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Biomedical subjects

J W Lance

Publications and source records attributed to J W Lance.

At least 37 records · Page 2Linked to original sources
PubMed1994

Negative myoclonus.

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Electromyography↗
PubMed1994

The mystery of one red ear.

Flushing and a sensation of tightness or pain in one ear lobe was a presenting complaint of 3 patients. In one case the symptoms were confined to the ear, another was associated with sensory impairment in the distribution of the C2 and C3 segments, while the 3rd patient experienced discomfort in the area of the 1st division of the trigeminal nerve on the same side. Two out of 3 patients had evidence of hypertrophy of the ipsilateral C2-3 facet joint and the symptoms of the 3rd patient were improved by an ipsilateral C2-3 root block. A possible mechanism could be the antidromic release of vasodilator peptides from afferent nerve terminals in response to irritation of the C3 root which supplies sensory innervation to the pinna.

Adult↗
PubMed1993

Site of autonomic deficit in harlequin syndrome: local autonomic failure affecting the arm and the face.

The site of autonomic deficit was investigated in 4 patients with loss of thermoregulatory flushing and sweating on one side of the face but no associated miosis (harlequin syndrome). In 2 patients the sudomotor deficit included the hand. Signs of postganglionic sympathetic deficit included pathological lacrimal sweating (2 patients) and supersensitivity to 1% phenylephrine eyedrops (3 patients). One or both pupils constricted excessively to 0.0625% pilocarpine eyedrops (3 patients), consistent with ocular parasympathetic deficit. These findings suggest that pre- or postganglionic cervical sympathetic fibers, and parasympathetic neurons in the ciliary ganglia, are compromised in harlequin syndrome. The finding of cholinergic supersensitivity in the iris muscles of patients with harlequin syndrome indicates a relationship with Holmes-Adie syndrome, Ross's syndrome, and the persistent autonomic deficit occasionally associated with Guillain-Barré syndrome.

Adult↗
PubMed1993

Current concepts of migraine pathogenesis.

Migraine is a neurovascular reaction to sudden changes in the internal or external environment. Each individual has a hereditary "migrainous threshold," with the degree of susceptibility depending on the balance between excitation and inhibition at various levels of the nervous system. The mechanism of migraine has been presented as an unstable trigeminovascular reflex with a segmental defect in the pain control pathway. This defect permits excessive discharge of part of the spinal nucleus of the trigeminal nerve and its thalamic connections in response to excessive afferent input or corticobulbar drive. The end result is the interaction of brain stem and cranial blood vessels, with the afferent impulses from the latter creating the throbbing (pulsating) character of the headache. Diffuse projections from the locus ceruleus to the cerebral cortex could initiate cortical oligemia and possibly spreading depression. Activity in this system could account for the migrainous aura that may occur quite independently of the headache. The headache phase may be interrupted by therapy aimed at either the central or peripheral end of the trigeminovascular afferent pathway. Strong evidence suggests that serotonin (5-hydroxytryptamine, 5-HT) plays an important part in the genesis of migraine. Whether 5-HT is effective in central pain control pathways, the serotonergic projection to the cerebral cortex, its direct action on the cranial blood vessels, or its action at all three sites remains uncertain. It seems probable that the 5-HT agonists act to terminate migraine through the cerebral and extracranial circulations, whereas medications used for prophylaxis may act centrally.

Cerebrovascular Circulation↗
PubMed1992

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.

Adult↗
PubMed1992

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.

Brain Stem↗
PubMed1991

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.

Acute Disease↗
PubMed1991

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.

Action Potentials↗
PubMed1991

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.

Adult↗
PubMed1991

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.

Adolescent↗