Perisulcal infarcts: Lesions caused by hypotension during increased intracranial pressure

Janzer, Robert C.; Friede, Reinhard L.

doi:10.1002/ana.410060504

Cited by 14 publications

(2 citation statements)

References 22 publications

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“…Of interest, ULG is seldom addressed in the epileptologic literature (Cusmai et al., ; Wolf et al., ; Lopez‐Gonzalez et al., ; Marin‐Padilla et al., ; Villani et al., ), and several reports are case studies from the pre‐MRI era (Janzer & Friede, ; Norman, ). Underreporting of ULG and epilepsy may result from the frequent association with cerebral palsy (which dominates the clinical picture and is the main focus of attention in these children) but also from the potential confusion with PMG.…”

Section: Discussionmentioning

confidence: 99%

Bilateral perisylvian ulegyria: An under‐recognized, surgically remediable epileptic syndrome

et al. 2013

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SUMMARYPurpose: Interest in the association of epilepsy and pseudobulbar palsy was rekindled since the identification through magnetic resonance imaging (MRI) of bilateral perisylvian polymicrogyria (PMG). Seizures are often intractable, but resective epilepsy surgery has not been recommended. However, a similar clinical picture can be encountered in patients with bilateral perisylvian destructive lesions, which fit the description of ulegyria (ULG). We report a series of patients with epilepsy and pseudobulbar palsy due to bilateral perisylvian ULG (BP-ULG), show that hippocampal sclerosis (HS) is often associated and highlight the fact that in this entity, unlike in malformative bilateral perisylvian PMG, seizures may be surgically treated. Methods: The motor, cognitive, epileptologic, and imaging features of 12 patients with perisylvian ULG followed at three institutions are described. For patients with refractory seizures, we detail extracranial and intracranial electrographic recordings, surgical strategies, histopathologic analyses of the resected tissue, and outcome of surgical treatment. Descriptive statistics were used for quantitative and categorical variables. Student's t-test was used to compare means, and a p < 0.05 was considered significant. Key Findings: Pseudobulbar palsy and mental retardation were present in all patients with symmetrical BP-ULG. Five had refractory seizures. There was no relationship between the severity of the pseudobulbar palsy or of the mental retardation and the degree of seizure control with medication. The five patients in whom seizures were refractory to medication had significantly earlier age of onset and longer duration of epilepsy (p < 0.05). Dual pathology with associated unilateral HS was present in four. One patient with dual pathology had a temporolimbic electroclinical picture and had an anterior temporal lobectomy (ATL) based upon noninvasive evaluation. The other four had ictal semiology suggesting involvement of both temporolimbic and perisylvian cortex. Intracranial electroencephalography (EEG) showed concomitant seizure onset in the anterior temporal region and in the ipsilateral ULG in three of the four with dual pathology and in the ulegyric cortex in the one without HS. Resection guided by a combination of semiology, MRI, and extra and intracranial EEG led to complete seizure control in two and almost complete seizure control (Engel class II) in two other patients. The only surgical failure was an isolated ATL in a patient with dual pathology, and concomitant seizure onset in both lesions according to semiology and intracranial EEG. Significance: Our findings suggest that BP-ULG mimics the clinical features of bilateral perisylvian PMG. In patients with refractory seizures, recognition of this entity should lead to consideration of resective surgery despite the bilateral ULG.

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Section: Discussionmentioning

confidence: 99%

Bilateral perisylvian ulegyria: An under‐recognized, surgically remediable epileptic syndrome

et al. 2013

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“…These perisulcal white matter lesions may reflect diminished cerebral perfusion in the face of elevated intracranial pressure (13,14). It has been suggested that the occipital cortex is particularly resistant to hyperammonemic-hyperglutaminergic encephalopathy (2,15).…”

Section: Protracted Cortical Visual Loss In a Child With Ornithine Trmentioning

confidence: 99%

Randot Stereoacuity Test and Multiple Sclerosis

Wiwanitkit¹

2010

Journal of Neuro-Ophthalmology

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The Neuropathology of Autism

Casanova

2014

Handbook of Autism and Pervasive Developmental Disorders, Fourth Edition

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The multitude of neuropathological results in autism spectrum disorder (ASD) should be critically assessed taking into consideration the use of medications, comorbidities, and the agonal/preagonal condition of the patients. The often‐quoted Purkinje cell loss, in many cases, may be a reactive phenomenon to seizures and/or usage of anticonvulsant medications. There is, however, a convergence of clinical and neuropathological evidence that indicates developmental abnormalities of the cerebral cortex in ASD. The presence of heterotopias, laminar effacement, and a minicolumnopathy suggest irregularities both of germinal cell divisions and in the subsequent migration of daughter cells. Clinical heterogeneity may be dictated by variability in the interplay between exogenous factors, genetic vulnerability, and the timing during brain development that frame the action of the multifactorial components.

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Perisulcal infarcts: Lesions caused by hypotension during increased intracranial pressure

Cited by 14 publications

References 22 publications

Bilateral perisylvian ulegyria: An under‐recognized, surgically remediable epileptic syndrome

Bilateral perisylvian ulegyria: An under‐recognized, surgically remediable epileptic syndrome

Randot Stereoacuity Test and Multiple Sclerosis

The Neuropathology of Autism

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