各種神経変性疾患における髄液somatostatin, substance P の検討

抄録

The cerebrospinal fluid (CSF) levels of somatostatin-like immunoreactivity (SSLI) and substance P-like immunoreactivity (SPLI) were measured by radioimmunoassay in 12 cases of amyotrophic lateral sclerosis (ALS), 20 cases of Parkinson's disease (PD), 19 cases of spinocerebellar degeneration (SCD) and 20 normal controls.
In the control group, the levels of SSLI and SPLI were 15.3±2.1 (mean± SD) fmol/ml and 5.36±1.66 fmol/ml, respectively, and these levels were not related to age or sex, nor was diurnal fluctuation observed.
In the ALS group, the levels of SSLI and SPLI were 19.2±3.0 fmol/ml and 5.05±2.05 fmol/ml. respectively, with the former being significantly increased (P<0.01). However, duration of the disease, degree of neurological impairment and spasticity were not related to the increase of SSLI. This suggests that the elevation of SSLI level occurs as a consequence of the pathological process of ALS.
In the PD group, the levels of SSLI and SPLI (14.9±3.6 fmol/ml and 4.59±1.51 fmol/ml, respectively) were not significantly changed. We divided parkinsonian patients into those with the slight disability (stage I, II), moderate disability (stage III) and severe disability (stage IV, V). The last group showed significant reductions of SSLI (10.6±1.4 fmol/ml, P<0.0 1) and SPLI (3.91 ± 0.97 fmol/ml, P<0.05) levels compared with those of controls. However, there was no correlation between SSLI and SPLI levels and the clinical characteristics of the parkinsonians including duration of disease, symptoms and duration of drug treatment. These findings support the speculation that somatostatinergic and substance P containing neurons as well as dopaminergic neurons are involved in patients with advanced Parkinson's disease.
In the SCD group, the levels of SSLI and SPLI (16.1±4.6 fmol/ml and 4.76±1.73 fmol/ml, respectively) were similar to those in controls. Classifying SCD into 4 groups : olivopontocerebellar atrophy, Menzel type of hereditary ataxia, late cortical cerebellar atrophy, and Holmes type cerebellar atrophy, the SPLI levels were slightly decreased in olivopontocerebellar atrophy (4.37±1.53 fmol/ml) and Menzel type of hereditary ataxia (4. 53 ± 0.90 fmol/ml), especially in those with orthostatic hypotension, whereas the SSLI level was slightly elevated (20.2±4.8 fmol/ml) in the latter. This suggests that the reduction of CSF SPLI in SCD may reflect autonomic dysfunction.