Treatment Objectives
Treatment of Neuropathic Pain
Treatment for Neuropathic Pain
To treat neuropathic pain, drug treatments are oftentimes the best strategy, particularly when coupled with other available therapies for pain management. The current drug treatments for neuropathic pain  are focused on dampening the neuronal input to patient consciousness. This is done by suppressing axonal function. It is also achieved by interfering with neurotransmission.
The drugs used to treat neuropathic pain can be divided into two types:
- Medications that treat other conditions (but also useful in neuropathic pain)
- Analgesics
Often working out a better management system for the causative disease or disorder can, in turn, reduce its neuropathic pain. Efficient management of the condition also has the potential to prevent further nerve damage.
Unfortunately, neuropathic pain often responds poorly to over the counter pain treatments. For some patients, their pain can worsen and turn into a serious disability. Combining therapies have been found to offer the best result in providing relief from neuropathic pain.
To relieve the discomfort from neuropathic pain, some patients opt to use non-steroidal anti-inflammatory drugs. This may work for a select few, but many patients find the relief to be mild and of little consequence.  Examples of this kind of medication:
- Aleve
- Motrin
Most patients experiencing neuropathic pain require a medication that packs more punch. To gain this kind of pain relief, many will consume medications containing morphine.
Anticonvulsant medications (neuroleptic drugs)Â
- carbamazepine
- felbamate
- valproic acid
- clonazepam
- phenytoin.
Antidepressant drugs called tricyclic antidepressants (TCA’s)
- Amitriptyline
- Nortriptyline
Local anaesthetics (intravenous application)Â
- lidocaine
- tocainide
- mexiletineÂ
- Physical therapy
- Working with a counsellor
- Relaxation therapy
- Massage therapy
- Acupuncture
- Implantable Device – electrical stimulation of nerves
Medicinal Cannabis Treatment for Neuropathic Pain
Endocannabinoid System and Pain
Cannabinoid receptors, specifically CB1 are well distributed throughout the endogenous pain modulation pathway. Key areas in pain transmission include the periaqueductal grey matter, rostral ventromedial medulla and the primary afferent neurones. Studies have shown that up-regulation of the endocannabinoid system is known to produce an analgesic effect.
Primary Afferent Neurons
Studies in mice in which CB1 receptors were removed from primary afferent nociceptive sensors showed an increased sensitivity to noxious stimuli. From this, the researchers proposed CB1 receptors are involved in primary pain transmission from the periphery to the spine. Furthermore, these rats were found to be hypersensitive to noxious stimuli, which supports the hypothesis. Transient potential vanilloid receptors are also found on the primary afferent neurones and suggested to work synergistically with cannabinoid receptors to reduce pain transmission when activated by cannabinoids.
Periaqueductal Gray Matter
The PAG is considered the relay centre for pain in the brain. PAG electrical stimulation is well known to produce analgesic effects in rats. CB1 receptors are densely concentrated through the PAG. Studies have shown that injection of cannabinoids into the PAG produce a similar analgesic effect that was reversed by a CB1 antagonist. Analgesic effect is generated in PAG via transmission of pain signals to the descending nociceptive pathway. The degree to which pain is modulated in this area of the brain is determined by GABA and glutamate excitation. Glutamate stimulation is known to have an analgesic effect. Conversely, GABA excitation is inhibitory to the descending antinociceptive pathway. Traditional opioid analgesics produce a slightly stronger antinociceptive effect than cannabinoids. Opioid treatment results in a decrease of spinal opioid receptors, whereas CB1 receptors are unregulated in neuropathic pain.
Rostral Ventromedial Medulla
RVM contains two cell types which are know to influence the descending antinociceptive pathway. ON cells are associated with increased pain signalling. OFF cells are associated with the analgesic effect. Cannabinoid receptor agonists have been shown to reduce the ON cell burst and decrease the OFF cell pause.
Cannabinoid receptors, specifically CB1 are well distributed throughout the endogenous pain modulation pathway. Key areas in pain transmission include the periaqueductal grey matter, rostral ventromedial medulla and the primary afferent neurones. Studies have shown that up-regulation of the endocannabinoid system is known to produce an analgesic effect.
Primary Afferent Neurons
Studies in mice in which CB1 receptors were removed from primary afferent nociceptive sensors showed an increased sensitivity to noxious stimuli. From this, the researchers proposed CB1 receptors are involved in primary pain transmission from the periphery to the spine. Furthermore, these rats were found to be hypersensitive to noxious stimuli, which supports the hypothesis. Transient potential vanilloid receptors are also found on the primary afferent neurones and suggested to work synergistically with cannabinoid receptors to reduce pain transmission when activated by cannabinoids.
Periaqueductal Gray Matter
The PAG is considered the relay centre for pain in the brain. PAG electrical stimulation is well known to produce analgesic effects in rats. CB1 receptors are densely concentrated through the PAG. Studies have shown that injection of cannabinoids into the PAG produce a similar analgesic effect that was reversed by a CB1 antagonist. Analgesic effect is generated in PAG via transmission of pain signals to the descending nociceptive pathway. The degree to which pain is modulated in this area of the brain is determined by GABA and glutamate excitation. Glutamate stimulation is known to have an analgesic effect. Conversely, GABA excitation is inhibitory to the descending antinociceptive pathway. Traditional opioid analgesics produce a slightly stronger antinociceptive effect than cannabinoids. Opioid treatment results in a decrease of spinal opioid receptors, whereas CB1 receptors are unregulated in neuropathic pain.
Rostral Ventromedial Medulla
RVM contains two cell types which are know to influence the descending antinociceptive pathway. ON cells are associated with increased pain signalling. OFF cells are associated with the analgesic effect. Cannabinoid receptor agonists have been shown to reduce the ON cell burst and decrease the OFF cell pause.
Statistics for Neuropathic Pain in Australia
29 percent of Australians experience chronic pain., which if you think about it, this means around three out of every ten people are suffering in some way, shape or form. (Stollznow Research for Pfizer Australia, 2010).
Pain can be distinguished as either acute or chronic. Acute pain is the body’s response to a single event such as tissue damage. The neurophysiology of acute pain is well understood and most occurrences are resolved with the discontinuation of the stimulus.
Chronic pain continues relentlessly and is often attributed to impairment of the nervous system. This type of chronic pain results from either unresolved disease causing nerve stimulation (nociceptive pain) or from physiological changes within the nervous system (neuropathic pain). Chronic pain is often debilitating to sufferers and resistant to traditional pharmaceuticals
Pain Physiology
Nociceptors are specialised receptors responsible for the detection of noxious stimuli and translating these sensations into electrical signals, which are then relayed to the brain. These receptors are triggered by physical (bumps or knocks), thermal (hot or cold) or chemical (inflammatory mediators or corrosive agents) stimuli. Once a noxious stimulus has been detected, primary afferent fibres relay the signal into the spinal cord via the dorsal horn. Secondary afferent fibres transmit these signals to higher brain areas, specifically the thalamus and somatosensory cortex. This pathway from stimulus to the brain is called the spinothalamic tract.
Pain Inhibition
The endogenous system responsible for nociceptive pain control is called the descending pathway. The descending pathway is the nociceptive modulatory system, which, when activated either chemically or electrically produces an analgesic effect. Important sections of this route include the periaqueductal grey (PAQ) and the rostral ventromedial medulla (RVM). These parts have been well characterised as fundamental in the pain cascade.
What is Neuropathic Pain?
Neuropathic pain is caused by disease or injury and signifies damage to the nerves. Usually, when a person experiences pain, the pain signal is validated by specialised nerve endings which sense that something is wrong with the body. Pain signals are then delivered to the spinal cord and brain. The issue with neuropathic pain is that when nerves have been damaged or injured, the signals sent to the brain are faulty. These false signals can tell the brain that there is a pain when there shouldn’t be. Diabetes is an example of a condition that can cause neuropathic pain. Unfortunately,  the resulting neuropathic pain experienced is often severe and can be difficult to treat.
Neuropathy – damage to a nerve
Neuralgia – describes pain in a nerve pathway that has resulted out of nerve damage.
Causes of Neuropathic Pain:
- Diabetes
- Shingles
- Sciatica
- Alcoholism.
- Back, leg, and hip problems.
- Chemotherapy.
- Facial nerve problems.
- HIV infection or AIDS.
- Multiple sclerosis.
- Spine Surgery
Symptoms of Neuropathic Pain
- Burning pain
- Tingling
- Numbness
Clinical Studies / References:
