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Early accounts of epilepsy: a synopsis
  1. J M S PEARCE
  1. 304 Beverley Road, Anlaby, East Yorkshire HU10 7BG, UK

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    The writings on a Babylonian tablet from the British Museum and an Assyrian duplicate represent a missing chapter on epilepsy from a Babylonian textbook of medicine*, the Sakikku, written around 1067–46bc.1-3 Galen of Pergamon (ad130–200) deduced that epilepsy was a brain disorder due to an accumulation of thick humours.4

    Vesalius recognised focal epilepsy: “ . . .a certain aura or vapour . . .carried from the leg through the hip, then the scapula, upward to the head; then the left leg is agitated by the vehemence of the disease and convulsed . . .”5

    Willis observed that convulsions arose “most often from the head itself . . .the fault both of Blood sending, and of the Brain receiving . . .morbifick matter.6. . . . “The evil disposition of the brain is either hereditary or acquired.” Injury, “prolonged intemperance”, or chronic illness might initiate epilepsy. He described focal and spreading aurae.The mechanism was an “explosion”, “transmitted into various parts of the nervous system . . .as if grains of gunpowder were laid in a long train to be fired successively.”—the kindling phenomenon anticipated.

    The nature of the epileptic phenomena

    Theories included excess phlegm in the brain; according to Paracelsus, a boiling up of the vital spirits (spiritus animalis). In the 17th century Willis visualised an “explosion”. A century later Marshall Hall talked of abnormal irritability in the afferent limb or central section of the reflex arc. However, the primary source was in the cervical cord, loss of consciousness in a fit being the result of secondary cerebral venous congestion. Brown-Séquard in 1858 ascribed an important role to peripheral afferent nerve irritability, and the medulla was the central component of the reflex mechanism. Reflex cerebral vasospasm, rather than cerebral venous congestion, was the cause of loss of consciousness. Jacobus Schroeder van der Kolk (1797–1862),7 Professor of Anatomy and Physiology at Utrecht in 1826 performed autopsies and used an early microscope to study the brains of epileptics. His conclusions were given in: On the minute structure and functions of the medulla oblongata and the proximate causes and rational treatment of epilepsy (1859). He found: “dilatation of the veins which appeared filled with blood in the cortex, medulla and spinal cord”. The medulla “showed a fatty degeneration” . . . “The first cause of epilepsy . . . is exalted sensibility and excitability of the medulla oblongata . . .liable to discharge upon itself . . . and followed by involuntary reflex movements . . .”8

    Of the origins of the fit, Robert Bentley Todd9believed that “in all instances the hemispheric lobes are first disturbed, next follow the corpora quadrigemina, and upon the intensity of the disturbance depends the extent to which the medulla oblongata and the spinal cord are engaged.”10 Nothnagel had referred to “the convulsive centre” adjacent to the centre for respiration. Hammond in his A treatise on the diseases of the nervous system (1871) , like van der Kolk thought that the seat of epilepsy lay in the medulla; lesions in the cortex excited the medulla to produce the convulsive fit.

    Gowers clearly favoured the cortex: “ . . .all the phenomena of the fits of idiopathic epilepsy may be explained by the discharge of grey matter; that the hypothesis of vascular spasm is as unneeded as it is unproved; . . .that epilepsy is a disease of the grey matter, and has not any uniform seat.”11

    It was Hughlings Jackson (1834–1911) who finally formulated a physiological and rational definition: “A convulsion is but a symptom, and implies only that there is an occasional, an excessive, and a disorderly discharge of nerve tissue on muscles.”12

    Jackson reported that in focal attacks postmortem disclosed “coarse” diseases of the brain . . . The site of such lesions could be inferred from the onset of the fit. This was an important early step forward in rational cerebral localisation from clinical signs. His lucid and minute descriptions embraced the diverse intellectual,psychic, dreamy states, sensory, motor, and aphasic contents of various types of seizures, as well as the several postepileptic states.13 14 A convulsion was a positive phenomenon as opposed to the negative phenomena of paralysis. His deductions received ample confirmation and acknowledgement from David Ferrier’s experimental work15 and the galvanic stimulation of the brain carried out by Fritsch and Hitzig.

    Pharmacological and surgical treatments were to follow.

    References

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    Footnotes

    • * If in his fit he loses consciousness and foam comes from his mouth, it is miqtu. (cf major generalised fit)

    • (If in his fit) he loses consciousness and his arms and legs bend round to the same side as his neck, it is miqtu.

    • If at the end of his fit his limbs become paralysed . . .(cf Todd’s palsy)

    • If before his fit a half of his body is “heavy” for him and pricks him . . .(Jacksonian sensory aura)

    • If his seizure (or, possession) always takes place in the evening, it is the seizure of a ghost (nocturnal epilepsy).

    • . . .if he cries “My heart, my heart!”, if he blinks his eyes, has hot flushes (?), rubs involuntarily the tip of his nose and the tips of his fingers and toes are cold; if he remains conscious but when you try to speak with him he acts strangely- hand of Lilu-la’bi. (autonomic disturbances and automatisms of complex partial (temporal lobe) fits).

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