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Biomedical subjects

M L Granström

Publications and source records attributed to M L Granström.

At least 37 records · Page 2Linked to original sources
PubMed1992

Psychomotor development in children of mothers with epilepsy.

The risk of psychomotor retardation and the prevalence of mental subnormality are slightly increased in offspring of mothers with epilepsy. The prevalence rates of mental deficiency observed in population-based studies have been lower than those in reports of hospital-based studies. In addition to use of antiepileptic drugs (AEDs), several other factors associated with maternal epilepsy, such as seizures during pregnancy, inherited brain disorders, and nonoptimal psychosocial environment, can affect the child's psychomotor development. None of the major AEDs carries any special risk for mental retardation. However, polytherapy and inherited deviations in AED metabolism in the fetus probably do increase the risk for mental retardation.

Anticonvulsants↗
PubMed1992

Minor anomalies in children of mothers with epilepsy.

Minor anomalies are small, structural deviations that result from alterations in morphogenesis during gestation. Multiple minor anomalies are clinically significant, because they are associated with an increased risk of major developmental defects in the affected individuals. Children of mothers with epilepsy have an excess of minor and major anomalies as compared with the incidence in children of parents without epilepsy. Of the typical minor anomalies described in offspring of mothers with epilepsy, most features appear to be genetically linked with epilepsy. Only distal digital hypoplasia seems to be a specific marker for phenytoin teratogenicity. In most children, distal digital hypoplasia is not associated with serious developmental disorders. Genetic defects in the mechanisms of drug detoxification in the fetus and treatment of the mother with more than one antiepileptic drug during pregnancy increase the risk of severe teratogenic effects in offspring.

Abnormalities, Drug-Induced↗
PubMed1991

Monitoring of concentrations of clobazam and norclobazam in serum and saliva of children with epilepsy.

Clobazam was added to the previous antiepileptic drug therapy of 90 children suffering from drug resistant epilepsy. Ten patients became seizure free, although four of these later developed tolerance. Thirty-three patients experienced a decrease in seizure frequency, and 24 of these, too, developed tolerance. Forty-four patients showed no change in seizure frequency, and three experienced an increase. The best results were experienced by patients with myoclonic seizures, whereas patients with complex partial seizures usually developed tolerance. The concentrations of clobazam and its active metabolite norclobazam were measured in 251 serum and 57 saliva samples. The group of seizure-free patients had the lowest clobazam and norclobazam concentrations; tolerance was associated with the highest concentrations. Beneficial side effects were associated with low, and adverse effects with high, concentrations of norclobazam. The concentrations of clobazam and norclobazam in saliva correlated with concentrations in serum. Monitoring of serum and salivary concentrations of clobazam and norclobazam is of limited value only, and no therapeutic target range can be given.

Adolescent↗
PubMed1991

The psychomotor development during the first year of life of infants exposed to intrauterine alcohol of various duration. Fetal alcohol exposure and development.

The developmental abilities of 80 children exposed to alcohol of various duration in utero were assessed 1 to 3 times during their first year of life. The occurrence of developmental delay increased towards the end of the first year. The longer the exposure the more common and severe was the developmental delay. If alcohol consumption could be reduced by the second trimester only a slight abnormality of motor development was seen at the age of 12 months. If heavy maternal drinking continued throughout the second trimester cognitive development was also delayed. Psychomotor retardation by the age of one year occurred in 38% of children who had been exposed to continuous heavy alcohol consumption during pregnancy. The psychomotor retardation diagnosed at the age of one year could be found earlier in 80% of the children but pure motor or pure cognitive delay only in some cases. The beneficial effect of reducing maternal alcohol consumption before the last trimester of the child's development was clear.

Alcohol Drinking↗
PubMed1991

The effect of intrauterine alcohol exposition in various durations on early cognitive development.

Fifty-three children exposed to alcohol of various duration were examined at 18 to 19 months of age. No significant difference was found in developmental outcome between non-exposed (n = 56) and during the I trimester exposed children (n = 21). Exposure until the III trimester (n = 19) or continuous exposure (n = 13) caused significantly lower scores in language and total mental assessment. The procentual numbers of children with possible developmental risk (failure or pass at acceptance limit) in various developmental fields grew with increasing duration of intrauterine alcohol exposure. Failures in gross or fine motor items differed significantly between the non-exposed and the two long exposed children but in language items only between the non-exposed and the children exposed until the III trimester. A high number of exposed children scored just the limit values indicating a milder form of developmental delay. In comparison with the developmental results of one year of age an increase in delay in cognitive development was seen. The incidences of other teratogenic effects (pre- or postnatal growth retardation, facial dysmorphia) of fetal alcohol exposure were highest in the continuous exposed group. Five (38%) of the continuous exposed children had typical fetal alcohol syndrome and only 1 (5%) of the children exposed until the III trimester.

Child, Preschool↗
PubMed1991

Landau-Kleffner syndrome: epileptic activity in the auditory cortex.

The Landau-Kleffner syndrome (LKS) is characterized by electroencephalographic spike discharges and verbal auditory agnosia in previously healthy children. We recorded magnetoencephalographic (MEG) spikes in a patient with LKS, and compared their sources with anatomical information from magnetic resonance imaging. All spikes originated close to the left auditory cortex. The evoked responses were contaminated by spikes in the left auditory area and suppressed in the right--the latter responses recovered when the spikes disappeared. We suggest that unilateral discharges at or near the auditory cortex disrupt auditory discrimination in the affected hemisphere, and lead to suppression of auditory information from the opposite hemisphere, thereby accounting for the two main criteria of LKS.

Aphasia↗
PubMed1990

Head circumference in children of epileptic mothers: contributions of drug exposure and genetic background.

Head circumference after the first year of life was investigated in 144 children of epileptic mothers ('study group'). Fifty-two children had been exposed to phenytoin monotherapy, 19 to carbamazepine monotherapy, 27 to drug combinations including barbiturates, 29 to other drug combinations, and 17 children had not been exposed to antiepileptic drugs (AEDs) during pregnancy. The prevalence of microcephaly (2.1%) was no higher than that in the general population. Head circumference was measured at 5.5 years in 121 of the study group children, in 105 control children, and in the majority of their parents (118 mothers and 89 fathers in the study group, and 103 mothers and 65 fathers in the control group). The sex-adjusted head circumferences of the children showed a significant variation according to exposure subgroup, with the barbiturate and carbamazepine monotherapy exposed children having the lowest mean values. This result is similar to our previous findings in the same children at birth and at 18 months of age. Paternal head circumference was also below average in the same subgroups. After further adjustment for parental head circumference, the significant variation between the subgroups of children disappeared, even though the barbiturate exposed children continued to have the lowest mean value. Genetic causes may thus contribute to the relatively small head circumference in some AED exposed children of epileptic mothers. However, a mild drug effect in the barbiturate and carbamazepine exposed children cannot be excluded.

Adult↗
PubMed1990

Specific cognitive dysfunction in children with epileptic mothers.

Specific cognitive abilities and motor function were investigated at 5.5 years in 104 children with epileptic mothers and in 105 control children, all with normal general intelligence. The majority (89 per cent) of the children of epileptic mothers had been exposed to anti-epileptic drugs during pregnancy, most commonly phenytoin (69 per cent). Maternal seizures had occurred during pregnancy in 52 per cent. A significant difference, with poorer performance in the study group, was found in block design (WPPSI) and auditory closure (ITPA). Significantly more study than control children had some type of specific cognitive dysfunction. Within the study group, increased risk was associated with maternal partial seizures, with seizures occurring during pregnancy, and with low paternal education, but not with exposure to anti-epileptic drugs. Three possible mechanisms of this effect are suggested: subtle brain-damage associated with fetal asphyxia during the mothers' generalized convulsions; genetically transmitted brain abnormalities; and psychosocial disadvantage limiting partner choice.

Anticonvulsants↗
PubMed1988

Prediction of perinatal brain damage by cord plasma vasopressin, erythropoietin, and hypoxanthine values.

For an assessment of whether cord plasma arginine vasopressin, erythropoietin, and hypoxanthine concentrations are predictors of perinatal brain damage, these concentrations were measured in 62 infants born after preeclampsia of pregnancy, 31 acutely asphyxiated infants, and 38 control infants. Follow-up at 2 years included neurologic examination and the determination of a Bayley mental score. Clear abnormality (death, cerebral palsy, or developmental delay) was found in four infants in the preeclampsia group and five in the asphyxia group; slight abnormality was found in 12 and 6 infants, respectively; and no abnormality was found in the remainder. Neither arginine vasopressin values nor hypoxanthine values predicted adverse outcome in either study group. A high erythropoietin level was found in infants born after preeclampsia regardless of outcome: normal outcome (geometric mean (GM), 102; 95% confidence interval [CI], 69 to 153 mU/ml), slightly abnormal outcome (GM, 100; 95% CI, 37 to 270 mU/ml) or clearly abnormal outcome (GM, 84; 95% CI, 19 to 378 mU/ml). However, asphyxiated infants with clearly abnormal outcome had higher erythropoietin values (GM, 67; 95% CI, 33 to 137 mU/ml; p less than 0.05) than the normal infants (GM, 37; 95% CI, 23 to 59 mU/ml). We conclude that a high erythropoietin level after normal pregnancy, but not after preeclampsia, indicates an increased risk for cerebral palsy or death.

Arginine Vasopressin↗
PubMed1988

Minor anomalies in offspring of epileptic mothers.

In a prospective study, 121 children of mothers with epilepsy (study group) and 105 control children were examined in a blinded fashion at age 5 1/2 years for 80 minor physical anomalies, including nine typical features previously reported characteristic of fetal hydantoin syndrome. Of the study group, 106 children had been exposed to antiepileptic drugs (82 to phenytoin) during pregnancy; 44 (36%) mothers had had generalized convulsions during pregnancy. One hundred fourteen mothers and 87 fathers of study group children and 101 mothers and 58 fathers of control children were also examined. A significant excess of minor anomalies considered characteristic of hydantoin syndrome was observed in children of epileptic mothers and in epileptic mothers, compared with the control group. There was no excess of other minor anomalies studied. Several minor anomalies previously regarded as typical of fetal hydantoin syndrome were shown to be genetically linked to epilepsy. Only hypertelorism and digital hypoplasia were associated with phenytoin exposure. The current concept of the syndrome seems to be incorrect; most of the "typical" characteristics are not caused by phenytoin. None of the phenytoin-exposed children had all of the main characteristics of hydantoin syndrome (typical acrofacial features, intellectual deficiency, growth retardation, and microcephaly). The risk of developmental disturbance associated with intrauterine phenytoin exposure seems to be much lower than the 7% to 11% risk of fetal hydantoin syndrome reported earlier.

Abnormalities, Drug-Induced↗
PubMed1988

Intelligence of children of epileptic mothers.

Intellectual performance was investigated in a group of 148 children of epileptic mothers enrolled in a prospective study during pregnancy, and in 105 control children; 121 of the 148 children (82%) were examined together with the control group at the age of 5 1/2 years. The intelligence of 116 study and 104 control children was assessed by both verbal (Wechsler Preschool and Primary Scale of Intelligence) and nonverbal (Leiter International Performance Scale) methods. The prevalence of mental subnormality among the remaining 32 study children was calculated on the basis of psychologic assessments done outside our study, or school achievement, or both. Of the 148 study group children, 131 had been exposed in utero to antiepileptic drugs, most commonly phenytoin (103 exposed). The prevalence of mental deficiency in the study group (1.4%) was either the same or only slightly elevated in comparison with that in the general population. In the control group, there were no mentally deficient children. The mean intelligence quotients obtained at the 5 1/2-year examination were significantly lower in the study group than in the control group. There was no increased risk of low intelligence attributable to fetal exposure either to antiepileptic drugs below toxic levels or to brief maternal convulsions. In a few cases, there seemed to be a genetic connection between epilepsy in the mother and poor intellectual performance in the child. A high number of minor anomalies was associated with a lower mean intelligence quotient in both the study and the control groups. However, those features previously reported as typical of children of epileptic mothers, and those shown to be associated with phenytoin exposure in a previous phase of this study, did not predict low intelligence in the affected children.

Child, Preschool↗
PubMed1987

Estradiol, estriol, progesterone, prolactin, and human chorionic gonadotropin in pregnant women with alcohol abuse.

Serum estradiol, estriol, progesterone, PRL, and hCG concentrations were measured at 4-week intervals in 40 pregnant women who chronically abused alcohol and in 20 abstinent pregnant women. Sixteen alcohol users gave birth to infants with the fetal alcohol syndrome (FAS), whereas the remaining 24 infants of alcohol users and all infants of the abstinent women were healthy. The women whose infants had the FAS had decreased estradiol and estriol levels throughout pregnancy. Progesterone levels also tended to be low. In contrast, the alcohol users had increased PRL levels during the 16-24th weeks of pregnancy compared with those in the abstinent women, but this rise was not related to the FAS. The concentrations of hCG fluctuated widely, without any consistent difference between alcohol users and abstinent women. Thus, heavy maternal abuse of alcohol resulting in FAS is accompanied, primarily or secondarily, by reduced estrogen concentrations throughout pregnancy and increased PRL levels during the 16-24th weeks of pregnancy.

Adult↗
PubMed1987

Prediction of fetal alcohol syndrome by maternal alpha fetoprotein, human placental lactogen and pregnancy specific beta 1-glycoprotein.

No diagnostic measures exist for the fetal alcohol syndrome (FAS). Therefore, maternal serum alpha-fetoprotein (AFP), human placental lactogen (HPL) and pregnancy specific beta-1-glycoprotein (SP 1) were followed in 35 pregnant problem drinkers and 14 abstinent control women throughout pregnancy. Thirteen women gave birth to infants with FAS. These women had low levels of AFP and SP 1, but the levels of HPL were normal. Low AFP predicted FAS correctly in 59% with a relative risk of 2.46. Low SP 1 predicted FAS in 56% of the cases with FAS, and a relative risk was 3.29. HPL assay was useless in the detection of FAS. Low AFP and SP 1 may reflect primary or secondary effects of ethanol abuse in pregnancy and appear useful in predicting FAS. These tests can be recommended for routine use in the antenatal care of drinking women.

Adult↗
PubMed1986

Alpha-fetoprotein, human placental lactogen, and pregnancy-specific beta 1-glycoprotein in pregnant women who drink: relation to fetal alcohol syndrome.

To determine the usefulness of the assays of maternal serum alpha-fetoprotein, human placental lactogen, and pregnancy-specific beta 1-glycoprotein in prenatal diagnosis of fetal alcohol syndrome, these proteins were followed in 35 problem drinkers (greater than 100 gm of ethanol weekly) and in 14 abstinent women throughout gestation. Thirteen women gave birth to infants with fetal alcohol syndrome, and these women had low levels of alpha-fetoprotein and pregnancy-specific beta 1-glycoprotein but levels of human placental lactogen were normal. Low alpha-fetoprotein correctly predicted fetal alcohol syndrome in 59% with a relative risk of 2.46. Low pregnancy-specific beta 1-glycoprotein predicted fetal alcohol syndrome in 56%, and a relative risk was 3.29. Low alpha-fetoprotein and pregnancy-specific beta 1-glycoprotein may reflect primary or secondary effects of ethanol abuse in pregnancy and appear to be useful in predicting fetal alcohol syndrome.

Adult↗
PubMed1983

Serum folate concentrations during pregnancy in women with epilepsy: relation to antiepileptic drug concentrations, number of seizures, and fetal outcome.

Serum folate concentrations, blood counts, and antiepileptic drug concentrations were measured during 133 pregnancies of 125 women with epilepsy. There was an inverse correlation between serum folate concentrations and concentrations of phenytoin and phenobarbitone. The number of epileptic seizures during pregnancy showed no association with serum folate concentrations. No cases of maternal tissue folate deficiency or fetal damage attributable to low maternal serum folate were observed. Maternal serum folate concentrations for infants with structural birth defects, "fetal hydantoin syndrome," or perinatal death were similar to those for healthy babies. A low dose (100 to 1000 micrograms daily) of folate supplement appeared sufficient for pregnant women with epilepsy despite the antifolic action of antiepileptic medication. Monitoring folate concentrations in pregnant women with high serum concentrations of phenytoin or phenobarbitone is recommended.

Carbamazepine↗
PubMed1983

EEG in neonatal herpes simplex encephalitis.

The EEGs of 21 newborns with herpes simplex encephalitis were analysed. The diagnosis was based on the demonstration of herpes simplex infection in association with neurological symptoms, other etiological factors being excluded. Sixteen of 21 babies (76%) showed in their EEGs electrical seizures, either focal or unilateral. These paroxysms consisted of sharp waves or slow waves repeating at pseudo-periodic intervals, usually of 0.5-2 sec. Individual paroxysms had a duration of 10-20 sec in 6 babies and 1-2 min in 10 patients. During the same period, 20 other babies displayed the same EEG finding. Of these, 11 had encephalitis of unknown etiology. In our series there appeared to exist a correlation between both the duration of the electrical seizures and the degree of EEG background abnormality and the clinical outcome. Babies with markedly abnormal background and long-lasting paroxysms tended to have a poor prognosis. It is concluded that in newborns with clinical signs of encephalitis who show in their EEGs paroxysms of the type described, the possibility of herpes simplex encephalitis should be considered.

Electroencephalography↗