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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 32  |  Issue : 3  |  Page : 145-149

Is tactile acuity altered in individuals with acute mechanical neck pain?


1 Department of Physiotherapy, Ramaiah Medical College, Bengaluru, Karnataka, India
2 Department of Physiotherapy, Global Hospital, Mumbai, Maharashtra, India
3 Center For Rehabiliitation, Ramaiah Memorial Hospital, Bangalore, Karnataka, India

Date of Web Publication31-Dec-2018

Correspondence Address:
Assoc Prof. Shobhalakshmi S Holla
Department of Physiotherapy, Ramaiah Medical College, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpn.ijpn_20_18

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  Abstract 

Background: Tactile acuity measured by point discrimination (TPD) refers to the precision by which we can sense touch.An increase in TPD threshold (loss of tactile acuity) is considered suggestive of disruptions to S1 cortical maps of that specific body part. In some chronically painful conditions, reduced tactile acuity is a manifestation of Central sensitization (CS).The other symptoms include hyperalgesia and allodynia due to repeated activation of spinal nociceptors. A recent study has shown that tactile acuity is affected in individuals with chronic neck pain. While there seems to be adequate evidence stating that tactile acuity is reduced in individuals with chronic pain, CS may not be limited to chronic pain states. There is a paucity of literature with respect to the tactile acuity of a person with acute neck pain. A measurement of tactile acuity of the affected body area in acute pain, may suggest the extent of the altered threshold of sensory discriminative aspect of pain experience. Objectives: To compare the two-point discrimination over C7 spinous process between the symptomatic individuals with mechanical neck pain and age matched healthy controls. Methods: 30 individuals with mechanical neck pain & 30 age matched normals were assessed for two point discrimination using mechanical calipers, The two sharp points of the caliper were vertically placed against the skin surface over C7 spinous process, commencing with 5mm, which was stretched out till the subject appreciated the two points. Values were noted down in millimeters. Results: An independent t – test showed a significant difference in the two point discrimination between the 2 groups (P < 0.000). Conclusion: It can be concluded that individuals with acute mechanical neck pain demonstrated a change in tactile acuity.

Keywords: Acute pain, mechanical neck pain, tactile acuity, two-point discrimination


How to cite this article:
Holla SS, Vats T, Nagpal P. Is tactile acuity altered in individuals with acute mechanical neck pain?. Indian J Pain 2018;32:145-9

How to cite this URL:
Holla SS, Vats T, Nagpal P. Is tactile acuity altered in individuals with acute mechanical neck pain?. Indian J Pain [serial online] 2018 [cited 2019 Jan 19];32:145-9. Available from: http://www.indianjpain.org/text.asp?2018/32/3/145/249097


  Introduction Top


Tactile acuity measured by two-point discrimination (TPD) refers to the precision by which we can sense touch.[1] It has been widely used in the clinical practice for the evaluation of peripheral nerve injuries and monitoring patient's recovery and response to the treatment.[2] It is a somatosensory information that ascends through the lemniscal pathway. It primarily consists of large myelinated axons, arising from A-beta sensory end organs (cutaneous mechanoreceptors that respond to pressure and vibration) located in the dermis of the skin.[3] Tactile acuity is dependent not only on the innervation density and intact neural pathways but also on the response profiles of the primary sensory cortex (S1) cells and the sensory neuraxis.[4] Tactile acuity is considered a clinical signature of S1 representation. Therefore, an increase in TPD threshold (loss of tactile acuity) is considered suggestive of disruptions to S1 cortical maps of that specific body part.[5]

In some chronically painful conditions, reduced tactile acuity is a manifestation of central sensitization (CS).[5] The other symptoms include hyperalgesia and allodynia due to repeated activation of the spinal nociceptors. CS is also associated with increased activity of pain facilitation pathways[6],[7] and malfunctioning of descending pain inhibitory pathways, thereby resulting in dysfunctional endogenous analgesic control.[8]

Notably, a recent study has shown that tactile acuity is affected in individuals with chronic neck pain.[9] Neck pain generally affects 45%–54% of population and is one of the causes of disability worldwide.[10] While there seems to be adequate evidence stating that tactile acuity is reduced in individuals with chronic pain,[11] CS may not be limited to chronic pain states.[8] For example, in patients with whiplash-associated disorders, abnormal sensory processing may appear quite rapidly (<7 days) after the initial whiplash trauma, and once present, it has an important predictive ability for the development of chronicity.[12]

There is a paucity of literature with respect to the tactile acuity of a person with acute pain. A measurement of tactile acuity of the affected body area in acute pain may suggest the extent of the altered threshold of sensory discriminative aspect of pain experience. Literature also suggest that tactile training approaches might normalize S1 reorganization and reduce pain.[13],[14],[15] Hence, it is important for clinicians to rapidly identify CS in patients with acute pain for the early identification of the risk for chronicity and aim treatments at improving the tactile acuity of acute pain conditions.

This study primarily aims at determining the tactile acuity of symptomatic individuals with acute mechanical neck pain. The objective of the study is to compare the TPD over C7 spinous process between the symptomatic individuals with acute mechanical neck pain and age-matched healthy controls.


  Materials and Methods Top


A cross-sectional study with a sample size of 60 was taken for the study (30 symptomatic individuals mechanical neck pain and 30 age-matched healthy controls).

Sample size estimation – A study carried out on “Tactile Acuity is disrupted in Osteoarthritis but is unrelated to disruptions in motor imagery performance,”[16] has revealed that the TPD threshold values of mean and standard deviation among the patients with a knee osteoarthritis as compared to controls were 45.1 (11.8) and 29.4 (8.8). Based on the above findings of the study with an alpha error of 1% and power of study at 99%, it is estimated that 21 subjects need to be recruited under each of the groups – acute pain and age-matched healthy controls. However, it was proposed to recruit a larger number of individuals for any subgroup analysis based on the intensity of pain, etc.

The individuals were taken from the outpatient department of orthopedics and physiotherapy through simple random sampling.

Inclusion criteria

  • Symptomatic individuals with mechanical neck pain
  • Onset <2 weeks
  • Age-matched asymptomatic individuals
  • Males and females aged between 18 and 40 years
  • Pain around C7 spinous process.


Exclusion criteria

  • Osteoporosis
  • Malignant tumors
  • Inflammatory arthritis
  • Any motor or sensory deficit
  • Neck pain due to trauma
  • Previous fracture of the neck or back
  • Structural abnormality affecting neck posture
  • Radiating neck pain.


Procedure for data collection

After receiving the approval from the Ethical Committee of the medical college, individuals satisfying the inclusion criteria were selected and assessed for measuring TPD values in the study. Individuals with and without mechanical neck pain, both males and females, were included in this study.

Purpose of this study was explained to each patient, and an informed consent was obtained from 60 patients. A detailed assessment of the patients was taken before the study. The assessment included history of the presenting illness, assessment of pain, postural screening for any deformities in the spine, palpation of the area of pain, range of motion and flexibility assessment, screening for neurological deficits and systemic illness, and performing provocative tests when required.

Individuals, who fulfilled the inclusion criteria and gave their consent, were taken up for the study. The painful area around the neck was palpated through palpatory method. Symptomatic individuals with mechanical neck pain and age-matched healthy controls were assessed for TPD, using mechanical calipers (Ocean Economy Vernier Caliper 0–150 mm), by a coinvestigator who was blinded to the study.

TPD was assessed with neck lying in a neutral position and the individual looking downward through the face hole of the plinth. It was assessed using a mechanical caliper, where the two sharp points of the caliper were vertically placed against the skin surface over the C7 spinous process, commencing with 5 mm, which was stretched out till the individual appreciated the two points. Values were noted down in millimeters.

The mechanical caliper was placed on the skin surface by applying pressure with its sharp tip so as to blanch the skin. Individual's feet were supported on a pillow placed under the ankles. Individuals were instructed to report after each application, “one” if they felt one point or “two” if they felt two points. If they were unsure, then they were instructed to report as one point,[17] under optimum room temperature and patient at ease. Readings obtained were measured from both the group of symptomatic individuals with mechanical neck pain and age-matched healthy controls and were compared for the significant difference, if any [Figure 1].
Figure 1: Assessment of two-point discrimination

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  Results Top


Data analysis was done using SPSS for windows, version 16.0, (Chicago, USA). Independent t-test was used to compare the mean TPD between symptomatic individuals with mechanical neck pain and age-matched healthy controls. A total of 60 individuals between the age groups of 18 and 40 years whose mean age was 30.23 years were included for the study [Table 1].
Table 1: Comparison of two-point discrimination between symptomatic individuals with mechanical neck pain and age-matched healthy controls

Click here to view


[Table 1] shows that there is a significant difference in the TPD value between the symptomatic individuals with neck pain and age-matched healthy controls, with P < 0.000.

[Graph 1] shows a strong negative correlation between the onset of pain and tactile acuity. This indicates that as the number of days from onset of pain increases, there is a decrease in the value of TPD (mm), with P < 0.005 and a correlation coefficient of r = −0.85.




  Discussion Top


The study aimed to compare the tactile acuity between symptomatic individuals with mechanical neck pain and age-matched healthy controls.

In this study, we have found that there is an alteration in tactile acuity in symptomatic individuals when compared with the age-matched healthy controls (P < 0.000). The results showed that the TPD was increased in individuals with neck pain, thereby reflecting decreased tactile acuity.

Our results also showed a negative correlation between the number of days from the onset of pain and tactile acuity in the individuals with mechanical neck pain. It showed that as the number of days from the onset of pain increased, the value of TPD decreased (P < 0.005).

The results obtained were in accordance with a recent study conducted by Adamczyk et al. on acute low back pain. The study showed an altered tactile acuity in an induced nociceptive low back pain. They also found that deterioration of pain occurred immediately after pain induction and was related to the intensity of pain perception.[18]

While the phenomenon for the observed changes in tactile acuity is unknown, it is hypothesized that the changes are based on some peripheral and central mechanisms.

The cortical regions that are frequently activated by pain, receive noxious and innocuous somatosensory inputs from somatosensory thalamus.[19] Evidence indicate that the parietal operculum and the anterior insula are also involved in the cortical representation of pain. Electrophysiological data in humans and clinical observations in patients with cortical lesions suggest that the inner surface of the parietal operculum, between the classical SII area and the insula, contains a nociceptive area.[20] Literature suggests that this area is activated very early after the onset of phasic noxious stimuli.[19],[20] Early disruptions to the parietal operculum, anterior insula, and the S1 cortical map could probably be one of the reasons for the increased TPD that is seen in acute neck pain.

Literature also suggests that in acute pain, the sensory discriminative aspect of the pain is altered when the nociceptors are excited after being stimulated via a noxious stimulus (here, mechanical), thereby conveying the information to the projection neurons within the dorsal root ganglion of the spinal cord and projecting the information to the somatosensory cortex via the thalamus.

Once the mechanical stimulus is carried out by the primary afferent terminal to the dorsal root ganglion, the receptor potentially activates the voltage-gated channels, where voltage-gated calcium channel plays a key role in the release of neurotransmitter from the central or peripheral nociceptor terminals which produces pain or neurogenic inflammation. In an acute phase of pain, the threshold of sensory discriminative part of pain could have hereby increased, thus lowering the pain threshold.[21]

Our results probably cannot be explained through central mechanisms only. The tissue damage that has taken place due to the inflammation following the acute neck pain could have led to the formation of inflammatory mediators activated by nociceptors such as serotonin, histamine, glutamate, adenosine triphosphate, adenosine, substance P, calcitonin gene-related peptide, bradykinin, prostaglandins, thromboxanes, leukotrienes, endocannabinoids, nerve growth factor, tumor necrosis factor-α, interleukin-1 β, extracellular proteases, and protons, which is also known as “inflammatory soup.” These act directly on the activated nociceptor by binding to one or more cell surface receptors consisting of G protein-coupled receptors, Transient receptor potential (TRP) channels, acid-sensitive ion channels, two-pore potassium channels, and receptor tyrosine kinases, which masks the effect of the other sensory receptors responsible for touch perception thereby, altering the tactile acuity at the peripheral level.[21]

While there is consistent evidence exhibiting tactile acuity deficits in people with chronic low back pain[22],[23] and complex regional pain syndrome,[24],[25],[26] the evidence on neck pain is limited. A recent study on tactile acuity in people with chronic neck pain showed tactile deficits in the neck when compared to healthy controls. Deficits in TPD were also seen at nonpainful sites, suggesting that reduced sensory precision could spread beyond the painful region.[9],[11] All of these suggest that the alterations in tactile acuity occur as a result of cortical reorganization.

Limitations

The limitations of the study could be the assessment of the spasm of cervical muscles, as it is subjectively quantified in symptomatic individuals with mechanical neck pain. A digital vernier caliper could have provided better reliability when compared to a mechanical sliding caliper.

Although TPD threshold is the most common measure of tactile acuity[27] as it is easy to assess, it has been criticized for the unexplained variability observed within individuals,[28] between individuals, and between studies.[29]


  Conclusion Top


With the present study, it can be concluded that tactile acuity is altered in individuals with acute mechanical neck pain.

Future research

Tactile acuity scores can be assessed at other areas such as the knee and other regions with acute pain. The study can be undertaken with the intervention provided to the symptomatic individuals with mechanical neck pain and follow-ups to see the alterations in tactile acuity. Future studies can also consider other measures to assess tactile acuity.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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