NMC case report journal最新文献

Meningiomas are benign tumors outside the brain parenchyma that usually progress slowly but occasionally develop suddenly. We report a 40-year-old woman who presented with symptoms of cerebral herniation within a few hours of the onset of a headache. She felt no particular change until going to bed, when she noticed a headache, vomited, and fell into a coma. At the time of admission, she had a large anisocoria on the right side. A computed tomographic scan revealed a tumor of more than 6 cm in the right frontal region, and cerebral angiography showed tumor staining in multiple branches of the anterior cerebral artery. Intracranial perfusion was slow, suggesting severe intracranial hypertension. An emergency craniotomy was performed, and severe brain swelling was found after the dural incision, requiring an additional craniotomy. The tumor was prone to bleeding, which prolonged the operation time; consequently, the tumor was only partially removed and external decompression with duraplasty was required. After the cerebral swelling improved, tumor-feeding vessel embolization was performed, and then the remaining tumor was completely resected. The pathological diagnosis was atypical meningioma. Eleven months after surgery, the patient can walk by herself despite sensory impairment on the left side, and there has been no evidence of tumor recurrence. Emergency surgery may be required for meningiomas and may have to be performed in a situation where preoperative examinations are not sufficient. In such situations, it is desirable to select an appropriate surgical procedure, including two-stage surgery, and to perform prompt treatment.

A lumbar facet joint cyst is a relatively uncommon lumbar spinal disease that includes synovial and ganglion cysts associated with the adjacent facet joint. Some studies have suggested that posterior decompression surgery is linked to the development of facet joint cysts due to postoperative local instability. Although an interlaminar approach may be anatomically suitable for resecting lumbar facet joint cysts, it can be technically challenging after interlaminar decompression surgery because of epidural adhesions and scar tissue. Full-endoscopic surgery via a transforaminal approach under local anesthesia is 1 of the least invasive spine surgery techniques. A 52-year-old woman presented with right leg radicular pain caused by a facet joint cyst at the L4-5 level following a partial laminectomy. Conservative treatment was not effective, and she opted for additional surgery. To minimize invasiveness, we performed a full-endoscopic ventral facetectomy and resection of the facet joint cyst via a transforaminal approach under local anesthesia. At the beginning of the procedure, facet joint arthrography with indigo carmine injection was performed to stain the facet joint cyst blue for easier visualization during the full-endoscopic procedure. Following the resection of the facet joint cyst, the patient's right leg resolved immediately. One year post-surgery, there has been no recurrence of the facet joint cyst or evidence of intervertebral instability. When resecting lumbar facet joint cysts after laminectomy, the full-endoscopic ventral facetectomy technique using a transforaminal approach under local anesthesia, combined with intraoperative facet joint arthrography and indigo carmine injection, can be a useful method to make the surgery less invasive and safer.

Spontaneous internal carotid artery dissection is a relatively common cause of stroke in younger patients. The occurrence of spontaneous internal carotid artery dissection with lower cranial nerve palsy is quite rare. However, few studies have reported its natural course or an effective treatment policy. We received a 42-year-old man with spontaneous internal carotid artery dissection presenting with multiple lower cranial nerve palsies. He exhibited difficulty in swallowing, dysarthria, and tongue deviation. After 2 months of conservative therapy, stent placement with coils was performed because the symptoms did not improve. The patient was discharged 4 days after the operation without any complications and showed evident improvement in symptoms. We reviewed cases of multiple lower cranial nerve palsies reported in the literature up to January 2025 and discussed the appropriate period of observation and the effectiveness of endovascular therapy for spontaneous internal carotid artery dissection with multiple lower cranial nerve palsies.

Intraosseous arteriovenous fistulas are rare vascular anomalies, with an increasing number of reports describing successful endovascular treatments in recent years. Although some cases of acute subdural hematoma caused by intraosseous arteriovenous fistulas have been reported, the precise mechanism remains unclear. In this study, we present a case of surgical treatment for an intraosseous arteriovenous fistula with acute subdural hematoma. A 58-year-old woman presented to our hospital with a sudden headache and nausea. Computed tomography revealed a left acute subdural hematoma with an abnormal diploic space in the frontal bone. Digital subtraction angiography confirmed an intraosseous arteriovenous fistula supplied by the middle meningeal artery and draining into the diploic vein. Because of concerns about potential tumor involvement, direct surgery was performed. Intraoperatively, vascularized tissue surrounding the fistula extended through the dural defect and connected to the subdural space, suggesting a possible cause of the acute subdural hematoma. The feeder and draining vein were dissected and removed along with the abnormal tissue. Histopathological analysis revealed fibrous tissue with hemorrhage and increased vascularity but no tumorous changes. Postoperative angiography confirmed successful arteriovenous fistula occlusion, and the patient recovered with minimal neurological deficit. This case suggests that intraosseous arteriovenous fistulas may cause acute subdural hematoma owing to the anatomical feature of vascularized tissue around the fistula extending through the dural defect into the subdural space.

Occlusion of the posterior communicating artery in isolation, without tandem lesions, is extremely rare. To our knowledge, only one prior report has described mechanical thrombectomy on a pure posterior communicating artery occlusion. This report describes the diagnostic and technical nuances involved in treating such an occlusion via mechanical thrombectomy. A 70-year-old male was admitted to our emergency department with left-sided hemiparesis. A computed tomography scan excluded intracranial hemorrhage. Follow-up computed tomography angiography and perfusion imaging were performed. The right P1 segment cannot be appreciated on computed tomography angiography, suggesting occlusion. Mechanical thrombectomy with a combined stent-aspiration technique achieved thrombolysis in cerebral infarction grade 3 in one pass. The patient tolerated the procedure well and was discharged to a rehabilitation hospital with a modified Rankin Scale score of 2. Posterior communicating artery occlusion is extremely rare, with only one documented report to date. The pressure difference between the internal carotid artery and the posterior cerebral artery across the posterior communicating artery is considerably low; thus, the likelihood of a thrombus passing from either side through the posterior communicating artery is low. In our case, the right posterior communicating artery fetal type with a normal posterior cerebral artery, where the right posterior cerebral artery is naturally hypoplastic, while the contralateral posterior cerebral artery was normal in size, thus misleading us into assuming the occlusion was in the P1 segment. We used a stent-retrieving into an aspiration catheter technique, which proved feasible and resulted in complete recanalization. Mechanical thrombectomy with the combined aspiration-stent retriever technique is feasible and safe for treating posterior communicating artery occlusion.

Spontaneous internal carotid artery dissection is a rare condition that generally affects middle-aged individuals. Most cases of reported spontaneous internal carotid artery dissections are unilateral, but approximately 10%-20% involve bilateral internal carotid arteries. Spontaneous internal carotid artery dissection generally presents with neck pain, ischemic cerebral symptoms, and/or Horner's syndrome. Pulsatile tinnitus is present in around 5%-10% of spontaneous internal carotid artery dissection cases. However, this is generally accompanied by other major internal carotid artery dissection symptoms. Herein, we report a case of bilateral spontaneous internal carotid artery dissection that presented with unilateral pulsatile tinnitus of sudden onset as an isolated symptom. An otherwise healthy 50-year-old man visited a neurosurgical clinic complaining of right temporal pulsatile tinnitus that had begun 1 day prior. In addition to tinnitus, a thorough symptom interview revealed mild heavy-headedness. Magnetic resonance angiography showed bilateral extracranial internal carotid artery dissections and severe stenosis of the true lumen of the right internal carotid artery. No cerebral ischemic lesions were observed. Administration of 5 mg/day amlodipine and 100 mg/day aspirin was initiated. Following the 9th day after onset, the pulsatile tinnitus gradually improved. Around the 40th day after onset, the pulsatile tinnitus disappeared, and magnetic resonance angiography showed an improvement of the right internal carotid artery stenosis. Magnetic resonance angiographies at 5 and 9 months after onset revealed complete disappearance of the false lumen and slight stenosis of the right internal carotid artery at the entrance of the carotid canal. This case suggests that the sudden onset of isolated unilateral pulsatile tinnitus can be a clue to the diagnosis of spontaneous internal carotid artery dissection.

Reversible cerebral vasoconstriction syndrome is characterized by severe headaches and diffuse, segmental constriction of cerebral arteries. We report a rare pediatric case of triptan-induced reversible cerebral vasoconstriction syndrome, complicated by both subarachnoid hemorrhage and cerebral infarction. A 10-year-old boy presented with persistent severe headaches initially suspected to be migraines, for which he was prescribed rizatriptan. Five days after starting rizatriptan, he developed impaired consciousness (Japan Coma Scale 10) and partial right-sided hemiparesis, prompting emergency hospitalization. A head computed tomography scan revealed subarachnoid hemorrhage in the left frontal cortical region. Cerebral angiography showed stenotic changes in the internal carotid artery, middle cerebral artery, anterior cerebral artery, and posterior cerebral artery. Suspecting triptan-induced reversible cerebral vasoconstriction syndrome, rizatriptan was discontinued, and verapamil treatment was initiated. Subsequent magnetic resonance imaging and magnetic resonance angiography revealed cerebral infarction in the right cerebellum, left middle cerebral artery territory, and right occipital lobe, with persistent stenotic changes from earlier findings. Edaravone was added to the treatment regimen. The patient's condition gradually improved, and follow-up magnetic resonance angiography showed almost complete resolution of the prior stenotic changes. His partial right-sided hemiparesis nearly resolved, and he was discharged home. Triptans should be used with caution, as they may precipitate reversible cerebral vasoconstriction syndrome or exacerbate cerebral vasoconstriction. Careful monitoring and vascular imaging are essential for patients presenting with symptoms following triptan administration.

Iatrogenic cerebral amyloid angiopathy is a rare yet clinically relevant condition that may develop decades after cadaveric dura mater transplantation. We present the case of a 48-year-old man who experienced recurrent, bilateral, multilobar intracerebral hemorrhages approximately 40 years after childhood dura mater transplantation. Pathological examination confirmed amyloid β protein deposition around small cerebral blood vessels in the brain parenchyma. Genetic testing excluded mutations associated with hereditary cerebral amyloid angiopathy. According to the patient's operative record, at age 7 years, a left parietal bone tumor and the adjacent dura mater were removed, and a cadaveric dural patch was transplanted onto the intact brain surface. This case suggests that exogenous amyloid β protein can be transmitted through cadaveric dura mater, even when placed on intact brain tissue with preserved glymphatic and dural lymphatic drainage function, manifesting decades after transplantation.

Posterior reversible encephalopathy syndrome is a well-known condition that causes reversible vasogenic edema, mainly in the occipital lobe. However, no guideline for its diagnosis or treatment has been established to date. While many atypical cases have been reported in recent years, posterior reversible encephalopathy syndrome associated with cranioplasty has not yet been reported. A man in his 50s underwent right decompressive craniectomy for brain swelling secondary to ischemic stroke. He was transferred to another hospital for rehabilitation 9 months later and was again admitted for cranioplasty after 2 months. Because of sustained brain distension, right cranioplasty was performed simultaneously with ventriculoperitoneal shunting. No sudden change in blood pressure occurred during the perioperative period. However, generalized convulsions occurred postoperatively. Magnetic resonance imaging showed signal changes in the right frontal lobe, left basal ganglia, left thalamus, and right occipital lobe. When cranioplasty was performed simultaneously with ventriculoperitoneal shunting for a skull defect complicated by brain distension, intraoperative cerebrospinal fluid drainage and continuous cerebrospinal fluid drainage by shunts may have caused a sudden decrease in intracranial pressure and an increase in cerebral perfusion pressure, possibly leading to the development of posterior reversible encephalopathy syndrome.

Composite or collision tumors in the central nervous system can significantly impact disease progression and metastasis, potentially affecting treatment efficacy. Studying the mechanisms associated with these tumors can provide neuro-oncologists with insights into tumor diversity, progression, and aid in the development of novel treatments. We encountered an 84-year-old female with memory disturbance who presented with tumors consistent with wild-type isocitrate dehydrogenase high-grade glioma and low-grade B-cell lymphoma at the same site. Magnetic resonance imaging revealed a solid enhanced mass in the right frontal lobe. A pre-operative suspicion of primary central nervous system lymphoma led to a brain biopsy. Histologically, 2 types of lesions were observed; the first consisted of atypical glial cells with diffuse infiltration and mitoses, positive for glial fibrillary acidic protein and negative for anti-isocitrate dehydrogenase 1 (IDH1)-R132H, characterized by partial amplification of PDGFRA and homozygous deletion of CDKN2A. The second type consisted of small atypical lymphoid positive forCD20, showing immunoglobulin heavy chain(IgH) rearrangement, and minimal invasion of vessel walls while filling the perivascular space. Based on these findings, collision neoplasms of high-grade gliomas and marginal zone B-cell lymphomas were suspected. To our knowledge, this is the first reported co-existence of a glioma and intracranial lymphoma.