Guillain-Barré syndrome (GBS) is an acute immune-mediated disorder of the peripheral nervous system in which autoantibodies — triggered by molecular mimicry between pathogen surface antigens and peripheral nerve gangliosides — attack the myelin sheath or axons of spinal nerve roots and peripheral nerves, producing a characteristic pattern of rapidly ascending symmetric limb weakness, hyporeflexia or areflexia, and variable sensory disturbance that reaches its nadir within 4 weeks of onset. It is distinguished from chronic inflammatory demyelinating polyneuropathy (CIDP) by its time course — GBS is monophasic and self-limiting, progressing to nadir within 4 weeks and then plateauing, whereas CIDP progresses or relapses over more than 8 weeks — and from transverse myelitis by its peripheral (rather than spinal cord) localization and the absence of a sensory level or bowel/bladder dysfunction in classic presentations. The pathophysiological mechanism varies by subtype: the most common form, AIDP (acute inflammatory demyelinating polyneuropathy), involves T-cell and antibody-mediated demyelination of nerve roots and proximal nerves; the axonal variants AMAN and AMSAN involve direct complement-mediated axonal injury, typically driven by anti-GM1 or anti-GD1a antibodies following Campylobacter jejuni infection; and Miller Fisher syndrome (MFS) is defined by the triad of ophthalmoplegia, ataxia, and areflexia driven by anti-GQ1b antibodies. The cerebrospinal fluid (CSF) finding of albuminocytologic dissociation — elevated protein with normal white cell count — is the hallmark laboratory abnormality and supports the diagnosis, though it may be absent in the first week of illness. In ICD-10-CM, all subtypes including AIDP, AMAN, AMSAN, and Miller Fisher syndrome map to the single billable code G61.0 — there are no separate codes for subtype specificity — making detailed clinical documentation essential for research and quality metrics even though it does not change the code assignment.
French neurologist at the Salpêtrière Hospital, Paris; co-described the syndrome in a landmark 1916 paper reporting on two French soldiers with ascending paralysis and the characteristic CSF finding
Barré
Jean Alexandre Barré (1880-1967)
French neurologist; co-author of the 1916 paper; contributed clinical electrophysiological and CSF characterization of the syndrome
syndrome
French syndrome, from Greek σύνδρομον (súndromon), from syn- (“together”) + dromos (“running, course”)
“running together” — a cluster of signs and symptoms that concurrently characterize a disease condition
Guillain-Barré syndrome is an eponym — a condition named for the clinicians who described it — not a term with roots in anatomical or pathophysiological Greek/Latin terminology. The condition was first described by French physician Jean-Baptiste Octave Landry in 1859, who documented the pattern of ascending paralysis now bearing his name (Landry’s ascending paralysis). The formal characterization with CSF findings was published in 1916 by Georges Guillain, Jean Alexandre Barré, and André Strohl, who described two French soldiers during World War I — notably, Strohl’s contributions to the electrophysiological characterization have been historically underrecognized and he is absent from the modern eponym. The syndrome has also been called Guillain-Barré-Strohl syndrome in some European literature in recognition of this omission. The acronym GBS is universally used in clinical, billing, and research contexts. The medical root family underlying the condition’s pathophysiology — poly- + neuro- + -pathy — generates the formal pathological name acute inflammatory demyelinating polyneuropathy (AIDP), linking GBS to the broader polyneuropathy and radiculopathy terminology families.
🔀 ALIASES / ALTERNATE TERMS
GBS(universal clinical acronym; used in all settings — inpatient, outpatient, rehab, billing, and research — as the shorthand for Guillain-Barré syndrome)
AIDP (Acute Inflammatory Demyelinating Polyneuropathy)(the most common subtype, ~85-90% of GBS cases in Western countries; demyelinating pattern on NCS; anti-ganglioside antibodies variable; treated with IVIG or plasmapheresis; codes G61.0)
AMAN (Acute Motor Axonal Neuropathy)(axonal variant; pure motor involvement; associated with anti-GM1/GD1a antibodies; strongly associated with Campylobacter jejuni infection; more common in Asia; codes G61.0)
AMSAN (Acute Motor and Sensory Axonal Neuropathy)(axonal variant with both motor and sensory involvement; more severe course; higher rate of residual deficits; codes G61.0)
Miller Fisher syndrome (MFS)(the classic triad of ophthalmoplegia, ataxia, and areflexia; anti-GQ1b antibody positive in ~90%; ICD-10-CM explicitly includes MFS as an inclusion term under G61.0)
Landry’s ascending paralysis(historical eponym for the clinical pattern of ascending flaccid paralysis; the original 1859 description by Jean-Baptiste Octave Landry; now synonymous with GBS in ICD-10-CM indexing; codes G61.0)
Acute (post-)infective polyneuritis(ICD-10-CM inclusion term under G61.0; used in documentation when the provider links GBS to a preceding infection — most commonly Campylobacter jejuni, cytomegalovirus, EBV, or SARS-CoV-2)
Acute idiopathic polyradiculoneuritis(alternate clinical descriptor emphasizing the nerve root [radicular] involvement; maps to G61.0; highlights that the pathology begins at the most proximal nerve roots before spreading distally)
CIDP (Chronic Inflammatory Demyelinating Polyneuropathy)(the chronic relapsing/progressive counterpart to GBS; defined by progression or relapse beyond 8 weeks; coded G61.81 — a distinct billable code, NOT G61.0; critical differential in coding and clinical management)
🔗 RELATED TERMS
CIDP (Chronic Inflammatory Demyelinating Polyneuropathy) — the chronic counterpart of GBS; defined by a disease course exceeding 8 weeks with progressive or relapsing-remitting course; coded G61.81, not G61.0; the most clinically critical distinction for coding — a patient initially coded G61.0 who continues to deteriorate beyond 8 weeks should trigger a provider query to re-evaluate whether CIDP is the correct diagnosis
Albuminocytologic dissociation — the hallmark CSF finding in GBS: elevated protein (typically >45 mg/dL, often dramatically elevated) with a normal white cell count (<10 cells/µL); absent in the first week in up to 50% of cases; confirmed by lumbar puncture coded 62270
Demyelination — destruction or loss of the myelin sheath surrounding peripheral nerve axons; the primary pathological mechanism in AIDP; results in slowed nerve conduction velocities and conduction block on NCS; distinguished from the axonal injury seen in AMAN/AMSAN
Areflexia — absence of deep tendon reflexes; a cardinal clinical feature of GBS; reflects disruption of the monosynaptic reflex arc at the level of the nerve root or peripheral nerve; coded as a sign/symptom R29.2 when documented independently
Molecular mimicry — the immunological mechanism underlying GBS in which structural similarity between pathogen surface antigens (e.g., Campylobacter lipooligosaccharides) and peripheral nerve gangliosides (GM1, GD1a, GQ1b) triggers cross-reactive autoantibody production
Campylobacter jejuni — the most common identified infectious trigger for GBS, preceding ~25-30% of cases; the C. jejuni infection itself is coded A04.5 when documented; GBS onset follows diarrheal illness by 1-3 weeks
Anti-GQ1b antibodies — highly specific autoantibodies (present in ~90% of MFS cases) targeting the GQ1b ganglioside, which is concentrated in the paranodal regions of oculomotor and other cranial nerve myelin; the confirmatory serological test for Miller Fisher syndrome
Ascending paralysis — the classic clinical pattern of GBS progression: weakness beginning symmetrically in the distal lower extremities and ascending proximally toward the trunk, respiratory muscles, and cranial nerves; the “20-30-30 rule” estimates 20% of patients require mechanical ventilation
Autonomic dysfunction (GBS) — dysregulation of autonomic nervous system function occurring in up to 70% of GBS patients; manifests as cardiac arrhythmias, blood pressure lability, ileus, urinary retention, and diaphoresis; a major driver of ICU-level care and inpatient resource utilization
Respiratory failure — the most life-threatening complication of GBS; occurs when ascending weakness involves the diaphragm and intercostal muscles; approximately 20-30% of patients require mechanical ventilation; coded J96.01 (acute with hypoxia) or J96.02 (acute with hypercapnia) as an additional code, sequenced after G61.0 per etiology/manifestation convention
Dysphagia (neurogenic) — impaired swallowing due to cranial nerve involvement (CN IX, X, XII) in GBS; coded R13.10 or R13.19 as an additional code; a clinical indicator of bulbar involvement and aspiration risk that often drives SLP consultation and PEG placement decisions on inpatient profee claims
Plasmapheresis / Plasma exchange — first-line immunotherapy for GBS; removes circulating autoantibodies and complement from the plasma; coded CPT 36514; typically administered as 5 sessions over 1-2 weeks; supported by Class I evidence equally alongside IVIG
IVIG (Intravenous Immunoglobulin) — first-line immunotherapy for GBS; replaces pathological autoantibodies and modulates immune response; administered 0.4 g/kg/day × 5 days or 1 g/kg/day × 2 days; coded CPT 96365 (initial hour) + 96366 (each additional hour); HCPCS J-code for the drug billed separately
Nerve conduction study (NCS) — the primary electrodiagnostic tool for confirming GBS and differentiating demyelinating from axonal subtypes; shows reduced conduction velocities and conduction block in AIDP vs. reduced amplitude with preserved velocity in AMAN/AMSAN; coded 95907-95913 by number of studies
Serum neuropathy (post-vaccination neuropathy — if GBS is triggered by vaccine, still code G61.0 per ICD-10-CM index; G61.1 is reserved for direct serum-injection neuropathy)
G61.81
Chronic inflammatory demyelinating polyneuropathy (CIDP — the chronic form; distinct code, NOT G61.0; assign when course exceeds 8 weeks)
G61.82
Multifocal motor neuropathy (MMN — distinct entity with anti-GM1 IgM antibodies; asymmetric motor neuropathy; do NOT confuse with AMAN)
G61.89
Other inflammatory polyneuropathies
G61.9
Inflammatory polyneuropathy, unspecified
Respiratory Complications (Assign as Additional Codes with G61.0)
Code
Description
J96.00
Acute respiratory failure, unspecified whether with hypoxia or hypercapnia
Nerve conduction studies; 13 or more studies (comprehensive bilateral upper and lower extremity NCS panel — standard for GBS electrodiagnostic workup to characterize demyelinating vs. axonal subtype)
95912
Nerve conduction studies; 11-12 studies
95911
Nerve conduction studies; 9-10 studies
+95886
Needle EMG, each extremity, with NCS; complete (5 or more muscles) — add-on to NCS code; per extremity; used to assess denervation and axonal loss severity
62270
Spinal puncture, lumbar, diagnostic (lumbar puncture for CSF analysis; confirms albuminocytologic dissociation; required for GBS workup documentation)
36514
Therapeutic apheresis; for plasmapheresis (plasma exchange — first-line GBS treatment; typically 5 sessions; each session billed separately; verify payer prior authorization requirements)
IV infusion, therapy/prophylaxis/diagnosis; initial, up to 1 hour (IVIG administration — initial hour; pair with HCPCS J-code for the immunoglobulin product e.g., J1459, J1556)
+96366
IV infusion; each additional hour (add-on to 96365; IVIG infusions typically run 4-6 hours; document infusion start and stop times)
71046
Radiologic examination, chest; 2 views (baseline and serial chest X-rays to monitor respiratory status and aspiration risk)
94760
Noninvasive ear or pulse oximetry for oxygen saturation; single determination (serial O₂ sat monitoring in GBS respiratory monitoring)
Therapeutic activities (15 min); functional movement retraining — PT/OT during GBS rehabilitation
92526
Treatment of swallowing dysfunction and/or oral function for feeding (SLP treatment for GBS-related dysphagia and bulbar weakness)
⚠️ Coding Note:G61.0 is the sole ICD-10-CM code for all recognized GBS subtypes — AIDP, AMAN, AMSAN, Miller Fisher syndrome, Landry’s ascending paralysis, and acute post-infective polyneuritis all index to G61.0 per the ICD-10-CM Alphabetic Index and Tabular instructions; document the subtype clearly in the medical record for clinical quality purposes even though it does not affect code assignment. The most critical inpatient profee undercoding alert for GBS: when a patient with G61.0 develops respiratory failure requiring intubation or mechanical ventilation, respiratory failure (J96.01 or J96.02) must be assigned as an additional code — this is a CC/MCC-level complication that significantly impacts MS-DRG assignment and is missed on a high proportion of GBS inpatient profee claims when the focus is solely on the neurological diagnosis; the documentation trigger is any provider note referencing “intubated,” “mechanical ventilation,” “respiratory decompensation,” “VC < 20 mL/kg,” or “20-30-30 rule.” For IVIG billing (96365/+96366), the infusion administration codes report the service itself — the immunoglobulin product (e.g., J1459 Immune globulin, Privigen; J1556 Immune globulin, Bivigam) must be billed separately via HCPCS J-code; most payers require a prior authorization and documented diagnosis of G61.0 before approving inpatient or outpatient IVIG for GBS. GBS vs. CIDP coding split: if a patient initially coded G61.0 continues to deteriorate or fails to plateau by 8 weeks, query the provider to evaluate for CIDP (G61.81) — this is a direct recode situation with DRG and treatment-authorization implications. Do not code the preceding infection (e.g., A04.5 Campylobacter) as the principal diagnosis on a GBS admission — G61.0 is the reason for the encounter; the infection is an additional code if still clinically active.
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