Abstract

The formation of stable radiation damage in crystalline solids often proceeds via complex dynamic annealing processes, involving migration and interaction of ballistically-generated point defects. The dominant dynamic annealing processes, however, remain unknown even for crystalline Si. Here, we use a pulsed ion beam method to study defect dynamics in Si bombarded in the temperature range from −20 to 140 °C with 500 keV Ar ions. Results reveal a defect relaxation time constant of ~10–0.2 ms, which decreases monotonically with increasing temperature. The dynamic annealing rate shows an Arrhenius dependence with two well-defined activation energies of 73 ± 5 meV and 420 ± 10 meV, below and above 60 °C, respectively. Rate theory modeling, bench-marked against this data, suggests a crucial role of both vacancy and interstitial diffusion, with the dynamic annealing rate limited by the migration and interaction of vacancies.

Highlights

  • These DA processes are complex and remain poorly understood even for crystalline Si, which is the most extensively studied and arguably best understood material[1]

  • We use a novel pulsed ion beam technique[7,8,9,10] to measure the T dependence of the DA time constant (τ) in Si bombarded with 500 keV Ar ions in a regime of relatively high ion doses when damage accumulation is dominated by inter-cascade DA processes

  • This effect is due to the interaction of mobile defects generated in different pulses and, in different cascades

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Summary

Introduction

These DA processes are complex and remain poorly understood even for crystalline Si, which is the most extensively studied and arguably best understood material[1]. Such large inconsistency in the Eas reported (~0.2–1.7 eV) highlights the complexity and currently limited understanding of the fundamental physics governing DA even for Si. Here, we use a novel pulsed ion beam technique[7,8,9,10] to measure the T dependence of the DA time constant (τ) in Si bombarded with 500 keV Ar ions in a regime of relatively high ion doses when damage accumulation is dominated by inter-cascade DA processes (i.e., by the interaction of mobile defects generated in different collision cascades).

Results
Conclusion

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