AVM not seen after bleed

38 y o male, a known case of left parietal AVM.

DSA dated 21-11-11 show an obvious nidus of left parietal AVM with left ACA as feeder and ultimately draining into superior Sagittal sinus.

After a month readmitted for a recent onset right sided weakness.

On admission MRI shows a focal left parietal para sagittal bleed with low signal intensity hemosiderin staining on T2*GRE, T1 bright Meth Hb, a sub acute stage blood degradation product. It’s a secondary intra cranial haemorrhage as site was atypical for bleed and cause is ruptured AVM as per previous MRI and DSA details.
MRI Brain is immediately followed by Non contrast 3D TOF MR Brain Angiography revealed no obvious AVM. Even strange is that DSA also was normal.

An arteriovenous malformation is a tangled cluster of vessels, in which arteries connect directly to veins without any intervening capillary bed.

When AVM Bleeds it may not be obvious on immediate follow up MRA or even on DSA. The reason may be mass effect of hematoma and perilesional odema over the nidus or it may have gone out of cerebral circulation due to rupture of feeder itself.
In such cases follow up MRI studies may be needed to rule out an underlying cause of bleed like AVM or any other vascular malformation which may not be obvious on a single MRI study performed immediately after bleed.

Secondary Intracerebral Hemorrhage

Young male admitted to casualty for stroke. 

On admission CT 

Follow up CT after a week

Follow up MRI

2 D TOF MR Venogram

T2*GRE

T2WI

Findings:
Right parietal lobar bleed.
The subependymal venous angioma noted along choroid plexus of right lateral ventricle on follow up CT and T2w images.
Multiple fine T2 flow voids clustured in right temporal lobe adjacent to the hematoma.
Faint dystrophic calcification along the vascular malformation in right temporal region adjacent to the hematoma depicted on CT.
Dilated right side posterior mesencephalic vein, basal vein and vein of Galen noted on MR.
Superior sagittal sinus show absence of normal T2 flow voids. Sinus is not bulky rather smaller in caliber, eccentric dots of T2 flow voids in the region of sinus are partially recanalised channels which show poor flow related signal on 2 D TOF MR Venogram appears to be a chronically thrombosed sinus.


Impression:

This MRI study shows:
Right parietal lobar bleed - a secondary intra parenchymal hemorrhage.
An associated venous Angioma.
Chronic dural sinus thrombosis. 

There is known association of dural venous sinus thrombosis (CVT)  with conditions like venous angioma and av fistulas. Now it is under debate that whether venous angiomas and fistula secondarily result into CVT as a result of altered blood dynamics or chronic CVT is first to occur resulting in  development of alternate abnormal vascular channels.

An intracerebral hemorrhage account for ~15% of all strokes and is the one of the most disabling forms of stroke.
Divided in to two major types primary and secondary.
A. Primary ICH develops in the absence of any underlying vascular malformation or coagulopathy. Primary intracerebral hemorrhage is more common than secondary. Hypertension and Amyloid angiopathy to 2/3 rd of causes primary haemorrhages. Some time it may be difficult to identify the underlying cause.  Hypertension related bleed are more common in basal ganglia along external capsule the reason appears to be high pressure within the Circle of Willis resulting in smooth cell proliferation followed by smooth muscle cell death. Whereas Amyloid angiopathy affects leptomeningeal and intraparenchymal cortical vessels explains the occurrence of large superficial lobar haemorrhages with amyloid angiopathy.
B. Secondary ICH occure secondary to underlying causes like vascular malformation, sinus thrombosis, hemorrhagic conversion of an ischemic stroke, embolic stroke, coagulopathy, intracranial tumor, hemorrhagic metastasis etc. Arteriovenous malformations, aneurysm account for majority of underlying vascular malformations. Venous Angioma are most the time asymptomatic, noted as an incidental finding and is a rare cause of bleed.


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Cavernoma with venous-angioma