Athletic Training and Sports Health Care

Pearls of Practice 

Performing a Neurological Examination on Patients With Musculoskeletal Extremity Symptoms: Part II. Integration of Quantitative Sensory Testing

Dhinu J. Jayaseelan, DPT, OCS, FAAOMPT; Erik B. Lineberry, DPT; Scott E. Resetar, DPT; Eric M. Magrum, DPT, OCS, FAAOMPT

Abstract

Part 1 of this two-part series described the clinical reasoning and statistical utility behind performing neurological examinations for individuals with extremity symptoms. Neurological examinations can assist in determining the integrity of the nervous system and localizing dysfunction to a peripheral or central problem. Neurological examinations are often performed when symptoms refer beyond the primary tissue(s) at fault or to determine the presence of red flags. In cases when symptoms spread or do not fit a typical pattern, identifying a specific tissue at fault can be challenging secondary to altered pain processing and sensitivity. As such, some authors suggest identifying dominant pain processing mechanisms (nociceptive, peripheral neuropathic, or central sensitization) to more effectively treat individuals with musculoskeletal symptoms.1 A review of differentiating and treating pain processing mechanisms is beyond the scope of this article, but readers are encouraged to further investigate these interesting topics.2,3 The purpose of this Part 2 article is to describe the potential integration of quantitative sensory testing (QST) into neurological examinations in attempts to identify the primary pain processing mechanism(s) at fault and subsequently guide treatment.

Pain spreading beyond the local site of tissue involvement (when present) may be a sign of increased responsiveness and/or reduced threshold of nociceptors to stimulation in their receptive field. This phenomenon is referred to as sensitization, or amplification. Sensitization can occur peripherally at the target tissue level (peripheral sensitization) or within the central nervous system itself (central sensitization), the latter of which is associated with normal or subthreshold afferent stimuli leading to hyperalgesia.4 This should be of particular relevance to orthopedic and sports clinicians because central and somatosensory changes may present bilaterally, even with unilateral symptom presentations. For example, some individuals with patellofemoral pain syndrome have demonstrated widespread hyperalgesia5 and bilateral tactile sensitivity deficits.6

QST is frequently used in research settings using mechanical, vibratory, or thermal detection thresholds to measure the degree of nervous system dysfunction in individuals with painful musculoskeletal conditions.2 Anecdotally, pain pressure thresholds (PPTs) measured using pressure algometers (Figure 1A) appear to be the most feasible method for QST in the rehabilitation setting. However, pressure algometers are not widely used clinically given the relative expense and lack of versatility. Although not currently validated for the measurement of PPTs, the primary author (DJJ) has used the rounded tip applicator on handheld dynamometers for this purpose (Figure 1B). The handheld dynamometer seems to be more readily available than pressure algometers in the orthopedic and sports settings due to the additional benefit of quantifying force output. Regardless of the type of tool used, obtaining objective data through QST and clustering findings with subjective and objective findings can assist in uncovering primary pain mechanisms at fault.

When assessing PPTs, force is applied perpendicular to the target tissue with gradually increasing pressure until the patient first subjectively reports pain instead of pressure.7 The mean of three trials is typically recorded in kilopascals (kPa) and testing is performed bilaterally. PPT has demonstrated good intrarater reliability (intraclass correlation coefficient = 0.94 to 0.97) and an intrarater minimal detectable change ranging from 42.7 to 137.0 kPa depending on the region tested.8 Lower values are indicative of a reduced threshold to non-noxious stimuli, or more pain perceived with less input. Reduced PPT values near the site of involvement can be representative of peripheral sensitization, whereas reduced readings at sites remote to the pain or bilaterally in the presence of unilateral dysfunction are more indicative of aberrant central pain processing.7

Consider a patient with chronic unilateral patellofemoral pain syndrome. The clinician has used appropriate exercise prescription and training/load modifications, but the patient has made little progress. The clinician…

Part 1 of this two-part series described the clinical reasoning and statistical utility behind performing neurological examinations for individuals with extremity symptoms. Neurological examinations can assist in determining the integrity of the nervous system and localizing dysfunction to a peripheral or central problem. Neurological examinations are often performed when symptoms refer beyond the primary tissue(s) at fault or to determine the presence of red flags. In cases when symptoms spread or do not fit a typical pattern, identifying a specific tissue at fault can be challenging secondary to altered pain processing and sensitivity. As such, some authors suggest identifying dominant pain processing mechanisms (nociceptive, peripheral neuropathic, or central sensitization) to more effectively treat individuals with musculoskeletal symptoms.1 A review of differentiating and treating pain processing mechanisms is beyond the scope of this article, but readers are encouraged to further investigate these interesting topics.2,3 The purpose of this Part 2 article is to describe the potential integration of quantitative sensory testing (QST) into neurological examinations in attempts to identify the primary pain processing mechanism(s) at fault and subsequently guide treatment.

Pain spreading beyond the local site of tissue involvement (when present) may be a sign of increased responsiveness and/or reduced threshold of nociceptors to stimulation in their receptive field. This phenomenon is referred to as sensitization, or amplification. Sensitization can occur peripherally at the target tissue level (peripheral sensitization) or within the central nervous system itself (central sensitization), the latter of which is associated with normal or subthreshold afferent stimuli leading to hyperalgesia.4 This should be of particular relevance to orthopedic and sports clinicians because central and somatosensory changes may present bilaterally, even with unilateral symptom presentations. For example, some individuals with patellofemoral pain syndrome have demonstrated widespread hyperalgesia5 and bilateral tactile sensitivity deficits.6

QST is frequently used in research settings using mechanical, vibratory, or thermal detection thresholds to measure the degree of nervous system dysfunction in individuals with painful musculoskeletal conditions.2 Anecdotally, pain pressure thresholds (PPTs) measured using pressure algometers (Figure 1A) appear to be the most feasible method for QST in the rehabilitation setting. However, pressure algometers are not widely used clinically given the relative expense and lack of versatility. Although not currently validated for the measurement of PPTs, the primary author (DJJ) has used the rounded tip applicator on handheld dynamometers for this purpose (Figure 1B). The handheld dynamometer seems to be more readily available than pressure algometers in the orthopedic and sports settings due to the additional benefit of quantifying force output. Regardless of the type of tool used, obtaining objective data through QST and clustering findings with subjective and objective findings can assist in uncovering primary pain mechanisms at fault.

Pressure pain threshold assessment of the quadriceps using a (A) pressure algometer and (B) handheld dynamometer.

Figure 1.

Pressure pain threshold assessment of the quadriceps using a (A) pressure algometer and (B) handheld dynamometer.

When assessing PPTs, force is applied perpendicular to the target tissue with gradually increasing pressure until the patient first subjectively reports pain instead of pressure.7 The mean of three trials is typically recorded in kilopascals (kPa) and testing is performed bilaterally. PPT has demonstrated good intrarater reliability (intraclass correlation coefficient = 0.94 to 0.97) and an intrarater minimal detectable change ranging from 42.7 to 137.0 kPa depending on the region tested.8 Lower values are indicative of a reduced threshold to non-noxious stimuli, or more pain perceived with less input. Reduced PPT values near the site of involvement can be representative of peripheral sensitization, whereas reduced readings at sites remote to the pain or bilaterally in the presence of unilateral dysfunction are more indicative of aberrant central pain processing.7

Consider a patient with chronic unilateral patellofemoral pain syndrome. The clinician has used appropriate exercise prescription and training/load modifications, but the patient has made little progress. The clinician performs QST and identifies decreased PPT readings on the contralateral limb and in both upper extremities. This likely indicates altered central pain processing mechanisms, which could benefit from additional conservative treatments such as manual therapy, aerobic activity, targeted psychosocial intervention, and/or a multi-disciplinary approach.7

Current evidence supports the potential benefit of understanding pain input and processing mechanisms in the evaluation and treatment of musculoskeletal dysfunction, but clinical practice does not necessarily reflect this. Having quantitative data to support findings can help create a specific treatment plan, track progress, and determine whether other practitioners are required (ie, psychology). In addition to performing a neurological examination to determine the integrity of the nervous system and screen out red flags, the authors propose the potential integration of QST into neurological examinations in attempts to match appropriate interventions to pain mechanisms to optimize patient/athlete outcomes.

References

  1. Vardeh D, Mannion RJ, Woolf CJ. Toward a mechanism-based approach to pain diagnosis. J Pain. 2016;17:T50–T69. doi:10.1016/j.jpain.2016.03.001 [CrossRef]
  2. Smart KM, Blake C, Staines A, Doody C. The discriminative validity of “nociceptive,” “peripheral neuropathic,” and “central sensitization” as mechanisms-based classifications of musculoskeletal pain. Clin J Pain. 2011;27:655–663. doi:10.1097/AJP.0b013e318215f16a [CrossRef]
  3. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152:S2–S15. doi:10.1016/j.pain.2010.09.030 [CrossRef]
  4. International Association for the Study of Pain. IASP Taxonomy. https://www.iasp-pain.org/Taxonomy. Published December 14, 2017.
  5. Pazzinatto MF, de Oliveira Silva D, Barton C, Rathleff MS, Briani RV, de Azevedo FM. Female adults with patellofemoral pain are characterized by widespread hyperalgesia, which is not affected immediately by patellofemoral joint loading. Pain Med. 2016;17:1953–1961. doi:10.1093/pm/pnw068 [CrossRef]
  6. Jensen R, Hystad T, Kvale A, Baerheim A. Quantitative sensory testing of patients with long lasting patellofemoral pain syndrome. Eur J Pain. 2007;11:665–676. doi:10.1016/j.ejpain.2006.10.007 [CrossRef]
  7. Courtney CA, Kavchak AE, Lowry CD, O'Hearn MA. Interpreting joint pain: quantitative sensory testing in musculoskeletal management. J Orthop Sports Phys Ther. 2010;40:818–825. doi:10.2519/jospt.2010.3314 [CrossRef]
  8. Walton DM, Macdermid JC, Nielson W, Teasell RW, Chiasson M, Brown L. Reliability, standard error, and minimum detectable change of clinical pressure pain threshold testing in people with and without acute neck pain. J Orthop Sports Phys Ther. 2011;41:644–650. doi:10.2519/jospt.2011.3666 [CrossRef]
Authors

From the School of Medicine and Health Sciences, George Washington University, Washington, DC (DJJ); and the Virginia Orthopedic Manual Physical Therapy Institute, Charlottesville, Virginia (DJJ, EBL, SER, EMM).

The authors have no financial or proprietary interest in the materials presented herein.

Correspondence: Dhinu J. Jayaseelan, DPT, OCS, FAAOMPT, 2000 Pennsylvania Avenue NW, Suite 2000, Washington, DC 20006. E-mail: dhinuj@gwu.edu

10.3928/19425864-20180809-01

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