Acute Flaccid Myelitis Treatment: How Supportive Care and Rehabilitation Are Planned

A six-year-old who was running through sprinklers on Saturday cannot lift her right arm on Wednesday. There was a cold the week before, a fever that came and went, nothing anyone would have written down. Now a pediatric neurologist is standing at the bedside using a word the family has never heard, and the first question is the one every parent asks: what do you do about it?

The honest answer to that question is the reason this article exists. Acute flaccid myelitis treatment is not built around a drug that switches the illness off. It is built around protecting the body while the spinal cord is under attack, watching breathing hour by hour, and then starting the long, deliberate work of rehabilitation before the inflammation has even settled.

That can feel unsatisfying when you want a fix. But understanding how the plan is actually assembled, and where the evidence is thin, gives families something more durable than false certainty: a way to ask the right questions at the right time.

What acute flaccid myelitis treatment actually involves, step by step

Acute flaccid myelitis, usually shortened to AFM, is a sudden injury to the gray matter of the spinal cord, the central column of nerve cells that sends movement commands out to the muscles. “Flaccid” describes what the affected limb looks like: limp, floppy, with reflexes that are reduced or gone, rather than stiff. The Centers for Disease Control and Prevention (CDC) describes it as rare but serious, with most confirmed cases occurring in young children.

Treatment unfolds in layers rather than as a single event. The first layer is stabilization. Because the same gray matter that moves an arm also drives the diaphragm and the muscles of swallowing, the earliest hours are spent measuring how well a child is breathing and whether they can protect their airway. The second layer is diagnosis, since several conditions can mimic AFM and some of those have specific treatments. Magnetic resonance imaging (MRI), a detailed scan of the spinal cord, and a lumbar puncture, which samples the fluid around the cord, are the two workhorses here.

The third layer is the one families find hardest to hear. Clinicians may consider medicines that calm the immune system, but the CDC’s clinical guidance is candid that none has been shown in well-designed studies to change the course of AFM. Decisions are made case by case by the neurology team, weighing possible benefit against known risks.

The fourth layer starts early and lasts longest: rehabilitation. Physical and occupational therapists often meet a patient while they are still in intensive care, because positioning, stretching and preventing joint stiffness matter from day one. For some patients with lasting weakness, a fifth layer, nerve transfer surgery, is discussed months later. Each layer hands off to the next, and the treating team decides how heavily to lean on any one of them.

Why there is no single proven treatment for AFM

Two facts explain the gap. AFM is rare, and its timing is unpredictable. The CDC reports that fewer than one to two children per million develop it in a typical year, and that recognized clusters have tended to arrive in late summer and early fall, roughly every other year. A condition that appears in small bursts, in scattered places, is extraordinarily hard to study in the randomized trials that establish whether a treatment works.

The cause complicates matters further. The strongest evidence points to enteroviruses, a large family of common viruses that usually cause nothing more than a cold or a stomach upset, and in particular a strain called enterovirus D68. The CDC notes that most patients had a mild respiratory illness or fever about one to two weeks before weakness began. Yet the virus is rarely found in spinal fluid by the time paralysis appears, which suggests the damage may come from the body’s response as much as from the virus itself. Treatments aimed at the virus and treatments aimed at the immune system therefore both have a plausible rationale, and neither has proof.

What clinicians do have is experience from related conditions, such as poliomyelitis, which attacks the same part of the spinal cord, and from other inflammatory spinal cord disorders. Those parallels shape supportive care with reasonable confidence. They are much weaker guides for choosing medicines, which is why the CDC’s guidance for health professionals lists options that “may be considered” while stating plainly that there is no clear evidence of benefit for any of them.

For families, the useful translation is this: when a neurologist says “we do not know if this will help,” that is not hesitation or a lack of expertise. It is an accurate description of the state of the science.

The first 72 hours: breathing, swallowing and the intensive care question

Ask a neurologist what they worry about most in early AFM and the answer is rarely the weak arm. It is the diaphragm. The nerve cells that drive breathing sit in the cervical spinal cord, the neck segment, and this is precisely where AFM lesions often appear. The CDC and the National Institute of Neurological Disorders and Stroke (NINDS) both flag that some patients progress to respiratory failure and need mechanical ventilation, a machine that breathes for the patient through a tube placed in the windpipe.

Because weakness can worsen over hours to days, most children with suspected AFM are admitted to a hospital where breathing can be watched continuously. Nurses measure oxygen levels, count breaths, and often check the strength of a cough or the volume a child can exhale. A child who is talking in shorter sentences, using neck and shoulder muscles to breathe, or becoming unusually sleepy may be moved to intensive care before any crisis develops, so that intubation, if needed, happens in a controlled setting rather than an emergency.

Swallowing gets the same scrutiny. Weak throat muscles allow food and saliva to slip into the lungs, so speech and language therapists may perform bedside swallow tests, and some patients are fed by tube for a period. Blood pressure and heart rate can also fluctuate when the autonomic nerves, which regulate those functions automatically, are involved.

Alongside monitoring, the team starts basic protective care: turning to prevent pressure sores, gentle movement to keep joints supple, and bowel and bladder management if those are affected. None of this feels like treatment in the dramatic sense. All of it is what determines whether a child comes through the acute phase safely.

Which medicines are sometimes considered in AFM treatment options, and what we honestly know

Neurologists caring for AFM generally weigh four categories of medicine. Each is described here by mechanism and by what the CDC’s clinical guidance says about the evidence. The choice, the timing and the decision to use nothing at all belong to the treating team.

Intravenous immunoglobulin, usually shortened to IVIG, is a concentrated preparation of antibodies pooled from many donors, given by infusion. The rationale is that it might neutralize virus or modulate a harmful immune response. The CDC notes it is often used in practice but that there is no clear evidence it improves outcomes in AFM.

Corticosteroids are powerful anti-inflammatory medicines. In AFM the concern is that they could also blunt the body’s defense against a virus that may still be active. The CDC suggests they may be considered in specific situations, such as significant swelling of the spinal cord, but again without proof of benefit.

Plasma exchange, sometimes called plasmapheresis, removes a patient’s plasma and its circulating antibodies and replaces it with donor plasma or a substitute. It is used in some other immune-mediated nerve disorders. For AFM, the CDC reports no evidence of benefit and highlights the procedural risks, which include line infections and blood pressure changes.

Antiviral approaches have been explored, including fluoxetine, an antidepressant that showed activity against enterovirus D68 in laboratory studies. When examined in patients, it did not improve strength, and the CDC does not recommend it for AFM. No antiviral currently has demonstrated effectiveness.

Pain control, muscle relaxants for spasm, and medicines for bladder function may be used to manage symptoms. Families should expect a frank conversation about uncertainty, and should never adjust or stop any prescribed medicine without speaking to the prescribing clinician.

Who is usually treated in hospital, and who is asked to wait and watch

Nearly everyone with suspected AFM is admitted, at least initially. The reason is the unpredictability of the first days: a child who looks stable at noon may need breathing support by midnight. The CDC advises that all patients with suspected AFM be hospitalized for monitoring, and this holds regardless of how mild the initial weakness appears.

Within the hospital, the intensity of treatment is matched to risk. Patients with weakness in the neck, shoulders or breathing muscles, those with lesions high in the cervical cord on MRI, and those whose weakness is still spreading are the ones most likely to be in intensive care and to have immune-based therapies discussed. Patients with a single weak limb, a stable examination over 48 hours and a normal breathing assessment may be watched on a general pediatric or neurology ward with rehabilitation starting right away.

“Waiting” in AFM has a specific meaning. It does not mean sending a child home to see what happens; it means holding off on treatments of unproven benefit while confirming the diagnosis and observing the trajectory. Some teams deliberately delay corticosteroids, for instance, until MRI and spinal fluid results have excluded conditions where steroids would be harmful or where a different therapy is clearly indicated.

Adults are a minority of cases. The CDC reports that more than 90% of confirmed cases have been in children, with a median age of about five. Adults are managed on the same principles, though the differential diagnosis, the list of look-alike conditions, is broader and may include stroke of the spinal cord or an autoimmune disorder.

The consistent thread is that admission is nearly universal, intervention is selective, and the neurology team, not a protocol, decides where a given patient sits on that spectrum.

How AFM is confirmed before treatment decisions are made

Because several conditions produce sudden limb weakness in a child, and some of them have treatments that genuinely work, the diagnostic workup is not a detour from treatment. It is part of it.

MRI of the entire spinal cord is the cornerstone. In AFM, the scan typically shows a bright signal confined largely to the gray matter, often stretching across several vertebral levels. The Mayo Clinic notes that this pattern may be subtle or absent in the first day or two, so a normal early scan does not rule out AFM and repeat imaging may be requested. Brain imaging is often added to look for brainstem involvement, which raises concern about breathing and swallowing.

A lumbar puncture, in which a needle draws a small amount of cerebrospinal fluid from the lower back, usually shows an increased number of white blood cells. The CDC uses this alongside MRI findings and the clinical picture to classify cases. The procedure is done under local anesthetic, sometimes with sedation for children, and the commonest aftereffect is a headache.

Samples from the nose, throat, stool and blood are sent for viral testing. The CDC asks clinicians to collect these as early as possible, because enteroviruses are more likely to be detected in respiratory and stool specimens than in spinal fluid. A positive result does not change bedside management today, but it helps public health tracking and may guide future research.

The conditions the team is working to exclude include Guillain-Barré syndrome, an immune attack on peripheral nerves that often responds to IVIG or plasma exchange; transverse myelitis, which involves white matter and is typically treated with corticosteroids; and spinal cord compression, which may need urgent surgery. Getting this step right is why medicine decisions sometimes wait a day.

Supportive care in acute flaccid myelitis at a glance

Supportive care sounds passive. In practice it is a coordinated set of interventions, each addressing a specific way the illness can cause harm. The table below summarizes the main elements as described in guidance from the CDC and NINDS, and what each is designed to prevent or manage.

Element of care	What it involves	Why it matters in AFM
Respiratory monitoring	Continuous oxygen measurement, breathing rate, cough strength and breathing tests	Weakness can spread to the diaphragm within hours; early recognition allows controlled ventilation rather than emergency intubation
Airway and swallow assessment	Bedside swallow tests, speech therapy review, temporary tube feeding if needed	Prevents food or saliva entering the lungs and causing pneumonia
Circulatory monitoring	Blood pressure and heart rate tracking	Autonomic nerve involvement can cause unstable pressure or rhythm
Skin and pressure care	Regular repositioning, pressure-relieving surfaces	A limb that cannot move cannot shift weight off bony points
Joint and muscle care	Passive range-of-motion exercises, splinting	Reduces contractures, the permanent tightening of joints that follows disuse
Bladder and bowel management	Catheterization or scheduled programs when nerves to these organs are affected	Protects kidney function and comfort
Pain management	Assessment and symptom-directed medicines chosen by the team	Limb and neck pain are common early and can interfere with therapy
Early rehabilitation	Physical, occupational and, where needed, speech therapy from the acute phase	Sets the foundation for functional recovery and prevents secondary complications

Notice what is absent from the table: a disease-modifying medicine. That absence is not an oversight. The measures above are the components with the clearest rationale and the fewest downsides, which is why they form the backbone of care while the evidence for anything more targeted remains unsettled.

How AFM rehabilitation is planned: physical, occupational and speech therapy

Rehabilitation in AFM is not something that begins after treatment. It is the treatment with the most consistent support across clinical guidance, and it starts while a child may still be attached to a monitor.

The first goals are protective. A physical therapist moves each weak joint through its full range every day so that ligaments and tendons do not shorten into a fixed position. Splints hold a wrist or ankle in a neutral posture during sleep. When a shoulder is paralyzed, careful positioning prevents the joint from stretching painfully under the weight of the arm.

As the acute phase settles, the plan shifts toward function. Therapists map exactly which muscles have some remaining activity and which have none, because AFM is famously patchy: a child may have a strong hand at the end of a shoulder that cannot lift. Strengthening focuses on what still works; compensatory strategies teach the body to accomplish tasks in new ways. An occupational therapist, whose specialty is daily activities, might work on dressing with one hand or adapting a fork grip, while a physical therapist addresses standing, transfers and walking, often with orthoses, the braces that support a weak ankle or knee.

Speech and language therapists stay involved where swallowing or voice was affected, and respiratory therapists teach breathing exercises and airway clearance for those with lingering chest weakness.

Intensity varies with the child’s age, fatigue and pain, and the schedule is revisited as strength changes. The Johns Hopkins overview of AFM describes rehabilitation as continuing for months to years, with the expectation that gains may be slow and uneven. Families are typically trained to carry out home programs, because the volume of repetition needed far exceeds what any clinic schedule can provide. The therapy team sets the plan; the family’s kitchen table is where much of it happens.

Nerve transfer surgery: when it is discussed and why timing matters

For a subset of patients whose weakness does not improve, surgeons may raise a procedure that sounds like science fiction and is in fact well established from injuries to the arm’s nerve network: nerve transfer.

The concept is a rewiring. AFM destroys nerve cells in the spinal cord, but the nerves running from those cells to the muscle, and the muscle itself, are initially intact. A surgeon can take a healthy, expendable nerve branch, one that supplies a muscle with a backup, and connect it to the nerve of a paralyzed muscle. Over months, the nerve fibers grow down the new pathway and the muscle regains a signal, though it now responds to a different command that the patient must learn.

Timing is the crucial variable. A muscle that receives no nerve input gradually loses the ability to be reconnected, and the Johns Hopkins overview notes that surgeons generally aim to operate within roughly the first year after onset, once it is clear that natural recovery has plateaued. This is why neurologists and rehabilitation teams track strength so carefully in the early months: the decision window is finite.

Candidacy depends on which muscles are affected, whether suitable donor nerves exist, and the child’s overall health. Shoulder and elbow function in the arm are the most frequently targeted goals; procedures for the legs and for the diaphragm have also been described. Results vary widely, and no guideline offers a reliable figure for how much strength returns, so families should treat any specific percentage with caution.

Nerve transfer is not offered to everyone, is not a substitute for rehabilitation, and requires an intensive therapy program afterward to retrain the brain. The surgical team, together with neurology and rehabilitation, decides whether and when it is appropriate.

Acute flaccid myelitis recovery time: what the following weeks and months usually look like

Recovery from AFM does not follow a neat curve, and no guideline provides a reliable timetable. What clinical descriptions from the CDC, NINDS and the Mayo Clinic do support is a general shape.

The first one to two weeks are dominated by the acute phase: weakness reaches its worst point, breathing and swallowing are monitored, and the diagnosis is confirmed. Hospital stays vary from days to many weeks, with the longest stays among children who needed ventilation.

The following weeks bring the transition to rehabilitation. Some children move to an inpatient rehabilitation unit where therapy happens several hours a day; others go home with outpatient sessions. During this period, pain often eases and any early improvement in strength tends to begin. Muscles that were weak but not completely paralyzed are the most likely to recover first, because their nerve cells were injured rather than lost.

Over the following months, the pattern becomes clearer. NINDS notes that some people recover fully while many are left with persistent weakness, and that the degree of improvement varies enormously from person to person. Muscles with no movement at all at the peak of the illness are the ones most likely to stay weak. Growth in a child adds its own dimension: a limb that is weaker can grow more slowly and may develop differences in length or joint alignment that need monitoring by an orthopedic team.

Beyond the first year, further natural recovery is generally modest, which is why the nerve transfer conversation, when it happens, tends to fall in this window. Fatigue, reduced exercise tolerance and the need for braces or mobility aids may persist. Follow-up with neurology, rehabilitation medicine and often pulmonology continues for years, with the frequency set by the treating team according to how the child is doing.

Acute flaccid myelitis prognosis: what the evidence actually shows

Families deserve a straight answer, and the straight answer is that the outlook is highly variable and often includes lasting weakness. The CDC states that most people with AFM have ongoing weakness in at least one limb, while some improve substantially. NINDS uses similar language, describing a spectrum from full recovery to permanent paralysis.

Several patterns are consistent across clinical descriptions, even if precise numbers are not. Proximal muscles, those close to the trunk such as the shoulder and hip, tend to be affected more severely than distal muscles in the hand and foot, and tend to recover less. Limbs that retained some movement at the worst point of the illness have a better chance of improvement than limbs that were completely paralyzed. Children who needed ventilation often do come off the breathing machine as the illness settles, although some require support for extended periods.

Deaths from AFM are uncommon and are typically related to respiratory complications during the acute phase, which is the principal reason monitoring is so intensive early on. Beyond the acute phase, the challenge is one of disability rather than danger to life.

Because AFM is rare, long-term data remain limited. Registries and follow-up studies are ongoing, and any figure quoted for “chance of walking” or “chance of full recovery” should be traced to its source before it is trusted. The most reliable individual predictor is the trajectory in the first weeks, which is why the neurology team will resist forecasting at the bedside on day two.

None of this diminishes the value of rehabilitation. Even when strength does not fully return, function often improves through adaptation, bracing and, for some, surgery. Outcome and quality of life are not the same measurement.

What people often get wrong about acute flaccid myelitis treatment

Misconceptions about AFM cluster around a few themes, and most of them stem from the natural wish for a clear answer.

The first is that AFM is polio. It resembles polio closely in where it strikes the spinal cord and what it does, and the poliovirus is itself an enterovirus, but the CDC has confirmed that poliovirus has not been detected in confirmed AFM cases. The polio vaccine does not protect against AFM, and AFM does not indicate a polio resurgence.

The second is that a specific medicine exists and is being withheld. IVIG, corticosteroids and plasma exchange are all available, and clinicians may use them, but the evidence that any of them changes outcomes is absent. A team that chooses observation is following the CDC’s stated position, not neglecting a known remedy.

The third is that rehabilitation only starts once the illness is “over.” The opposite is true. Therapy begins in the acute phase, and delay allows joints to stiffen and muscles to shorten in ways that are harder to reverse later.

The fourth is that a weak limb that has not moved in a few weeks is permanently lost. Improvement often continues for months, and for some muscles nerve transfer offers a further option within a defined time window. Equally, the reverse error, promising a child will be back to normal, is unsupported by what is known.

The fifth is that AFM is contagious in the way a cold is. The viruses linked to AFM spread easily, but the paralysis itself is extraordinarily rare among the millions infected each season. Ordinary hygiene, handwashing, covering coughs and staying home when ill, is the sensible level of precaution the CDC recommends, no more.

Correcting these ideas does not make the illness easier. It does make the plan make sense.

Questions to ask your care team about AFM treatment

Families in the acute phase are often too overwhelmed to know what to ask, and by the time the questions form, the specialist has left the room. Writing them down helps. The list below is a starting point, not a script; the answers will be specific to your child and to the treating team’s judgment.

• How are you monitoring breathing and swallowing, and what would prompt a move to intensive care?
• Which conditions are you still ruling out, and would any of them change the treatment?
• Are you considering IVIG, corticosteroids or plasma exchange? What is the reasoning for or against in this case, and what side effects would you watch for?
• When will rehabilitation start, and who is on the therapy team?
• Which muscles have some movement and which have none, and what does that tell you about the likely pattern of recovery?
• How often will strength be formally reassessed in the coming months?
• At what point would nerve transfer surgery be discussed, and who would evaluate for it?
• What signs at home should bring us straight back to the hospital?
• Who coordinates follow-up across neurology, rehabilitation, pulmonology and orthopedics?
• Are there registries or research studies our child could be part of?
• How do we support a sibling, or explain this at school?
• What written information and contact numbers can we take with us?

A good team will welcome these questions and will be comfortable answering “we do not know yet” where that is the truth. If a question falls outside a clinician’s specialty, ask who can answer it and when. Keep a running notebook or shared document; the details that seem unforgettable on day three blur by week six, and rehabilitation teams find a family’s own record of early strength and milestones genuinely useful when planning the months ahead.

When to call your doctor

AFM is a hospital illness in its acute phase, but many of its most important moments happen at home: before the diagnosis, when a limb first goes weak, and after discharge, when complications can surface quietly. Knowing when to act matters at both ends.

Before any diagnosis, seek emergency care immediately if a child develops sudden weakness or limpness in an arm or leg, especially following a recent cold or fever. The CDC lists this as the hallmark sign and urges prompt evaluation. Weakness that spreads, a drooping face, difficulty swallowing, slurred speech, a change in voice, or any trouble breathing is a reason to call emergency services rather than drive to an appointment. Severe neck or back pain with weakness, or new problems passing urine, also warrant urgent assessment.

After discharge, call the treating team the same day if you notice increasing shortness of breath, a weaker cough, noisy or rattling breathing, coughing or choking during meals, fever with a cough, or unusual sleepiness. Any of these could signal a chest infection or worsening respiratory weakness, which are the complications that most commonly bring children back to hospital. New or worsening weakness in a limb that had been stable, sudden severe pain, or skin redness over a bony point that does not fade within a few hours should also prompt a call.

Emotional and behavioral changes count too. A child who becomes withdrawn, stops sleeping, or refuses therapy may be in pain or struggling with the psychological weight of the illness, and the team can involve psychology or pain specialists.

When in doubt, call. Teams caring for AFM expect these calls and would rather hear about a false alarm than miss a real one. Every decision about investigation and treatment sits with the clinicians who know your child’s case.

Frequently asked questions

What are the main AFM treatment options available right now?

The main options are supportive care, rehabilitation and, for selected patients, nerve transfer surgery. Supportive care protects breathing, swallowing, skin and joints during the acute phase. Immune-based medicines such as intravenous immunoglobulin, corticosteroids or plasma exchange may be considered case by case, but the CDC notes there is no clear evidence any of them improves outcomes. The treating neurology team decides which measures fit an individual patient.

Is there a specific medicine that treats acute flaccid myelitis?

No. According to the CDC, no medicine has been proven to treat AFM or reverse the spinal cord injury. Antiviral approaches have been studied, including fluoxetine, which showed laboratory activity against enterovirus D68 but did not improve strength in patients. Clinicians may still use immune-modulating therapies on a case-by-case basis, weighing possible benefit against known risks, and decisions about any medicine rest with the prescribing team.

How long is acute flaccid myelitis recovery time?

There is no fixed recovery time. The acute phase typically lasts one to two weeks, followed by months of rehabilitation. NINDS and the CDC describe outcomes ranging from full recovery to persistent weakness, with most improvement occurring in the first several months and further gains becoming modest beyond the first year. The pattern of weakness at its worst point is the most useful guide to what a given person can expect.

What does AFM rehabilitation involve for a child?

AFM rehabilitation combines physical therapy for movement, standing and walking, occupational therapy for daily tasks such as dressing and feeding, and speech therapy where swallowing or voice was affected. It begins in the hospital with stretching, splinting and positioning to prevent stiff joints, then shifts toward strengthening muscles that still work and teaching new ways to accomplish tasks. Families are trained to continue exercises at home between sessions.

What is the acute flaccid myelitis prognosis?

The prognosis varies widely. The CDC reports that most people have some lasting weakness, while some recover substantially. Muscles near the trunk, such as the shoulder and hip, tend to be affected more severely and recover less than hand and foot muscles. Limbs that kept some movement at the peak of the illness have a better chance of improving. Because AFM is rare, long-term data are still limited.

Why do children with suspected AFM need to be in hospital?

Weakness in AFM can spread over hours to days and may reach the muscles that control breathing and swallowing. The CDC advises hospital admission for all suspected cases so that oxygen levels, breathing effort and swallowing can be monitored continuously and a ventilator can be started in a controlled way if needed. Hospital care also allows the diagnostic tests that rule out look-alike conditions with different treatments.

Is AFM the same as polio?

No. AFM affects the same gray matter of the spinal cord and looks similar clinically, but the CDC has confirmed that poliovirus has not been found in confirmed AFM cases. The leading suspected trigger is a different enterovirus, particularly enterovirus D68. The polio vaccine does not protect against AFM, and AFM cases do not signal a return of polio.

When is nerve transfer surgery considered for AFM?

Nerve transfer is considered for patients whose weakness has stopped improving and who have a suitable healthy donor nerve nearby. Surgeons generally aim to operate within roughly the first year after onset, according to the Johns Hopkins overview, because a muscle without nerve input gradually loses its ability to be reconnected. The procedure is followed by intensive therapy to retrain movement, and candidacy is decided jointly by surgery, neurology and rehabilitation teams.

Can AFM spread from one child to another?

The viruses linked to AFM spread easily and cause common colds and stomach illnesses, but the paralysis itself is extremely rare among those infected. The CDC recommends ordinary precautions: handwashing with soap and water, covering coughs and sneezes, avoiding close contact with people who are ill, and disinfecting frequently touched surfaces. No special isolation is required beyond what is used for any respiratory illness.

Does AFM affect adults, and is the treatment different?

Adults account for a small minority of cases, since more than 90% of confirmed cases have been in children according to CDC data. The treatment principles are the same: supportive care, monitoring of breathing and swallowing, case-by-case consideration of immune-based therapies and early rehabilitation. In adults, the list of alternative diagnoses is broader, so the workup may include additional tests before AFM is confirmed.

References

• CDC: About Acute Flaccid Myelitis
• MedlinePlus: Acute Flaccid Myelitis
• NIH NINDS: Acute Flaccid Myelitis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.