ABSTRACT
AIM: The anatomic characters and applicability of the extended pterional transtemporal transtentorial (EPTT) approach versus the subtemporal transtentorial (ST) approach for surgical treatment of petroclival tumors were evaluated. MATERIAL AND METHODS: Ten sides from five adult Chinese injected cadavers were manipulated using both two approaches. Four deep bony anatomic landmarks were specified in the skull base to create two adjoining triangles that were respectively located in the anterior and posterior petroclival region. The real, projected area and the percentage of the projected area were determined and calculated to compare the deep exposure from the two approaches. RESULTS: There was no difference regarding the percentage of the projected area was calculated in the anterior triangles (EPTT, 21.5±12.5%; ST, 28.8±14.9%; p=0.1948), but a significant difference was present in the posterior triangles (EPTT, 74.0±4.5%; ST, 51.5±4.3%; p < 0.01). Compared with the ST approach, the EPTT approach provides an equivalent percentage of projected area in the middle cranial fossa and a wider exposed area in the posterior cranial fossa. CONCLUSION: Through anatomic comparative analysis the EPTT approach provides better exposure and is more appropriate than the ST approach for large and giant petroclival tumors predominantly in the posterior cranial fossa with extensive invasion to parasellar structures and the cavernous sinus.
Subject(s)
Cranial Fossa, Posterior/anatomy & histology , Craniotomy/methods , Petrous Bone/anatomy & histology , Adult , Anatomic Landmarks , Cadaver , Cranial Fossa, Posterior/surgery , Humans , Petrous Bone/surgery , Temporal Lobe/anatomy & histology , Temporal Lobe/surgeryABSTRACT
Traumatic brain injury (TBI)-released excessive glutamate resulted in the activation of glutamate receptors including the metabotropic glutamate receptor 5 (mGluR5). To investigate the expression and cell distribution of mGluR5 in the rat cortex following TBI, western blot and quantitative real-time PCR were used to study the protein and mRNA level of mGluR5 respectively while immunohistochemistry analysis and double immunofluorescence with neural cell marker were used to define the cell distribution of mGluR5. Furthermore, we examined the effects of post-TBI administration of (R,S)-2-chloro-5-hydroxyphenylglycine (CHPG), a selective mGluR5 agonist, on the neuronal degeneration in the cortex. In the present study, we found that the protein level of mGluR5 was up-regulated by traumatic brain injury, while TBI-induced mGluR5 mRNA expression displayed biphasic changes with up-regulation in the early time and down-regulation in the late time after TBI. And neuron, astrocyte and microglia in the cortex after TBI all expressed mGluR5. Moreover, CHPG treatment significantly reduced the number of degenerating neurons detected by Fluoro-Jade C staining. These findings demonstrate that expression of mGluR5 differentially changes both spatially and temporally after TBI and may be related to the neuroprotection after TBI. Therefore, understanding the expression and cell distribution of mGluR5 after TBI may give insight into pathophysiology after TBI and provide a new target for the therapy of TBI.