Penetrating brain injuries are rare in head trauma, but nerve damage, vascular injury, and infections must be considered de pending on the type and trajectory of penetration. We report a case of a penetrating brain injury caused by an automatic nail gun.

A 59–year–old man attempted suicide by driving a nail into his right temporal region with an automatic nail gun. Upon admission, the patient was conscious but exhibited mild paralysis in the left upper and lower limbs. A head CT scan showed that the nail had penetrated the right temporal bone and reached the right frontal lobe, with no significant bleeding around the nail. A head CT angiography confirmed no contact with major arteries, indicating that nail removal was feasible.

On the day of admission, the removal of the intracranial foreign body was performed under general anesthesia. A 6 cm linear skin incision was made around the nail, and a diameter of 3 cm area of bone surrounding the nail was exposed. Two burr holes created two bone fragments: one fragment enclosing the nail and another larger fragment around the first. The outer bone fragment was carefully removed to avoid displacing the nail embedded in the dura. The inner fragment containing the nail was cautiously extracted, minimizing the force transmitted to the subdural space. There was no cerebrospinal fluid leakage or active bleeding at the removal site, and intraoperative CT confirmed no worsening of intracranial hemorrhage. Postoperatively, the patient experienced no deterioration in consciousness or motor function. Follow–up CT revealed minor bleeding near the nail tip, which did not progress. Sulbactam sodium and ampicillin sodium were administered postoperatively, with no signs of intracranial infection observed. The patient was transferred for rehabilitation.

While nail–induced penetrating brain injuries are rare, careful planning of the removal method and management of postoperative complications is crucial. In this case, creating two bone fragments —one enclosing the nail and another larger fragment surrounding the first— proved effective and safe.

Severe head trauma；Hemostasis；Endovascular therapy Severe head trauma can cause bleeding from the face and pharynx, making it difficult to stop the bleeding. Herein, we present two patients suffered head bleeding by traffic accident, in which we performed endovascular treatment..

Case 1: A 58–year–old woman was transported to the emergency room after traffic accident involving a light vehicle and a tanker truck. Bleeding from the head continued, so cerebral angiography was performed. It revealed bleeding from the sphenopalatine artery (SPA) and ascending pharyngeal artery (APA), and both were embolized with coils to stop the bleeding.

Case 2: A 87–year–old man was transported to the emergency room collision with a passenger car while walking. Bleeding from the Nasopharynx continued, so cerebral angiography was per formed. It revealed bleeding from the bilateral 3rd segment of internal maxillary artery (IMA), and both were embolized with coils to stop the bleeding.

Hemostasis in endovascular therapy for head trauma can be per formed under local anesthesia, hemostasis can be achieved in a short period of time, and multiple bleeding sources can be embolized simultaneously. This treatment should be considered as an option when bleeding is difficult to control or anemia progresses.

A 70–year–old man fell off a stepladder and was promptly transported to the hospital. Five days after admission, he presented with orthostatic headache, and was diagnosed with cerebrospinal fluid (CSF) hypotension syndrome by contrast–enhanced magnetic resonance imaging (MRI). Due to the persistence of symptoms despite conservative treatment, and the subsequent development of hearing loss and chronic subdural hematoma, he was referred to our department. Epidural blood patch therapy failed to improve his symptoms. Based on the findings of the whole–spine MRI, we performed CT myelography targeting the upper cervical spine, which revealed contrast agent spreading into the extradural space on the left side of the C1 ⁄ C2 level, thereby localizing the CSF leakage site. Surgical dural repair was performed, resulting in symptomatic improvement. In case of treatment–resistant CSF hypotension, it is important to identify the precise leakage site utilizing multiple modalities.

Introduction: Adult moyamoya disease is typically managed conservatively when perfusion studies indicate mild hemodynamic disturbance. However, whether traumatic intracranial hemorrhage increases the risk of ischemic stroke in these patients remains poorly understood. Here we presents two cases of adult moyamoya disease who developed ischemic stroke following traumatic intracranial hemorrhage.

Case 1: A 46–year–old woman with bilateral moyamoya disease was initially managed conservatively following a nonaneurysmal subarachnoid hemorrhage. Two years after the diagnosis, she had a head injury in a traffic accident. A head CT scan revealed a small traumatic subarachnoid hemorrhage, predominantly in the left frontal lobe, for which conservative treatment was selected. The day after the injury, asymptomatic multiple ischemic strokes were identified in the left insular gyrus and frontal cortex, despite no significant changes detected on magnetic resonance angiography and perfusion studies. The patient remained asymptomatic and was discharged on day 16 with a modified Rankin Scale (mRS) score of 0.

Case 2: A 79–year–old woman with asymptomatic moyamoya disease was on antiplatelet therapy for stroke prevention. Six years after the diagnosis, she had a head injury due to a fall. An initial head CT revealed a diffuse subarachnoid hemorrhage and right acute subdural hematoma. An emergency craniotomy was performed, and her level of consciousness improved postoperatively. However, seven days after the surgery, she developed ischemic stroke in the left parietal lobe. Despite resumption of antiplatelet therapy, multiple cerebral infarctions progressed, and the patient died fourteen days after the surgery.

Discussion: Many patients with moyamoya disease who are asymptomatic or have mild hemodynamic disturbance are managed conservatively. However, even in the absence of significant hemodynamic disturbance, such patients may exhibit reduced tolerance to microcirculatory disturbances such as dehydration, anemia, and vasospasm following head trauma and trigger ischemic stroke. Our cases suggested even in patients with mild hemodynamic disturbance, we should carefully avoid dehydration, promptly correct anemia, and judiciously administer antiplatelet therapy. Active imaging surveillance may be also crucial to detect early signs of ischemic stroke and guide timely intervention.

We present a rare case of infected subdural hematoma (ISH) in a patient with pancreatic head adenocarcinoma and severe cholangitis. A 78–year–old woman with pancreatic cancer and liver metastases presented one day after a fall, complaining of impaired mobility. She had poorly controlled diabetes (HbA1c 10.1%) and was scheduled for chemotherapy. On arrival, her Glasgow Coma Scale score was E3V4M6, with no focal deficits. Blood tests revealed leukocytosis (WBC 2.6×10⁴/μL), elevated CRP (16.8 mg/dL), thrombocytopenia (Plt 9.0×10³/μL), and liver ⁄ kidney dysfunction. Head computed tomography (CT) showed a right acute subdural hematoma with slight midline shift. Abdominal CT revealed bile duct dilatation due to pancreatic cancer, and she was diagnosed with severe cholangitis. Due to bleeding risk and impaired consciousness likely related to cholangitis, conservative management was selected for the hematoma, and cholangitis treatment was prioritized.

On the second day after head trauma, endoscopic retrograde cholangiopancreatography revealed distal bile duct stenosis, and a biliary stent was placed. Escherichia coli was detected in blood and bile cultures, and antibiotics were adjusted accordingly. Her condition improved, and she was transferred to a rehabilitation hospital on day 17 with a Glasgow Outcome Scale (GOS) score of 4.

However, on day 21, she developed decreased consciousness and left hemiparesis. Inflammatory markers had re–elevated, and head CT revealed hematoma enlargement with marked midline shift. Emergency burr hole drainage yielded brownish, purulent fluid. Escherichia coli was identified from the abscess culture, supporting the diagnosis of ISH. Antibiotic therapy was adjusted accordingly. The patient showed clinical improvement, and follow–up CT confirmed resolution of the abscess. She was transferred back to rehabilitation on day 52 with a GOS score of 3.

This case highlights the importance of considering ISH in patients with underlying conditions complicated by systemic infection.