James W. Lance

Observations on 500 cases of migraine and allied vascular headache

Title: OBSERVATIONS ON 500 CASES OF MIGRAINE AND ALLIED VASCULAR HEADACHE1 Authors: Selby G, Lance J W Published: 1960 Migraine: the clues were there 50 years ago, suggests James W Lance, Professor Emeritus of Neurology, University of New South Wales, Sydney In the 1950s, before the Ad Hoc Committee on the Classification of Headache and the more detailed criteria devised by the International Headache Society from 2004 onwards, the separation of headache entities was far from clear. During that period I had the privilege of having George Selby as a mentor while attending the Northcott Neurological Centre in Sydney. He was a meticulous clinician with a particular interest in migraine, a condition that was in ample supply in that outpatient clinic, which had been established to provide neurological advice to returned servicemen and their families after World War II. Retrospective analysis of data was aided by a set pattern of history taking and typed records. Why did we refer to ‘allied vascular headaches’? The occurrence of severe episodes …

The control of muscle tone, reflexes, and movement Robert Wartenbeg Lecture

My pleasure at being invited to give the Wartenberg lecture this year was enhanced by the admiration I hold for the writings of Wartenberg, who pruned the eponymous tree in which so many clinicians of the past had sought to roost forever. Vast numbers of named reflexes evoked by stroking, squeezing, or tapping some bodily appendage were shown to be different ways of testing the same mechanism.’S2 Wartenberg’s analysis simplified neurology by clearing away unnecessary and confusing terminology. Robert Wartenberg was born in the Russian city of Grodno in 1887, graduated in medicine with distinction from the University of Rostock in Germany and became Physician-in-Chief of the Nerve Clinic in Freiburg before fleeing from Germany in the dark days of 193!X3 For 20 years, until his death in 1956, Wartenberg served American neurology well, becoming Clinical Professor of Neurology at the University of California School of Medicine, San Francisco, in 1952. He was a fellow of the American Academy of Neurology and an associate editor of Neurology. To those who knew him, he combined precision of thought and a sharp critical faculty with a capacity for warmth and humor. Dr. Robert Aird recalls his rejecting compromise with the zestful cry “By the great Babinski, Professor Sigvald Refsum told me of an occasion when Wartenberg was demonstrating the physical signs of a patient with double athetosis. Wartenberg commented that the patient’s facial movements resembled those of someone chewing gum. He was startled when the patient said, “But I am chewing gum,” removing the gum from his mouth and displaying it to the laughing audience. Wartenberg promptly retorted, “Then this is double double athetosis.” In honored memory of such a man, it is my privilege to dedicate this lecture. My own interest in neurology was aroused as a medical student because the explanation of many physical signs did not ring true. Was spasticity really the same as decerebrate rigidity? Was the cogwheel phenomenon in Parkinson disease caused by the combination of the classical tremor and rigidity when some patients did not have a perceptible tremor? How could degeneration of the dorsal columns abolish tendon jerks in Friedreich ataxia? Why did so many muscles contract when the radius was tapped in a spastic patient? My opportunity to study the motor system arrived when Dr. Peter Bishop, now Professor of Physiology in the Australian National University, Canberra, started a brain research unit in the University of Sydney and encouraged me to work on the pyramidal tract. The outcome of those early years was the finding of two groups of fibers with distinctive properties in the cat pyramidal tract,* the mapping of their origin from the ~ o r t e x , ~ their distribution in the cord6 and the fact that they made no attempt to regenerate after the pyramidal tract was sectioned.’ It is probable that the more slowly conducting group is related to the maintenance of posture and the rapidly conducting group to phasic movement8 but the interaction of the two groups may be comple~ .~

Brainstem Influences on the Cephalic Circulation: Experimental Data From Cat and Monkey of Relevance to the Mechanism of Migraine

SYNOPSIS

Harlequin syndrome: the sudden onset of unilateral flushing and sweating.

Facial flushing and sweating were investigated in five patients who complained of the sudden onset of unilateral facial flushing in hot weather or when exercising vigorously. One patient probably suffered a brainstem infarct at the time that the unilateral flush was first noticed, and was left with a subtle Horners syndrome on the side opposite to the flush. The other four had no other neurological symptoms and no ocular signs of Horners syndrome. Thermal and emotional flushing and sweating were found to be impaired on the non-flushing side of the forehead in all five patients whereas gustatory sweating and flushing were increased on that side in four of the five patients, a combination of signs indicating a deficit of the second sympathetic neuron at the level of the third thoracic segment. CT and MRI of this area failed to disclose a structural lesion but latency from stimulation of the motor cortex and thoracic spinal cord to the third intercostal muscle was delayed on the non-flushing side in one patient. The complaint of unilateral flushing and sweating was abolished in one patient by ipsilateral stellate ganglionectomy. The unilateral facial flushing and sweating induced by heat in all five patients was thus a normal or excessive response by an intact sympathetic pathway, the other side failing to respond because of a sympathetic deficit. The onset in the four cases of peripheral origin followed strenuous exertion, which suggested that an anterior radicular artery may have become occluded at the third thoracic segment during torsion of the thoracic spine.

Differential effects on the internal and external carotid circulation of the monkey evoked by locus coeruleus stimulation.

Electrical stimulation at 1-200/s of the locus coeruleus in 12 Macaca nemestrina monkeys caused a frequency-dependent drop in vascular resistance in the extracerebral circulation which was twice as great on the side stimulated. Accompanying this dilatation of the extracerebral vasculature was a frequency-dependent rise in internal carotid vascular resistance, usually seen only on the side ipsilateral to stimulation. This constrictor response was maximal at low frequencies of stimulation and minimal at higher frequencies. Neither the dilator nor constrictor responses were affected by sectioning of the vagus nerve or sympathetic trunk in the neck. The simultaneous occurrence of intracranial vasoconstriction and extracranial vasodilatation has not been demonstrated previously, and bears a remarkable resemblance to the vascular changes of migraine.

Oral sumatriptan in acute migraine

The efficacy in acute migraine of oral sumatriptan was assessed in a double-blind, randomised, placebo-controlled, crossover study of 61 patients (mean age 39 [SD 10] years). 41 completed treatment of four attacks, two with sumatriptan 100 mg and two with placebo. The response rate (reduction in headache from moderate or severe to mild or absent at 2 h) was 51% (45/89) with sumatriptan and 10% (9/93) with placebo (p less than 0.01); rescue medication was needed at 2 h in 41% and 88%, respectively. Of 28 patients headache-free at 24 h, 11 (39%) had recurrent headache within 24 h. There were no substantial side-effects. Thus, sumatriptan is an effective well-tolerated treatment for acute migraine attacks.

Ophthalmoplegic migraine: a recurrent demyelinating neuropathy?

The demonstration by magnetic resonance imaging (MRI) scanning of thickening and enhancement of the cisternal part of the oculomotor nerve in patients diagnosed as ‘ophthalmoplegic migraine’ prompts reconsideration of this uncommon disorder. The case histories of five patients, three male and two female, varying in age from 6 to 30 years, are presented here. Recurrent painful ophthalmoplegia started in infancy in two cases, childhood in two instances and adult life in one. One child had his first attacks at 3, 5 and 12 months of age, on each occasion 10 days after an injection of triple vaccine. The possibility of this condition being a recurrent demyelinating neuropathy is considered and its possible relationship to migraine explored.

Stimulation of the Trigeminal ganglion increases flow in the extracerebral but not the cerebral circulation of the monkey

The trigeminal ganglion of 9 anesthetized paralysed artificially ventilated Macaca nemestrina monkeys was electrically stimulated with frequencies varying from 0.2 to 200 Hz. This stimulation led to a frequency-dependent decrease in external carotid resistance but no significant change in internal carotid resistance was recorded. The response is probably mediated as previously described in the cat, i.e. predominantly through the greater superficial petrosal branch of the facial nerve and a small proportion through antidromic activation of the trigeminal system. Elucidation of the physiological and pharmacological mechanisms underlying such a response may aid in a better understanding of the pathophysiology of vascular headache.

The red ear syndrome

The complaint of a painful, burning, red ear may be associated with irritation of the third cervical root, temporomandibular joint dysfunction, or thalamic syndrome.It may also occur without obvious structural cause in response to touch or heat. The condition may be an example of the ABC (Angry Back-firing C-nociceptor) syndrome with the increase in ear temperature being caused by the antidromic release of vasodilator peptides. NEUROLOGY 1996;47: 617-620

Effects of locus coeruleus stimulation on carotid vascular resistance in the cat

The locus coeruleus was stimulated in 62 cats in order to investigate the effect on cephalic blood flow and cephalic vascular resistance. Flow was measured by electromagnetic flow probes applied to the common carotid artery. Stimulation over a range of frequencies (0.2-200 s-1) produced a frequency-dependent fall in carotid vascular resistance, greater on the ipsilateral side. This response was not affected by either cervical sympathectomy or spinal cord section. The response was blocked by bilateral section of the facial nerve but was not abolished by classical cholinergic, histaminergic or adrenergic blocking agents. Stimulation of the locus coeruleus also resulted in a pressor response through spinal mechanisms in which coeruleo-hypothalamic projections were not involved. A post-stimulation constriction in the carotid vasculature followed the dilator response and was attributed to release of catecholamines from the adrenal medulla.