Physical Therapy (13:30 ～16:00 Lecture Room 3)
Chaired by the academic adviser of each presenter

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DEVELOPMENT OF AN INSTRUMENT FOR MEASURING PATELLAR MOBILITY ANDITS CLINICAL APPLICATION
S. Ota1), M.Kawamura1)
1) Department of Physical Therapy, School of Health Sciences, Nagoya University, Nagoya, Japan

Introduction
Passive patellar mobility was believed to be one of theimportant forms of assessment for patient withpatellofemoral pain (PFP) and the decreased range of motion(ROM) at the knee joint. Moreover, it shows the laxity of theknee joint which could also contribute to sports knee injuries.
However, there is no methods to assess the quantitative
measurment of patellar mobility in clinical situation. Given
the need for objective measurements of patellofemoral (PF)joint impairments, we have developed a clinical device(patellofemoral joint arthrometer [PFA]) to quantify mediolateral patellar displacement.
The purposes of this research were 1) to assess the validyof prototype PFA, 2) to apply PFA to the person with PF andto compare with the healthy subjects, 3) to investigate therelationship of patellar mobility and knee ROM after total
knee arthroplasty (TKA).
Materials and Methods
Study 11)
Subjects: A total of 26 individuals (24 females and 2
males) participated, and 14 were asymptomatic with PFP.
The average ± SD age, height and body mass of theparticipants was 27 ± 4 years, 164 ± 5 cm, and 59 ± 8 kg,
respectively. Twelve of the participants had a current historyof patellofemoral pain at the time of testing, while 14 wereasymptomatic.
Methods: A custom designed prototype PFA was used toassess the amount of lateral patellar displacement. PFA wassecured to the femoral condyle, and the femur was refer tothis measurement. The adjustable arm allowed the medial
border of the patella to be localized in the frontal plane withrespect to the fixed ruler. Subjects were measure thedisplacement of lateral patella between quadriceps relaxed
and isometirc contracted by PFA. Following assessment oflateral patellar displacement using the PFA, participants
underwent MRI of the patellofemoral joint. The sameprocedures of using PFA was performed on using MRI.
Bisect offset index and patellar tilet angle was measured thetrue lateral patellar displacment. The comparion of thesepatellar mobilities using both methods was performed as thevalidity study.
Study 22)
Subjects: The study comprised 22 females with PFP (PFP
group) and 22 females who had no knee pain (control group)
who were matched to the subjects with PFP based on age,height, and body mass index.
Mehtods: Patellar mobility was measured objectively
using PFA. Measurements of lateral and medial patellar
displacement, patellar mobility balance (lateral minus medialpatellar displacement), lateral patellar mobility index (LPMI:
lateral patellar displacement/ patellar width), and medialpatellar mobility index (MPMI: medial patellar displacement/
patellar width) were used.

Figure 1. Patellofemoral arthorometer

Figure 2. Initial positon of the patellar mobility (set 0 mm ofthe digital caliper)
The PFA was clamped to the femoral condyles aligned
parallel to the table. The digital caliper was positioned at anangle of 90 degrees to the line between the center of the patella
and the ASIS using the plane adjuster. Before each subject wasmeasured, the amount of force (approximately 80N) to be used
to move the patella for testing was practiced using a hand-helddynamometer, MicroFET2 (Hoggan Health Industries Inc.,
West Jordan, UT) to enable the examiner “to feel” what it was
like to apply an 80N force. For testing, relaxation of themusculature was confirmed by palpation of the quadriceps andpassively moving the patella in the lateral and medial
directions.17 To measure lateral patellar mobility, the lateralborder of the patella was palpated and located with a laser using
the adjustable laser module arm, and the digital caliper was
zeroed, setting this point as the initial position. Lateraldisplacement of the patella was then achieved by manuallypushing the patella laterally (applying approximately 80N offorce), at which point the lateral border of the patella was again

PT-1located by sliding the laser module arm on the caliper andreading the measurement. Medial passive patellar mobility
was assessed in the same manner except for the force
application being applying toward the medial direction. Allof these procedures for passive patellar mobility were
performed by the same tester for all subjects.
Study 33)
Subjects: Fifty-one patients [osteoarthritis (OA) group:
34 knees; rheumatoid arthritis (RA) group: 22 knees] were
examined after TKA.
Methods: Patellar mobility was measured preoperatively
and 1, 2, and 6 months postoperatively using a patellofemoral
arthrometer (PFA) fixed to the femoral condyles to measure
medial and lateral patella displacement at 30 degrees of knee
joint. Knee joint ROM was also measured in each of these 4
sessions.
All participates in these studies were approved by each
Ethics Committee of the University of Southern California
and the school of Health Sciences, Nagoya University.
Data analysis: Patellar mobility was measured threetimes, and the averages of the displacements were used inthese studies.
For the validity study was used intra-class correlation(ICC2,k), and t test was performed to compare thedisplacements between PFP group and control group in study
2. For the analysis of the relationship between patellar
mobility and ROM in the study 3 were used the Pearson
correlation. The differences between each session was using
ANOVA and Tukey’s procedure. Significance was set at
P<0.05.
Results
Study 1: The ICC assessing the level agreement between
the MRI and PFA measures of lateral patellar displacement
was good (0.86). Excellent intratester (ICCs of 0.96 and0.97) and intertester reliability (ICC 0.92) was demonstrated.
Study 2: Lateral and medial patellar mobility values were
not significantly different between the individuals in the PFP
and control groups. When normal patellar mobility wasarbitrarily defined as the average ± 2SD based on the datafrom the control group, normal lateral patellar displacement
was within a range of 7.2 to 17.6 mm and normal medialpatellar displacement was within a range of 6.8 to 14.0 mm.
Study 3: In the OA group, lateral patellar mobility was
positively correlated with knee flexion angle, while there wasno correlation between medial patellar mobility and knee
flexion angle. Knee joint extension was not correlated witheither lateral or medial patellar mobility. In the RA group,
both lateral and medial patellar mobility were positively
correlated with knee joint flexion/extension 1 and 2 months
after TKA.
Although, knee ROM were significantly improved from 1
month to 6 months after TKA, medial and lateral patellar
mobility were not improved.
Discussion
From the study 1, the validity of the prototype PFA
compared to MRI method was acceptable range in theclinical application. This prototype was made ofpolyethylene for using in side of MR imaging.
Study 2 was introduced to PFA to apply the clinicalevaluation. PFA was adjusted the patellar mobility using
equipped the adjustable lever, lever joints and laser. Based on

an arbitrarily defined normal range of values calculated using
the mean ± 2SD of the patellar displacements measured for theindividuals in the control group, we note that the distribution of
the data points are very similar between the 2 groups, with only
few subjects with PFP falling outside what we considered anormal range of scores. From the results of this study, abnormal
patellar mobility might not be a factor in female adults withmild symptoms of PFP.

Figure 3. Changes of knee flexion angle and patellar
mobility in OA group
In the study 3, although patellar mobility was shown to berelated to knee ROM after TKA, there were differences in therelationship between OA and RA groups. In both groups, lateral
patellar mobility was positively related to knee flexion angle 1
and 2 months after TKA. In the OA group, knee extension was
not associated with patellar mobility, while lateral and medialpatellar mobility were related to knee ROM (flexion andextension) after TKA in the RA group. Although these features
should be taken into consideration in planning of physicaltherapy treatment regimens to improve patellar mobility after
TKA, the relations identified in the present study represent only
cross-sectional findings. However, our findings demonstrated
that medial and lateral patellar mobility had no sufficientlongitudinal relationship with knee ROM after TKA.
Conclusions
We have developed PFA to asess the patellar mobility
quantitatively, and we apllied it to patients with PFP and after
TKA. The patellar mobility might not be a factor in thisresearch sujects with PFP (mild symptom). The knee ROM after
TKA could not be related to medial and lateral patellar
displacement. This study woulbe a framework for a future
clinical trial on patellar mobility in patient with knee disorder.
References[1]Ota S, Ward SR, Chen YJ, Tsai YJ, Powers CM. Concurrent
criterion-related validity and reliability of a clinical device
used to assess lateral patellar displacement. J Orthop Sports
Phys Ther. 2006;36(9):645-652.
[2]Ota S, Nakashima T, Morisaka A, Ida K, Kawamura M.
Comparison of Patellar Mobility in Female Adults With andWithout Patellofemoral Pain. J Orthop Sports Phys Ther.
2008;38(7):396-402.
[3]Ota S, Nakashima T, Morisaka A, Omachi T, Ida K,
Kawamura M. Is latero-medial patellar mobility related to
the range of motion of the knee joint after total knee
arthroplasty? Manual Therapy. 2010 (in press)
Author address

E-Mail: s-ota@met.nagoya-u.ac.jp

PT-1

CD105 POSITIVE MESENCHYMAL STEM CELLS FROM MOUSE ES CELLSSHOW HIGH POTENTIAL FOR DIFFERENTIATION
N. Ninagawa1), E. Isobe2), R. Murakami2) and S. Torihashi1), 2)
1) Program in Physical and Occupational Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan
2) Department of Physical Therapy, School of Health Sciences, Nagoya University, Nagoya, Japan
Introduction
Mesenchymal stem cells (MSCs) have a potential todifferentiate into any mesenchymal cell type such as
osteocytes, chondrocytes, adipocytes and muscular cells.
Recently, adipose tissues are indicated as a useful and richsource of adipose tissue-derived mesenchymal stem cells(ADSCs). Although ADSCs have therapeutic efficiency inrepairing damaged mesenchymal tissues, isolation andpurification of ADSCs from adult adipose tissue still requires
complicated and troublesome processes[1,2]. Mouseembryonic stem cells (ES cells) are pluripotent, and theirinduction to adipogenesis has been well described[3,4]. We
initially supposed that MSCs would differentiate through theprocess of adipogenesis from undifferentiated ES cells(Figure 1). The aim of this study was to establish a method
for the induction and collection of MSCs using a typical cellsurface marker CD105 through adipogenesis from ES cells
without genetic manipulation.

Results
Appearance and Sorting of CD105+ Cells
After 10 days of induction to adipogenesis, small, round
CD105+ cells appeared, began to increase, and reached theirmaximum population on day 14. After that adipocytes thenincreased and CD105+ cells alternately decreased. Since double
staining with CD105 and BODIPY demonstrated that
adipocytes did not express CD105, sorting by MACS wasusually carried out on day 14. The efficiency of sorting by
MACS was confirmed by FACS analysis, and more than 91%
of cells were CD105+ after MACS separation. Sorted CD105+
cells were uniformly bipolar in a shape similar to that of the
ADSCs previously reported.
Differentiation Potential of CD105+ cells to Mesenchymal
lineages in vitro
CD105+ cells showed a high potential for differentiation into
mesenchymal cells in vitro, when both CD105+ and CD105cells were induced to mesenchymal cells and compared witheach other. After induction of adipogenesis, almost all CD105+
cells differentiated into adipocytes. CD105- cells, however, did
not produce large Oil Red O-positive oil droplets. CD105+ cells
turned Alizarin Red-positive after induction of osteogenesis.
The CD105- cells did not survive under the condition of
osteogenesis and disappeared. Under the pellet culture forchondrogenesis, the CD105+ cells formed small ball likeaggregations. When a cryo-section of the aggregations was
stained with Alcian blue, the matrix surrounding thechondrocytes turned blue. The matrix produced by CD105+
cells also expressed collagen type II immunoreactivity, while
the CD105- cells did not form cell aggregations and were notstained with either Alcian blue or anti-collagen type II antibody.
When CD105+ cells differentiated into skeletal muscle cells,
they became thin and fibrous, and began to express M-cadherin.
They ran in the same direction and distributed parallel to eachother. They finally constructed sarcomeres exhibiting bands
with myosin and actin filaments regularly arrayed.
A few CD105- cells expressed M-cadherin immunoreactivity,
but they did not form myotubes under the same condition.

Materials and Methods
ES cells (G4-2; kind gifts from Dr. Niwa) carrying theenhanced green fluorescent protein —EGFP— gene under
the control of cytomegalovirus/chicken β-actin promoter
were expanded their population and embryoid bodies (EBs)were formed in hanging drops. EBs were cultured in aretinoic acid containing medium. After washing, they weresettled on culture dishes and maintained with adipogenesis
medium (insulin / triiodo-thyronine). After the increase ofCD105+ cells, we isolated and sorted them by a magnetic
cell sorter (MACS; Miltenyi). Purification of CD105+ cells
using MACS was confirmed by flow cytometry (FACS).
CD105+ cells were then differentiated into mesenchymal
cells such as adipocytes, osteocytes, chondrocytes, andskeletal muscles. Differentiation was examined by oil red O,
alizarin red, alcian blue, and M-cadherin and/or skeletal
muscle myosin heavy-chain (MHC) immuno-staining,respectively. Expression of each cell type-specific mRNA
was analyzed by RT-PCR. Obtained CD105+ cells were theninjected into tibialis anterior muscles of immunodeficient(SCID) mice to demonstrate their potential for differentiationin vivo.

Adipogenesis

CD105(endoglin)
Osteogenesis

Magnetic Cell Sorting（MACS）

MSCs

Chondrogenesis
Musculogenesis

ES cells

Adipogenesis

Adiposecells

Fig. 1 Schematic view of the induction and isolation of MSCs from ES cells
PT-2Potential of CD105+ cells for differentiation into
mesenchymal cells was confirmed as well by the expressionof their specific mRNAs detected by RT-PCR.
After the induction of adipocytes and the formation of lipid
droplets, CD105+ cells expressed PPAR-γ and LPL mRNAs.
Following the formation of osteogenic cells, they displayed
both Runx-2 and Osterix mRNAs. The small ball-likestructures observed after the induction of chondrogenesis
expressed Collagen2 and agglycan mRNAs. Skeletal muscle
cells differentiating from CD105+ cells expressed Myogenin,
M-cadherin, MyoD and Myf5 mRNAs.
Differentiation Potential in vivo; Transplantation to
Immunodeficient (SCID)Mice
Potential for differentiation into mesenchymal cells in vivo
was examined by transplantation to SCID mice. CD105+
cells were transplanted into injured tibialis anteriol muscles
24 hours after clamping. Transplanted cells located at the
injected area were clearly distinguished from host cells by
their EGFP immunoreactivity. After 1 week oftransplantation, EGFP-positive cells showed M-cadherin
immunoreactivity. Some of them express MHC
immunoreactivity. Their nuclei were located at the center ofthe cells and occasionally appeared as multinuclear cells in
the cross section. After 2 weeks of transplantation, EGFP and
MHC-double positive cells increased and became large
enough to involve several nuclei in the cross section. Fromthe HE staining, many blood vessels invaded the colony oftransplanted cells. Flk1-positive cells indicated angiogensis.
Discussion
Expression and Specificity of CD105
CD105, also know as endoglin, is a homodimeric typetransmembrane glycoprotein that binds to TGF-β1 and TGFβ3 to form a receptor complex comprised of TGF-β receptors
I and II. TGF signaling plays important roles in cell growth,differentiation and migration, and is also known as afunctional marker for the isolation of mesenchymal stem
cells including ADSCs. Almost all reports describing
mesenchymal stem cells have demonstrated the expression of
CD105 on the cell surface, further gene expression profilesof mesenchymal stem cells have involved CD105 [2,5]. Afterthe completion of adipogenesis, mature adipocytes did not
express CD105. This indicates that only stem cells orprogenitor cells express CD105, whereas mature
mesenchymal cells themselves lose the expression. Therefore,
CD105 was confirmed as a useful marker to separate andcollect mesenchymal cells in our system. The isolation
efficiency rate by MACS was more than 91%. This was
further enhanced using a technique of adhesion separation
after sorting by MACS.
Potential of Differentiation into Mesenchymal Cells invitor and in vivo Indicates MSCs
CD105+ cells demonstrated a high potential fordifferentiation into mesenchymal-type cells, i.e., adipocytes,
chondrocytes, osteogenic cells and skeletal muscles in vitro
and in vivo. Their differentiation potential indicates that
CD105+ cells were mesenchymal stem cells (MSCs). Our
MSCs were easily differentiated into skeletal muscles,
though ADSCs have been described as hardly differentiating
into muscles [6]. In general, the requirement of the provision
for specific ADSCs does not in fact involve the potential forskeletal muscle differentiation [2]. The prominent potentialof our MSCs to differentiate into skeletal muscle probably
depends on the medium containing insulin and T3 for

adipogenesis before sorting by MACS. Skeletal muscle cells are
sensitive to insulin and the IGF family as growth factors. IGF-II
promotes myogenesis through Rho-ROCK activity and induces
myoD1 [7]. The receptors of insulin and/or IGFs may be highly
expressed before induction of myogenesis in our MSCs. Culture
conditions generating our MSCs showed advantages overmyogenesis in our method.
Transplantation to the injured tibialis anterior muscles
differentiated MSCs into skeletal muscles in vivo. This suggestthat the fate of MSCs ultimately depends on their microenvironments as already described [2]. Induction factors fromhost tissues surrounding MSCs regulate their differentiation intoa certain mesenchymal cell type. Further studies of themolecular mechanisms of differentiation into specificmesenchymal cell type by MSCs should advance the MSC celltherapies.
Conclusions
We developed MSCs with a high potential fordifferentiation into mesenchymal cell lineages, including
skeletal muscles in vitro from ES cells using CD105 as a cellsurface marker without gene manipuration. Depending on theirsurrounding micro-environments in vivo, MSCs differentiatedinto skeletal muscles of injured tibialis anterior muscles. All
properties of our MSCs proved very beneficial to cell-derived
regeneration and therapeutic usage.
References[1]Izadpanah R, Trygg C, Patel B, Kriedt C, Dufour J, Gimble
JM, Bunnell B A. Biologic properties of mesenchymal stem
cells derived from bone marrow and adipose tissue. J Cell
Biochem. 2006;99:1285-1297.
[2] Schäffler A, Büchler C. Concise review: adipose tissuederived stromal cells--basic and clinical implications for novel
cell-based therapies. Stem Cells. 2007;25:818-827.
[3] Kawaguchi J. Generation of Osteoblast and Chondrocytes
from Embryonic Stem Cells. In: Turksen K, ed. Embryonic
Stem Cell Protocols Differentiation Models. Second Edition.
Totowa, NEw Jersey: Humana Press Inc. 2007; 135-148.
[4] Dani C, Smith AG, Dessolin S, Leroy P, Staccini
L,Villageois P, Darimont C, Ailhaud G. Differentiation ofembryonic stem cells into adipocytes in vitro. J Cell Sci.
1997;110 ( Pt 11):1279-1285.
[5] Trivedi P, Hematti P. Derivation and immunologicalcharacterization of mesenchymal stromal cells from humanembryonic stem cells. Exp Hematol. 2008;36:350-359.
[6] Bunnell BA, Flaat M, Gagliardi C, Patel B, Ripoll C.
Adipose-derived stem cells: isolation, expansion anddifferentiation. Methods. 2008;45:115-120.
[7] Wilson EM, Rotwein P. Control of MyoD function duringinitiation of muscle differentiation by an autocrine signaling
pathway activated by insulin-like growth factor-II. J Biol
Chem. 2006;281:29962-29971.
Author address
E-Mail: ninagawa.nana@b.mbox.nagoya-u.ac.jp

PT-2

EFFECTS OF FORCED IMPAIRED FORELIMB USE ON CENTRAL NERVOUS SYSTEMAFTER SMALL INTERNAL CAPSULE HEMORRHAGE IN RATS
A. Ishida1), 2), M. Hamakawa1), K. Tamakoshi1), H.Nakashima1), H.Shimada1), H. Hida2), K. Ishida3)
1) Program in Physical and Occupational Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan
2) Neurophysiology and Brain Science, Nagoya City University Graduate School of Medicine, Nagoya, Japan
3) Department of Physical Therapy, School of Health Sciences, Nagoya University Nagoya, Japan
Introduction
Forced impaired forelimb use (FLU) is known as aneffective method to promote functional recovery of theaffected forelimb after hemiplegic stroke (e.g., constraintinduced movement therapy) [1,2]. However, the detailed
mechanism of FLU effect on the brain was still unclear. In
this study, we investigated whether FLU induces functional
recovery after small intracerebral hemorrhage (ICH) and how
the dominant use induces improvement of motor functions.
Materials and Methods
Experimental setup: Adult male Wistar rats (250-300g)
were housed at a 12 h light/dark cycle with food and water ad
libitum. Rats were randomly assigned to four groups: ICH(n=8), ICH-FLU (n=9), Sham (n=5) and Sham-FLU (forcedpreffered limb use: n=6). All experimental procedures were
performed in accordance with the animal care guidelines of
the Nagoya University. Figure 1 shows a timeline of theperformed experiments.
Intracerebral hemorrhage: In the present study, we usedinternal capsule hemorrhage model [3]. Under deep
anesthesia, 1.4 μl Collagenase (15 Units/ml, Type IV;
Sigma-Aldrich, St. Louis, MO, USA) were injected into theinternal capsule contralateral to the preferred forepaw. Figure
2 shows a typical histological appearance of hemorrhage.
Forced-impaired limb use: FLU-treated animals werefitted with a 1-sleeve plaster cast 24hrs after ICH surgery.
The upper torso and the unimpaired/unpreferred forelimbwere wrapped in soft felt and Plaster of Paris strips. Rats
were forced to completely rely on either their
impaired/preferred forelimb for 1 week.
Behavioral assessment: After restraint, rats were assessedvarious forelimb motor functions, such as skilled reaching(assessed by single pellet reaching test), coordinated forelimb
stepping (by ladder test), spontaneous use of the impaired
forepaw (by cylinder test), and tactile-evoked forelimb
placing (contact placing response). Figure 3 shows theappearances of these tests. Assessment was carried out at
postoperative day 10-12 and 26-28. Before ICH, single pellet
reaching test and ladder test were pre-trained and determinedbaseline performance.
Lesion volume: After the completion of behavioral testing,all animals were deeply anesthetized and perfusedtranscardially with 0.9% saline followed by 4% phosphatebuffered paraformaldehyde (pH 7.4). The brains were
removed and postfixed, and then 40 μm thick coronal
sections were obtained using a cryostat. These sections were
processed with hematoxyline–eosin staining and volume oflesion was determined.
Retrograde labeling of corticospinal tract: An additionalgroup of rats (ICH; n=6, ICH-FLU; n=6, Sham; n=9) wasused for quantification of the remaining corticospinal tract.
After same FLU treatment, animals were anesthetized andtheir spinal cords were exposed at the C6–C8 level using
laminectomy. 4% fluorogold (FG; Biotium, Hayward, CA)
was injected into the spinal cord with a glass micropipette.

Each animal had four injections of 250 nl of FG spaced at 0.5mm, along the spinal cord (0.75 mm lateral from the midline
and 1.2 mm below the spinal cord surface). Seven days after
injection, animals were perfused and processed forcryosectioning. Series of 30 μm brain cross sections (with 180
μm gaps) were used for quantification of labeled cells.
Real-time PCR: Separate cohorts of animals exposed to thesame FLU treatment were used for quantitative transcription
polymerase reaction (PCR) analysis (ICH; n=6, ICH-FLU; n=6,
Sham; n=6, Sham-FLU; n=6). Sensorimotor cortex forelimb
region harvested at the end of the FLU period was analyzed byreal-time PCR of brain-derived neurotrophic factor (BDNF) andgrowth-associated protein 43 (GAP43).
Statistical analyses: One-way ANOVA followed by aTukey post hoc test was used for statistical analyses of
behavioral tests, FG-positive cell number, and real-time PCR
assay. Student’s t-test was used for lesion volume. All statisticalanalyses were conducted using the statistical software SPSS
(release 12.0). Data are presented as means ±SEM.
Results
Behavioral assessment: After FLU treatment, improvementof the skilled reaching task in single pellet reaching test was
found in the ICH-FLU in comparison with ICH rats.
Additionally, the reaching style of ICH-FLU group was morenormally than ICH group. Better performance of skilled
stepping in ladder test was also shown in the ICH-FLU groupthan ICH group. However, no significant differences were
found in cylinder test and contact placing response amongexperimental groups.
Lesion volume and remaining corticospinal tract: Injectionof low-dose collagenase caused small hemorrhage localized theinternal capsule (see figure 2). However, lesion volume was notdifference between ICH and ICH-FLU group. In parallel, thenumber of FG-positive neurons in sensorimotor cortex
decreased significantly after ICH, but FG-positive neuron
number was similar between ICH and ICH-FLU group.
Real-time PCR: BDNF and GAP43 are known as growthpromoting factor and involved plastic change of central nervous
system. After FLU treatment, mRNA expression of BDNF and
GAP43 was significantly enhanced in ICH-FLU animals
compared with ICH and Sham animals. These changes were
found in the sensorimotor cortex contralateral side to the forceduse side forelimb (ipsilateral side to collagenase injection), but
not in ipsilateral side (contralateral to injection).
Discussion
In this study, we demonstrated early FLU promotefunctional recovery of the skilled movement of forelimb(reaching, ladder stepping). Furthermore, upregulation of BDNF
and GAP43 was shown in the sensorimotor cortex contralateral
to the forced-use forelimb. These data suggested that usedependent plastic alterations in the forelimb sensorimotor area
would be induced by FLU after ICH, causing skilled functional
recovery with relation to enhanced expressions of BDNF and
GAP-43.

PT-3

In addition, brain lesion volume and damage ofcorticospinal tract were mostly unchanged by early FLU.
Some previous research has reported immediate FLU after
cortical insult enlarged lesion volume and exaggeratedfunctional recovery [4,5]. In this study we used subcorticallesion model, therefore these discrepancy might be related topathological conditions (cortical vs. subcortical lesion).

A

Conclusions
Forced-use of impaired forelimb after capsularhemorrhage induced better recovery of skilled reaching andstepping of the impaired limb. This functional recovery
might be related use-dependent alterations of the growthpromoting factors expression in the sensorimotor cortex.
References[1]Wolf SL, Winstein CJ, Miller JP, Taub E, Uswatte G,
Morris D, Giuliani C, Light KE, Nichols-Larsen D. Effectof constraint-induced movement therapy on upper
extremity function 3 to 9 months after stroke: the
EXCITE randomized clinical trial. JAMA. 2006; 296:
2095-104.
[2]Maier IC, Baumann K, Thallmair M, Weinmann O, SchollJ, Schwab ME. Constraint-induced movement therapy in
the adult rat after unilateral corticospinal tract injury. J
Neurosci. 2008;28:9386-403.
[3]Masuda T, Hida H, Kanda Y, Aihara N, Ohta K, Yamada
K, Nishino H. Oral administration of metal chelator
ameliorates motor dysfunction after a small hemorrhage
near the internal capsule in rat. J Neurosci Res.
2007;85:213-22.
[4]Kozlowski DA, James DC, Schallert T. Use-dependent
exaggeration of neuronal injury after unilateral
sensorimotor cortex lesions. J Neurosci. 1996;16:4776-86.
[5]Dromerick AW, Lang CE, Birkenmeier RL, Wagner JM,
Miller JP, Videen TO, Powers WJ, Wolf SL, Edwards DF.
Very Early Constraint-Induced Movement during Stroke
Rehabilitation (VECTORS): A single-center RCT.
Neurology. 2009;73:195-201.
Author address

E-Mail: ishida.akimasa@c.mbox.nagoya-u.ac.jp

Figure 1. Timeline of the experiments

C

B

D

E

F

G

Figure 3. Behavioral tests(A-B) Single pellet reaching test: A shows the apparatus of
single pellet reaching test. Reaching to retrieve pellets through anarrow slit by their impaired forelimb was analyzed (B).
(C-D) Ladder test: Crossing the 1-m long ladder was videotaped
and assessed the rate of correct step and fall. C demonstrated
correct step (midportion of limb placed on rung) and D showed
fall.
(E) Cylinder test: Rats were placed in a plexiglas cylinder 5min,and the percentage of the impaired limb use when touching thecylinder wall was analyzed.
(F-G) Contact placing response: Rats were held with theforelimb suspended, and advanced until the dorsum of theforepaw touched the edge of a table (F). Normally, rats show aplacing response by extending the forepaw digits and putting
them on the table (G).

Figure 2. Typical photograph of internal capsulehemorrhage
Hematoxylin and eosin staining 30 days after ICH shows
small hemorrhage localized the internal capsule (arrow).

PT-3

RECURRENT RISKS AFTER MILD ISCHEMIC STROKE IN A JAPANESE POPULATION
Yuji Kono1), Sumio Yamada2), Kenta Kamisaka3), Amane Araki4), Yusuke Fujioka4),
Keizo Yasui4), Yasuhiro Hasegawa4), Yasuo Koike2)
1) Program in Physical and Occupational Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan
2) Department of Physical Therapy, School of Health Sciences, Nagoya University, Nagoya, Japan
3) Rehabilitation Center, The Tazuke Kofukai Kitano Hospital, Osaka, Japan
4) Department of Neurology, Nagoya Daini Red Cross Hospital, Nagoya, Japan

Materials and Methods
Subjects: From December 2005 to September 2006,
patients with acute TIA or IS who met criteria of modified
Rankin Scale 0~2, no communication disability andemergent admission to a sophisticated acute hospital in
Nagoya city district were consecutively enrolled in this study.
Patients with age over 80 years old, cardiogenic stroke,
severe dementia, psychiatry disorder and extracorporenal
dialysis were excluded. During hospitalization, we assessed
sex, family history, age, height, weight, stroke subtype, bloodpressure, lipid profile, fasting glucose, HbA1c, smoking,alcohol consumption, exercise habits, waist circumference,
and ankle-brachial pressure index (ABI). And we also
assessed physical activity and salt-intake at 3 month after
discharge. We divided into 4 groups followed by physicalactivity and salt intake. Primary outcome was recurrence ofstroke or other vascular events such as myocardial infarction,
angina pectoris, and peripheral artery disease during 3 years.
Statistical analysis: Continuous variables are expressed asmeanstandard deviation (SD). Univariate associations
between pathophysiological / lifestyle factors and recurrence
were assessed using Kaplan–Meier survival analysis, andsignificance was determined using the log rank test with
continuous variables analyzed as median value. Hazard ratios(HRs) for recurrence were determined by univariate Cox
proportional hazards regression analyses and variables with a
P value of <0.1 at univariate analysis were entered into a
multivariate Cox model to determine HRs. All statisticalanalyses were performed with the SPSS 16.0 software
package (SPSS Japan, Tokyo, Japan), and a P value of <0.05
was considered significant.

・Outcome at 3 years
Figure 1 shows the Kaplan–Meier estimates of cumulative
recurrence rates of stroke for all subjects. Twenty-five out of
102 patients (24.5%) had stroke recurrence, 4 (3.9%) had acoronary event, 2 (2%) died due to cancer, and 1 (1%) had no
fixed residence. Eight patients of the 25 who had recurrent
strokes had a severe stroke (mRS ≥ 3).

・Pathophysiological factors
In univariate analyses in patients with LVD, abnormal ABI
and MetS were significantly associated with higher recurrence
rates. In multivariate Cox regression analyses, LVD (HR:2.81,
CI:1.13-6.96, P=0.025), abnormal ABI (HR:3.30, CI:1.33-8.20,
P=0.009) and MetS (HR:2.67, CI:1.23-5.80, P=0.013) wereselected as significant independent predictors for strokerecurrence or cardiovascular events.

・Lifestyle factors
In univariate analyses, higher salt intake was associated withhigher recurrence (HR: 2.43, CI:1.04-5.68, P=0.040) and lower
physical activity tended to be associated with higher
recurrence(HR: 1.10, CI: 0.36 - 3.33, P=0.076). When divided
into four groups, the poor lifestyle management group was
associated with higher stroke recurrence (HR:1.62, CI:1.10-2.39,
P=0.013). In multivariate Cox regression analyses, the poor
lifestyle management group remained associated withrecurrence. Kaplan–Meier survival curves for lifestyle
management are presented in Figure 2.

Cumulative recurrence rate

Introduction
The high rate of stroke recurrence during several years
after first ever stroke has suggested in Hisayama study inJapan. Furthermore, the 70% of ischemic stroke patients havemild motor paresis. However, stroke recurrence has notstudied depends on the severity of the paresis, so precise datain the recurrence rate and predictive variables for strokerecurrence in mild stroke remained unknown. Threfore, This
study aimed to estimate 3 year cumulative recurrence rates
and identified independent predictors of vascular events after
TIA and mild ischemic stroke (IS).

60%

Recurrence rate
1 year : 18.9%
2 year : 23.8%
3 year : 29.0%

40%

20%

0%
0

Results
・Study population
A total of 102 patients (78 men and 24 women) weresuccessfully followed for 3 years. The mean follow-up period
was 1134±80 day. The mean age at study entry was 65.0±
10.5 years.

200

400 600 800
Day from onset

1000 1200

Figure 1.
Kaplan–Meier estimates of cumulative recurrence rates ofstroke. Deaths without stroke recurrence were censored.

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LS Groups
Step ＜5800steps, Salt ＞10.7g
Step≧5800steps, Salt ＞10.7g
Step＜5800steps, Salt ≦10.7g

Cumulative recurrence rate

60%

Step≧5800steps, Salt ≦10.7g

40%

P=0.037

20%

0%
0

200

400
600
800
Day from onset

1000

1200

Figure 2.
Kaplan–Meier estimates of cumulative recurrence rates
of stroke according to lifestyle management.
Discussion
The results of the present study showed thatapproximately 30% of mild ischemic stroke patients
experienced vascular events during the 3 years after onset.
To our knowledge, this report is the first study todemonstrate the high recurrence rate in Japanese patientswith mild strokes. Moreover, the findings of this study
provide several predictive risk factors which include not only
pathophysiological factors but lifestyle factors for vascular
events.
In the present study, the 3-year risk of recurrence after
mild stroke was approximately 30%, exceeding the 10% to
20% rates reported in previous community-based studies
which included mild to severe stroke. There might be several
reasons for this discrepancy. First, a high proportion of LVD
in the present study might have influenced the recurrence rate.
For the background behind this higher recurrence rate,increasing prevalence of recurrent risk factors may raise therate of recurrence. These risk factors have gradually
increased during the past decade in Japanese population.
Secondly, race may be a possible reason for high strokerecurrence. High stroke recurrence results in increase of
severity of the effects of stroke. Indeed, approximately 30%
of cases of stroke recurrence in the present study resulted insevere disability.
Pathophysiological factors for recurrent predictors
The results of the present study indicated that abnormal
ABI, MetS and LVD were independent predictive factors for
3-year vascular events. This suggests that advances ofarthrosclerosis or complexity of traditional risk factors are
essential for moderate-term vascular events in mild stroke.
Low ABI, a subclinical marker for lower extremity
arterial disease. Previous study showed that ABI is inversely
related to traditional risk factors for vascular disease andrepresents a marker for atherosclerotic changes in othervascular beds. Thus the etiology of abnormal ABI isatherothrombosis. Prevalence of abnormal ABI with otheratherothorombosis like stroke in this study has reported toresult in poor prognosis. The findings of this study are in linewith these previous reports, suggesting abnormal ABI can bea powerful prognostic factor for stroke recurrence in mild stroke.
MetS shows that obesity with visceral fat accumulation
closely associates with atherosclerotic vascular events.
Moreover visceral fat obesity is closely related to adipose tissue.
Several studies have demonstrated that adipose tissue actively
produces a variety of locally and systemically functioning
bioactive molecules, including tumour necrosis factor-α,
plasminogen-activator inhibitor type-1 and adipocytokine, that
also interact in cardiovascular diseases. Especially, adiponectine
and leptine effect on increase blood pressure, sympathetic
nervous system activity, and expressed within atherosclerotic
plaques.[1]Lifestyle factors for recurrent predictors
High salt intake and lower physical activity were also
indicated as independent predictive factors for stroke recurrence.
This result highlights that lifestyle modification can help toprevent vascular events. Results from Japanese populationbased prospective cohort studies have showed significant
associations between salt intake and stroke incidence[2]. As
reported in a previous study, stroke mortality has a strong
relationship to dietary salt intake independent of blood pressure.
The mechanism responsible for the association between salt
intake and strokes is still unknown, but may be related to arterythickness, stiffness and platelet reactivity.
Physical activity also tended to be associated with strokerecurrence. In a meta-analysis, lower physical activity had a
33% higher risk of stroke incidence compared with more active
individuals[3]. Although the association between physicalactivity and strokes has not been well established, it has beenclearly demonstrated that insulin resistance and HDLcholesterol, which contribute to prevent the progression ofatherosclerosis, are related to higher physical activity.
Improvement of endothelial dysfunction by exercise is also
other possible mechanism for the prevention of strokerecurrence.
Conclusions
The findings of the present study suggest that the recurrence
rate in mild strokes has increased in conjunction with increased
prevalence of cardiovascular risk factors. The results alsosuggest that risk reduction through a combination of medicationand lifestyle intervention will improve this higher recurrence
rate.
Reference[1] Okamoto Y, Kihara S, Funahashi T, Matsuzawa Y, Libby P:
Adiponectin: a key adipocytokine in metabolic syndrome.
Clin Sci (Lond). 2006;110:267-278[2] Takachi R, Inoue M, Shimazu T, et al: Consumption of
sodium and salted foods in relation to cancer andcardiovascular disease: the Japan Public Health Center-based
Prospective Study. Am J Clin Nutr. 2010;91:456-464[3] Lee CD, Folsom AR, Blair SN: Physical activity and stroke
risk: a meta-analysis. Stroke. 2003;34:2475-2481
Author: Yuji Kono

E-Mail: el-condor-pasa@tiara.ocn.ne.jp
Corresponding Author: Sumio Yamada

E-Mail: yamadas@met.nagoya-u.ac.jp

PT-4

LOCOMOTOR IMAGERY TRAINING IMPROVES GAIT PERFORMANCE IN PEOPLE
WITH CHRONIC HEMIPARETIC STROKE
Su-Jin Hwang1), Hye-Seon Jeon1), Chung-hwi Yi1), Oh-Yun Kwon1), Sang-Hyun Cho1), Sung-Hyun You1)
1) Department of Physical therapy, College of Health Sciences, Yonsei University, Kangwon-do, Korea

Introduction
Motor imagery practice is an active practice in which thepatient imagines or visualizes the performance of a function, amovement, or a task without overt physical therapy.11
Beneficial effects of motor imagery practice have been
supported through studies of brain-imaging. The same areas of
the central nervous system are activated during real
performances and during motor imagery practice of theequivalent tasks.12,13 Neuroplasticity of motor activity arisingfrom physical therapy is also reproduced on the neural substratein the brain involving motor imagery practice of the sameactivity.12,14 Recently, motor imagery of gait training forindividuals with stroke has been introduced by someresearchers.5-7 Most studies on motor imagery practice arefocused on treating loss of upper extremity function11 and on
improving performance in activities of daily living.15 There are
not full studies of intervening in lower extremity and gait
dysfunction5-7,11
Dickstein et al. (2004) reported remarkable improvement inspatiotemporal parameters after gait-focused motor imagery
practice. Locomotor imagery training (LIT) for persons withhemiparetic stroke is a motor imagery training technique that
improves gait performance without requiring actual movementsby paretic or less paretic limbs. LIT may be beneficial forpatients who unable to participate in physical gait training
secondary to fatigue, severe paralysis, or improper balance.
The purpose of this study was to evaluate whether motor
imagery for gait training improves spatiotemporal parameters
on gait, related kinematic gait variables and clinical measures
for gait in individuals with hemiparetic stroke.
Materials and Methods
Participants: Thirteen hemiparetic hemiparetic subjects
were experimental group. Then we recruited same number ofage, lesion, sex, post-stroke duration matched control groupsubjects. However, two subjects in the control group were dropout before completing post-test. The study was approved by thehuman research ethics committee of all participating
institutions, and all subjects signed an informed consent form
after they received information about the study’s purpose,procedure, possible benefits and risks, privacy and use of data.
The inclusion criteria were (1) six months or more sincestroke onset, (2) ability to walk independently over-ground forat least 10 m with or without use of an ankle foot orthosis or
assistive device, (3) absence of any cognitive impairment(scores above 24 on the Mini Mental State Examination),16 (4)ability to understand verbal instructions, (5) no cerebellar
lesion, (6) no significant body or visuospatial hemineglect, and(7) a good ability for imagery functioning (a score of 32 or
higher on the revision of movement imagery questionnaire).17
Table 1 explains the general characteristics of the LIT andcontrol groups
Interventions: The subjects in the LIT group participated infour weeks of LIT five-times weekly, with each session lasting
25 to 30 minutes. Subjects in the control group watcheddocumentary television programs for the same period of time.
The first week of the four-week training focused onfamiliarizing patients with normal gait sequences andidentifying their own problems in gait by studying thedifferences between the first knowledge of performance of thesubject’s gait and that of the normal gait. Normal gait
sequences were described on the eight phases of gait cycle
including initial contact, loading response, midstance, terminal
stance, preswing, initial swing, midswing, and terminal swing.
The therapist explained the kinematic changes in each phasehip, knee, ankle, and foot. During the last three weeks, the LITgroup performed motor imagery practice according to a fivestage protocol: progressive relaxation, external imagery(analysis of task sequences), problem identification, internal
imagery, and mental rehearsal. This protocol was developed
based on the “active relaxation, imagery, and mental rehearsal(AIM)” strategy, which is commonly used in studies of motor
imagery practice for sports.18 A detail description of the fivestage protocol is shown in Appendix 1.
Outcome Measures and Analysis: 3-dimensional motion
analysis system and workstation software, Activities-specificbalance confidence scale, Berg balance scale, Dynamic gait
index.
Statistics: Pre-treatment demographic data of the subjects
were compared between the LIT and control groups using
independent t-tests and chi-square (χ2) tests. Independent t-tests
were used to determine whether the changes from the pretest to
the posttest of the spatiotemporal, kinematic, clinicalparameters significantly differed between the two groups. An
alpha level of P<.05 was used as statistical significance. All
statistical analyses were performed using the SPSS statisticalpackage 12.01.
Results
Spatiotemporal parameters
The increase of walking velocity from the pretest to posttest
was significantly greater in the LIT group than in the control
group (P=0.034) (Figure 2). However, the changes between thepretest and posttest for cadence were not significantly different
between the two groups (P=0.722). The changes of affected
and less affected limbs stride length between the pretest andposttest were significantly greater in the locomotor imagery
training group (Figure 3). Spatiotemporal parameters except forwalking velocity and stride length of both limbs were notsignificantly different between the groups.
Kinematic data
In the affected hip joint, the peak-to-peak extension-toflexion angular displacement increased from 31.95±9.68°
during the pretest to 38.08±5.51° after the locomotor imagery
training. However, the peak-to-peak joint angular displacementof hip extension-to-flexion in the control group decreased
1.46±4.30°. In the affected knee joint, the peak-to-peakextension-to-flexion angular displacement increased from30.25±14.27° during the pretest to 41.20±12.37° after the
locomotor imagery training. However, the peak-to-peak joint
angular displacement of knee extension-to-flexion in thecontrol group decreased by 3.73±6.26°. This change wassignificantly greater in the locomotor imagery training groupcompared with the control group (P=0.001). However, the test
1

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SPSS Inc, 233 S Wacker Dr, Chicago, IL, USA 60606

changes of other joint motions were not significantly different
between the two groups (P>0.05).
In less affected hip joint, the peak-to-peak angulardisplacement of rotation decreased by 8.77±10.57°, from
22.18±11.63° during the pretest to 13.41±5.15° at the posttest,in the locomotor imagery training group. However, the peak-topeak joint angular displacement of hip rotation in the control
group decreased by 0.21±9.17°. This change was significantly
greater in the locomotor imagery training group compared withthe control group (P=0.048). However, the test changes ofother joint motions were not significantly different between thetwo groups (P>0.05).
Clinical measures
The changes in the scores of ACTIVITIES-SPECIFICBALANCE CONFIDENCE scale BBT, and DGI weresignificantly greater in the locomotor imagery training groupcompared with the control group (Table 2) (P=0.000). The total
mEFAP time scores was more decrease in the locomotor
imagery training group than in the control group. The change oftime scores was significantly greater decreased in locomotor
imagery training group compared with control group (P=0.035).
The performance time in performing all mEFAP (floor, carpet,up & go, obstacles, and stairs) decreased upon termination of
the experiment in both the groups. The change of time scores inlocomotor imagery training group were significantly greater inall subtests except for up & go compared with those of thecontrol group.
Conclusion
The LIP is a cost effective and relatively safe motor
rehabilitation intervention for individuals with stroke.9
Locomotor imagery training maximizes practice opportunities
for individuals with stroke with hemiakinesia, low-level
functional ability, and little or no movement in the paralyzed
limb. locomotor imagery training is possible form of early gait
training despite focusing cognitive stage in motor learning
without overt motor output.
Key Words
Gait, Locomotor imagery training, Motion analysis, Stroke
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walking ability in people with stroke: a synthesis of theevidence. Expert Rev Neurother 2007; 7(10): 1417-36.
[2]Lord SE, McPherson K, McNaughton HK, Rochester L,
Weatherall M. Community ambulation after stroke: how
important and obtainable is it and what measures appear
predictive? Arch Phys Med Rehabil 2004; 85(2): 234-9.
[3]Stevens JA, Stoykov ME. Using motor imagery in the
rehabilitation of hemiparesis. Arch Phys Med Rehabil
2003; 84: 1090-2.
[4]O’SullivanSB, Schmitz TJ. Physical rehabilitation, fifth
edition. F.A. Davis, 2007.
[5]Dickstein R, Dunsky A, Marcovitz E. Motor imagery for
gait rehabilitation in post-stroke hemiparesis. Phys Ther
2004; 84(12): 1167-77.
[6]Dunsky A, Dickstein R, Ariav C, Deutsch J, Marchvitz E.
Motor imagery practice in gait rehabilitation of chronic
post-stroke hemiparesis: four case studies. Int J Rehabil
Res 2006; 29: 351-6.
[7]Dunsky A, Dickstein R, Marcovitz E, Levy S, Deutsch J.
Home-based motor imagery training for gait rehabilitationof people with chronic poststroke hemiparesis. Arch Phys
Med Rehabil 2008; 89: 1580-8.

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research as a guide to clinical practice. Altern Complement
Med 2004; 10: 84-9.
[9]Dickstein R, Deutsch J. Motor imagery in physicaltherapist practice. Phys Ther 2007; 87(7): 942-53.
[10]Mahoney MJ, Avener M. Psychology of the elite athlete:
an exploratory study. Cognit Ther Res 1977; 1: 135-41.
[11]Jackson PL, Lafleur MF, Malouin F, Richards C, Doyon J.
Functional cerebral reorganization following motor
sequence learning through mental practice with motor
imagery. Neuroimage 2003; 20: 1171-80.
[12]Lafleur MF, Jackson PL, Malouin F, Richards CL, Evans
AC, Doyon J. Motor learning produces parallel dynamic
functional changes during the execution and imaginationof sequential foot movements. Neuroimag 2002; 16: 14257.
[13]de Vries S, Mulder T. Motor imagery and stroke
rehabilitation: a critical discussion. J Rehabil Med 2007;
39: 5-13.
[14]Lacourse MG, Turner JA, Randolph-Orr E, Schandler SL,
Cohen MJ. Cerebral and cerebellar sensorimotor plasticity
following motor imagery-based mental practice of asequential movement. J Rehabil Res Dev 2004; 41: 505-24.
[15]Yoo E, Park E, Chung B. Mental practice effect on linetracing accuracy in persons with hemiparetic stroke: apreliminary study. Arch Phys Med Rehabil 2001; 82:1213-8.
[16]Folstein MF, Folstein SE, McHugh PR. Mini-mental
state: a practical method for grading the cognitive state ofpatients for the clinician. J Psychiat Res 1975; 12: 189198.
[17]Sharma N, Pomeroy VM, Baron J. Motor imagery: abackdoor to the motor system after stroke? Stroke 2006;
37: 1941-52.
[18]Sheikh AA, Korm ER. Imagery in sports and physicalperformance: imagery and human development series,
New York, Baywood Publishing Company Inc, 1994.
[19]Botner EM, Miller WC, Eng JJ. Measurement propertiesof the activities-specific balance confidence scale amongindividuals with stroke. Disabil Rehabil 2005; 27(4): 15663.
[20]Kornetti DL, Fritz SL, Chiu YP, Light KE, Velozo CA.
Rating scale analysis of the Berg balance test. Arch Phys
Med Rehabil 2004; 85: 1128-35.
[21]Marchetti GF, Whitney SL. Construction and validationof the 4-item dynamic gait index. Phys Ther 2006;
86(12): 1651-60.
[22]Baer HR, Wolf SL. Modified Emory functional
ambulation profile: an outcome measure for the
rehabilitation of poststroke gait dysfunction. Stroke 2001;
32(4): 973-9.
[23]Carr JH, Shepherd RB. Stroke rehabilitation: guidelines
for exercise and training to optimize motor skill, Seatle,WA, Butterworth-Heinemann Medical Books, 2003.
[24]Chen G, Patten C, Kothari DH, Zajac FE. Gait differences
between individuals with post-stroke hemiparesis andnon-disabled controls at matched speeds. Gait Posture2005; 22: 51-6.
[25]Olney SJ, Richards C. Hemiparetic gait following stroke.
Part I: characteristics. Gait Posture 1996; 4: 136-48.
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first edition. Thorofare, SLACK Incorporated, 1992.
[27]Kirtley C. Clinical gait analysis: theory and practice, firstedition. Philadelphia, Churchill Livingstone, 2006.
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Philadelphia, Lippincott Williams & Wilkins, 2006.

[29]Shumway-Cook A, Wollacott MH. Motor control:translating research into clinical practice, third edition.
Philadelphia, Lippincott Williams & Wilkins, 2007.
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Human Kinetics, 2005.
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Author address

E-Mail: hyeseonj@yonsei.ac.kr

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Memo

The effects of an isometric knee extension with hip adduction (KEWHA) exercise on
selective VMO muscle strengthening
Bo-ram Choi1), Hye-seon Jeon2)
1) Department of Rehabilitation Therapy, The Graduate School, Yonsei University, Wonju, Republic of Korea
2) Department of Physical Therapy, College of Health Science, Yonsei University, Wonju, Republic of Korea

Methods
Design: The training effect was evaluated using a onegroup pretest–posttest study design. We measured EMG onset
times during pre- and post-stair ascending tasks. We
determined whether VMO muscle onsets were earlier thanthose of the VL muscle and whether the times of EMG onsetchanged after training.
Participants: Thirty-three participants with no known lower
extremity surgical, musculoskeletal, or neurological history
participated in the pretest session of this study. Participants
showed faster VL muscle than VMO muscle EMG onset times
when they ascended stairs, were selected as participants for the
4-week training using the knee extension with hip adduction(KEWHA) exercise.
Equipment: Muscle EMG activities were recorded using a
Noraxon Telemyo 2400T (Noraxon Inc., Scottsdale, AZ, USA)with two bipolar Ag–AgCl surface electrodes (Blue sensor,
Olystyke, Denmark) during a stair-ascending task. Custommade stairs were used in this study and consisted of two steps,
20 cm in height, leading to a 60-cm-long platform. The firststair had a run of 28 cm, and the second stair had a run of 90cm.
The stair ascending task: During the pre-test, the stairascending task was used to identify subjects with earlier VL
muscle onsets, as described previously (Cowan et al., 2001;
Crossley et al., 2004; Hinman et al., 2002). Participants placed
the non-dominant foot on the floor, 20 cm away from thedominant foot which was on top of the first step, with the hipand knee joints at approximately 45°; their arms were relaxedby their sides. Both feet were parallel and shoulder-width apart,with no hip rotation and no pelvic rotation. Weight-bearing was
mainly on the non-dominant foot, with minimal weight-bearing
on the dominant foot where it was in contact with the stair(controlled by an EMG biofeedback program, threshold 1.0–
2.0µV). The participants were instructed to ascend with theirPT-6

non-dominant foot, to keep their trunk in an upright position,and to maintain a steady gaze to the front. Ascending speed
was at a rate of 96 steps per min, as paced by a metronome,
because it is not known if onset time is affected by different
walking speeds. Ascending began randomly when the examinersounded a bell. Prior to the examination, participants practiced
ascending the stairs to ensure they were able to step in time tothe metronome. The EMG onsets for the VMO and VL musclesin the stair-ascending task during the pre-test were used to
select participants with a 10-ms later onset for the VMO
muscle than for the VL muscle (Cowan et al., 2002).
Intervention: Subjects were selected on the basis of thepretest participated in the 4-week KEWHA exercise.
Participants sat on the Noland–Kickoff table (N-K table) andperformed isometric knee extension exercises with 15° hip
adduction, as described by Monteiro-Pedro et al. (1999). The
subjects performed the exercise 3 days a week with a trainerand 2 days a week at home for a total of 4 weeks. Each session
consisted of five trials of 10 repetitions (resting for 5 s between
repetitions). One trial involved alternating legs to prevent
asymmetry between the strength of the right and left quadriceps
muscles. Subjects were seated with their arms folded acrosstheir chests and used a back-rest set at a hip angle of 130°. A
belt was attached to both the pelvis (from the anterior superior
iliac spine [ASIS] line to the chair) and the trunk (under theinferior angle of the scapula to the chair) to prevent motion of
the pelvis and the trunk. The chair height was adjusted so thatboth feet were off the floor.
Results
Effect of the knee extension with hip adduction (KEWHA)
exercise on VMO and VL muscles onset time differences
The means ± SDs of the EMG onset time differences in the
pre- and post-tests are shown in Figure 1. There was no
significant difference among the EMG onset time differences
for the VMO muscle compared with the VL muscle between
the pre- (7.72 ± 95.88) and post-tests (-4.22 ± 40.98) (p = 0.63)
when data at two SDs of the mean baseline activity wereanalyzed. Very large variations in individual onset times wereobserved. When data at three SDs of the mean baseline activity
were analyzed, less variation in individual onset times wasfound, and there was a significant difference in the onset timedifferences for the VMO muscle compared to the VL muscle
between the pre- (23.78 ±13.61) and post-tests (-15.44 ±34.70)(p = 0.00).
EMG onset time difference(ms)Introduction
In general, patellofemoral rehabilitation involves
maximizing quadriceps strength while minimizing thepatellofemoral joint reaction forces and stress (Tang et al.,2001). There are many types of quadriceps strengthening
exercises. Traditionally, quad sets (Cerny, 1995) and kneeextension exercises have been used (Hanten and Schulthies,1990). However, these are designed to strengthen the wholequadriceps femoris. The VL muscle is naturally stronger thanthe VMO muscle; therefore, sustained exercise of bothfacilitates further strengthening of the VL muscle. In addition,
during these exercises, lateral and medial forces are notadequately balanced, and increased lateral displacement of thepatella into the trochlear groove occurs (Grabiner et al., 1994).
This continued imbalance between the VMO and VL muscles
accentuates PFPS (Hanten and Schulthies, 1990).
In this study, we investigated the 4-week training effects ofknee extension with hip adduction on onset timing of EMG
activity for the VL muscle and VMO muscle in asymptomaticparticipants. We also compared different methods for thedetermination of EMG onset times.

2SD
3SD

30
20
10
0
-10
-20
-30
Pre

Post

Pre

Post

Figure 1. Mean EMG onset time differences (OTD)
between VMO and VL during ascending stair task. The dot
indicates the mean EMG OTD and the each line indicates thestandard deviation (SD). Two and three standard deviations of
the mean baseline activity; (2SD, 3SD), VL onset time fasterthan VMO onset time; (VMO < VL), VMO onset time fasterthan VL onset time; (VMO > VL).
Discussion
The results of this study indicate that participants with adelayed onset time for the VMO muscle showed a decreased
difference between VMO and VL muscles onset time after
performing the KEWHA exercise for 4 weeks. These results
are in accordance with those of Cowan et al. (2002), who
conducted studies during a McConnell-based rehabilitation
program. However, their study focused on the effects of theposition of hip adduction on VMO muscle onset time during
the knee-extension exercise, not on a complex exercise
program. In addition, our investigations showed that when thethreshold for activity was set at two SDs of the mean baseline
activity, the results were more variable than those using athreshold of three SDs.
Knee extension with hip-adduction (KEWHA) exercise
Hip adduction exercises can be used to selectively
strengthen the VMO muscle (Coqueiro et al., 2005). Previous
studies combined hip adduction and open- or closed-chain
exercises performed by asymptomatic subjects. The VMO
muscle exhibited a significantly greater amount of activity thanthe VL muscle during open chain hip-adduction exercises(Hanten and Schulthies, 1990). No change in the activity of the
VMO muscle was found during a combination of isometric hip
adduction and open-chain knee extension, although VL muscle
activity was significantly less than that of the VMO muscle.
These data indicate that extensor mechanisms can reinforce
decreased VL muscle activity (Rice et al., 1995). Earl et al.
(2001) produced more overall activity in the quadriceps by
combining isometric hip adduction with a closed-chain minisquat. However, this exercise did not specifically support theactivity of the VMO muscle, as VMO and VL muscles activity
increased by the same amount. Reports on the activation of the
VMO and VL muscles s during open- or closed-chain exercises
cannot be applied to our study, as they are not directly related
to it. We did not consider open- or closed-chain exercises, as
we modified the methods of traditional quadriceps
strengthening exercises that use extension of the knee joint
from 90° flexion to full extension on the N-K table.
Furthermore, the purpose of our study was to investigate thedifferences in onset times that arise from changes in motor
control as well as the differences in quadriceps activation after
exercise. Herrington and Pearson (2006) found no significant
differences in onset times between open- and closed-chain knee
extension exercises. This suggests that the interactions between
the VMO and VL muscles s remain fairly constant irrespectiveof the type of exercise.
Conclusion
The knee extension exercise is an established 'self-exercise'used for knee pathology treatment and strengthening exercises.
However, if therapists do not adequately instruct the subject onproper positioning, the patella will receive a negative impact
due to an imbalance in the activation of the VMO muscle andVL muscles. This study describes the 4-week training effects of
the KEWHA exercise, which was used in an attempt todecrease the onset-time difference between the VMO muscle
and VL muscles. This is one factor that influences the lateral
tracking of the patella. As a result of the 4-week training period,
the onset time difference between the VMO and VL muscles
was decreased. In our study, the KEWHA exercise removed

PT-6

one of the PFPS risk factors that reduced the onset timedifference between the VMO muscle and VL muscle.
Furthermore, we suggest that the use of a correct KEWHA
exercise may reduce the risk of lateral tracking of the patella.
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Author address
E-Mail:boram@yonsei.ac.kr