ABSTRACT
Objective To evaluate the value of heart rate variability (HRV ) and sympathetic skin response (SSR) in differential diagnosis of Parkinson's disease (PD) .Methods We selected 36 PD ,17 essential tremor (ET) and 59 Parkinsonism-Plus (PD-plus) patients diagnosed in our department .We recorded HRV during the period of quiet breath ,deep breath and Vasaval as well as SSR incubation period of the upper limbs and lower limbs . Results ① During the period of quiet breath ,HRV decreased significantly in PD group compared with that in ET group (P< 0 .05) ,and abnormality rate of HRV in PD group was higher than that in ET group .HRV did not significantly differ between PD and PD-plus .HRV did not significantly differ among the three groups during the period of deep breath and Vasaval .② SSR incubation period showed no significant difference among PD ,PD-plus and ET groups .③ The specificity and sensibility of HRV in PD and PD-plus differential diagnosis were 22 .8% and 82 .6% , while for PD and ET differential diagnosis the values were 66 .9% and 82 .6% . The specificity and sensibility of SSR in PD and PD-plus differential diagnosis were 39 .0% and 52 .6% , 29 .4% and 52 .6% , respectively ,for PD and ET differential diagnosis .Conclusion Compared with those in ET patients ,HRV in PD patients decreases and HRV abnormality rate increases .HRV is of great value in differential diagnosis of PD and ET but not in differential diagnosis of PD and PD-plus .Determining SSR incubation period does not have much value in differential diagnosis of PD ,PD-plus and ET .
ABSTRACT
<p><b>OBJECTIVE</b>To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate (NMDA) receptor (MK-801) and antagonist of Ca(2+) channels (nimodipine) on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ([Ca(2+) ](i)) in synaptosomes or content of Evans Blue (EB).</p><p><b>METHODS</b>95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. [Ca(2+) ](i) was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with [(3)H]-MK-801 in the neuronal membrane of cerebral cortex.</p><p><b>RESULTS</b>The levels of water content and EB content of brain tissues, and [Ca(2+) ](i) in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P<0.05). The water content and [Ca(2+) ](i) increased with the duration of infectious brain edema. Nimodipine administered after the injection of PB could significantly decrease the water content, EB and [Ca(2+) ](i) (P<0.05). MK-801 could significantly decrease the water content, EB and [Ca(2+) ](i) in 4 h and 24 h groups (P<0.05). The Kd values were 30.5 nmol/L+/-3.0 nmol/L and 42.1 nmol/L+/-4.2 nmol/L in PB group and NS group respectively (P<0.05), and Bmax were 0.606 pmol/mg.pro+/-0.087 pmol/mg.pro and 0.623 pmol/mg.pro+/-0.082 pmol/mg.pro respectively, without statistical significance (P>0.05).</p><p><b>CONCLUSIONS</b>The changes in the permeability of blood-brain barrier (BBB) and Ca(2+)-overload may participate in the pathogenesis of infectious brain edema. Treatment with nimodipine can dramatically reduce the damage of brain edema and demonstrate neuroprotective effect on brain edema by inhibiting the excess of Ca(2+) influx and reducing the permeability of BBB. MK-801 pretreatment may inhibit the delayed Ca(2+) influx into the neurons. The infectious brain edema is not only cytotoxic brain edema (intracellular edema) but also vasogenic brain edema (extracellular edema) followed by earlier BBB breakdown, so infectious brain edema is complicated with brain edema.</p>