Week 5- Chronic Pain Flashcards
What are the three hypothetical types of pain and what fibers are associated with each?
If you split the pain experience into adaptive and maladaptive, what are types of pain?
- Superficial: sharp (a-delta) and dull (C). Sharp can be in response to mechano of temp stimuli, but C fibers can also respond to chemo stimuli
- Visceral: C fibers
- Referred: C fibers
Adaptive:
- Nociceptive
- Inflammatory (this results from increased sensitivity of the receptors)
Maladaptive
- Neuropathic: results from damage to the nervous system. Can be peripheral or central
- Functional: is the abnormal operation of the nervous system
What lamina and what type of cell fo nociceptive fibers synapse onto in the spinal cord?
First they travel in lissauer’s tract, then
- a-delta (sharp pain, myelinated): mostly I onto NS
- C-fibers: onto an interneuron in II (substantia gelatinosa) and then in V onto WDR
WDRs are found near the “wide” part of the spinal cord…
Describe what happens in peripheral and central sensitization.
Peripheral (out in the skin…)
- Nociceptor sensitivity is increased by phosphorylation and by more transcription of receptors
Central sensitization (spinal cord and up….) has two phases
- Acute: “wind-up”- feed forward. progressive increase in dorsal horn neuron response to the same stimuli via phosphorylation and the addition of NMDA receptors and the removal of the Mg blockade on the NMDA receptor
- Persistent phase: changes in gene regulation, structural reorganization ( loss of inhibitory interneurons (=disinhibtion), a-beta fiber sprouting and forming novel synapses)
- the death of interneurons and the forming of novel synapses is phenotype conversion which leads to intractable changes
Define neuralgia
pain in the distribution of one nerve
What are the first line drugs for chronic pain? What are their MOAs? What are their main uses?
TCAs:
- are 5-HT and NE reuptake inhibitors. This enhances descending inhibition.
- diabetic neuropathy, postherpetic neuralgia
- e.g Desipramine
Ca alpha-2-delta ligands (e.g. Gabapentin…doesn’t actually bind the GABA channel, it binds a calcium channel): has wider range of applications…most chronic neuropathic pain
anticonvulsants: e.g. carbamazepine is a Na channel blocker. Used mainly for trigeminal neuralgia (first line) or second line for other types of pain. Many potential SE including Stevens-Johnson syndrome
What is the MOA of TCAs? Is the analgesic or anti-depressant dose higher? What are the most serious side effects?
TCA’s are 5-HT and NE reuptake inhibitors- they strengthen descending inhibition
Analgesic dose is lower.
Blind as a bat, mad as a hatter, red as a beet, hot as Hades, dry as a bone, the bowel andbladder lose their tone, and the heart runs alone.
What are second line agents for management of chronic pain? 3rd and 4th line?
Second line:
- SSNRIs (e.g. venlafaxine)
3rd/4th line:
- opioids
- tramadol (synthetic opioid, extended release, relative lack of SE (major organ toxicity or respiratory depression), low abuse potential)
- SSRIs
- capsaicin (depletes substance P)
- cannabinoids (approved for MS neuropathic pain)
What drugs to NOT give in chronic pain
preparations with hypnotics/sedatives (e.g. barbituates) because they have higher abuse potential
e.g. butalbital
Canadian Consensus Guidelines Treatment Algorithm
What is the diagnostic criteria for migraine with and without aura? Chronic migraine?
2 of:
- unilateral
- throbbing
- worse on exertion
- moderate to severe intensity (rated based on functionality)
AND
1 of:
- nausea +/- vomiting
- stimulus sensitivity (e.g. light, sound)
AND
- 5 attacks
- 1 yr history
- normal physical exam (exclude secondary headaches)
AND aura (if migraine with aura :p)
- an important feature of aura is that you don’t lose awareness. You have some combo of visual, sensory and cognitive symptoms that last 4-60 minutes, and the headache follows <60 minutes
Chronic migraines are:
- Headache fro 15/30 days
- At least 8/30 days meet the migraine criteria
- Average length is usually ~ 4hrs
Recurrent sinus headaches are a type of …
Migraine, according to Dr. Robinson
What are trigeminal autonomic cephalalgias?
Unilateral headache pain in the distribution of the trigeminal nerve with autonomic symptoms
e.g. cluster headaches are severe orbital pain with tearing/ptosis/miosis that occur in clusters (up to 8/day)
What is the pathophysiology of migraine?
Cortical spreading depression. A wave of activity starts somewhere (“migraine generator”) that spreads across the cortex. According to the quiz, it starts in the occipital lobe and spreads anteriorly.
This explains the aura and activation fo trigeminal efferents. There is reflex change in blood vessel, and they become more permeable and there is irritaiton of the dura
Acute migraine management
General:
- Simple analgesics (ASA, acetaminophen)
- NSAIDs
- Combo
- Opiods
Specific
- triptans
- ergotamine
What are the main drugs used for migraine relief and prophylaxis? Contrast with cluster headaches and chronic migraines.
Migraines
- Relief:
- Triptans: mild vasoconstrictor. slow and fast onset exist
- Ergotamines
- Prophylaxis- tailor to pt, only use if migraines cannot be acutely controlled
- beta blockers
- TCAs
- CCBs
- Anticonvulsants
- Botox
Cluster headaches:
- acute: nasal sumatriptan and oxygen
- preventative: verapami +/- prednisone…no idea why….
Chronic Migraines:
- # 1 Avoid triggers- especially deal with “medication overuse migraines”
- # 2 triptans
- # 3 botox
