Search

placental anomalies can affect fetal and maternal outcome due to severe maternal hemorrhage potentially resulting in hysterectomy and cord accident including abruption that can determine fetal damage or death. The aims of our study are to determine if the rate of placental and umbilical cord anomalies are more common in IVF singleton pregnancies compared to spontaneous pregnancies; to evaluate the role of ultrasound in screening for these anomalies and to investigate if oocyte donor fertilization is an additional risk factor for the development of these anomalies.this was a prospective cohort study involving two tertiary centers. Patients with a singleton pregnancy conceived with IVF and patients presenting with a spontaneous conception were recruited between 1IVF pregnancies had a significantly higher risk of low-lying placenta, placenta previa, bilobed placenta and velamentous cord insertion (VCI) compared with spontaneous pregnancies. In the heterologous subgroup there was a significant increased incidence of placenta accreta spectrum (PAS) disorders than in spontaneous pregnancies. All these anomalies were identified prenatally on ultrasound imaging and confirmed at birth.IVF pregnancies in general and those resulting from donor oocyte in particular are at higher risk of placental and umbilical cord abnormalities compared to spontaneous pregnancies. These anomalies can be diagnosed accurately at the mid-trimester detailed fetal anomaly scan and our findings support the need for a targeted ultrasound screening of these anomalies in IVF pregnancies.

Background The role of central and/or peripheral nervous system dysfunction is basically fundamental in fibromyalgia. Aim The aim of this position statement on behalf of the Neuropathic Pain Study Group of the Italian Society of Neurology is to give practical guidelines for the clinical and instrumental assessment of fibromyalgia (FM) in the neurological clinical practice, taking into consideration recent studies. Methods Criteria for study selection and consideration were original studies, case-controls design, use of standardized methodologies for clinical practice, and FM diagnosis with ACR criteria (2010, 2011, 2016). Results ACR criteria were revised. For diagnostic procedure of small-fiber pathology, 47 studies were totally considered. Recent diagnostic criteria should be applied (ACR, 2016). A rheumatologic visit seems mandatory. The involvement of small fibers should request at least 2 among HRV + SSR and/or laser-evoked responses and/or skin biopsy and/or corneal confocal microscopy, eventually followed by monitoring of metabolic and/or immunological/ and or/paraneoplastic basis, to be repeated at 1-year follow-up. Conclusions The correct diagnostic approach to FM could promote the exclusion of the known causes of small-fiber impairment. The research toward common genetic factors would be useful to promote a more specific therapeutic approach.

The aim of this study was to evaluate the possibility to modulate pain perception with cerebellar transcranial Direct Current Stimulation (ctDCS) in phantom limb pain (PLP). Patients underwent ctDCS (anodal or sham, 2.0 mA, 20’ per day, five days a week). Clinical scores (VAS) and electrophysiological parameters (Laser Evoked Potentials, LEPs) were assessed before tDCS, at the end of 5-days treatment, two weeks and one month after ctDCS completion. LEPs were obtained using a Nd:YAP laser (wavelength 1.04 μm, pulse 164 duration 2–20 ms). The amputated limb was stimulated by laser pulses with short duration (5 ms) and small diameter spots (5 mm). Anodal tcDCS reduced non-painful phantom limb sensations (p

Aims The incidence of chronic pain after total knee replacement (TKR) is approx. 20%, why preoperative risk factors for the development of chronic postoperative pain are highly warranted. Studies have indicated that preoperative inflammatory markers hold prognostic information for the development of chronic postoperative pain. Long-non-coding-RNA (lncRNA) regulates the expression of genes related with e.g. inflammation. The current study aimed to investigate the preoperative influence of lncRNA on the development of chronic postoperative pain following TKR. Methods 24 patients, who developed chronic postoperative pain and 12 patients with painfree recovery, were sampled from a larger clinical study. Preoperative serum samples were obtained from all patients and analyzed for potential lncRNA candidates. Briefly, total RNA was extracted from serum using miRNeasy Mini kit.cDNA samples were pre-amplified with RT2lncRNAPreAMP Primer Mix that contained specific set of primers to target genes of Human RT2lncRNA Inflammatory Response & Autoimmunity PCR Array. Further, the reaction (25μl) will be aliquoted into the wells of RT2lncRNA PCR Array Human Inflammatory Response & Autoimmunity. LncRNA-expressions were compared between the two groups using student’s t-test. Results 19 patients were excluded due to the “cut-off” of the statistical analysis’s software that not included the samples because of genomic contamination, retro transcription and amplification’s low efficiency. A total of 13 patients were included (7 with pain, 6 without pain). The preliminary analysis found that the MEG3-lncRNA (implicated in tumor vascularization suppressing) were downregulated in patients who developed chronic postoperative pain compared to patients with a normal recovery (fold change: − 9.56, P < 0.05). Conclusions Preoperative MEG-3 is downregulated in patients in risk of developing chronic postoperative pain following TKR. Future research, in larger cohorts should further investigate the role of MEG3 and hence the improvement of the cartilage vascularization and other lncRNAs as predictive indicators for the development of chronic postoperative pain.

To investigate whether among children and adolescents with attention deficit and hyperactivity disorder (ADHD) those with Tuberous Sclerosis (TS) show specific abnormalities of event-related potentials (ERPs). We recruited 10 ADHD patients: 5 with TS (mean age: 12.6 ± 4.3 years) and 5 without TS (mean age: 11.6 ± 3 years). By using an oddball paradigm, auditory mismatch negativity (MMN) and P3b responses were recorded from Fz and Pz electrodes, respectively. All patients were administered with cognitive, executive functioning, and behavioural questionnaires. No difference was found in cognitive and executive functioning between two groups. The P3b amplitude was significantly higher in TS patients (15.6 ± 9 μV) than in children and adolescents without TS (5.5 ± 2.7 μV) (p = 0.04). The MMN amplitude was higher in TS patients (19 ± 18 μV) than in those without TS (9 ± 6.9 μV), although the difference was not significant (p = 0.3). Our results show that P3 and MMN amplitudes are higher in ADHD patients with TS than in those without TS. This means that among children and adolescents with ADHD involuntary and mostly voluntary attention capabilities are better in those with TS. Since this difference was not found by neuropsychological testing, ERP recording can be useful to unravel subclinical differences between two groups.

To investigate whether the electrode implantation in the thalamus for deep brain stimulation can damage the somatosensory pathway. A Parkinsonian patient underwent electrode implantation in the ventralis intermediate (VIM) nucleus of the thalamus. The somatosensory evoked potentials (SEPs) were recorded to median nerve stimulation in the operatory room, immediately after surgery, and in the laboratory, 5 days after surgery. Both low-frequency SEPs and high-frequency oscillations (HFOs) were recorded from the scalp and the VIM electrode contacts. Immediately after VIM targeting, the low-frequency SEP amplitudes obtained from both the scalp and the VIM electrode contacts were decreased, but they recovered after 5 days. The HFOs underlying the VIM low-frequency SEPs showed the same behaviour. In particular, the HFO modifications due to electrode implantation mainly involved the higher-frequency HFOs (1500 Hz), rather than the lower-frequency HFOs (800 Hz). Our results suggest that the somatosensory fibers are transitorily damaged by electrode implantation in the thalamus. The HFO analysis allowed us to determine that it was the higher-frequency HFOs to be particularly impaired. Since the higher-frequency HFOs have a postynaptic origin, we suggest that electrode implantation in the thalamus can lead to a reversible damage of the neurons of the ventral posterolateral (VPL) nucleus.

Preoperative evaluation, by means of intracerebral electrodes, in patients presenting with symptomatic drug resistant epilepsy, provides an opportunity to explore neural generators of P300, Mismatch Negativity (MMN) and also N140. We studied 5 pediatric patients with drug resistant epilepsy. ERPs and SEPs (to median and tibial nerve stimulation) were recorded from the intracerebral electrode contacts referred to the earlobe ipsilateral to the stimulation. P300 was recorded by electrodes located in hippocampus with a clear inversion of signals in posterior hippocampus; MMN was also well recorded by electrodes placed in opercular-insular cortex without a clear inversion of signal; N140, increased in amplitude during attention condition, showed the maximum amplitude in the frontal electrode contacts and in the opercular-insular traces. Numerous investigations revealed that generators of Event Related Potentials are independent and also with a cortical-subcortical distribution. In this short case series, we could show some brain areas clearly involved in the generation of P300, MMN and N140 components.

The cerebellum is involved in a number of integrative functions, but its role in pain perception and nociceptive processing is poorly understood. We evaluated the effects of transcranial cerebellar direct current stimulation (tcDCS) by studying changes in perceptive threshold (PT), pain intensity (VAS) and laser evoked potentials (LEPs). Twenty-five subjects were studied before and after anodal, cathodal and sham tcDCS. LEPs were obtained using a Nd:YAP laser. VAS was evaluated by delivering laser pulses at two different intensities, respectively two and three times the PT. Cathodal polarization dampened the perceptive threshold and increased the VAS score, while anodal one had opposite effects (p tcDCS modulates pain perception and its cortical correlates. As it is effective on N1 and N2/P2 components, we speculate that the cerebellum modulates the activity of both somatosensory and cingulate cortices, thus interfering with the sensory-discriminative and affective-emotional dimensions of pain. Our findings prompt investigation of the tsDCS as a novel and safe therapeutic tool in pain syndromes.

This study aimed to verify the hypothesis that somatosensory activity recorded from the Pedunculopontine nucleus (PPTg) comes from the dorsal column nuclei (DCN) (Insola et al., 2015). In one parkinsonian patient implanted in the PPTg for DBS, both tibial and median nerve SEPs were recorded from the PPTg electrode. The finding obtained from this patient was compared with that issued from another patient implanted with an epidural electrode at Cv2 level for pain relief. The triphasic waform and HFOs recorded from the PPTg after tibial nerve stimulation were very similar to the low- and high-frequency components recorded from the Cv2 epidural electrode, known to be generated in the DCN (Insola et al., 2010). Therefore, the present results suggest that both the low-frequency triphasic waveform and the HFOs recorded from the PPTg are generated from the DCN.

Background: We describe a group of previously normal children who developed severe focal epilepsy after an acute/sub-acute illness resembling encephalitis. Methods: This is a retrospective study. An acute phase (encephalitis/encephalopathy period) and a chronic phase (chronic focal resistant epilepsy) were defined. Results: Eight patients were enrolled. The median age at onset was 6.6 years (range 8 months–17.6 years). In the acute phase, fever was the first symptom in all cases and was associated with seizures and status epilepticus. All patients had focal seizures arising in both hemispheres. Seizure onset occurred in the frontal and temporal regions. EEGs showed slowing background activity associated with focal or diffuse slow waves with rare epileptiform abnormalities. Cerebrospinal fluid oligoclonal bands were observed in four out of six patients tested. MRI images showed bilateral peri-insular hyperintensity in four cases. Five patients received corticosteroids, and in four cases, they were given along with intravenous immunoglobulins. The median duration of the acute phase was 19 days (range 15–30 days). During the chronic phase, which followed the acute phase without interval, patients presented with drug-resistant focal seizures and neuropsychological deficits, which ranged from hyperactivity and attention deficits to short-term verbal memory deficit, pervasive developmental disorders, and language delay. Conclusion: Considering the clinical presentations, EEG findings, and the associated occurrence of non-specific immunological activations, a possible immune-mediated pathogenesis can be hypothesized, although firm conclusions cannot be drawn out.

Scalp somatosensory evoked potentials (SEPs) are later in latency after sural than after tibial nerve stimulation. This led to hypothesize that different spinal pathways could be involved in the scalp SEP generation (Rossini et al., 1986). Our aim was to investigate the SEP latencies at different subcortical sites after sural and tibial nerve stimulation. We studied 7 patients. Four patients with Parkinson’s disease (PD) were implanted with intracerebral electrodes for DBS: one in the thalamus bilaterally (Vim nucleus), and 3 in the Pedunculopontine nucleus (PPTg). The remaining 3 patients were implanted with cervical epidural electrodes for intractable pain. SEPs were recorded from the scalp and the deep recording electrodes after both tibial and sural nerve stimulation. In all our patients, the scalp SEP latencies were later after sural than after tibial nerve stimulation. On the contrary, SEPs recorded at all subcortical sites showed similar latencies for both sural and tibial nerve stimulation. In conclusion, sural and tibial nerve scalp SEPs are mediated by the same spinal pathway. The difference in latency observed between the scalp SEPs after sural and tibial nerve stimulation is probably due to the orientation of the dipolar sources generating these components.

In our study, preparation of voluntary movement was used to physiologically activate the motor cortex areas and the effect of this activation on CO(2) laser-evoked potentials (LEPs) was explored. LEPs were recorded from 31 scalp electrodes in 10 healthy subjects after painful stimulation of the right C6-C7 skin dermatomes. LEP stimuli were delivered in the time interval between a visual warning stimulus followed after 1 s. by an imperative stimulus. The imperative stimulus triggered: (i) no task in the baseline condition (Pain); (ii) flexion-extension movements of the second finger of the right hand in the movement condition (Pain + Movement); (iii) cognitive task (mathematic computation) in the distraction condition (Pain + Cognition). The experimental conditions were also repeated during application of laser stimuli on the left C6-C7 skin dermatomes. Compared with the baseline condition (no task required), during preparation of right-hand voluntary movement there was a significant reduction in LEP amplitude and subjective pain rating after right- but not after left-hand stimulation, which suggests that the observed effect cannot be attributed to a nonspecific reduction in attention toward painful stimulus. During preparation of a cognitive task, LEP amplitude was reduced compared to baseline. Our results represent the first neurophysiological suggestion that physiological activation of the motor cortex, occurring during movement preparation, inhibits cortical pain processing by a centrifugal mechanism.

Six patients with alternating hemiplegia of childhood (AHC) underwent motor evoked potentials (MEPs), somatosensory evoked potentials (SEPs) and blink reflex recording. No SEP abnormality was found. As for MEP recording, central conduction time did not differ between patients studied during either interictal or ictal phase, and normal subjects, suggesting that the pyramidal system function is spared. In blink reflex recording, the latencies of both the ipsilateral (iR2) and contralateral (cR2) R2 components were significantly longer ( P < 0.01) in patients during the interictal phase than in normal subjects. Moreover, the iR2 and cR2 areas were significantly reduced ( P < 0.01) in patients during the interictal phase, compared with normal subjects. During the ictal phase, the ipsilateral R2 latency was significantly decreased after stimulation of the hemiplegic side, compared with the interictal phase ( P < 0.05). The blink reflex abnormalities suggest a brainstem dysfunction, which may be linked to the pathophysiological mechanisms of the disease.

The present study aimed to investigate whether tonic cutaneous pain exerts any effect on the cortical processing of nociceptive input and if this effect may involve only body parts in pain. Tonic cutaneous pain was obtained in nine healthy human subjects by infusion of a hypertonic saline (5%) in the s.c. tissue over the hypothenar muscles (10 ml/h for 20 min). Nociceptive cutaneous CO2 laser-evoked potentials were recorded after stimulation of the right hand dorsum, which was adjacent to the painful area, and the right perioral region, corresponding to the adjacent cortical sensory area. Laser-evoked potentials were obtained before saline injection, at the peak pain and 20 min after pain disappeared. During saline infusion, the laser-evoked pain to right hand stimulation was reduced and the vertex laser-evoked potentials (N2a-P2, mean latency 181 ms and 319 ms for the N2a and the P2 potentials, respectively), which are generated in the anterior cingulate cortex, were significantly decreased in amplitude compared with the baseline. Moreover, the topography of these potentials was modified by cutaneous pain, shifting from the central toward the parietal region. Dipolar modeling showed that the dipolar source in the anterior cingulate cortex moved backward during saline infusion. This result suggests that cutaneous pain may modify the relative activities of the anterior and posterior anterior cingulate cortex parts, which are thought to be devoted to encode different aspects of pain sensation. No laser-evoked potential change was observed after stimulation of the right perioral region, suggesting that functional changes in the nociceptive system are selective for the painful regions and not for areas with cortical proximity.

Fourteen patients, suffering from chronic pain resistant to pharmacological treatment, underwent epidural electrode implant on the cervical spinal cord (CSC) for neuromodulation. After the median nerve stimulation, somatosensory evoked potentials (SEPs) were recorded from the epidural electrode contacts, from the frontal and the parietal regions contralateral to the stimulated side, from an electrode placed over the sixth cervical vertebra and from the Erb's point. SEPs were recorded at rest and during a voluntary flexion–extension movement of the stimulated wrist. The epidural electrode contacts recorded a triphasic potential (P1–N1–P2). The epidural potential amplitude was significantly decreased during voluntary movement compared with the rest, thus suggesting that the effect of movement on SEPs occurs also at CSC level.

Cardiac syndrome X (SX) is characterised by angina-like chest pain and ST segment depression on the ECG during stress. Our study aimed at investigating whether in patients with cardiac syndrome X the cerebral processing of the nociceptive inputs is impaired and whether this abnormality can play a primary role in generating pain. We observed that the habituation to experimental pain was assessed in 16 SX patients by evaluating the amplitude modification of the scalp potentials to CO 2 laser pulses (laser evoked potentials, LEPs) after repetitive stimulation of the right hand and chest. The LEP amplitude habituation in SX patients was compared with that in 13 control subjects (CS). While CS showed a significant habituation of both the LEP amplitude and pain rating, in SX patients neither the LEP amplitude nor the pain rating showed any significant reduction. The lack of habituation to experimental pain observed in SX patients can be due to an abnormal excitability of the cerebral areas involved in pain processing and can be relevant in the pathophysiology of cardiac syndrome X.

Objective : To identify low and high-frequency median nerve (MN) somatosensory evoked potential (SEP) generators by means of chronically implanted electrodes in the parietal lobe (SI and neighbouring areas) of two epileptic patients. Methods : Wide-pass short-latency and long-latency SEPs to electrical MN stimulation were recorded in two epileptic patients by stereotactically chronically implanted electrodes in the parietal lobe (SI and neighbouring areas). To study high-frequency responses (HFOs) an off-line digital filtering of depth short-latency SEPs was performed (500–800 Hz, 24 dB roll-off). Spectral analysis was performed by fast Fourier transform. Results : In both patients we recorded a N20/P30 potential followed by a biphasic N50/P70 response. A little negative response in the 100 ms latency range was the last detectable wide-pass SEP in both patients. Two HFOs components (called iP1 and iP2) were detected by mere visual analysis and spectral analysis, and were supposed to be originated within the parietal cortex. Conclusions : This was the very first study that recorded wide bandpass and high frequency SEPs by electrodes, exploring both the lateral and the mesial part of the parietal lobe and particularly that of the post-central gyrus.

Preoperative evaluation, by means of intracerebral electrodes, provides an opportunity to explore neural generators of ERPs and also N140 (a long latency SEP that is modulated by attention manipulations). We studied 5 pediatric patients with drug resistant epilepsy. ERPs and SEPs (to median and tibial nerve stimulation) were recorded from the intracerebral electrode contacts referred to the earlobe ipsilateral to the stimulation. The analysis was addressed to the electrode contacts where an inversion of neurophysiological component polarity was observed, or where the EP amplitude was higher. P300 was recorded by electrodes located in hippocampus; MMN was also well recorded by electrodes placed in opercular-insular cortex; N140, increased in amplitude during attention condition, showed the maximum amplitude in the frontal electrode contacts and in the opercular-insular traces. Numerous investigations revealed that generators of ERPS are independent and with a cortical-subcortical distribution too. In this short case series, we could show some brain areas clearly involved in the generation of P300, MMN and N140 components.

Neck flexion may play a role in the pathogenesis of Hirayama disease. Upper limb somatosensory evoked potentials were recorded in five patients with Hirayama disease, six patients with ALS, and 14 healthy subjects. Neck flexion caused a significant amplitude decrease of the N13 cervical response only in patients with Hirayama disease. Direct cord compression or microvascular changes can in theory account for this position-related dysfunction.

Objective: To study whether sensorimotor cortical areas are involved in Essential Tremor (ET) generation. Background: It has been suggested that sensorimotor cortical areas can play a role in ET generation. Therefore, we studied median nerve somatosensory evoked potentials (SEPs) in 10 patients with definite ET. Methods: To distinguish SEP changes due to hand movements from those specifically related to central mechanisms of tremor, SEPs were recorded at rest, during postural tremor and during active and passive movement of the hand. Moreover, we recorded SEPs from 5 volunteers who mimicked hand tremor. The traces were further submitted to dipolar source analysis. Results: Mimicked tremor in controls as well as active and passive hand movements in ET patients caused a marked attenuation of all scalp SEP components. These SEP changes can be explained by the interference between movement and somatosensory input (‘gating’ phenomenon). By contrast, SEPs during postural tremor in ET patients showed a reduction of N20, P22, N24 and P24 cortical SEP components, whereas the fronto-central N30 wave remained unaffected. Conclusions: Our findings suggest that in ET patients the physiological interference between movement and somatosensory input to the cortex is not effective on the N30 response. This finding thus indicates that a dysfunction of the cortical generator of the N30 response may play a role in the pathogenesis of ET. q 2002 Elsevier Science Ireland Ltd. All rights reserved.

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.

To elucidate whether the selective electrical stimulation of muscle as well as cutaneous afferents evokes modality-specific responses in somatosensory evoked potentials (SEPs) recorded on the scalp of humans, we compared scalp SEPs to electrical stimuli applied to the median nerve and to the abductor pollicis brevis (APB) motor point. In three subjects, we also recorded SEPs after stimulation of the distal phalanx of the thumb, which selectively involved cutaneous afferents. Motor point and median nerve SEPs showed the same scalp distribution; moreover, very similar dipole models, showing the same dipolar time courses, explained well the SEPs after both types of stimulation. Since the non-natural stimulation of muscle afferents evokes responses also in areas specifically devoted to cutaneous input processing, it is conceivable that, in physiological conditions, muscle afferents are differentially gated in somatosensory cortex. The frontocentral N30 response was absent after purely cutaneous stimulation; by contrast, it was relatively more represented in motor point rather than in mixed nerve SEPs. These data suggest that the N30 response is specifically evoked by proprioceptive inputs.

Objective cerebellum is involved in a wide number of integrative functions; its role in pain processing has been scarcely investigated. We tried to clarify this aspect using transcranial cerebellar direct current stimulation (tcDCS) and studying changes in perceptive threshold (PT), pain intensity (VAS) and laser evoked potentials (LEPs) responses (N1 and N2/P2). Materials and methods Fifteen subjects were studied before and after anodal, cathodal and sham tcDCS. LEPs were obtained using a Nd:YAP laser; signals were amplified, band pass filtered. The left hand dorsum was stimulated by laser pulses with short duration (5 ms) and small diameter spots (5 mm). VAS was evaluated by delivering laser pulses at two different intensities, respectively two and three times the pain threshold (PT). Results Cathodal polarization dampened the PT and increased the VAS score, while the anodal one had opposite effects ( p p Discussion tcDCS modulates pain perception and its cortical correlates. As it is effective on N1 and N2/P2 components and these responses are generated by parallel and partially segregated spinal pathways reaching different cortical targets, we speculate that the cerebellum modulates the activity of both somatosensory and cingulate cortices, interfering with the sensory-discriminative as well as emotional dimensions of pain. Conclusions Present findings prove Cerebellum involvement in pain processing and prompt further investigations on tcDCS employments as novel therapeutic tool in chronic pain patients.

Question The cerebellum is involved in a wide number of integrative functions, but its role in pain perception and nociceptive processing is poorly understood. We evaluated the effects of transcranial cerebellar direct current stimulation (tcDCS) by studying the changes in perceptive threshold (PT), pain intensity (VAS) and laser evoked potentials (LEPs) variables (amplitude and latency of both N1 and N2/P2 responses). Methods Fifteen subjects were studied before and after anodal, cathodal and sham tcDCS. LEPs were obtained using a Nd:YAP laser (wavelength 1.04 μm, pulse 164 duration 2–20 ms, maximum energy 7 J). The laser beam was transmitted from the generator to the stimulating probe via a 10 m length optical fibre; signals were then amplified, band pass filtered (0.1–200 Hz, time analysis 1000 ms). The dorsum of the left hand was stimulated by laser pulses (individual variability: 3.89–15.75 J/cm2) with short duration (5 ms) and small diameter spots (5 mm). VAS was evaluated by delivering laser pulses at two different intensities, respectively two and three times the PT. Results Cathodal polarization dampened the PT and increased the VAS score, while the anodal one had opposite effects. Conclusions TcDCS modulates pain perception and its cortical correlates. As it is effective on N1 and N2/P2 components and these responses are generated by parallel and partially segregated spinal pathways reaching different cortical targets, we speculate that the cerebellum modulates the activity of both somatosensory and cingulate cortices, thus interfering with the sensory-discriminative and emotional dimensions of pain. Present findings prompt investigation of the tsDCS as a novel, safe therapeutic tool in chronic pain patients. Download : Download high-res image (428KB) Download : Download full-size image

Adenoid cystic carcinoma (ACC) of Bartholin's gland is an extremely rare tumor of the female genital tract, representing about 5%-15% of Bartholin's gland malignancies. Approximately 80 cases have been reported in the literature. The authors describe the case of a 54-year-old woman with locally advanced ACC of Bartholin's gland treated with surgery and adjuvant radiotherapy (RT). She underwent radical hemivulvectomy associated with ipsilateral inguinal and femoral lymph node dissection. Subsequently, she received postoperative three-dimensional conformal RT. Total dose prescribed was 56 Gy in 28 fractions of two Gy each. After 20 months of follow up, there was no evidence of local failure or distant progression.

Objectives The study aimed to investigate the site of the movement related inhibition of the human dorsal column nuclei. Methods Median nerve somatosensory evoked potentials (SEPs) were recorded from 18 patients suffering from Parkinson’s disease, who underwent electrode implantation in the pedunculopontine (PPTg) nucleus. SEPs were recorded at rest and during active or passive movement of the thumb of the stimulated wrist. Results The PPTg electrode recorded a triphasic potential generated in the cuneate nucleus. The PPTg potential was subtended by 2 high frequency oscillation (HFO) components: (1) an earlier one with 1000 Hz frequency and (2) a later one with 1700 Hz frequency. Both HFO components were reduced by movement. No major difference between the effects of either active or passive movement was found. Discussion PPTg electrode can record SEPs generated in the dorsal column nuclei (DCN). We suggest that the 1000 Hz and 1700 Hz HFO bursts are generated at pre- and post-synaptical level, respectively. Conclusion Movement exerts both pre- and post-synaptic inhibition on dorsal column nuclei. Significance Investigating the effect of movement on the DCN activity by an intracerebral electrode located at the human PPTg level confirms what early studies in animals suggested.

OBJECTIVES Recording techniques permit the separate analysis of the response from cauda equina roots and the spinal potential that is probably generated by the activation of dorsal horn cells. To improve the functional assessment of focal lesions of the lumbosacral cord, lower limb somatosensory evoked potentials (SEPs) were measured by multisegmental stimulation. METHODS Common peroneal and tibial nerves SEPs were recorded in 14 patients in whom MRI demonstrated compressive cord damage ranging from T9 to L1 levels. SEPs were recorded in each patient at the lumbar level (cauda equina response), lower thoracic level (spinal response), and from the scalp (cortical response). RESULTS Abnormalities in spinal response occurred in 50% and 70% of tibial and common peroneal nerve SEPs respectively; these findings were well explained by the radiological compression level, involving in most of the patients lumbar rather than sacral myelomeres. The SEPs were often more effective than the clinical examination in showing the actual extension of damage. CONCLUSIONS The recording of spinal SEPs after multisegmental lower limb stimulation proved useful in assessing cord dysfunction and determining the cord levels mainly involved by the compression.

To elucidate whether the frontal components of scalp somatosensory evoked potentials (SEPs) depend on the type of peripheral input, we compared scalp SEPs in response to electrical stimuli applied to: (i) the proximal phalanx of the thumb, involving both deep and cutaneous afferents; and (ii) the distal phalanx of the thumb, involving cutaneous afferents, but excluding joint inputs coming from the interphalangeal articulation. We applied the same dipolar model that we built to explain the scalp SEP distribution to median nerve stimulation in previous investigations. Cortical SEPs after proximal stimulation were generated by three dipolar sources, one of which was likely to account for the frontal scalp N30. When we analyzed SEPs for distal (purely cutaneous) stimulation, the frontal and central recordings showed a clear reduction in amplitude of the negative responses having a latency of about 30 ms. Moreover, when applying the dipole model derived from analysis of responses to proximal stimulation to SEPs to distal stimulation, the source corresponding to the N30 distribution showed no activity, suggesting a strong relationship between joint and tendinous inputs and the activity of the N30 generator.

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.