AFM Education Center
AFM 101: What is acute flaccid myelitis
Acute Flaccid Myelitis, or Acute Flaccid Paralysis is a polio-like condition where a child loses the ability to move their muscles after experiencing cold or flu-like symptoms. The CDC defines AFM as an “onset of acute limb weakness on or after August 1, 2014, and a magnetic resonance image (MRI) showing a spinal cord lesion largely restricted to gray matter in a patient age ≤21 years.”(1) Although AFM has been recognized since 2014, earlier reports suggest that the disease may in fact not be new.(2,3)The primary viruses thought to be responsible for AFM are enterovirus D68 and A71 and coxsackievirus A16. So far adults are believed to immune from AFM. Children typically experience a typical cold, but within a few days of the onset of symptoms, high fevers may occur in conjunction with loss of muscle tone or paralysis. Approximately 1 in 4 children will lose the ability to breathe for themselves, requiring a ventilator for at least a few days to months. Most children will lose function of one or both arms and/or legs. Typically, the paralysis involves the shoulder and often at the elbow as well. Loss of hand function is less common. Some children are unable to walk, and others lose the ability to sit or even head control.
AFM 102: Understanding the disease
Based on animal studies,(1,2) it is believed that AFM is caused by a viral infection from the same family of viruses as the polio virus (enteroviruses). The virus gets into the blood stream of a child, and targets the muscles for infection. Once inside the muscle, the virus replicates (uses the machinery of the muscle cell to makes copies of itself) and often kills parts of the muscle in the process. In some children, the virus crosses the neuromuscular junction (the place where a nerve meets a muscle) and travels up the motor nerve axons via retrograde axoplasmic flow to the cell body within the anterior horn of the spinal cord. Once inside the spinal cord, it can infect other motor nerve cells. Afferent and autonomic nerve cells are spared by the virus, but may be injured by the body as the immune system fights the virus. We do not know why the virus only targets motor nerves and spares other nerve types.
AFM 201: Nerve Transfers
So far, the only treatment for AFM the has shown some efficacy is nerve transfer. Nerve transfers involve taking redundant parts of a child’s nerves and transferring them to nerves that are not working.(1) The concept is similar to hot-wiring a car. So far, nerve transfers have shown about 80% efficacy in restoring meaningful elbow bending and straightening. Hand function restoration has even better odds. Shoulder function, however, has proven more resistant to treatment with nerve transfers, with rates of overhead reach at about 20% and rotation of the shoulder at 40%. There is limited experience with restoring the ability to breathe, but so far results are promising. In order to be a candidate for nerve transfers, children must have some redundancy in their nerve function. These redundant nerves are referred to as donors. Children must also have discrete muscle functions that need to be restored that are controlled by a single nerve. These nerves that have lost their function are called recipients.
AFM 301: oberlin Transfer
This video demonstrates a nerve transfer where one or two fascicles of the ulnar nerve are transferred to the musculocutaneous nerve branch to the biceps muscle (Oberlin transfer). This can be performed for Acute Flaccid Myelitis as well as for Brachial Plexus Palsies and other nerve injuries.
AFM 302: Spinal accessory to suprascapular nerve transfer
The Spinal Accessory nerve can be used to power some of the muscles of the rotator cuff, the supraspinatus and infraspinatus. The spinal accessory nerve normally controls the lower trapezius muscle, which serves only to adduct the scapula to the spine, a function that is expendable and also redundant in patients with working rhomboid muscles.
AFM 401: thoracoscopic intercostal to phrenic nerve transfer
Children with AFM can lose the ability to breathe when their phrenic nerve is injured. Some children, however, may be able to have their respiratory function restored if just one of the intercostal nerves is functioning. The intercostal nerve can be transferred to the phrenic nerve to regain power to the muscle. Pacers that are used to shock the diaphragm will not function long-term in patients with AFM and should be used only as temporary adjuncts to support ventilatory function until either the child recovers spontaneously or, after 9-12 months of observation, is indicated for an intercostal nerve transfer.