Ion-beam-induced amorphization in Si has attracted significant interest since the beginning of the use of ion implantation for the fabrication of Si devices. A number of theoretical calculations and experiments were designed to provide a better understanding of the mechanisms behind the crystal-to-amorphous transition in Si. Nowadays, a renewed interest in the modeling of amorphization mechanisms at atomic level has arisen due to the use of preamorphizing implants and high dopant implantation doses for the fabrication of nanometric-scale Si devices. In this paper we will describe the most significant experimental observations related to the ion-beam-induced amorphization in Si and the models that have been developed to describe the process. Amorphous Si formation by ion implantation is the result of a critical balance between the damage generation and its annihilation. Implantation cascades generate different damage configurations going from isolated point defects and point defect clusters in essentially crystalline Si to amorphous pockets and continuous amorphous layers. The superlinear trend in the damage accumulation with dose and the existence of an ion mass depending critical temperature above which it is not possible to amorphize are some of the intriguing features of the ion-beam-induced amorphization in Si. Phenomenological models were developed in an attempt to explain the experimental observations, as well as other more recent atomistic models based on particular defects. Under traditional models, amorphization is envisaged to occur through the overlap of isolated damaged regions created by individual ions (heterogeneous amorphization) or via the buildup of simple defects (homogeneous amorphization). The development of atomistic amorphization models requires the identification of the lattice defects involved in the amorphization process and the characterization of their annealing behavior. Recently, the amorphization model based on the accumulation and interaction of bond defects or IV pairs has been shown to quantitatively reproduce the experimental observations. Current understanding of amorphous Si formation and its recrystallization, predictive capabilities of amorphization models, and residual damage after regrowth are analyzed.

A comprehensive model of the nucleation, growth, and dissolution of B clusters in Si is presented. We analyze the activation of B in implanted Si on the basis of detailed interactions between B and defects in Si. In the model, the nucleation of B clusters requires a high interstitial supersaturation, which occurs in the damaged region during implantation and at the early stages of the postimplant anneal. B clusters grow by adding interstitial B to preexisting B clusters, resulting in B complexes with a high interstitial content. As the annealing proceeds and the Si interstitial supersaturation decreases, the B clusters emit Si interstitials, leaving small stable B complexes with low interstitial content. The total dissolution of B clusters involves thermally generated Si interstitials, and it is only achieved at very high temperatures or long anneal times.

Using molecular-dynamics simulation techniques, we have investigated the role that point defects and interstitial-vacancy complexes have on the silicon amorphization process. We have observed that accumulation of interstitial-vacancy complexes in concentrations of 25% and above lead to homogeneous amorphization. However, we have determined the basic properties of the interstitial-vacancy complex, and showed that it is not as stable at room temperature as previously reported by other authors. From our simulations we have identified more stable defect structures, consisting of the combination of the complex and Si self-interstitials. These defects form when there is an excess of interstitials or by incomplete interstitial-vacancy recombination in a highly damaged lattice. Unlike the interstitial-vacancy complex, these defects could survive long enough at room temperature to act as embryos for the formation of extended amorphous zones and/or point defect clusters.

Carbon often appears in Si in concentrations above its solubility. In this article, we propose a comprehensive model that, taking diffusion and clustering into account, is able to reproduce a variety of experimental results. Simulations have been performed by implementing this model in a Monte-Carlo atomistic simulator. The initial path for clustering included in the model is consistent with experimental observations regarding the formation and dissolution of substitutional C-interstitial C pairs (C s-C i). In addition, carbon diffusion profiles at 850 and 900°C in carbon-doping superlattice structures are well reproduced. Finally, under conditions of thermal generation of intrinsic point defects, the weak temperature dependence of the Si interstitial undersaturation and the vacancy supersaturation in carbon-rich regions also agree with experimental measurements.

We use kinetic nonlattice Monte Carlo atomistic simulations to investigate the physical mechanisms for boron cluster formation and dissolution in complementary metal-oxide semiconductor ͑MOS͒ processing, and the role of Si interstitials in the different processes. For this purpose, B implants in crystalline Si as well as B implants in preamorphized Si are analyzed. For subamorphizing B implants, a high concentration of Si interstitials overlaps with the B profile and this causes a very quick B deactivation for both low-and high-dose B implants. For B implants in preamorphized silicon, B is activated during the regrowth of the amorphous layer if the B concentration is lower than 10 20 cm −3 and remains active upon annealing. However, if B concentrations higher than 10 20 cm −3 are present, as occurs in the formation of extensions in p-channel MOS transistors, B atoms are not completely activated during the regrowth. Moreover, the injection of Si interstitials from the end-of-range defects leads to additional B deactivation in the regrown layer during subsequent annealing. If the end-of-range defects overlap with a B profile, even of relatively low concentration, as it occurs for B pockets in n-channel MOS transistors, very quick and local B deactivation occurs in the high Si-interstitial concentration region.