Biomedical subjects

A J Terkelsen

Publications and source records attributed to A J Terkelsen.

3 recordsLinked to original sources

PubMed2004

Mental stress inhibits pain perception and heart rate variability but not a nociceptive withdrawal reflex.

AIM: Do distraction from- or attention to sural nerve stimulation affect pain, heart rate variability, and a spinal withdrawal reflex? MATERIAL AND METHODS: In 26 male volunteers, electrical stimulation at the distal cutaneous receptive field of the sural nerve elicited pain and a nociceptive withdrawal reflex. Intensity of pain was rated on a numeric rating scale. Electromyographic reflex responses were measured from biceps femoris muscle. Cardiac autonomic function was estimated by heart rate variability measures and was expressed in the time domain as mean of RR-intervals for normal heart beats (mean-RR) and standard deviation of all normal RR-intervals (SD-NN) and, in the frequency domain, where pure vagal activity was assessed by high frequency power (0.15-0.4 Hz). Low frequency power (0.04-0.15 Hz) reflects both parasympathetic and sympathetic control. Effect parameters were recorded before and during random distraction and attention. Distraction from sural nerve stimulation was induced by a mental arithmetic test, paced auditory serial addition task (PASAT), while attention was induced by concentrating on painful foot stimulation. RESULTS: Paced auditory serial addition task decreased mean-RR and SD-NN, frequency domain parameters, as well as pain (P<0.001). In contrast, PASAT did not change the spinal withdrawal reflex. Attention did not affect any effect parameter. CONCLUSION: Distraction by PASAT altered autonomic activity and inhibited pain but failed to affect withdrawal reflex responses, while attention had no effect on either parameter. Psychological distraction and attention may have different effects on noxious evoked pain perception and autonomic activity. Pain relief during PASAT probably involves supraspinal mechanisms.

Adult↗

PubMed2001

Has basic research contributed to chronic pain treatment?

Our understanding of nociceptive processing and of plastic changes after persistent noxious input has increased immensely within the last two decades. It is now clear that long-lasting noxious stimulation or damage to the nervous system give rise to a neuronal hyperexcitability and that this sensitisation of the nervous system plays an important role for development and maintenance of chronic pain. The manifestations of such hyperexcitability are numerous and include among others: increased neuronal response to a suprathreshold stimulus, expansion of the peripheral areas from where a central neurone can be activated and the recruitment of previous non-responding nociceptive neurones. Furthermore, it has been possible to modulate this neuronal hyperexcitability by the discovery of molecular targets for pain, by sequencing DNA of ion channels and receptors and by development of new molecules that exert their effects on these molecular targets. The changes in responsiveness appear to be partly time and intensity dependent and partly dependent on the cause of injury. Whereas relatively short-lasting and moderate noxious input leads to reversible plastic changes, more intense and long-lasting noxious stimulation implies a risk for persistent and more profound alterations in transmitters, receptors, ion channels and in neuronal connectivity. Despite the explosion of new knowledge in pain processing and in molecular background for neuroplasticity, this progress has unfortunately not resulted in a corresponding improvement of our ability to treat chronic pain. The number of patients with chronic unrelieved pain is still high and newer types of treatment have so far not resulted in a substantially better treatment. Nevertheless, there is now an ongoing systematic research in which chronic pain conditions are assessed in a fashion so that mechanisms underlying pain can be dissected. Moreover, controlled clinical trials together with systematic reviews are carried out which in the future should permit formulation of treatment algorithms for chronic pain. Finally, it is likely that the development of new specific types of treatment will show efficacy if they are evaluated and analysed not on the global pain experience, but more specifically on those targets and elements of the pain experience they are aimed to deal with.

Animals↗

PubMed2001

Effects of heterotopic- and segmental counter-stimulation on the nociceptive withdrawal reflex in humans.

A nociceptive withdrawal reflex in 12 human volunteers was elicited by painful electrical stimulation applied to the cutaneous innervation area of the sural nerve. The evoked electromyographic reflex activities were recorded with surface electrodes placed on the short head of the biceps femoris muscle ipsi-lateral to sural nerve stimulation, before, during and after conditioning stimuli. The nociceptive withdrawal reflex was conditioned by nociceptive and non-nociceptive, heterotopic and segmental counter-stimulation. Heterotopic nociceptive counter-stimulation and segmental nociceptive counter-stimulation were induced by ice water applied to the contra-lateral hand and foot, respectively. Heterotopic nociceptive counter-stimulation produced a significant inhibition of the nociceptive withdrawal reflex and the associated pains rating to sural nerve stimulation. Segmental nociceptive counter-stimulation inhibited the pain rating and tended to inhibit the nociceptive withdrawal reflex. There was no obvious correlation between visual analogue scale (VAS) and the nociceptive withdrawal reflex elicited by sural nerve stimulation neither in the group nor in the individual subject. This suggests that the nociceptive withdrawal reflex cannot always be used as a quantitative measure of pain.

Adult↗