Background: Guillain–Barré syndrome (GBS) is an immune-mediated disorder of the nervous system that shows acute or subacute onset. It is also known as Landry\'s paralysis. It is characterized by muscle weakness of legs and arms, limb paresthesias, and total or relative areflexia. Acute motor sensory axonal neuropathy (AMSAN) is a distinct subtype of GBS. It is not only a rare but severe variant that involves axonal degeneration in motor and sensory nerve fibers and has a prolonged recovery course.
Case description: A 60-year-old male presented to the emergency department having complaints of weakness, numbness, and tingling sensation in feet for the last fortnight, which ascended gradually towards the calves. He was observed to have a sensory disorder in hands, but not flaccid paralysis. The patient history and nerve conduction studies were indicative of AMSAN variant of GBS.
Discussion: In patients of AMSAN, the reduction of sural nerve amplitude is more pronounced as compared to acute inflammatory demyelinating polyneuropathy (AIDP) patients. In case of our patient, the electrophysiological feature indicated a more than 50% decrease in SNAP. A marked reduction in sensory nerve action potential and compound muscle action potential with only slightly decreased conduction velocities is a requirement for the diagnosis of axonal neuropathies, which is the trait seen in the reported case.
Goldman AS, Schmalstieg EJ, Freeman DH, et al. What was the cause of Franklin Delano Roosevelt's paralytic illness? J Med Biogr 2003;11(4):232–240. DOI: 10.1177/096777200301100412.
Gorson KC, Ropper AH. Guillain-Barré syndrome (acute inflammatory demyelinating polyneuropathy) and related disorders. In: Katirji B, Kaminski HJ, Preston DC, et al., editors. Neuromuscular disorders in clinical practice. Boston, Mass: Butterworth-Heinemann; 2002. p. 544–566.
Srivastava M. Nehal S, Seema N. Guillain- Barré syndrome: demographics, clinical profile and seasonal variation in a tertiary care centre of central India. Indian J Med Res 2017;145(2):203–208. DOI: 10.4103/ijmr.IJMR_995_14.
Hughes RAC, Cornblath DR. Guillain-Barré syndrome. Lancet 2005;366(9497):1653–1666. DOI: 10.1016/S0140-6736(05)67665-9.
Liu DY, Hollenbach JR, Gregorin JA, et al. A case of acute motor sensory axonal neuropathy: a variant of Guillain-Barré syndrome, with possible syndrome of irreversible lithium-effectuated neurotoxicity, Case Rep Med 2020;2020:4683507. DOI: 10.1155/2020/4683507.
Chowdhury D, Arora A. Axonal Guillain-Barré syndrome: a critical review. Acta Neurol Scand 2001;103(5):267–277. DOI: 10.1034/j.1600-0404.2001.103005267.x.
Arcila-Londono X, Lewis R. Guillain-Barré syndrome. Semin Neurol 2012;32(3):179–186. DOI: 10.1055/s-0032-1329196.
Sung EJ, Kim DY, Chang MC. Prediction of functional outcome in axonal Guillain–Barré syndrome. Ann Rehabil Med 2016;40(3):481–488. DOI: 10.5535/arm.2016.40.3.481.
Akbayram S, Akgün C, Sayin R, et al. Clinical features and prognosis with Guillain–Barré syndrome. Ann Indian Acad Neurol 2011;14(2):98–99. DOI: 10.4103/0972-2327.82793.
Forsberg A, Press R, Holmqvist LW. Residual disability 10 years after falling ill in Guillain–Barré syndrome: a prospective follow-up study. J Neurol Sci 2012;317(1–2):74–79. DOI: 10.1016/j.jns.2012.02.026.
Kuwabara S, Yuki N. Axonal Guillain-Barré syndrome: concepts and controversies. Lancet Neurol 2013;12(12):1180–1188. DOI: 10.1016/S1474-4422(13)70215-1.
Yadegari S, Nafissi S, Kazemi N. Comparison of electrophysiological findings in axonal and demyelinating Guillain-Barré syndrome. Iran J Neurol 2014;13(3):138–143. PMID: 25422732; PMCID: PMC4240930.