Central and peripheral diaphragmatic neural function in chronic obstructive pulmonary disease assessed by magnetic stimulation

In chronic obstructive pulmonary disease [COPD], the diaphragm may contribute to respiratory decompensation. Factors responsible for such impairment are complex and not completely studied. Little is known about the state of neural diaphragmatic pathways particularly in milder grades of the disease. This study aimed to evaluate the cortical and peripheral diaphragmatic neuronal function in COPD using magnetic stimulation. Twenty patients with mild/moderate COPD with mean age of 52.5 +/- 8.5 years, were included. Diaphragmatic function was assessed by transcranial magnetic stimulation of the motor cortex followed by stimulation of the cervical roots of the phrenic nerves. The following parameters were measured: diaphragmatic resting motor threshold, cortical motor evoked potential [MEP] latency and amplitude, phrenic nerve latency and amplitude and central conduction time [CMCT]. Correlations were done between different electrophysiological parameters and age, duration of illness and variables of pulmonary function testing. Compared to controls, patients demonstrated significant prolongation of cortical [n=9] and cervical [n=3] MEP latencies and CMCT [n=9], reduced phrenic nerve amplitude [n=5] and increased resting motor threshold [n=11]. Significant correlations were identified between different electrophysiological parameters and age, duration, severity of disease and degree of hypoxemia. All patients with phrenic nerve abnormalities had cortical abnormalities [n=9]. We concluded that diaphragmatic neural dysfunction occurs in early stages of COPD. Central impairment [cortico-spinal] seems to occur earlier than peripheral [neuropathy of the phrenic nerve]. This information has important clinical and therapeutic implications. It will be important to study the effect of therapies as non-invasive ventilation and specific pharmacological interventions on these changes

Plasma and bronchoalveolar lavage fluid [balf] prostaglandin F2 [PGF2] in bronchial asthma patients

Plasma and BALF PGF[2alpha] were estimated in 30 patients with bronchial asthma and 10 apparently healthy subjects in order to clarify its role in the pathogenesis of bronchial asthma and its possible relation to the disease severity.The results showed a significant increase in plasma PGF[2alpha] [3 folds] and a highly significant increase in BALF PGF[2alpha] [5 folds] in bronchial asthma pateints. This rise was apparent in different subgroups of asthmatic pateints [extrinsic intrinsic mild, moderate and severe] when compared with the control group. A significant positive correlation was observed between plasma PGF[2alpha] and BALF PGF[2alpha] While a non-significant negative correlation between both plasma PGF[2alpha] and BALF PGF[2alpha] and either FEV[1]/FVC% or blood eosinophil count. In conclusion the highly raised bronchoalveolar lavage fluid PGF[2alpha] [5 times] in bronchial asthma patients suggests its local release and the slightly raised plasma PGF[2alpha] [3folds] in bronchial asthma patient may be a reflection of its local production