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The carotid body (CB) is the main peripheral chemoreceptor that senses the arterial PO2, PCO2 and pH. In response to hypoxemia, hypercapnia and acidosis, carotid chemosensory discharge elicits reflex respiratory, autonomic and cardiovascular adjustments. The classical construct considers the CB as the main peripheral oxygen sensor, triggering reflex physiological responses to acute hypoxemia and facilitating the ventilatory acclimation to chronic hypoxemia at high altitude. However, a growing body of experimental evidence supports the novel concept that an abnormally enhanced CB chemosensory input to the brainstem contributes to overactivation of the sympathetic nervous system, and consequent pathology. Indeed, the CB has been implicated in several diseases associated with increases in central sympathetic outflow. These include hypertension, heart failure, sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome. Indeed, ablation of the CB has been proposed for the treatment of severe and resistant hypertension in humans. In this review, we will analyze and discuss new evidence supporting an important role for the CB chemoreceptor in the progression of autonomic and cardiorespiratory alterations induced by heart failure, obstructive sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome.

The results of this limited study indicate that despite the higher incidence of cardiovascular symptoms in PD patients with dementia than in those without dementia, there is no consistent association between OH or PPH and cognitive deficits in PD. The lack of correlation between OH, gastrointestinal and urinary symptoms with cognitive impairment suggests that cognitive and autonomic involvement progresses independently from each other and variably among PD patients.

Recessive dystrophic epidermolysis bullosa is a painful condition characterised by repeated blistering of the skin. Von Bischhoffshausen et al. report that in this condition, small sensory fibres in the skin are injured leading to neuropathic pain. These findings support the use of neuropathic pain treatment in recessive dystrophic epidermolysis bullosa.

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We sought to determine whether there was an association between specific neuropsychiatric deficits and autonomic dysfunction in patients with Alzheimer's disease (AD). We studied 20 patients and 20 age-matched control subjects with neuropsychiatric tests (Blessed, Cornell depression and NPI scores) and autonomic tests (Deep breath (HRdb), 30:15 ratio and orthostatic hypotension (Bpoh)). The 30:15 ratio was consistently reduced in AD patients as compared to control subjects (1.05+/-0.07 for patients and 1.18+/-0.1 for controls, p 0.001). Whereas there were no significant differences in the HRdb and presence of Bpoh. In AD patients with an abnormal 30:15 ratio, there were significant abnormalities in the Blessed score and in the apathy, delusions and aberrant motor behavior items of the NPI. The other autonomic tests did not correlate with any neuropsychiatric score. The relationship between abnormal cortical function and impaired 30:15 ratio suggested that a lack of cortical modulation of autonomic circuits may underlie cardiovascular instability in these patients.

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