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Biomedical subjects

N Callaghan

Publications and source records attributed to N Callaghan.

At least 37 records · Page 2Linked to original sources
PubMed1978

Carbamazepine as a single drug in the treatment of epilepsy. A prospective study of serum levels and seizure control.

Serum levels and seizure control were investigated in a prospective study when carbamazepine was given as a single drug to 32 patients with a variety of seizures. The patients included 13 previously untreated patients (group 1), and 19 who were unresponsive to other anticonvulsant drugs used in different combinations or as a single treatment (group 2). Thirteen patients (10 from group 1, and three from group 2) became seizure-free, and a greater than 50% reduction in seizure frequency occurred in 10 patients (nine from group 2, and one from group 1). Less than 50% reduction in seizure frequency occurred in five patients from group 2. As a wide range of serum levels was associated with complete freedom from seizures, or a greater than 50% reduction in seizure frequency, it was not possible to define a therapeutic range for carbamazepine. Side effects occurred at the start of treatment or after a dose increase. A wide range of serum levels was associated with side effects, and some patients could not tolerate levels greater than 42 mumol/l.

Adolescent↗
PubMed1978

Cerebral transmitter precursors and metabolites in advanced renal disease.

Patients with chronic renal disease had low plasma total tryptophan but an abnormally high proportion of this was in the free state. The subjects with encephalopathy had raised plasma free tryptophan, CSF tryptophan, and CSF 5-hydroxyindoleacetic acid. CSF tryptophan correlated better with plasma free than with plasma total tryptophan. Plasma and CSF tyrosine concentrations were normal but CSF homovanillic acid was raised especially in subjects with encephalopathy. The possible significance of these changes in advanced renal disease is discussed.

Adult↗
PubMed1977

The effect of anticonvulsant drugs which induce liver microsomal enzymes on derived and ingested phenobarbitone levels.

A comparison was made between the levels of derived Phenobarbitone in three groups of patients who were taking Primidone as a single drug, Primidone with Phenytoin and Primidone in combination with Phenytoin and Carbamazepine. The levels of ingested Phenobarbitone when this drug was taken as a single drug were compared with the levels when Phenobarbitone was taken in combination with Phenytoin in two other groups of patients. A significant increase in derived Phenobarbitone levels occurred when Primidone was used in combination with Phenytoin alone or with Phenytoin and Carbamazepine. The highest level occurred in a group of patients taking the three drug combination. There was no significant difference between the levels of ingested Phenobarbitone when this drug was used as single therapy or in combination with Phenytoin. We suggest that the increase in derived Phenobarbitone levels relates to the effect of Phenytoin on liver enzyme systems, and that the greater increase with triple therapy was related to the combined effect of Carbamazepine and Phenytoin on microsomal enzymes. As there was no increase in ingested Phenobarbitone levels when this drug was taken in combination with Phenytoin, we were unable to confirm previous suggestions that Phenytoin either inhibits the hydroxylation of Phenobarbitone or impairs its renal excretion.

Adolescent↗
PubMed1977

The effects of toxic and non-toxic serum phenytoin levels on carbohydrate tolerance and insulin levels.

The effect of toxic and non-toxic phenytoin levels on carobhydrate tolerance and insulin levels was studied in 18 patients with epilepsy and 17 control subjects. Toxic levels were defined as a serum level greater than 20 microgram/ml. Toxic levels occurred in 11 patients and nontoxic levels in seven patients. Blood glucose and insulin levels were measured at 30-min intervals for a period of 3 h following the ingestion of 50 g glucose. Blood glucose levels were measured by the ferricyanide method, and serum insulin levels by immunoassay of insulin with insulin antibody precipitate. Serum phenytoin levels were measured by gas liquid chromatography. The insulin profiles were the same for all three groups, but there was a significant delay in reaching peak glucose concentrations in patients with toxic levels of phenytoin. It was therefore confirmed that non-toxic levels of phenytoin do not affect carbohydrate tolerance or insulin levels when phenytoin is used in the routine treatement of epilepsy, and it has also been shown that toxic levels of phenytoin do not affect carbohydrate tolerance when the high levels are detected at an early stage.

Adolescent↗
PubMed1977

Relapsing neurological disorder associated with rubella virus infection in two sisters.

A disseminated relapsing neurological disorder presented simultaneously in two sisters. Encephalitic features were present in one case. The illness was associated with a significant increase in rubella specific IgM in both sisters. Despite the absence of a rubella rash, this increase would be compatible with a recent infection by the rubella virus as a basis for the illness, and the persistent elevation, with active antigenic stimulation. It is suggested that both patients might represent the clinical manifestations of perivenous demyelination caused by the rubella virus, which, in view of the relapsing nature of the illness, has progressed to plaque formation.

Adolescent↗
PubMed1975

Piribedil (ET 495) in the treatment of Parkinson's disease combined with amantadine or levodopa.

The further therapeutic benefit of piribedil when combined with amantadine or Levodopa was studied by a double-blind, cross-over trial in 15 patients with Parkinson's disease. A significant improvement at the 5 per cent level for akinesia, gait, speech disorder and facial expression occurred when piribedil was added to Levodopa; and a more highly significant improvement at the 1 per cent level for akinesia, facial expression and finger dexterity occurred with piribedil and amantadine. No significant improvement occurred for special timed tests. Improvement was associated with side effects in both groups of patients. Side effects occurred with both placebo and active piribedil. Only nausea during piribedil and Levodopa treatment reached statistical significance when compared with the placebo. Piribedil did not give rise to any haematological or biochemical complications. Our findings suggest that piribedil is of further therapeutic benefit when added to amantadine or Levodopa. It was suggested that the improvement which occurred together with amantadine could be due to the combined action of both drugs on dopamine receptors.

Aged↗
PubMed1974

Linoleate and fatty-acid patterns of serum lipids in multiple sclerosis and other diseases.

The linoleic acid content of serum lipids was measured in 47 patients with multiple sclerosis, 29 patients with other neurological diseases, 35 patients with acute non-neurological illnesses, and 49 healthy control subjects. Reduced linoleic acid content of serum lipids was not specific to multiple sclerosis and occurred in all ill patients with acute non-neurological illness. The fatty-acid pattern of serum lipids in illness resembles that of essential fatty-acid deficiency. It seems that this pattern of reduced linoleic acid content with increased oleic, palmitic, and palmitoleic acid content may be a general phenomenon in ill patients.

Acute Disease↗
PubMed1973

Dietary intake of linoleic acid in multiple sclerosis and other diseases.

The linoleic acid intake of patients with multiple sclerosis is not significantly different from that of healthy control subjects. This is true both in absolute terms and when linoleic acid intake is expressed as a percentage of total fat intake. In the other categories of illness, included as control groups, linoleic acid intake was significantly decreased only in patients with acute non-neurological illness and in this case only when considered in absolute terms. In all groups studied the daily linoleic acid intake was in excess of 1·7% of the total calorie intake and in the case of multiple sclerosis was 2·7% of the total calories ingested. Since other workers have shown that linoleic acid absorption is not altered in multiple sclerosis and we have shown that the diet is not deficient, it seems that the decrease in linoleic acid content is due to some process occurring after the absorption of this essential fatty acid.

Adult↗