Chronic subdural hematoma (CSDH), a common disease in neurosurgery, is mostly due to head trauma. CSDH is also one of the postoperative complications. CSDH can infrequently occur after craniotomy. CSDH is usually caused by supratentorial surgery. The incidence of CSDH after craniotomy is approximately 1.1% [2]. One of the causes is excessive cerebrospinal fluid (CSF) drainage during the procedure, as this can cause the bridging vein to stretch and rupture [10,11,15]. Venous bleeding, in turn, can produce subdural hematomas. Another possible cause of a hematoma is compression of jugular veins because of intraoperative position [20]. The compression of the jugular vein increases intracranial venous pressure and leads to subdural hemorrhage. Burr hole trephination is the treatment of choice for the management of CSDH. After burr hole trephination, the recurrence rate of CSDH is about 10% [17]. We introduce a patient who has undergone middle meningeal artery (MMA) embolization due to the recurrence of CSDH after microvascular decompression (MVD) for trigeminal neuralgia (TN). We want to discuss the risk factors of CSDH after infratentorial craniotomy and the efficacy of MMA embolization in patients at high risk of CSDH recurrence.

A 70-year-old man was diagnosed with right TN eight years ago. He took carbamazepine 300 mg three times a day and gabapentin 300 mg three times a day to relieve his facial pain. However, the treatment was not sufficient enough. He then underwent Gamma Knife radiosurgery (GKS) for TN five years ago. The problem was initially relieved after GKS, but TN relapsed four months later. Afterward, he underwent two times percutaneous nerve block and two times radiofrequency ablation. Meanwhile, he had developed essential tremor twenty years ago, and he took clonazepam 0.25 mg once a day and propranolol 60 mg twice a day. Also, he took aspirin for an unclear purpose. For persistent and medically intractable TN, the patients eventually underwent MVD. He stopped taking aspirin two weeks before surgery and did not take it again after surgery. In the supine position, his head was turned to the left less than 90 degrees, and the neck was flexed, with vertex being parallel to the floor. During skin incision and craniotomy, the bleeding tendency was detected, but not to the extent that it could not be controlled surgically. His preoperative clotting profile was within the normal range. When the dura was opened, the usual amount of CSF was drained with the typical speed. Arachnoid dissection was performed around the trigeminal nerve and surrounding vessels in the usual manner. Due to the age-related atrophic brain, additional CSF drainage was not necessary to make working space. A superior cerebellar artery was adhered to the trigeminal nerve and compressed the nerve at the root entry zone and mid-cisternal segment. Large superior petrosal veins were crossing over the surgical approach field of view. During the dissection between the offending vessel and the trigeminal nerve, the superior petrosal vein was slightly stretched, resulting in venous bleeding. Bleeding was entirely controlled by compression and using hemostatic materials. The offending vessel was successfully transposed not to conflict with the trigeminal nerve, and Teflon was inserted between the nerve and the vessel. There was no unusual finding except a mild degree of pneumocephalus on immediate postoperative brain computed tomography (CT). The patient’s pain alleviated immediately after surgery. He stopped taking carbamazepine and gabapentin. However, due to the recent aggravation of his essential tremor, he started taking topiramate 50 mg once a day in addition to propranolol and clonazepam. On the 4th day after surgery brain CT, an extra-axial fluid collection with CSF density with 7 mm thickness along the right cerebral convexity was observed. Still, there was no mass effect, and the patient was discharged (Fig. 1). A month later, he presented with worsening dizziness and headache. He tended to veer to the left and reported left-sided weakness without a history of head trauma. Brain CT showed CSDH in the right cerebral convexity. He underwent burr hole trephination to evacuate the CSDH. Although CSDH was completely drained, the brain was not fully re-expanded on 2nd day after the surgery brain CT, and there was still an excessive subdural space filled with CSF (Fig. 2). A month later, his subsequent CT scan showed a larger amount of CSDH mixed with acute stage hematoma in the right convexity. He underwent a repeated burr hole trephination, and a subdural catheter was inserted. A small amount of acute staged hematoma remained in the subdural space on the day after surgery brain CT. We considered that the patient was at high risk of CSDH recurrence due to age-related atrophic brain and bleeding tendency in the first intraoperative findings. Thus, we performed additional MMA embolization. There was still excessive subdural space filled with subacute staged hemorrhage on CT scan a month later, but the subdural space extent did not increase. Brain CT 3 months after the second surgery showed complete CSDH resolution and full expansion of the brain parenchyma. After that, he did not suffer from a recurrence of CSDH (Fig. 3).

MMA embolization is an effective way to treat repetitive CSDH after craniotomy. For patients at high risk of CSDH recurrence due to brain atrophy and bleeding tendency, upfront MMA embolization would help reduce recurrence.