| Heroin Spongiform Leukoencephalopathy (HSLE), a neurological disorder mainly revealing spongiform vacuoles degeneration of the white matter, is related with inhalation of the pyrolysate of heroin. 47 cases in Netherlands were first reported in 1982, which had following features: i. An outbreak after inhalation of heated heroin pyrolysate[1]; ii. The clinical symptoms began with apathy, bradyphrenia, cerebellar dysarthria and ataxia; iii. Medical imagings showed cerebral and cerebellar white matter hypodensities; iv. The autopsy showed there was spongiform white matter degeneration in the cerebrum and cerebellum. Within the following two decades, no more than 20 individual cases were reported in Germany, Italy, Spain, Switzerland, Norway, Taiwan, Belgium, Italy and the United States[2~14]. The mass occurrence (28 cases) in Guangdong province of China was first reported by Dr Lu-Binxun[15"16] in 2000. The majority of cases had a history of inhaling heated herion vapor, and acute onset was characterized by signs of cerebellar and pyramidal tract lesions. Their CT, MRI and neuropathological findings were quite similar with those reported before in Netherlands. The disease was designated as HSLE for inhalation of heated heroin vapor; the spongiform vacuole degeneration of white matter was the main morphological change; and the second mass occurrence of spongiform leukoencephalopathy had happened in the world; the clinical features of HSLE were different from acute or chronic heroin toxication, delayed leukoencephalopathy, the known CNS diseases related with heroin and others characterized with spongiform change as well. But currently, the etiology and pathogenesis of HSLE are still unclear for quite limited neuropathological documents and various findings. Therefore, it is very important of neuropathological research for further exploration of HSLE.To make clear the main morphological changes about HSLE and the difference among HSLE, acute or chronic heroin toxication, delayedleukoencephalopathy, and the diseases having similar spongiform degeneration in white matter, we carried out this research on both pathology and immunohistochemistry of HSLE brain tissues. Moreover, Myelin basic protein (MBP) may enter cerebrospinal fluid (CSF) and serum to provide information about a status of central nervous system (CNS) myelin damage[17-21]. Quantitative researches about the brain myelin sheath lesions of HSLE had not been documented. To make clear the myelin sheath changes of HSLE, we investigated the relationship between myelin basic protein (MBP) and HSLE by detecting and analyzing the serum and CSF amounts of MBP and Anti-MBP in the patients with HSLE. Materials andMathods31 cases of HSLE aged within the range of 23-45 years were enrolled in this study during the period from March 2000 to August 2002, including brain autopsies of 4 cases and brain biopsies of 8 cases with electron microscope observation. Several stains were carried out, such as HE, Weils, Loyez, Bielschowsky silver, Gallyas-Braak, GFAP immunocytochemistry, and MBP immunohistochemistry. The levels of MBP and Anti-MBP in CSF and sera of 28 patients with HSLE, 23 heroin addicts without corresponding clinical symptoms, 27 patients with multiple sclerosis (MS) and 30 normal controls (NC) were detected by enzyme-linked immunosorbent assays (ELISA). Applying the method of immunohistochemistry assay, the MBP polyclonal antibodies were detected in 6 cases with HSLE, 5 cases with inflammatory disease of CNS (ED) and 6 normal controls, in which the immunoreactivity of MBP was quantitatively evaluated with positive unit (PU). ResultsHistological examination showed that the most important character about HSLE was spongiform vacuolar degeneration of the CNS white matter and neurons hi grey matter did not decrease in all cases. The extent and the intensity of these spongiform degeneration were variable. The damaged white matter, especially in deep white matter, displayed countless vacuoles which coalesced to form larger cavities. Foci of necrosis were no...
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