SummaryThe detrimental effect of stress on the immune response increases with age, though the mechanisms responsible are not fully understood. The physiological response to stress is regulated in part by the adrenocortical system. Adrenal hormones dehydroepiandrosterone sulphate (DHEAS) and cortisol have opposing effects on the innate immune system, DHEAS enhances while cortisol suppresses immunity and the molar ratio of cortisol to DHEAS increases with age. We found that elderly hip fracture patients produced a robust neutrophilia after injury, but circulating neutrophils showed an impaired antibacterial response. We therefore proposed that adrenocortical hormones mediate the heightened immunosuppression seen in the elderly after injury. We examined neutrophil function and adrenocortical hormone levels in elderly (> 65 years) hip fracture patients and age-matched healthy controls. Thirteen out of 35 elderly patients acquired infections following hip fracture. Neutrophil superoxide production was lower in elderly hip fracture patients compared with controls ( P < 0.005) and lower in patients who acquired infection following injury compared with those who did not ( P < 0.05). Serum cortisol:DHEAS ratio was higher in elderly hip fracture patients (0.56 ± ± ± ± 0.38) compared with either age-matched controls (0.36 ± ± ± ± 0.21; P < 0.05) or young fracture patients (0.087 ± ± ± ± 0.033; P < 0.0001). Moreover, cortisol: DHEAS was increased in elderly patients who succumbed to infection compared with those who did not (0.803 ± ± ± ± 0.42 vs. 0.467 ± ± ± ± 0.28; P < 0.02). In vitro cortisol significantly decreased neutrophil superoxide generation ( P < 0.05) and this was prevented by coincubation with DHEAS. We propose that increased cortisol:DHEAS ratios may contribute to reduced immunity following physical stress in the elderly.

Previous work has demonstrated an age-related decline in neutrophil function, including a decline in phagocytic capacity, with age in healthy individuals. This decline in function may contribute to increased susceptibility to bacterial infections in the elderly population. The present study has investigated the effects of age on susceptibility to infection and neutrophil function in elderly humans following mild trauma. Specifically, we have measured neutrophil function in 44 patients, all of whom had no significant co-morbidity, were over 65 years old (mean age 82.5 years) and had sustained a fractured neck of femur. We obtained neutrophils and examined the process of microbial engulfment by phagocytosis and the bactericidal mechanism of superoxide production. In the 5-week period after trauma, almost half of the elderly trauma patients succumbed to bacterial or fungal infection, with a predominance of chest and urinary tract infections. When examining neutrophil function, a decline in superoxide production was observed in neutrophils from the elderly trauma group at the time of hip fracture when compared with those from healthy elderly controls, and this was maintained 5 weeks after trauma. This was accompanied by an age-related reduction in phagocytic function during this period. We propose that trauma and an age-related decline in neutrophil function combine to decrease the immune response to bacteria in the elderly.

We investigated the response of chronic neck and shoulder pain to decompression of the carpal tunnel in 38 patients with whiplash injury. We also determined the plasma levels of substance P (SP) and calcitonin gene-related peptide (CGRP), which are inflammatory peptides that sensitise nociceptors. Compared with normal control subjects, the mean concentrations of SP (220 v 28 ng/l; p < 0.0001) and CGRP (400 v 85 ng/l; p < 0.0005) were high in patients with chronic shoulder and neck pain before surgery. After operation their levels fell to normal. There was resolution of neurological symptoms with improvement of pain in 90% of patients. Only two of the 30 with chronic neck and shoulder pain who had been treated conservatively showed improvement when followed up at two years.In spite of having neuropathic pain arising from the median nerve, all these patients had normal electromyographic and nerve-conduction studies. Chronic pain in whiplash injury may be caused by 'atypical' carpal tunnel syndrome and responds favourably to surgery which is indicated in patients with neck, shoulder and arm pain but not in those with mild symptoms in the hand. Previously, the presence of persistent neurological symptoms has been accepted as a sign of a poor outcome after a whiplash injury, but our study suggests that it may be possible to treat chronic pain by carpal tunnel decompression.

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