Case Report: Recurrent Guillain–Barré Syndrome in a 56‐Year‐Old Male

ABSTRACT

Recurrent Guillain–Barré syndrome (GBS) is an uncommon variant of immune‐mediated polyradiculoneuropathy. We report a 56‐year‐old male who had two distinct episodes of acute inflammatory demyelinating neuropathy within the span of 3 months. The first episode presented with an episode of ascending paralysis and areflexia, with nerve conduction studies showing marked demyelination. He showed improvement after six sessions of plasma exchange. Three months later, he had a second acute relapse following a diarrheal illness, again demonstrating demyelinating changes. The infectious and metabolic workups were unremarkable. He responded to repeat plasma exchange and required no ventilatory support. This case emphasizes the importance of recognizing recurrent GBS and distinguishing it from acute‐onset CIPD, as timely immunotherapy remains critical in treatment.

Key Clinical Message

Recurrent GBS is a rare but important consideration in patients with previous GBS episodes. Clinicians should maintain a high index of suspicion for recurrence, especially in those with antecedent infections. Early recognition and treatment can improve outcomes and reduce morbidity in these patients.

1. Introduction

Guillain–Barré syndrome (GBS) is an acute, immune‐mediated polyradiculoneuropathy characterized by rapidly progressive weakness and areflexia [1]. It is most often triggered by preceding respiratory or gastrointestinal infections, although vaccination and other immune stressors have also been implicated [1, 2]. The worldwide incidence is approximately 1–2 per 100,000 individuals per year, and while most patients experience a single monophasic illness, recurrence has been described in 2%–6% of cases [1, 2]. The exact epidemiology of recurrent GBS remains less well described due to its rarity. However, certain factors such as antecedent infections, immunological susceptibility, and specific electrophysiological subtypes may contribute to recurrence risk [2]. Recurrent GBS is defined by the occurrence of two or more discrete episodes separated by a period of near‐complete recovery [3]. Distinguishing recurrent GBS from chronic inflammatory demyelinating polyneuropathy (CIDP) is clinically important, as the management and prognosis differ significantly. We present the case of a 56‐year‐old man with two distinct episodes of acute inflammatory demyelinating polyneuropathy (AIDP), confirmed on neurophysiological studies, within a 3‐month period [4, 5].

2. Case History and Examination

A 56‐year‐old previously healthy man, with no history of diabetes, autoimmune disease, or prior neuropathy, presented with progressive weakness. Five days prior to admission, he developed dull lower back pain followed by progressive bilateral lower limb weakness that ascends to involve the upper limbs. There was no preceding respiratory or gastrointestinal illness, though he reported receiving the COVID‐19 vaccination in 2020. He denied recent surgery or toxin exposure. On examination, he was alert and oriented. The cranial nerves were intact. Motor examination revealed profound weakness: muscle power was 0/5 in both lower limbs and 1/5 in the upper limbs on the Medical Research Council (MRC) scale. He was unable to ambulate independently. Deep tendon reflexes were absent throughout, while sensory examination, including vibration and pinprick, was intact. No autonomic dysfunction was observed. These findings are consistent with the classical GBS presentation.

3. Methods (Differential Diagnosis, Investigations, and Treatment)

Routine laboratory investigations, including complete blood count, renal and liver function tests, thyroid profile, calcium, magnesium, phosphate, albumin, and serum potassium, were within normal limits. CSF analysis showed protein‐cytologic dissociation, with elevated protein of 3000 mg/dL (normal: 15–45 mg/dL) and a white blood cell count of 6 cells/mm³ (normal < 5 cells/mm³) [1, 2]. MRI of the lumbosacral spine revealed degenerative disc herniation, which was considered incidental. Nerve conduction studies demonstrated markedly reduced conduction velocities (Median nerve: 30.7 m/s; Ulnar: 27.0 m/s; Tibial: 22.8 m/s), absent F‐waves, and absent sensory responses, consistent with an acquired demyelinating polyneuropathy. Several alternative diagnoses were considered and excluded:

1. Cervical or lumbar myelopathy—excluded by normal sensory level, absence of sphincter involvement, and MRI showing only incidental disc disease without cord compression.

2. Electrolyte disturbances (hypokalemia, hypocalcemia, hypophosphatemia, hypomagnesemia)—ruled out by normal laboratory values.

3. Myasthenia gravis—less likely due to symmetrical ascending weakness, areflexia, and absence of fatigability or ocular involvement.

4. Botulism—ruled out by absence of bulbar palsy, pupillary involvement, or autonomic instability.

5. Acute transverse myelitis—excluded by normal sensory function, no spinal cord lesion on imaging, and preserved bowel/bladder function.

He underwent six sessions of plasma exchange, which is the first‐line treatment in GBS. Each session involved the exchange of approximately 40 mL/kg of body plasma volume with replacement fluids (5% albumin and normal saline). He tolerated the procedure without complications. Progressive clinical improvement was noted, and by 2 months he had regained independent ambulation.

3 months after the first attack, the patient presented again with acute onset weakness following a three‐day history of watery diarrhea. This time, he also reported mild shortness of breath and nasal flaring on exertion. During the second episode, weakness progressed rapidly over 4 days and reached maximum severity within 1 week. Examination revealed quadriparesis, with muscle power graded at 1/5 in the upper limbs and 0/5 in the lower limbs. Head holding was sustained only for 30 s. Reflexes were absent throughout, cranial nerves remained intact, and sensory modalities were preserved. The autonomic function was stable. Repeat serum electrolytes, calcium, phosphate, magnesium, thyroid function, and albumin levels were normal. Infectious screening including HIV, hepatitis B and C, CMV, and EBV were negative; stool cultures for Campylobacter were pending. Repeat NCS/EMG findings were consistent with demyelinating polyneuropathy, showing persistent conduction slowing, absent F‐waves, and reduced sensory responses. Differential diagnosis of CIDP was considered but excluded given the acute monophasic course (< 4 weeks to nadir), full recovery between episodes, and distinct relapses separated by remission. Thus, the clinical, electrophysiological, and recovery pattern supported a diagnosis of recurrent AIDP subtype of GBS.

The patient was initiated on a second course of plasma exchange and completed three sessions at the time of reporting, with gradual recovery in muscle strength. He did not require mechanical ventilation during either episode.

The patient reported significant emotional distress during recurrence due to fear of permanent paralysis. He expressed reassurance after receiving treatment and reported satisfaction with functional recovery.

4. Results and Outcome

Functional disability was assessed using the Guillain‐Barre Disability Scale [GBS‐DS] [6]. Retrospectively estimated, during the first episode, the patient had a GBS‐DS score of 4 that implies bedridden or chair‐bound. Following six sessions of plasma exchange, he improved to a GBS‐DS score of 2 at 2 months, regaining independent ambulation.

During the second episode, his GBS‐DS score again reached 4 at nadir. After repeating plasma exchange, gradual improvement was observed. At 6‐month follow‐up from the initial presentation, i.e., 3 months after the second episode, he was ambulatory with mild residual lower limb weakness [GBS‐DS score of 2]. No further relapses occurred during follow‐up. The timeline of events is shown in Table 1.

TABLE 1.

Timeline of events.

Event	Time point	Clinical details
Episode 1 onset	Day 0.	Progressive ascending weakness over 5 days.
Hospital admission	Day 5.	Quadriparesis (LL 0/5, UL 1/5), Areflexia.
Treatment 1	Week 1.	6 sessions of plasma exchange.
Recovery	2 months after the first episode.	Independent ambulation was regained.
Symptom‐free interval	4 weeks after recovery.	Full functional recovery.
Episode 2 onset	3 months after the first episode.	Acute quadriparesis after diarrheal illness.
Second hospital admission	3 months after the first episode.	Rapidly progressive quadriparesis after acute diarrheal illness, reflexes absent and respiratory effort mildly affected.
Treatment 2	After admission.	Repeat plasmapheresis.
Follow‐up	6 months total follow‐up.	Gradual recovery, ambulatory with mild residual weakness.

5. Discussion

Recurrent GBS is rare but recognized in 2%–6% of patients [1, 2]. The hallmark features are discrete episodes of acute flaccid paralysis, each reaching maximum severity within 4 weeks [4, 5]. This was followed by substantial recovery and subsequent relapse after a variable symptom‐free interval. Our patient experienced two attacks separated by a three‐month period of complete recovery.

It remains unclear why a subset of patients experience recurrence. Potential mechanisms include repeated exposure to immunological triggers or persistence of autoreactive memory T‐cells and antibodies against gangliosides [2]. In this case, the first episode was not clearly associated with infection, while the second followed a diarrheal illness.

The immunopathogenesis of recurrent GBS is not completely understood. Proposed mechanisms include persistence of autoreactive memory lymphocytes, repeated exposure to infectious triggers, and molecular mimicry leading to renewed antiganglioside antibody production through molecular mimicry [2]. The diarrheal illness before the second episode may represent a triggering immune stimulus.

Treatment‐related fluctuation [TRF] in GBS is defined as clinical deterioration occurring within 8 weeks of onset after initial stabilization. In contrast, our patient experienced a second episode approximately 12 weeks after the first onset, following a complete functional recovery interval. This temporal separation makes TRF less likely [7]. While TRF occurs in approximately 10% of patients, true recurrence is significantly rarer. Recent large‐scale cohort data and systematic reviews estimate the recurrence rate of GBS to be between 1% and 5% [2]. Our patient's 12‐week interval and complete recovery significantly exceed the standard 8‐week TRF window, aligning with these epidemiological definitions of RGBS [2].

Acute‐onset CIDP typically presents progression beyond 8 weeks or with multiple relapses without full recovery [5]. In this case, both episodes reached nadir within 4 weeks, were separated by complete recovery, and demonstrated no chronic progression, supporting recurrent GBS rather than CIDP.

Electrophysiological findings in both episodes revealed severe demyelination with absent F‐waves and slowed conduction velocities, aligned with AIDP. The absence of autonomic instability in both episodes is noteworthy, as dysautonomia is present in up to two‐thirds of classic GBS cases [1].

Management of recurrent GBS is similar to that of primary GBS, with intravenous immunoglobulin (IVIG) and plasma exchange being equally effective as first‐line therapies. Our patient underwent plasma exchange in both episodes, which led to gradual functional recovery. Plasma exchange was selected due to institutional availability and the patient's favorable response during the first episode. Both plasma exchange and intravenous immunoglobulin (IVIG) are considered equally effective first‐line therapies for Guillain–Barré syndrome according to current evidence‐based guidelines [3]. According to the American Academy of Neurology (AAN) guidelines, corticosteroids are not recommended as they have not demonstrated benefit in GBS [3]. Comparison of our case with previously reported cases is presented in Table 2.

TABLE 2.

Comparison of present case with previously reported cases of recurrent GBS.

Author (Year)	Age/Sex	Interval between episodes	Clinical variant	Trigger	Treatment	Outcome
Kuitwaard et al. (2009) [8]	45 year old/M	6 years	AIDP → AIDP	URI	IVIG	Full recovery
Ruts et al. (2010) [5]	Multiple cases	Variable	GBS vs. CIDP overlap	Variable	IVIG/PLEX	Variable
Present Case	56 year old/M	3 months	AIDP → AIDP	Diarrheal illness	Plasmapheresis	Full recovery

5.1. Strengths and Limitations

The strength of this report lies in the documentation of two clinically and electrophysiologically confirmed demyelinating episodes within a short interval. Limitations include the absence of antiganglioside antibody testing and a relatively short follow‐up duration.

6. Conclusion

This case highlights the diagnostic challenge of recurrent GBS, particularly in distinguishing it from CIDP and other acute neuromuscular disorders. Vigilant follow‐up is essential, as recurrence can occur after complete recovery. Prompt initiation of immunotherapy and supportive care remains the cornerstone of management to minimize morbidity.

Author Contributions

Farah Sadiq: conceptualization, validation, visualization. Moeez Ahmad Saeed: validation, visualization, writing – original draft, writing – review and editing. Shayan Nawaz: visualization, writing – original draft. Fahad Bilal: conceptualization, writing – original draft, writing – review and editing. Kashaf Imtiaz: conceptualization, writing – original draft, writing – review and editing. Ali Gohar: writing – original draft, writing – review and editing. Hafiza Manahil Majeed: conceptualization, validation, visualization. Wasfa Shafiq: validation, writing – original draft, writing – review and editing. Muhammad Husnain Ahmad: validation, visualization.

Funding

The authors have nothing to report.

Ethics Statement

The authors have nothing to report.

Consent

A written informed consent was obtained from the patient based on the journal's policies.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The authors have nothing to report.