Acquired brain injuries (ABIs), such as stroke and traumatic brain injury (TBI), represent global health challenges, stroke ranking as the third leading combined cause of death and disability, and TBI contributing to over 7 million disability-adjusted life years. Functional recovery in ABIs is influenced by age, older individuals showing poorer recovery. Axonal plasticity, a form of structural neuroplasticity, holds promise for understanding and promoting recovery. Injuries were carried out in 14-month-old male Wistar rats. Focal stroke was induced by unilateral intracerebral administration of endothelin-1 (ETH-1), and a unilateral controlled cortical impact (CCI) was used to induce TBI. Functional outcomes were evaluated for 21 days post-surgery using the Montoya staircase test (MST) and a modified neurological severity score (mNSS). Endothelin-1-induced stroke resulted in deficits in forelimb use, evidenced by MST, and overall neurological impairment, as indicated by mNSS. In CCI, forelimb deficits were observed, although overall neurological function remained unaffected. Histological analysis revealed increased neuroinflammation and a reduction in neurons post-injury, as measured by the astrocytic marker GFAP and neuronal marker NeuN, respectively, in ETH-1 and CCI groups – compared to sham-operated groups. Axonal plasticity was assessed using biotinylated dextran amine (BDA), injected 14 days before tissue collection. ETH-1-induced stroke led to an increase in contralaterally derived BDA-labelled axons in the perilesion region, while CCI-induced TBI resulted in a decrease in contralaterally derived BDA-labelled axons perilesionally. These findings show the intricate relationship between axonal plasticity, histological changes, and functional outcomes, in different ABIs, offering insights for future therapeutic interventions focused on plasticity.