This is often a cause of pain, including chronic tension headache. Treatment is directed at reduc tion of the spasm in a variety of ways, including psychotherapy, sedation and the use of a centrally-acting muscle relaxant as well as non-narcotic analgesics, e.g. baclofen, diazepam; clinical efficacy is variable (see Other muscle relaxants, p. 357). Local infiltration with lignocaine (lidocaine) is sometimes appropriate. Hzanidine is an a2-adrenoreceptor agonist that may be used to relieve muscle spasticity in multiple sclerosis, spinal cord injury or disease.
NEURALGIAS (NEUROPATHIC PAIN)
These include postherpetic neuralgia, phantom limb pain, peripheral neuropathies of various causes, central pain, e.g. following a stroke, compression neuropathies, and the complex regional pain syndromes (comprising causalgia, when there is nerve damage, and reflex sympathetic dystrophy, when there is tissue but no nerve injury); they present the most challenging problems.
A tricyclic antidepressant and/or an antiepilepsy drug are commonly used in their management; analgesics play a subsidiary part.
• Amitriptyline is most frequently used, starting with 10 mg at night increasing to 75 mg. Nortriptyline is better tolerated by some patients. Their general action is to inhibit noradrenaline (norepinephrine) re-uptake by nerve terminals and benefit in neuropathic pain may follow enhanced activity in noradrenergic pain inhibitory paths in the spinal cord.
• Gabapentin is the most commonly used antiepilepsy drug in this setting; phenytoin (which raises the threshold of nerve cells to electrical stimulation) or sodium valproate are used for resistant neuralgias.
• Transcutaneous electrical nerve stimulation (TENS) helps some sufferers; it may act by promoting the release of endorphins. Ketamine (see p. 353) or lidocaine (lignocaine) (by i.v. infusion) are used in special circumstances. Pain due to nerve compression may be relieved by a corticosteroid injected loccally.
• When these measures fail, and an opioid appears necessary, methadone, dextroproxyphene, tramadol and oxycodone are preferred; all possess NMDA-receptor antagonist activity as well as being opioid |J.-receptor agonists.
Trigeminal neuralgia differs from other peripheral neuropathies in its management. The antiepilepsy drug, carbamazepine (p. 417), was accidentally discovered to be effective, probably by reducing excitability of the trigeminal nucleus. The initial dose should be low, and individuals generally soon learn to alter it themselves during remissions and exacerbations (200-1600 mg/d). It is not used for prophylaxis. Resistant cases may obtain benefit from oxcarbazepine, gabapentin or lamotrigine.
Postherpetic neuralgia. The pain of acute herpes zoster (shingles) is mitigated by NSAIDs and opioids (as well as by oral aciclovir started within 48 h of the rash). Whether the incidence of postherpetic neuralgia is reliably reduced by early treatment with an antivirus drug has yet to be proved. Amitrip-tyline is an appropriate initial choice, failing which gabapentin may be used. A topical application of capsaicin, derived from Capsicum spp (pepper and chilli), may be applied as a counter-iritant, although the initial intense burning sensation may limit its use. Conventional analgesics are ineffective.
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