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Biomedical subjects

B Melgaard

Publications and source records attributed to B Melgaard.

At least 37 records · Page 2Linked to original sources
PubMed1988

Misonidazole neuropathy. A prospective study.

The frequency with which polyneuropathy developed was investigated in patients with cancer of the larynx and pharynx who participated in a double-blind trial of the radiosensitizing drug misonidazole. Fourteen of 36 patients receiving misonidazole (total dose of about 11 g/m2) developed neuropathy, while this occurred in only 2 of 34 patients in the placebo group. Vibration perception threshold increased in all patients who developed neuropathy, but also in 12 (5 misonidazole and 7 placebo treated) without other symptoms or signs of neuropathy. Pharmacokinetic studies of misonidazole revealed a correlation between development of neuropathy and a high 'peak plasma concentration/g misonidazole in each fraction' and especially a high 'area under plasma concentration curve/g misonidazole in each fraction'.

Adult↗
PubMed1988

A cluster survey of mortality due to neonatal tetanus in Kenya.

Three house-to-house surveys were conducted in three different districts in Kenya, using a cluster survey technique for estimation of neonatal tetanus death rates. The results showed neonatal death rates of 10, 16 and 23 per 1000 livebirths and neonatal tetanus death rates of 6, 11 and 16 per 1000 livebirths respectively. A recall method based on interviews with women attending antenatal clinics gave much lower rates. The community surveys indicate a total neonatal tetanus death rate of 8 per 1000 livebirths and it is estimated that each year between 8000 and 12,000 children die in Kenya from this preventable disease.

Epidemiologic Methods↗
PubMed1988

Creatine kinase BB release into cerebrospinal fluid after lateral ventricle cannulation.

Creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB) activities were measured in ventricular CSF obtained by lateral ventricle cannulation in patients suspected of normal pressure hydrocephalus. Lateral ventricle cannulation resulted in highly and variably elevated CK and CK-BB levels. The results emphasise the interference of these CK and CK-BB elevations in studies on the prognostic value of CSF CK and CK-BB levels in head trauma patients with respect to outcome.

Catheterization↗
PubMed1987

Discordance between the cortisol response to insulin-hypoglycemia and 30-minute ACTH stimulation test in chronic alcoholic men.

An insulin hypoglycemia test and a 30-min ACTH stimulation test was performed in 10 chronic alcoholic men, who had been abstinent from alcohol for at least one month. Attenuated serum cortisol responses were found in six of the patients despite a normal ACTH test. Four patients showed normal responses to both the insulin hypoglycemia test and the short ACTH test. No correlation was demonstrated between the cortisol response and the severity of alcoholism, cerebral atrophy, and peripheral neuropathy. It is concluded that in chronic alcoholism the short ACTH test may fail in disclosing hypofunction of the integrated hypothalamic-pituitary-adrenocortical (HPA) axis as assessed with the insulin hypoglycemia test.

Adrenocorticotropic Hormone↗
PubMed1986

Ataxia and cerebellar atrophy in chronic alcoholics.

Forty-five alcoholics were examined clinically and by CT scanning in order to evaluate the relationship between ataxia, cerebellar atrophy and peripheral neuropathy. A significant relationship was found between ataxia and cerebellar atrophy as well as between ataxia and peripheral neuropathy.

Alcohol Withdrawal Delirium↗
PubMed1986

Symptoms and signs of polyneuropathy and their relation to alcohol intake in a normal male population.

In a normal population of 468 45-year-old males symptoms and signs of polyneuropathy were investigated and related to self-reported alcohol consumption and associated problems. Sensory disturbances in the feet were claimed by 3.4%, 5.8% had abolished Achilles tendon reflexes, and 7.7% increased vibratory perception thresholds. Significant correlations were found between persons with signs of neuropathy and persons with physical or social consequences of alcohol abuse.

Alcohol Drinking↗
PubMed1985

Frequency, diagnosis, and prognosis of spinal cord compression in small cell bronchogenic carcinoma. A review of 817 consecutive patients.

A retrospective review of 817 consecutive patients with small cell bronchogenic carcinoma disclosed 29 cases of spinal cord compression (frequency, 3.5%). Twelve patients (group 1) presented with symptom of cord compression, whereas the remaining 17 patients (group 2) developed this complication during therapy. Clinical features differed in the two groups: pain was present in 83% of the patients in group 1 and in 47% of those in group 2. Pain preceded motor dysfunction in 75% and 12% of the two groups, respectively. Radiologic bone destruction of the spine was found in 11 of 12 patients in group 1 and in 3 of 16 patients in group 2. Myelography was performed in 8 patients in group 1 and in 14 patients from group 2. A complete block was found in seven and none of the patients in each of the two groups, respectively. Treatment with irradiation and/or laminectomy rarely resulted in a significant improvement of preexisting neurologic impairment but it frequently prevented the progression of symptoms, leading to preservation of sphincter control and ambulatory function in eight of nine and seven of eight patients, respectively. Careful evaluation is mandatory for patients presenting with back pain and radiographic evidence of bone destruction, as 11 of 26 such patients were found to have spinal cord compression. It is concluded that spinal cord compression presents in two distinct ways. One with early onset, pain, evidence of bone destruction, and complete myelographic block. The second is characterized by motor impairment with no evidence of bone destruction and only partial myelographic block. Treatment rarely ameliorates symptoms but prevents deterioration, making early diagnosis important.

Carcinoma, Bronchogenic↗
PubMed1984

Sympathetic vasoconstrictor nerve function in alcoholic neuropathy.

The peripheral sympathetic vasomotor nerve function was investigated in 18 male chronic alcoholics admitted for intellectual impairment or polyneuropathy. By means of the local 133Xenon washout technique, the sympathetic veno-arteriolar axon-reflex was studied. This normally is responsible for a 50% decrease in tissue blood flow, when the ankle is lowered 40 cm below heart level in the supine individual. The patients with moderate to severe polyneuropathy, taken as a group, did not differ significantly from the group of patients with no or only mild polyneuropathy, although a lesser response was seen (18% and 48% decrease respectively). However, in three patients with moderate neuropathy, and in one patient with no signs of neuropathy, this veno-arteriolar reflex was absent, indicating dysfunction of the peripheral sympathetic adrenergic nerve fibres. The three patients also showed a lesser degree of arteriolar constriction during 45 degrees passive head-up tilt, although none developed symptoms of orthostatic hypotension. Anhidrosis of the feet was found in only three patients. This study lends support to the view that individual differences in the susceptibility to the deleterious effect of alcohol comprise not only the peripheral sensory and motor nerve fibres, but also the thin pseudomotor and vasomotor nerves.

Adult↗
PubMed1984

Misonidazole neuropathy.

Neurotoxic side effects of misonidazole with peripheral neuropathy was investigated in two series of patients. The first series consisted of eight patients with carcinoma of the pharynx, larynx or lung who, during treatment with misonidazole, developed peripheral neuropathy dominated by severe sensory symptoms and signs localized mainly to the lower extremities. Misonidazole was given for three to seven weeks in a total dose of 9.6 - 12.6 g/m2 (11 g/m2 or more in four of the patients). The symptoms subsided partially within a few months after cessation of the therapy. Electrophysiological and histological findings indicated axonal neuropathy with loss of large fibres and secondary demyelination. The second series consisted of 70 patients with carcinoma of the pharynx or larynx who, in addition to radiotherapy, were given either placebo or misonidazole over four weeks in a total dose of 11 g/m2. Fourteen patients out of 36 receiving misonidazole (38%) developed peripheral polyneuropathy, mostly in the feet, while this occurred in only two of the 34 patient placebo group.

Aged↗
PubMed1983

The neurotoxicity of ethanol.

Alterations in nervous system functioning following acute and chronic ethanol exposure have been studied in a great number of experimental investigations. Results from many of these investigations can be difficult to interpret, particularly since a variety of techniques and exposure models are employed. This review emphasizes those studies which, in the opinion of the author, fit into a pattern where results from studying one function of the nervous system is in accordance with results from studying another. Thus, the fluidizing effect of ethanol on the neuronal membrane - an effect which ethanol shares with anaesthetics - leads to a change in protein function which in turn affects ion transport such as Na+ and Ca++ across the membrane due to changes in the ion channels. Cation influx is probably directly coupled to neurotransmitter release which is in agreement with the finding that ethanol exposure results in inhibition of Na+ and Ca++ current as well as acetylcholine release. The sensitization of the dopaminergic system after ethanol exposure may also be related to the changes in cation flux, and the changes in this system probably play a crucial rôle in the development of tolerance and withdrawal symptoms. Other aspects such as impairment of protein synthesis, altered GABA function of impairment of neuron excitability and conduction are more difficult to place in proper perspective. The rôle of acetaldehyde in acute as well as chronic ethanol intoxication also remains a controversy. These may, however, be secondary phenomena to primary changes in different part of the nervous system not necessarily important in the clinical situation. Behavioural and anatomical studies particularly from recent years have shown that experimental animals develop memory disturbances following chronic exposure even when kept on sufficient diet. These findings argue strongly for a direct toxic effect of ethanol, and are furthermore compatible with behavioural changes in chronic alcoholics, dominated by memory impairment. Since it has been argued that the cholinergic system plays a significant rôle for memory function, a possible explanation for some of the psychological and anatomical deficits caused by ethanol is thus the changes in the function of the cholinergic system particularly in the hippocampal regions.

Acetylcholine↗
PubMed1982

Misonidazole Neuropathy: a clinical, electrophysiological, and histological study.

We studied eight patients with carcinoma of the pharynx and larynx (five cases) or lungs (three cases) who, during treatment with the radiosensitizing drug misonidazole, developed peripheral neuropathy dominated by severe sensory symptoms and signs mainly localized to the lower extremities. The symptoms partially subsided within months after cessation of therapy. Electrophysiological and histological findings indicated an axonal neuropathy with loss of large fibers and secondary demyelination. The neurotoxic property of misonidazole limits its therapeutic use.

Aged↗