Orthostatic symptoms, which include lightheadedness, dizziness, or syncope upon standing and loss of postural reflex tachycardia, occur in 78% of patients.

[1] Constipation or diarrhea, emesis, anorexia, early satiety, and abdominal pain are common symptoms of gastrointestinal dysmotility, which affects 70% of patients.

[1] Although about a quarter of patients report neuropathic symptoms such as tingling in the distal extremities, sensory examination and nerve conduction studies are normal.

In idiopathic AAG, the body's own immune system targets a receptor in the autonomic ganglia, which is part of a peripheral nerve fiber.

[3] Antibodies against the neuronal nicotinic acetylcholine receptor found in autonomic ganglia are present in approximately 50% of AAG patients.

Mice with genetically engineered null mutations in the 3 subunit have reduced autonomic ganglionic transmission, resulting in urinary retention, dilated and nonreactive pupils, and higher mortality rates.

Active immunization of rabbits against the 3 subunit results in gastrointestinal hypomotility, urinary retention, and a reduced number of gACh receptors on postsynaptic ganglionic neurons, as well as impaired synaptic transmission.

Some individuals with paraneoplastic autonomic neuropathy have ganglionic AChR antibodies, therefore occult small cell carcinoma or thymoma should be explored.

[1] One should rule out Guillain-Barré syndrome if the patient exhibits acute or subacute autonomic instability accompanied by weakness, as this condition frequently results in ileus, constipation, and blood pressure swings.