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Neurodevelopment abnormal

Clinical concern Transient hypothyroxinemia of prematurity (THOP) occiu s in 50% of extremely low gestational age neonates (ELGANs 24-28 weeks) and is a major factor of neurodevelopment abnormalities (cognitive delay, cerebral palsy, hearing loss, mental retardation, blindness or epilepsy) [9 ]. THOP characterised by very low total and free T4 levels and normal TSH may be safely treated with continuous infusion of 4 gg/kg/day levothyroxine for 42 days to produce a biochemical euthyroid state (phase I/II trials) [1(P]. There is a pressing need for a phase III trial of thyroid hormone that is of sufficient duration and size to determine whether a clinically important reduction in risk of developmental impairments in ELGANs can be achieved [11 ]. [Pg.636]

Prenatal cocaine exposure has been associated with subependymal hemorrhage and subependymal cyst formation in term neonates and more recently in preterm neonates (<36 weeks of gestation) (325). Medical records and cranial sonograms obtained during 1 year on 122 premature infants showed an increased incidence of subependymal cysts in preterm cocaine-exposed infants (8 of 18) compared with non-exposed infants (8 of 99). There was no increase in the incidence of major structural abnormalities. All subependymal cysts resolved by 4 months of age. The authors noted that the neurodevelop-mental implications of such cyst formation are unknown. [Pg.520]

Rujescu D, Bender A, Keck M, Hartmann AM, Ohl F, Raeder H, Giegling I, Genius J, McCarley RW, Moller HJ, Grunze H. A pharmacological model for psychosis based on N-methyl-D-aspartate receptor hypofunction molecular, cellular, functional and behavioral abnormalities. Biol. Psychiatry 2006 59 721-729. Mouri A, Noda Y, Enomoto T, Nabeshima T. Phencyclidine animal models of schizophrenia approaches from abnormality of glutamatergic neurotransmission and neurodevelopment. Neu-rochem. Int. 2007 51 173-84. [Pg.2291]

Another line of research is focused on the neurobiological development of the human brain in relation to schizophrenia. It has been hypothesised that schizophrenia is due to abnormal neurodevelopment, which results in a static encephalopathy that usually becomes manifest in adolescence. This abnormal development leads to morphological deviations such as enlarged or reduced brain structures, a disrupted communication between different brain structures, alterations in neuron density or decreased neuron size, and abnormal neuronal... [Pg.21]


See other pages where Neurodevelopment abnormal is mentioned: [Pg.89]    [Pg.89]    [Pg.191]    [Pg.34]    [Pg.83]    [Pg.185]    [Pg.115]    [Pg.34]    [Pg.426]    [Pg.427]    [Pg.752]    [Pg.1798]    [Pg.1798]    [Pg.1799]    [Pg.349]    [Pg.1210]    [Pg.280]    [Pg.261]    [Pg.1148]    [Pg.65]   
See also in sourсe #XX -- [ Pg.3 , Pg.111 , Pg.380 , Pg.381 , Pg.382 ]




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Neurodevelopment

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