Nociceptive Electrical Stimulation Research Articles

Pharmacological modulation of ventral tegmental area neurons elicits changes in trigeminovascular sensory processing and is accompanied by glycemic changes: Implications for migraine.

Imaging migraine premonitory studies show increased midbrain activation consistent with the ventral tegmental area, an area involved in pain modulation and hedonic feeding. We investigated ventral tegmental area pharmacological modulation effects on trigeminovascular processing and consequent glycemic levels, which could be involved in appetite changes in susceptible migraine patients. Serotonin and pituitary adenylate cyclase-activating polypeptide receptors immunohistochemistry was performed in ventral tegmental area parabrachial pigmented nucleus of male Sprague Dawley rats. In vivo trigeminocervical complex neuronal responses to dura mater nociceptive electrical stimulation, and facial mechanical stimulation of the ophthalmic dermatome were recorded. Changes in trigeminocervical complex responses following ventral tegmental area parabrachial pigmented nucleus microinjection of glutamate, bicuculline, naratriptan, pituitary adenylate cyclase-activating polypeptide-38 and quinpirole were measured, and blood glucose levels assessed pre- and post-microinjection. Glutamatergic stimulation of ventral tegmental area parabrachial pigmented nucleus neurons reduced nociceptive and spontaneous trigeminocervical complex neuronal firing. Naratriptan, pituitary adenylate cyclase-activating polypeptide-38 and quinpirole inhibited trigeminovascular spontaneous activity, and trigeminocervical complex neuronal responses to dural-evoked electrical and mechanical noxious stimulation. Trigeminovascular sensory processing through modulation of the ventral tegmental area parabrachial pigmented nucleus resulted in reduced circulating glucose levels. Pharmacological modulation of ventral tegmental area parabrachial pigmented nucleus neurons elicits changes in trigeminovascular sensory processing. The interplay between ventral tegmental area parabrachial pigmented nucleus activity and the sensory processing by the trigeminovascular system may be relevant to understand associated sensory and homeostatic symptoms in susceptible migraine patients.

Neuromuscular adaptations to experimentally induced pain in the lumbar region: systematic review and meta-analysis.

Experimental pain models are frequently used to understand the influence of pain on the control of human movement. In this systematic review, we assessed the effects of experimentally induced pain in the lumbar region of healthy individuals on trunk muscle activity and spine kinematics. Databases were searched from inception up to January 31, 2022. In total, 26 studies using either hypertonic saline injection (n = 19), heat thermal stimulation (n = 3), nociceptive electrical stimulation (n = 3), or capsaicin (n = 1) were included. The identified adaptations were task dependent, and their heterogeneity was partially explained by the experimental pain model adopted. Meta-analyses revealed an increase of erector spinae activity (standardized mean difference = 0.71, 95% confidence interval [CI] = 0.22-1.19) during full trunk flexion and delayed onset of transversus abdominis to postural perturbation tasks (mean difference = 25.2 ms, 95% CI = 4.09-46.30) in the presence of pain. Low quality of evidence supported an increase in the activity of the superficial lumbar muscles during locomotion and during voluntary trunk movements during painful conditions. By contrast, activity of erector spinae, deep multifidus, and transversus abdominis was reduced during postural perturbation tasks. Reduced range of motion of the lumbar spine in the presence of pain was supported by low quality of evidence. Given the agreement between our findings and the adaptations observed in clinical populations, the use of experimental pain models may help to better understand the mechanisms underlying motor adaptations to low back pain.

The Two Arrows of Pain: Mechanisms of Pain Related to Meditation and Mental States of Aversion and Identification

ObjectivesAccording to the core Buddhist psychology models of the “two arrows of pain” and “co-dependent origination,” pain is the resultant of bodily and mental factors, which can be regulated by meditation states and traits. Here we investigated how pain and the related aversion and identification (self-involvement) experiences are modulated by focused attention meditation (FAM), open monitoring meditation (OMM), and loving kindness meditation (LKM), as well as by meditation expertise.MethodsTheravada Buddhist long-term meditators were matched with a group of short-term meditators. Nociceptive electrical stimulation was administered during FAM, OMM, and LKM, and in a non-meditative rest condition. Experience reports of pain, aversion, and identification were collected in each trial.ResultsPain thresholds were higher in long-term meditators than in short-term meditators. In the short-term meditators, as compared to rest, pain was reduced in FAM and OMM, and aversion and identification in all meditation conditions. In the long-term meditators, pain was reduced only in LKM. Identification was reduced in the three forms of meditation, while aversion was not affected by meditation. Further analyses with a particular focus on long-term meditators showed that pain was predicted to increase with meditation expertise, aversion, and identification. Granger causality analysis revealed that aversion and pain, as well as aversion and identification, causally influenced each other; identification causally influenced pain. This pattern of results about the relationships between pain, aversion, and identification was largely overlapping in the group of short-term meditators.ConclusionsThe findings reveal mechanisms of pain in interaction with aversive and identification mental states, as well as their modulation by meditation states and traits. They also suggest that pain feeling is the resultant of coupling of sensory and mental factors, thus highlighting the relevance of the second arrow of pain and providing a clarification of the epistemological gap between sensory causation and mental state causation of pain, in terms of a co-production mechanism with multiple stages. In particular, the evidence about the causal influences of identification on pain highlights a self-related factor of relevance in pain experiences that can be modulated by mindfulness. The study also inspires new testable neuroscientific hypotheses, and sheds new light on core Buddhist psychology models, based on evidence from a controlled experimental setting and experience dimension reports by long-term meditators with enhanced mindfulness skills.

The influence of nociceptive and neuropathic pain states on the processing of acute electrical nociceptive stimulation: A dynamic causal modeling study

IntroductionDespite the worldwide increase in prevalence of chronic pain and the subsequent scientific interest, researchers studying the brain and brain mechanisms in pain patients have not yet clearly identified the exact underlying mechanisms. Quantifying the neuronal interactions in electrophysiological data could help us gain insight into the complexity of chronic pain. Therefore, the aim of this study is to examine how different underlying pain states affect the processing of nociceptive information. MethodsTwenty healthy participants, 20 patients with non-neuropathic low back-related leg pain and 20 patients with neuropathic failed back surgery syndrome received nociceptive electrical stimulation at the right sural nerve with simultaneous electroencephalographic recordings. Dynamic Causal Modeling (DCM) was used to infer hidden neuronal states within a Bayesian framework. ResultsPain intensity ratings and stimulus intensity of the nociceptive stimuli did not differ between groups. Compared to healthy participants, both patient groups had the same winning DCM model, with an additional forward and backward connection between the somatosensory cortex and right dorsolateral prefrontal cortex. DiscussionThe additional neuronal connection with the prefrontal cortex as seen in both pain patient groups could be a reflection of the higher attention towards pain in pain patients and might be explained by the higher levels of pain catastrophizing in these patients. ConclusionIn contrast to the similar pain intensity ratings of an acute nociceptive electrical stimulus between pain patients and healthy participants, the brain is processing these stimuli in a different way.

Effects of Intrahippocampal Injections of Melipramin on EEG, Brain Self-Stimulation, and Behavioral Indices of Rats under Conditions of Neurogenic Stress

In young (3-month-old) male Wistar rats, we studied the effects of intrahippocampal microinjections of melipramin under conditions of emotional stress induced by sessions of electrical nociceptive stimulation of the limbs. In most cases, seven-day-long stressing resulted in suppression of electrical activity of the hippocampus, exerted ambivalent effects on the frequency of brain self-stimulation (BSS) events, decreased the communicability of animals in the two-chamber test, and increased the latencies of going of the animal from the arena center and grooming episodes in the open field test. Injections of melipramin interfered with the development of stress-induced disorders in the hippocampus, decreased the normalized content of beta oscillations in the neocortex and the theta-index in the hypothalamus, increased the BSS frequency, and decreased the level of negativation of the behavioral manifestations of this phenomenon. The duration of stay of a rat near the partition in the two-chamber test increased, the mobility and number of grooming episodes in the open field enhanced, but the latency of leaving the arena center also increased (similarly to what was observed in the control). On the 8th–9th day of the poststress period, behavioral disorders of rats of the control group in the two-chamber test were smoothed to a significant extent. The stability of the examined indices or the reverse development of stress-induced disorders within the above period in animals injected with melipramin were indicative of a significant role of the hippocampus in the formation of central effects of this antidepressant and also of adaptogenic and stress-protective properties of this drug.

Neural Habituation to Painful Stimuli Is Modulated by Dopamine: Evidence from a Pharmacological fMRI Study.

In constantly changing environments, it is crucial to adaptively respond to threatening events. In particular, painful stimuli are not only processed in terms of their absolute intensity, but also with respect to their context. While contextual pain processing can simply entail the repeated processing of information (i.e., habituation), it can, in a more complex form, be expressed through predictions of magnitude before the delivery of nociceptive information (i.e., adaptive coding). Here, we investigated the brain regions involved in the adaptation to nociceptive electrical stimulation as well as their link to dopaminergic neurotransmission (placebo/haloperidol). The main finding is that haloperidol changed the habituation to the absolute pain intensity over time. More precisely, in the placebo condition, activity in left postcentral gyrus and midcingulate cortex increased linearly with pain intensity only in the beginning of the experiment and subsequently habituated. In contrast, when the dopaminergic system was blocked by haloperidol, a linear increase with pain intensity was present throughout the entire experiment. Finally, there were no adaptive coding effects in any brain regions. Together, our findings provide novel insights into the nature of pain processing by suggesting that dopaminergic neurotransmission plays a specific role for the habituation to painful stimuli over time.

The importance of measuring skin resistance for electrical nociceptive stimulation in standing horses

The importance of measuring skin resistance for electrical nociceptive stimulation in standing horses

Pain modulation as a function of hypnotizability: Diffuse noxious inhibitory control induced by cold pressor test vs explicit suggestions of analgesia

The aim of the present study was to compare the effects of explicit suggestions of analgesia and of the activation of the Diffuse Noxious Inhibitory Control (DNIC) by cold pressor test on pain perception and heart rate in healthy participants with high (highs, N=18), low (lows, N=18) and intermediate scores of hypnotizability (mediums, N=15) out of hypnosis. Pain reports and the stimulus-locked heart rate changes induced by electrical nociceptive stimulation of the left hand were studied in the absence of concomitant stimuli (Control), during suggestions of analgesia (SUGG, glove analgesia) and during cold pressor test used as a conditioning stimulus to the right hand (DNIC, water temperature=10–12°C) in the REAL session. Participants were submitted also to a SHAM session in which the DNIC water temperature was 30°C and the suggestions for analgesia were substituted with weather forecast information. Both suggestions and DNIC reduced pain significantly in all subjects; however, the percentage of reduction was significantly larger in highs (pain intensity=55% of the control condition) than in mediums (70%) and lows (80%) independently of the REAL/SHAM session and of the specific pain manipulation. Heart rate was not modulated consistently with pain experience. Findings indicate that both suggestions and DNIC influence pain experience as a function of hypnotizability and suggest that both sensory and cognitive mechanisms co-operate in DNIC induced analgesia

Systemic blood pressure alters cortical blood flow and neurovascular coupling during nociceptive processing in the primary somatosensory cortex of the rat

Inference on nociceptive and pain-related processes from functional magnetic resonance imaging is made with the assumption that the coupling of neuronal activity and cerebral hemodynamic changes is stable. However, since nociceptive stimulation is associated with increases in systemic arterial pressure, it is essential to determine whether this coupling remains the same during different levels of nociception and pain. The main objective of the present study was to compare the amplitude of local field potentials (LFP) and cerebral blood flow (CBF) changes in the primary somatosensory cortex during nociceptive electrical stimulation of the contralateral or ipsilateral forepaw in isoflurane-anesthetized rats, while manipulating mean arterial pressure (MAP). MAP changes induced by nociceptive stimulation were manipulated by transecting the spinal cord at the upper thoracic segments (T1–T2), which interrupts sympathetic pathways and prevents nociception-related MAP increases, while sensory pathways between the forepaws and the brain remain intact. Intensity-dependent increases in MAP and CBF were observed and these effects were abolished or significantly decreased after spinal transection (p<0.001 and p<0.05, respectively). In contrast, the intensity-dependent changes in LFP amplitude were decreased for the contralateral stimulation but increased for the ipsilateral stimulation after spinal transection (p<0.05). Thus, neurovascular coupling was altered differently by stimulus-induced MAP changes, depending on stimulus intensity and location. This demonstrates that CBF changes evoked by nociceptive processing do not always match neuronal activity, which may lead to inaccurate estimation of neuronal activity from hemodynamic changes. These results have important implications for neuroimaging of nociceptive and pain-related processes.

The cardiovascular status of isoflurane-anaesthetized horses with and without dexmedetomidine constant rate infusion evaluated at equivalent depths of anaesthesia

ObjectiveTo compare cardiac index and oxygen extraction at equivalent depths of anaesthesia between isoflurane-anaesthetized horses and horses anesthetized with isoflurane and dexmedetomidine CRI. Study designSequential, blinded, randomized, balanced, crossover study. AnimalsEight horses weighing a mean ± standard deviation of 478 ± 58 kg. MethodsHorses were premedicated with 0.03 mg kg−1 acepromazine intramuscularly (IM) and 8 μg kg−1 dexmedetomidine intravenously (IV). Anaesthesia was induced with 2.5 mg kg−1 ketamine and 0.1 mg kg−1 midazolam IV and maintained with isoflurane in oxygen and air. Horses were mechanically ventilated. Fractional concentration of end-tidal isoflurane (Fe’Iso) was stabilized at 1.7% with a CRI of 0.9% NaCl (IsoNaCl), or at 1.1% with 1.75 μg kg−1 hour−1 dexmedetomidine (IsoDex). Mean arterial blood pressure was maintained above 60 mmHg by dobutamine infusion. Following nociceptive electrical stimulation, Fe’Iso was stabilized at a 0.1% lower concentration and nociceptive stimulation was repeated. This procedure was continued until the horse moved. Fe’Iso values prior to the concentration at which movement occurred were considered to indicate equivalent depths of anaesthesia between treatments. Cardiac index and oxygen extraction were compared at equivalent depths of anaesthesia using a paired Student’s t-test. ResultsCardiac index differed between IsoNaCl at 61 ± 12 mL kg−1 minute−1 and IsoDex at 48 ± 10 mL kg−1 minute−1 (p = 0.047). In addition, oxygen extraction differed between IsoNaCl at 3.4 ± 0.8 mL kg−1 minute−1 and IsoDex at 4.5 ± 0.5 mL kg−1 minute−1 (p = 0.0042). Two horses receiving IsoNaCl were administered dobutamine at equivalent depths of anaesthesia (7.0 and 28.8 μg kg−1 hour−1, respectively). Conclusions and clinical relevanceCardiovascular function in horses receiving isoflurane and 1.75 μg kg−1 minute−1 dexmedetomidine is more compromised than in horses receiving a higher concentration of isoflurane and 0.9% NaCl CRI.

Inhibitory effects of heterotopic noxious counter-stimulation on perception and brain activity related to Aβ-fibre activation.

Heterotopic noxious counter-stimulation (HNCS) inhibits pain and pain processes through cerebral and cerebrospinal mechanisms. However, it is unclear whether HNCS inhibits non-nociceptive processes, which needs to be clarified for a better understanding of HNCS analgesia. The aim of this study was to examine the effects of HNCS on perception and scalp somatosensory evoked potentials (SEPs). Seventeen healthy volunteers participated in two counter-balanced sessions, including non-nociceptive (selective Aβ-fibre activation) or nociceptive electrical stimulation, combined with HNCS. HNCS was produced by a 20-min cold pressor test (left hand) adjusted individually to produce moderate pain (mean±SEM: 42.5±5.3 on a 0-100 scale, where 0 is no pain and 100 the worst pain imaginable). Non-nociceptive electrical stimulation was adjusted individually at 80% of pain threshold and produced a tactile sensation in every subject. Nociceptive electrical stimulation was adjusted individually at 120% of RIII-reflex threshold and produced moderate pain (45.3±4.5). Shock sensation was significantly decreased by HNCS compared with baseline for non-nociceptive (P<0.001) and nociceptive (P<0.001) stimulation. SEP peak-to-peak amplitude at Cz was significantly decreased by HNCS for non-nociceptive (P<0.01) and nociceptive (P<0.05) stimulation. These results indicate that perception and brain activity related to Aβ-fibre activation are inhibited by HNCS. The mechanisms of this effect remain to be investigated to clarify whether it involves inhibition of spinal wide-dynamic-range neurons by diffuse noxious inhibitory controls, supraspinal processes or both.

Blink reflex in subjects with different hypnotizability: New findings for an old debate

Hypnotizability is associated with attentional characteristics whose neurophysiological bases are still under debate. Aim of the study was the assessment of possible hypnotizability-related differences in blink reflex (BR) which has a nociceptive component, is sensitive to attentional-emotional traits and states and is modulated by the brain dopamine content.In 10 high (highs) and 10 low hypnotizable participants (lows) BR was induced by electrical nociceptive stimulation of the right supraorbital nerve in the absence (noW) and in the presence of a visual cue preceding the electrical stimulation by 0.1ms (W01) and by 1ms (W1). The studied variables were: the amplitude of BR components (R1, R2, R3), the amplitude of the quick change (TO) of heart rate (“turbulence”) induced by stimulation and its recovery slope (TS), the role of the Behavioral Inhibition/Activation System (BIS/BAS) in the variability BR and cardiac turbulence.Repeated measures ANOVA did not show any significant difference between highs and lows in blink reflex. TO indicated stimulation related HR increase in highs and decrease in lows, TS was larger in highs. BIS and BAS accounted for the warning effects on the BR amplitude and modulated the hypnotizability and warning effects on TO and TS. Findings do not support dopamine based hypnotizability-related attentional abilities. In contrast, they indicate that hypnotizability modulates the short-lasting cardiac response to electrical nociceptive stimulation.

Influences of smoking and caffeine consumption on trigeminal pain processing.

BackgroundMany human and animal studies have shown the influence of nicotine and caffeine on pain perception and processing. This study aims to investigate whether smoking or caffeine consumption influences trigeminal pain processing.MethodsSixty healthy subjects were investigated using simultaneous recordings of the nociceptive blink reflex (nBR) and pain related evoked potentials (PREP) following nociceptive electrical stimulation on both sides of the forehead (V1). Thirty subjects were investigated before and after smoking a cigarette, as well as before and after taking a tablet of 400 mg caffeine.ResultsAfter smoking PREP showed decreased N2 and P2 latencies indicating central facilitation at supraspinal (thalamic or cortical) level. PREP amplitudes were not changed. NBR showed a decreased area under the curve (AUC) indicating central inhibition at brainstem level. After caffeine intake no significant changes were observed comparing nBR and PREP results before consumption.ConclusionsSmoking influences trigeminal pain processing on supraspinal and brainstem level. In the investigated setting, caffeine consumption does not significantly alter trigeminal pain processing. This observation might help in the further understanding of the pathophysiology of pain disorders that are associated with excessive smoking habits such as cluster headache. Previous smoking has to be taken into account when performing electrophysiological studies to avoid bias of study results.

Effects of dexmedetomidine and xylazine on cardiovascular function during total intravenous anaesthesia with midazolam and ketamine and recovery quality and duration in horses

ObjectivesTo compare cardiovascular effects and recovery quality and duration of total intravenous anaesthesia (TIVA) with xylazine-ketamine-midazolam or dexmedetomidine-ketamine-midazolam. Study designProspective, randomized experimental cross-over trial. AnimalsEight adult warmblood horses. MethodsAfter sedation with acepromazine and either xylazine [0.5 mg kg−1, intravenously (IV)] or dexmedetomidine (3.5 μg kg−1 IV) anaesthesia was induced with ketamine and midazolam and maintained with a constant rate infusion (CRI) of xylazine (1 mg kg−1 hour−1) [XKM] or dexmedetomidine (7 μg kg−1 hour−1) [DKM] in combination with midazolam (0.1 mg kg−1 hour−1), and ketamine infusion (initially 3 mg kg−1 hour−1) for 120 minutes. Ketamine infusion rate was increased in response to positive reactions to electrical nociceptive stimulation performed every 30 minutes. Heart rate (HR), mean arterial blood pressure (MAP) and cardiac output ( Q˙t) were measured before treatment (baseline), after sedation (not Q˙t), and during anaesthesia. Xylazine, dexmedetomidine, midazolam and ketamine kinetics were calculated, from plasma drug concentrations. Twenty minutes after end of TIVA, flumazenil (0.01 mg kg−1 IV) was administered. Recovery quality and duration were assessed. Two-way analysis of variance with repeated measurements or Wilcoxon signed rank test as relevant were used to analyse data with an alpha of 5%. ResultsCompared to baseline, MAP did not change, while similar, but limited, decreases in HR and Q˙t were observed in both TIVA’s. Mean ketamine doses of 3.7 mg kg−1 hour−1 were required with both treatments. Plasma concentrations of dexmedetomidine and xylazine showed high intra- and inter-individual changes with elimination half-lifes of 46 ± 7 minutes and 64 ± 13 minutes, respectively. Recovery quality was good to excellent with mean duration of 37 ± 16 and 46 ± 21 minutes after stopping TIVA with XKM and DKM, respectively. Conclusions and clinical relevanceBoth drug combinations are suitable to maintain anaesthesia for two hours, with good cardiovascular and good to excellent recovery conditions.

Assessment of the wind-up phenomenon in the equine nociceptive trigeminal system

Repeated sub-threshold nociceptive electrical stimulation resulting in temporal summation of the limb nociceptive withdrawal reflex is a well-established non-invasive model to investigate the wind-up phenomenon in horses. Due to structural similarities of the trigeminal sensory nucleus to the dorsal horn of the spinal cord, temporal summation should be evoked by repeated transcutaneous electrical stimulation of trigeminal afferents. To evaluate this hypothesis repeated transcutaneous electrical stimulation was applied to the supraorbital and infraorbital nerves of 10 horses. Stimulation intensities varied between 0.5 and 1.3 times the trigemino-cervical reflex threshold defined for single stimulation. Evoked electromyographic activity of the orbicularis oculi, splenius and cleidomastoideus muscles was recorded and the signals analysed in the previously established epochs typical to the early and late component of the blink reflex and to the trigemino-cervical reflex. Behavioural reactions were evaluated with the aid of numerical rating scale.The nociceptive late component and the trigemino-cervical reflex were not elicited by sub-threshold intensity repeated transcutaneous electrical stimulation. Furthermore, the median reflex amplitude for the 10 horses showed a tendency to decline over the stimulation train so temporal summation of afferent trigeminal inputs could not be observed. Therefore, the modulation of trigeminal nociceptive processing attributable to repeated Aδ fibre stimulations seems to differ from spinal processing of similar inputs as it seems to have an inhibitory rather than facilitatory effect. Further evaluation is necessary to highlight the underlying mechanism.

A New Dimension in the Study of Human Functional Joint Instability

Functional joint instability is common after joint soft tissue injuries. We present in this report our pilot finding in a study of functional ankle instability. Although past studies have suggested multiple pathological factors for functional ankle instability, none of those factors has been confirmed in the past studies. More importantly, no known factor can provide an explanation for an ankle giving way phenomenon which is a key element in defining a functional ankle instability. In this pilot study, we tested five subjects with functional ankle instability using a dynamic ankle stretching device combined with nociceptive electrical stimulation. Three out of five subjects showed a drastic reaction in which they totally gave up their control of upright standing after their affected ankles were under the combined ankle stretch and nociceptive stimuli. Such drastic reaction was not observed in the same ankles under only the ankle stretch. There was no such drastic reaction in the unaffected ankle under either testing condition. This pilot finding indicates a possibility of a hyper-reactivity to unloading reaction in the ankles with functional ankle instability

Lateralized central facilitation of trigeminal nociception in cluster headache

To investigate whether central facilitation of trigeminal pain processing is part of the pathophysiology of cluster headache (CH). Sixty-six patients with CH (18 episodic CH inside bout, 28 episodic CH outside bout, 20 chronic CH) according to the International Classification of Headache Disorders-II classification, as well as 30 healthy controls, were investigated in a case-control study using simultaneous recordings of the nociceptive blink reflex (nBR) and pain-related evoked potentials (PREP) following nociceptive electrical stimulation on both sides of the forehead (V1). nBR latency ratio (headache side/nonheadache side) was decreased in all CH patients independent from CH subtype compared with healthy controls indicating central facilitation at brainstem level. Area under the curve ratio was increased in patients with episodic CH inside bout only. PREP showed decreased N2 latency ratio in patients with chronic CH indicating central facilitation at supraspinal (thalamic or cortical) level. Asymmetric facilitation of trigeminal nociceptive processing predominantly on brainstem level was detected in patients with CH. This alteration is most pronounced in the acute pain phase of the disease, but appears to persist in remission periods. Only chronic CH patients show additional changes of PREP prompting to supraspinal changes of pain processing related to the chronic state of disease in regard to neuronal plasticity, which exceeds changes observed in episodic CH.

A comparative study of cortical responses evoked by transcutaneous electrical vs CO 2 laser stimulation

Objectives A novel non-invasive method for nociceptive electrical stimulation of the skin has been recently introduced by using a planar concentric stimulating electrode (CE). We compared the cortical potentials induced by a CE vs laser stimulator in healthy subjects using a multichannel recording. Methods Cortical potentials were recorded in 11 healthy subjects by 54 scalp electrodes, stimulating the skin of the right hand and the right supra-orbital zone by the CE and laser stimulator settled two levels above the individual pain threshold. Results The latency difference between N1, N2, and P2 evoked by the CE vs laser stimulator was larger than the receptor activation time of 40 ms and larger following stimulation of the upper limbs than of the head. The amplitudes and topographic distribution of the cortical waves did not differ between the two stimulation types. Conclusions A-beta fibre co-activation may be induced by CE electrodes, as suggested by latency gaps. Nevertheless, CE-evoked potentials showed similarity in amplitude, morphology and topographic representation with laser-induced ones. Significance At present, CE-evoked potentials cannot be considered a reliable measure of nociceptive pathway function.

Electrically evoked nociceptive potentials for early detection of diabetic small‐fiber neuropathy

This study investigated the utility of pain-related evoked potentials (PREP's) elicited by a nociceptive electrical stimulation of the skin (= electrically evoked nociceptive potentials) in early detection of diabetic small-fiber neuropathy. We studied 36 'young' (19-35 years) and 24 'older' (36-65 years) healthy subjects as well as 35 patients (35-64 years) with diabetes and neuropathic symptoms and 22 patients (34-64 years) with diabetes without neuropathic symptoms. Only patients with normal standard nerve conduction testing were included. In patients with neuropathic symptoms, we found a significant increase in PREP latencies and decrease of amplitudes elicited from both, upper and lower limbs. In non-symptomatic diabetic patients, we observed PREP abnormalities from lower limbs only. These data suggest that the method of pain-related evoked potentials elicited by a nociceptive electrical stimulation of the skin may contribute to the early detection of diabetic sensory neuropathy.

Can Preoperative Electrical Nociceptive Stimulation Predict Acute Pain After Groin Herniotomy?

Preoperative identification of patients at risk for high-intensity postoperative pain may be used to predict patients at risk for development of a persistent pain state and allocate patients to more intensive specific pain therapy. Preoperative pain threshold to electrocutaneus stimulation has recently been shown to correlate to acute postoperative pain after cesarean section, but the findings have not been confirmed in larger studies or other procedures. Preoperative electrical pain detection threshold and pain tolerance were assessed in patients undergoing a primary unilateral groin hernia repair. The correlation between the pain data for electrical stimulation was compared with the postoperative pain during the first week in 165 patients, whereof 3 were excluded. Preoperative electrical pain detection threshold and electrical pain tolerance threshold did not correlate to postoperative pain (rho = -0.13, P = .09, and rho = -1.2, P = .4, respectively. Although preoperative electrical nociceptive stimulation may predict patients at risk of high-intensity acute pain after other surgical procedures, this was not the case in groin hernia repair patients receiving concomitant treatment with acetaminophen and ibuprofen.