Georges Guillain

Biography

• 1876 – Born March 3 in Rouen, France, to Louis Guillain (engineer) and Gabrielle Lemaignent.
• 1894 – Entered medical studies in Rouen.
• 1898 – Transferred to Paris for clinical and neurological training; published first paper on brachial plexus injuries with Pierre Duval.
• 1902 – Received Doctorat de Médecine (PhD), Paris; thesis on syringomyelia. Trained under Pierre Marie (1853–1940). Undertook pioneering research trip to major US neurology centres.
• 1906 – Appointed Chef de Clinique under Pierre Marie at Bicêtre and Salpêtrière.
• 1906 – Appointed Médecin des Hôpitaux.
• 1910 – Gained agrégation; became chef de clinique Salpêtrière Hospital
• 1914–1918 – Served in WWI; headed Neurology Centre of the Sixth French Army.
• 1916 – With Jean Alexandre Barré and André Strohl, described acute inflammatory demyelinating polyneuropathy with albuminocytologic dissociation in CSF in WWI soldiers – later Guillain-Barré syndrome.
• 1920 – Published Travaux neurologiques de guerre. Member of the Académie de Médecine (1920), President (1942)
• 1923 – Appointed Chair of Nervous System Diseases, Salpêtrière, succeeding Pierre Marie.
• 1927 – Eponym “Guillain–Barré syndrome” first used at Brussels neurology congress.
• 1931 – With Mollaret and Krépeline, described the dentato-rubro-olivary loop (Guillain–Mollaret triangle)
• 1947 – Retired from clinical chair at Salpêtrière
• 1949 – Appointed Commandeur de la Légion d’honneur.
• 1951 – Member of the Académie des Sciences de Paris
• 1961 – Died June 29 in Paris, aged 85.
• International honours: Commander of the Order of the Star of Romania; Commander of the Order of Ouissam Alaouite (Morocco); Knight of the Order of Dannebrog (Denmark); Knight of the Crown of Italy

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Medical Eponyms

Guillain- Barré syndrome (1916)

Guillain–Barré syndrome (GBS) refers to a group of acute immune-mediated polyneuropathies, including the classic acute inflammatory demyelinating polyradiculoneuropathy (AIDP), as well as axonal variants. It remains a core diagnosis in neurology and intensive care, though its subtypes are now more precisely defined by electrophysiology and pathology. The eponymous term is still widely used today. [*aka Landry palsy; Landry-Guillain–Barré–Strohl syndrome]

1916 – Over a two week period in 1916, Guillain and Barré admitted two patients to the army hospital with motor difficulties, areflexia, preservation of cutaneous reflexes, parasthesias, muscle tenderness, alteration in nerve conduction and increased albumin in the absence of lymphocyte elevation (which differentiated it from the more common condition of poliomyelitis at that time).

These clinical observations were confirmed with nerve conduction studies by the physician André Strohl (1887-1977).

The syndrome is characterised by motor disorders, abolition of the tendon reflexes with preservation of the cutaneous reflexes, paraesthesias with slight disturbance of objective sensation, pain on pressure of the muscle masses, marked modifications in the electrical reactions of the nerves and muscles, and remarkable hyperalbuminosis of the cerebrospinal fluid with absence of cytological reaction (albuminocytological dissociation).

This syndrome seemed to us to depend on a concomitant injury of the spinal roots, the nerves, and the muscles, probably of infectious or toxic nature

Guillan, Barré, Strohl. 1916

Guillain and Barré termed the syndrome “notre syndrome” (our syndrome) and excluded Strohl, with there being no clear explanation for this. Some speculate it was related to his younger age, him not being a neurologist or him being from Alsace.

• Guillain G, Barré JA, Strohl A. Sur un syndrome de radiculo-névrite avec hyperalbuminose du liquide céphalo-rachidien sans réaction cellulaire. Remarques sur les caractères cliniques et graphiques des réflexes tendineux. Bulletins et mémoires de la Société médicale des hôpitaux de Paris, 1916; 40: 1462-1470

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Guillain-Mollaret triangle (1931)

The Guillain–Mollaret triangle (GMT) — also called the dentato-rubro-olivary pathway — is a pivotal neuroanatomical circuit linking the contralateral dentate nucleus, ipsilateral red nucleus, and inferior olivary nucleus, via the central tegmental tract and cerebellar peduncles. Lesions affecting this triangle result in hypertrophic olivary degeneration and are classically associated with palatal myoclonus, now termed oculopalatal tremor (OPT).

This triangular feedback loop is fundamental in rhythmic motor coordination, and damage along its path may cause rhythmic involuntary movements. While first described in 1931 by Georges Guillain and Pierre Mollaret, based on detailed clinical observation of synchronized myoclonus, its modern relevance persists in neuroradiology (MRI signal changes in the inferior olive), movement disorders, and brainstem pathology.

Today, the triangle is frequently referenced in the context of hypertrophic olivary degeneration on T2-weighted imaging, and is increasingly studied using tractography and DTI.

1931 – Guillain and Mollaret publish on synchronized myoclonus involving the soft palate, eyes, diaphragm, and larynx – Deux cas de myoclonies synchrones et rythmées vélo-pliaryngo-oculo-diaphragmatiques

1933 – Anatomical lesion clarified by Guillain, Mollaret and Bertrand Sur la lesion responsable du syndrome myoclonique de tronc cerebral.

In the 1950s the term “Guillain–Mollaret triangle” adopted, based on this defined circuit: dentate nucleus → red nucleus → inferior olive.

Goyal et al (2000) describe MRI evolution of hypertrophic olivary degeneration following damage to GMT. Murdoch et al (2010) highlight cases of delayed oculopalatal tremor and its imaging correlates. Show variable clinical expression and poor response to treatment.

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Garcin-Guillain syndrome (1927)

Garcin–Guillain syndrome, more commonly referred to as Garcin syndrome, describes the rare occurrence of unilateral cranial nerve palsies — involving most or all of the twelve cranial nerves on one side — without signs of long tract involvement or raised intracranial pressure. It typically results from infiltrative lesions at the skull base, most commonly due to lymphoepithelioma or nasopharyngeal carcinoma.

The syndrome was initially mentioned by Georges Guillain in 1926 in collaboration with Théophile Alajouanine (1890–1980) and Raymond Garcin (1897–1971). However, it was Garcin’s 1927 Paris thesis that gave the first comprehensive clinical description, hence the naming predominance as “Garcin syndrome.”

The condition reflects peripheral cranial nerve involvement, usually from extracranial or parameningeal malignancy, with sparing of the brain parenchyma. Though exceedingly rare, it remains a key diagnostic consideration in progressive cranial neuropathies with imaging evidence of skull base pathology.

1926 – Guillain, Alajouanine, and Garcin co-author a note on a new form of cranial nerve paralysis – Le syndrome paralytique unilatéral global des nerfs crâniens

1927 – Raymond Garcin publishes his landmark thesis – Le syndrome paralytique unilatéral global des nerfs craniens: contribution à l’étude des tumeurs de la base du crâne

1930s–1950s – The syndrome is further observed in association with nasopharyngeal carcinomas, including the Schmincke type, and base of skull sarcomas.

Later 20th century – Often used synonymously with cranial polyneuropathy of neoplastic origin, the eponym persists in European neurology.

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Guillain sign (1923)

Guillain sign — originally termed Le réflexe médio-pubien — was described in 1923 by Georges Guillain and Théophile Alajouanine. It is a bone reflex elicited by percussion over the pubic symphysis, which produces a double muscular response: (1) contraction of the abdominal muscles (especially rectus abdominis), and (2) contraction of the hip adductors (notably the pectineus and adductor longus).

The reflex was proposed as a tool for segmental spinal cord localization, particularly in the lower thoracic and upper lumbar regions. Guillain emphasized that it was absent or asymmetric in cases of hemiplegia, paraplegia, or spinal cord compression, and particularly useful in differentiating flaccid from spastic paraplegia. It also served as a proxy to explore automated medullary responses when traditional reflexes were absent.

Though once a topic of intense neurophysiological interest, the reflex is rarely used in modern practice. Its use has largely been replaced by imaging and more standardised neurological testing.

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Guillain-Betrand-Lereboullet syndrome (1934)

Guillain–Bertrand–Lereboullet syndrome refers to a rare movement disorder characterised by unilateral arrhythmic myoclonus of the limbs resulting from a lesion of the dentate nucleus of the cerebellum. This syndrome represents one of the cerebellar variants of choreiform or myoclonic syndromes, reflecting disrupted coordination between cerebellar output and motor control pathways.

Described in 1934 by Georges Guillain, Igor Bertrand, and J. Lereboullet, the condition offered early evidence of the cerebellum’s role in movement modulation and involuntary motor discharge, at a time when cerebellar contributions to motor rhythm and pattern were only beginning to be anatomically elucidated.

While the syndrome is rarely referenced in contemporary practice, it remains of historical interest in the evolution of cerebellar neurophysiology, and sometimes emerges in differential diagnosis of asymmetric myoclonus or unilateral action tremors.

1934 – Guillain, Bertrand, and Lereboullet publish – Myoclonies arythmiques unilaterales des membres par lésion du noyau dentlé du cervelet. They describe cases of arrhythmic, irregular jerking affecting one side of the body, linked pathologically to damage of the cerebellar dentate nucleus.

1930s–1950s – Syndrome occasionally referenced in French neurology literature as part of the cerebellar myoclonus spectrum.

Late 20th century onward – The term falls into disuse, but cerebellar-induced myoclonus and tremor remain active fields of investigation, often revisiting the dentate nucleus as a key structure.

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Guillain-Thaon syndrome (1905)

Guillain–Thaon Syndrome is a historical term describing a rare neurological condition characterized by spastic paraplegia resulting from syphilitic meningomyelitis in the context of tertiary neurosyphilis. First described in 1905 by Georges Guillain and Pierre Thaon, the syndrome presents with clinical features that bridge syphilitic myelitis, tabes dorsalis, and general paresis. The condition reflects the diverse manifestations of neurosyphilis, particularly in its late stages, and underscores the importance of considering syphilitic involvement in patients presenting with progressive myelopathy.

In contemporary clinical practice, the eponym is largely of historical interest. Advances in diagnostic techniques and a deeper understanding of neurosyphilis have led to more precise classifications, rendering the term “Guillain–Thaon Syndrome” less commonly used. However, its historical significance remains as a testament to early efforts in delineating the neurological sequelae of syphilis.

1905 – Georges Guillain and Pierre Thaon publish initial observations on a clinical form of neurosyphilis exhibiting features intermediate between syphilitic myelitis, tabes dorsalis, and general paresis – Sur une forme clinique de la syphilis du névraxe réalisant la transition entre les myélites syphilitiques, le tabes et la paralysie générale

1913 – Mme L. Pilate, née Martsinkhvitsch, presents and defends her thesis Le syndrome de Guillain-Thaon in front of the Faculté de médecine de Montpellier le 24 mai 1913, further detailing cases of spastic paraplegia associated with syphilitic meningomyelitis, building upon the earlier work of Guillain and Thaon.

1914 – Georges Guillain publishes additional insights into the syndrome, emphasizing its distinct clinical presentation and its place within the spectrum of neurosyphilitic disorders in Travaux du centre neuropsychiatrique de la Vie armée.

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Controversies

The omission of André Strohl’s name from later references to Guillain–Barré syndrome remains a subject of historical debate. The initial 1916 description included Strohl’s electrophysiological contributions. The name “Guillain–Barré syndrome” became established after a 1927 congress presentation by Barré, without clear explanation for the omission.

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Major Publications

• Duval P, Guillain G. Pathogénie des accidents nerveux consécutifs aux luxations et traumatismes de l’épaule. Arch Gén Méd. 1898;2:143–191.
• Guillain G. La forme spasmodique de la syringomyélie. La névrite ascendante et le traumatisme dans l’étiologie de la syringomyélie. 1902
• Guillain G. Thaon P. Sur une forme clinique de la syphilis du névraxe réalisant la transition entre les myélites syphilitiques, le tabes et la paralysie générale. Comptes rendus des séances de la Société de biologie et de ses filiales 1905; 49-53 [Guillain-Thaon syndrome]
• Guillain G. Thaon P. Etude sur une forme clinique de la syphilis du névraxe réalisant la transition entre les myélites syphilitiques, le tabes et la paralysie générale. Bulletins et Mémoires de la Société médicale des hôpitaux de Paris 1907; 24: 661 [Guillain-Thaon syndrome]
• Marie P, Guillain G et al. La pratique neurologique. 1911
• Guillain G. Travaux du centre neuropsychiatrique de la Vie armée. Revue Neurologique. 1914; 28(2): 1198–1201.
• Guillain G, Barré JA, Strohl A. Le réflexe médico-plantaire: Étude de ses caracteres graphiques et de son temps perdu. Bulletins et mémoires de la Société médicale des hôpitaux de Paris, 1916; 40: 1459-1462.
• Guillain G, Barré JA, Strohl A. Sur un syndrome de radiculo-névrite avec hyperalbuminose du liquide céphalo-rachidien sans réaction cellulaire. Remarques sur les caractères cliniques et graphiques des réflexes tendineux [1916] Ann Med Interne (Paris). 1999 Jan;150(1):24-32.
• Guillain G, Barré JA, Strohl A. Sur un syndrome de radiculo-névrite avec hyperalbuminose du liquide céphalo-rachidien sans réaction cellulaire. Remarques sur les caractères cliniques et graphiques des réflexes tendineux. Bulletins et mémoires de la Société médicale des hôpitaux de Paris, 1916; 40: 1462-1470 [Guillain–Barré syndrome]
• Guillain G, Barré JA. Étude anatomo-clinique de quitanze cas de section totale de la moelle. Annales de médecine. 1917; 2: 178–222
• Guillain G. Etudes neurologiques. Paris: Masson 1922
• Guillain G. Alajouanine Th. Le réflexe médio-pubien. Comptes rendus des séances de la Société de biologie, Paris, 1923; 89: 874, 1215. [Guillain sign]
• Guillain G. Alajouanine Th, Garcin R. Le syndrome paralytique unilatéral global des nerfs crâniens. Bulletins et mémoires de la Société médicale des hôpitaux de Paris, 1926; 50: 456-460 [Garcin – Guillain syndrome]
• Guillain G, Mollaret P. Deux cas de myoclonies synchrones et rythmées vélo-pliaryngo-oculo-diaphragmatiques. Le problème anatomique et physio-pathologique de ce syndrome. Revue Neurologique 1931; 2: 545–566. [Guillain-Mollaret triangle]
• Guillain G, Mollaret P, Bertrand IG. Sur la lesion responsable du syndrome myoclonique de tronc cerebral. Revue Neurologique. 1933; 62: 666–674. [Guillain-Mollaret triangle]
• Guillain G, Bertrand IG. Lereboullet, J. Myoclonies arythmiques unilaterales des membres par lésion du noyau dentlé du cervelet. Revue Neurologique. 1934; 63(2): 73–78. [Guillain – Betrand – Lereboullet syndrome]

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References

Biography

• Pietrzak K, Grzybowski A, Kaczmarczyk J. Georges Guillain (1876–1961). J Neurol. 2016; 263(10): 2148–2149.
• Georges Guillain (1876-1961) BNF Data
• Walusinski O. Georges Guillain 1876-1961. Le Bâillement
• Fresquet JL. Georges Charles Guillain (1876-1961). Historia de la Medicina

Eponymous terms

• Pilate L. Le syndrome de Guillain-Thaon: thèse présentée et publiquement soutenue devant la Faculté de médecine de Montpellier le 24 mai 1913
• Garcin R. Le syndrome paralytique unilatéral global des nerfs craniens : contribution à l’étude des tumeurs de la base du crâne; thèse de médecine de Paris n° 34, 1927. [Garcin-Guillain syndrome]
• Afifi AK. The landry-guillain-barré strohl syndrome 1859 to 1992 a historical perspective. J Family Community Med. 1994 Jan;1(1):30-4.
• Goyal M, Versnick E, Tuite P, Cyr JS, Kucharczyk W, Montanera W, Willinsky R, Mikulis D. Hypertrophic olivary degeneration: metaanalysis of the temporal evolution of MR findings. AJNR Am J Neuroradiol. 2000 Jun-Jul;21(6):1073-7. 
• Murdoch S, Shah P, Jampana R. The Guillain-Mollaret triangle in action. Pract Neurol. 2016 Jun;16(3):243-6.
• Turgut AÇ, Tubbs RS, Turgut M. Georges Charles Guillain (1876-1961) and Pierre Mollaret (1898-1987) and their legacy to neuroanatomy: the forgotten triangle of Guillain-Mollaret. Childs Nerv Syst. 2021 Feb;37(2):349-350.