Epileptic and imaging findings in perinatal hypoxic-ischemic encephalopathy with ulegyria

Villani, Flavio; D’Incerti, Ludovico; Granata, Tiziana; Battaglia, Giorgio; Vitali, Paolo; Chiapparini, Luisa; Avanzini, G.

doi:10.1016/s0920-1211(03)00121-9

Cited by 45 publications

(62 citation statements)

References 21 publications

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“…Similar histopathological alterations have been reported in a variety of multicausal human perinatal injuries and insults (Rorke, 1992;Villani et al, 2003). Evidence is presented for a postinjury transformation of the damaged and spared neocortex, with the possibility of surviving cortical neurons adapting by transforming their structure (hypertrophy) and connectivity (increase in dendritic spines) to compensate for the massive laminar and columnar neuronal loss seen at the early timepoint (P30).…”

Section: Resultssupporting

confidence: 68%

“…Microgyral malformations in the parasagittal cortex of the HItreated epileptic rats from the late group are analogous with numerous human resective and autopsy studies of ulegyric/polymicrogyric tissue. Similarly located in watershed zones in neonates and children, they are thought to have a common pathogenic mechanism related to perfusion failure in that area (Villani et al, 2003). To our knowledge, this finding has never been reported for this model.…”

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confidence: 44%

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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: Resultssupporting

confidence: 68%

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confidence: 44%

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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“…From these 43 patients, eight (19 %) had a diagnosis of ulegyria based on commonly accepted brain MRI criteria [2,22]: 1) Poorly demarcated lesions located on watershed areas, between territories of the major cerebral arteries; 2) Atrophy and thinning of the cortex involving mainly the deep portion of the convolution and sparing the apex, resulting in mushroom-shaped gyri; 3) White matter signal abnormalities using T2 weighted and FLAIR sequences; 4) Wide sulci between the affected convolutions, more pronounced in the deeper portions, where abnormal signals of the cortex can also be detected. Brain MRI, EEG, and neuropsychological testing were performed in all patients, video-EEG monitoring with ictal recordings in five, and histological analysis in two individuals who were operated on for treatment of their epilepsy.…”

Section: Methodsmentioning

confidence: 99%

Occipital lobe epilepsy secondary to ulegyria

et al. 2005

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In this group of adult epileptic patients with ulegyria brain MRI, ictal semiology, and neurological examination are consistent with occipital lobe epilepsy. Most patients have severe epilepsy, but in some of them epilepsy can be controlled with antiepileptic drugs, while in others surgical treatment can be effective. Brain MRI criteria of ulegyria are well established, and in two cases it was possible to confirm their diagnosis with histological analysis.

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“…Multipli celulalarni i molekularni mehanizmi, jedinstveni za nesazreli CNS, doprinose patogenezi neonatalne hipoksično-ishemijske moždane povrede: neuropatologija moždanog oštećenja zavisi od gestacionog razdoblja, prirode i trajanja inzulta i drugih strukturnih i funkcionalnih varijabli. Stoga je, veliki broj neuropatoloških varijanti prepoznat, ali je njihovo prekelapanje evidentno (144).…”

Section: Među Ovim Tehnikama Ubrajaju Se Magnetna Rezonanca Spektroskunclassified

“…Ipak se, najčešće, ovakvi događaji od radiologa opisuju kao raniji moždani infarkti u sklopu perinatalne povrede. Danas se pretpostavlja da su u ovakvim slučajevima prava etiopatogenetska osnova "blage" malformacije kortikalnog razvoja (lisencefalija, polimikrogirija, hemimegancefalija, ulegirija i nodularna heterotopija) ili fokalne kortikalne displazije (145,144). U jednoj prehirurškoj seriji od 567 operisanih bolesnika, 25 bolesnika (4,4%) je imalo pre ili perinatalnu traumu i nalaz koji je odgovarao takvoj povredi, što je skoro identičan procenat kao i u našoj seriji.…”

Section: Među Ovim Tehnikama Ubrajaju Se Magnetna Rezonanca Spektroskunclassified

Correlation of the patterns of behavior in focal epileptic seizures and localization of the epileptic lesions

Ristić¹

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Epileptic and imaging findings in perinatal hypoxic-ischemic encephalopathy with ulegyria

Cited by 45 publications

References 21 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

Occipital lobe epilepsy secondary to ulegyria

Correlation of the patterns of behavior in focal epileptic seizures and localization of the epileptic lesions

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