John Hughlings Jackson Research Paper

When Jackson left school he was at once apprenticed to a general practitioner in York. Two years later, in 1852, he enrolled at the York Medical School and in 1855 he proceeded to St. Bartholomew’s Hospital in London. He qualified in 1856 and returned to the York Dispensary for three years as a resident medical officer. In 1860 he submitted a thesis (the title of which is unrecorded) to the University of St. Andrews and was awarded the MD.

By this time Jackson had returned to London. He had become increasingly interested in philosophy and seriously considered abandoning medicine for this field. He was dissuaded by his friend Jonathan Hutchinson (who later became one of the leading surgeons and ophthalmologists of his day). About this time (Hutchinson records) Jackson came under the influence of C E Brown-Sequard who ‘told him strongly, that it was foolish to waste his efforts in wide observation of disease in general, and that if he wished to attain anything he must keep to the nervous system’ (Hutchinson 1925). As a result, Jackson was appointed in 1862 to the staff of Brown-Sequard’s hospital, the National Hospital for the Paralysed and Epileptic in Queen Square. In the same year he became a clinical assistant at the Royal London Ophthalmic Hospital (now known as the Morefields Eye Hospital) in London and in the following year he was appointed to the London Hospital. These three institutions provided him with the experience on the basis of which he made his fundamental contributions to our understanding of the organization of nervous function.

Jackson was a shy, modest, self-effacing individual, much loved by his students and colleagues. His wife died after only eleven years of marriage. A place at the lunch table was always set for him at the home of his colleague Dr. Thomas Buzzard. Jackson came to lunch irregularly and without notice. As Buzzard’s son recalled, ‘… he would pull a chair up to the table, exchange a few remarks, perhaps tell a humorous story with only a twinkle of the eye disturbing the solemnity of his features, and after five, perhaps ten minutes he would mumble something about remembering an engagement and leave the room’ (Buzzard 1934). In his last years Jackson lived an even more solitary, though serene life. He retained an interest in the lives of his pupils and their families to the end. He died on the October 7, 1911. His contribution was widely acknowledged by the academic world during his lifetime, but to the surprise of all he received no national honor.

Jackson’s contemporaries and pupils recorded that he was a meticulous observer of clinical phenomena, and from his earliest days in medicine he was committed to the necessity for pathological verification of clinical inferences. His understanding of the nervous system based on this approach was molded by two main influences. The first derived from his teacher at medical school, Dr. Thomas Laycock (later Professor of Medicine in Edinburgh) who was interested in psychology and in nervous function and dysfunction. The other influence was the writings of the philosopher Herbert Spencer with whom Jackson corresponded up to the beginning of the twentieth century. It was from Spencer that Jackson derived the notion of the evolution of nervous function, which led to his idea of a hierarchical arrangement of functions, and that disease (neurological and psychiatric) led to a successive regression from the ‘least automatic’ and ‘least deeply organised’ to the ‘most automatic’ and ‘most deeply organised’ levels. As Walshe (1961) has pointed out, these ideas derived from Jackson’s life-long study of five kinds of clinical phenomena: focal seizures, chorea, hemiplegia, speech disorders, and mental disorders.

A remarkable consequence of Jackson’s work was his prediction, on the basis of unaided clinical observation, of a number of physiological principles which were later confirmed experimentally. One of them is the concept of localized cerebral discharges generating focal seizures, and that such focal seizures are caused by local brain disease. The comparison between the clinical symptomatology and subsequent neuropathology showed that the distribution of focal motor and sensory signs depended on the site of the lesion. The topographical structure–function relationships laid the ground for the topological functional organization of the cortex long before cytoarchitectonic anatomical maps were established. The general idea of the functional specialization of the cortex had already been proposed by Gall (1825). His phrenology was derived from the attribution of certain personality features to the individual ‘microstructure’ of the scalp as inferred from palpation. Gall’s postulate that cerebral function must be localized was correct in principle but based on inadequate evidence. The first real evidence came from Jackson, who published his first account of epilepsy in 1861, almost 10 years before his clinically based concept was confirmed by using electrical stimulation of the cortex (Fritsch and Hitzig 1870, Ferrier 1876).

The first pioneers of cortical neurophysiology indeed recognized the pivotal role of Jackson in the development of the concept of epileptogenic discharges in distinct areas generating focal seizures as the following two quotations show: ‘… I was precisely the first one, now some thirty or more years ago, to confirm by physiological experiment and to define more closely that which Hughlings Jackson had concluded from clinical facts’ (Hitzig 1900); ‘… Dr. Hughlings Jackson who from a clinical and pathological standpoint anticipated many of the more important results of recent experimental investigation into the functions of the cerebral hemispheres… (Ferrier 1886).

Another concept put forward by Jackson related to the effect of lesions on function. In order to understand the pathophysiology of the effects of lesions he introduced the term ‘negative and positive elements.’ The negative elements were derived from the more global effects of epileptic seizures as apparent from dreamy states and the loss of consciousness. This was regarded as a dissolution ‘of so many nervous elements of the highest centres’ by the epileptic discharge, so that the ‘most special and complex sensorimotor arrangements’ would affect the adjustment of the organism as a whole to the environment. Convulsions were recognized as due to excessive neuronal discharge. From his clinical observations Jackson deduced that ‘there are two ways in which nerve tissue suffers. It may be destroyed, and then there is loss of function. It may be unstable, and then there is disorder of function—‘discharge’ (Jackson 1931, Vol. 1, p. 29).

The ‘positive element’ was exemplified by speech disturbances, where the inability to express oneself demonstrates the negative effect of a brain lesion, whereas the paraphasia—the insertion of wrong words or inadequate sentence formations—would show the effect of the damaged part on the function of the remaining neural circuitry. These views later inspired Sigmund Freud’s contributions to aphasia, in particular his early insight into the emotional determinants of speech disruptions. The positive and negative elements also had an impact on subsequent hypotheses on psychotic disorders.

Jackson’s explanation of the clinical deficits associated with lesions was based on his view of the three levels in the evolution of the nervous system. Each element of each level was seen to contain a complete representation of the next lower level. Consequently, each element of the middle and highest levels would contain a representation of the entire body. If the nervous system is damaged the clinical impairment is not due just to the damaged part, but represents the compensatory action of the lower level circuitry that would then partially compensate for the function of the destroyed tissue.

The concept of evolution of the nervous system was therefore instrumental to his view that dissolution of the nervous system due to the effects of lesions results from the function of the remaining, nondamaged parts being liberated from control by the damaged part. This approach to understanding the pathophysiology and nature of the neurological signs and symptoms was later replaced by ‘localizationists’ who considered these to be deficits in a mechanical framework, i.e., saw them as loss of function of the destroyed tissue. It soon became clear that phenomena like spasticity, tremor etc., could not be explained in this way. With the advent of new, experimentally-based conceptions of the brain as a complex, densely interconnected and re-entrant network, the Jacksonian views were basically confirmed.

Jackson’s contribution was not limited to the conceptual advances we have described. His skill in precise clinical observation, together with his analytical and deductive powers, led to advances of practical value in clinical neurology. For example, he was one of those who pioneered the introduction of the Helmholtz ophthalmoscope to medicine, his first paper on the topic appearing in 1863. His papers of 1871 and 1873 on ‘optic neuritis’ from intracranial disease, and the diagnosis of brain tumours, represented a major advance. He made contributions to neuro-ophthalmology, particularly in relation to eye movement, and to the effects of syphilis on the nervous system.

The writings of Jackson have a reputation for being difficult to read, being filled as they are with qualifications in the text and in extensive footnotes, as he strove to get as close as possible to the truth about inherently complex problems; they are still illuminating. Many appeared in Brain (of which he was a cofounder) but many others appeared in journals which are now difficult to obtain. Fortunately a comprehensive selection was published in 1931 and reprinted in 1958.

Bibliography:

1. Buzzard E F 1934 Hughlings Jackson and his influence on neurology. Lancet 2: 909–13
2. Critchley M and Critchley E A 1998 John Hughlings Jackson. Father of English Neurology. Oxford University Press, New York, p. 228
3. Ferrier D 1876 The Function of the Brain. Smith, Elder, London
4. Ferrier D 1886 The Function of the Brain, 2nd edn. Putnam, New York, p. 498
5. Fritsch G T, Hitzig E 1870 Uber die elektrische Erregbarkeit des Großhirns. Archi fur Anatomie und Physiologie 300–32 (Engl. Trans. Wilkins H 1963 Neurosurgical classics. Journal Neurosurgery 20: 904–16)
6. Gall F J 1825 Fonction du Cerveau. Balliere, Paris
7. Hitzig E 1900 Hughlings Jackson and the cortical motor centres in the light of physiological research. Brain 23: 545–81
8. Hutchinson J 1925 Recollections of a lifelong friendship. In: Taylor J (ed.) Neurological Fragments. Oxford University Press, Oxford, UK
9. Jackson J H 1925 Neurological Fragments. In: Taylor J (ed.) Oxford University Press, Oxford, UK
10. Jackson J H 1931 Selected Writings of John Hughlings Jackson. Hodder and Stoughton, London
11. Spurzheim G 1825 Phrenology in Connection with the Study of Physiogonomy. Part I. Characters. Treuttel, Wurtz and Richter, London
12. Walshe F M R 1961 Contributions of John Hughlings Jackson to neurology. Archives of Neurology 5: 119–31