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Neoplasm: astrocytoma, lymphoma, metastasis

Subacute infarction

Active demyelination/inflammation: MS or ADEM

Vascular lesion: Capillary Telangiectasia, DVA.

Vascular malformations

Characteristic angiographic appearance

AVM

Venous angioma/Developmental Venous Anomaly

Angiographically occult

Cavernous angioma/Cavernous malformation

Capillary Telangiectasia.

Site: Characteristically, but not exclusively, within the pons (White et al., 1958; McCormick et al., 1968)

Size: Usually small, < 2 cm

Prevalence at autopsy: estimated at 0.4% (Sarwar and McCormick, 1978).

Histopathology

Ectatic, dilated capillaries with walls devoid of smooth muscle and elastic fibers

Interposed normal brain parenchyma

No gliosis

No hemosiderin deposition.

Cavernous angiomas

Spongy, blood-filled large sinusoidal vascular spaces

Compression and hemosiderin staining of surrounding parenchyma

No interposed normal neural tissue.

Angiographically occult

CT: generally not identified

MR

Small enhancing lesions

Not detectable on conventional T1 and T2 weighted images

GRE: dark due to succeptibility effects.

Contrast enhamcement

Ectatic capillary-type blood vessels with slow flow.

GRE hypointensity

Succeptibility dephasing could be due to air, calcium, melanin, hemosiderin, or deoxyhemaglobin

Deoxyhemaglobin best source – static blood in ectatic vessels partially desaturates (signal loss on GRE not as evident on T2WI).

Vs. Cav mal

Contain numerous hemosiderin laden macrophages resulting in marked signal loss on T2 and GRE

Blood products evident on T1WI

Typically not enhancing.

Part of a continuum/spectrum with cavernous malformations (Rigamonti et al., 1991)

Vessel walls of cav mal and capillary telangiectasias are indistinguishable

Cavernous angiomas frequently coexist with capillary telangiectasias in same patient

Transitional lesions with mixed characteristics: “cavernous form” of capillary telangiectasias

35% of otherwise typical cavernous lesions demonstrated brain parenchyma within the center.