Ioan-Paul Muresan, MD; Pascal Favrole, MD; Pierre Levy, MD; et al.
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Arch Neurol. 2010;67(11):1323-1328. doi:10.1001/archneurol.2010.265
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Editorial
The Sooner, the Better
José Biller, MD
Arch Neurol
Richard A. Rudick, MD; Jar-Chi Lee, MS; Gary R. Cutter, PhD; et al.
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Arch Neurol. 2010;67(11):1329-1335. doi:10.1001/archneurol.2010.150
ObjectiveTo investigate the value of Expanded Disability Status Scale (EDSS) worsening sustained for at least 6 months and other parameters as predictors for disability status.DesignRetrospective analysis of the Multiple Sclerosis Collaborative Research Group study data.SettingThe intramuscular interferon beta-1a pivotal trial was a double-blind, placebo-controlled phase 3 study.ParticipantsPatients with relapsing-remitting multiple sclerosis who received at least 2 years of treatment and completed an EDSS evaluation 8 years postrandomization.InterventionThirty micrograms of intramuscular interferon beta-1a or placebo once weekly during the 2-year clinical trial.Main Outcome MeasuresPositive predictive values for 6-month sustained progression during 2 years were calculated to determine the ability to predict disability status at 8 years. A multivariate logistic regression model was used to assess the relationship between predictors and EDSS milestones at follow-up.ResultsForty-five patients had sustained 6-month EDSS progression during the clinical trial and 115 did not. Progression during the trial was the strongest predictor of reaching EDSS milestones at the follow-up visit, 8 years after randomization. Other independent predictors were treatment arm assignment and baseline EDSS score.ConclusionIn this phase 3 clinical trial of intramuscular interferon beta-1a, compared with effects of treatment, baseline EDSS score, and number of relapses during the study, worsening of 1 point or more on EDSS from baseline lasting 6 months was the strongest predictor of clinically significant disability 8 years after randomization into the clinical trial.
Matthew A. Warner, BS; Teddy S. Youn, MD; Tommy Davis, PhD, MPH; et al.
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Arch Neurol. 2010;67(11):1336-1344. doi:10.1001/archneurol.2010.149
ObjectivesTo determine the spatial distribution of cortical and subcortical volume loss in patients with diffuse traumatic axonal injury and to assess the relationship between regional atrophy and functional outcome.DesignProspective imaging study. Longitudinal changes in global and regional brain volumes were assessed using high-resolution magnetic resonance imaging鈥揵ased morphometric analysis.SettingInpatient traumatic brain injury unit.Patients or Other ParticipantsTwenty-five patients with diffuse traumatic axonal injury and 22 age- and sex-matched controls.Main Outcome MeasureChanges in global and regional brain volumes between initial and follow-up magnetic resonance imaging were used to assess the spatial distribution of posttraumatic volume loss. The Glasgow Outcome Scale鈥揈xtended score was the primary measure of functional outcome.ResultsPatients underwent substantial global atrophy with mean whole-brain parenchymal volume loss of 4.5% (95% confidence interval, 2.7%-6.3%). Decreases in volume (at a false discovery rate of 0.05) were seen in several brain regions including the amygdala, hippocampus, thalamus, corpus callosum, putamen, precuneus, postcentral gyrus, paracentral lobule, and parietal and frontal cortices, while other regions such as the caudate and inferior temporal cortex were relatively resistant to atrophy. Loss of whole-brain parenchymal volume was predictive of long-term disability, as was atrophy of particular brain regions including the inferior parietal cortex, pars orbitalis, pericalcarine cortex, and supramarginal gyrus.ConclusionTraumatic axonal injury leads to substantial posttraumatic atrophy that is regionally selective rather than diffuse, and volume loss in certain regions may have prognostic value for functional recovery.
Lynette G. Sadleir, MBChB, MD; Ingrid E. Scheffer, MBBS, PhD
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Arch Neurol. 2010;67(11):1345-1349. doi:10.1001/archneurol.2010.155
ObjectivesTo establish whether early electroencephalography (EEG) or later sleep-deprived EEG (SD-EEG) has a higher yield of epileptiform and background abnormalities in children with new-onset seizures, and to use EEG results to assist in diagnosis of electroclinical epilepsy syndromes at presentation.DesignProspective analysis blinded to EEG protocol and epilepsy diagnosis.SettingRegional service capturing a pediatric population of 121聽000.PatientsConsecutive untreated children aged 2 to 16 years presenting to emergency departments with new-onset seizures (excluding myoclonic and absence seizures).InterventionEach child had 2 EEG protocols: an early EEG study (within 24 hours following a seizure) and an SD-EEG study (48 hours to 4 weeks following a seizure). Epilepsy diagnosis was made independently by 2 pediatric epileptologists.Main Outcome MeasuresRate of epileptiform abnormalities and slowing in the 2 EEG studies. The secondary outcome measure was diagnosis of epilepsy syndrome where possible.ResultsOf 92 children studied, 50 (54%) had a single seizure; 42 (46%) had 2 or more seizures at presentation. Seizures were focal in 61 children (66%) and generalized in 19 (21%). Epileptiform discharges occurred in 56 SD-EEGs (61%) and 52 early EEGs (57%) (P聽=聽.27). Background slowing occurred in 26 SD-EEGs (28%) and 42 early EEGs (46%) (P聽<聽.001). Parents preferred early EEG (65 parents [71%]) to later SD-EEG (14 parents [15%]) because of availability of earlier results and epilepsy diagnosis. Forty-two of 92 children (46%) were diagnosed with a specific electroclinical syndrome.ConclusionsEarly EEG and SD-EEG studies have a similar yield of epileptiform abnormalities. Background abnormalities are more frequent in early EEGs. The EEG results at presentation in new-onset seizures support epilepsy diagnosis, with electroclinical syndromes diagnosed in almost 50% of children.
Ignacio F. Mata, PhD; Min Shi, PhD; Pinky Agarwal, MD; et al.
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Arch Neurol. 2010;67(11):1350-1356. doi:10.1001/archneurol.2010.279
Norbert Brüggemann, MD; Johann Hagenah, MD; Kathrin Reetz, MD; et al.
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Arch Neurol. 2010;67(11):1357-1363. doi:10.1001/archneurol.2010.281
Martha Storandt, PhD; John C. Morris, MD
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Arch Neurol. 2010;67(11):1364-1369. doi:10.1001/archneurol.2010.272
Owen Carmichael, PhD; Christopher Schwarz; David Drucker; et al.
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Arch Neurol. 2010;67(11):1370-1378. doi:10.1001/archneurol.2010.284
Melissa E. Murray, PhD; Matthew L. Senjem, MS; Ronald C. Petersen, MD; et al.
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Arch Neurol. 2010;67(11):1379-1385. doi:10.1001/archneurol.2010.280