Intracerebral cavernous hemangioma is also known as intracerebral parenchymal cavernous hemangioma. It has been shown that cavernous hemangioma is an autosomal dominant disorder with incomplete episomal dominance, with the gene located on chromosome 7. It is now believed that intracerebral cavernous hemangioma is a vascular malformation that originates at the level of the capillaries in the brain. The main clinical symptoms are epilepsy, motor and sensory disorders. It is believed that about 1/3 of patients may present with multiple lesions. It is generally believed that intracerebral cavernous hemangiomas are commonly found in the cortex and subcortex of the cerebral hemispheres, as well as in the parietal ventricles, etc. With the development of MRI techniques, cavernous hemangiomas of the brainstem have received increasing attention. Extracerebral cavernous hemangiomas are most often found at the base of the middle cranial fossa and paracranial areas. It has been suggested that they originate from the extracerebral dural vascular system or from the dilatation of microarteries. Compared with intracerebral lesions, dural cavernous hemangiomas of the middle cranial fossa are more common in middle-aged women, with a relatively long history and clinical symptoms such as headache and cranial nerve palsy. Because of the thin blood sinus wall of intracerebral type cavernous hemangioma, it is easy to rupture and bleed. Secondary pathological changes such as slow blood flow, deposition of hemorrhagic components at different periods after repeated bleeding and thrombosis and calcification are the main imaging bases of intracerebral type cavernous hemangioma. Intracerebral cavernous hemangioma can grow and expand due to enlargement of the vascular lumen within the lesion, neovascular growth or repeated rupture and bleeding of thin-walled vessels, as well as hemorrhagic mechanization, fibrous hyperplasia or cystic lumen formation. Intracerebral cavernous hemangioma appears as a well-defined round or oval shaped equal to slightly dense shadow on CT, and may be combined with speckled calcification. Except for acute hemorrhage or large lesions, there is usually no perifocal edema and no signs of occupancy. The magnitude of enhancement after contrast injection depends mainly on the degree of thrombosis and calcification within the lesion. MRI can show the signal changes of the hemorrhagic component more clearly than CT at different periods. Recurrent chronic hemorrhage within the nidus and fresh thrombus contain dilute free ortho-hemoglobin, making it high signal in all imaging sequences. Intra-lesional glial septa and deposited iron-containing hemoglobin exhibit lattice-like long T1 and short T2 signal bands. Older thrombi as well as reactive gliosis showed long T1 and long T2 signals. Calcifications were low signal on both T1WI and T2WI. Iron-containing heme deposits were seen around the lesion forming a long T1 and short T2 low signal ring. Thus, a typical intracerebral cavernous hemangioma appears as a lattice-like or mulberry-shaped mixed-signal mass surrounded by a low-signal ring. This is generally considered to be the specific signal for the diagnosis of intracerebral cavernous hemangioma. Due to the magnetic susceptibility effect of ferritin, gradient echo images can show more multiple small lesions than T2WI. However, gradient echo images should be analyzed together with T1WI and T2WI performance to help overcome the interference of iron-containing heme artifacts on the correct diagnosis. Differential diagnosis Intracerebral cavernous hemangioma should be differentiated from hypertensive cerebral hemorrhage and intracerebral tumor hemorrhage. Dural cavernous hemangioma of the middle cranial fossa should be differentiated from meningioma, nerve sheath tumor, pituitary tumor, etc.