Co-Analgesics


Concomitant or Co-Analgesics were originally developed to treat medical conditions other than pain but have been found to have pain-relieving properties.


They are used
 

  • to enhance the analgesic efficacy of analgesics
     
  • to treat concurrent symptoms that intensify pain
     
  • to provide independent analgesia for specific types of pain like neuropathic pain

 


The main classes of co-analgesics are


Anticonvulsants (e.g. gabapentin, pregabalin)



Anticonvulsants inhibit the neuronal excitation and stabilise nerve membranes through the blocking of ion channels in the CNS.

Gabapentin binds to a subunit of presynaptic voltage-dependent calcium channels. The binding reaction reduces release of pre-synaptic transmitters. As a consequence, an analgesic effect occurs.

Pregabalin provides its analgesic effect by interacting with special N-type calcium channels and – as a consequence – regulating neurotransmitter release.

With regard to pain therapy, the main indication for anticonvulsants is shooting neuropathic pain (e.g. trigeminal neuralgia, postherpetic and other neuralgias).

 

Antidepressants (e.g. amitriptyline, duloxetine)


Antidepressants – SNRI - TCA - action.png

 

Tricyclic Antidepressants – TCA (e.g. amitriptyline)

TCA inhibit the neuronal re-uptake of noradrenaline or serotonine from the synaptic cleft.

The resulting increased transmitter concentration affects supraspinal structures of pain processing. Furthermore, the increased noradrenaline and serotonine levels intensify the descending pain inhibition pathway. Thus TCA provide analgesia. Indications for the use of TCA in pain therapy include neuropathic pain, complex regional pain syndrome (CRPS) or tension headache.

Selective Serotonin and Noradrenaline re-uptake inhibitors – SNRI (e.g. duloxetine)

SNRIs selectively inhibit the neuronal re-uptake of noradrenaline and serotonine from the synaptic cleft.

The resulting increased transmitter concentration affects supraspinal structures of pain processing. Furthermore, the increased noradrenaline and serotonine levels intensify the descending pain inhibition pathway.

SNRIs such as venlafaxine and duloxetine are safer to use than TCAs and are a better option in patients with cardiac disease. SNRIs do not have relevant affinity to adrenergic, cholinergic or histaminergic receptors (selective inhibitors) and, thus, do not evoke respective side-effects.

 

Anxiolytics (e.g. diazepam)

 

Neuroleptics (e.g. haloperidol)

 

Corticosteroids (e.g. prednisolone)