Abstract:Objective: To investigate the role of 99m Tc-TRODAT-1 SPECT in diagnosis and assessing severity of idiopathic Parkinson's disease (PD). Methods: Thirty-eight patients with primary, tentative diagnosis of PD and eighteen age-matched normal controls were studied with 99m Tc-TRODAT-1 SPECT imaging. The regions of interests (ROIs) were drawn manually on cerebellum (CB), occipital cortex (OC) and three transverse plane slice-views of striatums, the semiquantitative BG (background)/[(OC+CB)/2] were then calculated. Results: A lower uptake of 99m Tc-TRODAT-1 in striatums were displayed in thirty-six out of thirty-eight PD patients by visual inspection, compared to controls. In twenty-four PD cases with HYS (Hoehn and Yahr scale) stage I, a greater loss of DAT uptake was found in striatum and its subregions contralateral striatum to the affected limbs than in the same regions of the controls, although the striatal uptake was bilaterally reduced. Using Spearman correlation analysis showed that the reduction of the uptake ratios significantly correlated with the UPDRS in striatum and all its subregions in the PD group (P<0.05), a similar change was also found in the putamen by using the rating scale of Hoehn and Yahr (P<0.05). However, analysis of variance (ANOVA) did not show any relationship between the decreasing uptake of 99m Tc-TRODAT-1 and increasing severity of PD patients, although the specific uptake of 99m Tc-TRODAT-1 was continuously decreased in the striatum by visual inspection with the progress of PD from HYS stage I to III. Conclusion:99m Tc-TRODAT-1 SPECT imaging may serve as a useful method for improving the correct diagnosis of PD. In assessing the role of 99m Tc-TRODAT-1 SPECT in disease severity of PD, UPDRS can offer a comprehensive index, although the Hoehn and Yahr assessment may be available in part.

The sensitivity and specificity of immunocytochemical staining of mycobacterial antigens in the cytoplasm of cerebrospinal fluid (CSF) macrophages for diagnosis of tuberculous meningitis (TBM) was prospectively compared with Ahuja criteria from 393 consecutive CSF specimens. The assay can play an important role for the diagnosis of TBM, with sensitivity of 73.5% and specificity of 90.7%.

Background:Mitochondrial diseases are a group of multisystem heterogeneous diseases caused by pathologic dysfunction of the mitochondrial respiratory chain. A wide range of clinical expression has been described. However, pulmonary hypertension has rarely been described in association with mitochondrial disease until the past decade, and there is no currently recognized treatment for the pulmonary hypertension complicated with mitochondrial disorder.Patient concerns:We reported the case of a 15-year-old boy who presented with shortness of breath and exercise limitation after a cold, and the diagnosis of pulmonary hypertension was confirmed by right heart catheter. Other examinations, such as blood tests, high- resolution chest computed tomography scan, and pulmonary function test, excluded other associated diseases as causes of pulmonary hypertension.Diagnoses and Outcomes:The initial diagnosis was idiopathic pulmonary arterial hypertension and an injection of vasodilator (Treprostinil) was given. However, the dyspnea and fatigue subsequently got worsened. Tracing back his family history, together with the electromyography, nerve conduction studies, and the result of muscle biopsy, mitochondrial disease was confirmed. After treatment with vitamin E, vitamin B2, ATP, and coenzyme Q10, the patient's condition improved.Conclusion:Pulmonary hypertension should be considered as another potential manifestation of mitochondrial disease. Both mechanism and treatment for pulmonary hypertension complicated with mitochondrial disease are unclear. Further study is necessary.

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