Stewart A Factor

Emory University, Atlanta, Georgia, United States

Are you Stewart A Factor?

Claim your profile

Publications (192)1072.03 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive impairment is a common and disabling problem in Parkinson disease (PD) that is not well understood and is difficult to treat. Identification of genetic variants that influence the rate of cognitive decline or pattern of early cognitive deficits in PD might provide a clearer understanding of the etiopathogenesis of this important nonmotor feature.
    JAMA Neurology 09/2014; · 7.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Quantitative MRI of neuromelanin (NM) containing structures (referred to as NM-MRI) in the brainstem, namely the locus coeruleus (LC) and substantia nigra (SN), may assist with the early detection of Parkinson's disease (PD) and Alzheimer's disease (AD) as well as differential diagnosis in the early disease stages. In this study, two gradient echo (GRE) sequences with magnetization transfer contrast (MTC) preparation pulses were developed to simultaneously image the LC and SN. This has been a challenge with NM-MRI techniques used in previous studies due to the relatively high specific absorption rate (SAR) induced by these techniques. In addition, a semi-automated quantitative analysis scheme was applied to estimate volumes and contrast-to-noise ratios (CNR) of the LC and SN based on segmentation of both structures. Compared to a T1-weighted turbo spin echo (TSE) sequence typically used for simultaneous imaging of the LC and SN, the two GRE-MTC sequences exhibited improved performance in terms of higher sensitivity (in CNR) in imaging the SN and lower SAR during the scans. A multiple-measurement protocol was adopted as well, so that motion degraded measurements could be removed and artifacts associated with motion corrected. The presented approach has demonstrated advantages in imaging acquisition (lower SAR and higher sensitivity), imaging pre-processing (with motion correction) and quantitative image analysis (segmentation-based estimation of volume and CNR) as compared with existing NM-MRI approaches. This approach has potential for detection and monitoring of neurodegeneration in LC and SN in disease states including AD and PD.
    Magnetic resonance imaging. 07/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive impairment, including dementia, is common in Parkinson's disease (PD). The Mini-Mental State Examination (MMSE) has been recommended as a screening tool for Parkinson's disease dementia (PDD), with values below 26 indicative of possible dementia. Using a detailed neuropsychological battery, we examined the range of cognitive impairment in PD patients with an MMSE score of 26 or higher. In this multicenter, cross-sectional, observational study, we performed neuropsychological testing in a sample of 788 PD patients with MMSE scores of 26 or higher. Evaluation included tests of global cognition, executive function, language, memory, and visuospatial skills. A consensus panel reviewed results for 342 subjects and assigned a diagnosis of no cognitive impairment, mild cognitive impairment, or dementia. Sixty-seven percent of the 788 subjects performed 1.5 standard deviations below the normative mean on at least one test. On eight of the 15 tests, more than 20% of subjects scored 1.5 standard deviations or more below the normative mean. Greatest impairments were found on Hopkins Verbal Learning and Digit Symbol Coding tests. The sensitivity of the MMSE to detect dementia was 45% in a subset of participants who underwent clinical diagnostic procedures. A remarkably wide range of cognitive impairment can be found in PD patients with a relatively high score on the MMSE, including a level of cognitive impairment consistent with dementia. Given these findings, clinicians must be aware of the limitations of the MMSE in detecting cognitive impairment, including dementia, in PD. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 07/2014; · 5.63 Impact Factor
  • Donald L Bliwise, Michael K Scullin, Stewart A Factor
    Journal of neurology. 06/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Increased gut permeability, inflammation, and colonic α-synuclein pathology are present in early Parkinson's disease (PD) and have been proposed to contribute to PD pathogenesis. Peptidoglycan is a structural component of the bacterial cell wall. Peptidoglycan recognition proteins (PGRPs) maintain healthy gut microbial flora by regulating the immune response to both commensal and harmful bacteria. We tested the hypothesis that variants in genes that encode PGRPs are associated with PD risk. Participants in two independent case-control studies were genotyped for 30 single-nucleotide polymorphisms (SNPs) in the four PGLYRP genes. Using logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) adjusted for potential confounding variables, we conducted analyses in each study, separately and pooled. One SNP failed the assay, and three had little to no variation. The ORs were similar in both study populations. In pooled analyses, three of seven PGLYRP2 SNPs (rs3813135, rs733731, rs892145), one of five PGLYRP3 SNPs (rs2987763), and six of nine PGLYRP4 SNPs (rs10888557, rs12063091, rs3006440, rs3006448, rs3006458, and rs3014864) were significantly associated with PD risk. Association was strongest for PGLYRP4 5'untranslated region (UTR) SNP rs10888557 (GG reference, CG OR 0.6 [95%CI 0.4-0.9], CC OR 0.15 [95%CI 0.04-0.6]; log-additive P-trend, 0.0004). Common variants in PGLYRP genes are associated with PD risk in two independent studies. These results require replication, but they are consistent with hypotheses of a causative role for the gut microbiota and gastrointestinal immune response in PD. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 05/2014; · 5.63 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Parkinson's disease (PD) is complex and heterogeneous. The numerous susceptibility loci that have been identified reaffirm the complexity of PD but do not fully explain it; e.g., it is not known if any given PD susceptibility gene is associated with all PD or a disease subtype. We also suspect that important disease genes may have escaped detection because of this heterogeneity. We used presence/absence of family history to subdivide the cases and performed genome-wide association studies (GWAS) in Sporadic-PD and Familial-PD separately. The aim was to uncover new genes and gain insight into the genetic architecture of PD. Employing GWAS on the NeuroGenetics Research Consortium (NGRC) dataset stratified by family history (1565 Sporadic-PD, 435 Familial-PD, 1986 controls), we identified a novel locus on chromosome 1p21 in Sporadic-PD (PNGRC = 4x10-8) and replicated the finding (PReplication = 6x10-3; PPooled = 4x10-10) in 1528 Sporadic-PD and 796 controls from the National Institutes of Neurologic Disease and Stroke (NINDS) Repository. This is the fifth PD locus to be mapped to the short of arm of chromosome 1. It is flanked by S1PR1 and OLFM3 genes, and is 200 kb from a multiple sclerosis susceptibility gene. The second aim of the study was to extend the stratified GWAS to the well-established PD genes. SNCA_ rs356220 was associated with both Sporadic-PD (OR = 1.37, P = 1x10-9) and Familial-PD (OR = 1.40, P = 2x10-5). HLA_rs3129882 was more strongly associated with Sporadic-PD (OR = 1.38, P = 5x10-10) than Familial-PD (OR = 1.12, P = 0.15). In the MAPT region, virtually every single nucleotide polymorphism (SNP) had a stronger effect-size and lower P-value in Familial-PD (peak P = 8x10-7) than in Sporadic-PD (peak P = 2x10-5). We discovered and replicated a new locus for Sporadic-PD which had escaped detection in un-stratified GWAS. This demonstrates that by stratifying on a key variable the power gained due to diminished heterogeneity can sometimes outweigh the power lost to reduced sample size. We also detected distinct patterns of disease associations for previously established PD susceptibility genes, which gives an insight to the genetic architecture of the disease and could aid in the selection of appropriate study population for future studies.
    BMC Genomics 02/2014; 15(1):118. · 4.40 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The underlying etiology of parkinsonian anterocollis has been the subject of recent debate. The purpose of this study is to test the hypothesis that anterocollis in parkinsonian syndromes is associated with dystonia of the deep cervical flexors (longus colli and capitis). Eight patients with anterocollis, six in the setting of a Parkinsonism and two primary cervical dystonia control subjects with anterocollis underwent prospective structured clinical evaluations (interview, examination and rating scales), systematic electromyography of the cervical extensor musculature and 18 F-FDG PET/CT studies of cervical muscles to examine evidence of hypermetabolism or overactivity of deep cervical flexors. Subjects with parkinsonian anterocollis were found to have hypermetabolism of the extensor and sub-occipital muscles but not in the cervical flexors (superficial or deep). EMG abnormalities were observed in all evaluated patients, but only one patient was definitely myopathic. Meanwhile, both dystonia controls exhibited hypermetabolism of cervical flexors (including the longus colli). In conclusion, we were able to demonstrate hypermetabolism of superficial and deep cervical flexors with muscle 18 F-FDG PET/CT in dystonic anterocollis patients, but not in parkinsonian anterocollis patients. The hypermetabolic changes seen in parkinsonian anterocollis patients in posterior muscles may be compensatory. Alternative explanations for anterocollis include myopathy of the cervical extensors, or unbalanced rigidity of the cervical flexors, but this remains to be proven.
    Journal of the neurological sciences 01/2014; · 2.32 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Antidepressants have appeared to be more effective than placebo treatment in treating depressive syndromes in patients with Parkinson’s disease (PD). Objective To identify factors that predict improvement in depressive symptoms during antidepressant treatment in depressed PD patients. Methods A secondary analysis was performed on the dataset of the Randomized Placebo-controlled Study of Antidepressants in PD (SAD-PD), in which 76 patients received active treatment with either paroxetine or venlafaxine extended release (XR), and 39 patients received placebo treatment. Backward stepwise regression analyses were conducted with change in 24-item Hamilton Depression Rating Scale (HAMD-24) score between assessments at baseline and week 12 as the main outcome measure, and sex, age, baseline HAMD-24 score, Unified Parkinson’s Disease Rating Scale section III (UPDRS-III) score, Mini-Mental State Examination (MMSE), and the Clinical Anxiety Scale (CAS) as independent variables. Results In both the active treatment and placebo groups, higher baseline HAMD-24 score and lower UPDRS-III score were associated with greater reduction in HAMD-24 score. Higher anxiety scores predicted less response in the active treatment group. Higher MMSE scores predicted greater response only in the placebo treated group. Sex and age were no predictors of response. Conclusions Higher pre-treatment depression scores and lower pre-treatment anxiety scores are the two most important predictors for improvement during antidepressant treatment in depressed PD patients, which is in line with those found in treatment studies of depressed non-PD patients. Furthermore, our results indicate the requirement for different or more intensive treatment for depressed PD patients with more severe anxiety symptoms.
    Parkinsonism & Related Disorders 01/2014; · 3.27 Impact Factor
  • Stewart A Factor, Joseph Jankovic
    Journal of the American Society for Experimental NeuroTherapeutics 12/2013; · 5.38 Impact Factor
  • Haydeh Payami, Stewart A Factor
    [Show abstract] [Hide abstract]
    ABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by a heterogeneous array of motor and non-motor features. Anti-PD drugs that are in use target only the motor symptoms, may lose efficacy over time, and can cause serious adverse effects such as dyskinesia and psychosis. There are currently no preventative or disease modifying treatments. All attempts to develop disease modifying drugs have failed. Pharmacogenomics (PGx) has the potential to change the way new drugs are developed and the way drugs are prescribed. By using genetic markers that correlate with, and can therefore predict drug response, clinical trials can be designed to be enriched with individuals who are most likely to benefit from the drug, maximizing drug's efficacy, minimizing its adverse effects, and boosting the odds of successful drug discovery. Clinical application of PGx will help physicians to quickly and accurately determine the right drugs and the right doses for individuals, avoiding the lengthy trial and error approaches and adverse effects. In combination with known protective factors such as nicotine and caffeine, PGx may enable development of personalized methods for PD prevention and, by extension, care.
    Journal of the American Society for Experimental NeuroTherapeutics 11/2013; · 5.38 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: IMPORTANCE Data on the long-term cognitive outcomes of patients with PARKIN-associated Parkinson disease (PD) are unknown but may be useful when counseling these patients. OBJECTIVE Among patients with early-onset PD of long duration, we assessed cognitive and motor performances, comparing homozygotes and compound heterozygotes who carry 2 PARKIN mutations with noncarriers. DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 44 participants at 17 different movement disorder centers who were in the Consortium on Risk for Early-Onset PD study with a duration of PD greater than the median duration (>14 years): 4 homozygotes and 17 compound heterozygotes (hereafter referred to as carriers) and 23 noncarriers. MAIN OUTCOMES AND MEASURES Unified Parkinson Disease Rating Scale Part III (UPDRS-III) and Clinical Dementia Rating scores and neuropsychological performance. Linear regression models were applied to assess the association between PARKIN mutation status and cognitive domain scores and UPDRS-III scores. Models were adjusted for age, education, disease duration, language, and levodopa equivalent daily dose. RESULTS Carriers had an earlier age at onset of PD (P < .001) and were younger (P = .004) at time of examination than noncarriers. They performed better than noncarriers on the Mini-Mental State Examination (P = .010) and were more likely to receive lower scores on the Clinical Dementia Rating (P = .003). In multivariate analyses, carriers performed better than noncarriers on the UPDRS-III (P = .02) and on tests of attention (P = .03), memory (P = .03), and visuospatial (P = .02) cognitive domains. CONCLUSIONS AND RELEVANCE In cross-sectional analyses, carriers demonstrated better cognitive and motor performance than did noncarriers with long disease duration, suggesting slower disease progression. A longitudinal follow-up study is required to confirm these findings.
    JAMA neurology. 11/2013;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Historically, association of disease with the major histocompatibility complex (HLA) genes has been tested with HLA alleles that encode antigen-binding affinity. The association with Parkinson disease (PD), however, was discovered with noncoding SNPs in a genome-wide association study (GWAS). We show here that several HLA-region SNPs that have since been associated with PD form two blocks tagged by rs3129882 (p = 9 × 10(-11)) and by rs9268515 and/or rs2395163 (p = 3 × 10(-11)). We investigated whether these SNP-associations were driven by HLA-alleles at adjacent loci. We imputed class I and class II HLA-alleles for 2000 PD cases and 1986 controls from the NeuroGenetics Research Consortium GWAS and sequenced a subset of 194 cases and 204 controls. We were therefore able to assess accuracy of two imputation algorithms against next-generation-sequencing while taking advantage of the larger imputed data sets for disease study. Additionally, we imputed HLA alleles for 843 cases and 856 controls from another GWAS for replication. PD risk was positively associated with the B(∗)07:02_C(∗)07:02_DRB5(∗)01_DRB1(∗)15:01_DQA1(∗)01:02_DQB1(∗)06:02 haplotype and negatively associated with the C(∗)03:04, DRB1(∗)04:04 and DQA1(∗)03:01 alleles. The risk haplotype and DQA1(∗)03:01 lost significance when conditioned on the SNPs, but C(∗)03:04 (OR = 0.72, p = 8 × 10(-6)) and DRB1(∗)04:04 (OR = 0.65, p = 4 × 10(-5)) remained significant. Similarly, rs3129882 and the closely linked rs9268515 and rs2395163 remained significant irrespective of HLA alleles. rs3129882 and rs2395163 are expression quantitative trait loci (eQTLs) for HLA-DR and HLA-DQ (9 × 10(-5) ≥ PeQTL ≥ 2 × 10(-79)), suggesting that HLA gene expression might influence PD. Our data suggest that PD is associated with both structural and regulatory elements in HLA. Furthermore, our study demonstrates that noncoding SNPs in the HLA region can be associated with disease irrespective of HLA alleles, and that observed associations with HLA alleles can sometimes be secondary to a noncoding variant.
    The American Journal of Human Genetics 10/2013; · 11.20 Impact Factor
  • Source
  • Leslie J Cloud, Deepti Zutshi, Stewart A Factor
    [Show abstract] [Hide abstract]
    ABSTRACT: Tardive dyskinesia (TD) is a serious, often disabling, movement disorder that is caused by medications that block dopamine receptors (i.e., neuroleptics, anti-emetics). There is currently no standard treatment approach for physicians confronted with such patients. This may be the result of notions that TD is disappearing because of the switch to second-generation antipsychotic agents and that it is largely reversible. In this article we demonstrate that second-generation antipsychotics do, indeed, cause TD and, in fact, the frequency is likely higher than expected because of growing off-label uses and a tripling of prescriptions written in the last 10 years. In addition, studies demonstrate that TD actually remits in only a minority of patients when these drugs are withdrawn. Furthermore, neuroleptic agents are often utilized to treat TD, despite prolonged exposure being a risk factor for irreversibility. The outcome of these trends is a growing population afflicted with TD. We review non-neuroleptic agents that have shown positive results in small, early-phase, blinded trials, including tetrabenazine, amantadine, levetiracetam, piracetam, clonazepam, propranolol, vitamin B6, and Ginkgo biloba. Other options, such as botulinum toxin and deep brain stimulation, will also be discussed, and a suggested treatment algorithm is provided. While these agents are reasonable treatment options at this time there is a need, with a concerted effort between neurology and psychiatry, for full-scale drug development, including multicenter, randomized, blinded trials to confirm the effectiveness of the agents that were positive in phase 2 trials and the development of newer ones.
    Journal of the American Society for Experimental NeuroTherapeutics 10/2013; · 5.38 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sleep disturbances are common in many neurodegenerative diseases and may include altered sleep duration, fragmented sleep, nocturia, excessive daytime sleepiness, and vivid dreaming experiences, with occasional parasomnias. Although representing the "gold standard," polysomnography is not always cost-effective or available for measuring sleep disturbance, particularly for screening. Although numerous sleep-related questionnaires exist, many focus on a specific sleep disturbance (e.g., restless legs, REM Behavior Disorder) and do not capture efficiently the variety of sleep issues experienced by such patients. We administered the 12-item Neurodegenerative Disease Sleep Questionnaire (NDSQ) and the Epworth Sleepiness Scale to 145 idiopathic Parkinson's disease patients. Principal component analysis using eigenvalues greater than 1 suggested five separate components: sleep quality (e.g., sleep fragmentation), nocturia, vivid dreams/nightmares, restless legs symptoms, and sleep-disordered breathing. These results demonstrate construct validity of our sleep questionnaire and suggest that the NDSQ may be a useful screening tool for sleep disturbances in at least some types of neurodegenerative disorders.
    Journal of the neurological sciences 09/2013; · 2.32 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dystonia is a neurological disorder characterized by involuntary twisting movements and postures. The neck is among the most commonly affected regions, and diagnosis can be made readily through a simple clinical evaluation. The goal of this study was to explore how long it took patients to receive a diagnosis of cervical dystonia after symptom onset. A structured questionnaire was administered at outpatient clinics of a tertiary care academic medical center to 146 consecutively evaluated patients. The questionnaire addressed the length of time from symptom onset to diagnosis, the numbers and types of providers seen before reaching a diagnosis, and treatments attempted prior to receiving botulinum toxin. A total of 108 patients saw a mean of 3.5 providers over a mean period of 44months from symptom onset to diagnosis. For patients with symptom onset in the last decade only, patients saw a mean of 3.0 providers over a mean of 14months. Although cervical dystonia is the most common form of dystonia with clinical features readily identifiable by a simple history and examination, patients typically see multiple providers over more than a year before reaching a diagnosis and receiving optimal therapy. Improved awareness of the clinical features will enable patients to obtain appropriate therapy more rapidly.
    Journal of the neurological sciences 08/2013; · 2.32 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Impulsive behavior and poor sleep are important non-motor features of Parkinson's disease (PD) that negatively impact the quality of life of patients and their families. Previous research suggests a higher level of sleep complaints in PD patients who demonstrate impulsive behaviors, but the nature of the sleep disturbances has yet to be comprehensively tested. Consecutive idiopathic PD patients (N = 143) completed the Minnesota Impulse Disorder Interview and a sleep questionnaire that assessed sleep efficiency, excessive daytime sleepiness, restless legs symptoms, snoring, dreams/nightmares, and nocturia. Patients were also given a Unified Parkinson's Disease Rating Scale motor examination and they completed cognitive testing. Impulsive PD patients endorsed more sleep complaints than non-impulsive PD patients. The group difference was primarily attributable to poor sleep efficiency (e.g., greater nocturnal awakenings), p < .01, and greater daytime sleepiness, p < .01, in the impulsive PD patients. Interestingly, restless legs symptoms were also greater in the impulsive PD patients, p < .05. The results could not be explained by medications or disease severity. Poor sleep efficiency, restless legs symptoms, and increased daytime sleepiness are associated with impulsivity in PD. Longitudinal studies are needed to determine whether sleep disturbances precede impulsivity in PD.
    Parkinsonism & Related Disorders 07/2013; · 3.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: Preladenant is a selective adenosine A2A receptor antagonist under investigation for Parkinson's disease treatment. METHODS: A phase 2 36-week open-label follow-up of a double-blind study using preladenant 5 mg twice a day as a levodopa adjunct in 140 subjects with fluctuating Parkinson's disease was conducted. The primary end point was adverse event (AE) assessment. Secondary (efficacy) analyses included hours/day spent in OFF and ON states and dyskinesia prevalence/severity. RESULTS: The 36-week open-label phase was completed by 106 of 140 subjects (76%). AE-related treatment discontinuations occurred in 19 subjects (14%). Treatment-emergent AEs, reported by ≥15% of subjects, were dyskinesia (33%) and constipation (19%). Preladenant 5 mg twice a day provided OFF time reductions (1.4-1.9 hours/day) and ON time increases (1.2-1.5 hours/day) throughout the 36-week treatment relative to the baseline of the double-blind study. CONCLUSIONS: Long-term preladenant treatment (5 mg twice a day) was generally well tolerated and provided sustained OFF time reductions and ON time increases. © 2013 Movement Disorder Society.
    Movement Disorders 06/2013; 28(6):817-820. · 5.63 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The most common forms of dystonia are those that develop in adults and affect a relatively isolated region of the body. Although these adult-onset focal dystonias are most prevalent, knowledge of their etiologies and pathogenesis has lagged behind some of the rarer generalized dystonias, in which the identification of genetic defects has facilitated both basic and clinical research. This summary provides a brief review of the clinical manifestations of the adult-onset focal dystonias, focusing attention on less well understood clinical manifestations that need further study. It also provides a simple conceptual model for the similarities and differences among the different adult-onset focal dystonias as a rationale for lumping them together as a class of disorders while at the same time splitting them into subtypes. The concluding section outlines some of the most important research questions for the future. Answers to these questions are critical for advancing our understanding of this group of disorders and for developing novel therapeutics. © 2013 Movement Disorder Society.
    Movement Disorders 06/2013; 28(7):926-43. · 5.63 Impact Factor
  • Source
    Dataset: DOMINION

Publication Stats

5k Citations
1,072.03 Total Impact Points

Institutions

  • 2005–2014
    • Emory University
      • Department of Neurology
      Atlanta, Georgia, United States
    • Rhode Island Hospital
      Providence, Rhode Island, United States
  • 2013
    • Wadsworth Center, NYS Department of Health
      • Division of Genetics
      Albany, New York, United States
  • 2011
    • Medical University of South Carolina
      • Department of Neurosciences (College of Medicine)
      Charleston, SC, United States
    • University of Maryland, Baltimore
      • Department of Neurology
      Baltimore, MD, United States
  • 2010–2011
    • New York State Department of Health
      New York City, New York, United States
  • 1989–2009
    • Albany Medical College
      • • Neuroscience Institute
      • • Department of Neurology
      Albany, New York, United States
  • 2006–2008
    • University of Washington Seattle
      • • Department of Epidemiology
      • • International Clinical Research Center (ICRC)
      Seattle, WA, United States
    • Kansas City VA Medical Center
      Kansas City, Missouri, United States
  • 2005–2008
    • Albany Stratton VA Medical Center
      Albany, New York, United States
  • 1999–2005
    • Parkinson's and Movement Disorders Center Of Maryland
      Maryland, United States
  • 1988–2004
    • University of Miami
      • Department of Neurology
      Coral Gables, FL, United States
    • University of Miami Miller School of Medicine
      • Department of Neurology
      Miami, FL, United States
  • 2002
    • Mayo Clinic - Scottsdale
      Scottsdale, Arizona, United States
  • 2000
    • University of Southern California
      Los Angeles, California, United States
    • Memorial Hospital of Rhode Island
      Pawtucket, Rhode Island, United States
    • University of South Florida
      • Department of Neurology
      Tampa, FL, United States
  • 1997
    • University of Toronto
      Toronto, Ontario, Canada
    • Beth Israel Deaconess Medical Center
      • Department of Neurology
      Boston, MA, United States