Dear G members, the powerpoint version is much simpler, =) but I've uploaded the detailed version in case you wanted to know more, cheers
Pain Management
Pain
Nociceptive pain
responds better to anti-inflammatory and opioid
Neuropathic pain
responds better to antiepileptics and antidepressants
Psychological pain
responds to anti-depressants, neuroleptics, lithium & other measures e.g. psychotherapy, counselling, etc.
Therapy
Pain has two components: emotional (mental) and physical
Pain can be worsened during episodes of depression, stress or any other negative emotions and also lessens when the individual has happy emotions like while watching a comedy show. To tackle the emotional aspect of pain, the patient’s social support and history could be elicited from a well taken history. Management of pain in the emotional aspect would be tailored according to a patient’s history. Encouragement and a supportive environment would be highly effective. Counseling sessions would be highly useful for patients who are undergoing depression or any other troubles. Encouraging patients to indulge in their hobbies would definitely help relieve their stress levels.
Patients are also advised not to indulge or refrain as much as possible from activities that might potentially exacerbate their condition and to seek proper help or employ the help of medical social workers if need be.
Physical aspect, it would be divided into a few categories: surgical, pharmacological and non surgical and pharmacological therapy (physiotherapy, occupational therapy, acupuncture, chiropractitioners and more).
Surgical therapy: in the event of pain caused by a spinal cord compression due to tumors, lesions or fractures of the vertebrae, surgery would be the best option for pain relief. For phantom pains, the surgery to kill off the nerves are the sources of the problems could be instant relief of physical and mental pain of patients.
Pharmacological therapy: Tailored to nociceptive and neuropathic pain (peripheral or central) with reference to their condition
Nociceptive pain responds well to opioids while neuropathic pain opioids is not considered a first line treatment but sometimes there is no clear distinction of pain and both nociceptive and neuropathic pain might occur alongside.
Nociceptive Pain
WHO analgesic ladder
Mild pain
Non-opioid e.g. aspirin & paracetamol
Adjuvant analgesics
Mild to moderate pain
Simple analgesic – Paracetamol
Weak opioid – codeine, tramadol, propoxyphene, pentazocine, oxycodone, hydrocodone, meperidine
Severe pain
Strong opioids e.g. Morphine, alfentanil, methadone, diacetylmorphine (heroin)
Adjuvant analgesics
-Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. Voltaren, diclofenac for bone pain, inflammatory pain
-Anticonvulsants e.g. gabopentin/pregabalin for neuropathic pain
-Tricyclic antidepressants e.g. amitriptyline for neuropathic pain and depression
-Biphosphonates e.g. disodium pamidronate for metastatic bone disease
-Dexamethasone for headache from cerebral oedema due to brain tumour
Antidepressants
Activation of the descending norepinephringeic and serotonergic pathways (inhibitory) to the spinal cord limit pain signals sent to the brain. Compounds such as duloxetine, venlafaxine and milnacipran block both serotonin and norepinephrine reuptake improves neuropathic pain. Tricyclic antidepressants may also work on the sodium channels in peripheral nerves.
Anticonvulsants
Pregabalin and gabapentin work by blocking specific calcium channels on neurons. Carbamazepine and oxcarbazepine especially effective on trigeminal neuralgia are principally on sodium channels
Opioids
Narcotics are used as an important treatment for chronic pain. Methodone and ketobemidone possess NMDA antagonism. (NMDA: N-methyl-D-aspartic acid mimics the effect of glutamate and is an excitotoxin) NMDAR is an ionotropic receptor that allows transfer of electrical signals between brain and spinal column.
Others
Stimulation - transcutaneous electrical nerve stimulation (TENS) and spinal cord stimulation
TENS
Transcutaneous electrical nerve stimulation (TENS) currently is one of the most commonly used forms of electroanalgesia. Use to reduce low back pain (LBP), myofascial and arthritic pain, sympathetically mediated pain, bladder incontinence, neurogenic pain, visceral pain, and postsurgical pain
The currently proposed mechanisms by which TENS produces neuromodulation include the following:
• Presynaptic inhibition in the dorsal horn of the spinal cord
• Endogenous pain control (via endorphins, enkephalins, and dynorphins)5
• Direct inhibition of an abnormally excited nerve
Restoration of afferent input
Spinal sord stimulation
For spinal cord stimulation (SCS) to control your pain, you must have a small system placed in your body. An SCS system looks and works a lot like a pacemaker. In fact, SCS systems are sometimes called “pacemakers for pain.” An SCS system generates mild electrical pulses and sends them to your spinal cord. These electrical pulses replace the feeling of pain with a tingling or massaging sensation.
Nerve blocks
-Somatic blocks
(a) peripheral nerve & plexus injections
(b) epidural & spinal analgesia
-Sympathetic blocks
(a) sympathetic ganglia injections
(b) central epidural & spinal sympathetic blockade
Topical agents
Some forms of neuropathy like post-herpetic neuralgia, topical application of local anesthetics like lidocaine can provide relief.
Cannabinoids
Marijuana is an example and this class is commonly used on HIV-related peripheral neuropathy. Cannabinoid type I is found mainly in the brain (basal ganglia, limbic, hippocampus, cerebellum) and including reproductive systems are responsible for the euphoric and anticonvulsive effects.
Cannabinoid type II is found almost exclusively in the immune system with greatest density in the spleen. They are responsible for the anti-inflammatory effects of cannaboids.
Dietary supplements
Alpha lipoic acid and benfotiamine has shown in many studies to be effective treatments of diabetic neuropathy (microvascular disease, glucose binds to many proteins with non enzymatic covalent bonding, protein kinase C increase nerve conduction velocity, polyol pathway [increase in oxygen radicals, decrease in glutathione due to increase glucose levels, pathway dependent on aldose reductase]
Hyperglycaemic state causes the affinity of aldose reductase for glucose rises, increasing sorbitol levels but lower NADPH levels. NADPH is used for nitric oxide and glutathione production. Glutathione deficiencies can lead to haemolysis caused by oxidative stress and nitric oxide is for vasodilation. NAD+ is used for necessary for reducing radical oxygen molecules.
Increase in sorbitol levels causes a lower reuptake of myoinsitol, lowering the Na+/K+ ATPase pump
Neuromodulators
Spinal cord stimulators and implanted spinal pumps: electrodes placed adjacently to but outside the spinal cord and deliver medication directly to subarachnoid space respectively
Motor cortex stimulation: Stimulation of the primary motor cortex through electrodes placed within the skull outside dura mater.
Deep brain stimulation: implantation of a brain pacemaker which sends electrical signals to specific parts of the brain
References:
1. Kumar & Clark, Clinical Medicine, 7th Edition
2. http://www.poweroveryourpain.com/sb/learn_about/how_scs_works
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