REHABILITATION mortality over and above standard medical factors.

Experimental evidence for neuro-immune interaction was also pre- sented by Kiecolt-Glaser et al. (4), who studied immune response in participants suffering from long term stress. In an interesting design, immune system function of individuals responsible for pro- viding care for close family members with Alzheimer’s disease was compared to that of control participants. All subjects underwent a biopsy procedure to create an experimental wound. The authors reported that healing times were nearly 25% longer in care givers compared to controls and concluded that these increased recovery times were, as they hypothesised, due to the chronic life stress experienced by the experimental group. The authors suggested the relative failure of the normal immune inflammatory response was a major factor in producing the results. A similar experimental study by Marucha (5) examined wound healing time in students at two times of the year, an examination period hypothesised to be high- ly stressful, and a vacation period. Results supported those of Kiecolt-Glaser (4) in times of intense stress the healing process required a significantly greater period of time to operate. Several other authors have also reported neural-immune links. For exam- ple, Suinn (6) demonstrated that anger may compromise immune system function, while Liebeskind (7), demonstrated the adverse affect of pain on immune and endocrine function.

MECHANISMS OF NEURO-IMMUNE INTERACTION Traditionally the immune and nervous system were thought of as separate and independent systems, each with their own specific cells and regulators. It is now recognised that there is considerable interchange between these two systems and that these also inter- act with the endocrine system. Communication between these sys- tems occurs via the release of numerous messenger molecules in the extracellular fluid. These molecules (small peptides, steroids, amines and glycoproteins) activate autocrine, paracrine, synaptic and hormonal activity. The central nervous system (CNS) constant- ly monitors the concentration of many of these molecules as well as controlling the activity of the autonomic nervous system and endocrine systems. Both the CNS and endocrine systems have extensive bi-directional communications with the immune systems. When activated by noxious stimulation (eg. pain from soft tissue trauma), small diameter afferent nerve fibres (C-fibres) from peripheral nocicepter endings, release neural peptides (substance P) into the surrounding tissue causing neurogenic inflammation. Impulses are also sent to the dorsal horn of the spinal cord and then through the anterior lateral tract of the spinal cord to the brain stem and hypothalamus. Increased activity then occurs in the hypothalamic-pituitary-adrenal axis culminating in increased output from the sympathetic nervous system. Reciprocally, emotional factors effecting the neural, endocrine and immune system arise largely from the limbic system and hypothalamus. As can be seen from Figure 1, the limbic system exerts considerable influence over the pituitary gland as well as the auto- nomic nervous system (affecting human growth hormone and adrenocorticotrophic hormone to name just two). This altered neuronal functioning affects metabolic processes in peripheral tissues resulting in marked changes in immune functioning includ- ing stress-induced suppression of the immune system.

IMPLICATIONS OF PNI FOR PRACTITIONERS The evidence presented above suggests not only that subcon-

20 Hypothalamus CRH Locus ceruleus

Nucleus of the tractus solitarius

ACTH

Pituatary gland

Adrenal glands

Sympathetic nervous system

Immune organs

Vagus nerve

Immune cells

Note: Cytokines stimulate the hypothalamus through the blood stream or via the vagus nerve. Corticotropin releasing hormones activate the hypothalamic- pituitary-adrenal axis. The release of

cortisol depresses the immune

response. Corticotrophin releasing hormone stimulates the sympathetic centres that leads to the release of noradrenaline in immune organs and regulates inflammatory responses throughout the body.

Figure 1: Neuro-endocrine-immune system interactions

scious psychological processes might influence immune function (eg. conditioning (1)), but that conscious and everyday psycho- logical processes such as stress might have similar effects. In fact processes such as emotions (eg. anger), moods (anxiety), mood disorders (eg. chronic depression), cognitions (eg. pain), and even personality dispositions/coping styles (eg. pessimism), might impact negatively on immune system function. Logically, if it is accepted that optimal immune system functioning - along- side appropriate diagnosis, treatment, rest and rehabilitation - is one aspect of recovery from injury, practitioners should seek to minimise the effects of such potentially harmful psychological processes. To do so practitioners must be aware of circumstances that may elicit such processes, such as stress relating to injury/ illness, finance, relationships or career, grief, faulty belief systems and even phobias and addictions (many athletes may be addicted to one or more aspects of their sport, and withdrawal from that sport due to injury may result in a range of negative emotions not dissimilar to withdrawal from an addictive substance). Optimal treatment outcomes might only be possible in situations in which either the client is experiencing positive emotional and cognitive states (arguably an unreasonable expectation in the case of an elite or professional athlete with an injury precluding training and competition), or one in which the practitioner is able to minimise the impact of negative emotional and cognitive states on immune function.

Of the psychological processes listed above, stress, in any of its many forms, is likely to be the most frequently experienced by patients. Both acute and chronic stress are frequently experienced by the injured athlete, and may be manifest as any of a number of psychological states such as denial, anger, depression, anxiety

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Cortisol

Cortisol

Cytokines