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E M Airaksinen

Publications and source records attributed to E M Airaksinen.

At least 19 recordsLinked to original sources
PubMed2000

A population-based study on epilepsy in mentally retarded children.

PURPOSE: This study presents data on cumulative risk of seizures, cause, comorbidity, and remission of epilepsy among mentally retarded (MR) children followed until the age of 22 years. METHODS: A total of 151 MR children were identified at the age of 8 or 9 years by screening four birth cohorts of 12,882 children born from 1969 to 1972 in the Finnish province of Kuopio. Information about epilepsy was gathered longitudinally when children were 9 to 10, 17, and 22 years old. The guidelines for epidemiological studies on epilepsy proposed by the International League Against Epilepsy were followed. RESULTS: By the age of 10 years, 29 of the 151 MR children (19%) had epilepsy. The cumulative risk for epilepsy at 22 years was 21%. The probability of developing epilepsy was increased fivefold in severely MR children compared with mildly MR children, i.e., in 27 of the 77 severely MR children (35%) versus 5 of the 74 mildly MR children (7%). Postnatal causes of mental retardation or association with cerebral palsy increased the risk for epilepsy, especially in the mildly MR children. When these risk factors were not present, the mildly MR children exhibited only a 3% risk for epilepsy, whereas the respective risk was about 10-fold in severe mental retardation. The cumulative probability of epilepsy being in remission for 5 years by the age of 22 was 32%. CONCLUSIONS: The cumulative risk of epilepsy varies according to the severity and the cause of the retardation as well as the presence of additional disabilities. The cumulative probability of epilepsy remission tended to increase with age.

Adolescent↗
PubMed1996

Osmolality and electrolytes in cerebrospinal fluid and serum of febrile children with and without seizures.

UNLABELLED: During acute febrile diseases mild disturbances of water and electrolyte balance occur frequently. It has been suggested that changes in electrolyte balance, in particular hyponatraemia, might predispose a child to convulsions during febrile illness; however, the changes of electrolytes in the CSF are not known. We have studied the effects of fever and convulsions on water and electrolyte balance in CSF and serum by measuring osmolality and electrolyte concentrations in children. The febrile population consisted of 60 children, 36 of whom had seizures during fever. Twenty-one children without convulsions and nine children with epileptic symptoms were nonfebrile controls. We noticed that CSF is subject to changes in osmolality and electrolyte concentration during fever, while convulsions do not exhibit such changes. CSF osmolality and sodium concentrations were lower in febrile children than in nonfebrile controls. The osmolality in febrile children with convulsions was 3.8% (P < 0.01) and without seizures 3.5% (P < 0.01) lower than in nonfebrile nonconvulsive children. The changes in CSF sodium concentration, and to a lesser extent potassium and chloride concentrations, paralleled those of CSF osmolality. A positive correlation was observed between the CSF and serum osmolatities (r = 0.73, P < 0.0001), and sodium concentrations (r = 0.63, P < 0.0001). A negative correlation between the body temperature and both CSF osmolality (r = -0.66, P < 0.0001) and sodium concentration (r = -0.59, P < 0.0001) exhibits also the important regulative role of increased body temperature. CONCLUSION: Fever is an important factor for disturbances in fluid and electrolyte balance. The alterations in CSF osmolality and sodium concentration do not, however, give an unambiguous explanation for the susceptibility to simple febrile seizures.

Child↗
PubMed1995

Histamine in cerebrospinal fluid of children with febrile convulsions.

Febrile convulsions (FC) are frequent acute neurologic disturbances of childhood. The cellular and neurochemical mechanisms causing FC are unclear. Among other mechanisms, the CNS histamine (HA) has been suggested to participate in seizure control and thermoregulation. We evaluated the possible role of HA in regulation of FC by measuring HA and tele-methylhistamine (t-MH) concentrations in the cerebrospinal fluid (CSF) of children with FC. The study group consisted of 35 children treated for acute FC in the hospital. The control groups consisted of (a) feverish children without seizures (n = 23), (b) convulsive children without fever (n = 7), and (c) children with neither fever nor convulsions (n = 21). HA was assayed by high-performance liquid chromatography (HPLC) with fluorescence detection, and t-MH was measured by gas chromatography-mass spectrometry. CSF HA concentration in the group of febrile children without seizures was significantly higher (0.69 +/- 0.16 pmol/ml, mean +/- SE) than in children with FC (0.36 +/- 0.07 pmol/ml, p < 0.05, analysis of variance, ANOVA). HA concentration was 0.37 +/- 0.18 pmol/ml in the group of nonfebrile convulsive children and 0.36 +/- 0.08 pmol/ml in the nonfebrile nonconvulsive group. No statistical differences in t-MH were detected between groups. The increased susceptibility to seizures during fever may be connected to the lack of increase in CSF HA in the FC group. The data support the hypothesis that the central histaminergic neuron system may be involved in inhibition of seizures associated with febrile illnesses in childhood.

Child↗
PubMed1995

The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions.

In febrile convulsions glucose concentrations are known to increase both in the blood and cerebrospinal fluid (CSF). The reason behind this increase is, however, incompletely understood. We have studied the effects of convulsion and fever on the CSF and blood glucose concentrations in four different groups of children: febrile and non-febrile children, with and without convulsions. The concentration of glucose in the CSF was significantly higher in febrile children with (4.4 +/- 0.1 mmol/l, mean +/- SEM n = 35, p < 0.01. ANOVA, Duncan's test) and without convulsions (3.9 +/- 0.2 mmol/l, n = 22, p < 0.05) than in non-febrile, non-convulsive children (3.3 +/- 0.1 mmol/l, n = 21). In non-febrile convulsive children, the CSF glucose concentration was 3.7 +/- 0.2 mmol/l (n = 10). Both fever and seizures increased the CSF glucose levels (p < 0.0001) and p = 0.028, respectively, analysis of covariance). There was a linear correlation between the body temperature and concentration of glucose in the CSF (r = 0.454, p < 0.0001, n = 88, Pearson's correlation analysis). The changes in blood glucose concentrations between the groups paralleled those found in the CSF. Our results show that hyperglycaemia and an increase in the CSF glucose concentration in febrile convulsions is not explained just by a stress reaction, evoked by the seizure, as has been hypothesized earlier, but by the influence of increased body temperature as well.

Blood Glucose↗
PubMed1995

Low sodium levels in serum are associated with subsequent febrile seizures.

Fever plays an important role in causing disturbances in fluid and electrolyte balance. Hyponatraemia has been thought to enhance the susceptibility to seizures associated with febrile illnesses in childhood. We have studied serum electrolyte levels in children with simple and complicated febrile convulsions. Sodium levels were lower in those children with complicated convulsions in comparison with those having simple convulsions (136.07 +/- 3.06 mmoll-1, mean +/- SD, n = 42, and 137.62 +/- 2.63 mmoll-1, n = 71, respectively; p < 0.01, Student's t-test). The sodium concentrations were lowest in children with repeated seizures (134.20 +/- 2.30 mmoll-1, n = 15) compared with children having simple (p < 0.01, ANOVA, Duncan's test) or other complicated types of febrile convulsions: focal seizures (137.08 +/- 3.82 mmoll-1, n = 12, p < 0.01), seizures lasting longer than 15 minutes (138.00 +/- 2.45 mmoll-1, n = 5, p < 0.05) and children over 5 years (136.70 +/- 2.06 mmoll-1, n = 10, p < 0.05). Serum potassium levels showed no statistically significant differences between the patient groups. Our results show that hyponatraemia may increase the risk for multiple convulsions during the same febrile illness.

Child, Preschool↗
PubMed1994

Diurnal and age-related changes in cerebrospinal fluid tele-methylhistamine levels during infancy and childhood.

Histamine is a neurotransmitter participating in many physiological functions and behavior, including control of arousal and modulation of the circadian rhythms. Diurnal variation in cerebrospinal fluid (CSF) levels of tele-methylhistamine (t-MH), the main histamine metabolite, has been detected in several animal studies. In humans, such changes have not been described. Little is known on the development of histaminergic neurons in human brain. In children, the levels of CSF t-MH are not known. Therefore, we have measured the concentrations of CSF t-MH in 81 children, age ranging from 3 months to 14.6 years. t-MH levels were higher in infants, and near adult values were measured in adolescents, the relation between CSF t-MH and age being; CSF t-MH = -0.217 years + 7.31 (n = 81, r = 0.26, p = 0.021). The mean t-MH concentration was higher during the daytime (7.07 +/- 0.46 pmol/ml, mean +/- SEM) than in the night (5.35 +/- 0.60 pmol/ml, p = 0.0019, ANOVA). The results show a development change in the concentration of t-MH during childhood and a difference in t-MH levels between the daytime and night indicating a more active metabolism of brain HA in the waking period.

Adolescent↗
PubMed1990

Taurine in normal and diseased human skeletal muscle.

Taurine content of 199 clinical muscle biopsies was determined and correlated to histometric data of 121 cases. Taurine concentration in muscles was markedly dependent on fiber type distribution, taurine being more abundant in the slow, oxidative type 1 fibers than in the type 2 fibers. Taurine concentration rose slightly with age and tended to be higher in denervations, muscular dystrophies and myotonias, but the differences from the control values were non-significant.

Adolescent↗
PubMed1988

The neurological condition of the newborn infant with maternal hypertension, examined at term.

The aim of this prospective study was to examine the effect of maternal hypertension on the neurological condition of the newborn infant. Of the babies born between April 1984 and March 1986, 54 preterm, 151 full-term AGA and 24 full-term SGA neonates with maternal hypertension were compared, respectively, with 128 preterm, 144 full-term AGA and 73 full-term SGA neonates without maternal hypertension. Preterms were examined at term +/- 1 week and full-term neonates at 3-5 days postpartum by the Dubowitz method (Clinics in Developmental Medicine, Vol. 79, Heinemann, London, 1981). The respective full-term groups differed mostly in regard to movement and tone, with preterm groups differing in the predominant state and in auditory orientation. The differences were clearest between preterm AGA groups. The neurological condition of the infants was affected more by pre-eclampsia than by hypertension as such. Statistical analysis was carried out with the t-test, chi2-test and stepwise discriminant analysis.

Adult↗
PubMed1987

Biochemical and clinical studies on epileptic patients during two phase I trials with the novel anticonvulsant taltrimide.

Taltrimide (2-phthalimidoethanesulphon-N-isopropylamide), a lipophilic derivative of taurine and a potent anticonvulsant in animal studies, was administered in daily doses of 1 and 2 g for 2 weeks with an interval of 2.5 months in 2 phase I clinical trials to 9 drug-resistant epileptic patients. Seizures and EEG were recorded, and routine laboratory studies conducted. Concentrations of antiepileptic drugs in plasma, of amino acids in urine and plasma, and contents of amino acids, homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and cyclic nucleotides in the cerebrospinal fluid were determined. Although no clinical or neurophysiological effects were observed, an increase in the cerebrospinal fluid contents of HVA and cyclic nucleotides and changes in the concentrations of antiepileptic drugs and amino acids were found. The concentrations of HVA correlated with those of 5-HIAA and also with those of the main active metabolite of taltrimide. Biochemical changes due to taltrimide treatment resembled only partly those found after taurine treatment.

Adult↗
PubMed1985

Hereditary recurrent brachial plexus neuropathy with dysmorphic features.

A Finnish pedigree comprising 13 members in 3 generations with recurrent brachial plexus neuropathy is described. The disease was characterized by repeated attacks of pain in the upper limb/shoulder region, followed by muscle weakness and atrophy. The first episode usually occurred in childhood after a mild infection. Symptoms varied in intensity and seldom left marked neurological deficiencies. Patients had typical features including hypotelorism, small palpebral fissures and a small oral opening. The distribution of the affected members in the pedigree was compatible with autosomal dominant inheritance with high penetrance. Despite the limitation of the symptoms to the upper limbs, sural nerve biopsy showed tomaculous neuropathy in an affected member of the family. The structural changes of tomaculous neuropathy probably reflect a genetically determined generalized abnormality of the Schwann cells predisposing the patients to the recurrent palsies by exogenous factors.

Abnormalities, Multiple↗
PubMed1982

Decrease of GABA in the cerebrospinal fluid of patients with progressive myoclonus epilepsy and its correlation with the decrease of 5HIAA and HVA.

The degenerative type of progressive myoclonus epilepsy (PME) is a hereditary disease with grand mal seizures, stimulus sensitive myoclonus, characteristic EEG and mental deterioration in the late stage. GABAergic antiepileptic drugs are the most effective ones in this disease, with an unknown etiology. In this study, the GABA concentration in the CSF of 15 PME patients was measured and compared with values of sex- and age-matched epileptic controls. It was correlated with the concentrations of 5HIAA and HVA in the CSF, which were determined earlier from the same patients. The GABA concentration in the PME patients was statistically significantly decreased, to about 75% of that of the epileptic controls. It correlated with HVA and 5HIAA concentrations in the PME patients, but not in the epileptic controls. It is unknown whether these findings are related to the primary cause of PME or whether they are only secondary, owing to a loss of respective neurons or synapses.

Adult↗
PubMed1980

Taurine and other amino acids of platelets and plasma in retinitis pigmentosa.

The biochemical cause of human retinitis pigmentosa (RP) is unknown, although in kittens it is related to taurine deficiency. The concentrations of free amino acids were therefore determined in the plasma and platelets of 16 patients with RP and 27 controls. No statistically significant change was found in the plasma, but the concentration of taurine and aspartic acid of platelets calculated per number of platelets were significantly (p < 0.05) lower in RP patients than in controls. This finding correlates with the decreased uptake of taurine by platelets of RP patients and may be connected with the pathogenesis of this disease.

Adolescent↗
PubMed1979

Uptake of taurine by platelets in retinitis pigmentosa.

Uptake of 3H-taurine by platelets from twelve patients with retinitis pigmentosa (R.P.) and from healthy controls was measured. Platelets were incubated in autologous plasma with 3H-taurine for different times and at different substrate concentrations. The uptake of taurine by R.P. platelets at each incubation time was about two-thirds of the control value, the difference being statistically significant. Km was about the same, but Vmax was lower in R.P. platelets. The results suggest that R.P. is a disease affecting not only the eye but also taurine transport and/or storage in general.

Adolescent↗
PubMed1979

Uptake of taurine, GABA, 5-HT, and dopamine by blood platelets in progressive myoclonus epilepsy.

The uptakes of four neurotransmitters (taurine, GABA, 5-HT, and dopamine) by blood platelets from patients with degenerative-type progressive myoclonus epilepsy (PME) and from controls were studied using different incubation times and different concentrations. Only the uptakes of taurine differed significantly between patients and controls: patients' uptakes were 70% to 80% of control values at 10, 30, 60, and 120 min of incubation time. Km values were approximately the same, but Vmax values in PME patients were lower, showing quantitative but not qualitative differences in taurine uptake by platelets in PME. These results suggest that a defect or an inhibitory mechanism of some factor needed in the transport or binding of taurine (but not of GABA, 5-HT, and dopamine) is present in PME.

Adolescent↗