Case Report: Atypical AMAN Strikes During Active Pneumonia, Prompting Urgent IVIG and Full Recovery
Acute motor axonal neuropathy, known by the acronym AMAN, is one of the more severe subtypes of Guillain-Barré syndrome (GBS). While GBS encompasses a family of immune-mediated nerve disorders, AMAN stands apart because it attacks the axons themselves, the conducting cables of nerve cells, rather than the protective myelin sheath that surrounds them. Axonal damage is generally harder for the body to repair than myelin damage, which means AMAN patients can face deeper and more prolonged weakness. The condition is more commonly seen in Asia than in Western countries, and it is frequently associated with infections by Campylobacter jejuni, the bacterium behind many cases of food-related gastroenteritis.
The classic pattern of AMAN follows a predictable sequence: a triggering infection occurs, the body mounts an immune response, and then, one to four weeks after the infection has passed, the nervous system begins to malfunction. Antibodies that were originally made to fight the infection mistakenly target components of motor nerves, a process known as molecular mimicry. Weakness starts in the legs and moves upward, potentially reaching the respiratory muscles, which can require mechanical ventilation. The post-infectious timing is so well recognized that doctors are trained to expect it, and a diagnosis of GBS or AMAN in someone who is still acutely ill with infection is considered unusual.
A case report published in Cureus in November 2025 by authors Mohit Vaid and Monika Singh describes exactly that kind of unusual presentation. The patient, a 36-year-old woman, arrived at the hospital with rapidly ascending, flaccid weakness in all four limbs along with bulbar symptoms including difficulty swallowing and facial weakness. Her condition deteriorated quickly, requiring four days of mechanical ventilation for respiratory failure. What made this case particularly striking was the timeline: her neurological symptoms began on the fourth day of an active febrile illness that turned out to be community-acquired pneumonia. There was no post-infectious gap. The paralysis arrived while the lung infection was still in progress.
Reaching the correct diagnosis required careful testing to exclude other causes. Muscle enzyme levels, including creatine phosphokinase and CK-MB, were completely normal, which ruled out the possibility that muscle disease or myopathy was driving the weakness. Nerve conduction velocity studies then showed a characteristic pattern of axonal motor polyneuropathy without sensory involvement, meaning the electrical signals in motor nerves were compromised while sensory nerves remained intact. Cerebrospinal fluid analysis revealed albuminocytologic dissociation, a classic finding in GBS in which protein levels are elevated but white blood cell counts are not, supporting the autoimmune nerve diagnosis.
Once AMAN was identified, the clinical team moved quickly. Intravenous immunoglobulin (IVIG) was started alongside broad-spectrum antibiotics to treat the concurrent pneumonia. The patient was successfully weaned from the ventilator and demonstrated impressive motor recovery by the time she was discharged. The authors emphasize that this case illustrates a phenomenon called parainfectious AMAN, meaning the nerve attack occurs during active infection rather than after it. For clinicians, the lesson is significant: AMAN should remain on the diagnostic radar even when a patient is still visibly unwell with another illness. Waiting for a post-infectious period before considering the diagnosis could delay IVIG by days, and in a rapidly progressing condition, that delay can have serious consequences for recovery.
Source: Cureus, November 25, 2025. Vaid M, Singh M. This summary is for informational purposes only and does not constitute medical advice. Please consult a qualified healthcare provider for guidance specific to your situation.