Neuropathic pain: burning and tingling 

Neuropathic pain commonly is described as hot burning, throbbing, shooting, lancinating, stabbing, sharp, cramping, gnawing, aching, heavy, tender, splitting, tiring, exhausting, sickening, fearful, punishing, cruel, icy cold, tingling, pins and needles, intense and itch like.

Medical descriptors are

• allodynia (pain due to a stimulus which does not normally provoke pain),
• hyperalgesia (an increased response to a stimulus which is normally painful),
• hyperaesthesia (increased sensitivity to stimulation, excluding the special senses), dysaesthesia (an unpleasant abnormal sensation, whether spontaneous or evoked),
• hyperpathia (a painful syndrome characterised by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold) and
• neuralgia (pain in the distribution of a nerve or nerves not necessarily of paroxysmal quality).

Neuropathic pain: also disturbance of mood, sleep and other problems 

Neuropathic pain may be associated with mood changes, sleep disturbance, fatigue and may have an impact on physical and social functioning.^[1] A central element is to help patients become experts in understanding and managing their pain, then addressing the toll it has taken on their emotions, daily activities, and important relationships. ^[2]

The prevalence of neuropathic pain

The prevalence of peripheral neuropathy rises from 2.4% in the general population to 8% in subjects older than 55 years.^[3] In diabetic patients the prevalence of peripheral neuropathy is around 50%.^[4] Neuropathic pain in diabetic patients is prevalent in 8% to14% of the patients. Diabetic type 2 patients suffer more from neuropathy and neuropathic pain then type 1 patients.^[5]

Neuropathic pain: etiology and pathophysiology 

The relationship between aetiology, pathophysiology and symptoms in neuropathic pain is complex. After a nerve injury, stimulus independent pain may be evoked by an accumulation of sodium channels in the injured neurons, the expression of α-adrenoreceptors on injured axons, sprouting of sympathic axons into the dorsal root ganglion and disinhibition of dorsal horn neurons. This disinhibition is thought to be due to a reduction in GABA, down regulation of GABA and Opioid receptors at dorsal horn neurons and loss of inhibition by interneurons of the dorsal horn. Stimulus dependent pain is thought to be due to sensitisation of dorsal horn neurons mediated by glutamate and stimulation of NMDA receptor.

These mechanisms offer a framework for pharmacotherapy of neuropathic pain.

Therapy resistance of neuropathic pain!

Neuropathic pain has been shown to be therapy resistant. Usually a list of possible effective agents is tried until an agent and dose is found that provides satisfactory control of the pain for that individual patient. However, the treatment effect of conventional agents is disappointing and if an effect is observed it is usually transient. A number of agents have been used in neuropathic pain including NSAID’s, opioids, antidepressants, anticonvulsants, excitatory amino acid antagonists, GABA-ergic agonists, Substance P antagonists etc.

Low doses of carbamazepine and amitriptyline have been recommended for neuropathic pain in general. However, there is no acknowledged standard treatment for the neuropathic pain in the EU. In several European countries carbamazepine and amitriptyline are used off-label for this indication. In some Member states gabapentin has been approved for the treatment of neuropathic pain.  

Source

March 2010, Jan M. Keppel Hesselink, MD, PhD, David J. Kopsky MD

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