| In Focus |
spotlight on the may 15 issue.
- Gross, Robert, MD, PhD, Editor-in-Chief, Neurology. Pages: 1541
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| Editorials |
from patterns to patients: what can we tell people with newly diagnosed epilepsy?.
- Penovich, Patricia, Gruenthal, Michael, MD, PhD. Pages: 1542-1543
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hyperexcitability and amyotrophic lateral sclerosis.
- Kiernan, Matthew, PhD, DSc, Petri, Susanne. Pages: 1544-1545
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decision support for diagnosis: co-evolution of tools and resources.
- Segal, Michael, MD, PhD, Schiffmann, Raphael. Pages: 1546-1547
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| Articles |
patterns of treatment response in newly diagnosed epilepsy.
- Brodie, M.J., Barry, S.J.E., Bamagous, G.A., Norrie, J.D., Kwan, P., MD, PhD. Pages: 1548-1554
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Objective: To delineate the temporal patterns of outcome and to determine the probability of seizure freedom with successive antiepileptic drug regimens in newly diagnosed epilepsy.Methods: Patients in whom epilepsy was diagnosed and the first antiepileptic drug prescribed between July 1, 1982, and April 1, 2006, were followed up until March 31, 2008. Outcomes were categorized into 4 patterns: A) early and sustained seizure freedom; B) delayed but sustained seizure freedom; C) fluctuation between periods of seizure freedom and relapse; and D) seizure freedom never attained. Probability of seizure freedom with successive drug regimens was compared. Seizure freedom was defined as no seizures for >=1 year.Results: A total of 1,098 patients were included (median age 32 years, range 9-93). At the last clinic visit, 749 (68%) patients were seizure-free, 678 (62%) on monotherapy. Outcome pattern A was observed in 408 (37%), pattern B in 246 (22%), pattern C in 172 (16%), and pattern D in 272 (25%) patients. There was a higher probability of seizure freedom in patients receiving 1 compared to 2 drug regimens, and 2 compared to 3 regimens (p < 0.001). The difference was greater among patients with symptomatic or cryptogenic than with idiopathic epilepsy. Less than 2% of patients became seizure-free on subsequent regimens but a few did so on their sixth or seventh regimen.Conclusions: Most patients with newly diagnosed epilepsy had a constant course which could usually be predicted early. The chance of seizure freedom declined with successive drug regimens, most markedly from the first to the third and among patients with localization-related epilepsies.GLOSSARY: AED: antiepileptic drugILAE: International League Against EpilepsyIQR: interquartile rangeNGPSE: National General Practice Study of Epilepsy.(C)2012 American Academy of Neurology
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altered microstructural connectivity in juvenile myoclonic epilepsy: the missing link.
- Vollmar, C., O'Muircheartaigh, J., Symms, M.R, Barker, G.J., Thompson, P., Kumari, V., Stretton, J., Duncan, J.S., FMedSci, FRCP, Richardson, M.P., FRCP, PhD, Koepp, M.J., MD, PhD. Pages: 1555-1559
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Objectives: Juvenile myoclonic epilepsy (JME) is characterized by myoclonic jerks of the upper limbs, often triggered by cognitive stressors. Here we aim to reconcile this particular seizure phenotype with the known frontal lobe type neuropsychological profile, photosensitivity, hyperexcitable motor cortex, and recent advanced imaging studies that identified abnormal functional connectivity of the motor cortex and supplementary motor area (SMA).Methods: We acquired fMRI and diffusion tensor imaging (DTI) in a cohort of 29 patients with JME and 28 healthy control subjects. We used fMRI to determine functional connectivity and DTI-based region parcellation and voxel-wise comparison of probabilistic tractography data to assess the structural connectivity profiles of the mesial frontal lobe.Results: Patients with JME showed alterations of mesial frontal connectivity with increased structural connectivity between the prefrontal cognitive cortex and motor cortex. We found a positive correlation between DTI and fMRI-based measures of structural and functional connectivity: the greater the structural connectivity between these 2 regions, the greater the observed functional connectivity of corresponding areas. Furthermore, connectivity was reduced between prefrontal and frontopolar regions and increased between the occipital cortex and the SMA.Conclusion: The observed alterations in microstructural connectivity of the mesial frontal region may represent the anatomic basis for cognitive triggering of motor seizures in JME. Changes in the mesial frontal connectivity profile provide an explanatory framework for several other clinical observations in JME and may be the link between seizure semiology, neurophysiology, neuropsychology, and imaging findings in JME.GLOSSARY: DTI: diffusion tensor imagingFA: fractional anisotropyJME: juvenile myoclonic epilepsyMNI: Montreal Neurological InstituteSMA: supplementary motor area(C)2012 American Academy of Neurology
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development of a suspicion index to aid diagnosis of niemann-pick disease type c.
- Wijburg, F.A., MD, PhD, Sedel, F., MD, PhD, Pineda, M., MD, PhD, Hendriksz, C.J., Fahey, M., MB, BS, Walterfang, M., MBBS, PhD, Patterson, M.C., Wraith, J.E., Kolb, S.A.. Pages: 1560-1567
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Objectives: Niemann-Pick disease type C (NP-C) is a rare, autosomal recessive lysosomal lipid storage disorder that is invariably fatal. NP-C diagnosis can be delayed for years due to heterogeneous presentation; adult-onset NP-C can be particularly difficult to diagnose. We developed a Suspicion Index tool, ranking specific symptoms within and across domains, including family members who have NP-C, to provide a risk prediction score to identify patients who should undergo testing for NP-C.Methods: A retrospective chart review was performed in 5 centers in Europe and 2 in Australia (n = 216). Three patient types were selected: classic or variant filipin staining NP-C cases (n = 71), NP-C noncases (confirmed negative by filipin staining; n = 64), or controls with at least 1 characteristic symptom of NP-C (n = 81). NP-C signs and symptoms were categorized into visceral, neurologic, or psychiatric domains. Logistic regression was performed on individual signs and symptoms within and across domains, and regression coefficients were used to develop prediction scores for NP-C. Internal validation was performed with the bootstrap resampling method.Results: The Suspicion Index tool has good discriminatory performance with cutpoints for grading suspicion of NP-C. Neonatal jaundice/cholestasis, splenomegaly, vertical supranuclear gaze palsy, cataplexy, and cognitive decline/dementia were strong predictors of NP-C, as well as symptoms occurring in multiple domains in individual patients, and also parents/siblings or cousins with NP-C.Conclusions: The Suspicion Index tool is a screening tool that can help identify patients who may warrant further investigation for NP-C. A score >=70 indicates that patients should be referred for testing for NP-C.GLOSSARY: CI: confidence intervalNP-C: Niemann-Pick disease type CROC: receiver operating characteristic.(C)2012 American Academy of Neurology
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csf biomarkers for alzheimer disease correlate with cortical brain biopsy findings.
- Seppala, T.T., Nerg, O., Koivisto, A.M., MD, PhD, Rummukainen, J., MD, PhD, Puli, L., Zetterberg, H., MD, PhD, Pyykko, O.T., Helisalmi, S., Alafuzoff, I., MD, PhD, Hiltunen, M., Jaaskelainen, J.E., MD, PhD, Rinne, J., MD, PhD, Soininen, H., MD, PhD, Leinonen, V., MD, PhD, Herukka, S.-K., MD, PhD. Pages: 1568-1575
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Objective: To assess the relationship between Alzheimer disease (AD)-related pathologic changes in frontal cortical brain biopsy and AD biomarkers in ventricular vs lumbar CSF, and to evaluate the relationships of AD biomarkers in CSF and cortical biopsy with the final clinical diagnosis of AD.Methods: In 182 patients with presumed normal pressure hydrocephalus (152 with known APOE carrier status), A[beta] plaques and tau in the cortical brain biopsies were correlated with the ventricular and lumbar CSF A[beta]42, total tau, and p-tau levels measured by ELISA. In a median follow-up of 2.0 years, 51 patients developed AD dementia.Results: The patients with A[beta] plaques in the cortical biopsy had lower (p = 0.009) CSF A[beta]42 levels than those with no A[beta] plaques. The patients with tau in the cortical biopsy had lower (p = 0.014) A[beta]42 but higher (p = 0.015) p-tau 181 in CSF as compared to those with no tau in the cortical biopsy. The patients with amyloid + tau + biopsies had the lowest A[beta]42 and highest tau and p-tau 181 levels in CSF. The A[beta]42 levels were lower and the tau and p-tau 181 higher in the ventricular vs corresponding lumbar CSF samples. In multivariate analysis, the presence of cortical A[beta] was independently predicted by the APOE [epsilon]4 carrier status and age but not by CSF A[beta]42 or tau levels.Conclusions: Amyloid plaques and hyperphosphorylated tau in cortical brain biopsies are reflected by low CSF A[beta]42 and high CSF tau and p-tau levels, respectively.GLOSSARY: A[beta]42: 42 amino acid isoform of amyloid [beta]AD: Alzheimer diseaseCDR: Clinical Dementia RatingDSM-IV: Diagnostic and Statistical Manual of Mental Disorders, 4th editionICP: intracranial pressureiNPH: idiopathic normal pressure hydrocephalusKUH: Kuopio University HospitalNPH: normal pressure hydrocephalusPiB: Pittsburgh compound Bt-tau: total tau(C)2012 American Academy of Neurology
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short-term clinical outcomes for stages of nia-aa preclinical alzheimer disease.
- Knopman, D.S., Jack, C.R., Wiste, H.J., Weigand, S.D., Vemuri, P., Lowe, V., Kantarci, K., Gunter, J.L., Senjem, M.L., Ivnik, R.J., PhD, LP, Roberts, R.O., Boeve, B.F., Petersen, R.C., MD, PhD. Pages: 1576-1582
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Objective: Recommendations for the diagnosis of preclinical Alzheimer disease (AD) have been formulated by a workgroup of the National Institute on Aging and Alzheimer's Association. Three stages of preclinical AD were described. Stage 1 is characterized by abnormal levels of [beta]-amyloid. Stage 2 represents abnormal levels of [beta]-amyloid and evidence of brain neurodegeneration. Stage 3 includes the features of stage 2 plus subtle cognitive changes. Stage 0, not explicitly defined in the criteria, represents subjects with normal biomarkers and normal cognition. The ability of the recommended criteria to predict progression to cognitive impairment is the crux of their validity.Methods: Using previously developed operational definitions of the 3 stages of preclinical AD, we examined the outcomes of subjects from the Mayo Clinic Study of Aging diagnosed as cognitively normal who underwent brain MRI or [18F]fluorodeoxyglucose and Pittsburgh compound B PET, had global cognitive test scores, and were followed for at least 1 year.Results: Of the 296 initially normal subjects, 31 (10%) progressed to a diagnosis of mild cognitive impairment (MCI) or dementia (27 amnestic MCI, 2 nonamnestic MCI, and 2 non-AD dementias) within 1 year. The proportion of subjects who progressed to MCI or dementia increased with advancing stage (stage 0, 5%; stage 1, 11%; stage 2, 21%; stage 3, 43%; test for trend, p < 0.001).Conclusions: Despite the short follow-up period, our operationalization of the new preclinical AD recommendations confirmed that advancing preclinical stage led to higher proportions of subjects who progressed to MCI or dementia.GLOSSARY: AA: Alzheimer's AssociationAD: Alzheimer diseaseAVLT: Auditory Verbal Learning TestBNT: Boston Naming TestCN: cognitively normalDSM-IV: Diagnostic and Statistical Manual of Mental Disorders, 4th editionFDG: fluorodeoxyglucoseHVa: hippocampal volume adjusted for total intracranial volumeIQR: interquartile rangeMCI: mild cognitive impairmentMCSA: Mayo Clinic Study of AgingNIA-AA: National Institute on Aging and Alzheimer's AssociationPiB: Pittsburgh compound BROI: region of interestSNAP: suspected non-Alzheimer pathwayTMT: Trail Making TestWAIS-R: Wechsler Adult Intelligence Scale-RevisedWMS-R: Wechsler Memory Scale-Revised.(C)2012 American Academy of Neurology
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prevalence and comorbidity of nocturnal wandering in the us adult general population.
- Ohayon, M.M., MD, DSc, Mahowald, M.W., Dauvilliers, Y., MD, PhD, Krystal, A.D., MD, MS, Leger, D., MD, PhD. Pages: 1583-1589
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Objective: To assess the prevalence and comorbid conditions of nocturnal wandering with abnormal state of consciousness (NW) in the American general population.Methods: Cross-sectional study conducted with a representative sample of 19,136 noninstitutionalized individuals of the US general population >=18 years old. The Sleep-EVAL expert system administered questions on life and sleeping habits; health; and sleep, mental, and organic disorders (DSM-IV-TR; International Classification of Sleep Disorders, version 2; International Classification of Diseases-10).Results: Lifetime prevalence of NW was 29.2% (95% confidence interval [CI] 28.5%-29.9%). In the previous year, NW was reported by 3.6% (3.3%-3.9%) of the sample: 1% had 2 or more episodes per month and 2.6% had between 1 and 12 episodes in the previous year. Family history of NW was reported by 30.5% of NW participants. Individuals with obstructive sleep apnea syndrome (odds ratio [OR] 3.9), circadian rhythm sleep disorder (OR 3.4), insomnia disorder (OR 2.1), alcohol abuse/dependence (OR 3.5), major depressive disorder (MDD) (OR 3.5), obsessive-compulsive disorder (OCD) (OR 3.9), or using over-the-counter sleeping pills (OR 2.5) or selective serotonin reuptake inhibitor (SSRI) antidepressants (OR 3.0) were at higher risk of frequent NW episodes (>=2 times/month).Conclusions: With a rate of 29.2%, lifetime prevalence of NW is high. SSRIs were associated with an increased risk of NW. However, these medications appear to precipitate events in individuals with a prior history of NW. Furthermore, MDD and OCD were associated with significantly greater risk of NW, and this was not due to the use of psychotropic medication. These psychiatric associations imply an increased risk due to sleep disturbance.GLOSSARY: CI: confidence intervalDSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revisionICSD-II: International Classification of Sleep Disorders, version 2MDD: major depressive disorderNREM: non-REMNSAID: nonsteroidal anti-inflammatory drugNW: nocturnal wanderingOCD: obsessive-compulsive disorderOR: odds ratioSSRI: selective serotonin reuptake inhibitor.(C)2012 American Academy of Neurology
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effect of insurance status on postacute care among working age stroke survivors.
- Skolarus, L.E., MD, MS, Meurer, W.J., MD, MS, Burke, J.F., MD, MS, Prvu Bettger, J., Lisabeth, L.D.. Pages: 1590-1595
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Objective: Utilization of postacute care is associated with improved poststroke outcomes. However, more than 20% of American adults under age 65 are uninsured. We sought to determine whether insurance status is associated with utilization and intensity of institutional postacute care among working age stroke survivors.Methods: A retrospective cross-sectional study of ischemic stroke survivors under age 65 from the 2004-2006 Nationwide Inpatient Sample was conducted. Hierarchical logistic regression models controlling for patient and hospital-level factors were used. The primary outcome was utilization of any institutional postacute care (inpatient rehabilitation or skilled nursing facilities) following hospital admission for ischemic stroke. Intensity of rehabilitation was explored by comparing utilization of inpatient rehabilitation facilities and skilled nursing facilities.Results: Of the 33,917 working age stroke survivors, 19.3% were uninsured, 19.8% were Medicaid enrollees, and 22.8% were discharged to institutional postacute care. Compared to those privately insured, uninsured stroke survivors were less likely (adjusted odds ratio [AOR] 0.53, 95% confidence interval [CI] 0.47-0.59) while stroke survivors with Medicaid were more likely to utilize any institutional postacute care (AOR = 1.40, 95% CI 1.27-1.54). Among stroke survivors who utilized institutional postacute care, uninsured (AOR = 0.48, 95% CI 0.36-0.64) and Medicaid stroke survivors (AOR = 0.27, 95% CI 0.23-0.33) were less likely to utilize an inpatient rehabilitation facility than a skilled nursing facility compared to privately insured stroke survivors.Conclusions: Insurance status among working age acute stroke survivors is independently associated with utilization and intensity of institutional postacute care. This may explain differences in poststroke outcomes among uninsured and Medicaid stroke survivors compared to the privately insured.GLOSSARY: AHRQ: Agency for Healthcare Research and QualityAOR: adjusted odds ratioCI: confidence intervalED: Emergency DepartmentHCUP: Healthcare Cost and Utilization ProjectICD: International Classification of DiseasesIRF: inpatient rehabilitation facilityNIS: Nationwide Inpatient SampleOR: odds ratioPAC: postacute careSNF: skilled nursing facility(C)2012 American Academy of Neurology
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decreased motor cortex [gamma]-aminobutyric acid in amyotrophic lateral sclerosis.
- Foerster, B.R., Callaghan, B.C., Petrou, M., MA, MBChB, Edden, R.A.E., Chenevert, T.L., Feldman, E.L., MD, PhD. Pages: 1596-1600
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Objectives: To determine if there are in vivo differences in [gamma]-aminobutyric acid (GABA) in the motor cortex and subcortical white matter of patients with amyotrophic lateral sclerosis (ALS) compared with healthy controls using proton magnetic resonance spectroscopy (1H-MRS).Methods: In this cross-sectional study, 10 patients with ALS and 9 age- and sex-matched healthy controls (HCs) underwent 3T edited 1H-MRS to quantify GABA centered on the motor cortex and the subcortical white matter.Results: Compared with healthy controls, patients with ALS had significantly lower levels of GABA in the left motor cortex (1.42 +/- 0.27 arbitrary institutional units vs 1.70 +/- 0.24 arbitrary institutional units, p = 0.038). There was no significant difference in GABA levels between groups in the subcortical white matter (p > 0.05).Conclusion: Decreased levels of GABA are present in the motor cortex of patients with ALS compared to HCs. Findings are consistent with prior reports of alterations in GABA receptors in the motor cortex as well as increased cortical excitability in the context of ALS. Larger, longitudinal studies are needed to confirm these findings and to further our understanding of the role of GABA in the pathogenesis of ALS.GLOSSARY: ALS: amyotrophic lateral sclerosisGABA: [gamma]-aminobutyric acid1H-MRS: proton magnetic resonance spectroscopyHC: healthy controlLMN: lower motor neuronNAA: N-acetylaspartatePRESS: point resolved spectroscopySCWM: subcortical white matterTE: echo timeTR: repetition timeUMN: upper motor neuron(C)2012 American Academy of Neurology
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myasthenia gravis and neuromyelitis optica spectrum disorder: a multicenter study of 16 patients.
- Leite, M.I., Coutinho, E., Lana-Peixoto, M., Apostolos, S., Waters, P., Sato, D., Melamud, L., Marta, M., Graham, A., Spillane, J., Villa, A.M., Callegaro, D., Santos, E., da Silva, A., Jarius, S., Howard, R., Nakashima, I., Giovannoni, G., Buckley, C., Hilton-Jones, D., Vincent, A., FRS, FMedSci, Palace, J.. Pages: 1601-1607
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Objective: To describe 16 patients with a coincidence of 2 rare diseases: aquaporin-4 antibody (AQP4-Ab)-mediated neuromyelitis optica spectrum disorder (AQP4-NMOSD) and acetylcholine receptor antibody (AChR-Ab)-mediated myasthenia gravis (AChR-MG).Methods: The clinical details and antibody results of 16 patients with AChR-MG and AQP4-NMOSD were analyzed retrospectively.Results: All had early-onset AChR-MG, the majority with mild generalized disease, and a high proportion achieved remission. Fifteen were female; 11 were Caucasian. In 14/16, the MG preceded NMOSD (median interval: 16 years) and 11 of these had had a thymectomy although 1 only after NMOSD onset. In 4/5 patients tested, AQP4-Abs were detectable between 4 and 16 years prior to disease onset, including 2 patients with detectable AQP4-Abs prior to thymectomy. AChR-Abs decreased and the AQP4-Ab levels increased over time in concordance with the relevant disease. AChR-Abs were detectable at NMOSD onset in the one sample available from 1 of the 2 patients with NMOSD before MG.Conclusions: Although both conditions are rare, the association of MG and NMOSD occurs much more frequently than by chance and the MG appears to follow a benign course. AChR-Abs or AQP4-Abs may be present years before onset of the relevant disease and the antibody titers against AQP4 and AChR tend to change in opposite directions. Although most cases had MG prior to NMOSD onset, and had undergone thymectomy, NMOSD can occur first and in patients who have not had their thymus removed.GLOSSARY: Ab: antibodiesAChR-Ab: acetylcholine receptor antibodyAChR-MG: acetylcholine receptor antibody-mediated myasthenia gravisAQP4-Ab: aquaporin-4 antibodyAQP4-NMOSD: aquaporin-4 antibody-mediated neuromyelitis optica spectrum disorderIgG: immunoglobulin GIS: immunosuppressiveLETM: longitudinally extensive transverse myelitisMG: myasthenia gravisNMO: neuromyelitis opticaNMOSD: neuromyelitis optica spectrum disorderOCB: oligoclonal bandsON: optic neuritisSLE: systemic lupus erythematosusVGKC: voltage-gated potassium channel(C)2012 American Academy of Neurology
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value of nmo-igg determination at the time of presentation as cis.
- Costa, C., Arrambide, G., Tintore, M., PhD, MD, Castillo, J., Sastre-Garriga, J., Tur, C., Rio, J., PhD, MD, Saiz, A., Vidal-Jordana, A., Auger, C., Nos, C., Rovira, A., Comabella, M., Horga, A., Montalban, X., PhD, MD. Pages: 1608-1611
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Background: Despite the availability of diagnostic criteria, an overlap between neuromyelitis optica (NMO) and multiple sclerosis (MS) exists, particularly in the early stage of the disease.Objective: To study the value of NMO-immunoglobulin G (IgG) determination in Caucasian patients with a first demyelinating episode who develop a relapsing form of optic neuritis or myelitis.Methods: This study was based on a prospectively acquired cohort of patients regarded as having a clinically isolated syndrome (CIS) at the time of presentation. From this cohort, 2 different groups were selected: group 1 (NMO phenotype), consisting of a first attack involving the optic nerve or the spinal cord, and at least a second event affecting either topography, and group 2 (negative control group), consisting of a first attack involving the brainstem or the cerebral hemispheres and at least 1 relapse in any topography. Group 3 was composed of patients with NMO according to the 2006 revised diagnostic criteria. Serum NMO-IgG was determined by indirect immunofluorescence.Results: A total of 3.1 of the group 1 patients were positive for NMO-IgG in comparison to 3.9% of group 2 and 44.5% of group 3, NMO. One of the positive patients in group 1 evolved to NMO.Conclusions: NMO-IgG determination is crucial in detecting patients who will develop NMO; however, its value as a routine test in cases presenting with symptoms of the type seen in MS is low, and should only be performed in those patients in which the initial diagnosis is not clear.GLOSSARY: AQP4: aquaporin-4CIS: clinically isolated syndromeIgG: immunoglobulin GMS: multiple sclerosisNMO: neuromyelitis opticaOCB: oligoclonal bands(C)2012 American Academy of Neurology
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| Clinical Implications of Neuroscience Research |
mitochondrial dynamics: general concepts and clinical implications.
- Milone, Margherita, MD, PhD, Benarroch, Eduardo. Pages: 1612-1619
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GLOSSARY: ADOA: autosomal dominant optic atrophyATP: adenosine triphosphateCMT: Charcot-Marie-Tooth diseaseDLP1: dynamin-like protein 1DLP1: dynamin-like protein 1 geneDRP1: dynamin-related protein 1DRP1: dynamin-related protein 1 geneEGR2: early growth response 2 geneEOP: early-onset Parkinson diseaseGDAP1: ganglioside-induced differentiation-associated protein 1GDAP1: ganglioside-induced differentiation-associated protein 1 geneGST: glutathione-S-transferaseHAP1: huntingtin-associated proteinLHON: Leber hereditary optic neuropathyMFF: mitochondrial fission factorMFN: mitofusinMFN2: mitofusin 2 geneMIEF: mitochondrial elongation factormtDNA: mitochondrial DNAOPA1: optic atrophy type 1 genePARK2: parkin genePARL: presenilin-associated rhomboid-like proteinPINK1: PTEN-induced putative kinase protein-1PINK1: PTEN-induced kinase 1 genePD: Parkinson disease(C)2012 American Academy of Neurology
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| Clinical/Scientific Notes |
reversible paraneoplastic tonic pupil with pca-tr igg and hodgkin lymphoma.
- Horta, Erika, McKeon, Andrew, Lennon, Vanda, MD, PhD, Benarroch, Eduardo. Pages: 1620-1622
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| Correction |
effects of fetal antiepileptic drug exposure: outcomes at age 4.5 years.
Pages: 1622
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| Resident and Fellow Section |
media & book reviews: app review: neuro toolkit.
- Krishnan, Vaishnav, MD, PhD. Pages: e124
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teaching video neuroimages: asymptomatic subclavian-carotid double steal phenomenon due to innominate artery stenosis.
- Munoz, Roberto, MD, PhD, Pulido, Laura, Gallego, Jaime, MD, PhD. Pages: e125
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teaching neuroimages: intracranial optic nerve enlargement in infantile krabbe disease.
- Shah, S., Freeman, E., Wolf, V., Murthy, S., MBBS, MPH, Lotze, T.. Pages: e126
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