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Senior Clinician

Mary Kay Floeter, M.D., Ph.D.

Motor Neuron Disorders Unit

Office of the Clinical Director
Building 10-CRC Room 1D45
10 Center Drive, MSC 1404 MSC1404
Bethesda MD 20892-1404
Office: 301-496-7428
Lab: 301-496-7428
Fax: 301-451-9805

Dr. Floeter received her MD and PhD at Washington University in St. Louis and completed residency training in Neurology at the University of California, San Francisco. After postdoctoral work in physiology at UCSF, she came to NIH as a senior staff fellow in the Laboratory of Neural Control to study the physiology of motor neurons and mammalian spinal cord circuits controlling movement. She joined the EMG section as a clinical associate in Clinical Neurophysiology three years later and served as Chief of the NINDS EMG Section 1996-2014. She was appointed as the NINDS Deputy Clinical Director in 2006, and became a Senior Clinician in 2008. Dr. Floeter’s current research focuses on two rare motor neuron disorders: primary lateral sclerosis and C9ORF72-associated amyotrophic lateral sclerosis and frontotemporal dementia.

The NINDS Motor Neuron Disorders Unit studies neurodegenerative disorders that affect corticospinal and spinal motor neurons that control voluntary movement. Primary lateral sclerosis (PLS) and amyotrophic lateral sclerosis (ALS) are examples of rare disorders in which neurons responsible for voluntary movements undergo degeneration. Corticospinal (upper) motor neurons degenerate in both disorders; spinal (lower) motor neurons also degenerate in ALS, but are relatively spared in PLS. We are interested in understanding how these disorders are related and finding biomarkers of disease progression or prognosis. We hypothesize that functional changes will precede structural changes, with a sequence reflecting cell death, inflammation, axonal breakdown and tissue remodeling. Multimodal imaging and physiology studies are being used to explore these questions. 

ALS, PLS, and frontotemporal dementia (FTD) have been proposed to form a spectrum of neurodegenerative disease because of overlapping clinical symptoms and pathological features. In 2011, a hexanucleotide repeat expansion in the gene C9ORF72 was found to cause ALS and FTD, extending the evidence for this proposal to  genetics. To better understand the range of clinical presentations of this mutation in C9ORF72 and how clinical symptoms progress, we are carrying out a prospective longitudinal study of C9ORF72-related disorders, with imaging, physiological, and biofluid studies. This study of C9ORF72-related disease is highly collaborative, with investigators in laboratories at NINDS, NIA, and outside institutions, including agreements for sharing biospecimens.

6 Months Spread of White Matter Changes in C9orf72 ALS-FTD

Research Image

Diffusion tensor imaging of a group of C9orf72 mutation carriers shows a frontal predominance of white matter disruption, with spread of regions with reduced fractional anisotropy (upper panel) from the initial scan (red) and a second scan 6 months later. White matter regions with increased mean diffusivity (lower panel) at the initial scan (blue) extend further posteriorly and into the temporal lobe 6 months later (green).

Clinical Protocols

  • Structural and Function Brain Imaging Markers of Upper Motor Neuron Function 12-N-0060

  • Natural History and Biomarkers of C9ORF72 ALS and FTD 13-N-0188

  • Investigating Complex Neurodegenerative Disorders 17-N-0131

Staff Image
  • Michael Clark, B.S.
    Post baccalaureate IRTA Fellow

  • Laura Danielian, M.S.
    Biomedical Engineer

  • Jennifer Farren, R.N.

  • Caleb Huang, B.S.
    Post baccalaureate IRTA Fellow

  • Rachel Smallwood, Ph.D.
    Postdoctoral Fellow

  • Alice Tran, B.S.
    Post baccalaureate IRTA Fellow

  • 1) Floeter MK, Danielian LE, Braun LE, Wu T. (2018)
  • Longitudinal diffusion imaging across the C9orf72 clinical spectrum
  • J Neurol Neurosurg Psychiatry, 89, 53-60
  • 2) Floeter MK, Traynor BJ, Farren J, Braun LE, Tierney M, Wiggs EA, Wu T (2017)
  • Disease progression in C9orf72 mutation carriers
  • Neurology, 89, 234-241
  • 3) Cardenas AM, Sarlls JE, Kwan JY, Bageac D, Gala ZS, Danielian LE, Ray-Chaudhury A, Wang H-W, Miller KL, Foxley S, Jbabdi S, Welsh RC, Floeter MK (2017)
  • Pathology of callosal damage in ALS: An ex-vivo, 7T diffusion tensor MRI study
  • Neuroimage Clin., 15, 200-208
  • 4) Schanz O, Bageac D, Braun L, Traynor BJ, Lehky TJ, Floeter MK (2016)
  • Cortical hyperexcitability in patients with C9ORF72 mutations: Relationship to phenotype.
  • Muscle Nerve, 54(2), 264-269
  • 5) Floeter MK, Bageac D, Danielian LE, Braun LE, Traynor BJ, Kwan JY (2016)
  • Longitudinal imaging in C9orf72 mutation carriers: Relationship to phenotype
  • Neuroimage Clin. , 12, 1035-1043.
  • 6) Statland JM, Barohn RJ, Dimachkie MM, Floeter MK, Mitsumoto H (2015)
  • Primary Lateral Sclerosis
  • Neurology Clinics, 33(4), 749-760
  • 7) Meoded A, Morrissette AE, Katipally R, Schanz O, Gotts SJ, Floeter MK (2015)
  • Cerebro-cerebellar connectivity is increased in primary lateral sclerosis
  • Neuroimage Clinical, 7, 288-296
  • 8) Flynn L, Stephen M, and Floeter MK (2014)
  • Disease Spread through Contiguity and Axonal Tracts in Primary Lateral Sclerosis
  • Muscle & Nerve, 49, 439-441
  • 9) Floeter MK, Katipally R, Kim MP, Schanz O, Stephen M, Danielian L, Wu T, Huey ED, Meoded A. (2014)
  • Impaired corticopontocerebellar tracts underlie pseudobulbar affect in motor neuron disorders
  • Neurology, 83, 620-627
  • 10) Meoded A, Kwan JY, Peters TL, Huey ED, Danielian LE, Wiggs E, Morrissette A, Wu T, Russell JW, Bayat E, Grafman J, Floeter MK (2013)
  • Imaging findings associated with cognitive performance in primary lateral sclerosis and amyotrophic lateral sclerosis
  • Dement Geriatr Cogn Dis, 16, 233-250
  • 11) Kwan JY, Jeong SY, Van Gelderen P,Deng H-X, Quezado MM, Danielian LE, Butman JA,Chen L, Bayat E, Russell J, Siddique T, Duyn JH, Rouault TA, Floeter MK (2012)
  • Iron Accumulation in Deep Cortical Layers Accounts for MRI Signal Abnormalities in ALS: Correlating 7 Tesla MRI and Pathology
  • PLoSOne, 7(4), e35241
  • 12) Kwan Jy, Meoded A, Danielian LE, Wu T, Floeter MK (2012)
  • Structural imaging differences and longitudinal changes in primary lateral sclerosis and amyotrophic lateral sclerosis
  • Neuroimage Clin, 2, 151-160
  • 13) Iwata NK, Kwan JY, Danielian LE, Butman J, Tovar Moll F, Bayat E, Floeter MK (2011)
  • White matter alterations differ in primary lateral sclerosis and amyotrophic lateral sclerosis
  • Brain
  • 14) Danielian LE, Iwata NK, Thomasson DM, Floeter MK (2010)
  • Reliability of longitudinal fiber tracking measurements in diffusion tensor imaging
  • Neuroimage, 49, 1572-1580
  • 15) Bai O, Lin P, Huang D, Fei DY, Floeter MK (2010)
  • Towards a user-friendly brain-computer interface: Initial tests in ALS and PLS patients
  • Clin Neurophysiol, 121, 1293-303
  • 16) Huey ED, Koppel J, Armstrong N, Grafman J, Floeter MK (2010)
  • A pilot study of the prevalence of psychiatric disorders in PLS and ALS
  • Amyotroph Lateral Scler, 11, 293-7
  • 17) Floeter MK and Mills R (2009)
  • Progression in primary lateral sclerosis: a prospective study
  • Amyotrophic Lateral Sclerosis , 10, 339-346
  • 18) Peters TL and Floeter MK (2009)
  • Usage of Support Services in Primary Lateral Sclerosis.
  • Amyotrophic Lateral Sclerosis, 10, 187-191.
  • 19) Lupu VD, Danielian L, Johnsen JA, Vasconcelos OM, Prokhorenko OA, Jabbari B, Campbell WW, Floeter MK. (2008)
  • Physiology of the motor cortex in polio survivors.
  • Muscle Nerve, 37(2), 177-82
  • 20) Butman JA, Floeter MK. (2007)
  • Decreased thickness of primary motor cortex in primary lateral sclerosis.
  • AJNR Am J Neuroradiol., 28(1), 87-91
  • 21) Bai O, Vorbach S, Hallett M, Floeter MK. (2006)
  • Movement-related cortical potentials in primary lateral sclerosis
  • Ann Neurol , 59, 682-690
  • 22) Floeter MK, Zhai P, Saigal R, Kim Y, Statland J. (2005)
  • Motor neuron firing dysfunction in spastic patients with primary lateral sclerosis.
  • J Neurophysiology, 94, 919-927
  • 23) Lin JZ, Floeter MK. (2004)
  • Do F-wave measurements detect changes in motor neuron excitability?
  • Muscle Nerve, 30, 289-94
  • 24) Zhai P, Pagan F, Statland J, Butman JA, Floeter MK (2003)
  • Primary lateral sclerosis: a heterogeneous disorder composed of different subtypes?
  • Neurology, 60, 1258-1265
  • 25) Puls I, Jonnakuty C, LaMonte BH, Holzbaur EL, Tokito M, Mann E, Floeter MK, Bidus K, Drayna D, Oh SJ, Brown RH Jr, Ludlow CL, Fischbeck KH (2003)
  • Mutant dynactin in motor neuron disease
  • Nature Genetics, 33(4), 455-6
  • 26) Floeter MK (2003)
  • Cutaneous silent periods
  • Muscle and Nerve, 28, 391-401
  • 27) Perez M, Field-Fote E, Floeter MK (2003)
  • Patterned sensory stimulation induces plasticity in reciprocal Ia inhibition in humans
  • J Neuroscience, 23, 2014-8
  • 28) Wilson, RH, Lehky T, Thomas R, Quinn M, Floeter MK, Grem JL (2002)
  • Acute oxaliplatin-induced peripheral nerve hyperexcitability
  • J Clin Oncol, 20, 1767-1774
  • 29) Molloy FM, Dalakas MC, Floeter MK (2002)
  • Increased brainstem excitability in Stiff Person syndrome
  • Neurology, 59, 449-451
  • 30) Molloy FM, Floeter MK, Syed NA, Sandbrink F, Culcea E, Steinberg SM, Dahut W, Pluda J, Kruger E, Reed E, Figg WD (2001)
  • Thalidomide neuropathy in patients treatedfor metastatic prostate cancer
  • Muscle Nerve , 24, 1050-1057
  • 31) Sandbrink F, AD Klion, MK Floeter (2001)
  • Psuedo-conduction block in a patient with vasculitic neuropathy
  • Electromyogr Clin Neurophysiol , 41, 195-202
  • 32) NA Syed, F Sandbrink, CA Luciano, G Alterescu, T Weibel, R Schiffman, MK Floeter (2000)
  • Cutaneous silent periods in Fabry disease
  • Muscle Nerve, 23, 1179-1186
  • 33) Jabbari, B, Molloy FM, Erikson M, and Floeter MK (2000)
  • Bilateral painful hand - moving fingers: Electrophysiological assessment of the central nervous system oscillator
  • Movement Disorders, 15, 1259-1263
  • 34) Sandbrink F, NA Syed, M Fujii, MC Dalakas, and MK Floeter (2000)
  • Motor cortex excitability in Stiff-Person Syndrome
  • Brain, 123, 2231-2239
  • 35) Syed NA, A Delgado, F Sandbrink, A Schulman, M Hallett, MK Floeter (1999)
  • Blink reflex recovery in facial weakness: an electrophysiological study of adaptive changes
  • Neurology, 52, 834-838
  • 36) Manconi F, NA Syed, and MK Floeter (1998)
  • Mechanisms underlying spinal motor neuron excitability during the cutaneous silent period in humans
  • Muscle Nerve, 21, 1256-1264
  • 37) Floeter MK, C Gerloff, J Kouri and M Hallett (1998)
  • Cutaneous withdrawal reflexes of the upper extremity in humans.
  • Muscle Nerve, 21, 591-598
  • 38) Floeter MK , J Valls-Sole, C Toro, D Jacobowitz and M Hallett (1998)
  • Physiological studies of spinal inhibitory pathways in patients with Stiff-person syndrome.
  • Neurology, 51, 85-93
  • 39) Kohn AF, MK Floeter, M Hallett (1997)
  • Presynaptic inhibition versus homosynaptic depression as an explanation for soleus H-reflex depression in humans
  • Exp Brain Res, 116, 375-380
  • 40) Floeter MK and AF Kohn (1997)
  • Differential sensitivity of H-reflexes of different sizes to low frequency depression
  • Electroenceph Clin Neurophys, 106, 470-475
  • 41) Floeter, MK, F Andermann, E Andermann, M Nigro, and M Hallett (1996)
  • Physiological studies of spinal inhibitory pathways in patients with hereditary hyperekplexia.
  • Neurology, 46, 766-772.
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