Biomedical subjects

M Besser

Publications and source records attributed to M Besser.

At least 55 records · Page 3Linked to original sources

PubMed1992

Anaerobic osteomyelitis in patients with Gaucher's disease.

Bone involvement in patients with Gaucher's disease is common, and some of its clinical manifestations may resemble acute osteomyelitis. In addition, many studies have emphasized the high risk of secondary infection when surgical procedures are performed at the site of the involved bone. Nevertheless, these infections have never been well documented in the literature. Presentation of a patient with Gaucher's disease and osteomyelitis due to Prevotella (Bacteroides) melaninogenica provided us the opportunity to review 10 other similar case reports documented in the literature since 1966. This review suggests that acute hematogenic osteomyelitis is an uncommon complication of Gaucher's disease, but it is of interest that in most cases it is due to unusual organisms, particularly anaerobes.

Adult↗

PubMed1992

Controversies in the management of brainstem cavernous angioma: report of two cases.

Two cases of cavernous angioma involving the medulla oblongata are presented. Both cases underwent surgical excision with excellent outcome. The use of surgery via craniectomy is contrasted with stereotactic radiosurgery in light of the known natural history of the lesions. As a result, it is suggested that surgical excision provides immediate protection from the risks of recurrent haemorrhage, establishes a tissue diagnosis, allows complete removal at the primary intervention, avoids complications of radiation-induced damage and is performed more easily in these vascular anomalies due to the presence of a capsule with surrounding gliotic tissue. Additionally, it is implied that the natural history of lesions in this region is still unclear. For these reasons, it is suggested that surgical excision should be the primary therapeutic intervention for cavernous angiomata that involve the brainstem.

Adult↗

PubMed1992

Spinal cord compression in prostate cancer. A 10-year experience.

Of 478 patients treated at a single institution for prostate cancer, 29 developed spinal cord or cauda equina compression. In 5 patients, spinal cord compression was the first evidence of malignancy. Clinical features were predominantly pain, weakness, sensory and sphincter disturbance. The median duration of symptoms was 2 weeks, although the diagnosis was made rapidly at presentation. Clinical diagnosis correlated well with myelographic findings. Only 1 patient suffered neurological deterioration as a consequence of myelography. The functional outcome was dependent on the ability to walk prior to treatment. The median survival in those who were bedridden following treatment was 6 weeks (range 3.5-13) and 21 weeks (range 7-110+) in those who were ambulant following therapy.

Cauda Equina↗

PubMed1992

Interleukin-1 beta and interleukin-6 specifically increase the release of prostaglandin E2 from rat hypothalamic explants in vitro.

It has previously been shown that the cytokines interleukin-1 beta and interleukin-6 (IL-1 beta and IL-6) stimulate directly the release of corticotrophin-releasing-hormone-41 from the rat hypothalamus in vitro, while IL-1 beta can also stimulate the release of somatostatin. These effects can be antagonized by drugs which block prostaglandin (PG) synthesis. PGs are also involved in the control of hypothalamic neuropeptides by other neurotransmitters. In the present study, we have characterized the production of PGs from the rat hypothalamus in vitro, and investigated the effects of IL-1 beta and IL-6, as well as the neurotransmitters norepinephrine, acetylcholine and 5-hydroxytryptamine, on the acute release of PGs, using a well-validated acute hypothalamic incubation system. The rate of release of PGs [PGE2, PGF2 alpha, 6-keto-PGF1 alpha (6KPGF1 alpha) and thromboxane B2 (TXB2) in the medium was found to stabilize after 60 min of preincubation and thereafter remain constant, with TXB2 being the predominant species. Twenty-minute incubation in the presence of human recombinant IL-1 beta or IL-6, in the dose range 1-100 U/ml, had no effect on the release of PGF2 alpha, 6KPGF1 alpha or TXB2; however, the release of PGE2 was significantly increased by both IL-1 beta and IL-6. The effect of IL-1 beta was antagonized by both indomethacin and dexamethasone. None of the other neurotransmitters tested had any effect on the release of any of the PGs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Management of prolactinomas.

The management of prolactinomas requires a complex interaction of medical, surgical and radiotherapeutic intervention. With the judicious use of all these modalities, patients can usually be managed with great success and, perhaps more importantly, their presenting complaints (gonadal dysfunction and infertility) are usually completely corrected.

Bromocriptine↗

PubMed1991

Adrenergic stimulation of the human pituitary-adrenal axis is attenuated by an analog of met-enkephalin.

It has previously been suggested that endogenous opioid peptides may suppress the pituitary-adrenal axis in man by inhibiting an excitatory alpha 1-adrenoceptor input to neural mechanisms liberating corticotrophin-releasing factor or factors (CRFs). This hypothesis has been tested here by investigating the effect of the met-enkephalin analog, DAMME (FK-33,824), on the elevation in serum cortisol induced by the catecholamine-releasing agent d-amphetamine (10 and 25 mg p.o.) and the direct alpha 1-adrenoceptor agonist methoxamine (6 micrograms/kg/min i.v.) in two groups of 6 normal male subjects. In both studies, the rise in serum cortisol was significantly attenuated by the analog of met-enkephalin. These data suggest that exogenous opioids act as a site downstream to the alpha 1-adrenoceptor input to CRF release; it appears that opioids modulate adrenocorticotrophic hormone release in man at a minimum of two distinct and separate sites.

Adrenal Glands↗

PubMed1990

Cushing's disease cycling over ten years.

Cycles of excessive cortisol secretion have been reported interposed with phases of remission lasting from few days to several months. In this study we report a ten year follow up on a patient who had four episodes of hypercortisolism and Cushing's syndrome associated with hypokalemia and edema and three long lasting spontaneous remissions. This was all caused by corticotroph pituitary adenoma. She demonstrated the longest phase of remission yet recorded in this condition, 4.5 years. The precipitating factors for the recurrence in cyclical Cushing's syndrome are not well defined, but the last recurrence in our patient appeared two months after delivery. We have discussed the continuing uncertainty of the standard dynamic tests in the differential diagnosis of Cushing's syndrome.

Adenoma↗

PubMed1990

The role of alpha-2-adrenoceptors in the control of ACTH secretion; interaction with the opioid system.

This study examined the effects of an alpha-2-adrenoceptor antagonist on the secretion of ACTH basally and in response to the opioid antagonist naloxone, which is known to stimulate ACTH secretion by an adrenergic mechanism. Eight normal men were given, in double-blind, random order, intravenous infusions of normal saline (placebo), idazoxan (alpha-2-adrenoceptor antagonist), naloxone and the combination of idazoxan and naloxone. Naloxone increased plasma ACTH and cortisol concentrations in comparison to placebo. Idazoxan significantly enhanced the ACTH and cortisol responses to naloxone but had no effect on plasma ACTH or cortisol concentrations when given alone. These findings suggest that during some conditions of increased ACTH secretion, inhibitory alpha-2-adrenoceptors are activated and that these receptors limit the ACTH response. This provides an explanation for some of the apparent contradictions in interpreting the data from previous studies on the effects of catecholamines on the secretion of ACTH.

Adrenergic alpha-Antagonists↗

PubMed1990

Opiate receptor subtype regulation of CRF-41 release from rat hypothalamus in vitro.

We have previously shown that the release of corticotrophin-releasing factor 41 (CRF-41) induced by a variety of neurotransmitters and depolarizing agents from the rat hypothalamus in vitro is inhibited by morphine. In order to further characterize the opiate receptors mediating this inhibitory action, we have now investigated the effects of a variety of opioid compounds with relatively high selectivity for mu-, kappa- and delta-opiate receptors on K(+)-stimulated CRF-41 release. The selective mu-opioid receptor agonist 202-250 inhibited K(+)-evoked CRF-41 release in a dose-dependent manner with a maximum inhibition of approximately 60% at 10(-5) M (p less than 0.01), as did the kappa-selective agonists PD-117,302 and U-50,488, with a similar plateau in response of approximately 40% inhibition at 10(-6) M (p less than 0.05). The effects of these agonists were specifically reversed by the mu- and kappa-receptor antagonists naloxone and MR2266, respectively, while the specific delta-receptor antagonist ICI 154,129 was ineffective. Both naloxone and MR2266 slightly but significantly increased the basal release of CRF-41. The delta-agonist D-Pen2,5-enkephalin was without significant effect in the same dose range. These data suggest that both mu- and kappa-receptors, but not delta-receptors, mediate the inhibitory effect of opiates on stimulated CRF-41 release from the rat hypothalamus.

Animals↗

PubMed1990

Vasopressin mediates alpha 1-adrenergic stimulation of adrenocorticotropin secretion.

In conscious rats bearing venous and cerebroventricular cannulae, central administration of the alpha 1-adrenergic agonist methoxamine stimulated the secretion of ACTH, and the effect was reduced by the alpha 1-antagonist prazosin. Methoxamine was more potent in stimulating ACTH secretion when injected icv than peripherally, suggesting that the stimulant alpha 1-adrenoceptors are located in the brain rather than in the periphery. In order to investigate the relative roles of hypothalamic CRF-41 and vasopressin as mediators of the stimulant effects of alpha 1-adrenoceptors on ACTH secretion, we examined the effects of equipotent doses of antagonists to CRF-41 and vasopressin on the ACTH responses to methoxamine. The effect of methoxamine was reduced by the vasopressin antagonist dPTyr(Me) arginine vasopressin but not by the CRF-41 antagonist alpha-helical CRF-9-41, suggesting that vasopressin is more important than CRF-41 in mediating the effects of alpha 1-adrenoceptors on ACTH secretion. However, the combination of the two antagonists caused a reduction in the ACTH response to methoxamine that was greater than that of the vasopressin antagonist alone. This suggested that CRF-41 plays some role in this response, possibly by enhancing the activity of vasopressin in a synergistic manner. These two hypothalamic peptides seem to account for most of the ACTH releasing activity of alpha 1 adrenoceptor activation.

Adrenocorticotropic Hormone↗

PubMed1990

Brattleboro rats have deficient adrenocorticotropin responses to activation of central alpha 1-adrenoceptors.

This experiment was designed to test further the hypothesis that vasopressin is the major mediator of the ACTH response to activation of central alpha 1-adrenoceptors in the rat. The alpha 1-adrenergic agonist methoxamine was given intracerebro-ventricularly to conscious vasopressin-deficient (homozygous Brattleboro) and normal rats bearing venous and intracerebro-ventricular cannulae. Methoxamine stimulated the secretion of ACTH in the normal, but not in the vasopressin-deficient, rats. The data confirm that vasopressin, rather than CRH-41 or oxytocin, is the major hypothalamic peptide that mediates the effects of central alpha 1-adrenoceptors on the pituitary corticotrophs.

Adrenocorticotropic Hormone↗

PubMed1989

Timing of surgery for cerebral aneurysms: a plea for early referral.

Two groups of patients with aneurysmal subarachnoid haemorrhages--111 patients who underwent surgery within three days of haemorrhage, and 203 patients who underwent operations four or more days after the haemorrhage--were compared. No significant differences were found in outcome between the two groups. This indicates that early operation, which has the advantage of minimizing the risk of recurrent haemorrhage, is safe. The importance of the early diagnosis of subarachnoid haemorrhage and of an urgent referral for neurosurgical management is stressed.

Emergencies↗

PubMed1989

Interleukin-1 directly stimulates the release of corticotrophin releasing factor from rat hypothalamus.

While interleukin-1 (IL-1), a monocyte-derived polypeptide, clearly stimulates the hypothalamo-pituitary-adrenal (HPA) axis, its precise site of action is controversial. In these studies, the possibility of a hypothalamic and/or a pituitary site of action was investigated in vitro, using incubated rat hypothalami and perifused dispersed pituitary cells. Both forms of IL-1, IL-1 alpha and IL-1 beta, produced a dose-dependent stimulation of CRF-41 release from incubated rat hypothalami in the dose range of 1-100 U/ml (p less than 0.01). However, concentrations of both interleukins of 1-1,000 U/ml given as 10-min infusions had no effect on ACTH release from dispersed pituitary cells. Moreover, IL-1 beta, used in the concentration range of 1-100 U/ml, was unable to potentiate CRF-41-induced ACTH release. These data therefore provide evidence that at least the acute stimulatory effects of IL-1 on the HPA axis are predominantly mediated via a direct stimulation of hypothalamic CRF-41, suggesting that the hypothalamus may provide an interface between the neuroendocrine and immune axes.

Animals↗

PubMed1989

Morphine directly modulates the release of stimulated corticotrophin-releasing factor-41 from rat hypothalamus in vitro.

The actions of opioids and opiates on the hypothalamo-pituitary-adrenal axis are currently controversial. In the rat, morphine is reported to both stimulate and inhibit ACTH and corticosterone secretion, but the precise sites and mechanisms of these effects have remained unclear. To analyze further the hypothalamic actions of morphine, we have investigated its effect on hypothalamic fragments in vitro and measured the major CRF, CRF-41, by a specific RIA. The acute effects of morphine on both basal and stimulated ACTH release from dispersed pituitary cells were also investigated. Morphine (10(-8)-10(-6) M) did not significantly alter the basal secretion of CRF-41. However, similar concentrations of morphine inhibited CRF-41 release stimulated by norepinephrine in a dose-dependent manner. Similarly, morphine (10(-6) M) inhibited acetylcholine (10(-9) M)- and serotonin (10(-7) M)-stimulated CRF-41 release. The stimulatory effect on CRF-41 release induced by veratridine (10(-6) M) was inhibited by approximately 50% in the presence of morphine. KCl (28 nM)-mediated CRF-41 release was also significantly inhibited by morphine. Naloxone (10(-7)-10(-5) M) had no significant effect on either basal or norepinephrine-induced CRF-41 release, but reversed the inhibitory effect of morphine on norepinephrine-induced CRF-41 secretion in a dose-dependent manner. Morphine (10(-6)-10(-5) M) had no effect on either basal or CRF-41-stimulated ACTH release from dispersed pituitary cells. These data suggest that the predominant effect of morphine on hypothalamic CRF-41 release in vitro is suppression of the release induced by a variety of putative neurotransmitters and depolarizing agents. This inhibitory effect is reversed by naloxone, suggesting that it is mediated by opiate receptors, presumably situated directly on CRF-41 neurons.

Adrenocorticotropic Hormone↗

PubMed1988

Terguride--a new dopamine agonist drug: a comparison of its neuroendocrine and side effect profile with bromocriptine.

Terguride, the C9-10 dihydrogenated derivative of lisuride, is a new drug which inhibits pituitary prolactin (PRL) secretion. It has mixed dopaminergic-antidopaminergic and alpha 2-antiadrenergic activity, and has proved useful in the clinical management of hyperprolactinemia. However, no trial comparing its use with the standard dopamine agonist bromocriptine has been reported. We have therefore compared three doses of terguride with bromocriptine 2.5 mg and placebo in a randomized double-blind crossover trial in eight normal volunteers. Terguride showed a potent dose-dependent PRL-inhibiting and growth hormone (GH)-releasing effect, while no significant changes were observed in thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), or luteinizing hormone (LH) in comparison to placebo. The neuroendocrine profile of terguride 1 mg was identical to that of bromocriptine, with a significant reduction in PRL still evident at 24 hours. However, in this small group of normal subjects, the side effects experienced at any dose of terguride were significantly less than with bromocriptine. Terguride 1 mg was always preferred to bromocriptine, while the lower doses were indistinguishable from placebo. Terguride is therefore likely to play an important role in the treatment of hyperprolactinemia.

Adult↗

PubMed1988

Cerebrospinal fluid diversion in the treatment of benign intracranial hypertension.

Thirty-six patients from a consecutive series of 41 patients with benign intracranial hypertension (BIH) were treated by cerebrospinal fluid shunting. In 12 patients this was selected as the primary treatment due to the severe deterioration of vision or concern regarding the possible adverse effects of steroids; all 12 patients showed rapid and complete resolution of the disease, although eight patients still have a shunt in place. In 24 patients a shunt was inserted when other forms of treatment failed; all of these patients showed rapid resolution of the condition, although 20 patients still have a shunt in place. Three patients had the shunt removed without sequelae, and one patient in whom the shunt was removed because of low-pressure symptoms remains symptomatic with persistent papilledema (over 6 years). The percutaneous lumboperitoneal (LP) shunt was associated with the lowest revision and complication rates. Cisternal shunting to either the atrium or pleural cavity was next most effective, whereas valved LP shunts inserted via a laminectomy were least effective; ventricular shunts were used in only two cases. Shunting is therefore very effective in the treatment of BIH, but the significant complication rate and the possibility of inducing shunt dependence must be recognized.

Adolescent↗

PubMed1987

Moyamoya disease: presentation and treatment of two cases by surgery.

Stroke prophylaxis in patients with moyamoya disease has not been described previously in Australia. Two cases are presented in which superficial temporal to middle cerebral arterial bypass has been successful in halting the progress of the disease. The presentation, investigation and management of this occlusive vasculopathy are discussed.

Arterial Occlusive Diseases↗

PubMed1987

Short latency somatosensory-evoked potentials in children--Part 1. Normative data.

Spinal, subcortical, and short latency cortical somatosensory-evoked potentials (SEPs) following electrical stimulation of the median or tibial nerve were studied in 100 children aged 4 weeks to 13 years. Standard neurophysiological methods of recording surface SEPs were used in sedated and nonsedated children. The morphology of the SEPs was similar to that obtained in adults; however, the initial components of the cortical SEP following median nerve stimulation did show maturational changes in both interpeak latencies and morphology. The negative peak latencies recorded over Erb's point (N9 equivalent) and the second cervical vertebra (N13 equivalent) following median nerve stimulation, and over the lumbothoracic junction (N14 equivalent) following tibial nerve stimulation were directly related to patient age and limb length. There was no correlation between age and the latencies of either the initial negativity (N18 equivalent) or the initial positivity (P28 equivalent) of the cortical SEPs following respective median and tibial nerve stimulation. The central somatosensory conduction time decreased slowly during the first decade and attained adult values after 8 years of age. The lumbar spine to scalp transit time showed no direct relationship to age. Comparisons of SEPs recorded in the same subject when awake and under general anesthesia showed that the latencies of the subcortical, spinal, and N1-P1 complex of the cortical SEP are identical; however, the later components of the cortical SEP vary both in latency and amplitude with anesthesia. This study represents normative data against which SEP in children with disorders of the central nervous system may be compared.

Adolescent↗