The difference between concussions in high school and in professional sports

This article explains the difference between concussions in high school sports and concussions in professional sports.

No sports enthusiast will ever forget the goal line collision between Pittsburgh Steelers' Le'Veon Bell and Baltimore Ravens' Jimmy Smith or when Detroit Tigers Catcher Alex Avila was drilled by David Ross of the Boston Red Sox.

Both of these plays caused two serious concussions and both of these athletes returned to play about a week later.

But that's professional sports.

When a high school athlete suffers a severe concussion, it could take weeks before they are back on the field. That's for multiple reasons.

"They too have to go through certain criteria, just like our high school athletes do. However, they are being monitored 24/7. Seven days a week, 365 days a year by the medical staff. They have somebody with them pretty much at all times," said Mike Casselman, HealthWorks.

In high school, it's a different story.

"Though we have athletic trainers there on a daily basis, there might be a day or two gap where the communication isn't there," Casselman added.

The issue of 'chronic encephalipathy' in many NFL players has been receiving a great deal of media attention. In the cases of retired players, it appears most had long careers in the NFL after playing in both high school and college.

In most cases, they played football for more than 20 years and suffered multiple concussions in addition to hundreds of other blows to the head.

But its not just football players that can receive a concussion and its not just from helmet to helmet impact.

"It can be by whip lash. It could be from a quick fall," said Frank Moore, Marion County Athletic Director. "Football would be one you would think. But soccer has a lot of concussions, along with basketball."

Casselman agreed.

"I'm telling you. A big one is cheerleading. People might not think that. It's very competitive in this area. You have the bases that are catching the flyers. They take an elbow, they take a knee," Casselman said.

While many professional athletes blame concussions for their memory loss and depression, little is known about the long term effects concussions can have on high school athletes.

"No concussion is the same and you need to take a very serious approach if they have any of the signs and symptoms," Moore said.

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Study: Auditory verbal hallucinations may be due to epilepsy

A study claims that epilepsy can cause auditory verbal hallucinations in some people.

According to a new study, epilepsy patients with damage to the left temporal cortex are at risk of experiencing complex, auditory verbal hallucinations (AVHs) – suggesting there is a neurological, as well as psychiatric, origin of these phenomena.

While AVHs are well documented in people with psychiatric conditions, reports from neurological patients are rare and have not been extensively studied.

Now, though, researchers from the Swiss Federal Institute of Technology in Lausanne and University Hospital Geneva have suggested epilepsy patients with prevalent language deficits, as well as damage to posterior and basal language areas in the left temporal cortex, sometimes hallucinate voices.

The study, which is published in this month’s edition of the journal Epilepsy Behaviour, comprised an examination of more than 350 people with epilepsy.

Nine of these subjects – all of whom had drug-resistant forms of the neurological condition – were found to experience AVHs, underlining the rarity of the phenomenon. They were studied by means of a semistructured interview, neuropsychological tests and multimodal imaging. The scientists used a combination of functional and structural neuroimaging data, and surface and intracranial EEG, to locate the damaged brain tissue from which their epilepsies originated.

They found the occurrence of AVHs in epilepsy patients was associated with the neurodevelopmental problems outlined above.

Subjects’ AVHs also followed common patterns – they heard single voices at a time, speaking in their native languages and of the same gender as the patient. The hallucinations also had consistent spatial features – most subjects reported they heard voices that seemed to come from external space, contralateral to the parts of their brain tissue that were damaged.

“We argue that the consistent location of AVHs in the contralesional external space, the prominence of associated language deficits and the prevalence of lesions to the posterior temporal language areas characterise AVHs of neurological origin, distinguishing them from those of psychiatric origin,” the report’s authors commented.

Read more here

Pediatric migraines may be caused by environment

Different environmental factors, such as sleep deprivation, diet, and school, could play a role in pediatric migraines.

Environmental stressors play a large role in triggering migraines in children, according to Dr. Eric Pearlman.

"Migraine is definitely a pediatric disorder. It peaks in young adulthood, but it definitely occurs in kids," Dr. Pearlman, chair of the department of pediatrics at Mercer University in Savannah, Ga., said at the annual meeting of the American Academy of Pediatrics.

Epidemiologic data suggest that migraine occurs in 10.5% of 10- to 15-year-old children and 3% of 7-year-olds, and that headaches – possibly including migraines – occur in 4% of 3-year-olds. By about 13 years of age, the prevalence of migraines starts reaching adult levels of about 6% in males, and 18% in females.

Environmental factors such as sleep deprivation, dehydration, dietary factors, school stressors, hidden stressors (like peers), and hormonal fluctuations represent triggers that can be particularly pronounced in children, he noted.

With International Classification of Headache Disorders, third edition (ICHD-III) criteria, migraines can be differentiated from acute, acute recurrent, and chronic progressive or chronic nonprogressive headaches if a child has experienced at least five attacks lasting up to 72 hours (whether untreated or unsuccessfully treated), if nausea and/or vomiting or photophobia and phonophobia are present, and if the child has at least two of four characteristics, including unilateral location, pulsating quality, moderate to severe intensity, and a tendency to be aggravated by – or avoid – routine physical activity.

In children, photophobia and phonophobia can be inferred (if they report having to lie down in a dark, quiet room, for example), as many have difficulty describing or understanding these symptoms

Unilateral headaches are rare in children, Dr. Pearlman noted.

If a diagnosis of migraine is established, it is important to make the diagnosis known to the child, and to educate the child about the condition and treatments.

Consider providing handouts and referring to websites (such as theAmerican Headache Society or the National Headache Foundationsites), to help educate patients and to manage their expectations, as they need to understand you cannot cure their migraine, he advised.

Involving both the patient and their parents in decision making can improve compliance with treatment recommendations, he said.

Pharmacologic interventions can include nonspecific short-term therapies, migraine-specific therapies, and preventive treatment.

Nonspecific short-term therapies may include acetaminophen, nonsteroidal anti-inflammatory drugs, or combination drugs. Migraine-specific therapies include ergotamine and dihydroergotamine, and the "triptans."

Seven triptans are available, including two that are approved for use in children; rizitriptan (Maxalt) is approved for children older than age 6 years, and almitriptan (Axert) is approved for those aged 12-17 years.

Maxalt comes in both an oral and orally disintegrating form, and is available as a generic drug. Generic sumitriptan (Imitrex) also is available.

"There are good data for most of the triptans for adolescents aged 12 and older," Dr. Pearlman said.

Rescue medications for those who have an inadequate response to short-term therapy can include a combination of an analgesic like a nonsteroidal and an antiemetic, or an opiate and an antiemetic if the patient used a nonsteroidal initially. Rescue medications may be needed "because nothing is going to work 100% of the time," he said.

Read more here

Ecstasy may help those with Anxiety and PTSD

A study shows that the way Ecstasy acts on the brain could benefit those with anxiety and PTSD.

Researchers say they've discovered how the club drug Ecstasy acts on the brain, and their findings suggest the drug might be useful in treating anxiety and post-traumatic stress disorder.

The study included 25 volunteers who underwent two functional MRI brain scans -- one after taking Ecstasy (MDMA) and one after taking a placebo. Both times, the participants did not know which substance they had been given.

Ecstasy decreased activity in the brain's limbic system, which is involved in emotional responses. The drug also reduced communication between the brain's medial temporal lobe and medial prefrontal cortex, which is involved in emotional control, according to the study, which was published online Jan. 13 in the journal Biological Psychiatry.

These effects are the opposite of brain patterns that occur in people with anxiety, said the researchers, from Imperial College London, in England.

The researchers also found that Ecstasy increased communication between the amygdala and the hippocampus. Previous research has shown that people with post-traumatic stress disorder (PTSD) have reduced communication between these brain areas.

"We found that MDMA caused reduced blood flow in regions of the brain linked to emotion and memory," study author Dr. Robin Carhart-Harris, of the department of medicine, said in a college news release. "These effects may be related to the feelings of euphoria that people experience on the drug."

"In healthy volunteers, MDMA seems to lessen the impact of painful memories," Carhart-Harris said. "This fits with the idea that it could help patients with PTSD revisit their traumatic experiences in psychotherapy without being overwhelmed by negative emotions, but we need to do studies in PTSD patients to see if the drug affects them in the same way."

Another researcher advised caution in applying the study results to other groups of people.

"The findings suggest possible clinical uses of MDMA in treating anxiety and PTSD, but we need to be careful about drawing too many conclusions from a study in healthy volunteers," study co-leader David Nutt, a professor of neuropsychopharmacology, said in the news release. "We would have to do studies in patients to see if we find the same effects."

A recent pilot study in the United States investigated the use of MDMA along with psychotherapy in the treatment of PTSD patients and yielded positive results, the researchers said.

Read more here

Sleeping during the day can hurt your genes

This study shows that sleeping during the day can mess up a third or a person's genes.

Sleeping during the day -- a necessity for jet-lagged travelers and those who work overnight shifts -- disrupts the rhythms of about one-third of your genes, a new study suggests.

What's more, shifted sleep appears to disrupt gene activity even more than not getting enough sleep, according to the research.

For the new study, which was published in this week's issue of the journal Proceedings of the National Academy of Sciences, British researchers put 22 healthy, young volunteers in a dimly lit sleep lab for three days.

During the first day, they disrupted the participants' sleep at regular intervals to reset their body clock to its innate rhythm. On the second and third days, the volunteers ate and slept on a 28-hour schedule, so their longest period of sleep was from noon until about 6:30 p.m.

The researchers drew blood samples all three days so they could watch what happened to the timing of gene activity.

During the first day, when the body reset its circadian rhythm, nearly 1,400 genes -- about 6.4 percent of all genes that were analyzed -- were in sync with that rhythm. On the days of shifted sleep, however, the number of genes tied to the body's clock dropped dramatically, to 228 genes, or only 1 percent of genes analyzed.

The researchers estimated that the sleep disruptions would ultimately impact about a third of a person's genes.

That's an even greater disruption than scientists saw in a previous study when they tested the effects of sleep deprivation on gene activity. In that study, which had study volunteers sleeping about five and half hours each night, the number of genes that were in sync with the body's clock dropped from about 9 percent to 7 percent.

"These are quite fundamental processes that are being affected," said senior study author Derk-Jan Dijk, a professor of sleep and physiology at the University of Surrey, in the United Kingdom.

"We think that may be related to the negative health outcomes associated with long-term shift work," Dijk said. Shift workers are at higher risk for many health problems, including obesity, diabetes, high blood pressure, heart disease, disrupted menstrual cycles and cancer, he said.

This study didn't directly connect health problems and night-shift work, but experts said it does start to help them understand why sleep might have such a powerful influence on a person's health.

"This study suggests that mistimed sleep can alter circadian rhythms, so the cycling of many, many genes is impaired," said Dr. Mark Wu, assistant professor of neurology, medicine, genetic medicine and neuroscience at Johns Hopkins University. "What this could cause, they can't really say -- except it's probably not good." Wu was not involved in the new research.

Genes carry the instructions for making proteins. Proteins make up just about every kind of chemical signal, hormone and tissue in the body, the researchers said.

The timing of when proteins are made is important because their production should correspond to our behaviors, said Frank Scheer, a neuroscientist at Harvard and director of the Medical Chronobiology Program at Brigham and Women's Hospital in Boston.

When the body anticipates a meal, for example, the liver has to stop releasing into the blood the carbohydrates it has stored and the pancreas has to make more insulin, while the muscles have to become more sensitive to insulin that's released so they can take in blood sugar, Scheer said.

"If these processes are working in concert and they're synchronized to when you eat and when you fast, then the system is very efficient and effective at absorbing these sugars quickly and minimizing any adverse consequences of elevated blood sugar levels," Scheer said.

"If these are not rhythmic, then you can easily imagine that, during the nighttime, you have this machinery up and running without need," he said. "During the daytime, when you actually do need it, it's only running half speed."

Read more here

Challenges for college students with ADHD

This article looks into challenges that college students with ADHD face.

Many students with Attention Deficit Hyperactivity Disorder (ADHD) attend college. College students with ADHD face a number of challenges, including choosing a supportive school and community where they can:

• find and access medical services


• get help with organizing their schedule and life


• succeed academically

Most people with ADHD are diagnosed before college. However, some people may not recognize the signs and symptoms of ADHD until they are at college. Trying to balance school work and the freedom of living away from home for the first time may be challenging. It can be natural to feel unfocused, distracted, overwhelmed, or disorganized when attending college. However, if these issues have caused significant problems in the past and are getting in the way of current functioning, the student may have ADHD.

If a student is struggling, it may be helpful to seek consultation with a qualified mental health professional. The diagnosis of ADHD is made based on a comprehensive clinical assessment. This may include information from multiple sources, including rating scales, getting history from the student, family, or past teachers if possible. There is no single test (brain imaging, blood testing, or psychological testing) that can reliably diagnose ADHD. Research shows that medication is the most effective treatment for ADHD. Cognitive-behavioral therapy, social skills training, and academic support can also be helpful.

There are many ways to successfully manage ADHD before and during college.

Preparing for and Staying Organized While at College

• Consider the best college environment to meet your needs, such as class size, workload, academic calendar, and availability of support services. Resources to help you find the best college include: high school counselors, parents, friends who are in or have attended college, and national ADHD organizations or websites.


• Learn about the medical services available at colleges before choosing where to go. Some college and university health centers do not prescribe ADHD medications. You may need to find a doctor in the surrounding community. Think about the transportation options and ease of access to that provider.


• Talk with your doctor about how to best manage your medications when at college. Do not make changes in your medication without consulting your doctor. Ask your current doctor and the doctor at college to coordinate care. It is also helpful to have a history of your medications and your response to those medications for your new doctor.


• If you have used tutors or support before college, think about continuing at college, at least for a little while.


• If you need specific support or accommodations, register at the college disability office. If you have a summary of treatment or any psychological tests that were done within the last 3 years, bring them to the visit.


• Practice using planners, calendars, or scheduling apps while still in high school. The demands on time management and organization increase greatly in college. Even if your parents helped you in the past, it is important to learn to do it yourself.

Managing Medications at College

• Many medications prescribed for ADHD have to be monitored regularly. While at college, you need to schedule and keep your own medical appointments. Changes to your medication should only be made after talking with your doctor.


• Learn how to use pharmacy services. Pay attention to prescription start dates and expiration dates. Many medications prescribed for ADHD are “controlled substances” so states may have additional rules on how these medicines can be provided, including limits on how often prescriptions can be refilled.


• Taking medication that is not prescribed for you, sometimes called “diversion” or “academic doping,” is illegal and unsafe. Your medications were prescribed by your doctor who knows you and your medical history. They should only be taken by you. There are serious cardiac, neurological, and psychological risks of misusing ADHD medications. There can also be serious risks to mixing medications with alcohol or other drugs.


• Keep medications safely stored or hidden to protect against theft. If medications are stolen, report it to campus or local police.

Adjusting to the academic, social, and organizational demands of college is difficult for most students. It can be especially difficult for students with ADHD. Arranging for support from medical and school professionals can help students with ADHD have a successful college experience, as well as a long career after graduation.

Read more here

New surgery option for people with migraines

This is an interesting area of literature that is developing with a small number of articles comparing efficacy and surgical techniques.
For instance, see this article  JR


UT Southwestern is offering a new surgery to help people who suffer from migraine headaches.

A new surgery for migraine headache relief is being pioneered at UT Southwestern Medical Center in Dallas, and the results thus far have been incredibly promising.

The news comes by way of a release from UT Southwestern, which tells the story of 18 year-old Meredith Messerli, whose prospects of being able to attend college were hampered by persistent, debilitating migraine headaches, which were so life-altering that the teen missed two years of high school as a result of her hypersensitivity to light and a headache that literally never went away. “Once I got a headache, it never went away,” Meredith explained in a recent interview. “Having a headache for that long changes your personality. You don’t want to talk to anyone. You don’t want to do anything.”

For years, Meredith and her family searched for medical answers to her severe migraines, which in themselves still remain a partial mystery to researchers. She and her family had consultations who tested her for a wide range of different causes and prescribed almost fifty different types of medicines. She was even admitted to the hospital several times for for weeks in order to receive D.H.E. 45 treatments, which is considered to be a last-resort medication prescribed for migraines. However, this past summer, Meredith underwent a novel procedure for migraines at UT Southwestern, which has since then relieved her never-ending headaches.

The procedure, known as nerve decompression surgery, has recently gained in popularity as an alternative therapy for chronic headache sufferers that has shown to offer migraine headache relief to those who have not been able to find relief elsewhere. The first stage of the procedure is a process for identifying the compressed nerves that are causing the migraine, usually through the use of Botox and nerve blocks. Once the problem areas have been identified, surgeons sever the tiny muscles and tissues that cause the compression of these nerves, thus relieving the pain once and for all.

Migraine surgery involves first identifying the compressed nerves through a clinical history and exam or use of Botox and nerve blocks. Then, the pressure causing the migraines is relieved by severing tiny muscles and other tissues pressing on and irritating these headache-trigger nerves.

Dr. Bardia Amirlak, an Assistant Professor of Plastic Surgery at UT Southwestern who performed the surgery on Meredith, has quickly established himself as a leading pioneer of the surgery, having successfully performed more than 100 such procedures over the past two years. Dr. Amirlak has refined the surgery with his own method of using an endoscope to target smaller blood vessels, and as a result, has also improved on the procedure’s outcome. “This surgery is an option for patients with chronic headaches, nerve-compression headaches, occipital neuralgia, new daily persistent headaches, episodic migraines, and chronic migraines,” said Dr. Amirlak. “However, before considering surgery, all patients should first be evaluated by a neurologist and try medical management.”

From Dr. Amirlak’s own accounts, the surgery is quickly becoming a popular approach to migraine headache relief, thanks to its relatively high success rate: Amirlak reports that 60 percent of his patients get complete relief after the surgery, and for the remaining 40 percent, nearly 90 percent of those experience at least a 50 percent reduction in pain.

As a result, he is currently performing two to three migraine surgeries a week. “Patients are coming from all over the country as well as from other countries,” he said.

Of course, the surgery is not an option for everyone looking for relief from migraines, as the procedure is an invasive one. “Not all migraine sufferers are candidates. We must be careful selecting candidates for this type of surgery,” Dr. Amirlak. However, the doctor does believe that is a particularly well-suited surgery for young patients like Meredith who are otherwise healthy, but whose migraines are having major life-altering consequences. “I would rather operate on a young patient to prevent lifelong pain and suffering than to wait many years after their school, work, and social life has suffered. Here at UT Southwestern we are trying to establish standard protocols for migraine surgery in children,” he added.

Both Meredith and her family attest to Dr. Amirlak’s commitment to helping her get out of pain, and his expertise in the field of treating migraines. “He spent an hour talking to us. He seemed really passionate about helping people, and we felt we had a bond with him,” Meredith said, adding, “I wouldn’t be in college right now if not for Dr. Amirlak. I can do everything I used to do before. I’m excited to be myself again.”

Read more here

Effects of sleep deprivation on the pediatric electroencephalogram

Many are surprised to learn that the yield of a single EEG is limited.  A normal EEG does not exclude epilepsy.  

Neurologists request sleep deprivation with the goal of acquiring sleep tracing on the EEG and hopefully to provoke abnormalities.

This article is helpful in showing the yield may be higher in children over 3  and those who have already had a seizure. 

As an aside, a calm outpatient environment is also important in promoting sleep in an EEG.

JR 

Effects of sleep deprivation on the pediatric electroencephalogram.

Steven T DeRoos, Kipp L Chillag, Martina Keeler, Donald L Gilbert

View Original ArticleLikeCommentShare

1. Steven T. DeRoos, MD^a,
2. Kipp L. Chillag, DO^a,
3. Martina Keeler, MD^b,
4. Donald L. Gilbert, MD^c

1. ^aDivisions of Pediatric Neurology
2. ^bPediatric Hospitalists, Helen DeVos Children's Hospital, Grand Rapids, Michigan
3. ^cDivision of Pediatric Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio

Abstract

BACKGROUND. The routine electroencephalogram aids in epilepsy syndrome diagnosis. Unfortunately, routine outpatient electroencephalogram results are normal in roughly half of children with epilepsy. To increase the yield, practice guidelines recommend electroencephalograms with sleep and sleep deprivation. The purpose of this study was to rigorously evaluate this recommendation in children.

METHODS. We conducted a randomized, blinded comparison of routine electroencephalograms versus sleep-deprived electroencephalograms in 206 children aged 0 to 18 years. Electroencephalograms were ordered for standard indications after a neurologist's clinical assessment indicated ≥1 seizure (83%) or unclear spell (17%). The primary outcome was the proportion of normal routine electroencephalogram results versus sleep-deprived electroencephalogram results. Logistic regression modeling was used to assess the influence of sleep, as well as other clinical factors.

RESULTS. Although children with sleep-deprived electroencephalograms had less sleep the night before (4.9 vs 7.9 hours) and more sleep during electroencephalograms (73% vs 55%), the increase in electroencephalogram yield was borderline significant (56% normal sleep-deprived electroencephalogram versus 68% normal routine electroencephalogram). Moreover, sleep during the electroencephalogram did not increase its diagnostic yield. Sleep-deprived electroencephalogram yield tended to be higher in children with preelectroencephalogram clinical diagnosis of seizure(s) and at older ages (>3 years).

CONCLUSIONS. Sleep deprivation, but not sleep during the electroencephalogram, modestly increases the yield of the electroencephalogram in children diagnosed with seizures by neurologists. Compared with a routine electroencephalogram, the number needed to test with sleep-deprived electroencephalogram to identify 1 additional child with epileptiform discharges is ∼11.

Key Words:

• Child neurology Epilepsy Serving Houston Sugar land Katy Cypress The Woodlands San antonio Seguin

REVIEW: PORTABLE DIAGNOSTIC DEVICES FOR IDENTIFYING OSA IN CMV DRIVERS

  VOLUME  35, ISSUE  11  

REVIEW: PORTABLE DIAGNOSTIC DEVICES FOR IDENTIFYING OSA IN CMV DRIVERS
Portable Diagnostic Devices for Identifying Obstructive Sleep Apnea among Commercial Motor Vehicle Drivers: Considerations and Unanswered Questions

http://dx.doi.org/10.5665/sleep.2194

Chunbai Zhang, MD, MPH^1,3,4; Mark Berger, MD²; Atul Malhotra, MD^3,4; Stefanos N. Kales, MD, MPH^1,4,5

 ¹Environmental and Occupational Medicine and Epidemiology, Harvard School of Public Health, Boston, MA; ²Precision Pulmonary Diagnostics, 8275 El Rio Street, Houston, TX; ³Division of Sleep Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA; ⁴Division of Sleep Medicine, Harvard Medical School, Boston, MA; ⁵Employee and Industrial Medicine, Cambridge Health Alliance, Cambridge, MA

Obstructive sleep apnea (OSA), a syndrome defined by breathing abnormalities during sleep, can lead to fatigue and excessive daytime sleepiness (EDS) with an increased risk of motor vehicle crashes. Identifying commercial motor vehicle operators with unrecognized OSA is a major public health priority. Portable monitors (PMs) are being actively marketed to trucking firms as potentially lower-cost and more accessible alternatives to the reference standard of in-laboratory polysomnography (PSG) in the diagnosis of OSA among commercial motor vehicle operators. Several factors regarding PMs remain uncertain in this unique patient population: their sensitivity and specificity; the cost-benefit ratio of the PMs versus PSG; potential barriers from human factors; and evolving technologic advancement. Human factors that alter test accuracy are a major concern among commercial drivers motivated to gain/maintain employment. Current available data using PMs as a diagnostic tool among CMV operators indicate relatively high data loss and high loss to follow-up. Loss to follow-up has also been an issue using PSG in commercial motor vehicle operators. Furthermore, PM testing and PM results interpretation protocols may have no sleep specialist oversight, and sometimes minimal physician oversight and involvement. Additional studies comparing unattended and unmonitored PMs directly against full in-laboratory PSG are needed to provide evidence for their efficacy among commercial motor vehicle operators.

Citation:

Zhang C; Berger M; Malhotra A; Kales SN. Portable diagnostic devices for identifying obstructive sleep apnea among commercial motor vehicle drivers: considerations and unanswered questions. SLEEP2012;35(11):1481-1489.

Does a child with CP have a developmental regression? Think EEG abnormalities in sleep.

Does a child with CP have a developmental regression? Think EEG abnormalities in sleep. 

Early thalamic lesions in patients with sleep-potentiated epileptiform activity

Objective: To compare the prevalence and type of early developmental lesions in patients with a clinical presentation consistent with electrical status epilepticus in sleep either with or without prominent sleep-potentiated epileptiform activity (PSPEA).
                    

Methods: We performed a case-control study and enrolled patients with 1) clinical features consistent with electrical status epilepticus in sleep, 2) ≥1 brain MRI scan, and 3) ≥1 overnight EEG recording. We quantified epileptiform activity using spike percentage, the percentage of 1-second bins in the EEG tracing containing at least 1 spike. PSPEA was present when spike percentage during non-REM sleep was ≥50% than spike percentage during wakefulness.

                    

Results: One hundred patients with PSPEA (cases) and 47 patients without PSPEA (controls) met the inclusion criteria during a 14-year period. Both groups were comparable in terms of clinical and epidemiologic features.

Early developmental lesions were more frequent in cases (48% vs 19.2%, p = 0.002). Thalamic lesions were more frequent in cases (14% vs 2.1%, p = 0.037).

The main types of early developmental lesions found in cases were vascular lesions (14%), periventricular leukomalacia (9%), and malformation of cortical development (5%). Vascular lesions were the only type of early developmental lesions that were more frequent in cases (14% vs 0%, p = 0.005).
                    

Conclusions: Patients with PSPEA have a higher frequency of early developmental lesions and thalamic lesions than a comparable population of patients without PSPEA. Vascular lesions were the type of early developmental lesions most related to PSPEA.

http://www.neurology.org/content/78/22/1721.full

Premature infants on parenteral nutrition hurt by the national zinc shortage

Zinc Deficiency–Associated Dermatitis in Infants During a Nationwide Shortage of Injectable Zinc — Washington, DC, and Houston, Texas, 2012–2013

Weekly

January 17, 2014 / 63(02);35-37

Duke Ruktanonchai, MD1, Michael Lowe, PhD1, Scott A. Norton, MD2, Tiana Garrett, PhD1, Lamia Soghier, MD3, Edward Weiss, MD4, June Hatfield, MS3, Jeffrey Lapinski, MS3, Steven Abrams, MD4, Wanda Barfield, MD5 (Author affiliations at end of text)

Injectable zinc, a vital component of parenteral nutrition (PN) formulations, has been in short supply in the United States since late 2012. In December 2012, three premature infants with cholestasis hospitalized in Washington, DC, experienced erosive dermatitis in the diaper area and blisters on their extremities, a condition that can be associated with zinc deficiency (1). All three infants were receiving PN because they had extreme cholestasis and were unable to be fed by mouth or tube. The PN administered to each infant was zinc deficient. Injectable zinc normally is added to PN for premature or medically compromised infants (e.g., those with cholestasis) by the hospital pharmacy because the amount of zinc needed by each patient differs; however, the pharmacy had run out of injectable zinc. No alternatives were available; other preparations of parenteral trace elements either contained insufficient zinc to meet infants' requirements or had the potential to cause trace element toxicity in infants with cholestasis (2). The dermatitis of one infant resolved after the patient was able to take nutrition by mouth. The other two infants were found to have low serum zinc levels. In January 2013, CDC was notified of four additional cases of zinc deficiency among infants with cholestasis who received zinc-deficient PN in a hospital in Houston, Texas. In collaboration with the Food and Drug Administration (FDA), the two hospitals obtained emergency shipments of injectable zinc. No additional cases were reported. Current injectable zinc supplies have been increasing as FDA collaborates with pharmaceutical companies to import emergency supplies. FDA is working to establish temporary backup sources should future shortages occur.

On December 18, 2012, three cases of zinc deficiency disorder in premature infants were diagnosed in Washington, DC. Among the three infants, two were born at 24 weeks' gestation, and one was born at 29 weeks' gestation. Birth weights ranged from 551 g to 734 g (Table). The hospital caring for the infants had exhausted its supply of injectable zinc in November 2012. Infants typically receive injectable zinc and other trace elements as part of PN. Because of extreme cholestasis and prematurity in all three infants, they were unable to receive zinc through oral or enteral feedings. Among cholestatic infants, other preparations of zinc-containing parenteral trace elements might cause trace element toxicity; therefore, no alternatives to the injectable zinc supplements were available. On January 3, 2013, the District of Columbia Department of Health and CDC began case investigations. For this investigation, a case of zinc deficiency disorder was defined as an infant receiving zinc-deficient PN who had either a below-normal serum zinc level (<70 i="" nbsp="" style="margin: 0px; padding: 0px;">µ

g/dL) or dermatitis consistent with zinc deficiency disorder. The objectives of the investigation were to 1) identify and describe cases of zinc deficiency disorder among infants at greatest risk for zinc deficiency, including those who were born at <37 2="" 3="" and="" at="" birth="" cause="" chronic="" deficiency="" describe="" during="" dysfunction="" g="" gastrointestinal="" gestation="" injectable="" investigate="" micronutrient="" monitor="" need="" of="" or="" p="" permanent="" shortage="" shortages.="" symptoms="" the="" those="" to="" weeks="" weighing="" with="" zinc="">

After consulting with CDC, on January 10, 2013, the American Academy of Pediatrics (AAP) informed its members, which include approximately 3,000 neonatologists and 800 neonatal intensive care units nationwide, of the injectable zinc shortage. The members were asked to report to AAP and their respective state health department if their hospitals were experiencing a critical shortage of zinc. AAP compiled and forwarded all responses to CDC. On January 21, a neonatologist in Houston, Texas, reported four additional cases of zinc deficiency disorder to CDC. Among these four infants, two were born at gestational ages >37 weeks; one was born at 33 weeks, and one was born at 25 weeks. All four infants had cholestasis. Birth weights of these four infants ranged from 690 g to 2,950 g (Table). The Houston hospital also had exhausted its supplies of injectable zinc in November 2012. By January 22, 2013, a total of 17 hospitals in 10 states had reported shortages of zinc and other micronutrients. No additional cases of zinc deficiency disorder were identified. By the end of January, FDA was able to facilitate emergency shipment of injectable zinc to all 17 hospitals.

Each of the seven infants experienced zinc deficiency disorder after receiving zinc-deficient PN as a result of the nationwide shortage. The time from initiation of PN to diagnosis of zinc deficiency disorder ranged from 4 to 34 weeks; the exact number of weeks each infant was on zinc-deficient PN is unknown. Six patients were characterized as having low serum zinc levels (range:14–56 µg/dL [normal: 70–120 µg/dL]) and low alkaline phosphatase levels (range: 32–125 U/L [normal: 150–420 U/L]). Alkaline phosphatase levels typically are high in patients with cholestasis, but the zinc deficiency disorder in these infants resulted in low alkaline phosphatase levels. The serum zinc level for the first patient was not measured because suspicion of zinc deficiency disorder occurred after the infant had taken oral feedings containing zinc and the dermatitis had resolved.

All seven infants had cholestasis. Six of the seven had dermatitis consistent with zinc deficiency disorder, and three experienced bacterial infections. One infant experienced recurrent sepsis and liver failure before receiving zinc-deficient PN. This infant did not have dermatitis but had a low serum zinc level (Table). The infant died, and an autopsy was not performed. It is uncertain whether zinc deficiency disorder had a role in his death. After an emergency shipment of zinc was received by two hospitals, the remaining six infants received zinc in their PN, and all six infants improved clinically. Zinc and alkaline phosphatase levels returned to normal ranges, and the infants' skin lesions resolved. Five of the six infants were discharged home. One infant remained hospitalized for 6 months for treatment of conditions unrelated to zinc deficiency disorder; that infant died in October 2013 from conditions unrelated to zinc deficiency disorder.

According to FDA, only two domestic manufacturers' injectable zinc compounds are used in PN (American Regent and Hospira, Inc.). In fall 2012, American Regent informed FDA that it would be experiencing shortages of multiple chemicals, including zinc sulfate, because of delays in manufacturing. These delays resulted from drug quality concerns identified by the company, which included problems of particulate matter in the injectable products. FDA then contacted Hospira to determine whether they could meet the increase in zinc demand. Hospira representatives stated that the company was operating at maximum capacity and was unable to meet the increased demand; thus, the shortage continued to worsen in early January 2013. American Regent was able to release injectable zinc sulfate on January 22, but shortages continued. Hospira planned to release injectable zinc sulfate again by the end of 2013. One foreign manufacturer, Laboratoire Aguettant, and its authorized U.S. distributor, Baxter Healthcare, in conjunction with the FDA, have initiated temporary importation of an injectable zinc solution into the U.S. market to address this shortage.

FDA is continuing to work with American Regent and Hospira to expedite release of injectable zinc sulfate. Information for health-care providers regarding the zinc shortages and expected release dates of new supplies of injectable zinc is provided by FDA on its drug shortage website (http://www.fda.gov/drugs/drugsafety/drugshortages/ucm050792.htm). Finally, FDA is working with pharmaceutical companies to establish temporary backup sources for micronutrients should future shortages occur. When FDA uses regulatory discretion to allow a company to import a drug temporarily during a shortage, FDA ensures that the overseas manufacturing facility meets FDA quality standards and that its products (in terms of formulation and labeling) do not present undue risks for patients.

Editorial Note

Zinc is an essential trace element that functions as a cofactor for certain enzymes involved in metabolism and cell growth (2,3); zinc supports immune function, protein metabolism, development of the gastrointestinal tract, and genetic processes (3). Acute zinc deficiency disorder is characterized by dermatitis around the limbs and body orifices, diarrhea, and impaired immune function, whereas chronic zinc deficiency disorder can lead to liver or kidney failure (2). A rare genetic disorder, acrodermatitis enteropathica, shares the same clinical manifestations as acute zinc deficiency disorder but is a metabolic disorder of zinc absorption. Zinc is a standard component in PN. Premature infants administered PN require 400 µg/kg/body weight/day of zinc to maintain serum levels and promote growth, whereas 200 µg/kg/body weight/day of zinc is sufficient for full-term infants on PN (4). Additionally, PN might be needed for prolonged periods for very low birth weight infants (<1 and="" chronic="" dysfunction.="" g="" gastrointestinal="" i="" infants="" with="">

Studies have reported progressively decreasing serum zinc levels among infants on zinc-deficient PN, particularly premature infants and low birth weight infants (3,5). Although zinc deficiency disorder can have serious health implications among all age groups, infants are particularly vulnerable because their systemic zinc reserves are not fully developed and they are totally dependent on breast milk or formula. Therefore, the American Society for Clinical Nutrition recommends adding injectable zinc to PN for all infants and children, with priority for those who are premature, have low birth weight, or have chronic gastrointestinal dysfunction (4).

Zinc deficiencies among infants are difficult to identify for multiple reasons, including nonspecific signs and symptoms. The most common signs of zinc deficiency disorder include dermatitis and growth impairment, which can be attributed to multiple causes. Zinc deficiency disorder–associated dermatitis, which is a physical manifestation, is present in only the most severe cases. For premature infants, withdrawl of the amount of blood required to measure the serum zinc level might compromise the health of the infant; therefore, routine testing is not performed, which might explain, in part, why no other cases were reported.

Physicians who prescribe PN should recognize the potential risks for micronutrient deficiency, including zinc deficiency, among premature infants who require increased amounts or are unable to receive adequate doses. During shortages, clinicians might need to reserve micronutrients for the most vulnerable populations. According to FDA, shortages also are ongoing for other PN micronutrient components (e.g., selenium, chromium, and copper); FDA is working with manufacturers to prioritize which micronutrients to produce and to identify other sources for the micronutrients. Until the manufacture of these micronutrients increases, shortages will continue. Hospitals with limited stocks of injectable zinc should consider reserving available supplies for infants with the highest risk for deficiency. Whenever PN without the standard micronutrients is administered to patients, either as a result of shortages or other considerations, monitoring for signs and symptoms of micronutrient deficiencies is recommended. Health-care providers should always consider the specific clinical situation when applying these guidelines for individual clinical care.

Acknowledgments

Billie Lou Short, MD, Dept of Neonatology, Children's National Medical Center, Washington, DC. Valerie Jensen, Susan Lance, PhD, Andrei Perlloni, PhD, Food and Drug Administration. Jim Couto, MA, American Academy of Pediatrics. Diana Bensyl, PhD, Scientific Education and Professional Development Office, CDC.

1EIS officers, CDC; 2Dept of Dermatology, 3Dept of Neonatology, Children's National Medical Center, Washington, DC; 4Scientific Education and Professional Development Office, Office of Public Health Scientific Svcs, CDC; 5Texas Children's Hospital, Houston, Texas; 6Div of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion. CDC (Corresponding author: Duke Ruktanonchai, druktanonchai@cdc.gov, 512-776-2497)

References

1. CDC. Notes from the field: zinc deficiency dermatitis in cholestatic extremely premature infants after a nationwide shortage of injectable zinc—Washington, DC, December 2012. MMWR 20013;62:136–7.
2. Greene HL, Hambidge KM, Schanler R, Tsang RC. Guidelines for the use of vitamins, trace elements, calcium, magnesium, and phosphorus in infants and children receiving total parenteral nutrition: report of the Subcommittee on Pediatric Parenteral Nutrient Requirements from the Committee on Clinical Practice Issues of the American Society for Clinical Nutrition. Am J Clin Nutr 1988;48:1324–42.
3. Burjonrappa SC, Miller M. Role of trace elements in parenteral nutrition support of the surgical neonate. J Pediatr Surg 2012;47:760–71.
4. Krebs N. Update on zinc deficiency and excess in clinical pediatric practice. Ann Nutr Metab 2013;62(Suppl 1):19–29.
5. Prasad AS. Impact of the discovery of zinc deficiency on health. J Am Col Nutr 2009;28:257–65.

What is already known on this topic?

Nationwide shortages of parenteral micronutrients have continued to occur in recent years. These shortages can lead to clinically significant micronutrient deficiencies among patients who depend on prolonged parenteral nutrition. Premature infants are especially vulnerable, and certain micronutrient deficiencies can be lethal.

What is added by this report?

The nationwide shortage of injectable zinc that began in late 2012 led to seven reported cases of zinc deficiency disorder in vulnerable infants. Among these infants, six experienced severe dermatitis, and three experienced invasive bacterial infections. The Food and Drug Administration is now temporarily permitting the importation and sale of an injectable zinc product.

What are the implications for public health practice?

Hospitals with limited stocks of injectable zinc should consider reserving supplies for infants with the highest risk for deficiency (e.g., those who are premature [born at <37 and="" birth="" chronic="" crucial.="" deficiencies="" dysfunction="" for="" g="" gastrointestinal="" gestation="" have="" if="" is="" low="" micronutrient="" monitoring="" nutrition="" occur="" of="" on="" or="" p="" parenteral="" patients="" permanent="" shortages="" signs="" symptoms="" those="" very="" weeks="" weight="" with="">

TABLE. Seven infants with physician-diagnosed zinc deficiency disorder, by selected characteristics — Washington, DC, and Houston, Texas, 2012–2013
Patient	Sex	Gestational age (wks)	Birth weight (g)	Cholestasis	Race/ Ethnicity	Received PN	Dermatitis	PN duration before diagnosis (wks)	Serum zinc level (µg/dL)*	Serum  alkaline phosphatase level (U/L)†	Bacterial infection	Infant death
1	M	24	734	Yes	Black, non-Hispanic	Yes	Yes	10	NA	192	No	No
2	M	24	673	Yes	Black, non-Hispanic	Yes	Yes	15	14	62	No	No
3	F	29	551	Yes	Black, non-Hispanic	Yes	Yes	10	56	32	No	No
4	M	37	2,950	Yes	White, Hispanic	Yes	Yes	18	16	74	No	No
5	M	25	690	Yes	White, non-Hispanic	Yes	Yes	34	41	73	Yes§	Yes
6	F	37	2,620	Yes	White, Hispanic	Yes	Yes	5	25	110	Yes¶	Yes
7	M	33	1,599	Yes	Black, Hispanic	Yes	No	4	34	92	Yes**	No
Abbreviations: PN = parenteral nutrition; NA = not available. * Lowest serum zinc level measured by laboratory testing; normal range = 70–120 µg/dL. † Lowest serum alkaline phosphatase level measured by laboratory testing; normal range = 150–420 U/L. § Staphylococcus aureus. ¶ Methicillin-resistant Staphylococcus aureus. ** Escherichia coli and Kluyvera ascorbata.

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