Molecular dynamics simulations, with a modified Tersoff potential, were used to investigate cascade overlap, damage accumulation and amorphization processes in 3C-SiC at dose-levels which were comparable to experimental conditions. A large number of 10keV displacement cascades were randomly generated in a model crystal in order to produce damage and cause amorphization. At low doses, the damage state was dominated by point defects and small clusters, whose concentration increased sigmoidally with increasing dose. The coalescence and growth of clusters at intermediate and higher doses was an important mechanism which led to amorphization in SiC. The homogeneous nucleation of small clusters at low doses was the basis of the homogeneous-like amorphization observed in SiC. A large increase in the number of antisite defects at higher doses indicated that both interstitials and antisite defects played an important role in producing high-energy states that led to amorphization in SiC. The topology (total pair correlation function, bond-angle, bond-length distribution) of damage accumulation in the crystal suggested that a crystalline-to-amorphous transition occurred at about 0.28dpa. This value was in qualitative agreement with the experimental value of 0.27dpa observed under similar irradiation conditions. When the model crystal had transformed to the fully amorphous state, the long-range order was completely lost while the short-range order parameter saturated at a value of about 0.49.

Cascade Overlap and Amorphization in 3C-SiC - Defect Accumulation, Topological Features and Disordering. F.Gao, W.J.Weber: Physical Review B, 2002, 66[2], 024106 (10pp)