Cavernous malformations can be grouped into four types based on MRI appearances using the Zabramski classification 1).
The Zabramski classification of cerebral cavernous malformations has been proposed as a way of classifying cerebral cavernous malformations, and although not used in clinical practice it is useful in scientific publications that seek to study cavernous malformations.
The classification was proposed in 1994 , and at the time of writing (June 2016) remains the most commonly used classification of cavernous malformations in the literature.
Based on MRI characteristics:
| Type | MRI Features | Description |
|---|---|---|
| Type I | Hyperintense on T1 and T2, no hemosiderin rim | Recent hemorrhage with blood degradation products |
| Type II | Mixed signal intensity on T1 and T2, hemosiderin rim | “Popcorn-like” lesion with chronic hemorrhage and thrombosis |
| Type III | Hypointense on T1 and T2 | Chronic resolved hemorrhage, gliosis, and hemosiderin deposits |
| Type IV | Only visible on GRE/SWI sequences | Tiny capillary telangiectasia-like lesions (micromalformations) |
T1: hyperintense
T2: hypo or hyperintense
: most common type - classic “popcorn” lesion
T1: mixed signal intensity centrally
T2: mixed signal intensity centrally
Low signal rim with blooming on T2* sequences
: chronic haemorrhage
T1: hypointense to isointense centrally
T2: hypointense centrally
low signal rim with blooming on T2* sequences
: multiple punctate microhaemorrhages
T1: difficult to identify
T2: difficult to identify
T2* Gradient Echo: “black dots” with blooming
Difficult to distinguish from small capillary telangiectasias
It is worth noting a couple of point about type IV cavernous malformations.
Firstly, the classification proposed in 1994 by Zabramski predates SWI and as such some authors have suggested that care should be taken in assuming that lesions only seen on SWI (but not on T2* sequences) are type 4 cavernous malformations.
Secondly, how these differ from micro haemorrhages from other causes (e.g. cerebral amyloid angiopathy) is unclear in the absence of genetic evidence of familial multiple cavernous malformation syndrome, as the absence of central T1 / T2 abnormality makes a definite diagnosis of cavernous malformation (in the absence of histology) difficult.