[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.

Cognitive event-related potentials and reaction time in presenile subjects with initial mild cognitive decline or probable Alzheimer-type dementia.

The so-called contingent negative variation (CNV) is a slow brain potential representing a complex of variously overlapped "endogenous" components of behavior related to different reasonably well-known neurocognitive processes. CNV complex evoked with a standard paradigm (S1-2 sec-S2-motor response) and reaction time (RT) to imperative signal (S2) were recorded and measured in 11 patients with initial presenile idiopathic cognitive decline (PICD), 8 with presenile Alzheimer-type dementia (PAD) and 10 healthy age-matched controls. Significant group differences were obtained for measures of some CNV components, particularly of the late pre-S2 CNV.

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.

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.

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.

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).

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).

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).

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.

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.

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.

[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.

[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.