Neuronal migration disorders: Positron emission tomography correlations

Lee, Namsoo; Radtke, Rodney A.; Gray, Linda; Burger, Peter C.; Montine, Thomas J.; DeLong, G. Robert; Lewis, Darrell V.; Oakes, W. Jerry; Friedman, Allan H.; Hoffman, John M.

doi:10.1002/ana.410350308

Cited by 104 publications

(40 citation statements)

References 26 publications

(1 reference statement)

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“…Recent technologies in high resolution magnetic resonance imaging (MRI) allow the identification of neuronal migration disorders (NMD) in humans (Guerrini et al, 1992;Lee et al, 1994). NMD have a wide range of clinical and histological features that reflect the presence of different disturbances in cortical development (Anderman and Palmini, 1992).…”

Section: Introductionmentioning

confidence: 99%

Transplacentally induced neuronal migration disorders: An animal model for the study of the epilepsies

Germano

Sperber

1998

J. Neurosci. Res.

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Recent clinical and laboratory data suggest that there is a link between neuronal migration disorders (NMD) and increased seizure threshold. To characterize an animal model with features similar to human NMD and to assess seizure susceptibility, NMD were induced in the rat at the time of neuroblastic division (PG15) and three other gestational ages (PG 13, PG14, PG16) by transplacental exposure to methylaxozymethanol (MAM, 25 mg/kg). Offspring pups were monitored for spontaneous and electrographic seizures. At postnatal day 14, randomly selected rat pups were sacrificed for histological examination. In other MAM-exposed pups and controls, status epilepticus was induced by intraperitoneal administration of kainic acid. On histology, NMD were found in all PG 15 MAM-exposed rats, in comparison to 63% of PG 13, 70% of PG 14, 80% of PG16. Histological features included cortical laminar disorganization, ectopic neurons in the subcortical white matter and in cortical layer I, persistent granular layer, marginal glioneuronal heterotopia, and discrete areas of neuronal ectopia in the CA1 subfield of the hippocampus. Based on the severity of the neuronal migration abnormalities, rats were divided into three categories: severe, moderate, and mild. Severe and moderate NMD were only found in the PG 15 MAM-exposed rats. EEG recording in rats with NMD did not disclose spontaneous seizures; however, rats with severe NMD had higher slow wave activity compared to controls (P < .05). MAM-exposed rats with severe NMD were more susceptible to kainic-induced seizures compared to controls (P < .05). In rats with severe NMD, kainic acid-induced status epilepticus produced hippocampal damage in the CA3/4 region. These results demonstrate that MAM-induced NMD have histological and electrographic characteristics similar to human NMD. The severity of neuronal abnormality depends on the time of transplacental exposure as the most severe NMD were found after exposure to MAM at the time of neuroblastic division. The degree of NMD positively correlates with seizure susceptibility, since only rats with severe NMD have decreased seizure threshold. The occurrence of status epilepticus-induced hippocampal damage in pups with severe NMD suggests that the severely compromised hippocampus is less resistant to seizure-induced injury than the normal developing brain.

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Section: Introductionmentioning

confidence: 99%

Transplacentally induced neuronal migration disorders: An animal model for the study of the epilepsies

Germano

Sperber

1998

J. Neurosci. Res.

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“…heterotopia demonstrated glucose uptake that was similar to normal cortex (11). Focal hypometabolism was found using 18 FDG-PET in 9/15 patients with neuronal migration disorders (11).…”

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confidence: 96%

Magnetic resonance perfusion imaging in malformations of cortical development

2007

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“…In contrast to this, for the neuronal migration disorder in the right parietooccipital region, a displaced metabolic activity of normal gray matter was demonstrated. For the latter, hypometabolism as well as displaced gray matter metabolic activity to an area of white matter has been observed [ 12]. Furthermore, although the lateral part of the right temporal lobe appeared structurally normal, a severe reduction of rCMRGlc most pronounced in this region was observed.…”

Section: Discussionmentioning

confidence: 94%

Adult‐Onset Complex Partial Seizures as the Presenting Sign in Colpocephaly: MRI and PET Correlates

Wunderlich¹,

Schlaug

Jäncke³

et al. 1996

Journal of Neuroimaging

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In a 30-year-old man, adult-onset complex partial seizures were associated with colpocephaly as evident from magnetic resonance images. The structurally normal lateral neocortex of the right temporal lobe showed a severe reduction in regional glucose consumption corresponding to the epileptic focus as judged from the surface electroencephalogram. In contrast to previously reported patients, this patient had no focal neurological signs, and neuropsychological testing revealed normal general intelligence. Thus, this patient adds a benign variant to the clinical spectrum of this cerebral developmental disorder.

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Neuronal migration disorders: Positron emission tomography correlations

Cited by 104 publications

References 26 publications

Transplacentally induced neuronal migration disorders: An animal model for the study of the epilepsies

Transplacentally induced neuronal migration disorders: An animal model for the study of the epilepsies

Magnetic resonance perfusion imaging in malformations of cortical development

Adult‐Onset Complex Partial Seizures as the Presenting Sign in Colpocephaly: MRI and PET Correlates

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