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  • br Discussion Delayed expansion of a contralateral EDH after


    Discussion Delayed expansion of a contralateral EDH after decompressive surgery for an acute SDH is rare, with an incidence ranging from 1.3% to 5.7%. In the literature, the longest period for an occurrence of the enlargement of a delayed contralateral EDH following the initial surgery is 4 days, as reported by Su et al. Our patient developed a delayed expansion of the EDH 14 days after the initial surgery, an extensive period never reported in the literature according to our research. Intraoperative levosimendan swelling, postoperative neurologic deterioration, and uncontrollable, elevated ICP may imply a delayed expansion of the contralateral EDH. A decompressive craniectomy may be a predisposing factor for a delayed expansion of the EDH. An immediate postoperative CT scan is recommended for patients with an acute SDH and a contralateral skull fracture to detect this rare but life threatening delayed expansion of the contralateral EDH, which levosimendan has devastating consequences such as neurologic deficits and even death. Shen et al reviewed 37 patients with an expansion of a contralateral acute EDH following acute SDH evacuation, of whom 81% (30/37) had contralateral skull fractures and only one was aged > 60 years. The low prevalence of EDH formation among elderly patients may be attributed to increased adherence between the dura and the inner table of the skull. The precise mechanism of the delayed formation of a contralateral EDH following a decompressive craniectomy is unclear. It has been hypothesized that the initial impact causes a contrecoup injury with SDH and intracerebral hematoma formation, in addition to a coup injury with a skull fracture and bleeding from the fracture site or the dura mater. The SDH with mass effect probably increases the ICP and produces a tamponade effect on the contralateral epidural bleeding source, which subsequently induces delayed EDH enlargement after the mass effect has subsided or the SDH is removed. Therefore, measures such as decompressive surgery, the use of hyperosmolar agents, and TH are undertaken to reduce the elevated ICP, which may decrease the tamponade effect and promote delayed formation or expansion of a contralateral EDH. In our reported case, the uncontrollable ICP was frequently >35 mmHg with considerable Cushing\'s triad despite treatment with various osmotic agents. Repeat CT (Figure 2) confirmed that the intracranial hypertension was induced by brain swelling rather than by the rare but life threatening delayed expansion of the contralateral EDH. Sadaka and Veremakis et al reviewed the most recent 18 studies using TH for ICP management in patients with traumatic brain injury, concluding that ICP was always significantly lower in the TH group than in the normothermia group. We started TH as a second-line therapeutic option; the ICP was <20 mmHg, and no TH-induced coagulopathy or other side effects were observed. A decompressive craniectomy is a predisposing factor for the delayed expansion of an EDH. The prolonged use of hyperosmolar agents and TH may further reduce the ICP and gradually decrease the tamponade effect, which is attributed to the etiology of this devastating delayed expansion of the contralateral EDH. Based on our research, no other study has reported the delayed expansion of a contralateral EDH occurring up to 14 days after the initial surgery. Neurosurgeons should be aware that the rare but life threatening delayed expansion of a contralateral EDH can occur within an extensive period after the initial surgery. Additional studies should be conducted to determine whether contralateral EDHs should be managed during the initial surgery.
    Introduction Brain tumors and intracranial aneurysms are commonly encountered in neurosurgical practice. However, the coexistence of an intracranial tumor and an aneurysm is rare, with a reported incidence of 0.3–1%. From an anatomic perspective, the middle cranial fossa and the nearby middle cerebral artery are the most typical locations for both lesions, and their occurrence at these locations is related to an increased regional blood flow. The association between tuberculum sellae meningioma (TSM) and anterior communicating artery (AComA) aneurysm is extremely rare. Here, we report the case of an unruptured AComA aneurysm embedded within a TSM. The importance of the prompt early detection of an intratumoral aneurysm prior to surgery is critical to avoiding intraoperative disaster. Treatment strategies for these two coexistent lesions are also discussed.