8. Headache Flashcards
1
Q
list and describe the 4 main types of headaches
A
- Sinus: pain is behind the brow bone and in the area of cheekbones
- cluster: pain in and around one eye
- tension: pain is like a band squeezing the head
- migraine: pain, nausea and visual changes are typical of the classic form
2
Q
this is the most common of the headache disorders. the pathophysiology is unknown but is likely to be multifactorial
A
tension type headache (TTH)
3
Q
list some risk factors of tension type headaches
A
- female
- fatigue/sleep disturbance/sleep disorder
- psychological stress (stress can cause low cortisol levels which may also contribute)
- migraine hx
- depression hx
- alcohol
4
Q
true or false: if you are experiencing a TTH, you cannot have another type of headache
A
false - TTH can coexist with other primary h/a disorder (e.g. an individual can have migraines and still experience a TTH)
5
Q
how does pain typically present in tension type headaches (TTH)?
A
- usually mild to moderate but infrequently may be severe
- explained as “dull” “pressure” “head fullness” “like a tight cap” “band-like” or “heavy weight on head or shoulders”
6
Q
what muscle in the head creates the “tight band” like sensation in tension type headaches (TTH)?q
A
cranial muscle tenderness
7
Q
this is the second most common primary headache disorder; episodic disorder with severe headache as centrepiece
- most people have positive fam history of this
- more common in females
- more than 80% of these people experience some degree of disability
patho: primary neuronal dysfunction leads to a sequence of changes intracranially and extracranially; maybe some cranial vasodilation
A
migraine
8
Q
this is a wave of neuronal depolarization that spreads across the cerebral cortex, which causes an aura, activates trigeminal nerves and alters BBB permeability; activation of the trigeminovascular system, causes a cascade of inflammatory neuropeptides which contribute to cerebral vascular pathology and pain transmission
A
cortical spreading depression
9
Q
this neurotransmitter likely plays an important role in migraines. most acute migraine therapies agonize this NT
A
serotonin (5HT)
10
Q
this class of medications are agonists of vascular and neuronal 5HT receptors, resulting in cerebral vasoconstriction, inhibition of vasoactive neuropeptides and pain signal transmission
A
triptans
11
Q
this is a neuropeptide in trigeminal ganglia nerves; it is a potent vasodilator of cerebral vessels which passes along pain signals
A
CGRP
12
Q
explain the features of migraine prodrome
A
- occurs in 77% of patients
- appear 24 to 48 hours prior to onset of headache
- light &/or sound sensitivity, fatigue, neck pain, food cravings, yawning
- cognitive sx’s such as irritability or euphoria and changes to bowel function
13
Q
explain the features of migraine aura
A
- occurs in 25% of patients
- focal neurological sx’s are present, usually a mix of positive and negative sx’s
- usually visual, develop over 5 mins and last less than an hour
14
Q
what are some positive migraine aura sx’s
A
visual:
- bright lines, shapes or objects
auditory:
- tinnitus, noises, music
somatosensory:
- burning, pain, parenthesis
motor:
- jerking or repetitive rhythmic movements
15
Q
what are some negative migraine aura sx’s
A
indicate ana bsence or loss of function
- loss of vision
- loss of hearing
- loss of feeloing
- inability to move a certain part of the body
16
Q
how does pain typically present in migraine headaches?
A
- unilateral
- throbbing/pulsating
- pain is rated 10/10
- severity increases over 1 to several hours
- patients frequently experience n/v, photo/phonophobia
- routine physical acuity or exercise may worsen the head pain
17
Q
how is the pain in migraine headaches usually caused?
A
caused by the activation of nerve fibres within the walls of the brain blood vessels travelling inside the meninges and scalp
18
Q
in adults, how long does an untreated migraine headache usually last?
A
as little as 4 hours and as long as several days
19
Q
this is the stage of a migraine headache where the patient feels drained or exhausted (some may feel the opposite and experience mild elation or euphoria). can have light or sound sensitivity or food cravings. typically last hours up to one day
A
migraine prodrome
20
Q
this is a secondary headache that occurs when overuse of acute medications to treat other headache disorders results in an increased headache burden
A
medication overuse headache (MOH)
21
Q
true or false: MOH is restricted to individuals who already have other headache disorders. MOH does not develop in individuals with no previous headache hx
A
true
22
Q
true or false: acute exposure to triptans or other analgesics could lead to down regulation of serotonin receptors and changes in central inhibitory pathways that translate to an impairment of antinocieptive activity and a permanent feeling of head pain
A
false - this occurs with chronic exposure to triptans and other analgesics
23
Q
> __ days a month of using triptans or opioids can cause MOH
A
9
24
Q
> __ days a month of using NSAIDs or acetaminophen can cause MOH
A
14
25
what is the hallmark sign of MOH
early morning headache
- manifests as a headache that is present or develops upon awakening
- thought to be due to a nocturnal withdrawal of acute therapies
26
what is a common symptom that accompanies MOH
neck pain
27
true or false: in MOH, severity increases after a period without the drug
true - which causes the individual to want to use the offending medication more which causes a vicious cycle
28
when should a patient be referred to the emergency room?
- suspected stroke, TIA, meningitis or head trauma
- a new headache that presents with cognitive change
- any headache that becomes progressively severe, changes in headache pattern (particularly in elderly folks)
- headache with unilateral eye pain with red eye, fixed and dilated pull or diminished vision
- if the headache came on suddenly
- if the headache is the patients worst headache
- headache occurs with fever, neck stiffness or impaired consciousness
- headache is associated with tenderness in the temporal artery
29
if a patient > 50 presents with a new, undiagnosed headache what are we worried about
Temporal Arteritis
(inflammation of the temporal artery may be visible)
*blood flow is worse in an inflamed artery and the temporal artery supplies O2 to the optic nerve and if the optic nerve goes w/o O2 for an extended period of time, this can cause blindness
30
what are some non-emergent referrals to the patients primary care provider
- MOH (tx needs to be optimized)
- if patient is on any medications that can cause headaches (e.g. tetracyclines, SMX/TMP, ACEIs, beta-blockers, CCBs, birth control, corticosteroids, HRT, decongestants, SSRI's, PPIs)
- withdrawal from medications
- uncontrolled HTN
- shingles and post-herpetic neuralgia
- sinusitis, otitis media or a dental abscess (may be able to recommend analgesics for sinusitis/otitis media - people with dental abscess usually need to be on Abx)
- chronic TTH or frequent migraines
31
what are some non-pharm treatments for headaches
- headache diary (helps identify triggers so they can be avoided)
- rest in a dark, quiet room
- apply cold cloth to head
- physio and chiropractic care
32
what are some potential diet triggers of headaches
- missing meals
- chocolate
- caffeine intake or withdrawal
- red wine and alcohol
- dairy products
33
what are some potential medications that a may trigger headaches
- cimetidine
- birth control
- nifedipine
- withdrawal of analgesics, decongestants, BDZ
34
what are some potential environmental triggers of headaches
- strong smells/perfumes
- loud noises
- tobacco smoke
- weather
- bright/flickering lights
35
what are some potential behavioural triggers of headaches
- fatigue
- stress/anxiety
- menses/menopause
- prolonged exercise
36
what pharmacological treatment is preferred as acute treatment for tension type headaches
simple analgesics (acetaminophen or NSAIDs)
*no more than 2 days/week to avoid MOH
37
true or false: codeine is recommended for acute treatment of tension headaches
false - not recommended due to increased potential for MOH, more s/e and limited evidence for effectiveness
38
this agent may be found in combination with other analgesics to help with tension type headaches; it is a vasoconstrictor therefore it helps constrict the dilated blood vessels that are causing the headache pain
caffeine
e.g.: Tylenol Ultra Relief (acetaminophen 500mg + caffeine 65mg)
39
these are older agents that were used for tension headaches but are not used much anymore as they are known to increase propensity for MOH and they also have the potential for the development of tolerance, dependancy and toxicity
combo products with opioids and butalbital or both
e.g. Fiorinol (ASA/caffeine/butalbital)
Fiorinol C 1/2 and C 1/4 (ASA/caffeine/butalbital/codeine)
40
true or false: there is no evidence for efficacy of muscle relaxants for the acute treatment of tension type headache
true
41
what options are used in the acute treatment of migraines
triptan and/or NSAID and/or antiemetic
if patient is a reg. migraine sufferer may use only triptan, most likely won't need NSAID
if patient has severe migraines, may use triptan AND NSAID for acute tx
42
true or false: opioids and barbiturates are used for acute treatment of migraines
false - AVOID these due to risks of MOH, s/e and overdose
43
when should acute medications be taken with regards to the onset of a headache
within 30 mins of mild pain
44
what is an adequate triptan trial
try a selected triptan for 3 attacks (with repeated dosing PRN and/or increased dose)
if failure, try at least 2 other triptans
*triptans have different PK properties therefore if one does not work, another may
45
how do triptans work
bind to 5HT 1B and 1D receptors to inhibit the release of vasoactive neuropeptides and cause vasoconstriction of the pain-sensitive blood vessels
46
if a patient has reoccurring headaches, what type of triptan would be most beneficial
longer acting
e.g. Frovatriptan (onset ~2hrs/half-life ~25 hrs) or Naratriptan (onset ~1-3 hrs/half-life ~ 6 hours)
47
if a patient has rapid escalating headaches, what type of triptan would be most beneficial
short onset
e.g. almotriptan, rizatriptan, eletriptan (onset: 30-60 mins/half-life: 2-4 hrs)
48
which triptan comes in an ODT
rizatriptan
49
which two triptans come in a nasal spray
Zolmitriptan and Sumatriptan
50
which triptan comes in a SC injection
sumatriptan
51
these triptan dosage forms may be suitable for someone who has rapidly escalating headaches, but they have an increased cost
nasal spray and SC
52
which triptans have a decreased incidence of nausea
Frovatriptan and Naratriptan because they have slower onset
53
what dosage forms of triptans would be suitable if nausea and vomiting is present with headaches
choose nasal spray or waterless formulation (wafers, rapid melts)
54
what are some side effects of triptans
- chest discomfort or tightness (triptan sensations)
- dizziness/drowsiness
- fatigue
- nausea
- facial flushing
- paresthesia (tingling of arms/legs)
- serotonin syndrome
55
who is at risk of coronary venospasm potential
females with aura are at increased risk
56
true or false; caution should be taken in patients with CV or cerebrovascualr disease or uncontrolled hypertension when starting a triptan
true
57
what should triptans not be used within 24 hours of due to additive vasoconstriction/coronary venospasm?
Dihydroergotamine or other triptans
58
true or false: triptans can be used in someone who takes an MAOI
false - high risk of serotonin syndrome
MAOI must be discontoinued for two weeks before a triptan is started
59
true or false: triptans can be used in someone who takes an SSRI
true - counsel on signs of serotonin syndrome (agitation, excitement, tremor, weakness, fever, chills, diarrhea) but risk is low
60
what should be done at baseline before an individual is started on a triptan for females > 40 and males >50
Cardiac evaluation for females > 40 and males > 50
61
these medications may be used for mild migraines
simple analgesics (NSAIDs, acetaminophen)
62
which NSAIDs show the most evidence for benefit in migraines
ASA (not used much), ibuprofen and naproxen
63
what are some important points to keep in mind when choosing an NSAID for someone with mild migraines
- avoid EC or slow release b/c want fast absorption/action for migraines
- take on empty stomach as food will slow absorption
64
if someone is taking NSAIDs chronically, what would be important to assess
renal function and CV risk
65
this type of medication is last line due to decreased efficacy and increased nausea
ergots (5-HT partial agonist and vasoconstrictor)
66
what is a counseling point for someone starting on an ergot
high incidence of nausea therefore recommended to take with an anti-emetic (e.g. domperidone or metoclopramide)
*note: has same side effect profile as triptans*
67
this class of medication are used for acute migraine treatments and work by inhibiting the action of CGRP which reduces both pain transmission and reducing intracranial vasodilation. they have a fast onset, convenient dosing and mild to moderate side effects
CGRP (calcitonin gene-related peptide) inhibitors
68
true or false: CGRP inhbitors can be used in a patient that has CV risk factors
true
69
this medication is a nasal spray; it is a mixed opioid agonsit/antagonist and is typically only used if other meds have failed. it has dependancy potential or can cause withdrawal symptoms in those on long term opioids.
Butorphanol
70
these medications are what are used in practice to treat associated n/v for someone who has a diagnosis of migraines
dopamine antagonists (metoclopramide or domperidone)
71
this medication may be used to treat n/v in someone who does not have a confirmed diagnosis of migraines
dimenhydrinate
72
what is the first line acute therapy for headache in pregnancy
acetaminophen
*note: ideally optimize prophylactic tx so they don't have to use acute agents during pregnancy
73
true or false: NSAIDs and triptans should be avoided in pregnancy
true
- Sumatriptan may be considered if absolutely necessary (risk vs. benefits)
74
when should prophylactic tx be considered for a patient
- if their attacks significantly interfere with patients daily routine desire acute tx
- frequent attacks (at least 4/month)
- contraindications to, failure of or over-use of acute tx's
- adverse rxn to acute tx
75
what is a reasonable expectation to counsel patients on regarding successful prophylaxis
successful prophylaxis is a decrease in severity or frequency by 50%
76
when starting someone on prophylactic tx, how often should the dose be increased when getting to target dose
increase the dose q 1-2 weeks until target dose is reached
77
what is an adequate trial of prophylactic therapy (when can we determine whether or not this agent is working for this pt)
8-12 weeks
- may not see any benefit until 4-8 weeks
78
true or false: prophylactic tx is always dosed once daily
false
- can be administered episodically prior to known triggers (e.g. menstruation, exercise)
79
what should be done if a single prophylactic agent is ineffective
switch to another agent
80
what should be done if a single prophylactic agent is partially effective
try a combination of agents (add another agent to current therapy)
81
true or false: prophylactic therapy can help with MOH
false - if patient has MOH and it is not addressed, prophylactic tx won't work until MOH is addressed
82
what is the first line choice for prophylactic therapy
beta blockers (e.g. metoprolol and propanolol)
83
what are some s/e of beta-blockers
fatigue, decreased HR and BP, mask hypoglycaemia in T2DM & vivid dreams (propranolol)
84
if a patient uses rizatriptan for acute therapy when needed and is now getting prescribed propranolol for prophylaxis, what needs to be considered in this case?
propanolol inhibits the metabolism of rizatriptan therefore rizatriptan may need to be dose decreased or switched
85
besides beta-blockers, which other agents have the most evidence for use in prophylactic tx and may be more beneficial if someone has comrobid depression
TCA's
- amitriptyline HS is first line
(also may use nortriptyline/Aventyl)
86
what are some s/e of TCA
anticholinergic (4 cants) and increased weight
87
this is a possible 1st line prophylactic option. it is a teratogen and is contraindicated in pregnancy therefore it would not be a good option for women of childbearing age; may be used if patient failed a beta blocker and TCA or had comorbid seizure d/o?
topiramate
88
true or false: candesartan is a possible 1st line prophylactic option
true
89
these two herbals are second line agents for prophylactic therapy. they are usually well tolerated but may cause some nausea and diarrhea
Magnesium (oxide & citrate) and Riboflavin (vitamin B2)
90
this class of medications is second line for prophylactic therapy. they are humanized monoclonal antibodies. they are available as SC and given monthly and are very costly
CGRP antagonists
- Fermanezumab (Ajovy)
91
this class of medications is a second line for prophylactic therapy. there is limited evidence than TCA's but may be tolerated better
SNRIs
- venlafaxine and duloxetine
e.g. if was on a TCA and it was working but they were having anticholinergic s/e, may switch to an SNRI as they are known as "clean TCA's"
92
this medication is a second line prophylactic therapy (Kieley said its more like third line due to s/e and DI's). side effects include decreased BP, HR, constipation
CCBs (verapamil and flunarizine)
93
this medication is a second line agent for prophylactic therapy. it is just as effective as topirmate but it is more costly and not as well tolerated. side effects include: sedation, nausea, hair loss, weight gain & rash. It is contraindicated in pregnancy
divalproex
94
what are some third line agents for prophylactic therapy
- gabapentin
- other herbals: coenzyme Q10, feverfew, butterbur
- botox
95
if someone needs prophylactic therapy and is also a smoker, what may be a good option to recommend for this patient
nortriptyline
96
if someone needs prophylactic therapy and also has insomnia, what may be a good option to recommend for this patient
amitriptyline
97
if someone needs prophylactic therapy and also has hypertension, what may be a good option to recommend for this patient
beta blocker or cadesartan first line.
verapamil may be second line and lisinopril third
98
if someone needs prophylactic therapy and also has chronic pain, what may be a good option to recommend for this patient
amitriptyline or topiramate first line. venlafaxine or duloxetine may be used second line and gabapentin may be used as third line
99
if someone needs prophylactic therapy and also has depression, what may be a good option to recommend for this patient
amitriptyline, venlafaxine or duloxetine may be beneficial
100
what are some questions that you can use to approach someone who seems like they may be experiencing MOH?
"it seems as though you're not getting adequate pain relief.."
"do you know that some of these medications can actually make your headache worse overtime?"
*avoid the word abuse and "you shouldn't be taking so many pain medications"
101
what are the 3 options for managing MOH
1. stop the overused medication abruptly
2. stop or taper the overused medications while starting prophylactic medication
3. start prophylactic medications only (as headaches decrease, overused meds can be decreased)
102
what are some signs of withdrawal sx's if someone is stopped on their medication that they are overusing
headaches will increase in severity and frequency before they improve
anxiety, n/v and problems with sleep can occur
103
when are withdrawal sx's typically seen
symptoms usually last 2-10 days, but can be up to 2-4 weeks
104
true or false: simple analgesics, triptans and ergotamine can be stopped abruptly
true
105
true or false: options and butalbital can be sopped abruptly
true - if only periodic use; if chronic use and high dose, MUST taper (over 2-4 weeks)
106
if a patient is stopping their triptan due to MOH and is being put on metoprolol for prophylaxis, and they are experiencing unmanageable withdrawal symptoms, can their be any other medications added to temporarily help here?
NSAIDs, prednisone, metoclopramide
AVOID: opioids & barbituates
