Neuro Flashcards
What are the four recesses of the third ventricle?
Chiasmatic (supraoptic) recess
Infundibular Recess
Suprapineal Recess
Pineal Recess
What is the massa intermedia of the third ventricle?
Interthalamic adhesion - gray and white matter structure that passes through the third ventricle to connect the bilateral thalami.
What connects the third and fourth ventricles?
Cerebral aqueduct (of Sylvius)
How does the fourth ventricle drain?
Continues inferiority as the central canal of the spinal cord. Into the subarachnoid space and basal cisterns via the paired foramina of Luschka (lateral) and single foramen of MAgendie (medial).
Where are the choroid plexi located?
Body and temporal horn of each lateral ventricle
Roof of third ventricle
Roof of fourth ventricle
No choroid plexus in the cerebral aqueduct or occipital or frontal horns of the lateral ventricles.
What are the volumes of the ventricles and subarachnoid space? How much CSF is produced per day?
Ventricular volume = 25 mL
Subarachnoid space = 125 mL
Total = 150
Produce about 500 ml/day
Replenish CSF 3-4 times per day.
Where is vasogenic edema primarily seen?
White matter - more interstitial space
Caused by increased capillary permeability.
What are the complications of subfalacine hernation?
Compression of the anterior cerebral artery (ACA) against the falx.
Contralateral hydrocephalus from foramen of Monro obstruction
What are the complications of transtentorial herniation?
Ipsilateral CN III (oculomotor nerve) compression - pupillary dilation and CN III palsy (down and out).
Compression of ipsilateral PCA and cause medial temporal/occipital infarct.
Upper brainstem Duret hemorrhages - shearing of perforating vessels due to downward force on the brainstem.
Compression of contralateral cerebral peduncle against Kernohan’s notch - hemiparesis ipsilateral to the herniated side.
What is communicating hydrocephalus and what are the causes?
Ventricular enlargement w/o obstructing lesion.
SAH - impeding arachnoid granulation reabsorption of CSF.
NPH- normal mean CSF pressure and clinical triad of dementia, ataxia, and incontinence.
What are the basal cisterns
CSF-filled spaces surrounding the midbrain and pons.
Suprasellar cistern Prepontine cistern Interpeduncular cistern Ambient cistern Quadrigeminal cistern
Causes of T1 shortening (hyperintensity)
Gadolinium Fat Proteinaceous substances Some paramagnetic stages of blood - intra- and extra-cellular methemoglobin Melanin Mineralization - copper, iron, manganese Slowly-flowing blood Calcium - rarely, if dispersed, not in bone.
Causes of T2 hypointensity
Most paramagnetic stages of blood - except hyperacute and extracellular methemoglobin
Calcification
Fibrous lesion
Highly cellular tumors (i.e. lymphoma and medulloblastoma)
Vascular flow-void
Mucin - desiccated mucin
How is Flair different from a T1 sequence?
T1: white matter is brighter than gray matter b/c fatty myelinated white matter has a shorter T1 time.
FLAIR: White matter is darker than gray matter.
What is the benefit of proton density images?
highest signal to noise ratio
Used for MS
What is the DDx for diffusion restriction?
Acute stroke Bacterial abscess Cellular tumors - such as lymphoma or medulloblastoma Epidermoid cyst Herpes encephalitis Creutzfeld-Jakob disease
What is a gradient recall echo (GRE) sequence?
Captures the T2* signal.
The 180-degree rephasing pulse is omitted, GRE images are susceptible to signal loss from magnetic field inhomogeneities.
Hemosiderin and calcium produce inhomogeneities- creates blooming artifacts on GRE.
DDx for dark spots on GRE sequences?
Hypertensive microbleeds - basal ganglia, thalami, cerebellum, and pons
Cerebral amyloid angiopathy - subcortical white matter, most commonly the parietal and occipital lobes
Familial cerebral cavernous malformation
Axon shear injury
Multiple hemorrhagic metastases
What are the things measured in magnetic resonance spectroscopy?
N-acetylaspartate - normal marker for neuronal viability - decreases in most abnormalities. In tumors NAA decrases and choline increases, but nonspecific.
Cr provides information about cellular energy stores
Measured in alphabetical order- Choline (cho), creatinine (cr), and NAA.
Hunter’s angle - connecting points - like plane taking off
What forms the blood brain barrier?
Astrocytic foot processes of brain capillary endothelial cells and prevents direct communication between the systemic capillaries and the protected extracellular fluid of the brain.
What CNS regions do not have a blood brain barrier?
No BBB = will enhance.
Choroid plexus
Pituitary and pineal glands
Tuber cinereum (controls circadian rhythm, located in inferior hypothalamus)
Area postrema (controls vomiting located at inferior aspect of 4th ventricle)
What is the tuber cinereum?
Located in inferior hypothalamus - controls circadian rhythm
What is the area postrema?
Located at inferior aspect of 4th ventricle - controls vomiting.
What are the causes of periventricular enhancement (intra-axial)?
Primary CNS lymphoma - can be periventricular enhancement, solitary brain mass, or multiple brain masses.
Infectious ependymitis - MC caused by cytomegalovirus. Usually features thin linear enhancement along the margins of the ventricles.
Primary Glial Tumor
MS
Causes of gyriform enhancement (intra-axial)?
Herpes encephalitis
Meningitis
Subacute infarct - 6 days to 6 weeks after ischemic event
PRES
What causes nodular subcortical enhancement (intra-axial)?
Hematogenously disseminated metastatic disease - arterial
Where are venous brain metastases found?
Posterior fossa through the retroclival venous plexus and Batson prevertebral venous plexus
Mnemonic for ring enhancing lesion?
MAGIC DR Metastasis Abscess Glioma Infarct Contusion Demyelination - C-shaped Radiation
DWI findings of an abscess
Diffusion restriction centrally due to high viscosity of central necrosis
Enhancement pattern of demyelinating disease?
Incomplete and “C” shaped. Lack of significant mass effect
What is pachymeningeal enhancement?
Dural enhancement.
No BBB in dura, but no water molecules in dura.
Dural enhancement on MRI is an indication of dural edema rather than BBB breakdown.
DDx of pachymeningeal enhancement?
Intracranial hypotension - vasogenic edema of dura
Postoperative
Post-lumbar puncture
Meningeal neoplasm - such as meningioma - can produce focal area of dural enhancement called dural tail, due to reactive changes in the dura.
Granulomatous disease - typically basal meninges (skull base)
Cancers that metastasize to the dura?
Breast and Prostate - irregular dural enhancement.
What is leptomeningeal enhancement?
Pia-arachnoid enhancement
DDx of leptomeningeal enhancement?
Meningitis
Leptomeningeal carcinomatosis - primary or metastatic disease
Viral encephalitis
Slow vascular flow
Mnemonic for primary CNS tumors that cause leptomeningeal enhancement
GEMCLOG
Glioblastoma Ependymoma Medulloblastoma Choroid plexus tumor Lymphoma Oligodendroglioma Germinoma
Causes of subarachnoid FLAIR hyperintensity
Meningitis and leptomeningeal carcinomatosis - with leptomeningeal enhancement
SAH - no enhancement - has susceptibility
Oxygen or propofol therapy.
What is the most common primary brain tumor to hemorrhage?
Glioblastoma
What intracranial metastases hemorrhage?
Melanoma, RCC, thyroid, and choriocarcinoma.
Lung and breast are less frequently hemorrhagic.
What brain tumors are hypointense on T2?
Metastases containing desiccated mucin - such as GI adenocarcinomas.
Hypercellular metastases - including lymphoma, germinoma, and some glioblastomas.
What brain tumors are hyperintense on T1?
Metastatic melanoma
Fat-containing tumors- such as dermoid or teratoma.
Hemorrhagic metastasis - RCC, thyroid, choriocarcinoma, and melanoma.
What types of intracranial lesions tend to have cysts?
Low-grade tumors
What is a glioma?
Primary CNS tumor arising from a glial cell - astrocytes, oligodendrocytes, ependymal cells, and choroid plexus cells.
What is an astrocyte?
Provide biochemical support to the endothelial cells that maintain the BBB, to maintain extracellular ion balance, and aid in repair after neuronal injury.
Throughout brain and spinal cord.
What is an oligodendrocyte?
Maintain myelin around CNS axons. Single can maintain myelin of dozens of axons. Throughout brain and spinal cord.
Counterpart is a schwann cell in a peripheral nerve.
What are ependymal cells?
Circulate CSF with its multiple cilia. Line ventricles and central canal of the spinal cord.
What is a Junvenile Pilocytic Astrocytoma (JPA)?
Pilocytic = “hair-like”
Benign, typically in the posterior fossa in children.
Well-circumscribed cystic mass with an enhancing nodule and relatively little edema.
May compress 4th ventricle if in posterior fossa. Can occur along the optic pathway with NF1. Posterior fossa JPA is not associated with NF1.
What does a low-grade astrocytoma look like?
Hyperintense mass on T2 without enhancement
What does an anaplastic astrocytoma look like?
Range of appearances from thickened cortex (similar to low-grade astrocytoma) to an irregularly enhancing mass that may appear identical to glioblastoma.
Will eventually progress to glioblastoma.
What is the DDx of a transcallosal mass?
GBM, lymphoma, or demyelinating disease.
What is Gliomatosis Cerebri and what does it look like?
Diffuse infiltrative mid-grade astrocytoma that affects multiple lobes.
Diagnostic criteria- involvement of at least two lobes plus extra-cortical involvement of structures such as the basal ganglia, corpus callosum, brainstem, or cerebellum.
Poor prognosis and may degenerate into GBM.
Exerts mass effect, but does not enhance.
What is an Oligodendoglioma and what does it look like?
Slow-growing cortical-based mass.
Young to middle aged patient with seizures.
Propensity to calcify (about 75%).
What is an ependymoma?
Tumor of ependymal cells that tends to occur in the posterior fossa in children and in the spinal cord in older adults.
What is a Lhermitte-Duclos tumor?
Dysplastic cerebellar gangliocytoma - part hamartoma and part neoplasm.
Associated with Cowden syndrome.
Corduroy or tiger-striped striated lesion in the cerebellar hemisphere. Enhancement is rare.
What are the embryonal/primitive neuroectodermal tumors (PNET)?
Atypical teratoid/rhabdoid tumor (ATRT)
Medulloblastoma
What is an Atypical Teratoid/Rhabdoid Tumor (ATRT)?
Agrgressive tumor that may appear similar to medulloblastoma, but occurs in slightly younger patients. Majority occur in posterior fossa.
Associated with malignant rhabdoid tumor of kidney.
What is a medulloblastoma?
Small-blue-cell origin tumor. One of the most common pediatric brain tumors.
MC occurs in midline cerebellar vermis. Slightly hyperattenuating on CT due to densly packed cells and is hypointense on T2 and has low ADC values. Avidly enhancing and may appear heterogeneous due to internal hemorrhage and calcification.
What are the most common childhood posterior fossa tumors?
Medulloblastoma, ependymoma, and pilocytic astrocytoma.
What are the brain tumors with a cyst and an enhancing nodule?
Juvenile Pilocytic Astrocytoma
Hemangioblastoma
Pleomorphic Xanthoastrocytoma
Ganglioglioma
What is a hemangioblastoma?
Cystic mass with enhancing mural nodule. Prominent vessels are often seen as tubular areas of flow void. Often associated with syrinx in spinal cord.
Highly vascular tumor associated with VHL
Most commonly in the cerebellum, medulla, or spinal cord.
30% of hemangioblastomas have VHL.
Hemangioblastoma in patient with VHL has a worse prognosis.
What is a Pleomorphic Xanthoastrocytoma?
Low grade astrocytoma variant.
Rare tumor of childhood and adolescents- typically with history of chronic epilepsy.
MC location is temporal lobe- supratentorial cortical cystic mass with an enhancing mural nodule. The overlying dura may be thickened and enhancing.
Main DDx is a ganglioglioma- however, ganglioglioma does not usually cause dural thickening.
What is the main imaging difference between a ganglioglioma and pleomorphic xanthoastrocytoma?
PXA causes dural thickening
What is a Ganglioglioma?
Rare, slow-growing neuroglial tumor- adolescent or young adult with medically refractory temporal lobe epilepsy.
Temporal lobe cyst and enhancing mural nodule, often with calcification. May cause calvarial remodeling and scalloping.
What tumors are associated with medically refractory temporal lobe epilepsy?
Pleomorphic Xanthoastrocytoma and Ganglioglioma
What are the intraventricular tumors?
Central neurocytoma Choroid Plexus Papilloma/carcinoma Intraventricular Meningioma Subependymal Giant Cell Asrocytoma (SEGA) Subependymoma
What is a central neurocytoma?
Low-grade tumor likely of neuronal origin that occurs in young adults.
Lobulated mass attached to the septum pellucidum with numerous intratumoral cystic areas. Calcification is common.
Lobulated mass attached to the septum pellucidum with numerous intratumoral cystic areas. Commonly with calcification.
Central Neurocytoma
What is a choroid plexus papilloma?
Rare intraventricular tumor. Arising from choroid plexus epithelial cells.
Lobulated, heterogeneous mass that avidly enhances. MC in the atrium of the lateral ventricle in children. In adults, the fourth ventricle is the most common.
Where are intraventricular meningiomas commonly found?
Trigone of the lateral ventricle.
What is a Subependymal Giant Cell Astrocytoma (SEGA)?
Low-grade astrocytoma variant that is associated with tuberous sclerosis.
Other findings of tuberous sclerosis - subependymal nodules and hamartomas (cortical and subcortical).
Classically- enhancing mass in the lateral ventricle near the foramen of Monro.
What is a Subependymoma?
Nonehancing low-grade tumor- thought to arise from subependymal astrocytes, ependymal cells lining the ventricles, or common precursor cells.
Tumor of middle age and older adults.
MC in obex of 4th ventricle (inferior 4th ventricle) or at formen of Monro in the lateral ventricle. Doesn’t enhance.
Nonenhancing mass arising from the inferior 4th ventricle?
Subependymoma
What type of lymphoma is primary CNS lymphoma?
Most commonly diffuse large B-cell lymphoma. Immature blast cells form lymphoid aggregates around small cerebral blood vessels in a periventricular location.
Brain does not contain native lymphoid tissue.
What is the appearance of primary CNS lymphoma in general?
Appearance of PCNSL depends on the immune status of the patient, but always periventricular location and high cellularity (hyperattenuating on CT, relatively hypointense on T2 and reduced diffusivity.
What is the appearance of primary CNS lymphoma in immunocompetent patients?
Enhancing periventricular mass in immunocompetent, often crossing the corpus callosum. Involvement of the frontal lobes and basal ganglia is most common.
What is the appearance of primary CNS lymphoma in immunocompromised patients?
Periventricular ring-enhancing lesion in the basal ganglia, due to central necrosis.
Difference between primary CNS lymphoma in immunocompetent and immunocompromised patients?
In immunocompromised- ring-enhancing due to central necrosis.
DDx of ring-enahncing basal ganglia mass in immunocompromised patient?
Lymphoma and toxoplasmosis
Ways to differentiate between lymphoma and toxoplasmosis for a ring-enhancing basal ganglia lesion in immunocompromised patient
Emperitcal anti-toxoplasmosis therapy and short-interval follow-up.
Thallium scanning- Lymphoma is thallium avid and toxo is not.
PET- lymphoma tends to be high grade and metabolically active. Toxo usually does not have avid FDG uptake.
Perfusion scanning- lymphoma has increased relative cerebral blood volume while toxo is hypovascular.
What does secondary CNS lymphoma look like?
Tends to involve the meninges and may cause leptomeningeal carcinomatosis or epidural cord compression. Less commonly may present as a parencymal mass.
MC primary tumors to cause CNS parencymal metastases
Lung, breast, and melanoma.
Where do meningiomas arise from?
Meningoepithelial cells called arachnoid “cap” cells.
What are multiple meningiomas associated with?
NF-2 or following radiation therapy.
MC tumors to metastasize to the dura
Breast (MC), lymphoma, small cell lung cancer, and melanoma.
Posterior fossa mass in a child that is hyperattenuating on CT with low ADC on MRI?
Medulloblastoma
Posterior fossa mass in child that is cystic with an enhancing mural nodule?
Juvenile Pilocystic Astrocytoma
Posterior fossa mass in a child that is intraventricular and pushes through fourth ventricular foramina?
Ependymoma
Posterior fossa mass in a child that is cystic with enhancing mural nodule and flow voids with history of VHL?
Hemangioblastoma
Posterior fossa mass in a child with slightly younger age that medulloblastoma, with similar imaging of an aggressive, heterogeneous mass? Renal mass present?
Atypical teratoid/rhabdoid tumor
Posterior fossa mass in an adult with history of primary malignancy? Enhancing mass with edema? Multiple lesions?
Metastasis
Posterior fossa mass in an adult that is cystic with enhancing mural nodule and flow voids? History of VHL?
Hemangioblastoma
Posterior fossa mass in an adult with minimal or little mural enhancement?
Astrocytoma
Posterior fossa mass in young adult, lateral location?
Medulloblastoma
What are the important structures of the CP angle?
CNV, CNVII, CNVIII, and AICA
What are the intracranial manifestations of VHL?
Hemangioblastoma - cerebellar hemisphere fluid-secreting tumor with a cyst and enhancing nodule. Prominent flow voids feeding the tumor.
Endolymphatic sac tumor - occurs along the posterior petrous ridge.
What is the only segment of the trigeminal nerve that does not traverse the cavernous sinus?
V3 - Exits inferiorly from Meckel’s cave through foramen ovale.
How does the abducens nerve (VI) enters the petrous portion of the temporal bone through what?
Dorello’s canal
What is the only nerve that travels in the medial venous sinusoids of the cavernous sinus?
VI
What is the only nerve in the cavernous sinus that does not exit the superior orbital fissure?
Maxillary nerve (V2) - exits the foramen rotundum.
What forms the pituitary gland?
Rathke’s pouch - superior invagination from the primitive oral cavity.
DDx of intrinsic pituitary mass
Pituitary adenoma, Rathke’s cleft cyst, and hypophysitis.
Craniopharyngioma may rarely occur in the sella, but essentially never occurs within the pituitary gland itself.
What is a pituitary microadenoma?
<10 mm in size
Usually symptoms due to hormone excess, not mass effect.
What is a pituitary macroadenoma?
> 10 mm in size. Usually present with mass effect (compression of optic chiasm) rather than endocrine dysfunction.
Usually encase the carotid, but tend not to narrow it. In contrast, meningiomas or metastases can narrow the carotid.
How to tell difference between macroadenoma and meningioma or metastases on imaging?
Macroadenoma usually encase the carotid, but tend not to narrow it. Meningiomas or metastases can narrow the carotid.
What is pituitary apoplexy?
Clinical syndrome of severe headache and endocrine dysfunction caused by hemorrhage into an otherwise normal pituitary.
What is lymphocytic hypophysitis?
Autoimmune inflammatory disorder usually seen in peripartum women that may affect the pituitary and infuncibulum. Present with DI, HA, visual impairment, and endocrine dysfunction.
Thickening and enhancment of the pituitary stalk.
What is granulomatous hypophysitis?
Granulomatous inflammation of the pituitary and infundibulum- can be secondary to sarcoid, Wegener granulomatosis, TB, and LCH.
MC suprasellar lesion in child vs adult?
Child- craniopharyngioma.
Adult- Pititary macroadenoma that has extended superiorly.
Mnemonic for extra-pituitary masses
SATCHMO
Sarcoidosis/Suprasellar extension of an adenoma
Aneurysm
Teratoma (dermoid cyst)/Tolosa Hunt
Craniopharyngiomia/Cleft cyst (Rathke’s)
Hypothalamic glioma (adults)/Hypothalamic hamartoma (children)
Meningioma/Metastasis
Optic nerve glioma
Second most common suprasellar mass in children?
Optic pathway astrocytoma.
Craniopharyngioma is MC.
Low-grade tumor in children. Aggressive tumor in adults.
What is the MC intracranial germ cell tumor?
Germinoma - 80% arise from the pineal region. 20% parasellar. Primarily seen in children and adolescents.
What is a Hypothalamic Hamartoma?
Ectopic hypothalamic neural tissue. Presents with precocious puberty and gelastic seizures (laughing spells).
Characteristically appears as a sessile mass between the pituitary stalk and the mammillary bodies. Does not enhance and is isointense to gray matter.
Suprasellar mass in child that is calcified, complex cystic mass, distinct from pituitary?
Craniopharyngioma
Suprasellar mass in child that is T2 hyperintense, enhancing mass with secondary signs of NF1?
Optic pathway glioma
Suprasellar mass in a child that avidly enhancing midline? Contains fat?
Germ cell tumor
Suprasellar mass in a child that is nonenhancing, gray-matter isointense mass? Presents with gelastic seizures and precocious puberty?
Hypothalamic hamartoma
Suprasellar mass in a child that is enhancing, enlarged pituitary stalk, with DI?
Langerhans Cell Histiocytosis Hypophysitis
Suprasellar mass in an adult that expands up from the sella with expansion of the sella?
Pituitary macroadenoma extension
Suprasellar mass in an adult with intense enhancement with a normal sella? Enhancing dural tail? Adjacent hyperostois? Narrows adjacent vasculature?
Meningioma
Suprasellar mass in an adult that is calcified, enhancing, complex cystic mass? Distinct from pituitary?
Craniopharyngioma
Suprasellar mass in an adult that is nonenhancing cystic mass without calcification?
Rathke’s cleft cyst
Suprasellar mass in an adult with enhancement equal to blood pool? Calcified rim (if thrombosed)?
Aneurysm
Suprasellar mass in an adult that is enhancing with enlarged pituitary stalk with DI?
Lymphocytic or granulomatous hypophysitis
Lymphocytic if peripartum; granulomatous if otherwise
What is the principal neuronal cell of the pineal gland? What is it’s function?
Pinealocyte - modified retinal neuronal cell that is innervated by the sympathetic plexus originating in the retina. Releases melatonin. Does not have a blood brain barrier.
What can a mass within the pineal gland cause?
Compression of the midbrain, compression of the cerebral aqueduct of Sylvius, or compression of the tectal plate - produces Parinaud syndrome- inability to look up, pupillary light dissociation, and nystagmus.
What is Parinaud Syndrome?
Upward gaze paralysis, pupillary light dissociation, and nystagmus.
Caused by compression of tectal plate - pineal gland lesion.
A mass of the pineal gland is intra or extra-axial?
Extra-axial
DDx of pineal masses?
Germ cell tumor, Pineal cyst, Pineocytoma, Pineaoblastoma, or metastases
What are the 2 most common pineal region tumors?
Germinoma and teratoma
What is a Pineocytoma?
Low-grade slow-growing pinealocyte tumor. Any solid component should enahnce. Pineocytoma may feature cystic change, however, which can make differentiation from a pineal cyst difficult.
What is a Pineoblastoma?
Highly malignant tumor of young children, of same primitive neuroectodermal tumor (PNET) type as medulloblastoma.
Trilateral retinoblastoma is used with bilateral retinoblastomas are also present (retina and pineal gland are light-sensing organs). The sella is additionally involved in quadrilateral retinoblastoma.
Presents with obstructive hydrocephalus. Poorly defined pineal mass that may invade into adjacent structures. High cellularity = restricted diffusion.
What is a trilateral retinoblastoma?
Bilateral retinoblastomas and a pineoblastoma.
When sella is involved = quadrilateral retinoblastoma.
What is the difference between a Pineocytoma and Pineoblastoma?
Pineocytoma - low-grade, slow-growing pinealocyte tumor.
Pineoblastoma - highly malignant tumor of young children.
Difference between a pineal germinoma and a pineaoblastoma?
Germinoma - engulfs and induces calcification of the pineal gland.
Pineoblastoma - peripherally calcifies in a pattern that looks like “exploded” calcifications.
What is a Vein of Galen Aneurysm?
Not a true aneurysm. Dilation of the vein of Galen due to an AVF between the anterior or posterior circulation and the venous plexus leading to the vein of Galen.
What is a quadrigeminal plate lipoma associated with?
Can be seen in isolation or associatd with agenesis or hypoplasia of the corpus callosum.
What is the MC cause of SAH?
Trauma
What is the grading of diffuse axonal injury?
Grade I - only the gray-white matter junctions
Grade II - involves the corpus callosum
Grade III - involves the dorsolateral midbrain
Sulcus that separates the motor strip from the sensory cortex?
Central sulcus.
Segments of the ICA?
Cervical (C1) Petrous (C2) Lacerum (C3) Cavernous (C4) Clinoid Segment (C5) Supraclinoid (C6-C7)
Branches of the cavernous (C4) segment of the ICA?
Meningohypophyseal trunk - supplies the pituitary tentorium, and dura of the clivus.
Inferolateral trunk - Supplies the 3rd, 4th, and 6th cranial nerves as well as the trigeminal ganglion.
Branches of the supraclinoid (C6-C7) segment of the ICA?
Opthalamic artery - just above carotid ring - can cause SAH, treated more aggressively.
Posterior Communicating Artery
Anterior Choroidal Artery - supplies the optic chiasm, hippocampus, and posterior limb of internal capsule.
Why are opthalmic artery aneurysms treated aggressively?
Just above superior carotid ring, can cause SAH.
What does the anterior choroidal artery supply?
Optic chiasm, hippocampus, and posterior limb of internal capsule.
Most distal branch of ICA before bifurcation into ACA and MCA.
Where does the recurrent artery of Heubner arise and what does it supply?
A1 segment - supplies the caudate head and anterior limb of the internal capsule.
Where do the medial lenticulostriate perforator vessels arise and what do they supply?
A1 segment - supply the medial basal ganglia.
Where do the lateral lenticulostriate perforator vessels arise and what do they supply?
MCA - supply the lateral basal ganglia including the lateral putamen, extrnal capsule, and the posterior limb of the internal capsule.
Where do the thalamoperforator vessels arise and what do they supply?
Posterior communicating artery and posterior cerebral artery - supplies the thalamus.
What symptom does a P-comm aneurysm cause?
CN III palsy.
What is the Artery of Percheron and where does it arise?
Variant where there is a dominant thalamic perforator supplying the ventromedial thalami bilaterally and the rostral midbrain. Arises from the P1 PCA segment.
Infarct will cause bilateral ventromedial thalamic infarction, with or without midbrain infarction.
What does a Artery of Percheron infarct look like?
Infarct of bilateral ventromedial thalami with or without midbrain infarction.
What circle of willis malformation is associated with aneurysms?
Double or plexiform A-comm
What circle of willis malformation is associated with holoprosencephaly?
azygos ACA - common ACA
What is the M1 segment of the MCA?
From the ICA terminus to the origin of the sylvian fissure
What is the M2 segment of the MCA?
Extends from the bottom to the top of the sylvian fissure
What is the M3 segment of the MCA?
Extends from the top of the sylvian fissure to the cortical surface
What is the M4 segment of the MCA?
Represents small cortical branches.
Where does the recurrent artery of Heubner arise?
MC from the A1 segment of the ACA, proximal to the AComm.
Supplies the head of the caudate and the anterior limb of the internal capsule.
What is the most common persistent carotid-basilar connection?
Persistent trigeminal artery - courses adjacent to the trigeminal nerve. Trident or tau sign on angio.
Associated with aneurysms.
What are the less common carotid to basilar connections?
Otic, hypoglossal, and proatlantal intersegmental arteries are rare.
Persistent trigenimal artery is most common.
What artery supplies the anterior limb of the internal capsule?
Recurrent artery of Heubner. Along with the head of the caudate.
What artery supplies the posterior limb of the internal capsule?
Anterior Choroidal artery. Along with the optic chiasm and hippocampus.
What is the goal of stroke imaging?
Who would benefit from therapy.
What is the only CT finding that absolutely precludes IV tPA within 3 hours of onset of stroke?
Hemorrhage.
Intra-arterial thrombolysis may be performed for an MCA thrombus within how may hours?
6 hours of stroke onset who are not candidates for IV tPA. No time frame for posterior circulation.
Additional exclusion criteria (besides hemorrhage) for tPA
Larger (>1/3 MCA territory)
Occlusion of distal ICA and proximal MCA and ACA (T-shaped occlusion).
Absence of penumbra of salvagable brain that represents at least 20% of the region of abnormal perfusion may preclude treatment with IV tPA.
What is the penumbra?
Does receive some perfusion, but reduced. <20 mL/100g tissue per minute compared to ~60mL/100g tissue per minute for normal gray matter.
What are the stages of evolution of an infarct?
Hyperacute (0-6 hours) Acute infarct (6-72 hours) Early subacute infarct (1.5 days - 5 days) Late subacute infarct (5 days - 2 weeks) Chronic
What happens in the hyperacute stage of infarction?
Na-K ATPase pump that maintains normal low intracellular Na fails. Sodium and water diffuse into cells - cell swelling and cytotoxic edema. Calcium diffuses into cells - triggers cascades that contribute to cell lysis.
DWI hyperintensity with ADC map hypointensity.
Why is diffusion restricted in hyperacute infarct?
0-6 hours
Shift from extracellular to intracellular water due to Na/K ATPase pump failure.
Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein.
What happens in the acute phase of an infarct?
6-72 hours
Characterized by increase in vasogenic edema and mass effect.
Damaged endovascular cells cause leakage of extracellular fluid and increase the risk of hemorrhage. Sulcal effacement and mass effect which peaks at 3-4 days - overlap between acute and early subacute phases.
Hyperintense on T2 of infarct core, best seen on FLAIR. Usually confined to the gray matter. DWI still positive. May see arterial enhancement via collateral flow.
What characterizes the acute phase of an infarct?
Increase in vasogenic edema and mass effect. Endothelial cell damage causes leakage of extracellualr fluid and increase risk of hemorrhage.
What happens in early subacute phase of infarct?
1.5 days to 5 days
Blood flow to affected brain is re-established by leptomeningeal collaterals and ingrowth of new vessels into the region of infarction. Have incomplete BBB = increase in vasogenic edema and mass effect, peaks 3-4 days.
Marked hyperintensity on T2 in both gray and white matter (early is just gray matter). ADC maps becomes less dark or even resolves, but DWI remains bright due to T2 shine through
In which phase does ADC normalize in an infarct?
Early subacute (1.5 -5 days).
DWI still positive due to T2 shine through.
What happens in Late subacute infarct?
5 days - 2 weeks
Resolution of vasogenic edema and reduction in mass effect.
Key imaging finding is gyriform enhancement - may be confused with neoplasm, but no mass effect. Enhancement can be seen from about 6 days to 6 weeks after initial infarct. “2-2-2 rule” - enhancement begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
DWI remains bright due to T2 shine through. ADC back to normal or show increased diffusivity.
What is the 2-2-2 rule of stroke?
Enhancment of subacute infarct begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
What happens in chronic infarct?
> 2 weeks
Cellular debris and dead brain tissue are removed by macrophages and replaced by cystic encephalomalacia and gliosis.
What is Wallerian Degeneration?
Atrophy of contralateral corticospinal tract due to cortical infarct.
What is cortical laminar necrosis?
Deposition of lipid-laden macrophages after ischemia - hyperintensity of T1 and T2 images.
Can be seen instead of encephalomalacia.
What are the high-flow vascular malformations?
AVM and dural AVF
What are the low-flow vascular malformations?
Cavernous malformation (cavernoma)
DVA (venous angioma)
Capillary telangiectasia
What is an arteriovenous malformation (AVM)?
Congenital high-flow vascular malformation. Directly connecting arteries and veins without capillary bed.
Present with seizures or bleeding
Spetzier-Martin scale helps evaluate surgical risk of AVM resection. Large draining to a deep vein in eloquent cortex is high risk.
AVM replaces rather than displaces brain - minimal mass effect.
What is the Spetzler-Martin scale?
Helps evaluate surgical risk for AVM resection.
Large AVM draining to a deep vein in eloquent cortex is high risk.
Small AVM draining into a superficial vein in non-eloquent cortex is low risk.
What does an AVM do to surrounding brain tissue?
Replaces rather than displaces brain. Minimal mass effect.
What is a Vein of Galen Malformation?
AVF from thalamoperforator branches into the deep venous system. The enlarged vein is actually an enlarged median prosencephalic vein.
MC cause of extracardiac high output cardiac failure. Can cause Parinaud syndrome due to mass effect in the pineal region.
What are Dural AVFs?
High-flow lesions characterized by AV shunts between the meningeal arterioles and dural venules.
Primary prognostic feature - presence and degree of cortical venous drainage.
Cognard classification.
Carotid-cavernous fistula (CCF) is subtype of dAVF - often caused by trauma with resultant fistula between cavernous carotid artery and the cavernous sinus. Enlargement of the superior orbital vein and shunting within the cavernous sinus can lead to eye symptoms such as proptosis and CN palsy.
What is the Cognard classification?
Prognostic indicator of dural AVFs. Shows increased risk of bleeding.
I: No cortical venous drainage. Lowest risk.
II: Reflus into dural sinus but not cortical veins.
IIB: Reflux into cortical veins: 10-20% hemorhage rate.
III: Direct cortical venous drainage: 40% hemorrhage rate
IV: Direct cortical venous drainage with venous ectasia: 66% hemorrhage rate
V: Spinal venous drainage. May cause myelopathy.
What is a Carotid-Cavernous fistula?
Subtype of dAVF often caused by trauma.
Fistula between cavernous carotid artery and the cavernous sinus. Enlargement of the superior orbital vein and shunting within the cavernous sinus can lead to eye symptoms such as proptosis and CN palsy.
What causes enlargement of the superior orbital vein and shunting within the cavernous sinus that can lead to eye symptoms such as proptosis and CN palsy?
CC fistula. Fistula between the cavernous carotid artery and the cavernous sinus.
What is a cavernous malformation?
AKA - cavernoma.
Vascular hamartoma with very small but definite bleeding risk. May cause seizures.
Often associated with adjacent developmental venous anomaly (DVA). Increased bleeding risk if DVA present, but DVA itself does not have any bleeding risk.
Multiple = familial cavernomatosis
Can be induced by radiation.
What is associated with multiple cavernomas?
Familial cavernomatosis
What is a Developmental Venous Anomaly (DVA)?
Abnormal vein that provides functional venous drainage to normal brain.
If resected, the patient will suffer a debilitating venous infarct.
What is a capillary telangectasia?
Astymptomatic vascular lesion of dilated capillaries with interspersed normal brain. Do not touch.
Faint, brush-stroke-like enhancing lesion in the brainstem or pons, without mass effect or surrounding edema. GRE may show blooming.
Angiographically occult, like cavernous malformation.
Overall, what is the MC cause of SAH?
Trauma.
Aneurysm rupture is by far the MC of non-traumatic SAH.
DDx of high attenuation material in the subarachnoid space
SAH (by far MC)
Meningitis
Leptomeningeal carcinomatosis
Intrathecal contrast administration
If clinical suspicion for SAH is high and CT is negative what is standard of care to do next?
LP for xanthochromia.
What can cause increased FLAIR signal in the subarachnoid space on MRI?
SAH, meningitis, leptomeningeal carcinomatosis, and residual contrast material.
Recent oxygen or propofol can also cause.
What are the MC sites of aneurysm?
AComm (33%)
PComm (33%)
MCA (20%)
Basilar tip (5%)
What is the Hunt and Hess score?
Clinical grading scale for aneurysmal SAH based solely on symptoms without imaging.
What is the Fisher Grade?
Classifies CT appearance of SAH. Grade 1 is negative on CT; grades 2 and 3 are <1 mm and >1mm thick respectively; grade 4 is diffuse SAH or intraventricular or parenchymal extension.
What is superficial siderosis?
Iron overload of pial membranes due to chronic repeated SAH.
Present with sensorineural deafness and ataxia.
Iron causes hypointensity on T2-weighted images outlining the affected sulci.
What is perimesencephalic SAH?
Type of nonaneurysmal SAH that is Dx of exclusion with much better prognosis than hemorrhage due to ruptured aneurysm.
Must be limited to cisterns directly anterior to the midbrain. Standard of care is to do perform catheter anigio twice, one week apart. Must be negative.
Unknown cause, but thought to represent angiographically occult venous bleeding.
What is reversible cerebral vasoconstriction syndrome (RCVS)?
Cause of nontraumatic, nonaneurysmal SAH and ischemia.
Presents with thunderclap HA and is characterized by prolonged (but reversible) vasoconstriction.
What are the inherited and non-inherited risk factors for the development of saccular aneurysms?
Inherited: Connective tissue diseases such as Marfan and Ehlers-Danlos, polycystic kidney disease, and NF 1.
Non-inherited: HTN and inflammatory vascular disease such as Takayasu or giant cell arteritis.
Fusiform aneurysms are usually due to atherosclerosis.
What is a fusiform aneurysm?
Segmental arterial dilation w/o a defined neck. Usually due to atherosclerosis, but may arise from chronic dissection
Do not occur at branch points. Vertebrobasilar system affected more commonly than anterior circulation.
Much less common than saccular
What is an Oncotic aneurysm?
Aneurysm caused by neoplasm.
Benign left atrial myxoma may peripherally embolize and cause a distal oncotic aneurysm.
Which transverse sinus is usually hypoplastic?
Left transverse sinus
What is the confluence of the superior sagittal sinus, transverse sinus, and the straight sinus called?
Torcular Herophili
What are the dural sinuses?
Superior sagittal sinus- drains the motor and sensory strips
Paired transverse sinuses
Sigmoid sinuses - connects to the jugular bulbs
Torcular Herophili is confluence.
What are the deep cerebral veins?
Paired internal cerebral veins, basal vein of Rosenthal, and Vein of Galen
Venous angle is intersection of the septal vein and the thalamostriate veins. Angiographic landmark for the foramen of Monro.
What is the Venous angle?
Intersection of the septal vein and the thalamostriate veins. Angiographic landmark for the foramen of Monro.
What is the angiographic langmark for the foramen of Monro?
Venous angle - intersection of the septal vein and the thalamostriate veins.
What are the superficial cerebral veins?
Vein of Troclard - connects superficial cortical veins to the superior sagittal sinus.
Vein of Labbe - drains the temporal convexity into the transverse or sigmoid sinus. Traction on during surgery can cause venous infarction and aphasia.
What is the Vein of Troclard?
Connects the superficial cortical veins to the superior sagittal sinus
What is the vein of Labbe?
Drains the temporal convexity into the transverse or sigmoid sinus.
What are the risk factors for venous thrombosis?
Pregnancy, oral contraceptives, thrombophilia, malignancy, and infection.
What does infarction of the parasagittal high convexity cortex suggest?
Superior sagittal sinus thrombosis
What does infarction of the bilateral thalami suggest?
Deep venous system thrombosis
What does infarction of the posterior temporal lobe suggest?
Transverse sinus thrombosis
What are the stages of iron in hemoglobin as it evolves?
Intracellular oxyhemoglobin –> deoxygenation –> Intracellular deoxyhemoglobin –> oxidation –> Intracellular methemoglobin –> cell lysis –> extracellular methemoglobin –> chelation –> Hemosiderin and ferritin
What stage of blood breakdown is bright on T1?
Methemoglobin stages - all others are dark on T1
Bright on both T1 and T2
What do the methemoglobin stages of blood break down look like?
Bright on T1 and T2, except for intracellular methemoglobin, which is dark on T2.
What are the stages of parenchymal hematoma on MR?
Hyperacute hematoma (0-6 hours) Acute hematoma (6-72 hours) Early subacute hematoma (3 days - 1 week) Late subacute (1 week - months) Chronic hematoma
What is a hyperacute parenchymal hematoma?
<6 hours
Intracellular oxyhemoglobin
Primarily intact RBCs containing oxygenated hemoglobin, which is diamagnetic
Center of the hematoma will be isointense on T1 and iso to slightly hyperintense on T2.
Key is peripheral rim of hypointensity on T2 due to deoxygenation of the most peripheral red cells.
What are the imaging findings of hyperacute parenchymal hematoma?
T1 isointense; T2 iso to hyperintense with dark rim.
What is an acute parenchymal hematoma?
6-72 hours
Intracellular deoxyhemoglobin
RBCs desaturate (lose oxygen), entire hematoma becomes hypointense on T2 and iso to mildly hypointense on T1
What is an early subacute parenchymal hematoma?
3 days to 1 week
Intracellular methemoglobin
Characterized by methemoglobin, which is paramagnetic and undergoes proton-electron dipole-dipole interactions (PEDDI) with water. PEDDI shortens T1 to cause hyperintensity on T1 images. Intracellular and extracellular methemoglobin and both hyperintense on T1.
In early subacute, blood remains hypointense on T2 images due to the paramgnetic effects of methemoglobin, which remains trapped in the red cells.
What is a late subacute parenchyaml hematoma?
1 week to months Extracellular methemoglobin (after RBC lysis)
Methemoglobin PEDDI effec persists are cell lysis- continued hyperintensity on T1.
Paramagnetic effects of methemoglobin lessens. Signal intensity on T2 images increases to that of CSF, due to RBC lysis and decrease in protein concentration.
May be peripheral enhancement of subacute to chronic infarct.
What are the T1 and T2 characteristics of blood in a hyperacute parenchymal hematoma on MR?
T2 isointense
T2 iso to hyperintense with dark rim.
What are the T1 and T2 characteristics of blood in a acute parenchymal hematoma on MR?
T1 iso or hypointense
T2 hypointense
What are the T1 and T2 characteristics of blood in a early subacute parenchymal hematoma on MR?
T1 hyperintense
T2 hypointense
What are the T1 and T2 characteristics of blood in a late subacute parenchymal hematoma on MR?
T1 hyperintense
T2 hyperintense
What are the T1 and T2 characteristics of blood in a chronic parenchymal hematoma on MR?
T1 iso or hypointense
T2 hypointense
How does chronic hypertension cause intraparenchymal hemorrhage?
Arteriolar smooth muscle hyperplasia, which eventually leads to smooth muscle death and replacement with collagen. The resultant vascular ectasia predisposes to hemorrhage.
What is the main clinical clue that hemorrhage is due to cerebral amyloid angiopathy?
Normotensive elderly adult
What is the primary imaging feature to suggest hemorrhage is due to cerebral amyloid angiopathy?
Location of hematoma - almost always lobar or cortical - usually in the parietal or occipital lobes.
MC primary brain tumor to cause hemorrhage?
Glioblastoma
Extracranial primary tumors to cause hemorrhagic metastases
Choriocarcinoma Melanoma Thyroid Carcinoma RCC Breast cancer - maybe
Patients on what drug may be at increased risk for hemorrhagic metastasis
Bevacizumab - Avastin, Genentech
Clues to the diagnosis of an underlying tumor causing hemorrhage
More than expected edema surrounding a hyperacute hematoma and heterogeneous blood product signal, suggesting varying breakdown stages of hemoglobin.
Presence of multiple enhancing masses.
If unclear- follow-up MRI once initial hemorrhage improves. May show a delay in the expected evolution of blood products, persistent edema, and enhancement of the underlying tumor.
What is a cavernoma?
Cavernous malformation - vascular hamartoma that consists of low-flow endothelial-lined blood vessels w/o intervening normal brain.
Angiographically occult.
What does vasculitis look like on MRI?
MC presentation is cerebral ischemia. Less commonly, may present with frank hemorrhage.
Multiple foci of T2 prolongation in the basal ganglia and subcortical white matter.
What is Moyamoya?
Non-atherosclerotic vasculopathy characterized by progresive stenosis of the intracranial ICA and their proximal branches, which leads to proliferation of fragile lenticulostriate collateral vessels.
Angio- enlarged basal perforating arteries gives a puff of smoke appearance.
Ivy Sign - FLAIR MRI shows tubular branching hyperintense structures within the sulci, representing cortical arterial branches that appear hyperintense due to slow collateral flow.
Susceptible to aneurysm, especially in the posterior circulation.
What is the Ivy Sign with Moyamoya?
FLAIR tubular branching hyperintense structures within the sulci, representing cortical arterial branches that appear hyperintense due to slow collateral flow.
What are people with Moyamoya susuceptible to?
Aneurysm formation, especially in the posterior circulation.
Intraparenchymal hemorrhage etiology in elderly adult with HTN? Hemorrhage in basal ganglia, cerebellum, or thalamus? Multiple basal ganglia microbleeds on T2*? Prior lacunes and periventricular WM disease?
Hypertensive hemorrhage
Intraparenchymal hemorrhage etiology in lobar or cortical hemorrhage? Elderly adult w/o HTN? Multiple parenchymal microbleeds on T2*?
Amyloid angiopathy
Intraparenchymal hemorrhage etiology with extensive subarachnoid blood? Aneurysm adjacent to hematoma?
Aneurysmal hemorrhage
Intraparenchymal hemorrhage etiology with parenchymal hemorrhage in a young patient? Enlarged feeding artery? Adjacent encephalomalacia?
AVM
Intraparenchymal hemorrhage etiology with hemorrhage adjacent to cavernous sinus or in posterior fossa? Enlarged meningeal artery or cortical vein?
dAVF
Intraparenchymal hemorrhage etiology with adjacent DVA on post-contrast images? Multiple dark spots on T2* (familial variant)?
Cavernous malformation
Intraparenchymal hemorrhage etiology with parasagittal or bilateral thalamic hemorrhage? Young patient, especially female? Increased density in cortical vein or dural sinus?
Venous thrombosis
Intraparenchymal hemorrhage etiology with more edema than expected? More heterogeneous signal than expected? Multiple enhancing lesions?
Hemorrhagic neoplasm
Intraparenchymal hemorrhage etiology with clinical history of infarct? History of thrombolytic therapy?
Hemorrhagic infarct
Intraparenchymal hemorrhage etiology with multifocal T2 prolongation in deep WM? History of systemic vasculitis? Multifocal stenosis/dilation on angiography?
CNS Vasculitis
Intraparenchymal hemorrhage etiology with occlusion of internal carotid arteries? Multiple collateral vessels?
Moyamoya
What is the key imaging finding of demyelinating disease?
Minimal mass effect relative to lesion size.
Enlarged Virchow-Robin spaces and a J-shaped sella can be seen in what?
Mucopolysaccharidoses.
What is Ependymitis Granularis?
Frontal horn periventricular hyperintensity on T2-weighted images due to interstitial CSF backup.
Despite “-itis”, ependymitis granularis is not associated with inflammation.
What are the two main clinical presentations of MS?
Relapsing-remitting (most common): partial or complete resolution of each acute attack.
Progressive: No resolution or incomplete resolution between attacks.
- Primary progessive: slow onset without discrete exacerbations
- Secondary progressive: Similar to relapsing-remitting but with less complete resolution between attacks, leading to progressive disability.
What is the cause of MS?
Lymphocytes attacking oligodendrocytes (which make CNS myelin).
What do you need to make a diagnosis of MS?
Lesions separated in space (different areas of CNS) and time (new lesions across scans).
What are the findings of chronic MS on MRI spectroscopy?
Decreased NAA, Increased choline, Increased lipids, and increased lactate.
What does spinal cord involvement in MS look like?
Usually short-segment and unilateral.
What is Concentric (Balo) sclerosis?
Very rare variant of MS with pathognomonic alternating concentric bands of normal and abnormal myelin.
More often seen in younger patients.
What is the pathognomonic finding in concentric (Balo) sclerosis?
Alternating concentric bands of normal and abnormal myelin.
What is the Marburg Variant of MS?
Fulminant manifestation of MS, leading to death within months.
What is Devic Disease (Neuromyelitis Optica)?
Demyelinating disease, distinct from MS, which involves both the optic nerves and spinal cord.
Worse prognosis than MS.
NMO-IgG, an antibody to aquaporin 4, is highly specific for Devic disease. NMO-IgG activates the complement cascade and induces demyelination.
Imaging shows MS-type lesions with involvement of the optic tracts and spinal cord. Brain lesions, if present, tend to be periventricular.
What is the antibody for Devic Disease (Neuromyelitis Optica)?
NMO-IgG, an antibody for aquaporin 4.
Activates the complement cascade and induces demyelination.
What are the imaging finds of Devic Disease (Neuromyelitis Optica)?
MS-type lesions with involvement of the optic tracts and spinal cord. Brain lesions, if present, tend to be periventricular.
What causes osmotic demyelination?
Caused by rapid change in extracellular osmolality, typically after aggressive correction of hyponatremia.
Quick osmotic gradient change causes endothelial damage, BBB breakdown, and release of extracellular toxins, which damage myelin.
Typically in the pons, but may occur elsewhere in the brainstem and deep gray nuclei. Bilateral central T2 prolongation in the affected region.
What is Marchiafava-Bignami?
Fulminant demyelinating disease of the corpus callosum seen in male alcoholics.
Fulminant demyelinating disease of the corpus callosum seen in male alcoholics.
Marchiafava-Bignami
What is Wernicke Encephalopathy?
Ataxia, confusion, and oculomotor dysfunction - caused by alcoholism or generalized metabolic disturbances, such as bariatric surgery.
T2 prolongation and possible enhancement within the mamillary bodies and medial thalamus. Non-alcoholic form may also affect the cortex.
What is PRES associated with?
Acute HTN, eclampsia, sepsis, autoimmune disorders, multidrug chemotherapy, and solid or stem cell transplantation.
What is Progressive Multifocal Leukoencephalopathy (PML)?
Demyelinating disease of immunocompromised patients caused by reactivation of the JC virus. Progressive demyelination with lack of inflammatory response.
AIDS defining illness, but also in patients with malignancy, s/p organ transplant, or autoimmune disorders.
Asymmetric multifocal white matter lesions that may become confluent. Rarely mass effect or enhancement. The arcuate (subcortical U) fibers are typically involved.
Imaging findings of Progressive Multifocal Leukoencephalopathy (PML)?
Asymmetric multifocal white matter lesions that may become confluent. Rarely mass effect or enhancement. The arcuate (subcortical U) fibers are typically involved.
What is the DDx of white matter lesions in AIDS patients? How to tell the difference?
PML and HIV encephalitis
PML is asymmetric that may become confluent. Involves subcortical white matter and lack of atrophy.
HIV encephalitis is usually bilateral (and symmetric), spares the subcortical white matter, and is associated with cerebral atrophy.
What is subacute sclerosing panencephalitis (SSPE)?
Subacute sclerosing panencephalitis (SSPE) is a demyelinating disease caused by reactivation of measles virus, usually after a long latent period
Periventricular white matter lesions, but SSPE lesions tend to have surrounding edema and mass effect.
Imaging findings of subacute sclerosing panencephalitis (SSPE)?
Periventricular white matter lesions, but SSPE lesions tend to have surrounding edema and mass effect.
White matter disease caused by reactivation of measles virus?
Subacute sclerosing panencephalitis (SSPE)
What is Acute Disseminated Encephalomyelitis (ADEM)?
Monophasic demyelinating disoder seen primarily in children that typically occurs after viral infection or vaccination. Majority make full recovery.
Imaging can be identical to MS- brain, brainstem, and spinal cord.
What are the brain complications of radiation injury?
Acute (during therapy): Edema due to endothelial injury
Early delayed (several weeks to 6 months): Demyelination
Late delayed (months to years): White matter injury or focal radiation necrosis - Mass effect, edema, and enhancement - ring-enhancing.
Other complications - development of meningiomas, capillary telangectasias, cavernous malformations, and/or moyamoya.
Causes of cerebral pyogenic abscesses?
Hematogenous dissemination, direct spread from paranasal sinusitis or mastoiditis, or a complication of bacterial meningitis.
What is the difference in imaging between cerebral abscess and glioma or metastasis?
Rim-enhancing lesion - thin and smooth.
Hypointense rim on T2-weighted images.
What is a Tuberculoma?
Localized tuberculosis granuloma. Not always possible to differentiate a tuberculoma from a pyogenic abscess.
Tends to have central hypointensity on T2-weighted image (in contrast to pyogenic abscess, which is hyperintense). A cystic tuberculoma, however, may mimic a pyogenic abscess. Similar to pyogenic abscess, tuberculomas tend to show restricted diffusion.
Imaging Lyme Disease?
Can cause white matter disease with nonspecific imaging appearance of T2 prolongation predominantly in the frontal subcortical white matter.
Associated enhancement of multiple cranial nerves or meningeal enhancement may suggest the diagnosis.
What is the most common CNS fungal infection in patients with AIDS?
Cryptococcus - Cryptococcus neoformans
Cryptococcus
Third MC CNS infection in AIDS overall, after HIV encephalopathy and toxoplasmosis.
CD4 count less than 100, similar to toxoplasmosis.
MC clinical presentation is chronic basilar meningnitis. MC imaging finding is hydrocephalus, which is nonspecific.
Spreads along the basal ganglia periventricular spaces, leaving behind gelatinous pseudocysts, which appear as round water-signal lesions on T2 and T2 weighted MRI.
Prediliction for spread to the choroid plexus, producing ring-enhancing granulomas (called cryptococcomas) within the ventricles.
Treatment with antifungal agents including fluconazole and amphotericin B.
Top 3 most common CNS infections in AIDS
HIV encephalopathy
Toxoplasmosis
Cryptococcus
At what CD4 count do CNS infections (Toxo and Crypto) present?
<100
Most common presentation and imaging findingns of Cryptococcus CNS infection?
Chronic basilar meningnitis. MC imaging finding is hydrocephalus, which is nonspecific.
Spreads along the basal ganglia periventricular spaces, leaving behind gelatinous pseudocysts, which appear as round water-signal lesions on T2 and T2 weighted MRI.
Prediliction for spread to the choroid plexus, producing ring-enhancing granulomas (called cryptococcomas) within the ventricles.
Most common parasitic CNS infection of immunocompetent patients?
Neurocysticercosis
What is Neurocysticercosis?
MC parasitic CNS infection of immunocompetent patients. Caused by tapeworm Taenia solium and clinically presents with seizures.
Four stages:
1. Viable/vesicular - several CSF-intensity cysts, without enahncement. Many of these cystic lesions may demonstrate an eccentric “dot” representing the scolex.
- Colloidal - Least specific imaging findingns, ring enhancing lesions. In contrast to pyogenic abscess, the lesions feature increased diffusivity.
- Nodular/granular - Edema decreases as the cyst involutes and the cyst wall thickens.
- Calcified - Imaging showed small parenchymal calcifications (on CT) and small foci of susceptibility (GRE)
What are the stages of Neurocysticercosis?
Four stages:
1. Viable/vesicular - several CSF-intensity cysts, without enahncement. Many of these cystic lesions may demonstrate an eccentric “dot” representing the scolex.
- Colloidal - Least specific imaging findingns, ring enhancing lesions. In contrast to pyogenic abscess, the lesions feature increased diffusivity.
- Nodular/granular - Edema decreases as the cyst involutes and the cyst wall thickens.
- Calcified - Imaging showed small parenchymal calcifications (on CT) and small foci of susceptibility (GRE)
What is the MC mass lesion in AIDS patients?
Toxoplasmosis
Toxoplasma gondii
Second most common CNS infection in AIDS patients, with HIV encephalitis being the most common.
Appearance of CNS toxoplasmosis?
Single or multiple ring-enhancing lesions in the basal ganglia.
Asymmetric target sign - not frequently seen, but relatively specific - eccentric nodule of enhancement along the enhancing wall of the toxoplasmosis lesion.
Primary DDx of a basal ganglia mass in immunocompromised patient is CNS lymphoma. Toxo does not demonstrate reduced diffusivity and does not demonstrate increased relative cerebral blood volume on perfusion.
Will be hypometabolic on PET and not avid on thallium scintigraphy.
What is the DDx of basal ganglia mass in immunocompromised patients?
Toxoplasmosis vs CNS lymphoma.
Toxo does not demonstrate reduced diffusivity and does not demonstrate increased relative cerebral blood volume on perfusion.
Toxo is hypometabolic on PET and not avid on thallium scintigraphy.
DDx of medial temporal lobe lesions?
Herpes encephalitis MCA infarction Infiltrating glioma Limbic encephalitis Seizure-related changes.
Fever is typically absent in infarction and glioma.
MC CNS infection in AIDS patients?
HIV encephalopathy
Progressive neurodegenerative disease caused by direct infection of CNS lymphocytes and microglial cells (CNS macrophages) by the HIV virus.
Imaging findings of HIV encephalopathy?
Diffuse cerebral atrophy and symmetric T2 prolongation in the periventricular and deep white matter.
In contrast to PML, HIV encephalitis spares the subcortical U-fibers and tends to be symmetric.
Who does Cytomegalovirus (CMV) encephalitis involve?
Only affects the immunosuppressed, typically when CD4 cell count is less than 50.
MC CNS manifestation of CMV infection?
Ventriculitis or meningoencephalitis.
Subependymal FLAIR hyperintensity and enhancement throughout the ventricular system.
In neonates, CMV is one of the most common TORCH infections and causes atrophy, encephalomalacia, ventricular enlargement, and periventricular calcification.
MRI findings of Creutzfeldt-Jakob Disease (CJD)
Cortical ribboning - ribbonlike FLAIR hyperintensity and restricted diffusion of the cerebral cortex. The basal ganglia and thalami are also involved. Often sparing the motor cortex.
Pulvinar sign - bright DWI and FLAIR signal within the pulvinar nucleus of the thalamus.
Hockey stick sign - bright DWI and FLAIR signal within the doromedial thalamus.
MRI findings of liver disease
Hyperintense signal on T1 in the globus pallidus and substantia nigra, thought to be due to manganese deposition.
MRI findings of hypoglycemia
Bilateral T2 prolongation in the gray matter, including the cerebral cortex, hippocampi, and basal ganglia.
MRI findings of Hypoxic Ischemic Encephalopathy (HIE)
FLAIR and/or DWI hyperintensity of the affected regions - usually gray matter, including the cerebral cortex, hippocampi, and basal ganglia. Distribution tends to be similar to that of severe hypoglycemia. Involvement of basal ganglia portends a worse prognosis.
MRI findings of Methanol Poisoning
Can present as optic neuritis as first symptom.
Hemorrhagic necrosis of the putamen and white matter edema may follow.
MRI findings of Carbon Monoxide
Symmetric T2 prolongation and restricted diffusion of the globus pallidus.
What is the retropharyngeal space?
Potential space located posterior to the pharynx, separated from the pharynx by the pharyngobasilar fascia.
Extends from the base of the skull to the upper mediastinum. Directly lateral to the retropharyngeal space are the carotid and parapharyngeal spaces.
What separates the pharynx from the retropharyngeal space?
Pharyngobasilar fascia.
What separates the retropharyngeal space from the danger space?
Alar fascia
What is the prevertebral space?
Anterior compartment of the perivertebral space in the suprahyoid neck - located just anterior to the vertebral body and is bounded anteriorly by the prevertebral fascia.
What is the sublingual space?
Potential space located at base of the tongue - nestled between the genioglossus and geniohyoid muscles medially and the sling of the mylohyoid muscle inferiorly and laterally.
What muscles make up the boundaries of the sublingual space?
Between the genioglossus and geniohyoid muscles medially. Sling of the mylohyoid muscle inferiorly and laterally.
What is Ludwig Angina?
Cellulitis of the floor of the mouth. Can involve the submental, sublingual, and submandiular spaces.
Tongue can become posteriorly displaced.
Causes of retropharyngeal infection in children and adults?
Children- Spread of an upper respiratory tract infection, such as pharyngitis. Enlargement of retropharyngeal lymph nodes that drain the pharynx may lead to subsequent suppuration and rupture.
Adults- Most often due to penetrating injury, such as fish bone ingestion or instrumentation.
What is Lemierre Syndrome?
Venous thrombophlebitis of the tonsillar and peritonsillar veins, often with spread to the internal jugular vein. Immunocompetent adolescents and young adults are typically affected.
MC is anaerobe Fusoacterium necrophorum, which is part of the normal mouth flora.
Imaging - enlargement, thrombosis, and mural enhancement of the affected veins.
Metastatic pulmonary abscesses may be present.
What is a Bezold Abscess?
Complication of otomastoiditis where there is necrosis of the mastoid tip and resultant spread of infection into the adjacent soft tissue.
Imaging- opacification of the middle ear and mastoid air cells, often with bony erosion of the mastoid.
What is a Ranula?
Mucus retention cyst that arises from the sublingual gland as a sequella of inflammation.
Plunging ranula 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.
What is the difference between a dermoid and an epidermoid?
Dermoid is a teratomatous lesion that contains at least two germ cell layers, while an epidermoid contains only ectoderm.
Both appear as fluid-attenuation lesion, most commonly in the midline of the floor of the mouth. Pathognomonic MRI finding of dermoid is the sack of marbles appearance from floating fat globules. In absence - epidermoid and dermoid can be indistinguishable in this location on MRI.
What is a thyroglossal duct cyst?
Persistence of the thyroglossal duct - follows the midline descent of the embryonic thyroid gland from the base of the tongue (foramen cecum) to its normal position of in the neck.
Present in childhood as an enlarging neck mass that elevates with tongue protrusion.
Majority are infrahyoid- the rest found at the level of the hyoid or above.
Most midline, but may be slightly off midline, especially when infrahyoid.
Where is a first branchial cleft cyst located?
Near the parotid or the external auditory canal
What is the most common branchial cleft cyst?
Second - Most occur near the angle of the mandible, anterior to the SCM, posterior to the submandibular gland, and closely associated with the carotid bifurcation.
MC location of a second branchial cleft cyst
Can occur at any point along the path extending from the palatine tonsil to the supraclavicular region- most near the angle of the mandible, anterior to the SCM, posterior to the submandibular gland, and closely associated with the carotid bifurcation.
Difference between superinfected second branchial cleft cyst and submandibular abscess?
Submandibular abscess is usually due to dental disease and is typically located immediately inferior to the mandible.
What are the three types of lymphatic malformations?
Cystic hygroma (MC)
Cavernous lymphangioma
Capillary Lymphangioma - smallest cystic spaces
What is a cystic hygroma?
MC type of lymphatic malformation. Majority being present at birth and associated with chromosomal anomalies including Turner and Down syndromes.
Large lymphatic spaces.
MC location is the posterior triangle of the neck.
What are cystic hyromas associated with?
Present at birth and associated with chromosomal anomalies including Turner and Down syndromes.
MC location of a cystic hygroma?
Posterior triangle of the neck.
What is a Thornwaldt cyst?
Notochordal remnant that is usually asymptomatic, but may be a cause of halitosis. Typically in the midline nasopharynx.
What are the cartilaginous components of the larynx?
Epiglotis, thyroid cartilage, cricoid cartilage, and arytenoids.
What are the aryepiglottic folds?
Extension of the mucosa covering the epiglottis and mark the entrance to the larynx. Connect the epiglottis anteriorly to the arytenoids posteriorly.
What structure marks the entrance to the larynx?
Aryepiglottic folds
What are the false focal cords?
Mucosal infoldings superior to the laryngeal ventricle.
Can be identified by the presence of the paraglottic fat laterally.
What is the supraglottic larynx?
Extends from the epiglottis to the ventricle. Contains the false vocal cords, the aryepiglottic folds, and the arytenoid cartilages.
What are the structures in the supraglottic larynx?
False vocal cords, the aryepiglottic folds, and the arytenoid cartilages.
What is the glottis?
Includes the true vocal cords and the thyroarytenoid muscle. The medial fibers of the thyroarytenoid muscle comprise the vocalis muscle.
True vocal cords are identified in the axial plane on CT or MRI by identifying the transition of paraglottic fat to muscle (thyroarytenoid muscle) within the wall of the larynx.
What makes up the vocalis muscle?
The medial fibers of the thyroarytenoid muscle comprise the vocalis muscle.
How to identify the true vocal cords?
True vocal cords are identified in the axial plane on CT or MRI by identifying the transition of paraglottic fat to muscle (thyroarytenoid muscle) within the wall of the larynx.
What is the subglottic larynx?
Begins 1 cm inferior to the apex of the laryngeal ventricle and extends to the first tracheal ring.
What is the MC mass lesion to cause of vocal cord paralysis?
Mediastinal or thoracic mass. Can have enlargement of the left atrium or pulmonary arteries may cause cardiovocal syndrome due to recurrent laryngeal nerve compression.
MC cause is iatrogenic trauma from neck surgery.
Innervation of the laryngeal musculature
Recurrent laryngeal nerve innervates all laryngeal musculature except the cricothyroid muscle which is innervated by the superior laryngeal nerve.
What is a Laryngocele?
Dilation of the laryngeal ventricle- may be caused by high laryngeal pressures. Trumpet players, glassblowers, and patients with COPD have increased risk of developing a laryngocele. May be filled with air or fluid.
Can get ventricular obstruction by neoplasm (MC is SCC), which typically causes a fluid-filled laryngocele.
What is the ostiomeatal unit (OMU)?
Common drainage pathway for the maxillary, frontal, and anterior ethmoid sinuses - all drain into the middle meatus.
Made up of the maxillary sinus ostium, infundibulum, uncinate process, hiatus semilunaris, ethmoid bulla, and middle meatus.
What structures drain the maxillary, frongal, and anterior ethmoid sinuses?
Ostiomeatal unit to the middle meatus.
Obstruction of what causes isolated sinus disease of the maxillary sinus?
Obstruction of maxillary sinus ostium or infundibulum.
Obstruction of what causes sinus disease affecting the maxillary, frontal, and anterior ethmoid sinuses?
Obstruction of the hiatus semilunaris
What structure demarcates the boundary between the anterior and posterior ethmoids?
Basal lamella
Where do the anterior ethmoids drain?
Via the frontal recess into the middle meatus (via the ostiomeatal unit)
Where do the posterior ethmoids drain?
Via tiny ostia underneath the superior turbinate into the superior meatus.
Where does the frontal sinus drain?
Drains into the ethmoid infundibulum via the frontal recess.
The frontal sinus is absent at birth and represents an enlarged anterior ethmoid cell.
Where does the sphenoid sinus drain?
Drains into the ethmoid air cells via the sphenoethmoidal recess - then the posterior ethmoids drain into the superior meatus via individual unnamed ostia.
What structures drain into the superior meatus?
Posterior ethmoids and sphenoid sinus (via the sphenoethmoidal recess)
What structures drain into the middle meatus?
Common drainage pathway of the maxillary, frontal, and anterior ethmoid sinuses via the ostiomeatal unit.
What structures drain into the inferior meatus?
Drainage pathway of the lacrimal duct.
What is an Agger Nasi Cell?
The most anterior ethmoid air cell.
Large agger nasi cell may cause obstruction of the frontal recess.
What is a Haller Cell?
Ethmoid cell located inferior to the orbit, which may compromise the maxillary ostium if the Haller cell becomes large or inflamed.
What is an Onodi Cell?
The most posterosuperior ethmoid air cell, which is located directly inferomedial to the optic nerve. May be mistaken for a sphenoid sinus endoscopically, potentially placing the optic nerve at risk.
What is the Concha Bullosa?
Formed when the inferior bulbous portion of the middle turbinate is pneumatized.
Usually incidental, but may cause septal deviation and narrowing of the infundibulum when large.
Most anterior ethmoid air cell. Can cause obstruction of the frontal recess
Agger nasi cell
Ethmoid air cell located inferior to the orbit which may compromise the maxillary ostium if becomes enlarged or inflamed.
Onodi Cell
Formed when the inferior bulbous portion of the middle turbinate is pneumatized.
Concha Bullosa
What is a Pott’s Puffy Tumor?
Osteomyelitis of the frontal bone which may cause a subgaleal abscess with associated soft tissue edema.
Imaging findings of chronic allergic fungal sinusitis
Affected sinus is expanded and airless, with thin deossified walls. The sinus contents are typically mixed attenuation with heterogeneous curvilinear high attenuation.
What causes acute invasive fungal sinusitis?
Aggressive infection that occurs in immunosuppressed patients.
Aspergillus and Zygomycetes are the MC organisms.
Aspergillus can cause acute fulminant disease.
Imaging findings of acute invasive fungal sinusitis
Nonspecific sinus mucosal thickening. Later in disease process there is often local invasion, bony destruction, and intracranial and intraorbital spread.
Unlike chronic allergic fungal sinusitis, invasive fungal sinusitis is not hyperdense on CT.
What is an Antrochoanal Polyp?
Benign polyp extending from the maxillary sinus into the nasal cavity with characteristic widening of the involved ostium. It may erode bone and extend into the nasopharynx.
What is an inverted papilloma?
Benign lobulated epithelial tumor of the sinus mucosa - can be associated with SCC 10-20% of the time.
Classic imaging finding on an enhanced study is a cerebriform pattern of enhancement - curvilinear, gyriform enhancement. In contrast to a mucocele or obstructed secretions, the entire solid tumor will enhance. Tends to remodel bone.
What is used as the demarcation of the superficial and deep lobes of the parotid gland?
Surgeons use facial nerve
Radiologists use the retromandibular vein
What is the main parotid gland duct?
Stensen’s Duct
Which salivary gland contains intrinsic lymphoid tissue?
Parotid - last major salivary gland to become encapsulated.
Course of facials nerve after it exits the skull base
Exits the stylomastoid foramen and subsequently passes anterior to the posterior belly of the digastric and lateral to the styloid process before entering the parotid gland.
What structure separates the floor of the mouth from the neck?
Posterior margin of the mylohyoid muscle.
MC minor salivary gland tumor?
Benign pleomorphic adenoma.
Tumor of a minor salivary gland origin is much more likely to be malignant than submandibular or parotid.
What is the MC parotid gland tumor?
Pleomorphic adenoma
Small firm mass in a middle-aged patient.
2nd MC is Warthin tumor
Why are pleomorphic adenoma’s resected?
Can transform into carcinoma ex pleomorphic adenoma.
Can’t distinguish between benign pleomorphic adenoma and malignant mucoepidermoid carcinoma by imaging.
MRI characteristics of Pleomorphic adenoma
Similar to water, but enhancement is typical.
What is a Warthin Tumor?
2nd MC benign parotid tumor. No risk of malignant transformation.
Generally appear as a cystic neoplasm, but unlike pleomorphic adenoma, Warthin tumors do not enhance.
What are the benign parotid neoplasms?
Pleomorphic adenoma and Warthin tumor
What are the malignant parotid neoplasms?
Mucoepidermoid Carcinoma
Adenoid Cystic Carcinoma
Carcinoma ex pleomorphic adenoma
SCC
What is a Mucoepidermoid Carcinoma?
MC primary parotid malignancy
Appears as an enhancing mass that is hyperintense on T2. Indistinguishable from benign pleomorphic adenoma on MRI.
What is the MC primary parotid malignancy?
Mucoepidermoid carcinoma
Adenoid cystic carcinoma is 2nd
What is an Adenoid Cystic Carcinoma?
MC submandibular and sublingual gland malignancy - 2nd MC parotid gland malignancy.
Tends to spread along the nerves (perineural spread) and often presents with cranial nerve palsy or paresthesia.
Key imaging feature is an enhancing mass with perineural spread
MC submandibular and sublingual gland malignancy?
Adenoid cystic carcinoma
Which salivary gland malignancy tends to spread along the nerves?
Adenoid cystic carcinoma
Which salivary glad tumor presents with cranial nerve palsy or paresthesia?
Adenoid cystic carcinoma
What is a Carcinoma ex pleomorphic adenoma?
Malignant degeneration of a benign pleomorphic adenoma
Elderly with rapid enlargement of an existing mass.
Hypointense on both T1 and T2
MRI characteristics of carcinoma ex pleomorphic adenoma
Hypointense on both T1 and T2
In which gland do a majority of salivary calculi occur?
Submandibular - 80-90%
What is Uveopoarotid fever?
Bilateral uveitis, parotid enlargement, and facial nerve palsy - pathognomonic for sarcoidosis
What are the findings of Sjogren syndrome in the salivary glands?
Atrophy and fatty replacement of the salivary glandular tissue with multiple nodules, abnormal enhancement, numerous small cystic foci and punctate calcification.
Risk of lymphoma is increased.
What are HIV lymphoepithelial lesions?
Parotid manifestations of lymphoid dysfunction in patients with HIV - multiple bilateral lymphepithelial cysts and solid masses.
Only parotid glands affected b/c only salivary glands to contain lymphoid tissue.
What does the pterygopalatine fossa act as a bridge between?
Face and brain - is an important potential pathway for the spread of tumor or infection.
Where does the pterygopalatine fossa sit?
Posterior to the maxillary sinus and inferior to the inferior orbital fissure.
3D box with each of the six sides leading to important structures in the face.
What are the contents of the pterygopalatine fossa?
Pterygopalatine ganglion and branches of the internal maxillary artery.
What are the foramina of the pterygopalatine fossa and central skull base?
Pterygomaxillary fissure - lateral exit of the pterygopalatine fossa - leads to the masticator space.
Sphenopalatine Foramen - Medial exit of the pterygopalatine fossa - leads to the nasopharynx via the superior meatus. The nasal margin of the spheopalatine foramen is though to the the site of origin of juvenile nasopharyngeal angiofibroma.
Foramen Rotundum - posterior opening to the middle cranial fossa. CN V2 travels through.
Inferior Orbital Fissure - the “roof” of the pterygopalatine fossa and opens anteriorly into the orbit. The infraorbital nerve and artery travel through the inferior orbital fissure.
Vidian Canal - located directly below the foramen rotundum. Contains the vidian canal and artery, also known as the nerve and artery of the pterygoid canal.
Pterygopalatine Canal - the “floor” of the pterygopalatine fossa - leads to the oral cavity via the greater and lesser palatine foramina. The pterygopalatine canal transmits the descending palatine nerve and artery.
What is the Pterygomaxillary fissure?
lateral exit of the pterygopalatine fossa - leads to the masticator space
What is the lateral exit of the pterygopalatine fossa leading to the masticator space?
Pterygomaxillary fissure
What is the Sphenopalatine Foramen?
Medial exit of the pterygopalatine fossa - leads to the nasopharynx via the superior meatus. The nasal margin of the spheopalatine foramen is though to the the site of origin of juvenile nasopharyngeal angiofibroma.
What is the Foramen Rotundum?
Posterior opening of the pterygopalatine fossa to the middle cranial fossa. CN V2 travels through.
What is the Inferior Orbital Fissure?
The “roof” of the pterygopalatine fossa and opens anteriorly into the orbit. The infraorbital nerve and artery travel through the inferior orbital fissure.
What structures travel through the Inferior Orbital Fissure?
Infraorbital nerve and artery
What is the Vidian Canal?
Part of the pterygopalatine fossa. Located directly below the foramen rotundum. Contains the vidian canal and artery, also known as the nerve and artery of the pterygoid canal.
Where is the Vidian canal in relation to the foramen rotundum?
Vidian canal is located directly below the foramen rotundum.
What is the Pterygopalatine Canal?
the “floor” of the pterygopalatine fossa - leads to the oral cavity via the greater and lesser palatine foramina. The pterygopalatine canal transmits the descending palatine nerve and artery.
What makes up the “floor” of the pterygopalatine fossa?
Pterygopalatine Canal - leads to the oral cavity via the greater and lesser palatine foramina. The pterygopalatine canal transmits the descending palatine nerve and artery.
What travels through the foramen spinosum?
Middle meningeal artery
What travels through foramen ovale?
CN V3
What is a Juvenile Nasopharyngeal Angiofibroma (JNA)?
Benign, highly vascular tumor seen in adolescent males. MC presentation is nasal obstruction and epistaxis.
Lack of metastatic behavior, is very locally aggresive and insinuates through adjacent skull base foramina.
Arises from within the nasal aspect of the sphenopalatine foramen, which is the medial boundary of the pterygopalatine fossa.
Enhances very avidly and is centered in the nasopharynx. Can extend into the pterygopalatine fossa or orbits as it continues to grow.
Classic findings:
Nasopharyngeal mass, expansion of the pterygopalatine fossa and anterior bowing or displacement of the posterior maxillary sinus wall.
Usually embolized prior to resection.
Where does a Juvenile Nasopharyngeal Angiofibroma (JNA) arise?
Arises from within the nasal aspect of the sphenopalatine foramen, which is the medial boundary of the pterygopalatine fossa.
Classic findings of a Juvenile Nasopharyngeal Angiofibroma (JNA) ?
Nasopharyngeal mass, expansion of the pterygopalatine fossa and anterior bowing or displacement of the posterior maxillary sinus wall.
What cells do meningiomas arise from?
Arachnoid villi rests
Important findings to describe with malignant anterior skull base neoplasms
Presence of bony destruction, invasion into the brain parenchyma, and extension into the orbit and cavernous sinus.
What is an Esthesioneuroblastoma?
Olfactory Neuroblastoma - malignant neural crest tumor that arises from specialized olfactory epithelium. Histology similar to other neural crest tumors, such as small cell lung cancer and neuroblastoma
Bimodal age distribition - peak in the teenage years and middle age.
Aggressive mass that is slightly hyperattenuating on CT and indeterminate intensity on both T1 and T2 images due to high cellularity. Calcification is often present.
Presence of peripheral tumor cysts that occur at the margins of the intracranial portion of the mass is classic
Another name for Esthesioneuroblastoma?
Olfactory Neuroblastoma - malignant neural crest tumor that arises from specialized olfactory epithelium. Histology similar to other neural crest tumors, such as small cell lung cancer and neuroblastoma
Imaging findings of Esthesioneuroblastoma
Aggressive mass that is slightly hyperattenuating on CT and indeterminate intensity on both T1 and T2 images due to high cellularity. Calcification is often present.
Presence of peripheral tumor cysts that occur at the margins of the intracranial portion of the mass is classic
MC malignancy of the paransal sinuses?
SCC.
Maxillary antrum is MC primary site.
Enhancement is the key differentiating feature from benign inflammatory processes such as sinonasal polyposis or mucocele.
What is Adenoid Cystic Carcinoma?
May arise from minor salivary glands in the sinonasal cavity.
Lymphatic spread is rare, distant metastases are seen commonly.
Demonstrates water signal on T1 and T2 images, but unlike a cyst, enhancement is characteristic.
Adenoid cystic carcinoma arising in the region of the anterior skull base has a high rate of trigeminal nerve perineural spread. Post-contrast evaluation of the cranial nerves offers the highest sensitivity to evaluate for subtle perineural spread.
MC head and neck tumor in children?
Rhabdomyosarcoma
What makes up the external ear?
External auditory canal (EAC)
What makes up the middle ear?
Tympanic membrane
Ossicles (malleus, incus, stapes)
Stapedius Muscle
Facial Nerve
What makes up the inner ear?
Cochlea Semicircular Canals Vestibule Utricle Saccule Vestibular Aqueduct Cochlear Aqueduct
What is the function of the labyrinth and what makes it up?
Cochlea, vestibule, and semicircular canals
Balance and position sense.
What pathology can affect the external auditory canal?
Congenital EAC stenosis, hypoplasia and atresia
Acute external otitis
EAC exostosis (surfer’s ear)
Necrotizing external otitis (malignant otitis externa)
Keratosis Obturans
Cholesteatoma
EAC Malignancy
Is it possible to get EAC and inner ear congential abnormalities in the same person?
EAC and inner ear have different embryologic origins, so it is uncommon for both an EAC and inner ear abnormality to be present.
What are also likely to be absent in EAC atresia?
Malleus and incus - 1st branchial cleft structures.
What is EAC exostosis?
AKA surfer’s ear - bony exostosis of the EAC seen in those who swim/surf in cold waters.
What is necrotizing external otitis?
AKA malignant otitis externa - severe complication of external otitis seen in elderly diabetic or immunocompromised patients.
Pseudomonas aeruginosa in diabetics and Aspergillus fumigatus in immunocompromised.
Fast spreading and aggressive with potential involvement of the middle or inner ear structures, or skull base extension.
Extensive enhancement centered around the external ear with bony erosion.
Causes of necrotizing external otitis in diabetics and immunocompromised?
Pseudomonas aeruginosa in diabetics and Aspergillus fumigatus in immunocompromised.
What is Keratosis Obturans?
Keratin plugs w/in an enlarged EAC.
Typically seen in young patients with sinusitis and bronchiectasis - usually bilateral.
What are the muscles of the middle ear?
Tensor tympani and stapedius
What does the footplate of the stapes articulate with?
The oval window.
What is the interface between the air-filled middle ear and the fluid-filled inner ear?
The oval window.
What is Glomus Tympanicum?
Extra-adrenal pheochromocytoma (paraganglioma) isolated to the middle ear.
MC primary middle ear tumor. Pulsatile tinnitus or conductive hearing loss.
MC primary middle ear tumor?
Glomus Tympanicum
What are the segments of the Facial nerve?
Labrynthine Segment - courses from the IAC to the geniculate ganglion, which is located superior to the cochlea. Greater superficial petrosal nerve innervates salivation.
Tympanic (horizontal) segment - Courses under the lateral semicircular canal.
Mastoid (descending) segment - Courses inferiority, then exits the temporal bone at the stylomastoid foramen. Nerve to stapedius and Chorda Tympani (taste to anterior 2/3 of tongue)
What is the Labrynthine segment of the facial nerve?
Courses from the IAC to the geniculate ganglion, which is located superior to the cochlea.
Greater superficial petrosal nerve innervates salivation.
What is the Tympanic (horizontal) segment of the facial nerve?
Courses under the lateral semicircular canal.
What is the Mastoid (descending) segment of the facial nerve?
Courses inferiority, then exits the temporal bone at the stylomastoid foramen.
Nerve to stapedius and Chorda Tympani (taste to anterior 2/3 of tongue)
What nerve provides taste to anterior 2/3 of the tongue?
Chorda Tympani - branch of the mastoid (descending) segment of the facial nerve
What are the MC segments of the facial nerve involved with schwannomas?
Geniculate ganglion, followed by the labyrinthine and tympanic segments.
What is a cholesterol granuloma?
AKA a cholesterol cyst - MC benign petrous apex lesion, but may occur in the middle ear.
Caused by giant cell reaction to cholesterol crystals thought to be intially incited by an obstructed air cell.
Blue mass behind the tympanic membrane.
Cholesterol granuloma and cholesteatoma are often considered together in the DDx of a soft tissue middle ear mass with bony erosion.
Cholesteatoma will show restricted diffusion and will appear as a white mass on otoscopic examination.
Cholesterol granuloma is typically hyperintense on T1.
DDx of a soft tissue middle ear mass with bony erosion
Cholesterol granuloma and cholesteatoma
Cholesteatoma will show restricted diffusion and will appear as a white mass on otoscopic examination.
Cholesterol granuloma is typically hyperintense on T1.
What is a cholesteatoma?
Non-neoplastic lesion of the temporal bone - skin in the wrong place.
Does not contain fat and is not neoplastic - despite it’s name.
An intracranial, extra-axial “cholesteatoma” is an epidermoid cyst.
What is an intracranial, extra-axial “cholesteatoma” called?
Epidermoid cyst
What structures need to be looked at when evaluating a cholesteatoma?
Lateral semicircular canal, the tegmen tympani (bony roof separating the mastoids from the brain), and the facial nerve.
CT findings of a cholesteatoma?
Well-circumscribed soft-tissue mass with adjacent bony erosion, blunting of the scutum, and erosion of the ossicles.
CT can’t tell the difference between cholesteatoma and cholesterol granuloma.
What are the most specific MRI sequences to evaluate for cholesteatoma?
Diffusion- hyperintense - combination of T2 shine through and restricted diffusion.
Post-contrast - do not enhance.
Intermediate to slightly hyperintense on T2 and of variable signal intensity on T1.
What is the bony superstructure containing the fluid-filled spaces of the cochlea, vestibule, and semicircular canals?
Otic capsule - densest bone in the body.
Function of the cochlea and vestibule?
Cochlea - allows us to hear - two-and-a-half turn spiral containing numerous neuroepithelial hair cells of the organ of Corti - send electrical impulses to the spiral ganglia of the cochlea in response to mechanical bending.
How does the cochlea allow us to hear?
Contains numerous neuroepithelial hair cells of the organ of Corti - send electrical impulses to the spiral ganglia of the cochlea in response to mechanical bending.
Hydralic pressure created in the perilymph by the vibrations of the stapes against the oval window ascends to the apex of the cochlea by the scala vestibuli. Pressure waves descend back to the basal turn through the scala tympani. Vibrations from the scala tympani are transmitted through the round window, where the energy is dissipated.
What is the structure in which hydralic pressure is transmitted up the cochlea?
Scala Vestibuli
What is the structure in which hydralic pressure is transmitted up the cochlea?
Scala Tympani and out through the round window.
What inner ear structures are involved with balance?
Vestibule and semicircular canals.
What structure connects the semicircular canals to the subarachnoid space?
Vestibular aqueduct connects the crus common (common channel of the superior and posterior semicircular canals) to the subarachnoid space in the IAC and is thought to be involved in pressure equalization between the CSF and the inner ear.
What is cochlear dysplasia?
Mondini Deformity - MC form of congenital cochlear dysplasia - incomplete development of the normal two and a half turns of the cochlea, resulting in confluence of the apical and middle turns and preservation of a distinct basilar turn
Strong association between cochlear dysplasia and enlarged vestibular aqueduct.
What is Michel Aplasia?
Very rare complete lack of development of the entire inner ear.
What is enlarged vestibular aqueduct syndrome?
Spectrum of congenital hearing loss associated with an enlarged vestibular aqueduct - the vestibular aqueduct does not have a direct function in the physiology of hearing.
Clinically, enlarged vestibular aqueduct syndrome may lead to progressive hearing loss while playing contact sports.
The vestibular aqueduct should not be larger than the posterior semicircular canal, which is often seen at the same level in the axial plane.
What is Otospongiosis?
AKA otosclerosis.
A primary bone dysplasia of the otic capsule characterized by replacement of normal endochondral bone by irregular spongy bone - MC in young and middle-aged women - bilateral 85% of the time.
Fenesteral - anterior to the oval window
Retrofenestral - more severe - involvement of the otic capsule in addition to the lateral wall of the labyrinth.
What are the two types of otospongiosis?
Fenestral - more common - occurs as the fissula ante fenestrum (located directly anterior to the oval window), and usually affects the oval window.
Retrofenestral (cochlear) - thought to represent more severe form with involvement of the otic capsule in addition to the lateral wall of the labyrinth.
What is the DDx of cochlear demineralization?
Retrofenestral otospongiosis, osteogenesis imperfecta in a child, fibrous dysplasia in a young adult, and Paget disease in an older adult.
What are the three stages of Labyrinthitis?
Acute Labyrinthitis - pus in the inner ear. Enhancement of the affected inner ear structures.
Fibrous Labyrinthitis - Replacement of endolymph and perilymph with fibrous strands that cause decreased signal intensity on T2. May be mild (but decreased) residual post-contrast enhancement of the affected structures.
Labyrinthitis Ossificans - final stage - calcified debris replaces the normal endolymph and perilymph. Calcification on CT with decreased signal intensity on T2 with lack of enhancement.
What are the two types of temporal bone fractures?
Longitudinal (MC) and Transverse
What is a longitudinal temporal bone fracture associated with?
MC - likely to involve the ossicles and result in conductive hearing loss. 20% associated with facial nerve injury.
What is a transverse temporal bone fracture associated with?
More likely to involve the bony labyrinth and result in sensorineural hearing loss. 50% result in facial nerve injury.
Which orientation of temporal bone fracture is associated with ossicle involvement and results in conductive hearing loss?
Longitudinal
Which orientation of temporal bone fracture is associated with involvement of the bony labyrinth and sensorineural hearing loss?
Transverse
Which orientation of temporal bone fracture is more likely to result in facial nerve involvement?
Transverse (50%)
Longitudinal (20%)
What is the petrous apex?
Most medial portion of the temporal bone
Bridge between the suprahyoid neck inferiorly and the intracranial component above. Adjacent to several important structures such as Dorello’s canal, Meckel’s cave and the petrous portion of the ICA
Normally bone marrow and dense bone. Pneumatized in 10% of the population which increases the risk for development of cholesterol cyst or apical petrositis.
What structure passes through Dorello’s Canal?
Cranial nerve VI
What structure passes through Meckel’s cave?
Trigeminal ganglion.
A pneumatized petrous apex increases the risk for development of?
cholesterol cyst or apical petrositis
What is the MC primary petrous apex lesion?
Cholesterol cyst
Can also occur in the mastoid portion of the temporal bone or the middle ear.
What is apical petrositis (petrous apicitis)?
Rare complication of infectious otomastoiditis - infection extends medially into a pneumatized petrous apex.
Gradenigo Triad - Otomastoiditis, facial pain due to trigeminal neuropathy at Meckel’s Cave, and lateral rectus palsy from CN VI palsy at Dorello’s canal.
What is the Gradenigo Triad and what causes it?
Apical Petrositis
Otomastoiditis, facial pain due to trigeminal neuropathy at Meckel’s Cave, and lateral rectus palsy from CN VI palsy at Dorello’s canal.
Where are acquired cholesteatomas located?
Middle ear
Congenital - can be located anywhere in the temporal bone, including the petrous apex.
What is Langerhans Cell Histiocytosis (LCH)?
Neoplastic proliferation of eosinophils and Langerhans Cells
Temporal bone is MC site of skull base involvement.
Where does a skullbase chondrosarcoma arise from?
Midline from the clivus or slightly off midline from the petroclival synchondrosis.
Petrous apex lesion with fluid w/in petrous apex?
Apical petrositis
Petrous apex lesion with bony erosion? Restricted diffusion?
Congenital cholesteatoma
Petrous apex lesion with no restricted diffusion? T1 hyperintense?
Cholesterol Granuloma
Petrous apex lesion with dural tail?
Meningioma
Petrous apex lesion with well circumscribed lytic lesion in a child?
Eosinophilic granuloma
Petrous apex lesion with smooth enhancement? Adjacent bony remodeling? Intralesional cysts?
Schwannoma
Petrous apex lesion that is aggressive appearing?
Mets/Myeloma
Petrous apex lesion that is aggressive appearing? Hyperintense on T2?
Chondrosarcoma/Chordoma
What is a Chordoma?
Locally invasive tumor arising in the midline from notochord remnants
50% near the sacrum, 35% near the clivus, and remainder in the vertebral column.
MC tumor to metastasize to the clivus?
Breast cancer
What are Paragangliomas?
Glomus Tumors - neoplasms of paraganglionic tissue that arise from sympathetic glomus bodies. Histologically identical to extra-adrenal pheochromocytoma. Occur in a few predictable locations in neck.
Associated with MEN 1 and NF1.
Highly vascular and enhance avidly.
Classic MRI appearance is salt and pepper appearance due to intratumora flow voids.
What syndromes are paragangliomas associated with?
MEN 1 and NF1.
What are the common locations of paragangliomas in the head and neck?
Glomus Jugulare Glomus tympanicum Glomus Jugulotympanicum Carotid Body Tumor (glomus caroticum) Glomus Vagale
What is a Glomus Jugulare?
MC primary neoplasm of the jugular foramen - woman in late middle age presenting with pulsatile tinnitus and conductive hearing loss.
Moth-eaten bony destruction typical of paragangliomas centered around the jugular foramen.
Schwannoma and meningioma features smooth bony remodeling and meningioma causes hyperostosis.
What is a Glomus Tympanicum?
Paraganglioma isolated to the middle ear
Vascular, red, retro-tympanic mass
DDx of vascular, red, retro-tympanic mass
Glomus tympanicum
Aberrant carotid artery
Tympanic membrane hemangioma
What is a Glomus Jugulotympanicum?
Glomus jugular that has spread into the middle ear
What is a Carotid Body Tumor?
Glomus Caroticum - paraganglioma of the carotid body
Characteristically splays the internal and external carotid arteries.
What is a Glomus Vagale?
Paraganglioma of the vagus nerve - typically occuring at the same level of the neck as the carotid body tumor
Displaces the carotid artery (both internal and external branches) medially and anteriorly. In contrast, a carotid body tumor splays the internal and external carotids.
Schwannoma of the vagus nerve may occur in the same location and will also displace the carotid artery medially and anteriorly. Generally less vascular. May enhance avidly, but would show the flow voids of typical glomus vagale.
Tumor that splays the internal and external carotid arteries?
Carotid Body Tumor
Tumor that displaces the carotid artery (both internal and external branches) medially and anteriorly?
Glomus Vagale
Bones that make up the orbit
Frontal, ethmoid, nasal, zygomatic, and maxilla.
Structures that pass through the optic foramen?
Optic nerve
Opthalmic artery
Structures that pass through the superior orbital fissure?
All cranial nerves of the cavernous sinus except V2 (exits via the foramen rotundum and enters the orbit via the inferior orbital fissure).
CN III (oculomotor) CN IV (trochlear) CN V1 (opthalmic division of trigeminal nerve) CN VI (abducens) Superior opthalmic vein
Function of CN III
Oculomotor Nerve - Innervates the superior, medial, and inferior rectus, and the inferior oblique
Function of CN IV
Trochlear Nerve - Innervates the superior oblique
Function of CN V1
Opthalmic division of the trigeminal nerve - provides sensory innervation to the upper face
Function of CN VI
Abducens Nerve - innervates the lateral rectus
The superior opthalmic vein passes through what?
Superior orbital fissure
Structures that pass through the inferior orbital fissure
CN V2
Infraorbital artery
Function of CN V2
Maxillary division of the trigeminal nerve - provides sensory innervation to the inferior eyelid, upper lip, and nose.
5 compartments of the orbit
Preseptal Postseptal Extraconal Conal Intraconal Globe
What divides the preseptal and postseptal compartments?
Orbital septum
Contents of the extraconal compartment of the orbit?
Lacrimal gland, fat, and bony orbit.
Where do the conal muscles arise from?
All the muscles except the inferior oblique muscle arise from a common fibrous ring called the annulus of Zinn - located at the apex of the orbit at the optic foramen and medial superior orbital fissure.
The inferior oblique arises from the medial orbital floor.
Contents of the intraconal compartment of the orbit?
Optic nerve-sheath complex, sensory and motor nerves of the orbit, lymph nodes, and fat.
MC etiology of orbital infection
Direct spread of infection from the paranasal sinuses
Can get from trauma, foreign body, and odotogenic
Types of orbital infection
Preseptal infection Orbital cellulitis/phlegmon Subperiosteal abscess Orbital abscess Cavernous sinus thrombosis
DDx of orbital masses
Hemangioma Orbital Lymphoma Lymphangioma Schwannoma/Neurofibroma Metastases Lacrimal Gland Lesion
Two types of orbital hemangiomas
Cavernous hemangioma - seen in adults - MC adult orbital mass, typically presents with proptosis. Usually intraconal, but may be extraconal. Ovoid enhancing intra or extraconal mass. Isointense on T1 and hyperintense on T2 with patchy enhanement that progressively fills in.
Capillary hemangioma - seen only in the first year of life. Analogous to and often present in conjunction with skin lesions - typically enlarges over first few months of life before spontaneously involuting.
MC site of orbital lymphoma
Lacrimal gland- usually associated with systemic disease. Painless downward proptosis.
Hypercellular tumor that is hyperdense on CT and hypointense on both T1 and T2.
Molds to the globe like orbital pseudotumor, but pseudotumor presents with pain.
Similarities and differences between orbital lymphoma and pseudotumor
Both mold to the globe.
Pseudotumor typically presents with pain.
What is an orbital lymphangioma?
Benign hamartomatous lesion seen in the pediatric population - low flow lymphatic malformation
Most commonly involve the extraconal compartment but may be found anywhere in the orbit.
Multilocular cystic mass, often with complex internal contents with fluid levels from prior hemorrhage. Slight peripheral and septal enhancement.
Multilocular cystic mass in the orbit, often with complex internal contents with fluid levels from prior hemorrhage. Slight peripheral and septal enhancement.
Lymphangioma
MC location for schwannoma/neurofibroma in the orbit
Sensory branches of V1 - characteristic location in the superior orbit
MC tumor to metastasize to the orbit
Breast, lung, thyroid, renal cell, and melanoma.
Diseases that can affect the lacrimal gland
Epithelial salivary gland tumors - 50% benign (pleomorphic adenoma) and 50% malignant (adenoid cystic and mucoepidermoid carcinoma)
Diseases of lymphoid tissue - sarcoidosis and lymphoma
May become enlarged in orbital pseudotumor
What causes thyroid opthalmopathy?
Mediated by lymphocytes that produce hyaluronic acid - leads to fibrosis of the extraocular muscles.
Can occur with any thyroid disorder, MC with Graves.
Initially increase in intra-orbital fat, which may demonstrate stranding due to inflammatory change, then extraocular muscles become enlarged.
I’M SLow
Inferior rectus –> Medial Rectus –> Superior Rectus –> Lateral rectus
Isolated lateral rectus enlargement?
Very uncommon in thyroid opthalmopathy - prompt search for alternative diagnosis such as orbital pseudotumor.
Thyroid opthalmopathy tends to be bilateral and spares the muscle tendons.
What is orbital pseudotumor?
Idiopathic orbital inflammation mediated by an infiltrate of lymphocytes, plasma cells, and macrophages.
Painful proptosis (in contrast to lymphoma which is painless)
Dx of exclusion
Lacrimal gland is MC involved orbital structure. Several other structures in the orbit may be affected, including the anterior structures (producing uveitis) and the extraocular muscles.
Stranding w/in the orbit fat, increased orbital soft tissue, and enlargement of the extrocular muscles.
Tx with steroids
Presentation of orbital pseudotumor
Painful proptosis (in contrast to lymphoma which is painless)
MC involved orbital structure with orbital pseudotumor?
Lacrimal gland is MC involved orbital structure. Several other structures in the orbit may be affected, including the anterior structures (producing uveitis) and the extraocular muscles.
Findings of orbital pseudotumor
Stranding w/in the orbit fat, increased orbital soft tissue, and enlargement of the extrocular muscles.
What is Tolosa-Hunt Syndrome?
Same pathologic process as orbital pseudotumor (inflammation mediated by an infiltrate of lymphocytes, plasma cells, and macrophages), but involving the cavernous sinus
What is an optic nerve glioma?
MC Tumor to arise from the optic nerve-sheath complex.
In children: typically low-grade astrocytoma with indolent course. Associated with NF1 and often bilateral. Variable appearance with fusiform enlargement of optic nerve and variable nehancement. May have a cyst and nodule appearance like low-grade pilocytic astrocytomas of the posterior fossa.
Adulthood: usually anaplastic astrocytoma or GBM with poor prognosis. Aggressive enhancing mass, often extends intracranially to involve the optic chiasm. May involve any part of optic tract, including the optic radiations.
MC Tumor to arise from the optic nerve-sheath complex.
Optic nerve glioma
Findings of optic nerve glioma in children
Typically low-grade astrocytoma with indolent course. Associated with NF1 and often bilateral. Variable appearance with fusiform enlargement of optic nerve and variable nehancement. May have a cyst and nodule appearance like low-grade pilocytic astrocytomas of the posterior fossa.
Findings of optic nerve glioma in adults
Usually anaplastic astrocytoma or GBM with poor prognosis. Aggressive enhancing mass, often extends intracranially to involve the optic chiasm. May involve any part of optic tract, including the optic radiations.
What is an optic nerve meningioma?
2nd MC optic nerve-sheath tumor- arising from arachnoid cells within the leptomeninges surrounding the optic nerve
Middle aged female with slowly progressive visual impairment, classically with preservation of the central visual field.
Nerve-sheath tends to be circumferentially thickened, with uniform contrast enhancement. The enhancing peripheral tumor and the nonenhancing, central optic nerve produce the tram-track sign on axial image.
2nd MC optic nerve-sheath tumor
Optic nerve meningioma
Presentation of optic nerve meningioma
Middle aged female with slowly progressive visual impairment, classically with preservation of the central visual field.
Imaging findings of optic nerve glioma
Nerve-sheath tends to be circumferentially thickened, with uniform contrast enhancement. The enhancing peripheral tumor and the nonenhancing, central optic nerve produce the tram-track sign on axial image.
Causes of optic neuritis
MS (MC) Viral infection Sarcoidosis Vasculitis Toxin exposure
Optic neuritis associated with spinal demyelination (in absence of brain lesions)
Devic Syndrome
What is Retinoblastoma?
MC primary malignant tumor of the globe
Almost always seen in children under 5 and typically presents with leukocoria (white pupillary reflex)
Hyperattenuating, enhancing retinal mass with calcification, in normal-sized globe.
“Trilateral” retinoblastoma = bilateral retinoblastoma with pineal-gland pineoblastoma
“Quadrilateral” retinoblastoma = bilateral retinoblastoma, pineoblastoma, and suprasellar retinoblastoma
MC primary malignant tumor of the globe
Retinoblastoma
Presentation of Retinoblastoma
Almost always seen in children under 5 and typically presents with leukocoria (white pupillary reflex)
Findings of retinoblastoma
Hyperattenuating, enhancing retinal mass with calcification, in normal-sized globe.
What is “Trilateral” retinoblastoma?
bilateral retinoblastoma with pineal-gland pineoblastoma
What is “Quadrilateral” retinoblastoma?
bilateral retinoblastoma, pineoblastoma, and suprasellar retinoblastoma
What is Coat Disease?
Vascular disease of the retina that affects boys and features lipoproteinaceous subretinal exudates that lead to retinal detachment.
Slightly older than those affected by retinoblastoma
Globe is normal in size, but features subretinal soft tissue that does not enhance.
Vascular disease of the retina that affects boys and features lipoproteinaceous subretinal exudates that lead to retinal detachment.
Coat Disease
Normal size globe that features subretinal soft tissue that does not enhance.
Coat Disease
What is Retinopathy of Prematurity?
Seen only premature infants and due to prolonged oxygen therapy. Abnormal vascular development, hemorrhage, and retinal detachment.
Both eyes tend to be affected equally.
Bilateral microthalmia (small globes), with increased attenuation of the globes due to prior hemorrhage.
Intraocular calcifications may be present (similar to retinoblastoma), but distinguished by microphthamia
End-stage is phthisis bulbi - shrunken, nonfunctioning globe.
Cause of Retinopathy of Prematurity
Prolonged oxygen therapy. Abnormal vascular development, hemorrhage, and retinal detachment.
Imaging of Retinopathy of Prematurity
Bilateral microthalmia (small globes), with increased attenuation of the globes due to prior hemorrhage.
Intraocular calcifications may be present (similar to retinoblastoma), but distinguished by microphthalmia
End-stage is phthisis bulbi - shrunken, nonfunctioning globe.
DDx of calcifications in globe
Retinopathy of prematurity and Retinoblastoma
ROP has microphthalmia
What is Persistent Hyperplastic Primary Vitreous (PHPV)?
Persistent embryonic vasculature w/in the vitreous that leads to loss of vision from hemorrhage, cataracts, and retinal detachment. Affected infants are typically full term.
Eye is small (microphthalmia) with increased attenuation of the vitreous
Distinguished from retinoblastoma and ROP by absence of calcifications
Persistent embryonic vasculature w/in the vitreous that leads to loss of vision from hemorrhage, cataracts, and retinal detachment.
Persistent Hyperplastic Primary Vitreous (PHPV)
Findings of Persistent Hyperplastic Primary Vitreous (PHPV)
Eye is small (microphthalmia) with increased attenuation of the vitreous
Distinguished from retinoblastoma and ROP by absence of calcifications
Difference between Retinoblastoma, Persistent Hyperplastic Primary Vitreous (PHPV), and Persistent Hyperplastic Primary Vitreous
Calcifications = Retinoblastoma and Retinopathy of prematurity - ROP = small globe
Small globe = Retinopathy of Prematurity and Persistent Hyperplastic Primary Vitreous - PHPV = no calcifications
What is Coloboma?
Incomplete fusion of the embryonic introcular fissure, which can result in an elongated or malformed globe.
Associated with numerous syndromes - trisomies 13 and 18, and CHARGE and VATER associations
Cone-shaped or notch-shaped deformity. Optic nerve colobomas can have outpouchings posteriorly, while iris colobomas are anterior. Colobomas that involve the uvea tend to have microphthalmos and a cyst.
Incomplete fusion of the embryonic introcular fissure, which can result in an elongated or malformed globe.
Coloboma
Associations with Coloboma
Numerous syndromes - trisomies 13 and 18, and CHARGE and VATER associations
Orbital cone-shaped or notch-shaped deformity.
Coloboma
Optic nerve colobomas can have outpouchings posteriorly, while iris colobomas are anterior. Colobomas that involve the uvea tend to have microphthalmos and a cyst.
Sphenoid wing dysplasia is seen in
NF 1
Transmission of CSF pulsation through the sphenoid wing defect may classically produce pulsatile exophthalmos.
What is septo-optic dysplasia?
Optic nerve hypoplasia and agenesis of the septum pellucidum.
Often associated with schizencephaly, a full-thickness cleft in the cerebral hemisphere that creates a communication between the ventricles and the extra-axial subarachnoid space.
Optic nerve hypoplasia and agenesis of the septum pellucidum.
Septo-optic dysplasia
Associated with septo-optic dysplasia
Schizencephaly, a full-thickness cleft in the cerebral hemisphere that creates a communication between the ventricles and the extra-axial subarachnoid space.
Optic nerve hypoplasia and agenesis of the septum pellucidum.
What is the pharynx divided into?
Nasopharynx - Top of the pharynx behind the nasal cavity
Oropharynx - From level of the palate to the hyoid bone, behind the oral cavity. The posterior 1/3 of the tongue is part of the oropharynx
Oral Cavity - Space defined by the anterior 2/3 of the tongue, bounded superiorly by the palate and inferiorly by the floor of the mouth
Hypopharynx - From the hyoid bone to the esophagus (posterior)
Larynx - From the hydoid bone to the trachea (anterior)
What makes up the Nasopharynx?
Top of the pharynx behind the nasal cavity
What makes up the Oropharynx?
From level of the palate to the hyoid bone, behind the oral cavity. The posterior 1/3 of the tongue is part of the oropharynx
What makes up the Oral Cavity?
Space defined by the anterior 2/3 of the tongue, bounded superiorly by the palate and inferiorly by the floor of the mouth
What makes up the Hypopharynx?
From the hyoid bone to the esophagus (posterior)
What makes up the Larynx?
From the hydoid bone to the trachea (anterior)
What is the Masticator Space?
Located directly anterior to the parotid and contains the muscles of mastication, the mandible, and cranial nerve V3.
CN V3 (manidbular division) exits the skull through foramen ovale and innervates the muscles of mastication. If lesion is seen in masticator space, need to check for perineural spread along V3.
What is the course and function of CN V3?
CN V3 (manidbular division) exits the skull through foramen ovale and innervates the muscles of mastication. If lesion is seen in masticator space, need to check for perineural spread along V3.
DDx of Masticator Space Lesion
Odontogenic Abscess - dental disease is MC masticator space pathology, which can lead to abscess
Mandibular Lesion - Osteosarcoma and metastasis are the two MC malignant mandibular lesions.
Rhabdomyosarcoma - MC head and neck tumor of childhood.
MC malignant mandibular lesions
Osteosarcoma and metastasis
MC head and neck tumor of childhood
Rhabdomyosarcoma
What is the carotid space?
AKA post-styloid parapharyngeal space. Incomplete fascial ring surrounding the carotid artery and jugular vein.
Extends from the skull base to the aortic arch
Contents: carotid artery, carotid body, jugular vein, and several cranial nerves. Vagus nerve (CN X) is the only CN that remains w/in the carotid space the entire way into the thorax. CN IX, XI, and XII pass transiently through the carotid space. Lymph nodes are seen surrounding it, but not contained within it.
Contents of the carotid space?
Carotid artery, carotid body, jugular vein, and several cranial nerves. Vagus nerve (CN X) is the only CN that remains w/in the carotid space the entire way into the thorax. CN IX, XI, and XII pass transiently through the carotid space. Lymph nodes are seen surrounding it, but not contained within it.
DDx of carotid space mass
Paraganglioma - benign highly vascular neoplasm of neural crest cells - intense enhancement and a characteristic salt and pepper appearance on MRI due to intra-tumoral flow voids.
Paraganglioma of the carotid body (carotid body tumor) splays the external and internal carotid arteries at the carotid bifurcation
Paraganglioma of the vagal nerve (glomus vagale) displaces the internal and external carotid aarteries anteromedially.
Schwannoma - Similar to glomus vagale, schwannoma (MC of the vagus nerve) also displaces the carotid arteries anteromedially. Schwannoma, however, is not nearly as vascular as paraganglioma and usually does not enhance as homogeneously.
Neurofibroma - Almost always associated with NF1. Neurofibroma and schwannoma are indistinguishable by MRI.
What is a carotid body tumor?
Paraganglioma - benign highly vascular neoplasm of neural crest cells - intense enhancement and a characteristic salt and pepper appearance on MRI due to intra-tumoral flow voids.
Paraganglioma of the carotid body (carotid body tumor) splays the external and internal carotid arteries at the carotid bifurcation
Paraganglioma of the vagal nerve (glomus vagale) displaces the internal and external carotid aarteries anteromedially.
Difference between carotid body tumor and glomus vagale?
Paraganglioma of the carotid body (carotid body tumor) splays the external and internal carotid arteries at the carotid bifurcation
Paraganglioma of the vagal nerve (glomus vagale) displaces the internal and external carotid aarteries anteromedially.
What is the parapharyngeal space?
Triangular fat-filled space with no significant contents aside from occasional ectopic minor salivary gland tissue.
Direction of displacement by a mass lesion in an adjacent compartment is predictable and helpful in determining from which compartment a given mass originates.
Masticator space lesions (e.g. masticator abscess) displaces the PPS posteromedially.
Parotid lesions (e.g. pleomorphic adenoma) displace the PPS anteromedially.
Carotid space lesions (e.g. paraganglioma) displace the PPS anteriorly.
What is the prevertebral space?
Formed by the deep layer of cervical fascia, which wraps entirely around the prevertebral and paraspinal muscles. Is the anterior component of the perivertebral space. The perivertebral space is in the suprahyoid neck; the paravertebral space is the analgous region in the thoracolumbar spine.
Contents include the vertebral arteries, paraspinal muscles, spinal column, and exiting nerves.
Contents of the prevertebral space?
Vertebral arteries, paraspinal muscles, spinal column, and exiting nerves
What are Level I lymph nodes?
Submental and submandibular nodes, which are superior to the hyoid bone and inferior to the mandible and mylohyoid.
- IA nodes are submental, lying between the medial margins of the anterior bellies of the digastrics.
- IB nodes are submandibular, lateral to the medial margin of the anterior belly of the digastric and extending to the posterior margin of the submandibular gland.
What are Level IA lymph nodes?
Submental, lying between the medial margins of the anterior bellies of the digastrics.
What are Level IB lymph nodes?
Submandibular, lateral to the medial margin of the anterior belly of the digastric and extending to the posterior margin of the submandibular gland.
What are Level II lymph nodes?
Upper internal jugular nodes, extending from the skull base to the inferior margin of the hyoid bone.
- IIA nodes are anterior to the posterior margin of the internal jugular vein (IJV).
- IIB nodes are posterior to the IJV but anterior to the posterior margin of the sternocleidomastoid muscle.
What are Level IIA lymph nodes?
IIA nodes are anterior to the posterior margin of the internal jugular vein (IJV).
What are Level IIB lymph nodes?
IIB nodes are posterior to the IJV but anterior to the posterior margin of the sternocleidomastoid muscle.
What are Level III lymph nodes?
Level III lymph nodes are middle jugular nodes, extending craniocaudally from the inferior aspect of the hyoid to the inferior aspect of the cricoid cartilage. The posterior edge of the sternocleidomastoid is the shared posterior margin for both level III and level IIB nodes.
What is the shared posterior margin for both level III and level IIB nodes?
Posterior edge of the sternocleidomastoid
What are the Level IV lymph nodes?
Level IV nodes are inferior jugular nodes, extending from the inferior aspect of the
cricoid cartilage to the clavicle. Superiorly, the posterior border is the posterior aspect
of the sternocleidomastoid muscle (similar to level III and IIB nodes). Inferiorly, the
posterior border is the posterior aspect of the anterior scalene muscle.
What are Level V lymph nodes?
Level V lymph nodes are posterior cervical nodes.
- VA nodes are superior, extending from the skull base to the inferior cricoid cartilage.
- VB nodes are inferior, extending from the inferior cricoid cartilage to the clavicle.
What are Level VA lymph nodes?
VA nodes are superior, extending from the skull base to the inferior cricoid cartilage.
What are Level VB lymph nodes?
VB nodes are inferior, extending from the inferior cricoid cartilage to the clavicle.
What are level VI lymph nodes?
Level VI nodes are pretracheal nodes, which are often simply called “pretracheal.” They are located anteromedially in the lower neck and bounded laterally by the carotid sheaths. Level VI extends craniocaudally from the inferior aspect of the hyoid bone to the top of the manubrium.
What is another name from Level VI lymph nodes?
Pretracheal
What are Level VII lymph nodes?
Level VII nodes are superior mediastinal nodes, which are also commonly described by their location. They are inferior to level VI and medial to the carotid sheaths, extending craniocaudally from the superior aspect of the manubrium to the brachiocephalic vein.
How can spinal tumors be classified?
Intramedullary
Intradural Extramedullary
Extradural
What are the Intramedullary spinal tumors?
ependymoma
astrocytoma
hemangioblastoma
demyelinating lesion
What are the Intradural Extramedullary spinal tumors?
schwannoma neurobroma meningioma myxopapillary ependymoma epidermoid/dermoid arachnoiditis
What are the Extradural spinal tumors?
degenerative disease vertebral neoplasm epidural metastasis hemangioma epidural lipomatosis
What two diagnoses make up 95% of intramedullary tumors?
Astrocytoma and Ependymoma
Astrocytoma - more common in children
Ependymoma - more common in adults
What is a spinal astrocytoma?
Astrocytoma is the most common intramedullary tumor in children. Most spinal astrocytomas are low grade.
Usually extends over several vertebral levels and causes fusiform dilation of the spinal cord.
Cystic components are seen in approximately 1/3 and a syrinx may be present. Tumors almost always enhance despite being low grade. In contrast to ependymoma,
hemorrhage is rare.
Astrocytoma cannot be reliably differentiated from ependymoma based on imaging features. Hemorrhage is more commonly seen with ependymoma and may occasionally be a helpful discriminating feature.
Most commonly seen difference between spinal Astrocytoma and Ependymoma
Hemorrhage more common with ependymoma.
What is a spinal Ependymoma?
Ependymoma is the most common intramedullary tumor in adults, arising from ependymal cells that line the central spinal canal. Ependymoma is associated with neurofibromatosis type 2, especially when seen in children.
Often hemorrhagic, leading to a heterogeneous MRI appearance. Peripheral hemosiderin deposition causes a dark rim on T2-weighted images. Most ependymomas enhance. Classically, there is extensive formation of both tumoral cysts and nontumoral polar cysts. Tumoral cysts are surrounded by enhancement and must be resected with the mass. A classic radiographic finding of ependymoma is scalloping of the vertebral bodies;
however, that finding is associated with advanced disease and is rarely seen today.
When a spinal ependymoma is seen in children it is most often associated with?
NF 2
What is a spinal hemangioblastoma?
Rare intramedullary tumor (distant third most common
behind astrocytoma) associated with von Hippel–Lindau (VHL). One third of hemangioblastomas are associated with this syndrome.
Marked enhancement, cyst formation, and numerous flow voids. Up to 15% have both intramedullary and intradural–extramedullary components.
Spinal hemangioblastomas are associated with?
VHL.
1/3 of hemangioblastomas are associated with VHL.
What are Intradural-extramedullary spinal lesions?
Located within the dura but outside the spinal cord.
Most of the time, intradural–extramedullary
lesions are located in the subarachnoid space.
A cleft of CSF can sometimes be seen between the lesion and the spinal cord.
Nerve-sheath tumors (neurofibromas and schwannomas) and meningiomas together make up 90%
How is a spinal schwannoma treated?
Encapsulated - can be treated by a nerve-sparing approach, which is accomplished by “shelling out” the tumor.
Neurofibroma is associated with NF1, younger patients and lacks a capsule. The complete circumference of the nerve is involved and treatment therefore necessitates nerve resection.
How is a spinal neurofibroma treated?
Lacks a capsule. The complete circumference of the nerve is involved and treatment therefore necessitates nerve resection.
Sign seen with spinal nerve-sheath tumors (schwannoma and neurofibroma)
Target Sign - Central hypointensity on T2 surrounded by a hyperintense periphery, suggests benignity.
What is a Myxopapillary Ependymoma?
An ependymoma variant that occurs exclusively within
the conus medullaris or the filum terminale. It is the most common tumor of the conus and filum and arises from ependymal cells in the filum.
Characterized by slow growth, classically leading to vertebral scalloping and spinal canal enlargement.
Highly vascular, hemorrhagic tumor, featuring
a complex, lobulated MRI appearance with internal hemorrhage. Peripheral hemosiderin is often present, producing hypointensity on T2-weighted images and
blooming on GRE.
Most common tumor of the conus and filum?
Myxopapillary Ependymoma
Imaging findings of Myxopapillary Ependymoma?
Highly vascular, hemorrhagic tumor, featuring
a complex, lobulated MRI appearance with internal hemorrhage. Peripheral hemosiderin is often present, producing hypointensity on T2-weighted images and
blooming on GRE.
What is spinal arachnoiditis?
inflammation of the arachnoid surrounding the nerve roots, which produces a fibrinous exudate and secondary dural adhesions. In the past, tuberculosis and syphilis were common causes of arachnoiditis. Today, lumbar spine surgery is a far more common cause. Arachnoiditis may be a cause of persistent back pain after lumbar surgery.
Three types of spinal arachnoiditis?
Group 1: Central conglomerations of nerve roots within the thecal sac.
Group 2: Peripheral clumping of nerve roots, causing the empty thecal sacsign.
Group 3: Obliteration of the subarachnoid space. Imaging shows increased soft tissue within the thecal sac. This is the most severe form of arachnoiditis.
MC tumors to metastasize to the spinal column?
Breast, lung, and prostate
Marrow should always be more hyperintense on T1-weighted images than the intervertebral discs.
Focal decrease in intensity on T1-weighted images is concerning for metastasis
Diffuse decrease in intensity on T1-weighted images is abnormal but nonspecific. The differential for diffusely decreased T1 marrow signal includes leukemia, lymphoma, myelofibrosis, HIV, and idiopathic causes.
Focal decrease in intensity on T1-weighted images of the bone marrow is concerning for
Metastases
DDx of diffuse decrease in T2 intensity of the bone marrow
Abnormal but nonspecific. Leukemia, lymphoma, myelofibrosis, HIV, and idiopathic causes
Findings of a hemangioma on MRI
Hyperintense on both T1- and T2-weighted images
What are the primary osseous vertebral body tumors of middle-aged and older adults?
Chordoma -
Malignant tumor of older adults that arises from a notochord remnant. Occurs most commonly in the sacrococcygeal region and second most commonly in the clivus. Up to 15% may occur in the vertebral bodies. Appears as a destructive, hyperintense mass on T2-weighted images. It avidly enhances.
Plasmacytoma -
Lytic, expansile bony lesion of late adulthood that is thought to be a precursor of multiple myeloma. A plasmacytoma is a solitary lesion. The presence of multiple plasmacytomas implies the diagnosis
of multiple myeloma.
Chondrosarcoma -
low-grade malignancy that appears as a hyperintense mass on T2-weighted images, similar to chordoma. Chondroid rings-and-arcscalcification may be seen
What is a Chordoma?
Malignant tumor of older adults that arises from a notochord remnant.
Occurs most commonly in the sacrococcygeal region and second most commonly in the clivus. Up to 15% may occur in the vertebral bodies.
Appears as a destructive, hyperintense mass on T2-weighted images. It avidly enhances.
What is the difference between a disc protrusion and extrusion?
Protrusion - focal herniation where the diameter of the neck is greater than the diameter of the dome.
Extrusion - Focal herniation where the diameter of the neck is less than the diameter of the dome.
What are the terms used to describe the medial-lateral position of a herniation?
Central
Paracentral (adjacent to the subarticular facet joint)
Foraminal
Far-lateral (extra-foraminal)
Medial hernation (central or paracentral) will affect the descending nerve root corresponding to the level below the disc.
A lateral herniation (foraminal or far-lateral) will affect the exiting nerve root.
A medial hernation (central or paracentral) will affect which nerve root?
Descending nerve root corresponding to the level below the disc.
A lateral herniation (foraminal or far-lateral) will affect which nerve root?
The exiting nerve root.
What are Modic changes?
Degenerative changes in the spine are associated with vertebral body endplate and subchondral marrow signal changes that were described and classified by Modic
What are Modic Type 1 endplate changes?
Hyperintense on T2-weighted images and hypointense on T1-weighted images, reflecting bone marrow edema and inflammation. These changes may be associated with active back pain and their presence predicts a better outcome following lumbar spine surgery.
What are Modic Type 2 endplate changes?
Hyperintense on both T2- and T1-weighted images and reflect fatty proliferation within the affected marrow, thought to be secondary to chronic marrow ischemia. Modic 2 changes are less likely to be associated with active symptoms.
What are Modic Type 3 endplate changes?
Hypointense on both T2- and T1-weighted images and are thought to represent sclerosis. Their clinical significance is unclear.
What is a Tarlov Cyst?
Perineural cyst of the sacrum, formed within the nerve root sheath, usually asymptomatic.
Not associated with facet arthropathy, in contrast to a synovial cyst.
What does contrast in a postoperative lumbar MRI tell you?
Distinguish between recurrent disc disease and scar tissue.
Both disc and scar appear hypointense on T2-weighted MRI. In theory, scar tissue should enhance throughout, while recurrent disc demonstrates only peripheral enhancement.
If there is recurrent disc herniation, further surgical intervention may be indicated. In general, however, the presence of scar tissue would decrease the chance of successful relief of symptoms.
Mechanism of discitis/osteomyelitis.
Typically from a hematogenous source. Staphylococcus aureus is the most common agent.
In adults, the vascularized subchondral bone is the initial site of infection, which spreads to the disc. In children, however, the intervertebral disc is initially infected, with subsequent spread to the vertebral endplates.
Imaging findings of discitis/osteomyelitis
The key imaging appearance of discitis/osteomyelitis is marrow hypointensity on T1-weighted images centered on both sides of an abnormal intervertebral disc that is hyperintense on T2-weighted images. Loss of adjacent endplate definition is usually present. On radiography, the only initial clue may be loss of disc space height. Later in the course of infection, there may be vertebral collapse.
Adjacent soft tissue infection (paraspinal or epidural) is often present
What is Tuberculous Osteomyelitis?
Also called Pott disease, tuberculous osteomyelitis represents infection of the vertebral body with Mycobacterium tuberculosis.
Unlike pyogenic discitis/osteomyelitis, the discs are usually spared as M. tuberculosislacks the proteolytic enzymes necessary to break down the disc substance.
Classically causes wedge-shaped compression of the anterior aspect of the vertebral body, often leading to a gibbus deformity centered at the infected vertebra.
Gibbus deformity is an acutely angled kyphosis. Gibbus deformity may result from a vertebral compression fracture or can be seen in congenital syndromes including achondroplasia and the mucopolysaccharidoses (Hunter and Hurler syndromes)
Difference between pyogenic discitis/osteomyelitis and tuberculous osteomyelitis?
Unlike pyogenic discitis/osteomyelitis, the discs are usually spared as M. tuberculosislacks the proteolytic enzymes necessary to break down the disc substance.
Imaging findings of Tuberculous Osteomyelitis
Classically causes wedge-shaped compression of the anterior aspect of the vertebral body, often leading to a gibbus deformity centered at the infected vertebra.
Gibbus deformity is an acutely angled kyphosis. Gibbus deformity may result from a vertebral compression fracture or can be seen in congenital syndromes including achondroplasia and the mucopolysaccharidoses (Hunter and Hurler syndromes)
What is Gibbus deformity?
Gibbus deformity is an acutely angled kyphosis. Gibbus deformity may result from a vertebral compression fracture (can be seen with Tuberculous osteomyelitis) or can be seen in congenital syndromes including achondroplasia and the mucopolysaccharidoses (Hunter and Hurler syndromes)
MC spinal vascular malformation?
Dural arteriovenous fistula (dAVF)
Imaging findings of a dural arteriovenous fistula in the spine?
MRI of dAVF shows flow voids surrounding the cord. The cord is often swollen, with abnormal intramedullary T2 prolongation. CT myelography shows serpiginous filling defects in the subarachnoid space.
Where is spinal cord infarction most commonly seen?
Most common in the upper thoracic or thoracolumbar spine due to more precarious blood supply. The predominant blood supply to the distal cord is the artery of Adamkiewicz.
Imaging findings of spinal cord infarction
Imaging of spinal cord infarction shows hyperintensity of the affected cord regions on T2-weighted images. The cord may be enlarged. Diffusion images typically show restricted diffusion. Concomitant vertebral body infarction may be present, which is more common in sickle cell disease and chronic steroid use.
