Contact Heat Evoked Potentials Research Articles

Contact heat evoked potentials and habituation measured interictally in migraineurs.

BackgroundA lack of habituation of different evoked potential modalities in migraine patients in-between attacks has been suggested.MethodsThis study investigates cortical response after painful stimuli evaluated by contact heat evoked potentials (CHEPs) and quantitative sensory testing (QST) during the migraine-free interval. We enrolled 22 migraine patients and 22 healthy subjects.ResultsCortical potentials after contact heat stimulation of the cheeks and the volar forearm at a temperature of 51°C showed significantly reduced A-δ-amplitudes in patients and healthy controls. When the subjects’ attention was drawn to an arithmetic task, a partial lack of habituation of amplitude could be seen in migraine patients. QST did not show any difference between migraineurs and controls.ConclusionOur findings can be primarily deemed to demonstrate that patients and healthy controls show significantly lower amplitudes while performing the calculation task. Without performing the calculation task we could not show the expected lack of habituation in migraineurs. Yet, while performing the calculation task our results partly suggest that hypothesis.

71. Functional reorganization of brain networks in patients with painful chronic pancreatitis

To investigate the organization of brain networks involved in nociceptive processing in patients with painful CP. Contact heat-evoked potentials (CHEPs) were recorded in 15 CP patients and in 15 healthy volunteers. The upper abdominal area (sharing spinal innervation with the pancreatic gland) was used as a proxy of ‘pancreatic stimulation’, while stimulation of the right forearm was used as a control. The brain source organization of CHEPs components were analysed. After abdominal stimulation, brain source analysis revealed abnormalities in the cingulate/operculo-insular network. A posterior shift of the operculo-insular source ( p = 0.004) and an anterior shift of the cingulate source ( p < 0.001) were seen in CP patients, along with a decreased strength of the cingulate source ( p = 0.01). The operculo-insular shift was positively correlated with the severity of pain ( r = 0.61; p = 0.03). CP patients showed abnormal cerebral processing after stimulation of the upper abdominal area. These changes correlated with the severity of pain, probably reflecting maladaptive neuroplastic changes.

The role of neurophysiology.

The role of neurophysiology.

EHMTI-0306. Contact heat-evoked potentials (CHEPS) in healthy subjects and patients with episodic or chronic migraine

Habituation and 1st block amplitude of sensory evoked potentials are commonly reduced in episodic migraine between attacks, whereas in chronic migraine 1st block amplitude is increased and habituation tends to normalize like during an attack. The aim of our study was to compare Contact Heat-Evoked Potentials (CHEPs) in healthy subjects (HS), episodic migraine without aura (EM) and chronic migraine (CM).

P144: Contact heat evoked potentials (CHEPs) in healthy subjects – no laterality effect

P144: Contact heat evoked potentials (CHEPs) in healthy subjects – no laterality effect

Contact heat-evoked potentials as a useful means in patients with Guillain–Barré syndrome

Few objective methods have been utilized to identify the small myelinated fiber impairment causing neuropathic pain in Guillain-Barré syndrome (GBS). In this study, contact heat-evoked potentials (CHEPs) were applied to study the nociceptive pathway in GBS. Sixty GBS patients and fifty healthy controls were enrolled. The 60 GBS patients were divided into two subgroups presenting with or without subjective lower limb paresthesia (21/39). CHEPs were recorded at Cz and Pz with a peak thermal stimuli of 47 °C applied to the skin of the leg above the internal malleolus (AIM) and of the waist at the anterior superior iliac spine (ASIS) level. The N2 latency and N2-P2 amplitude of CHEPs were compared. When the skin of the leg AIM was stimulated, the N2 latency was significantly postponed (425.23 ± 28.66 vs. 402.30 ± 19.48 ms, P < 0.05) and the N2-P2 amplitude significantly decreased in GBS patients as compared to controls (32.71 ± 7.49 vs. 42.77 ± 8.71 μV, P < 0.05). Slower nerve conduction velocity was observed in GBS patients (11.84 ± 1.45 vs. 13.28 ± 0.66 ms, P < 0.05). However, no differences in N2 latency or N2-P2 amplitude were detected between the two subgroups of GBS patients with or without subjective lower limb paresthesia (P all >0.05). Moreover, there were no differences in N2 latency and N2-P2 amplitude among different groups when the waist was stimulated at the ASIS level. Our study suggested that CHEPs could be utilized as an objective and non-invasive tool to detect small myelinated fiber damage in GBS patients, especially for those without subjective paresthesia.

Heterotopic and homotopic nociceptive conditioning stimulation: Distinct effects of pain modulation

Within an area, habituation and sensitization represent well-established modulatory effects to repetitive noxious input. Less is known regarding the nociceptive conditioning effects between body sites - i.e., how stimulating one site may affect another. Therefore, we investigated the effects of nociceptive stimulation of anatomically distinct locations (shoulder and hand) on pain rating and evoked potentials (i.e., contact heat-evoked potentials). The effect of stimulation order was assessed in eight healthy subjects. The shoulder was examined before the hand or the hand before the shoulder. All subjects underwent both conditions (shoulder before hand and hand before shoulder) on separate days. In an additional 30 subjects (total n = 38), between retesting the shoulder or the hand, conditioning stimulation in the respective other location (i.e., hand or shoulder) was applied. Both analyses focused upon changes in the magnitude of evoked pain responses in relation to the respective area being conditioned by heterotopic stimulation. When the shoulder was stimulated before the hand, N2P2 amplitude was significantly reduced. In contrast, stimulating the hand before the shoulder resulted in significant response increments (shorter N2 latency). Additionally, conditioning stimulation of the hand resulted in increased pain rating to shoulder stimulation. Overall, these findings indicate that response modulation to noxious contact heat stimulation depends upon conditioning stimulus location. These effects represent changes beyond conventional habituation due to repeated stimulation in the same area.

Functional reorganization of brain networks in patients with painful chronic pancreatitis

The underlying pain mechanisms of chronic pancreatitis (CP) are incompletely understood, but recent research points to involvement of pathological central nervous system processing involving pain-relevant brain areas. We investigated the organization and connectivity of brain networks involved in nociceptive processing in patients with painful CP. Contact heat-evoked potentials (CHEPs) were recorded in 15 patients with CP and in 15 healthy volunteers. The upper abdominal area (sharing spinal innervation with the pancreatic gland) was used as a proxy of 'pancreatic stimulation', while stimulation of a heterologous region remote to the pancreas (right forearm) was used as a control. Subjective pain scores were assessed by visual analogue scale. The brain source organization and connectivity of CHEPs components were analysed. After pancreatic area stimulation, brain source analysis revealed abnormalities in the cingulate/operculo-insular network. A posterior shift of the operculo-insular source (p = 0.004) and an anterior shift of the cingulate source (p < 0.001) were seen in CP patients, along with a decreased strength of the cingulate source (p = 0.01). The operculo-insular shift was positively correlated with the severity of patient clinical pain score (r = 0.61; p = 0.03). No differences in CHEPs characteristics or source localizations were seen following stimulation of the right forearm. CP patients showed abnormal cerebral processing after stimulation of the upper abdominal area. These changes correlated to the severity of pain the patient was experiencing. Since the upper abdominal area shares spinal innervation with the pancreatic gland, these findings likely reflect maladaptive neuroplastic changes, which are characteristic of CP.

Differences in contact heat-evoked potentials (CHEPs) between healthy subjects and patients with episodic or chronic migraine

Differences in contact heat-evoked potentials (CHEPs) between healthy subjects and patients with episodic or chronic migraine

Assessment of Spinothalamic Tract Function Beyond Pinprick in Spinal Cord Lesions

Background. Although a mainstay of clinical sensory examination after damage in the spinal cord, pinprick sensation represents only one afferent modality conveyed in the spinothalamic tract. As an objective outcome, complementary information regarding spinothalamic tract conduction may be elucidated by measuring contact heat evoked potentials (CHEPs). Objective. To assess the value of CHEPs to measure spinothalamic tract function in spinal cord disorders compared with pinprick scoring. Methods. CHEPs were examined using a standard (35°C) and increased baseline (42°C) contact heat temperature. Pinprick sensation was rated as absent, impaired, or normal according to the International Standards for the Neurological Classification of Spinal Cord Injury. Results. Fifty-nine dermatomes above, at, and below the sensory level of impairment were analyzed in 37 patients with defined spinal cord disorder. In dermatomes with absent or impaired pinprick sensation, CHEPs using a standard baseline temperature were mainly abolished (3/16 and 8/35, respectively). However, when applying an increased baseline temperature, CHEPs became recordable (absent: 11/16; impaired: 31/35). Furthermore, CHEPs with increased baseline temperature allowed discerning between dermatomes with absent, impaired, and normal pinprick sensation when using an objective measure (ie, N2P2 amplitude). In contrast, the pain perception to contact heat stimulation was independent of pinprick scores. Conclusion. Applying pinprick testing is of limited sensitivity to assess spinothalamic tract function in spinal cord disorders. The application of CHEPs (using standard and increased baseline temperatures) as an objective readout provides complementary information of spinothalamic tract functional integrity beyond pinprick testing.

Modulation of thermal somatosensory thresholds within local and remote spinal dermatomes following cervical repetitive magnetic stimulation

Background: Repetitive magnetic stimulation (rMS) modulates thermal somatosensory function at both low (0.2–1.0Hz) and high (5.0–20.0Hz) frequencies within the conditioned dermatome. However the effects of 1Hz and 20Hz cervical (C6-C7) rMS on thermosensory thresholds and contact heat evoked potentials (CHEPs) tested within local and remote spinal dermatomes are not known. Methods: Thirty healthy subjects participated in the study. Warm and cold detection threshold, heat and cold pain thresholds, and Cz/Fz CHEPs were evaluated within the C6, T10 and extrasegmental V3 control dermatome, before and after random assignment of subjects to sham, 1 or 20Hz C6-C7 rMS. Results: Following both 1 and 20Hz cervical rMS, warm detection threshold increased within the local C6 dermatome. Furthermore 1Hz cervical rMS increased warm detection threshold within the remote T10 dermatome, but not within the V3-trigeminal control area. Cervical rMS failed to modulate cold detection threshold, heat and cold pain threshold or Cz/Fz CHEP amplitude from the dermatomal test sites. Conclusion: Both 1 and 20Hz cervical rMS modulated warm detection threshold within the locally conditioned C6 dermatome. The concomitant increase in warm detection threshold within the T10 dermatome following 1Hz rMS provides evidence for remote neuromodulation of thermosensory function via intraspinal control mechanisms.

Differences in Spinothalamic Function of Cervical and Thoracic Dermatomes

After spinal cord injury, contact heat evoked potentials (CHEPs) may represent a means to refine the clinical assessment of sensory function from each spinal cord segment by quantifying nociception, including conduction along the spinothalamic tract. The influence of stimulation site (i.e., dermatomes) on CHEPs and thermal thresholds in 19 healthy subjects (mean age, 45.2 ± 18.3 years) divided into 2 age classes (younger subjects, n = 10; mean age, 28.8 ± 5.2 years; older subjects, n = 9; mean age, 63.4 ± 3.4 years) at 5 different dermatomes (C4, C5, C6, C8, and T4) was assessed. In terms of distance from the body midline (i.e., spinal cord entry), there was a reduction in CHEP amplitudes from proximal (C4 and T4) to distal (C6 and C8) dermatomes with a corresponding reduction in nociceptive perception (i.e., pain threshold and rating). Within primary and secondary cortical sensory areas, including areas associated with affective noxious processing, the cortical source density analysis showed a similar current density distribution between C4 and C8 dermatomes but consistent higher current densities for C4. The study supports CHEPs as a feasible tool for assessing discrete dermatomes corresponding to spinal cord segments. The results suggest that the proximodistal pattern in the intensity of perceived pain and CHEP amplitudes is likely attributable to the distribution of heat nociceptors and the increase in conduction distance from proximal to distal dermatomes. The present findings emphasize on the importance that if patients are assessed segment by segment, the underlying topographical differences need to be accounted for.

Differential Effects of a 5% lidocaine medicated patch in peripheral nerve injury

We examined the effect of topical lidocaine on the function of small and large fibers in patients with peripheral neuropathic pain due to traumatic or postoperative nerve injury. In an open-label study, 24 patients were treated with a 5% lidocaine patch for up to 12 weeks. We recorded contact heat evoked potentials (CHEPs) and performed quantitative sensory testing (QST) before and after treatment with the contralateral side as control. Twenty-one patients (mean age 47.6 ± 13.5 years) completed the study. Lidocaine increased cold pain threshold (P = 0.04) and reduced CHEP amplitude (P = 0.007) with no effect on other QST parameters. Patients responding to treatment had less cold detection deficit on the affected side and had a larger increase in cold pain detection threshold following treatment than nonresponders. Controlled trials are warranted to further understand the mechanisms mediating the effects of topical lidocaine.

Clinical and neurophysiologic profiles of sensory neuron disease

To explore the clinical and electrophysiological characteristics of sensory neuron disease (SND). The clinical and electrophysiological characteristics were analyzed from November 2007 to November 2012 in 57 patients with sensory neuron disease and another 95 with sensory polyneuropathy. Nerve conduction studies of median nerve, ulnar nerve, tibial nerve, peroneal nerve and sural nerve and electromyogram (EMG) of bulbar, cervical, thoracic and lumbosacral region, somatosensory evoked potential (SEP) and contact heat evoked potential (CHEP) were performed. The amplitude of sensory nerve action potential (SNAP) decreased in 50 SND patients and disappeared in another 7. The parameters of SEP and CHEP were abnormal. The amplitude of SNAP was lower in median and ulnar nerve than in sural nerve ((0.6 ± 0.2) µV, (0.7 ± 0.2) µV vs (1.5 ± 0.5) µV; t = 2.42, 2.38; P < 0.05). The latencies of SEPs were longer in SND patients than in those with sensory polyneuropathy (t = 1.99, 1.99, 2.00, 2.07, 1.99; 1.98, 1.99, 2.02, 1.98, 1.99; P < 0.05).Comparing with those with sensory polyneuropathy, the latencies of CHEP were longer in SND patients when the stimuli was applied at hand dorsum, proximal volar forearm and anticus tibialis (t = 2.01, 2.00, 2.02; P < 0.05). No difference existed in latencies between 2 groups when the stimuli was at the levels of C7 and T12 (t = 0.97, 0.68; P > 0.05). Sensory neuron diseases usually present with sensory symptoms and ataxia. The amplitude of SNAP decreases or disappears especially in upper extremities. Both SEP and CHEP are abnormal.

Improved diagnosis of spinal cord disorders with contact heat evoked potentials

To evaluate the sensitivity of contact heat evoked potentials (CHEPs) compared with dermatomal somatosensory evoked potentials (dSSEPs) and clinical sensory testing in myelopathic spinal cord disorders (SCDs). In a prospective cohort study, light-touch (LT) and pinprick (PP) testing was complemented by dermatomal CHEPs and dSSEPs in patients with a confirmed SCD as defined by MRI. Patients with different etiologies (i.e., traumatic and nontraumatic) and varying degrees of spinal cord damage (i.e., completeness) were included. SCD was distinguished into 3 categories according to MRI pattern and neurologic examination: a) complete, b) incomplete-diffuse, and c) central or anterior cord damage. Seventy-five patients were included (complete n = 7, incomplete-diffuse n = 33, central/anterior n = 35). In total, 319 dermatomes were tested with combined CHEPs and dSSEPs. CHEPs, dSSEPs, and clinical sensory testing were comparably sensitive to detect the myelopathy in complete (CHEPs 100%, dSSEPs 91%, PP and LT 82%) and incomplete-diffuse (CHEPs 92%, dSSEPs and PP 86%, LT 81%, p > 0.05 for all comparisons) cord damage. In central/anterior cord damage, CHEPs showed a significantly higher sensitivity than dSSEPs (89% compared with 24%, p < 0.001) and clinical sensory testing (PP 62%, LT 57%, p < 0.05). A subclinical sensory impairment was detected more frequently by CHEPs than dSSEPs (60% compared with 29%, p = 0.001). Assessment of spinothalamic pathways with CHEPs is reliable and revealed the highest sensitivity in all SCDs. Specifically in incomplete lesions that spare dorsal pathways, CHEPs are sensitive to complement the clinical diagnosis.

Effects of Propofol, Sevoflurane, Remifentanil, and (S)-Ketamine in Subanesthetic Concentrations on Visceral and Somatosensory Pain–evoked Potentials

Although electroencephalographic parameters and auditory evoked potentials (AEP) reflect the hypnotic component of anesthesia, there is currently no specific and mechanism-based monitoring tool for anesthesia-induced blockade of nociceptive inputs. The aim of this study was to assess visceral pain-evoked potentials (VPEP) and contact heat-evoked potentials (CHEP) as electroencephalographic indicators of drug-induced changes of visceral and somatosensory pain. Additionally, AEP and electroencephalographic permutation entropy were used to evaluate sedative components of the applied drugs. In a study enrolling 60 volunteers, VPEP, CHEP (amplitude N2-P1), and AEP (latency Nb, amplitude Pa-Nb) were recorded without drug application and at two subanesthetic concentration levels of propofol, sevoflurane, remifentanil, or (s)-ketamine. Drug-induced changes of evoked potentials were analyzed. VPEP were generated by electric stimuli using bipolar electrodes positioned in the distal esophagus. For CHEP, heat pulses were given to the medial aspect of the right forearm using a CHEP stimulator. In addition to AEP, electroencephalographic permutation entropy was used to indicate level of sedation. With increasing concentrations of propofol, sevoflurane, remifentanil, and (s)-ketamine, VPEP and CHEP N2-P1 amplitudes decreased. AEP and electroencephalographic permutation entropy showed neither clinically relevant nor statistically significant suppression of cortical activity during drug application. Decreasing VPEP and CHEP amplitudes under subanesthetic concentrations of propofol, sevoflurane, remifentanil, and (s)-ketamine indicate suppressive drug effects. These effects seem to be specific for analgesia.

Neurophysiology and Intraoperative Nociception

Neurophysiology and Intraoperative Nociception

Effect of intrathecal baclofen on evoked pain perception: An evoked potentials and quantitative thermal testing study

Somatic antinociceptive effects of baclofen have been demonstrated in animal models. We hypothesized that if enhanced thermal or pain sensitivity is produced by loss of gamma-aminobutyric acid (GABA)-ergic tone in the central nervous system, spinal administration of GABA agonists might be predicted to be effective in thermal and/or pain perception changes and pain-related evoked potentials in candidates for intrathecal baclofen (ITB) treatment. Eleven patients with severe spinal cord injury (SCI) who suffered from severe spasticity were evaluated during a 50-μg ITB bolus test. Warm and heat pain thresholds, evoked heat pain perception, and contact heat-evoked potentials (CHEPs) were determined above SCI level from the right and left sides. Nine age- and gender-matched healthy volunteers undergoing repeat testing without any placebo injection served as control group. In patients, heat pain perception threshold increased, and evoked pain perception and amplitude of CHEPs decreased significantly after ITB bolus application in comparison with baseline (p < 0.005), with no change in warm perception threshold. In controls, no significant changes were observed in repeat testing over time. Our findings indicate that ITB modulates heat pain perception threshold, evoked heat pain perception and heat pain-related evoked potentials without inducing warm perception threshold changes in SCI patients. This phenomenon should be taken into account in the clinical evaluation and management of pain in patients receiving baclofen.

Improving the acquisition of nociceptive evoked potentials without causing more pain

Following nociceptive heat or laser stimulation, an early contralateral and later vertex potential can be recorded. Although more indicative of the nociceptive input, the acquisition of the contralateral N1 after contact heat stimulation (contact heat-evoked potentials [CHEPs]) remains difficult. An advantage of contact heat is that the baseline skin temperature preceding peak stimulation can be controlled. Increasing the baseline temperature may represent a novel strategy to improve the acquisition of CHEPs without resulting in more subjective pain to stimulation. A study was undertaken in 23 healthy subjects to examine the effects of increasing the baseline temperature but not the perceived intensity of contact heat stimulation. A combined standard averaging and single-trial analysis was performed to disclose how changes in averaged waveforms related to latency jitter and individual trial amplitudes. By increasing the baseline temperature, the acquisition of N1 was improved among subjects with a low-amplitude response (greater than −4μV) following 35°C baseline temperature stimulation (P<.05). Based on standard averaging, N2/P2 amplitudes were also significantly increased with and without an accompanying change in the rating of perceived pain when the baseline temperature was increased (P<.05). In contrast, automated single-trial averaging revealed no significant difference in N2 amplitude when the baseline temperature was increased to 42°C and the peak temperature reduced. These findings suggest that 2 mechanisms underlie the improved acquisition of CHEPs: increased synchronization of afferent volley, yielding larger-amplitude evoked potentials in response to the same rating of intensity; and reduced inter-trial variability.

The effect of nerve compression and capsaicin on contact heat-evoked potentials related to Aδ- and C-fibers

Brief noxious heat stimuli activate Aδ- and C-fibers and allow contact heat-evoked potentials (CHEPs) to be recorded from the scalp. Under normal conditions, only late responses related to Aδ-fibers can be recorded. This study aimed to demonstrate C-fiber responses to contact heat stimuli. A preferential A-fiber compression blockade of the superficial radial nerve was applied in 22 healthy subjects. Quality and intensity of heat-evoked pain and CHEPs were examined at baseline, during nerve compression, and during nerve compression with simultaneous application of topical capsaicin (5%). During the A-fiber block, three subjects had CHEPs with latencies below 400ms, eight subjects within 400–800ms and six subjects (29%) later than 800ms. Pain intensity to contact heat stimuli after compression was reduced and fewer subjects reported the heat stimuli as stinging. Following nerve compression and capsaicin application, ultralate CHEPs with latencies >800ms could be recorded in 13 subjects (62%), pain intensity to the contact heat stimuli was increased and the warm/hot-burning pain quality became more intense. The main results of our study are the demonstration of ultralate C-fiber-related CHEPs following A-fiber blockade in 29% of healthy subjects increasing to 62% when the blockade was combined with capsaicin. After blockade of Aδ-fibers we recorded responses with latencies in the range between the latencies of Aδ- and C-fibers suggesting release of Aδ-fibers with slower conduction velocity than normally recorded with CHEPs.