哮喘联盟

   摘要
   引言：慢性干咳是肺部疾病的主要并发症，也可在很多没有确诊的人中发生。咳嗽人群共同的临床联系是呼吸系统高反应性从而刺激引起过度咳嗽。这种“咳嗽高反应性综合症”的病因尚不清楚，但是认为与支配呼吸道和肺的感觉神经通路高反应性有关。
   方法：在本研究中，我们采用功能性脑成像来比较健康人和咳嗽高反应性人群在吸入性辣椒素刺激气道后的中枢神经反应。
   结果：与对照组人群的正常敏感性相似，对吸入性辣椒素的高反应性与楔形核(左侧: p<0.001; 右侧: p<0.001)和中脑水管灰质(p=0.008)包绕的中脑区域的神经活性增加一致。中脑区域增强的神经活性与慢性疼痛患者的相似，因此为咳嗽和疼痛存在神经生物学相似性的说法提供实验性证据。此外，与正常人群相比，咳嗽高反应性患者存在咳嗽控制困难，证明在辣椒素刺激时不能很好的抑制咳嗽（例如，减少咳嗽频率）(p=0.046)。咳嗽抑制与前脑网络（包括背内侧额前叶和前中扣带回）活性降低有关。另外，咳嗽频率与右侧额下回和右前脑岛的活性有关，这些区域被认为是与自主咳嗽抑制相关的区域。
   结论：本研究观察了咳嗽高反应性的中枢神经生物学改变，且提示采用咳嗽感觉输入的中枢扩大和抑制咳嗽运动行为的能力降低来共同定义问题性咳嗽患者。

 

（苏欣 审校）
Thorax. 2016 Feb 9. pii: thoraxjnl-2015-207425.doi:10.1136/thoraxjnl-2015-207425. [Epub ahead of print]


 

Neural correlates of cough hypersensitivity in humans: evidence for central sensitisation and dysfunctional inhibitory control.
 

Ando A1, Smallwood D2, McMahon M3, Irving L2, Mazzone SB4, Farrell MJ5.
 

Abstract
INTRODUCTION:Chronic non-productive coughing is a major complication of pulmonary disease and can also occur in many individuals without identifiable underlying pathology. The common clinical link in patients with cough is an enhanced sensitivity of the respiratory system to stimuli that subsequently evoke excessive coughing. The aetiology of this 'cough hypersensitivity syndrome' is unclear but believed to involve hypersensitivity of the sensory neural pathways that innervate the airways and lungs.
METHODS:In the present study, we used functional brain imaging to compare central neural responses to airway stimulation using inhaled capsaicin in healthy people and patients with cough hypersensitivity.
RESULTS:Hypersensitivity in response to inhaled capsaicin coincided with elevated neural activity in the midbrain in a region encompassing the nucleus cuneiformis (left: p<0.001; right: p<0.001) and periaqueductal gray (p=0.008) in comparison to normal sensitivity in controls. The enhanced activity noted in the midbrain is similar to that occurring in patients with chronic pain, thus providing empirical evidence to support the notion that cough and pain share neurobiological similarities. Furthermore, patients with cough hypersensitivity displayed difficulty controlling their cough, which manifested as a failure to suppress cough during capsaicin challenge (ie, reduced cough frequency) in controls compared with patients with coughhypersensitivity (p=0.046). Cough suppression was associated with reduced activity in a forebrain network that included the dorsomedial prefrontal and anterior mid-cingulate cortices. Additionally, cough frequency was correlated with activity in the right inferior frontal gyrus (R2=0.6, p<0.001) and right anterior insula (R2=0.6, p<0.001), regions previously implicated in voluntary cough suppression.
CONCLUSIONS:These findings provide insight into the central neurobiology of cough hypersensitivity and suggest that both central amplification ofcough sensory inputs and reduced capacity to suppress cough motor behaviours define patients with problematic cough.
 

Thorax. 2016 Feb 9. pii: thoraxjnl-2015-207425.doi:10.1136/thoraxjnl-2015-207425. [Epub ahead of print]