Studies on Adenosine Deaminase(ADA) Activity in the Cerebrospinal Fluid of Tuberculous Meningitis(TBM)

BACKGROUND & PURPOSE: Confirmation of etiology in various types of meningitis is the essential step for the treatment with respect to the underlying organism. Although the definite diagnosis of TBM depends on identifying M. tuberculosis in the CSF, the acid fast bacilli are rarely shown in smears of CSF and are cultured in only some patients. Increased levels of ADA in systemic tuberculous effusion have been observed. This study is to evaluate the diagnositc significance & value as a laboratory index of disease activity of ADA in TBM. METHODS: We assayed the activity of ADA in the CSF of 117 patients with various types of meningitis (tuberculous, viral, and bacterial) from 1995 through 1996 at Chungnam National University Hospital. We established several diagnostic criteria for TBM: characteristic CSF findings, such as lymphocytic pleocytosis, cloudy or ground-glass appearance, increased protein content, and decreased sugar level, positive acid fast bacilli in CSF smear, brain CT or MRI findings compatible with TBM. RESULTS: The mean ADA value in CSF was higher in TBM(15.5+/-4.6 U/liter) than in other meningitis. The sensitivity of the test for diagnosing TBM was 0.80 and specificity, 0.98. Increased CSF protein in TBM(271.23+/-78.2) showed in parallel with ADA activity in CSF(p<.05). A gradual decline in level of this enzyme was observed during the first two weeks of therapy in concordance with the clinical improvement. The mean interval for normalizing ADA activity was 37.6 days from the onset of treatment. CONCLUSION: The quantification of ADA in CSF is a rapid and economic test that is useful for early diagnosis of TBM and sensitive as an indicator for disease activity.

Central pain after thalamic stroke: clinical and radiological characteristics

BACKGROUND AND OBJECTIVES: Although pain resulting from thalamic stroke was described by D jerine & Roussy in 1906, its pathomechanism & anatomical substrate have not been defined yet. Several clinical & experimental studies suggest that laterality of lesion for generation of central pain is as important as location of lesion. We performed this study to evaluate clinical features of thalamic pain syndrome, including incidence, onset interval from stroke, nature, distribution, accompaniments, and to assess the relationships between laterality & location of lesion and occurrence of pain. METHODS: We reviewed the medical records and brain imaging of all patients with thalamic stroke from 1990 to 1997. Patients with thalamic pain syndrome due to a single well-demarcated thalamic stroke were included, and excluded tumoral, non-vascular etilogy, and patients with sensory deficit without pain and excluded patients who had multiple cerebral lesions even they have thalamic pain syndrome. RESULTS: One-hundred one cases were selected under the inclusion criteria, and twenty-four patients(24%) with thalamic pain syndrome were identified from 101 thalamic stroke. Pain onset within the first week poststroke was 17(71%). The patients with allodynia were 8(33%), increased by movement, stress, and thermal contact. The painful area distributed mainly limbs(50%), especially arm(35%), face plus hemibody(34%), and hemibody below face(8%). Thalamic pain syndrome accompanied with the pain and temperature loss was 17(71%). Thirteen patients had a right-sided lesion, 11 left-sided lesion. The lesion causing thalamic pain syndrome mainly located in the posterolateral areas(75%). CONCLUSIONS: We conclude that the thalamic pain syndrome resulting from mainly posterolateral thalamic lesion cause the spontaneous pain on the contralateral body, especially upper extrimity, and accompanied with pain & tempterature loss. The laterality of lesion is not represent for generation of thalamic pain syndrome. Key word : thalamic stroke, central pain.