Osteoarthritis, KneePhase 2NCT02854176
Somatosensory Stimulation in Knee Osteoarthritis
A Phase 2 study testing Somatosensory electrical stimulation in people with Osteoarthritis, Knee, run by Menno Veldman.
Trial summary
Worldwide, 9.6% of men and 18% of women aged over 60 years suffer from osteoarthritis (OA), most of which involve the knee. Within the OA patient population, 80% of the OA patients have limitations of movement, and 25% cannot perform the majority of their daily activities (WHO). Read more about this study
- Who is it for?
- Ages 18 to 75 years
- Conditions the study is for
- Osteoarthritis, Knee
- What is being tested?
- Somatosensory electrical stimulation
- Type of treatment
- Surgery or procedure
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 20 participants
- Where
- No sites listed yet
- Study dates
- Sep 2016to Aug 2017
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 75 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- 18 to 45 years.
- Unilateral symptomatic KOA.
- Patient in waitlist at the Schulthess Clinic for knee arthroplasty.
- Patient has mild to average pain levels
- Living place: Canton of Zurich or neighbouring Cantons.
- Signed written informed consent.
Who cannot join
- Symptomatic OA in lower extremity joints other than the knee.
- Bilateral symptomatic KOA.
- Usage of walking aids.
- Surgery to the lower limbs in the prior 12 months.
- BMI >35 kg/m2.
- Disorders that affect visuomotor function.
About this study
Official title: Somatosensory Electrical Stimulation to Improve Motor Control in Patients Suffering From Knee Osteoarthritis
Worldwide, 9.6% of men and 18% of women aged over 60 years suffer from osteoarthritis (OA), most of which involve the knee. Within the OA patient population, 80% of the OA patients have limitations of movement, and 25% cannot perform the majority of their daily activities (WHO). Some of these symptoms contribute to arthrogenic muscle inhibition (AMI), a reflexive decrease in motor output to the muscles surrounding the affected joint.
AMI is characterized by abnormal afferent information transmitted to the central nervous system, resulting in altered afferent feedback to the quadriceps motoneurons (MN) which in turn results in reduced excitability of that particular pool. The altered afferent input is suggested to stem from stimulation of mechanoreceptors, via joint effusion or excessive movements, nociceptors as a response to pain, or loss of joint receptors (Palmieri-Smith et al., 2009). Although the evidence concerning the role of the central nervous system is scarce, pre- and postsynaptic spinal mechanisms directly affecting alpha-MNs seem affected. Dysfunction of γ-loops also seems to be involved (Konishi et al., 2002). These mechanisms together result in AMI that manifests through aberrations in voluntary quadriceps torque, force control, and reflex excitability often measured by the H-reflex (Hopkins et al., 2000).
Besides the evident role of motor efferents, sensory afferents also influence motor control (Gentilucci et al., 1997) and poor proprioceptive function is predictive of poor chair-stand performance (Sharma et al., 2003). Reduction of the sensory deficits could potentially increase motor function in knee OA. The present study aims to evaluate whether low-intensity peripheral electrical nerve stimulation, a form of increasing afferent input, could potentially improve OA patients' motor function. The most limiting factor in OA patients, however, is pain, experienced at rest and during movement. Although previous paradigms used high-frequency stimulation and the lack of physiological explanations concerning pain reductions after peripheral electrical nerve stimulation, it is possible that reductions in experienced pain are mediated by reduced analgesia, i.e., decreased excitability of nociceptive neurons.
Read the detailed description
Worldwide, 9.6% of men and 18% of women aged over 60 years suffer from osteoarthritis (OA), most of which involve the knee. Within the OA patient population, 80% of the OA patients have limitations of movement, and 25% cannot perform the majority of their daily activities (WHO). OA is a progressive articular cartilage disorder involving motor and sensory dysfunctions, including a decreased range of motion, muscle weakness, impaired proprioception, and pain. Some of these symptoms contribute to arthrogenic muscle inhibition (AMI), a reflexive decrease in motor output to the muscles surrounding the affected joint that is most likely mediated by GABAergic inhibitory mechanisms.
AMI is characterized by abnormal afferent information transmitted to the central nervous system, resulting in altered afferent feedback to the quadriceps motoneurons (MN) which in turn results in reduced excitability of that particular pool. The altered afferent input is suggested to stem from stimulation of mechanoreceptors, via joint effusion or excessive movements, nociceptors as a response to pain, or loss of joint receptors. Although the evidence concerning the role of the central nervous system is scarce, pre- and postsynaptic spinal mechanisms directly affecting alpha-MNs seem affected. Dysfunction of γ-loops also seems to be involved. These mechanisms together result in AMI that manifests through aberrations in voluntary quadriceps torque, force control, and reflex excitability often measured by the H-reflex.
Motor dysfunction thus is an important limiting factor for OA patients and involves motor and sensory factors. Besides the evident role of motor efferents, sensory afferents also influence motor control and poor proprioceptive function is predictive of poor chair-stand performance. Reduction of the sensory deficits could potentially increase motor function in knee OA. The present study aims to evaluate whether low-intensity peripheral electrical nerve stimulation, a form of increasing afferent input, could potentially improve OA patients' motor function. The most limiting factor in OA patients, however, is pain, experienced at rest and during movement. High-frequencies stimulation paradigms are normally used to reduce pain, but 40-50 minutes of low-frequency electrical stimulation (4 Hz, < MT intensity) can also be effective in reducing pain at rest, pain during movement, and pain sensitivity, although a recent systematic review questions consistency of these effects considering the limited evidence. Although, to the best of our knowledge, there is no clear physiological explanation concerning pain reductions after peripheral electrical nerve stimulation, it is possible that reductions in experienced pain are mediated by reduced analgesia, i.e., decreased excitability of nociceptive neurons.
Electrical stimulation of peripheral nerves and muscles has been applied in various forms to modulate muscle strength, motor skill, spinal- and cortical excitability. Neuromuscular electrical stimulation (NMES) evoked forces can generate torques up to 112% of maximal voluntary contraction force and increases with increasing stimulation frequency up to 70-80 Hz.
Whereas NMES is primarily focused on increasing muscle strength, low-intensity somatosensory electrical stimulation (SES) has been used to increase motor skill acquisition in neurologic patients and healthy participants. SES excites group Ia, Ib, and II afferents, as well as secondary muscle afferent fibers. SES increases motor performance the most when applied to a peripheral nerve at high sensory intensities (2-3 times perceptual threshold) at 10 Hz (SES applied in 1 Hz trains consisting of 5 pulses at 10 Hz). High-frequency transcutaneous electrical nerve stimulation (TENS) and sensorimotor training can both repositioning error reflecting impaired knee proprioception in patients with knee OA. Both TENS and SES thus excite afferent fibers involved in knee proprioception. Impaired knee proprioception has been associated with impaired ability to accurately and steadily control force and impaired eccentric strength. In contrast with NMES, in which induced increases in muscle force most likely involve changes in metabolism, hypertrophy, and possibly spinal mechanisms, and TENS, where large diameter primary afferents are pivotal in pain reductions, SES targets sensory pathways, both cutaneous and proprioceptive, which seem an appropriate target to reduce sensory deficits involved in OA.
SES can improve stroke patients' motor function but whether such improvements can occur in patients with knee AO is unknown. Excitation of primary afferents by SES could serve as a physiological basis for the hypothesis that SES positively influences the afferent input to α-MN of the quadriceps muscles surrounding the dysfunctional joint and reduce pain. The increased afferent input by SES, as shown previously in healthy participants and stroke patients, is expected to increase motor control, measured by an increase in tracking performance in the dysfunctional knee joint. As a task variant to visuomotor tracking, force steadiness and accuracy are expected to increase after SES because these measures are associated with proprioception, an outcome SES is known to improve through excitation of muscle afferents. If this expectation is correct, SES could then be used in future studies and rehabilitation protocols as a primer to potentiate the effects of NMES and other exercise therapies designed to improve quadriceps strength and power. Second, if SES reduces pain and increases motor control, SES can possibly postpone surgery and can serve as an adjuvant for patients for patients who are unsuitable for or resist a total knee replacement to improve activities of daily and therefore quality of life.
Therefore, the present study will examine the acute and delayed effects of 60 minutes of SES (five pulses in 1 Hz trains at 10 Hz at motor threshold intensity) of the femoral nerve in patients suffering from knee OA. Figure 1 depicts a schematic overview of the proposed study design. As an initial step, a pilot experiment in 5-6 healthy individuals should reveal whether there are some effects or trends observed after 30 minutes of SES, a duration probably would be more optimal at 60 minutes considering the 120 minutes standard used for improving neurological patients' hand function. The primary outcomes of the study is motor coordination evaluated using target tracking based on knee position and not based on quadriceps force, because position vs. force is less affected by the influences of pain and therefore more suitable in the current context. Secondary outcomes are motor control and proprioception reflected by increased force steadiness and accuracy, maximal voluntary strength and daily physical function. The investigators hypothesize based on previous data that afferent input induced by SES reduces abnormalities in sensory input as a result of OA, and therefore increases motor control.
- Conditions
- Osteoarthritis, Knee
- Being tested
- Somatosensory electrical stimulation, Control
- Medical subject headings
- Osteoarthritis, Knee
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Somatosensory electrical stimulationProcedure or surgery
ControlProcedure or surgery
| Study group | Role | What they receive |
|---|---|---|
| Somatosensory electrical stimulation | Experimental | Not described Receives: Procedure: Somatosensory electrical stimulation |
| Control | Sham comparator | Not described Receives: Procedure: Control |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mean absolute deviation from a preprogrammed template during target tracking with the injured knee
Measured: Change from before to after 60 minutes of somatosensory electrical stimulation applied to the femoral nerve
Secondary outcomes (1)
Quadriceps force accuracy and steadiness of the injured leg during isometric force at 50 and 100 Newton
Measured: Change from before to after 60 minutes of somatosensory electrical stimulation applied to the femoral nerve
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Aug 2016 (estimated)
- Study startSep 2016
- Primary completionDec 2016 (estimated)
- Study completionAug 2017 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (24)Papers the sponsor has linked to this study.
- Other trials for Osteoarthritis, KneeStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Enrolment
- 20 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Menno Veldman
- Sponsor type
- University, hospital or other
- Collaborators
- Schulthess Klinik
- Responsible party
- Sponsor-investigator, Menno Veldman, University Medical Center Groningen
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02854176
- Sponsor's protocol ID
- Somatosensory stimulation
- Status last verified
- Jul 2016
- First submitted
- 26 Jul 2016
- Last updated
- 3 Aug 2016
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Celnik P, Hummel F, Harris-Love M, Wolk R, Cohen LG. Somatosensory stimulation enhances the effects of training functional hand tasks in patients with chronic stroke. Arch Phys Med Rehabil. 2007 Nov;88(11):1369-76. doi: 10.1016/j.apmr.2007.08.001.
PubMed 17964875Courtney CA, O'Hearn MA, Hornby TG. Neuromuscular function in painful knee osteoarthritis. Curr Pain Headache Rep. 2012 Dec;16(6):518-24. doi: 10.1007/s11916-012-0299-2.
PubMed 23054978Gentilucci M, Toni I, Daprati E, Gangitano M. Tactile input of the hand and the control of reaching to grasp movements. Exp Brain Res. 1997 Mar;114(1):130-7. doi: 10.1007/pl00005612.
PubMed 9125458Herzig D, Maffiuletti NA, Eser P. The Application of Neuromuscular Electrical Stimulation Training in Various Non-neurologic Patient Populations: A Narrative Review. PM R. 2015 Nov;7(11):1167-1178. doi: 10.1016/j.pmrj.2015.03.022. Epub 2015 Mar 31.
PubMed 25839763Hopkins JT, Ingersoll CD, Edwards JE, Cordova ML. Changes in soleus motoneuron pool excitability after artificial knee joint effusion. Arch Phys Med Rehabil. 2000 Sep;81(9):1199-203. doi: 10.1053/apmr.2000.6298.
PubMed 10987162Hortobagyi T, Garry J, Holbert D, Devita P. Aberrations in the control of quadriceps muscle force in patients with knee osteoarthritis. Arthritis Rheum. 2004 Aug 15;51(4):562-9. doi: 10.1002/art.20545.
PubMed 15334428Hortobagyi T, Scott K, Lambert J, Hamilton G, Tracy J. Cross-education of muscle strength is greater with stimulated than voluntary contractions. Motor Control. 1999 Apr;3(2):205-19. doi: 10.1123/mcj.3.2.205.
PubMed 10198150Kaelin-Lang A. Enhancing rehabilitation of motor deficits with peripheral nerve stimulation. NeuroRehabilitation. 2008;23(1):89-93.
PubMed 18356592Kaelin-Lang A, Luft AR, Sawaki L, Burstein AH, Sohn YH, Cohen LG. Modulation of human corticomotor excitability by somatosensory input. J Physiol. 2002 Apr 15;540(Pt 2):623-33. doi: 10.1113/jphysiol.2001.012801.
PubMed 11956348Konishi Y, Fukubayashi T, Takeshita D. Mechanism of quadriceps femoris muscle weakness in patients with anterior cruciate ligament reconstruction. Scand J Med Sci Sports. 2002 Dec;12(6):371-5. doi: 10.1034/j.1600-0838.2002.01293.x.
PubMed 12453165Maffiuletti NA, Bizzini M, Schatt S, Munzinger U. A multi-joint lower-limb tracking-trajectory test for the assessment of motor coordination. Neurosci Lett. 2005 Aug 12-19;384(1-2):106-11. doi: 10.1016/j.neulet.2005.04.064.
PubMed 15885904Palmieri-Smith RM, Thomas AC. A neuromuscular mechanism of posttraumatic osteoarthritis associated with ACL injury. Exerc Sport Sci Rev. 2009 Jul;37(3):147-53. doi: 10.1097/JES.0b013e3181aa6669.
PubMed 19550206Poortvliet PC, Tucker KJ, Finnigan S, Scott D, Sowman P, Hodges PW. Cortical activity differs between position- and force-control knee extension tasks. Exp Brain Res. 2015 Dec;233(12):3447-57. doi: 10.1007/s00221-015-4404-8. Epub 2015 Aug 21.
PubMed 26292962Radhakrishnan R, Sluka KA. Deep tissue afferents, but not cutaneous afferents, mediate transcutaneous electrical nerve stimulation-Induced antihyperalgesia. J Pain. 2005 Oct;6(10):673-80. doi: 10.1016/j.jpain.2005.06.001.
PubMed 16202960Roos EM, Klassbo M, Lohmander LS. WOMAC osteoarthritis index. Reliability, validity, and responsiveness in patients with arthroscopically assessed osteoarthritis. Western Ontario and MacMaster Universities. Scand J Rheumatol. 1999;28(4):210-5. doi: 10.1080/03009749950155562.
PubMed 10503556
Study at a glance
From the registry record, last updated by the sponsor on 3 Aug 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Somatosensory Electrical Stimulation to Improve Motor Control in Patients Suffering From Knee Osteoarthritis
- ClinicalTrials.gov ID
- NCT02854176
- Acronym / sponsor ID
- Somatosensory stimulation
- Conditions
- Osteoarthritis, Knee
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 20 participants (estimated)
- Lead sponsor
- Menno VeldmanUniversity, hospital or other
- Collaborators
- Schulthess Klinik
- Study start
- Sep 2016
- Primary completion
- Dec 2016 (estimated)
- Study completion
- Aug 2017 (estimated)
- First posted
- 3 Aug 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Worldwide, 9.6% of men and 18% of women aged over 60 years suffer from osteoarthritis (OA), most of which involve the knee. Within the OA patient population, 80% of the OA patients have limitations of movement, and 25% cannot perform the majority of their daily activities (WHO). Some of these symptoms contribute to arthrogenic muscle inhibition (AMI), a reflexive decrease in motor output to the muscles surrounding the affected joint.
AMI is characterized by abnormal afferent information transmitted to the central nervous system, resulting in altered afferent feedback to the quadriceps motoneurons (MN) which in turn results in reduced excitability of that particular pool. The altered afferent input is suggested to stem from stimulation of mechanoreceptors, via joint effusion or excessive movements, nociceptors as a response to pain, or loss of joint receptors (Palmieri-Smith et al., 2009). Although the evidence concerning the role of the central nervous system is scarce, pre- and postsynaptic spinal mechanisms directly affecting alpha-MNs seem affected. Dysfunction of γ-loops also seems to be involved (Konishi et al., 2002). These mechanisms together result in AMI that manifests through aberrations in voluntary quadriceps torque, force control, and reflex excitability often measured by the H-reflex (Hopkins et al., 2000).
Besides the evident role of motor efferents, sensory afferents also influence motor control (Gentilucci et al., 1997) and poor proprioceptive function is predictive of poor chair-stand performance (Sharma et al., 2003). Reduction of the sensory deficits could potentially increase motor function in knee OA. The present study aims to evaluate whether low-intensity peripheral electrical nerve stimulation, a form of increasing afferent input, could potentially improve OA patients' motor function. The most limiting factor in OA patients, however, is pain, experienced at rest and during movement. Although previous paradigms used high-frequency stimulation and the lack of physiological explanations concerning pain reductions after peripheral electrical nerve stimulation, it is possible that reductions in experienced pain are mediated by reduced analgesia, i.e., decreased excitability of nociceptive neurons.
Detailed description
Worldwide, 9.6% of men and 18% of women aged over 60 years suffer from osteoarthritis (OA), most of which involve the knee. Within the OA patient population, 80% of the OA patients have limitations of movement, and 25% cannot perform the majority of their daily activities (WHO). OA is a progressive articular cartilage disorder involving motor and sensory dysfunctions, including a decreased range of motion, muscle weakness, impaired proprioception, and pain. Some of these symptoms contribute to arthrogenic muscle inhibition (AMI), a reflexive decrease in motor output to the muscles surrounding the affected joint that is most likely mediated by GABAergic inhibitory mechanisms.
AMI is characterized by abnormal afferent information transmitted to the central nervous system, resulting in altered afferent feedback to the quadriceps motoneurons (MN) which in turn results in reduced excitability of that particular pool. The altered afferent input is suggested to stem from stimulation of mechanoreceptors, via joint effusion or excessive movements, nociceptors as a response to pain, or loss of joint receptors. Although the evidence concerning the role of the central nervous system is scarce, pre- and postsynaptic spinal mechanisms directly affecting alpha-MNs seem affected. Dysfunction of γ-loops also seems to be involved. These mechanisms together result in AMI that manifests through aberrations in voluntary quadriceps torque, force control, and reflex excitability often measured by the H-reflex.
Motor dysfunction thus is an important limiting factor for OA patients and involves motor and sensory factors. Besides the evident role of motor efferents, sensory afferents also influence motor control and poor proprioceptive function is predictive of poor chair-stand performance. Reduction of the sensory deficits could potentially increase motor function in knee OA. The present study aims to evaluate whether low-intensity peripheral electrical nerve stimulation, a form of increasing afferent input, could potentially improve OA patients' motor function. The most limiting factor in OA patients, however, is pain, experienced at rest and during movement. High-frequencies stimulation paradigms are normally used to reduce pain, but 40-50 minutes of low-frequency electrical stimulation (4 Hz, < MT intensity) can also be effective in reducing pain at rest, pain during movement, and pain sensitivity, although a recent systematic review questions consistency of these effects considering the limited evidence. Although, to the best of our knowledge, there is no clear physiological explanation concerning pain reductions after peripheral electrical nerve stimulation, it is possible that reductions in experienced pain are mediated by reduced analgesia, i.e., decreased excitability of nociceptive neurons.
Electrical stimulation of peripheral nerves and muscles has been applied in various forms to modulate muscle strength, motor skill, spinal- and cortical excitability. Neuromuscular electrical stimulation (NMES) evoked forces can generate torques up to 112% of maximal voluntary contraction force and increases with increasing stimulation frequency up to 70-80 Hz.
Whereas NMES is primarily focused on increasing muscle strength, low-intensity somatosensory electrical stimulation (SES) has been used to increase motor skill acquisition in neurologic patients and healthy participants. SES excites group Ia, Ib, and II afferents, as well as secondary muscle afferent fibers. SES increases motor performance the most when applied to a peripheral nerve at high sensory intensities (2-3 times perceptual threshold) at 10 Hz (SES applied in 1 Hz trains consisting of 5 pulses at 10 Hz). High-frequency transcutaneous electrical nerve stimulation (TENS) and sensorimotor training can both repositioning error reflecting impaired knee proprioception in patients with knee OA. Both TENS and SES thus excite afferent fibers involved in knee proprioception. Impaired knee proprioception has been associated with impaired ability to accurately and steadily control force and impaired eccentric strength. In contrast with NMES, in which induced increases in muscle force most likely involve changes in metabolism, hypertrophy, and possibly spinal mechanisms, and TENS, where large diameter primary afferents are pivotal in pain reductions, SES targets sensory pathways, both cutaneous and proprioceptive, which seem an appropriate target to reduce sensory deficits involved in OA.
SES can improve stroke patients' motor function but whether such improvements can occur in patients with knee AO is unknown. Excitation of primary afferents by SES could serve as a physiological basis for the hypothesis that SES positively influences the afferent input to α-MN of the quadriceps muscles surrounding the dysfunctional joint and reduce pain. The increased afferent input by SES, as shown previously in healthy participants and stroke patients, is expected to increase motor control, measured by an increase in tracking performance in the dysfunctional knee joint. As a task variant to visuomotor tracking, force steadiness and accuracy are expected to increase after SES because these measures are associated with proprioception, an outcome SES is known to improve through excitation of muscle afferents. If this expectation is correct, SES could then be used in future studies and rehabilitation protocols as a primer to potentiate the effects of NMES and other exercise therapies designed to improve quadriceps strength and power. Second, if SES reduces pain and increases motor control, SES can possibly postpone surgery and can serve as an adjuvant for patients for patients who are unsuitable for or resist a total knee replacement to improve activities of daily and therefore quality of life.
Therefore, the present study will examine the acute and delayed effects of 60 minutes of SES (five pulses in 1 Hz trains at 10 Hz at motor threshold intensity) of the femoral nerve in patients suffering from knee OA. Figure 1 depicts a schematic overview of the proposed study design. As an initial step, a pilot experiment in 5-6 healthy individuals should reveal whether there are some effects or trends observed after 30 minutes of SES, a duration probably would be more optimal at 60 minutes considering the 120 minutes standard used for improving neurological patients' hand function. The primary outcomes of the study is motor coordination evaluated using target tracking based on knee position and not based on quadriceps force, because position vs. force is less affected by the influences of pain and therefore more suitable in the current context. Secondary outcomes are motor control and proprioception reflected by increased force steadiness and accuracy, maximal voluntary strength and daily physical function. The investigators hypothesize based on previous data that afferent input induced by SES reduces abnormalities in sensory input as a result of OA, and therefore increases motor control.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Somatosensory electrical stimulation | Experimental | Procedure: Somatosensory electrical stimulation |
| Control | Sham comparator | Procedure: Control |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (6 listed)
- 18 to 45 years.
- Unilateral symptomatic KOA.
- Patient in waitlist at the Schulthess Clinic for knee arthroplasty.
- Patient has mild to average pain levels
- Living place: Canton of Zurich or neighbouring Cantons.
Key exclusion criteria (6 listed)
- Symptomatic OA in lower extremity joints other than the knee.
- Bilateral symptomatic KOA.
- Usage of walking aids.
- Surgery to the lower limbs in the prior 12 months.
- BMI >35 kg/m2.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Somatosensory electrical stimulation | Procedure or surgery | Somatosensory electrical stimulation |
| Control | Procedure or surgery | Control |
Primary outcome
Mean absolute deviation from a preprogrammed template during target tracking with the injured knee
Time frame: Change from before to after 60 minutes of somatosensory electrical stimulation applied to the femoral nerve
1 secondary outcome
Quadriceps force accuracy and steadiness of the injured leg during isometric force at 50 and 100 Newton
Time frame: Change from before to after 60 minutes of somatosensory electrical stimulation applied to the femoral nerve
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Aug 2016.
- Background: PubMed 17964875Celnik P, Hummel F, Harris-Love M, Wolk R, Cohen LG. Somatosensory stimulation enhances the effects of training functional hand tasks in patients with chronic stroke. Arch Phys Med Rehabil. 2007 Nov;88(11):1369-76. doi: 10.1016/j.apmr.2007.08.001.
- Background: PubMed 23054978Courtney CA, O'Hearn MA, Hornby TG. Neuromuscular function in painful knee osteoarthritis. Curr Pain Headache Rep. 2012 Dec;16(6):518-24. doi: 10.1007/s11916-012-0299-2.
- Background: PubMed 9125458Gentilucci M, Toni I, Daprati E, Gangitano M. Tactile input of the hand and the control of reaching to grasp movements. Exp Brain Res. 1997 Mar;114(1):130-7. doi: 10.1007/pl00005612.
- Background: PubMed 25839763Herzig D, Maffiuletti NA, Eser P. The Application of Neuromuscular Electrical Stimulation Training in Various Non-neurologic Patient Populations: A Narrative Review. PM R. 2015 Nov;7(11):1167-1178. doi: 10.1016/j.pmrj.2015.03.022. Epub 2015 Mar 31.
- Background: PubMed 10987162Hopkins JT, Ingersoll CD, Edwards JE, Cordova ML. Changes in soleus motoneuron pool excitability after artificial knee joint effusion. Arch Phys Med Rehabil. 2000 Sep;81(9):1199-203. doi: 10.1053/apmr.2000.6298.
- Background: PubMed 15334428Hortobagyi T, Garry J, Holbert D, Devita P. Aberrations in the control of quadriceps muscle force in patients with knee osteoarthritis. Arthritis Rheum. 2004 Aug 15;51(4):562-9. doi: 10.1002/art.20545.
- Background: PubMed 10198150Hortobagyi T, Scott K, Lambert J, Hamilton G, Tracy J. Cross-education of muscle strength is greater with stimulated than voluntary contractions. Motor Control. 1999 Apr;3(2):205-19. doi: 10.1123/mcj.3.2.205.
- Background: PubMed 18356592Kaelin-Lang A. Enhancing rehabilitation of motor deficits with peripheral nerve stimulation. NeuroRehabilitation. 2008;23(1):89-93.
- Background: PubMed 11956348Kaelin-Lang A, Luft AR, Sawaki L, Burstein AH, Sohn YH, Cohen LG. Modulation of human corticomotor excitability by somatosensory input. J Physiol. 2002 Apr 15;540(Pt 2):623-33. doi: 10.1113/jphysiol.2001.012801.
- Background: PubMed 12453165Konishi Y, Fukubayashi T, Takeshita D. Mechanism of quadriceps femoris muscle weakness in patients with anterior cruciate ligament reconstruction. Scand J Med Sci Sports. 2002 Dec;12(6):371-5. doi: 10.1034/j.1600-0838.2002.01293.x.
- Background: PubMed 15885904Maffiuletti NA, Bizzini M, Schatt S, Munzinger U. A multi-joint lower-limb tracking-trajectory test for the assessment of motor coordination. Neurosci Lett. 2005 Aug 12-19;384(1-2):106-11. doi: 10.1016/j.neulet.2005.04.064.
- Background: PubMed 19550206Palmieri-Smith RM, Thomas AC. A neuromuscular mechanism of posttraumatic osteoarthritis associated with ACL injury. Exerc Sport Sci Rev. 2009 Jul;37(3):147-53. doi: 10.1097/JES.0b013e3181aa6669.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Somatosensory electrical stimulation in people with Osteoarthritis, Knee, run by Menno Veldman.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 6 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 3 Aug 2016. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Mean absolute deviation from a preprogrammed template during target tracking with the injured knee (time frame: Change from before to after 60 minutes of somatosensory electrical stimulation applied to the femoral nerve). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02854176, which also lists 24 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 Aug 2016.