- Modulation of soleus stretch reflexes during walking in people with chronic incomplete spinal cord injury. [Journal Article]
- EBExp Brain Res 2019 Jul 15
- In people with spasticity due to chronic incomplete spinal cord injury (SCI), it has been presumed that the abnormal stretch reflex activity impairs gait. However, locomotor stretch reflexes across a…
In people with spasticity due to chronic incomplete spinal cord injury (SCI), it has been presumed that the abnormal stretch reflex activity impairs gait. However, locomotor stretch reflexes across all phases of walking have not been investigated in people with SCI. Thus, to understand modulation of stretch reflex excitability during spastic gait, we investigated soleus stretch reflexes across the entire gait cycle in nine neurologically normal participants and nine participants with spasticity due to chronic incomplete SCI (2.5-11 year post-injury). While the participant walked on the treadmill at his/her preferred speed, unexpected ankle dorsiflexion perturbations (6° at 250°/s) were imposed every 4-6 steps. The soleus H-reflex was also examined. In participants without SCI, spinal short-latency "M1", spinal medium latency "M2", and long-latency "M3" were clearly modulated throughout the step cycle; the responses were largest in the mid-stance and almost completely suppressed during the stance-swing transition and swing phases. In participants with SCI, M1 and M2 were abnormally large in the mid-late-swing phase, while M3 modulation was similar to that in participants without SCI. The H-reflex was also large in the mid-late-swing phase. Elicitation of H-reflex and stretch reflexes in the late swing often triggered clonus and affected the soleus activity in the following stance. In individuals without SCI, moderate positive correlation was found between H-reflex and stretch reflex sizes across the step cycle, whereas in participants with SCI, such correlation was weak to non-existing, suggesting that H-reflex investigation would not substitute for stretch reflex investigation in individuals after SCI.
- Botulinum Toxin Type A and Physiotherapy in Spasticity of the Lower Limbs Due to Amyotrophic Lateral Sclerosis. [Journal Article]
- TToxins (Basel) 2019 Jul 01; 11(7)
- Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease (unknown pathogenesis) of the central nervous system that causes death within 1-5 years. Clinically, flabby paralysis, a…
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease (unknown pathogenesis) of the central nervous system that causes death within 1-5 years. Clinically, flabby paralysis, areflexia, muscular atrophy, and muscle fasciculations, signs of II motor neuron damage, appear. Sometimes, clinical manifestations of damage of the I motor neuron come out in lower limbs; spastic paralysis, iperflexia, and clonus emerge, and they impair deambulation and management of activities of daily living, such as personal hygiene or dressing. Thus, the first therapeutic approach in these patients involves antispasmodic drugs orally followed by botulinum toxin type A injection (BTX-A). In this study, we study the efficacy of BTX-A and physiotherapy in lower limb spasticity due to ALS and no response to treatment with oral antispastic drugs. We evaluated 15 patients (10 male and five female), with a mean age of 48.06 ± 5.2 with spasticity of adductor magnus (AM), at baseline (T0, before BTX-A treatment) and in the following three follow-up visits (T1 30 days, T2 60 days, and T3 90 days after infiltration). We evaluated myometric measure of muscle tone, the Modified Ashworth Scale of AM, Barthel Index, Adductor Tone Rating Scale, and Hygiene Score. The study was conducted between November 2018 and April 2019. We treated AM with incobotulinum toxin type A (Xeomin®, Merz). Spasticity (myometric measurement, Adductor Tone Rating Scale, and Modified Ashworth Scale) and clinical (Barthel Index and Hygiene Score) improvements were obtained for 90 days after injection (p < 0.05). Our study shows the possibility of using BTX-A in the treatment of spasticity in patients with ALS and no response to oral antispastic drugs, with no side effects. The limitation of the study is the small number of patients and the limited time of observation; therefore, it is important to increase both the number of patients and the observation time in future studies.
- Complete Atlantoaxial Dislocation After Odontoid Synchondrosis Fracture: A 2-Year Follow-up Study: A Case Report. [Journal Article]
- JCJBJS Case Connect 2019 Apr-Jun; 9(2):e0327
- CONCLUSIONS: The case presented demonstrates one option for an otherwise nonreducible odontoid synchondrosis fracture with complete atlantoaxial dislocation: transoral reduction and open posterior instrumentation. This proved to be a practical technique and provided a good clinical result in this case. These injuries are rare, but when they do occur, the examination can be surprisingly subtle given the severity of the injury. Plain films should be scrutinized carefully and advanced imaging obtained when necessary to confirm the diagnosis.
- The loss of slow skeletal muscle isoform of troponin T in spindle intrafusal fibres explains the pathophysiology of Amish nemaline myopathy. [Journal Article]
- JPJ Physiol 2019 May 31
- CONCLUSIONS: The pathogenic mechanism and the neuromuscular reflex-related phenotype (e.g. tremors accompanied by clonus) of Amish nemaline myopathy, as well as of other recessively inherited TNNT1 myopathies, remain to be clarified. The truncated slow skeletal muscle isoform of troponin T (ssTnT) encoded by the mutant TNNT1 gene is unable to incorporate into myofilaments and is degraded in muscle cells. By contrast to extrafusal muscle fibres, spindle intrafusal fibres of normal mice contain a significant level of cardiac TnT and a low molecular weight splice form of ssTnT. Intrafusal fibres of ssTnT-knockout mice have significantly increased cardiac TnT. Rotarod and balance beam tests have revealed abnormal neuromuscular co-ordination in ssTnT-knockout mice and a blunted response to a spindle sensitizer, succinylcholine. The loss of ssTnT and a compensatory increase of cardiac TnT in intrafusal nuclear bag fibres may increase myofilament Ca2+ -sensitivity and tension, impairing spindle function, thus identifying a novel mechanism for the development of targeted treatment.
- Ossification of the yellow ligament in the cervical spine - an unusual location. [Journal Article]
- BBiomedicine (Taipei) 2019; 9(2):14
- Ossification of the yellow ligament (OYL) or ligamentum flavum, usually occurs in the thoracic spine. Focal OYL occurring in the cervical spine is considered rare and is sparsely reported in the lite…
Ossification of the yellow ligament (OYL) or ligamentum flavum, usually occurs in the thoracic spine. Focal OYL occurring in the cervical spine is considered rare and is sparsely reported in the literature. We came across a 30-year-old male patient with progressive left upper limb and bilateral lower limb weakness over a period of 3 months, associated with an unsteady gait. Clinical examination revealed bilateral generalized hyper-reflexia in both upper and lower limbs, inverted supinator jerk, Hoffman's sign and clonus. Myelopathy due to cord compression was suspected and further investigations were done. MRI and CT scans revealed a bony mass in relation to the C6 spinous process projecting anterosuperiorly and narrowing the cervical spinal canal causing cord signal changes from C4 to C6 levels. In view of the deteriorating neurological status, immediate surgery in the form of decompression and posterior stabilization from C4-C6 was performed. Patient gradually recovered after surgery and attained full functional status. We report this case considering the unusual location of OYL and its successful management.
- The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre-eclampsia: A pragmatic guide for first-trimester screening and prevention. [Journal Article]
- IJInt J Gynaecol Obstet 2019; 145 Suppl 1:1-33
- Pre‐eclampsia (PE) is a multisystem disorder that typically affects 2%–5% of pregnant women and is one of the leading causes of maternal and perinatal morbidity and mortality, especially when the con…
Pre‐eclampsia (PE) is a multisystem disorder that typically affects 2%–5% of pregnant women and is one of the leading causes of maternal and perinatal morbidity and mortality, especially when the condition is of early onset. Globally, 76 000 women and 500 000 babies die each year from this disorder. Furthermore, women in low‐resource countries are at a higher risk of developing PE compared with those in high‐resource countries. Although a complete understanding of the pathogenesis of PE remains unclear, the current theory suggests a two‐stage process. The first stage is caused by shallow invasion of the trophoblast, resulting in inadequate remodeling of the spiral arteries. This is presumed to lead to the second stage, which involves the maternal response to endothelial dysfunction and imbalance between angiogenic and antiangiogenic factors, resulting in the clinical features of the disorder. Accurate prediction and uniform prevention continue to elude us. The quest to effectively predict PE in the first trimester of pregnancy is fueled by the desire to identify women who are at high risk of developing PE, so that necessary measures can be initiated early enough to improve placentation and thus prevent or at least reduce the frequency of its occurrence. Furthermore, identification of an “at risk” group will allow tailored prenatal surveillance to anticipate and recognize the onset of the clinical syndrome and manage it promptly. PE has been previously defined as the onset of hypertension accompanied by significant proteinuria after 20 weeks of gestation. Recently, the definition of PE has been broadened. Now the internationally agreed definition of PE is the one proposed by the International Society for the Study of Hypertension in Pregnancy (ISSHP). According to the ISSHP, PE is defined as systolic blood pressure at ≥140 mm Hg and/or diastolic blood pressure at ≥90 mm Hg on at least two occasions measured 4 hours apart in previously normotensive women and is accompanied by one or more of the following new‐onset conditions at or after 20 weeks of gestation: 1.Proteinuria (i.e. ≥30 mg/mol protein:creatinine ratio; ≥300 mg/24 hour; or ≥2 + dipstick); 2.Evidence of other maternal organ dysfunction, including: acute kidney injury (creatinine ≥90 μmol/L; 1 mg/dL); liver involvement (elevated transaminases, e.g. alanine aminotransferase or aspartate aminotransferase >40 IU/L) with or without right upper quadrant or epigastric abdominal pain; neurological complications (e.g. eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, and persistent visual scotomata); or hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular coagulation, hemolysis); or 3.Uteroplacental dysfunction (such as fetal growth restriction, abnormal umbilical artery Doppler waveform analysis, or stillbirth). It is well established that a number of maternal risk factors are associated with the development of PE: advanced maternal age; nulliparity; previous history of PE; short and long interpregnancy interval; use of assisted reproductive technologies; family history of PE; obesity; Afro‐Caribbean and South Asian racial origin; co‐morbid medical conditions including hyperglycemia in pregnancy; pre‐existing chronic hypertension; renal disease; and autoimmune diseases, such as systemic lupus erythematosus and antiphospholipid syndrome. These risk factors have been described by various professional organizations for the identification of women at risk of PE; however, this approach to screening is inadequate for effective prediction of PE. PE can be subclassified into: 1.Early‐onset PE (with delivery at <34+0 weeks of gestation); 2.Preterm PE (with delivery at <37+0 weeks of gestation); 3.Late‐onset PE (with delivery at ≥34+0 weeks of gestation); 4.Term PE (with delivery at ≥37+0 weeks of gestation). These subclassifications are not mutually exclusive. Early‐onset PE is associated with a much higher risk of short‐ and long‐term maternal and perinatal morbidity and mortality. Obstetricians managing women with preterm PE are faced with the challenge of balancing the need to achieve fetal maturation in utero with the risks to the mother and fetus of continuing the pregnancy longer. These risks include progression to eclampsia, development of placental abruption and HELLP (hemolysis, elevated liver enzyme, low platelet) syndrome. On the other hand, preterm delivery is associated with higher infant mortality rates and increased morbidity resulting from small for gestational age (SGA), thrombocytopenia, bronchopulmonary dysplasia, cerebral palsy, and an increased risk of various chronic diseases in adult life, particularly type 2 diabetes, cardiovascular disease, and obesity. Women who have experienced PE may also face additional health problems in later life, as the condition is associated with an increased risk of death from future cardiovascular disease, hypertension, stroke, renal impairment, metabolic syndrome, and diabetes. The life expectancy of women who developed preterm PE is reduced on average by 10 years. There is also significant impact on the infants in the long term, such as increased risks of insulin resistance, diabetes mellitus, coronary artery disease, and hypertension in infants born to pre‐eclamptic women. The International Federation of Gynecology and Obstetrics (FIGO) brought together international experts to discuss and evaluate current knowledge on PE and develop a document to frame the issues and suggest key actions to address the health burden posed by PE. FIGO's objectives, as outlined in this document, are: (1) To raise awareness of the links between PE and poor maternal and perinatal outcomes, as well as to the future health risks to mother and offspring, and demand a clearly defined global health agenda to tackle this issue; and (2) To create a consensus document that provides guidance for the first‐trimester screening and prevention of preterm PE, and to disseminate and encourage its use. Based on high‐quality evidence, the document outlines current global standards for the first‐trimester screening and prevention of preterm PE, which is in line with FIGO good clinical practice advice on first trimester screening and prevention of pre‐eclampsia in singleton pregnancy.1 It provides both the best and the most pragmatic recommendations according to the level of acceptability, feasibility, and ease of implementation that have the potential to produce the most significant impact in different resource settings. Suggestions are provided for a variety of different regional and resource settings based on their financial, human, and infrastructure resources, as well as for research priorities to bridge the current knowledge and evidence gap. To deal with the issue of PE, FIGO recommends the following: Public health focus: There should be greater international attention given to PE and to the links between maternal health and noncommunicable diseases (NCDs) on the Sustainable Developmental Goals agenda. Public health measures to increase awareness, access, affordability, and acceptance of preconception counselling, and prenatal and postnatal services for women of reproductive age should be prioritized. Greater efforts are required to raise awareness of the benefits of early prenatal visits targeted at reproductive‐aged women, particularly in low‐resource countries. Universal screening: All pregnant women should be screened for preterm PE during early pregnancy by the first‐trimester combined test with maternal risk factors and biomarkers as a one‐step procedure. The risk calculator is available free of charge at https://fetalmedicine.org/research/assess/preeclampsia. FIGO encourages all countries and its member associations to adopt and promote strategies to ensure this. The best combined test is one that includes maternal risk factors, measurements of mean arterial pressure (MAP), serum placental growth factor (PLGF), and uterine artery pulsatility index (UTPI). Where it is not possible to measure PLGF and/or UTPI, the baseline screening test should be a combination of maternal risk factors with MAP, and not maternal risk factors alone. If maternal serum pregnancy‐associated plasma protein A (PAPP‐A) is measured for routine first‐trimester screening for fetal aneuploidies, the result can be included for PE risk assessment. Variations to the full combined test would lead to a reduction in the performance screening. A woman is considered high risk when the risk is 1 in 100 or more based on the first‐trimester combined test with maternal risk factors, MAP, PLGF, and UTPI. Contingent screening: Where resources are limited, routine screening for preterm PE by maternal factors and MAP in all pregnancies and reserving measurements of PLGF and UTPI for a subgroup of the population (selected on the basis of the risk derived from screening by maternal factors and MAP) can be considered. Prophylactic measures: Following first‐trimester screening for preterm PE, women identified at high risk should receive aspirin prophylaxis commencing at 11–14+6 weeks of gestation at a dose of ~150 mg to be taken every night until 36 weeks of gestation, when delivery occurs, or when PE is diagnosed. Low‐dose aspirin should not be prescribed to all pregnant women. In women with low calcium intake (<800 mg/d), either calcium replacement (≤1 g elemental calcium/d) or calcium supplementation (1.5–2 g elemental calcium/d) may reduce the burden of both early‐ and late‐onset PE.
- Defining the spectrum of spasticity-associated involuntary movements. [Journal Article]
- PRParkinsonism Relat Disord 2019 May 12
- CONCLUSIONS: Most spastic patients experience spasticity-associated involuntary movements of variable phenomenology and impact. However, only half of these patients experience significant improvement with the current management strategies. More research is needed to explore better treatment options for spasticity-associated involuntary movements with focus on phenomenology-specific approaches.
- StatPearls: Neuroanatomy, Upper Motor Nerve Signs [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- The initiation and coordination of movement are under the control of an immense network of nerves in the central nervous system (CNS) that originate from the cerebral cortex and course through the in…
The initiation and coordination of movement are under the control of an immense network of nerves in the central nervous system (CNS) that originate from the cerebral cortex and course through the internal capsule, brainstem, and spinal cord. The impulses for movement are carried by nerves known as upper motor neurons (UMN). The pyramidal tract is the primary tract which propagates signals necessary for voluntary movement. The pyramidal tract divides into the corticospinal tract and the corticobulbar tract. Injury to UMNs in these tracts is common because of the large areas covered by the motor neuron pathway. Any injury to these tracts is known as UMN lesions. Damage to UMNs results in characteristic clinical manifestations colloquially termed “upper motor neuron signs” or “upper motor neuron syndrome.” The symptoms include muscle weakness, spasticity, hyperreflexia, and clonus. Damage to UMNs of the corticobulbar tract can manifest as dysphagia and dysarthria. Distinguishing upper motor neuron signs from lower motor neuron signs is essential in the neurological physical exam.
- Spinal Cord Diffuse Midline Glioma in a 4-Year-Old Boy. [Case Reports]
- CNChild Neurol Open 2019; 6:2329048X19842451
- CONCLUSIONS: High-grade spinal cord gliomas are very rare but should be considered in the differential diagnosis of pediatric myelopathy. Tissue biopsy is recommended in indeterminate cases to facilitate diagnosis and to guide management.
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- Early α-linolenic acid exposure to embryo reduces pentylenetetrazol-induced seizures in zebrafish larva. [Journal Article]
- PLProstaglandins Leukot Essent Fatty Acids 2019; 143:15-20
- Over the past few years, there has been a tremendous increase in interest of general population toward food-based therapies for management of chronic clinical conditions due to their lesser adverse e…
Over the past few years, there has been a tremendous increase in interest of general population toward food-based therapies for management of chronic clinical conditions due to their lesser adverse effects with prolonged use over pharmacotherapies. Foods enriched with omega-3 fatty acids have shown some promising results in case of epilepsy. The present study was envisioned to investigate the effect of early exposure of α-linolenic acid (ALA), an essential omega-3 fatty acid in developing zebrafish (Danio rerio) embryos toward pentylenetetrazol (PTZ)-induced seizure susceptibility. The healthy wild-type zebrafish embryos were incubated in system water or system water containing different ALA concentrations (1-20 µM) till 7 dpf (days post fertilization). Each larva at 7 dpf was placed in 8 mM PTZ solution and seizure event was recorded. ALA incubation at 10 µM and 20 µM concentrations showed a dose-dependent reduction in PTZ-mediated hyperactive responses in larvae indicated by a marked decrease in total distance travelled and speed, as compared to vehicle control. Furthermore, both the treated groups showed increase in the latency to PTZ-induced clonus-like seizures in larvae, as compared to vehicle control. ALA incubated larvae at 10 µM and 20 µM concentrations also showed a significant reduction in c-fos mRNA level. A marked increase in the level of ALA and docosahexaenoic acid was also observed in the larvae incubated at highest effective concentration of ALA. The present study concluded that embryonic exposure of ALA reduced PTZ-induced seizures in zebrafish larva.