Book p. 1022 · asked once in NTRUHS papers

In one breath

A handful of words describe how pain sensitivity has gone wrong: hyperalgesia (lowered threshold), hypoalgesia (raised threshold), analgesia (none at all), hyperpathia (an exaggerated reaction once pain is felt) and allodynia (pain from a stimulus that should not hurt, like light touch). The named syndromes then follow: causalgia, a burning pain after nerve trauma that outlives the injury and is maintained by sympathetic fibers; inflammatory pain, the commonest of all; neuropathic pain from nerve injury, which responds poorly to analgesics; tic douloureux, or trigeminal neuralgia; thalamic syndrome after a posterior thalamic stroke; and toothache, from the richly innervated dental pulp.

Builds on: Pain: concepts, receptors and fibers · Endogenous pain control and gate control theory · Leads to: Trigeminal pathway and trigeminal neuralgia · Thalamus: nuclei, functions and thalamic syndrome · Sensory lesions and sensory function tests

Terminologies

TermWhat it means
Hyperalgesiagreater sensitivity, lowered threshold to painful stimuli
Hypoalgesia (hypalgesia)less sensitivity, raised threshold
Analgesiacomplete loss of pain sensation
Hyperpathiapain perception is faulty, but the reaction is exaggerated once pain is perceived
Allodyniaexcessive response to a mild stimulus
  • Hyperalgesia: inflamed skin is the everyday cause.
  • Analgesia need not take the other sensations with it; pain alone can be lost (Sensory lesions and sensory function tests).
  • Hyperpathia: the reaction to other stimuli is increased as well, not only to painful ones.
  • Allodynia: the classic example is light touch, which is never painful in health, producing pain.

Hyperalgesia, hyperpathia, allodynia

Three words that get swapped in vivas. Pin them to the stimulus:

  • Hyperalgesia — a painful stimulus hurts more than it should.
  • Allodynia — a harmless stimulus hurts at all.
  • Hyperpathia — the reaction to the stimulus is out of proportion, and other stimuli are over-reacted to as well.

Assessing a patient’s pain

Six things the physician notes:

  1. How it began.
  2. Its quality — burning, stabbing, aching.
  3. Its location, and any referral (Visceral and referred pain).
  4. Its intensity and duration.
  5. What provokes it and what relieves it.
  6. The physiological and behavioural responses that go with it.

Causalgia

  • A burning pain that follows traumatic injury of a peripheral nerve.
  • It is continuous, and usually carries hyperalgesia and allodynia with it.
  • The striking thing: it persists even after the nerve damage has fully recovered.
  • The sympathetic fibers are thought to keep it going, because it is relieved by sympathectomy or by adrenergic blockers.
  • The mechanism proposed: noradrenergic sympathetic fibers grow into the dorsal root ganglia serving the injured area. After that, every sympathetic discharge produces pain there.

Applied: why a pain can be sympathetically maintained

Normally the sympathetic system has nothing to do with sensation. In causalgia the sprouted noradrenergic fibers hand it a line straight into the sensory neurons of the DRG, so ordinary sympathetic traffic now produces pain — which is why removing or blocking the sympathetic supply relieves it.

Inflammatory pain

  • Inflammation is the commonest cause of pain, and inflammation follows injury.
  • The mediators, including cytokines and substance P, raise sensitivity and lower the pain threshold in the injured area.
  • So a minor painful stimulus now produces severe pain: these substances increase pain perception.
  • It is one of the two kinds of pathologic pain (Pain: concepts, receptors and fibers).

Neuropathic pain

  • Pain caused by injury to a nerve. Neuralgia is the general term for it.

  • Trigeminal neuralgia from herpes zoster, causalgia included, is the book’s example.

  • Other causes: diabetic neuropathy, nerve injury, the polyneuropathies, root irritation as in a prolapsed disc, and spinal cord injury.

  • It usually comes with hyperesthesia (increased cutaneous sensitivity), hyperalgesia, hyperpathia and allodynia.

  • It does not respond well to analgesics. Treatment climbs in steps:

    • usually helpful: an epidural injection of analgesic together with a steroid;
    • in severe cases, cutting the pathway —
      • nerve section: cut the nerve carrying sensation from the injured site;
      • dorsal rhizotomy: cut the pain fibers in the dorsal root;
      • anterolateral cordotomy, also called spinothalamic tractotomy: cut the ascending spinothalamic fibers in the cord.
  • Worth knowing, though not in your pages: the reason anterolateral cordotomy is done on the side opposite the pain is that the second-order fibers have already crossed in the cord (Pain pathways and perception).

Tic douloureux

  • Another name for trigeminal neuralgia.
  • Severe, stabbing, acute facial pain that lasts only briefly each time.
  • Most patients get it after compression of the trigeminal nerve roots (Trigeminal pathway and trigeminal neuralgia).

Thalamic syndrome

  • Chronic, severe and extremely unpleasant pain, arising spontaneously or from a trivial stimulus.
  • The pain is felt in the brain, with no peripheral pathology at all.
  • Cause: an ischemic or hemorrhagic lesion of the posterior thalamic nuclei, after obstruction of the thalamogeniculate branch of the posterior cerebral artery (Thalamus: nuclei, functions and thalamic syndrome).
  • Treatment: the pain is cured by stereotaxic destruction of the posterior thalamic nucleus.

Central pain, not peripheral

Thalamic syndrome is the standard example of central pain: cut every nerve to the limb and the pain stays, because the pain is generated in the thalamus. Compare causalgia, where the trigger sits in the periphery.

Toothache

  • Teeth are full of nociceptors.
  • They are supplied by axons of the maxillary and mandibular divisions of the trigeminal nerve — C, Aδ and Aβ fibers.
  • Route of the fibers: in through the root apex, branching within the pulp, ending in the pulp plexus.
  • Enamel and cementum carry no nerve fibers. The pulp is the sensitive part, and enamel is its cover and shield.
  • So exposure of the pulp, or inflammation of it, is what hurts.
  • Four things set a toothache off: heat, cold, inflammation, and probing the pulp mechanically.

Exam-answer skeleton: "Define hyperalgesia, hypoalgesia, hyperpathia and allodynia, and give an example of each" (short note)

  1. One line on pain threshold, and on inflammation lowering it, so the definitions have something to hang on.
  2. Hyperalgesia: lowered threshold, greater sensitivity; example, inflamed skin.
  3. Hypoalgesia: raised threshold; example, a local anesthetic or a partial nerve lesion.
  4. Analgesia: complete loss of pain, which may spare the other sensations.
  5. Hyperpathia: faulty perception with an exaggerated reaction once pain registers, and over-reaction to other stimuli too.
  6. Allodynia: pain from a stimulus that should not hurt; example, light touch.
  7. Where they cluster in practice: inflammatory pain (hyperalgesia, allodynia), neuropathic pain and causalgia (all four, plus hyperesthesia).
  8. Close with the six points a physician records when assessing pain.

Asked in exams