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Biomedical subjects

T S Jensen

Publications and source records attributed to T S Jensen.

At least 19 recordsLinked to original sources
PubMed2002

Human masseter inhibitory reflexes evoked by repetitive electrical stimulation.

OBJECTIVES: The relationship between the masseter inhibitory reflex (MIR) and nociceptive processing in the trigeminal region was studied in 10 healthy subjects. Based on the known increase in perceived sensory intensity following repetitive stimulation of the nociceptive system, we examined the hypothesis that the MIR reflects noxious activity in the trigeminal system by determining the possible relation between changes in MIR and perceived sensory intensity. METHODS: The MIR was quantitated and compared with psychophysical measures following repetitive peri-oral electrical stimulation (5 square wave pulses of 0.5ms repeated at 2Hz). In addition to the early (ES1) and late (ES2) periods of exteroceptive suppression, two periods with apparent excitation could be distinguished from the background electromyografical activity: (a) the inter-suppression period (ISP) between the ES1 and the ES2, and (b) the post-suppression period (PSP) after the ES2. A computer algorithm was used to detect and quantitate ES1, ES2, ISP, and PSP. The response variables were (a) onset latencies and (b) magnitudes of suppression (ES1 and ES2) and excitation (ISP and PSP). RESULTS: Consistent reduction of the magnitude of ES2 suppression in response to repetitive stimuli was observed below as well as above the pain detection threshold. CONCLUSIONS: The observed reduction of the magnitude of ES2 suppression is not specifically related to nociceptive processing. Habituation or net inhibitory effects on inhibitory pre-motor neurones (i.e. disinhibition) are possible mechanisms for the observed reduction of the magnitude of ES2 suppression after repetitive stimulation.

Adult↗
PubMed2001

Experimental brush-evoked allodynia activates posterior parietal cortex.

OBJECTIVE: To study the brain activation pattern of coexisting experimental ongoing pain and brush-evoked allodynia (pain evoked by innocuous brush) with the use of PET. BACKGROUND: Neuropathic pain usually has two essential phenomena: ongoing pain and brush-evoked allodynia, which coexist and may influence each other. Capsaicin induces both ongoing pain and brush-evoked allodynia. METHODS: Eight healthy right-handed volunteers participated in eight H2(15)O PET scans with two blocks of four randomized conditions: 1) rest, 2) brush, 3) capsaicin pain, and 4) capsaicin pain + brush (brush-evoked allodynia). Capsaicin was injected intradermally on the nondominant forearm and the subjects rated pain intensity and unpleasantness on 100-mm visual analogue scales. RESULTS: Pain intensity and unpleasantness were significantly higher during brush-evoked allodynia (74 +/- 4 and 67 +/- 4 mm) compared with capsaicin pain alone (60 +/- 4 and 51 +/- 5 mm). Brush-evoked allodynia, but not capsaicin pain alone, increased blood flow significantly in the contralateral right sensory association cortex Brodmann area (BA) 5/7, and in bilateral prefrontal cortex BA 9/10/47 and insula. No significant activity was seen in thalamus or primary somatosensory cortex (SI). Direct comparison between capsaicin pain and brush-evoked allodynia revealed significant increase in contralateral BA 5/7 only. CONCLUSIONS: The specific activation of contralateral BA 5/7 indicates that this brain region is important to the processing of brush-evoked allodynia. The involvement of BA 5/7 in brush-evoked allodynia is claimed to reflect multisensory input to this region, its role in conscious pain perception, and its neuroplastic properties.

Adult↗
PubMed2001

The clinical picture of neuropathic pain.

Neuropathic pains refer to a heterogeneous group of pain conditions characterised by lesion or dysfunction of the normal sensory pathways. Clinical characteristics include: delayed onset of pain after nervous system lesion, pain in area of sensory loss, spontaneous and different evoked types of pains. It has so far only been possible to classify these pains on basis of underlying cause or on anatomical location. The mechanisms underlying neuropathic pain are not yet clear, but neuronal hyperexcitability in those neurons that have lost their normal patterned input seems to be a common denominator for many, if not all types, of neuropathic pains. Along these lines, a mechanism-based classification has recently been proposed, which is an attractive approach because it provides a frame for a rationally based therapy of neuropathic pains. The clinical manifestations of neuronal hyperexcitability due to nervous system lesions is described.

Animals↗
PubMed2001

Handicap after acute whiplash injury: a 1-year prospective study of risk factors.

BACKGROUND: Exposure to a whiplash injury implies a risk for development of chronic disability and handicap, with reported frequencies ranging from 0% to 50% in follow-up studies. The exact risk for development of chronic whiplash syndrome is not known. OBJECTIVE: To prospectively determine the sensitivity and specificity of five possible predictors for handicap following a whiplash injury. METHODS: In a 1-year prospective study of persons with acute whiplash injury (n = 141) and control subjects who had acute ankle distortion (n = 40), pain intensity, number of nonpainful neurologic complaints, cervical mobility, workload during extension and flexion of the neck, and results of psychometric assessment were recorded. The consecutively sampled injured persons were assessed with structured and semistructured questionnaires, and underwent neurologic examination after 1 week and 1, 3, 6, and 12 months. After 3 to 4 years, participants with whiplash injury were questioned about legal issues. RESULTS: After 1 year, 11 (7.8%) persons with whiplash injury had not returned to usual level of activity or work. The best single estimator of handicap was the cervical range-of-motion test, which had a sensitivity of 73% and a specificity of 91% (p < 0.01, Cox regression analysis). Accuracy and specificity increased to 94% and 99% when combined with pain intensity and other complaints. This increase was gained at the expense of a reduced sensitivity. Initiation of lawsuit within first month after injury did not influence recovery. CONCLUSION: The cervical range-of-motion test has a high sensitivity in prediction of handicap after acute whiplash injury. The value of cervical range-of-motion test is further improved by additional recording of symptoms and pain intensity.

Adult↗
PubMed2001

Lamotrigine for central poststroke pain: a randomized controlled trial.

OBJECTIVE: Central poststroke pain (CPSP) is usually difficult to treat. Amitriptyline, the only oral preparation shown to be effective in a randomized controlled trial, is often associated with a range of side effects related to the many mechanisms of actions of tricyclic antidepressants. We investigated the effect of lamotrigine, a drug that reduces neuronal hyperexcitability, on poststroke pain. METHODS: Thirty consecutive patients with CPSP (median age 59 years, range 37 to 77; median pain duration 2.0 years, range 0.3 to 12) from two centers participated in a randomized, double-blind, placebo-controlled cross-over study. The study consisted of two 8-week treatment periods separated by 2 weeks of wash-out. The primary endpoint was the median value of the mean daily pain score during the last week of treatment while treated with 200 mg/d lamotrigine. Secondary endpoints were median pain scores while on lamotrigine 25 mg/d, 50 mg/d, and 100 mg/d; a global pain score; assessment of evoked pain; areas of spontaneous pain; and allodynia/dysesthesia. RESULTS: Lamotrigine 200 mg/d reduced the median pain score to 5, compared to 7 during placebo (p = 0.01) in the intent-to-treat population of 27 patients. No significant effect was obtained at lower doses. Twelve patients (44%) responded to the treatment. There was a uniform tendency to reduction of all secondary outcome measures, but lamotrigine only had significant effects on some of the secondary outcome measures. Lamotrigine was well tolerated with few and transient side effects. Two mild rashes occurred during lamotrigine treatment, one causing withdrawal from study. CONCLUSIONS: Oral lamotrigine 200 mg daily is a well tolerated and moderately effective treatment for central poststroke pain. Lamotrigine may be an alternative to tricyclic antidepressants in the treatment of CPSP.

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

Pain and dysesthesia in patients with spinal cord injury: A postal survey.

STUDY DESIGN: A postal survey. OBJECTIVES: To assess the prevalence and characteristics of pain and dysesthesia in a community based sample of patients with spinal cord injury (SCI) with special focus on neuropathic pain. SETTING: Community. Western half of Denmark. METHODS: We mailed a questionnaire to all outpatients (n = 436) of the Viborg rehabilitation centre for spinal cord injury. The questionnaire contained questions regarding cause and level of spinal injury and amount of sensory and motor function below this level. The words pain and unpleasant sensations were used to describe pain (P) and dysesthesia (D) respectively. Questions included location and intensity of chronic pain or dysesthesia, degree of interference with daily activity and sleep, presence of paroxysms and evoked pain or dysesthesia, temporal aspects, alleviating and aggravating factors, McGill Pain Questionnaire (MPQ) and treatment. RESULTS: Seventy-six per cent of the patients returned the questionnaire, (230 males and 100 females). The ages ranged from 19 to 80 years (median 42.6 years) and time since spinal injury ranged from 0.5 to 39 years (median 9.3 years). The majority (> 75%) of patients had traumatic spinal cord injury. Of the respondents, 77% reported having pain or unpleasant sensations, and 67% had chronic pain or unpleasant sensations at or below lesion. Forty-eight per cent reported that P/D could be evoked by non-noxious stimulation of the skin indicating that allodynia is present in almost half of the patients. Forty-three per cent of respondents took analgesics, 7% received antidepressants or anticonvulsants. CONCLUSION: This survey suggests that pain and dysesthesia are common and serious complaints in SCI patients. Unexpectedly, only 7% of the patients were treated with drugs considered to be most effective in neuropathic pain. This emphasizes the need for a continued research and education on P/D in SCI.

Adult↗
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↗
PubMed2001

Acute pain induces insulin resistance in humans.

BACKGROUND: Painful trauma results in a disturbed metabolic state with impaired insulin sensitivity, which is related to the magnitude of the trauma. The authors explored whether pain per se influences hepatic and extrahepatic actions of insulin. METHODS: Ten healthy male volunteers underwent two randomly sequenced hyperinsulinemic-euglycemic (insulin infusion rate, 0.6 mU x kg(-1) x min(-1) for 180 min) clamp studies 4 weeks apart. Self-controlled painful electrical stimulation was applied to the abdominal skin for 30 min, to a pain intensity of 8 on a visual analog scale of 0-10, just before the clamp procedure (study P). In the other study, no pain was inflicted (study C). RESULTS: Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Differences in glucose oxidation rates were not statistically significant. The suppression of isotopically determined endogenous glucose output during hyperinsulinemia tended to be decreased after pain (1.67+/-0.48 mg x kg(-1) x min(-1) in study P vs. 2.04+/-0.45 mg x kg(-1) x min(-1) in study C; P = 0.06). Pain elicited a twofold to threefold increase in serum cortisol (P < 0.01), plasma epinephrine (P < 0.05), and serum free fatty acids (P < 0.05). Similarly, circulating concentrations of glucagon and growth hormone tended to increase during pain. CONCLUSIONS: Acute severe pain decreases insulin sensitivity, primarily by affecting nonoxidative glucose metabolism. It is conceivable that the counterregulatory hormonal response plays an important role. This may indicate that pain relief in stress states is important for maintenance of normal glucose metabolism.

Acute Disease↗
PubMed2001

Recent advances in pain research: implications for chronic headache.

Within the last 2 decades there has been an explosion in new information on mechanisms underlying pain. Unfortunately this information has not resulted in a similar improvement of our handling of patients with chronic pain including chronic musculoskeletal pain. Neuronal hyperexcitability, which apparently is a key phenomenon in many (if not all) types of chronic pain results in changes in the nervous system from the level of the peripheral nociceptor to the highest cortical centers in the brain. The neuronal plastic changes in chronic pain conditions makes the nociceptive system amenable for treatment with several traditional as well as nontraditional types of interventions. Two treatment areas that seem worth exploring within chronic pain including headache concerns preventive measures and endogenous pain modulation.

Animals↗
PubMed2000

Pharmacologic treatment of pain in polyneuropathy.

Tricyclic antidepressants and anticonvulsants have become the mainstay in the treatment of pain in polyneuropathy. Within the last decade, controlled trials have shown that numerous other drugs relieve such pain. To estimate the efficacy of the different treatments, the authors identified all placebo-controlled trials and calculated numbers needed to treat (NNT) to obtain one patient with more than 50% pain relief. The NNT was 2.6 for tricyclic antidepressants, 6.7 for selective serotonin reuptake inhibitors, 2.5 for anticonvulsant sodium channel blockers, 4.1 for the anticonvulsant calcium channel blocker gabapentin, and 3.4 for the mixed opioid and monoaminergic drug tramadol, as calculated from a sufficiently large number of patients. Favorable point estimates of NNT of 1.9 for the NMDA-antagonist dextromethorphan and 3.4 for L-dopa were determined from a limited number of data. For capsaicin, the NNT calculated from many exposed patients was 5.9, but most of the data are controversial owing to trial methodology. Finally, the NNT for the antiarrhythmic sodium channel blocker mexiletine was 38, but this value may be biased because of a lack of dichotomous data in several positive trials. Tricyclic antidepressants are at the moment still the drugs of first choice, and drugs such as gabapentin, carbamazepine, and tramadol may be tried if contraindications or tolerability problems are encountered with the tricyclics.

Anticonvulsants↗
PubMed2000

Duration and distribution of experimental muscle hyperalgesia in humans following combined infusions of serotonin and bradykinin.

The present study examined distribution and duration of muscle hyperalgesia to pressure stimuli after intramuscular bolus-infusions of serotonin (5-HT, 20 nmol) and bradykinin (BKN, 10 nmol) in 10 volunteers. Infusions were given into the tibialis anterior (TA) muscle over 20 s with an inter-infusions interval of 3 min. Infusions of isotonic saline (NaCl, 0.9%) were given as control. Pain intensity was continuously scored on a visual analogue scale (VAS), and subjects drew the distribution of the pain areas on an anatomical map. Pressure pain thresholds (PPTs) were assessed with an electronic algometer at the injection site (10 cm below the patella), 2, 5, and 10 cm distal from the injection site, and at the ankle. Control assessments of PPTs were done at the contralateral TA and ankle. Skin sensibility was assessed with a Von Frey hair at the same sites. All measurements were done before and 5, 20, 40, and 60 min after infusions. The VAS-peak after BKN was significantly higher (P<0.05) compared with 5-HT and the second infusion of NaCl. The duration of the increase in VAS after 5-HT+BKN was significantly longer (P<0.05) compared with the infusions of NaCl. The local pain area after infusion of BKN was significantly larger (P<0.05) compared with 5-HT and control infusions. Cutaneous sensibility to tactile stimuli was not affected by any of the combinations. PPTs at the injection site and 2 cm (5, 20, and 40 min) were significantly decreased (P<0.05) after 5-HT+BKN compared with baseline and isotonic saline. In addition, PPTs were significantly decreased (P<0.05) after 5-HT+BKN at 5 cm (5 and 20 min) and 10 cm (5 min). Serotonin may enhance the effect of bradykinin in producing experimental muscle pain and muscle hyperalgesia to mechanical stimuli. The combination of serotonin and bradykinin can produce muscle hyperalgesia, lasted for up to 40 min and located within the muscle. No widespread hyperalgesia to the ankle and other leg (tested at 10 cm below the patella and ankle) was observed suggesting a predominant peripheral origin of the experimentally induced hyperalgesic stage.

Adult↗
PubMed2000

Intramuscular and intradermal injection of capsaicin: a comparison of local and referred pain.

The present study compared capsaicin-induced muscle and skin pain in humans. Twelve healthy subjects received, in a randomised, balanced order, 3 intramuscular (i.m.) injections into the brachioradial muscle: capsaicin 100 microg/1 ml, capsaicin 100 microg/20 microl or 1 ml solvent (Tween 80), and one intradermal injection (i.d.): capsaicin 100 microg/20 microl. Local and referred pain intensities and areas were assessed from 0 to 60 min after injection. Intradermal capsaicin produced more intense local pain than i.m. capsaicin in the first min (skin: 68+/-6, muscle: 51+/-6 mm VASxmin, P<0.05). In contrast, the local pain offset was later (muscle: 38+/-5, skin: 23+/-5 min, P<0.05) and referred pain was more frequent (muscle: 9/12, skin: 1/12 subjects, P<0.01) following i.m. capsaicin compared with i.d. capsaicin. Capsaicin (1 ml) produced significantly more pain than 20 microl i.m. (pain in the first min: 1 ml: 71+/-6, 20 microl: 51+/-6 VASxmin, P<0.05, offset: 1 ml: 50+/-4, 20 microl: 38+/-5 min, P<0.05). The different local and referred pain following identical noxious stimulation of muscle and skin indicates that the neurophysiological mechanisms underlying skin and muscle pain differs. The model with identical noxious stimulation of muscle and skin may be suitable for the study of differences in deep and superficial pain as seen in the clinic.

Adult↗
PubMed2000

Relationship between mechanical sensitivity and postamputation pain: a prospective study.

Limb amputation is followed by stump and phantom pain in a large proportion of amputees and postamputation pain may be associated with signs of hyperexcitability such as hyperalgesia to mechanical stimulation. The present study examined the possible relationship between mechanical pain threshold of the limb and early (after 1 week) and late (after 6 months) phantom pain. Thirty-five patients scheduled for amputation of the lower limb were examined before, 1 week and 6 months after amputation. On all three examination days pressure-pain thresholds were measured and compared with the simultaneous recording of ongoing pain intensity assessed on a visual analogue scale (VAS). There was a weak but significant inverse relationship between preamputation thresholds and early stump and phantom pain. There was no relationship between preamputation thresholds and late stump and phantom pain. One week after amputation there was a significant and inverse relationship between mechanical thresholds and phantom pain but no relationship was found after 6 months. The findings suggest that although tenderness of the limb before and after amputation is related to early stump and phantom pain, the relationship is weak. Neuronal sensitization peripherally or centrally may play a role in the development of phantom pain.

Aged↗
PubMed2000

Repetitive intradermal capsaicin: differential effect on pain and areas of allodynia and punctate hyperalgesia.

This study examined the effect of repeated intradermal capsaicin injections on capsaicin pain intensity and areas of allodynia and punctate hyperalgesia. Seventeen healthy volunteers participated in four sessions separated by at least 5 days. Each session included four intradermal injections of 10 microg of capsaicin. In one session injections were given with 0.5 cm and 6 min intervals, in a second with 0.5 cm and 15 min intervals, in a third with 0.5 cm and 24 min intervals, and in a fourth session with 4 cm and 15 min intervals. Following each injection capsaicin pain intensity was measured in the first 5 min, the area of allodynia at 5 min and area of punctate hyperalgesia at 10 min. With 6 min and 0.5 cm between repeated injections, capsaicin pain intensity decreased significantly whereas areas of allodynia and punctate hyperalgesia increased. In contrast, both capsaicin pain intensity and areas of allodynia and punctate hyperalgesia increased when the interval between injections was 24 min and 0.5 cm or 15 min and 4 cm. With 15 min and 0.5 cm between injections, capsaicin pain intensity did not change, whereas areas of allodynia and punctate hyperalgesia increased. There were no significant relations between capsaicin pain intensity and areas of allodynia and punctate hyperalgesia after first injections. The findings indicate that the response to intradermal injection of capsaicin is dependent on the time and distance between injections. The lack of significant relation between capsaicin pain intensity and area of allodynia and punctate hyperalgesia suggests that the two phenomena are mediated by different central mechanisms.

Adult↗
PubMed2000

Peripheral lidocaine but not ketamine inhibits capsaicin-induced hyperalgesia in humans.

We examined the effect of the subcutaneous infiltration of ketamine, lidocaine and saline before injury on capsaicin-induced pain and hyperalgesia. Twelve healthy volunteers participated in two separate, randomized, double-blind, placebo-controlled crossover experiments. In experiment 1, 100 micrograms capsaicin was injected intradermally in one volar forearm 10 min after the skin had been pretreated with lidocaine 20.0 mg in 2.0 ml or 0.9% saline 2.0 ml at the capsaicin injection site. In experiment 2, a similar capsaicin test was given 10 min after the skin had been pretreated with ketamine 5 mg in 2.0 ml or 0.9% saline 2.0 ml. To control for possible systemic effects, the capsaicin injection site was pretreated by injection of saline into the skin and the contralateral arm was treated with active drug, and vice versa. Outcome measures were spontaneous pain, pain evoked by punctate and brush stimuli, and areas of brush-evoked and punctate-evoked hyperalgesia. Lidocaine reduced all measures compared with placebo (P < 0.001), whereas ketamine failed to change any measures. Pain scores and areas of hyperalgesia were not affected when the contralateral site was infiltrated with ketamine or lidocaine. Lidocaine produced no side-effects, whereas ketamine produced paraesthesia, dizziness and sleepiness in six out of 24 (25%) cases. Blocking peripheral sodium channels with locally administered lidocaine reduces spontaneous pain and capsaicin-induced hyperalgesia but local block with the NMDA-type glutamate receptor antagonist ketamine has no effect on capsaicin-induced pain and hyperalgesia.

Analgesics↗