Final Flashcards

(75 cards)

1
Q

What’s a disease?

A
  • A medical condition with a specific cause or causes and recognizable signs and symptoms
  • If we know what’s going on, it’s a disease
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2
Q

What’s a syndrome?

A
  • A collection of signs, symptoms, and medical problems that tend to occur together, but are not related to a specific, identifiable cause
  • If we don’t know what’s going on/don’t know the cause, it’s a syndrome
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3
Q

What are the most to least common diseases?

A
  1. Hypertension
  2. Type 2 Diabetes
  3. Ischemic heart disease
  4. Atrial Fibrillation
  5. Dementia
  6. COPD
  7. Cancer
  8. Heart failure
  9. Stroke
  10. Obesity
  11. Chronic liver disease
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4
Q

List different syndromes by medical specialty

A
  • Gastroenterology: Irritable Bowel Syndrome, non-ulcer dispepsia
  • Gynaecology: pre-menstrual syndrome, chronic pelvic pain
  • Rheumatology: fibromyalgia
  • Cardiology: atypical or non-cardiac chest pain
  • Respiratory medicine: hyperventilation syndrome
  • Infectious disease: chronic (postviral) fatigue syndrome
  • Neurology: tension headache
  • Dentistry: temporomadibular joint dysfunction (TMJ), atypical face pain
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5
Q

What are the 3 types of clinical pain?

A

1) Acute pain (Acute Pain Service)
- Emergency room
- Post-operative
2) Cancer pain (Oncology, Palliative Care)
3) Chronic non-cancer pain (Chronic Pain Service)
- Inflammatory
- Neuropathic
- Idiopathic/functional/nociplastic
- Headache
- How these things are managed in medicine
- If you go on to work in pain management as a healthcare worker, then you will be assigned to work with 1 of 3 types of clinical pain

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6
Q

Describe acute pain service

A
  • People coming in with trauma
  • Lots of pain going on in the emergency room
  • Triage: #1 priority is if you can’t breathe and #2 priority is if you’re bleeding out and pain is at the bottom of triage list
  • # 1 goal is that you don’t die
  • Burst appendix is a type of pain that is recognized as if it’s not attended to, it can lead to infection
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7
Q

Describe the causes of acute pain

A

1) Burns
- Heat injury and the thing to do with it is make it cold
- The heat is doing the damage
- 1st degree burn: through the epidermis
- 2nd degree burn: through the epidermis and dermis
- 3rd degree burn: all skin layers
- 2 things that matter with burns: severity and extent of it
- Treatment is incredibly painful (need to debride the skin everyday so it heals back properly and this debridement is extremely painful)
2) Fractures
- Ex: fractured leg that’s swollen
3) Dislocated shoulder or rotator cuff injuries
4) Mouth pain (ex: tooth pain, gum issue, TMJ, impacted molar)
- Dentists deal with pain a lot
5) Back pain
- 3 distinctions: acute back pain, sub-acute back pain, chronic back pain
- Acute: single episode resolved in 6-7 weeks from onset
- Sub-acute: episode resolved between 7-12 weeks from onset
- Chronic: episode lasting more than 12 weeks (3 months)

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8
Q

Describe Postsurgical Pain Prevention

A
  • Knowing surgeries are going to be painful, people have put a lot of thought about what to do about them
  • Analgesia during
  • Is giving analgesia after the surgery a good idea? Or is giving it before the surgery a good idea?
  • Presurgical analgesia (preemptive analgesia - giving it before a surgery)
  • Postsurgical (giving it after surgery)
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9
Q

Describe the Scott Reuben Fraud

A
  • The majority of the evidence supporting the use of presurgical analgesia was from Scott Reuben who as it turns out made up everything
  • These studies never occurred
  • This is one of the worst examples of discovered scientific fraud
  • This is thus a concept that sounds reasonable but there is no data confirming that it’s true as all the evidence is fake
  • The pain is going to be there it just won’t be conscious
  • The point was that it seemed like a reasonable idea that if you’re going to use analgesics, you definitely want to use them after surgeries but should instruct patients that maybe want to use it before as well because it’ll block more input and reduce the chance of post-surgical pain
  • A lot of the evidence that it really does work was faked by Scott Reuben
  • A lot of people use it because it seems reasonable and probably won’t hurt
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10
Q

Describe Chronic Postsurgical Pain (CPSP)

A
  • When someone has an operation and 4 or more months later, they still have pain
  • Even though your chances of developing it are reasonable
  • Most of the time, if you have a surgery, you won’t develop CPSP
  • The incidence is fairly low but there are so many operations
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11
Q

Describe McCrae, Br. J. (2008) depiction of the approximate numbers of operations carried out in England and the US and incidence of CPSP (most to least)

A
  • Total operations:
  • UK (# of ops in 2005-6) = 7 125 000
  • US (# of ops in 1994) = 22 629 000

1) Amputation
- Incidence of chronic pain: 50-85%
- UK: 15 000
- US: 132 000
2) Thoracotomy
- Incidence of chronic pain: 5-65%
- UK: 0
- US: 660 000
3) Cardiac surgery
- Incidence of chronic pain: 30-55%
- UK: 29 000
- US: 501 000
4) Mastectomy
- Incidence of chronic pain: 20-50%
- UK: 18 000
- US: 131 000
5) Cholecystectomy
- Incidence of chronic pain: 5-50%
- UK: 51 000
- US: 667 000
6) Hernia repair
- Incidence of chronic pain: 5-35%
- UK: 75 000
- US: 689 000
7) Hip replacement
- Incidence of chronic pain: 12%
- UK: 61 000
- US: 0
8) Caesarean section
- Incidence of chronic pain: 6%
- UK: 139 000 (most common)
- US: 858 000 (most common)

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12
Q

What are some non-essential surgeries associated with CPSP?

A
  • Cosmetic surgery: 21-50% CPSP
  • Breast augmentation: 13% CPSP
  • Vasectomy: 15% CPSP
  • Suggesting that surgical consent forms probably should list the risk of developing CPSP
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13
Q

Why doesn’t the risk of developing CPSP appear in surgical consent forms?

A

Surgeons are the ones that develop the consent forms and surgeons don’t care that much about CPSP (probably care more about making money)

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14
Q

What are the causes of CPSP?

A
  • Some CPSP is the surgeon’s fault (ex: neuropathic pain from surgeon nicking a nerve)
  • Could also be the patient’s fault (more vulnerable to it)
  • Unlike other pain syndromes, with CPSP, you know exactly when the pain started
  • A lot of things are known with CPSP
  • Hard to know with fibromyalgia
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15
Q

Describe Acute-to-Chronic Pain Transitioning

A
  • Big thing lately in pain research field
  • People are very polarized on whether they think this is a thing
  • There are 2 hypotheses on what’s happening:
    1) You have acute pain from (ex: a surgery - physiological pain) where pain intensity is highest
  • Then one of 2 things happen during a transition period: either the pain goes away (pain is resolved) or in some % of people, it doesn’t resolve and because it’s still there, now it’s pathological pain but it’s the same thing
  • Becomes chronic pain
    2) Chronic pain either starts or doesn’t start but postoperative pain and chronic pain are independent of each other and postoperative pain resolves in everyone
  • A lot of people believe in this and a lot of people don’t
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16
Q

Describe Parisien/Lima et al. (2023) UK Biobank Study on whether blocking inflammation is the cause of acute-to-chronic pain transitioning?

A
  • 502k Ps that agreed to go in and answer a bunch of questions about them and their medical history
  • Gave a bunch of biological samples (ex: urine, blood, brain imaging)
  • Ps came and gave info at 2 diff times (T0 and T1 ~4.4-7.7 years later)
  • At T0, 130k of them had back pain
  • They were asked how long they had had this back pain
  • At T0, 40.5k had acute back pain
  • At T1, 2.6k had chronic back pain
  • Researchers looked at difference of 2.6k people who transitioned to chronic back pain
  • Found 2 statistically significant differences:
    1) Neutrophils: importance of the immune system
  • The pathology of chronic pain is much more likely to be an immune system problem
    2) NSAIDs
  • People who took NSAIDs were 1.67x more likely to develop chronic pain
  • Blocked inflammation which is bad
  • Good for the acute pain but blocks processes that would occur to lead to resolution
  • This is also true for steroids
  • Evidence is starting to emerge that if you have a new painful inflammatory injury, you’ll want to take NSAIDs but you shouldn’t
  • Bad idea since this injury will probably turn into CRPS
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17
Q

Describe the prevalence (most to least) of the different types of cancer with moderate to severe pain (Lipman (ed.), 2004)

A

1) Bone (80-90%)
2) Oral (80-90%)
3) Genitourinary (male - 70-80%)
4) Genitourinary (female - 65-75%)
5) Breast (50-55%)
6) Bronchus (40-50%)
7) Lymphoma (20-25%)
8) Leukemia (5-10%)

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18
Q

Describe cancer pain

A
  • Eventually cancers metastasize and they metastasize to the bone and bone cancer is almost always painful
  • Differences in pain: probably about whether or not the tumour is being secreted
  • Tumours are growing and pressing on nerves
  • When people have cancer pain, it’s not always levelled
  • You’ll get spikes of cancer pain throughout the day
  • This requires a different strategy to manage cancer pain
  • Solution: give you 2 drugs
  • One drug is around the clock medication to manage the spikes of pain and the background pain that’s always present
  • Other drug is a strong opioid which is the only thing strong enough to deal with the breakthrough pain
  • Often the breakthrough pain is so painful that the opioid isn’t doing anything
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19
Q

Describe chemotherapy-induced peripheral neuropathy (CIPN)

A
  • Standard chemotherapy drugs
  • These work very well if you give them at high doses but you can’t give them at high doses because you’ll cause CIPN
  • Problem with chemotherapeutic drug treatment is that patients won’t be able to keep taking it
  • But could get rid of pain and cancer
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20
Q

Describe the chemotherapy-induced peripheral neuropathy (CIPN) symptoms (most to least prevalent)

A

1) Tingling in feet (~86% “quite a bit” and “very much”)
2) Numbness in feet (~81% “quite a bit” and “very much”)
3) Tingling in hands (~76% “quite a bit” and “very much”)
4) Numbness in hands (~69% “quite a bit” and “very much”)
5) Pain in feet (~31% “quite a bit” and “very much”)
6) Pain in hands (~21% “quite a bit” and “very much”)

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21
Q

What are the 2 types of arthritis?

A

Osteoarthritis (OA) and rheumatoid arthritis (RA)

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22
Q

Osteoarthritis (OA) vs rheumatoid arthritis (RA)

A
  • OA is what you get when you get old
  • Affects many people (~20% of population right now)
  • Bone ends rub together
  • Thinned cartilage (cartilage in time or with age is getting thinner)
  • The synovial fluid isn’t replenishing
  • Whether there’s inflammation in OA or not depends
  • RA is what you get much younger
  • Autoimmune disease
  • Occurs because of the autoimmune problem, the joint swells up and the hand swells up
  • Pretty rare
  • Characterized by bone erosion, swollen inflamed Synovial membrane
  • OA or RA can either be painful or not
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23
Q

What do words that end with -itis mean?

A

Inflammation

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24
Q

What’s a joint?

A

Where 2 bones meet

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25
Describe Rheumatoid Arthritis Treatment
- Treatment for RA are pretty good 1) Painkillers - Results: moderate pain relief - Side Effects: few - Ex: Tylenol 2) NSAIDs - Results: mild/severe pain relief - Side Effects: moderate - Ex: Ibuprofen, celecoxib 3) Glucocorticoids - Results: pain, inflammation & joint damage relief - Side Effects: severe - Ex: Prednisone and Dexamethasone 4) Biologic Response Modifiers - Results: pain, inflammation & joint damage prevention - Side Effects: few - Ex: Abatacept, Adalimumab, Etanercept, Infliximab 5) Disease-modifying antirheumatic drugs (DMARDs) - Results: pain, inflammation & joint damage relief - Side Effects: severe - Ex: Methotrexate (designed to treat the actual joint degeneration - doesn't work very well)
26
Describe the different drugs and their usual dosing regimen for RA treatment
1) Infliximab (Remicade): initially given at the clinic or at an infusion centre as an IV at a dose of 3-5mg/kg (according to body weight) at weeks, 0, 2, and 6 2) Etanercept (Enbrel): initially 50 mg once a week or 25mg 2x a week as a self-administered subcutaneous injection 3) Adalimumab (Humira): initially 40mg every other week as a self-administered subcutaneous injection 4) Certolizumab (Cimzia): initially 400mg on week 0, 2, and 4 as a self-administered subcutaneous injection 5) Golimumab (Simponi): 50mg once per month as a self-administered subcutaneous injection
27
What does RA treatment target?
- TNF-alpha, interleukin-1 - There have been a bunch of -mabs that have been developed to get rid of TNF-alpha - Have to be given intravenously
28
Describe Silas Weird Mitchell
- 1829-1914 - Thought of as the father of medical neurology - Civil war doctor that saw all kinds of soldiers with bullet wounds - Many of the soldiers were left with neuropathic pain - He was referring to a disease he named "causalgia" - Discovered the existence of neuropathic pain - He was also the inventor of the "rest cure" - He would usually prescribe this to women and wouldn't let them leave their bed for months and months - "Perhaps few persons who are not physicians can realize the influence which long-continued and unendurable pain may have on both body and mind. ... Under such torments the temper changes, the most amiable grow irritable, the bravest soldier becomes coward, and the strongest man is scarcely less nervous than the most hysterical girl. Nothing can better illustrate the extent to which these statement may be true than the case of burning pain, or, as I prefer to term it, Causalgia, the most terrible of all tortures which a nerve wound may inflict" - S. W. Mitchell
29
Chronic pain can be divided into what?
- Cancer - Other non-cancer chronic pain - Inflammatory pain - Neuropathic pain - Everything else
30
What are the causes of chronic neuropathic pain?
1) Nerve trauma - If you cut a nerve either completely or partially, this will lead to neuropathy - Sometimes neuropathies are painful and sometimes they aren't - Ex: stump pain, phantom limb, CRPS2 (causalgia), bone fractures, penetrating injuries 2) Iatrogenic nerve injury (ex: surgery, radiotherapy, chemotherapy) - Ex: scar pain, post-thoracotomy pain, post-mastectomy pain, accidental intramural injection, vincristine neuropathy 3) Nerve compression due to entrapment - Pressure on nerves that's not supposed to be there can cause it to malfunction - Ex: carpel tunnel, ulnar n. entrapment, foramina (lateral) stenosis 4) Nerve entrapment by: tumour, artery, edema, herniated intervertebral disc - Ex: many cancer pains, sciatica's trigeminal neuralgia 5) Parasitic, bacterial or viral infection - If it attacks nerves, this can cause neuropathy - Ex: nerve abscess, Hanson's disease (leprosy), tabes dorsals, postherpetic neuralgia, HIV/AIDS neuropathy 6) Inflammation (sterile) - Either of the nerve itself or of the tissue surrounding the nerve - Ex: acute and chronic demyelinating neuropathy, dorsal root ganglionitis, tumour infiltration of nerves or innervated tissues 7) Metabolic/nutritional/ischemic - Ex: diabetic neuropathy, sickle cell anemia, occlusive/ischemic antipathy, alcoholic neuropathy, vitamin deficiency 8) Toxic - Ex: lead, mercury, ethanol, vincristine neuropathy (and other chemotherapeutics) 9) Ionizing radiation - Ex: radiation burns, radiation therapy for cancer 10) Hereditary neuropathies - Ex: some Marie-Charcot-Tooth neuropathies, Fairy's disease 11) Autoimmune, idiopathic - Ex: Guillian-Barré, small fibre neuropathies, paraproteinemia, Sjogren syndrome - Anything that can cause a nerve to malfunction will produce neuropathy by definition and some percentage of those neuropathies are painful whereas others aren't
31
What's Carpel Tunnel Syndrome?
Nerves in your hand are pretty complex and compacted and one nerve can only go to where it's going to through a small opening and this can sometimes cause compression
32
Describe neuropathic pain
- Cause: injury to the nervous system, or injury to nerves, often accompanied by maladaptive changes in the nervous system - Descriptors: lancinating, shooting (going from place to place), electric-like, stabbing, burning, sharp pain - Sensory deficits: common (ex: numbness, tingling, pricking) -> paraesthesia and dysesthesia - Motor deficits: neurological weakness may be present if a motor nerve is affected; dystonia or spasticity may be associated with CNS lesions and sometimes peripheral lesions (ex: complex regional pain syndrome) - Hypersensitivity: pain often evoked by non-painful (allodynia) or pain (exaggerated response) stimuli; secondary hyperalgesia common - Character: distal radiation common - Paroxysms: exacerbations common and unpredictable - Autonomic signs: colour changes, temperature changes, swelling, or sudomotor (sweating) activity occur in 1/3 to 1/2 of patients
33
Describe nociceptive pain
- Inflammatory pain is often referred to or lumped into nociceptive pain - Cause: damage or potential damage to tissues - Descriptors: throbbing, aching, pressure-like pain, dull, localized - Sensory deficits: uncommon; if present they have a non-dermatomal or non-nerve distribution - Motor deficits: may have pain induced weakness - Hypersensitivity: uncommon, expect for hypersensitivity in the immediate area of an acute injury - Character: distal radiation less common; proximal radiation more common - Paroxysms: exacerbations less common and often associated with activity - Autonomic signs: uncommon
34
What are the most common neuropathic pains?
- Painful diabetic peripheral neuropathy (PDN or DPN) - Post-Herpectic Neuralgia (PHN) - Phantom Limb Pain (PLP) - Complex Regional Pain Syndrome (CRPS)
35
Describe Painful Diabetic Peripheral Neuropathy (PDN or DPN)
- Location is almost always the feet - Diabetes causes a bunch of bad metabolic states that all have the ability to damage nerves - Causes neuropathy - Gunshot - Polyneuropathy because all the nerves are damaged, but they aren’t all damaged equally because they're the longest, which makes them more fragile (cell body is keeping a 1-2 meter of nerve alive) - First nerves to die or stop working are going to be the longest ones in your feet (because most fragile) - Then gets more proximal - Symptoms (in feet): - Pins & needles - Burning - Tingling - Painful cold - Electric shock
36
Describe Shingles and Post-Herpetic Neuralgia (PHN)
* Varicella -> control of primary infection -> Latency -> failed immune control, virus reactivation -> Zoster -> Postherpetic neuralgia (for ~15% of elderly patients) * PHN is when the pain from shingles fails to resolve * Usually the rash resolves and if the pain doesn't go away after the rash is resolved * PHN is basically the chicken pox virus going dormant in one of your dorsal ganglion * In ~15% of people with shingles, the rash resolves but not the pain * Chance of getting shingles before you die is 1 in 2 (50%) and then chance of pain not going away after (PHN) is 15% * There are highly effective vaccines for shingles (ex: Zostavax, Shingrix) * These vaccines are also good at reducing your risk of dementia
37
Describe Lazzarine et al. (2012) depiction of % of people (most to least) and their mean age for the main conditions associated with lower extremity amputation
1) Type 2 Diabetes (~53%, mean age = 67) - Can't keep their sugar levels in check - Often need to have their feet amputated 2) Peripheral arterial disease (non-diabetes - PAD) (~18%, mean age = 68) 3) Trauma (8%, mean age = 36) 4) Type 1 Diabetes (7%, mean age = 52) 5) Malignant tumours (~5%, mean age = 56) 6) Joint deformity (~4%, mean age = 55) 7) Emboli (~2%, mean age = 69) 8) Neuropathy (~2%, mean age = 48) 9) Infection (0.5%, mean age = 84)
38
What is Phantom Limb Pain (PLP) usually caused by?
- An amputation - If you have an amputation, by definition you have a neuropathy
39
Describe Davidson et al. (2010) depiction of the chances of developing post-amputation pain
1) Upper Limb (N = 17) - Post-Amputation Pain Present (94%) - Severity (Moderate to Severe = 64%) and (No pain to mild = 35%) - Frequency (most days to every day = 94%) and (no pain to once a week = 6%) 2) Lower Limb (N = 39) - Post-Amputation Pain Present (64%) - Severity (Moderate to Severe = 28%) and (No pain to mild = 72%) - Frequency (most days to every day = 33%) and (no pain to once a week = 68%) - Shows pain is worse for upper limb amputation and upper limb amputations are less frequent
40
Describe Phantom Limb symptoms
1) Pain - Classic symptoms of neuropathic pain: cramping, shooting, stabbing, burning (from closest to furthest location on limb away from body and from level of amputation) 2) Itch, vibration, temperature 3) Movement - Some people feel like their amputated limb is moving its position not under their control 4) Size, shape, position 5) Rings, etc. - Some people can still feel the rings on their phantom limb 6) Referred phantom sensation (ex: face touching felt in phantom limb) - If you touch some person's part of their body, in addition of where you touched, they'll feel like you're touching them on their phantom limb 7) Telescoping - Feels overtime that the person's phantom arm is retracting into their stomach - Usually associated with a clenching of their fist, they feel like their fist is slowly clenching into itself - This is described as very annoying - Some people describe feeling their nails dig into their phantom hand
41
Describe the debate of the causes of Phantom Limb Pain (PLP)
Debate between those that say that the cause of the pain is all central and due to central changes (going on in the brain or spinal cord) vs others that say the cause of the pain is due to peripheral changes
42
Describe PLP Interventions
- Traditional treatment methods (ex: drugs) <30% effective one year after injury - One thing that really works is Lidocaine blocks - Works even better if you do it near the spinal cord - Spinal block (in DRG): PLP "always" gone (almost 100% of the time that you do a spinal block, the phantom pain will stop for a small amount of time) - Nerve/plexus block: PLP eliminated in ~50% of patients - Plexus block is done peripherally (can be done closer to the stump) - Mirror box: - The mirror convinces them that their other arm is there - Humans are so reliant on our visual sense - This didn’t hold up - People are still doing things that are reminiscent of mirror box - Study on mirror box shows people with PLP develop subconscious weird notions of size and shape of limb they lost - Show that if you show the limb to patient
43
Describe Complex Regional Pain Syndrome (CRPS)
* Rather common disorder * CRPS is divided into 2 types: CRPS 1 (RSD) and CRPS 2 (causalgia) * Example of lumping 2 things together and calling them CRPS when there's every reason to be kept separate
44
Describe CRPS 1
- Used to be called Reflex Sympathetic Dystrophy (RSD) - Precipitating event: sometimes - Single peripheral nerve involvement: sometimes - Physiologic changes in affected limb: yes (loss of hair, nail changes, sweating) - Cardinal signs: spontaneous pain, swelling, different skin temperatures - Circumferential in distribution - Good response to sympathetic blocks - No response to nerve blocks - Often happens in hand or feet - Often not sure why they're experiencing this - Usually injuries people can come up with are very minor - Might be the easiest thing in the world to diagnose - Big problems physiologically in affected area (they turn red, hair falls out, changes in sweating, nail fungus) - With these types of changes, we suspect the SNS is involved - Sympathetic block temporarily relieves the symptoms and the physiologically changes
45
Describe CRPS 2
- Causalgia - What S. Weir Mitchell discovered and called causalgia - Precipitating event: yes - Single peripheral nerve involvement: yes - Physiologic changes in affected limb: no - Cardinal signs: burning pain, allodynia, hyperalgesia - Follows discrete nerve distribution - Variable response to sympathetic blocks - Responds well to nerve blocks - Classic mono neuropathy - One nerve is involved and was damaged - CRPS 2 if we know the precipitating event and that only a single peripheral nerve is involved - All of our animal models of neuropathic pain are mimicking this - Signs: shooting, lancinating, etc. - In general, the limb looks fine
46
What causes CRPS?
- Inflammation - Central sensitization - Cortical plasticity - Sympathetic processes - Psychological factors - Genetic predisposition - Peripheral sensitization
47
Describe Fibromyalgia
- Always been a huge mystery - Idiopathic, functional, nosiplastic pain - Been considered a rheumatic condition: - When you ask people where the pain is, they tend to point to their joints - A condition that affects the joints and/or soft tissues, causing chronic pain - Significant pain and fatigue (#1 symptoms) - We know now that this isn't true - But not a form of arthritis: - Usually arthritis is a particular joint vs fibromyalgia is many joints - No inflammation or damage to joints, muscles, or tissues - But does produce pain in soft tissues around joints and in skin and organs throughout body - Other symptoms too: - Cognitive (“fibro fog”) - Numbness and tingling (might lead you to believe it's neuropathic) - The usual comorbidities (sleep, anxiety, depression, etc.) - Very common in women (especially middle-to-late age - 40-80) - Huge disparity between sexes (not as common in men)
48
Describe the Fibromyalgia Tender Points
* ~19 fibromyalgia tender points in the body * Allodynia * There's nothing special about the tender points * Tender points are tender but also areas between * Been shown that people with fibromyalgia are hypersensitive everywhere and not just touch but also every other sense (ex: sensitive to sounds)
49
Describe the history of fibromyalgia
* For a long time, most of the medical establishment didn't believe fibromyalgia was real * Because it was mostly found in middle-aged women * Thought they had angst and ennui because of their role in culture and that this expresses itself through pain and they're being hysterical * A lot of medical doctors though this wasn't real * What really changed people not believing in fibromyalgia, was the beginning of brain imaging (ex: fMRI) * Brains of fibromyalgia patients agrees with their complaints * Wasn't psychological magnification of pain but rather cortical magnification of pain * This fMRI evidence went a long way to remove some of the stigma around fibromyalgia and helping these patients
50
What causes fibromyalgia?
- Different hypotheses - You can predict who's going to develop it and their prognosis by looking at catastrophizing scores and anxiety levels same as other pain syndromes (risk factors) - 3 hypotheses: 1) Increased windup in fibromyalgia 2) Decreased Conditioned Pain Modulation in Fibromyalgia 3) Small-Fiber Neuropathy
51
Describe the hypothesis of Increased windup in fibromyalgia
* Fibromyalgia patients have more ascending pain info * They have increased windup * Windup: proxy for how much ascending pain info you're getting (how much sensitization is occurring) * Staud (2006) study: * Looked at windup pain ratings of normal control (NC) and fibromyalgia syndrome (FM) patients * All subjects received 15 mechanical stimuli (taps) to the adductor policies muscles of the hands at interstimulatory intervals of 3s and 5s * FM patients showed mechanical hyperalgesia during the first tap and greater temporal summation than NCs at both inter stimulatory intervals
52
Describe the fibromyalgia hypothesis of Decreased Conditioned Pain Modulation in Fibromyalgia
* Unable to inhibit their pain input using the normal mechanisms that have been developed using conditioned pain modulation * Chalaye et al. (2014) study: * Study shows that women with FM have the same pain intensity before and after cold pressor test, whereas healthy women have more pain intensity before vs after the cold pressor test * Argument is that life comes with a small amount of pain * Normal aches and pains and these are inhibited completely by descending modulation
53
Describe the fibromyalgia hypothesis of Small-Fiber Neuropathy
Fibromyalgia patients don’t have nosiplastic disorder but rather a neuropathic disorder
54
Describe the overlap between idiopathic pain conditions
* All the idiopathic and nosiplastic conditions have overlapping symptoms * Chronic fatigue syndrome (unrefreshing sleep and headaches) * Fibromyalgia (myalgia/arthralgia and tender points) * Irritable Bowel Syndrome (diarrhea/constipation, abdominal pain, bloating) * Anxiety (panic attacks and avoidant behaviour) * Depression (loss of motivation and loss of pleasure) * What they all have in common: prolonged fatigue states (fatigue, pain, poor concentration, irritable mood)
55
List some of the conditions comorbid with fibromyalgia
* Ex: IBS, tension/migraine headaches, TMJ, restless-legs syndrome, allergies, anxiety disorders, Lyme disease, RA, thyroid dysfunction, OA, PMS, Depression, carpal tunnel syndrome, tendinitis, lead poisoning * All kind of idiopathic conditions * Syndromes where we don't really know their cause * In general, women are more sensitive to them * These have generally been dismissed * Also all comorbid with each other * Maybe this is a lumping and splitting problem
56
Describe pain location in idiopathic pain syndromes
- There's more and more data suggesting that they're not quite as focused on the body as we think - In Irritable Bowel Syndrome: - People with IBS are complaining about their butt (where the pain is) - As it turns out, they're hypersensitive across the board - Study by Stabell et al. (2014) - Found IBS patients had significantly more nonabdominal chronic pain and psychological distress than controls - Also found IBS patients had significantly lower pain threshold than controls for heat pain, pressure (fingernail) pain and pressure (shoulder) pain - In Vestibulodynia: - Study by Pukall et al. (2002) - Looked at mechanical allodynia - Found they're hypersensitive in the vulva vestibule but also in many other locations (far away) from the vulva (ex: L minus, deltoid, forearm) - Many people believe that the diagnosis has less to do with your pain and more to do with the type of specialist you were referred to - Evidence that the problem here might be central and not peripheral
57
What are the different types of headaches?
- Sinus: pain is behind brow bone and/or cheekbones - Cluster: pain is in and around one eye - Tension: pain is like a band squeezing the head (most common) - Migraine: pain, nausea and visual changes are typical of classic form (usually unilateral) - Such a big pain problem in terms of prevalence - What distinguishes these are their locations
58
Describe Gantenbein & Sandor (2007) comparison of the diagnostic criteria for frequent episodic tension-type headache and migraine without aura from the International Heachache Classification
1) Frequent episodic tension-type headache - Number of episodes: at least 10 - Number of days with such headache: more or equal to 1 day and less than 15 days per months (for at least 3 months) - Duration of the headache: 30 mins to 7 days - Pain characteristics (at least 2 of these): pressing/tightening (non-pulsating) quality, mild or moderate intensity, bilateral location, no aggravation by walking stairs or similar routine physical activity - Accompanying symptoms (both of these): no nausea or vomiting (anorexia may occur) and photophobia (light phobia) or phonophobia (sound phobia) or none 2) Migraine without aura - Number of episodes: at least 5 - Number of days with such headache: less than 15 days per month (untreated or unsuccessfully treated) - Duration of the headache: 4-72hrs - Pain characteristics (at least 2 of these): pulsating/throbbing quality, moderate or severe pain intensity, unilateral location, aggravation by or causing avoidance of routine physical activity - Accompanying symptoms (at least one of the following): nausea and/or vomiting and photophobia (light phobia) or phonophobia (sound phobia)
59
Describe the stages of a migraine
1) Prodome - Symptoms may occur days before actual pain hits - Lasts ~1-2 days - ~1/2 of all migraine sufferers experience this stage, which is characterized by symptoms of light and sound sensitivity, depression, irritability and lack of appetite - A lot of migraine patients know they're going to get a migraine soon 2) Aura - Auras usually occur up to 1 hr prior to the headache (immediately preceding the headache) - 20% of migraine sufferers experience migraine aura - A phase characterized by changes in visual perception, flashing lights and geometric patterns obscuring vision 3) Headache - Headache pain can be moderate to severe, lasting up to 3 days - Migraine pain may start on one or both sides of the head - Other symptoms may include intolerance of light and noise, nausea and vomiting, sensitivity to movement and speech difficulties 4) Postdrome - Symptoms can last several days after the headache, and have been described as a "migraine hangover" - Lasts ~1-2 days - Most migraine sufferers may be irritable and fatigued - They may have difficulty concentrating and experience mood changes - The scalp may also be very tender - Certain symptoms last for a long time - Overall these different stages account for ~5 days for 1 migraine attack - Migrainers can have a few migraines per month - Why headaches are one of the most debilitating
60
Describe Aura and Cortical Spreading Depression (CSD)
* Theory that auras are caused by cortical spreading depression (CSD) * Electrophysiological phenomenon that goes over the surface of the cortex * Starts at the back of the brain and then goes forward * Spreading wave of cortical hyperexcitability * Progresses from the posterior pole of the brain toward the frontal lobe until the self-limited process terminates * Best evidence of this: the speed of the electrophysiological movement of this disturbance is exactly the same speed that the visual disturbance moves through the visual field
61
What are the most common reported migraine triggers?
1) Stress/tension (most common) 2) Menstruation 3) Lack of sleep 4) Hunger/not eating 5) Specific foods/drinks 6) Visual disturbance
62
Describe migraine triggers
* Migraineurs are often quite convinced that their migraines are triggered by environmental events * Stress is the most common trigger * After this there's lots of disagreement from one study to another * Interesting how convinced migraineurs are of their triggers * A lot of migraine specialists are skeptical about these triggers because it's pretty easy to do good controlled experiments on migraineurs * You can take people who are migraineurs into the lab who aren't currently experiencing a migraine and give them a migraine * This can be done 100% of the time by giving them nitroglycerin * If you give nitroglycerin to a non-migraineur you'll probably just give them a headache * Migraine researchers have good control in their experiments * People have done the experiments with triggers * Bring migraineurs in the lab who aren't currently experiencing a migraine and give them their trigger and see what happens -> usually no migraine happens * Most of the time people's migraine triggers don't survive being put to the test * Triggers could be due to nocebo * You can try to get people stressed in the lab but how stressed can they really get in a lab? * The question of whether triggers are real or just nocebo is a very contentious question * Lots of debate between migraine specialists
63
Describe the evidence for the cause of migraine being due to vasoldilation vs neuronal
* Never gotten to the bottom of the issue of whether the cause of migraine has to do with your vascular system or if the cause is completely neuronal * Might be immune as well * There's a bunch of reasons to believe that the cause is vasodilation related * Migraine pain throbs approx at the same frequency as your heart rate * Throbbing has something to do with the blood going through the arteries * Computed tomography angiogram of the superficial temporal and occipital arteries which form the basis of Wolff's theory of extracranial vascular pain (Shevel, 2011) * Current leading theory for the cause of migraine (Burnstein & Jakubowski, J., 2005): * The problem ultimately is in the dura and the nerves that are going through the dura * Migraine pain is ultimately dural inflammation or something else in the dura that causes the neuronal pathway from SpV to Th to be activated * Not sure of this is true * Part of the problem of not knowing this is due to the lack of animal models for this
64
Describe migraine treatments
1) Acute (you're having a migraine what can you do about it): - OTC Analgesics (NSAIDs are still popular treatments for acute migraines) - Triptans (only work for migraines - serotonin drugs) - CGRP antagonists (“gepants” - new ones) -> people were hoping these would work better - There are some people who don't respond to triptans and respond to gepants and vice versa 2) Prophylatic (what can you take to prevent migraines): - Anti-epileptics - Beta-Blockers - Antidepressants - Botox - Neuromodulation - CGRP antagonists (“Mabs”) - None of these work particularly well - But the mabs work well (they're better) - Beat placebo by a few headache days per month - Hardly a cure
65
Describe Belvis et al. (2009) depiction of the effectiveness of the different triptans for headaches (most to least effective)
1) Rizatriptan - Headache response at 2 hours: 70-77% - Complete relief of pain at 2 hours: 40-44% 2) Eletriptan 80mg - Headache response at 2 hours: 65-80% - Complete relief of pain at 2 hours: 37% 3) Zolmitriptan 5mg - Headache response at 2 hours: 65% - Complete relief of pain at 2 hours: 38% 4) Zolmitriptan 2.5mg - Headache response at 2 hours: 64% - Complete relief of pain at 2 hours: 33% 5) Eletriptan 40mg - Headache response at 2 hours: 65% - Complete relief of pain at 2 hours: 29% 6) Samatriptan - Headache response at 2 hours: 50-61% - Complete relief of pain at 2 hours: 30-32% 7) Almotriptan 12.5mg - Headache response at 2 hours: 57-65% - Complete relief of pain at 2 hours: 20-25% 8) Natatriptan 2.5mg - Headache response at 2 hours: 45-52% - Complete relief of pain at 2 hours: 21-27% 9) Frovatriptan 2.5mg - Headache response at 2 hours: 38-40% - Complete relief of pain at 2 hours: 23-28%
66
Describe Deen et al. (2017) depiction of the effectiveness of different mab drugs in beating placebo at reducing the mean monthly migraine headache days (most to least)
1) Erenumab 140mg and 70mg (most -> reduction by almost 7 days) 2) Fremanezumab 675 mg 3) Fremanezumab 225 mg 4) Eptinezumab 1000mg iv 5) Galcanezumab 150 mg 6) Erenumab 70mg 7) Erenumab 21mg 8) Erenumab 7mg (least -> reduction by a bit more than 2 days)
67
Who has more training in pain than our doctors?
- Us who have taken this class - Have had more than 30 hours worth of pain education - This training doesn't occur as much in medical programs - If you add pain course, then you have to remove a class from medical school curricula - Lots of backlash for this because people take pride in their courses - McGill's medical school was put in probation in 2011 - Medical training program was lacking in a number of ways - One of the problems in the report was that they had inadequate instruction on the management of pain - Added 5 hours in consequent of this - Problems were identified by students - Vets and dentists get good instruction on pain - Courses on pain at the undergraduate level are very rare (only ~4 in the world)
68
Describe the discovery of cannabis
* Interesting parallel with the development of cannabis and opioids * Cannabis (scientific name) * Plants that are the sources of these medical compounds * Cannabis was initially used for other purposes (ex: paper, harnesses for horses) * People realized that if you took the flower and you extracted the oils from within the flower you could generate some psychoactivity
69
Describe historical perspectives on opium
- Homer in the Odyssey was thought to be describing opium when speaking of Helen of Troy (ex: "she cast into the wine a drug to quiet all pain and strife to bring forgetfulness of every ill") - Galen (great Roman physician) wrote in the 2nd Century AD about opium - Stated that pretty much anything you could think of, opium was the cure (ex: headaches, vertigo, deafness, epilepsy, asthma, menstruation, melancholy, coughs) - ‘‘Among the remedies which it has pleased Almighty God to give to man to relieve his sufferings, none is so universal and so efficacious as opium.’’ – Thomas Sydenham (1692) - There was this feeling thousands of years ago that opium was a great healing plant - There was a huge interest - Opium was used by these physicians for treatment of pain
70
Describe historical perspectives on cannabis
* Culpeper's Complete Herbal (1653) * Manual for Herbal Remedies * Back then there wasn't any pharmaceuticals so plant remedies were what people went to for treatment * They were boiling the roots, the seeds and not just the flowers * There was a lot of historical use of cannabis * Hampstead in Montreal is named after Hempstead * Hemp was widely used * CBD is a non-psychoactive compound
71
Describe the opium wars
* Info about opium began to reach European attention * There were 2 massive opium wars * The trafficking of opium from China to England * Story of colonialism, power, and greed * A lot of geopolitics today started with the opium wars of the 1600s * There was a tremendous interest in trafficking opium in the world * Continues to show its effects in modern wars and political conflicts today
72
Describe the possible reasons for the US opioid epidemic
1) Physician related - Inadequate and inaccurate training on opioid pharmacology and risks - Lack of access to multidisciplinary chronic pain care - Ease of prescribing opioids compared to other chronic pain therapies 2) Patient related - Strong appeal of immediate pain relief provided by opioids - Focus on pain rather than physiological distress as a treatment target - More value placed on pain relief than functional improvement (ex: they were getting constipation and other quality of life defects but cared about the pain relief and not that) 3) Society and health-system related - Acceptance of right to pain treatment and interpretation of this right in terms of access to opioid therapy - Better insurance coverage for medications than for other chronic pain therapies - Aggressive marketing of sustained-release opioids by pharmaceutical companies
73
Describe when people started to recognize the recreational purposes of opium and cannabis
* During the enlightenment, a bunch of writers got together and consumed these drugs and then wrote about them * Ex: The Hasheeh Eater (Life of a Pythagorean) and Confessions of an English Opium Eater * Hasheesh (cannabis rolled into a ball) * Consumed cannabis and opium * Rise in recognition of these 2 drugs * Not just of their medical value but also non-medical use
74
Describe the rise of opium and cannabis as pharmaceuticals
* Emerging industry trying to take these plant based compounds and put them into medicinal products * These found their way in early pharmacies * Opium was supposedly used by Queen Elizabeth for her menstrual cramps * Opium and cannabis extracted with alcohol
75
Describe the United Nations Office on Drugs and Crime timelines of 100 years of drug control
* Drug policies started coming out * What happened to cannabis? * From 1936-37 onward, cannabis became illegal * Why? * History of racism with cannabis: * Cannabis was being brought in the US by Mexican labourers (called marijuana) and Americans were afraid of them and their use of cannabis * Also jazz black musicians used cannabis * Allegations of these people consuming cannabis harassing women * Believed cannabis was making people mad, sexually depraved * Reaction was to make it illegal (initially just wanted to tax it) * Through the 1900s * At one point, cannabis was considered as having no medical use at all * Completely shut down * No more research on it * Cannabis and opium then became illicitly trafficked * Now modern scientists were trying to find what was the active compound of these plants that was helping people with their pain * Development of synthetics, pharmaceutical companies and the FDA * Opium began to get extracted * Morphine was identified in the early 40s as the active ingredient used for medicine * The synthetic chemists in 1960s made heroin (variant of molecule of morphine) * Cannabis was much slower in this process * Until ~1970s