Computerized Cranial Transverse Axial Tomography (CTAT) in 145 Patients with Primary and Secondary Generalized Epilepsies – West Syndrome, Myoclonic-Astatic Petit Mal, Absence Epilepsy

Lagenstein, I; Kühne, D; Hj, Sternowsky; Rothe, Marti Jill

doi:10.1055/s-0028-1085310

Cited by 9 publications

(5 citation statements)

References 7 publications

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“…Alternatively, atrophy observed following steroids is likely multifactorial and may be reversible following steroid withdrawal (Gordon 1980;Lagenstein et al 1979). Both Gordon and Langenstein reported reversal of steroid-related atrophy after discontinuation of steroids in infants (Gordon 1980;Lagenstein et al 1979). The literature in adults with atrophy reversal is scant and most likely due to the fact that most adults who received steroids usually remained on these drugs chronically (Ostrov et al 1982).…”

Section: Discussionmentioning

confidence: 92%

“…The atrophy reported following anoxia is presumed to be ischemic in nature and is usually irreversible (Belet et al 2004;Gale and Hopkins 2004;Gordon 1980;Hopkins et al 2005a). Alternatively, atrophy observed following steroids is likely multifactorial and may be reversible following steroid withdrawal (Gordon 1980;Lagenstein et al 1979). Both Gordon and Langenstein reported reversal of steroid-related atrophy after discontinuation of steroids in infants (Gordon 1980;Lagenstein et al 1979).…”

Section: Discussionmentioning

confidence: 94%

“…months) several studies report rapid atrophy within days to a few weeks of a precipitating event. Rapid cerebral atrophy occurs following hypoxemic encephalopathy and steroid use in preterm infants and anoxia and steroid use in adults (Belet et al 2004;Gordon 1980;Lagenstein et al 1979). The atrophy reported following anoxia is presumed to be ischemic in nature and is usually irreversible (Belet et al 2004;Gale and Hopkins 2004;Gordon 1980;Hopkins et al 2005a).…”

Section: Discussionmentioning

confidence: 99%

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Neurologic Changes during Critical Illness: Brain Imaging Findings and Neurobehavioral Outcomes

Suchyta

Jephson

Hopkins

2009

Brain Imaging and Behavior

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Encephalopathy and other neurologic morbidities are common in critical illness, sepsis, and prolonged mechanical ventilation. We assessed structural changes on brain imaging and neuropsychological outcomes in critically ill patients who developed neurological changes during their intensive care unit (ICU) stay. Patients who underwent brain imaging for neurological changes were included in the study. Medical, neuroradiological, and outcome data were obtained from patient medical records. Sixty-four patients underwent brain imaging for neurological changes. Forty-one (64%) patients had abnormalities on brain imaging. There were no differences for age, hospital length of stay, ICU length of stay, duration of mechanical ventilation or APACHE II scores for patients with normal compared to abnormal brain imaging. Cognitive impairments occurred in 48% of survivors and 6% developed psychiatric disorders. Our study demonstrates that abnormalities on brain imaging are common in critically ill patients. We also confirm previous findings that survivors of critical illness have cognitive impairments post-ICU discharge. This study further illustrates the adverse effects of critical illness on the brain and highlights the need for additional research in this emerging area.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Neurologic Changes during Critical Illness: Brain Imaging Findings and Neurobehavioral Outcomes

Suchyta

Jephson

Hopkins

2009

Brain Imaging and Behavior

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“…It is important to note that studies have reported brain atrophy may occur over a period of days rather than months, (63–66) raising the possibility that atrophic processes for these patients may have occurred during hospitalization. Animal studies have also shown significant hippocampal cell loss within hours of sepsis induction using a lipopolysaccharide model (67), although in our investigation, no such association was identified.…”

Section: Discussionmentioning

confidence: 99%

The association between brain volumes, delirium duration, and cognitive outcomes in intensive care unit survivors

Gunther

Morandi

Krauskopf

et al. 2012

Critical Care Medicine

257

186

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Objective Delirium duration is predictive of long-term cognitive impairment (LTCI) in Intensive Care Unit (ICU) survivors. Hypothesizing that a neuroanatomical basis may exist for the relationship between delirium and LTCI, we conducted this exploratory investigation of the associations between delirium duration, brain volumes and LTCI. Design, Setting, and Patients A prospective cohort of medical and surgical ICU survivors with respiratory failure or shock. Measurements Quantitative high resolution 3-Tesla brain magnetic resonance imaging was used to calculate brain volumes at discharge and three-month follow-up. Delirium was evaluated using the Confusion Assessment Method for the ICU; cognitive outcomes were tested at three- and twelve-month follow-up. Linear regression was used to examine associations between delirium duration and brain volumes, and between brain volumes and cognitive outcomes. Results A total of 47 patients completed the MRI protocol. Patients with longer duration of delirium displayed greater brain atrophy as measured by a larger ventricle-to-brain ratio (VBR) at hospital discharge [0.76, 95% confidence intervals (CI) (0.10, 1.41); p=0.03] and at 3-month follow-up [0.62 (0.02, 1.21), p=0.05]. Longer duration of delirium was associated with smaller superior frontal lobe [−2.11 cm3 (−3.89, −0.32); p=0.03] and hippocampal volumes at discharge [−0.58 cm3 (−0.85, −0.31), p<0.001] – regions responsible for executive functioning and memory, respectively. Greater brain atrophy (higher VBR) at three months was associated with worse cognitive performances at twelve months [lower RBANS battery score −11.17 (−21.12, −1.22), p=0.04]. Smaller superior frontal lobes, thalamus, and cerebellar volumes at three months were associated with worse executive functioning and visual attention at twelve months. Conclusions These preliminary data show that longer duration of delirium is associated with smaller brain volumes up to three months after discharge, and that smaller brain volumes are associated with LTCI up to 12 months. We cannot, however, rule out that smaller preexisting brain volumes explain these findings.

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“…Generalized subcortical atrophy on cranial computerized tomography had been reported in groups of patients with symptoms similar to MAE prior to the 1989 classification (Gastaut et al., 1966; Lagenstein et al., 1979). However, the pathologic significance of generalized subcortical atrophy is difficult to determine as it may result from repeated seizures, episodes of status epilepticus, or from hormonal treatment.…”

Section: Phenotypic Featuresmentioning

confidence: 99%

Dissecting the genetic basis of myoclonic‐astatic epilepsy

Tang

Pal

2012

Epilepsia

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Summary Herman Doose first described the generalized childhood epilepsy syndrome of myoclonic astatic epilepsy (MAE) in 1970, attributing a genetic cause from this first description. However, although the International League Against Epilepsy (ILAE) defined criteria for MAE in 1989, the diagnostic boundaries of the syndrome continue to be debated. Moreover, 40 years since Doose's first description of MAE, although a genetic predisposition is acknowledged and many studies have demonstrated familial aggregation of seizures within MAE families, the actual genetic determinants of MAE still remain unknown. Although initially thought to be within the same spectrum as severe myoclonic epilepsy of infancy, the exclusion of SCN1A mutations in non‐generalized epilepsy with febrile seizures plus (GEFS+) MAE cases has confirmed the genetic distinction of MAE. In this critical review, we shall trace the historical evolution of concepts around MAE and its distinction from Lennox‐Gastaut syndrome, review the described phenotypic features of MAE from updated studies that will allow its distinction from other overlap epilepsy syndromes, review the evidence of genetic influences and clues for genetic heterogeneity, and discuss strategies that may be helpful in elucidating the etiology of MAE in light of current genetic techniques.

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Computerized Cranial Transverse Axial Tomography (CTAT) in 145 Patients with Primary and Secondary Generalized Epilepsies – West Syndrome, Myoclonic-Astatic Petit Mal, Absence Epilepsy

Cited by 9 publications

References 7 publications

Neurologic Changes during Critical Illness: Brain Imaging Findings and Neurobehavioral Outcomes

Neurologic Changes during Critical Illness: Brain Imaging Findings and Neurobehavioral Outcomes

The association between brain volumes, delirium duration, and cognitive outcomes in intensive care unit survivors

Dissecting the genetic basis of myoclonic‐astatic epilepsy

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