR intensity within the pulvinar nucleus of the thalamus. It is indicative of Creutzfeld-Jakob disease. |
| What is the "Hockey Stick Sign" and what does it signify? | DWI and FLAIR intensity in the dorsomedial thalamus which mimics the appearance of a hockey stick. It is indicative of Creutzfeld-Jakob disease. |
| Describe the classic MR appearance of a brain affected by Liver Disease. What is the mechanism behind this appearance? | T1 intensity in the globus pallidus and substancia nigra, which is thought to be due to manganese deposition. |
| What changes can be seen on MR in the brain of a patient affected by severe hypoglycemia? | Bilateral T2 intensity in the gray matter of the cerebral cortex, hippocampi, and basal ganglia |
| What causes hypoxic ischemic encephalopathy (HIE)? | Circulatory or Respiratory arrest leading to global hypoxia/anoxia. |
| Which structures are typically affected by hypoxic ischemic encephalopathy. Involvement of which of these structures confers the worst prognosis? | The grey matter of the cerebral cortex, hippocampi, and basal ganglia (similar to severe hypoglycemia). These structures will demonstrate DWI and/or FLAIR intensity. Involvement of the basal ganglia confers the worst prognosis. |
| What are the CT signs of hypoxic ischemic encephalopathy? | Diffuse, global loss of grey-white differentiation, Diffuse cerebral hypoattenuation, and sulcal effacement. |
| Describe the "White Cerebellum Sign" and what it signifies. | The white cerebellum sign describes the typical sparing of te cerebellum in hypoxic ischemic encephalopathy. It appears white due to relative hyperattenuation in contrast to the hypoattenuating (affected) supratentorium. |
| What is the first clinical symptom often seen in cases of Methanol intoxication? | Optic Neuritis |
| What brain changes can be seen in patients experiencing Methanol intoxication? | Hemorrhagic necrosis of the putamen in association with white matter edema. |
| What are the MR imaging findings associated with carbon monoxide poisoning? | T2 intensity in the region of the globus pallidus |
| Describe, in general, Ludwig's Angina. | Cellulitis of the floor of the mouth which can involve the submental, sublingual, and submandibular spaces. The tongue can become rapidly posterior displaced due to edema, risking airway patency. Imaging reveals stranding/edema at the floor of the mouth. |
| In children, what is the most common cause of retropharyngeal abscess? | Spread of an upper respiratory tract infection such as pharyngitis. Enlargement and suppuration of the lymph nodes which drain the pharynx may lead to this spread. |
| In adults, what is the most common cause of retropharyngeal abscess? | Penetrating injury such as that of a fish bone piercing the posterior pharynx, allowing for direct innoculation. Instrumentation via the same mechanism is also a common cause. |
| What is the classic (buzzword) presentation of peritonsillar abscess? | "Hot Potato voice". Peritonsillar abscess is caused by suppuration and rupture of peritonsillar lymph nodes. |
| Describe Lemierre's Syndrome. | Venous thrombophlebitis of the tonsillar and peritonsillar veins, often with spread to the internal jugular vein. Metastatic pulmonary abscesses may be present. |
| Which patient population is at greatest risk of Lemierre's Syndrome. | Immunocompromised adolescents/young adults. |
| Which bug is most often responsible for Lemierre's Syndrome. | Fusobacterium necrophorum (typically normal mouth flora) |
| What are the imaging findings associated with Lemierre's syndrome? | Enlargement, thrombosis, and mural enhancement of the affected veins |
| Describe, in general, a Bezold abscess. | Bezold abscess is a complication of otomastoiditis where there is necrosis of the mastoid tip and resultant spread of infection into the adjacent soft tissues. |
| What are the imaging findings seen in Bezold abscess? | Opacification of the middle ear and mastoid cells often with bony erosion of the mastoid. |
| Describe, in general, a Ranula. | Mucous retention cyst that arises from the sublingual gland as a sequelae of inflammation. |
| From which gland do all Ranulas arise? | Sublingual gland(s) - thus all ranulas begin in the sublingual space |
| Describe a plunging Ranula. | A ranula which extends from the sublingual space into the submandibular space by protruding posteriorly over the free edge of the mylohyoid or by extending directly through a defect in the mylohyoid to below of the level of the mandible |
| Describe the difference in location of Plunging Ranula vs. Dermoid cyst. | Both can extend below of the mandible, but a dermoid is general midline while a plunging ranula is often eccentric/peripherally located. |
| Describe the histological difference between Dermoids and Epidermoid cysts. | Dermoids are teratomatous lesions which contain at least 2 germ cell layers while Epidermoids contain only ectoderm. |
| What is the major imaging finding which differentiates Dermoid from Epidermoid found in the oral cavity? | Both appear as fluid-attenuating lesions in the midline of the floor of the mouth. However, on MR, Dermoid will appear as a "sack of marbles" due to the presence of float fat globules. Without this finding, these entities are indistinguishable on imaging. |
| Describe, in general, a thyroglossal duct cyst. | TDC is due to a persistent thyroglossal duct. IT follows the midline descent of the embyronic thyroid gland from the base of the tongue (foramen cecum) to its normal position in the neck. |
| What is the common clinical presentation of a thyroglossal duct cyst? | A child with a midline, enlarging neck mass which elevates with tongue protrusion. |
| Describe the different potential positioning of thyroglossal duct cysts. | The majority (65%) are infrahyoid. The rest are found at the level of the hyoid or above. The majority are in the midline. |
| What is a rare malignant complication of thyroglossal duct cysts which occurs in 1% of cases? | Thyroid carcinoma of the papillary variety. |
| Which malignancies are most common at the floor of the mouth? | Papillary carcinoma from the thyroid and squamous cell carcinoma from the base of the tongue or tonsils which metastasize to this location. Both tend to be cystic in appearance. |
| Describe the characteristics and appearance of a FIRST branchial cleft cyst. | Rare. Usually located near the parotid or external auditory canal. It may first appear as a simple cyst though may eventually become heterogenous if infected. |
| Describe the location of SECOND branchial cleft cysts. | They occur along the path from the palatine tonsil to the supraclavicular region though most occur at the angle if the mandible. Classic location is anterior to SCM, posterior to submandibular gland, in close proximity to the carotid bifurcation. |
| What is the most common of the 4 types of branchial cleft cysts? | Second branchial cleft cyst is most common |
| Describe the difference between an infected second branchial cleft cyst and a submandibular abscess in terms of location. | Submandibular abscess is due to dental disease, located immediately below the mandible. Second BCC is general posterior to this location. |
| What is the standard treatment of submandibular/masticator abscess? | Aspiration + Antibiotics |
| Name the three types of lymphatic malformations which can be seen in the neck, from largest to smallest in appearance. | 1) Cystic hygroma (usually in posterior triangle of the neck), 2) Cavernous lymphangioma, and 3) Capillary lymphangioma |
| With which chromosomal abnormalities are Cystic Hygromas most often associated? | Down Syndrome and Turner's Syndrome |
| Describe a Thornwaldt Cyst. Where does it typically occur? | Notochordal remnant that is usually asymptomatic but may be a cause of halitosis. Typical location is in the midline of the pharynx. |
| Describe a Lingual Thyroid. | Ectopic thyroid tissue which has incompletely descended and remains at the floor of the mouth. Its usually the only functioning thyroid tissue so must confirm of lack of a normally positioned/functioning gland. Its susceptible to all thyroid pathology. |
| In which sex is lingual thyroid more commonly found? | Females |
| What is the most common cause of vocal cord paralysis? What are the less common causes? | Iatrogenic trauma from neck surgery. Less common causes include a mass along the course of the vagus or recurrent laryngeal nerve or enlargement of the left atrium causing compression of the recurrent laryngeal nerve ("cardiovocal syndrome") |
| What is the most common type of mass to cause vocal cord paralysis? | Mediastinal/Thoracic mass. |
| How do paralyzed vocal cord appear on CT imaging? | Thickened, medialized aryepiglottic fold and enlargement of the piriform sinus on the affected side |
| What structures does the recurrent laryngeal nerve innervate? | All laryngeal musculature except the cricothyroid which is innervated by the superior laryngeal nerve. |
| Describe a Laryngocele. Which populations are at risk for development of this phenomenon? | Dilation of the laryngeal ventricle which may be caused by high pressure. IT may be filled with fluid or air. Trumpet players, glassblowers, and patients with COPD are at increased risk of developing this. |
| Which differential diagnoses should be considered in laryngocele? | Laryngeal ventricular obstruction by squamous cell carcinoma (typically causes fluid filled laryngocele) |
| What is the most common type of cancer to affect the larynx? | Squamous cell, detected via direct visualization for biopsy. Lymphoma and Chondrosarcoma are more rare and occur submucosally so they are not seen via laryngoscope. |
| What is the most important imaging determination for a radiologist to provide in the case of laryngeal cancer? | Extent/Location - Supraglottic (30%), Glottic (65%), or Subglottic (5%). |
| What is a "transglottic" laryngeal cancer? | One which corsses the laryngeal ventricle to involve both the true and false vocal cords. This diagnosis changes surgical/treatment management. |
| What is the treatment for supraglottic/glottic laryngeal tumor vs. subglottic/transglottic laryngeal tumor? | Supraglottic/glottic = laser resection, Subglottic/transglottic = total laryngectomy (an extremely morbid procedure) |
| What type of damage can occur to the larynx during intubation? | Arytenoid dislocation. |
| Which cartilagenous structures in the neck are subject to fracture in the event of blunt trauma? (2) | Thyroid cartilage and cricoid cartilage, though this may be difficult to distinguish in kids in whom these structures may be incompletely ossified. |
| Which structures does the Ostiomeatal unit drain? (3) | 1) Maxillary sinus, 2) Frontal sinus, and 3) Ethmoid sinuses |
| Several air passages and a single bony structure make up the ostiomeatal unit - name the bony structure. | Uncinate process. Bonus: the passages include the maxillary sinus ostium, infundibulum, hiatus semilunaris, ethmid bulla, and middle meatus +/- frontal recess (depending upon author). |
| Isolated maxillary sinus disease is due to obstruction of which structure(s)? | Maxillary sinus ostium and/or infundibulum |
| Combined sinus disease involving the maxillary, frontal, and anterior ethmoid sinuses is due to obstruction of which structure(s)? | Hiatus semilunaris |
| Which structure demarcates the anterior from posterior ethmoid sinuses? | Basal lamella |
| Name the thin bone that forms the lateral wall of the ethmoid sinuses, separating them from the orbit. | Lamina Papyracea |
| The frontal sinus drains via which structure? | Frontal recess (into the ethmoid infundibulum) |
| The sphenoid sinus drains into the ethmoid cells via which structure? | Sphenoethmoid recess |
| To which meatus do the posterior ethmoid sinuses drain? | Superior meatus |
| To which meatus do the frontal, maxillary, and anterior ethmoid sinuses drain? | Middle Meatus |
| To which meatus do the lacrimal ducts drain? | Inferior Meatus |
| What disorder does FESS (Functional endoscopic sinus surgery) treat? | Chronic sinusitis |
| Describe a dehiscent lamina papyracea and its clinical relevance. | Medial bulging of the lamina papyracea into the orbit. IT is important to mention this in a report, to avoid a surgeon accidentally entering an orbit during surgery. |
| Describe a dehiscent cribiform plate and its clinical relevance. | Inferior bulging of the frontal lobe and cribiform plate. It is important to mention this in a report, to avoid a surgeon accidentally entering the frontal lobe during surgery. |
| What is the BEST imaging modality for evaluation of routine sinus disease? | CT (a low dose CT has the same radiation exposure as a 4 view x-ray series and secretions can vary far too greatly on MR to make definitive diagnoses). An exception for use of MR of the sinuses is to detect potential osteomyelitis. |
| Describe an Agger Nasi cell. What structure may it obstruct? | The most anterior and lateral ethmoid air cell which may cause obstruction of the frontal recess. |
| Describe a Haller cell. Why is it clinically significant? | An ethmoid air cell posterior to the orbit. It may compromise the maxillary ostium if it becomes enlarged or inflamed. |
| Describe an Onodi cell. What is its clinical relevance? | The most posterosuperior ethoid air cell, located directly inferomedial to the optic nerve. IT may be mistaken for the sphenoid sinus endoscopically, potentially placing the optic nerve at risk. |
| What is a concha bullosa? | Concha bullosa is formed when the ifnerior bulbous portion of the middle turbinate is pneumatized. IT is usually incidental but may cause septal deviation and narrowing of the infundibulum when large, |
| List the potential orbital complications of sinusitis. (3) | 1) Subperiosteal abscess, 2) orbital cellulitis, 3) ophthalmic vein thrombosis |
| List the potential intracranial complications of sinusitis. (3) | 1) Cavernous sinus thrombosis, 2) meningitis, 3) Intraparenchymal/Epidural/Subdural abscesses |
| List the potential bony complications of sinusitis. | 1) Periostitis, 2) Osteomyelitis |
| What is a "Pott's Puffy Tumor" | Osteomyelitis of the frontal bone causing a subgaleal abscess with associated soft tissue edema |
| Describe, in general, Allergic Fungal Sinusitis. Who suffers from this disorder? | A noninvasive disease caused by a hypersensitivity reaction to fungi. Most patients are immunocompetent but have a history of asthma. |
| Describe the imaging findings seen in Allergic Fungal Sinusitis. | The affected sinus will be expanded, airless, and filled with mixed attenuation /heterogeneous contents. The walls of the affected sinus will be thin and deossified. |
| Describe, in general, Acute Invasive Fungal Sinusitis. Who suffers from this disease and which bugs are the most common culprits? | An aggressive infection that occurs in immunosuppressed patients. Aspergillus and Zygomycetes are the most common organisms. Aspergillus can cause fulminant disease, acutely. |
| Describe the imaging findings seen in Acute Invasive Fungal Sinusitis. | Early imaging findings are nonspecific and including mucosal thickening. Later, more progressive findings include local invasion, bony destruction, and intracranial/intraorbital spread. |
| Which imaging feature most effectively differentiates allergic fungal sinusitis from acute invasive fungal sinusitis. | Invasive fungal sinusitis is NOT hyperdense on CT (but allergic fungal sinusitis can be) |
| What is an Antrochoanal polyp? | A benign polyp extending from the maxillary sinus into the nasal cavity with characteristic widening of the involved ostium. IT may erode bone an extend into the nasopharynx. It requires complete resection to prevent recurrence. |
| What is a Mucocele? | An expanded, airless sinus that results from obstruction of the sinus ostia. It may be secondary to inflammatory sinus disease. |
| Describe the imaging findings associated with mucocele. | Thinning of the walls of the affected sinus. Sinus contents appear homogeneous on CT imaging. T1 signal increases and T2 signla decreases as secretions dessicate. |
| What is an inverted papilloma? | A benign lobulated epithelial tumor of the sinus mucosa which is associated with squamous cell carcinoma in 10-20% of cases. The tumor tends to remodel bone. Treatment is surgical resection, which still results in recurrence ~15% of the time. |
| What is the classic imaging finding associated with inverted papilloma? | "Cerebriform" (curvilinear/gyriform) pattern of enhancement. This is incontrast to a mucocele which will not enhance. |
| What landmark demarcates the superficial lobe from deep lobe of the parotid gland in surgery (vs. on imaging. | The facial nerve, which courses through the gland is used for demarcation by surgeons. However, the facial nerve is not visible on imaging so radiologists rely on the position of the retromandibular vein for demarcation purposes. |
| Name the main duct of the parotid gland. | Stenson's duct. |
| Which is the only salivary gland to contain lymphatic tissue? Why? | Parotid gland (because it is the last to become encapsulated during embryological development) |
| Through which foramen does the facial nerve exit the skull, just before entering the parotid gland? | Stylomastoid foramen |
| Which are the smallest major salivary glands? | Sublingual glands |
| What is the most common benign salivary gland tumor, particularly of the parotid gland? | Benign pleomorphic adenoma (80% of all parotid tumors). It often presents as a small firm mass in a middle aged female. |
| How do minor salivary glands vary from the other (major) salivary glands (ie - submandibular, parotid) in terms of malignant potential of tumors arising from them? | Tumors of the minor salivary glands are much more likely to be malignant than tumors of the major salivary glands |
| Although they are benign, treatment of pleomorphic adenoma consists of complete surgical resection. Why? | Left unexcised they can continue to grow quite large, which increases their potential for malignant transformation to "carcinoma ex pleomorphic adenoma" |
| It is impossible to differentiate between benign pleomorphic adenoma and which other tumor of the parotid by imaging alone? | Malignant mucoepidermoid carcinoma |
| Why is preservation of the tumor capsule of a benign pleomorphic adenoma during resection of paramount importance? | To prevent diffuse tumor seeding. |
| What is the preferred imaging modality for evaluating small parotid tumor, benign pleomorphic adenoma in particular? | MR - T1 and T2 characteristics are the same as water. However, unlike a simply cyst, pleomorphic adenomas will enhance. |
| What is the second most common benign tumor of the parotid gland? Who typically gets these tumors? | Warthin tumor (~15% of benign parotid tumors). Elderly male patients with a history of smoking are at highest risk. |
| Is there any potential malignant transformation potential for Warthin tumors? | No - none whatsoever. |
| How does Warthin tumor appear on imaging and which characteristic differentiates it from Pleomorphic Adenoma? | It appears as a cystic neoplasm. Unlike Pleomorphic Adenoma, it does not enhance. |
| What is the most common maligant neoplasm of the Parotid gland? | Mucoepidermoid carcinoma (though in generally it is pretty rare, <5% of all salivary gland tumors, it is the most common malignant tumor). |
| Describe the imaging characteristics of Mucoepidermoid carcinoma. | Enhancing mass which is T2 intense. Indistinguishable from pleomorphic adenoma. |
| What is the most common malignant tumor of the submandibular and sublingual glands? (also happens to be the second most common malignant neoplasm of the parotid gland) | Adenoid Cystic Carcinoma. These are aggressive tumors which tend to both recur after resection as well as demonstrate metastasis. |
| Describe the feature which is unique to adenoid cystic carcinoma, not demonstrated by other neoplasms of the salivary gland (either benign or malignant). | Adenoid cystic carcinoma has a predilection for perineural spread such that it often presents with cranial nerve palsies/parasthesias. An enhancing mass with perineural spread is characteristic. |
| If a patient experiences rapid enlargement of a preexisting salivary gland mass, what is the most likely diagnosis? | Malignant conversion of Benign Pleomrophic Adenoma to Carcinoma Ex Pleomorphic Adenoma. |
| Describe the imaging difference between benign pleomorphic adenoma and carcinoma ex pleomorphic adenoma. | Benign pleomorphic adenoma is T2 hyperintense. The carcinoma version is hypointense on both T1 and T2. |
| What is the rarest carcinoma seen in the Parotid gland. | Squamous cell carcinoma because there are normally no squamous cells present in the parotid gland. However, prolonged inflammation can cause squamous metaplasia and thus, SCC. |
| What is the most common site of sialolithiasis and sialoadenitis? Give 3 reasons why. | Submandibular gland due to 1) its relative viscous secretions, 2) the alkalinity of the its secretions, and 3) its upward course which predisposes to stasis. |
| Which salivary gland is typically involved in Sarcoidosis? | Parotid gland, where it typically presents as bilateral painless swelling. |
| Describe the triad of symptoms associated with Uveoparotid Fever? What is this condition pathognomonic for? | Bilateral uveitis, parotid enlargement, and facial nerve palsy - pathognomic for sarcoidosis. |
| What is the very classic finding associated with salivary gland invovlvment in sarcoidosis seen on Gallium-67 scintigraphy? | "Panda Sign" due to increased uptake of Gallium-67 by the parotid and lacrimal glands. |
| What are the primary organs affected by Sjogren's Syndrome? Who is most often affected? | The Salivary and Lacrimal glands (of middle aged females). |
| What are the imaging characteristics seen in the salivary glands of a patient with Sjogren's Syndrome? | Atrophy and fatty replacement with multiple nodules, enhancement, numerous small cystic foci, and pubctate calcifications |
| The risk of which malignancy is increased in patient's with Sjogren's Syndrome? | Lymphoma, particularly of the parotids and/or head/neck |
| How are the parotids of patients with HIV affected? | HIV-infected parotid glands often demonstrate lymphoid dysfunction in the form of multiple bilateral lymphoepithalial cysts and solid masses. |
| Cranial nerve V2 traverses which foramen to exit the skull? | Foramen Rotundum |
| Cranial nerve V3 transverse which foramen to exit the skull? | Foramen Ovale |
| Describe, in general, Juvenile Nasopharyngeal Angiofibroma | Benign, highly vascular tumor seen in adolescent males. It often presents with nasal obstruction and epistaxis. Can be locally aggressive, traveling through adjacent foramen. Frequently recurs even if resected. |
| From which foramen do Juvenile Nasopharyngeal Angiofibromas arise? | Sphenopalatine Foramen (its nasal aspect) |
| Describe the imaging appearance of Juvenile Nasopharyngeal Angiofibroma. | Avidly enhancing mass, centered in the nasopharynx +/- extension into the pterygopalatine fossa or orbits. 3 classic findings: 1) Nasopharyngeal mass, 2) Expansion of the pterygopalatine fossa, 3) anterior bowing of posterior maxillary sinus wall |
| What pre-operative consideration must be made prior to surgical resection of juvenile nasopharyngeal angiofibroma? | Embolization, to prevent bleeding due its highly vascular nature |
| Describe, in general, Olfactory Groove Meningioma. | Similar appearance to Meningiomas elsewhere in the skull (avid enhancement, dural tail, adjacent reactive bony sclerosis). Simply found at olfactory groove in the skull base. |
| Describe, in general, Enthesioneuroblastoma (aka Olfactory Neuroblastoma) | Malignant neural crest tumor arising from specialized olfactory epithelium. Incidence is bimodal, peaking in teenage years and middle age. |
| Describe the imaging characteristics of Enthesioneuroblastoma. | Aggressive mass which is slightly hyperattenuating on CT and intermediate signal on T1 and T2 due to high cellularity. Calcifications are often present. |
| What is the pathognomic finding associated with Enthesioneuroblastoma? | Peripheral tumor cysts that occur at the margins on the intracranial portion of the mass. |
| What is the most common malignancy of the paranasal sinuses? What is the most common primary site for this malignancy? | Squamous Cell Carcinoma. Most commonly arising from the maxillary antrum. |
| What is the most common head/neck tumor in kids? | Rhabdomyosarcoma |
| Which type of cancer can occur both within the saivary glands and paranasal sinuses which appears cyst-like (water-type characteristics on MR) but demonstrates avid enhancement? | Adenoid cystic carcinoma |
| Which middle ear structures are typically absent in the case of external auditory canal atresia? (2) | Malleus and Incus (both, along with the EAC, are first branchial cleft cyst structures) |
| Who is at risk of external auditory canal exostosis? | People who swim or surf in cold waters |
| What is Necrotizing otitis externa (aka malignant otitis externa) are who is affected by this disorder? | Severe, fast-spreading, aggressive external otitis +/- bony erosion seen in elderly diabetic or immunocompromised patients. Pseudomonas is the most common organism is diabetics and Aspergillus is the most common organism in the immunocompromised. |
| Describe Keratosis obturans. | Bilateral keratin plugs within enlarged external auditory canals, typically seen in young patients with sinusitis and bronchiectasis. |
| Can Cholesteatomas affect the external auditory canal? | Yes, though it is seen more often in the middle ear |
| What is Glomus tympanicum? | Extra-adrenal pheochromocytoma (paraganglioma) isolated to the middle ear. It presents clinically with pulsatile tinnitus or conductive hearing loss. A vascular, red mass may be seen behind the tympanic membrane. |
| What is the most common malignant tumor of the middle ear? | Glomus tympanicum. |
| Schwannoma of which cranial nerve can affect the middle ear? | Facial nerve (CN VII). Within the temporal bone, these tend to be slow growing and most commonly involve the geniculate ganglion, followed by the labyrinthine and tympanic segments. |
| What innervation is provided by the labyrinthine segment of the facial nerve? | Salivation (via greater superficial petrosal nerve) |
| What innervation is provided by the mastoid/descending segment of the facial nerve? | Taste (via chorda tympani) and sound conduction via ossicular function of the stapedius (via nerve to stapedius) |
| Describe the imaging findings associated with Facial nerve Schwannoma. | Enlargement of the bony canal through which the affected portion of the facial nerve courses and brisk contrast enhancement. |
| What is the most common benign lesion of the petrous apex? | Cholesterol granuloma (cyst) - though it may also occur in the middle ear |
| Describe, in general, Cholesterol granuloma (cyst). | A soft tissue cyst formed by giant cell reaction to cholesterol crystals thought to initially be incited by an obstructed air cell. One may be a blue lesion behind the tympanic membrane. |
| How can one distinguish cholesteatoma from a cholesterol granuloma on imaging? | Cholesteatoma will have restricted diffusion but cholesterol granuloma will not. Also, Cholesterol granuloma will be T1 hyperintense. |
| What lesion is indicated by a white mass behind the tympanic membrane on physical exam? | Cholesteatoma |
| What are the differential diagnoses from lesions behind the tympanic membrane of the following colors: 1) red, 2) white, and 3) blue | 1) Red lesion = Glomus tympanicum, 2) White lesion = Cholesteatoma, 3) Blue lesion = Cholesterol granuloma |
| Describe, in general, Cholesteatoma. | Non-neoplastic lesion of the temporal bone which can be described as "skin in the wrong place". In the middle ear, they are almost always acquired (98%). In any other location within the temporal bone, they are almost always congenital. |
| Why is the name "cholesteatoma" deceptive? | Because they do not contain any fat. Nor are the neoplastic. |
| What is the Intracranial, extra-axial equivalent of a cholesteatoma? | Epidermoid cyst |
| Describe the clinical sequela of middle ear cholesteatoma. | Recurrent ear disease, eutachian tube obstruction, chronic ear discharge, and mixed sensorineural/conductive hearing loss. |
| Which 3 structures MUST be mentioned when describing the extent of a cholesteatoma on imaging? | 1) Lateral semicircular canal, 2) Tegmen tympani (the bony roof separating the mastoid air cells from the brain), and 3) Facial nerve |
| What are the most specific MR sequences on which to evaluate a cholesteatoma? (2) | DWI and Post-contrast sequences (Cholesteatomas demonstrate restrcited diffusion but do not enhance - same characteristics of intra-cranial/extra-axial epidermoid cysts) |
| Is the restricted diffusion demonstrated by cholesteatomas truly restricted diffusion? | Not entirely - the restricted diffusion demonstrated by cholesteatomas is a combination of true restricted diffusion and T2 shine through |
| What is Mondini Deformity (aka Cochlear dysplasia)? | Incomplete development of the cochlea. The most common form is lack of the normal 2.5 turns of the cochlea (loss of apical and middle turns) while the final basilar turn is preserved. |
| Mondini deformity is associated with which additional ear abnormality? | Enlarged vestibular aqueduct |
| What is Michel Aplasia? | Complete lack of development of the entire inner ear (Very rare) |
| An enlarged vestibular aqueduct may lead to what symptom in which scenario? | While in doesnt play a direct role in hearing, an enlarged vestibular aqueduct may cause progressive conductive hearing loss while playing contact sports. |
| What is Otospongiosis? What is another name for this entity and which population does it affect? | "Otosclerosis" is a primary dysplasia of the bone of the otic capsule characterized by replacement of normal endochondral bone by irregular spongy bone. It occurs in young to middle aged women and is often bilateral. |
| What are the two main types of Otospongiosis/Otosclerosis? | 1) Fenestral (more common, affects the oval window) and 2) Retrofenestral ("Cochlear type", more severe, affects the otic capsule and lateral wall of the labyrinth) |
| What are the 3 differential diagnoses for Retrofenestral Otospongiosis/Otosclerosis as divided by age? | 1) Osteogenesis imperfecta (in a child), Fibrous dysplasia (young adult), 3) Paget disease (older adults) |
| What is the best imaging modality to evaluate Otospongiosis/Otosclerosis? | CT (will show increased lucency of the affect bone) |
| Describe Labyrinthitis. What are the 3 stages of this disorder? | Inflammation of the inner ear which may be infectious or autoimmune. 1) Acute, 2) Fibrous, and 3) Ossificans. |
| What defines acute labyrinthitis? | Earliest stage of this disorder, presents as pus in the inner ear. The only MR imaging finding is enhancement of the affected inner ear structures. |
| What is the main differential diagnosis in a case of acute labyrinthitis? | Cochlear or intralabyrinthine schwannoma. |
| What defines Fibrous labyrinitis? | Replacement of the endolymph and perilymph with fibrous strands of decreased T2 signal intensity. |
| What defines Labyrinthitis ossificans? | Calcified debri replaces the fibrous strands left by the prior stage. Thus, CT is the best modality to evaluate this stage. |
| Disruption of the tympanic membrane is associated with development of which ear finding? | Cholesteatoma. |
| Which type of hearing loss is associated with longitudinal fracture of the temporal bone? | Conductive hearing loss |
| Which type of hearing loss is associated with transverse fracture of the temporal bone? | Sensorineural hearing loss |
| Which type of temporal bone fracture is more likely to cause facial nerve injury? | Transverse (50%). Longitudinal fractures only result in facial nerve injury approximately 20% of the time. |
| What is the Petrous apex? | The most medial portion of the temporal bone |
| Which 3 important structures are located adjacent to the petrous apex? | 1) Dorello's canal, 2) Meckel's cave, 3) the petrous portion of the internal carotid artery |
| Which nerve passes through Dorello's cave? | Cranial Nerve 6 |
| What structure resides in Meckel's cave? | Trigeminal ganglion |
| Which 8 pathologies can affect the Petrous Apex? What is the mnemonic? | ACGME MC's: 1) Apical petrositis, 2) Cholesteatoma (congenital), 3) Granuloma (cholesterol), 4) Meningioma, 5) Eosinophilic granuloma (LCH), 6) Schwannoma 7) Myeloma/Metastasis, 8) Chondrosarcoma/Chordoma |
| Describe Apical Petrositis/Petrous Apicitis. | A relatively rare cmplication of infectious otomastoiditis which occurs when infection extends medially into a pneumatized petrous apex causing fluid opacification of the petrous air cells, bony demineralization/resorption, and localized osteomyelitis. |
| What are the 3 components of Gradenigo Triad? | 1) Otomastoiditis, 2) Facial pain due to trigeminal nueropathy at Meckel's cave, and 3) Lateral rectus palsy due to compression of CN6 at Dorello's canal. |
| What are the two main vascular complications of apical petrositis? | 1) Internal carotid arteritis and 2) Dural venous thrombosis |
| Petroud apex schwannoma may originate from one of which 3 cranial nerves? | 5, 7, or 8 |
| What is the most common site of skull base involvement seen in Langerhan's Cell Histiocytosis? | Temporal bone |
| Describe, in general, Langerhan's Cell Histiocytosis. | Aka - Eosinophilic granuloma. Neoplastic proliferation of both eosinophils and Langerhan's cells. |
| What are the CT image findings of Langerhan's Cell histiocytosis (eosinophilic granuloma)? How about MR imaging findings? | CT: Well-circumscribed destructive lesion of bone with nonsclerotic margins. MR: soft tissue masses surrounded by bone marrow and edema which demonstrate enhancement. |
| Describe Chondrosarcoma in relation to its location at the clivus vs. petrous apex. | Malignant neoplasm which affects the clivus (arises in the midline) or the petroclival synchondrosis (arises slightly off the midline). |
| What are CT imaging findings (particularly of the internal composition) of chondrosarcoma at the clivus/petrous apex? | "Ring and arc" chondroid matrix |
| What are the MR imaging charactersitics of chondrosarcoma at the clivus/petrous apex? | Lobular, cauliflower-like lesion which is T2 intense |
| Describe Chordoma in relation to how it may come to affect the petrous apex. | Malignant lesion which most commonly arises from the clivus but it may expand laterally to involve the petrous apex. Can be disfficult to distinguish from chondrosarcoma. |
| Describe the normal MR signal of the clivus in adults. How does this vary from its signal in children? | In adults, the clivus should demonstrate fatty marrow appearance on T1. However, in kids, clival fatty marrow signal may be low due to the presence of hematopoeitic marrow. This appearance in adults should suggest neoplastic disease. |
| Which type of cancer has a propensity for metastasis to the clivus? | Breast Cancer |
| Describe, in general, the characteristics of Chordoma. | Locally invasive tumor which arises from notochord remnants. While it is the most common tumor of the clivus, it appears at the sacrum more commonly (50%). The remainder occur in the vertebral column. |
| Do Chordomas have internal matrix (like chondrosarcomas)? | No, they do not. However, the may contain calcifications which represent fragments of eroded bone. Also, similar to Chondrosarcoma, Chordoma will appear T2 intense. |
| From what type of tissue do Glomus tumors (aka - Paragangliomas) arise? | Sympathetic glomus body cells (as such, they are histologically identical to extra-adrenal pheochromocytoma) |
| Are most glomus tumors (paragangliomas) malignant? | No, most are benign but they can be locally aggressive. Less than 5% undergo malignant degeneration. |
| With which disorders are Paragangliomas often associated? (2) | MEN type 1 and Neurofibromatosis type 1 (often multiple in number) |
| Describe the classic MR appearance of Paragangliomas (Glomus Tumors). | "Salt and Pepper" appearance due to intratumoral flow voids (these are highly vascular tumors and as such, they enhance avidly) |
| What is the most common tumor of the Jugular Foramen? Who is most often affect by these tumors? | Glomus jugulare (type of glomus tumor/paraganglioma) - most often affect late middle aged woman who present with pulsatile tinnitus and conductive hearing loss. |
| Describe the classic CT appearance of a Glomus Jugulare tumor. | "Moth Eaten" bony destruction structured around the jugular foramen. |
| Which two types of tumors may occur near the jugular foramen, similar to a Glomus jugulare? | Schwannoma (smooth bony remodeling, will not appear moth eaten) or Meningioma (causes hyperostosis) |
| Where does glomus tympanicum typically arise? | Middle Ear (red vascular mass behind the tympanic membrane) |
| Which 3 differentials should be considered when a "Red vascular mass behind the tympanic membrane" is seen? | 1) Glomus tympanicum, 2) Aberrant carotid artery, 3) Tympanic membrane hemangioma |
| What is a Glomus jugulotympanicum? | A glomus jugulare tumor which has spread into the middle ear |
| Where does a Glomus caroticum typically arise? | The carotid body (aka "carotid body tumor") where it characteristically splays the internal from external carotid artery. |
| Describe, in general, Glomus vagale. | Paraganglioma of the vagus nerve which typically occurs at the same level as teh carotid body tumor. |
| How does the displacement of the carotid artery/branches vary in glomus caroticum vs glomus vagale? | Carotid body tumor = separates the internal from the external carotid arteries. Glomus vagale = will push both the internal and external carotid artery medially and anteriorly |
| What is the main differential diagnosis for glomus vagale? | Schwannoma of the vagus nerve (it displaces the interal and external carotid arteries medially and anteriorly, just like gomus vagale). However, while both will enhance avidly, Schwannoma will not have the associated "salt and pepper" flow voids. |
| Name the 5 types of glomus tumors in the head/neck. | 1) Glomus vagale, 2) Glomus caroticum, 3) Glomus jugulare, 4) Glomus tympanicum, 5) Glomus jugulotympanicum |
| Which cranial nerve in the cavernous sinus does NOT pass through the superior orbital fissure on its exit from the sinus? | V2 (exits via foramen rotundum then enters the orbit via the inferior orbital fissure) |
| Which vessel accompanies the V2 nerve through the inferior orbital fissure? | Infraorbital artery |
| Which nerves exit the cavernous sinus and pass through the superior orbital fissure? Which vessel accompanies them? | CN 3, 4, 6, and V1. The Superior ophthalmic vein accompanies them. |
| Portions of which 5 bones converge to form an orbit? | 1) Frontal, 2) Ethmoid, 3) Nasal, 4) Zygomatic, and 5) Maxilla |
| Which two structures pass through the optic foramen? | Optic nerve and ophthalmic artery |
| What are the two main divisions of the orbit? | Preseptal orbit and postseptal orbit |
| What structures are contained in the preseptal vs. postseptal orbit? | Preseptal orbit is a superficial potential space which does not contain any structures. Postseptal orbit is basicallt the whole orbit (divided into extraconal, conal, and intraconal compartments as well as the globe) |
| What structures are contained in the Extraconal compartment of the postseptal orbit? (3) | Lacrimal gland, fat, bony orbit |
| What structures does the conal compartment of the postseptal orbit contain? | Extraocular muscles |
| What structures does the intraconal compartment of the postseptal orbit contain? | 1) optic nerve and its nerve sheath, 2) sensory and motor nerves of the orbit, 3) lymph nodes, 4) fat |
| Within the conal compartment of the postseptal orbit, from what structure do all (except for 1) extraocular muscles arise? From which structure does the single exception arise from? | All the extraocular muscles except the inferior oblique arise from a fibrous ring called the annulus of Zinn. the inferior oblique arises from the medial orbital floor. |
| What is the most common route of spread for development of orbital infection? | Direct spread from the paranasal sinuses |
| Describe the clinical presentation of preseptal orbital infection. | Infection of the preseptal space with swelling and erythema of the eyelids |
| Describe the characteristics of orbital cellulitis/phlegmon. | Infection within the orbit that is not yet organized or ring-enhancing. May predispose to intracranial infection via spread through the valveless ophthalmic veins. |
| Describe the characteristics and treatment of orbital subperiosteal abscess. | Organizing infection underneath the orbital periosteum which presents with exophthalamos and visual impairment. It is a surgical emergency (needs drainage) due to risk of blindness from elevated intraocular pressure. |
| Which is more severe, orbital abscess or subperiosteal abscess? | Orbital abscess |
| Describe the characteristics of orbital abscess. | Abscess involving the subperiosteum and entireity of the orbital bone which presents with ophthalmoplegia and exophthalamos |
| Aside from blindness, what is the most feared complication of orbital infections? | Cavernous sinus thrombosis. Can present with multiple cranial nerve palsies plus symptoms of orbital abscess. |
| What are the 6 main differential diagnoses for orbital masses (not involving the optic nerve/sheath)? | 1) Hemangioma, 2) Orbital lymphoma, 3) Lymphangioma, 4) Schwannoma/neurofibroma (usually V1), 5) Metastasis, 6) Lacrimal gland lesions |
| What are the two different varieties of orbital hemangioma? Which is more common and which populations does each affect? | Cavernous hemangioma (adults, most common) or capillary hemangioma (first year of life) |
| Describe the imaging findings of orbital cavernous hemangioma. | Usually intraconal, composed of vascular channels filled with slow moving blood. CT: ovoid enhancing mass +/- bony remodeling. MR: T1 isointense, T2 hyperintense with early patchy enhancement that progressively fills in. |
| Which cutaneous manifestions often accompan the presence of an orbital capillary hemangioma? | Port wine stains and strawberry hemangiomas. Like these lesions, the capillary hemangioma may enlarge overthe first few months of life then spontaneously regress/involute. |
| What orbital organ is most commonly affected by lymphoma? What is the classic clinical presentation? | Lacrimal gland. Classically presents with painless downward proptosis. |
| Describe the imaging characteristics of orbital lymphoma. | Cellular mass that is hyperattenuating on CT and hyperintense of both T1/T2. |
| What is the main clinical difference that may differentiate orbital lymphoma from orbital pseudotumor? | While both tend to deform the globe, orbital pseudotumor is generally painful while lymphoma is generally painless. |
| Describe the general characteristics of intraorbital lymphangioma. | Benign hamartomatous lesion seen in the pediatric population. Also known as low flow lymphatic malformation. Usually found in extraconal region. |
| What are the imaging findings associated with intraorbital lymphangioma? | Multilocular cystic mass often with complex internal contents and fluid levels from prior hemorrhage. Slight peripheral and septal enhancement is often seen. |
| What nerve is most commonly affected by schwannoma in the orbit? How does this appear on imaging? Which similar entity can be indistinguishable from intraorbital schwannoma? | V1. They demonstrate T1 hypointensity, T2 hyperintensity, and enhancement. Intraorbital schwannoma can be indistinguishable from neurofibroma though schwannoma is more common. |
| Where does Scirrhous breast cancer most often metastasize to? How does it appear? | The orbit where it causes fibrosis which can prevent exophthalamos, or even create frank enophthalmos. |
| Which malignancy preferentially metastasized to the orbit in kids, causing a sunburst periosteal reaction in at the nearby bone? | Neuroblastoma |
| Describe the percentage of benign vs. malignant lesions which affect the lacrimal gland. | About 50/50. Because the gland contains epithelial salivary tissue, it is subject to pleomorphic adenoma (benign) and adenoid cystic or mucoepidermoid carcinoma (malignant). It also contains lymphoid tissue (subject to sarcoidosis and lymphoma) |
| What is the most common structure affected by intraorbital lymphoma? | Lacrimal gland |
| What substance mediates the intraorbital inflammatory response seen in thyroid ophthalmopathy? | Hyaluronic acid, which usually leads to fibrosis via persistent inflammation. |
| Which thyroid pathology is most often associated with thyroid ophthalmopathy? | Graves Disease (may even precede changes in lab values) |
| What is the first change seen in Thyroid ophthalmopathy? What is the second change? | Increased intra-orbital fat occurs first, which may demonstrate stranding due to inflammation. Enlargement of the extraocular muscles occurs next. |
| In what order (first to last) are the extraocular muscles affected? | The mnemonic is "I'M SLow"... I(nferior rectus), M(edial rectus), S(uperior rectus), and L(ateral rectus) |
| What factors help distinguish between the diagnosis of orbital pseudotumor vs. thyroid ophthalmopathy? | Thyroid eye disease will eventually affect all 4 rectus muscles while pseudotumor affects only the lateral rectus. Also, thyroid eye disease is bilateral and spares the extraocular muscle tendons while pseudotumor is unilateral and does affect the tendons |
| What is the treatment of thyroid ophthalmopathy? | Steroids. Though up to 20% of cases will require surgical decompression to preserve the optic nerve. |
| Describe, in general, the entity known as orbital pseudotumor. | Idiopathic orbital inflammation mediated by an infiltrate of lymphocytes, plasma cells, and macrophages. It can only be diagnosed after other causes of orbital inflammation are ruled out. |
| Which process is synonomous with Orbital Pseudotumor (idiopathic inflammation causing eye pain), except that it occurs in the cavernous sinus? | Tolosa-Hunt Syndrome |
| Describe, in general, the characteristics of Optic Nerve Glioma. | Tumor that affects both kids and adults but has a different course/outcome depending on age. Kids get slow, indolent astrocytoma growth. Adults, however, get anaplastic astrocytoma or GBM which carries a much worse prognosis. |
| What is the most common tumor of the sheath of the optic nerve? Second most common? | Optic Nerve Glioma is the most tumor of the optic nerve sheath. Meningioma is the second most common (arises from the arachnoid cells within the leptomeninges surrounding the optic nerve. |
| What syndrome is associated with optic nerve gliomas in kids? | Neurofibromatosis type 1. |
| Describe the typical patient diagnosed with meningioma of the optic nerve sheath. | Middle aged female with slowly progressive vision impairment, classically with preservation of the central visual field. |
| Describe the classic imaging characteristics of optic nerve sheath meningioma. | The nerve sheath tends to be circumferentially thickened with uniform contrast enhancement. The enhancing peripheral tumor and non-enhancing optic nerve create the classic "Tram Track" sign on axial imaging. |
| Describe the clinical presentation of optic neuritis. | Non-neoplastic inflammation of the optic nerve resulting in pain, subacute vision loss, and reduced color vision. |
| What is the most common cause of optic neuritis? | Multiple Sclerosis. |
| Which syndrome is characterized by the combination of optic neuritis and spinal demyelination? | Devic Syndrome |
| Describe the imaging findings of optic neuritis. | Optic nerve enhancement and T2 hyperintensity. Enhancement suggests active disease. Chronically, the nerve will atrophy. |
| Lesions of the globe are primarily seen in which patient population? | Pediatric population |
| What is the most common primary malignancy of the globe? | Retinoblastoma |
| What is the typically presentation of retinoblastoma? | Leukocoria (white pupillary reflex) in kids <5 years old |
| Describe the distribution of retinoblastoma lesions when they are sporadic vs. familial. | Sporadic = unilateral. Familial (usually due to p53 mutations) = bilateral. |
| What are the classic imaging characteristics of retinoblastoma? | Hyperattenuating, enhancing retinal mass (posterior aspect of globe) with calcifications in a normal sized globe. |
| Describe Coat disease. | Vascular disease of the retina causing lipoproteinaceous subretinal exudates that lead to retinal detachment, seen in boys. |
| Describe the imaging characteristics seen in Coat disease. | Normal sized globe with scattered/multiple calcifications and peripheral/posterior high attenuation material which doesn't enhance. |
| Describe the general characteristics of Retinopathy of Prematurity. | Retinopathy in premature infants due to prolonged oxygen exposure for neonatal care. One may seen abnormal vascular development, hemorrhage, and retinal detachment. Usually bilateral with *small* globes. |
| Describe the imaging characteristics of Retinopathy of Prematurity. | Small globe with increased attenuation due to prior hemorrhage. Multiple calcifications. End stage findings include phthisis bulbi. |
| Which main feature distinguishes Retinopathy of prematurity from retinoblastoma? | While both demonstrate calcifications, the globe is normal sized in retinoblastoma and reduced in size in retinopathy of prematurity. |
| Describe the general characteristics of Persistent Hyperplastic Primary Vitreous (PHPV). | Persistent embryonic vasculature within the vitreous that leads to loss of vision from hemorrhage, cataracts, and retinal detachment. |
| Is Persistent Hyperplastic Primary Vitreous usually associated with prematurity? | No, it usually occurs in full term infants. |
| How does one distinguish Persistent Hyperplastic Primary Vitreous from Retinoblastoma and Retinopathy or prematurity? | PHPV has no calcifications while the others do. |
| What causes coloboma? | Incomplete fusion of the embryonic intraocular fissure, which results in an elongated or malformed globe. |
| Which 4 pediatric syndromes is Coloboma associated with? | 1) CHARGE, 2) VATER, 3) Trisomy 13, and 4) Trisomy 18 |
| Which syndrome can result in sphenoid wing dysplasia? | Neurofibromatosis type 1 |
| What is Septo-optic dysplasia? | Optic nerve hypoplasia and agenesis of the corpus callosum. Often associated with Schizencephaly (ful thickness cleft in a cerebral hemisphere that creates a communication between the ventricles and subarachnoid space) |
| Which structures form the masticator space? | Muscles of mastication, the mandible, and V3 |
| What are the 3 main differentials for masticator space lesion? | 1) Odontogenic disease (may lead to abscess), 2) Mandibular lesion (Osteosarcoma and metastasis are the two main offenders), and 3) Rhabdomyosarcoma |
| Which structures form the carotid space? | Carotid artery, carotid body, jugular vein, and the vagus nerve (CN 9, 11, and 12 pass through the carotid space transiently). |
| What are the 3 main differentials for carotid space lesion? | 1) Paraganglioma, 2) Schwannoma, and 3) Neurofibroma |
| Which structures form the parapharyngeal space? | Fat... there are no significant contents aside from occasional ectopic minor salivary gland tissue. |
| How does the displacement of the parapharyngeal space by an adjacent mass lesion hint at where the lesion arises? | The specific direction of displacement will give away the location of the mass. |
| Displacement of the parapharyngeal space in a posteromedial direction hints at a lesion in which space? | Masticator space |
| Displacement of the parapharyngeal space in a anteromedial direction hints at a lesion in which structure? | Parotid lesion |
| Displacement of the parapharyngeal space in a anterior direction hints at a lesion in which space? | Carotid space |
| Which structures are contained by the perivertebral space? | Vertebral arteries, paraspinal muscles, spinal column, and exiting nerves |
| Which lymph nodes are included in the group 1A nodal chain? | Submental nodes (lying between the medial margins of the anterior bellies of the diagastrics) |
| Which lymph nodes are included in the group 1B nodal chain? | Submandibular nodes (lateral to the medial margin of the anterior belly of the digastric and extending to the posterior margin of the submandibular gland. |
| Which lymph nodes are included in the group 2A nodal chain? | Upper internal jugular nodes anterior to the posterior margin of the internal jugular vein |
| Which lymph nodes are included in the group 2B nodal chain? | Upper internal jugular nodes posterior to the internal jugular vein but anterior to the posterior margin of the sternocleidomastoid muscle |
| Which lymph nodes are included in the group 3 nodal chain? | Middle jugular nodes extending craniocaudally from the inferior hyoid to to the inferior aspect of the cricoid cartilage, posteriorly to the sternocleidomastoid |
| Which lymph nodes are included in the group 4 nodal chain? | Inferior jugular nodes extending from the inferior cricoid cartilage to the clavicle, the superoposterior border is the sternocleidomastoid, the inferoposterior border is the anterior scalene muscle. |
| Which lymph nodes are included in the group 5A nodal chain? | Superoposterior cervical nodes extending from the skull base to the inferior cricoid cartilage. |
| Which lymph nodes are included in the group 5B nodal chain? | Inferoposterior cervical nodes extending from the inferior cricoid cartilage to the clavicle. |
| Which lymph nodes are included in the group 6 nodal chain? | Pretracheal lymph nodes (bounded laterally by the carotid sheaths) |
| Which lymph nodes are included in the group 7 nodal chain? | Superior mediastinal lymph nodes |
| What are the differential diagnoses for intramedullary (deep to the pia) spinal lesions? (4) | 1) Astrocytoma (including GBM), 2) Ependymoma, 3) Hemangioblastoma, and 4) Demyelinating lesions (ie - MS) |
| What are the differential diagnoses for intradural-extramedullary (deep to the dura but external to the pia) spinal lesions? | 1) Schwannoma/Neurofibroma, 2) Meningioma, 3) Dermoid cyst, 4) Epidermoid cyst, 5) Myxopapillary ependymoma, 6) Arachnoiditis |
| Describe the myxopapillary variant of ependymoma. | Ependymoma which occurs exclusively within the conus medullaris or filum terminale. Grows very slowly. Causes vertebral scalloping and canal enlargement. Highly vascular/hemorrhagic tumor with peripheral hemosiderin often present. |
| Describe, in general, arachnoiditis. | Inflammation of the arachnoid surrounding the nerve roots which produces fibrinous exudate and secondary dural adhesions. In the past syphilis and TB were common causes but now a days, its usually spinal surgery. |
| Which three patterns of arachnoiditis are seen on imaging? | Group 1: Central conglomerations of nerve roots in the thecal sac, Group 2: Peripheral clumping of the nerve roots causing "empty thecal sac sign", Group 3: Obliteration of subarachnoid space (increased soft tissue attenuation in thecal sac, most severe) |
| What is the differential diagnosis of extradural spinal lesions? | 1) Degenerative disease (osteophytes, herniated discs), 2) Metastasis, 3) Discitis/Osteomyelitis, 4) Hemangioma, 5) Chordoma, 6) Plasmacytoma, 7) ABC, 8) Chondroblastoma, 9) Osteoid osteoma, 10) Osteosarcoma, 11) Epidural Lipomatsis |
| What buzzword is typically used to describe the appearance of a hemangioma within a vertebral body? | "Corduroy appearance" (will be hyperintense on T1 and T2) |
| Describe the cause and appearance of epidural lipomatosis. | Rare overgrowth of fat in the extradural space which can compress adjacent neural elements (potentially, cauda equina syndrome). Can be caused by steroid use, Cushing's disease, or morbid obesity. |
| Describe the appearance of Plasmacytoma. | Lytic, expansile bony lesion of late adulthood that is thought to be a precursor of multiple myeloma. Generally a solitary lesion but multiple implies MM. Urine and serum electrophoresis abnormalities may not change for years following their appearance. |
| Describe the difference between intervertebral disc bulge vs herniation (protrusion vs. extrusion). | Broad base bulge: >180 degrees of the disc circumference extends beyond the vertebral body margin. Herniation is divided; Protrusion: focal herniation where the base is wider than the dome, Extrusion: focal herniation where dome is wider than the base. |
| Where (above or below) do the spinal nerve roots exit in the cervical vs. thoracic vs. lumbar spine? | Cervical: nerve roots exit above their named vertebral body, Thoracic/Lumbar: nerve roots exit below their named vertebral body |
| What are the 4 distinct terms used to describe the medial-lateral position of a posterior intervertebral disc space herniation? | Central, paracentral, foraminal, and far lateral (extra foraminal) |
| Describe what a "sequestered fragment" of herniated intervertebral disc is. | Once protruded, disc material may separate from its parent disc and migrate inferiorly or superiorly. |
| What is a Schmorl's node? | Inferior or superior herniation of an intervertebral disc into the adjacent vertebral body endplate which creates a distinct-appearing bony defect. Acutely, they may contribute to back pain. |
| What are "Modic" changes of the spine? | Degenerative changes in the spine that are associated with vertebral body endplate and subchondral marrow signal changes. There are 3 types. |
| Describe Modic type 1 changes. | Vertebral body bone marrow edema and inflammation. Hyperintense on T2, hypointense on T1. Associated with upper back pain. Convey better outcome following lumbar spine surgery. |
| Describe Modic type 2 changes. | Reflect fatty proliferation within the vertebral body marrow secondary to chronic marrow ischemia. Hyperintense on both T1/T2. Not likely to be associated with active symptoms. |
| Describe Modic type 3 changes. | Represent sclerosis of the bone marrow of the vertebral bodies. . Are of unclear significance. Hypointense on T1/T2. |
| Describe a "Tarlov Cyst" in the spine. | In contrast to a synovial cyst, a Tarlov cyst is not associated with facet arthropathy. Its a perineural cyst of the sacrum, formed within the nerve root sheath, which is usually asymptomatic. |
| Describe a "Synovial Cyst" in the spine. | Epidural cyst that is associated with facet arthropathy. They are hyperintense on T2 with variable T1 signal depending on the presence or absence of associated internal bleeding. |
| A thin linear segment of T2 hyperintensity in the annulus fibrosis may be described as what entity? | Annular fissure or annular tear (fissure is preferred because tear implies trauma though this finding is usually due to disc degeneration. |
| Describe the findings seen in Diffuse Skeletal Hyperostosis (DISH). | Flowing anterior osteophytes extending at least 4 vertebral levels. The intervertebral disc spaces will be spared. The peri-aortic areas of the vertebral bodies will be spared. May predispose to fracture due to decreased spinal column mobility. |
| With which additional degenerative spinal condition is DISH associated? | Ossification of the posterior longitudinal ligament (OPLL). |
| Describe the findings seen in Ossification of the Posterior Longitudinal Ligament (OPLL). | Calcification and ossification of the posterior longitudinal ligament of the spine which can lead to spinal stenosis and anterior compression of the cord. Best seen on CT at the anterior aspect of the spinal canal. Generally seen in the cervical spine. |
| Which is the most common causative organism in Pyogenic discitis/osteomyelitis? | Staph aureus. |
| How does spread of pyogenic discitis/osteomyeitis vary between kids and adults? | Adults: Infection starts in the vertebral body then spreads to the disc, Kids: Infection starts in the disc then spreads to the vertebral body |
| What are the hallmark MR image findings in bacterial discitis/osteomyelitis? | T1 hypointensity in the vertebral bodies on both sides of an abnormal intervertebral disc. The abnormal disc will be T2 hyperintense. |
| Describe Pott's Disease. What is the causative agent? | Osteomyelitis of the spine due to Tuberculosis infection. Classically causes wedge shaped compression deformity of the anterior aspect of the vertebral body, leading to gibbus deformity at the center of the vertebral body. |
| What is the most unique imaging characteristic of Pott's Disease? | Its tendency to spare the intervertebral discs. Tuberculosis lacks the proteolytic enzymes (that most bacteria have) needed to break down the disc. |
| What is Gibbus deformity (in relation to the spine)? In which group of disorders is this phenomenon seen? | Acute angulation of the anterior aspect of a vertebral body leading to kyphosis. Mucopolysaccharidoses (except Morquio). |
| What % of patients with Pott's disease have active pulmonary TB? | 10% |
| What is the most common vascular malformation of the spinal cord? | Dural arteriovenous fistula (dAVF). Typically affects older males with back pain and progressive myelopathy. |
| Which Cognard classification do all spinal dAVFs belong to? | Type V |
| What are the imaging findings associated with spinal dAVF? | Flow voids will be seen surrounding the cord. The cord will be swollen with abnormal intramedullary T2 prolongation. CT myelography shows serpiginous filling defects in the subarachnoid space. |
| Where in the spinal cord is infarction most likely to occur? | Upper thoracic or thoracolumbar spine due to precarious blood supply. |
| What is the predominant vessel supplying blood to the distal spinal cord? | Artery of Adamkiewicz. |
| What is the classical clinical presentation of a patient with spinal cord infarction? | Loss of bowel and bladder control, loss of perineal sensation, and impairment of motor and sensory function of the legs |
| What are the major risk factors for spinal cord infarction? (6) | 1) Aortic surgery, 2) Aortic aneurysm, 3) Arteritis, 4) Sickle Cell disease, 5) Vascular malformation, and 6) Disc herniation |
| What is Tethered Cord Syndrome? | Congenital syndrome which features back and leg pain , gait spasticity, and decreased lower extremity sensation when the conus medullaris is tethered in the lower spinal column by a thick/fatty filum or lipoma. |
| What is Diastematomyelia? | Congenitally split spinal cord |
| Which which spinal conditions is Diastematomyelia associated? (2) | Scoliosis and fatty filum terminale. |
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stephanie.prater
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