Positron emission tomography in the newborn

Perlman, Jeffrey M.; Herscovitch, Peter; Kreusser, Katherine L.; Raichle, Marcus E.; Volpe, Joseph J.

doi:10.1212/wnl.35.2.244

Cited by 32 publications

(8 citation statements)

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“…CBF-metabolism coupling is probably developed in the preterm infants by 32 wk of gestation, if not earlier (67). Excessive neuronal activity during seizures has been associated with increased CBF and CBF velocity in term newborn and preterm infants, respectively (23,150). Changes in the regional distribution of CBF during infancy and childhood correlate with changes in the local pattern of glucose utilization in the brain (35), supporting the concept of CBF-metabolism coupling in the developing brain.…”

Section: Cerebral Blood Flow-metabolism Coupling In the Pre-mentioning

confidence: 74%

Cerebral vascular regulation and brain injury in preterm infants

Brew

Walker

Wong

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Cerebrovascular lesions, mainly germinal matrix hemorrhage and ischemic injury to the periventricular white matter, are major causes of adverse neurodevelopmental outcome in preterm infants. Cerebrovascular lesions and neuromorbidity increase with decreasing gestational age, with the white matter predominantly affected. Developmental immaturity in the cerebral circulation, including ongoing angiogenesis and vasoregulatory immaturity, plays a major role in the severity and pattern of preterm brain injury. Prevention of this injury requires insight into pathogenesis. Cerebral blood flow (CBF) is low in the preterm white matter, which also has blunted vasoreactivity compared with other brain regions. Vasoreactivity in the preterm brain to cerebral perfusion pressure, oxygen, carbon dioxide, and neuronal metabolism is also immature. This could be related to immaturity of both the vasculature and vasoactive signaling. Other pathologies arising from preterm birth and the neonatal intensive care environment itself may contribute to impaired vasoreactivity and ineffective CBF regulation, resulting in the marked variations in cerebral hemodynamics reported both within and between infants depending on their clinical condition. Many gaps exist in our understanding of how neonatal treatment procedures and medications have an impact on cerebral hemodynamics and preterm brain injury. Future research directions for neuroprotective strategies include establishing cotside, real-time clinical reference values for cerebral hemodynamics and vasoregulatory capacity and to demonstrate that these thresholds improve long-term outcomes for the preterm infant. In addition, stimulation of vascular development and repair with growth factor and cell-based therapies also hold promise.

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Section: Cerebral Blood Flow-metabolism Coupling In the Pre-mentioning

confidence: 74%

Cerebral vascular regulation and brain injury in preterm infants

Brew

Walker

Wong

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The arterial hypertension and increased CBF associated with seizure activity in the adult are also seen in many experimental models of neonatal seizures, and possibly in humans (Monin et al, 1990;Wagerle and Delivoria-Papdopoulos, 1990). Increases in local CBF were obseked during focal penicillin seizures in newborn macaque monkeys (Hosokawa et al, 1977), generalized seizures in newborn dogs (Young et al, 1985) and piglets (Clozel et al, 1985;Park et al, 1987;Monin et al, 1990), and were observed by positron emission tomography (PET) in an asphyxiated human infant during a focal motor seizure (Perlman et al, 1985). On the other hand, studies of bicuculline-induced seizures in newborn marmoset monkeys showed large increases in brainstem blood flow but little or no increase in forebrain structures .…”

Section: Cerebral Blood Flow and Metabolism In Neonatal Sementioning

confidence: 99%

Pathophysiological Mechanisms of Brain Damage from Status Epilepticus

Wasterlain¹,

Fujikawa²,

et al. 1993

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Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.

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“…Studies with radiolabelled water suggest that after intraventricular haemorrhage there is marked impairment of regional cerebral blood flow in the hemisphere containing an apparently restricted intracerebral haematoma [8]. Furthermore, parasagittal cerebral blood flow is disturbed in asphyxiated term infants [9], and the flow increases in the hemisphere opposite to the lesion during a one-sided focal seizure [10].…”

Section: Introductionmentioning

confidence: 99%

Repeated fluorodeoxyglucose positron emission tomography of the brain in infants with suspected hypoxic-ischaemic brain injury

et al. 1993

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Positron emission tomography (PET) permits the study of cerebral metabolism in vivo. We performed repeated PET studies with fluorine-18 fluorodeoxyglucose (FDG) as a tracer to measure cerebral glucose metabolism for estimation of neurological prognosis in infants with suspected hypoxic-ischaemic brain injury. Fourteen infants (gestational age 35.3 +/- 4.67 weeks) were examined during the neonatal period (at age 38.4 +/- 2.7 weeks) and again at the age of 3.5 +/- 0.7 months; one further infant was studied only once at the age of 2.5 months. All children also underwent ultrasound examinations. Electroencephalography and computed tomography or magnetic resonance imaging were performed according to their clinical condition and their neurological development has been followed. FDG accumulated most actively in the subcortical areas (thalami, brainstem and cerebellum) and the sensorimotor cortex during the neonatal period. The repeated PET study showed that the uptake of FDG was markedly high and increased in all brain sections of infants with normal development (n = 11), whereas those with delayed development (n = 4) had significantly lower values (P < or = 0.005).

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Positron emission tomography in the newborn

Cited by 32 publications

References 0 publications

Cerebral vascular regulation and brain injury in preterm infants

Cerebral vascular regulation and brain injury in preterm infants

Pathophysiological Mechanisms of Brain Damage from Status Epilepticus

Repeated fluorodeoxyglucose positron emission tomography of the brain in infants with suspected hypoxic-ischaemic brain injury

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