✓ A 48-year-old man presented with a rare intraparenchymal schwannoma of the medulla oblongata. After he underwent gamma knife surgery, the patient's condition deteriorated and the mass, which at the time was thought to be a glioma, became larger on magnetic resonance images. The mass was resected through a suboccipital craniectomy via the transcerebellomedullary fissure approach. The tumor, which was moderately firm but distinct from the surrounding parenchyma, was removed totally. Postoperative histological and immunohistochemical examinations confirmed the diagnosis of a benign schwannoma. Brainstem schwannomas can be cured by microneurosurgery. It is important to distinguish these tumors from glioma. The main theories on the cause(s) of this lesion are briefly reviewed.
Jiangkai Lin, Hua Feng, Fei Li, Bingmei Zhao and Qiaonan Guo
Jingyu Chen, Zhi Chen, Fei Li, Jiangkai Lin, Hui Meng and Hua Feng
The purpose of this study was to review 14 rare cases of cerebral paragonimiasis that first manifested as intracranial hemorrhage (ICH), and to investigate the characteristics of clinical manifestation, diagnosis, and treatment of the disease.
The authors have encountered 14 cases of cerebral paragonimiasis in patients between the ages of 6 and 16 years (mean age 11.5 years) who presented with sudden headache, nausea, and vomiting. Three of them were affected with varying degrees of limb hemiplegia, and in 1 this was combined with high fever; the blood eosinophil count and enzyme-linked immunosorbent assay showed positive results too. The ICHs were observed with cranial CT and MR imaging, and lung lesions were also detected in 5 cases on chest CT scans. Ten of the diagnosed cases were treated with oral praziquantel. Three of these patients were given carbamazepine from the beginning of parasiticidal treatment to prevent seizures; 4 of the remaining 7 patients experienced epileptic seizures during the treatment process. Four patients needed surgery to remove the lesions, and these individuals received praziquantel treatment right after the surgery.
Pathological examinations demonstrated eosinophilic granuloma in these patients. There was no disease recurrence or epilepsy in 11–40 months of follow-up; however, mild hemiplegia could still be observed in 2 cases after 12 months and 17 months of follow-up.
The possibility of cerebral paragonimiasis should be considered when ICH is detected in young patients who are either from an endemic area or have recently visited such an area; the relatively small amount of hemorrhage in cerebral paragonimiasis is often represented as small lesions surrounded by disproportionately larger edema on the imaging study. Preventive antiepileptic drugs should be used along with the administration of parasiticide.
Rong Hu, Jianjun Zhou, Chunxia Luo, Jiangkai Lin, Xianrong Wang, Xiaoguang Li, Xiuwu Bian, Yunqing Li, Qi Wan, Yanbing Yu and Hua Feng
A glial scar is thought to be responsible for halting neuroregeneration following spinal cord injury (SCI). However, little quantitative evidence has been provided to show the relationship of a glial scar and axonal regrowth after injury.
In this study performed in rats and dogs, a traumatic SCI model was made using a weight-drop injury device, and tissue sections were stained with H & E for immunohistochemical analysis. The function and behavior of model animals were tested using electrophysiological recording and the Basso-Beattie-Bresnahan Locomotor Rating Scale, respectively. The cavity in the spinal cord after SCI in dogs was observed using MR imaging.
The morphological results showed that the formation of an astroglial scar was defined at 4 weeks after SCI. While regenerative axons reached the vicinity of the lesion site, the glial scar blocked the extension of regrown axons. In agreement with these findings, the electrophysiological, behavioral, and in vivo MR imaging tests showed that functional recovery reached a plateau at 4 weeks after SCI. The thickness of the glial scars in the injured rat spinal cords was also measured. The mean thickness of the glial scar rostral and caudal to the lesion cavity was 107.00 ± 20.12 μm; laterally it was 69.92 ± 15.12 μm.
These results provide comprehensive evidence indicating that the formation of a glial scar inhibits axonal regeneration at 4 weeks after SCI. This study reveals a critical time window of postinjury recovery and a detailed spatial orientation of glial scar, which would provide an important basis for the development of therapeutic strategy for glial scar ablation.