Gordon Holmes

Biographical Timeline

• 1876 – Born February 22 in Castlebellingham, County Louth, Ireland, to Gordon Holmes and Kathleen (née Morgan).
• 1897 – Graduated B.A., Senior Moderator in Natural Science, and MB from Trinity College Dublin.
• 1898–1901 Studied neuroanatomy in Frankfurt under Ludwig Edinger (1855–1918) and Carl Weigert (1845–1904); published work on Goltz’s forebrainless dog in J Physiol (1903).
• 1902 – Returned to London; became House Physician at National Hospital for Nervous Diseases, Queen Square.
• 1903 – Awarded MD.
• 1906 – Appointed Director of Clinical Research at National Hospital.
• 1908 – Began collaboration with Sir Henry Head (1861–1940); jointly described thalamic sensory function.
• 1909 – Appointed Honorary Physician, National Hospital; also served at Charing Cross and Moorfields Eye Hospitals.
• 1911 – Co-authored seminal paper Sensory Disturbances from Cerebral Lesions with Henry Head
• 1914–1918 WWI: Initially rejected for service due to myopia; later served in France as Consulting Neurologist to the British Expeditionary Force alongside Percy Sargent (1873–1933). Treated brain and spinal injuries; published 18 wartime papers.
• 1915 – Delivered Goulstonian Lectures on spinal injury.
• 1917 – Appointed Companion of the Order of St Michael and St George (CMG).
• 1918 – Married Dr Rosalie Jobson, an Oxford graduate and wartime colleague.
• 1919 – Appointed Commander of the Order of the British Empire (CBE).
• 1920 – Co-authored Studies in Neurology with W.H.R. Rivers, James Sherren, et al..
• 1922 – Delivered Croonian Lectures on cerebellar function to the Royal College of Physicians.
• 1922–1937 Editor of the journal Brain.
• 1931 – Described Holmes-Adie syndrome independently from William John Adie (1886–1935).
• 1932 – Co-founded the Association of British Neurologists; hosted inaugural meeting at his home in London.
• 1933 – Elected Fellow of the Royal Society (FRS).
• 1935–1938 President of International Congresses of Neurology (1935, 1936, 1938).
• 1939–1945 WWII: Consultant to Emergency Medical Services; oversaw national neurological service during war.
• 1941 – Retired from National Hospital, Queen Square.
• 1944 – Delivered Ferrier Lecture of the Royal Society.
• 1951 – Knighted for services to medicine.
• 1965 – Died December 29 at home in Farnham, Surrey, aged 89.

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Medical Eponyms

Holmes-Adie syndrome (1931)

Holmes-Adie syndrome (Adie syndrome) is a benign, typically unilateral neurological condition characterised by a tonic pupil, light–near dissociation, and absent deep tendon reflexes.

1931 – William John Adie (1886-1935) described six cases of patients (five women) with tonic pupils and areflexia, without evidence of syphilis in Pseudo-Argyll Robertson Pupils with Absent Tendon Reflexes: A Benign Disorder Simulating Tabes Dorsalis. Adie emphasised the benign nature of the disorder and its frequent misdiagnosis as neurosyphilis

I wish to draw attention to a benign symptomless disorder characterized by pupils which react on accommodation but not to light, and by absent tendon reflexes…Though harmless in itself it merits recognition because it is often mistaken for a manifestation of syphilis of the nervous system, with unfortunate consequences…

Adie, May 1931

1931 – Holmes identified 19 patients with myotonic pupils and presented his paper Partial iridoplegia to the Ophthalmological Society of the United Kingdom

By very slow contraction on convergence, and even slower relaxation. The reflex to light is often lost too. One or both eyes may be affected.… In the present state of our knowledge a separation of those cases in which the tendon jerks are absent from those in which they persist is unjustifiable…the similarity of the symptoms in all these cases naturally suggests a common aetiology.

Holmes, 1931

1936 – Edwin Bramwell (1873–1952) formally proposes the eponym “Holmes-Adie Syndrome” at the March meeting of the Medico-Chirurgical Society of Edinburgh. Noting the condition’s frequent misdiagnosis as tabes dorsalis or neurosyphilis, he advocated naming the syndrome to improve recognition.

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Stewart-Holmes Sign / Manoeuvre / Test (1904)

The Stewart-Holmes sign, also referred to as the rebound phenomenon, is a clinical test used to assess cerebellar function and muscle tone regulation. Holmes and Thomas Grainger Stewart (1877–1957) reported on the Symptomatology of cerebellar tumors: A study of forty cases in 1904.

The manoeuvre involves asking a patient to flex the forearm against resistance, which is then suddenly removed. In healthy individuals, the antagonistic muscles act reflexively to prevent excessive movement, but in cerebellar disease, this corrective response fails, and the limb overshoots or may strike the body.

This phenomenon highlighted the cerebellum’s role in coordinated muscle inhibition and anticipatory motor control and is still employed in neurological examinations today.

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Gordon Holmes syndrome (1908)

A rare, autosomal recessive, adult-onset neurodegenerative disorder. The syndrome is characterised by progressive cerebellar ataxia combined with cognitive decline or early-onset dementia, and may include additional features such as chorea, myoclonus, or hypogonadism.

Holmes’ original cases published as A form of familial degeneration of the cerebellum described familial ataxia with both cerebellar and cortical involvement, making one of the earliest clinical connections between motor incoordination and cognitive dysfunction.

Neuropathological findings typically include degeneration of the cerebellum and inferior olivary nuclei. In modern practice, the term has been applied to genetically defined conditions with similar phenotypes, including mutations in RNF216, PNPLA6, and related genes.

This was one of the earliest descriptions to associate cerebellar degeneration with cognitive impairment, anticipating the now-recognised cerebellar cognitive affective syndrome.

The phenomenon to which we wish especially to refer occurs when resistance to a flexed arm is suddenly withdrawn. In normal individuals, the limb is checked by the antagonistic muscles. In our cerebellar patients, the limb flies back unchecked, sometimes with considerable force, and in one case struck the patient’s face.

We believe this sign to be of particular value in distinguishing cerebellar lesions from those of the cerebral cortex, as it indicates a failure in coordinated inhibitory response rather than simple muscular weakness.

Brain, 1908

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Bálint-Holmes syndrome (1909, 1918)

Bálint-Holmes syndrome is a rare neuropsychological disorder caused by bilateral lesions of the posterior parietal lobes, resulting in a triad of simultagnosia, optic ataxia, and oculomotor apraxia.

1909 – First described by the Hungarian neurologist Rudolf Bálint (1874–1929) in a patient with bilateral parietal damage. He identified a “psychic paralysis of gaze” (Seelenlähmung des Schauens); a spatial disorder of attention (räumliche Störung der Aufmerksamkeit); and coined the term optic ataxia (optische Ataxie) to describe the imprecise, misdirected hand movements during visually guided reaching.

Bálint recognised that this was not due to visual or motor deficits alone, but a failure of coordination between visual input and motor execution.

1918 – Holmes described six soldiers with bilateral parieto-occipital injuries sustained during World War I, who presented with similar visuomotor disturbances. Holmes documented profound gaze instability, difficulty with visual fixation, and spatial disorientation, yet made no reference to Bálint’s prior work. Holmes highlighted the hallmark of optic ataxia:

The most striking symptom in these cases is an inability to coordinate vision with movement, the hand frequently bearing no relation to the object aimed at

Holmes, 1918

The earliest identified usage of the combined eponym “Bálint-Holmes syndrome” appears to be Ennio De Renzi’s 1982 monograph Disorders of Space Exploration and Cognition. De Renzi used the eponymous term to group the triad of symptoms described independently by Bálint and Holmes and acknowledged their independent descriptions of higher-order visuospatial dysfunction.

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Head-Holmes syndrome (1911)

Head-Holmes syndrome refers to the complex sensory changes produced by lesions of the cerebral cortex and thalamus, first detailed by Henry Head (1861–1940) and Holmes in their 1911 publication Sensory disturbances from cerebral lesions (Brain, 34: 102–254).

Lesions of the parietal cortex, particularly the postcentral gyrus, were shown to result in loss or distortion of joint position sense and tactile perception contralaterally. Despite preserved primary motor function, patients often displayed sensory inattention, impaired spatial discrimination, and ataxia, emphasising the role of cortical integration in higher sensory processing.

In contrast, Head and Holmes demonstrated that circumscribed lesions of the optic thalamus produced a distinct syndrome of hemianaesthesia, astereognosis, impaired tactile localisation, and altered limb awareness, frequently accompanied by disturbances of taste and smell on the opposite side. As they wrote:

In lesions confined to the optic thalamus the most constant phenomena are impairment of taste and smell upon the opposite side, associated with a diminution of tactile localisation, astereognosis, and a sense of unreality or strangeness in the affected limbs.

Head, Holmes 1911

This dual emphasis on cortical versus thalamic sensory deficits was foundational in mapping the functional anatomy of sensation and in shaping clinical neurological examination throughout the 20th century.

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Holmes Syndrome (Cerebellar and Visual Disorientation Syndromes)

The term “Holmes syndrome” has historically been applied to more than one neurological entity. The better-known usage refers to Holmes systematic descriptions of cerebellar dysfunction, in which he defined the core clinical signs of ataxia, adiadochokinesia, asthenia, and rebound. These features were comprehensively presented in his Croonian Lectures of 1922 the Clinical Symptoms of Cerebellar Disease and Their Interpretation. These syndromes highlighted the cerebellum’s essential role in the regulation of tone, coordination, and anticipatory motor control, and remain foundational in clinical neurology.

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Key medical Contributions

Barognosis and Sensory Integration

Holmes investigated the faculty of barognosis, the ability to discriminate between weights using cutaneous, muscle, tendon, and joint senses. After 1910, he demonstrated that patients with unilateral cerebellar disease tended to overestimate weights placed in the ataxic hand, reflecting impaired integration of proprioceptive and motor feedback. He also noted that similar disturbances could occur in parietal cortical lesions, highlighting the contribution of both cerebellar and cortical systems to higher sensory processing.

Sensory Disturbances and the Thalamus

In collaboration with Henry Head, Holmes published Sensory Disturbances from Cerebral Lesions in 1911, a landmark work that distinguished between cortical and thalamic contributions to sensory processing. They showed that thalamic lesions produced contralateral deficits in taste, smell, tactile localisation, and stereognosis, often accompanied by altered limb perception, while cortical lesions impaired higher sensory integration and spatial awareness. This paper shaped the methodology of sensory testing for decades.

Spinal Cord Injury and War Neurology

Holmes played a central role in the neurological services of the First World War, particularly in the assessment of spinal cord injuries from gunshot wounds. His Goulstonian Lectures of 1915 on spinal injuries provided one of the first systematic accounts of missile lesions of the cord, their pathological anatomy, and clinical course. His observations during wartime laid the foundation for modern neurotraumatology and rehabilitation practices.

Academic Leadership and Publications

Beyond his clinical discoveries, Holmes exerted lasting influence through his editorship of Brain (1922–1937), where he set high standards for neurological publication. His Introduction to Clinical Neurology (1946) codified neurological examination for post-war generations, and his contributions to Studies in Neurology (1920) reflected his broad interest in both clinical and experimental aspects of the nervous system.

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Major Publications

• Stewart TG, Holmes GM. Symptomatology of cerebellar tumors: A study of forty cases. Brain, 1904; 27: 522-591. [Stewart-Holmes syndrome]
• Holmes GM. A form of familial degeneration of the cerebellum. Brain, 1908; 30(4): 466-489. [Holmes degeneration, Gordon Holmes syndrome]
• Head G, Holmes GM. Sensory disturbances from cerebral lesions. Brain, 1911; 34(2-3): 102–254. [Head-Holmes syndrome]
• Holmes G. The symptoms of acute cerebellar injuries due to gunshot injuries. Brain 1917; 40(4): 461-535.
• Holmes G. Disturbances of visual orientation. British Journal of Ophthalmology. 1918 Sep;2(9):449-68 and 1918 Oct;2(10):506-16 [Balint-Holmes syndrome]
• Holmes G. Clinical Symptoms of Cerebellar Disease and Their Interpretation. Lecture I. The Lancet 1922; 199(5155): 1177-1182 and Lecture II. 1922; 199(5156): 1231-1237
• Holmes GM. Observations on ocular palsies. Br Med J. 1931 Dec 26; 2(3703): 1165–1167
• Holmes GM. Partial iridoplegia associated with symptoms of other disease of the nervous system. Transactions of the Ophthalmological Societies of the United Kingdom, 1931; 51: 209-228. [Holmes-Adie Pupil]
• Holmes G. The cerebellum of man. Brain, 1939; 62(1): 1-62

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References

Biography

• Walshe FMR. Gordon Morgan Holmes, 1876-1965. Fellows of the Royal Society. November 1966
• Penfield W. Sir Gordon Morgan Holmes (1876-1965). J Neurol Sci. 1967 Jul-Aug;5(1):185-90.
• Sak JJ, Grzybowski A, Baj J. Sir Gordon Morgan Holmes (1876-1965): one of the founders of modern neurology. Neurol Sci. 2018 Jan;39(1):169-171
• Pearce JMS. Gordon Morgan Holmes MD., FRS. Hektoen International
• Sir Gordon Morgan Holmes. Inspiring Physicians. RCP

Eponymous terms

• Balint R. Seelenlähmung des “Schauens”, optische Ataxia, räumliche Störung der Aufmerksamkeit. Monatsschrift für Psychiatrie und Neurologie, 1909; 25: 51-81.
• Haines DE, Manto MU. Clinical symptoms of cerebellar disease and their interpretation. Cerebellum. 2007; 6(4): 360-374.
• Bodranghien F, Bastian A, Casali C, et al. Consensus Paper: Revisiting the Symptoms and Signs of Cerebellar Syndrome. Cerebellum. 2016;15(3):369-391.