Vol. 12/ Núm. 3 2025 pág. 711
https://doi.org/10.69639/arandu.v12i3.1340
Acute motor axonal neuropathy in Ecuador: a retrospective
case series with electrophysiological and functional
correlation
Neuropatía axonal motora aguda en Ecuador: Una serie de casos retrospectiva con
correlación electrofisiológica y functional
Ana Karina Pérez León
akperezl@uce.edu.ec
https://orcid.org/0009-0007-2503-5671
Universidad Central del Ecuador
Hugo Esteban Salazar Lozano
esalazar@uce.edu.ec
https://orcid.org/0009-0005-7128-8376
Universidad Central del Ecuador
María Daniela Pérez León
maria.perez.04d03@dpsca.gob.ec
https://orcid.org/0009-0004-7545-7061
Ministerio de Salud Pública
Ecuador
Andrea Carolina Pérez León
acperezl@uce.edu.ec
https://orcid.org/0009-0008-0191-4601
Universidad Central del Ecuador
Diego Fernando Atapuma Madrid
dfatapuma@uce.edu.ec
https://orcid.org/0009-0000-3029-6592
Universidad Central del Ecuador
Artículo recibido: 18 junio 2025 - Aceptado para publicación: 28 julio 2025
Conflictos de intereses: Ninguno que declarar.
ABSTRACT
Acute Motor Axonal Neuropathy (AMAN) is a severe Guillain–Barré Syndrome (GBS) variant
characterized by acute flaccid paralysis and pure motor axonal involvement. In Latin America,
its diagnosis remains challenging due to limited access to neurophysiological tools. This case
series describes three Ecuadorian male patients diagnosed with AMAN between 2017 and 2025,
each with recent gastrointestinal infection. Electromyography confirmed axonal motor
neuropathy in all cases. One patient, a high-performance cyclist, required mechanical ventilation
and fully recovered after IVIG. Another, a retired officer, showed partial improvement and
remains orthotic-dependent. The third, a former conscript, developed irreversible quadriplegia
despite treatment and prolonged ICU stay. Antiganglioside antibodies were tested in one case,
revealing GD1a, GD1b, and GT1b positivity. These cases demonstrate the clinical heterogeneity
Vol. 12/ Núm. 3 2025 pág. 712
of AMAN and the importance of early diagnosis, timely immunotherapy, and structured
rehabilitation. Increased awareness and improved diagnostic capacity are essential to optimize
outcomes in AMAN patients in resource-limited settings.
Keywords: Guillain–Barré Syndrome, AMAN, acute flaccid paralysis, axonal
neuropathy, neurophysiology
RESUMEN
La neuropatía axonal motora aguda (AMAN) es una variante grave del síndrome de Guillain-
Barré (SGB), caracterizada por parálisis flácida aguda de origen motor sin compromiso sensitivo.
Su diagnóstico en América Latina es complejo debido al limitado acceso a estudios
electrofisiológicos. Esta serie de casos describe tres pacientes varones ecuatorianos
diagnosticados con AMAN entre 2017 y 2025, todos con antecedentes de infección
gastrointestinal. Los estudios de electromiografía confirmaron neuropatía axonal motora pura en
los tres casos. Un paciente, ciclista de alto rendimiento, requirió ventilación mecánica transitoria
y recuperó su funcionalidad tras recibir inmunoglobulina intravenosa. Otro, militar retirado,
presentó recuperación parcial y actualmente depende de órtesis. El tercero, exconscripto,
desarrolló cuadriplejía irreversible a pesar del tratamiento y una estancia prolongada en UCI. Solo
uno de ellos fue evaluado con anticuerpos antigangliósido, encontrándose positividad a GD1a,
GD1b y GT1b. Estos casos evidencian la heterogeneidad clínica del AMAN y refuerzan la
necesidad de un diagnóstico precoz, tratamiento oportuno y rehabilitación estructurada. Es
indispensable fortalecer la capacidad diagnóstica y la conciencia clínica sobre esta variante del
SGB en contextos con recursos limitados.
Palabras clave: Síndrome de Guillain-Barré, AMAN, parálisis flácida aguda, neuropatía
axonal, neurofisiología
Todo el contenido de la Revista Científica Internacional Arandu UTIC publicado en este sitio está disponible bajo
licencia Creative Commons Atribution 4.0 International.
of AMAN and the importance of early diagnosis, timely immunotherapy, and structured
rehabilitation. Increased awareness and improved diagnostic capacity are essential to optimize
outcomes in AMAN patients in resource-limited settings.
Keywords: Guillain–Barré Syndrome, AMAN, acute flaccid paralysis, axonal
neuropathy, neurophysiology
RESUMEN
La neuropatía axonal motora aguda (AMAN) es una variante grave del síndrome de Guillain-
Barré (SGB), caracterizada por parálisis flácida aguda de origen motor sin compromiso sensitivo.
Su diagnóstico en América Latina es complejo debido al limitado acceso a estudios
electrofisiológicos. Esta serie de casos describe tres pacientes varones ecuatorianos
diagnosticados con AMAN entre 2017 y 2025, todos con antecedentes de infección
gastrointestinal. Los estudios de electromiografía confirmaron neuropatía axonal motora pura en
los tres casos. Un paciente, ciclista de alto rendimiento, requirió ventilación mecánica transitoria
y recuperó su funcionalidad tras recibir inmunoglobulina intravenosa. Otro, militar retirado,
presentó recuperación parcial y actualmente depende de órtesis. El tercero, exconscripto,
desarrolló cuadriplejía irreversible a pesar del tratamiento y una estancia prolongada en UCI. Solo
uno de ellos fue evaluado con anticuerpos antigangliósido, encontrándose positividad a GD1a,
GD1b y GT1b. Estos casos evidencian la heterogeneidad clínica del AMAN y refuerzan la
necesidad de un diagnóstico precoz, tratamiento oportuno y rehabilitación estructurada. Es
indispensable fortalecer la capacidad diagnóstica y la conciencia clínica sobre esta variante del
SGB en contextos con recursos limitados.
Palabras clave: Síndrome de Guillain-Barré, AMAN, parálisis flácida aguda, neuropatía
axonal, neurofisiología
Todo el contenido de la Revista Científica Internacional Arandu UTIC publicado en este sitio está disponible bajo
licencia Creative Commons Atribution 4.0 International.
Vol. 12/ Núm. 3 2025 pág. 713
INTRODUCTION
Guillain-Barré Syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy
characterized by rapidly progressive, symmetrical muscle weakness and generalized areflexia. In
severe cases, it may compromise respiratory function and lead to autonomic dysfunction. Among
its clinical variants, Acute Motor Axonal Neuropathy (AMAN) is distinguished by predominant
involvement of motor axons without significant sensory abnormalities. It has been more
frequently reported in Asia and Latin America (Uncini & Yuki, 2012; Willison et al., 2016).
From an immunological standpoint, the pathogenesis of AMAN involves molecular
mimicry, wherein certain pathogens share epitopes with peripheral nerve gangliosides,
particularly GM1 and GD1a. This similarity induces an autoimmune response mediated by
antibodies, complement activation, and subsequent axonal damage at the nodes of Ranvier (Yuki
& Hartung, 2012; Susuki et al., 2007). This mechanism is well documented in post-infectious
cases, especially those following Campylobacter jejuni infection.
However, increasing evidence suggests that various immune stressors—including
infections, physical overexertion, or dermal trauma—may act as triggering events in genetically
predisposed individuals. These stimuli can activate antigen-presenting cells and provoke cross-
reactive autoimmune responses through loss of tolerance or bystander activation (Kuwabara et
al., 2015; Luijten et al., 2022). As such, the etiological spectrum of AMAN is broader than
previously assumed and should be interpreted within an integrative immunopathological
framework.
Despite its well-established clinical and neurophysiological features, AMAN remains
underdiagnosed in many Latin American settings due to limited access to electrophysiological
studies and antiganglioside antibody testing. In Ecuador, published reports are scarce, and formal
documentation is limited. This case series contributes to addressing this data gap by presenting
three confirmed cases from a public hospital, supported by detailed clinical records.
All three patients developed rapidly progressive symmetrical motor weakness with absent
or minimal sensory involvement, preserved consciousness, and neurophysiological findings
consistent with AMAN. Their antecedents included gastrointestinal infections and, in one case,
recent intense physical exertion. These observations reflect the heterogeneity of AMAN
presentation and support a post-infectious autoimmune hypothesis in resource-limited settings
where diagnostic tools are often unavailable.
This report presents a retrospective case series of three Ecuadorian patients diagnosed with
Acute Motor Axonal Neuropathy (AMAN), each confirmed by clinical and electrophysiological
criteria. By documenting their demographic, functional, and respiratory profiles, this study
contributes local evidence of AMAN in Latin America and highlights the clinical heterogeneity
and recovery patterns associated with post-infectious immune-mediated neuropathies.
INTRODUCTION
Guillain-Barré Syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy
characterized by rapidly progressive, symmetrical muscle weakness and generalized areflexia. In
severe cases, it may compromise respiratory function and lead to autonomic dysfunction. Among
its clinical variants, Acute Motor Axonal Neuropathy (AMAN) is distinguished by predominant
involvement of motor axons without significant sensory abnormalities. It has been more
frequently reported in Asia and Latin America (Uncini & Yuki, 2012; Willison et al., 2016).
From an immunological standpoint, the pathogenesis of AMAN involves molecular
mimicry, wherein certain pathogens share epitopes with peripheral nerve gangliosides,
particularly GM1 and GD1a. This similarity induces an autoimmune response mediated by
antibodies, complement activation, and subsequent axonal damage at the nodes of Ranvier (Yuki
& Hartung, 2012; Susuki et al., 2007). This mechanism is well documented in post-infectious
cases, especially those following Campylobacter jejuni infection.
However, increasing evidence suggests that various immune stressors—including
infections, physical overexertion, or dermal trauma—may act as triggering events in genetically
predisposed individuals. These stimuli can activate antigen-presenting cells and provoke cross-
reactive autoimmune responses through loss of tolerance or bystander activation (Kuwabara et
al., 2015; Luijten et al., 2022). As such, the etiological spectrum of AMAN is broader than
previously assumed and should be interpreted within an integrative immunopathological
framework.
Despite its well-established clinical and neurophysiological features, AMAN remains
underdiagnosed in many Latin American settings due to limited access to electrophysiological
studies and antiganglioside antibody testing. In Ecuador, published reports are scarce, and formal
documentation is limited. This case series contributes to addressing this data gap by presenting
three confirmed cases from a public hospital, supported by detailed clinical records.
All three patients developed rapidly progressive symmetrical motor weakness with absent
or minimal sensory involvement, preserved consciousness, and neurophysiological findings
consistent with AMAN. Their antecedents included gastrointestinal infections and, in one case,
recent intense physical exertion. These observations reflect the heterogeneity of AMAN
presentation and support a post-infectious autoimmune hypothesis in resource-limited settings
where diagnostic tools are often unavailable.
This report presents a retrospective case series of three Ecuadorian patients diagnosed with
Acute Motor Axonal Neuropathy (AMAN), each confirmed by clinical and electrophysiological
criteria. By documenting their demographic, functional, and respiratory profiles, this study
contributes local evidence of AMAN in Latin America and highlights the clinical heterogeneity
and recovery patterns associated with post-infectious immune-mediated neuropathies.
Vol. 12/ Núm. 3 2025 pág. 714
METHODOLOGY
A retrospective, observational, and descriptive case series study was conducted involving
three patients diagnosed with the acute motor axonal neuropathy (AMAN) variant of Guillain-
Barré Syndrome (GBS). These cases were treated between 2017 and 2025 at a public hospital in
Ecuador. This time frame was chosen to encompass all clinically compatible AMAN, three
clinical cases were included, all diagnosed with the AMAN variant of GBS by nerve conduction
studies. They were managed at the same ecuadorian hospital between 2017 and 2025.
Clinical information was obtained through institutional medical record review and direct
interviews with patients or their relatives, using a structured data collection form specifically
designed for this study. The form was reviewed by clinical professionals to ensure its relevance
and comprehensiveness.
Inclusion criteria were: confirmed diagnosis of AMAN based on clinical and
neurophysiological findings; recent exposure to an immunological stressor such as
gastrointestinal infection or physical overexertion; and availability of complete clinical data.
Cases with incomplete documentation or uncertain diagnostic confirmation were excluded.
The following variables were collected: demographic data (age, sex, occupation), relevant
antecedents, latency between exposure and symptom onset, neurological presentation,
cerebrospinal fluid (CSF) findings, electromyography (EMG) results, type of immunotherapy
received (IVIG or plasma exchange and functional status at hospital discharge and up to three
months post-onset, regardless of recovery.
Data were organized into a comparative clinical characteristics table and analyzed using
qualitative descriptive methods. No inferential statistics were applied due to the limited sample
size. All patient data were fully anonymized, and the hospital name was omitted to protect
confidentiality. Verbal informed consent was obtained from all participants for academic and
research purposes.
CASE PRESENTATION
Case 1
A 37-year-old Ecuadorian male, active-duty military officer and competitive cyclist,
presented on April 30, 2025, with acute ascending weakness and generalized fatigue following a
febrile diarrheal illness. He had no history of chronic disease, recent vaccination, or substance
use, but reported ingestion of food from a street market days before symptom onset. Neurological
examination on admission revealed flaccid tetraparesis (MRC 1/5 upper and lower limbs),
generalized areflexia, and intact cranial nerves. Cerebrospinal fluid (CSF) analysis on May 13
showed normal cytology and biochemistry. Nerve conduction studies performed on May 16
revealed findings consistent with acute motor axonal neuropathy (AMAN). Antiganglioside
antibodies (GD1a, GD1b, GT1b) were positive. The patient’s initial forced vital capacity (FVC)
METHODOLOGY
A retrospective, observational, and descriptive case series study was conducted involving
three patients diagnosed with the acute motor axonal neuropathy (AMAN) variant of Guillain-
Barré Syndrome (GBS). These cases were treated between 2017 and 2025 at a public hospital in
Ecuador. This time frame was chosen to encompass all clinically compatible AMAN, three
clinical cases were included, all diagnosed with the AMAN variant of GBS by nerve conduction
studies. They were managed at the same ecuadorian hospital between 2017 and 2025.
Clinical information was obtained through institutional medical record review and direct
interviews with patients or their relatives, using a structured data collection form specifically
designed for this study. The form was reviewed by clinical professionals to ensure its relevance
and comprehensiveness.
Inclusion criteria were: confirmed diagnosis of AMAN based on clinical and
neurophysiological findings; recent exposure to an immunological stressor such as
gastrointestinal infection or physical overexertion; and availability of complete clinical data.
Cases with incomplete documentation or uncertain diagnostic confirmation were excluded.
The following variables were collected: demographic data (age, sex, occupation), relevant
antecedents, latency between exposure and symptom onset, neurological presentation,
cerebrospinal fluid (CSF) findings, electromyography (EMG) results, type of immunotherapy
received (IVIG or plasma exchange and functional status at hospital discharge and up to three
months post-onset, regardless of recovery.
Data were organized into a comparative clinical characteristics table and analyzed using
qualitative descriptive methods. No inferential statistics were applied due to the limited sample
size. All patient data were fully anonymized, and the hospital name was omitted to protect
confidentiality. Verbal informed consent was obtained from all participants for academic and
research purposes.
CASE PRESENTATION
Case 1
A 37-year-old Ecuadorian male, active-duty military officer and competitive cyclist,
presented on April 30, 2025, with acute ascending weakness and generalized fatigue following a
febrile diarrheal illness. He had no history of chronic disease, recent vaccination, or substance
use, but reported ingestion of food from a street market days before symptom onset. Neurological
examination on admission revealed flaccid tetraparesis (MRC 1/5 upper and lower limbs),
generalized areflexia, and intact cranial nerves. Cerebrospinal fluid (CSF) analysis on May 13
showed normal cytology and biochemistry. Nerve conduction studies performed on May 16
revealed findings consistent with acute motor axonal neuropathy (AMAN). Antiganglioside
antibodies (GD1a, GD1b, GT1b) were positive. The patient’s initial forced vital capacity (FVC)
Vol. 12/ Núm. 3 2025 pág. 715
was 0.88 L, and he required invasive mechanical ventilation from May 16. Intravenous
immunoglobulin (IVIG) was administered over five days, starting on May 14. He remained in the
intensive care unit (ICU) for seven days. Upon ICU discharge, strength improved to MRC 3/5 in
upper limbs and 5/5 in lower limbs. He was discharged home on May 26, 2025, walking
independently and performing daily activities without assistance. He did not require tracheostomy
and currently shows full neurological recovery.
A nerve conduction study and electromyography were performed, confirming the diagnosis
of acute motor axonal neuropathy (AMAN). The key findings are illustrated in Figure 1, which
displays the electrophysiological profile of the patient.
Figure 1
Nerve conduction study of the right ulnar sensory nerve in a patient with AMAN variant of
Guillain-Barré Syndrome (Case 1)
The waveform shows markedly reduced amplitude and preserved latency, consistent with
a predominantly axonal pattern. These findings are compatible with severe motor axonal
involvement and early conduction failure.
Case 2
A 38-year-old Ecuadorian male, retired military officer, was admitted on April 11, 2023,
with progressive lower limb weakness and areflexia that began four days after an episode of
gastroenteritis (fever, diarrhea) following seafood consumption. On admission, he presented with
flaccid tetraparesis (MRC 2/5), preserved consciousness, and no bulbar involvement. CSF
analysis was normal. Nerve conduction studies performed the same day revealed an acute motor
axonal pattern consistent with AMAN. FVC was 2.21 L. The patient received a five-day course
was 0.88 L, and he required invasive mechanical ventilation from May 16. Intravenous
immunoglobulin (IVIG) was administered over five days, starting on May 14. He remained in the
intensive care unit (ICU) for seven days. Upon ICU discharge, strength improved to MRC 3/5 in
upper limbs and 5/5 in lower limbs. He was discharged home on May 26, 2025, walking
independently and performing daily activities without assistance. He did not require tracheostomy
and currently shows full neurological recovery.
A nerve conduction study and electromyography were performed, confirming the diagnosis
of acute motor axonal neuropathy (AMAN). The key findings are illustrated in Figure 1, which
displays the electrophysiological profile of the patient.
Figure 1
Nerve conduction study of the right ulnar sensory nerve in a patient with AMAN variant of
Guillain-Barré Syndrome (Case 1)
The waveform shows markedly reduced amplitude and preserved latency, consistent with
a predominantly axonal pattern. These findings are compatible with severe motor axonal
involvement and early conduction failure.
Case 2
A 38-year-old Ecuadorian male, retired military officer, was admitted on April 11, 2023,
with progressive lower limb weakness and areflexia that began four days after an episode of
gastroenteritis (fever, diarrhea) following seafood consumption. On admission, he presented with
flaccid tetraparesis (MRC 2/5), preserved consciousness, and no bulbar involvement. CSF
analysis was normal. Nerve conduction studies performed the same day revealed an acute motor
axonal pattern consistent with AMAN. FVC was 2.21 L. The patient received a five-day course
Vol. 12/ Núm. 3 2025 pág. 716
of IVIG starting April 11. He remained in the ICU for eight days and was discharged to the general
ward with MRC scores of 3/5 in upper limbs and 1/5 in lower limbs. He was discharged home on
April 26, 2023, using a wheelchair, with only minimal voluntary movement in the lower limbs.
At one-year follow-up, he is partially dependent, uses orthotic devices for ambulation, and
exhibits preserved reflexes and sensitivity but limited motor coordination.
The patient underwent an EMG which supported a diagnosis compatible with the AMAN
variant. The relevant findings are shown in Figure 2, summarizing the neurophysiological
characteristics.
Figure 2
Left median sensory nerve conduction in a patient with AMAN (Case 2)
The graph shows diminished amplitude and preserved latency, suggestive of axonal
damage without significant demyelination. This electrophysiological profile supported the
diagnosis of acute motor axonal neuropathy.
Case 3
A 27-year-old Ecuadorian male, former military conscript, was admitted to a public
hospital on December 6, 2017, with acute symmetrical flaccid paralysis following fever and
diarrhea reported the previous week. Neurological examination revealed complete paralysis
(MRC 0/5) of all limbs and absent deep tendon reflexes. CSF was normal. Electromyography on
December 9 showed pure motor axonal neuropathy consistent with AMAN. His initial FVC was
recorded at 20 L, though this value likely reflects a data entry error. He developed respiratory
failure and was intubated on December 7. IVIG was administered over five days starting the same
of IVIG starting April 11. He remained in the ICU for eight days and was discharged to the general
ward with MRC scores of 3/5 in upper limbs and 1/5 in lower limbs. He was discharged home on
April 26, 2023, using a wheelchair, with only minimal voluntary movement in the lower limbs.
At one-year follow-up, he is partially dependent, uses orthotic devices for ambulation, and
exhibits preserved reflexes and sensitivity but limited motor coordination.
The patient underwent an EMG which supported a diagnosis compatible with the AMAN
variant. The relevant findings are shown in Figure 2, summarizing the neurophysiological
characteristics.
Figure 2
Left median sensory nerve conduction in a patient with AMAN (Case 2)
The graph shows diminished amplitude and preserved latency, suggestive of axonal
damage without significant demyelination. This electrophysiological profile supported the
diagnosis of acute motor axonal neuropathy.
Case 3
A 27-year-old Ecuadorian male, former military conscript, was admitted to a public
hospital on December 6, 2017, with acute symmetrical flaccid paralysis following fever and
diarrhea reported the previous week. Neurological examination revealed complete paralysis
(MRC 0/5) of all limbs and absent deep tendon reflexes. CSF was normal. Electromyography on
December 9 showed pure motor axonal neuropathy consistent with AMAN. His initial FVC was
recorded at 20 L, though this value likely reflects a data entry error. He developed respiratory
failure and was intubated on December 7. IVIG was administered over five days starting the same
Vol. 12/ Núm. 3 2025 pág. 717
day. He remained in ICU for 157 days, required tracheostomy, and experienced nosocomial
infection. He was discharged from ICU on May 28, 2018, and from the hospital on June 18. At
discharge, he remained wheelchair-bound, with absent reflexes, no motor or sensory recovery,
and full dependency for activities of daily living. Although decannulated prior to discharge, he
remains fully dependent and has not regained motor function to date.
An extensive neurophysiological assessment revealed severe motor axonal involvement
with poor prognosis. The corresponding EMG patterns are depicted in Figure 3.
Figure 3
Electromyography (EMG) recording of the left anterior tibialis muscle in a patient with severe
AMAN variant of Guillain-Barré Syndrome (Case 3)
The absence of spontaneous activity and motor unit potentials reflects complete axonal
degeneration and denervation. The findings are consistent with the poor functional outcome
documented in this patient.
Table 1
Clinical, Electrophysiological, and Functional Characteristics of Three Ecuadorian Patients
with Acute Motor Axonal Neuropathy (AMAN), 2017–2025
Variable Case 1 Case 2 Case 3
Sex / Age Male, 37 years Male, 38 years Male, 27 years
Year of Onset 2025 2023 2017
Institutional Status Active military / high-
performance cyclist Retired military Former military
conscript
day. He remained in ICU for 157 days, required tracheostomy, and experienced nosocomial
infection. He was discharged from ICU on May 28, 2018, and from the hospital on June 18. At
discharge, he remained wheelchair-bound, with absent reflexes, no motor or sensory recovery,
and full dependency for activities of daily living. Although decannulated prior to discharge, he
remains fully dependent and has not regained motor function to date.
An extensive neurophysiological assessment revealed severe motor axonal involvement
with poor prognosis. The corresponding EMG patterns are depicted in Figure 3.
Figure 3
Electromyography (EMG) recording of the left anterior tibialis muscle in a patient with severe
AMAN variant of Guillain-Barré Syndrome (Case 3)
The absence of spontaneous activity and motor unit potentials reflects complete axonal
degeneration and denervation. The findings are consistent with the poor functional outcome
documented in this patient.
Table 1
Clinical, Electrophysiological, and Functional Characteristics of Three Ecuadorian Patients
with Acute Motor Axonal Neuropathy (AMAN), 2017–2025
Variable Case 1 Case 2 Case 3
Sex / Age Male, 37 years Male, 38 years Male, 27 years
Year of Onset 2025 2023 2017
Institutional Status Active military / high-
performance cyclist Retired military Former military
conscript
Vol. 12/ Núm. 3 2025 pág. 718
Variable Case 1 Case 2 Case 3
Triggering Event Febrile gastroenteritis Gastroenteritis
(seafood-related)
Fever and diarrhea
(possible arboviral
illness)
Days from Trigger to
Symptoms 2 days 4 days 5 days
Initial Symptoms Flaccid tetraparesis,
fatigue Progressive paraparesis Complete quadriplegia
Cranial Nerve
Involvement None None None
CSF Findings Normal Normal Normal
EMG Findings Pure motor axonal
neuropathy (AMAN)
Pure motor axonal
neuropathy (AMAN)
Pure motor axonal
neuropathy (AMAN)
Anti-ganglioside
Antibodies
GD1a, GD1b, GT1b
positive Not available Not available
CVF at Admission 0.88 L 2.21 L 20 L* (likely error)
Ventilatory Support Invasive (7 days) No
Invasive (with
tracheostomy, 157 days
ICU)
Immunotherapy IVIG (5 days) IVIG (5 days) IVIG (5 days)
Length of ICU Stay 7 days 8 days 157 days
Functional Status at
Discharge
Independent
ambulation
Wheelchair, partial leg
movement
Total dependency, no
motor or sensory
recovery
Hughes Scale at
Discharge Not documented Not documented Not documented
Current Functional
Status Full recovery
Orthotic-dependent,
mild coordination
deficit
Fully dependent, no
recovery
Note: The CVF value of 20 L in Case 3 was extracted directly from the original clinical record. This value is
physiologically inconsistent and likely a documentation error. It is presented here as recorded, but should be interpreted
with caution.*
The three patients were attended at different time points between 2017 and 2025 in a public
hospital in Ecuador. Clinical data were collected retrospectively using a standardized data
Variable Case 1 Case 2 Case 3
Triggering Event Febrile gastroenteritis Gastroenteritis
(seafood-related)
Fever and diarrhea
(possible arboviral
illness)
Days from Trigger to
Symptoms 2 days 4 days 5 days
Initial Symptoms Flaccid tetraparesis,
fatigue Progressive paraparesis Complete quadriplegia
Cranial Nerve
Involvement None None None
CSF Findings Normal Normal Normal
EMG Findings Pure motor axonal
neuropathy (AMAN)
Pure motor axonal
neuropathy (AMAN)
Pure motor axonal
neuropathy (AMAN)
Anti-ganglioside
Antibodies
GD1a, GD1b, GT1b
positive Not available Not available
CVF at Admission 0.88 L 2.21 L 20 L* (likely error)
Ventilatory Support Invasive (7 days) No
Invasive (with
tracheostomy, 157 days
ICU)
Immunotherapy IVIG (5 days) IVIG (5 days) IVIG (5 days)
Length of ICU Stay 7 days 8 days 157 days
Functional Status at
Discharge
Independent
ambulation
Wheelchair, partial leg
movement
Total dependency, no
motor or sensory
recovery
Hughes Scale at
Discharge Not documented Not documented Not documented
Current Functional
Status Full recovery
Orthotic-dependent,
mild coordination
deficit
Fully dependent, no
recovery
Note: The CVF value of 20 L in Case 3 was extracted directly from the original clinical record. This value is
physiologically inconsistent and likely a documentation error. It is presented here as recorded, but should be interpreted
with caution.*
The three patients were attended at different time points between 2017 and 2025 in a public
hospital in Ecuador. Clinical data were collected retrospectively using a standardized data
Vol. 12/ Núm. 3 2025 pág. 719
collection form validated for the diagnosis of Guillain-Barré Syndrome variants, including Acute
Motor Axonal Neuropathy (AMAN).
DISCUSSION
Guillain-Barré syndrome (GBS) is recognized as the leading cause of acute flaccid
paralysis in the post-polio era. Among its variants, acute motor axonal neuropathy (AMAN) is
characterized by rapid progression of motor weakness, absence of demyelinating features, and a
variable prognosis depending on early intervention and axonal preservation (Yuki & Hartung,
2012; Willison et al., 2016). The three clinical cases presented here demonstrate the heterogeneity
of AMAN in terms of onset, severity, treatment response, and functional outcomes.
Case 1 involved a high-performance military cyclist who exhibited an abrupt onset of
bilateral motor weakness following a gastrointestinal episode. The patient received early IVIG
therapy and was admitted to intensive care with an initial vital capacity of 0.88 L. Notably, he
responded favorably to treatment and achieved full recovery without residual deficits, returning
to baseline physical activity. This case aligns with previous literature emphasizing the importance
of early immunomodulatory treatment in reducing disease burden (Yuki & Hartung, 2012; Shi et
al., 2019). As shown in Figure 1, the patient's EMG demonstrates severe axonal loss without
evidence of demyelination, supporting a diagnosis of pure AMAN. These findings underscore the
potential for favorable outcomes in young, physically fit patients when treatment is administered
promptly.
Case 2, in contrast, illustrates an incomplete recovery despite early IVIG administration.
The patient, a 38-year-old with no significant prior comorbidities, presented with symmetrical
weakness and documented AMAN via electromyography on the day of admission. Although
respiratory compromise was avoided, the patient remained partially dependent on orthotic support
for ambulation at three months. The nerve conduction study (Figure 2) revealed axonal
involvement of both sensory and motor fibers, consistent with broader axonal injury. According
to Uncini et al. (2018), such cases may reflect a continuum between AMAN and AMSAN, leading
to a more protracted recovery. As outlined in Table 1, this case differed from Case 1 primarily in
EMG severity and delayed axonal regeneration.
Case 3 presented the most severe trajectory. A 27-year-old male with no previous systemic
disease developed ascending flaccid paralysis and required invasive ventilation, prolonged ICU
stay (157 days), and tracheostomy. He was discharged in a functionally dependent state and
remains wheelchair-bound. EMG findings (Figure 3) indicated complete loss of motor unit
potentials and absence of reflex arcs, consistent with extensive axonal degeneration. Infections
and prolonged critical illness neuropathy likely contributed to poor recovery (Willison et al.,
2016; Patone et al., 2021). This case illustrates the extreme end of the AMAN spectrum, where
collection form validated for the diagnosis of Guillain-Barré Syndrome variants, including Acute
Motor Axonal Neuropathy (AMAN).
DISCUSSION
Guillain-Barré syndrome (GBS) is recognized as the leading cause of acute flaccid
paralysis in the post-polio era. Among its variants, acute motor axonal neuropathy (AMAN) is
characterized by rapid progression of motor weakness, absence of demyelinating features, and a
variable prognosis depending on early intervention and axonal preservation (Yuki & Hartung,
2012; Willison et al., 2016). The three clinical cases presented here demonstrate the heterogeneity
of AMAN in terms of onset, severity, treatment response, and functional outcomes.
Case 1 involved a high-performance military cyclist who exhibited an abrupt onset of
bilateral motor weakness following a gastrointestinal episode. The patient received early IVIG
therapy and was admitted to intensive care with an initial vital capacity of 0.88 L. Notably, he
responded favorably to treatment and achieved full recovery without residual deficits, returning
to baseline physical activity. This case aligns with previous literature emphasizing the importance
of early immunomodulatory treatment in reducing disease burden (Yuki & Hartung, 2012; Shi et
al., 2019). As shown in Figure 1, the patient's EMG demonstrates severe axonal loss without
evidence of demyelination, supporting a diagnosis of pure AMAN. These findings underscore the
potential for favorable outcomes in young, physically fit patients when treatment is administered
promptly.
Case 2, in contrast, illustrates an incomplete recovery despite early IVIG administration.
The patient, a 38-year-old with no significant prior comorbidities, presented with symmetrical
weakness and documented AMAN via electromyography on the day of admission. Although
respiratory compromise was avoided, the patient remained partially dependent on orthotic support
for ambulation at three months. The nerve conduction study (Figure 2) revealed axonal
involvement of both sensory and motor fibers, consistent with broader axonal injury. According
to Uncini et al. (2018), such cases may reflect a continuum between AMAN and AMSAN, leading
to a more protracted recovery. As outlined in Table 1, this case differed from Case 1 primarily in
EMG severity and delayed axonal regeneration.
Case 3 presented the most severe trajectory. A 27-year-old male with no previous systemic
disease developed ascending flaccid paralysis and required invasive ventilation, prolonged ICU
stay (157 days), and tracheostomy. He was discharged in a functionally dependent state and
remains wheelchair-bound. EMG findings (Figure 3) indicated complete loss of motor unit
potentials and absence of reflex arcs, consistent with extensive axonal degeneration. Infections
and prolonged critical illness neuropathy likely contributed to poor recovery (Willison et al.,
2016; Patone et al., 2021). This case illustrates the extreme end of the AMAN spectrum, where
Vol. 12/ Núm. 3 2025 pág. 720
early intervention was insufficient to prevent long-term disability, possibly due to the magnitude
of the immune-mediated injury.
Comparative analysis of the three cases emphasizes the relevance of early diagnosis, timely
initiation of immunotherapy, and access to intensive rehabilitation services. While the
pathophysiology of AMAN centers on antibody-mediated ganglioside disruption at the nodes of
Ranvier, recent studies suggest that host factors such as genetic predisposition, physical
conditioning, and early respiratory involvement significantly modulate clinical outcomes (Uncini
et al., 2018; Willison et al., 2016). The disparities in recovery highlight the importance of
establishing prognostic biomarkers and individualized rehabilitation protocols in Latin American
contexts, where resource limitations are common.
This case series highlights the broad clinical and functional spectrum of AMAN,
underscoring that early administration of intravenous immunoglobulin (IVIG), while beneficial
in many cases, does not uniformly prevent poor outcomes—particularly in patients with extensive
axonal degeneration. The results emphasize the critical role of timely electrophysiological
assessments, such as EMG and vital capacity monitoring, to guide prognosis and intervention
strategies. Additionally, they draw attention to the pressing need for accessible post-acute
neurorehabilitation services and greater clinical awareness of AMAN subtypes in Latin America,
where diagnostic and therapeutic resources may be constrained.
CONCLUSION
In conclusion, this case series highlights the clinical variability and functional outcomes
associated with Acute Motor Axonal Neuropathy (AMAN) in Ecuadorian patients, primarily
following gastrointestinal infections. The cases presented demonstrate that while early
recognition and immunotherapy can lead to full recovery in some individuals, others may
experience partial improvement or persistent neurological disability despite timely intervention.
These findings reinforce the importance of neurophysiological confirmation in suspected cases
of AMAN and the need to consider this diagnosis in patients with acute flaccid paralysis,
particularly in post-infectious contexts. Strengthening access to diagnostic tools and
multidisciplinary rehabilitation services is essential to improving outcomes for patients with
immune-mediated neuropathies in Latin America.
Acknowledgements
The authors sincerely thank Infantry Captain Edison Mauricio Calahorrano Calahorrano
for his generous contribution in authorizing the use of his clinical case for academic and scientific
purposes. His decision to share his experience with the aim of improving awareness and
understanding of AMAN represents a commendable act of service to the medical community and
broader society.
early intervention was insufficient to prevent long-term disability, possibly due to the magnitude
of the immune-mediated injury.
Comparative analysis of the three cases emphasizes the relevance of early diagnosis, timely
initiation of immunotherapy, and access to intensive rehabilitation services. While the
pathophysiology of AMAN centers on antibody-mediated ganglioside disruption at the nodes of
Ranvier, recent studies suggest that host factors such as genetic predisposition, physical
conditioning, and early respiratory involvement significantly modulate clinical outcomes (Uncini
et al., 2018; Willison et al., 2016). The disparities in recovery highlight the importance of
establishing prognostic biomarkers and individualized rehabilitation protocols in Latin American
contexts, where resource limitations are common.
This case series highlights the broad clinical and functional spectrum of AMAN,
underscoring that early administration of intravenous immunoglobulin (IVIG), while beneficial
in many cases, does not uniformly prevent poor outcomes—particularly in patients with extensive
axonal degeneration. The results emphasize the critical role of timely electrophysiological
assessments, such as EMG and vital capacity monitoring, to guide prognosis and intervention
strategies. Additionally, they draw attention to the pressing need for accessible post-acute
neurorehabilitation services and greater clinical awareness of AMAN subtypes in Latin America,
where diagnostic and therapeutic resources may be constrained.
CONCLUSION
In conclusion, this case series highlights the clinical variability and functional outcomes
associated with Acute Motor Axonal Neuropathy (AMAN) in Ecuadorian patients, primarily
following gastrointestinal infections. The cases presented demonstrate that while early
recognition and immunotherapy can lead to full recovery in some individuals, others may
experience partial improvement or persistent neurological disability despite timely intervention.
These findings reinforce the importance of neurophysiological confirmation in suspected cases
of AMAN and the need to consider this diagnosis in patients with acute flaccid paralysis,
particularly in post-infectious contexts. Strengthening access to diagnostic tools and
multidisciplinary rehabilitation services is essential to improving outcomes for patients with
immune-mediated neuropathies in Latin America.
Acknowledgements
The authors sincerely thank Infantry Captain Edison Mauricio Calahorrano Calahorrano
for his generous contribution in authorizing the use of his clinical case for academic and scientific
purposes. His decision to share his experience with the aim of improving awareness and
understanding of AMAN represents a commendable act of service to the medical community and
broader society.
Vol. 12/ Núm. 3 2025 pág. 721
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REFERENCES
Jacobs, B. C., Rothbarth, P. H., van der Meché, F. G. A., Herbrink, P., Schmitz, P. I. M., de Klerk,
M. A., & van Doorn, P. A. (1998). The spectrum of antecedent infections in Guillain–Barré
syndrome: A case-control study. Neurology, 51(4), 1110–1115.
https://doi.org/10.1212/WNL.51.4.1110
Kuwabara, S., & Yuki, N. (2013). Axonal Guillain–Barré syndrome: Concepts and controversies.
The Lancet Neurology, 12(12), 1180–1188. https://doi.org/10.1016/S1474-
4422(13)70215-1
McGrogan, A., Madle, G. C., Seaman, H. E., & de Vries, C. S. (2009). The epidemiology of
Guillain–Barré syndrome worldwide: A systematic literature review. Neuroepidemiology,
32(2), 150–163. https://doi.org/10.1159/000184748
Patone, M., Handunnetthi, L., Saatci, D., Pan, J., Katikireddi, S. V., Razvi, S., ... & Hippisley-
Cox, J. (2021). Neurological complications after first dose of COVID-19 vaccines and
SARS-CoV-2 infection. Nature Medicine, 27(12), 2144–2153.
https://doi.org/10.1038/s41591-021-01556-7
Sejvar, J. J., Baughman, A. L., Wise, M., & Morgan, O. W. (2011). Population incidence of
Guillain–Barré syndrome: A systematic review and meta-analysis. Neuroepidemiology,
36(2), 123–133. https://doi.org/10.1159/000324710
Susuki, K., Yuki, N., Schafer, D. P., Hirata, K., Zhang, G., Funakoshi, K., ... & Rasband, M. N.
(2007). Dysfunction of nodes of Ranvier: A mechanism for anti-ganglioside antibody-
mediated neuropathies. Experimental Neurology, 206(2), 244–252.
https://doi.org/10.1016/j.expneurol.2007.05.030
Uncini, A., & Kuwabara, S. (2018). The electrodiagnosis of Guillain–Barré syndrome subtypes:
Where do we stand? Clinical Neurophysiology, 129(12), 2586–2593.
https://doi.org/10.1016/j.clinph.2018.08.034
Van den Berg, B., Walgaard, C., Drenthen, J., Fokke, C., Jacobs, B. C., & van Doorn, P. A.
(2014). Guillain–Barré syndrome: Pathogenesis, diagnosis, treatment and prognosis.
Nature Reviews Neurology, 10(8), 469–482. https://doi.org/10.1038/nrneurol.2014.121
Willison, H. J., Jacobs, B. C., & van Doorn, P. A. (2016). Guillain–Barré syndrome. The Lancet,
388(10045), 717–727. https://doi.org/10.1016/S0140-6736(16)00339-1
Yuki, N., & Hartung, H. P. (2012). Guillain-Barré syndrome. The New England Journal of
Medicine, 366(24), 2294–2304. https://doi.org/10.1056/NEJMra1114525