Abstract
Third cranial nerve palsy (3cnP) following traumatic brain injury (TBI) is a worrying neurological sign and is often associated with an expanding mass lesion, such as extradural or acute subdural haematomas. Isolated 3cnP can be found in the absence of posttraumatic space-occupying mass lesion, yet it is often considered as a devastating prognostic factor in the context of diffuse axonal injury (DAI). Through the analysis of five exemplificative cases and a thorough review of the literature, we identified four possible mechanisms leading to 3cnP: (1) a partial rootlet avulsion at the site of exit from the midbrain, representing a direct shearing injury to the nerve; (2) a direct traction injury due to the nerve stretching against the posterior petroclinoid ligament at the base of the oculomotor triangle secondary to the downward displacement of the brainstem at the time of impact; (3) a direct vascular compression as a result of internal carotid artery (ICA) dissection or pseudoaneurysm; (4) an indirect injury caused by impaired blood supply to the third nerve in addition to the detrimental biochemical effects of the underlying brain injury itself. Understanding the exact mechanism underlying the onset of 3cnP is key to provide an informed clinical decision-making to the patients and ensure their best chances of recovery. Our experience corroborates data from the literature showing that, even in Grade III DAI, prompt recognition of isolated 3cnP can guide adequate treatment. Nonetheless, even when an overall good neurological outcome is achieved, recovery of isolated 3cnP is dismal, and only rarely the visual deficit completely resolves.