ObjectivesThe causes and nature of insensitivity to pain in schizophrenia remain unknown. The role of endorphins and the association of cognitive dysfunction and negative symptoms are postulated.MethodsIn this study, 43 patients with schizophrenia, five first-degree relatives, and 34 healthy controls were examined. Participants’ plasma concentrations of substance P, β-endorphin, and calcitonin gene-related peptide (CGRP) were assessed. In patients, the Trail-Making Test, the Color Reading Interference Test (Stroop test), and the Positive and Negative Syndrome Scale Negative Syndrome subscale (PANSS N) test were performed. We also evaluated pain threshold using nociceptive reflex (RTIII) testing.ResultsThe mean β-endorphin concentration was about 20% higher in patients than in healthy controls (P<0.05). CGRP concentrations were significantly higher in patients than in controls (5.34 ng/mL versus 4.16 ng/mL; P<0.01). Subjects treated with antipsychotic polytherapy had higher concentrations of CGRP than did patients treated with second-generation antipsychotic monotherapy (5.92 ng/mL versus 5.02 ng/mL; P<0.05). There were no correlations between any biochemical parameters and Trail-Making Test, Stroop test, and PANSS N scores. There were no differences in RTIII among study groups. Strong negative correlation (P<0.001) was found between PANSS N scores and subjective pain threshold on the right lower limb.ConclusionThe insensitivity to pain in schizophrenia is a complex phenomenon that is probably not related to changes in nociceptive pathways. Increase in β-endorphin level may be related to this issue, but it is uncertain if such concentration ensures analgesic effect. It is unknown if patients with schizophrenia in fact experience less pain. Cognitive impairment and excess negative symptoms may strongly influence the patient’s expression of pain.

POEMS syndrome is a rare multisystem disorder, characterized by the presence of polyneuropathy, organomegaly, endocrinopathy, monoclonal protein and skin changes. The variety of clinical pictures and asynchronous manifestation of dominant features make diagnosis difficult. We report a case of a 42-year-old man with polyneuropathy who was initially negative for monoclonal protein and so Guillain-Barré syndrome was diagnosed. Other signs and symptoms, including monoclonal gammopathy, developed later in the course of the disease and finally POEMS syndrome was diagnosed.

1 Pracownia EMG w Poradni Neurologicznej i Oddziale Dziennym Neurologicznym Centralnego Szpitala klinicznego instytutu stomatologii uniwersytetu Medycznego w Łodzi 2 oddział neurologii iii szpitala Miejskiego im dr. karola Jonschera w Łodzi 3 klinika chorób układu Pozapiramidowego uniwersytetu Medycznego w Łodzi A -przygotowanie projektu badania, B -zbieranie danych, C -analiza statystyczna, D -interpretacja danych, E -przygotowanie maszynopisu, F -opracowanie piśmiennictwa, G -pozyskanie funduszyPourazowe uszkodzenie nerwów obwodowych wymaga szczegółowej diagnostyki za pomocą badania przewodnictwa (eng) we włóknach ruchowych (McV) i czuciowych (scV) oraz elektromiografii (eMg). opierając się na klasyfikacji seddona i sunderlanda wyróżnia się zmiany świadczące o uszkodzeniu osłonki mielinowej (neurapraksja) i aksonu oraz struktur otaczających nerw (postaci aksonotmesis i neurotmesis). Badania wykonane bezpośrednio po urazie dają niepełny obraz i w celach rokowniczych zaleca się powtórzenie tych badań po 2-3 tygodniach, a w razie braku poprawy -po 3 miesiącach. W przypadku neurapraksji rokowanie jest korzystne. W eng stwierdza się zwolnienie szybkości przewodzenia i blok na wysokości uszkodzenia nerwu. W przypadku aksonotmesis rokowanie zależy od stopnia uszkodzenia nerwu, w eng obecne jest uszkodzenie o charakterze aksonalnym. odnerwienie w mięśniach pojawia się w okresie od 10 dni do 2 tygodni od momentu urazu i pozwala na rozróżnienie neurapraksji od uszkodzenia aksonu (aksonotmesis lub neurotmesis). Jeżeli dochodzi do pełnego uszkodzenia nerwu wraz z jego strukturami podtrzymującymi (neurotmesis) w zajętych mięśniach nie obserwuje się reinerwacji. regeneracja nerwu jest wtedy praktycznie niemożliwa. diagnostyka eng/eMg utrudniona jest przez częste występowanie urazów mnogich (również ośrodkowego układu nerwowego) oraz obecność wariantów unerwienia na wszystkich poziomach anatomicznych. Badanie neurofizjologiczne pozwala na lokalizację uszkodzenia, ocenę ewolucji zmian, umożliwia kwalifikację do zabiegu, jest również ważne w trakcie postępowań odszkodowawczych. Słowa kluczowe: elektromiografia, urazy nerwów, elektroneurografia.

Introduction: Altered sensitivity to pain in schizophrenia has been described in literature, but the knowledge of this issue is insufficient. Objectives: Case reports describing schizophrenia patients with painful medical conditions reported little or no pain. In all published studies except one, subjective test methods of pain were used. AIims: The study assessed pain threshold using objective test method and relationship between concentration of β-endorphin, substance P,CGRP and pain insensitivity in schizophrenia. The influence of negative symptoms and cognitive disorders on pain sensitivity was evaluated. Methods: 43 patients with schizophrenia, 5 healthy first degree relatives and 34 healthy volunteers were included in the study. All patients were in stable mental state and received neuroleptics. The concentration of β-endorphin, substance P,CGRP was measured and PANSS N , Trail Makin Test and Stroop test were performed. To assess pain threshold nociceptive reflex test (RIII) was used. Results: Concentration of β-endorphin and CGRP was 20% higher among patients compared with healthy subjects. Study groups did not differ in subjective and objective pain threshold. Negative correlation between Stroop Test performance and subjective pain threshold was found. Negative correlation between TMT performance and nociceptive reflex was observed. A strong negative correlation (p < 0.001) between PANSS N scores and nociceptive reflex was found. Conclusions: Patients with schizophrenia do not differ in objective pain threshold from healthy control. Insensitivity to pain could be the result of negative symptoms or working memory disorder. It is also possible that increased level of β-endorphin is related to hypoalgesia.

Progressive muscular atrophy (PMA), or the lower motor neuron disease, is a sporadic disorder characterized by onset in adulthood, pure lower motor neuron involvement and relatively benign course. Muscle atrophy and weakness may be symmetrical or asymmetrical, but they are always bilateral. We present a male patient with exclusively left-side flaccid paresis due to lower motor neuron disease without electromyographic evidence of neurogenic lesion of contralateral muscles and with no signs of corticospinal tracts involvement. The rapid disease progression was typical of the generalized phenotype of PMA and it suggested the relation to the aggressive course of classical ALS.