The Pathogenesis of Subacute Subdural Hematoma: A Report of 3 Cases and Literature Review.

OBJECTIVE: To discuss the pathologic mechanism of subacute subdural hematoma (sASDH). METHODS: Three typical cases of sASDH were reported, and related literature in Chinese published in the past 15 years was reviewed. RESULTS: Intervals from onset of acute subdural hematoma to surgery or symptom deterioration resulting in sASDH were 12.5-15.5 days (mean 14.1 days). Delayed liquefaction of hematoma clots occurred in all 3 reported cases. One patient achieved good curative effect after administration of dexamethasone, and another patient relapsed owing to poor drainage after evacuation of hematoma. CONCLUSIONS: The conversion of acute subdural hematoma to sASDH is an inflammatory reaction process with very regular in time, and it is speculated that the pathologic mechanism may be a delayed hypersensitivity reaction. Antigen released during the liquefaction process of blood clot, with subdural neomembrane cells as antigen-presenting cells, is presented to the T lymphocytes released from the capillaries in the neomembrane and forms sensitized T lymphocytes. When the subsequent antigen is released from the blood clots with a delayed liquefaction and is exposed to sensitized T lymphocytes, the delayed hypersensitivity process occurs.

Antitumor activity of photodynamic therapy with a chlorin derivative in vitro and in vivo.

Chlorin derivatives are promising photosensitive agents for photodynamic therapy (PDT) of tumors. The aim of the current study is to investigate the PDT therapeutic effects of a novel chlorin-based photosensitizer, meso-tetra[3-(N,N-diethyl)aminomethyl-4-methoxy]phenyl chlorin (TMPC) for gliomas in vitro and in vivo. Physicochemical characteristics of TMPC were recorded by ultraviolet visible spectrophotometer and fluorescence spectrometer. The rate of singlet oxygen generation of TMPC upon photo-excitation was detected by using 1,3-diphenylisobenzofuran (DPBF). The accumulation of TMPC in gliomas U87 MG cells was measured by fluorescence spectrometer. The efficiency of TMPC-PDT in vitro was analyzed by MTT assay and clonogenic assay. The biodistribution and clearance of TMPC were determined by fluorescence measuring. Human gliomas U87 MG tumor-bearing mice model was used to evaluate the antitumor effects of TMPC-PDT. TMPC shows a singlet oxygen generation rate of 0.05 and displays a characteristic long wavelength absorption peak at 653 nm (ε = 15,400). The accumulation of TMPC increased with the increase of incubation time. In vitro, PDT using TMPC and laser showed laser dose- and concentration-dependent cytotoxicity to U87 MG cells. In U87 MG tumor-bearing mice, TMPC-PDT significantly reduced the growth of the tumors. Both in vitro and in vivo, TMPC showed little dark toxicity. In vitro and in vivo studies, it found that TMPC has excellent antitumor activities. It suggests that TMPC is a potential photosensitizer of photodynamic therapy for cancer.