COVID-19 Updates and Survey Opportunity

Since the beginning of the COVID-19 pandemic, SRNA has kept an updated information page to keep our community informed on the latest updates throughout the pandemic. We compiled resources and information on the status COVID-19 and rare neuroimmune disorders, and we asked members of our Medical and Scientific Council to give the expertise into how COVID-19 may impact people diagnosed with ADEM, AFM, MOGAD, NMOSD, ON, and TM. Some of the resources are:

For a full list of resources, please visit the COVID-19 section of our Resource Library. The information and resources provided are meant to be an educational resource and do not constitute medical advice. For specific information about treatments, symptoms you may be experiencing or questions about personal exposure as someone with a rare neuroimmune disorder or as a caregiver, please contact your physician directly.

Dr.Benjamin Greenberg will be giving a talk on COVID-19 and Rare Neuroimmune Disorders at our upcoming Virtual Rare Neuroimmune Disorders Symposium (RNDS). The RNDS will take place this Saturday, August 29th and is free to attend. You can register for the event here.

SRNA recently launched a research study, Experiences during COVID-19 Pandemic Among Those with Rare Neuroimmune Disorders. The intention of this research project is to describe the experiences of individuals with rare neuroimmune disorders during the COVID-19 pandemic. If you are interested in participating in the study, you can find information and the link to sign up on the study page here.

If you have any questions about COVID-19 and rare neuroimmune disorders, please share them with us using this form.

New Q&A Sessions on COVID-19 with SRNA’s Medical and Scientific Council

Over the past several weeks, SRNA has collected questions from our community on COVID-19 and how it may impact people with rare neuroimmune disorders. Recently, we had the chance to ask several members of our Medical and Scientific Council to shed light on this developing situation and answer the most frequently asked questions we collected. You can view these FAQs here.

Please note that our medical experts are answering questions to the best of their current medical knowledge, and information is changing rapidly. Please also keep in mind that SRNA cannot provide individualized medical advice. The information provided here is for informational purposes only and is not intended to take the place of consultation with your physician. If you have concerns about your health or treatment, please contact your physician, pharmacist, or other medical professional.

Dr. Benjamin Greenberg of University of Texas Southwestern answered general questions regarding COVID-19, including prevention techniques, when you should start wearing a mask, and how to safely bring in groceries from the store. He also answered many questions specific to the rare neuroimmune disorder community, such as “Because I have TM, can I be around other people?” and “Are there special precautions for caring for one at home who is ventilator dependent?” Additionally, Dr. Greenberg answered several questions about medications and supplements such as anti-inflammatory medications and Vitamins C and D.

Dr. Michael Levy of Massachusetts General Hospital and Harvard Medical School also took time to answer some of the frequently asked questions from our community. In an interview with SRNA’S Associate Director of Research and Education GG deFiebre, Dr. Levy answered questions about the relationship between COVID-19 and long-term medications such as Rituxan and azathioprine. He also discussed the changes that hospitals and medical centers are implementing to keep patients safe and the considerations someone should take into account before deciding whether to visit a hospital for non-emergency treatment (such as IVIG infusions) and check-up MRIs. Finally, Dr. Levy discussed ways to properly sanitize mobility devices, and he discussed the possible risks associated with acute treatments for individuals who are newly diagnosed with a rare neuroimmune disorder or who are experiencing a relapse.

Dr. Carlos Pardo of the Johns Hopkins University School of Medicine responded to the remaining questions from our community in an interview with GG. He answered questions about the susceptibility of people with rare neuroimmune disorders and other autoimmune diseases to becoming infected with COVID-19, and he described the reaction of the immune system in those infected with this coronavirus. Dr. Pardo explained the ways in which this coronavirus is similar and different from other viruses, and he discussed what we have learned so far from observing the situations in China and Italy. Finally, Dr. Pardo emphasized that the best precautions people can take are to follow CDC’s guidelines on isolation, quarantine recommendations, and extreme care to protect family members that are exposed to higher risk because they have rare neuroimmune disorders.

The Patient Experience with Transverse Myelitis: a Book Review

By Allen Rucker

Allen Rucker grew up in Bartlesville, Oklahoma and has degrees from Washington University, St Louis, the University of Michigan, and Stanford. In the 1970’s, he co-founded the pioneering video group, TVTV, winning the Columbia-duPont Journalism Award. In the 80’s he wrote sketch comedy with Martin Mull, Harry Shearer, Fred Willard, and others, winning the WGA Annual Award for Comedy and two CableAce Awards. In 1996, he became paralyzed from the waist down from transverse myelitis. Post-paralysis, he has written or co-written eleven books, including three books on “The Sopranos,” one of which was a #1 New York Times bestseller, and a memoir of life after TM, “The Best Seat in The House.” He is chair of the WGA Writers with Disabilities Committee and the annual Media Access Awards and writes regularly for New Mobility magazine and the Christopher Reeve Foundation website.

Sandy Siegel is a force of nature. I have known him for almost twenty-three years and am continually blown away by the energy, commitment, and compassion he’s freely given to people with transverse myelitis and associated disorders. Like many of you, Sandy was the first person I talked to after my own injury who knew more than a few medical-school facts about TM. When you first speak to Sandy, you intuitively grasp the mantra often repeated in this expansive and definitive book on living with this weird and mysterious disorder – you are not alone.

Sandy claims early on in the book that “no one in the world has spoken to more people with TM” than he has. Without a doubt. He then explains why. “This is likely to be the case until the end of time, as it would be difficult to imagine another human being stupid enough to post their home phone number all over the internet.”

Sandy’s “anthropological” overview of TM – he’s not a doctor but knows this specialty cold from a laymen’s point of view – begins and ends with his late wife, Pauline, who first contracted TM in 1994. She taught him, as have many other sufferers, what he knows about living with rare neuroimmune disorders. This book is grounded in the myriad of personal, and often personally told, stories and the myriad of approaches or solutions to the inevitable presence of pain, loss of bodily function, self-doubt, and social anxiety associated with TM, not to mention how to deal with pesky matters like incontinence and airplane travel. Here Sandy, more than in any other book I know of on the subject, went to the source – actual TM’ers and their caregivers and friends.

The book is long, goodness knows, but never tedious or dry. Sandy can tell and retell stories and they are not only full of both the emotional and medical components of TM, they are infused with the main thing that makes this book great – Sandy’s voice. Throughout, Sandy is kind, patient, and non-judgmental in describing one’s adjustment to TM, even for those who push people away and never transcend the bitterness and loss.

Sandy is the rabbi of transverse myelitis — there to help and give comfort and not to profit personally. Answering the phone at 11:30 on a Thursday night to listen to and advise someone newly faced with TM is not a pathway to personal aggrandizement or even a decent night’s sleep.

Not that he hasn’t faced his own dark moments of guilt and inadequacy. Speaking as husband and caregiver stunned by his wife’s misfortune, he asks: “How does one experience an intense tragedy and life-changing event without running headlong into some self-doubt? I have had significant questions about my character throughout this entire experience with Pauline’s illness. I have experienced significant inner struggle between who I am and the person I would like to be.…

As he delineates the reality of living with one of these disorders, Sandy is sympathetic but never less than blunt about the often-ugly consequences. He occasionally writes in sentences so direct and unsentimental that they almost read as aphorisms. Here is a sampling:

  • “Pain, depression, and fatigue can conquer the soul of the strongest of human beings.”
  • “There is nothing more demoralizing for a person with transverse myelitis than to have regular bowel and bladder accidents.”
  • “TM complicates a good marriage. TM is going to obliterate a bad marriage.”
  • “Nerve pain is the game changer with TM… For people who are paralyzed and have nerve pain, paralysis is the least of their burdens.”

Sandy’s role throughout Pauline’s long illness was that of caregiver and despite his doubts, he was a stellar one. Very few caregivers know as much about the most intimate details of life with TM – spasticity, bowel/bladder failure, sexual dysfunction, infections, UTI’s, thoughts of suicide, the awful, often silent presence of fatigue – and what he doesn’t know, he has found some remarkable people to tell their own tales.

Some of these stories are heartbreaking. I will never forget Elisa Holt’s account of discovering that her first-born son, Noah, had contracted, at six months of age, Acute Flaccid Myelitis (AFM). In the blink of an eye, Noah went from healthy to paralyzed from the waist down. In facing what she calls “a parent’s worst nightmare; a nightmare I didn’t even know existed,” Elisa and her husband guide their little boy through what will surely be years of intense physical therapy in their collective effort to “take back AFM.” Her parting advice to any parent in the same situation: “You’ll make it through the wilderness.”

Sandy knows a hundred of such stories of struggle and courage and his empathy seems to know no bounds. One of my favorite passages in the whole book involves those with TM, even if they are physically impaired, who have many ongoing side effects that others can’t easily see. Sandy offers up his sage if acerbic advice: “Perhaps people with TM should think about wearing a sign with print that says, ‘I haven’t peed in eight years. My feet and legs and butt are in so much burning pain that I would scream all day long if I were allowed…my fatigue has me so totally exhausted that I need a nap ten minutes after I wake up. I have transverse myelitis…and because you can’t see the symptoms…doesn’t give you a pass to make judgements about me in any way.’

I could go on picking out sound bites of hard facts and insights into the mindset of someone with TM and still feel I’ve failed to convey the scope, depth, and magnanimous spirit of this definitive “brain dump,” as Sandy calls it. As it began with Pauline, so it ends with Pauline. She is his lodestar on this journey. Without Pauline’s illness and her openness about it, and Sandy’s remarkable tenacity and passion, there probably would never have been a Transverse Myelitis Association -now called Siegel Rare Neuroimmune Association – and hundreds of thousands of sufferers, myself included, would be left not knowing how to deal with the next day, or the day after, how to find expert medical help, or how to discover a community of people who know exactly what you’re talking about. Sandy has helped build a public edifice of knowledge and goodwill that will far outlive him, and he has now written a book full of the wisdom of a lifetime dealing with TM.

We all owe him our supreme gratitude.

You can order a copy of the The Patient Experience with Transverse Myelitis by Sanford J. Siegel, PhD on Amazon here. Both paperback ($18) and Kindle ($2.85) versions are available. The book is self-published. All proceeds from sale of the book are donated to SRNA.

New AFM Information Sheet

The term Acute Flaccid Myelitis (AFM) was coined in 2014, but it is likely that many individuals with initial presentation of flaccid limb weakness and/or paralysis were diagnosed as having transverse myelitis or Guillain Barre Syndrome in previous years. As scientists and clinicians learn more about this disorder, SRNA strives to keep our community updated on their findings and to provide timely and accurate information and resources. As a part of this effort, we have recently updated our AFM disease information sheet so that information on AFM is easily accessible in a concise and helpful manner. The AFM information sheet has sections on Epidemiology, Signs and Symptoms, Diagnosis, Acute Treatments, Prognosis, and Rehabilitation and Symptom Management. You can find the AFM information sheet here.

Acute Flaccid Myelitis

Acute Flaccid Myelitis (AFM) is a type of inflammation in the spinal cord that has specific clinical and MRI features. AFM abnormalities noted on MRI are predominantly found in the gray matter (lower motor neuron) of the spinal cord. In 2012, an outbreak of AFM occurred in California and more cases were reported in the summer and fall of 2014, 2016, and 2018 across the United States. Non-polio enteroviruses have been implicated as potential causal factors in the development of AFM. The enterovirus D68 and enterovirus A71 have been suspect in many of these cases, although others such as coxsackie viruses have been implicated as well. Enterovirus D68 most often causes a respiratory illness and has been circulating in the United States during the summer and fall every two years since 2014, which coincides with the increase of cases of AFM seen every other year. It has not been definitively proven that these particular viruses have directly caused cases of AFM but the temporal onset of neurological symptoms with infections produced by those viruses implicate them as direct or indirect triggers of the neurological problem.

Epidemiology

There are no conclusive studies that identify the actual numbers of individuals specifically affected by AFM, but from 2014 to 2018, the CDC confirmed over 500 reports of those affected by AFM. Not all cases are reported to the CDC nor confirmed by the CDC, so this number is likely an underestimation. There have been reports of AFM in both children and adults, but AFM cases primarily affect children under the age of 18.

Until the recent characterization of AFM in 2014, it is likely that many individuals with initial presentation of flaccid limb weakness and/or paralysis have been diagnosed as having transverse myelitis or Guillain Barre Syndrome in previous years.

Signs & Symptoms

Most of those diagnosed with AFM report having a respiratory or gastrointestinal illness before the onset of weakness. The predominant presentation is a rapid onset of weakness that may affect the limbs, face, oropharyngeal muscles, or the muscles that control breathing. Those with AFM may not be able to breathe, swallow, or move their eyes normally. Weakness varies greatly ranging from mild to very severe. AFM may result in weakness, partial paralysis, or total paralysis of just one limb or all limbs. The pattern of paralysis and how individuals present are widely variable. Weakness most often occurs in proximal muscles, meaning the muscles closest to the center of the body. Pain in the neck, back, or limb may be an early symptom. Autonomic instability, such as issues with heart rate, may occur as well. Since it is mainly the gray matter of the spinal cord that is damaged in individuals with AFM, they may not have bladder or bowel dysfunction or issues with sensation. However, some individuals may have inflammation in both the white and gray matter of the spinal cord (upper and lower motor neuron), so some of those with AFM may experience impaired sensation, bladder, and/or bowel dysfunction.

Diagnosis

Acute flaccid myelitis is diagnosed based upon clinical exam, magnetic resonance imaging (MRI) of the spinal cord, and analysis of cerebrospinal fluid (CSF) (usually with increased white blood cells or pleocytosis). On MRI of the spinal cord, AFM lesions are longitudinal throughout the grey matter (the anterior horn cells). Sometimes imaging may appear normal early in the disease, but repeat imaging shows the lesions. In some situations, electrophysiological studies of the nerves and muscle (called nerve conduction and electromyogram [NCS/EMG]) may help to determine if there is injury to the lower motor neuron. Testing may also include blood draws, respiratory tract samples or collection of other bodily fluids to determine if a viral or infectious cause is present.

Acute Treatments

Specific treatments and intervention for AFM have not yet been identified, but some of the treatments available for transverse myelitis have been used (high dose intravenous (IV) steroids, intravenous immunoglobulin (IVIG), and plasma exchange (PLEX)). The purpose of the treatments is to attempt to reduce inflammation in the spinal cord and further prevent the individual’s immune system from causing damage. IVIG has antibodies that may have effect on limiting inflammation or neutralization or replication of enteroviruses and is widely used in treating AFM. The data on use of steroids or PLEX are mixed. Fluoxetine was used in several centers in the US in 2016 and was well tolerated but was not associated with improved outcomes among treated children. As is usual with treatment of rare neuroimmune disorders, in which placebo-controlled trials are difficult to perform, treatment must be individualized. Physical and occupational therapy are also believed to be significant for recovery in AFM.

Prognosis

Recovery varies among individuals with AFM. Most do not recover fully, but patients do regain strength and motor function over time to varying degrees. The most affected muscle may be the least likely to recover. Again, physical and occupational therapy are also believed to be critical for recovery in AFM.

Rehabilitation and Symptom Management

After the acute phase, rehabilitative care to improve functional skills and prevent secondary complications of immobility involves both psychological and physical accommodations. Rehabilitation may begin in the intensive care unit with the goal to transition individuals to an inpatient or outpatient rehabilitation program. There is very limited information in the medical literature specifically dealing with rehabilitation after AFM. However, much has been written regarding recovery from spinal cord injury (SCI), in general, and this literature applies. The physical issues include speech and oral motor skills training, bowel and bladder management, maintenance of skin integrity, spasticity, activities of daily living (i.e., dressing), mobility, sexual dysfunction (for adults), and pain.

The long-term management of AFM requires attention to a number of issues. These are the residual effects of any spinal cord injury, including AFM. In addition to chronic medical problems, there are the ongoing issues of ordering the appropriate equipment, reentry into school, re-socialization into the community, and coping with the psychological effects of this condition by the patients and their families. During the early recovery period, family education is essential to develop a strategic plan for dealing with the challenges to independence following return to the community.

Rehabilitation

It is important to begin occupational and physical therapies early during the course of recovery to prevent the inactivity related problems of skin breakdown and soft tissue contractures that lead to a decreased range of motion. Assessment and fitting for splints designed to passively maintain an optimal position for limbs that cannot be actively moved is an important part of the management at this stage.

Activity-based rehabilitation includes weight-bearing exercise, functional electrical stimulation (FES), locomotor training, task-specific practice, and massed practice. Individuals with AFM may not respond to FES, but therapists can adjust FES parameters to try to get a better muscle contraction. FES even without obvious muscle contraction may have benefits. Weight-bearing exercise has been shown to improve bone mineral density, range of motion, muscle tone, and bowel function. Vibration during weight bearing may also activate denervated muscles. Weight-bearing exercises can progress to locomotor training on the treadmill with appropriate orthotics. Aqua therapy can be helpful for stretching tight muscles. Task specific practice involves relearning functions that were lost due to AFM such as bed mobility and coming to a seated position, feeding, dressing, and personal hygiene. Some children who were younger when AFM onset occurred will have to learn these for the first time. Massed practice involves repetition and increased level of activity. It has been shown that children can tolerate up to 5 hours of therapy a day. It is important to keep in mind that spinal cord injuries in children result in risks of skeletal subluxations and decreased bone mineral density which can result in fractures.

Other rehabilitation factors to consider are pulmonary management for those with ventilator dependence, and speech and language pathologists for those children with difficulty swallowing (dysphagia) and talking (dysphonia).

Individuals with AFM may find ordinary tasks such as dressing, bathing, grooming, and eating very difficult. Many of these obstacles can be mastered with training and specialized equipment. For example, long handled sponges can make bathing easier as can grab bars, portable bath seats and hand-held shower heads. For dressing, elastic shoe-laces can eliminate the need to tie shoes while other devices can aid in donning socks. Occupational therapists are specialists in assessing equipment needs and helping people with limited function perform activities of daily living. A home assessment by an experienced professional is often helpful. Physical therapists assist with mobility. Besides teaching people to walk and transfer more easily, they can recommend mobility aids. This includes everything from canes (single point vs. small quad cane vs. large quad cane) to walkers (static vs. rolling vs. rollator) and braces. For a custom-fabricated orthotic (brace), an orthotist is necessary. Careful thought should go into deciding whether the brace should be an ankle-foot orthosis, whether it should be flexible or stiff, and what angle the foot portion should be in relationship to the calf portion. Some will benefit by a knee-ankle foot orthosis. Each person should be evaluated individually. The best results occur when a physician coordinates the team so that the therapists and orthotists are united on what is to be achieved. The physician best trained to take this role is the physiatrist.

Nerve Transfers

Some individuals may benefit from nerve transfer procedures, which is when nerves are taken from one area of the body and are transferred to a denervated nerve. The previous experience derived from obstetric brachial plexus injury has guided some of the approaches in patients with AFM. The value in recovery of selected upper extremity muscle groups in AFM patients appears promising although there is still need for a well-documented and validated approach to prove their beneficial outcomes. There are some cases reported in the literature of successful nerve transfers, but additional studies are needed to learn the correct timing for when nerve transfers should occur after onset.

Bladder Function

Bladder dysfunction may not occur in all individuals with AFM. Immediately after the onset of AFM, there is frequently a period of transient loss or depression of neural activity below the involved spinal cord lesion, referred to as “spinal shock,” which lasts about 3 weeks. Following this period, two general problems can affect the bladder. The bladder can become overly sensitive, and empty after only a small amount of urine has collected, or relatively insensitive, causing the bladder to become over extended and overflow. An overly distended bladder increases the likelihood of urinary tract infections and, in time, may threaten the health of the kidneys. Depending on the dysfunction, treatment options include timed voiding, medicines, external catheters for males (a catheter connected to a condom), padding for females, intermittent internal self-catheterization, an indwelling catheter, or electrical stimulation. Surgical options may be appropriate for some people.

Bowel Function

Another major area of concern is effective management of bowel function. A common problem in spinal cord injury is difficulty with evacuation of stool, although fecal incontinence can also occur. The neurologic pathways for defecation are similar to those of the bladder. Many lacking voluntary control of the bowel may still be able to achieve continence by diet, strategic use of stool softeners and fiber, and the technique of rectal stimulation. Other aids include suppositories, mini-enemas, anal irrigation, and oral medications. A high-fiber diet, adequate and timely fluid intake, and medications to regulate bowel evacuations are the basic components of success. Regular evaluations by medical specialists for adjustment of the bowel program are recommended to prevent potentially serious complications. There are some surgical options, although this is rarely necessary.

Sexual Dysfunction

Sexual dysfunction involves similar innervation and analogous syndromes as those found in bladder dysfunction. Treatment of sexual dysfunction in adults diagnosed with AFM should take into account baseline function before the onset of AFM. Until we learn more about this issue in AFM, individuals experiencing sexual dysfunction may want to refer to the strategies used in individuals with other rare neuroimmune disorders or spinal cord injuries.

Skin Breakdown

Skin breakdown occurs if the skin is exposed to pressure for a significant amount of time, without sensation or the strength to shift position as necessary. Sitting position should be changed at least every 15 minutes. This can be accomplished by standing, by lifting the body up while pushing down on armrests, or by just leaning and weight shifting. Wheelchairs can be supplied with either power mechanisms of recline or tilt-in-space to redistribute weight bearing.

A variety of wheelchair cushions are available to minimize sitting pressure. Redness that does not blanch when finger pressure is applied may signal the beginning of a pressure ulcer. Good nutrition, vitamin C, and avoidance of moisture all contribute to healthy skin. Pressure ulcers are much easier to prevent than to heal.

Spasticity

Spasticity may be an issue in AFM, particularly when a cervical spine lesion involved both the gray matter and the white matter. Damage to the white matter in the neck leads to a spastic weakness in the legs and can be seen in some AFM patients. The goal is to maintain flexibility with a stretching routine using exercises for active stretching and a bracing program with splints for a prolonged stretch. These splints are commonly used at the ankles, wrists, or elbows. Also recommended are appropriate strengthening programs for the weaker of the spastic muscles acting on a joint and an aerobic conditioning regimen. These interventions are supported by adjunctive measures that include antispasticity drugs (e.g., diazepam, baclofen, dantrolene, tizanidine), therapeutic botulinum toxin injections, and serial casting. The therapeutic goal is to improve the function of the individual in performing specific activities of daily living (i.e., feeding, dressing, bathing, hygiene, mobility) by improving the available joint range of motion, teaching effective compensatory strategies, and relieving pain.

Pain

Pain is common following AFM. The first step in treating pain effectively is obtaining an accurate diagnosis. Unfortunately, this can be very difficult. Causes of pain include muscle strain from using the body in an unaccustomed manner, nerve compression (i.e., compression of the ulnar nerve at the elbow due to excessive pressure from resting the elbow on an armrest continuously) or dysfunction of the spinal cord from the damage caused by the inflammatory attack. Muscle pain might be treated with analgesics, such as acetaminophen (Tylenol), non-steroidal, anti-inflammatory drugs such as naproxen or ibuprofen (Naprosyn, Aleve, Motrin), or modalities such as heat or cold. Nerve compression might be treated with repositioning and padding (i.e., an elbow pad for an ulnar nerve compression).

Nerve pain can be a significant challenge to find effective treatment. Nerve messages traveling through the damaged portion of the spinal cord may become scrambled and misinterpreted by the brain as pain. Besides the treatments listed above, certain antidepressants such as amitriptyline (Elavil), or anticonvulsants, such as carbamazepine, phenytoin, or gabapentin (Tegretol, Dilantin, Neurontin) may be helpful. Stress and depression should also be addressed since these conditions make pain harder to tolerate.

Depression

Individuals with AFM should be educated about the effect of AFM on mood regulation and routinely screened for the development of symptoms consistent with clinical depression. Warning signs that should prompt a complete evaluation for depression include failure to progress with rehabilitation and self-care, worsening fixed low mood, pervasive decreased interest, and/or social and professional withdrawal. A preoccupation with death or suicidal thoughts constitutes a true psychiatric emergency and should lead to prompt evaluation and treatment. Depression in AFM is similar to the other neurologic symptoms patients endure, which are mediated by the effects of the immune system on the brain. While the prevalence of depression among individuals with AFM is not known, depression is remarkably prevalent in TM, occurring in up to 25% of those diagnosed at any given time, and is largely independent of the patient’s degree of physical disability. Depression is not due to personal weakness or the inability to “cope.” It can have devastating consequences; not only can depression worsen physical disability (such as fatigue, pain, and decreased concentration) but it can have lethal consequences. Despite the severity of the clinical presentation of depression in AFM, there is a very robust response to combined aggressive psychopharmacologic and psychotherapeutic interventions.

Autonomic Dysreflexia

Autonomic dysreflexia can occur when a spinal cord is damaged above the T6 level. Symptoms can include nausea, sweating, fast heart rate and/or profound blood pressure changes (up or down). Episodes can be triggered by urinary tract infections, catheterizations, constipation or painful events in the lower extremities. Care should be given to minimize triggers and manage any blood pressure variations during an event.

Respiratory Dysfunction

A subset of patients with aggressive forms of AFM may experience marked respiratory and diaphragmatic dysfunction. It may occur when the neurons that control diaphragm movement innervated by the phrenic nerve, or intercostal muscles that partially control the mechanics of breathing, fail due to damage of motor neurons in the spinal cord. Thus, patients can have difficulty breathing and require long term ventilatory support. Over months or years patients can be weaned from the ventilator as motor control of the diaphragm comes back, but in some patients it has not yet returned. Strategies such as a diaphragm pacer are being used now although there is still need for a validated demonstration of its efficacy. Those with respiratory issues may also experiences issues with heart rate, like tachycardia (high heart rate) and bradycardia (low heart rate).

CDC Case Confirmation for Acute Flaccid Myelitis

For children and adults diagnosed with Acute Flaccid Myelitis (AFM) in the United States, the process of confirming their case with Centers for Disease Control and Prevention (CDC) can be overwhelming. The Transverse Myelitis Association (SRNA) and the Acute Flaccid Myelitis Association (AFMA) recently teamed up to create the following information sheet to explain the process of reporting a case of AFM to CDC.

You can find the CDC Case Confirmation for Acute Flaccid Myelitis information sheet in SRNA’s Resource Library here.

What is Acute Flaccid Myelitis?

In recent years we’ve seen an uptick in reports of children and adults being diagnosed with Acute Flaccid Myelitis (AFM). Cases have peaked every 2 years since 2012, and there have been over 500 cases confirmed by the Centers for Disease Control and Prevention (CDC) since 2014. Most individuals diagnosed with AFM are children, although there have also been cases in adults. Symptoms usually include a febrile respiratory illness followed by sudden onset of limb weakness/paralysis and the loss of muscle tone and reflexes. Some individuals have cranial nerve involvement and have a facial droop/weakness, difficulty moving the eyes, drooping eyelids, or difficulty swallowing or slurred speech. Some individuals may also experience respiratory failure where breathing assistance is necessary.

Although a definitive cause for AFM has not yet been established, many experts think it is due to infection from a non-polio enterovirus (EV), such as EV-D68 or EV-71. To better understand the potential causes, optimal treatment, and outcomes of AFM, health departments across the United States are conducting enhanced surveillance for AFM cases.

When children or adults are diagnosed with AFM, cases are reported to CDC, who then publish the data. The process for getting cases to CDC is clunky and, in many cases, parents or patients never hear back if their case was confirmed. The AFM community’s long held fear is that cases are underreported to CDC, and as a result, AFM is not getting the attention it deserves. It’s critical that CDC has an accurate count of cases so that research for AFM can be properly funded. Better treatment protocols and outcomes should follow research–and it all hinges on CDC having all the information it needs. The details for the case confirmation process are as follows:

How do cases get reported to CDC?

Be a voice! Please urge your clinician to report you or your child’s AFM diagnosis to the local health department. Below you can find the steps for cases to be reported to CDC.

1. Clinicians submit the Patient Summary Form, Medical Records and MRI to State/Local Health Departments.

2. State Health Departments pass this information along to CDC.

3. CDC evaluates the case (confirmed, probable) and updates the State Health Department.

4. The State Health Department updates the clinician.

5. The clinician updates the parent or patient.

How do I find out if my case was confirmed by CDC?

If you have not heard back about your case, these are the steps you can take to make sure it was reported.

1. Call your state health department. Find the contact for Infectious Disease or Epidemiology (if that fails, find the press person!)

2. Say, “My child/I was/were diagnosed with AFM in (Month/Year) in (County) and I would like to know my case’s status (confirmed, probable, pending) with CDC.”

  • If they say your case was confirmed, ask if it was reported back to the clinician.
  • If it wasn’t confirmed, determine where the breakdown occurred. Did they get the information from the clinician? Was it passed along to CDC? Are they waiting to hear back from CDC?
    • If the clinician never submitted information, contact your clinician.
    • If the State Health Department sent the information to CDC and are still waiting to hear back from CDC, it is likely the case has not yet been classified. CDC alerts health departments as soon as cases are classified. However, if the health department is unsure of the status, they can contact CDC with the patient’s case ID number for an update.

3. If all else fails, email [email protected] and they can try to contact State Health Departments. Please be sure to let them know which county/state you live in. CDC will still not be able to verify if your or your child’s case was confirmed because their data are anonymous, but they can help connect you with someone at the state department who will follow up with you and provide you that information. But call your state first —that helps raise awareness of AFM!

For your Clinician: AFM Classification Information

  • An illness with acute limb weakness and:
    • Confirmed: A magnetic resonance image (MRI) showing spinal cord lesion largely restricted to gray matter** and spanning one or more spinal segments.

    • Probable: Cerebrospinal fluid (CSF) showing pleocytosis (white blood cell count>5 cells/mm3, may adjust for presence of red blood cells by subtracting 1 white blood cell for every 500 red blood cells present).

** Normal or negative MRI images within the first 72 hours of symptoms does NOT rule out AFM. Terms used in the spinal cord MRI report such as “affecting mostly gray matter”, “affecting the anterior horn or anterior horn cells”, affecting the central cord”, “anterior myelitis” or “poliomyelitis” would all be consistent with this terminology. If you are unsure if this criterion is met, consider consulting the neurologist or radiologist directly.

Specimen Collection and Submittal

Urge clinicians to collect specimens on suspect cases as early as possible, preferably on the day of onset of limb weakness/paralysis, to increase the chance of virus detection.

The following is a check list of specimens and tests the clinician should submit to the health department.

1. MRI (performed within 72 hours) √
2. Nose and mouth swabs for viral detection √
3. Antibody levels (serum) collected prior to any treatments √
4. Lumbar Puncture √
5. Stool and urine samples √.

Additional Resources

The Siegel Rare Neuroimmune Association
www.wearesrna.org

Acute Flaccid Myelitis Association
www.afmanow.org

Centers for Disease Control and Prevention
https://www.cdc.gov/acute-flaccid-myelitis

*Some sections were adapted from the California Department of Public Health – November 2018 Acute Flaccid Myelitis (AFM) Quicksheet: ow.ly/GnpX30nHhh1

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Facts About Rare Neuroimmune Disorders: The 5 W’s

SRNA currently advocates for individuals with six rare neuroimmune disorders: acute disseminated encephalomyelitis (ADEM), acute flaccid myelitis (AFM), MOG antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), optic neuritis (ON), and transverse myelitis (TM). While these conditions are similar in some ways, each disorder has a distinct criteria for diagnosis. In order to help our community understand the connections between the disorders as well as the differences, Dr. Cynthia Wang compiled the following information on the 5 W’s: who, where, what, which, and why.

You can find the Facts about rare neuroimmune disorders: The 5 W’s information sheet in SRNA’s Resource Library here.



Neuroimmune disorders, such as acute disseminated encephalomyelitis (ADEM), acute flaccid myelitis (AFM), MOG antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), optic neuritis (ON), and transverse myelitis (TM) are conditions in which a person’s immune system mistakenly attacks parts of the central nervous system (CNS) – brain, spinal cord, optic nerve. 

Who gets these illnesses? 

  • ADEM tends to affect young children, typically ages 4-8, without a significant bias for specific gender or ethnic background.
  • AFM tends to affect children as well, and increases in cases have occurred every other year since 2012.
  • We are still learning about who is more likely to get MOG-Ab disease. Some studies have shown that those with MOG Antibody Disease are on average younger and are likely to be male compared to those with aquaporin-4 (AQP-4) positive NMOSD. Those with MOGAD may be more likely to have bilateral involvement of the optic nerves.
  • NMOSD associated with AQP-4 antibodies tends to disproportionately affect non-Caucasian women in their 30-40s.
  • TM can affect individuals of all ages, ethnicities, and either gender.
  • ON is more common in women and develops in most patients between the ages of 20 and 45. Additionally, ON typically occurs more frequently in Caucasians than African Americans.

Where in the nervous system do these disorders affect?

  • inflammation in optic nerves = optic neuritis (ON)
  • inflammation of spinal cord, primarily the white matter of the spinal cord = transverse myelitis (TM)
  • inflammation of spinal cord, primarily the grey matter of the spinal cord = acute flaccid myelitis (AFM)
  • inflammation of brain = encephalitis
  • inflammation of brain and spinal cord (and sometimes optic nerve) = encephalomyelitis (acute disseminated encephalomyelitis (ADEM) is a subtype that may or may not include spinal cord involvement)
  • inflammation of brain, optic nerves, and/or spinal cord = neuromyelitis optica spectrum disorder (NMOSD) or MOG antibody disease (MOGAD)

What does monophasic or relapsing mean?

Some of these disorders are monophasic, meaning a one-time confused reaction of the immune system, without any further episodes of inflammation (TM, AFM, ADEM, ON).

Other disorders are known as relapsing, in which a persistently confused immune system can continue to cause inflammatory episodes (NMOSD and MOGAD, although ADEM, TM, and ON can be initial presentations of these relapsing diseases) 

For the disorders that can be relapsing, people are given long-term therapies to diminish the chance of future episodes or to lessen their impact should they occur.  

Testing for AQP-4 and MOG antibodies can help predict if someone will have a monophasic or relapsing course.  

If antibody testing is negative, the longer one goes without another attack, the more likely it is that the condition is monophasic.

Which of these conditions tend to be relapsing or recurring?

Multiple sclerosis and neuromyelitis optica spectrum disorder associated with aquaporin-4 (AQP-4) antibodies are the two most well recognized forms of relapsing CNS autoimmune disorders.

60-80% of individuals with optic neuritis and longitudinally extensive transverse myelitis (involvement of greater or equal to the length of 3 vertebrae) have antibodies to aquaporin-4 (AQP-4), a water channel in astrocytes, a type of support cell in the central nervous system.

A proportion of individuals who test negative for AQP-4 and some of those diagnosed with recurrent ON or ADEM are now known to have antibodies against another target, called myelin oligodendrocyte glycoprotein (MOG). MOG is a protein on myelin and oligodendrocytes, the myelin-producing cells of the central nervous system and are thought to have MOGAD. Individuals who continue to test positive for MOG antibodies 6-12 months after their initial attack are at risk for recurrent disease and should discuss with their provider if chronic immunosuppression is warranted.

Why do people get these disorders?

This is a central question in neuroimmunology and currently we still don’t know for sure. It is hypothesized that these disorders result from a specific set of circumstances, namely 1) a person whose immune system may be primed to overreact or get confused, or a genetic predisposition to autoimmunity and environmental triggers, and 2) a life event, perhaps a bodily stressor, such as an infection, to trigger the attack. We do not yet know the genetics or environmental factors that lead to these conditions.



Author

Dr. Cynthia Wang received her medical degree from University of Texas Southwestern Medical Center in Dallas, Texas and completed a pediatrics and pediatric neurology residency at Mott Children’s Hospital, University of Michigan Health System in Ann Arbor, Michigan. Dr. Cynthia Wang completed her James T. Lubin Fellowship under the mentorship of Dr. Benjamin Greenberg at The University of Texas Southwestern and Children’s Health. Her research study was a prospective, longitudinal study on acute disseminated encephalomyelitis (ADEM) to identify the clinical characteristics, treatment methods, and follow-up interventions that are associated with better and worse patient-centered outcomes.

Q&A on Relapsing vs Monophasic Rare Neuroimmune Disorders with Dr. Cynthia Wang

Individuals who are diagnosed with a rare neuroimmune disorder sometimes experience new or worsening symptoms months or years after the initial onset of their inflammatory attack. Understandably, this causes concern that a relapse of their disorder has occurred. To help our community understand the difference between a relapse and worsening symptoms, we asked Dr. Cynthia Wang to answer some questions about relapsing versus monophasic rare neuroimmune disorders and what to do if you think you may be experiencing a relapse.

You can find the Relapsing vs Monophasic Rare Neuroimmune Disorders fact sheet in SRNA’s Resource Library here.



Are diseases such as transverse myelitis (TM), acute flaccid myelitis (AFM), optic neuritis (ON), acute disseminated encephalomyelitis (ADEM), MOG antibody disease (MOGAD), or neuromyelitis optica spectrum disorder (NMOSD) one-time or relapsing diseases?

It depends. TM, ON, and syndromes resembling ADEM can occur in the setting of relapsing conditions, such as multiple sclerosis, neuromyelitis optica associated with aquaporin-4 antibodies (AQP-4), and some systemic/ rheumatologic diseases. Once an individual has undergone sufficient workup for these conditions and they have been ruled out, the likelihood he or she has idiopathic transverse myelitis or monophasic ADEM increases, which are considered one-time disorders. In the past year, clinicians have also been able to test for a new antibody called MOG (myelin oligodendrocyte glycoprotein). Like AQP-4, MOG antibodies can be assessed with good accuracy through a blood sample. Although the MOG story is still unfolding, many physicians following patients who continue to test positive for MOG antibodies 6-12 months after the initial episode have reported relapsing disease in this population and are thought to have MOG antibody disease.

I had transverse myelitis (TM), optic neuritis (ON), or acute disseminated encephalomyelitis (ADEM) in the past and was told I don’t have multiple sclerosis or neuromyelitis optica spectrum disorder (NMOSD). I am now experiencing new or worsening neurological symptoms? What should I do?

It is very important for you and your provider to determine if the worsening symptoms are related to new inflammation (i.e., a relapse), or from some temporary disturbance in your body’s normal state unmasking symptoms from a prior injury, without new inflammation (pseudo-relapse).

For symptoms that last over 24 hours and do not improve with rest, hydration, being in a comfortable temperature, and/or recovery from an acute illness (e.g., respiratory or urinary tract infection), contact your neurology provider. He or she may order blood or urine tests to make sure you are not experiencing any acute infections or metabolic disturbances. If ruled out, additional tests may include an MRI of suspected area of new inflammation (i.e., brain, spine, and/or optic nerves).

Evidence of new inflammation on MRI and/or symptoms related to a part of the nervous system that was not affected in the past suggests a new acute inflammatory episode. This should be treated with immunotherapy such as corticosteroids to stop ongoing inflammation, and trigger a discussion with your clinician about whether ongoing immunotherapy to prevent another attack is needed.

If I am concerned I have a relapsing disorder, what should I do?  

Discuss this concern with your neurology provider, and ask if you would be an appropriate candidate to test for AQP-4 and MOG antibodies (available through Mayo Medical Laboratories as “CDS1” order).  

My doctors say they can still see TM or an area of damage on my MRI. Does this mean I have a relapsing disorder?

During an inflammatory attack in the spinal cord, as occurs in TM, there may be evidence of inflammation on MRI (areas of contrast enhancement indicating compromise of the blood-brain-barrier) or an increase in inflammatory cells in cerebrospinal fluid. After this inflammation subsides, there may be evidence of where this attack occurred, or an area showing previous damage (T2/ FLAIR abnormalities), but not ongoing inflammation (e.g., continued contrast enhancement). Gliosis, essentially a scar in the brain, can be seen for months or years and does not indicate ongoing inflammation or relapsing disease. An MRI that shows new inflammation suggests a new acute inflammatory episode.

My doctor told me I am AQP-4 positive, now what?

An episode consistent with neuromyelitis optica spectrum disorder and a single positive test for AQP-4 in blood or spinal fluid are typically adequate to establish a diagnosis of NMOSD. These individuals should be placed on immunosuppressive therapy, which we currently advise be continued indefinitely. This is because NMOSD attacks can be severe, cause lasting visual or motor impairment, and are very likely to recur unless treated.

My doctor told me I am MOG positive, now what?

This depends on when MOG antibodies were tested in relation to your demyelinating event. If MOG antibodies were detected at the time of the attack or in the first 6 months following attack, we recommend retesting for MOG antibodies 6-12 months after your event. If you become MOG negative, you are unlikely to have future relapses.

If MOG antibodies are positive again, you are considered to have MOG antibody disease, and may be at risk for future demyelinating episodes. You should speak to your neurologist about whether you should be placed on a therapy to prevent the likelihood of a relapse.

For individuals who undergo MOG testing for the first time 12 months or greater after their demyelinating event, one positive MOG test would be sufficient to diagnosis persistent MOG antibodies and then you should have a discussion with your physician as above about chronic immunotherapy.

I already have any existing diagnosis of multiple sclerosis or neuromyelitis optica spectrum disorder. Should I be tested for MOG?

It depends on your clinical history and if you have tested positive for AQP-4. MOG testing is reasonable in people who’ve been told their presentation is atypical for multiple sclerosis and neuromyelitis optica spectrum disorder and previously have been negative on AQP-4 testing. AQP-4 positive patients with symptoms consistent with NMOSD do not need MOG testing, as being double positive (MOG and AQP-4 positive) is exceedingly rare. In addition, this information ultimately would not change management as recurrent MOG and AQP-4 associated NMOSD are currently managed very similarly.

People with presumptive multiple sclerosis who do not respond as well as expected to MS drugs should have a discussion with their doctor about MOG testing as MOG syndromes can be misdiagnosed as MS. A positive MOG test may change medical management as some MS therapies might be ineffective or perhaps even exacerbate MOG antibody disease.

People with MRI and spinal fluid studies consistent with multiple sclerosis should not be routinely screened for MOG antibodies, but decided on a case- by-case basis after discussion with a neurologist.

Glossary

Central Nervous System: Includes the brain, spinal cord, and optic nerve.

Monophasic rare neuroimmune disorder: A disorder that causes only one episode of inflammation in the central nervous system.

Recurrent or relapsing rare neuroimmune disorder:
A disorder that causes more than one episode of inflammation in the central nervous system.

Relapse: New inflammation in the central nervous system.

Pseudo-relapse: Temporary disturbance in the body’s normal state unmasking or worsening symptoms from a prior injury, without new inflammation in the central nervous system.

Attack: An event of inflammation in the central nervous system.

Onset: The first symptoms of a rare neuroimmune disorder. Typically, the first attack.

Inflammation: Part of the body’s immune system meant to eliminate noxious agents. In rare neuroimmune disorders, the immune system mistakenly attacks the brain, spinal cord, or optic nerve, causing inflammation in these areas.


DisorderAreas of CNS InvolvementSpecific Diagnostic TestsRelapsing or MonophasicOngoing Immuno-suppresion indicated?
ADEMBrain
Spinal Cord
Optic Nerve

None if monophasic

___________________________

MOG Antibody

If MOG negative 6-12 months after onset, typically monophasic

__________________________

If MOG positive 6-12 months after onset, might be recurrent (MOGAD)


No

_________________________

Yes

AFMSpinal Cord (primarily grey matter)Enterovirus PCR in CSF (though virus is very difficult to isolate), positive enterovirus/rhinovirus on respiratory specimen is supportiveMonophasicNo
Mog-Ab DiseaseBrain
Spinal Cord
Optic Nerve
MOG AntibodyUncertain, persistence of MOG antibodies are associated with relapsing diseaseYes, if relapses occur
MSBrain
Spinal Cord
Optic Nerve
None, though CSF oligoclonal bands are supportiveRelapsingYes
NMOSDBrain
Spinal Cord (typically lesions more than 3 vertebral segments in length)
Optic Nerve
Aquaporin-4 antibodyRelapsingYes
ONOptic NerveNoneDepends if ON is a part of MS, NMOSD, or MOGADTypically yes if relapsing
TMSpinal Cord (primarily white matter)NoneMonophasic

_________________

In very rare cases can be recurrent

No

__________________

Case-by-case


Author

Dr. Cynthia Wang received her medical degree from University of Texas Southwestern Medical Center in Dallas, Texas and completed a pediatrics and pediatric neurology residency at Mott Children’s Hospital, University of Michigan Health System in Ann Arbor, Michigan. Dr. Cynthia Wang completed her James T. Lubin Fellowship under the mentorship of Dr. Benjamin Greenberg at The University of Texas Southwestern and Children’s Health. Her research study was a prospective, longitudinal study on acute disseminated encephalomyelitis (ADEM) to identify the clinical characteristics, treatment methods, and follow-up interventions that are associated with better and worse patient-centered outcomes.

Frequently Asked Questions about AFM

The recent increase in cases of Acute Flaccid Myelitis (AFM) is causing concern across the United States. SRNA has received many questions from the community about AFM, so at the 2018 Regional Rare Neuroimmune Disorders Symposium in Boston, we asked Dr. Benjamin Greenberg of the University of Texas Southwestern Medical Center to respond to the most commonly asked questions we have received. You can view his responses below. You can also view the rest of the videos from the symposium on our YouTube page here. You can find more resources on AFM in our Resource Library, including our 2018 Podcast on Acute Flaccid Myelitis and Dr. Greenberg’s presentation on AFM at the 2018 Regional RNDS.


What is acute flaccid myelitis?




What causes acute flaccid myelitis?




Is acute flaccid myelitis contagious?



Will someone who already has TM or another neuroimmune disorder be susceptible to AFM?



What are the symptoms of acute flaccid myelitis?



What should a parent do when they suspect symptoms of acute flaccid myelitis?



Where should treatment be sought?



How do you diagnose acute flaccid myelitis?



What are the treatments for acute flaccid myelitis?



Is there a relation between vaccinations and acute flaccid myelitis?



Can acute flaccid myelitis be prevented?



Is there a cure for acute flaccid myelitis?



What is the relationship between EVD68 and acute flaccid myelitis?


Does my child need an IEP or 504?

By Beth Schwartz

Beth is the mother of a child with NMOSD and has attended the SRNA Quality of Life Family Camp. You can find Beth’s blog at https://thesurpriseturn.blogspot.com/.

Your child is out of the hospital, hopefully has a diagnosis and now is ready to go back to school. Now what?

Depending on your child’s needs, you can talk to your child’s school about different levels of support.

My daughter had a seizure, so the first thing the school needed was a seizure action plan. This is a plan the doctor created with directions on what to do if she had another seizure. I needed to provide the school with the seizure action plan (signed by her doctor) and a medical form (also signed by her doctor) for her prescription rescue medication before she could go back to school.

A similar protocol is often used for children diagnosed with diabetes. Schools may require a diabetes action plan that is signed by the doctor and includes information on how to manage the child’s diabetic needs.

If your child is doing well in school and able to do things like he or she did before? That is awesome. Do a little happy dance!

Some children, though, need more. For our daughter, we saw that her school success was being hindered by the visual and memory problems that resulted from her NMO. She didn’t need special instruction or therapies, but she did need some accommodations. We met with the school staff and determined that she was eligible for a 504 plan. 504 plans are based on the individual needs of the child and can allow for things such as extra time and preferential seating.

Some children require specialized instruction or therapies. In these situations, students may need to be evaluated to see if the qualify for an IEP (Individualized Education Plan). This requires an evaluation process in which the school district often does both cognitive and academic testing.

What’s the difference between a 504 and an IEP? They are both individualized plans. A 504 provides accommodations to the general education instruction, where as an IEP is providing specialized instruction. IEPs include specific goals for areas of need. These goals can be related to specific areas such as academics, behavior, speech, occupational therapy and physical therapy. 504 plans do not include goals. Information from the doctor, your child’s teacher and school evaluations can help you determine if your child is eligible for one of these plans.

Not sure what to do? Call your child’s school. They can meet with you to talk about your concerns and determine what the next steps should be for your child’s success.

Recent Spike in Cases of Acute Flaccid Myelitis

Reports have been circulating across the United States concerning the recent spike in cases of Acute Flaccid Myelitis (AFM), a subtype of Transverse Myelitis. AFM is inflammation of the spinal cord, and it predominantly affects children. From August 2014 through August 2018, the Centers for Disease Control and Prevention (CDC) has received information on a total of 362 cases of AFM across the U.S.1 The exact cause of AFM has not yet been determined, but it usually follows a respiratory infection and is believed to be caused by a common virus. However, most children who are infected by the virus do not contract AFM.

The most common symptom of AFM is weakness in the limbs and can result in partial or full paralysis in some cases. AFM is diagnosed based upon clinical exam, MRI findings, lumbar puncture, and may also include a nerve conduction study (EMG) to determine if there is injury to the lower motor neuron. Testing may also include blood draws, respiratory tract samples, or collection of other bodily fluids to determine if a viral or infectious component is present. A diagnosis of AFM differs from classically described Transverse Myelitis in that abnormalities on an MRI are predominantly found in the gray matter of the spinal cord in cases of AFM.

To date, there have not been any conclusive studies that prove a viable treatment for AFM; however, treatments available for Transverse Myelitis have been used. These treatments include high dose IV steroids, IVIG, and plasma exchange (PLEX). The CDC does not recommend the use of steroids, IVIG, or plasma exchange in AFM because of a lack of controlled data, but individuals with AFM or caregivers of children with AFM should discuss treatment recommendations with their physician. Multiple centers have used these therapies with variable results. Physical therapy is believed to be critical for recovery in AFM.

If you or someone you know has a child experiencing symptoms consistent with AFM, it is important to seek emergency care immediately. SRNA will be hosting a special podcast on AFM next week with Dr. Benjamin Greenberg of UT Southwestern Medical Center. We will announce the podcast once all details are finalized. Information and support for those affected by AFM can be found using the following resources:

Membership Form: https://wearesrna.org/join//

Information Sheet on AFM: https://tma.ong/2y9Ie5v

AFM Resources: https://tma.ong/AFM-resources

Management of AFM: https://www.youtube.com/watch?v=mpe-TkQhrD4&feature=youtu.be&list=PLXi60bECkjnXxzgkf2bk3J12iwVU1Q4ML

Q&A and Podcast: https://wearesrna.org/acute-flaccid-myelitis-understanding-recent-outbreak/

2017 Collaborative Meeting on AFM: https://wearesrna.org/collaborative-meeting-acute-flaccid-myelitis/

Parents of Children with AFM Share Stories: https://wearesrna.org/resources/power-sharing-stories/2/

AFM – What Is It?: https://files.wearesrna.org/resources/Newsletter_Articles/2015_04_15_afm.pdf

[1] AFM Investigation. (2018, October 5). Retrieved October 11, 2018, from https://www.cdc.gov/acute-flaccid-myelitis/afm-surveillance.html