Conventional Somatosensory Evoked Potentials Research Articles

Cortical somatosensory processing after botulinum toxin therapy in post-stroke spasticity.

In dystonic and spastic movement disorders, abnormalities of motor control and somatosensory processing as well as cortical modulations associated with clinical improvement after botulinum toxin A (BoNT-A) treatment have been reported, but electrophysiological evidence remains controversial. In the present observational study, we aimed to uncover central correlates of post-stroke spasticity (PSS) and BoNT-A-related changes in the sensorimotor cortex by investigating the cortical components of somatosensory evoked potentials (SEPs). Thirty-one chronic stroke patients with PSS of the upper limb were treated with BoNT-A application into the affected muscles and physiotherapy. Clinical and electrophysiological evaluations were performed just before BoNT-A application (W0), then 4 weeks (W4) and 11 weeks (W11) later. PSS was evaluated with the modified Ashworth scale (MAS). Median nerve SEPs were examined in both upper limbs with subsequent statistical analysis of the peak-to-peak amplitudes of precentral P22/N30 and postcentral N20/P23 components. At baseline (W0), postcentral SEPs were significantly lower over the affected cortex. At follow up, cortical SEPs did not show any significant changes attributable to BoNT-A and/or physiotherapy, despite clear clinical improvement. Our results imply that conventional SEPs are of limited value in evaluating cortical changes after BoNT-A treatment and further studies are needed to elucidate its central actions.

Combination of Single- and Paired-Pulse Somatosensory Evoked Potentials in Ischemic Monitoring: Preliminary Investigation in Carotid Endarterectomy.

IntroductionSevere ischemia induces cerebral excitability imbalance before completion of infarct. To investigate the clinical availability of this imbalance with ischemic monitoring, paired-pulse somatosensory evoked potentials (SEPs) were performed in conjunction with conventional SEPs during carotid endarterectomy.MethodsFor carotid endarterectomy patients with hemodynamic deficits of the middle cerebral artery area (n = 34), the excitability imbalances (Q) were measured by paired-pulse SEPs, wherein the second response (A2) was divided by the first (A1; Q = A2/A1). Regional cerebral saturation (rSO2) was also measured. Occlusion was performed twice using shunting.ResultsEach carotid occlusion induced a significant decrease in mean A1 and rSO2, and an increase in mean Q values (p < 0.001), which returned to the baseline level after occlusion. While neuronal imbalances were mostly transient, persistently increased Q values were observed in four cases (11.8%), all indicating postoperative abnormalities in diffusion-weighted magnetic resonance imaging (100%). Meanwhile, A1 detected the postoperative abnormality in only one case (25%). Preoperative Q values at the time of surgery were significantly higher in symptomatic patients having the upper limb deficits than those without (p < 0.01), indicating persistent or permanent imbalances.ConclusionPaired-pulse SEPs reliably identified transient, persistent or permanent neuronal imbalances, depending on the ischemic severity. These preliminary results indicated that paired-pulse SEPs, in combination with conventional SEPs (A1), may offer better ischemic monitoring.

A Novel Electrophysiological Method in the Diagnosis of Pudendal Neuropathy: Position-related Changes in Pudendal Sensory Evoked Potentials

To examine the diagnostic value of pudendal somatosensory evoked potentials (SEPs) in pudendal nerve entrapment (PNE) neuropathy by stimulating the 2 sides separately after provocation by a standard sitting position. Routine pudendal SEPs performed in the supine position with bilateral simultaneous stimulation may fail to show the abnormality because the complaints of PNE appear or worsen in the sitting position. Forty-nine patients with PNE and 16 controls were included. SEP recordings were performed by stimulating the dorsal nerve of penis or clitoris on either side. The recordings were performed at the initial supine position, at the beginning and end of the provocation by sitting position, and at the second supine position. Amplitude loss in the SEP responses after prolonged sitting was significantly more pronounced on the symptomatic sides of the patients. Approximately 45% decrease in the SEP amplitude or an amplitude value less than 1.5 µV at the end of sitting are the parameters to be used with high selectivity. The dynamic pudendal SEP study described herein seems to be more helpful in PNE diagnosis than in conventional SEPs.

ID 10 – A novel electrophysiological method in the diagnosis of pudendal neuropathy: Position related changes in pudendal sensory evoked potentials

Pudendal nerve entrapment (PNE) is a common cause of resistant and disabling perineal pain. Although it is diagnosed clinically, neurophysiological tests are used for the diagnosis. Since the complaints worsen in the sitting position, routine pudendal somatosensory evoked potentials (SEP) performed in the supine position with midline stimulation may fail to show the PNE. We hypothesized that diagnostic value of SEP can be increased by stimulating the right and left sides separately along with provocation by maintained sitting position (dynamic SEP). Forty-nine patients with PNE and 16 healthy controls were included. SEP recordings were performed by stimulating the dorsal nerve of penis/clitoris on either side. The recordings were performed at the first supine position, at the beginning and end of a standardized sitting posture and at the second supine position. Regarding the patients with recordable responses, we might suggest that approximately 45% decrease in SEP amplitude or an amplitude value less than 1.5 mV at the termination of the sitting position (and their reversal with switching to the supine position again) are the parameters to be used with high selectivity. The dynamic pudendal SEP study described herein seems to be more valuable in PNE diagnosis than conventional SEPs.

Dissociated behavior of low-frequency responses and high-frequency oscillations after systemic morphine administration in conscious rats

It has been proposed that high-frequency oscillations (HFOs) and underlying conventional somatosensory-evoked potentials (SEPs) have different brain origins. To further explore the neural mechanism of HFOs, we recorded the SEPs responding to high-intensity electrical stimulation applied to the hind paw of conscious, freely moving rats. We also investigated the effect of systemic morphine on HFOs and the conventional SEPs. HFOs after high-intensity electrical stimulation showed a widespread distribution in frontal and temporal regions of the brain. The amplitude of HFOs was significantly decreased by systemic morphine, whereas the primary conventional SEP components remained unaffected. The different changes in HFOs and primary SEP components after systemic morphine administration provided further evidence for the hypothesis that HFOs and underlying conventional SEP components have different origins.

Dermatomal laser-evoked potentials: a diagnostic approach to the dorsal root. Norm data in healthy volunteers and changes in patients with radiculopathy

We conducted a cross-sectional study of 40 radiculopathy patients in comparison with norm data from healthy subjects using a new electrophysiological method. Early manifestations of dorsal root impairment escape objective diagnosis by conventional somatosensory-evoked potentials due to the overlapping innervation of the affected dermatome by thickly myelinated mechanoreceptive afferents projecting to adjacent intact roots. Evidence suggested less intersegmental overlap for thermonociceptive afferents rendering laser-evoked potentials (LEP) sensitive to monosegmental dorsal root damage. Therefore we used this new method to study acute manifestations of monosegmental dorsal root pathology. Dorsal root function was tested in 12 healthy subjects and 40 sciatica patients by intraindividual interside comparison. Mechanosensibility and thermosensibility were clinically investigated. LEP were induced by moderately painful laser stimuli. The LEP were evaluated by amplitude and latency of the averaged electroencephalogram. Normal interside differences of LEP for amplitude were +/-22% (lower limb) and +/-35% (upper limb) and +/-15 to +/-16% for latency. Twenty-six patients (65%) showed significant LEP changes, mainly amplitude decreases. Six of these patients exhibited latency prolongations. Clinical testing yielded more frequent pathological results for pain compared to mechanosensibility. The study confirmed our preliminary evidence of LEP sensitivity to objectively document dorsal root impairment in patients suffering from acute monosegmental radiculopathy. This result opens the perspective of electrophysiologically differentiating the presence or absence of dorsal root pathology in patients with similar clinical symptoms but possibly different prognoses, which require different therapies.

Dissociated changes of somatosensory evoked low-frequency scalp responses and 600 Hz bursts after single-dose administration of lorazepam

Electrical stimulation of upper limb nerves allows one to record two types of scalp responses, that is conventional low-frequency somatosensory evoked potentials (SEPs), and bursts of high-frequency (about 600 Hz) wavelets. To further clarify the functional meaning of both types of responses, we investigated whether changes of GABAergic drive could cause significant modifications of conventional as well as high-frequency SEPs. We recorded median nerve SEPs from six healthy volunteers before and after a single oral administration of lorazepam. In order to explain scalp SEP distribution before and after lorazepam administration, we performed the brain electrical source analysis of raw data. After lorazepam administration, conventional scalp SEPs showed a significant amplitude decrease of all cortical components including the primary N20/P20 response, while the subcortical P14 response remained substantially unchanged. Similarly, dipolar analysis showed a significant strength decrease of all cortical dipoles, whereas the strength of both subcortical dipoles (possibly located at the level of the brainstem and thalamus, respectively) remained unchanged. By contrast, no significant changes of high-frequency SEPs were induced by drug intake. Therefore, our findings suggest that the inhibitory effect induced by lorazepam mainly affects intracortical circuitry. Tonic increase of the inhibitory drive, possibly mediated by GABAA receptors, can account for the reduced activity of first order deep spiny neurons generating the primary N20/P20. Conversely, intrinsic firing properties of the cell population generating high-frequency SEP responses are unaffected by the increase of GABAergic drive. This finding lends further substance to the hypothesis that conventional and high-frequency SEPs are generated by different cell populations.

Contribution of GABAergic cortical circuitry in shaping somatosensory evoked scalp responses: specific changes after single-dose administration of tiagabine

Objectives: To determine whether conventional as well as high-frequency somatosensory evoked potentials (SEPs) to upper limb stimulation are influenced by GABAergic intracortical circuitry.Methods: We recorded SEPs from 6 healthy volunteers before and after a single-oral administration of tiagabine. Conventional low-frequency SEPs have been obtained after stimulation of the median nerve, as well as after stimulation of the first phalanx of the thumb, which selectively involves cutaneous finger inputs. Median nerve SEPs have been further analyzed after digital narrow-bandpass filtering, to selectively examine high-frequency responses. Lastly, in order to explain scalp SEP distribution before and after tiagabine administration, we performed the brain electrical source analysis (BESA) of raw data.Results: After tiagabine administration, conventional scalp SEPs showed a significant amplitude increase of parietal P24, frontal N24 and central P22 components. Similarly, BESA showed a significant strength increase of the second peak of activation of the first two perirolandic dipoles, which are likely to correspond to the N24/P24 and P22 generators. By contrast, no significant changes of high-frequency SEPs were induced by drug intake.Conclusions: Our findings support the view that both N24/P24 and P22 SEP components are probably generated by deep spiny cell hyperpolarization, which is strongly increased by inhibitory inputs from GABAergic interneurons. By considering the clear influence of inhibitory circuitry in shaping these SEP components, conventional scalp SEP recording could be useful in the functional assessment of the somatosensory cortex in different physiological and pathological conditions. By contrast, intrinsic firing properties of the cell population generating high-frequency SEP responses are unaffected by the increase of recurrent GABAergic inhibition.

Somatosensory evoked potential recovery in myotonic dystrophy

Objective: To evaluate recovery functions of the sensory cortex using somatosensory evoked potentials (SEPs) elicited by paired stimuli of the median nerve in patients with myotonic dystrophy (MD). Subjects/methods: Twelve MD patients were enrolled in the present investigation. Five patients with facioscapulohumeral muscular dystrophy (FSH) and 12 healthy volunteers were studied as control groups. SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Single pulse or paired-pulse stimuli at various interstimulus intervals (ISIs) (10, 20, 40, 60, 80, 100, 150, 200 and 300 ms) were given. Recovery functions of N9, N20onset-N20peak, N20–P25 and P25–N33 components were studied. Results: Conventional SEPs to a single stimulus were normal in the latency and amplitude in all the patients. Recovery functions of both N9 and N20o–N20p components were normal in the patients. In contrast, in MD patients, disinhibited or hyperexcitable recovery pattern was observed in recovery curves of the N20–P25 or P25–N33 components, whereas those were normal in FSH patients. Conclusions: Disinhibited cortical excitability (or hyperexcitability) is present in the sensory cortex in patients with myotonic dystrophy. This may reflect cortical pathology or functional alteration of the sensory cortex in MD.

Pain-Related somatosensory evoked potentials.

The authors reviewed basic and clinical reports of pain-related somatosensory evoked potentials (SSEP) after high-intensity electrical stimulation [pain SSEP(E)] and painful laser stimulation [pain SSEP(L)]. The conduction velocity of peripheral nerves for both pain SSEP(E) and pain SSEP(L) is approximately 10 to 15 m/second, in a range of Adelta fibers. The generator sources are considered to be the secondary somatosensory cortex and insula, and the limbic system, including the cingulate cortex, amygdala, or hippocampus of the bilateral hemispheres. The latencies and amplitudes are clearly affected by vigilance, attention-distraction, and various kinds of stimulation applied simultaneously with pain. Abnormalities of pain SSEP(L) reflect an impairment of pain-temperature sensation, probably relating to dysfunction of A5 fibers of the peripheral nerve and spinothalamic tract. In contrast, conventional SSEP after nonpainful electrical stimulation reflects an impairment of tactile, vibratory, and deep sensation, probably relating to dysfunction of Aalpha or Abeta fibers of the peripheral nerve and dorsal column. Therefore, combining the study of pain SSEP(L) and conventional SSEP is useful to detect physiologic abnormalities, and sometimes subclinical abnormalities, of patients with peripheral and central nervous system lesions.

Abnormal subcortical somatosensory evoked potentials indicate high cervical myelopathy in achondroplasia.

Children with achondroplasia may have high cervical myelopathy due to stenosis of the cranio-cervical junction resulting in neurological disability and an increased rate of sudden death. To detect myelopathy we recorded somatosensory evoked potentials (SEPs) after median nerve stimulation in 30 patients with achondroplasia aged 13 months to 18 years (mean 6 years). In addition to the conventional technique of recording the cortical N20 and the central conduction time (CCT), we employed a noncephalic reference electrode recording the subcortical waveforms N13b and P13. generated near the cranio-cervical junction. The findings were related to the clinical status and MRI results. Eighteen patients had MRI evidence of spinal cord compression with indentation or narrowing of the upper cervical cord, and 13 showed signs of myelomalacia. Seven patients had neurological abnormalities. The sensitivities of the SEPs were 0.89 for cervical cord compression, 0.92 for myelomalacia and 1.0 for the clinically symptomatic patients. There were no false-positive results. The subcortical SEPs were more sensitive than the conventional recordings. However, the conventional SEPs were highly specific in the most severely affected patients; here the specificity was 1.0 for patients with myelomalacia and 0.96 for symptomatic patients. Postoperative SEPs improved after occipital decompression in two children. The analysis of somatosensory evoked potentials, in particular of subcortical tracings, is useful in the detection of early cervical myelopathy in children with achondroplasia. Early neurosurgical decompression may prevent irreversible damage.

Pain-related somatosensory evoked potentials following CO 2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO 2 laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO 2 laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.

Physiological functions of the ascending spinal tracts in HTLV-I-associated myelopathy (HAM)

Physiological functions of the spinothalamic tract (STT) and the posterior column (PC) were studied in 19 Japanese patients with HTLV-I-associated myelopathy (HAM). The former was evaluated by pain-related somatosensory evoked potentials (SEPs) following CO 2 laser stimulation, and the latter by conventional SEPs following electrical stimulation. Conduction velocity of STT and PC was significantly decreased in 9 and 14 patients, respectively, and more than half of them showed no clinical impairment of sensations (subclinical abnormality).

Somatosensory and spinal evoked potentials in patients with cervical syringomyelia.

We recorded somatosensory evoked potentials (SEPs) from the skin surface and spinal evoked potentials (SpEP) from the posterior epidural space after median nerve stimulation in 11 patients with cervical syringomyelia. We compared SEPs with SpEP to assess the possible feasibility of using these techniques to localize the offending lesion. SEP abnormalities were present on one or both sides of 7 patients (9 of 22 upper limbs; 41%). The abnormal SEP pattern was the attenuation or loss of N13, which was of little value for delineating the lesion. In patients with abnormal SEPs, three types of abnormal SpEPs were noted. In the Type A abnormality (three limbs), potentials were attenuated in all cervical segments, suggesting that the syrinx itself had enlarged to involve the posterior column. In Type B (two limbs), there was reduced amplitude or absent upper cervical potentials, probably a result of the accompanying tonsilar herniation. Finally, the Type C (four limbs) abnormality was a mixture of Type A and B abnormalities in that the attenuated cervical potentials were again affected in the most upper cervical segment. We concluded that SpEP revealed various kinds of involvement of the dorsal column pathway in the syringomyelic patients, a finding not expressed with conventional SEPs.

Somatosensory evoked potentials recovery (SEP-R) in myoclonic patients

Recovery of somatosensory evoked potentials (SEPs) was studied by paired stimulation of the median nerve in patients with various kinds of myoclonus. This technique revealed the hyperexcitability of the central nervous system (CNS) which could not be detected by the conventional SEP technique using a single stimulus. This technique would be useful for studying the excitability of the CNS.

Skin and epidural recording of spinal somatosensory evoked potentials following median nerve stimulation: correlation between the absence of spinal N13 and impaired pain sense

A clinical lesion study and intraoperative epidural recordings were made to test the origin and clinical significance of the spinal N13 and P13 of somatosensory evoked potentials (SEP) that follow median nerve stimulation. Intraoperatively, the respective peak latencies of spinal P13 and N13 coincided with those of the N1 component of the dorsal cord potential and its phase reversed positivity. On both the ventral and dorsal sides of the cervical epidural space, maximal amplitude was at the C5 vertebral level to which nerve input from the C6 dermatome is the main contributor. The modality of sensory impairment in the hand dermatome was examined in selected patients with cervical lesions, who showed such normal conventional SEP components as Erb N9, far-field P9, P11, P14, N18 and cortical N20, with or without loss of spinal N13. Statistically, the loss of spinal N13 was associated with decrease of pain sensation in the C6 dermatome. This was interpreted as being due to damage to the central grey matter of the cord, including the dorsal horn. Our results suggest the spinal N13 and P13 originate from the same source in the C6 spinal cord segment and that they are good indicators for the detection of centromedullary cervical cord damage.