BACKGROUND: Gelastic seizure (GS) is a rare type of epilepsy that most commonly appears in patients with hypothalamic hamartoma. It is rarely associated with other types of brain damage. This particular type of epilepsy is relatively rare and has few links to other brain lesions. Temporal lobe malacia is mostly caused by cerebral infarction or cerebral hemorrhage, which can lead to seizures. We report a case of GS in a woman with temporal lobe malacia which was reported for the first time in the literature.
METHODS: A 73-year-old female, diagnosed case of GS, presented with repetitive stereotyped laughter a month prior to presentation, happening multiple times daily and with each time lasting for 5-15s. Electroencephalogram displayed a focal seizure seen in the right temporal region. Magnetic resonance imaging head with contrast showed a right temporal lobe malacia. The patient was started on levetiracetam daily. The patient indicated that they had fully recovered and were not experiencing any recurrent or stereotyped laughter during their daily routines. These results remained consistent even after a one-year follow-up period.
CONCLUSIONS: GS can be caused by temporal lobe malacia, which is an uncommon but potentially grave condition. The outcome of this present case exhibited the importance of the temporal lobe in the genesis of GS.

Carotid webs cause ischemic stroke in young people and are associated with a high rate of stroke recurrence. Histopathological examination is crucial for clarifying the pathogenesis and mechanisms underlying the occurrence of carotid webs, although the mechanisms generally remain unclear. Here, we report a case of a symptomatic carotid web in a woman in her 50s who had a medical history of two ischemic strokes. She was diagnosed with a right carotid web and underwent carotid endarterectomy 18 days after the second stroke. Histopathological examination clearly revealed several phases of intimal hyperplasia. Furthermore, a thrombus attached to the carotid web showed invasion by fibroblasts and capillaries, and organization had begun. We presume that after the appearance of the carotid web, the thrombus formed by stagnant flow and became organized, causing the carotid web to grow and change in shape.

Lung biopsy is an important interventional radiology procedure allowing the characterization of lesions with suspected malignancy. The most frequent complications are pneumothorax and hemorrhage. Air embolism is a rare but potentially fatal occurrence. In this case report, we present an air embolism after core needle CT-guided biopsy showing CT and MRI features that radiologists should expect in the everyday clinical practice.

Cerebral air embolism (CAE) occurs in various clinical situations such as surgery, angiography, and hemodialysis; most are iatrogenic. Here we report the case of a 57-year-old man who developed CAE immediately after air-powder abrasive treatment, which is commonly used in dentistry. The patient underwent air-powder abrasive treatment for peri-implantitis, and immediately after the treatment, cardiac arrest occurred and cardio- pulmonary resuscitation was performed. After resuscitation, brain computed tomography performed in the emergency room showed scattered dark density presumed to be air. The day after admission, the patient showed right hemiplegia and a multifocal cerebral infarction was observed on brain magnetic resonance imaging. Therefore, CAE was strongly suspected. After hyperbaric oxygen treatment (HBOT), which started 4 days after the incident, the patient regained consciousness and showed improvement in cognitive impairment, and only grade 4 muscle weakness was observed in the right lower extremity on the manual muscle test. This case highlights the importance of considering CAE as a possible cause of neurological symptoms occurring during clinical procedures involving air, and adds to the accumulation of evidence of therapeutic effects of delayed HBOT.

A 59-year-old male was found unconscious in a car filled with smoke. On arrival, he was in a semi-comatose state with hemorrhagic shock due to deep lacerations on his wrist. His carboxyhemoglobin level was 16.6%. Electrocardiography showed ST segment elevation at the precordial leads with troponin T positivity. Magnetic resonance imaging showed spotty ischemic lesions in his brain. He was treated with 100% oxygen by mechanical ventilation; however, he also developed acute respiratory distress syndrome due to an inhalation injury. His condition was complicated by bloody stools, which were judged to have been caused by ischemic colitis based on computed tomography and were managed by observation. After regaining consciousness and the improvement of the heart, lung, and bowel conditions, the patient was transported to a psychiatric hospital due to concerns regarding self-harm. Due to the small number of reported cases, the accumulation of similar cases of ischemic colitis after carbon monoxide (CO) poisoning is needed to clarify the characteristics of ischemic colitis after carbon monoxide poisoning.

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BACKGROUND: Cases of multiple cerebral aneurysms are rare. In this case report, we describe a male patient with multiple, enlarging, and ruptured aneurysms. The two aneurysms were believed to be dissecting aneurysms.
METHODS: A 47-year-old man presented with left limb paralysis. Magnetic resonance imaging revealed a cerebral infarction. Digital subtraction angiography (DSA) identified an aneurysm and occlusion in the right middle cerebral artery (MCA). The MCA aneurysm was remarkably enlarged on the eighth day after cerebral ischemia and was treated using endovascular techniques. Two weeks after the endovascular treatment, the patient experienced a severe headache and became comatose, and a subarachnoid re-hemorrhage was confirmed. The fourth DSA revealed an enlarging dissecting aneurysm in the posterior cerebral artery. The patient died without further treatment.
CONCLUSIONS: Some dissecting aneurysms rapidly enlarge and rupture.

Cerebral vasospasm is a well-known phenomenon that has been associated with subarachnoid hemorrhage due to aneurysmal bleeding. It can lead to serious outcomes if not recognized and treated promptly. It happens most frequently following cases of aneurysmal subarachnoid hemorrhage. Other causes include traumatic brain injury, reversible cerebral vasoconstriction syndrome, post-tumor resection, and non-aneurysmal subarachnoid hemorrhage. We describe a case of severe clinical vasospasm following acute on top of chronic spontaneous subdural hematoma in a patient with corpus callosum agenesis. Also, a small literature review of the possible risk factors of such occurrence is discussed.

BACKGROUND: Superficial temporal artery-middle cerebral artery (STA-MCA) bypass helps treat cerebral ischemia. However, the STA is not available for bypass in some conditions. Therefore, with some technical tips, the authors introduced a bypass technique using the occipital artery (OA).
METHODS: Two female patients complained of hemiparesis. Brain magnetic resonance imaging (MRI) indicated contralateral infarction from the MCA steno-occlusion. On Diamox single photon emission computed tomography or perfusion MRI, the contralateral front parietotemporal reserve was diminished. On transfemoral cerebral angiography, the STA was thin with a weak flow; however, the OA was prominent. Direct OA-MCA end-to-side extracranial-intracranial bypass surgery was implemented instead of STA because the caliber was too narrow. The postoperative course was uneventful in both cases, with well-maintained bypass patency and neurological stability during follow-up.
CONCLUSIONS: OA might be an acceptable alternative for MCA cerebral ischemic cases with an unsuitable STA.

It has been reported that bevacizumab, an agent administered as an adjuvant therapy for high-grade gliomas, causes thromboembolic complications. We report a cerebral infarction with newly developed cerebral artery stenosis occurring during treatment with bevacizumab for an anaplastic astrocytoma. A 48-year-old female underwent excision surgery for an anaplastic astrocytoma on the right temporal lobe and received radiation therapy and chemotherapy with temozolomide. Twenty months after the maintenance therapy, treatment with bevacizumab was introduced for tumor recurrence. After the 14th course of bevacizumab at 6 months, 27 months after radiation therapy, the patient began experiencing mild right hemiparesis. Magnetic resonance imaging revealed scattered cerebral infarcts on the left frontal lobe and diffuse cerebral artery stenosis of the bilateral internal carotid artery system both inside and outside the radiation-treated area. Antiplatelet medication was commenced, and there was no recurrence of ischemic stroke. The morphological transition of the cerebral arteries should be carefully monitored via magnetic resonance angiography during post-radiation treatment with bevacizumab.