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Can the use of QST lead to more targeted pediatric chronic pain treatment?



A question often asked: how would performing quantitative sensory testing (QST) affect

my treatment?


This is indeed a very legitimate question. We know that performing QST can assist in diagnostic queries like: is there a neuropathic aspect to this pain, do we see hypo-, hyperesthesia or allodynia, is there central sensitization? But does QST influence prescription habits of treating physicians?


In a very recent retrospective study out of McGill University in Canada (Bruneau, 2022) medical records of children treated in an outpatient interdisciplinary complex pediatric pain program were assessed. Medical records of 106 female adolescent patients (9-17 years old) for whom QST data were available, were compared to 102 medical records of age and gender matched patient for whom not QST data were available. The researchers’ objective was to determine whether the availability of patients’ sensory phenotype would affect prescription habits and whether it would have an impact on the duration of the treatment.


Patients with chronic primary pain and chronic secondary pain were treated. In patients with chronic secondary pain a disease is the underlying cause and the pain is part of the symptomatology of this disease, for example: chronic post-operative pain or chronic neuropathic pain. In contrast chronic primary pain includes diagnoses like complex regional pain syndrome or chronic primary headache.

Treatment was ceased when the patient reported minimal (VAS <3/10) pain.


Comprehensive QST protocol

The QST protocol in this outpatient pain treatment program consists of pressure pain threshold, dynamic mechanical allodynia, mechanical temporal summation, mechanical detection threshold, vibration detection thresholds, temporal summation and conditioned pain modulation (CPM).


Thermal tonic temporal summation (TS) was performed using Medoc’s Q-Sense at a pain intensity of 5/10 visual analogue scale (VAS) for 2 minutes. De Computerized Visual Analogue Scale (CoVAS) was used to rate pain throughout the stimulus.


Conditioned Pain Modulation (CPM) was measured by using the tonic thermal pain stimulus of the Q-Sense as the test stimulus, while having a cold pressor as the conditioning stimulus.

Thus, there was information available on mechanical hypersensitivity, the presence of allodynia, function of Aβ-fibers, increase of excitatory postsynaptic potential through TS, or descending inhibition through CPM.


Chronic pain treatment

Patients were treated in a multidisciplinary team and received cognitive behavioral therapy as well as outpatient physical therapy.


Based on their QST results patients fit either Phenotype A (allodynia and/or TS), phenotype B (pressure pain sensitivity), or phenotype C (reduced CPM). Each phenotype has a first line and second line pharmacological treatment preference based on mechanistic approach from data of previous studies on chronic pain populations.


When no QST data was available, treatment choice was based on condition-based guidelines.

Interventional treatment was considered in more complex clinical situations, in the presence of multiple diagnoses, or varied clinical findings.


Patient groups compared

Patients did not differ in age, diagnoses, pain intensity, sleep, mood and function between the two groups at baseline. There was also no difference in the distribution of chronic primary pain and chronic secondary pain between groups.


In the QST group 65% of patients had the allodynia/TS phenotype, 61% had the pressure pain sensitivity phenotype, while 55% had the deficient CPM phenotype. Of all patients, 26% belonged to all phenotypes of sensory deficit.


QST vs. non-QST group

Patients in the QST group received opioids and anticonvulsants less frequently, while being prescribed other drugs, such as magnesium supplements, melatonin supplements etc. more often. These patients were prescribed smaller number of medications – 0.9 in QST group vs 1.4 in the standard group. They also received less interventional treatments.


The above results were specifically relevant for secondary chronic pain patients. In contrast, in primary chronic pain patients, there were no statistical differences in prescribing antidepressants, non-steroidal anti-inflammatory drugs (NSAIDs), opioids, anticonvulsants or interventional therapies. However, this group received more other types of drugs when QST was available.


In terms of treatment duration, there was no statistically significant difference between the QST group and the non-QST group.


Conclusion

More and more pain clinicians choose to base treatment choices on pain mechanisms, rather than primary diagnosis. The results of this study show the potential of QST to assist in providing such mechanism-based, targeted treatment and prevent over-prescription and costly interventions.



References




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