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Biomedical subjects

M Paganini

Publications and source records attributed to M Paganini.

32 records · Page 2Linked to original sources
PubMed1988

Age differences in contingent negative variation activity of healthy young adults and presenile subjects.

20 selected right-handed very healthy subjects (10 young adults and 10 presenile subjects mean age 28.3 and 59.6) were tested for CNV activity with a simple warned reaction time (RT) paradigm. EEG and CNV components (post-S1, N1, P2, P3; early CNV; N1200; late CNV; CNV resolution) were recorded from Fz, C3, Cz, C4, P3, Pz, and P4 referenced to linked mastoid electrodes. EOG, RT and stimuli were also recorded. The presenile group differed significantly from the younger group in the auditory post-S1 N1 and P3, and in the early (O-wave) and late (P-wave) CNV complex components. A progressive amplitude reduction only in frontal leads between O-wave and P-wave with the lowest point being reached in the P-wave was characteristic in the presenile group. Further, presenile subjects showed relatively flat CNV waveshapes of low amplitude and, as a whole, performed a little less well than young persons. This finding suggests that the statistically significant changes in post-S1 EPRs and CNV activity recorded in our presenile subjects, without appreciable deficits in behavioral and mental performance, could be alerting signs of early brain involutional processes related to minimal and subclinical decrement of orienting, attentiveness and response preparation capabilities. If such is the case and it could be confirmed in a larger sample of very healthy subjects, these age-related changes in the presenium could be of considerable practical importance for clinical and research applications.

Adult↗
PubMed1987

Lack of relationship between sodium valproate-induced adverse effects and the plasma concentration of its metabolite 2-propylpenten-4-oic acid.

The concentrations of valproic acid (VPA) and of its metabolites 3-oxo-VPA and 4-en-VPA were measured in the plasma of 12 selected epileptic patients 1, 2, 3, and 4 h after administration of a loading dose of VPA. Four of the patients, all on polytherapy, had had short-term adverse effects during chronic VPA treatment, and in them there has been abnormal NH3-values after a test doese of VPA. Eight patients (4 on monotherapy and 4 on polytherapy) had been free from adverse effects. No significant difference in the VPA, 3-oxo-VPA and 4-en-VPA concentrations was found between the three groups of patients. Accumulation of 4-en-VPA is not involved in the short-term adverse effects and hyperammonaemia induced by VPA.

Adolescent↗
PubMed1987

Long-term treatment with sodium valproate: monitoring of venous ammonia concentrations and adverse effects.

Adverse effects and venous blood ammonia concentrations were monitored over a period of 7 months in patients with epilepsy treated with valproate (VPA). During the 1st, 4th, 12th, 20th, and 28th weeks of therapy, blood samples for analysis of ammonia and anticonvulsants were taken immediately before the morning dose of VPA as well as 2 h after dosing. In all, 40 patients completed the follow-up; 16 of these (Group 1) received VPA alone, while the remaining 24 (Group 2) were treated simultaneously with VPA and other anticonvulsants (phenobarbital, phenytoin, and/or carbamazepine). In Group 1 patients, a slight though significant increase in ammonia concentrations was found during long-term VPA treatment; this trend was even more pronounced in Group 2 patients. The difference between postdose and predose ammonia levels in Group 2 patients was significant at each of the five follow-up examinations. In contrast, no such difference was demonstrated in patients of Group 1. VPA concentrations were found to be consistently higher in Group 2 patients than in Group 1. Twenty-three patients complained of various long-term adverse effects, while the other 17 remained symptom-free. The adverse effects reported included drowsiness, tremors, weight gain, hair loss, and gastrointestinal symptoms. Our data confirm the previously suggested hypothesis that changes in venous blood ammonia are particularly evident in patients taking VPA in combination with other antiepileptic drugs, such as phenobarbital and phenytoin.

Adolescent↗
PubMed1987

Contingent negative variation and reaction time in patients with presenile idiopathic cognitive decline and presenile Alzheimer-type dementia. Preliminary report on long-term nicergoline treatment.

Up to date 6 patients with initial presenile idiopathic cognitive decline (PICD) and 5 suffering from a presenile Alzheimer-type dementia (PAD) with a mean age of 59.5 were admitted to the trial. The 6 PICD patients were assigned to a double-blind nicergoline/placebo 6-month course with an oral dose of 30 mg twice a day. PAD patients were treated in an open design (nicergoline oral dose 30 mg twice a day) for at least 6 months. Until now only 4 PICD and 3 PAD patients have been treated regularly for 6 months. Two of 4 PICD patients showed a progressive enhancement of contingent negative variation (CNV), shorter reaction time (RT) and an improvement of clinical status. The other 2 PICD patients, on the contrary, showed a progressive mild worsening of CNV-RT and clinical patterns. The double-blind trial is not yet completed. CNV activity, RTs and clinical patterns progressively improved also in 2 PAD patients while in the 3rd they remained nearly unchanged or minimally worse during the 6-month treatment. The positive nicergoline effect on CNV-RT and clinical status noted in our patients appeared similar to that observed by other authors with DHEMT in patients with senile dementia of Alzheimer type. No adverse drug-related reactions were seen.

Alzheimer Disease↗
PubMed1985

Valproate-induced hyperammonaemia in two epileptic identical twins.

The cases of two epileptic identical twins are described, one of whom had presented an episode of valproate (VPA)-induced stupor associated with very high blood ammonia (NH3) concentrations. Both twins showed a similar marked increase of venous NH3 concentrations after the administration of a single loading dose of VPA (800 mg).

Adult↗
PubMed1985

Effect of associated antiepileptic treatment on valproate-induced hyperammonemia.

It has recently been shown that acute changes of venous blood ammonia (NH3) may predict short-term adverse effects of valproic acid (VPA). In the present study, the time course of NH3 concentration after a single oral dose of VPA (800 mg) was monitored in 68 epileptic patients. Patients were classified into four groups: previously untreated patients (group A, n = 21), patients under treatment with either phenobarbital (group B, n = 14) or phenytoin (group C, n = 13) or both (group D, n = 20). In each patient, venous blood for the NH3 assay was taken before the VPA dose (predose level) and at 1, 2, 3, and 4 h after the dose (postdose levels). While in patients receiving only VPA the postdose NH3 concentrations did not differ from the predose level, in each of groups B, C, and D the postdose concentrations appeared to be significantly higher than the predose concentration. The greatest increase was observed in group D. In the light of the data reported in the literature, those patients whose NH3 concentration after the VPA dose exceeds 100 micrograms/dl should be considered at higher risk for short-term, VPA-induced adverse effects during long-term therapy. Thus, our data suggest that caution should be exercised in adding VPA to anticonvulsant treatments including phenobarbital or phenytoin or both.

Adolescent↗
PubMed1984

Hyperammonemia and valproate-induced alterations of the state of consciousness. A report of 8 cases.

Sodium valproate was administered to 38 patients, admitted to our unit in the last 18 months, and chosen because they had: (1) poor control of their seizures; (2) therapeutic concentrations in their plasma of at least two major antiepileptic drugs. In 8 of them, a therapeutic dosage of VPA caused modifications of the state of consciousness ranging from coma to drowsiness and stupor. These patients also showed gastrointestinal disturbances, asterixis, ataxia, tremor and a worsening of EEG abnormalities. The side effects of the drug were constantly associated with increased concentration of blood ammonia. Better penetration of ammonia into the CNS of patients undergoing frequent seizures and possibly having imperfectly functioning biological barriers, could explain our observations. In view of the unusually high percentage of patients suffering from serious VPA side effects, it is probably advisable to carefully monitor ammonemia in the first few days of VPA therapy in every patient treated with multiple anticonvulsants.

Adult↗
PubMed1984

Acute changes of blood ammonia may predict short-term adverse effects of valproic acid.

Valproic acid (VPA) was given to 24 epileptic patients who were already being treated with other antiepileptic drugs. A standardized loading dose of VPA was administered, and venous blood was sampled at 0, 1, 2, 3, and 4 hours. Ammonia (NH3) was higher in patients who, during continuous therapy, complained of drowsiness (7 patients) than in those who were symptom-free (17 patients), although VPA plasma levels were similar in both groups. By measuring VPA-induced changes of blood NH3 content, it may be possible to identify patients at higher risk of obtundation when VPA is given chronically.

Adolescent↗
PubMed1983

Treatment of epileptic patients with valproic acid does not modify plasma and urine short-chain-fatty acids.

The purpose of this study was to evaluate the possible modifications of the plasma and urine short-chain-fatty acid (SCFA) patterns indiced by treatment with valproic acid (VPA). Increased amounts of SCFAs in patients under VPA treatment may explain the presence of VPA-induced hyperammonemia, toxic encephalopathies and rarer Rey-like syndromes recently observed. For this reason we assayed SCFA levels in the plasma and looked for propionic acid in the urine of 10 epileptic patients to whom it was decided to add VPA to their previously unsatisfactory anti-epileptic treatment. This was carried out prior to and during therapy with VPA. 5 of these patients developed toxic encephalopathy with hyperammonemia induced by VPA. Our data show that plasma and urine SCFAs are not modified by VPA treatment. This is so even in patients who have toxic encephalopathy with hyperammonemia indiced by this drug.

Adolescent↗
PubMedDate not supplied

[Alterations of smooth-pursuit ocular movements in Alzheimer's disease].

Recent findings suggest that patients affected by Alzheimer's disease (AD) have evident alterations of smooth-pursuit ocular movements induced by a sinusoidal predictable target. For a better understanding of the possible modifications of this performance in patients with AD we evaluated, using a quantitative method, the smooth-Pursuit induced by ramps with constant, unpredictable velocities. Twelve patients with probable AD were studied. These patients were compared with twelve age matched healthy volunteers. Visual inspection of our recordings shows that AD patients have frequent, large saccades intrusions which in some cases appeared to disrupt smooth tracking, particularly for low target speeds. Furthermore, the smooth-pursuit eye velocity induced by target of high speed is significantly reduced in respect to that present in our control group. Some significant correlations between altered smooth-pursuit parameters and abnormal psychometric scores were noted.

Aged↗
PubMedDate not supplied

[Alterations of the state of consciousness induced by valproic acid: 6 case reports].

Six epileptic patients are described to whom the addition of Valproic Acid (VPA) to a previously unsatisfactory antiepileptic treatment caused a toxic encephalopathy. This was characterized by alterations of the state of consciousness in all patients a few days after the beninning of the treatment with VPA. These ranged from a marked drowsiness to coma and were often associated with gastrointestinal and neurological (ataxia, asterixis) symptoms. In all cases very high blood ammonia values were found and the EEGs showed a diffuse slowing down of the activity. After the discontinuation of the drug the toxic symptoms quickly ceased and ammonia values returned to the normal values. It is hypothesized that the interference of VPA on the metabolism of ammonia could play an important role in the pathogenesis of the VPA-induced toxic encephalopathy.

Abdomen↗
PubMedDate not supplied

[Permanent amnesia as a result of a bilateral lesion of the hippocampus: description of a clinical case].

A case of permanent global amnesia resulting from a bilateral hippocampal lesion is reported, remarkable for its typical clinical picture and prolonged period of observation with repeated neuropsychological testing. No tendency toward spontaneous recovery was noted, even though extra-mnesic cognitive functions remained undamaged. No differences were observed between this amnesic syndrome and the neuropsychological picture during an acute episode of transient global amnesia.

Amnesia↗