- Email: [email protected]
A Novel Technique for Conduction Studies of the Infrapatellar Nerve
Original Research
A Novel Technique for Conduction Studies of the Infrapatellar Nerve Jeanna Tsenter, MD, Isabella Schwartz, MD, Michal Katz-Leurer, PhD, Zeev Meiner, MD, Diana Goldin, MD, Jean-Jacques Vatine, MD Objective: To introduce a noninvasive method for electrodiagnostic evaluation of the infrapatellar nerve (IPN). Design: A prospective cohort study. Setting: Electrodiagnostic laboratory, rehabilitation department, Hadassah University Hospital. Participants: A total of 38 healthy adults; 57 asymptomatic limbs were studied. Methods: Sensory nerve action potential of the IPN was recorded with surface electrodes placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. Transcutaneous antidromic electrical stimulation of IPN was applied above the medial femoral condyle and 8-10 cm proximally from the active surface electrode. Results: The sensory nerve action potential mean (n ⫽ 38) onset latency was 1.69 ⫾ 0.32 ms. Peak latency was 2.36 ⫾ 0.47 ms, and amplitude was 6.96 ⫾ 3.68 V. Conclusions: This article describes a novel and simple technique for IPN conduction electrodiagnostic examination. The method used provides a new tool to evaluate IPN injury in reference to anterior or inferior knee pain with associated sensory deficit. PM R 2012;4:682-685
INTRODUCTION Injury of the infrapatellar nerve (IPN), a branch of the saphenous nerve (SN), is not an uncommon event. It has been reported as a complication of arthroscopic procedures, surgery, and knee trauma [1-9]. In addition, a syndrome of IPN entrapment also has been reported [10]. Damage of the IPN may lead to hypesthesia, paresthesia, dysesthesia, and neuropathic pain [1,11,12]. Studies have shown a correlation between injury of the IPN and anterior knee pain syndrome [6,12], reflex sympathetic dystrophy [3], and poor outcome after knee surgery [1,9]. The SN passes the Hunter canal and becomes subcutaneous approximately 10 cm proximal to the medial epicondyle of the femur between the sartorius and gracilis muscles. Once it becomes subcutaneous, the nerve branches to form the IPN. The IPN emerges from the fascia medial to and at the level of the lower pole of the patella. It then divides into its branches approximately 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. A significant variability in IPN branching has been reported, but in the majority of cases, the IPN branches were distributed in the anterior knee area, between the lower border of the patella and the tibial tuberosity [4,8,11,13-15]. Although lesions of the IPN may be responsible for many clinical symptoms, the literature includes only one report in which the authors describe a method to evaluate the conduction of the IPN [16]. In that study a method of orthodromic stimulation of the IPN via the use of needle electrode recording in the inguinal area was described. In our article, we describe a noninvasive method for electrodiagnostic evaluation of the IPN that may be efficient for identification of specific lesions of the IPN in patients experiencing anterior knee pain.
PM&R
682
1934-1482/12/$36.00 Printed in U.S.A.
J.T. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital, Jerusalem, Israel Disclosure: nothing to disclose I.S. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital and Hadassah– Hebrew University Medical Center, Mount, Scopus, PO Box 24035, Jerusalem 91240 Israel. Address correspondence to: I.S.; email: [email protected] Disclosure: nothing to disclose M.K.-L. Department of Physical Therapy, School of Health Professions, Tel-Aviv University, Ramat-Aviv, Israel Disclosure: nothing to disclose Z.M. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital, Jerusalem, Israel Disclosure: nothing to disclose D.G. Outpatient and Research Division, Reuth Medical Center–Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel J.J.-V. Outpatient and Research Division, Reuth Medical Center–Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel Disclosure: nothing to disclose Part of this material was presented at the Annual Meeting of the Israeli Society of Clinical Neurophysiology, Kfar-Saba, 2001. Disclosure Key can be found on the Table of Contents and at www.pmrjournal.org. Submitted for publication January 24, 2012; accepted June 1, 2012.
© 2012 by the American Academy of Physical Medicine and Rehabilitation Vol. 4, 682-685, September 2012 http://dx.doi.org/10.1016/j.pmrj.2012.06.001
PM&R
Vol. 4, Iss. 9, 2012
683
METHODS Subjects The study was approved by the institutional review boards at our institutions. A total of 38 healthy subjects participated in our study. The sample consisted of 28 men (73.7%) and 10 women (26.3 %). Inclusion criteria stipulated that subjects would be 17 years of age or older (ages 17-78 years; mean ⫾ SD: 41 ⫾ 10 years). Fifty-seven asymptomatic limbs were studied: in 19 subjects, both legs were tested (38 limbs), whereas 19 additional subjects had only one leg tested (19 limbs). Exclusion criteria consisted of any history of soft tissue or bony injury around the knee (eg, trauma, fracture, surgery, scars, and contractures) or neurologic problems involving deficits in the lower limbs (eg, neuropathy, radiculopathy, myopathy, and brain or spine injury).
Electrodiagnosis All studies were performed at standard settings (Keypoint, Medtronic, v3.01, Dantec Medical, Denmark) with the lowfrequency filter set at 20 Hz, the high-frequency filter set at 10 kHz, stimulus duration set at 0.1 ms, stimulus intensity set at 35-50 mA, recording sensitivity set at 20 V/division, and sweep speed set at 1 ms/division. Signal averaging was used when the sensory nerve action potential (SNAP) was too small to be identified easily after a single stimulus (4-12 trials). Room temperature was maintained at 22°-25°C. Skin surface temperature was measured over the medial femoral condyle area. Mean skin temperature for all limbs was 31.85 ⫾ 0.6°C. No subjects had a skin temperature less than 31°C. The active surface electrode (disposable bar electrode, VIASIS Healthcare, Madison, WI,) was placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. The reference surface electrode was placed 3 cm distally to the active surface electrode. Transcutaneous antidromic electrostimulation was applied above the medial femoral condyle, 8-10 cm proximal to the recording electrode. The ground electrode (disposable ground electrode, VIASIS Healthcare) was placed somewhat laterally to the line between stimulation and pickup sites (Figure 1).
Measurements The following measurements were taken from the elicited potential: onset latency (first negative deflection), negative peak latency, and negative peak amplitude. Conduction velocities to onset and to peak were calculated with the use of conventional methods (9).
Statistics The calculation for adequate sample size was based on previous study results [16] demonstrating a mean amplitude
Figure 1. Method for antidromic stimulation (left leg) of the infrapatellar nerve. The active surface electrode (black) was placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar ligament. The reference surface electrode (red) was placed 3 cm distally to the active surface electrode. Transcutaneous antidromic electrostimulation was applied above the medial femoral condyle, 8-10 cm proximal to the recording electrode. The ground electrode (green) was placed somewhat lateral to the line between stimulation and pickup sites.
value of 1.3 V (⫾1.1) on the assumption that the mean amplitude in the current method will be one standard deviation higher than this value. On the basis of a type 1 error of 0.05, with the power of 0.8, a minimum number of 32 subjects were needed. For testing differences between sides, the Wilcoxon signed rank test was performed, and the Pearson correlation was used to quantify the association between conduction parameters within a person between sides (n ⫽ 16). The Mann-Whitney U test was computed to examine whether differences existed in conduction parameters among persons of different genders or ages (younger or older than 40 years). The results from a single leg of 38 subjects were used. One side was chosen randomly for each of the participants for whom data were recorded from both legs. Statistical significance was set at P ⬍ .05. All analyses were performed with SPSS 14.0 software (SPSS, Inc., Chicago, IL).
RESULTS SNAP was recorded in 54 of 57 examined limbs (94.8%; 16 pairs and 22 single legs). Among 3 of 19 subjects who had both legs tested, the potentials were obtained from one leg only. For 16 subjects for whom both leg SNAPs were obtained, correlation analysis with use of the Pearson test revealed a significant relationship between right and left leg conduction parameters values (rp ⬎ 0.7, P ⬍ .01), and therefore one side was chosen randomly (Table 1). The mean
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Tsenter et al
NOVEL TECHNIQUE FOR CONDUCTION STUDIES OF THE IPN
Table 1. Sensory nerve action parameters of infrapatellar nerve conduction study 16 Pairs Parameters Onset latency, ms Peak latency, ms Amplitude, V Conduction velocity onset, m/s Conduction velocity peak, m/s
38 Limbs
Right Limb
Left Limb
P Value*
1.69 ⫾ 0.32 [1.15-2.68] 2.36 ⫾ 0.47 [1.73-3.70] 6.96 ⫾ 3.68 [1.60-13.00] 57.75 ⫾ 7.78 [32.55-69.81] 41.78 ⫾ 5.96 [25.00-55.20]
1.64 ⫾ 0.38 [1.15-2.68] 2.31 ⫾ 0.57 [1.73-3.70] 5.84 ⫾ 2.74 [1.60-13.00] 58.9 ⫾ 9.14 [32.55-69.81] 42.2 ⫾ 6.67 [25.00-49.70]
1.62 ⫾ 0.33 [1.21-2.20] 2.18 ⫾ 0.43 [1.77-3.60] 6.51 ⫾ 2.87 [2.10-12.00] 59.37 ⫾ 6.87 [40.70-67.70] 44.07 ⫾ 4.86 [30.60-50.80]
.83 .10 .23 .88 .18
Values in table are mean ⫾ SD [min-max]. *Wilcoxon signed rank test.
SNAP onset latency of 38 limbs was 1.69 ⫾ 0.32 ms, peak latency was 2.36 ⫾ 0.47 ms, and amplitude was 6.96 ⫾ 3.68 V (Table 1). A significant difference in onset latency was found between the 8-cm versus 10-cm recording distances (1.47 ⫾ 0.28 versus 1.86 ⫾ 0.27 relatively, P ⬍ .01), but no significant difference regarding recording distances was found in peak latency, amplitude, or conduction velocity parameters. No differences in conduction parameters were found between genders and between age groups (MannWhitney U test, P ⬎.05, data not shown).
DISCUSSION The development of our technique for nerve conduction evaluations of the IPN was based on previous anatomic studies of the knees from cadavers, where accurate anatomy of IPN in the knee area has been described [4,6,8,11,17]. To allow maximal nerve stimulation and to prevent volume conduction from surrounding muscles, the SN stimulation was performed on a subcutaneous part of an SN after its exit from the Hunter canal [4]. The active surface electrode was placed at the area of IPN dispersion, far enough from the main SN trunk. The high rate of SNAP recording in our study shows good sensitivity of this technique despite a high known anatomic variability of the IPN described previously [8,10,11,14]. The anatomic studies showed a high rate variability of the IPN regarding its relationship to the sartorius muscle, the number of branches, and the area the nerve passes through [8,11]. This fact may explain the relatively high rate of 5.2% SNAP absence in our study (in 3 of 19 subjects who had both legs tested, the potentials were obtainable from only one leg). Furthermore, even assuming that side-to-side anatomic variability may exist [4,11], our study did not reveal significant electrodiagnostic differences between legs. Less range variation was found in SNAP onset latency compared with negative peak latency. Therefore we suggest that the SNAP onset latency is the most reliable parameter for
nerve conduction evaluation of IPN. A possible reason for the slight increase in SD is that the distance between the stimulation and recording electrodes varied from 8-10 cm depend on body habit. According to our results, a significant difference in onset latency was found between the 8-cm versus 10-cm recording distances. Thus for additional accuracy, we suggest that conduction velocity to onset that is not dependent on recording distance would be more reliable. As may be expected from the size of the IPN and its ramifications, the SNAP amplitude of IPN (onset to negative peak amplitude) was lower than the measured amplitude of the main trunk of the SN described in the literature [4,11]. However, the mean IPN amplitude observed in our study was markedly higher than the IPN amplitude described previously by Bademkiran et al [16] (6.96 ⫾ 3.68 V versus 1.3 ⫾ 1.1 V). Furthermore, we suggest that our method has the additional advantages of being simple, noninvasive, and faster than the previously mentioned near-nerve needle technique in the inguinal region. The technique presented in our study will allow a more practical approach to evaluation of infrapatellar neuropathy. This technique may be used in any case of anterior knee pain accompanied by hypesthesia, paresthesia, or dysesthesia suggestive of neuropathic involvement. It is recommended that the electrodiagnostician compare data from the involved limb, contralateral limb (when normal), and with normal conduction values presented in our study. Some limitations inherent to the methodology used in this study should be considered. First, the small number of patients makes it difficult to define the expected variation in latencies among the different age groups. Additional studies with a larger number of patients from various age groups will allow for expansion of the normal database. Second, the relatively high rate of SNAP absence found in the subgroup that had both legs tested is presumed to be a result of anatomic variability. Further studies of both legs in a larger population along with cadaveric studies will help to clarify this issue.
PM&R
Vol. 4, Iss. 9, 2012
CONCLUSION In this study we present a very simple noninvasive method for nerve conduction examination of the IPN. We found this technique to be reliable and easy to perform. It may be useful for establishing a definitive diagnosis of IPN injury and should be considered in cases of persistent anterior or inferior knee pain with sensory deficit of unknown origin.
8.
9. 10. 11.
REFERENCES 1. Johnson RJ, Kettelkamp DB, Clark W, Leaverton P. Factors effecting late results after meniscectomy. J Bone Joint Surg Am 1974;56:719-729. 2. Swanson AJ. The incidence of prepatellar neuropathy following medial meniscectomy. Clin Orthop 1983;181:151-153. 3. Poehling GG, Pollock FE Jr, Koman LA. Reflex sympathetic dystrophy of the knee after sensory nerve injury. Arthroscopy 1988;4:31-35. 4. Mochida H, Kikuchi S. Injury to infrapateller branch of saphenous nerve in arthroscopic knee surgery. Clin Orthop 1995;320:88-94. 5. Ikpeme JO, Gray C. Traumatic prepatellar neuralgia. Injury 1995;26: 225-229. 6. Tennent TD, Birch NC, Holmes MJ, Birch R, Goddard NJ. Knee pain and the infrapatellar branch of the saphenous nerve. J R Soc Med 1998;91:573-575. 7. Tifford CD, Spero L, Luke T, Plancher KD. The relationship of the infrapateller branches of the saphenous nerve to arthroscopic portals
12.
13.
14.
15. 16.
17.
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and incisions for anterior cruciate ligament surgery. Am J Sports Med 2000;28:562-567. Kartus J, Movin T, Karlsson J. Donor-site morbidity and anterior knee problems after anterior cruciate ligament reconstruction using autografts. Arthroscopy 2001;17:971-980. Mistry D, O’Meeghan C. Fate of the infrapatellar branch of the saphenous nerve post total knee arthroplasty. ANZ J Surg 2005;75:822-824. House JH, Ahmed K. Entrapment neuropathy of the infrapatellar branch of the saphenous nerve. Am J Sports Med 1977;5:217-224. Arthornthurasook A, Gaew-Im K. Study of the infrapatellar nerve. Am J Sports Med 1988;16:57-59. Ellen MI, Jackson HB, DiBiase SJ. Uncommon causes of anterior knee pain: A case report of infrapatellar contracture syndrome. Am J Phys Med Rehabil 1999;78:376-380. Le Corroller T, Lagier A, Pirro N, Champsaur P. Anatomical study of the infrapatellar branch of the saphenous nerve using ultrasonography. Muscle Nerve 2011;44:50-54. Hunter LY, Louis DS, Ricciardi JR, O’Connor GA. The saphenous nerve: Its course and importance in medial arthrotomy. Am J Sports Med 1979;7:227-230. Ebraheim NA, Mekhail AO. The infrapatellar branch of the saphenous nerve: An anatomic study. J Orthop Trauma 1997;11:195-199. Bademkiran F, Obay B, Aydogdu I, Ertekin C. Sensory conduction study of the infrapatellar branch of the saphenous nerve. Muscle Nerve 2007;35:224-227. Boon JM, Van Wyck MJ, Jordaan D. A safe area and angle for harvesting autogenous tendons for anterior cruciate ligament reconstruction. Surg Radiol Anat 2004;26:167-171.
A Novel Technique for Conduction Studies of the Infrapatellar Nerve Jeanna Tsenter, MD, Isabella Schwartz, MD, Michal Katz-Leurer, PhD, Zeev Meiner, MD, Diana Goldin, MD, Jean-Jacques Vatine, MD Objective: To introduce a noninvasive method for electrodiagnostic evaluation of the infrapatellar nerve (IPN). Design: A prospective cohort study. Setting: Electrodiagnostic laboratory, rehabilitation department, Hadassah University Hospital. Participants: A total of 38 healthy adults; 57 asymptomatic limbs were studied. Methods: Sensory nerve action potential of the IPN was recorded with surface electrodes placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. Transcutaneous antidromic electrical stimulation of IPN was applied above the medial femoral condyle and 8-10 cm proximally from the active surface electrode. Results: The sensory nerve action potential mean (n ⫽ 38) onset latency was 1.69 ⫾ 0.32 ms. Peak latency was 2.36 ⫾ 0.47 ms, and amplitude was 6.96 ⫾ 3.68 V. Conclusions: This article describes a novel and simple technique for IPN conduction electrodiagnostic examination. The method used provides a new tool to evaluate IPN injury in reference to anterior or inferior knee pain with associated sensory deficit. PM R 2012;4:682-685
INTRODUCTION Injury of the infrapatellar nerve (IPN), a branch of the saphenous nerve (SN), is not an uncommon event. It has been reported as a complication of arthroscopic procedures, surgery, and knee trauma [1-9]. In addition, a syndrome of IPN entrapment also has been reported [10]. Damage of the IPN may lead to hypesthesia, paresthesia, dysesthesia, and neuropathic pain [1,11,12]. Studies have shown a correlation between injury of the IPN and anterior knee pain syndrome [6,12], reflex sympathetic dystrophy [3], and poor outcome after knee surgery [1,9]. The SN passes the Hunter canal and becomes subcutaneous approximately 10 cm proximal to the medial epicondyle of the femur between the sartorius and gracilis muscles. Once it becomes subcutaneous, the nerve branches to form the IPN. The IPN emerges from the fascia medial to and at the level of the lower pole of the patella. It then divides into its branches approximately 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. A significant variability in IPN branching has been reported, but in the majority of cases, the IPN branches were distributed in the anterior knee area, between the lower border of the patella and the tibial tuberosity [4,8,11,13-15]. Although lesions of the IPN may be responsible for many clinical symptoms, the literature includes only one report in which the authors describe a method to evaluate the conduction of the IPN [16]. In that study a method of orthodromic stimulation of the IPN via the use of needle electrode recording in the inguinal area was described. In our article, we describe a noninvasive method for electrodiagnostic evaluation of the IPN that may be efficient for identification of specific lesions of the IPN in patients experiencing anterior knee pain.
PM&R
682
1934-1482/12/$36.00 Printed in U.S.A.
J.T. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital, Jerusalem, Israel Disclosure: nothing to disclose I.S. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital and Hadassah– Hebrew University Medical Center, Mount, Scopus, PO Box 24035, Jerusalem 91240 Israel. Address correspondence to: I.S.; email: [email protected] Disclosure: nothing to disclose M.K.-L. Department of Physical Therapy, School of Health Professions, Tel-Aviv University, Ramat-Aviv, Israel Disclosure: nothing to disclose Z.M. Department of Physical Medicine and Rehabilitation, Hadassah Medical Center–Hadassah University Hospital, Jerusalem, Israel Disclosure: nothing to disclose D.G. Outpatient and Research Division, Reuth Medical Center–Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel J.J.-V. Outpatient and Research Division, Reuth Medical Center–Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel Disclosure: nothing to disclose Part of this material was presented at the Annual Meeting of the Israeli Society of Clinical Neurophysiology, Kfar-Saba, 2001. Disclosure Key can be found on the Table of Contents and at www.pmrjournal.org. Submitted for publication January 24, 2012; accepted June 1, 2012.
© 2012 by the American Academy of Physical Medicine and Rehabilitation Vol. 4, 682-685, September 2012 http://dx.doi.org/10.1016/j.pmrj.2012.06.001
PM&R
Vol. 4, Iss. 9, 2012
683
METHODS Subjects The study was approved by the institutional review boards at our institutions. A total of 38 healthy subjects participated in our study. The sample consisted of 28 men (73.7%) and 10 women (26.3 %). Inclusion criteria stipulated that subjects would be 17 years of age or older (ages 17-78 years; mean ⫾ SD: 41 ⫾ 10 years). Fifty-seven asymptomatic limbs were studied: in 19 subjects, both legs were tested (38 limbs), whereas 19 additional subjects had only one leg tested (19 limbs). Exclusion criteria consisted of any history of soft tissue or bony injury around the knee (eg, trauma, fracture, surgery, scars, and contractures) or neurologic problems involving deficits in the lower limbs (eg, neuropathy, radiculopathy, myopathy, and brain or spine injury).
Electrodiagnosis All studies were performed at standard settings (Keypoint, Medtronic, v3.01, Dantec Medical, Denmark) with the lowfrequency filter set at 20 Hz, the high-frequency filter set at 10 kHz, stimulus duration set at 0.1 ms, stimulus intensity set at 35-50 mA, recording sensitivity set at 20 V/division, and sweep speed set at 1 ms/division. Signal averaging was used when the sensory nerve action potential (SNAP) was too small to be identified easily after a single stimulus (4-12 trials). Room temperature was maintained at 22°-25°C. Skin surface temperature was measured over the medial femoral condyle area. Mean skin temperature for all limbs was 31.85 ⫾ 0.6°C. No subjects had a skin temperature less than 31°C. The active surface electrode (disposable bar electrode, VIASIS Healthcare, Madison, WI,) was placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar tendon. The reference surface electrode was placed 3 cm distally to the active surface electrode. Transcutaneous antidromic electrostimulation was applied above the medial femoral condyle, 8-10 cm proximal to the recording electrode. The ground electrode (disposable ground electrode, VIASIS Healthcare) was placed somewhat laterally to the line between stimulation and pickup sites (Figure 1).
Measurements The following measurements were taken from the elicited potential: onset latency (first negative deflection), negative peak latency, and negative peak amplitude. Conduction velocities to onset and to peak were calculated with the use of conventional methods (9).
Statistics The calculation for adequate sample size was based on previous study results [16] demonstrating a mean amplitude
Figure 1. Method for antidromic stimulation (left leg) of the infrapatellar nerve. The active surface electrode (black) was placed 2.5 cm below the distal pole of the patella and 2 cm medially from the medial border of the patellar ligament. The reference surface electrode (red) was placed 3 cm distally to the active surface electrode. Transcutaneous antidromic electrostimulation was applied above the medial femoral condyle, 8-10 cm proximal to the recording electrode. The ground electrode (green) was placed somewhat lateral to the line between stimulation and pickup sites.
value of 1.3 V (⫾1.1) on the assumption that the mean amplitude in the current method will be one standard deviation higher than this value. On the basis of a type 1 error of 0.05, with the power of 0.8, a minimum number of 32 subjects were needed. For testing differences between sides, the Wilcoxon signed rank test was performed, and the Pearson correlation was used to quantify the association between conduction parameters within a person between sides (n ⫽ 16). The Mann-Whitney U test was computed to examine whether differences existed in conduction parameters among persons of different genders or ages (younger or older than 40 years). The results from a single leg of 38 subjects were used. One side was chosen randomly for each of the participants for whom data were recorded from both legs. Statistical significance was set at P ⬍ .05. All analyses were performed with SPSS 14.0 software (SPSS, Inc., Chicago, IL).
RESULTS SNAP was recorded in 54 of 57 examined limbs (94.8%; 16 pairs and 22 single legs). Among 3 of 19 subjects who had both legs tested, the potentials were obtained from one leg only. For 16 subjects for whom both leg SNAPs were obtained, correlation analysis with use of the Pearson test revealed a significant relationship between right and left leg conduction parameters values (rp ⬎ 0.7, P ⬍ .01), and therefore one side was chosen randomly (Table 1). The mean
684
Tsenter et al
NOVEL TECHNIQUE FOR CONDUCTION STUDIES OF THE IPN
Table 1. Sensory nerve action parameters of infrapatellar nerve conduction study 16 Pairs Parameters Onset latency, ms Peak latency, ms Amplitude, V Conduction velocity onset, m/s Conduction velocity peak, m/s
38 Limbs
Right Limb
Left Limb
P Value*
1.69 ⫾ 0.32 [1.15-2.68] 2.36 ⫾ 0.47 [1.73-3.70] 6.96 ⫾ 3.68 [1.60-13.00] 57.75 ⫾ 7.78 [32.55-69.81] 41.78 ⫾ 5.96 [25.00-55.20]
1.64 ⫾ 0.38 [1.15-2.68] 2.31 ⫾ 0.57 [1.73-3.70] 5.84 ⫾ 2.74 [1.60-13.00] 58.9 ⫾ 9.14 [32.55-69.81] 42.2 ⫾ 6.67 [25.00-49.70]
1.62 ⫾ 0.33 [1.21-2.20] 2.18 ⫾ 0.43 [1.77-3.60] 6.51 ⫾ 2.87 [2.10-12.00] 59.37 ⫾ 6.87 [40.70-67.70] 44.07 ⫾ 4.86 [30.60-50.80]
.83 .10 .23 .88 .18
Values in table are mean ⫾ SD [min-max]. *Wilcoxon signed rank test.
SNAP onset latency of 38 limbs was 1.69 ⫾ 0.32 ms, peak latency was 2.36 ⫾ 0.47 ms, and amplitude was 6.96 ⫾ 3.68 V (Table 1). A significant difference in onset latency was found between the 8-cm versus 10-cm recording distances (1.47 ⫾ 0.28 versus 1.86 ⫾ 0.27 relatively, P ⬍ .01), but no significant difference regarding recording distances was found in peak latency, amplitude, or conduction velocity parameters. No differences in conduction parameters were found between genders and between age groups (MannWhitney U test, P ⬎.05, data not shown).
DISCUSSION The development of our technique for nerve conduction evaluations of the IPN was based on previous anatomic studies of the knees from cadavers, where accurate anatomy of IPN in the knee area has been described [4,6,8,11,17]. To allow maximal nerve stimulation and to prevent volume conduction from surrounding muscles, the SN stimulation was performed on a subcutaneous part of an SN after its exit from the Hunter canal [4]. The active surface electrode was placed at the area of IPN dispersion, far enough from the main SN trunk. The high rate of SNAP recording in our study shows good sensitivity of this technique despite a high known anatomic variability of the IPN described previously [8,10,11,14]. The anatomic studies showed a high rate variability of the IPN regarding its relationship to the sartorius muscle, the number of branches, and the area the nerve passes through [8,11]. This fact may explain the relatively high rate of 5.2% SNAP absence in our study (in 3 of 19 subjects who had both legs tested, the potentials were obtainable from only one leg). Furthermore, even assuming that side-to-side anatomic variability may exist [4,11], our study did not reveal significant electrodiagnostic differences between legs. Less range variation was found in SNAP onset latency compared with negative peak latency. Therefore we suggest that the SNAP onset latency is the most reliable parameter for
nerve conduction evaluation of IPN. A possible reason for the slight increase in SD is that the distance between the stimulation and recording electrodes varied from 8-10 cm depend on body habit. According to our results, a significant difference in onset latency was found between the 8-cm versus 10-cm recording distances. Thus for additional accuracy, we suggest that conduction velocity to onset that is not dependent on recording distance would be more reliable. As may be expected from the size of the IPN and its ramifications, the SNAP amplitude of IPN (onset to negative peak amplitude) was lower than the measured amplitude of the main trunk of the SN described in the literature [4,11]. However, the mean IPN amplitude observed in our study was markedly higher than the IPN amplitude described previously by Bademkiran et al [16] (6.96 ⫾ 3.68 V versus 1.3 ⫾ 1.1 V). Furthermore, we suggest that our method has the additional advantages of being simple, noninvasive, and faster than the previously mentioned near-nerve needle technique in the inguinal region. The technique presented in our study will allow a more practical approach to evaluation of infrapatellar neuropathy. This technique may be used in any case of anterior knee pain accompanied by hypesthesia, paresthesia, or dysesthesia suggestive of neuropathic involvement. It is recommended that the electrodiagnostician compare data from the involved limb, contralateral limb (when normal), and with normal conduction values presented in our study. Some limitations inherent to the methodology used in this study should be considered. First, the small number of patients makes it difficult to define the expected variation in latencies among the different age groups. Additional studies with a larger number of patients from various age groups will allow for expansion of the normal database. Second, the relatively high rate of SNAP absence found in the subgroup that had both legs tested is presumed to be a result of anatomic variability. Further studies of both legs in a larger population along with cadaveric studies will help to clarify this issue.
PM&R
Vol. 4, Iss. 9, 2012
CONCLUSION In this study we present a very simple noninvasive method for nerve conduction examination of the IPN. We found this technique to be reliable and easy to perform. It may be useful for establishing a definitive diagnosis of IPN injury and should be considered in cases of persistent anterior or inferior knee pain with sensory deficit of unknown origin.
8.
9. 10. 11.
REFERENCES 1. Johnson RJ, Kettelkamp DB, Clark W, Leaverton P. Factors effecting late results after meniscectomy. J Bone Joint Surg Am 1974;56:719-729. 2. Swanson AJ. The incidence of prepatellar neuropathy following medial meniscectomy. Clin Orthop 1983;181:151-153. 3. Poehling GG, Pollock FE Jr, Koman LA. Reflex sympathetic dystrophy of the knee after sensory nerve injury. Arthroscopy 1988;4:31-35. 4. Mochida H, Kikuchi S. Injury to infrapateller branch of saphenous nerve in arthroscopic knee surgery. Clin Orthop 1995;320:88-94. 5. Ikpeme JO, Gray C. Traumatic prepatellar neuralgia. Injury 1995;26: 225-229. 6. Tennent TD, Birch NC, Holmes MJ, Birch R, Goddard NJ. Knee pain and the infrapatellar branch of the saphenous nerve. J R Soc Med 1998;91:573-575. 7. Tifford CD, Spero L, Luke T, Plancher KD. The relationship of the infrapateller branches of the saphenous nerve to arthroscopic portals
12.
13.
14.
15. 16.
17.
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