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Biomedical subjects

F Schon

Publications and source records attributed to F Schon.

At least 55 records · Page 3Linked to original sources
PubMed1987

Post-epileptic headache and migraine.

One hundred epileptic patients were questioned about their headaches. Post-ictal headaches occurred in 51 of these patients and most commonly lasted 6-72 hours. Major seizures were more often associated with post-epileptic headaches than minor attacks. Nine patients in this series of 100 also had migraine: in eight of these nine a typical, albeit a mild, migraine attack was provoked by fits. The post-ictal headache in the 40 epileptics who did not have migraine was accompanied by vomiting in 11 cases, photophobia in 14 cases and vomiting with photophobia in 4 cases. Furthermore, post-epileptic headache was accentuated by coughing, bending and sudden head movements and relieved by sleep. It is, therefore, clear that seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics. It is proposed that post-epileptic headache arises intracranially and is related to the vasodilatation known to follow seizures. The relationship of post-epileptic headache to migraine is discussed in the light of current ideas on migraine pathogenesis, in particular the vasodilation which accompanies Leao's spreading cortical depression.

Adult↗
PubMed1986

Optic neuritis following chickenpox in adults.

Three cases of bilateral optic neuritis, one of which also had transverse myelitis, are described in young adults following chickenpox. Severe bilateral loss of vision developed in all cases and was followed by good visual recovery in the two with isolated optic neuritis, but poor recovery in the patient with concomitant transverse myelitis. The interval between the initial rash and subsequent optic neuritis suggests an immunological pathogenesis for this complication.

Acyclovir↗
PubMed1986

The effect of 6-hydroxydopamine, reserpine and cold stress on the neuropeptide Y content of the rat central nervous system.

Neuropeptide Y has previously been detected in neurons throughout the rat brain and spinal cord. On histochemical grounds, the neuropeptide Y-containing cell bodies have been subdivided into two groups: those in the brain stem in which colocalization with noradrenaline and adrenaline has been demonstrated and those in other brain regions where no catecholamine coexistence is found. In this paper the regional distribution of neuropeptide Y has been investigated in the rat brain by a specific neuropeptide Y radioimmunoassay, before and after the destruction of catecholaminergic nerve terminals by the administration of intraventricular 6-hydroxydopamine. Despite massive reductions in brain catecholamines, the neuropeptide Y level was unchanged in the cerebral cortex, striatum, spinal cord and hippocampus. A minor reduction in neuropeptide Y was found in the hypothalamus. Reserpine treatment, which is known to deplete brain nerve terminal stores of catecholamines, likewise did not result in any loss of neuropeptide Y. Cold stress which increases noradrenergic turnover in the rat brain stem had no effect on neuropeptide Y levels. These results suggest that the bulk of neuropeptide Y in the rat brain and spinal cord may not be stored in catecholaminergic nerve terminals.

Animals↗
PubMed1986

Effect of reserpine, phenoxybenzamine and cold stress on the neuropeptide Y content of the rat peripheral nervous system.

The effect of reserpine treatment on the neuropeptide Y content of the rat adrenal gland, heart, kidney and vasculature was studied using a specific radioimmunoassay. One hour after reserpine administration (5 mg/kg) the neuropeptide Y concentration in the adrenal gland was significantly reduced and after 4 h a similar reduction was seen in the heart and kidney. After 48 h, neuropeptide Y concentrations were reduced in all tissues. The greatest reduction occurred in the cardiac septum (77%) and the least in the inferior vena cava (25%). Phenoxybenzamine (2 mg/kg) also caused a reduction in neuropeptide Y concentrations which was less marked than after reserpine, except in the adrenal gland where it was similar. Cold stress caused no change in neuropeptide Y concentrations. The neuropeptide Y depletion induced by reserpine was compared to that following 6-hydroxydopamine. In the heart and pial arteries both drugs caused a similar neuropeptide Y depletion whilst in the pineal gland and renal artery 6-hydroxydopamine had more effect than reserpine. The implications of these results on NPY storage sites are discussed.

Animals↗
PubMed1985

The effect of sympathectomy on calcitonin gene-related peptide levels in the rat trigeminovascular system.

The effect of sympathectomy on the calcitonin gene-related peptide (CGRP) level in the rat primary trigeminal sensory neurone was investigated. Six weeks after bilateral removal of the superior cervical ganglion there was a 70% rise in the CGRP content of the iris and the pial arteries, a 34% rise in the concentration in the trigeminal ganglion but no change in the brainstem. The CGRP rise in both end organs suggests that this phenomenon may be common to all peripheral organs receiving combined sensory and sympathetic innervations. The lack of any rise in the brainstem CGRP content raises the possibility that this process spares central terminations. In contrast, the level of neuropeptide Y, a peptide mainly contained in sympathetic terminals, fell to 35% of control values in the iris and pial arteries whilst the trigeminal ganglion and brainstem concentrations remained unchanged. The possible relevance of these observations to the clinical syndrome of postsympathectomy pain (sympathalgia) is discussed. There are similarities between the delayed onset of the human pain state and the delayed rise in sensory peptides after sympathectomy.

Animals↗
PubMed1985

Postsympathectomy pain and changes in sensory neuropeptides: towards an animal model.

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions. There is a characteristic interval of about 10 days between surgical sympathectomy and onset of pain. It is proposed that this pain in man is correlated with the delayed rise in sensory neuropeptides seen in rodents after sympathectomy. These chemical changes probably reflect the sprouting of sensory fibres and may result from the greater availability of nerve growth factor after sympathectomy. The balance between the sensory and sympathetic innervations of a peripheral organ may be determined by competition for a limited supply of nerve growth factor.

Animals↗
PubMed1985

Neuropeptide Y innervation of the rodent pineal gland and cerebral blood vessels.

Neuropeptide Y (NPY)-immunoreactivity has been shown to be present in sympathetic nerve fibres in the rat pineal gland and a dense network of NPY-containing nerve fibres demonstrated to innervate the rat circle of Willis. The NPY content of the major rabbit intracranial arteries was determined by radioimmunoassay and maximal levels found in the anterior cerebral arteries. After bilateral superior cervical ganglion (SCG) removal, no NPY was detectable in the rat pineal gland; however, significant NPY-immunoreactive nerve fibres remained throughout the rat vertebrobasilar arteries, and 47% of the assayable NPY was still present. Neither intraventricular 6-hydroxydopamine (6-OHDA) nor the combination of 6-OHDA treatment and SCG removal resulted in any further loss of NPY. In conclusion, the NPY innervation of the pineal gland originates exclusively from the peripheral sympathetic nervous system. In contrast the caudal portion of the rat circle of Willis contains NPY fibres which are resistant to sympathectomy.

Animals↗
PubMed1984

Presence of neuropeptide Y in human circle of Willis and its possible role in cerebral vasospasm.

Neuropeptide Y (NPY) has been demonstrated in the human circle of Willis by specific radioimmunoassay. Concentrations were similar in cadaver and peroperative specimens. NPY concentrations were highest around the basilar bifurcation (2.9 +/- 1.0 pmol/g), anterior cerebral artery (2.7 +/- 0.5 pmol/g), and carotid trifurcation (2.4 +/- 0.6 pmol/g). Concentrations were lowest in the basilar artery (1.0 +/- 0.4 pmol/g). Intracarotid administration of NPY (50 pmol to 2 nmol) to rats reduced mean cerebral cortical blood flow by 40-98%. This vasoconstriction lasted for at least 2 h. These findings suggest that NPY may be involved in the cerebral vasospasm which follows subarachnoid haemorrhage and in the maintenance of normal vascular tone.

Animals↗
PubMed1984

Subarachnoid haemorrhage in identical twins.

A pair of identical twins both of whom died of subarachnoid haemorrhage from ruptured anterior communicating artery aneurysms are reported. These twins are compared to the three other reported twins with ruptured cerebral aneurysms.

Adult↗