A 56-year-old female presented with transorbital penetrating injury caused by bamboo fragments, which resulted in brain abscess 2 weeks after the injury. Initial computed tomography (CT) of the head did not reveal the foreign bodies. However, follow-up CT demonstrated a well-defined hyperdense abnormality of 1.0 cm length in the left orbit and brain abscess in the left temporal lobe. The lesion corresponding to the hyperdense abnormality on CT appeared isointense on T 1 -weighted magnetic resonance (MR) imaging and hypointense on T 2 -weighted MR imaging. The bamboo fragments were surgically removed, and aspiration and continuous drainage were performed for the brain abscess. The postoperative course was uneventful and the patient was transferred to a local hospital with minor neurological deficits. Bamboo foreign bodies may show changes in properties on CT and MR imaging in the subacute stage. Careful radiological examination and follow-up monitoring are required for the correct diagnosis and treatment of such injuries.
We report three cases of traumatic microbleeds evaluated by sequential observation. Hypo-intensities on T2* gradient echo imaging (T2*GEI) appeared just 2-3 h after the injury (the hyper-acute period). However, these hypo-intensities on T2*GEI disappeared or became obscure 2-6 days after the injury (the subacute period). A follow-up MRI again revealed clear hypo-intensities on T2*GEI 1-3 months after the injury (the chronic period). Our cases indicate that hypo-intensities on T2*GEI might change dynamically from the hyper-acute to the chronic period. The differences of susceptibility effects by hematoma age might be the cause of this dynamic change.
A 43-year-old woman suffered clinical brain death after severe head injury. The patient met the criteria for the diagnosis of clinical brain death on Day 3. Aggressive hemodynamic and respiratory managements coupled with triple hormone therapy were performed at the family's request, resulting in continued cardiac activity for a prolonged period. Spinal reflexes and automatisms were observed until cardiac arrest. Ventilatory support was discontinued on Day 168, when cardiac death was confirmed, and her kidneys and eyeballs were removed for transplantation. The patient survived for 165 days after the diagnosis of clinical brain death, which is an extremely prolonged period of somatic support for an adult patient after brain death. An extensive and informed discussion on the end-of-life treatment of clinically brain-dead patients is urgently required in Japan to establish treatment guidelines for such patients.
A 69-year-old man consulted our department regarding further examination because cerebrovascular abnormalities were accidentally found during a medical checkup of the brain (brain dock). He did not have any history of head trauma or hypertension. Physical examination yielded completely normal results. Magnetic resonance imaging during the brain dock revealed anomalous venous ectasia of BVR (Fig. 1). Subsequent catheter angiography revealed a DAVF in the left sphenoid wing; the fistula was supplied by direct collateral from ethmoidal branches of the ophthalmic artery ( Fig. 2A) and MMA (Fig. 2B). Venous drainage from the fistula mainly consisted of a large collector vein located in the temporal tip (referred to as BATV), draining in an anterograde manner into the BVR and subsequently into the vein of Galen ( Fig. 2A, B). Some part of the venous drainage from BATV flowed into the deep middle cerebral vein (DMCV), refluxed into SMCV in the capillary phase, and finally flowed into the cavernous sinus (CS; Fig. 2C). Considering the angiography findings, the venous route may not have been accessible for transvenous embolization (TVE), and the risks of incomplete obliteration or damage to the central retinal artery that are associated with transarterial embolization (TAE) should not be ignored. This lesion may be easily accessible by a usual craniotomy procedure. We decided to proceed with open surgery rather than the endovascular approach. A left-sided frontotemporal craniotomy A 69-year-old man consulted our department regarding further examination because abnormal venous ectasia of the basal vein of Rosenthal (BVR) was accidentally found on magnetic resonance imaging. Angiography revealed a dural arteriovenous fistula (DAVF) in the left sphenoid wing; the fistula was supplied by the ophthalmic artery and the middle meningeal artery. Venous drainage from the fistula consisted of a large collector vein located in the temporal tip, which drained into the BVR. We selected open surgery because this lesion may be difficult to access and is associated with significant risks through an endovascular approach. After temporal clip ligation of the drainer, the superficial middle cerebral vein became the main drainage route directly in connection with the fistula. Therefore, both were ligated, after coagulation of feeding arterial networks on the dura around the sphenoid wing. The patient experienced no complications from the surgical procedure, and postoperative angiography demonstrated obliteration of the fistula. DAVF in the sphenoid wing with deep drainage is believed to carry a high risk of hemorrhage or venous infarction because of the presence of Galenic drainage, varix, and cortical venous reflux. Treatment is strongly recommended even if the symptoms are minimal. Open surgery appears to be safe and often the best therapeutic option.
Diffusion-weighted imaging (DWI) may detect hyperintense lesions in patients with transient hypoglycaemia-induced hemiparesis or coma, which are completely reversible after glucose infusion.1(-)3 In vivo animal studies have documented the visualisation of such hypoglycaemia-induced changes of signal intensity and the reversal by glucose intake in detail.4 However, the time necessary for hyperintense lesions on DWI to disappear after glucose infusion in humans is still unclear. A 54 year old woman presented comatose with brain stem signs and severe hypoglycaemia. DWI demonstrated hyperintense lesions in the corpus callosum and internal capsules. She was treated with IV glucose. These lesions had resolved significantly on imaging 2 hours later and completely resolved on repeat imaging 2 days later. This report documents the time course of recovery of neurological lesions induced by hypoglycaemia after treatment with IV glucose.
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