Neurophysiological Characterization of Dry Needling in People With Spasticity Due to Stroke--COBRE
Phase: NA
Conditions: Stroke, Spasticity, Muscle, CVA
Sponsor: Medical University of South Carolina

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PROTOCOL TITLE: 
Neurophysiological characterization of dry needling in people with spasticity due to stroke--
COBRE 
 
PRINCIPAL INVESTIGATOR: 
• 
Gretchen A. Seif, PT, DPT 
 
Associate Professor, College of Health Professions, Medical University of South Carolina 
 
 
 
 
 

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1.0 
Objectives / Specific Aims 
In individuals post-stroke and other CNS disorders, one of the most common and disabling 
problems is spasticity (12, 35, 36, 40), which is defined as a velocity-dependent reaction to passive 
range of motion, and often is demonstrated concurrently with increased resting muscle tone (12, 35-
39). In chronic situations, spasticity can lead to secondary changes in spinal and supraspinal 
pathways (1, 2) and when coupled with muscular weakness these reflex changes can ultimately limit 
joint motion and impair motor control. Furthermore, when untreated or treated inadequately, 
spasticity can contribute to increased pain and joint contractures, thereby negatively impacting 
quality of life (12, 35, 36, 40). Currently, the most common approaches to treat spasticity are 
pharmacological treatments (12, 3-13) and standard physical therapy (including stretches, massages, 
and transcutaneous electrical stimulation). Recently, as a potential adjunct to these approaches, an 
increasing number of physical therapists worldwide have started administering trigger point deep 
dry needling (DDN) to treat spasticity and associated pain in people with CNS injuries(14-22). 
Locally, DDN at myofascial trigger points (MTrP) disrupts dysfunctional motor end plates and 
increases the local blood flow and oxygenation (68, 69) while stimulating nociceptors (60). 
Conceivably, excitation of nociceptors would influence the excitability of multiple spinal and 
supraspinal pathways (for example A-b and A-d (group II/III) sensory afferents (60-64)). To date, 
the effects of DDN on spinal somatosensory processing are not well understood. To define the 
clinical utility of DDN in treating spasticity and related sensorimotor disorders, it is essential to 
understand its neurophysiological impact on CNS pathways.  The understanding of the 
neurophysiological effects of DDN will lead to the optimal use (e.g., timing, amount, and frequency 
of DDN administration) clinically to ultimately improve the overall quality of life in patients with 
spasticity secondary to stroke (herein referred to as ‘spasticity’).  
Available small studies, case reports (14-22), and our preliminary data (87) support that 
DDN likely produces neural plasticity at both spinal and supraspinal levels. Thus, our central 
hypothesis is that DDN at MTrP induces plasticity in the spinal and supraspinal pathways and 
produces therapeutic effects.  While the steady increase in therapeutic use of DDN implies its 
clinical potential, its optimal use is yet to be established, largely due to the limited mechanistic 
understanding of its neurophysiological effects. This pilot project is our first step towards 
understanding the neurophysiological mechanisms of DDN, specifically the spinal mechanisms of 
DDN-induced plasticity. This project evaluates these mechanisms via two specific aims: 
 
Aim 1. To evaluate the effects of DDN on proprioceptive reflexes in people with spasticity due 
to stroke. 
In people with spasticity the excitability of the H-reflex pathway (an electrical analog of 
spinal stretch reflex) becomes elevated and reciprocal inhibition of the plantarflexors by the 
dorsiflexors becomes impaired (25, 26). Thus, to investigate the effects of DDN at the medial 
gastrocnemius (MG) MTrP on excitatory and inhibitory proprioceptive reflexes, in 20 individuals 
with spasticity due to stroke we will measure the H-reflex – M-wave (H/M) recruitment curves and 
reciprocal inhibition in the triceps surae muscles before, immediately after, 90 minutes after, 24 
hours after, and 72 hours after DDN. One week prior to DDN, the same measurements will be 
repeated 5 times, with inter-measurement intervals matching to pre and post DDN measurements. 
We anticipate that decreases in H-reflex size and reciprocal inhibition will occur between pre and 
post DDN time points.   
 
Aim 2. To evaluate the effects of DDN on cutaneous reflexes in people with spasticity due to 
stroke. Modulation of cutaneous reflexes to non-noxious stimulation of the skin become abnormal 

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post-stroke, reflecting the altered somatosensory processing in this population (33, 34). Thus, in this 
project, we will examine cutaneous reflex responses to non-noxious stimulation of the distal limb 
(i.e., at or below the area treated with dry-needling) at the same time points as the proprioceptive 
reflexes before and after a single DDN session. We anticipate that cutaneous reflex amplitudes will 
be decreased after DDN.   
Additionally, to interpret these reflex changes related to typical clinical measures, we will 
measure passive and active dorsiflexion range of motion (ROM) and the Modified Ashworth scale, 
Fugl-Meyer, and 10-m walk test. These measurements will facilitate the development of future DDN 
clinical trials towards establishing spinal neurophysiological mechanisms of DDN. 
The findings from this project would also help clinicians estimate when post DDN motor 
practice/training therapies should be administered for improving motor function in persons with and 
without spasticity. The data obtained through this pilot project will significantly strengthen our 
future NIH R-series applications, through which we plan to test the hypothesis that a single 
administration of DDN procedures will produce lasting effects on spinal neurophysiology that 
support temporary relief/alleviation of sensorimotor impairments in people with spasticity due to 
chronic stroke. 
 
2.0 
Background 
 
Sensorimotor disorder after stroke 
Spasticity, conventionally seen as increased muscle tone and exaggerated stretch reflexes 
[12,35-39], is one of the most common and disabling motor control problems after stroke [12,35,36,40]. 
Together with weakened voluntary muscle contraction [41], it often limits joint movements and 
results in spastic movement disorders (e.g., circumduction gait). When untreated or treated 
inappropriately, spasticity may contribute to increased pain and joint contractures, and thereby affect 
quality of life. Malfunctioning spinal inhibition (including presynaptic inhibition), muscle 
hypertonus, secondary changes in spinal pathways, and impaired sensory afferent processing and 
contribution are known contributors to spastic sensorimotor disorders [1,2]. 
 
Currently, the most common methods to treat spasticity are pharmacological and physical 
therapies. Widely applied pharmacotherapy typically disables certain connections (e.g., botulinum 
toxin) or enhance general inhibition (e.g., baclofen). While its utility has been generally accepted, 
undesirable side effects may occur [3-13]. Standard methods used in physical therapy, including joint 
mobilization [42-44] and transcutaneous electrical nerve stimulation [45-47], can also help to reduce 
spasticity temporally. In recent years, among physical therapists across the US, Europe, and Asia, 
dry needling has become recognized as a potential alternative tool to treat muscle spasm, spasticity, 
and pain in people with orthopedic or CNS injuries [16-19,48,49].   
Dry needling 
 
As the therapeutic use of dry needling grows, mechanistic understanding of this approach 
has been building up [21,24,49], although slowly. Mechanically, dry needling that targets Myofascial 
Trigger Points (MTrP) would disrupt dysfunctional motor end plates; that is, needling of MTrPs can 
stretch the contracted cytoskeletal structures (i.e., shortened sarcomeres) [50] and thereby help to 
restore the resting level of sarcomere (i.e., muscle fiber) length. Change in the muscle fiber length 
will then affect the firing of group II muscle spindle afferent, which produces complex effects on 
the network of spinal inhibitory and excitatory pathways [26,51-54], as well as exciting motoneurons 
through spinal stretch reflex pathways [55-59].  
 
Physiologically, dry needling stimulates nociceptors (i.e., A-b and A-d (group II/III) sensory 
afferents,), which in turn, influences the excitability of multiple spinal pathways (including both 
excitatory and inhibitory interneurons) [60-64]. This may partly explain pain reduction as a result of 

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dry needling [19,48,65]. It has been suggested that dry needling also activate serotonergic and 
noradrenergic systems, which influence the impact of sensory inputs in the spinal dorsal horn [66,67].  
 
Dry needling also affects the local muscle blood flow and oxygen saturation [68,69], which 
presumably helps to reduce pain-producing substances (e.g., bradykinin, calcitonin gene-related 
peptide, and Substance P) that are accumulated at/around MTrPs [70,71]. Sustained contractures of 
taut bands (often felt as palpable contraction knots) cause local ischemia and hypoxia in the MTrPs. 
Hypoxia, together with myofascial tension, can increase the amount of acetylcholine release at the 
motor end plate, which can create a self-sustaining vicious cycle of muscle contraction. A drop in 
pH resulting from low oxygen levels could also excite muscle nociceptors, which sense the 
peripheral biochemical environment and mediate local blood supply. Sensitized muscle nociceptors 
have a lower excitation threshold (allodynia) and are more easily respond to muscle movement 
(mechanical hyperalgesia) [21]. Pain associated with spastic hypertonia can further involve central 
sensitization. Altered central processing of somatosensory input can be seen in impaired flexor 
withdrawal reflexes to noxious stimuli and/or impaired cutaneous reflexes to non-noxious stimuli 
(e.g., [34]). Central sensitization is also the mechanism of referred pain, and involves sensitization 
and an expansion of receptive fields [21]. For all these reasons, increasing the local blood flow and 
oxygenation appears to be a key mechanism of action of therapeutic dry needling.  
 
In sum, the current view/presumption is that dry needling can help to restore the functional 
state of end plate and alleviate hypertonia and hyperalgesia through its immediate mechanical effects 
on end plate and by increasing the local blood flow and oxygenation. However, to date, its 
neurophysiological effects on spinal and supraspinal somatosensory processing in people after 
stroke are not yet understood. To determine the clinical utility of dry needling in treating spasticity 
and/or related sensorimotor disorders after stroke, it is essential to understand its neurophysiological 
impact on CNS pathways involved in sensorimotor function. Thus, the goal of this project is to 
characterize neurophysiological effects of dry needling on spinal and supraspinal somatosensory 
pathways in people with spasticity due to chronic stroke. 
 
3.0 
Intervention to be studied 
This project is to examine the neurophysiological mechanisms of trigger point deep dry needling 
(DDN), a commonly practiced therapeutic method to treat spasticity and pain in individuals with 
neurological and non-neurological (orthopedic) injuries.  
 
4.0 
Inclusion and Exclusion Criteria/ Study Population 
Adults (≥18 years old) with spastic hyperreflexia due to stroke.  
 
Inclusion criteria are: 1) neurologically stable for >6 months (and >1 yr post stroke); 2) 
medical clearance to participate; 3) unilateral ankle and/or wrist spasticity, confirmed by Modified 
Ashworth Scale (MAS) > 1 and the presence of spastic hyperreflexia, 4) ability to ambulate at least 
10 m with or without an assistive device (except for parallel bars). For quantifying hyperreflexia, 
we will measure the H-reflex in the soleus for the lower extremity. We will enroll post-stroke 
individuals who exhibit abnormally large H-reflexes [25] and abnormally strong reflex activity 
during the simple motor task [26,72,73] (e.g., walking and reaching and grasping). The H-reflex is 
completely suppressed in neurologically normal individuals during the swing phase of walking [74], 
for example, and therefore, testing reflexes during these dynamic movements is useful for evaluating 
spasticity. 
 
Exclusion criteria are 1) motoneuron injury (i.e. the neurons that give rise to the axons 
innervating the muscles) with inadequate response to stimulation; 2) a cardiac condition ( history of 
myocardial infarction, congestive heart failure, pacemaker use, coronary artery disease, atrial 
fibrillation, congenital heart disease, uncontrolled hypertension); 3) a medically unstable condition 

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(including temporary infections and pregnancy); 4) age <18 years old; 5) cognitive impairment 
sufficient to interfere with informed consent or successful completion of the protocol; 6) metal 
allergies; 7) needle phobias; 8) lymphedema over a limb (due to risk of infection/cellulitis); 9) 
abnormal bleeding tendencies; 10) compromised immune system; 11) vascular disease; 12) 
uncontrolled diabetes; 13) history of epilepsy (as DDN generates strong somatosensory sensation); 
14) anxiety disorders or in distress; 15) botox injection in targeted muscle within 3 months prior to 
study procedures. 
 
5.0 
Number of Subjects 
Twenty adults (≥18 years old) with spastic hyperreflexia due to stroke are recruited from 
the community around the MUSC and a greater Charleston area. 
 
6.0 
Setting 
The entire procedures will be performed at the College of Health Professions Research 
Building on the Medical University of South Carolina campus. 
 
7.0 
Recruitment Methods 
 
 
Adults (≥18 years old) with spasticity due to stroke are recruited from the community 
around the MUSC and greater Charleston area. Individuals with stroke will be recruited through 
word of mouth (i.e. support group meetings, through clinicians, health care providers, and 
participants).  Subjects recruited in this manner will be directed to contact the research team 
directly. This study will also recruit from the Registry for Stroke Recovery (RESTORE-
Pro#00037803, IRB approved 9/6/14) which is a research tool sponsored by the National Institutes 
of Health (NIH) Center of Biomedical Research Excellence (COBRE) in Stroke Recovery with 
subjects consented for future contact to support stroke recovery research conducted at MUSC.  
RESTORE staff will query the registry for potential subjects and provide the Principal Investigator 
(PI) with the contact information of subjects who meet their criteria.  The PI or research staff will 
contact subjects via phone or email to further screen for potential enrollment.   
 The research coordinator will be the first study staff to make the contact with a potential 
participant, obtain the medical records, and pre-screen him/her for eligibility. During this process, 
the coordinator will mail or email the study consent form to the potential participant. For 
medical/neurological screening of participants, the pre-screened potential participant will be 
brought to MUSC for an appointment with the study therapist and investigators, if agreed. The 
coordinator will obtain the signed consent from the potential participant in person, prior to the in-
person medical or EMG screening (i.e., first preliminary session).  
 
The participant will be paid $45 for the second and fifth sessions, and $15 for the remaining 
5 sessions. S/he will also be provided with transportation reimbursement if needed. The participant 
will be reimbursed $0.56 per mile for transportation costs for any distance greater than or equal to 
1 mile; or if s/he is using a transportation service (CARTA, etc.), the fee may be reimbursed. The 
payment (including transportation expense) will be made with cash or ClinCard, even if the 
participant does not complete the sessions.     
 
8.0 
Consent Process 
 
At the beginning of each participant’s study participation, prior to the medical/neurological 
screening, the clinical research coordinator will meet a potential participant at MUSC, explain the 
proposed study, answer questions, and obtain the signed consent in person. The potential participant 
is encouraged to ask any questions during the consent process and anytime during his/her study 
participation. If preferred by the potential participant, s/he will directly contact the principal 

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investigator or co-investigator, for any questions or concerns. Prior to meeting with the coordinator 
in person, the potential participant will receive a consent form to review and will be given time to 
discuss this clinical study with anyone (including the PIs of this study) before making a decision.  
 
Individuals with the reduced mental capacity (e.g., due to medication, drug abuse, injury or 
disease) are excluded from this study (see the fifth exclusion criterion above). Neurophysiological 
measures to be made in this study require the participant to be able to respond to the investigator’s 
commands and questions during simple motor tasks, and therefore, individuals with known 
cognitive impairment will be excluded. This further excludes the individual who are not able to 
consent by him/herself.  
 
Sharing Data: The RESTORE registry (Pro#00037803), from which this study may recruit 
subjects, also serves as a data analysis tool by which interdisciplinary teams may share data across 
projects and provide MUSC’s stroke recovery research community with a more complete registry 
with key stroke elements. Some subjects may have participated or will participate in other stroke 
related research studies at MUSC. Sharing data from this and other stroke research studies with 
RESTORE will allow for more targeted recruitment efforts in the future and could reduce the burden 
placed on subjects by reducing the duplicative efforts of collecting common data and physical 
function assessments requested by multiple studies and storing them in one centralized and secure 
location. 
 
Subjects are informed in the consent process if they enroll into the RESTORE registry, their 
data from this study will be shared. Those who have participated in other stroke research will be 
asked to sign a Release of Study Records form to share data with RESTORE if they did not already 
authorize release. 
 
Subjects will be asked to sign a HIPAA authorization stating their health information may 
be disclosed to MUSC investigators requiring their data for their research projects upon approval 
by an Institutional Review Board. 
 
 
9.0 
Study Design / Methods 
This study is a partial cross-over waitlist control design, in which each of the 20 
participants post stroke will participate in 7 visits over a two-week period, during which 
measurements will be taken 10 times. Neurophysiological and functional measurements will be 
collected five times over 3 visits during the first week (treatment as usual control week), through 
which each participant will serve as their own “controls” for their second week of measurements. 
No sham or other treatment procedure will occur during this week. On the second week, all 
participants will transition to the DDN intervention week where five measurements will be 
collected over 3 visits (one pre-DDN baseline and four post-DDN measurements: immediately 
after, 90 minutes, 24 hours, and 72 hours). 
 
Deep Dry Needling (DDN) 
DDN procedures used in this project have been widely used in clinical practice to treat 
spasticity and pain in individuals with neurological and non-neurological (orthopedic) injuries 
[15,16,18,20,21,48,75].  
Each participant receives a single session of DDN, targeting the medial gastrocnemius. In 
each DDN session, first, localized hypersensitive spots in palpable taut bands of the targeted skeletal 
muscles (i.e., MTrPs)(75, 76) are identified with pincer palpation. Then, after cleaning the skin area 
over a MTrPs with alcohol swabs, a disposable stainless steel acupuncture needle is inserted into 
the skin, penetrating approximately 15 to 20 mm to the depth of the trigger point, until the local 
twitch response (LTR) is elicited. Once the LTR is confirmed, the needle is moved up and down 

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(~4-5 mm vertically) with a small piston motions (approximately at 1 Hz for 25 to 30 seconds) with 
no rotation at the MTrPs (9,10, 38). The same procedure is repeated at other MTrPs in the same 
local skin region as needed until the LTR is eradicated. After removing the needle, the needled area 
is rubbed to prevent bleeding and bruising.  Each participant will complete 5 repetitions of each of 
the following: ankle plantarflexion/dorsiflexion passive range of motion (PROM), sub-maximal 
concentric and eccentric contractions of the plantarflexors as would be typical in a clinical setting. 
 
 
Electromyography (EMG) and nerve stimulation 
 
At the beginning of each session, surface self-adhesive Ag-AgCl electrodes are placed over 
the TA, medial and lateral gastrocnemius (MG and LG), and soleus muscles of the studied leg. 
Throughout the study, all EMG activity is amplified, band-pass filtered (10-1000 Hz), sampled at 
3,200 Hz, and stored. Nerve stimulation protocol consists of 4 components: (1) single pulse posterior 
tibial nerve stimulation for the triceps surae H-reflex / M-wave (H/M) recruitment curve 
measurement, (2) single pulse common peroneal (CP) nerve stimulation for the TA H/M recruitment 
curve measurement, (3) multiple pulse (train) tibial nerve stimulation for cutaneous reflex 
measurement, and (4) multiple pulse (train) superficial peroneal (SP) nerve stimulation for 
cutaneous reflex measurement.  
(1) Single pulse posterior tibial nerve stimulation for triceps surae H/M recruitment curve: To 
elicit the triceps H-reflex, the tibial nerve is stimulated in the popliteal fossa, using surface Ag-
AgCl electrodes and isolated constant current stimulation. The stimulating electrode pair is 
placed so as to minimize the H-reflex threshold and to avoid stimulation of other nerves. For 
eliciting the H-reflex and M-wave, a 1-ms square stimulus pulse is delivered when the 
participant has maintained his/her natural standing level (typically, 10-20% of maximum 
voluntary contraction (MVC) level of EMG activity) of soleus EMG activity for at least 2 s. The 
minimum interstimulus interval is 5 s. An H/M recruitment curve is obtained by gradually 
increasing the stimulus intensity in increments of 1.2-2.5 mA from the H-reflex threshold to the 
maximum H-reflex (Hmax) to an intensity just above what is needed to elicit the maximum M-
wave (Mmax) [77-79], while the participant stands and maintains the above noted level of soleus 
EMG activity. About 10 different intensities are used to obtain a recruitment curve, and four 
EMG responses are averaged to measure the H-reflex and M-wave at each intensity. Then, about 
100 responses are elicited at the Hmax level of stimulus intensity (i.e., weak to mild intensity) 
while monitoring cortical electroencephalographic (EEG) activity.  
(2) Single pulse common peroneal (CP) nerve stimulation for TA H/M recruitment curve: To 
elicit the H-reflex and M-wave in the TA, the CP nerve is stimulated at the neck of the fibula, 
using surface Ag-AgCl electrodes and isolated constant current stimulation. For eliciting the H-
reflex and M-wave, a 0.5-ms square stimulus pulse is delivered when the participant has 
maintained his/her natural standing level of soleus EMG activity for at least 2 s, with the 
minimum interstimulus interval of 5 s. An H/M recruitment curve is obtained by gradually 
increasing the stimulus intensity from the H-reflex threshold to the Hmax to an intensity just 
above what is needed to elicit the Mmax [77-79], while the participant stands and maintains the 
above noted level of soleus EMG activity. About 10 different intensities are used to obtain a 
recruitment curve, and four EMG responses are averaged to measure the H-reflex and M-wave 
at each intensity. Then, about 100 responses are elicited at the Hmax level of stimulus intensity 
(i.e., weak to mild intensity) while monitoring cortical EEG activity. 
(3) Train of tibial nerve stimulation for cutaneous reflexes: The distal tibial nerve is stimulated 
on the medial surface of the ankle posterior to the medial malleolus by trains of five pulses at 
200 Hz, with a pulse width of 1.0 ms [34,80]. The stimulus electrodes are placed at a location at 
which strong radiating paresthesia is reported by the participant in the appropriate cutaneous 

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receptive fields (i.e., plantar surface of foot). While standing, the perceptual threshold, defined 
as the lowest stimulation detectable by the participant, and the radiating threshold (RT), defined 
as a clear radiating paresthesia, are determined. Perceptual threshold is thought to represent local 
activation of cutaneous receptors lying immediately underneath the recording electrodes, 
whereas RT is likely representing electrical activation of fascicles in the underlying cutaneous 
nerve [80,81]. 1´RT, 2´RT, and 3´RT of train of stimuli are delivered while the standing 
participant maintains the above described level of soleus EMG activity. Fifteen to 20 trials are 
averaged for each stimulus intensity, with the minimum inter-train interval of 5s.  
(4) Train of superficial peroneal (SP) nerve stimulation for the cutaneous reflexes: The SP nerve 
is stimulated on the anterior surface of the leg just near the crease of the ankle joint by trains of 
five pulses at 200 Hz, with a pulse width of 1.0 ms [34,80]; the stimulus location at which the 
participant receives strong radiating paresthesia in the appropriate cutaneous receptive fields 
(i.e., foot dorsum). While standing, the perceptual threshold and the RT are determined. 1´RT, 
2´RT, and 3´RT of train of stimuli are delivered while the standing participant maintains the 
above described level of soleus EMG activity. Fifteen to 20 trials are averaged for each stimulus 
intensity, with the minimum inter-train interval of 5s. 
 
Analysis of H-reflex and cutaneous reflexes 
 
The H-reflex and the M-wave amplitudes are measured as the peak-to-peak values in time 
windows determined for each participant. Typically, for the soleus, the H-reflex occurs in a time 
window of 30–50 ms post-stimulus 6–25 ms post-stimulus for the M-wave. For the MG, LG, and 
TA, the M-wave and H-reflex occur with shorter latencies [79]. For all muscles, the Hmax, Mmax, and 
Hmax/Mmax ratio are obtained from the recruitment curve measurement. 
 
To analyze cutaneous reflexes, the background (prestimulus) EMG is subtracted from the 
post-stimulus EMG trace [34,78]. Then, subtracted EMG traces from each muscle are analyzed for 
peak reflex amplitudes at two distinct epochs termed early (~50–75 ms to peak) and middle (~75–
120 ms to peak) latencies [78,83].  
 
 
Assessment of sensory and motor function 
 
Fugl-Meyer Assessment: Fugl-Meyer Assessment is one of the most widely used 
quantitative measures of motor impairment and recovery in post-stroke hemiparetic individuals. 
The assessment includes: motor function (upper extremity maximum score = 66; lower extremity 
maximum score = 34), sensory function (maximum score = 24), balance (maximum score = 14), 
joint range of motion (maximum score = 44), and joint pain (maximum score = 44). Each item is 
scored on a 3-point ordinal scale: 0 = cannot perform, 1 = performs partially, 2 = performs fully. 
The maximum score is 226.  
  
10-meter walk test: The participant is asked to walk at his/her fastest comfortable speed on 
an indoor flat straight walkway that has markers at 0, 2, 12, and 14 m, 3 times. The 10-meter speed is 
calculated from when the toes of the leading foot cross the 2-m marker to when they cross the 12-m 
marker. An assistive device (e.g., walker) can be used. If the participant’s device use changes during 
the study, the measurements will be made with both the new and old devices.  
  
Modified Ashworth Scale:  To measure spasticity, resistance to passive movement about a 
joint is tested at a range of velocities. The score ranges from 0-4 (i.e., 0: normal muscle tone; 4: rigid 
in flexion or extension [84]).  
 
Visual Analog Scale for Pain: To measure pain, participants rate the level of pain they are 
experiencing in the affected limb. The score ranges from 0 to 10 (0=”no pain” and 10=”worst 
imaginable pain”). 
 
Range of Motion: Range of motion in the affected limb is measured using a standard 

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goniometer. Both passive and active range of motion will be recorded. 
 
10.0 Data Management  
Data analysis: Reflex sizes are calculated in reference to each participant’s Mmax measured 
during natural standing. For example, the peak-to-peak H-reflex amplitude is normalized to the 
peak-to-peak Mmax amplitude, and the mean rectified H-reflex amplitude is normalized to the mean 
rectified Mmax amplitude.  
For comparing reflex sizes before and after dry needling, a two-way repeated measures 
ANOVA (studied side of the extremity ´ time) will be used, together with Student t-test with 
Bonferroni correction as a post-hoc test. For simple comparison between participants without known 
neurological conditions and participants after stroke (e.g., age and Mmax), and assessments of 
changes in sensory and motor function (i.e., only applicable to participants after stroke), a Student 
t-test will be used.  
 
Data management: The data will be managed by the PIs and research coordinator at the 
College of Health Professions (CHP). All EMG and assessment data are electronically stored in the 
secure CHP server with password protection. Only the investigators directly involved in this project 
have access to these data.  
 
Protection of participant confidentiality is essential in human clinical trials. The participants’ 
confidential information will be securely stored in locked cabinets of a locked room and a password-
protected computer, and only the principal and co-investigators and the research coordinator will 
have access to the participant’s confidential information. For the length of the study, limited 
personal information (specifically, the participant’s name, address, and social security number) will 
also be accessible to the program administrator for processing the participant reimbursement 
paperwork. Investigators and therapists, who run data collection sessions, will have access to the 
EMG and other collected data for the purpose of analysis, but will have no access to the participant’s 
confidential information. Alphanumeric codes will be assigned to each participant’s dataset to 
protect confidentiality. 
 
11.0 Provisions to Monitor the Data to Ensure the Safety of Subjects  
 
From the time of initial contact (before obtaining the informed consent for study 
participation) to the end of project (i.e., study publication), the confidentiality and rights of all the 
study participants and potential study candidates are protected. At the time of consent, the potential 
study candidate is assured that s/he has the right to stop participation in any or all parts of the study 
at any time with no penalty or loss of benefits to which s/he is otherwise entitled.  
 
After the pre-screening, the clinical research coordinator will discard all records of potential 
study candidates who are not eligible to participate in the study. For candidates after stroke, after 
the medical/neurological screening (by the study therapist) and the EMG screening, all records of 
non-eligible candidates will be discarded. For the eligible participants, who will therefore go through 
the study protocol, the medical, neurological, and personal information will be securely stored in 
locked cabinets of a locked room and on MUSC’s secure network storage, and only the principal 
and co-investigators and the research coordinator will have access to the participant’s confidential 
information. For the length of the study, limited personal information (specifically, the participant’s 
name, address, and social security number) will also be accessible to the program administrator for 
processing the participant reimbursement paperwork. Investigators and therapists, who run data 
collection sessions, will have access to the EMG and other collected data for the purpose of analysis, 
but will have no access to the participant’s confidential information. Alphanumeric codes will be 
assigned to each participant’s dataset to protect confidentiality.  
 
At the time of obtaining consent, the potential participant will be made aware of the fact that 

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we cannot guarantee the protection of the confidentiality of his/her records, although every 
reasonable effort will be made to protect it.  The consent form will clearly state as “By law, 
representatives of the sponsoring organization or other regulatory authorities may inspect these 
records. All personal information made available for inspection will be handled in strictest 
confidence and in accordance with data protection laws.” 
 
The coordinator will check with each participant for any discomfort or adverse events that 
s/he might have experienced after each session. If and when adverse effects or events and any 
protocol deviations occur, the coordinator or the PI will immediately report them to the department 
and the IRB.  
 
12.0 Withdrawal of Subjects  
• 
Some of the participants may find DDN to be stressful or painful (e.g., in case of individuals 
with needle phobias), even after careful screening with the above listed inclusion/exclusion 
criteria. All participants are assured that they have the right to stop participation at any part 
of the study procedures.  
• 
DDN is a commonly practiced therapeutic method to treat spasticity and pain in individuals 
with neurological and non-neurological (orthopedic) injuries. Careful screening with the 
above listed inclusion/exclusion criteria ensures safe administration of DDN. 
 
13.0 Risks to Subjects 
• 
There is a risk (1-10/100) of local bleeding, hematoma, and needling site pain.  In order to 
minimize this risk, the patient will be placed in a recumbent or comfortable position for the 
technique and gentle massage/hemostasis will be applied to the needling site post needling 
[86].  
• 
There is an uncommon risk (1-10/1000) of local or systemic infections or swelling.  In order 
to minimize this risk a clean technique will be utilized with the use of gloves and cleaning the 
skin around the region with an alcohol swab pre needling [86].   
• 
There is an uncommon risk (1-10/1000) for strong pain during the treatment, nerve irritation, 
nerve injury, headache, fatigue, vertigo, and nausea.  In order to minimize this risk the patient 
will be placed in comfortable position and will be monitored throughout needling.  At any 
point the subject can request that the needling be discontinued [86].   
• 
There is a rare risk (1-10/10000) for redness, itching, sweating, blood pressure changes, 
unconsciousness, tachycardia, breathing difficulties, or vomiting.  In order to minimize this 
risk the patient will be placed in comfortable position and will be monitored throughout 
needling.  At any point the subject can request that the needling be discontinued [86].   
• 
There is a very rare risk (<1/10000) for a broken needle.  This risk will be minimized by using 
the appropriate needle and not inserting the needle to the handle of the needle [86].   
• 
There is a very small possibility that the recording and stimulating electrodes will produce 
minor irritations, such as itchiness. This is extremely unlikely, since the electrodes we use 
are designed for sleep studies (Vermed., Inc). If itchiness does occur after the experiment, 
an over-the-counter topical steroid cream will be applied to the skin over which the 
electrodes were placed. Electrical stimulation of sensory or motor nerves may generate brief 
non-painful sensations. Careful adjustment of the stimulus intensity and electrode 
placement should minimize any discomfort. 

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Page 11 of 18 
 
• 
There is a risk of loss of confidentiality. From the time of initial contact (before obtaining 
the informed consent) to the end of the study, every reasonable effort will be made to 
protect the confidentiality and rights of all the study participants and potential study 
candidates. 
• 
There is a risk of falling when performing the 10 meter walk test. The participant can use an 
adaptive device during this assessment, and the risk of falling is no greater than when 
walking at home or in the community with the same device. The risk of falling will be 
minimized by study staff, who will walk beside the participant and assist if he/she becomes 
fatigued or experiences a loss of balance. 
• 
The experimental procedures may have unknown side effects. The researchers will inform 
study participants if any new side effect is discovered. 
 
14.0 Potential Benefits to Subjects or Others 
 
This study is experimental, and we promise no direct benefits to the study participants. 
However, some of the participants may benefit from the study intervention (i.e., dry needling). This 
possibility is supported by several existing studies [14-18,20,48]. Successful completion of this study 
will help to understand the neurophysiological mechanisms of action resulting from dry needling, 
which will then help to determine effective uses of this intervention for treating spasticity and related 
physiological problems in individuals after stroke. 
 
15.0 Sharing of Results with Subjects 
This project investigates neurophysiological mechanisms of action of dry needling 
that has been widely used in therapy clinics across the world, and thus, it is anticipated that 
to study participants, the immediate clinical value of study results are likely limited. Study 
results will not be shared directly with the participants. 
16.0 Devices 
 
Acupuncture needles used for dry needling will be stored in a locked cabinet in a locked 
room that can be accessed only by study staff. The physical therapist trained in dry needling will 
be the only study team member to handle the needles. Each needle is individually packaged in a 
sterile guide tube that is used to insert the needle into the skin. Following the dry needling 
procedure, the needle will be disposed of in a sharps container. 
 
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