Effect of Active and Passive Mechanical Thromboprophylaxis and Consensual Effect on the Venous Blood Flow Velocity Among Hemiparetic Patients.

Our aim was to measure the venous blood flow velocity (VBFV) in case of hemiparetic patients, after passive and active thromboembolic methods, as well as the consensual effect in the hemiparetic limb following the active venous exercises in the healthy limb. We examined 215 patients, with the median age of 58.0 (55.0-63.0) years. The VBFV was measured with a HADECO BIDOP ES-100 V II type Doppler ultrasound device, using an 8 MHz head, on the femoral vein at the level of the hip joint. For statistical analysis, SPSS version 22 was used. After passive movement, on the hemiparetic side, compared to the value in resting state, the VBFV significantly (12.6; 11.6-13.5 cm/s; P < .001) increased. Following active venous exercises performed on the healthy side, the VBFV significantly (18.0; 15.6-19.6 cm/s; P < .001) increased compared to the value in resting state. Following the active venous exercises performed on the healthy side, the VBFV measured on the hemiparetic side (consensual effect) was significantly (15.1 [14.1-16.5] cm/s; P < .001) higher than the value on the hemiparetic side in resting state. Active and passive mechanical thromboprophylaxis methods can be effective. Movements of the healthy limb significantly increase the VBFV in the inactive limb, and patients can perform it themselves several times a day.

Transient Expression of Interleukin-21 in the Second Hit of Acute Pancreatitis May Potentiate Immune Paresis in Severe Acute Pancreatitis.

OBJECTIVES: Interleukin-21 (IL-21) is a cytokine associated with tissue inflammation, autoimmune and infectious diseases. Organ dysfunction and death can occur in patients with acute pancreatitis (AP) in two distinct clinical phases. Initially, a systemic inflammatory response syndrome may be followed by systemic sepsis from infected pancreatic necrosis, known as the "second hit." The expression and possible role of IL-21 in AP has not been established. METHODS: Thirty-six patients with mild, moderate, and severe AP (SAP) were enrolled. Peripheral blood samples of patients were drawn on days 7, 9, 11, and 13. Reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed to determine the expression and concentration of IL-21. RESULTS: Interleukin-21 mRNA levels increased significantly at day 9 in severe (P = 0.002) pancreatitis compared with both the mild and control patient groups. At the protein level, IL-21 was elevated in SAP patients compared with those with mild pancreatitis, although this was not significant. Furthermore, day 9 IL-21 was elevated in septic SAP patients and patients with pancreatic necrosis. CONCLUSIONS: Interleukin-21 is transiently elevated in SAP compared with the mild/moderate group, and hence IL-21 may contribute to the immune imbalance that occurs in AP.

Idiopathic benign paroxysmal positional vertigo with persistent vertigo/dizziness sensation is associated with latent canal paresis, endolymphatic hydrops, and osteoporosis.

OBJECTIVE: The aim of the present study was to examine the association of neuro-otological examination, blood test, and scoring questionnaire data with treatment-resistant intractability in idiopathic benign paroxysmal positional vertigo (BPPV) patients. METHODS: We experienced 1520 successive vertigo/dizziness patients at the Vertigo/Dizziness Center in Nara Medical University during May 2014 to April 2018. Six hundred and eleven patients were diagnosed as BPPV (611/1520; 40.2%) according to the diagnostic guideline of the International Classification of Vestibular Disorder in 2015. Among BPPV patients, there were 201 intractable patients (201/611; 32.9%), 66 of whom were idiopathic and enrolled to be hospitalized and receive neuro-otological examinations, including the caloric test (C-test), vestibular evoked cervical myogenic potentials (cVEMP), subjective visual vertical (SVV), glycerol test (G-test), electrocochleogram (ECoG), inner ear magnetic resonance imaging (ieMRI), blood tests including anti-diuretic hormone (ADH) and bone alkaline phosphatase (BAP), and self-rating questionnaires of depression score (SDS). Sixty-six patients were diagnosed as horizontal type cupula (hBPPVcu; n=30), horizontal type canal (hBPPVca; n=10), posterior type (n=20), and probable and/or atypical BPPV (n=6). Data are presented as ratios (+) of the number of idiopathic BPPV patients with examination and questionnaire data outside of the normal range. RESULTS: The ratio (+) data were as follows: C-test=21.2% (14/66), cVEMP=24.2% (16/66), SVV=48.5% (32/66), G-test=18.2% (12/66), ECoG=18.2% (12/66), ieMRI=12.1% (8/66), ADH=9.1% (6/66), BAP=13.6% (9/66), and SDS=37.9% (25/66). Multivariate regression analysis revealed that the periods of persistent vertigo/dizziness were significantly longer in BPPV patients with hBPPVcu, C-test (+), endolymphatic hydrops (+), and BAP (+) compared with those with negative findings. CONCLUSION: Although patients with idiopathic BPPV are usually treatable and curable within 1 month, the presence of hBPPVcu, canal paresis, endolymphatic hydrops, and elevated BAP may make the disease intractable, and thus require additional treatments.

Exercise intensity affects acute neurotrophic and neurophysiological responses poststroke.

Aerobic exercise may acutely prime the brain to be more responsive to rehabilitation, thus facilitating neurologic recovery from conditions like stroke. This aerobic priming effect could occur through multiple mechanisms, including upregulation of circulating brain-derived neurotrophic factor (BDNF), increased corticospinal excitability, and decreased intracortical inhibition. However, optimal exercise parameters for targeting these mechanisms are poorly understood. This study tested the effects of exercise intensity on acute BDNF and neurophysiological responses. Sixteen ambulatory persons >6 mo poststroke performed three different 20-min exercise protocols in random order, approximately 1 wk apart, including the following: 1) treadmill high-intensity interval training (HIT-treadmill); 2) seated-stepper HIT (HIT-stepper); and 3) treadmill moderate-intensity continuous exercise (MCT-treadmill). Serum BDNF and transcranial magnetic stimulation measures of paretic lower limb excitability and inhibition were assessed at multiple time points during each session. Compared with MCT-treadmill, HIT-treadmill elicited significantly greater acute increases in circulating BDNF and corticospinal excitability. HIT-stepper initially showed BDNF responses similar to HIT-treadmill but was no longer significantly different from MCT-treadmill after decreasing the intensity in reaction to two hypotensive events. Additional regression analyses showed that an intensity sufficient to accumulate blood lactate appeared to be important for eliciting BDNF responses, that the interval training approach may have facilitated the corticospinal excitability increases, and that the circulating BDNF response was (negatively) related to intracortical inhibition. These findings further elucidate neurologic mechanisms of aerobic exercise and inform selection of optimal exercise-dosing parameters for enhancing acute neurologic effects. NEW & NOTEWORTHY Acute exercise-related increases in circulating BDNF and corticospinal excitability are thought to prime the brain for learning. Our data suggest that these responses can be obtained among persons with stroke using short-interval treadmill high-intensity interval training, that a vigorous aerobic intensity sufficient to generate lactate accumulation is needed to increase BDNF, that interval training facilitates increases in paretic quadriceps corticospinal excitability, and that greater BDNF response is associated with lesser intracortical inhibition response.

Thyroxine-induced periodic paralysis: a rare complication of nutritional supplements.

The consumption of daily nutritional supplements has risen dramatically all over the world. Many people believe that dietary supplements, if not useful, are at least safe to fulfil small dietary gaps. Many nutritional supplements have not been approved by Federal Drug Administration due to their unregulated active ingredients, but they are available as over the counter. One of the active ingredients, exogenous triiodothyronine (T3), has been reported in dietary supplements. We present a case of sudden onset of tetraparesis. Laboratory workup showed hypokalaemia, low thyroid-stimulating hormone and thyroxine (T4) but normal T3 and thyroglobulin levels. The radioiodine uptake scan also showed reduced uptake. After aggressive serum potassium correction and stopping supplements, his condition got improved. So the suspicion of exogenous T3-induced thyrotoxic periodic paralysis was confirmed.

Changes in Quadriceps Muscle Thickness, Disease Severity, Nutritional Status, and C-Reactive Protein after Acute Stroke.

BACKGROUND: Lower leg muscle wasting is common in stroke patients; however, patient characteristics in the acute phase are rarely studied. This study aimed to examine the relationship between changes in quadriceps muscle thickness and disease severity, nutritional status, and C-reactive protein (CRP) levels after acute stroke. METHODS: Thirty-one consecutive patients with acute intracerebral hemorrhage or ischemic stroke had quadriceps muscle thickness measured in the paretic and nonparetic limbs within 1 week after admission (first week) and 2 weeks after the first examination (last week) using ultrasonography. We also determined the relationship between the percentage change in muscle thickness and disease severity, nutritional status, and CRP levels on admission. RESULTS: There was a significant correlation between changes in muscle thickness for both paretic and nonparetic sides and National Institutes of Health Stroke Scale (NIHSS) scores (paretic limb: r = -.46, P = .01; nonparetic limb: r = -.54, P = .002, respectively); however, there was no significant correlation with nutritional status on admission. Quadriceps muscle thickness was reduced more in the CRP-positive (≥.3 mg/dL) patients than in the CRP-negative (<.3 mg/dL) patients in the nonparetic limb (positive: -21.4 ± 12.1, negative: -11.4 ± 16.4%; P = .039), but not in the paretic limb (positive: -23.4 ± 9.0, negative: -19.1 ± 15.7; P = .27). CONCLUSIONS: A high NIHSS score and a positive CRP on admission were both significantly correlated with decreased quadriceps muscle thickness after acute stroke. Nutritional status on admission was not correlated with changes in quadriceps muscle thickness for these patients.

Changes in serum growth factors in stroke rehabilitation patients and their relation to hemiparesis improvement.

Predicting recovery from hemiparesis after stroke is important for rehabilitation. A few recent studies reported that the levels of some growth factors shortly after stroke were positively correlated with the clinical outcomes during the chronic phase. The aim of this study was to examine the relationships between the serum levels of growth factors (vascular endothelial growth factor [VEGF], insulin-like growth factor-I [IGF-I], and hepatocyte growth factor [HGF]) and improvement in hemiparesis in stroke patients who received rehabilitation in a postacute rehabilitation hospital. Subjects were 32 stroke patients (cerebral infarction: 21 and intracerebral hemorrhage [ICH]: 11). We measured serum levels of VEGF, IGF-I, and HGF and 5 items of the Stroke Impairment Assessment Set (SIAS) for hemiparesis on admission and at discharge. Age-matched healthy subjects (n=15) served as controls. Serum levels of VEGF and HGF in cerebral infarct patients on admission were higher than those in control subjects, and the serum levels of IGF-I in stroke patients were lower than those in controls. The level of HGF in ICH patients on admission was negatively correlated with gains in SIAS, and higher outliers in HGF concentration were correlated with lower gains in SIAS. Focusing on the extremely high levels of these factors may be a predictor of the low recovery from hemiparesis after stroke.

Muscle atrophy, voluntary activation disturbances, and low serum concentrations of IGF-1 and IGFBP-3 are associated with weakness in people with chronic stroke.

BACKGROUND: The muscle weakness that is exhibited poststroke is due to a multifactorial etiology involving the central nervous system and skeletal muscle changes. Insulinlike growth factor 1 (IGF-1) and IGF binding protein 3 (IGFBP-3) have been described as biomarkers of neuromuscular performance in many conditions. However, no information about these biomarkers is available for people with chronic hemiparesis. OBJECTIVE: The purpose of this study was to investigate possible factors involved in muscle weakness, such as IGF-1 and IGFBP-3 serum concentrations, muscle volume, and neuromuscular performance of the knee flexors and extensors, in people with chronic hemiparesis poststroke. DESIGN: This was a cross-sectional study. METHODS: A cross-sectional study was performed on 14 individuals poststroke who were paired with healthy controls. Mobility, function, balance, and quality of life were recorded as outcome measures. Knee flexor and extensor muscle volumes and neuromuscular performance were measured using nuclear magnetic resonance imaging, dynamometry, and electromyography. The serum concentrations of IGF-1 and IGFBP-3 were quantified by enzyme-linked immunosorbent assay (ELISA). RESULTS: The hemiparetic group had low serum concentrations of IGF-1 (25%) and IGFBP-3 (40%); reduced muscle volume in the vastus medialis (32%), vastus intermedius (29%), biceps femoris (16%), and semitendinosus and semimembranosus (12%) muscles; reduced peak torque, power, and work of the knee flexors and extensors; and altered agonist and antagonist muscle activation compared with controls. CONCLUSIONS: Low serum concentrations of IGF-1 and IGFBP-3, deficits in neuromuscular performance, selective muscle atrophy, and decreased agonist muscle activation were found in the group with chronic hemiparesis poststroke. Both hemorrhagic and ischemic stroke were considered, and the data reflect a chronic poststroke population with good function.

Predicting the risk of venous thromboembolism recurrence.

Venous thromboembolism (VTE) is a chronic disease with a 30% ten-year recurrence rate. The highest incidence of recurrence is in the first 6 months. Active cancer significantly increases the hazard of early recurrence, and the proportions of time on standard heparin with an APTT ≥ 0.2 anti-X(a) U/mL, and on warfarin with an INR ≥ 2.0, significantly reduce the hazard. The acute treatment duration does not affect recurrence risk after treatment is stopped. Independent predictors of late recurrence include increasing patient age and body mass index, leg paresis, active cancer and other persistent VTE risk factors, idiopathic VTE, antiphospholipid antibody syndrome, antithrombin, protein C or protein S deficiency, hyperhomocysteinemia and a persistently increased plasma fibrin D-dimer. A recommendation for secondary prophylaxis should be individualized based on the risk for recurrent VTE (especially fatal pulmonary embolism) and bleeding. The appropriateness of secondary prophylaxis should be continuously reevaluated, and the prophylaxis stopped if the benefit no longer exceeds the risk.

Experimental subacute spinal cord compression: correlation of serial S100B and NSE serum measurements, histopathological changes, and outcome.

OBJECTIVE: To correlate serial measurements of serum S100B and neuron-specific enolase (NSE) with histopathological changes of the spinal cord and to assess their prognostic significance in a set-up of experimental spinal cord compression. METHODS: The thoracic cords of 22 rabbits were increasingly compressed and decompressed once paresis had developed. After decompression, outcome was rated as favorable or unfavorable. Following sacrifice of the animals, the cord was analyzed microscopically and morphometrically. Serum S100B and NSE were measured daily, and levels were correlated with initial degree of paresis, outcome after decompression, and histopathological changes of the cord. RESULTS: Regardless of the initial degree of paresis, animals with favorable outcome had significantly higher cell counts than animals with unfavorable outcome. The time course of S100B values following decompression was correlated with outcome. Animals with favorable outcome had either always normal levels or levels that were initially increased but normalized within 2 days. The values of animals with unfavorable outcome were elevated throughout (P<0.0001). No correlation was found between NSE levels and outcome. CONCLUSIONS: The initial degree of paresis is not a prognostic factor to predict outcome. Despite timely decompression, pronounced structural lesions of the cord may develop, resulting in an unfavorable outcome. In cases with favorable outcome, sufficient tissue is preserved to maintain function regardless of the initial extent of paresis. This different reaction of the cord may be followed indirectly with serial measurements of S100B serum levels. Thus, S100B is a reliable biochemical marker allowing for prediction of outcome. NSE does not have this prognostic significance.

[Pareses, myalgias, and massive CK elevation: a severe neurological disorder?]. / Paresen, myalgien und massive CK-erhöhung: eine schwere neurologische erkrankung?

CASE REPORT: The authors report on a 51-year-old patient with transient pareses, myalgias, and a massive creatine kinase elevation which had led to an intensive neurological work-up by the general practitioner. Despite refractory hypertension, primary aldosteronism was not excluded. At the authors' clinic, the patient was diagnosed to have Conn's syndrome. Laparoscopic adrenalectomy revealed a big adenoma of the left adrenal gland. CONCLUSION: Transient pareses, myalgias, and creatine kinase elevation can indicate primary aldosteronism among hypertensive patients. If clinically suspected, the aldosterone-renin ratio should be determined.

Haemorrhagic transformation of cerebral infarction in an AIDS patient--thrombophilia screen essential!

Patients with advanced HIV disease with low CD4 count are more prone to thrombo-embolism and various predisposing factors have been identified. These include the presence of anticardiolipin antibodies and the lupus anticoagulant, deficiencies of proteins C and S, heparin co-factor II and antithrombin. Increased levels of Von Willebrand factor and d-dimers have also been linked with thrombo-embolism, as has the presence of concurrent infections and malignancies. We report a case of an AIDS patient who presented with acute hemiparesis. He was severely immunosuppressed. Computed tomography of the head confirmed cerebral infarction with haemorrhagic transformation. He had no known risk factors apart from being severely immunocompromised and had high anticardiolipin antibodies and low free protein S.

Origin of ICU acquired paresis determined by direct muscle stimulation.

BACKGROUND: Acquired diffuse paresis in an intensive care unit (ICU) can result from critical illness myopathy or polyneuropathy. Clinical examination and conventional neurophysiological techniques may not distinguish between these entities. OBJECTIVE: To assess the value of direct muscle stimulation (DMS) to differentiate myopathic from neuropathic process in critically ill patients with diffuse severe muscle weakness. METHODS: 30 consecutive patients with ICU acquired diffuse motor weakness were studied. Responses of the right deltoid and tibialis anterior muscles to DMS and to motor nerve stimulation (MNS) were studied and compared with results of conventional nerve conduction studies and concentric needle electromyography (EMG). An original algorithm was used for differential diagnosis, taking into account first the amplitude of the responses to DMS, then the MNS to DMS amplitude ratio, and finally the amplitude of the sensory nerve action potentials recorded at the lower limbs. RESULTS: Evidence of neuropathy and myopathy was found in 57% and 83% of the patients, respectively. Pure or predominant myopathy was found in 19 patients. Other results were consistent with neuromyopathy (n = 5) and pure or predominant neuropathy (n = 2). Four patients had normal results with stimulation techniques, but spontaneous EMG activity and raised plasma creatine kinase suggesting necrotic myopathy. CONCLUSIONS: A neurophysiological approach combining DMS and conventional techniques revealed myopathic processes in a majority of ICU patients. Reduced muscle fibre excitability may be a leading cause for this. The diagnosis of myopathy in ICU acquired paralysis can be established by a combination of DMS, needle EMG, and plasma creatine kinase.

The increase of neuron-specific enolase in cerebrospinal fluid and plasma as a marker of neuronal damage in patients with acute brain infarction.

Our goal was to determine the neuron-specific enolase (NSE) concentration in cerebrospinal fluid (CSF) and plasma in patients with the acute brain infarction (BI) and analyze the correlation between the measured NSE concentration and infarct volume and the degree of neurological and functional deficit. The study included 55 patients aged 56-68 with BI in the acute phase. The control group consisted of 16 patients subjected to diagnostic radiculography. The results showed a significant increase of NSE concentration within the first seven days in patients compared to the controls (2.838 +/- 0.504 ng/ml CSF and 4.479 +/- 0.893 ng/ml plasma). A significant correlation was found between NSE concentration and infarction volume and the degree of neurological and functional deficit both in the CSF (r = 0.828, r = 0.735, r = 0.796; p < 0.001) and in plasma (r = 0.810, r = 0.681, r = 0.783; p < 0.001). The results suggest that an early determination of this marker in CSF and plasma in patients with BI could be a valuable diagnostic factor.

Critical illness polyneuropathy and myopathy in patients with acute respiratory distress syndrome.

OBJECTIVE: Critical illness polyneuropathy/myopathy (CIP/CIM) is frequently described in critically ill patients who survive severe sepsis. Clinically relevant paresis is major symptom of CIP/CIM. We aimed at determining risk factors and diagnostic value of electrophysiologic testing for CIP/CIM in patients with acute respiratory distress syndrome (ARDS). DESIGN: Single-center, retrospective analysis, using charts. SETTING: University medical center. PATIENTS: Fifty consecutive ARDS patients in our intensive care unit. INTERVENTIONS: Patient characteristics and clinical course were analyzed. All patients received early electrophysiologic testing. CIP/CIM was diagnosed by the presence of clinical relevant paresis. MEASUREMENTS AND MAIN RESULTS: Clinically relevant paresis was confirmed in 27 ARDS patients (60%), whereas in 18 patients no paresis was determined (controls); five patients died before clinical assessment of paresis was feasible. Patients with paresis were older, had more days on mechanical ventilation, and had increased intensive care unit length of stay compared with controls. Patients who developed paresis had elevated daily peak blood glucose levels during 28 days of intensive care unit treatment: 166 (134, 200) mg/dL in CIP/CIM patients vs. 144 (132, 161) mg/dL in controls (median, quartiles). Twenty-five of 27 patients with paresis revealed reduced motor unit potentials, fibrillation potentials, or positive sharp waves on early electrophysiologic testing indicating CIP/CIM, whereas 16 of 18 control patients did not. CONCLUSIONS: In ARDS patients, paresis is a frequent complication causing prolonged mechanical ventilation and intensive care unit length of stay. An association between hyperglycemia and CIP/CIM has been found. However, since this is a retrospective survey, a causal relation is not clearly supported. In this study, the use of early electrophysiologic testing in ARDS patients was a valuable diagnostic tool for detecting CIP/CIM.

Localized reversible reduction of apparent diffusion coefficient in transient hypoglycemia-induced hemiparesis.

BACKGROUND AND PURPOSE: The pathophysiology of hypoglycemia shares a common mechanism with cerebral ischemia, but so far, little is known regarding MRI of humans with hypoglycemia. METHODS: We report a patient with left hemiparesis and dysarthria associated with a blood glucose level of 1.7 mmol/L. The patient recovered completely after glucose infusion. RESULTS: The initial diffusion-weighted imaging (DWI) showed increased signal intensities and a reduction of apparent diffusion coefficient (ADC) values localized in the corpus callosum (splenium) and asymmetrically in the corona radiata. After 48 hours, follow-up revealed complete recovery of DWI and ADC signal abnormalities. CONCLUSIONS: To our knowledge, this is the first presentation of a case with transient hypoglycemia-induced focal neurological deficits revealing completely reversible MRI changes in terms of disturbed DWI and ADC with a peculiar as yet undescribed topography.

Interaction between the levels of hormones and minerals in sera of healthy and sick cows.

An interaction between blood levels of parathyroid hormone, calcitonin, 1.25-dihydroxycholecalciferol and levels of calcium, phosphorus and magnesium was examined in 85 cows, which included healthy cows and cows with ostemalacia, mastitis and paresis. Levels of parathyroid hormone (PTH) and calcitonin were determined in vitro using IMMULITE analyser (Diagnostic Products Corporation, USA), by means of immunometric assay. Levels of vitamin D were measured using the enzyme linked immunosorbent assay (ELISA). Levels of calcium, phosphorus and magnesium were determined using the automated Eos-Bravo analyser (Hospitex Diagnostics, Italy) with HOSPITEX reagents. The lowest blood levels of calcium (1.38 +/- 0.18 mmol/L) and phosphorus (0.65 +/- 0.12 mmol/L) were found in cows with parturient paresis. Decreased blood levels of phosphorus and magnesium were also determined in cows with osteomalacia. For cows with parturient paresis, which received a mineral supplement, the average serum level of calcium was by 20.7% higher than the level found in those which did not receive a supplement, and the level of phosphorus was by 23.6% higher, however, these levels remained low. The blood level of parathyroid hormone ranged from 3.47 to 5.20 pmol/L in healthy cows and from 3.95 to 15.21 pmol/L in sick cows. The highest and statistically significant increase in blood PTH level (up to 18.31 +/- 1.88 pmol/L) was found in cows with parturient paresis. The blood level of PTH correlated inversely with the level of calcium in cows with osteomaliacia (r = -0.89) and in cows with parturient paresis (r = -0.49 and r = -0.61, respectively). The serum level of calcitonin ranged from 1.46 pmol/L to 2.40 pmol/L in healthy and sick cows and the difference was not statistically significant. Lower serum levels of vitamin D were found in heifers-in-calf and in cows with mastitis. A clear correlation between levels of calcitonin, vitamin D and macronutrients was not found.