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Ole Kaeseler Andersen

Publications and source records attributed to Ole Kaeseler Andersen.

8 recordsLinked to original sources

Nociceptive withdrawal reflexes evoked by uniform-temperature laser heat stimulation of large skin areas in humans.

Nociceptive withdrawal reflexes (NWR) were evoked by brief (200 ms) painful CO(2) laser stimulation at five intensities (1.2, 1.4, 1.6, 1.8, and 2.0 x pain threshold) applied to nine sites (2 cm(2)) separated by 1.7 cm on the dorsal side of the foot and anterior part of the lower leg of 14 healthy volunteers. The purpose of the study was to investigate the characteristics of NWRs evoked by a natural stimulation modality. The reflexes were measured as the electromyographic response from the iliopsoas (ILI), quadriceps vastus lateralis (QVL), biceps femoris (BF), tibialis anterior (TA), and soleus (SOL) muscles. Stimulus-response relationships between heat intensity and the reflex magnitude and correlation between perceived pain intensity and reflex magnitude were observed in the ILI, QVL, BF, and TA but not the SOL. No significant differences in reflex magnitude were found between the stimulation sites. NWRs were evoked more often in flexor muscles than extensor muscles, indicating a non-site-specific reflex organization. The paper presents a new method to evoke NWRs by uniform-temperature laser heat stimulation of large skin areas in humans. These heat evoked reflexes had a stimulus-response relationship.

Adult↗

Transient cold pain has no effect on cutaneous vasodilatation induced by capsaicin: a randomized-control-crossover study in healthy subjects.

Cooling the skin induces sympathetically driven vasoconstriction, along with some vasoparalytic dilatation at lowermost temperatures. Neurogenic inflammation, on the other hand, entails vasodilatation. In the present study, we examined the dynamic vasomotor balance of capsaicin-induced vasodilatation within the area of the induced neurogenic inflammation, with and without superimposed cooling. In a randomized-control-crossover fashion, a sample of 14 healthy volunteers participated in three experiments: (1) exposure to each 0 degrees C cold pain stimulus and a neutral 30 degrees C stimulus (control) for 30 s to the volar forearms by contact thermal thermode (1.6x1.6 cm(2)), (2) injection of 50 microg intradermal capsaicin without cooling and (3) injection of capsaicin followed by application of 0 degrees C cold pain stimulation for 30 s within the area of the secondary hyperalgesia. Repetitive vascular measurements over skin area of 4.0x4.0 cm(2) of blood flux (BF) were acquired before and during the 5 min after stimulation. A marked increase in BF (i.e. vasodilatation) at the location of the cold stimulus in comparison to control (30 degrees C) (F=11.97, p=0.004) within the first 3 min was demonstrated. Two-way repeated-measures ANOVA indicated no interaction between the experimental conditions (capsaicin with or without cold) and time (F=0.934, p=0.454). The cold pain stimulation was found to be insignificant in its influence on BF evoked by capsaicin (F=0.018, p=0.894). The results of our study indicate that (1) transient cooling causes significant vasodilatation, (2) intradermal injection of capsaicin is dominant in inducing vasodilatation, and (3) the cold-pain-evoked vasodilatation has no modulative effect on the capsaicin-evoked cutaneous vasodilatation.

Adult↗

Effects of cold stimulation on secondary hyperalgesia (HA) induced by capsaicin in healthy volunteers.

Little is known about the sensory characteristics and underlying mechanisms behind secondary hyperalgesia (HA) (2 degrees HA). The aim of the present study was to investigate the relationships between two different noxious stimuli, mechanical and cold on capsaicin-induced 2 degrees HA. Fourteen healthy volunteers were exposed to three different cold stimuli (20, 10, 0 degrees C) 30 s each, on both forearms. The cold stimuli were applied before (baseline) and 8 min after intradermal administration of 50-microg capsaicin to the forearm, distally to the injection site in the inspected area of 2 degrees HA. Pain intensities were assessed immediately after each cold stimulus by means of a visual analogue scale (cold-VAS). Additionally, areas of mechanical HA (cm(2)) were assessed distally and proximally to the injection site at three different time points: 5, 8 (right after the second series of cold stimuli), and 30 min after the injection. No significant differences in cold-VAS were found between pre- and post-capsaicin injection at the tested forearm (P= 0.334), whereas significant reduction from pre- to post-injection was found in cold-VAS in the control forearm (P= 0.024). Further, 8 min after the injection, the cold stimulation led to an expansion of 2 degrees HA area (from 5.1+/-1.38 to 11.4+/-1.72 cm(2)) to punctuate stimuli distally but not proximally to the injection site (P<0.05). It is concluded that there is no HA to cold stimuli within the area of mechanical 2 degrees HA. However, cooling acts as a conditioning stimulus and expands the area of capsaicin-induced punctuate HA.

Adult↗

A human experimental capsaicin model for trigeminal sensitization. Gender-specific differences.

Migraine is much more common in women (18%) than in men (6%). Menstrual migraine in female migraineurs also varies from 7 to 19%. The main goals of the present study were (1) to investigate gender specific differences in an experimental capsaicin model of trigeminal sensitization (a proposed mechanism of migraine) and (2) to explore the influence of menstrual cycle phases. Twenty-eight healthy female and male volunteers were studied. Capsaicin (100 microg/0.1 ml) was injected intradermally to the forehead. Pain intensity and distribution together with the visual flare and allodynic area (central sensitization) were assessed for females (during their menstrual and luteal phases) and for males. Pain area significantly changed across the menstrual cycle with 19.2+/-2.0 cm x min at menstrual and 16.4+/-0.9 cm x min at luteal phase (P<0.001). The area was significantly larger in both phases for females compared to males (14.2+/-1.3 cm x min, P<0.0001). Flare area at menstrual phase (69.2+/-4.2 cm(2)) was significantly (P<0.0001) larger than luteal phase (58.6+/-2.1 cm(2)). Females, in both phases, showed larger flare area compared to males (44.9+/-3.6 cm(2), P<0.0001). Area of brush-evoked allodynia was also larger at the menstrual phase compared to the luteal phase (P<0.0001) and males (P<0.0001). A significant difference was found in the capsaicin-evoked pain distribution with a greater response in menstrual phase compared to the luteal phase (P<0.01) and men (P<0.0001). Capsaicin induced trigeminal sensitization and evoked gender specific sensory and vaso-motor responses, with menstruating females generally showing the strongest manifestations. The model may be further applied to explore mechanisms of human trigeminal sensitization.

Capsaicin↗

Acute pain increases heart rate: differential mechanisms during rest and mental stress.

The main aim was to investigate if acutely stressed subjects have abnormal heart rate variability responses to acute pain. Efferent cardiac autonomic activity was assessed by analyzing RR interval variation in 26 male volunteers. Heart rate variability was measured as mean and standard deviation of normal RR intervals (mean RR, SDNN) and by power spectral analysis where high frequency (HF) and low frequency (LF) power were used as indexes of vagal function and of sympatho-vagal interaction, respectively. Coefficient of component variance in the LF and HF bands (CCV-LF, CCV-HF) was estimated to adjust for possible influences of different mean RR levels on power amplitude. Subjects received painful and non-painful sural nerve stimulations during rest, during attention to pain, and during mental stress. Our results show that pain significantly decreased mean RR and increased LF power and CCV-LF during rest and during attention to pain. SDNN, HF power, and total power were not affected by pain. During mental stress, pain significantly decreased mean RR but failed to affect other heart rate variability parameters. We conclude that acute pain induced efferent cardiac sympathetic activation during rest and during attention to pain as LF power and CCV-LF increased without alterations of pure vagal heart rate variability measures. During mental stress, pain inhibited mean RR without changing heart rate variability measures suggesting that pain does not increase efferent cardiac sympathetic activity during mental stress. Pain induced decrease of mean RR during mental stress may be caused by the release of catecholamines into the systemic circulation.

Acoustic Stimulation↗

Vasomotor response to cold stimulation in human capsaicin-induced hyperalgesic area.

Cooling the skin induces sympathetically driven vasoconstriction, with some vasoparalytic dilatation at the lowest temperatures. Neurogenic inflammation, on the other hand, entails vasodilatation. In this study we investigated the balance between vasoconstriction and vasodilatation in an area of experimentally induced secondary hyperalgesia (2 degrees HA), in response to low-temperature stimulations. Fourteen healthy volunteers were exposed to three 30-s long cold stimuli (20, 10, and 0 degrees C) applied, at three adjacent sites, before (baseline) and 8 min after intradermal injection of 50 microg capsaicin to the volar forearm. The cold stimuli were applied distally to the injection site within the 2 degrees HA. Blood flux (BF) and skin temperatures were measured at four different regions (proximally, and distally to the capsaicin injection and at the 0, 10, and 20 degrees C thermode sites) all within the 2 degrees HA. The vascular measurements were conducted five times. Results showed a marked increase in BF after baseline cold stimulation (P<0.001) at the 0 degrees C compared with the three other sites. In addition, vasodilatory effect (elevated BF) was found following the capsaicin injection compared with baseline for all regions (P<0.001): the non-cooled area was dilated by 450+/-5.1%; The vasoconstrictive effect for the 10 and 20 degrees C did not overcome the capsaicin vasodilatation, but did reduce it, with dilatation of 364+/-7.0% and 329+/-7.3%, respectively. For 0 degrees C, a dilatation of 407+/-6.5% was seen. It is concluded that in this experimental model, and potentially in the equivalent clinical syndromes, vasodilatation induced by the inflammation is only slightly reduced by cold stimulation such that it is still dominant, despite some cold-induced vasoconstriction.

Adult↗

Multi-modal induction and assessment of allodynia and hyperalgesia in the human oesophagus.

BACKGROUND AND AIMS: Experimental pain models based on single stimuli have to some degree limited visceral pain studies in humans. Hence, the aim of this study was to investigate the effect of multi-modal visceral pain stimuli of the oesophagus in healthy subjects before and after induction of visceral hyperalgesia. We used a multi-modal psychophysical assessment regime and a neurophysiological method (nociceptive reflex) for the characterisation of the experimentally induced hyperalgesia. METHODS: A probe for multi-modal (cold, warm, electrical, and mechanical) visceral stimulation was positioned in the lower part of the oesophagus in eleven healthy subjects. Mechanical stimuli were applied as distensions with a bag, which also had electrodes mounted for electrical stimulation. Thermal stimulation with temperatures from 0 to 60 degrees C was applied with re-circulating water in the bag. To assess the interaction between visceral and somatic pathways, the nociceptive withdrawal reflex to electrical stimuli at the ankle was measured with and without simultaneous mechanical oesophageal distension to painful levels. Finally, the oesophageal sensitisation was induced by perfusion with hydrochloric acid. Multimodal responses (pain threshold, stimulus response function, size of nociceptive reflex, and referred pain areas) were assessed before and after the induced hyperalgesia. RESULTS: The multi-modal psychophysical responses and reflex sizes were assessed twice before sensitisation, and the parameters were reproducible. Sensitisation of the oesophagus resulted in hyperalgesia to electrical and mechanical stimuli (29 and 35% decrease in pain threshold) and allodynia to cold and warmth stimuli (11% increase in sensory rating). After sensitisation, the referred pain area to mechanical stimuli increased more than 300% with a change in the localisation of the referred pain to all stimuli, and the amplitude of nociceptive reflex increased 100%, all indicating the presence of central hyperexcitability. CONCLUSIONS: Visceral hyperalgesia/allodynia can be induced experimentally and assessed quantitatively by the newly introduced multi-modal psychophysical assessment approach. The significant changes of the experimentally evoked referred pain patterns and of the nociceptive reflex evoked from a distant somatic structure indicate that even short-lasting visceral hyperalgesia can generate generalised sensitisation.

Adult↗

Multimodal assessment of pain in the esophagus: a new experimental model.

A new multimodal pain assessment model was developed integrating electrical, mechanical, cold, and warmth stimuli into the same device. The device, with a bag and electrodes for electrical stimulation, was positioned in the lower part of the esophagus in 11 healthy subjects. Mechanical stimuli were delivered with an impedance planimetric system. Thermal stimuli were performed by circulating water of different temperatures (5-50 degrees C) inside the bag. All subjects reported both nonpainful and painful local and referred sensations to all stimuli. Temporal summation to repeated electrical stimuli could be studied. For all stimuli, there was a relationship between stimulus intensity and pain intensity. The referred pain area increased with increasing intensity of the electrical and mechanical stimuli. There were several differences between the sensations evoked by the four stimulus modalities, indicating activation of different visceral nerve pathways. This model offers the possibility for controlled multimodal stimuli activating the superficial and deeper layers of the human gut and should be used in basic, clinical, and pharmacological pain studies.

Adult↗