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Biomedical subjects

J W Lance

Publications and source records attributed to J W Lance.

At least 91 records · Page 5Linked to original sources

The peripheral pathway for extracranial vasodilatation in the cat.

The locus coeruleus was electrically stimulated in 27 cats with high spinal cord sections. Common carotid blood flow was measured using electromagnetic flow probes, and arterial resistance calculated from mean arterial blood pressure and flow. Activation of the locus coeruleus caused an ipsilateral decrease in common carotid resistance, an effect previously demonstrated to depend on the integrity of the facial nerve. This vasodilator response is now shown to be mediated approximately equally by the pterygopalatine (sphenopalatine) and otic ganglia.

Animals↗

Facial temperature in migraine, tension-vascular and tension headache.

The relationship between clinical features and changes in the extracranial circulation was studied during 209 separate attacks of headache affecting the anterior part of the head. Extracranial vascular changes were assessed thermographically and by the change in headache intensity when pressure was applied over the superficial temporal and common carotid arteries. In unilateral headaches, increased heat loss from the affected frontotemporal region was observed most frequently in attacks which were temporarily relieved by compression of the superficial temporal artery; thermographic asymmetry disappeared as the headache abated. Although such headaches were associated more frequently with migrainous features than attacks which did not respond to arterial compression, many headaches with clinical features of migraine had no vascular component detectable by thermography or vascular compression. Furthermore, the response to arterial compression was not consistent from one headache to another in the same patient. It was concluded that extracranial vascular changes recur intermittently in headache-prone patients, depending on the severity of pain and association with other features commonly regarded as migrainous. However, there was no clear demarcation point between entities diagnosed clinically as "migraine" and "tension headache".

Adolescent↗

Clinical diagnosis and computer analysis of headache symptoms.

The headache histories obtained from clinical interviews of 600 patients were analysed by computer to see whether patients could be separated systematically into clinical categories and to see whether sets of symptoms commonly reported together differed in distribution among the categories. The computer classification procedure assigned 537 patients to the same category as their clinical diagnosis, the majority of discrepancies between clinical and computer classifications involving common migraine, tension-vascular and tension headache. Cluster headache emerged as a clearly-definable syndrome, and neurological symptoms during headache were most prevalent in the classical migraine group. However, the classical migraine, common migraine, tension-vascular and tension headache categories differed in terms of the number, rather than the nature, of common migraine features. Whether the two extremes of this migraine-tension headache spectrum are different disorders can be determined only by studies of their pathophysiology.

Cluster Headache↗

Thermographic changes in cluster headache.

Eleven patients were examined thermographically during spontaneous cluster headaches and 22 during attacks induced by nitroglycerin or alcohol. In cluster headache, heat loss increased from the affected orbital region, and in some patients, this spread above and below the eye, down the nose, and to the affected temple. Inhalation of 100% oxygen reduced or abolished cluster pain in 22 of 25 instances, and asymmetry of heat loss then disappeared. Since the unilateral increase in blood flow usually followed the onset of pain in affected areas, the vascular changes of cluster headache are probably secondary phenomena, initiated by a vasodilator pathway, with the trigeminal nerve as the afferent and the greater superficial petrosal nerve as the efferent limb.

Adult↗

Intermittent claudication of one cerebral hemisphere.

A 13-year-old girl consistently developed unilateral sensory and motor symptoms on hyperventilation, suggesting the diagnosis of hysteria. Investigation disclosed hypoplasia of one internal carotid artery and part of the circle of Willis, responsible for compromising blood flow to one hemisphere sufficiently to produce ischemic deficit during hypocapnia.

Adolescent↗

Decreased carotid arterial resistance in cats in response to trigeminal stimulation.

Stimulation of the trigeminal nerve or ganglion in the cat caused a frequency-dependent reduction in carotid vascular resistance. Systemic arterial blood pressure (SABP) decreased at low frequencies (0.2 to 5 sec-1) and increased at higher frequencies, thus increasing carotid blood flow at the higher frequencies. The effect on resistance was predominantly ipsilateral and was unaltered by cervical sympathectomy, but was abolished or substantially reduced by section of the trigeminal root proximal to the ganglion. Diminution of carotid vascular resistance was replicated by stimulation of the greater superficial petrosal (GSP) nerve without any change in SABP. Section of the seventh cranial nerve reduced or abolished the response to stimulation of the trigeminal nerve but not that from the GSP nerve. The trigeminal response was prevented by ganglion-blocking drugs in seven out of eight cats. The resistance response was unaffected by noradrenergic, cholinergic, serotonergic, and histamine-2 blocking agents. No neural connection could be demonstrated between the GSP and the trigeminal ganglion, and the vascular response to GSP stimulation persisted after trigeminal section. It is concluded that activation of the trigeminal system increases carotid blood flow by a pathway involving the seventh cranial nerve, the GSP and Vidian nerves, and a parasympathetic synapse employing an unconventional transmitter. A varying proportion of the response (greatest in the third division) may be mediated by antidromic activation of trigeminal nerves. These findings may have clinical implications for the vascular changes of migraine and other facial pain.

Animals↗

Dilatation in the carotid vascular territory of the cat in response to activation of cell bodies in the locus coeruleus.

Electrical stimulation of the locus coeruleus in the monkey results in a frequency-dependent vasoconstriction in the internal carotid circulation, and a frequency-dependent vasodilatation in the external carotid circulation. In the cat we have studied the extracerebral vasodilator response using electrical stimulation at appropriately high frequencies. Further investigations reported here demonstrate that 1-glutamate, a non-specific neuronal excitant, reproduces the dilator response in the cat. This clearly shows that the response to electric stimulation of the locus coeruleus, previously reported, is due to excitation of cell bodies rather than fibres of passage.

Animals↗

Progressive myoclonic epilepsy, nerve deafness and spinal muscular atrophy.

A boy of Finnish descent developed nerve deafness at six years of age, action myoclonus two years later, generalized myoclonic seizures when 16 years old and muscular atrophy at the age of 17 years. Bulbar palsy caused his death from inhalational pneumonia when he was 19 years old. Autopsy disclosed no significant changes in the cerebral cortex, thalamus, striatum, Purkinje cells or dentate nucleus. The most striking histological finding was degeneration of motor neurones in cranial nerves and anterior horns of the spinal cord, with neuroaxonal dystrophy of nucleus gracilis and cuneatus. While nerve deafness and spinal muscular atrophy have been recorded (each in different families) in association with progressive myoclonic epilepsy, the combination of these features has not previously been reported. Reasons are put forward for regarding all the system degenerations found in PME, including Unverricht-Lundborg disease (Baltic myoclonus) and the Ramsay Hunt syndrome, as variations of the same disorder.

Adult↗

Neurovascular disturbances in headache patients.

The prevalence of icecream headache, icepick-like pains and premonitory symptoms (changes in mood, appetite and alertness one to 24 hours before headache onset) was studied in 530 patients referred for neurological assessment of headache. Pain in the head after icecream or cold drinks was reported by 37% of patients, more often by those whose headaches were associated with focal neurological symptoms and gastrointestinal disturbances. The affected region coincided with that of the customary headache in 33% of patients questioned. Icepick-like pains were reported by 39% of patients and were restricted to the distribution of the customary headache in 40% of these. Premonitory symptoms were noted by 30% of patients, particularly those with focal neurological symptoms before or during the attack. Premonitory symptoms may form part of a diffuse cerebral or hypothalamic disturbance preceding headache, while the prevalence of icecream headache and icepick-like pains suggests that pain pathways and neurovascular reflexes to sensory stimulation are hyperexcitable even between headache episodes. These phenomena favour a neurological origin of migrainous headache.

Adolescent↗

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.

Animals↗

Extracranial vascular changes and the source of pain in migraine headache.

The extracranial circulation of 66 migrainous patients was assessed during unilateral headache by recording the pulse amplitude of the superficial temporal artery and its main frontal branch, by facial thermography, and by changes in the intensity of headache when temporal or carotid arteries were compressed. Amplitude of pulsation of the superficial temporal artery did not differ between headache and headache-free sides but the amplitude of its frontal branch was increased on the headache side, specifically in a subgroup of patients whose headache was relieved by compressing the superficial temporal artery ("extracranial vascular" group). Facial thermograms demonstrated significant differences in heat loss from the temples and orbits between migrainous patients and controls, frontotemporal changes being more conspicuous in the extracranial vascular group. It was concluded that dilatation of the superficial temporal artery and its branches contributes substantially to migraine headache in only a minority of patients.

Carotid Arteries↗

Benign intracranial hypertension.

Benign intracranial hypertension is caused by defective cerebrospinal fluid (CSF) absorption which may sometimes be secondary to partial superior sagittal sinus obstruction. It may appear in obese young women for obscure hormonal reasons or may be a reaction to head injury, infections or certain medications. It commonly presents with headache and papilloedema, sometimes with associated ocular palsies. Conservative management comprises repeated lumbar puncture, salt and fluid restriction and the use of diuretics or steroids. Surgical treatment such as CSF shunting procedures, optic nerve decompression or subtemporal decompression may become necessary. The results of treatment have not been subjected to adequate evaluation, but the patient usually recovers well, although some 10% suffer severe visual impairment and 10% are subject to recurrence.

Adolescent↗

Facial flushing after thermocoagulation of the Gasserian ganglion.

The development of a facial flush during thermocoagulation of the Gasserian ganglion was monitored in 16 patients with pulse recording techniques and in a further 17 patients with thermography. There was a close association between the development of the facial flush in the distribution of one or more divisions of the trigeminal nerve and the subsequent demonstration of postoperative analgesia. In regions where significant changes took place, vascular pulsations increased 25-233% (mean 96%) and facial temperature rose 0.5-2.0 degrees C. The response persisted for up to an hour postoperatively, and was not diminished in patients with pre-operative analgesia from a previous procedure. Possible mechanisms for the facial flush, including stimulation of an active vasodilator system, the antidromic release of vasoactive substances from trigeminal nerve terminals and the release of tonic vasoconstriction are discussed. A practical application of the pulse recording technique used in the present investigation would be to monitor the distribution of vasodilatation at operation to avoid unwanted first division sensory loss.

Adult↗

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.

Adrenergic Fibers↗

What is a migraine?

The migrainous patient appears to differ in reaction to stress or environmental changes from nonmigrainous subjects quantitatively rather than qualitatively. An inherited pattern of monoamine metabolism may render the patient more susceptible to such changes, which represent a threat, real or imagined, to the integrity of the brain. The migraine attack may thus be interpreted as a neurohumoral reaction aimed at protecting the brain from some noxious influence by shunting blood away from the cortex. The headache itself may be a by-product of such a reaction, serving, like any pain, to alert the organism to potential danger. The predominantly unilateral site of migraine remains unexplained. A more comprehensive clinical classification of migraine is proposed in the hope that certain entities may prove to correlate with variations in pathophysiology and thus permit more selective therapy.

Catecholamines↗

Headache.

Present views on the cause and treatment of temporal arteritis, trigeminal neuralgia, pain arising from the neck, benign intracranial hypertension, and other headaches of intracranial origin are summarized. The clinical components of migraine are correlated with recent studies of cerebral blood flow, monoamine changes, and the platelet release reaction. Psychological, physiological, and pharmacological management is based on the holistic concept of migraine as an uninhibited protective reaction. Cluster headache is subdivided into three varieties which respond preferentially to different medication. Tension headache may depend more on vascular mechanisms than excessive muscle contraction, but treatment is still directed at behavioral management and relaxation training with the aid of antidepressant therapy.

Carotid Artery Diseases↗