Patient Portal

Baijayanta Maiti, MD, PhD

Assistant Professor, Neurology 

Specialty Areas

Movement Disorders
Parkinson disease
Dystonia
Tremor
Neurology - Adult

Board Certifications

Neurology
Neuromuscular Medicine

Hospital Affiliations

Barnes-Jewish Hospital
St. Louis Children's Hospital

Areas of Clinical Interest

Parkinson disease, dystonia, essential tremor, hemifacial spasm, Huntington disease, ataxia, Botulinum toxin injections for patients with dystonia, sialorrhea, spasticity, children with cerebral palsy 

  • Maps & Directions
  • Education
  • Publication & Research

Maps & Directions

Maps & Directions

Center for Advanced Medicine
Neuroscience Center

4921 Parkview Place
St. Louis, MO 63110

Suite: C
Floor: 6
Office Phone: 314-362-6908
Fax: 314-747-3258

Barnes-Jewish Hospital
McMillan Building

517 S. Euclid Avenue
St. Louis, MO 63110

Floor: Lower Level
Office Phone: 314-362-6908
Fax: 314-747-3258

Education

Education

Fellowship - Movement Disorders: Washington University School of Medicine, St. Louis MO 2016
Fellowship - Neuromuscular Medicine: Washington University School of Medicine, St. Louis, MO 2014
Residency - Neurology: Washington University School of Medicine, St. Louis, MO 2013
PhD - Human Genetics: University of Utah, Salt Lake City, UT 2009
Medical Degree: Calcutta Medical College, Calcutta, India 2003

Publication & Research

Publication & Research

Emergent Functional Network Effects in Parkinson Disease.
Gratton C, Koller JM, Shannon W, Greene DJ, Maiti B, Snyder AZ, Petersen SE, Perlmutter JS, Campbell MC
Cereb Cortex. 2018 Nov 12; doi: 10.1093/cercor/bhy229.

PMID:
    30418543
    [PubMed - as supplied by publisher]
Related citations


PET Imaging in Movement Disorders.
Maiti B, Perlmutter JS
Semin Nucl Med. 2018 Nov; 48(6)513-524. doi: 10.1053/j.semnuclmed.2018.07.006.

PMID:
    30322477
    [PubMed - indexed for MEDLINE]
Related citations


Cognitive reserve and β-amyloid pathology in Parkinson disease.
Lucero C, Campbell MC, Flores H, Maiti B, Perlmutter JS, Foster ER
Parkinsonism Relat Disord. 2015 Aug; 21(8)899-904. doi: 10.1016/j.parkreldis.2015.05.020.

PMID:
    26037458
    [PubMed - indexed for MEDLINE]
Related citations


Corrigendum: Translation from a DMD exon 5 IRES results in a functional dystrophin isoform that attenuates dystrophinopathy in humans and mice.
Wein N, Vulin A, Falzarano MS, Szigyarto CA, Maiti B, Findlay A, Heller KN, Uhlén M, Bakthavachalu B, Messina S, Vita G, Passarelli C, Brioschi S, Bovolenta M, Neri M, Gualandi F, Wilton SD, Rodino-Klapac LR, Yang L, Dunn DM, Schoenberg DR, Weiss RB, Howard MT, Ferlini A, Flanigan KM
Nat Med. 2015 May; 21(5)537. doi: 10.1038/nm0515-537c.

PMID:
    25951531
    [PubMed]
Related citations


Corrigendum: Translation from a DMD exon 5 IRES results in a functional dystrophin isoform that attenuates dystrophinopathy in humans and mice.
Wein N, Vulin A, Falzarano MS, Szigyarto CA, Maiti B, Findlay A, Heller KN, Uhlén M, Bakthavachalu B, Messina S, Vita G, Passarelli C, Gualandi F, Wilton SD, Rodino-Klapac LR, Yang L, Dunn DM, Schoenberg DR, Weiss RB, Howard MT, Ferlini A, Flanigan KM
Nat Med. 2015 Apr; 21(4)414. doi: 10.1038/nm0415-414b.

PMID:
    25849273
    [PubMed]
Related citations


Atypical CSF findings in West Nile neuroinvasive disease: A diagnostic and therapeutic conundrum.
Maiti B, Bucelli RC
Neurol Neuroimmunol Neuroinflamm. 2014 Jun; 1(1)e8. doi: 10.1212/NXI.0000000000000008.

PMID:
    25340064
    [PubMed]
Related citations


Translation from a DMD exon 5 IRES results in a functional dystrophin isoform that attenuates dystrophinopathy in humans and mice.
Wein N, Vulin A, Falzarano MS, Szigyarto CA, Maiti B, Findlay A, Heller KN, Uhlén M, Bakthavachalu B, Messina S, Vita G, Passarelli C, Brioschi S, Bovolenta M, Neri M, Gualandi F, Wilton SD, Rodino-Klapac LR, Yang L, Dunn DM, Schoenberg DR, Weiss RB, Howard MT, Ferlini A, Flanigan KM
Nat Med. 2014 Sep; 20(9)992-1000. doi: 10.1038/nm.3628.

PMID:
    25108525
    [PubMed - indexed for MEDLINE]
Related citations


The ZZ domain of dystrophin in DMD: making sense of missense mutations.
Vulin A, Wein N, Strandjord DM, Johnson EK, Findlay AR, Maiti B, Howard MT, Kaminoh YJ, Taylor LE, Simmons TR, Ray WC, Montanaro F, Ervasti JM, Flanigan KM
Hum Mutat. 2014 Feb; 35(2)257-64. doi: 10.1002/humu.22479.

PMID:
    24302611
    [PubMed - indexed for MEDLINE]
Related citations


DMD exon 1 truncating point mutations: amelioration of phenotype by alternative translation initiation in exon 6.
Gurvich OL, Maiti B, Weiss RB, Aggarwal G, Howard MT, Flanigan KM
Hum Mutat. 2009 Apr; 30(4)633-40. doi: 10.1002/humu.20913.

PMID:
    19206170
    [PubMed - indexed for MEDLINE]
Related citations


Clinical, histological and genetic characterization of reducing body myopathy caused by mutations in FHL1.
Schessl J, Taratuto AL, Sewry C, Battini R, Chin SS, Maiti B, Dubrovsky AL, Erro MG, Espada G, Robertella M, Saccoliti M, Olmos P, Bridges LR, Standring P, Hu Y, Zou Y, Swoboda KJ, Scavina M, Goebel HH, Mitchell CA, Flanigan KM, Muntoni F, Bönnemann CG
Brain. 2009 Feb; 132(Pt 2)452-64. doi: 10.1093/brain/awn325.

PMID:
    19181672
    [PubMed - indexed for MEDLINE]
Related citations


A mutation in the SEPN1 selenocysteine redefinition element (SRE) reduces selenocysteine incorporation and leads to SEPN1-related myopathy.
Maiti B, Arbogast S, Allamand V, Moyle MW, Anderson CB, Richard P, Guicheney P, Ferreiro A, Flanigan KM, Howard MT
Hum Mutat. 2009 Mar; 30(3)411-6. doi: 10.1002/humu.20879.

PMID:
    19067361
    [PubMed - indexed for MEDLINE]
Related citations


Proteomic identification of FHL1 as the protein mutated in human reducing body myopathy.
Schessl J, Zou Y, McGrath MJ, Cowling BS, Maiti B, Chin SS, Sewry C, Battini R, Hu Y, Cottle DL, Rosenblatt M, Spruce L, Ganguly A, Kirschner J, Judkins AR, Golden JA, Goebel HH, Muntoni F, Flanigan KM, Mitchell CA, Bönnemann CG
J Clin Invest. 2008 Mar; 118(3)904-12. doi: 10.1172/JCI34450.

PMID:
    18274675
    [PubMed - indexed for MEDLINE]
Related citations

Areas of Research Interest

Dr. Maiti’s research utilizes state of the art multimodal, non-invasive, functional imaging techniques to enhance our understanding of the pathophysiologic bases of dementia and gait impairment in Parkinson disease and thereby unravel new therapeutic targets.