Differentials Neuro

Question 1

hyperintensity on T1-weighted images (caused by T1 shortening)

Answer 1

hyperintensity on T1-weighted images (caused by T1 shortening) can be an
important clue to specific substances:

Fat.

Proteinaceous material.

Methemoglobin.

Melanin.

Minerals: gadolinium, copper, manganese, iron,
and calcium (rarely; when dispersed, not in
bone).

Question 2

hypointensity on T2-weighted images (caused by T2 shortening)

Answer 2

hypointensity on T2-weighted images (caused by T2 shortening) can be an
important clue to specific substances:

Most stages of blood (deoxyhemoglobin, intracellular methemoglobin, hemosiderin).

Calcification.

Fibrous tissue.

Highly cellular tumors with a high nucleus:cytoplasm ratio producing low lesional water content (for
instance, lymphoma and medulloblastoma).

Desiccated secretions in the paranasal sinuses.

Question 3

Diffusion restriction

Answer 3

reduced diffusion are diverse:

Neoplastic: e.g., lymphoma, glioblastoma, medulloblastoma.

Inflammatory: e.g., multiple sclerosis, acute disseminated encephalomyelitis.

Infectious: e.g., abscess,
empyema, ventriculitis, herpes encephalitis, Creutzfeldt-Jakob disease.

Vascular: e.g., arterial or venous infarction, global hypoxic-ischemic injury, posterior reversible
encephalopathy syndrome.

Toxic: e.g., carbon monoxide, methanol, ethylene glycol,
Wernicke encephalopathy, chemotherapy.

Metabolic: e.g., osmotic demyelination, hypoglycemic encephalopathy, hepatic encephalopathy.

Congenital: e.g., epidermoid cyst, mitochondrial diseases.

Traumatic: diffuse axonal injury, hematoma.

Seizure (status epilepticus).

Treatment: radiosurgery, antiangiogenic therapy.

Question 4

multiple dark spots on GRE/SWI reflects causes of
microhemorrhage:

Answer 4

multiple dark spots on GRE/SWI reflects causes of
microhemorrhage:

Hypertensive microangiopathy (primarily in the basal ganglia, thalami, cerebellum, and pons).

Cerebral amyloid angiopathy (primarily lobar in cortico-subcortical sites, sparing deep structures).

Familial cerebral cavernous malformation syndrome (inherited multiple cavernous malformations).

Radiation-induced cerebral vasculopathy.

Diffuse axonal injury (primarily at gray-white matter junction and corpus callosum).

Hemorrhagic metastases.

Fat embolism.

Complication of cardiac surgery (presumed to be rapidly developed microbleeds).

Question 5

Several CNS regions do not have a BBB, and therefore normally enhance:

Answer 5

Several CNS regions do not have a BBB, and therefore normally enhance:
Choroid plexus.
Pituitary and pineal glands.
Tuber cinereum (controls circadian rhythm, located in the inferior hypothalamus).
Area postrema (controls vomiti ng, located at inferior aspect of fourth ventricle).

The dura also lacks a BBB, but does not normally enhance. This phenomenon is subsequently explained in
the secti on on pachymeningeal (dural) enhancement.

Question 6

Peripheral (ring) enhancement

Answer 6

Metastasis: Hematogenous metastases are typically found at the subcortical gray-white
junction. Metastases are often multiple, but smaller lesions may not be ring-enhancing.

Abscess: A pyogenic abscess is formed as a result of organization and sequestration of an
infection, featuring a central region of viscous necrosis.
The key imaging findings of abscess are reduced diffusivity (bright on DWI and dark on ADC) caused by
high viscosity of central necrosis and a characteristic smooth, hypointense rim on T2-weighted images.

Glioma: High grade tumors such as glioblastoma typically have a thick and irregular wall.
Multivoxel MRI spectroscopy will be abnormal outside the margin of an enhancing high grade glial
neoplasm secondary to nonenhancing infiltrative tumor. This is in contrast to demyelinating lesion,
abscess, and metastasis, where the spectral pattern returns to normal at the margin of the lesion.
Perfusion MRI demonstrates elevated perfusion in a high grade glioma.

Infarct: Although subacute infarcts often demonstrate gyral enhancement, ring
enhancement can be seen in subacute basal ganglia infarcts.
In contrast to neoplasm or infection, a subacute infarct does not have significant mass effect.

Contusion: Both traumatic and nontraumatic intraparenchymal hemorrhage can show ring
enhancement in the subacute to chronic stage.

Demyelinating disease: The key finding in ring-enhancing demyelinating disease is lack of
significant mass effect. The “ring” of enhancement is often incomplete and “C” shaped.
Multiple sclerosis is the most common demyelinating disease. Enhancement suggests active disease.
Although the typical finding is an incomplete rim of enhancement, tumefactive demyelinating disease can
look identical to a high-grade tumor.

Radiation necrosis may look identical to a necrotic tumor such as high-grade tumor or
metastasis. On perfusion, cerebral blood volume is generally low in radiation necrosis and
typically increased in a high-grade glioma.

Question 7

Subarachnoid FLAIR hyperintensity may be due to:

Answer 7

Meningitis and leptomeningeal metastases both have increased subarachnoid FLAIR signal and leptomeningeal
enhancement.

Subarachnoid hemorrhage manifests as increased subarachnoid FLAIR signal, without leptomeningeal
enhancement. Blooming arti fact on GRE or SWI from blood products will help diff erenti ate subarachnoid
hemorrhage from leptomeningeal metastases.

Slow vascular flow appears as an intravascular distributi on of FLAIR hyperintensity due to “unmasking” of the
inherent high signal of blood, which remains in the plane of imaging as the enti re pulse sequence is obtained.

Slow
flow of peripheral vessels in moyamoya disease causes the ivy sign.

Subarachnoid FLAIR signal is is artifactually increased when the pati entis on oxygen or propofol therapy, without
abnormal enhancement.

Question 7

Superficial enhancement of the cortical (gyral) surface of the brain can be due to either
cerebral infection, inflammation, or ischemia.

Answer 7

Herpes encephalitis is a serious necrotizing infection of the brain parenchyma due to
reactivation of latent HSV-1 infection within the trigeminal ganglion. The medial temporal
lobes and cingulate gyrus are usually affected first and demonstrate gyral enhancement
due to inflammation, petechial hemorrhage, and resultant BBB breakdown. The involved
areas typically also demonstrate reduced diffusivity.
Meningitis may cause gyral enhancement in addition to the leptomeningeal enhancement
previously discussed.
Subacute infarct can demonstrate gyriform enhancement lasting approximately 6 days to 6
weeks after the initial ischemic event.
In contrast to the gyriform enhancement of subacute infarct, an acute infarct may demonstrate vascular
enhancement due to reactive collateral vasodilation and resultant hyperemia.
Enhancement related to subacute infarct is often associated with varying degree of T1 shortening
(hyperintensity) and this can be an important distinguishing feature in addition to volume loss that will
take longer time to manifest.
Posterior reversible encephalopathy syndrome (PRES) is a syndrome of vasogenic
white matter edema triggered by altered autoregulation that may demonstrate gyral
enhancement. PRES may rarely exhibit restricted diffusion.
SMART syndrome (stroke-like migraine attacks after radiation therapy) is a delayed
complication of radiotherapy, usually occurring years or decades after treatment. It is
characterized by contiguous cortical thickening, edema, gyriform DWI abnormality, and
enhancement. It can progressively worsen over months, but eventually stabilizes.

Question 8

differenti al diagnosis of
leptomeningeal enhancement

Answer 8

• Meningitis (either bacterial, viral, or fungal) is the primary considerati on when
  leptomeningeal enhancement is seen.
  Leptomeningeal enhancement in meningiti s is caused by BBB breakdown due to infl ammati on or
  infection.
  Fine, linear enhancement suggests bacterial or viral meningitis.
  Thicker, nodular enhancement suggests fungal meningitis.
• Viral encephaliti s may produce cranial nerve enhancement within the subarachnoid space.
• Leptomeningeal metastases, also called neoplastic meningitis, is spread of tumor cells into
  the subarachnoid space, which may be due to primary brain tumor or metastati c disease
  from an extra-CNS malignancy.
  CNS neoplasms that more commonly have leptomeningeal spread include medulloblastoma, choroid
  plexus tumor, lymphoma, ependymoma, glioblastoma, and germinoma.

Metastatic tumors known to cause leptomeningeal disease include lymphoma and breast cancer.

• Inflammatory amyloidosis oft en shows leptomeningeal enhancement with cortical edema
  and susceptibility.

Question 8

Differential diagnosis of
pachymeningeal enhancement

Answer 8

Intracranial hypotension: Prolonged decrease in CSF pressure can lead to vasogenic edema
in the dura.
Intracranial hypotension clinically presents as a postural headache exacerbated by standing upright.
Etiology may be idiopathic or secondary to CSF leak whether spontaneous or iatrogenic.
Imaging shows smooth, linear dural enhancement, enlargement of the pituitary gland and dural venous
sinuses, and “sagging” of the cerebellar tonsils. There may also be subdural hemorrhage due to traction
effect on the cerebral veins.

Postoperative: Dural enhancement may be seen postoperatively.

Post lumbar puncture: Diffuse dural enhancement is occasionally seen (<5% of the time)
after routine lumbar puncture.

Meningeal neoplasm, such as meningioma, can produce a focal area of dural enhancement
called a dural tail, due to reactive changes in the dura.

Metastatic disease to the dura, most
commonly breast cancer in a female and prostate cancer in a male, can cause irregular
dural enhancement.

Hypertrophic pachymeningitis: localized or diffuse dural thickening due to various causes,
including infectious (e.g., tuberculosis, fungal, syphilis), inflammatory (e.g., rheumatoid
arthritis, granulomatosis with polyangiitis), sarcoidosis, or can be idiopathic.

Question 9

High attenuation material in the subarachnoid space

Answer 9

High attenuation material in the subarachnoid space may be due to SAH (by far the most common
cause), meningitis, leptomeningeal metastases, or prior intrathecal contrast administration.

Question 10

hemorrhagic metastases, including:

Answer 10

hemorrhagic metastases, including:
Melanoma.
Renal cell carcinoma.
Choriocarcinoma.
Thyroid carcinoma.
Although breast and lung cancer rarely cause hemorrhage on a per-case basis, they are such common
cancers overall that they can always be considered when a hemorrhagic neoplasm is suspected.

Question 11

Non-traumatic etiology of intraparenchymal hemorrhage

Answer 11

Question 12

tumors involving the corpus callosum and crossing midline (butterfly tumors) are

Answer 12

primary central nervous system lymphoma and glioblastoma.

Question 12

cerebellopontine angle masses

Answer 12

vestibular schwannoma, meningioma, and
epidermoid cyst.

Question 13

pineal region tumors

Answer 13

are germ cell tumors, such as germinoma, followed by pineal
parenchymal tumors, such as pineoblastoma.

Question 14

The most common cortical (rather than subcortical) supratentorial brain tumors

Answer 14

pleomorphic
xanthoastrocytoma,

dysembryoplastic neuroepithelial tumor,

oligodendroglioma,

and
ganglioglioma.
The most common primary central skull base tumors are chordoma and chondrosarcoma

Question 15

primary central skull base tumors

Answer 15

are chordoma and chondrosarcoma.

Question 16

Adults vs children
suprasellar tumors

Answer 16

pituitary adenoma in adults and craniopharyngioma in children.

Question 17

Adults vs children
Posterior fossa tumours

Answer 17

posterior fossa tumors in adults are hemangioblastoma and metastases,

whereas
in children the most common are
1. pilocytic astrocytoma
2. medulloblastoma,
3. ependymoma, and
4. diffuse
midline/intrinsic pontine glioma.
5. AT/RT

Question 18

purely intraventricular masses in the atrium of the lateral ventricle

Answer 18

purely intraventricular masses in the atrium of the lateral ventricle are meningioma
and degenerative choroid plexus cyst/xanthogranuloma in adults

and choroid plexus papilloma in children.

Question 19

Foramen of monro lesions

Answer 19

foramen of Monro in adults is colloid cyst, whereas the most common in
children is subependymal giant cell astrocytoma.

Question 20

Calcified extra axial tumours

Answer 20

The most common extra-axial tumor that may calcify is meningioma.

The vast majority of
craniopharyngiomas are calcified.

Question 21

Intra-axial tumours calcifying

Answer 21

The most common intra-axial tumor that may calcify is astrocytoma. The vast majority of
oligodendrogliomas are calcified

Intracranial calcifications are most commonly physiologic/aging-related rather than tumoral, such as in the
choroid plexus, pineal gland, and dura of the tentorium and falx cerebri. However, these can be helpful in
localizing tumors based on their displacement: a tumor that engulfs pineal calcifications is more likely a
germ cell tumor, while one that disperses pineal calcifications to the periphery is more likely to be a pineal
parenchymal tumor.

Question 22

Cysts in brain tumours

Answer 22

Cysts are a feature of many low-grade tumors, typically at the periphery of the enhancing component. In contrast, although necrosis of a high-grade tumor may also follow CSF signal, necrosis tends to be central and surrounded by enhancing tumor. In the supratentorial brain, the most common cystic tumors with a mural nodule are ganglioglioma and pleomorphic xanthoastrocytoma. In the infratentorial brain, the most common cystic tumors with a mural nodule are pilocytic astrocytoma and hemangioblastoma. In the sellar region, the most common cystic lesions are pituitary adenoma, craniopharyngioma, and Rathke cleft cyst. Common extra-axial tumors that occasionally show cystic change include meningioma and schwannoma. The differential for cysts without nodular/thick enhancement includes nonneoplastic entities, such as arachnoid, dermoid, epidermoid, neuroenteric, pineal, colloid, neuroglial, choroidal fissure, hippocampal sulcus remnant, porencephalic, and parasitic cysts.

Question 23

Supratentorial cortical tumours

Answer 23

In addition to oligodendrogliomas, there are several rare, low-grade primary neoplasms of glial, neuronal, or mixed glial-neuronal lineage that are predominantly centered in the superficial cerebrum. The supratentorial cortical tumors can be remembered with the acronym P-DOG MD: Pleomorphic xanthoastrocytoma (PXA). Dysembryoplastic neuroepithelial tumor (DNET). Oligodendroglioma. Ganglioglioma. Multinodular and vacuolating neuronal tumor (MVNT). Desmoplastic infantile astrocytoma and ganglioglioma (DIA/DIG).