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Dive into the research topics where F. Monaco is active.

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Featured researches published by F. Monaco.


European Neurology | 1983

Carbamazepine versus Diphenylhydantoin in the Treatment of Myotonia

GianPietro Sechi; S. Traccis; L. Durelli; F. Monaco; Roberto Mutani

A double-blind controlled trial was performed on 6 patients affected with Steinerts disease in order to evaluate the efficacy of two different dosages of diphenylhydantoin (PHT, 200 and 300 mg/day) and carbamazepine (CBZ, 600 and 800 mg/day) on the myotonic afterdischarge. Both dosages of PHT and CBZ induced a significant improvement of myotonia. For PHT a trend towards decreased efficacy is pointed out at toxic or at high dosages.


Epilepsia | 1975

Free Amino Acids in Serum of Patients with Epilepsy: Significant Increase in Taurine

F. Monaco; R. Mutani; L. Durelli; M. Delsedime

More than half the amino acids determined in serum were lower in patients with epilepsy than in control subjects. Taurine was the only amino acid to be increased in epilepsy. The changes could represent a compensatory metabolic reaction to limit the imbalance of amino acids in epileptic brain and to facilitate uptake of taurine, which has an anticonvulsant action.


Epilepsia | 1975

Levels of Free Amino Acids in Serum and Cerebrospinal Fluid After Administration of Taurine to Epileptic and Normal Subjects

R. Mutani; F. Monaco; L. Durelli; M. Delsedime

The modifications associated with taurine treatment of the free amino acid content of serum and cerebrospinal fluid were investigated in epileptic and control subjects. In patients with epilepsy the main findings were, in the serum, the correction toward normal of the amino acid levels that were low prior to therapy, and in the cerebrospinal fluid, the increase up to above‐normal levels of glutamic acid, greatly diminished before treatment. Thus taurine, which has an anticonvulsant action, appears to partially correct the amino acid imbalance in epileptics. The monitoring of taurine‐induced glutamate changes in the cerebrospinal fluid could help to establish the correct therapeutic dose.


European Neurology | 1983

Long-term therapy with carbamazepine: Effects on nerve conduction velocity

S. Traccis; F. Monaco; GianPietro Sechi; A. Moglia; Roberto Mutani

Peripheral nerve function was evaluated in 30 epileptic patients on chronic therapy with carbamazepine (CBZ) and 20 healthy controls. The electrophysiological data indicated a mild progressive reduction of both motor and sensory conduction velocity in the patients on long-term treatment with the drug. The impairment of nerve function paralleled the duration of therapy (i.e. 1 through 3 years). CBZ plasma levels were constantly within the therapeutic range. Folic acid levels were below normal in about 50% of the subjects. In the absence of other evidence, the hypothesis cannot be excluded that folate deficiency may have played some role in the development of the peripheral nerve dysfunction.


Therapeutic Drug Monitoring | 1981

Ethosuximide in tears, saliva, and cerebrospinal fluid.

S. Piredda; F. Monaco

Ethosuximide (ESM) was determined by the EMIT technique in tears, saliva, cerebrospinal fluid (CSF), and plasma of epileptic subjects. CSF/ plasma, saliva/plasma and saliva/CSF ratios were in good agreement with gasliquid chromatography (GLC). The tears/plasma ratio was not significantly different from the saliva/plasma ratio, although the standard deviation was higher in the latter. These data indicate that ESM can be determined in a quantitatively similar manner in both saliva and tears by EMIT.


Epilepsia | 1981

Diphenylhydantoin and primidone in tears.

F. Monaco; S. Piredda; Camillo Mastropaolo; Massimo Tondi; R. Mutani

Summary: Diphenylhydantoin (PHT) and primidone (PRM) were determined by the EMIT® technique in the plasma, tears, saliva, and CSF of epileptic patients. Results indicate for PHT that tear values are more strictly correlated than are the saliva values to plasma and CSF concentrations. As for PRM, the data obtained show great interindividual variability of concentration in the different body fluids–in agreement with the wide range of both protein binding and half‐life of this drug.


European Neurology | 1979

Post-Convulsive Spinal Epidural Haematoma in Ankylosing Spondylitis

Virgilio Agnetti; F. Monaco; Roberto Mutani

A case of post-convulsive spinal spidural haematoma in a patient with ankylosing spondylitis is presented. As acute tetraplegia developed, surgery was performed with finding of blood clots in the extradural space from C6 to D8. Lethal evolution due to late referral to medical care stresses the need for prompt decompression of the injured spine.


Epilepsia | 1980

Carbamazepine‐10,11‐Epoxide Determined by EMIT Carbamazepine Reagent

F. Monaco; S. Piredda

Carbamazepine‐10,11‐epoxide (CBZ‐OX) was determined in physiological solutions by means of EMIT carbamazepine reagent. It was recognized as 12 to 20% of the total amount, the cross‐reaction being higher at lower CBZ‐OX concentrations. A correction for CBZ‐OX is necessary when one wants to correlate EMIT carbamazepine values with gas‐liquid chromatography values. However, this correction is relevant only for body fluids other than plasma, since the unbound fraction of CBZ‐OX would greatly influence the ultrafiltrate serum ratios.


Epilepsia | 1982

Brain Uptake of Carbamazepine in the Cat

F. Monaco; R. Mutani; S. Piredda; S. Traccis; Ramsay Re

Summary: Carbamazepine (CBZ) was determined by EMIT® assay in plasma, cerebrospinal fluid (CSF), and brain samples of cats after administration of the drug (40 mg/kg, i.p.). Plasma and CSF levels increase in a parallel manner from time 0 to 90 min after completion of injection, indicating a passive transport from one body fluid to the other. Brain levels reach a steady state at 15 min, with no significant difference being found between the concentrations at 15, 30, 60, and 90 min postinjection; this indicates that substantial early binding occurs in the brain. Since peak CSF concentrations occur at 90 min, concomitant with those for plasma, while brain levels are already high at 15 min, it is likely that CBZ enters the two compartments by independent mechanisms.


Neurological Sciences | 1979

Psychotic onset of multiple sclerosis

F. Monaco; R. Mutani; S. Piredda; A. Senini

A case is reported of a woman in whom acute manic attacks were followed later in life by neurological signs of multiple sclerosis, thus suggesting a possible correlation between the two clinical entities.SommarioÈ descritto il caso di una donna in cui la sclerosi multipla fu preceduta da attacchi acuti di tipo psicotico (maniacale).

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R. Mutani

University of Sassari

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