Designing a field trial of an equine grass sickness vaccine: A questionnaire-based feasibility study.

Without an experimental model of equine grass sickness (EGS), a randomised controlled field trial (RCT) represents the only method of evaluating the efficacy of Clostridium botulinum type C vaccination in preventing naturally occurring disease. Clinical trial feasibility is an important aspect of preliminary work undertaken prior to initiating RCTs, estimating parameters that are important for study design. This cross-sectional study aimed to assess the feasibility of conducting a nationwide RCT of a candidate vaccine for EGS based on responses from a sample of British equine veterinary practices (n = 119/284). Seventy-three percent of practices had attended ≥1 EGS case within the preceding 2 years (median four cases), and 51.3% regularly attended recurrently affected premises. Veterinary surgeons had greater confidence diagnosing acute/subacute EGS based solely on history and clinical signs compared to chronic EGS. Ninety-one percent of respondents (n = 103/113) considered the proposed RCT to be important/very important to equine veterinary research. Ninety-one percent of respondents (n = 102/112) indicated preparedness to assist in owner recruitment and 92.9% (n = 104/112) indicated willingness to participate in a RCT. The most frequent reasons for practices declining to participate were low incidence of EGS (n = 4), did not believe clients would wish to participate (n = 3) and amount of paperwork/data collection involved (n = 2). There was considerable support amongst participating veterinary practices for a RCT evaluating the efficacy of Clostridium botulinum vaccination for the prevention of EGS in Britain. Substantial proportions of participating practices would be prepared to participate in the RCT and regularly attended EGS-affected premises that would meet trial inclusion criteria.

Pharmacological Therapy for the Prevention and Treatment of Weakness After Critical Illness: A Systematic Review.

OBJECTIVES: ICU-acquired weakness is a common complication of critical illness and can have significant effects upon functional status and quality of life. As part of preliminary work to inform the design of a randomized trial of a complex intervention to improve recovery from critical illness, we sought to identify pharmacological interventions that may play a role in this area. DATA SOURCES: We systematically reviewed the published literature relating to pharmacological intervention for the treatment and prevention of ICU-acquired weakness. STUDY SELECTION: We searched MEDLINE, EMBASE, CINAHL+, Web of Science, and both U.S. and European trial registries up to July 2014 alongside reviews and reference lists from populations with no age or language restrictions. We included studies that reported a measure of muscle structure or physical function as an outcome measure. DATA EXTRACTION: We estimated pooled odds ratios and 95% CI using data extracted from published articles or where available, original data provided by the authors. Assessment of bias was performed using the Cochrane Collaboration's risk of bias tool. DATA SYNTHESIS: Ten studies met the inclusion criteria. The current body of evidence does not support the use of any pharmacological agent in this setting, although maintaining euglycemia may reduce the prevalence of critical illness polyneuropathy. CONCLUSIONS: At present, no pharmacological intervention can be recommended to prevent or treat ICU-acquired weakness. Further research is required into this field to include more novel agents such as myostatin inhibitors. Challenges in the conduct of research in this area are highlighted.

[Justifying standards of workup in patients with occupational polyneuropathy caused by physical overload].

The authors examined algorithm of investigations in occupational pathology centers for suspected occupational polyneuropathy due to physical overload. Suggestions included a procedure to investigate the patients, including medical specialists consultations, set of laboratory and instrumental studies divided into obligatory and by special indications.

Isoniazid-induced polyneuropathy in a tuberculosis patient - implication for individual risk stratification with genotyping?

BACKGROUND: Development of polyneuropathy (PNP) under treatment for tuberculosis (TB), including isoniazid (INH), is a highly relevant adverse drug effect. The NAT2 acetylation status is a predictor of potential toxic effects of INH. The question as to whether individual risk stratification by genotyping is useful to avoid suffering of patients and to lower costs for the health care system is of considerable clinical importance. CASE PRESENTATION: After drug treatment for TB, including INH, a 23-year-old man developed severe PNP. During the treatment, laboratory results have been indicating incipient liver and renal injury. Later, molecular genetic analyses were performed and revealed a variation in the NAT2 gene and the c1/c2 genotype of the CYP2E1 gene, both described to contribute to an elevated risk for anti-tuberculostatic-induced liver damages (ATIL). CONCLUSION: The combination of metabolizer genotypes should be taken into account as a cause for toxic effects and the development of PNP. Individual genotyping, performed before medication or at least if an elevation of liver parameters is observed, may reduce the risk of severe cases of PNP by early adjustment of treatment. Our case study indicates that evaluation of individual risk stratification with systematic pharmacogenetic genotyping of metabolizer gene combinations in the context of TB treatment should be addressed in clinical studies with larger cohorts.

Near-normoglycaemia and development of neuropathy: a 24-year prospective study from diagnosis of type 1 diabetes.

OBJECTIVE: Complete prevention of diabetic neuropathies has not been previously demonstrated. We sought to determine whether long-term near-normoglycaemia maintained from the diagnosis of type 1 diabetes is associated with polyneuropathy and cardiac autonomic dysfunction. DESIGN: Prospective observational study over 24 years. SETTING: Ambulatory care. PARTICIPANTS: 32 newly diagnosed patients with type 1 diabetes aged 20.3 ± 1.0 years, duration of diabetes 2.7 ± 0.3 weeks. INTERVENTION: Insulin therapy according to standards of care. PRIMARY AND SECONDARY OUTCOME MEASURES: Motor and sensory nerve conduction velocity (MNCV and SNCV), heart rate variability (HRV), and confirmed clinical polyneuropathy measured at 15 time points over 24 years and quantitative sensory testing (QST) determined over 20-22 years. RESULTS: 11 patients were well controlled over 24 years with mean glycated haemoglobin (HbA1c) <7.0% (6.5 ± 0.1%; group 1), whereas 21 patients were poorly controlled (mean HbA1c ≥ 7.0%: 8.3 ± 0.2%; group 2). After 24 years, MNCV was faster in group 1 versus group 2 in the median (55.5 ± 1.6 vs 48.9 ± 1.6 m/s), ulnar (56.5 ± 1.5 vs 49.3 ± 1.7 m/s) and peroneal nerve (44.7 ± 1.6 vs 36.8 ± 2.5 m/s), while SNCV was faster in the median (53.6 ± 1.6 vs 45.5 ± 2.8 m/s), ulnar (54.7 ± 1.8 vs 43.0 ± 3.9 m/s), and sural nerve (44.5 ± 1.8 vs 35.5 ± 2.6 m/s; all p<0.05). The annual decline in peroneal MNCV and sural SNCV in group 1 was sixfold and threefold faster in group 2 than in group 1, respectively. Likewise, impairment in QST and HRV developed at faster rates in group 2. After 24 years, 64% of patients in group 2, but none in group 1, developed confirmed clinical polyneuropathy. CONCLUSIONS: Near-normoglycaemia maintained from the diagnosis of type 1 diabetes over 24 years was associated with a complete prevention of the decline in hyperglycaemia-related peripheral and autonomic nerve function, and development of confirmed clinical polyneuropathy.

Demonstration of ameliorative effect of lacosamide: in a rat model of sepsis-induced critical illness polyneuropathy.

OBJECTIVES: Critical illness neuropathy (CIN) is a condition that may occur in diseases with severe systemic response, particularly in sepsis. The aim of this study is to investigate the potential anti-inflammatory and lipid-peroxidation inhibiting activities of lacosamide by measuring tumour necrotizing factor-alpha (TNF-alpha), C-reactive protein (CRP), malondialdehyde (MDA) and white blood cells (WBC) using electroneuromyography (ENMG) in rats with sepsis-induced critical illness neuropathy (SICIN). METHODS: Cecal ligation and puncture (CLP) procedure was performed on 39 rats to induce a sepsis model. The study groups were designed as follows: Group 1: normal (nonoperative); Group 2: (sham-operated); Group 3: CLP (untreated group); Group 4: CLP and lacosamide 20 mg/kg; Group 5: CLP and lacosamide 40 mg/kg. TNF-alpha, C reactive protein, MDA and WBC levels was measured and compound muscle action potential (CMAP) distal latans, amplitudes were measured by using ENMG in rats with SICIN. RESULTS: When untreated sepsis group was compared with both control and sham groups, CMAP amplitudes and latans were significantly lower (P < 000.1). When CLP, CLP+lacosamide 20 mg/kg and CLP+lacosamide 40 mg/kg groups were compared, plasma levels of TNF-alpha and MDA were significantly higher in the untreated CLP group (F = 12.74, P < 0.0001), (F = 19.43, P < 0.05). In the CLP+lacosamide 40 mg/kg group, CRP levels were significantly lower only compared to the CLP group (P < 0.001). DISCUSSION: We have showed that lacosamide may have beneficial effects on early SICIN by its potential anti-inflammatory and lipid peroxidation inhibiting activities; however, further comprehensive studies are required to clarify these effects.

Primer caso descrito de parálisis aislada, completa y fluctuante del III nervio craneal como forma de inicio de un mieloma múltiple / First case described of isolated, complete and fluctuating cranial nerve III palsy heralding multiple myeloma

Introducción. El mieloma múltiple es la neoplasia de células plasmáticas más frecuente. Al ser incurable, el tratamiento persigue obtener el mayor tiempo de supervivencia libre de clínica. Constituye una causa extremadamente rara de afectación de los nervios craneales y es producido habitualmente por un plasmocitoma intracraneal. Presentamos un caso de mieloma múltiple, que asociaba un plasmocitoma intracraneal y que comenzó clínicamente con parálisis aislada, completa y fluctuante del III nervio craneal. Caso clínico. Mujer de 63 años que acudió a urgencias por presentar un cuadro clínico oscilante, consistente en diplopía binocular horizontal y, posteriormente, cefalea. La exploración neurooftalmológica reveló una parálisis completa del III nervio craneal derecho. Se solicitó una tomografía axial computarizada craneal urgente, que reveló múltiples lesiones osteolíticas diploicas, asociando una de ellas componente de partes blandas en la hendidura esfenoidal derecha. La paciente fue ingresada, y se le diagnosticó posteriormente un mieloma múltiple IgA-k. Tras recibir inducción quimioterápica y ser sometida a un trasplante autólogo de progenitores hematopoyéticos, alcanzó la remisión completa. Conclusiones. El mieloma múltiple es un trastorno raro de los nervios craneales, una causa muy infrecuente de parálisis aislada y completa del III nervio craneal y menos aún fluctuante, y no se ha encontrado ningún caso publicado con este inicio clínico. Tener en cuenta las posibles manifestaciones neurooftalmológicas del mieloma múltiple puede contribuir a un diagnóstico precoz y a una incidencia positiva sobre el curso de esta enfermedad (AU)

Introduction. Multiple myeloma is the most common plasma-cell malignancy. To be incurable, treatment aims to obtain the longest non-clinical survival time. Cranial nerve palsy in multiple myeloma is extremely rare and is usually due to an intracranial plasmacytoma. We present a multiple myeloma case, with an intracranial plasmacytoma, which debuted clinically with isolated, complete and fluctuating cranial nerve III palsy. Case report. A 63-year-old woman presented an oscillating clinical picture, consisting of horizontal binocular diplopia and later, headache. The neuro-ophthalmologic examination revealed a complete cranial nerve III palsy of the right eye. An urgent cranial CT-scan was requested. It showed multiple diploic osteolytic lesions, associating soft-parts component in the right superior orbital fissure. The patient was admitted, being diagnosed subsequently of IgA-k multiple myeloma. After receiving induction-chemotherapy and undergoing autologous stem cell transplantation, she achieved full remission. Conclusions. Multiple myeloma is a rare cranial nerves disorder, very uncommon cause of cranial nerve III full isolated paralysis and even less fluctuating, not having found any case published with this clinical onset. Awareness of possible multiple myeloma neuro-ophthalmic manifestations may bring about an early diagnosis and a positive impact on the disease course (AU)

Interventions for preventing critical illness polyneuropathy and critical illness myopathy.

BACKGROUND: Critical illness polyneuropathy or myopathy (CIP/CIM) is a frequent complication in the intensive care unit (ICU) and is associated with prolonged mechanical ventilation, longer ICU stay and increased mortality. This is an interim update of a review first published in 2009 (Hermans 2009). It has been updated to October 2011, with further potentially eligible studies from a December 2013 search characterised as awaiting assessment. OBJECTIVES: To systematically review the evidence from RCTs concerning the ability of any intervention to reduce the incidence of CIP or CIM in critically ill individuals. SEARCH METHODS: On 4 October 2011, we searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL, MEDLINE, and EMBASE. We checked the bibliographies of identified trials and contacted trial authors and experts in the field. We carried out an additional search of these databases on 6 December 2013 to identify recent studies. SELECTION CRITERIA: All randomised controlled trials (RCTs), examining the effect of any intervention on the incidence of CIP/CIM in people admitted to adult medical or surgical ICUs. The primary outcome was the incidence of CIP/CIM in ICU, based on electrophysiological or clinical examination. Secondary outcomes included duration of mechanical ventilation, duration of ICU stay, death at 30 and 180 days after ICU admission and serious adverse events from the treatment regimens. DATA COLLECTION AND ANALYSIS: Two authors independently extracted the data and assessed the risk of bias in included studies. MAIN RESULTS: We identified five trials that met our inclusion criteria. Two trials compared intensive insulin therapy (IIT) to conventional insulin therapy (CIT). IIT significantly reduced CIP/CIM in the screened (n = 825; risk ratio (RR) 0.65, 95% confidence interval (CI) 0.55 to 0.77) and total (n = 2748; RR 0.70, 95% CI 0.60 to 0.82) population randomised. IIT reduced duration of mechanical ventilation, ICU stay and 180-day mortality, but not 30-day mortality compared with CIT. Hypoglycaemia increased with IIT but did not cause early deaths.One trial compared corticosteroids with placebo (n = 180). The trial found no effect of treatment on CIP/CIM (RR 1.27, 95% CI 0.77 to 2.08), 180-day mortality, new infections, glycaemia at day seven, or episodes of pneumonia, but did show a reduction of new shock events.In the fourth trial, early physical therapy reduced CIP/CIM in 82/104 evaluable participants in ICU (RR 0.62. 95% CI 0.39 to 0.96). Statistical significance was lost when we performed a full intention-to-treat analysis (RR 0.81, 95% CI 0.60 to 1.08). Duration of mechanical ventilation but not ICU stay was significantly shorter in the intervention group. Hospital mortality was not affected but 30- and 180-day mortality results were not available. No adverse effects were noticed.The last trial found a reduced incidence of CIP/CIM in 52 evaluable participants out of a total of 140 who were randomised to electrical muscle stimulation (EMS) versus no stimulation (RR 0.32, 95% CI 0.10 to 1.01). These data were prone to bias due to imbalances between treatment groups in this subgroup of participants. After we imputed missing data and performed an intention-to-treat analysis, there was still no significant effect (RR 0.94, 95% CI 0.78 to 1.15). The investigators found no effect on duration of mechanical ventilation and noted no difference in ICU mortality, but did not report 30- and 180-day mortality.We updated the searches in December 2013 and identified nine potentially eligible studies that will be assessed for inclusion in the next update of the review. AUTHORS' CONCLUSIONS: There is moderate quality evidence from two large trials that intensive insulin therapy reduces CIP/CIM, and high quality evidence that it reduces duration of mechanical ventilation, ICU stay and 180-day mortality, at the expense of hypoglycaemia. Consequences and prevention of hypoglycaemia need further study. There is moderate quality evidence which suggests no effect of corticosteroids on CIP/CIM and high quality evidence that steroids do not affect secondary outcomes, except for fewer new shock episodes. Moderate quality evidence suggests a potential benefit of early rehabilitation on CIP/CIM which is accompanied by a shorter duration of mechanical ventilation but without an effect on ICU stay. Very low quality evidence suggests no effect of EMS, although data are prone to bias. Strict diagnostic criteria for CIP/CIM are urgently needed for research purposes. Large RCTs need to be conducted to further explore the role of early rehabilitation and EMS and to develop new preventive strategies.

The beneficial effects of levetiracetam on polyneuropathy in the early stage of sepsis in rats: electrophysiological and biochemical evidence.

ABSTRACT Critical illness polyneuropathy (CIP) is a common complication in long (≥1 week) critical/intensive care hospitalizations. Rapidly progressing atrophy and weakness of the limb, trunk and, particularly, respiratory muscles may lead to severe morbidity or mortality. The aim of the present study was to investigate the protective effects of levetiracetam (LEV) on CIP in the early stage of sepsis in rats. We simulated CIP by a surgically induced sepsis model and verified it by lower-limb electromyography (EMG) (amplitude and duration of CMAP, and distal latency). We evaluated the effects of various doses of LEV treatment (300, 600, and 1200 mg/kg i.p.) on CIP by performing electrophysiology, and determining plasma tumor necrosis factor (TNF)-α, lipid peroxides (malondialdehyde, MDA) levels, and total antioxidant capacity (TAC). Our data showed: (1) significant suppression of CMAP amplitude and prolongation of distal latency in the saline-treated sepsis group, and distal latency as well as CMAP amplitudes benefiting best from the 600 mg/kg LEV treatment; (2) significant rise in plasma TNF-α and MDA levels in the saline-treated sepsis group, but significant ameliorations by the 600 and 1200 mg/kg LEV treatment; (3) highly significant suppression of TAC in the saline-treated group, but profound reversals in all LEV-treated groups. We conclude that 300, 600, and 1200 mg/kg i.p. doses of post-septic treatment by LEV has possibly acted in a dose-dependent manner to both protect and restore the affected peripheral nerves' axon and myelin following surgical disturbance of the cecum to induce sepsis and consequent polyneuropathy.

[Thalidomide in the treatment of multiple myeloma: focus on combination with bortezomib]. / Thalidomid v lécbe mnohocetného myelomu se zamerením na kombinaci s bortezomibem.

Thalidomide, the first clinically available immunomodulatory drug, reaches monotherapy treatment response in about 1/ 3 of significantly pretreated patients with multiple myeloma, and in combination with glucocorticoids approximately 50% response rate. After addition of conventional cytostatic into the triple combination, therapeutic response is achieved in 80% of untreated patients or about 60% of pretreated patients. Therapeutic response is achieved even in 1/3 of patients with refractory multiple myeloma resistant to other available treatment. With regard to the frequency of adverse effects, particularly peripheral polyneuropathy, its use as maintenance therapy was nearly abandoned. The combination of thalidomide and bortezomib has a high therapeutic potential that was accompanied by a high frequency of peripheral polyneuropathy in entry studies. After optimizing bortezomib schedule and route of administration, which lead to significant reduction in the frequency of polyneuropathy, this combination is currently a very interesting therapeutic alternative for clinical practice. This is one of the most economically available treatment regimens combining the benefits of two major drug classes in the treatment of multiple myeloma -  proteasome inhibitor and imunumodulatory drugs. There is also a renewed interest in thalidomide following sharp decline in its use in recent years in the Czech Republic. Comprehensive work is focused on summarizing the longterm experience with thalidomide, with special reference to combination with bortezomib.

Protective effect of coenzyme Q10 in paclitaxel-induced peripheral neuropathy in rats.

OBJECTIVE: To investigate the possible protective effect of coenzyme Q10 (CQ10) on neuropathy in rats. METHODS: Experiments were conducted in the Department of Pharmacology, Faculty of Medicine, Hacettepe University, Ankara, Turkey between January and March 2012. Forty rats were divided into 4 groups: group 1 (control), group 2 (paclitaxel), group 3 (control + CQ10), and group 4 (paclitaxel + CQ10). Group 2 and 4 rats received paclitaxel (2 mg/kg, intraperitoneally, on days 0, 2, 4, 6). Group 3 and 4 rats were treated with CQ10 (10 mg/kg, intraperitoneally, on days 0, 1, 2, 3, 4, 5, 6, 7, 8, 9). The rats that did not receive paclitaxel or CQ10 received vehicle. Mechanical allodynia tests were performed for each animal on day 0, 2, 6, 8, 10, 14, 16, 19, 39 and 41 for all groups with von Frey filaments. RESULTS: At day 0, mean mechanical withdrawal thresholds were similar among all groups. Starting from day 2, the threshold of the paclitaxel group decreased. Starting from day 10, paclitaxel+CQ10 treated rats had significantly higher thresholds compared with the paclitaxel group, but these values were still significantly lower than that of the controls. Control and control + CQ10 rats had similar threshold values during the protocol. CONCLUSION: The CQ10 treatment decreased the degree of paclitaxel-induced peripheral neuropathy in rats.

Whither pathogenetic treatments for diabetic polyneuropathy?

Diabetic distal symmetric polyneuropathy (DSPN) occurs in around one-third of patients with diabetes and is associated with significant morbidity and increased mortality. Diagnosis and clinical assessment of DSPN remain a challenge, not only for the physician in clinical practice but also for clinical trials. Optimal diabetes control is generally considered an essential first step in the prevention and management of DSPN. However, glycaemic control alone may be insufficient to prevent the development or progression of DSPN, especially in type 2 diabetes. Near-normoglycaemia is also difficult to achieve in a significant proportion of patients. Although considerable advances have been made in symptomatic pain management, these have not addressed the problem of sensory deficits and have no impact on the underlying pathogenesis of DSPN. There remains a lack of treatment options that effectively target the natural history of the disease. Several pathogenetic treatment approaches have been investigated, but evidence from clinical trials is limited with a number of treatments having shown disappointing results. However, some pathogenetic therapies have shown clinically relevant improvements in neuropathic endpoints in randomised controlled trials, in particular α-lipoic acid and Actovegin. These advances in DSPN disease modification need to be confirmed with further robust evidence from clinical trials together with a better understanding of the mechanisms of action of promising treatments.

Comparison of melatonin and oxytocin in the prevention of critical illness polyneuropathy in rats with experimentally induced sepsis.

BACKGROUND: Critical illness polyneuropathy is an acute neuromuscular disorder of critically ill patients and is characterized by limb and respiratory muscle weakness. The purpose of the study was to evaluate the neuroprotective effects of melatonin (MEL) and oxytocin (OT) on the early stage of sepsis by recording compound muscle action potentials and measuring plasma tumor necrosis factor (TNF)-α levels, lipid peroxidation (malondialdehyde; MDA), and total antioxidant capacity. MATERIALS AND METHODS: One hundred adult male Sprague-Dawley rats were included in the study. The cecal ligation and puncture (CLP) procedure was performed to induce the sepsis model. MEL (10, 20, and 40 mg/kg), OT (0.4, 0.8, and 1.6 mg/kg), and a combination of MEL (20 mg/kg) and OT (0.8 mg/kg) were administered intraperitoneally in the first hour of surgery. Electromyography (EMG) studies were achieved 24 h after CLP surgery and then blood samples were collected for biochemical measurements. RESULTS: EMG findings revealed that compound muscle action potential amplitude was significantly decreased and distal latency was prolonged in the CLP group compared with the sham group (P < 0.05 and P < 0.0005). Moreover, the animals that received CLP surgery showed significantly higher TNF-α and MDA levels and lower total antioxidant capacity values than the sham group. The administration of MEL and OT to rats significantly abolished the EMG alterations and suppressed oxidative stress and TNF-α release in CLP-induced rats. CONCLUSIONS: The inflammatory processes and imbalance in oxidative/antioxidative status play important roles in the pathogenesis of critical illness polyneuropathy. We suggest that both oxytocin and melatonin may have beneficial effects against sepsis-induced polyneuropathy in critical illness.

[Study about target-network of anti-cerebral infarction neuropathy based on theory of neurovascular unit and network pharmacology].

OBJECTIVE: Potention drug-targets on anti-neuropathy of stroke were summarized, and it will provide materials for developing innovation components traditional Chinese medicine on anti-cerebral infarction neuropathy. METHOD: This article had done a series of researching work about neurovascular unit which includes three kinds of cells: neuron, gliacyte,brain microvascular endothelial cell, then signal mechanism of cell death or apoptosis of each section of stroke neuropathy was analysised by the historical documents. RESULT: There are five important pathways: inflammatory factor-MMPs pathway- Caspases, Ca2+ -mitochondrial pathway-Caspases, Ca2+ -Phospholipase-PI-3K/AK pathway, Ca2+ -radical-MAPK pathway, Ca2+ -NO-protease pathway, among all the nodes, Caspases, Ca2+, NO were the most important ones. CONCLUSION: Developing the multi-mechanism and multilevel of traditional chinese medicine under the guidance of the theories of network pharmacology and neurovascular unit will play an important role in studying the key links of signal-network of stroke neuropathy.

The significance of folate deficiency in alcoholic and nutritional neuropathies: analysis of a case.

OBJECTIVE: To elucidate the significance of folate deficiency in alcoholic and nutritional neuropathies. METHODS: We preformed a comprehensive clinical screening of a patient with chronic alcoholism who manifested neuropathy, macrocytic anemia, liver dysfunction, and folate deficiency. RESULTS: A 33-y-old woman with chronic alcoholism presented with acutely progressive glove- and stocking-type sensorimotor polyneuropathy. Although an episode of neuropathy preceded the current episode by 2 y, its cause was never determined. The findings of nerve conduction studies were indicative of axonal neuropathy. Laboratory findings revealed macrocytic anemia and liver dysfunction. Her serum level of folate was reduced, whereas thiamine, riboflavin, and cobalamin levels were within normal range. The neuropathy and anemia showed gradual recovery after the initiation of folic acid supplementation. CONCLUSIONS: This case study indicates that folate deficiency should be monitored closely in patients with chronic alcoholism and associated malnutrition. Additionally, folate deficiency should be considered as a differential diagnosis of neuropathy.

Muscle weakness in septic patients requiring mechanical ventilation: protective effect of transcutaneous neuromuscular electrical stimulation.

PURPOSE: The aim of this study was to evaluate the effect of transcutaneous neuromuscular electrical stimulation (NMES) on muscle strength in septic patients requiring mechanical ventilation (MV). METHODS: Sixteen septic patients requiring MV and having 1 or more organ failure other than respiratory dysfunction were enrolled within 48 hours from admission to the intensive care unit. Neuromuscular electrical stimulation was administered twice a day on brachial biceps and vastus medialis (quadriceps) of 1 side of the body until MV withdrawal. Blinded investigators measured arm and thigh circumferences, biceps thickness by ultrasonography, and muscle strength after awakening with Medical Research Council scale. RESULTS: Two patients died before strength evaluation and were excluded from the analysis. Neuromuscular electrical stimulation was applied for 13 days (interquartile range, 7-30 days). Biceps (P = .005) and quadriceps (P = .034) strengths were significantly higher on the stimulated side at the last day of NMES. Improvement was mainly observed in more severe and weaker patients. Circumference of the nonstimulated arm decreased at the last day of NMES (P = .015), whereas no other significant differences in limb circumferences or biceps thickness were observed. CONCLUSION: Neuromuscular electrical stimulation was associated with an increase in strength of the stimulated muscle in septic patients requiring MV. Neuromuscular electrical stimulation may be useful to prevent muscle weakness in this population.

[Dynamics of blood concentration of neurospecific proteins and risk of neuropathy development in the conditions of 105-day confinement].

Six male volunteers (aged 25 to 40 years) were subjects in all-round psychophysiological, hormonal and immunological studies before, in and after 105-day isolation and confinement. Blood was drawn and the 16-factorial Cattell personality inventory was filled out every 30 days. Concentrations of blood hormones, neurospecific proteins and cytokines point to a close interrelation between antibody titers to myelin-associated glycoprotein and changes in the parameters of metabolism and reproduction-related hormones, as well as cytokines and individual psychophysiology (extra-introversion, dominance, intropunitiveness, social contact selectivity, etc.), and suggest a minimum risk of demyelinizing neuropathy due to exposure to the conditions of isolation and confinement.