Haymaker and Kernohan’s Landry-Guillain-Barré syndrome paper: an essential contribution for accurate understanding of its early pathophysiology

J. Berciano, J. Gazulla, J. Infante
Neurosciences and History 2025;13(1):48-70

Type of article: REVIEW

AUTHORS

J. Berciano¹, J. Gazulla², J. Infante^3
1Professor emeritus ad honorem, Universidad de Cantabria, Santander, Spain
²Neurology Department, Hospital Universitario Miguel Servet, Zaragoza, Spain
³Neurology Department, Hospital Universitario “Marqués de Valdecilla (IDIVAL)”, Biomedical Research Networking Center on Neurodegenerative Diseases (“CIBERNED”), and Universidad de Cantabria, Santander, Spain

ABSTRACT

Introduction. Autopsy studies in early (≤ 10 days after onset) or very early (≤ 4 days), classic Guillain-Barré syndrome (GBS) are scarce. In 1949, Webb Haymaker and James Kernohan reported 50 clinical pathology studies of fatal GBS cases, with 32 patients having died between days 2 and 10 after onset.

Objective. To analyze Haymaker and Kernohan’s GBS paper and its implications for establishing the boundaries of the syndrome, and their contributions in setting out a reliable interpretation of its early pathophysiology.

Development. The article is divided into two sections. The first includes brief biographies of Haymaker and Kernohan; their pioneering description of the inaugural endoneurial edema in spinal nerves; corroboration of these findings by Krücke, which were later questioned by Asbury and colleagues; and support of the pathogenic role of edema in experimental autoimmune neuritis. The second comprises six sections in which we review the nosological overturning of GBS through the work by Haymaker and Kernohan, and the enormous impact that their study has had on the current pathophysiology of the syndrome.

Conclusions. The contribution of Haymaker and Kernohan was pivotal in establishing the nosological boundaries of GBS, and in identifying the characteristics and topography of the inaugural histopathological changes. To a large extent, the current pathophysiology of the syndrome, in its very early stage, is based upon these changes.

KEYWORDS

Acute febrile polyneuritis; AIDP; AMAN; AMSAN; axonal degeneration; blood-nerve barrier; CSF; demyelination; electric root stimulation; endoneurial fluid pressure; experimental autoimmune neuritis; Guillain-Barré syndrome; Haymaker Webb; Kernohan James; Landry paralysis; MRI; nerve conduction study; NfL; nerve inexcitability; nerve inflammatory edema; nerve ischemia; peripherin; spinal nerve; spinal roots; triple stimulation technique; ultrasonography

Neurosciences and History 2025;13(1): 48-70