Clinical Analysis Of15Patients With Toxic Leukoencephalopathy

In the1970s, along with methotrexate usage in chemotherapy forhematological malignancy increasing, people found that it could lead to a seriesof neuropsychiatric symptoms. CT images of the patients showed low density inthe white matter. Combined with clinical symptoms and CT images, it wascalled methotrexate-related leukoencephalopathy. In the1980s,the appearanceand popularization of MRI led an increased incidence of leukoencephalopathy.And more and more substance that can cause leukoencephalopathy has beenreported. In1999, Filley indicated that the infectious agents of toxic includedradiation, chemotherapy drugs, immunosuppressants, environmental toxin. Theleukoencephalopathy caused by all above compounds could be referred to astoxic leukoencephalopathy. TL is a syndrome of a series of abnormalneurological symptoms caused by various exogenous substances. White matterchanges are given priority to nerve myelin damage. Clinical symptoms includethe disturbance of consciousness and mental symptoms, seizures, after contactwith pathogenic substances.Objective:To understand the TL correctly and comprehensively, along with providingclues and hints of diagnosis and treatment for clinical doctors.Methods:This respective study involved patients of TL that were treated in the neurologic department of the first affiliated hospital of JILIN university (fromJanuary2010to December2014). We analysed and evaluated their total clinicalfeatures, including age; gender; infectious agent; clinical manifestations;neuro-imaging; diagnosis and identification; as well as treatment and prognosis.Results:(1) The15patients consisted of10males and5females, the ration of genderwas2:1. The average age was42years(ranged from21to63years).(2)Pathogenic substances:4cases of organic solvent,3cases of CO,2cases ofheroin,1case of cyclophosphamide,1case of methotrexate,1case of arsenic,1case of pyrantelpamoate,1case of bromadiolone,1case with tetramine.(3)Clinical manifestations: In this study,13patients had acute onset,2patients hadsubacute onset;12patients presented with consciousness dysfunction, includingsomnolence, stupor, various coma, confusion;10patients presented withseizures, of which3patients presented with status epilepticus; headache occuredin8;5patients presented with mental behavior abnormality;5patients presentedwith tremor;5patients presented with dystaxia;3cases of patients withmeningeal stimulation; Other clinical manifestations included dizziness,vomiting, visual impairment, limb paralysis, positive Babinski sign.(4)Neuroimaging: CT and MRI were performed in all15patients in early onset ofsymptoms. CT showed the hypodensity lesions in8patients; and thecharacterized MRI neuroimagings were found in all patients. It was low signalintensity or isointense on T1-weighted images and high signal intensity on T2-weighted images and FLAIR images. Most TL lesions located predominantlyin the white matter of bilateral cerebral hemisphere, including subcortical whitematter, periventricular white matter, centrum semioval, and were not enhancedon T1-weighted images. Sometimes atypical lesions involved brainstem,cerebella, corpus callosum, cortical lesions. In our group, the neuroimagingfeatures included periventricular white matter involvement in14cases,subcortical white matter involvement in12patients, centrum semiovalinvolvement in8cases, gray matter/cortical involvement in5patients, brainstemand cerebella involvement were present in2and4patients separately. Corpuscallosum lesion occurred in2patient. Hemorrhage lesions were presented in1patients. In our group,10of15patients received repeated brain imaging. Thelesions were obviously disappeared in5patients, and completely reversible in5patients.(5) The main treatment measures included dehydration, loweringintracranial pressure, anti-epilepsy treatment, discontinuing the causativeimmunosuppressive or cytotoxic drugs, allopathic and supporting treatments,clinical manifestations disappeared in4patients, clinical manifestationsimproved markedly in8patients,3patients had not obvious change in clinicalmanifestations.Conclusion:1. For clinical acute or subacute onset, presented with the clinicalmanifestations, including the different levels of consciousness disorders,psychological and behavioral abnormalities, seizures and headache without fever, and imaging examination showing white matter of bilateral cerebral hemisphereinvolvement, we should consider the toxic or drug exposure and the happeningof the TL in patients.2. TL lesions locate predominantly in the white matter of bilateral cerebralhemisphere, including subcortical white matter, periventricular white matter,centrum semioval. The lesions shows hypodensity on CT scan, low signalintensity or isointense on T1-weighted images and high signal intensity onT2-weighted images and FLAIR images.3. Given the timely and effective treatment, clinical symptoms and imagingchanges can disappear obviously. For the TL patients without specific antidote,support and symptomatic treatment is primary, dehydration of intracranialpressure and termination of seizure is the key of treatment.