Pain

last authored: April 2012, David LaPierre
last reviewed:

 

Introduction

Pain is "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" (IASP, 1994). However, pain frequently involves aspects other than the body, and can include emotional pain, social pain, and spiritual pain.

Sensory

  • location
  • intensity
  • quality

Affective

  • emotional reaction
  • fear, anxiety
  • depression

Cognitive

  • interpretation
  • context/meaning
  • memory/past experience

 

 

 

 

 

Suffering is in many ways rooted in loss; what has the pain taken away?

Nociception, pain, suffering, behaviours, social.

Pain can normally be managed or completely resolved, though often at the expense of side effects.

 

 

 

Biology of Pain

Pain is an integral part of physiology, and has protective functions against damage. Acute pain is mediated by nociceptors (temperature, chemical, pressure) and usually involves inflammation. It is a sharp pain that is also discriminative. It is mainly carried by fast Aδ fibres. Pain carried by C fibres is usually dull, diffuse, and aching.

 

 

Causes of Pain

Pain can be nociceptive or neuropathic, but is often both. Given its importance, chronic pain is a topic of its own.

  • nociceptive pain
  • neuropathic pain
  • mixed

Nociceptive Pain

Nociceptive pain is caused by stimuli or tissue damage. Inflammation can pften play a role here.

Somatic pain is superficial, and is usually well-localized.

Free nerve endings are not anatomocally identifiable.

TRP: transient receptor potential

ASIC: acid sensitive ion channels

 

Examples include:

  • burn
  • fracture
  • arthritis
  • trauma,

 

 

Nociceptors fall into three broad groups:

  • thermal nociceptors activated above 45 C or below 5 C
  • mechanical nociceptors
  • chemical nociceptors
    • activated by ie acid, bradykinins, histamine, cytokines, and prostaglandins, often from damaged cells

nociceptors tend to increase firing with longer stimuli, as opposed to other receptors that adapt to increased stimuli. So faster APs increases pain experience

TRP channels and ASIC channels

 

Most axons are C fibres belonging to polymodal nociceptors, which respond to mechanical, thermal, and chemical pain

 

Myelinated Adelta fibres are mechanical and thermal nociceptors

 

glutamate, peptides, and others are invloved with transmission at the spinal cord

modulation can be excitatory or inhibitory

 

 

Deep nociceptive pain is visceral. It is usally poorly diffused.

 

Referred Pain

Viscera are rich in nociceptors which are noomally silent. When visceral pain does occur, the skin area innervated by the same nerve root, according to dermatomes.

Visceral pain is

Neuropathic Pain

Neuropathic pain may be peripheral, affecting nerves, or central.

 

Causes of peripheral pain include:

  • herpes zoster
  • diabetic neuropathy
  • carpal tunnel syndrome
  • diabetic neuropathy
  • post-herpetic neuralgia
  • post-trauma/surgery

 

Central Pain

  • Damage to the anterolateral system, particularly spinothalamic and spinoreticular fibres, can cause central pain
  • damage to the thalamus can also lead to central pain, particularly one-sided and following vascular problems
  • also central suppression of pain

Somatic Reflexes

  • flexor and crossed extensor reflexes: cutaneous pain causes limb withdrawal and contralateral limb extension
  • scratch reflex: cutaneous pain on the body causes limb movements to remove source of irritation
  • increased muscle tone

Autonomic Responses

  • mediated by the brainstem and hypothalamus
  • increased heart rate, respiration rate, blood pressure
  • nausea, vomiting, sweating, dilated pupils

emotional responses: anxiety, fear; mediated by cingulate cortex in the limbic system

  • learning and memory, possibly through hippocampal connections, can lead to pain avoidance, or to pain expectation and increased perception
  • burning
  • shooting
  • stabbing
  • squeezing
  • aching
  • throbbing
  • scalding
  • hypersensitivity
  • tingling pain

 

Treatments

Neuropathic pain may be treated in a number of ways. These include:

  • SSRIs
  • SNRI's
  • GABA

Mixed

Appear to be both neuropathic and nociceptive.

  • FM
  • CFS
  • chronic headaches
  • dysmenorrhea
  • TMJ dysfunction
  • chronic whiplash d/o
  • chronic LBP
  • IBS
  • interstitial cystitis/prostatits

May be better called 'central sensitivity syndromes'.

 

 

Assessment of Pain

 

 

Pain Processing

Pain processing is complex. It causes somatic reflexes, autonomic reflexes, changes in attention, emotion, memory.

The spinothalamic tract carries somatic pain and temperature information up the contralateral spinal cord to the ventral posterolateral thalamus, and thereby to the somatosensory cortex. This is a fast pathway conveying information about intensity and location. The spinal trigeminal tract carries pain and temperature information from the head to ventral posteromedial thalamus. A slow, indirect path travels through the reticular formation to the hypothalamus and cingulate cortex, mediating arousal levels.

 

It appears that every person has a different volume control setting on pain, and that this threshold setting can be altered by life's events, eg psyical or psychological trauma, illness.

 

 

 

Pain Modulation

 

Hyperalgesia and Allodynia

Cellular damage and C fibre signaling leads to local vasodilation and substance P release, inducing mast cell degranulation of histamine. This causes local redness and hyperalgesia.

Inflammation-induced kinins, prostaglandins, amines, protons, and ATP can increase pain sensitivity by lowering nociceptor thresholds. Peripheral inflammation also signals the cell body to increase sensitivity to pain biochemically.

Hyperalgesia and allodynia (pain caused by normally non-painful stimuli, such as touch or warmth) can spread beyond the area covered by the axon reflex, likely through changes in synapses in the spinal cord.

 

 

Modulation in the spinal cord

Persistent, chronic pain involves peripheral and central sensitization.

Numerous receptors modulate transmitter release. Inhibitory neurotransmitters include opiods, cannabinoids, and GABA, while excitatory transmitters include bradykinin and prostaglandins.

Calcium channels in nociceptor terminals are different than those in other synapses, allowing them to be selecively inhibited.

 

 

Spinal Gating

Aβ mechanoreceptors synapse on inhibitory neurons, which thereby inhibit the Adelta synapse in the spinal cord. Mechanical stimulation (rubbing) or transcutaneous electrical stimulation excite these large mechanoreceptors and reduce pain.

 

 

Descending control

Decsending neurons from the periaqueductal gray and medulla synapse on inhibitory interneurons, which release endorphins (enkephalins) and inhibit the Adelta synapse. There is also some evidence for descending excitatory pain.

DNIC can be controlled by focus.

 

 

 

Effects of Pain

 

Pain and Depression

If pain is present before depresssion, it lasted; if it came with the depression, it went away with depression.

RESPECT trial: (Kroenke et al, Pain, 2008)

Pain and Sleep

We are beginning to learn how sleep modulates pain and how pain influences sleep. We do know chronic pain reduces total sleep time and number of cycles; shorter duration in stages 3 and 4.

Sleep efficacy drops from 91% to 78%.

Pain causes microarousals: sleep fragmentation and poor sleep.

Acutely ill hospitalized patients report poor sleep.

 

 

 

Pain Management

  • medications
  • visceral pain
  • neuropathic
  • palliative
  • other forms of management

Medications

 

Somatic pain

The analgesic stepladder is a helpful way of considering

mild (1-3): NSAIDs, acetaminophen +/- adjuvants

  • topical NSAIDs are also an option

moderate (4-6): mild, weak opioids: codiene, tramadol

severe (7-10): potent opioids: morphine, hydromorphone, fentanyl

unresponsive severe pain: interventional radiology

 

Titrate every three days; if after a week or two, there is no benefit, move on and pick another drug.

Upper dose is determined by the presence of toxicity

 

Adjuvants may be used for pain but first optimize the opioid dose, and avoid polypharmacy if possible.

 

 

no one should be in pain for more than an hour; breakthrough doses are 10% of the total daily

if more that 3 prns/day implies the baseline dose is not high enough

 

pick a route of administration

oral is preferred because of ease

 

  • NSAIDs for bone pain
  • antidepressants
    • TCAs, amytryptaline, nortryptyline
    • NE/SE
  • anticonvulsants (gabapentin, pregabalin, tegredol, phenytoin)
  • steroids

Visceral Pain

Opioids can be helpful.

Other options include:

  • antemetic drugs, such as serotonin antagonists
  • anticholinergic drugs
  • PPIs

Neuropathic pain

A mainstay of treatment of neuropathic pain includes:

  • tricyclic antidepressants: nortryptiline, amitripyline

Other options include:

  • SSRIs: sertraline, citalopram
  • SNRIs: duloxetine, venlafaxine
  • anticonvulsants: gabapentin, pregabalin, carbamazepine
  • opioids and tramadol
  • topical agents: lidocaine, capsaicin

Palliative

 

In situations of advanced disease, pain control is of critical importance.

Opioids are necessary for many patients.

Other pain management options include:

  • corticosteroids

Other Forms of Management

 

education

therapuetic exercise

psychological technoqies

massage

trials of modality-based therapies

music therapy

acupuncture

 

For substantial pain for a condition such as cancer, consider other modalities, ie radiation, surgery.

 

 

Resources and References

International Association for the Study of Pain