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Biomedical subjects

A Ylinen

Publications and source records attributed to A Ylinen.

At least 55 records · Page 3Linked to original sources
PubMed1991

Behavioural, electrophysiological and histopathological changes following sustained stimulation of the perforant pathway input to the hippocampus: effect of the NMDA receptor antagonist, CGP 39551.

Sustained stimulation of the perforant path has been shown to damage the CA1 area and impair spatial memory in rats. The pattern of cell death is similar in human epileptics, who also exhibit memory deficits. In this study we demonstrate that the learning/memory impairment in water maze test and the development of interictal spikes that also followed stimulation-induced damage were antagonized by CGP 39551. Pretreatment with this NMDA receptor antagonist also slightly diminished somatostatin cell loss in the hilus but not CA1 pyramidal cell damage. These results indicate that the impairment of spatial learning/memory seems to be dependent not only on the degree of cell degeneration in the CA1 subfield of the hippocampus but also on the frequency of interictal spikes, at least in this model of epilepsy.

2-Amino-5-phosphonovalerate↗
PubMed1991

The effect of subchronic administration of vigabatrin on learning and memory in nonepileptic rats.

The present experiments investigated whether subchronic administration of vigabatrin, a GABA-mimetic drug, affects the performance of normal rats in the behavioural tasks assessing learning and memory. The effects of vigabatrin [50-200 mg/kg (IP)/day] administration on the acquisition and retention of water maze and passive avoidance task were studied. According to the results of three experiments, vigabatrin treatment did not markedly impair the acquisition or retention of water maze task. Furthermore, vigabatrin-treated rats were not inferior to saline-treated rats in reversal learning of water maze task. On the other hand, vigabatrin treatment slightly increased the speed of swimming in rats. The administration of vigabatrin did not affect the performance (training latency, number of training trials, testing latency) of rats in the passive avoidance task. According to these results, the effects of vigabatrin, a new antiepileptic drug, on the performance of nonepileptic rats were modest in behavioural tasks used to assess learning and memory.

Amino Acids↗
PubMed1991

Vigabatrin pre-treatment prevents hilar somatostatin cell loss and the development of interictal spiking activity following sustained simulation of the perforant path.

Somatostatin-containing neurons in the hilus of the dentate gyrus are known to be exceptionally vulnerable in experimental models of epilepsy, as well as in human temporal lobe epilepsy. The position of these cells in the circuitry of the dentate gyrus is ideal for gating the activation evoked by afferents from the entorhinal cortex. In the present study we have shown that the loss of hilar somatostatin-containing neurons, and the development of interictal spiking activity induced by sustained perforant pathway stimulation can be prevented by high doses (500 mg/kg), but not by low doses (100 mg/kg) of vigabatrin, an irreversible inhibitor of GABA-transaminase.

4-Aminobutyrate Transaminase↗
PubMed1991

Vigabatrin in drug-resistant partial epilepsy: a 5-year follow-up study.

We treated 75 patients with drug-resistant complex partial seizures and secondarily generalized seizures with vigabatrin as additional therapy for 6 months. Twenty-one patients either showed no benefit from vigabatrin treatment or had side effects. The remaining 54 patients entered into the long-term study. The median monthly seizure frequency decreased from 12.5 at baseline to 3.3 at the 3-month visit, and was 3.9 after 5 years of therapy in 28 patients who continued using the drug after the 5-year period. During 5 years of therapy with vigabatrin, 26 patients have withdrawn from the study because of various reasons: loss of efficacy (14), suspected side effects (5), noncompliance (3), administrative reasons (2), pregnancy (1), and epilepsy surgery (1). In all, 19 patients had a greater than 50% seizure frequency reduction at 5 years, representing 35% of the 54 patients who entered the long-term study, or 25% of the 75 patients who were initially recruited into the efficacy study.

Adolescent↗
PubMed1989

The importance of the electrocardiogram in ambulatory electroencephalographic recordings.

The role of an ambulatory electroencephalogram performed simultaneously with an electrocardiogram was studied in 861 neurologic inpatients. In total, 123 patients (14%) had interictal cardiac rhythm abnormalities, and 31 (4%) had neurologic symptoms considered to be of cardiac origin. The occurrence of cardiac arrhythmias was related to medical history of cardiovascular disease, but not to organic cerebral disorders. The ictal increase of heart rate was significantly higher and more abrupt in epileptic seizures than in psychogenic attacks. The ictal electroencephalogram/electrocardiogram may thus be applicable to the differential diagnosis between the epileptic and psychogenic seizures.

Ambulatory Care↗
PubMed1989

Cardiac arrhythmias in the differential diagnosis of epilepsy.

Symptomatic attacks or seizures associated with cardiac arrhythmias may cause difficulty in differential diagnosis. Two patients are reported in whom disturbances of cardiac conduction induced attacks which clinically resembled attacks of psychogenic and epileptic origin and were abolished after implantation of a demand-type pacemaker. A third patient is described who had epileptic seizures resulting in cardiac arrhythmias. In the differential diagnosis of these cases, simultaneous ambulatory EEG and ECG recording was essential.

Adult↗
PubMed1989

Somatostatin and beta-endorphin levels in cerebrospinal fluid of nonmedicated and medicated patients with epileptic seizures.

Neuropeptides have been proposed to play a role in regulation of the seizure threshold and interictal behavior in experimental models of epilepsy, but there are few studies concerning neuropeptides in human epilepsy. We compared the levels of two peptides, somatostatin (SLI) and beta-endorphin (BEP) in lumbar cerebrospinal fluid (CSF) of unmedicated (N = 18) and medicated (n = 24) epileptic patients with the levels of these peptides in control (n = 20). Peptide levels in the CSF of patients with panic disorder (8) were also evaluated. Patients with chronic medicated epilepsy had a SLl level 80% (p = 0.003, Mann-Whitney U-test) that of the controls, 76% (p = 0.011) that of unmedicated patients, and 84% (p = 0.028) that of the panic group. BEP in the CSF did not differ in unmedicated, medicated and control patients. On the other hand, patients with panic disorder had higher levels of BEP in CSF than did the controls (117%, p = 0.041). In panic patients SLl was at control level. The present study indicates that the peptidergic systems are affected differentially in epilepsy and in panic disorder. Furthermore, there seems to be selectivity in the affect on peptidergic systems during the period when the epilepsy becomes chronic.

Adolescent↗
PubMed1989

Cerebrospinal fluid GABA and seizure control with vigabatrin.

1. To evaluate the relationship between the clinical response and enhancement of GABAergic neurotransmission, for 6 months we administered vigabatrin (gamma-vinyl-GABA, GVG) to 75 patients with complex partial epilepsy. Total GABA (TGABA), free GABA (FGABA), homocarnosine (HC), and GVG concentrations were measured in CSF of these patients before and during GVG treatment. 2. Over 50% reduction in seizures was found in 55% of the patients. Dose-reduction resulted in a relapse, i.e. the return of seizures. 3. At baseline TGABA, FGABA, and HC did not differ in responders and nonresponders. After GVG treatment, the TGABA and HC levels were lower in nonresponders (P less than 0.001), but the GVG and FGABA levels did not differ. The GVG dose reduction resulted in a concomitant decrease in TGABA, FGABA, HC and GVG (P less than 0.001). 4. According to our results GVG is an effective anticonvulsant drug in complex partial seizures. In nonresponders the poor anticonvulsant response may be related to the lower elevation of the CSF markers of GABAergic neuronal activity in this group compared with the responders.

Adolescent↗
PubMed1989

Specificity of vigabatrin for the GABAergic system in human epilepsy.

The therapeutic action of vigabatrin (gamma vinyl GABA, GVG) has been reported to be mediated by GABAergic neurotransmission. In the present study, we evaluated different neurotransmitter systems in the cerebrospinal fluid (CSF) of patients with complex partial epilepsy, before and during GVG treatment. The markers of the GABAergic system (free GABA, total GABA, homocarnosine) showed a two- to threefold elevation. There was also an increase in glycine during the 6 months of GVG treatment. In contrast, we did not find any constant CSF changes in either excitatory amino acids or in markers of the cholinergic (acetylcholinesterase), dopaminergic (homovanillic acid), serotonergic (5-hydroxyindoleacetic acid), or peptidergic (somatostatin, prolactin, beta-endorphin) systems. This finding (except an elevation in glycine) was in agreement with previous studies which suggest a specific action of GVG on the GABAergic system. The role of glycine in antiepileptic efficacy of GVG needs further evaluation.

Adult↗
PubMed1988

Effect of gamma-vinyl GABA treatment on cholinergic and aminergic neurotransmission and on cyclic nucleotides in human complex partial epilepsy--a CSF study.

1. Gamma-vinyl GABA (GVG) is a new anticonvulsant drug that enhances levels of GABA in the brain by irreversibly inhibiting GABA transaminase. 2. To further evaluate the effects and mechanism of action of GVG in the human brain, we measured acetylcholinesterase (AChE) activity and levels of homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), cyclic nucleotides (cAMP, cGMP), total GABA (TGABA), and GVG in CSF of 78 patients with complex partial epilepsy. The CSF samples were taken at baseline and after 3 months of GVG administration (3 g GVG per day). Thereafter, the responders (= 50% decrease in number of seizures) were divided (double-blind) into two groups that received either 1.5 g or 3 g of GVG per day for the next 3 months. The third CSF sample was taken after this double-blind period. 3. TGABA levels were increased during the GVG treatment (p less than 0.001). In the whole group of patients AChE, HVA, 5-HIAA, and cAMP did not differ from baseline values, cGMP levels were slightly elevated after 3 months of GVG administration (p = 0.019), but were no longer elevated after 6 months. Responders had slightly lower AChE activity than nonresponders (p = 0.041). After 6 months of drug treatment the cGMP levels of patients receiving 1.5 g of GVG did not differ from those receiving 3 g. 4. In conclusion, GVG administration elevates levels of TGABA in the CSF without any clear of constant change to cholinergic and aminergic transmission or effect on cyclic nucleotides. Our study further emphasizes the specific mechanism of action of GVG via GABAergic transmission.

Acetylcholinesterase↗
PubMed1987

Amino acid levels in human CSF after generalized seizure.

We studied the possible role of excitatory and inhibitory amino acids and their balance during generalized convulsions. The levels of amino acids in postictal cerebrospinal fluid (CSF) were compared with amino acid concentrations in interictal CSF of ten patients with generalized tonic-clonic convulsions. Glu, Gln, Asp, Asn, Tau, Gly, total GABA (t-GABA), free GABA (f-GABA), and homocarnosine levels and Glu/Gln, Asp/Asn, t-GABA/Glu, f-GABA/Glu, f-GABA/Asp, and Glu/Asp ratios were similar in both samples (Student's paired t-test). Our results suggest that in humans possible changes in amino acids in brain tissue during the ictal stage are not reflected in the lumbar CSF.

Adult↗
PubMed1987

Somatostatin, beta-endorphin, and prolactin levels in human cerebrospinal fluid during the gamma-vinyl-GABA treatment of patients with complex partial epilepsy.

The anticonvulsant action of the new anticonvulsant drug gamma-vinyl-GABA (GVG) is obviously mediated by elevation of the concentration of GABA in the brain. The effect of GVG administration on other transmitter systems is not fully known in humans. We studied the possible interactions of GVG administration with peptidergic systems. Included in this study were 67 patients with complex partial epilepsy (CPS). The first CSF sample was taken before GVG administration. The second CSF sample was taken after 3 months of GVG treatment (3 g/day). Thereafter half of the responders (50% decrease in seizure frequency or clear improvement in global performance) received 3 g/day and the other half received 1.5 g/day for the next three months, after which the third CSF sample was taken. Somatostatin (SLI), beta-endorphin (beta-EP), and prolactin (PROL) levels in CSF were measured by radioimmunoassay. Total GABA (tGABA) and GVG levels in CSF were measured by high performance liquid chromatography. After 3 months of GVG treatment there was a slight increase in the beta-EP (p = 0.027, Student's paired t-test), which was not found after 6 months of GVG administration. Both SLI and PROL were stable during the study. Peptide levels were not connected to the clinical response to GVG, GVG dosage, or to tGABA levels in the CSF. In conclusion, the elevation of GABA levels in the brain during GVG treatment apparently does not induce long-term interactions with the peptidergic systems studied.

Adult↗
PubMed1986

Somatostatin-like immunoreactivity in the cerebrospinal fluid of patients with Parkinson's disease and its relation to dementia.

Acetylcholinesterase, somatostatin-like immunoreactivity, and homovanillic acid levels were measured in the cerebrospinal fluid of 36 patients with early stages of Parkinson's disease and in 19 control patients. In patients with Parkinson's disease the levels of somatostatin-like immunoreactivity were lower than in the controls (p less than 0.01); these values were lowest in the demented Parkinsonian patients. Concentrations of homovanillic acid were also significantly lower in Parkinsonian patients (p less than 0.05). In contrast, no changes were observed in the acetylcholinesterase activity of patients with Parkinson's disease. The reduced somatostatin-like immunoreactivity in CSF agrees with previous post-mortem studies and indicates that Parkinson's disease and Alzheimer's disease may have some neurochemical features in common.

Acetylcholinesterase↗
PubMed1981

Neurodevelopmental screening at five years of children who were at risk neonatally.

A neurodevelopmental screening test with cumulative scoring for abnormal test responses was performed on 845 five-year-old Finnish children who, in the newborn period, had had disorders which placed them in a high-risk group, and on 70 controls. The results showed a significant difference between the neurodevelopmental scores of the risk-group children and those of the controls. The scores were higher if the child had had many of the risk factors simultaneously. Boys had significantly higher scores than girls. The mean scores also varied between different risk factors. It is evident that slight neurodevelopmental deviations at the age of five years can derive from disorders in the newborn period.

Child, Preschool↗
PubMed1978

Occurrence of risk factors in newborn infants. A study of 22359 consecutive cases.

All the 22359 deliveries in 1971-1974 at the Institute of Midwifery, Helsinki, were analyzed for risk factors. 1196 infants (5.35%) had one or more risk factor at birth, the most common being an Apgar score of 6 or less at 5 or 15 minutes, hyperbilirubinaemia, and a birth weight of 2000 g or below. The other risk factors registered were neurological symptoms, respiratory difficulties, hypoglycaemia, newborn infants of diabetic mothers and cases with sepsis. 124 infants in the risk group died during the first week. This was 83% of the total neonatal mortality. Except for hyperbilirubinaemia, which was less frequent in 1974, there was no marked change in the composition of the risk group from 1971 to 1974.

Apgar Score↗