Nerve Pain       Sympathetic Pain      
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Anatomy and Physiology

Sympathetic pain is a type of nerve pain (neuropathy, neuralgia, neuritis), seen in the pain clinic, that arises due to an abnormality of the function of the sympathetic nervous system.

The sympathetic nervous system (SNS) is part of the autonomic nervous system (involuntary) and prepares the body for the "Fight or Flight" reaction. Its activity is normally balanced by that of the parasympathetic nervous system (PNS), which tends to favour digestive processes and returning the body to its normal state after a "Fight or Flight" episode.


  • SNS - Preganglionic nerves leave the central nervous system between T1 and L2 to join the sympathetic ganglia (junction box). The ganglia form a chain which runs down the front of the spinal vertebral bodies. Postganglionic nerves leave the ganglia to supply their target organ.
    • Of note is the fact that every part of the peripheral nervous system, from dorsal root ganglion all the way to the pain receptors in the periphery, has a post-ganglionic sympathetic supply which increases both sensory receptor sensitivity and nerve conduction speeds.
  • PNS - Preganglionic nerves leave the central nervous system via the 10th cranial nerve (Vagus) and also via the sacral parasympathetic nerves (Cranio-sacral Outflow). They join ganglia just before their target organ. Postganglionic nerves then leave the ganglia to supply their target organ.

Autonomic Physiology - this can be summarised in the table below:-

Physiological Parameter
Pupil Size
Heart Rate
Force of Heart Contraction
No Effect
Blood Flow Diversion
Brain, Heart, Muscle
Intestines, Liver
Airways (Bronchi)
Intestinal Motility / Secretion
Adrenaline Release (Adrenal)
No effect
Glucose Production (Liver)
No effect
Bladder Muscle
Sphincters (Anal, Bladder)
Blood Vessels
No Effect
No Effect
Heat Conservation
Hairs stand up on end
No Effect
Nerve Conduction Speed
No Effect
Pain Receptor Sensitivity
No Effect

CRPS I (Reflex Sympathetic Dystrophy)

Complex Regional Pain Syndrome I (CRPS I) was also known as Reflex Sympathetic Dystrophy (RSD) in the past. It's a chronic pain condition where there signs and symptoms to suggest overactivity of the sympathetic nervous system.


  • There is often a history of an injury, but in some patients none can be identified. In some patients the pain seems to be associated with injury to a peripheral nerve e.g. Colles wrist fracture with a tight plaster of Paris causing ischaemia (lack of oxygen) to the dorsal radial nerve of the wrist.
  • No one really knows why this condition starts - but research is ongoing. It's possible that genetics has a part to play, and that certain individuals are pre-disposed to developing this syndrome after minor injuries. It therefore may be familial.
  • The possible other causes of CRPS I include:-
    • Ephaptic Crosstalk - the insulating myelin layer in a nerve is damaged by the injury, allowing electrical signals to jump from one nerve fibre to an adjacent one. This causes the light touch and temperature sensory signals to get mixed up with the pain messages.
    • Dorsal Horn Reorganisation - after a nerve injury, the central connections for each sensory modality (light touch, pain, vibration, temperature) unplug like a telephone exchange, and become reconnected to the wrong socket. Thus light touch and temperature modalities become painful.
    • SNS changes - there may be an increase in the number of noradrenergic receptors on the surface of the peripheral nerves distant to the site of the nerve injury. This would make the nerve more sensitive to circulating adrenaline (released by stress), causing increased receptor sensitivity in the periphery, and also causing the nerve to fire off more readily.

Clinical Features

  • Allodynia is a cardinal sign, and must be present before the diagnosis can be confirmed. Allodynia may be vibrational (worse on light touch), or thermal (worse with immersion in hot / cold water). Pain is often disproportionate to the magnitude of any injury.
  • The pain usually starts in the periphery and may spread towards the centre over a number of months. The opposite limb may become involved if left untreated.
  • Signs of sympathetic overactivity include increased colour changes (blue / red), sweating, cold periphery with vasoconstriction, and piloerection (hairs standing up on end).
  • The affected limb may be > 2 deg C colder than the normal side, and this can be demonstrated with a thermogram .
  • A very common feature is guarding of the limb to prevent accidental knocking by persons or objects. Patients often refuse to use it, which over several months leads to peripheral swelling (oedema), muscle wasting, osteoporosis, joint and ligament contractures. Patients also may refuse to cut their finger and toe nails as the sensitivity is too much to bear. The quality of the nail and hair growth in the area may also be affected.
  • These trophic changes may be related to disuse secondary to pain, or they may be the effects of prolonged vasoconstriction causing oxygen starvation in the peripheral tissues.
  • Some patients find that their limb is most affected when they emotionally upset, increasing the degree of vasoconstriction and colour change. This may occur because emotional upset releases adrenaline from the adrenal glands, which then adds to the vasoconstriction in the affected limb. Being calm and relaxed can have the opposite effect.
  • A personal observation is that CRPS I is very unusual in non-smokers. I'm not sure of any research which shows an interaction between nicotine and CRPS I, but the pharmacology of nicotine does confirm that it is a potent vasoconstrictor of skin blood vessels.


  • Usually made from the history, examination findings, and the response to a sympathetic nerve block. In the later stages Bone Scans may suggest osteoporosis but these findings are not specific for CRPS I.


  • This is one of the few conditions that needs an urgent referral to a Pain Specialist. Poor outcomes are usually related to a delay in starting multi-disciplinary pain management .
  • Pain Relief Drugs
    • Amitriptyline (10 - 50 mg) plus either pregabalin or gabapentin can drastically reduce the degree of allodynia in some patients allowing them to participate in rehabilitation of the affected part.
    • Multiple action drugs e.g. tramadol (Zamadol), tapentadol (Palexia) block morphine, noradrenaline and serotonin receptors
    • Combinations of simple oral pain relieving medications like paracetamol + NSAIDs + weak or strong opioids should be considered in addition to specific nerve pain blocking treatments.
    • Ketamine 30 - 80 mg per day orally can be useful.
    • Nifedipine (calcium channel blocker) can reduce peripheral vasoconstriction.
  • Peripheral nerve blocks in those where the pain seems to be centred around an injury to a single peripheral nerve.
  • Sympathetic Blocks repeated a regular intervals can be useful but should not be used in isolation.
  • Physiotherapy and / or Occupational therapy is mandatory to maintain or improve limb function.
  • Psychological Support is essential.
  • Surgical Sympathectomy may be done at the T2/3 for the upper limb and at L2/3/4 for the lower limb, if the effects of sympathetic blocks are effective but short lasting.
  • Spinal Cord Stimulation can help with pain control and limb blood flow improvement.
CRPS II (Causalga)

Complex Regional Pain Syndrome II was also known in the past as Causalgia. It is similar to CRPS I but with some important differences:-

  • There is usually a serious injury to a major nerve trunk that is immediately obvious e.g. brachial plexus avulsion or gun shot wound to the sciatic nerve roots. CRPS I tends to be due to a minor peripheral nerve injury.
  • The allodynia symptoms start within hours in the affected limb and are far more severe. CRPS I tends to develop gradually over weeks and months. The pain from CRPS II has been rated as the only pain worse than labour (by women presumably !).
  • Pain treatment is required as an emergency:-
    • Brachial Plexus or Sciatic Blockade should be performed within hours preferably. Implantable catheters with local anaesthetic infusions can be very effective.
    • Sympathetic Blocks may also be used.
    • Combinations of simple oral pain relieving medications like paracetamol + NSAIDs + strong opioids should be considered in addition to specific nerve pain blocking treatments.
    • There is one series of patients in Lebanon in whom an oral sympathetic blocker called phenoxybenzamine proved effective. Doses in the range 10 - 40 mg three times a day were effective, but postural hypotension was a problem.
Sympathetically Mediated Pain
  • Sympathetically Maintained Pain (SMP) is a watered down version of CRPS I, where patients may develop milder symptoms over a longer period of time after various traumatic or surgical insults.
  • There seems to be a blurring between nerve pain and sympathetic pain as the main diagnosis in these patients.
  • The treatment is essentially the same as CRPS I, and the outcome is usually better as the disease process is not as advanced.
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