Pain Boards Flashcards
Describe the difference between migraines, cluster headaches, tension-type headaches, and chronic paroxysmal hemicrania.
Migraines
- Usually associated with nausea, vomiting, and sensitivity to light/sound/smells.
- An aura (visual/sensory/motor symptoms) may
precede the attack although migraine without aura is more common
- Pain is usually unilateral and throbbing
- Episodes can last hours to days
- Believed to involve cortical spreading depression, activation of the trigeminovascular system, and CNS modulation of the pain-producing structures of the cranium
- Can be triggered by abrupt decreases in levels of estrogen
Cluster headaches
- Associated with ipsilateral lacrimation, eye redness, eyelid edema, stuffy nose, rhinorrhea, and sweating
- Repetitive headaches that occur at the same time each day
- Episodes last minutes to hours.
- Can occur for a week to several months and are followed by a period of remission
- Can be treated with 100% oxygen
Tension-type headaches
- Bilateral, pressing/tightening sensation.
Chronic paroxysmal hemicrania is like a cluster headache, but episodes are shorter and more frequent.
How should you treat a pt with known contrast allergy, but who requires a procedure with contrast?
Pretreatment at 12 and 2 hours pre-procedure with Prednisone, Ranitidine, and Diphenhydramine. Pt should also receive 25 mg IV Diphenhydramine immediately pre-procedure.
What factors determine local anesthetic potency, speed of onset, and duration of action?
Potency- lipid solubility
Onset - pKa
Duration- protein binding
How does Botox work?
Botox produces localized flaccid paralysis by blocking the release of acetylcholine at the neuromuscular junction.
What is Carbamazepine used for? How does it work? What are the common side effects? What type of monitoring is required?
Drug of choice for trigeminal neuralgia
Selectively blocks Na channels on active nerve fibers, and has no effect on normally functioning C and A-delta fibers
Main side effects are nausea, vomiting, and sedation
Pts should have blood tests every 2 to 4 months, due to risk of agranulocytosis and aplastic anemia
What is Topiramate used for? How does it work? What are the side effects?
Used for neuropathic pain
Affects sodium and calcium channels, enhances the action of inhibitory GABA, and inhibits excitatory glutamate receptors
Side effects include weight loss, sedation, kidney stones, and ocular glaucoma
How do prostaglandins enhance the transmission of pain?
They increase the release of neurotransmitters such as substance P and glutamate from primary neurons, increase the sensitivity of second-order neurons, and inhibit the release of descending inhibitory neurotransmitters
What is Nabumetone? What are the benefits?
Nabumetone is an NSAID prodrug which needs to be converted to its active form
Theoretically has fewer gastric side effects, but this is unproven
How and where does Baclofen work?
Baclofen is a GABA-B receptor agonist that binds to presynaptic receptors in the dorsal horn of the spinal cord
What is the mechanism of action of various muscle relaxants (Baclofen, Carisoprodol, Tizanidine, Cyclobenzaprine)?
Baclofen - GABA-B agonist
Carisoprodol (SOMA) - inhibits descending reticular activating system
Tizanidine (Zanaflex) - central alpha-2 agonist
Cyclobenzaprine (Flexeril) - effects on brain stem
What are some common TNF inhibitors? What are they used for? How do they work?
Common inhibitors include Infliximab (Remicade), D2E7 (Humira), and Etanercept (Enbrel)
Used for the treatment of rheumatoid arthritis
Inhibit TNF, reduce markers of inflammation, and slow structural damage
Describe the effects that each opioid receptor is responsible for.
Mew-1
- supraspinal analgesia
Mew-2
- spinal analgesia
- dependence, respiratory depression, miosis, GI effects, pruritis
Delta
- supraspinal and spinal analgesia
- euphoria
Kappa
- spinal analgesia
- sedation, dysphoria, respiratory depression
What are the three molecular classes of opioids?
1) Pheneathrenes
- morphine, hydromorphone, codeine, oxycodone, oxymorphone, and hydrocodone
2) Phenylpiperidines
- meperidine, fentanyl, sufantanil, alfentanil, and remifentanil
3) Diphenylhepatanes
- methadone and propoxyphene
Aside from pain control, what use does Meperidine have? What are the side effects?
May have a beneficial effect in the setting of post-anesthetic shivering
Side effects include cardiac effects (orthostatic hypotension and cardiac depression), anticholinergic effects, neurotoxic effects due to accumulation of metabolite (worse with renal failure), potential for serotonin syndrome (when mixed with MAOIs, SSRIs, Tramadol, or Methadone), and local anesthetic effects
A pt with a clean history and I signs of misuse is requiring almost 5 times the originally prescribed oxycodone dose to control their pain. What is a possible explanation?
Pt may have genetically low levels of the cytochrome P450 enzyme required to metabolize oxycodone into oxymorphone
- Occurs in about 10% of pts
What nerve root is tested when checking the following reflexes: biceps, brachioradialis, triceps, patellar, Achilles
Biceps - C5
Brachioradialis - C6
Triceps - C7
Patellar - L4
Achilles- S1
What information can an EMG/NCS give you?
Site of injury (anterior horn, spinal root, plexus, nerve, NMJ, or muscle)
Type of nerve involved (motor, sensory, or autonomic)
Nature of pathology (demyelination or axonal degeneration)
Time course (acute or chronic)
How would you perform a maxillary nerve block?
- mandibular notch is identified
- 22 gauge needle is advanced perpendicular to the skin at the posterior inferior border of the notch
- needle is advanced until it hits the lateral ptyergoid plate
- needle is then withdrawn slightly and redirected anteriorly superiorly
- needle is advanced toward the pterygopalatine fossa until a parasthesia is obtained
When performing a lumbar sympathetic block, there can be inadvertent nerve block. Which nerve is most commonly blocked and how does it manifest?
The genitofemoral nerve is very susceptible at the L4-5 level
Manifests as weakness and numbness in the groin, anterior thigh, and quads
What is Tramadol’s mechanism of action? What type of patients should it be avoided in?
Mechanism includes agonism at the mu receptor and inhibition of norepinephrine and serotonin reuptake
Should be avoided in pts with seizure history (can lower seizure threshold) and in pts taking SSRIs (increases risk of serotonin syndrome)
Describe primary afferent neurons. What are the different types?
Primary afferent neurons have cell bodies in the DRG and axons that reach out to peripheral sites
- No spontaneous activity
- Increased activity corresponds with increased stimuli intensity
Three main types:
A-beta (large myelinated) - rapid speed - specialized endings
A-delta (small myelinated) - intermediate speed - low threshold - specialized endings
- responsible for “fast epicritic (1st) pain”
C (small unmyelinated) - slow speed - high threshold - free nerve endings
- responsible for “slow protopathic (2nd) pain”
What is the significance of the spinal rexed lamina?
Spinal rexed lamina are the site of secondary nociceptive neurons
Also the site of opioid receptors
Lamina I - marginal zone = “nociceptive specific”
Lamina II - substantia gelatinosa = highest density of nociceptors
Lamina V - nucleus proprius = “wide dynamic range” neurons
Describe the ascending pain pathways from the dorsal horn.
Spinoreticulothalamic tract = light touch
- ipsilateral, ventrolateral
Spinothalamic tract = pain
- contralateral, ventrolateral
- two main routes
1) lateral thalamus to somatosensory cortex = sensory and discriminative aspects of pain
2) medial thalamus to cingulate and insula = emotional aspects of pain and autonomic reflex responses
Define hyperalgesia, allodynia, paresthesia, dysesthesia, and hyperpathia.
Hyperalgesia = exaggerated nociceptive response to a moderately noxious stimuli
Allodynia = nociceptive response generated by a normally innocuous stimulus
Paresthesia = abnormal sensation (not necessarily pain)
Dysesthesia = spontaneous pain
Hyperpathia = a state in which pain is persistent, radiates, and may become amplified
Describe how tissue injury leads to peripheral and central sensitization. What receptor is involved in central sensitization?
Peripheral sensitization is due to:
- Persistent/increased spontaneous nociceptor discharge
- Enhanced response to stimuli
Central sensitization (“wind up”) due to:
- Repetitive C fiber input
- Increased response to stimuli from increased kinase activity and changes in gene transcription
- Enhanced receptive field size due to collateral nociceptor innervation
NMDA receptor is thought to be involved in central sensitization
- NMDA receptors are composed of NR1, NR2 (A, B, C, and D), and NR3 (A and B) subunits
- The NR2B subunit appears particularly important for nociception
Describe the changes/mechanisms that lead to neuropathic pain after nerve injury.
Widespread changes include increased activity of sodium channels and decreased activity of potassium channels, leading to increased afferent activity
Peripheral changes
- Retrograde chromatolysis
- Wallerian degeneration (starts distally; slow 1 mm/day; faster peripherally compared to centrally; motor faster than sensory)
- Sprouting and neuroma formation
- Invasion of inflammatory cells
Central changes
- Changes in the DRG including alteration of protein, channel, and receptor expression
- Increased DRG spontaneous activity
What is the mechanism by which opioids produce analgesia
Opioid receptors alter the conductance of potassium and calcium ion channels
Inhibit the release of neurotransmitters presynpatically
Inhibit neuronal firing via hyperpolarization postsynaptically
What are the concerns regarding migraine medications that contain Propoxyphene?
Issues with Propoxyphene:
- Daily use my cause rebound headaches
- Has been associated with cardiac dysrhythmias
- Metabolism occurs in the liver to norpropoxyphene which can cause toxic side effects
- Has not been shown to be any stronger than aspirin
Define physical dependence.
Physical dependence - state of adaptation that is manifested by a withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, and/or administration of an antagonist
What are the contraindications for stellate ganglion block?
Absolute contraindications
- Anticoagulation
- Pneumothorax on the contralateral side (due to high risk of pneumothorax on side of procedure)
- Recent MI (due to blockade of cardiac accelerator fibers)
Relative contraindications
- Glaucoma and impaired cardiac conduction
Placement of a spinal cord electrode at which cervical levels will cover the distribution for: upper neck pain, radial nerve pain, median nerve pain, and ulnar nerve pain?
Upper neck pain = C2-3
Radial nerve pain = C4-5
Median nerve pain = C5-6
Ulnar nerve pain = C6-7
If a stellate ganglion block is performed and shows technical success (ptosis, miosis, nasal congestion, etc.) but does not cause a change in temperature or pain, what is the likely reason?
In some cases the upper extremity may be supplied by the T2 and T3 grey rami communicantes (Kuntz fibers)
- Do not pass through the stellate ganglion
- Have been implicated in inadequate relief of sympathetically maintained pain despite a good stellate ganglion block.
Describe the metabolism of local anesthetics.
Amide local anesthetics are metabolized in the liver
Ester local anesthetics are metabolized in the plasma by plasma pseudocholinesterase
- Metabolism results in the formation of PABA, which is associated with allergic reactions
The genitofemoral nerve is made up of which nerve roots?
L1 and L2
Describe intervertebral disk anatomy
The inner nucleus pulposis is made up of mostly water but also some Type II collagen
The outer annulus fibrosis is mostly Type I collagen
What is the Dallas classification of IVD annular tears?
Grade 0 = normal disk
Grade 1 = contrast leaks to inner 1/3 of annulus
Grade 2 = contrast leaks to middle 1/3 of annulus
Grade 3 = contrast extends out to outer 1/3 of annulus
Grade 4 = contrast leaks to outer edge of annulus with concentric spread
Grade 5 = complete rupture
What receptors do opioids block in the spinal cord?
Mu and Kappa receptors
What is the treatment for a brachial plexus avulsion injury? What are the side effects?
Treatment is radiofrequency DREZ lesioning
Side effects include motor weakness, sensory deficits, and ataxia
How does nerve compression lead to neuropathic pain?
Nerve compression leads to hypoxia/damage to large myelinated nerve fibers
This loss of segmental inhibition leads to unopposed C fiber stimulation
Describe post-herpetic neuralgia
Caused by Herpes Zoster (Shingles)
- Virus stays dormant in DRG
Most commonly affects thoracic dermatomes
- Can also affect the opthalmic division of the trigeminal nerve (V1)
Characterized by pain that persists 30 days or more after rash onset
- Due to ischemic loss of myelinated fibers
Affects women more than men
What are the causes of central pain? What is the theorized mechanism? Are there any treatment options?
Causes:
- Stroke
- Almost 90% of all central pain is caused by CVAs, but less than 10% report pain within the first year - Spinal cord injury
- Multiple sclerosis
Mechanism is thought to involve disruption or injury of the spinothalamocortical tract
Motor cortex stimulation may be a possible treatment
What signs/symptoms are seen if local anesthetic is accidentally injected around the brain stem?
Bilateral headaches
4th or 6th nerve palsies
Pupillary changes
When performing a glossopharyngeal nerve block, which nerves are also commonly blocked??
Spinal accessory nerve
- Weakness of the SCM and trapezius
Vagus nerve
- Reflex tachycardia
The trigeminal ganglion lies in what structure?
Within Meckel’s cavity
Describe the “drug schedule”
The drug schedule ranks drugs based on abuse potential: Schedule V drugs have the lowest potential, while Schedule I drugs have no approved medical indications (ie Heroin)
Schedule II includes most opioids
Schedule III includes mixed acetaminophen-opioids and Tramadol
What is the best test to order if you are concerned about diskitis?
ESR
What are some excitatory neuromediators? What about inhibitory neuromediators?
Excitatory neuromediators: Glutamate Aspartate Substance P Neurokinin Bradykinin CGRP BDNF
Inhibitory neuromediators: GABA Glycine Enkephalin Beta-endorphin
Which part of the hypothalamus partly controls the sleep/wake patterns and may be altered in chronic pain?
The suprachiasmatic nucleus
Where are opioid precursors and their respective peptides found in the brain?
Amygdala
Hypothalamus
PAG matter
Raphe Magnus
What nerve is involved in cubital tunnel syndrome?
Ulnar nerve