Acute flaccid paralysis (AFP) is a clinical syndrome characterised by the sudden weakening or complete loss of function in the arms, legs, or respiratory muscles. The word “flaccid” is critical here: rather than becoming stiff or spastic, the affected muscles become loose, soft, and devoid of tone. Deep tendon reflexes diminish or disappear entirely.
AFP is not the name of a single disease but rather the shared clinical presentation of many different conditions. It is therefore defined in medicine as a syndrome — not one disease with a single cause, but a common clinical picture produced by a variety of underlying causes.
Why Does It Matter So Much?
AFP is a condition monitored with particular vigilance worldwide, especially in children. The primary reason for this is its association with poliomyelitis (polio). Under global polio eradication programmes, every child under the age of 15 who develops acute flaccid paralysis anywhere in the world must be reported to the World Health Organization. This surveillance system allows authorities to track whether the poliovirus is still circulating in a given population.
What Conditions Cause AFP?
The causes of AFP are classified according to which part of the nervous system is damaged.
Anterior horn cell damage of the spinal cord
Poliomyelitis is historically the most common and most significant cause of AFP. West Nile virus and Enterovirus D68 and A71 — causes that have been increasing in frequency in recent years — also fall into this category. Acute flaccid myelitis (AFM) is a newer and not yet fully understood condition that selectively affects anterior horn cells.
Peripheral nerve damage
Guillain-Barré syndrome is the most frequently encountered non-polio cause of AFP; the immune system attacks the myelin sheaths surrounding peripheral nerves. Traumatic neuritis can occur following incorrectly administered injections.
Neuromuscular junction damage
In botulism, the toxin blocks the nerve-muscle junction. Acute exacerbation of myasthenia gravis also falls within this category.
Muscle-related causes
Acute myopathies and electrolyte disturbances such as hypocalcaemia and hypokalaemia are evaluated within this group.
What Are the Clinical Features?
The cardinal features of the syndrome are sudden-onset weakness of one or more limbs, diminished or absent deep tendon reflexes, and a marked reduction in muscle tone. Pain may or may not accompany the weakness. When the respiratory muscles are affected, the situation becomes life-threatening — this is the most critical complication of AFP.
How Is It Diagnosed?
The diagnostic workup for AFP combines clinical examination, MRI of the spinal cord and brain, nerve conduction studies and electromyography (EMG), cerebrospinal fluid analysis, and viral testing including stool, throat, and CSF cultures. Identifying the underlying cause is of vital importance in determining the appropriate treatment plan.
Treatment
Management of AFP is largely guided by the underlying cause. There is no specific antiviral treatment for poliomyelitis; supportive care is the mainstay. In the early stages of Guillain-Barré syndrome, intravenous immunoglobulin (IVIG) or plasmapheresis is administered. Antitoxin is given in botulism. Mechanical ventilation may be required if the respiratory muscles are involved.
Prognosis
The likelihood and pace of recovery vary considerably depending on the aetiology and the extent of nerve damage. Most patients with Guillain-Barré syndrome recover substantially over a course of months, though the timeline can be prolonged. Poliomyelitis can result in permanent paralysis. In cases of acute flaccid myelitis, recovery is generally partial and long-term rehabilitation is typically required.