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DigiGait

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Overview

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Gait analysis is the study of the manner of walking. It is used worldwide to aid in the diagnosis and treatment of a wide range of ambulatory problems, including Parkinson’s disease, muscular dystrophy, and nerve injury. It is increasing being recognized as a useful preclinical assay to better understand how animal models may reflect the human condition, and to generate quantitative metrics of normal and abnormal gait.

Gait can be assessed in subjects walking voluntarily or on a treadmill. As in human life, however, when subjects walk voluntarily, the assessment of gait can be difficult depending on the subject’s speed.

DigiGait is now the most widely published ventral plane videography instrumentation available for gait analysis in laboratory animals. Voluntary and treadmill walking, DigiGait performs gait analysis of mice and rats over a range of walking and running speeds. Ventral Plane Imaging (VPI) Technology continuously images the underside of the animals walking atop of the patented motorized transparent treadmill belt, generating “digital paw prints” and dynamic gait signals. These dynamic gait signals, generated for each of the 4 limbs, describe the posture and kinematics of the animals that reflect strength, balance, and coordination. Animals can also be challenged to walk up an incline or down a decline to maximize the details about the subjects’ motor abilities.

See How They Run

How does DigiGait work?

DigiGait’s patented VPI Technology images the ventral view of animals as they walk on a motorized transparent treadmill belt. [By analogy, imagine yourself at the gym on a treadmill with clear belt, and a camera imaging the underside of your sneakers.] VPI Technology automatically computes the area of the advancing and retreating paws to quantify the spatial and temporal indices of gait. When the motor speed is set to zero, the animals are free to voluntarily traverse the walking corridor, from which images are captured and results generated. The motorized belt, however, enables numerous strides to be captured over a range of walking speeds (0.1 cm/s to 99.9 cm/s); goal boxes and other artifices to compel the animals to walk are not needed. Numerous strides at known and comparable speeds can be measured for all of the animals in a study. Over 50 indices of gait for each limb are reported in spreadsheet ready format.

Why use DigiGait?

DigiGait is the most widely applicable and comprehensive gait analysis instrumentation available. Key advantages over other devices you are considering:

Enables study of voluntary and treadmill walking
Enables study of hopping and running at high speeds
Enables study of gait in animals walking up inclines and down declines
Enables the capture of numerous strides at known and comparable speeds, eliminating speed differences as the most important confounder in the interpretation of gait differences
Data generated have lower standard errors and a higher degree of accuracy and repeatability
The entire ventral view of the subject is imaged, not just the portions of the paw that make contact with illuminated glass
Higher throughput, for data collection and data analysis
Early detection of subtle phenotypes; most subtle phenotypes require animals to be studied over numerous strides under challenging conditions, such as is often the case for humans
Motor Rater
Fine motor skills assessment

Who else uses DigiGait?

DigiGait is used worldwide at universities, biotechnology companies, and pharmaceutical giants. Clients include Harvard, Yale, Stanford, King’s College London, Biogen, Genzyme, and Pfizer to name a few (please ask for references as we respect our customers’ confidences). Research areas include amyotrophic lateral sclerosis, spinal cord injury, arthritis, traumatic brain injury, and nerve injury…to name a few…

If you are interested in more details or a price quote please Contact Us

DigiGait FAQTom Hampton2015-09-13T01:18:37+00:00

Gait Analysis

1. How does the DigiGait system compare to other gait analysis systems?

The DigiGait system does not require external reflective markers to be attached to the animal for gait analysis, whereas other systems may require markers. DigiGait directly collects digital video images of the underside of animals, whereas other systems may use a mirror to reflect the ventral view of the animal to a camera. As a consequence, image clarity, color, and shades are best preserved by DigiGait. The DigiGait system enables the user to select a range of walking speeds, whereas other systems expect the animal to walk [or not walk] at its preferred walking speed. This feature of DigiGait is important since there may be no gait abnormalities at a slow walking speed, but a high walking speed may demonstrate important differences. Moreover, even subtle differences in walking speed may have profound effects on gait indices. DigiGait empowers the user to study uphill and downhill walking, as subtle phenotypes might be highlighted with incline and decline locomotion. Standard errors are lower, repeatability is higher, throughput is higher, and data is more relevant from DigiGait.

2. Why is temporal resolution important in gait analysis?

Rodents may walk at speeds exceeding 90 cm/s. Mice walking at such speeds recruit their limbs more than 10 times each second. All the kinematic parameters are shortened at such a high speed. The braking duration of the forelimbs, for example, can be shorter than 40 ms. High temporal resolution, therefore, is important to provide exact information about subtle gait abnormalities.

3. What is the spatial resolution of the DigiGait system?

The spatial resolution of the DigiGait system exceeds 5,000 pixels per cm2.

4. How does the DigiGait system determine the correct swing time?

The treadmill belt of the DigiGait system is transparent, so that the high resolution digital video camera is able to image the ventral view of the paws even when they are not in contact with the treadmill belt. Among the thousands of lines of code and artificial intelligence algorithms within the DigiGait software are functions that detect not only the spatial coordinates of a pixel, but also its direction. An image pixel of a paw that has a linear direction parallel to the treadmill belt is in the stance phase of a stride. An image pixel of a paw that has a direction different from the direction of the belt is in the swing phase of stride.

5. How often does the treadmill belt need to be replaced?

One of the first DigiGait treadmills has been in service at the Pfizer Pharmaceutical Company for over 5 years, and the treadmill belt has been changed once. The belt can be exchanged in <10 minutes. The belt material has good transparency without comprising the animals’ tactile walking comfort. The belt can be cleaned with most laboratory cleaning agents, including ethanol.

6. Can spinal cord injured animals walk on the treadmill?

Spinal cord injured rodents are able to execute stepping on the treadmill. In animals with total hemisection, the forelimbs of the animals attempt to compensate for hind limbs paralysis. The DigiGait system is able to quantify the asymmetry between forelimb and hind limb stepping as the animals recover from spinal cord injury. Several gait metrics are of interest in spinal cord injured animals, including phase dispersion, paw placement angle, and toe spread.

7. How do the metrics of the DigiGait system compare to the BBB score?

The DigiGait system objectively reports over 30 metrics of posture and locomotion at a range of walking speeds. There are likely some functional measures of the Basso-Beattie-Bresnahan (BBB) score that relate to the DigiGait system’s quantitative metrics. However, most gait metrics are very sensitive to walking speeds, and walking speeds usually differ between animals in the open field. Stride lengths, for example, of a group of mice with cerebral infarction, may be significantly different at walking speeds of 20 cm/s vs. 25 cm/s, a velocity difference imperceptible to the eye. The DigiGait system also reports phase dispersion values that quantify interlimb coordination, differences which are relevant when animals are studied at comparable walking speeds.

8. Does the DigiGait system measure ground reaction forces?

The DigiGait system does not measure ground reaction forces. Only a system that includes force transducers can measure ground reaction forces. The qualitative shape and quantitative timings of gait signals obtained by the DigiGait system, however, have been shown to correlate to force development in rodents. For example, the protracted braking durations of forelimbs compared to hind limbs, and the briefer propulsion durations of hind limbs compared to forelimbs, indicate hind limb vs. forelimb functional differences in loading and force development. DigiGait, moreover, has demonstrated significant differences in several gait metrics in hamsters with muscular dystrophy that may be attributable to their muscle weakness.

9. Why did you patent the DigiGait system?

Scientists and engineers from Mouse Specifics, Inc. and The CuraVita Corporation invented the technology and analysis software for imaging small mammals’ gait from underneath a transparent treadmill belt, for which a United Sates patent was issued [US Patent (#6,899,686), Method and Apparatus for Monitoring Locomotion Kinematics for Ambulating Animals]. The system provides not only two-dimensional topography, but also three-dimensional kinematics from one camera placed ventrally. The patent exemplifies not only the system’s utility and novelty, but also our commitment to scientific leadership in the field. Imitators of our patented technology do not adhere to the same rigor in ensuring instrument accuracy or sensitivity, especially when most motor defects are subtle.

VIDEOS

DIGIGAIT DATA CAPTURE

1- Digigait Imager - Setup

2- Digigait Imager - Data Capture

3- Digigait Imager - Video Examples

DigiGait Data Analysis

1- Digigait Analysis - Overview

2- Digigait Analysis - Preprocessing

3- Digigait Analysis - Processing

4- Digigait Analysis - Postprocessing

5- Digigait Analysis - Correct

6- Digigait Analysis - Connect

7- Digigait Analysis - Exclude

Specifications

Accessories

Citations

2022

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Deng, P., Halmai, J., Beitnere, U., Cameron, D., Martinez, M. L., Lee, C. C., Waldo, J. J., Thongphanh, K., Adhikari, A., Copping, N., Petkova, S. P., Lee, R. D., Lock, S., Palomares, M., O’Geen, H., Carter, J., Gonzalez, C. E., Buchanan, F., Anderson, J. D., Fierro, F. A., … Fink, K. D. (2022). An in vivo Cell-Based Delivery Platform for Zinc Finger Artificial Transcription Factors in Pre-clinical Animal Models. Frontiers in molecular neuroscience, 14, 789913. https://doi.org/10.3389/fnmol.2021.789913 Read Abstract

Ong-Pålsson, E., Njavro, J. R., Wilson, Y., Pigoni, M., Schmidt, A., Müller, S. A., Meyer, M., Hartmann, J., Busche, M. A., Gunnersen, J. M., Munro, K. M., & Lichtenthaler, S. F. (2022). The β-Secretase Substrate Seizure 6-Like Protein (SEZ6L) Controls Motor Functions in Mice. Molecular neurobiology, 59(2), 1183–1198. https://doi.org/10.1007/s12035-021-02660-y Read Abstract

Yang, L., Li, M., Zhan, Y., Feng, X., Lu, Y., Li, M., Zhuang, Y., Lei, J., & Zhao, H. (2022). The Impact of Ischemic Stroke on Gray and White Matter Injury Correlated With Motor and Cognitive Impairments in Permanent MCAO Rats: A Multimodal MRI-Based Study. Frontiers in neurology, 13, 834329. https://doi.org/10.3389/fneur.2022.834329 Read Abstract

Yao, Y., Qu, D., Jing, X., Jia, Y., Zhong, Q., Zhuo, L., Chen, X., Li, G., Tang, L., Zhu, Y., Zhang, X., Ji, Y., Li, Z., & Tao, J. (2022). Molecular Mechanisms of Epileptic Encephalopathy Caused by KCNMA1 Loss-of-Function Mutations. Frontiers in pharmacology, 12, 775328. https://doi.org/10.3389/fphar.2021.775328 Read Abstract

2021

Gubert, C., Love, C. J., Kodikara, S., Mei Liew, J. J., Renoir, T., Lê Cao, K. A., & Hannan, A. J. (2021). Gene-environment-gut interactions in Huntington’s disease mice are associated with environmental modulation of the gut microbiome. iScience, 25(1), 103687. https://doi.org/10.1016/j.isci.2021.103687 Read Abstract

2019

David F. Wozniak, Pamela Valnegri, Joshua T. Dearborn, Stephen C. Fowler, and Azad Bonni. 2019. Conditional knockout of UBC13 produces disturbances in gait and spontaneous locomotion and exploration in mice. Sci Rep. 9: 4379. Read Abstract

Feng H, Larrivee CL, Demireva EY, Xie H, Leipprandt JR, Neubig RR. 2019. Mouse models of GNAO1-associated movement disorder: Allele- and sex-specific differences in phenotypes. PLoS One Jan 25;14(1) Read Abstract

Robertson L, Featherby T, Howell S, Hughes J, Thomas P. 2019. Paroxysmal and cognitive phenotypes in Prrt2 mutant mice. Genes Brain Behav. Jun;18(5):e12566 Read Abstract

2018

Falk DJ, Galatas T, Todd AG, Soto EP, Harris AB, Notterpek L. 2018. Locomotor and skeletal muscle abnormalities in trembler J neuropathic mice. Muscle Nerve. Apr;57(4):664-671. Read Abstract

2017

Claghorn, G. C., Z. Thompson, J. C. Kay, G. Ordonez, T. G. Hampton, and T. Garland, Jr. 2017. Selective breeding and short-term access to a running wheel alter stride characteristics in house mice. Physiological and Biochemical Zoology 90:533–545. Read Abstract

2016

Connell JW, Allison R, Reid E. Quantitative Gait Analysis Using a Motorized Treadmill System Sensitively Detects Motor Abnormalities in Mice Expressing ATPase Defective Spastin. PLoS One. 2016 Mar 28;11(3):e0152413. doi: 10.1371/journal.pone.0152413. eCollection 2016. Read Article

Heuermann RJ, et al. Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy. Neurobiol Dis. 2016 Jan;85:81-92. doi:10.1016/j.nbd.2015.10.005. Read Abstract

Hung YH, Walterfang M, Churilov L et al. Neurological Dysfunction in Early Maturity of a Model for Niemann-Pick C1 Carrier Status. Neurotherapeutics. 2016 Mar 4. [Epub ahead of print] Read Article

Miyuki Sakuma, et al. Lack of motor recovery after prolonged denervation of the neuromuscular junction is not due to regenerative failure. Eur J Neurosci. 2016 Feb;43(3):451-62. doi: 10.1111/ejn.13059. Epub 2015 Sep 28. Read Abstract

Xiao J, et al. Motor phenotypes and molecular networks associated with germline deficiency of Ciz1. Exp Neurol. 2016 Sep;283(Pt A):110-20. doi: 10.1016/j.expneurol.2016.05.006. Epub 2016 May 7. Read Abstract

2015

Chen L, et al. A53T human α-synuclein overexpression in transgenic mice induces pervasive mitochondria macroautophagy defects preceding dopamine neuron degeneration. J Neurosci. 2015 Jan 21;35(3):890-905. Read Abstrac

Del Mar N, et al. A novel closed-body model of spinal cord injury caused by high-pressure air blasts produces extensive axonal injury and motor impairments. Exp Neurol. 2015 Sep;271:53-71. Read Abstract

Gennarino VA et al. Pumilio1 haploinsufficiency leads to SCA1-like neurodegeneration by increasing wild-type Ataxin1 levels. Cell. 2015 Mar 12;160(6):1087-98. doi: 10.1016/j.cell.2015.02.012. Read Article

Jara JH, et al. Corticospinal Motor Neurons Are Susceptible to Increased ER Stress and Display Profound Degeneration in the Absence of UCHL1 Function. Cereb Cortex. 2015 Nov 25; (11):4259-72 Read Abstract

Lambert CS, et al . Analysis of gait in rats with olivocerebellar lesions and ability of the nicotinic acetylcholine receptor agonist varenicline to attenuate impairments. Behav Brain Res. 2015 Jun 3. pii: S0166-4328(15)30025-5. doi: 10.1016/j.bbr.2015.05.056. Read Abstract

Lasagna-Reeves CA, et al. Ataxin-1 oligomers induce local spread of pathology and decreasing them by passive immunization slows Spinocerebellar ataxia type 1 phenotypes. Elife. 2015 Dec 17;4. pii: e10891. doi: 10.7554/eLife.10891. Read Article

Liu YB, Tewari A, Salameh J, et al. A dystonia-like movement disorder with brain and spinal neuronal defects is caused by mutation of the mouse laminin β1 subunit, Lamb1. Elife. 2015 Dec 24;4. pii: e11102. doi: 10.7554/eLife.11102. Read Abstract

Neckel ND. Methods to quantify the velocity dependence of common gait measurements from automated rodent gait analysis devices. J Neurosci Methods. 2015 253:244-53. Read Abstract

Nori S, et al. Long-term safety issues of iPSC-based cell therapy in a spinal cord injury model: oncogenic transformation with epithelial-mesenchymal transition. Stem Cell Reports. 2015 Mar 10;4(3):360-73. Read Abstract

Pappas SS, et al. Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons. Elife. 2015 Jun 8;4:e08352 Read Abstract

Poulet B, et al. Intermittent applied mechanical loading induces subchondral bone thickening that may be intensified locally by contiguous articular cartilage lesions. Osteoarthritis Cartilage. 2015 Jun;23(6):940-8. Read Abstract

Rothaug M, et al. LAMP-2 deficiency leads to hippocampal dysfunction but normal clearance of neuronal substrates of chaperone-mediated autophagy in a mouse model for Danon disease. Acta Neuropathol Commun. 2015 Jan 31;3:6. Read Abstract

Samantaray S, et al. Inhibition of calpain activation protects MPTP-induced nigral and spinal cord neurodegeneration, reduces inflammation, and improves gait dynamics in mice. Mol Neurobiol. 2015 52(2):1054-66. Read Abstract

Sashindranath M, et al.. Evaluation of gait impairment in mice subjected to craniotomy and traumatic brain injury. Behav Brain Res. 2015 Jun 1;286:33-8. doi: 10.1016/j.bbr.2015.02.038. Read Abstract

Spinelli KJ, et al. Curcumin Treatment Improves Motor Behavior in α-Synuclein Transgenic Mice. PLoS One. 2015 Jun 2;10(6):e0128510. doi: 10.1371/journal.pone.0128510. eCollection 2015 Read Abstract

Wright DJ, et al. N-Acetylcysteine improves mitochondrial function and ameliorates behavioral deficits in the R6/1 mouse model of Huntington’s disease. Transl Psychiatry 2015 5:e492. doi:10.1038/tp.2014.131. Read Abstract

Yuengert et al. Origin of a non-Clarke’s column division of the dorsal spinocerebellar tract and the role of caudal proprioceptive neurons in motor function. Cell Rep. 2015 Nov 10; 13(6): 1258–1271. Read Abstract

Zhang B, et al. Age decreases macrophage IL-10 expression: Implications for functional recovery and tissue repair in spinal cord injury. Exp Neurol. 2015 273:83-91. Read Abstract

2014

Eftaxiopoulou T, et al. Gait compensations in rats after a temporary nerve palsy quantified using temporo-spatial and kinematic parameters. J Neurosci Methods. 2014; 232:16-23. Read Abstract

Jantzie LL, et al. Complex pattern of interaction between in utero hypoxia-ischemia and intra-amniotic inflammation disrupts brain development and motor function. J Neuroinflammation. 2014 11:131 Read Abstract

Lambert CS, et al. Gait analysis and the cumulative gait index (CGI): Translational tools to assess impairments exhibited by rats with olivocerebellar ataxia. Behav Brain Res. 2014 274:334-43. Read Abstract

Lu W, et al. Genetic deficiency of the mitochondrial protein PGAM5 causes a Parkinson’s-like movement disorder. Nat Commun. 2014 Sep 15;5:4930 Read Abstract

Müller D, Cherukuri P, Henningfeld K, Poh CH, Wittler L, Grote P, Schlüter O, Schmidt J, Laborda J, Bauer SR, Brownstone RM, Marquardt T. Dlk1 promotes a fast motor neuron biophysical signature required for peak force execution. Science. 2014 Mar 14;343(6176):1264-6. doi: 10.1126/science.1246448. PMID: 24626931. Read Abstract

Piochon C, et al. Cerebellar plasticity and motor learning deficits in a copy-number variation mouse model of autism. Nat Commun. 2014 5:5586. Read Abstract

2013

Cops EJ, et al. Tissue-type plasminogen activator is an extracellular mediator of Purkinje cell damage and altered gait. See comment in PubMed Commons below Exp Neurol. 2013 Nov;249:8-19. doi: 10.1016/j.expneurol.2013.08.001. Read Abstract

Dorman CW, et al. A comparison of DigiGait™ and TreadScan™ imaging systems: assessment of pain using gait analysis in murine monoarthritis. See comment in PubMed Commons below J Pain Res. 2013 Dec 24;7:25-35. doi: 10.2147/JPR.S52195. Read Abstract

Hansen ST, Pulst SM. Response to ethanol induced ataxia between C57BL/6J and 129X1/SvJ mouse strains using a treadmill based assay. Pharmacol Biochem Behav. 2013 Jan;103(3):582-8. doi: 10.1016/j.pbb.2012.10.010. Epub 2012 Oct 24 Read Abstract

Paumier KL, et al. Behavioral characterization of A53T mice reveals early and late stage deficits related to Parkinson’s disease. PLoS One. 2013 Aug 1;8(8):e70274. doi: 10.1371/journal.pone.0070274. Print 2013 Read Abstract

Takano M, et al. In vivo tracing of neural tracts in tiptoe walking Yoshimura mice by diffusion
tensor tractography. Spine (Phila Pa 1976). 2013 Jan 15;38(2):E66-72 Read Abstract

2012

Glajch KE, et al. Sensorimotor assessment of the unilateral 6-hydroxydopamine mouse model of Parkinson’s disease. Behavioural Brain Research. 2012 May 1;230(2):309-16. doi: 10.1016/j.bbr.2011.12.007. 2012. Read Abstract

Gonzalez-Reyes LE, et al. Sonic Hedgehog Maintains Cellular and Neurochemical Homeostasis in the Adult Nigrostriatal Circuit. Neuron. 2012 July 26; 75(2): 306–319. doi: 10.1016/j.neuron.2012.05.018. Read Abstract

2011

Hampton TG, et al. Gait Disturbances in Dystrophic Hamsters. Journal of Biomedicine and Biotechnology. Volume 2011 (2011), Article ID 235354, 8 pages doi:10.1155/2011/235354. Read Abstract

Goldberg N, et al. Profiling Changes in Gait Dynamics Resulting From Progressive 1-Methyl-4-Phenyl-1,2,3, 6-Tetrahydropyridine-Induced Nigrostriatal Lesioning. J Neurosci Res. 2011 Oct;89(10):1698-706. doi: 10.1002/jnr.22699.

Gomez C. et al. Skeletal Muscle IP3R1 Receptors Amplify Physiological and Pathological Synaptic Calcium Signals. The Journal of Neuroscience. 2011 26 Oct;31(43): 15269-15283 Read Abstract

Gong P, et al. Transgenic neuronal overexpression reveals that stringently regulated p23 expression is critical for coordinated movement in mice. Molecular Neurodegeneration. 2011 Dec 28;6:87. doi: 10.1186/1750-1326-6-87. Read Abstract

Kam GL. Determination of disease progression with early toxin-induced neuropathology in the aging mutant SOD mouse model of amyotrophic lateral sclerosis. A thesis submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in The Faculty of Graduate Studies (Experimental Medicine) The University of British Columbia (Vancouver) December 2011 Read Abstract

Mancuso R, et al. Evolution of gait abnormalities in SOD1(G93A) transgenic mice. Brain Res. 2011 Aug 11;1406:65-73. Epub 2011 Jul 5. Read Abstract

Puram SV, et al. A TRPC5-regulated calcium signaling pathway controls dendrite patterning in the mammalian brain. Genes Dev. 2011 December 15; 25(24): 2659–2673. doi: 10.1101/gad.174060.111 PMCID: PMC3248686 Read Abstract

2010

Ek CJ, et al. Spatio-temporal progression of grey and white matter damage following contusion injury in rat spinal cord. PLoS One. 2010 Aug 9;5(8):e12021. Read Abstract

Gómez-Sintes R, Lucas JJ. NFAT/Fas signaling mediates the neuronal apoptosis and motor side effects of GSK-3 inhibition in a mouse model of lithium therapy. J Clin Invest. 2010 Jul 1;120(7):2432-45. doi: 10.1172/JCI37873. Epub 2010 Jun 7. Read Abstract

Hampton TG, Amende I. Treadmill Gait Analysis Characterizes Gait Alterations in Parkinson’s Disease and Amyotrophic Lateral Sclerosis Mouse Models. Journal of Motor Behavior. 2010 Jan-Feb;42(1):1-4. doi: 10.1080/00222890903272025. Read Abstract

Kravitz AV, et al. Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia. Nature. 2010 Jul 29;466(7306):622-6. Epub 2010 Jul 7. Read Abstract

Springer JE, et al. The Functional and Neuroprotective Actions of Neu2000, a Dual Acting Pharmacological Agent, in the Treatment of Acute Spinal Cord Injury. J Neurotrauma. 2010 Jan;27(1):139-49

Xu YF, et al. Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits, and early mortality in transgenic mice. J Neurosci. 2010 Aug 11; 30(32):10851-9. Read Abstract

2009

Berryman ER, et al. Digigait™ quantitation of gait dynamics in rat rheumatoid arthritis model. J Musculoskelet Neuronal Interact. 2009 9:89-98. Read Abstract

Callaway JK, et al. Assessment of residual function and morphology after spinal cord contusion injury in rats: behavioral and histological evidence. 2009 Australian Neuroscience Annual Meeting.

Crone SA, et al. In Mice Lacking V2a Interneurons, Gait Depends on Speed of Locomotion. The Journal of Neuroscience. 2009 29:7098-7109.

Dai Y, et al. Striatal Expression of a Calmodulin Fragment Improved Motor Function, Weight Loss, and Neuropathology in the R6/2 Mouse Model of Huntington’s Disease. J Neuroscience. 2009 September 16; 29(37):11550 –11559. Read Abstract

Dodge JC, et al. Intracerebroventricular infusion of acid sphingomyelinase corrects CNS manifestations in a mouse model of Niemann–Pick A disease. Experimental Neurology. 2009 215:349-357. Read Abstract

Hurlock EC, et al. Rescue of Motor Coordination by Purkinje Cell-Targeted Restoration of Kv3.3 Channels in Kcnc3-Null Mice Requires Kcnc1. The Journal of Neuroscience. 2009 December 16; 29(50):15735–15744. Read Abstract

Kim HA, et al. Motor impairments in a mouse model of Huntington’s with selective ablation of D-1 Receptor- Expressing neurons in the Striatum. 2009 Australian Neuroscience Annual Meeting.

Lubjuhn J, et al. Functional testing in a mouse stroke model induced by occlusion of the distal middle cerebral artery Journal of Neuroscience Methods. 2009 184:195-103.

Pallier PN, Drew CJG, Morton JA. The detection and measurement of locomotor deficits in a transgenic mouse model of Huntington’s disease are task-and-protocol-dependent: Influence of non-motor factors on locomotor function. Brain Res Bull. 2009 78:347-55.

Piesla MJ, et al. Abnormal gait, due to inflammation but not nerve injury, reflects enhanced nociception in preclinical pain models. Brain Res. 2009 1295:89-98. Read Abstract

2008

Cashman NR, et al. METHODS AND COMPOSITIONS TO TREAT AND DETECT MISFOLDED-SOD1 MEDIATED DISEASES WIPO Patent Application WO/2007/098607. 2008.

Oien DB, et al. MsrA knockout mouse exhibits abnormal behavior and brain dopamine levels. Free Radic Biol Med. 2008 45:193-200. Read Abstract

Rohe, MS. Role of SORLA in the brain and its relevance for Alzheimer disease. Dissertation to obtain the academic degree of Doctor of Natural Sciences (Dr. rer. Nat.) Lodged in the Department of Biology, Chemistry, Pharmacy, Free University of Berlin presented by Mr. Dipl.-Biol. Michael Stephen Rohe August 2008.

Tabata RC, Chu TLH, Shaw CA. Genome British Columbia in Collaboration with the Student Biotechnology Network Research Exchange. Stigmasterol glucoside is a putative Neurotoxin: Behavioral and Neuropathological Evidence. 2008: Program 24.

2007

Cabrera-Salazar MA, et al. Timing of Therapeutic Intervention Determines Functional and Survival Outcomes in a Mouse Model of Late Infantile Batten Disease. Molecular Therapy. 2007 10:1782–1788. Read Abstract

Cummings CJ, et al. Method of treating neurological disorders using clotrimazole and derivatives thereof. United States Patent Application. 2007 0037800. 2008.

Ganguly M, et al. Effects of acute chondroitinase treatment and training on functional recovery following moderate spinal cord injury in rats. Program No. 405.6/TT10. 2007 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience. 2007. Online.

Hampton TG, et al. Gait disturbances in BIO 14.6 and BIO TO2 dystrophic hamsters. 2007 Experimental Biology meeting [on CD-ROM]. Abstract #558.3, 2007.

Hampton TG, et al. Does your mouse walk strangely? Gait analysis in rodent models of neuromuscular disease. 2007 BIO International Convention meeting abstracts [Online]. Abstract #4.

Huntington J, et al. Hind limb locomotor recovery following spinal cord injury in the rat: Comparison of automated paw print analysis at different gait speeds, open field scores, and recovery time. Program No. 75.18/GG18. 2007 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience. 2007. Online.

Luo E, et al. Neurturin protects against gait impairment and induced unilateral neurodegeneration model. Program No. 265.3/T22. 200. Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience. 2007. Online.

Rane J, et al. Emotional and cognitive deficits observed in early stages of Parkinson’s disease. Program No. 445.1. 2007. Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience. 2007. Online.

Rommelfanger KS, et al. Norepinephrine loss produces more profound motor deficits than MPTP treatment in mice Proc Natl Acad Sci U S A. 2007 104:13804-9. Read Abstract

Theriault BR, et al. Gait analysis of mice emerging from isoflurane anesthesia. 58th AALAS National Meeting. Accepted Abstract, 2007.

Vincelette J, et al. Gait analysis in a murine model of collagen-induced arthritis. Arthritis Res Ther. 2007 9(6):R123. Read Abstract

Zinkhan G. Paw print gait analysis in rats with spinal cord injury. Doctoral Dissertation] Dallas (TX): The University of Texas Southwestern Medical Center at Dallas. 2007.

2006

Hampton TG, et al. Propranolol attenuates sympathetic hyperfunction, delays motor dysfunction, and prolongs life in a mouse model of amyotrophic lateral sclerosis. Eur Heart J. 2006 27(Supp.):2161. 2006. [Online], P5469.

Hampton TG, et al. See how they run: gait in blind mice. Program No. 12.9. 2006 Abstract Viewer/Itinerary Planner. Atlanta, GA: Society for Neuroscience. 2006.

Lee G, et al. Neurotoxic susceptibility in a mouse model of ALS2 as revealed by behavioral analysis. Program No. 671.4. 2006 Abstract Viewer/Itinerary Planner. Atlanta, GA: Society for Neuroscience. 2006.

Piesla MJ, et al. Neuropathic and inflammatory pain alters gait and constitutes a novel measurement of therapeutic efficacy in the rat. Program No. 553.7. 2006 Abstract Viewer/Itinerary Planner. Atlanta, GA: Society for Neuroscience, 2006.

Prior to 2005

Amende I, et al. Gait deterioration in the SOD1 G93A mouse model of ALS Program No. 131.13. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience. 2005. Online.

Hampton TG, et al. Gait deterioration in the SOD1 G93A mouse model of ALS. Program No. 131.13. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience. 2005. Online.

Hampton TG, et al. Gait dynamics in Trisomic mice: Quantitative Neurological Traits of Down Syndrome Physiology & Behavior. 2004 82:381– 389. Read Abstract

Hampton TG, et al. How to characterize gait dynamics in mouse models of neuromuscular disease. Program No. 22.60. 2002 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience. 2002. CD-ROM.

Huebsch KA, et al. Mdm muscular dystrophy: interactions with calpain 3 and a novel functional role for titin’s N2A domain. Hum Mol Genet. 2005 14:2801-11. Read Abstract

Kale A, et al. Early detection of gait abnormalities in the MPTP mouse model of Parkinson’s disease. Movement Disorders. 2005 Congress Abstract Program.

Kale A, et al. Gait dynamics in mouse models of Parkinson’s disease and Huntington’s disease. J Neuroengineering Rehabil. 2005 Jul 25;2:20. Read Abstract

Kale A, et al. Ethanol’s effects on gait dynamics in mice investigated by ventral plane videography Alcohol Clin Exp Res. 2004 28:1839-48. Read Abstract

Li S, et al. Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury. Mol Cell Neurosci. 2005 1:26-39.

Piskorski K, et al. Non-invasive physiology in conscious mice. 2002 Fourth World Congress Alternatives Congress Trust Proceedings. 2004. ATLA 32, Supplement 1:195–201. Read Abstract

Sharma N, et al. Impaired motor learning in mice expressing torsinA with the DYT1 dystonia mutation. J Neurosci. 2005 25:5351-5. Read Abstract

Wooley CM, et al. Gait analysis detects early changes in transgenic SOD1(G93A) mice. Muscle Nerve. 2005 32:43-50. Read Abstract

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Researcher, Imperial College National Heart and Lung Institute