Biomedical subjects
J W Lance
Publications and source records attributed to J W Lance.
Pathological sweating and flushing accompanying the trigeminal lacrimal reflex in patients with cluster headache and in patients with a confirmed site of cervical sympathetic deficit. Evidence for parasympathetic cross-innervation.
Electrodermal responses (as a measure of sweating) and vascular responses to irritation of the eye were investigated in 11 cluster headache patients and, for comparison, in another 24 patients with a confirmed site of lesion in the cervical sympathetic pathway. Seven of the cluster headache patients had ocular and thermoregulatory signs of a postganglionic sympathetic lesion. In these patients, and in six of seven patients with a postganglionic sympathetic lesion from some other cause, the electrodermal response to ocular stimulation was far greater on the denervated side of the forehead than on the sympathetically intact side. This pathological response can be explained by lacrimotor fibres branching into vacant sympathetic sudomotor pathways. The response could account for excessive forehead sweating during attacks of cluster headache, in spite of the presence of Horner's syndrome, because parasympathetic outflow to the lacrimal glands increases during attacks. In patients with diminished sympathetic vasomotor outflow, the vascular response to ocular irritation was also greater on the denervated side of the forehead than on the sympathetically intact side, irrespective of the site of the lesion. The excessive vascular response in sympathetically denervated skin could be caused by adaptive supersensitivity to peptides such as vasoactive intestinal polypeptide, which is known to be released from parasympathetic terminals. The same mechanism might augment vasodilatation during attacks of cluster headache.
The E. Graeme Robertson Lecture. Interesting neurological syndromes.
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The pathophysiology of migraine: a tentative synthesis.
It is proposed that the migraine attack is explicable by an interaction between the brain and the cranial circulation in subjects with unstable vascular and pain-control mechanisms. While peptides are undoubtedly involved in vasodilatation, there is strong evidence that 5-HT plays an important part in the genesis of migraine. Whether the place of 5-HT lies in central pain-control pathways, in the serotonergic project to the cerebral cortex, in a direct action on the cranial blood vessels or in its action at all three sites remains uncertain. It seems probable that the primary action of sumatriptan or ergotamine in terminating migraine headache is exerted on the cerebral and extracranial circulation whereas medications employed in prophylaxis may act centrally.
The second Seah Cheng Siang Memorial Lecture. Clinical skills in an age of technology.
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[Association of 2 phacomatoses].
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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.
Multiple right-sided cranial nerve palsies.
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Cervical spinal cord neurons receiving sensory input from the cranial vasculature.
The superior sagittal sinus, middle meningeal artery or superficial temporal artery was stimulated electrically in anaesthetized cats. Field potential recordings were used to locate areas of maximum responses in the upper cervical cord, which were then further examined for responsive single units. Short latency units responded to stimulation of the superior sagittal sinus with a mean latency of 11.9 ms. Some units also responded at longer latencies in the 200-250 ms range. Spontaneous discharge rates of some units in a dorsolateral area of the cervical cord were accelerated by iontophoretic application of glutamic or homocysteic acid to these same units. Evoked action potentials were commonly multiphasic. Dorsolateral area units commonly received convergent input from two vessels and often had receptive fields on the face and limbs. Spontaneously active cells which respond to electrical stimulation were accelerated by the local application of bradykinin to the sinus and responses of dorsolateral area units could be reversibly blocked by local application of lignocaine to the sinus. It was concluded that the dorsolateral area is a relay area for the perception of pain from cranial vessels.
Solved and unsolved headache problems.
Two unusual cases of vascular headache, one caused by jugular venous compression from a goiter and one triggered by flushing associated with a CGRP-producing renal tumour, are reported. Their histories are compared with those experiencing other headaches of vascular origin. Two patients with a primary neural irritative lesion, one with a sphenoid sinus carcinoma and one with Tolosa-Hunt syndrome, presented with headaches resembling migraine. These case-histories are used to illustrate the interaction of nervous system and vascular system in the production of headache which has implications for the pathophysiology of migraine and cluster headache.
The hospital management of severe migrainous headache.
In a two year period, 47 patients with migraine were hospitalized for the management of severe headache; 18 had acute migraine (duration less than 72 hours), 17 had status migrainosus (duration by definition more than 72 hours), and 12 had chronic daily headaches qualitatively of a migraine type. Treatment in all comprised cessation of all previous medication, plus one of the following: intravenous DHE, intravenous lidocaine, a combination of lidocaine + DHE, or subcutaneous sumatriptan. Improvement from DHE, lidocaine, or both was slow and often incomplete. Sumatriptan was not used in patients with chronic daily headaches; in the 8 cases of acute migraine or status migrainosus in which it was used, improvement was rapid and complete in seven.
5-Hydroxytryptamine and its role in migraine.
Platelet 5-hydroxytryptamine (5-HT) is diminished during migraine headache and the injection of reserpine, which releases 5-HT from body stores, induces a typical headache in migrainous subjects. The intravenous injection of 5-HT relieves established migraine headache, but causes side-effects of nausea, faintness, paraesthesia and dyspnoea. The 5-HT1-like agonist sumatriptan exerts the beneficial effects of 5-HT with minimal side-effects. Receptors for 5-HT are present in cranial arteries and are also widely distributed in the central nervous system, where they play a role in the neural control of the cranial circulation and endogenous pain control system. The pathophysiology of migraine involves interaction between these central pathways and cranial blood vessels. It is probable that many prophylactic agents exert their action by central 5-HT2 antagonism, whereas termination of an established attack of migraine depends upon constriction of cranial vessels mediated by 5-HT1 receptors.
Parietal sensory loss simulating a peripheral lesion, documented by somatosensory evoked potentials.
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[Physiopathology of migraine].
In those subjects genetically susceptible to migraine, biological rhythms or excessive afferent stimulation trigger an episodic neurovascular reaction with focal neurological symptoms, headache and nausea as its most common manifestations. Mood changes and a craving for sweet foods point to a preliminary hypothalamic disturbance. The referral of ice-cream headache and ice-pick pains to the habitual site of migraine headache (even in the intervals between attacks) indicate defective control of trigeminal pathways. Laboratory experiments have demonstrated that projections from the brainstem, releasing monoamines and peptides as transmitter agents, can mimic the vascular changes of migraine. Serotonin released from platelets may sensitize vessels to respond to distension by generating pain-producing afferent discharges. Central depletion of monoamines can accentuate the perception of pain by reducing the efficacy of the endogenous pain control system. The intravenous injection of serotonin relieves migraine headache but produces side-effects. A new drug, sumatriptan, acting on a subtype of serotonin receptors, the 5HT1-like receptor, is undergoing clinical trial for the relief of acute attacks of migraine. Antagonist of the 5HT2 receptor are beneficial in interval therapy for the prevention of migraine. Increased knowledge of physiological mechanisms and neurotransmitters that can mediate the various components of the migraine attack opens the way for improvements in pharmacotherapy.
A concept of migraine and the search for the ideal headache drug.
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