During the nineteenth century, epilepsy moved into a new kind of medical framework. Seizures had long been described as disorders of the brain, but physicians still disagreed about where attacks began, what produced them and whether different forms of convulsion belonged to the same disease.
Between roughly 1840 and 1900, that changed dramatically. Clinical observation, post-mortem examination, experimental physiology and the emerging specialty of neurology began to converge. Physicians increasingly treated the seizure itself as a physiological event that could reveal where abnormal activity had begun and how it had spread through the nervous system.
John Hughlings Jackson became the central figure in this transformation, but he did not work in isolation. Robert Bentley Todd, John Russell Reynolds, Théodore Herpin, Louis Delasiauve, Charles-Édouard Brown-Séquard, Gustav Fritsch, Eduard Hitzig, David Ferrier, Victor Horsley and William Gowers all contributed to the nineteenth-century reconstruction of epilepsy.
This page is about that wider historical shift. Jackson’s detailed observations of spreading focal motor seizures — later called the Jacksonian march — belong to the next page in this history.
Neurology did not yet exist as a modern specialty
At the beginning of the nineteenth century, diseases of the nervous system were treated within general medicine, psychiatry, surgery and anatomy. The boundaries between those fields were still forming.
Physicians could describe paralysis, convulsion, aphasia and abnormal movement, but there was no EEG, no MRI and no modern system for classifying seizure types. The brain’s functional organisation was still disputed.
By the end of the century, specialist neurological hospitals, journals, societies and academic networks had begun to emerge. Epilepsy became one of the disorders through which the new discipline learned how to connect symptoms with specific parts of the nervous system.
Before Jackson: epilepsy was already changing
It would be inaccurate to tell the story as though nineteenth-century epileptology began suddenly with Hughlings Jackson.
In France, Théodore Herpin and Louis Delasiauve produced important clinical classifications of seizures in the mid-nineteenth century. In Britain, John Russell Reynolds published a major study of epilepsy in 1861. Charles-Édouard Brown-Séquard investigated convulsions experimentally and clinically.
These physicians helped shift attention toward the detailed phenomenology of attacks: how they began, what happened first, which body parts were affected and how consciousness changed.
That descriptive tradition created the clinical material from which later localisation theories could grow.
Robert Bentley Todd and an earlier electrical idea
Robert Bentley Todd deserves a particular place in the story because he proposed an electrical model of epilepsy before Jackson’s famous writings.
In his 1849 Lumleian Lectures, Todd drew on contemporary discoveries in electricity, including the work of Michael Faraday. He compared the brain to an electrical apparatus capable of accumulating and suddenly discharging nervous force.
He also performed electrical experiments in animals.
Later histories often credited Jackson with the first electrical theory of epilepsy, but historical scholarship has shown that Todd’s formulation came earlier. Jackson’s achievement was different: he built a powerful clinical and anatomical theory of seizure discharge and localisation from observations of patients.
The problem of where seizures began
One major nineteenth-century dispute concerned the origin of convulsions.
Many physicians believed that the crucial centres responsible for epileptic seizures lay in lower parts of the brain, particularly the medulla oblongata or other subcortical structures. The cerebral cortex was widely regarded as incapable of being directly excited in the way later experiments would demonstrate.
This assumption made cortical theories of epilepsy difficult to accept.
Jackson’s clinical work challenged it.
John Hughlings Jackson enters the story
John Hughlings Jackson was born in Yorkshire in 1835. In the early 1860s he began working at the National Hospital for the Paralysed and Epileptic at Queen Square in London and at the London Hospital.
He became fascinated by patients whose seizures began in one part of the body and then spread in an orderly sequence.
Instead of treating this pattern as an odd variation of epilepsy, Jackson treated it as evidence.
If a seizure began with movement of one hand, then progressed to the arm and face, he reasoned that the physiological disturbance producing the movement must itself be spreading through organised nervous tissue.
By combining seizure descriptions with paralysis, aphasia and post-mortem findings, he began to infer the functional arrangement of the cerebral hemispheres.
A seizure became a symptom, not a disease entity in itself
One of Jackson’s most important conceptual moves was to treat convulsion as a symptom produced by abnormal activity in nervous tissue.
In his 1870 paper A Study of Convulsions, he described a convulsion as the result of an excessive and disorderly discharge of nerve tissue onto muscles. Later, in 1873, he gave a more general formulation in which epilepsy was characterised by sudden, excessive, rapid and local discharge of grey matter.
This language was historically revolutionary because it shifted attention from the outward appearance of the attack to an underlying physiological event.
Jackson did not possess the modern concept of neuronal membrane potentials or synchronized cortical networks. His term ‘discharge’ belonged to nineteenth-century neurophysiology and ideas about nervous energy.
Nevertheless, it created a framework in which different seizure manifestations could be understood as different expressions of abnormal nervous activity.
The cortex becomes excitable
Jackson’s early reasoning was bold partly because many physiologists still considered the cerebral cortex electrically inexcitable.
That changed dramatically in 1870, when Gustav Fritsch and Eduard Hitzig reported experiments showing that electrical stimulation of particular areas of the exposed cerebral cortex of dogs produced movements on the opposite side of the body.
The result provided experimental evidence that movement was represented in organised cortical regions.
It also supported the kind of localisation Jackson had inferred from patients.
David Ferrier turns localisation into an experimental programme
David Ferrier extended cortical stimulation experiments in the 1870s, initially at the West Riding Lunatic Asylum in Wakefield.
Ferrier stimulated the brains of several animal species and mapped movements produced from different cortical sites. His 1873 work strengthened the case for cerebral localisation and had direct relevance to epilepsy.
Appropriately placed stimulation could produce focal motor convulsions that spread and sometimes developed into more generalised attacks. Ferrier concluded that focal and generalised convulsions could represent different stages of the same cortical process.
The clinical observations and laboratory experiments now reinforced one another: seizure pattern could reveal cortical organisation, while cortical stimulation could reproduce seizure-like motor sequences.
From ‘genuine epilepsy’ to focal epilepsy
Before this period, physicians often distinguished so-called ‘genuine’ or idiopathic epilepsy from ‘epileptiform’ attacks caused by visible brain disease.
Jackson increasingly rejected a fundamental physiological divide between them.
By around 1870 he argued that both could arise from the same basic process of abnormal discharge, differing in site, cause and spread rather than belonging to entirely separate mechanisms.
This helped establish focal epilepsy as a central neurological concept.
A seizure beginning in one limb was no longer simply an incomplete version of a ‘proper’ convulsion. It could carry anatomical information about where the disturbance started.
The National Hospital at Queen Square
The National Hospital for the Relief and Cure of the Paralysed and the Epileptic opened in London in 1860. It later became one of the world’s most important centres for neurology.
Between 1860 and 1910, Queen Square brought together an extraordinary group of clinicians and researchers, including Jackson, Ferrier, Victor Horsley and William Gowers.
Historical reviews describe this period as a revolution in epilepsy theory and practice. At Queen Square, physicians developed concepts of focal epilepsy, cortical localisation, seizure semiology, drug treatment and ultimately epilepsy surgery.
The institution mattered because large numbers of patients with neurological disease could be observed repeatedly over time, compared with one another and followed through illness and sometimes post-mortem examination.
The seizure as a map of the brain
For Jackson, the order of symptoms mattered.
If movement spread from thumb to hand, arm and face, that sequence was not random. It reflected the organisation and recruitment of nervous structures.
This made epilepsy unexpectedly useful to nineteenth-century neurology. A seizure was a pathological event, but it was also a natural experiment in functional anatomy.
By studying what function appeared first, what followed next and what was temporarily lost afterwards, physicians could infer how the brain was organised.
Post-seizure weakness also became evidence
Jackson paid close attention to temporary paralysis after focal seizures.
What would later be widely known as postictal paresis or Todd’s paralysis linked seizure activity with transient loss of function in the same motor systems.
The concept itself had earlier associations with Robert Bentley Todd, but Jackson incorporated post-seizure weakness into his broader reasoning about localisation.
Seizure and paralysis could therefore be read together: excessive function during the attack followed by reduced function afterwards.
Aphasia strengthened localisation theory
The nineteenth century also transformed ideas about language in the brain.
Following work by Paul Broca and others, aphasia became central to debates about cerebral localisation. Jackson studied patients with aphasia alongside patients with unilateral seizures and hemiplegia.
These overlapping clinical problems helped him develop a hierarchical view of nervous-system organisation and reinforced the idea that different functions could be represented in particular cerebral systems.
Jackson’s theory was not simply ‘electricity in the brain’
Modern summaries sometimes say Jackson discovered that epilepsy is caused by abnormal electrical activity.
That wording is convenient but historically imprecise.
Jackson spoke of nervous discharge, instability of grey matter and excessive activity. His ideas developed before neurons, synapses and cortical electrophysiology were understood in modern terms.
The electrical interpretation became increasingly plausible through experimental stimulation work, but Jackson’s own framework was fundamentally clinical and physiological rather than an EEG-era theory of electrical synchronisation.
Calling him the inventor of the modern electrical theory therefore compresses several distinct nineteenth-century developments into one slogan.
Hierarchy, positive symptoms and negative symptoms
Jackson developed a broader theory of nervous-system organisation in which higher levels controlled or integrated lower levels.
He distinguished ‘positive’ symptoms — abnormal activity such as convulsion — from ‘negative’ symptoms representing loss of normal function, such as paralysis.
This distinction influenced later neurological thinking far beyond epilepsy.
In a seizure, excessive activity could create positive motor phenomena, while temporary exhaustion or disruption could be followed by weakness or impaired function.
The language and theoretical details evolved across Jackson’s career, but the general approach helped neurologists interpret symptoms as expressions of altered nervous function rather than simply names of diseases.
Not every nineteenth-century neurologist agreed
The rise of cortical localisation was not immediate or uncontested.
Physicians debated whether functions were sharply localised, broadly distributed or hierarchically organised. Experimental results were challenged. Animal findings did not always translate neatly to human disease.
Jackson himself revised his ideas repeatedly.
The history therefore should not be told as one discovery followed by universal acceptance. Localisation emerged through argument among clinicians, physiologists, pathologists and surgeons.
Epilepsy helped create modern neurological examination
The new approach required clinicians to observe seizures with unusual precision.
Which finger moved first? Did the eyes or head turn? Did speech stop? Was consciousness impaired immediately or only after the movement spread? Was there weakness afterwards?
These details mattered because they could indicate where the pathological process had begun.
That style of examination became characteristic of neurology: careful description of function used to infer anatomy.
From localisation to surgery
Once physicians believed a focal seizure could identify a localised cortical abnormality, a new possibility emerged.
If the responsible area could be identified accurately, perhaps a surgeon could remove the underlying lesion.
Victor Horsley and the Queen Square physicians would turn that possibility into some of the earliest operations specifically guided by seizure localisation in the 1880s.
That development belongs to the later page on epilepsy surgery before the Montreal procedure, but its intellectual foundation was built during this nineteenth-century localisation revolution.
William Gowers brings clinical epileptology together
William Gowers, another major Queen Square physician, published Epilepsy and Other Chronic Convulsive Diseases in 1881.
His work drew on large numbers of patients and helped systematise knowledge about seizure manifestations, causes, prognosis and treatment.
Gowers belongs to the next stage of nineteenth-century epileptology: the consolidation of detailed clinical observation after localisation theory had begun to transform the field.
Because he has his own page later in this history sequence, his work is only placed in context here rather than repeated in detail.
What changed between 1850 and 1900?
The transformation can be summarised without pretending that every problem had been solved.
Epilepsy increasingly became understood as a disorder of nervous function rather than a mysterious constitutional illness defined only by dramatic convulsions.
Focal onset became medically meaningful.
The cerebral cortex became central to theories of seizure generation.
The sequence of symptoms became evidence for localisation.
Experimental stimulation connected physiology with bedside observation.
Specialist neurological institutions created environments where large numbers of patients could be studied systematically.
And localisation made targeted surgery conceptually possible.
What nineteenth-century neurology still did not know
There was no EEG. Neurons had not yet been understood in the modern electrophysiological sense. Genetics was in its infancy. Neuroimaging did not exist. Many underlying causes of epilepsy could not be detected during life.
Physicians continued to use broad categories such as idiopathic, symptomatic, grand mal and petit mal.
Treatments were limited. Bromides could reduce seizures in some people but had substantial adverse effects. Phenobarbital would not enter epilepsy treatment until the next century.
The nineteenth-century revolution therefore created a framework for modern epileptology without possessing most of the tools later used to test it.
Why Hughlings Jackson matters
Jackson’s importance lies less in one isolated discovery than in a method.
He treated seizure phenomena as physiological clues. He connected clinical sequence with anatomy. He argued that focal and more generalised convulsions could belong to the same underlying process. And he helped establish the concept of abnormal discharge in grey matter as central to epilepsy.
His work made seizures useful to neurology not only as symptoms to be controlled, but as events that could reveal how the brain was organised.
The central historical lesson
The nineteenth-century rise of neurology did not begin modern epilepsy science in a single moment.
It was a convergence.
Clinical observers described increasingly subtle seizure forms. Physiologists demonstrated that the cortex was excitable and functionally organised. Pathologists related symptoms to lesions. Neurological hospitals created concentrated clinical experience. Surgeons began to act on localisation.
Hughlings Jackson stood at the centre of that convergence, but the transformation depended on a network of physicians and experimenters around him.
By 1900, epilepsy had become one of the disorders through which neurology learned to read the brain from the pattern of symptoms.
Sources and further reading
Eadie MJ. The evolution of J. Hughlings Jackson’s thought on epilepsy. Clinical and Experimental Neurology. 1990.
Shorvon S. The evolution of epilepsy theory and practice at the National Hospital, Queen Square, between 1860 and 1910. Epilepsy & Behavior. 2014.
York GK, Steinberg DA. An Introduction to the Life and Work of John Hughlings Jackson. Medical History Supplement. 2007.
Eadie MJ. The role of focal epilepsy in the development of Jacksonian localisation. Journal of the History of the Neurosciences. 2009.
Reynolds EH. Todd, Hughlings Jackson, and the electrical basis of epilepsy. The Lancet. 2001.
Compston A. David Ferrier’s classical cerebral localisation researches of 1873. Clinical Medicine. 2023.
Eadie MJ. Cortical epileptogenesis and David Ferrier. Journal of Clinical Neuroscience. 2018.
Magiorkinis E et al. Highlights in the history of epilepsy: the last 200 years. Epilepsy Research and Treatment. 2014.
Iniesta I. John Hughlings Jackson and our understanding of the epilepsies 100 years on. Practical Neurology. 2011.
Historical evidence checked: September 2026.