Semin Neurol 2006; 26(2): 271-276
DOI: 10.1055/s-2006-939927
HISTORICAL NOTES

Copyright © 2006 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Latham and the Vasomotor Theory of Migraine

J.M.S. Pearce1
  • 1Emeritus Consultant Neurologist, Department of Neurology, Hull Royal Infirmary, and Hull York Medical School, United Kingdom
Further Information

Publication History

Publication Date:
21 April 2006 (online)

Among the lengthy annals of descriptive accounts of migraine and its mechanisms, the 19th century writings[1] are pre-eminent. This paper gives a précis of the vasomotor theory propounded by Latham, in On Nervous or Sick-Headache, written at the time of Edward Liveing's (1873) scholarly book[2] that supported the contrary neural hypothesis. Liveing was Registrar to the Royal College of Physicians of London and Assistant Physician to King's College Hospital. He favored “nerve storms” as the principal mechanism, the forerunner of modern neural theories.[3] In explaining his “nerve storm” theory,[4] he considered migraine along with other “neuroses” to be:

… a primary and often hereditary disposition of the nervous system itself; this consists in a tendency to the irregular accumulation and discharge of the nerve force.”

Hughlings Jackson also favored a neural initiation of migraine:

Some of the symptoms of migraine, the headache among others, are, I think, after-effects of the discharge producing the paroxysm.5

By “middle centres” Jackson referred to the basal nuclei, which in his concept were subservient to the cortex and associational areas that were the higher centres in terms of cerebral organization. Gowers[6] also adhered to the neurogenic hypothesis.[3]

Latham's idea was of a primary vascular mechanism with dilated arteries causing the pulsating headache and the preceding or accompanying vasoconstrictor phase that was thought to account for the diverse symptoms of the migraine aura. This theory was to be examined,[7] and much later was amplified particularly by the groundbreaking investigations of Harold Wolff[8] and his collaborators between 1930 and 1963. Before Latham, Du Bois-Reymond (1818-1896) in 1860 attributed migraine to:

… a Tetanus takes place in the muscular coats of the vessels of the affected half of the head; in other words a Tetanus of the cervical portion of the sympathetic.9

In his “hemikrania sympathicotonica,” Du Bois-Reymond postulated an increased sympathicotonic effect on the blood vessels of one side of the head. Migraine was not a disease of the brain or cranial blood vessels, but of the cilio-spinal center in the cord. Brown-Séquard, in respect of Du Bois-Reymond's paper, said that irritation of the cervical sympathetic did not cause pain.

REFERENCES

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  • 2 Liveing E. On Megrim, Sick Headache, and Some Allied Disorders: A Contribution to the Pathology of Nerve Storms. London; Churchill 1873
  • 3 Pearce J MS. Is migraine explained by Leão's spreading depression?.  Lancet. 1985;  2 763-766
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  • 5 Jackson J H. Diagnosis and treatment of brain diseases. In: Taylor J Selected Writings of JH Jackson. Vol. 2. London; Staples Press 1958: 371-372
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  • 11 Pearce J MS. Current Topics In Migraine. London; Heinemann 1975
  • 12 Airy H. On a Distinct Form of Transient Hemiopsia. Philosophical; Transactions 1870: 247
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  • 17 Rao N S, Pearce J MS. Hypothalamic-pituitary-adrenal axis studies in migraine with special reference to Insulin sensitivity.  Brain. 1971;  94 289-298
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  • 19 Goadsby P J. Advances in the understanding of headache.  Br Med Bull. 2005;  73-74 83-92
  • 20 Goadsby P J. Can we develop neurally acting drugs for the treatment of migraine?.  Nat Rev Drug Discov. 2005;  4 741-750
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J.M.S. PearceM.D. F.R.C.P. 

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