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Clinicopathological relations of cerebral cavernous angiomas: observations in eleven cases
H J Steiger1, T M Markwalder, H J Reulen
1Department of Neurosurgery, University Hospital, Bern, Switzerland.
Insights
Cerebral cavernous angiomas (cavernomas) can cause hemorrhage, epilepsy, and neurological deficits. Histological analysis suggests iron deposits from prior hemorrhages correlate with seizures, and cystic growth may stem from recurrent bleeding.
Area of Science:
- Neurology
- Neurosurgery
- Pathology
Background:
- Cerebral cavernous angiomas (cavernomas) are vascular malformations that can present with various neurological symptoms.
- Diagnosis and understanding of cavernoma pathogenesis remain areas of active research.
Purpose of the Study:
- To analyze clinical presentations, imaging findings, and histological features of cerebral cavernous angiomas.
- To investigate the relationship between histological findings, particularly iron deposits and encapsulation, and clinical manifestations.
Main Methods:
- Retrospective review of eleven cerebral cavernous angioma cases over three years.
- Analysis of clinical data, computed tomography (CT), angiography, and histological examination of resected lesions.
- Special attention to signs of previous hemorrhages (iron deposits) and lesion encapsulation.
Main Results:
- Common presentations included cerebral hemorrhage, epilepsy, focal neurological deficits, and papilledema.
- Unruptured lesions showed heterogeneous density on CT with minimal contrast enhancement; two had large cysts.
- Histological examination revealed iron deposits in all cavernomas and surrounding gliotic tissue, suggesting prior hemorrhages, with a likely link to epilepsy. Encapsulation varied, being minimal in ruptured lesions and prominent in cystic ones.
Conclusions:
- Iron deposits within cerebral cavernous angiomas are indicative of prior hemorrhages and likely contribute to epileptic seizures.
- The growth of cystic cavernomas may be attributed to recurrent microhemorrhages from the malformation and its associated neovascularized cyst membranes.
Abstract:
Eleven cases of cerebral cavernous angiomas (cavernomas) were observed within a period of 3 years. Two patients presented with cerebral hemorrhage, five with epilepsy, three each with a progressive focal neurological deficit, and one with papilledema. The unruptured lesions had a heterogeneous density on computed tomography with relatively little contrast enhancement. Two lesions contained major cysts. In one of these cases, the cyst measured 5.5 cm in diameter, had an enhancing membrane, and was surrounded by brain edema. Angiography did not show hypervascularity in any instance. During exploration and histological processing, special attention was paid to signs of previous silent hemorrhages and to the degree of encapsulation of the lesion. Iron deposits (signs of previous hemorrhages) were seen to varying degrees inside all cavernomas as well as in the surrounding gliotic cerebrum, and a causal relation between iron deposits and epileptic seizures seems likely. Encapsulation was minimal with the ruptured cavernomas and particularly prominent with the cystic lesions. The membrane of the giant cystic lesion with peripheral brain edema had a histological structure similar to that of the membranes of chronic subdural hematomas. It is suggested that continuous growth of cavernoma cysts is the result of recurrent hemorrhages from sinusoids of the malformation and from the neocapillary network of the cyst membranes.