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Background and purpose : Autoimmune encephalitides (AE) include a spectrum of neurological disorders whose diagnosis revolves around the detection of neuronal antibodies (Abs). Consensus‐based diagnostic criteria (AE‐DC) allow clinic‐serological subgrouping of AE, with unclear prognostic implications. The impact of AE‐DC on patients' management was studied, focusing on the subgroup of Ab‐negative‐AE. Methods: This was a retrospective multicenter study on patients fulfilling AE‐DC. All patients underwent Ab testing with commercial cell‐based assays (CBAs) and, when available, in‐house assays (immunohistochemistry, live/fixed CBAs, neuronal cultures) that contributed to defining final categories. Patients were classified as Ab‐positive‐AE [N‐methyl‐d‐aspartate‐receptor encephalitis (NMDAR‐E), Ab‐positive limbic encephalitis (LE), definite‐AE] or Ab‐negative‐AE (Ab‐negative‐LE, probable‐AE, possible‐AE). Results: Commercial CBAs detected neuronal Abs in 70/118 (59.3%) patients. Testing 37/48 Ab‐negative cases, in‐house assays identified Abs in 11 patients (29.7%). A hundred and eighteen patients fulfilled the AE‐DC, 81 (68.6%) with Ab‐positive‐AE (Ab‐positive‐LE, 40; NMDAR‐E, 32; definite‐AE, nine) and 37 (31.4%) with Ab‐negative‐AE (Ab‐negative‐LE, 17; probable/possible‐AE, 20). Clinical phenotypes were similar in Ab‐positive‐LE versus Ab‐negative‐LE. Twenty‐four/118 (20.3%) patients had tumors, and 19/118 (16.1%) relapsed, regardless of being Ab‐positive or Ab‐negative. Ab‐positive‐AE patients were treated earlier than Ab‐negative‐AE patients (P = 0.045), responded more frequently to treatments (92.3% vs. 65.6%, P < 0.001) and received second‐line therapies more often (33.3% vs. 10.8%, P = 0.01). Delays in first‐line therapy initiation were associated with poor response (P = 0.022; odds ratio 1.02; confidence interval 1.00–1.04). Conclusions: In‐house diagnostics improved Ab detection allowing better patient management but was available in a patient subgroup only, implying possible Ab‐positive‐AE underestimation. Notwithstanding this limitation, our findings suggest that Ab‐negative‐AE and Ab‐positive‐AE patients share similar oncological profiles, warranting appropriate tumor screening. Ab‐negative‐AE patients risk worse responses due to delayed and less aggressive treatments. [ABSTRACT FROM AUTHOR]

Background: In the neurophysiological assessment of patients with neuropathic pain, laser evoked potentials (LEPs), contact heat evoked potentials (CHEPs) and the evoked potentials by the intraepidermal electrical stimulation via concentric needle electrode are widely agreed as nociceptive specific responses; conversely, the nociceptive specificity of evoked potentials by surface concentric electrode (SE-PREPs) is still debated.Methods: In this neurophysiological study we aimed at verifying the nociceptive specificity of SE-PREPs. We recorded LEPs, CHEPs and SE-PREPs in eleven healthy participants, before and after epidermal denervation produced by prolonged capsaicin application. We also used skin biopsy to verify the capsaicin-induced nociceptive nerve fibre loss in the epidermis.Results: We found that whereas LEPs and CHEPs were suppressed after capsaicin-induced epidermal denervation, the surface concentric electrode stimulation of the same denervated skin area yielded unchanged SE-PREPs.Conclusion: The suppression of LEPs and CHEPs after nociceptive nerve fibre loss in the epidermis indicates that these techniques are selectively mediated by nociceptive system. Conversely, the lack of SE-PREP changes suggests that SE-PREPs do not provide selective information on nociceptive system function.Significance: Capsaicin-induced epidermal denervation abolishes laser evoked potentials (LEPs) and contact heat evoked potentials (CHEPs), but leaves unaffected pain-related evoked potentials by surface concentric electrode (SE-PREPs). These findings suggest that unlike LEPs and CHEPs, SE-PREPs are not selectively mediated by nociceptive system. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to explore the nociceptive system of patients affected by trigeminal neuralgia (TN) secondary to documented vascular contact who underwent microvascular decompression. For that purpose, we used the classical trigeminal reflexes and the trigeminal laser‐evoked potentials (tLEPs) before and after surgery, in order to verify any possible change after decompression and determine if there was any correlation between the neurophysiological parameters and the clinical outcome. Methods: Eleven patients affected by TN caused by trigeminovascular contact and 10 age‐matched controls underwent conventional trigeminal reflexes (bilateral Blink Reflex/BR and Masseter Inhibitory Reflex stimulating infraorbital and mental nerves/MIR V2 and V3) and tLEPs. Patients repeated neurophysiological tests one week after surgery. Results: Short‐latency BR and MIR were normal in all patients before surgery and there was no statistical difference before and after surgery. Conversely, in patients before surgery, tLEPs' amplitudes were significantly lower in the affected than in the healthy side (p = 0.017 for V2 and 0.037 for V3 branches). After surgery, on the affected side, tLEP amplitude increased and the pre/post‐operative difference was significant (p = 0.017 for V2 and 0.028 for V3 divisions). Nine patients referred satisfactory pain relief and the favourable clinical outcome correlated with the neurophysiological recovery. Conclusions: This study demonstrates that TN caused by trigeminovascular compression may be related to Aδ fibres impairment, and tLEPs are more sensitive than conventional trigeminal reflexes to reveal small fibre dysfunction and to monitor the post‐surgical outcome in these patients. [ABSTRACT FROM AUTHOR]

Background and purpose Alternating hemiplegia of childhood ( AHC) is a rare neurological disease characterized by recurrent paroxysmal attacks of hemiplegia. The aim of the study was to assess the recovery cycle of the somatosensory evoked potentials ( SEPs) in a group of AHC patients. Methods Seven AHC patients and 10 control age-matched subjects ( CS) were recruited. Right and left median nerve SEPs were recorded. The somatosensory system excitability was assessed by calculating the SEP changes after paired electrical stimuli. All patients were studied during the interictal phase, whilst four patients were studied also during the ictal phase. Results In AHC patients during the interictal phase, the amplitudes of the cervical N13 and of the cortical N20, P24 and N30 responses showed a faster recovery than in CS. In AHC patients during the ictal phase, the cortical N20 recovery cycle was prolonged compared with the interictal phase. Conclusions A shortened SEP recovery cycle in AHC during the interictal phase suggests multilevel somatosensory system hyperexcitability in AHC. A partial recovery of this phenomenon during the ictal phase possibly reflects a functional reset of the somatosensory system. Overall, there is a disinhibition of the somatosensory system in AHC, a functional change of brain function associated with a possible involvement of the Na+/ K+ channels. This abnormality and its partial recovery during the attacks might be linked to the pathophysiological and genetic mechanisms of the disease. [ABSTRACT FROM AUTHOR]

Background: 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. Methods: 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. Results: 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. Conclusions: 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. [ABSTRACT FROM AUTHOR]

Background & Aims Long-term diabetes mellitus ( DM) has been associated with neuronal changes in the enteric, peripheral and/or central nervous system. Moreover, abnormal visceral sensation and gastrointestinal ( GI) symptoms are seen in up to 75% of patients. To explore the role of diabetic autonomic neuropathy ( DAN) in patients with long-standing DM, we investigated psychophysical responses and neuronal activity recorded as evoked brain potentials and dipolar source modelling. Methods Fifteen healthy volunteers and 14 type-1 DM patients with DAN were assessed with a symptom score index characterizing upper GI abnormalities. Multichannel (62) electroencephalography was recorded during painful electrical stimulation of the lower oesophagus. Brain activity to painful stimulations was modelled using Brain Electrical Source Analysis ( besa). Results Diabetic patients had higher stimulus intensities to evoke painful sensation ( p ≤ 0.001), longer latencies of N2 and P2 components (both p ≤ 0.001), and lower amplitudes of P1-N2 and N2-P2 complexes ( p ≤ 0.001; p = 0.02). Inverse modelling of brain sources showed deeper bilateral insular dipolar source localization ( p = 0.002). Symptom score index was negatively correlated with the depth of insular activity ( p = 0.004) and positively correlated with insular dipole strength ( p = 0.03). Conclusion DM patients show peripheral and central neuroplastic changes. Moreover, the role of abnormal insular processing may explain the appearance and persistence of GI symptoms related to DAN. This enhanced understanding of DAN may have future clinical and therapeutical implications. [ABSTRACT FROM AUTHOR]

Background We investigated whether patients with painful chronic pancreatitis ( CP) present abnormalities in the cerebral response to experimental pain stimuli. Methods Contact heat-evoked potentials ( CHEPS) were recorded in 15 patients with CP and in 15 healthy volunteers during repetitive stimulation of the upper abdominal region (pancreatic 'viscerotome') and the right forearm (heterologous area). Three sequences of painful stimuli were applied at each site. Subjective pain scores were assessed by a visual analogue scale. Habituation was calculated as the relative change in CHEPS amplitudes between the first and the third stimulation sequence. Results As expected pain scores decreased in healthy volunteers during successive stimulations at both sites (i.e., habituation), while in the CP group, they remained unchanged. The cerebral response consisted of an early-latency, low-amplitude response (N1, contralateral temporal region) followed by a late, high-amplitude, negative-positive complex ( N2/ P2, vertex). During successive stimulation of the pancreatic area, N2/ P2 amplitude increased 25% in CP patients, while they decreased 20% in healthy volunteers ( p = 0.006). After stimulation of the forearm, N2/ P2 amplitudes increased 3% in CP patients compared to a decrease of 20% in healthy volunteers ( p = 0.06). Conclusions Taken together, CP patients had an abnormal cerebral response to repetitive thermal stimuli. This was most prominent after stimulation of the upper abdominal area. As this area share spinal innervation with the pancreatic gland, these findings likely mirror distinctive abnormalities in cerebral pain processing. [ABSTRACT FROM AUTHOR]

Background To investigate changes in heat pain threshold and modifications in heat pain processing during pregnancy and labour, seventy-six nulliparous pregnant women were enrolled in two studies. Methods In the first study (psychophysical), 60 pregnant women underwent a quantitative sensory testing ( QST) investigating heat perception in two body areas (right forearm and T10 dermatome) according to these groups: 32-33 gestational weeks ( GW), 39-40 GW, early stage of active labour and 24 h after the delivery. In the other study (neurophysiological), contact heat-evoked potentials ( CHEPs) were recorded in other 16 women at the 32nd GW and in 11 of these also at the 40th GW. Results The psychophysical study showed that heat pain threshold was significantly increased at the forearm at 32-33 GW (median ± IQR: 39.6 ± 0.7 ° C), at 39-40 GW (40.6 ± 1.1 ° C) and at early stage of active labour (40.8 ± 1.5 ° C) as compared to 20 non-pregnant controls ( p < 0.001). Heat pain threshold tested at T10 level was significantly increased at 32-33 GW (41.0 ± 1.6 ° C), at 39-40 GW (42.1 ± 1.8 ° C), and at early stage of active labour (42.3 ± 1.3 ° C) as compared to the non-pregnant women ( p < 0.001). The N2- P2 CHEP amplitude (main negative N2 and positive P2 components of the vertex biphasic potential) recorded from the pregnant women was significantly lower at the 40th than at the 32nd GW, after stimulation of both the forearm ( p < 0.001) and the abdomen ( p < 0.001). Conclusions In pregnant women, there is a progressive increase of heat pain threshold and a reduction of the CHEP amplitude, suggesting that a general inhibitory mechanism may be involved. [ABSTRACT FROM AUTHOR]

Aliment Pharmacol Ther 2011; 34: 878-887 Summary Background Pregabalin has a broad spectrum of analgesic and antihyperalgesic activity in both basic and clinical studies. However, its mechanisms and sites of action have yet to be determined in humans. Aims To assess the antinociceptive effect of pregabalin on experimental gut pain in patients with visceral hyperalgesia due to chronic pancreatitis and to reveal putative changes in corresponding central pain processing as assessed by evoked brain potentials. Methods Thirty-one patients were randomly assigned to receive increasing doses of pregabalin or placebo for three consecutive weeks. Perceptual thresholds to electrical stimulation of the sigmoid with recording of corresponding evoked brain potentials were obtained at baseline and study end. The brain source localisations reflecting direct neuronal activity were fitted by a five-dipole model projected to magnetic resonance imaging of the individuals' brains. Results As compared to placebo, pregabalin significantly increased the pain threshold to electrical gut stimulation from baseline ( P = 0.02). No differences in evoked brain potential characteristics were seen, neither after pregabalin nor placebo treatment (all P > 0.05). In agreement with this, brain source locations remained stable during study treatment (all P > 0.05). Conclusion Pregabalin was superior to placebo for attenuation of experimental visceral pain in chronic pancreatitis patients. We suggest its antinociceptive effects to be mediated primarily through sub-cortical mechanisms. (ClinicalTrials.gov, number NCT 00755573). [ABSTRACT FROM AUTHOR]

We describe a group of previously normal children who developed severe focal epilepsy after an acute/sub-acute illness resembling encephalitis. This is a retrospective study. An acute phase (encephalitis/encephalopathy period) and a chronic phase (chronic focal resistant epilepsy) were defined. 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. 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. [ABSTRACT FROM AUTHOR]

In our study, preparation of voluntary movement was used to physiologically activate the motor cortex areas and the effect of this activation on CO2 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. [ABSTRACT FROM AUTHOR]

The post-stroke aftermath of patients suffering from atrial fibrillation (AF) is investigated. A total of 104 consecutive patients (80 with AF and 24 without AF) were referred to a rehabilitation centre and enrolled. They underwent a rehabilitative programme. Disability was assessed by using the Functional Independence Measure (FIM), at the time of admission, discharge and after 1 year. Death was more frequent over the 1-year interval in AF group. Ten patients died (42%), whereas in the non-AF group death occurred in 15 cases (19%). By using chi-square test, the difference was significant (P < 0.02). The logistic regression analysis indicated that the unique variable affecting the FIM at follow-up was the FIM at discharge (P < 0.0001). AF was not a significant variable in the equation. The result can be attributed to subject attrition in the AF group, as the most severe patients died and survivors could benefit from a better functional status. [ABSTRACT FROM AUTHOR]

Logistic regression and nonparametric receiver operating characteristic (ROC) analysis was carried out to investigate the association of umbilical artery diameter in single-artery fetuses with FGR and low birthweight. Single umbilical artery (SUA) increases the risk of fetal growth restriction (FGR) and low birthweight. [Extracted from the article]

Conclusions Our data confirm that IVF pregnancies are at higher risks of placental and umbilical cord abnormalities including PAS. The association between I in vitro i fertilisation (IVF) and placental abnormalities is known but there are currently no data of the effects of the use of donor oocytes on placentation. The aim of our study was to prospectively quantify the incidence of placenta abnormalities in IVF pregnancies in a large cohort, and to assess whether heterologous fertilisation is an additional risk factor for the development of these abnormalities. [Extracted from the article]

The author comments on a paper by N. Silvestrini and P. Rainville entitled "After-effects of Cognitive Control on Pain," in the current issue of the periodical which discusses the effect of cognitive task on subsequent pain perception and nociceptive flexion reflex (NFR). He points out the need for elucidating and investigating some of the topics in future studies. He evaluates why the results of the paper can not be applied to clinical practice.

Our aim is to assess the incidence of second cancer in long-time surviving primary mediastinal B-cell lymphoma (PMBCL) patients treated with combined radiochemoimmunotherapy (standard methotrexate with leucovorin rescue, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin with rituximab and mediastinal radiation therapy at a dose of 30 to 36 Gy). For this purpose, 92 points were evaluated. After a median overall survival of 137 months (range 76-212), we recorded second cancer in 3 of 80 long-surviving patients (3.75%) with cumulative incidence of 3.47% at 15 years and 11% at 17 years, with a 17-year second cancer-free survival of 82%. We observed 2 papillary thyroid cancers with a standardized incidence ratio (SIR) of 7.97 and an absolute excess risk (AER) of 17. 84 and 1 acute myeloid leukemia (AML) with an SIR of 66.53 and an AER of 10.05. No breast cancer occurred. Although we should take into account the limits of the proposed statistical analysis, combined modality treatment was related to a significant SIR and AER for thyroid cancer and acute myeloid leukemia., (Copyright © 2017 John Wiley & Sons, Ltd.)

Aims: Opioids and antidepressants that inhibit serotonin and norepinephrine reuptake (SNRI) are recognized as analgesics to treat severe and moderate pain, but their mechanisms of action in humans remain unclear. The present study aimed to explore how oxycodone (an opioid) and venlafaxine (an SNRI) modulate spinal and supraspinal sensory processing., Methods: Twenty volunteers were included in a randomized, double-blinded, three-way (placebo, oxycodone, venlafaxine), crossover study. Spinal and full scalp cortical evoked potentials (EPs) to median nerve stimulation were recorded before and after 5 days of treatment. Assessment of the central effects of the three treatments involved: (i) amplitudes and latencies of spinal EPs (spinal level); (ii) amplitudes and latencies of the P14 potential (subcortical level); (iii) amplitudes and latencies of early and late cortical EPs (cortical level); (iv) brain sources underlying early cortical Eps; and (v) brain networks underlying the late cortical EPs., Results: In the venlafaxine arm, the spinal P11 and the late cortical N60-80 latencies were reduced by 1.8% [95% confidence interval (CI) 1.7%, 1.9%) and 5.7% (95% CI 5.3%, 6.1%), whereas the early cortical P25 amplitude was decreased by 7.1% (95%CI 6.1%, 8.7%). Oxycodone increased the subcortical P14 [+25% (95% CI 22.2%, 28.6%)], early cortical N30 [+12.9% (95% CI 12.5%, 13.2%)] amplitudes and the late cortical N60-80 latency [+2.9% (95% CI 1.9%, 4.0%)]. The brainstem and primary somatosensory cortex source strengths were increased by 66.7% (95% CI 62.5%, 75.0%) and 28.8% (95% CI 27.5%, 29.6%) in the oxycodone arm, whereas the primary somatosensory cortex strength was decreased in the venlafaxine arm by 18.3% (95% CI 12.0%, 28.1%)., Conclusions: Opioids and SNRI drugs exert different central effects. The present study contributed to the much-needed human models of the mechanisms of action of drugs with effects on the central nervous system., (© 2016 The British Pharmacological Society.)

Although the inhibitory action that tactile stimuli can have on pain is well documented, the precise timing of the interaction between the painful and non-painful stimuli in the central nervous system is unclear. The aim of this study was to investigate this issue by measuring the timing of the amplitude modulation of laser evoked potentials (LEPs) due to conditioning non-painful stimuli. LEPs were recorded from 31 scalp electrodes in 10 healthy subjects after painful stimulation of the right arm (C6-C7 dermatomes). Non-painful electrical stimuli were applied by ring electrodes on the second and third finger of the right hand. Electrical stimuli were delivered at +50, +150, +200 and +250 ms interstimulus intervals (ISIs) after the laser pulses. LEPs obtained without any conditioning stimulation were used as a baseline. As compared to the baseline, non-painful electrical stimulation reduced the amplitude of the vertex N2/P2 LEP component and the laser pain rating when electrical stimuli followed the laser pulses only at +150 and +200 ms ISIs. As at these ISIs the collision between the non-painful and painful input is likely to take place at the cortical level, we can conclude that the late processing of painful (thermal) stimuli is partially inhibited by the processing of non-painful (cutaneous) stimuli within the cerebral cortex. Moreover, our results do not provide evidence that non-painful inputs can inhibit pain at a lower level, including the spinal cord., (© 2015 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

Aims: The cortical response to nociceptive thermal stimuli recorded as contact heat evoked potentials (CHEPs) may be altered by morphine. However, previous studies have averaged CHEPs over multiple stimuli, which are confounded by jitter between sweeps. Thus, the aim was to assess single-sweep characteristics to identify alterations induced by morphine., Methods: In a crossover study 15 single-sweep CHEPs were analyzed from 62 electroencephalography electrodes in 26 healthy volunteers before and after administration of morphine or placebo. Each sweep was decomposed by a continuous wavelet transform to obtain normalized spectral indices in the delta (0.5-4 Hz), theta (4-8 Hz), alpha (8-12 Hz), beta (12-32 Hz) and gamma (32-80 Hz) bands. The average distribution over all sweeps and channels was calculated for the four recordings for each volunteer, and the two recordings before treatments were assessed for reproducibility. Baseline corrected spectral indices after morphine and placebo treatments were compared to identify alterations induced by morphine., Results: Reproducibility between baseline CHEPs was demonstrated. As compared with placebo, morphine decreased the spectral indices in the delta and theta bands by 13% (P = 0.04) and 9% (P = 0.007), while the beta and gamma bands were increased by 10% (P = 0.006) and 24% (P = 0.04)., Conclusion: The decreases in the delta and theta band are suggested to represent a decrease in the pain specific morphology of the CHEPs, which indicates a diminished pain response after morphine administration. Hence, assessment of spectral indices in single-sweep CHEPs can be used to study cortical mechanisms induced by morphine treatment., (© 2015 The British Pharmacological Society.)

Objectives: We aimed to study knee proprioception and somatosensory evoked potentials (SEPs) to stimulation of the common peroneal nerve (CPN) in 7 patients with lesion of the anterior cruciate ligament (ACL) before and after ACL reconstruction., Materials and Methods: We recorded the spinal N14 and scalp P27 potentials in 5 patients, while in the remaining 2 patients we calculated scalp SEP maps by 20 electrodes. The knee proprioception was tested by comparing the sensitivity to movement of both the knees., Results: Before surgery, all patients showed decreased knee position sense and lack of the cortical P27 potential on the side of the ACL lesion. Arthroscopic reconstruction of the ligament improved neither the knee proprioception nor the somatosensory central conduction., Conclusion: We suggest that the loss of the knee mechanoreceptors can be followed by modifications of the central nervous system, which are not compensated by other nervous structures.