Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC 50 value was 400 µM. The DNA fragment became evident after incubation of the cells with 300 µM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).

A case is presented of painful tic convulsif caused by schwannoma in the cerebellopontine angle (CPA), with right trigeminal neuralgia and ipsilateral hemifacial spasm. Magnetic resonance images showed a 4 cm round mass displacing the 4th ventricle and distorting the brain stem in the right CPA. The schwannoma, which compressed the fifth and seventh cranial nerves directly, was subtotally removed by a suboccipital craniectomy. Postoperatively, the patient had a complete relief from the hemifacial spasm and marked improvement from trigeminal neuralgia. The painful tic convulsif in this case was probably produced by the tumor compressing and displacing the anterior cerebellar artery directly.

ObjectiveThe spot sign is related with the risk of hematoma expansion in spontaneous intracerebral hemorrhage (ICH). However, not all spot sign positive patients undergo hematoma expansion. Thus, the present study investigates the specific factors enhancing the spot sign positivity in predicting hematoma expansion.MethodsWe retrospectively studied 316 consecutive patients who presented between March 2009 to March 2011 with primary ICH and whose initial computed tomography brain angiography (CTA) was performed at our Emergency Department. Of these patients, 47 primary ICH patients presented spot signs in their CTA. We classified these 47 patients into two groups based on the presence of hematoma expansion then analyzed them with the following factors : gender, age, initial systolic blood pressure, history of anti-platelet therapy, volume and location of hematoma, time interval from symptom onset to initial CTA, spot sign number, axial dimension, and Hounsfield Unit (HU) of spot signs.ResultsOf the 47 spot sign positive patients, hematoma expansion occurred in 26 patients (55.3%) while the remaining 21 (44.7%) showed no expansion. The time intervals from symptom onset to initial CTA were 2.42±1.24 hours and 3.69±2.57 hours for expansion and no expansion, respectively (p=0.031). The HU of spot signs were 192.12±45.97 and 151.10±25.14 for expansion and no expansion, respectively (p=0.001).ConclusionsThe conditions of shorter time from symptom onset to initial CTA and higher HU of spot signs are the emphasizing factors for predicting hematoma expansion in spot sign positive patients.

Pseudoaneurysm of internal maxillary artery (IMA) after trauma is rare, and most cases reported are caused by maxilla-facial blunt trauma. Pseudoaneurysm is discontinuity in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space producing pulsatile hematoma rapidly. A 44-years-old woman presented with a pulsatile swelling and pain in the left parotid region. She underwent the masticatory muscle reduction using needle injection in dentistry 1 month ago. The left facial pulsatile swelling developed after the procedure immediately and uncontrolled bleeding occurred on the day of visit to our institution. We performed emergency angiography and diagnosed pseudoaneurysm of left IMA. We treated by embolization with Histoacryl Glue through left IMA. IMA total occlusion was confirmed and symptoms improved. Pseudoaneurysm following blunt trauma of the face have been reported but are few. Furthermore, there is no report of IMA pseudoaneurysm due to direct injury by needle. Recently, many cosmetic surgery procedures using injection techniques have been performed, and it is necessary to pay attention to the direct vessel injury by the needle. And endovascular therapies can give early recovery with minimal morbidity and avoids injury to the facial nerve and its branches.