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Biomedical subjects

A Richens

Publications and source records attributed to A Richens.

At least 253 records · Page 14Linked to original sources
PubMed1970

Osteomalacia with long-term anticonvulsant therapy in epilepsy.

The investigation and treatment of osteomalacia are described in four patients with epilepsy treated with long-term anticonvulsant therapy. It is suggested that drug-mediated enzyme induction may be the mechanism responsible by causing a greatly increased inactivation of vitamin D in these patients.

Adolescent↗
PubMed1970

Disturbance of calcium metabolism by anticonvulsant drugs.

A survey of calcium metabolism in epileptic patients in a residential centre showed a subnormal serum calcium level in 22.5% of patients and a raised alkaline phosphatase in 29%. Hypocalcaemia was related to high dosage of anticonvulsant drugs, to multiple drug therapy, and to the use of individual anticonvulsant drugs in the following order, with decreasing order of importance: pheneturide, primidone, phenytoin, phenobarbitone. Subnormal serum calcium levels occurred more commonly in patients with a raised liver alkaline phosphatase isoenzyme than in those whose phosphatase was mainly of bone origin.Preliminary results of treatment with calciferol suggested that the disturbance of calcium metabolism was the result of vitamin D deficiency. It is possible that anticonvulsant drugs accelerate the breakdown of vitamin D by liver enzyme induction.

Adolescent↗
PubMed1969

The action of general anaesthetic agents on root responses of the frog isolated spinal cord.

1. The action of volatile and barbiturate general anaesthetic agents on synaptic transmission in the frog isolated spinal cord has been studied by recording ventral root synaptic potentials and spike discharges evoked by volleys in a dorsal root and in the lateral column fibres.2. Some observations on the distribution of the lateral column fibres and the characteristics of the dorsal root potentials have been presented.3. Volatile agents depressed and eventually abolished all components of the ventral root responses. Failure of motoneurone discharge was the result of two factors, a decrease in the slope of the synaptic potential and an elevation of the critical depolarization required to trigger propagated impulses.4. Barbiturate compounds, in contrast, readily abolished polysynaptic components of the ventral root responses, but the short latency discharge produced by lateral column stimulation was potentiated, and was accompanied by a lowering of the firing threshold of motoneurones. The mechanism of this potentiation by barbiturate compounds is discussed.5. It is concluded that volatile agents act predominantly on the initial segment and subsynaptic elements of the motoneurone, whereas barbiturate compounds depress the presynaptic or postsynaptic components of interneuronal synapses.

Anesthetics↗
PubMed1969

Microelectrode studies in the frog isolated spinal cord during depression by general anaesthetic agents.

1. Extracellular and intracellular potentials have been recorded from the isolated spinal cord of the frog during depression of synaptic transmission by volatile and barbiturate general anaesthetic agents.2. Volatile agents did not impair conduction in presynaptic terminals in concentrations which completely blocked synaptic transmission.3. Methohexitone consistently impaired conduction in presynaptic terminals long before transmission through polysynaptic pathways was blocked.4. Volatile agents depressed the excitability of the motoneurone membrane, as evidenced by impaired antidromic invasion, reduced excitability to direct stimulation, depression of the synaptic potential and elevation of firing threshold. It is concluded that these actions are responsible for the depressant effect of volatile agents on spinal reflexes.5. Methohexitone produced an increase in the excitability of the motoneurone membrane, as evidenced by enhanced antidromic invasion, increased excitability to direct stimulation and potentiation of short latency responses. Despite this excitatory action, the polysynaptic pathways through the cord were depressed by an action of the drug on conduction in presynaptic terminals.6. It is suggested that the sensitivity of the motoneurone membrane to volatile agents may contribute to the good muscle relaxant properties of these drugs in clinical use.

Anesthetics↗
PubMedDate not supplied

An update on sodium valproate.

Sodium valproate has been in clinical use for the treatment of epilepsy in Great Britain since 1973 and in the United States since 1978. It is chemically quite different from the existing antiepileptic drugs. Although most authorities concentrate on its modification of GABAergic inhibitory transmission in the central nervous system, its mechanism of action remains obscure. It has been shown to be an effective antiepileptic drug in a wide variety of seizure types, but clinically, its major use to date has been in generalized seizures. It is particularly effective in photosensitive epilepsy and myoclonus. Most adverse reactions to sodium valproate are mild and reversible, but with increasing experience, the drug's rare, idiosyncratic, adverse effects are becoming apparent, particularly hepatotoxicity and teratogenicity. The role of therapeutic drug monitoring in the management of patients taking sodium valproate is controversial.

Anticonvulsants↗
PubMedDate not supplied

A comparison of the acute effect of single doses of vigabatrin and sodium valproate on photosensitivity in epileptic patients.

The acute effect of oral administration of a single dose of vigabatrin, a new antiepileptic drug which acts by irreversible enzyme-activated inhibition of the brain enzyme, GABA-aminotransferase, on the photoconvulsive response in patients with photosensitive epilepsy, was compared with that of the established antiepileptic drug, sodium valproate. Both drugs significantly suppressed the photoconvulsive response in 3 out of 6 subjects. This result was interpreted as further evidence of vigabatrin's potential value in the future treatment of patients with epilepsy.

Adolescent↗