1.
Amyloid Angiopathy (AA)
Occurs by progressive deposition of amyloid within small and medium veins,
leading to fibrinoid necrosis and vascular fragility.
It's the major cause of lobar hemorrhage in the elderly,
the number of MHs increase the risk of such bleeding. The presence of multiple strictly lobar hemorrhages (including MHs) demonstrated highly specific for AA in older patients without another set of intracranial hemorrhage causes (trauma,
ischemic stroke,
tumor,
coagulopathy,
or excessive anticoagulation).
The distribution shows posterior cortical predominance,
tending to cluster in the same lobe in individuals with multiple lesions.
2.
Hypertension
Developed by intimal hyperplasia and hyalinosis in deep penetrating cerebral arterioles as a result of chronic hypertension. Unlike AA,
in chronic hypertension are most commonly found in the thalamus,
basal ganglia,
cerebellum and pons.
3.
Cavernous angioma
It is a type of vascular malformation demonstrated on MRI as sinusoidal spaces and venous lakes,
resembling "popcorn",
which would globular areas of hyperintensity on T1 hypointense surrounded by halo on T2 *,
representing hemosiderin deposited peripherally as a result of previous bleeding.
4 . Diffuse axonal injury (DAI)
Traumatic brain injury shear due to rapid acceleration or deceleration of the head most commonly in the gray/white junction,
splenium of the corpus callosum and dorsolateral brainstem.
It's seen as multiple small foci of hyperintensity on FLAIR ,
T2 and occasionally,
the diffusion,
due to the presence of white matter edema .
It may be accompanied by MHs,
and are more apparent in T2*weighted sequences and SWI.
5 .
CADASIL
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is an inherited form of cerebral artery that leads to early demyelination and ischemic stroke.
The underlying defect affects the smooth muscle cells of small vessels that are affected by type single negative amyloid angiopathy non-arteriosclerotic.
MRI may show symmetric confluent areas of high signal intensity in the white matter in the frontal and anterior temporal lobe and within the external capsule .
MHs have been reported in 25-70%,
but have no characteristic distribution.
6 . Embolism
Hematogenous dissemination of septic emboli from bacterial,
fungal and protozoal origin may even reach the cerebral vessels.
7.
Metastasis
It may manifest as MHs,
more related tod melanoma and renal cell carcinoma.