Pain Oriented Sensory Testing

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The examination of the somatosensory system is of great importance in the assessment of chronic pain, especially Neuropathic Pain and Nociplastic Pain. See also Numbness.


See also: Nociception
Figure 1. Electrical recordings from a sciatic nerve from a stimulus 80mm away. Shock strengths increase from top to bottom which results in stimulation of progressively smaller fibres.
Copyright Michael D Mann

Peripheral transmission follows transduction. Figure 1 shows a response being recorded from a sciatic nerve after an applied stimulus. The recording electrode experiences large changes in electrical potential. There are three major waves corresponding to three groups of nerves - A wave, B wave, and a smaller later C wave.

Velocities can be calculated, and we find that the diameter of the nerve fibres are proportional to their conduction velocities.

  • Large Fibres = Aα + Aβ. Aβ are found in skin, muscle, and viscera. They are important for discriminative touch, muscle spindles, Golgi tendon, and pain modulation.
  • Small Fibres = Aδ + C (+ Aγ). These provide sensory and autonomic function. They include preganglionic and postganglionic C fibres, plus efferent Aγ fibres. Small fibres cannot be tested using electrophysiology.

The Aα and Aγ nerves are largely made up of motor neurons. The Aβ waves are produced by large diameter sensory nerve fibres that information related to proprioception, touch, and pressure. All fibres capable of transmitting nociception are Aδ fibres or C fibres.

There is no such thing as a "pain fibre" or specific nociceptive fibre. There are a variety of nerve fibres that are capable of transmitting nociception, but that may not be their only function. In various situations there may be more than one fibre involved in transmitting nociceptive information.

Characteristics of peripheral nerve fibres
Nerve Fibre Myelin Diameter (µm) Conduction velocity (m/s) General Function
Aα (I) Yes   13-20   80-120 Proprioception: muscle spindle primary endings (Ia), golgi tendon organs (Ib), and alpha motor neurons
Aβ (II)   Yes   6-12   35-75 Discriminative sensitivity to mechanical stimuli (touch, vibration), proprioception, pain modulation (block nociceptive information, allodynia in sensitisation)
Aγ   Yes   4-8   15-40 Touch, pressure, and gamma motor neurons.
Aδ (III) Thin 1-5 5-30 "rapid" pain, crude touch, pressure, temperature. AMH type I for rapid mechanical pain (high heat threshold >53C), AMH type II for rapid heat pain (lower heat threshold 43-47C).
B No 1-3 3-14 preganglionic autonomic
C (IV) No 0.2-1.5 0.5-2.0 "second" pain, mechanical, chemical, thermal, pruritis, and postganglionic autonomic. polymodal

Stimulus Response

Main article: Allodynia and Alloknesis
Allodynia and hyperalgesia. Any reduction in pain threshold is allodynia, while any increased pain to supra-threshold stimuli is hyperalgesia.

Morphological and functional nervous system changes can lead to abnormal sensory signs. Hyperalgesia and allodynia are classic findings of neuropathic pain. Hyperalgesia reflects sensitisation of receptors, while allodynia is a central phenomenon mediated by large myelinated fibres.

Hyperaesthesia refers to both lowered thresholds and to increased response to suprathreshold stimuli.

Allodynia is essentially decreased pain threshold. "Pain due to a stimulus that does not normally provoke pain." It is a nociceptive sensation or aversive response elicited by a normally non-nociceptive stimulus. "allo" means other, and "dynia" means pain. It can occur with mechanical, thermal, or chemical stimuli (e.g. tactile allodynia, heat allodynia).

Hyperalgesia is essentially increased response (lowering of the pain threshold) to normally painful stimuli. It is defined by the IASP as "Increased pain from a stimulus that normally provokes pain." An example is the prick of a needle, which is normally painful, but with hyperalgesia there is a greater than normal magnitude and/or duration of pain.


There are three types of mechanical hyperalgesia and allodynia:

  1. Static allodynia and hyperalgesia: blunt gentle pressure on the skin elicits pain. Some term this static allodynia but others call it static hyperalgesia. This appears to be mediated by sensitised C nociceptors (and Aδ fibres?).
  2. Punctate hyperalgesia and allodynia: punctate hyperalgesia e.g. when tested with a stiff von Frey hair, and punctate allodynia e.g. when tested with a toothpick. This is mediated by sensitised Aδ fibre high-threshold mechanoreceptors.
  3. Dynamic allodynia: light brushing elicits pain. This is mediated by Aβ fibre low-threshold mechanoreceptors normally responsible for touch sensation, but in neuropathy can evoke Aβ pain due to central sensitisation.

There are two types of thermal hyperalgesia and allodynia:

  1. Cold hyperalgesia and allodynia: cold stimuli elicits pain. This is possibly due to a loss of cold Aδ fibres leading to cortical reorganisation
  2. Heat allodynia: warm and heat elicit pain. Some authors incorrectly call this heat hyperalgesia, but a lowering of the heat pain threshold means that pain occurs to a normally nonpainful warming. This process is possibly due to sensitisation of C fibres and their second order neurons.


Hyperpathia is essentially a type of allodynia and hyperalgesia that describes a complex sensory experience. The IASP define hyperpathia as "a painful syndrome characterised by an abnormally painful reaction to a stimulus, as well as an increased threshold."

Hyperpathia may occur alongside allodynia, hyperaesthesia, hyperalgesia, or dysaesthesia (dysaesthesia is an abnormal sensory experience, either unpleasant or evoked). Some view it has a type of hyperaesthesia, or even equate the two terms. There is both an elevation of the detection threshold and central hyperexcitability. It can occur in axonal loss and in central sensitisation states.

There are four main features of hyperpathia:

  1. Increased detection threshold: An increased threshold to noxious or non-noxious stimulation. This may be due to reduced afferent input.
  2. Delay: An abnormal latent period in the perception of the stimulus. This may be due to reduced large fibre afferent input.
  3. Summation: this refers to an increasingly painful sensation to a repetitive stimulus of steady intensity which unmasks hyperpathia. Summation can be seen as an explosive overshooting pain response that can occur with strong withdrawal movements and a vasomotor or vegetative reaction. There is a lack or insufficient relationship between the stimulus strength and sensation strength. There is poor localisation and the inability to identify the nature of the stimulus that elicited the pain, with a radiating sensation out from the point of sensation to wide adjacent areas. Summation may be due to afterdischarge in damaged sensory neurons, crossed afterdischarge in sensory neurons, coupling of adjacent nerves, and central sensitisation.
  4. Aftersensation: there is a long aftersensation or pain after the stimulus has ceased. This can occur for seconds, minutes, or hours after only brief periods of stimulation.


Main article: Dermatomes

In spinal cord disease the sensory level is often several segments below the level of the injury. If the sensory and motor levels disagree then the motor level is more accurate. The level of vertebral pain and tenderness is the most accurate indicator of the affected section. In radiculopathy sensory loss is less useful than motor and reflex changes.


  • Reflex hammer - Aα (Ia and II)
  • Camel hair brush or cotton wool - Aβ
  • Tuning fork - Aβ + Aδ
  • Fingertip - Aδ
  • Toothpicks - Aδ
  • Timer

Optional tools

  • Neurotips
  • Battery size D
  • Infrared thermometer
  • Paperclips
  • Tape measure



Below is a table comparing clinical vs QST methods that I have modified from several sources. One should compare both sides and sites.

  • Compare sides: compare sensation on opposite sides (mirror testing).
  • Compare sites: compare sensation at test site with a ‘normal’ (reference) site.
Summary of choice methods of assessing nerve function per sensation.
Fibres Sensation Finding Descriptor Clinical Relevance Testing Equipment and Instructions
Clinical QST Laboratory
Touch Dynamic mechanical allodynia Common to most NP. Central sensitisation. cotton wool or camel hairbrush - 2cm stroke over 1 second and repeat Von Frey filaments NCS, SEPs
Vibration Vibration detection threshold Infrequent but strongly suggestive of NP Tuning fork (128 Hz) Vibrameter† NCS, SEPs
Pinprick, sharp pain Punctate mechanical allodynia and hyperalgesia Common to most NP. Central sensitisation. Punctate mechanical allodynia - use a toothpick apply 2 stimuli per second (2 Hz) and repeat.

Punctate mechanical hyperalgesia - optionally tested with a neurotips needle.

Weighted needles LEPs, IENF
Touch Static or Pressure-evoked mechanical allodynia Common to most NP, also observed in inflammatory pain. Central sensitisation. Finger tip - apply pressure until blanching of nail bed for 1 second and repeat. Von Frey filaments
Cold Cold allodynia Infrequent but strongly suggestive of NP. Central sensitisation. Stainless steel 128 Hz tuning fork prongs applied to the skin for 1 second and repeat Thermode‡ None
Touch, Pain Temporal summation indicating hyperpathia Central sensitisation, test for "wind-up" Toothpick applied 2 stimuli per second (2Hz) for 30 seconds. Assess change in pre- and post- pain scores, and aftersensation.
C Warmth Warm allodynia Infrequent but strongly suggestive of NP. Peripheral sensitisation. Thermoroller or warmed C size battery at 45° applied for 1 second and repeat Thermode‡ LEPs, IENF
† or other device providing graded vibratory stimuli

‡ or other device providing graded thermal stimuli
NCS: nerve conduction studies, SEP: sensory evoked potentials, LEP: laser evoked potentials, IENF: intra-epidermal nerve fibre density. NP: neuropathic pain
Modified from various sources[1][2][3][4]

Simple Sensations

Reduced simple sensations define all important clinical sensory syndromes: peripheral nerve injury, radiculopathy, spinal cord syndromes, lateral medullary infarction, and thalamic and cerebral hemispheric syndromes.

Reduced Touch Sensation (Aβ): Touch the skin using a single “dabbing motion.” Assess qualitatively

Reduced Pain Sensation (Aδ): Apply stimulus with bent safety pin or broken wooden stick. Assess qualitatively.

Reduced pain sensation detects loss of small nerve fibres on skin biopsies with sensitivity of 88% and specificity of 81% with positive LR of 4.6 and negative LR of 0.2.[5]

Vibration Sensation (Aβ): Strike a 128-Hz tuning fork from a distance of 20cm against the heel of the clinician’s hand and apply to the tested structure.

Thresholds: 40 year old man should feel vibration over lateral malleolus for 11 seconds, and ulnar styloid for 15 seconds. Decreases by 2 seconds for every decade greater than 40.

Although vibration is is a highly developed sensation, there is no distinct vibration sense organ and the neuroanatomic pathways are not clear. Traditionally vibration is considered together with proprioception because impulses from both sensations ascend up the posterior columns of the spinal cord. However there can be dissociation of vibration and sensory loss in some peripheral neuropathies (diabetic polyneuropathy) and diseases of the dorsal column of the spinal cord (tabes dorsalis, multiple sclerosis, vitamin B deficiency).

Humans are most sensitive to 200-300Hz but we use a 128Hz tuning fork because of tradition and because normative values are based on 128Hz. Also interestingly bone is not more sensitive to vibration than soft tissue, it is equal or even better over soft tissues, but again normative values have used bone.

One disadvantage to vibration testing is that the vibrating impulse is conducted away from the tuning fork, and so you can't use it to define precise sensory boundaries in those with peripheral nerve injuries.

Cortical Sensations

One method of testing cortical sensation is through Two-point Discrimination (Aβ). You need to have normal simple sensations to be able to test this

Apply paper clip bent into a ∩ shape and apply stimulus for 1 second then repeat.


  • Fingertip  5mm
  • Palm + sole   10mm
  • Face   15mm
  • Limb + back + torso   40mm

Mechanical Sensation

Static Allodynia (Aδ): Apply pressure to soft tissues with tip of your index finger until the nail bed ‘blanches.’ Apply the stimulus for 1 second and repeat

Dynamic Allodynia (Aβ): Tangentially stroke the skin with a camel hair brush OR a cotton wool ball. Apply a 2 cm long brush-stroke over 1 second and repeat

Punctate Allodynia and Hyperalgesia (Aδ): Stimulate the skin with a toothpick. Apply 2 stimuli per second (2 Hz) and repeat

Neurotips test more for hyperalgesia, while toothpicks test more for allodynia.

Thermal Sensation

Cold Allodynia and Hyperalgesia (Aδ): Apply the cold prongs of a stainless steel tuning fork to the skin. Apply the stimulus for 1 second and repeat

Warm Allodynia (C) OPTIONAL: Warm a C-size battery in water bath at 45˚C for 5 minutes (use IR thermometer. Then apply base of the battery to the skin. Apply the stimulus for 1 second and repeat


Hyperpathia (Aδ): Stimulate the skin with a toothpick. Apply 2 stimuli per second (2Hz) and repeat, and ask a baseline pain score. Then apply stimulus at 2Hz continuously for 30 seconds.. Ask a final pain score immediately at the end of 30 seconds

Final pain > Baseline pain = hyperpathia

Pain continues after stimulation ceases = after-sensations

Infrared Thermometry

Infrared Thermometry tests the sympathetic fibres by using a hand-held infrared thermometer and measuring skin temperature in an area where altered sensory, sympathetic nervous system, or vascular function is suspected. For example this could be in CRPS or painful diabetic neuropathy.

Direct a hand-help infrared thermometer to an area of skin and compare with the opposite side (mirror measurements). A temperature difference of ≥ 1.0˚C is considered significant.

Chronic CRPS patients have a normal vasodilatory response to external heating. Skin temperature differences between the affected and unaffected lower limbs are highly variable during daytime and disappear during sleep. In other words part of the vasomotor regulation is suspected to be functional.[6]


See Also


  1. Cruccu & Truini. Tools for assessing neuropathic pain. PLoS medicine 2009. 6:e1000045. PMID: 19360134. DOI. Full Text.
  2. Zhu et al.. Concurrent validity of a low-cost and time-efficient clinical sensory test battery to evaluate somatosensory dysfunction. European journal of pain (London, England) 2019. 23:1826-1838. PMID: 31325385. DOI. Full Text.
  3. Backonja et al.. Value of quantitative sensory testing in neurological and pain disorders: NeuPSIG consensus. References 2013. 154:1807-1819. PMID: 23742795. DOI.
  4. Faculty of Pain Medicine. Pain Oriented Sensory Testing Guidelines. 2018.
  5. Walk D, Wendelschafer-Crabb G, Davey C, Kennedy WR. Concordance between epidermal nerve fiber density and sensory examination in patients with symptoms of idiopathic small fiber neuropathy. J Neurol Sci. 2007;255:23–26.
  6. Schilder JC, Niehof SP, Marinus J, van Hilten JJ. Diurnal and nocturnal skin temperature regulation in chronic complex regional pain syndrome. J Pain. 2015 Mar;16(3):207-13. doi: 10.1016/j.jpain.2014.11.012. Epub 2014 Dec 3. PMID: 25481495.