Background:
Solitary plasmacytoma is a localized lesion comprising monoclonal neoplastic proliferation of plasma cells. This disease is rarely encountered and few reports have described primary intracranial solitary plasmacytoma (PISP).
Case Description:
We report a case of PISP that presented initially as status epilepticus and exhibited massive intratumoral hemorrhage at the subcortical area. To the best of our knowledge, this is the first recorded presentation of this pathology in this manner. Following evacuation of the hematoma and decompressive craniectomy, the patient underwent radiation therapy and showed no sign of tumor recurrence at 3 years after diagnosis.
Conclusion:
This case reveals that PISP can present as subcortical intraparenchymal hemorrhage. It should be emphasized that the precise diagnosis of this disease is of utmost importance, because solitary plasmacytoma without a background of multiple myeloma responds well to radiation therapy.
Increased intracellular calcium and cytoskeletal damage play a crucial role in neuronal death following injury such as cerebral ischemia. The effect of brain temperature on early intracellular calcium increase and neuronal cytoskeletal damage following cerebral ischemia has not been rigorously investigated. In the current communication we evaluated calmodulin (CaM) and microtubule-associated protein 2 (MAP2) in the same brain section using a double labeling immunohistochemical technique, and obtained evidence that the brain temperature has a significant effect on the early calcium increase and cytoskeletal damage as well as the delayed neuronal death occurring in CA1 sector of the gerbil hippocampus after transient forebrain ischemia. In the normothermia (36.7 degrees C) group, CaM and MAP2 immunoreactivity were markedly decreased within 48 h after ischemia and thereafter dramatic neuronal death (grade 3) was seen in the CA1 sector at 7 days. Mild hypothermia (33.3 degrees C) significantly protected against all these changes, whereas cytoskeletal damage and delayed neuronal death were aggravated by mild hyperthermia (39.7 degrees C). We conclude that mild hypothermia protects the brain against transient forebrain ischemia by reducing early cytoskeletal damage and subsequent neuronal death.
Objective: A case of symptomatic cervical carotid artery stenosis with persistent primitive hypoglossal artery (PPHA) treated by carotid artery stenting (CAS) with appropriate embolic protection is reported.Case Presentation: The patient was a 65-year-old male presenting with left hemiplegia. MRI revealed infarction in the right cerebral hemisphere, and cerebral angiography demonstrated stenosis affecting the proximal segment of the internal carotid artery (ICA), proximal to the origin of the PPHA. Since blood flow was observed from the PPHA to the ICA during simultaneous obstruction of the common and external carotid arteries, a filter protection device was placed in the ICA along with proximal protection, and CAS could be performed without complications.
Conclusion:In performing CAS for symptomatic stenosis of the cervical carotid artery with PPHA, it is considered important to select appropriate embolic protection based on the evaluation of the direction of the blood flow of the ICA and PPHA under balloon occlusion conditions.Keywords▶ carotid artery stenting, persistent primitive hypoglossal artery, cervical internal carotid artery stenosis, endovascular surgery
Sequential changes in plasma fibronectin level in 17 patients with subarachnoid hemorrhage (SAH), with 16 due to ruptured cerebral aneurysms, were compared for patients with good and poor outcomes, and patients with and without vasospasm. Plasma fibronectin concentrations were measured by an immune diffusion method. The clinical outcome was evaluated 3 months after SAH according to the Glasgow Outcome Scale. Plasma fibronectin concentrations were significantly lower on days 3 (p < 0.02) and 9 (p < 0.05) after ictus in patients with poor outcomes (moderately disabled or worse) than in those with good outcomes (good recovery). Patients with vasospasm had lower fibronectin concentrations during the 4 weeks after ictus. Decreased levels of plasma fibronectin were correlated with poor outcomes, most related to vasospasm. Plasma fibronectin levels reflect the overall severity in patients with SAH and are a useful marker for prediction of the final clinical outcome.
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