Unilateral progressive muscular atrophy with fast symptoms progression.

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.

Neurophysiological and Ultrasound Correlations in Guillain Barré Syndrome and CIDP-Case Series.

INTRODUCTION: Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are inflammatory polyneuropathies with an autoimmune etiology. These diseases differ mainly in the timing of their course but also in certain clinical differences. Electroneurography and electromyography are crucial for fulfilling the primary (for CIDP) and secondary (for GBS) diagnostic criteria. High-resolution ultrasound (HRUS) is recognized as a complementary method in the diagnosis of CIDP and GBS. AIM: The aim of this study was to present the neurophysiological and ultrasound findings of patients with clinically diagnosed inflammatory neuropathies (GBS and CIDP). MATERIAL AND METHODS: We collected data from clinically confirmed patients with GBS (3 persons) and CIDP (6 persons). The neurography and high-resolution ultrasound examinations according to the UPSS scale were performed. RESULTS: The neurography tests of GBS and CIDP patients showed mainly demyelinating lesions of the examined nerves, often with abnormal F-wave recordings. Examination using HRUS in GBS patients showed mild and regional nerve swelling with hypoechoic bundles with a predilection for proximal segments and cervical spinal nerve roots. In contrast, CIDP patients had diffused nerve swelling with hypoechoic bundles of greater severity and extent than those with GBS. CONCLUSION: Neurophysiological tests and HRUS of peripheral nerves, plexi, and roots performed together can be very valuable, complementary diagnostic methods for the early diagnosis and effective treatment of inflammatory polyneuropathies.

Guillain-Barré syndrome as the first manifestation of POEMS syndrome.

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.

Management of an iatrogenic injury to the tibial nerve in a 24-year-old hurdle runner.

According to previously published papers, neurovascular injuries seem to be the most unfortunate complications after surgical procedures. In this report, we present our therapeutic approach to iatrogenic injury of the posterior tibial nerve that occurred during ankle arthroscopy in a 24-year-old patient. The outcome of the therapy was a full sensory return and partial motor return (S4 and M3 according to the Medical Research Council Grading System for Nerve Recovery). Our patient was able to resume her typical training. In comparison with available reports, our therapeutic approach enabled earlier functional recovery after nerve injury. While sensory return is beneficial, motor improvement is also important. However, we are conscious of the poor functional outcomes reported by other researchers.

Pain perception in schizophrenia: influence of neuropeptides, cognitive disorders, and negative symptoms.

OBJECTIVES: The 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. METHODS: In this study, 43 patients with schizophrenia, five first-degree relatives, and 34 healthy controls were examined. Participants' plasma concentrations of substance P, ß-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. RESULTS: The mean ß-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. CONCLUSION: The insensitivity to pain in schizophrenia is a complex phenomenon that is probably not related to changes in nociceptive pathways. Increase in ß-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.