This test looks for autoantibodies that target ganglionic nicotinic acetylcholine receptors (α3-AChR)—key “signal docks” inside the autonomic nervous system, which controls involuntary functions like blood pressure, heart rate, sweating, digestion, and bladder function.
If your immune system makes these antibodies, it can disrupt autonomic signaling and cause dysautonomia. The most specific condition is Autoimmune Autonomic Ganglionopathy (AAG).
Why Doctors Order It
Your clinician may order this test if you have unexplained autonomic symptoms, such as:
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Orthostatic hypotension (lightheadedness or fainting when standing)
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Dry mouth / dry eyes
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Abnormal sweating (too much or too little)
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Digestive issues (constipation, nausea, bloating, early fullness)
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Bladder problems (retention, urgency, incontinence)
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Pupil abnormalities (light sensitivity, blurry vision)
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Erectile dysfunction or heart-rate/blood-pressure instability
It’s also used when clinicians suspect paraneoplastic (cancer-related) neurologic disease—most often with small cell lung cancer or thymoma.
Typical Reference Range
Ranges vary by lab. Common interpretations:
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Negative: < 0.02 nmol/L
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Borderline / Indeterminate: 0.02–0.05 nmol/L
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Positive: > 0.05 nmol/L
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High positive (often more specific for AAG): > 0.20 nmol/L
Always interpret your exact value using the reference interval on your report.
Understanding Your Results
If Your Result is Elevated / Positive
What it suggests:
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Supports an autoimmune cause of dysautonomia, most notably AAG.
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Higher titers often track with more severe or widespread autonomic involvement, though exceptions exist.
What to do next:
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Share the result with your clinician. They may recommend:
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Autonomic function testing (tilt-table, QSART/sweat testing, heart-rate variability)
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Targeted cancer screening (e.g., CT chest, PET/CT, or other imaging) to rule out paraneoplastic causes
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Expanded autoantibody panels (paraneoplastic/neuronal antibodies)
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Discuss immunotherapy options where appropriate: IVIG, plasma exchange, corticosteroids, or steroid-sparing agents (e.g., rituximab, mycophenolate, azathioprine).
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Symptom-focused care for blood pressure, GI motility, bladder function, and temperature/sweating can improve daily life.
Practical tips while you wait for care:
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For orthostatic symptoms: rise slowly, hydrate well, consider compression stockings, and ask about salt/fluid strategies if safe for you.
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Track blood pressure and symptom patterns to share with your clinician.
If Your Result is Borderline / Indeterminate
What it suggests:
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Low-level positivity can occur with limited or early disease, other autoimmune conditions, or occasionally without clear disease.
What to do next:
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Correlate with symptoms and autonomic testing.
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Your clinician may repeat the test or add related antibody panels.
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Continue evaluation for common non-autoimmune causes of similar symptoms (medications, dehydration, diabetes, Parkinsonian syndromes, etc.).
If Your Result is Negative
What it suggests:
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Makes antibody-mediated AAG less likely, but does not fully exclude it. A minority of patients can be seronegative.
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Think broadly: medication side effects, volume depletion, neuropathies (e.g., diabetes), POTS, neurodegenerative conditions.
What to do next:
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If symptoms persist or are severe, ask about autonomic function testing, alternative antibodies, and evaluation for other causes of dysautonomia.
Related / Reflex Tests
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Autonomic reflex screen (tilt-table, QSART, heart-rate variability to deep breathing/Valsalva)
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Paraneoplastic antibody panel (e.g., anti-Hu/ANNA-1, CRMP-5, etc.)
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Cancer screening when clinically indicated (CT chest, PET/CT, mammography, colonoscopy, based on age/risk)
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Basic labs to rule out mimics: CBC, CMP, fasting glucose/HbA1c, B12, TSH, SPEP, autoimmune panels
Conditions Linked to Positive Ganglionic AChRAb
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Autoimmune Autonomic Ganglionopathy (AAG)
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Paraneoplastic autonomic neuropathy (notably small cell lung carcinoma)
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Thymoma-associated autoimmunity
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Occasionally seen with other systemic autoimmune diseases
Treatment & Outlook
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Many patients benefit from immunotherapy (IVIG, plasma exchange, corticosteroids; selected cases: rituximab or other immunosuppressants).
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Symptom-targeted therapies (midodrine, droxidopa, fludrocortisone for orthostatic hypotension; pro-motility agents for GI symptoms; bladder protocols) improve quality of life.
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Monitoring titers over time can help some clinicians track disease activity, but symptom changes and autonomic testing usually guide treatment decisions.
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Some patients recover partially or fully; others may have a chronic or relapsing course.
FAQs
Is a high titer always severe disease?
No. Higher levels often correlate with severity, but not perfectly. Clinical evaluation remains essential.
Can I have AAG with a negative test?
Yes—seronegative AAG exists. Diagnosis relies on symptoms + autonomic testing, not the antibody alone.
Should everyone with a positive test get cancer screening?
Your clinician will tailor screening to your age, risks, and symptoms, but a thoughtful search is common with positive results, especially at higher titers.
How fast do treatments work?
Response varies by therapy and disease severity. Some patients notice improvement within weeks, others months. Ongoing follow-up is important.
How to Use Your Result
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Match the number to your lab’s reference range.
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Document your symptoms (when they start, what triggers/worsens them).
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Share the result with your healthcare provider and discuss next steps (testing, screening, treatment).
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Track progress: blood pressure logs, hydration, and symptom diaries can guide care.
Safety Note
Seek urgent care for fainting with injury, chest pain, severe dehydration, or sudden neurologic changes.
What does it mean if your Ganglionic AChRab, Serum result is too high?
A high Ganglionic Acetylcholine Receptor Antibody (Ganglionic AChRAb) suggests an autoimmune cause of dysautonomia, most specifically Autoimmune Autonomic Ganglionopathy (AAG) or a paraneoplastic autonomic neuropathy. Titer (how high the number is) can correlate with severity, but clinical context is essential.
What “Elevated” Means
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Positive (> your lab’s cutoff, often >0.05 nmol/L): Supports an immune attack on ganglionic nicotinic AChR (α3) in autonomic ganglia.
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Higher-positive (e.g., >0.20 nmol/L): More strongly associated with AAG and moderate–severe autonomic failure, though exceptions occur.
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Borderline/low-positive: May indicate early/limited disease or overlap with other autoimmune conditions; repeat testing and clinical correlation are key.
Always interpret using the reference range printed on your report, as cutoffs vary by lab.
Why Levels Can Be High
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Autoimmune Autonomic Ganglionopathy (AAG) – primary association.
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Paraneoplastic autonomic neuropathy – most often linked to small cell lung carcinoma (SCLC); also reported with thymoma and some other malignancies.
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Other autoimmunity – occasionally seen with systemic autoimmune diseases (context-dependent).
Symptoms Often Seen with Elevated Results
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Cardiovascular: orthostatic hypotension (dizziness/fainting on standing), heart-rate variability.
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Sweat/temperature: too little or too much sweating, heat intolerance.
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Gastrointestinal: constipation, early satiety, nausea, bloating.
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Genitourinary: urinary retention, urgency, incontinence; erectile dysfunction.
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Eyes/pupils: light sensitivity, blurry vision.
Important Considerations
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Serology ≠ diagnosis: Some patients with classic AAG are seronegative, and some with low-positive results may have limited disease.
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Medications and mimics: Dehydration, diabetes neuropathy, Parkinsonian syndromes, medication side effects, and POTS can produce overlapping symptoms and should be reviewed.
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Trend, not just a point: Serial measurements may help track disease activity in context with symptoms and formal autonomic testing.
What to Do Next (Action Plan)
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Share the result with your clinician and review your full symptom history (include blood pressure/symptom logs).
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Autonomic testing: Tilt-table, QSART/sudomotor testing, heart-rate variability (deep breathing/Valsalva), pupillometry where available.
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Targeted cancer evaluation if clinically appropriate (especially with higher titers or red flags): CT chest, PET/CT, age-appropriate screenings.
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Extended antibody panels: Paraneoplastic and neuronal antibodies (e.g., anti-Hu/ANNA-1, CRMP-5) when suspicion is higher.
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Manage complications now:
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Orthostatic hypotension: fluid/salt strategies if safe, compression garments, head-of-bed elevation; discuss fludrocortisone, midodrine, or droxidopa with your clinician.
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GI dysmotility: nutrition/hydration planning; prokinetics as appropriate.
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Bladder dysfunction: timed voids, urology referral if needed.
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Treatment Pathways Often Discussed
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Immunotherapy: IVIG, plasma exchange, corticosteroids; in selected cases rituximab or other steroid-sparing agents.
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Symptom-directed care: BP support agents, GI motility treatments, bladder protocols, temperature/sweat management.
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Monitoring: Symptom diaries + periodic autonomic testing; consider repeating antibody titers per clinician guidance.
Questions to Ask Your Clinician
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Does my titer level change the urgency or type of evaluation?
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Which autonomic tests are most informative for my symptoms?
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Do I need cancer screening now? If so, which studies?
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Which immunotherapy is most appropriate for my situation, and how will we measure response?
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What at-home strategies can reduce fainting risk and GI/bladder symptoms?
When to Seek Urgent Care
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Recurrent fainting with injury, chest pain, signs of severe dehydration, or sudden, rapidly worsening neurologic symptoms.
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