DEVELOPMENT OF CHRONIC SUBDURAL HAEMATOMA FROM MILD HEAD INJURY: A CASE REPORT AND REVIEW OF CURRENT MALAYSIAN GUIDELINES ON TRAUMATIC BRAIN INJURY Delayed chronic subdural haematoma (cSDH) is a common but potentially serious complication following traumatic brain injury (TBI). Mild TBIs are commonly managed by primary care providers (PCPs), particularly in large, resource-limited settings such as Malaysia, where access to tertiary neurosurgical services may be delayed. Early identification of red-flag signs and symptoms and timely referrals are crucial to prevent clinical deterioration. We describe the case of a 66-year-old man who sustained mild head injury following a vasovagal syncope. His initial brain CT revealed evidence of a small traumatic subarachnoid haemorrhage over the left precentral sulcus, with resolution on an interval scan 24 hours later. He was discharged home without follow-up. Eleven weeks later, he developed bilateral lower-limb weakness and unsteady gait, which prompted an urgent referral by his general practitioner. Repeat CT revealed bilateral acute-on-chronic subdural haematomas, with mass effect requiring emergency burr-hole drainage. The patient showed excellent post-operative improvement and was discharged home on day 4, with no clinical or radiological recurrence on subsequent follow-up. This case highlights the risk of delayed cSDH in patients following mild TBI, even in those discharged with a normal CT scan. PCPs play a pivotal role in recognising high-risk patients, ensuring structured follow-up and facilitating timely specialist referral. We advocate for updating the Malaysian head injury guidelines to incorporate routine follow-up protocols for at-risk patients, modelled after international standards.

Vestibular schwannomas (VSs) are the most common cerebellopontine tumors. The natural history of smaller-sized VSs (<30 mm) has been well-studied, leading to the recommendation of a “watch and wait” approach. However, large VSs (>30 mm) have not been extensively studied, mainly because of their rarity. As such, most patients are conventionally offered surgery which carries a significant risk of neurological morbidity. Here, we report a case of a giant VS (>40 mm) in a 30-year-old man who regressed spontaneously. He was lost to follow-up for 18 years and, upon re-presentation, the symptomatology drastically improved and repeat imaging demonstrated a marked reduction in tumor size. Referring to similar cases in other studies, we postulate that most large and giant VSs undergo a phase of growth and stasis, followed by regression due to shifts in the balance between tumorigenic and regressive factors. Taken together with emerging molecular data, further studies are required to better understand the history of large and giant VSs to shape more personalized treatment options. This potentially includes non-operative management as a tenable option.