Is Guillain-Barré Syndrome (GBS) characterized by flaccid paralysis?

Yes, Guillain-Barré Syndrome is Characterized by Flaccid Paralysis

GBS is definitively a flaccid paralysis syndrome, characterized by acute, areflexic, bilateral weakness with reduced or absent reflexes—this is a core diagnostic feature that distinguishes it from upper motor neuron disorders. 1, 2

Core Clinical Features of Flaccid Paralysis in GBS

The flaccid nature of GBS paralysis manifests through several key characteristics:

• Acute areflexic weakness is the hallmark presentation, with decreased or absent reflexes present in most patients at presentation and almost all at nadir 2
• Bilateral ascending weakness typically starts in the legs and progresses to arms and cranial muscles, representing the classic pattern of lower motor neuron involvement 2
• Hypotonia and muscle flaccidity occur due to peripheral nerve dysfunction affecting motor neurons, as opposed to the spasticity seen in upper motor neuron lesions 3

Why GBS Produces Flaccid Rather Than Spastic Paralysis

The pathophysiology explains the flaccid presentation:

• Peripheral nervous system involvement causes demyelination or axonal damage to motor nerves, interrupting the connection between spinal cord and muscles 1
• Lower motor neuron dysfunction results in loss of muscle tone and reflexes, contrasting with central nervous system lesions that produce hyperreflexia and spasticity 3
• Polyradiculoneuropathy affects nerve roots and peripheral nerves, not the corticospinal tracts, which is why upper motor neuron signs are absent 1

Critical Diagnostic Distinction

Ascending bilateral symmetric flaccid weakness with areflexia strongly suggests GBS, while descending flaccid paralysis starting with cranial nerves indicates botulism until proven otherwise. 2

This distinction is clinically crucial:

• GBS pattern: Legs → arms → cranial nerves with areflexia 2
• Botulism pattern: Cranial nerves → trunk → extremities, also flaccid but descending 2, 4
• Preserved or normal reflexes with flaccid paralysis should raise suspicion for botulism or myasthenia gravis rather than GBS 2

Clinical Implications of Flaccid Paralysis

The flaccid nature of GBS paralysis creates specific clinical challenges:

• Respiratory muscle weakness develops in approximately 20% of patients, requiring mechanical ventilation, and can occur rapidly without obvious dyspnea 2, 5, 6
• Bulbar muscle involvement causes dysphagia and aspiration risk due to flaccid pharyngeal muscles 1
• Autonomic dysfunction frequently accompanies the flaccid paralysis, causing blood pressure instability and cardiac arrhythmias 2, 6

Variants and Subtypes

All GBS subtypes produce flaccid paralysis, though distribution varies:

• Classic sensorimotor GBS (30-85% of cases) presents with rapidly progressive symmetric flaccid weakness and sensory signs 1
• Pure motor variant (5-70% depending on region) shows flaccid weakness without sensory involvement 1
• Miller Fisher syndrome demonstrates flaccid ophthalmoplegia with ataxia and areflexia 1, 2
• Regional variants including pharyngeal-cervical-brachial weakness show localized flaccid paralysis patterns 1, 2

Monitoring and Management Considerations

The flaccid paralysis requires specific monitoring:

• Vital capacity and negative inspiratory force must be assessed serially to detect impending respiratory failure from flaccid respiratory muscles 2
• Patients are at imminent risk when vital capacity falls below 20 ml/kg or maximum inspiratory pressure is less than 30 cmH₂O 6
• Continuous cardiac monitoring is essential as autonomic involvement can cause life-threatening arrhythmias alongside the flaccid paralysis 2, 6