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Biomedical subjects

B H Eidelman

Publications and source records attributed to B H Eidelman.

At least 19 recordsLinked to original sources
PubMed1991

Anorectal sensory and motor function in neurogenic fecal incontinence. Comparison between multiple sclerosis and diabetes mellitus.

We measured anorectal sensory and motor function in 11 patients with multiple sclerosis and fecal incontinence, 11 continent patients with multiple sclerosis, 10 diabetics with fecal incontinence, and 12 healthy control subjects. The threshold volume at which patients with multiple sclerosis and fecal incontinence experienced rectal sensation was higher than that in healthy controls (42.7 +/- 6.2 mL vs. 13.3 +/- 2.8 mL; P less than 0.01) and was similar to that in incontinent diabetics (36.5 +/- 5.7 mL). Patients with multiple sclerosis and incontinent diabetics also showed increased thresholds of phasic external sphincter contraction compared with controls (P less than 0.05). Diabetics with incontinence had reduced resting and maximal voluntary anal sphincter pressures compared with controls (P less than 0.05), whereas patients with multiple sclerosis and incontinence showed only decreased maximal voluntary anal sphincter pressures (P less than 0.01 vs. controls and diabetics). Incontinent patients with multiple sclerosis also required smaller volumes of rectal distention to inhibit internal sphincter tone compared with diabetics and controls (P less than 0.01). Decreased maximal voluntary squeeze pressures were less severe in continent patients with multiple sclerosis than in incontinent patients with multiple sclerosis. We conclude that impaired function of the external anal sphincter and decreased volumes of rectal distention to inhibit the internal anal sphincter or both may contribute to fecal incontinence in multiple sclerosis. In addition, increased thresholds of conscious rectal sensation in some incontinent patients with multiple sclerosis and diabetes mellitus may contribute to fecal incontinence by impairing the recognition of impending defecation.

Adult↗
PubMed1990

Prevalence of bowel dysfunction in multiple sclerosis. A population survey.

An unselected outpatient population of 280 individuals with multiple sclerosis was surveyed to determine the prevalence of bowel dysfunction and to define their characteristics and their relationship to the nongastrointestinal manifestations of the disease. Constipation was present in 43%, was similar in frequency in both sexes, and was more common in patients, regardless of degree of disability, than in a control population. Frequency of constipation also correlated with duration of disease and genitourinary symptoms but did not correlate with use of any medications in mildly disabled patients. Fecal incontinence had occurred at least once in the preceding 3 mo in 51% of patients and once per week or more frequently in 25% of patients who were questioned in more detail with a follow-up questionnaire. Correlations of fecal incontinence with disability, duration of disease, and presence of genitourinary symptoms were similar to constipation. The prevalence of bowel dysfunction (constipation and/or fecal incontinence) in the multiple sclerosis population was 68%, and this manifestation was common even in mildly disabled subjects. Bowel dysfunction can be a source of considerable ongoing social disability in patients with multiple sclerosis. Further studies are needed to characterize the pathophysiology of this common disorder so that effective therapeutic strategies can be identified.

Adult↗
PubMed1990

Multiple cranial neuropathy as a feature of internal carotid artery dissection.

The traditional presentation of spontaneous internal carotid artery dissection includes ipsilateral hemicranial headache, oculosympathetic paresis, and contralateral focal cerebral ischemic deficits. However, we describe two cases with multiple cranial nerve involvement ipsilateral to the dissection as the principal feature. The first patient, a 36-year-old man, had involvement of the 9th, 10th, 11th, and 12th cranial nerves. The second case was a 53-year-old man with abnormalities of the 5th, 7th, 9th, 10th, and 12th cranial nerves. In both, magnetic resonance imaging revealed a ring-like area of abnormal signal intensity surrounding the carotid artery at the skull base. Carotid angiography was consistent with the suggestion of dissection on the magnetic resonance studies in both cases. The patients recovered without anticoagulation. Internal carotid artery dissection may thus present with multiple cranial nerve palsies, which could be mistaken for an infiltrating tumor of the skull base. Magnetic resonance imaging is useful in identifying the condition.

Adult↗
PubMed1989

Treatment of a cluster headache patient in a hyperbaric chamber.

A patient with severe cluster headaches was treated in a hyperbaric chamber on two occasions. Her symptoms had been refractory to other treatment modalities including conventional oxygen therapy. On both occasions her pain was promptly relieved while breathing 100% oxygen at two atmospheres of pressure. This is the first known reported case of a cluster headache treated with hyperbaric oxygen. A prospective study is needed to substantiate the efficacy of this treatment modality for cluster headaches.

Cluster Headache↗
PubMed1978

Potentiation of the cerebrovascular response to intra-arterial 5-hydroxytryptamine.

Infusion of 5-hydroxytryptamine (5HT) into the internal carotid artery of normal baboons was not accompanied by alteration of gray matter cerebral blood flow. In animals pretreated with depot estrogen and progesterone (dosage equivalent to oral contraceptive preparations), infusion of 5HT produced a marked decrease in gray matter blood flow. A similar decrease in flow was obtained when the 5HT was infused with a concentrate of beta-lipoprotein. Steroid substances appear to enhance the cerebrovascular constrictor responses to 5HT. A further series of six experiments has shown that the monoamine oxidase inhibitor tranylcypromine similarly produced constrictor responses to 5HT. It is possible that the steroids, the beta-lipoprotein, and the tranylcypromine produced constrictor responses to 5HT by the same mechanism (inhibition of cerebrovascular monoamine oxidase).

Animals↗
PubMed1978

The effect of intracarotid infusion of dexamethasone and 5-hydroxytryptamine on cerebral blood flow and metabolism in baboons.

The effect of intracarotid infusion of dexamethasone on cerebral blood flow and cerebral oxygen utilization was measured in baboons using the xenon-133 clearance technique. The cerebrovascular response to intracarotid infusion of 5-hydroxytryptamine (5-ht) was then determined during simultaneous infusion of the steroid. Infusion of dexamethasone alone and infusion with 5-HT produced no significant change in cerebral blood flow or cerebral oxygen utilization when compared to baseline values. The study indicates that neither dexamethasone nor 5-HT with dexamethasone modify cerebral blood flow when infused via the internal carotid artery.

Animals↗
PubMed1977

Barrier and uptake mechanisms in the cerebrovascular response to noradrenaline.

Cerebral blood flow (CBF) was measured in 20 baboons by the intra-arterial xenon-133 injection method. The CBF responses to intra-arterial infusions of noradrenaline (NA) were determined. These responses were normally found to be vasodilator and mediated by beta adrenoreceptors. After infusion of substances blocking extraneuronal uptake of NA or opening of the blood-brain barrier, this vasodilation was either abolished or converted to an alpha-receptor mediated vasoconstriction. This suggests that normally the cerebral circulation is protected against noradrenergic vasoconstriction by mechanisms reducing the concentration of NA in the tunica media to below threshold for alpha-adrenoreceptor stimulation.

Animals↗
PubMed1976

Cerebrovascular response to infused noradrenalin and its modification by a catecholamine metabolism blocker.

Despite many studies, the cerebrovascular action of infused noradrenalin is still unclear. The study reported here tested the hypothesis that infused noradrenalin is prevented from reaching the adrenoreceptors by being avidly taken up and metabolized in the vascular smooth muscle. Cerebral blood flow was measured by the xenon133 clearance technique in nine baboons before and during blockade of the enzyme catechol-O-methyl transferase, which is known to be important in inactivation of circulating noradrenalin. The cerebral blood flow responses to noradrenalin infused at 8, 16, and 32 mug per minute were also determined. Responses indicated vasodilatation before but vasoconstriction after blockade, with a significant noradrenalin. It is suggested that the cerebral circulation is normally protected against sympathetic vasoconstriction by the avid uptake and metabolism of noradrenalin in extraneuronal and possibly neuronal sites.

Animals↗
PubMed1975

Modification of the cerebrovascular response to noradrenaline by bile duct ligation.

The effects of intracarotid infusions of noradrenaline on the cerebral vasculature were studied in seven baboons with bile duct ligation. Infusion of 8 mug and 16 mug/min of noradrenaline resulted in a significant decrease in cerebral blood flow in the jaundiced animals. In normal baboons, these doses produced cerebrovascular dilatation. These results indicate that there is an increased cerebrovascular sensitivity to noradrenaline in the obstructive jaundice which follows bile duct ligation. It is postulated that noradrenaline smooth muscle uptake mechanisms are disturbed allowing a greater concentration of the amine at the receptor sites.

Animals↗
PubMedDate not supplied

Role of catecholamine degradative enzymes and the adrenergic innervation in determining the cerebrovascular response to infused norepinephrine.

Cerebral blood flow responses to intra-arterial infusion of norepinephrine (NE) at 0.55 microgram/kg/min and 1.1 microgram/kg/min were studied in 3 groups of baboons. The flow was measured by the intracarotid 133xenon clearance technique using a computer program to calculate flow (height over area--H/A) flow (initial slope--is) and cerebral metabolic utilization of oxygen (CMRO2). The normal response to NE was to increase flow without significant changes in CMRO2. Blockade of catechol-o-methyl transferase (COMT) produced vasoconstrictor responses to these same NE doses. Monoamine oxidase blockade abolished the normal vasodilation. Denervation of the cerebral circulation with intracisternal 6-hydroxydopamine produced vasoconstrictor responses with flow (H/A) but not with flow (is). It is concluded that the extra-neuronal COMT enzyme is important in limiting the access of blood-borne NE to cerebrovascular constrictor receptors.

Adrenergic Fibers↗
PubMedDate not supplied

The role of the carotid body in mediating the cerebrovascular response to altered arterial carbon dioxide tension.

The role of the carotid bifurcation chemoreceptors in mediating the cerebrovascular response to altered arterial PCO2 has been suggested to be large. In the present study the cerebrovascular response to raised PCO2 was measured in a group of baboons before and after bilateral inactivation of the carotid bodies. The results suggest that these chemoreceptors do play a part in the cerebral vasodilator response to raised PCO2. The role of the carotid body, however, appears to be relatively minor as it only accounted for +/- 40% of the total response and became significant only at arterial PCO2 levels of more than 50 mm Hg. It is postulated that the peripheral chemoreceptors in the carotid bifurcation mediate part of the cerebrovascular response to altered PaCO2 but the role is quantitatively small.

Animals↗