|Title||Ultrastructure of perinidal capillaries in cerebral arteriovenous malformations.|
|Publication Type||Journal Article|
|Year of Publication||2006|
|Authors||Tu J, Stoodley MA, Morgan MK, Storer KP|
|Pagination||961-70; discussion 961-70|
|Date Published||2006 May|
|Keywords||Adolescent, Adult, Blood-Brain Barrier, Capillaries, Child, Female, Humans, Intracranial Arteriovenous Malformations, Male, Middle Aged|
OBJECTIVE: The ultrastructure of perinidal capillaries in cerebral arteriovenous malformations (AVMs) was examined to clarify their pathomorphological features.
METHODS: Fifteen AVM specimens were dissected and divided into perinidal and intranidal groups and processed for ultrastructural study immediately after surgical removal. Eleven of the patients had presented with hemorrhage. Tissue from four normal controls was also studied. Electron microscopy was used to compare features of the blood-brain barrier and endothelial cells (ECs) of capillaries in perinidal, intranidal, and controls.
RESULTS: Perinidal capillaries demonstrated abnormal ultrastructure of the blood-brain barrier with no basement membranes and astrocytic foot processes. ECs had fenestrated luminal surfaces. Large gaps were observed at endothelial intercellular junctions. ECs contained numerous filopodia, large numbers of cytoplasmic processes, numerous micropinocytotic vesicles, and the cytoplasm contained more filaments than those observed in controls. Pericytes were rich in pinocytotic vesicles, vacuoles, and filaments. Their processes were in close contact with ECs. Weibel-Palade bodies were present in perinidal ECs.
CONCLUSION: The absence of blood-brain barrier components in perinidal capillaries may contribute to extravasation of red blood cells into the surrounding brain in the absence of major hemorrhage and explain the gliosis and hemosiderin occasionally seen around AVMs. Cellular differentiation and proliferation in perinidal capillaries should be included in a systematic study aimed at a better understanding of the mechanisms underlying the recurrence of surgically removed AVMs.