Neonatal Hypoxia and Epileptic Risk: A Clinical Prospective Study

Bergamasco, B.; Benna, Paolo; Ferrero, P.; Gavinelli, R

doi:10.1111/j.1528-1157.1984.tb04168.x

Cited by 101 publications

(63 citation statements)

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“…animal model; seizure clustering; cortical dysplasia; microgyri; porencephaly; dual pathology Hypoxic-ischemic (HI)-induced perinatal encephalopathies are the major cause of acute mortality and chronic neurologic morbidity, such as in epilepsy (Bergamasco et al, 1984;Aso et al, 1990;Lanska et al, 1991;Volpe, 2001;Ramaswamy et al, 2004). The multifactorial causative factors range from prematurity, low birth weight, traumatic/ prolonged labor, asphyxia, coagulation abnormalities, severe systemic cardiovascular hypotension, respiratory disorders, and maternal and fetal infections in the perinatal period …”

Section: Indexing Termsmentioning

confidence: 99%

Neuropathogical features of a rat model for perinatal hypoxic‐ischemic encephalopathy with associated epilepsy

Kadam

Dudek

2007

J of Comparative Neurology

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Hypoxic-ischemic (HI) encephalopathy is an important neurological problem of the perinatal period. Little is known of the long-term progression of HI insults or the maladaptive changes that lead to epilepsy. Using rats with unilateral carotid occlusion followed by hypoxia at postnatal day 7, this study provides an initial analysis of the epilepsy caused by a perinatal HI insult with chronic and continuous behavioral monitoring. The histopathology was investigated at postnatal day 30 and later at ≥6 months of age using cresyl violet, Timm, and rapid Golgi staining and immunocytochemistry. The resultant epilepsy showed an increase in seizure frequency over time, with a preponderance for seizure clusters and behavioral features of an ipsilateral cerebral syndrome. In addition to parasagittal infarcts and porencephalic cysts in severe lesions, columnar neuronal death was found with cytomegaly in isolated groups of dysmorphic cortical neurons. Cortical dysgenesis was seen in the form of deep laminar cell loss, microgyri, white matter hypercellularity, and blurring of the white and gray matter junction. Mossy fiber sprouting was not only detected in the atrophied ipsilateral dorsal hippocampus of HI rats with chronic epilepsy, but was also found in comparable grades in spared ipsi-and contralateral ventral hippocampi. The cortical lesions in this animal model show histological similarities with those found in humans after perinatal HI. The occurrence of cortical abnormalities that are associated with epilepsy in humans correlates with the consequent detection of spontaneous recurrent seizures. Indexing termsanimal model; seizure clustering; cortical dysplasia; microgyri; porencephaly; dual pathology Hypoxic-ischemic (HI)-induced perinatal encephalopathies are the major cause of acute mortality and chronic neurologic morbidity, such as in epilepsy (Bergamasco et al., 1984;Aso et al., 1990;Lanska et al., 1991;Volpe, 2001;Ramaswamy et al., 2004). The multifactorial causative factors range from prematurity, low birth weight, traumatic/ prolonged labor, asphyxia, coagulation abnormalities, severe systemic cardiovascular hypotension, respiratory disorders, and maternal and fetal infections in the perinatal period HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript (Courville, 1959;Golomb et al., 2001;Scher et al., 2002;Cowan et al., 2003;Nelson and Lynch, 2004). Refractory epilepsy is a common sequela (≈30%) in children who survive such insults (Marin-Padilla, 2000a). Autopsy and surgically resected neocortical tissues have revealed dysplasias and abnormal neuronal morphologies, which are thought to underlie the abnormal electrophysiological properties recorded during intraoperative and in vitro slice studies (Palmini et al., 1994;Avoli et al., 1999;Burneo et al., 2004;Najm et al., 2004;Calcagnotto et al., 2005;Matsumoto et al., 2005). A strong association has been found between disorders of cortical development and medically refractory epilepsy in children (Mischel et al., 1995...

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Section: Indexing Termsmentioning

confidence: 99%

Neuropathogical features of a rat model for perinatal hypoxic‐ischemic encephalopathy with associated epilepsy

Kadam

Dudek

2007

J of Comparative Neurology

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“…Neonatal seizures in the setting of hypoxic encephalopathy are associated with an increased risk of epilepsy later in life (Bergamasco et al, 1984;Bernes and Kaplan, 1994) and can be refractory to conventional anticonvulsant drugs that are effective in older children and adults (Painter et al, 1999). To investigate age-specific mechanisms of epileptogenesis in the neonatal brain, we used a rodent model that mimics the acute seizures and chronic proepileptogenic effects of neonatal hypoxia observed clinically.…”

Section: Introductionmentioning

confidence: 99%

AMPA/Kainate Receptor-Mediated Downregulation of GABAergic Synaptic Transmission by Calcineurin after Seizures in the Developing Rat Brain

Sánchez¹,

Dai²,

Levada³

et al. 2005

J. Neurosci.

103

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“…However, other early-life seizures may be related to long-term epilepsy, including the symptomatic neonatal seizures (such as those associated with hypoxic encephalopathy) or complex and recurrent febrile seizures in childhood (3,(5)(6)(7).…”

Section: Seizures In the Developing Human Brainmentioning

confidence: 99%

Acute and Chronic Effects of Seizures in the Developing Brain: Experimental Models

Jensen

1999

Epilepsia

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Summary: Clinical experience suggests two major components to the relationship between brain development and epilepsy. First, the maturational state of the immature brain appears to generally decrease seizure threshold and contribute to a different seizure phenotype from the adult. Second, certain forms of seizures, when present during development, may modify brain maturation to result in chronic epilepsy and/or other neurocognitive deficits.Maturational studies in animals suggest there are numerous factors developmentally regulated in such a way as to increase excitability in immature neuronal networks in the forebrain.The developing brain appears to exhibit a transient overexpression of glutamate receptors, glutamate receptor subunit composition permissive of enhanced excitatory neurotransmission, a relative lack of GABAergic inhibitory transmission, and ion channel expression and homeostasis which enhance neuronal excitability. The increased excitatory "drive" that is likely to be critical for normal brain development may share common mechanisms with those responsible for rendering the immature brain more susceptible to seizures, seizure induced plasticity (epileptogenesis), and neuronal injury. Furthermore, the coincidence of seizures during early postnatal brain development may modify many of these parameters, which in turn may promote long term epilepsy. SEIZURES IN THE DEVELOPING HUMAN BRAINClinical data indicate that the immature brain is highly susceptible to seizure activity. The incidence of seizures is highest in the first year of life (1). However, although neonatal seizures are relatively common, they represent a heterogeneous group in terms of prognosis (2,3). Neonatal and childhood seizures can be benign, such as in the case of hypocalcemic or hypoglycemic seizures in the first week of life or simple febrile seizures in childhood.Despite quite prominent clinical seizure activity, these seizures do not appear to increase the risk for later epilepsy or other neurologic deficits (3,4). However, other early-life seizures may be related to long-term epilepsy, including the symptomatic neonatal seizures (such as those associated with hypoxic encephalopathy) or complex and recurrent febrile seizures in childhood (3,(5)(6)(7).Clinical experience also suggests that the pharmacology of seizures in the immature brain is different from that in the adult. Antiepileptic drugs (AEDs) that are potent in the adult can be ineffective in treating early-life status epilepticus (SE) or seizures (3,6).

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Neonatal Hypoxia and Epileptic Risk: A Clinical Prospective Study

Cited by 101 publications

References 10 publications

Neuropathogical features of a rat model for perinatal hypoxic‐ischemic encephalopathy with associated epilepsy

Neuropathogical features of a rat model for perinatal hypoxic‐ischemic encephalopathy with associated epilepsy

AMPA/Kainate Receptor-Mediated Downregulation of GABAergic Synaptic Transmission by Calcineurin after Seizures in the Developing Rat Brain

Acute and Chronic Effects of Seizures in the Developing Brain: Experimental Models

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