Important: Contact your state representative to preserve access to epilepsy medications on current formulary.
Preserve open access to epilepsy medicine in Medicaid program
Sindi J. Rosales and Donna Stahlhut, For the Express-News
Published 12:00 am, Sunday, May 29, 2016
The Texas Legislature is considering a change to the state’s Medicaid program that could jeopardize access to epilepsy care by allowing insurers, not physicians, to choose what medications managed care plans would cover.
Drug formulary changes, intended to cut costs, often translate into medical complications that hurt the vulnerable beneficiaries served by the Medicaid program and are more costly to the state in the long run. Research shows that access to epilepsy medications leads to greater seizure control and less hospitalizations, and savings from restrictive formularies often lead to greater spending on medical complications that outweigh the savings.
Epilepsy medications are not interchangeable, and individuals often react quite differently to available treatments. With each medication comes side effects, often significant enough that quality of life is compromised and many people abandon their treatment. This is why people living with epilepsy need meaningful access to the full range of treatments available — and the specialists who know how to prescribe them.
Selecting the appropriate epilepsy medication to achieve seizure control requires consideration of a number of variables, including type and frequency of seizures, age, gender, and other health conditions. It often requires trial and error, along with close observation of blood levels and side effects. Open access to epilepsy medications in the Medicaid program ensures meaningful and timely access to epilepsy care.
The human toll of uncontrolled seizures is significant and extends beyond the individual living with epilepsy.
Delaying access to medications and interrupting proven treatment regimens leads to breakthrough seizures, related complications, and increased medical costs due to preventable seizures, including accidents, emergency room visits and hospitalizations. Along with a decreased quality of life and costly health complications, there also are the lost wages and productivity for individuals living with epilepsy, their families and their communities. Full article HERE
Insufficient sleep can adversely affect a variety of cognitive abilities, ranging from simple alertness to higher-order executive functions. Although the effects of sleep loss on mood and cognition are well documented, there have been no controlled studies examining its effects on perceived emotional intelligence (EQ) and constructive thinking, abilities that require the integration of affect and cognition and are central to adaptive functioning.
PATIENTS AND METHODS:
Twenty-six healthy volunteers completed the Bar-On Emotional Quotient Inventory (EQi) and the Constructive Thinking Inventory (CTI) at rested baseline and again after 55.5 and 58 h of continuous wakefulness, respectively.
Relative to baseline, sleep deprivation was associated with lower scores on Total EQ (decreased global emotional intelligence), Intrapersonal functioning (reduced self-regard, assertiveness, sense of independence, and self-actualization), Interpersonal functioning (reduced empathy toward others and quality of interpersonal relationships), Stress Management skills (reduced impulse control and difficulty with delay of gratification), and Behavioral Coping (reduced positive thinking and action orientation). Esoteric Thinking (greater reliance on formal superstitions and magical thinking processes) was increased.
These findings are consistent with the neurobehavioral model suggesting that sleep loss produces temporary changes in cerebral metabolism, cognition, emotion, and behavior consistent with mild prefrontal lobe dysfunction.
Sleep. 2010 Aug;33(8):1086-90.
The impact of partial sleep deprivation on moral reasoning in military officers. Olsen OK1, Pallesen S, Eid J.
The present study explores the impact of long-term partial sleep deprivation on the activation of moral justice schemas, which are suggested to play a prominent role in moral reasoning and the formation of moral judgments and behavior.
Participants judged 5 dilemmas in rested and partially sleep deprived condition, in a counterbalanced design.
In classroom and field exercises at the Norwegian Naval Academy and the Norwegian Army Academy.
Seventy-one Norwegian naval and army officer cadets.
MEASUREMENTS AND RESULTS:
The results showed that the officers' ability to conduct mature and principally oriented moral reasoning was severely impaired during partial sleep deprivation compared to the rested state. At the same time, the officers became substantially more rules-oriented in the sleep deprived condition, while self-oriented moral reasoning did not change. Interaction effects showed that those officers who displayed high levels of mature moral reasoning (n = 24) in the rested condition, lost much of this capacity during sleep deprivation in favor of a strong increase in rules-oriented moral reasoning as well as self-orientation. Conversely, officers at low levels of mature moral reasoning in rested condition (n = 23) were unaffected by sleep deprivation.
The present data show that long-term partial sleep deprivation has an impact on the activation of moral justice schemas, and consequently on the ability to make moral justice judgments.
PMID: 20815191 [PubMed - indexed for MEDLINE] PMCID: PMC2910538 Free PMC Article
Functional neuroimaging studies suggest a prominent role for the medial prefrontal cortex in the formation of moral judgments. Activity in this region has also been shown to decline significantly during sleep loss. We therefore examined the effects of 2 nights ofsleep deprivation on several aspects of moral judgment.
Participants made judgments about the "appropriateness" of various courses of action in response to 3 types of moral dilemmas at rested baseline and again following 53 hours of continuous wakefulness.
In-residence sleep laboratory at the Walter Reed Army Institute of Research.
Twenty-six healthy adults (21 men, 5 women).
MEASUREMENTS AND RESULTS:
Compared to baseline, sleep deprivation resulted in significantly longer response latencies (suggesting greater difficulty deciding upon a course of action) only for Moral Personal (i.e., emotionally evocative) dilemmas, whereas response times to Moral Impersonal (less emotionally evocative) and Non Moral dilemmas did not change significantly with sleep loss. The effect of sleep deprivation on the willingness to agree with solutions that violate personally held moral beliefs was moderated by the level of emotional intelligence, as measured by the Bar-On EQ-i. Persons high in emotional intelligence were less susceptible to changes in moral judgments as a function of sleep loss.
These findings suggest that sleep deprivation impairs the ability to integrate emotion and cognition to guide moral judgments, although susceptibility to the effects of sleep loss on this ability is moderated by the level of emotional intelligence.
The Developmental, Individual-differences, Relationship-based (DIR) model is a developmental model for assessing and understanding any child's strengths and weaknesses. It has become particularly effective at identifying the unique developmental profiles and developing programs for children experiencing developmental delays due to autism, autism spectrum disorders, or other developmental disorders. This Model was developed by Dr. Stanley Greenspan and first outlined in 1979 in his book Intelligence and Adaptation. However, it has been listed by the National Autism Center in their National Standards Project Phase 2 as having an "unestablished level of evidence." "The Play Project" - a version of DIR which was developed by Richard Solomon, established evidence-based status for their approach through a 3-year study by NIMH which was published last year.
The Developmental, Individual-difference, Relationship-based (DIR) model is the formal name for a new, comprehensive, individualized approach to assess, understand, and treat children who have developmental delays (including Autism Spectrum Disorder). Focusing on the building blocks of healthy development, this approach is also referred to as the "Floortime" or "DIRFloortime" approach. However, Floortime is actually a strategy within the DIR model that emphasizes the creation of emotionally meaningful learning exchanges that encourage developmental abilities.
The goal of treatment within the DIR model is to build foundations for healthy development rather than to work only on the surface of symptoms and behaviors. Here, children learn to master critical abilities that may have been missed along their developmental track. For example, Autism Spectrum Disorder (ASD) has three core/primary problems: (1) establishing closeness, (2) using emerging words or symbols with emotional intent, and (3) exchanging emotional gestures in a continuous way. Secondary symptoms (perseveration, sensory-processing problems, etc.) may also exist. Thus, treatment options are based on particular underlying assumptions. The DIR model is based on the assumption that the core developmental foundations for thinking, relating, and communicating can be favorably influenced by work with children’s emotions and their effects.
The DIR model was developed to tailor to each child and to involve families much more intensively than approaches have in the past. Through the DIR model, cognition, language, and social and emotional skills are learned through relationships that involve emotionally meaningful exchanges. Likewise, the model views children as being individuals who are very different and who vary in their underlying sensory processing and motor capacities. As such, all areas of child development are interconnected and work together beneficially.
The Interdisciplinary Council on Development and Learning (ICDL) holds registered trademarks in the United States and/or other countries for DIR, DIRFloortime, and Floortime.
The DIR model is broken down into milestones (AKA capacities) (i.e., stages of development) that are gauged in normally developing children (versus children who have developmental delays).
In babies from 0 to 2 months, Milestone One involves self-control/self-regulation and interest in the world. The focus here is shared attention, which involves learning and interacting socially. Children need to learn to stay calm, to focus, and to actively take in information from their experiences with others.
Milestone Two occurs in ages 2 to 6 months. It involves relating and engagement whereby babies learn to recognize patterns, such as patterns of language in the flow of conversation. From there, they can internalize and process those patterns into something meaningful; for example, they understand cognitively that they can use language to obtain a desire.
Milestone Three involves intentional two-way communication and occurs by 6 months, when babies begin to convert emotions into signals for communication. But in order for this to happen, primary caregivers must read and respond to babies’ signals while also challenging the babies to read and respond to theirs.
Milestone Four involves social problem-solving, formation of a sense of self, and mood regulation, which occurs between 9 and 18 months. Babies use two-way communication to solve problems by employing patterns that involve a few steps to achieve a desired goal. For example, the baby can engage a parent and use eye gaze to get a desired goal or can grab a caregiver’s hand and pull toward his/her plate to indicate the desire for more food. Later, this process helps children to put words together into a sentence. Progress here is built on emotional interactions that increasingly become more complex.
Milestone Five occurs around age one, involving the creation of symbols and the use of words/ideas. "Using ideas" is defined as the meaningful use of pictures, words, or symbols to communicate something (in contrast to scripting or repeating).
Milestone Six, which occurs in toddlers around two years of age, regards emotional thinking, a sense of reality, and logic. Here, to create a new understanding of reality, one must logically connect his/her own idea to someone else’s. Emotional investment in relationships helps children to recognize the differences between their own and others’ ideas and behaviors.
Milestone 7 presents multi-causal and triangular thinking in which a child between ages 5 and 7 begins to recognize and process multiple causes for emotions and events.
During Milestone 8, between ages 7 and 10, emotionally differentiated thinking and gray-area thinking occur. Here, the child begins to understand the varying degrees or relative influences of events, feelings, or phenomena (e.g., "I’m only a little sad").
Last, Milestone 9, which arrives between puberty and early adolescence, involves a growing sense of self and reflection on an internal standard. This means that more-complex emotional interactions are helping the adolescent to progress into thinking in relation to an internal standard of an expanding self (e.g., "I was more angry than usual").
These nine functional emotional-developmental capacities continue to develop throughout life, but they need to happen sequentially, building upon the prior capacity, in order for the child to adapt and develop healthily.
Global Maps: Why do the metabolome? With 2 cc of serum, we can screen for metabolic disease and altered nutritional states.
What is Metabolomics? Metabolomics is the study of small molecules and an integral technology for understanding the function of biological systems. It is the systematic measurement and biological interpretation of the low molecular weight (~50-1500 Da) biochemicals or “metabolites” within a biological sample, such as urine, plasma or tissue. Surveying these small molecules allows for better understanding of biological mechanisms, thereby creating a more complete picture of the phenotype (the observable characteristics of a living system).
Autism spectrum disorders (ASD) are a group of biological disorders with associated metabolic derangement. This study aimed to identify a pattern of metabolic perturbance in ASD using metabolomics in urinary specimens from 48 children with ASD and 53 age matched controls. Using a combination of liquid- and gas-chromatography-based mass spectrometry, we detected the levels of 82 metabolites (53 of which were increased) that were significantly altered between the ASD and the control groups using osmolality normalized data. Pattern analysis showed that the levels of several amino acids such as glycine, serine, threonine, alanine, histidine, glutamyl amino acids and the organic acid, taurine were significantly (p≤0.05) lower in ASD children. The levels of antioxidants such as carnosine were also reduced in ASD (p=0.054). Furthermore, several gut bacterial metabolites were significantly altered in ASD children who had gastrointestinal dysfunction. Overall, this study detected abnormal amino acid metabolism, increased oxidative stress, and altered gut microbiomes in ASD. The relationship of altered gut microbial co-metabolism and the disrupted metabolisms requires further investigation.
The incidence of individuals with autism spectrum disorders (ASDs) is on the rise; therefore, well-timed screening is important. Given that this is a nutritionally vulnerable population, it is imperative to conduct a detailed nutritional assessment so that timely and intensive interventions can be recommended. This review article summarizes the research, focusing on the nutritional status of individuals with ASDs based on their anthropometric measurements, biomarkers, and dietary assessments. Research examining anthropometric measurements reveals an abnormally accelerated rate of growth among children with autism but shows inconsistent findings on the prevalence of overweight/obesity in comparison with typically growing children. Although dysregulated amino acid metabolism, increased homocysteine, and decreased folate, vitamins B-6 and B-12, and vitamin D concentrations have been proposed as possible biomarkers for an early diagnosis of ASDs, research investigating their association with age, gender, severity, and other comorbid psychiatric/nonpsychiatric disorders is lacking. There is consensus that children with autism have selective eating patterns, food neophobia, limited food repertoire, and sensory issues. Although inadequate micronutrient but adequate macronutrient intakes are increasingly reported, there are inconsistent results about the extent and type of nutrient deficiencies. Identification and development of nutritional assessment indicators that serve as early warning signs during routine practice beginning at birth and extending throughout the child's growth are necessary. With this population aging, there is also a dire need to study the adult population. A more vigorous role by nutrition professionals is warranted because management of potential comorbidities and contributory factors may be particularly problematic.
Mitochondrial respiratory chain deficiencies are a group of more than 100 disorders of adults and children, with highly variable phenotypes. Their diagnosis is a great challenge, in spite of the fact that knowledge on their molecular genetic background has increased considerably during the last 20 years. Muscle biopsy is the key diagnostic procedure, including histological and biochemical analysis of mitochondria. Less invasive, specific and sensitive diagnostic tools based on serum biomarkers are still lacking. Recent technological developments, especially in mass spectrometry, enable novel tools for identification of local and global molecular consequences of mitochondrial respiratory chain dysfunction in patient samples. Furthermore, emerging disease models, especially genetically modified mice, offer unique materials to tackle pathophysiology with modern transcriptomic, proteomic, and metabolomic approaches. Identified molecular signals or metabolic fingerprints have the potential to be highly useful biomarkers for future diagnosis of mitochondrial respiratory chain disorders.
Our office is located in the Medical Office Building #1 at the Methodist Sugar Land Hospital. The facility provides outside parking at no charge. There is not a valet parking service.
From the Northeast:
Follow 59 South to Sugar Land, exit at Sweetwater Blvd; follow the feeder road and make a “U Turn” under the freeway; make an immediate right at the Methodist Sugar Land Hospital sign; follow the road about 200 yards; make a left into the hospital parking lot; make a left at the 3-way stop sign; follow the parking lot around to the Medical Office Building #1 entrance (MOB #1 is four-stories tall and faces the freeway). We are located on the third floor, Ste 320.
Take the Grand Parkway (Hwy 99) until it ends at Hwy 59; take 59 North two exits to Sweetwater Blvd; exit Sweetwater Blvd and stay on the feeder passing the stop light for Sweetwater Blvd, make an immediate right at the Methodist Sugar Land Hospital sign; follow the road about 200 yards; make a left into the hospital parking lot; make a left at the 3-way stop sign; follow the parking lot around to the Medical Office Building #1 entrance (MOB #1 is four-stories tall and faces the freeway). We are located on the third floor, Ste 320.
From the Memorial Area:
Go South on Beltway 8, exit onto 59 South; follow 59 South to Sugar Land, exit at Sweetwater Blvd; follow the feeder road and make a “U Turn” under the freeway; make an immediate right at the Methodist Sugar Land Hospital sign; follow the road about 200 yards; make a left into the hospital parking lot; make a left at the 3-way stop sign; follow the parking lot around to the Medical Office Building #1 entrance (MOB #1 is four-stories tall and faces the freeway). We are located on the third floor, Ste 320.
Take Hwy 6 North to Hwy 59 South; turn left onto the feeder road of Hwy 59 South; stay on the feeder to the next stoplight at Sweetwater Blvd; make a “U-Turn” under the freeway; make an immediate right at the Methodist Sugar Land Hospital sign; follow the road about 200 yards; make a left into the hospital parking lot; make a left at the 3-way stop sign; follow the parking lot around to the Medical Office Building #1 entrance (MOB #1 is four-stories tall and faces the freeway). We are located on the third floor, Ste 320.
Balance and coordination are products of complex circuitry involving the basal ganglia, cerebellum and cerebral cortex, as well as peripheral motor and sensory pathways. Malfunction of any part of this intricate circuitry can lead to imbalance and incoordination, or ataxia, of gait, the limbs or eyes, or a combination thereof. Ataxia can be a symptom of a multisystemic disorder, or it can manifest as the major component of a disease process. Ongoing discoveries of genetic abnormalities suggest the role ofmitochondrial dysfunction, oxidative stress, abnormal mechanisms of DNA repair, possible protein misfolding, and abnormalities in cytoskeletal proteins. Few ataxias are fully treatable, and most are symptomatically managed. A discussion of the ataxias is presented here with brief mention of acquired ataxias, and a greater focus on inherited ataxias. FREE article here
In December 2015, Steminent received US FDA Orphan Drug Designation for Stemchymal ® in the treatment of PolyQ SCAs. The US FDA’s Orphan Drug Designation program provides orphan status to drugs and biologics intended for both safe and effective treatment of rare indications that affect fewer than 200,000 people in the U.S.
The granted designation also allows Steminent to enjoy a 7-year market exclusivity upon approval of Stemchymal ® and other development incentives including tax credits for clinical research costs and Prescription Drug User Fee Act (PDUFA) fee exemption.
Stemchymal® is the proprietary, allogenicMSC product developed by Steminent for treatment of selected diseases with unmet or underserved medical needs.
The company’s SCA clinical study is now in the Phase II stage.