Head Aches Patho Flashcards
4 Types of Primary Head Aches
- Tension
- Migraine
- Cluster
- Medication overuse head ache
Treatment Primary Head Aches
- Abortive therapy
- non-specific
- specific - Preventative therapy
- Non pharmacological therapy
Tension Type Head Aches
Incidence, prevalence
Most common type of head ache
10-19 years
men = women
Tension Type Head Aches
Clinical S&S
Onset: gradual
Severity: mild to moderate
Quality: Tight band, bilateral, pressure, steady
Location: variable, usually temporal
Duration: hours to days
*Not aggravated by physical activity
Two types of tension type head aches
- Episodic
< 15 days per month - Chronic
>/= 15 days per month for 3 months
Abortive Treatment
Tension Type Head Aches
- Non-Specific
- Tylenol
- NSAIDS
- Ice
Pathophysiology
Tension Type Head Aches
NOCICEPTORS and MUSCLES
- Hypersensitivity trigeminal nerve nociceptors
- chronic - Hypersensitivity myofacial sensory nerves
- episodic
- peri-cranial muscles
*NOT due to vasoconstriction
*TRIPTANS do not work
MOA
Abortive Treatment
Tension Type Head Ache
NSAIDS
Acetaminophen
Ice
- NSAIDs
- block COX (periphery, central)
- prevent formation prostaglandins
- prostaglandins = fever (central)
- prostaglandins = chemotaxis WBC
- prostaglandins = vasodilation, vascular permeability -> edema, erythema, activation nociceptors
- Acetaminophen
- block COX (central)
- prevention fever and central pain - ICE
- Blocks pain signal? (see non pharm section)
Preventative Treatments
Tension Type Head Aches
Examples
- Tri-cyclic anti-depressants
- Serotonin norepinephrine reuptake inhibitors
- Tetracycline anti-depressants
- Botox
Examples
Preventative Treatments
Tension Type Head Aches
Tricyclic anti-depressants
- Nortriptyline
- Amitriptyline
Serotonin norepineprhine reuptake inhibitors
- venlafaxine
Tetracycline anti-depressants
- mirtazapine
MOA
Preventative Treatments
Tension Type Head Aches
TCA
- Tri cyclic anti-depressants
- inhibit reuptake of NE and 5HT
SNRI
- serotonin norepinephrine reuptake inhibitors
- Inhibit reuptake of NE and 5HT
Tetracycline anti-depressants
- Increase release of serotonin and NE by inhibiting pre-synaptic receptor
Contraindications
Drug-Drug Interactions
TCA, SNRI, Tetracycline anti depressants
*All drugs increase serotonin and NE
Serotonin syndrome and hypertensive crisis
- do not combine with
- MAOinhibitors
- Triptants
- SSRIs
- Together
Sedation
- Do not combine with CNS sedating drugs (alcohol, benzodiazepines, phenobarb, etc.)
SE
TCA
Tricyclic Antidepressants
- amytriptyline
- nortriptyline
MOA
- increase HT and NE by blocking reuptake
- *light effect on DA
SE
- ANTI CHOLINERGIC: dry mouth, urinary retention, constipation, gluacoma, sedation
- CARDIOTOXIC - dysrhythmias, conduction blocks
- SUICIDE
Prescribing considerations before starting TCA
ECG
- evaluation for bradycardia, branch blocks, dysrhythmias
TCAs can cause these
they are cardiotoxic
SE
SNRIs
- better tolerated than TCA
- *no anti-cholinergic
- *not cardiotoxic
Examples
- venlafaxine
MOA
- block NE and serotonin reuptake
SE
- insomnia, sweating, head ache, nausea, anorexia
- weight loss, hyponatremia
SUICIDE
SE
Tetracycline anti-depressants
Examples
- mirtazapine
MOA
- increases release of NE and serotonin
SE
- Hypercholesterolemia
- weight gain
- agranulocytosis
- CNS sedation
Why are preventative therapies not prescribed for children < 18 years
Increase risk of suicide
Botox
MOA, therapeutic effect, SE
Neuromuscarinic blockage
reduce HA by 2 / month
SE
paralysis
dysphagia
Normal physiological effect of NE and serotonin
Neuromodulators
Decrease pain transmission in the spinal cord
Therapies
- increase NE and serotonin = decrease pain transmission = decrease pain signals to the brain
ex.
TCAs
SNRIs
mirtazapine
Migraine HA
Incidence, prevalence
more common females
18-44 years of age
family history
MIgraine HA
Triggers
- Stress (before/after)
- weather
- periods
- food (tyramines - aged wine, cheese, smoked fish; nitrates - bacon; caffiene; chocolate)
- sleep (too much, too little)
- sensory overload (lights, smells)
Diagnostic criteria
Migraine HA
5 episodes, 4 hours - 72 hours duration, with at least 2:
- unilateral pain
- thobbing/pulsing
- moderate to severe
- avoidance / aggrevated by activity
at least 1 of the following:
- nausea/vomiting
- photophobia or phonophobia
REMEMBER
Tension head aches
- bilateral
- steady pain
- not aggrevated by activity
- mild to moderate
- gradual onset
4 Phases of Migraine HA
- Premonitory phase
- hours to days before
- tired, irritable, concentration, hunger
- PATHO: increased blood flow hypothalamus
- Aura phase (1/3 people)
- 1 hour before
- cortical spreading depression (CSD)
- depolarization from occiput across cortex
- depresses the threshold for firing (hyperactivity)
- Head ache phase (2/3)
- 4 hours to 72 hours
- Activation trigeminovascular system
- Trigeminal nerve hyperactivity -> projections dural intracranial blood vessels –>
inflammation
vasodilation
pain
- Recovery
- hours to days
- irritability, fatigue, depression
Neuromodulators
Protective vs. Not during HA phase
Serotonin
- neuromodulator
- protective
- vasoconstriction of the (trigeminovascular system)
*protective before, during, afterwards
Example medications
- SNRI
- TCA
- mirtazipine (tricyclic antidepressant)
- triptans
Calcitonin gene related protein (CGRP)
- released by trigeminovascular system
- increase inflammation and vasodilation
- worsen head aches
- calcium increases calcitonin release from thyroid (this is why dairy increases migraine head aches)
*increases during migraine
*caused by infusing it
tension type head ache vs. migraine head ache
tension type head ache
- hypersensitivity nociceptors trigeminal nerve
- hypersensitivity myofacial afferent nerves
migraine type head ache
- trigeminovascular system
- inflammation, vasodilation, irritation of meningeal vessels
Migraine HA
Trigeminovascular activation
- inflammation
- vasodilation
- hypersensitivity nociceptors
- pain
Abortive treatment
migraine head aches
- NSAIDS, tylenol (moderate)
Severe
1. triptans
2. ergot alkaloids
3. Calcitonin gene related protein blockers
4. opioids (last resort)
Preventative treatment
mIgraine head aches
- triptans
- beta blockers
- TCAs, SNRIs
- AEDs (gabapentin, topiramate, divalproex)
- estrogens
- injections
Example Triptans
Almotriptan
sumatriptan
Almotriptan
*approved for children in canada > 12 years
Serotonin syndrome
S&S
Neuro: aggitation, delirium, hallucinations
Heart: tachycardia, dysrhythmias
MSK: myocolonus, ataxia, tremors, hyperreflexia
GI: N/V/D
DEATH
Do not combine
- triptans
- ergot alkaloids
- SNRI
- SSRIs
- MAOinhibitors
Ergot Alkaloids
Indication and examples
Abortive therapy
Second line
if triptans do not work
Examples
- Ergotamine
- Dihydroergotamine (canada)
MOA
ergot alkaloids
Unknown
increase transmission at serotonin, dompamin and alpha adrenergic nerons
decrease release of pro-inflammatory NT (CRGP) from trigeminovascular ssystem
decrease vasomotor centres
ERgot alkaloids
SE
VASOCONSTRICTION
GI: n/v
Cardio: HTN, vasoconstriction, angina, dysrhythmias
PVS: vasoconstriction, ischemia, gangrene
Teratogenic
Ergot alkaloids
Contraindications
pregnancy - causes uterine contractions and labour
hepatic or kidney disease
CYP3A4 inhibitors
HTN, dysrhythmias
CAD, PVD
sepsis
*ischemia and gangrene
Drugs
- triptans
- washout of 24 hours needed
Pharmacokinetics
ergot alkaloids
IN, IM, Subcutaneous
Not PO - 100% first pass effect
Black box warning
Ergot alkaloids
ischemia and gangrene
increase risk
- increase use, longer duration
- CYP3A4inhibitors
- hepatic or renal disease
- CAD or peripheral vascular disease
- HTN
- sepsis
Calcitonin gene related peptide (CGRP) receptor antagonists
Examples
Ubrogepant
Atogepant
CGRP receptor antagonists
MOA
bind to receptor
block effect of CGRP (pro-inflammatory, released from trigeminovascular system)
CGRP receptor antagonists
SE
nausea, vomiting
teratogenic
Preventative Therapy
Migraine HA
Qualifications
Any age
> 3 HA in a month
Severe in quality
do not respond to abortive therapy
Preventative therapy
Migraine HA
Examples
- beta blockers
- propranolol
- SE: heart block, bradycardia, hypotension, HF, hypoglycemia, rebound tachycardia, bronchoconstriction
- ECG before start - AEDs
- divalproex (VPA)
- SE: teratogenic, hepatitis, pancreatitis, GI upset, ammonia
- topiramate
- SE: metabolic acidosis
- gabapentin
- TCA
- amitriptyline
- SE: anti-cholinergic, anti-histamine, suicide, cardiotoxicity (dysrhtyhmias, HTN), serotonin syndrome, hypertensive crisis
- ECG before you start - estrogens / Triptans - menstruation induced
- injections
- botox
- lidocaine/bupivicane nerve block - CGRP monoclonal antibodies
SE: immunogenicity, hypersensitivity, skin/GI, hepatotoxicity
Pathophysiology
Cluster head aches
- trigeminovascular system
- inflammation
- vasodilation - autonomic division trigeminal nerve
- occiput, cheek, temple
- dysfunciton ANS: rhinorrhea, lacrimnation, Horner’s sydnrom (Ptosis, anhydrosis, mydriasis) - hypothalamus
- pattern of attacks
Cluster head aches
Are also known as
Trigeminal Autonomic cephalalgias
Cluster head ache
incidence, prevalence, triggers
men > women
onset 20-50 years of age
triggers: alcohol, smoking, caffiene
no family history
Cluster head aches
clinical signs and symptoms
sudden onset
unilatera
severe stabbing pain (more debilitating than migraine)
clusters in time 8x per day, for hours to days, remission for years
associated: horner’s syndrome, ipsilateral lacrimation rhonorrhea
Treatment
Cluster head aches
abortion
First line: Triptan + oxygen + glucocorticoid
- First line: tripans
- Somatotriptan
- SE: vasoconstriction, angina, vasospastic angina, crushing chest pain (bronchoconstriction, pulmonary constriction, esophageal spasms, intercostal muscles, HTN, teratogenic - Second line: ergot alkaloids
- dihydroergotamine
- SE: black box warning vasoconstriction and gangrene, HTN, angina, muscular weakness/numbness/tingling, N/V - glucocorticoid
- methylprednisone, dexmethasone
- SE: GI ulcers, infection, hypernatremia, FVO, hypokalemia, osteoporosis, adrenal supression, hyperglycemia, striations, etc.
Preventative treatment
Cluster HA
- non-dihydropyridine calcium channel blockers
- Heart: decrease HR, conduciton, contraction
- VSM: prevent calcium influx and contraction, vasodilation
- SE: heart block, bradycardia, hypotension, flushing, HA, fainting, edema, eczema, constipation (ECG before administer)
- Lithium
- Suboccipital glucocorticoid injections
- decrease severity frequency
- repeat every 3 months
Lithium
MOA, therapeutic index, SE, contraindications
MOA: unknown
Therapeutic index: narrow 0.6-0.8 (toxicity 1.5)
SE:
toxicity
N/V/D, polyuria (blocks ADH), tremors, stupor, coma,
teratogenic
Contraindications:
diuretics
verapamil
MOA, SE, contraindications, monitoring
MOA: unclear for migraines
SE: heart block , bradycardia, heart failure, flushing, head ache, dizziness, eczema, constipatoin
monitoring; ECG before start, every 6 months of therapy
Medication over use head aches
Example medications
NSAIDS
Tylenol
Opioids
Triptans (mild, for days)
Ergot alkaloids (severe, for weeks)
Medicaiton over use head aches
when are you at risk?
> 2 x per week using abortive medications
- start preventative treatment to decrease amount of times having to use abortive medications
- higher dosages
Medication over use head aches are also known as
rebound head aches
drug induced head aches
MOA
medication induced head aches
unknown
Treatment
medication over use headaches
D/C medications
inform client HA will get worse
ergot alkaloids (severe, for weeks)
triptans (mild and for days)
lower dosage
start preventative therapy
addition non pharmacological therapy
Non pharmacological therapy for HA prevention
stress
eating regular intervals
exercise
water
CBT, accupuncture, biofeedback
HA diary to identify triggers, avoid triggers
sleep
