Headaches Flashcards
*Red Flag*
DDX…HA +
split second onset, unexpected, WOSRT HA EVER/never previously encountered, LOC, vertigo, vomiting
Consider DDX:
Aneurysmal Subarachnoid Hemorrhage
Cerebellar Hematoma
*Red Flag*
DDx to consider: HA +
Fever and skin rash
DDx:
Meningitis
*Red Flag*
DDx to consider: HA in immunosuppressed state
Crypto meningitis
Toxoplasmosis
*Red Flag*
DDx to consider: HA with coagulopathy/anticoagulation
Subdural hematoma
intradural hematoma
What type of drugs should never be used to treat a headache?
(1 example)
Opiods and narcotics
DO NOT USE: butalbital-acetaminophen combination therapy
[True/False]
Severity of the HA is key to clinically diagnose a migraine hHA
FALSE
Severisty is NOT A FEATURE of migraines
What are the three key clinical questions that would highly point to Migraines?
- Do you have NAUSEA or feel SICK to your STOMACH with your HA?
- Does LIGHT BOTHER you more than with a HA than withouth a HA?
- Does the HA LIMIT YOU from working, studying or doing what you need to do?
*IF yes to all three: sensivity 0.81, specificity 0/75
Typical clinical symtopms of a migraine (6):
Risk Factors (3):
a migraine POUNDS:
P: pulsatile
O: one-day duration
U: unilateral
N: nausea
D: disabling
S: stereotypical
INC Risk Factors: females, young, + family history
What are some typical triggers of migraines (8):
Stress
Lack of sleep
Hunger
Hormonal fluctuations
Foods (+/-)
Alcohol/nitrates
Weather changes
Smokes, scents, fumes
Name the 4 phases of a migraine:
PAPP
- PROdrome*
- AURA*
- Pain*
- POSTdrome*
- (PAPPs give me migraines)*
Phase 1 of Migraines:
When could the pt experience it?
What are signs the pt could experience?
Phase 1: Prodrome
Occurs: 6 hours to 48 hours before the HA (60% of patients)
SX: depression, irritability, drowsiness, fatigue, yawning, rhinorrhea/lacrimation, hunger/third (cause or reaction?)
Phase 2:
When can it occur?
How long can it last?
What are the different types?
Phase 2: Aura, due to spreading cortical depression
BEFORE > during >> after the HA
develops over 5-20 minutes and lasts usually <60 minutes
you can expect the HA within 60 minutes
Types: VISUAL (most common), sensory, motor, brainstem (dizziness/diplopia) or cortical (aphasia)
What is an acephalgic migraine?
An aura not associated with headache symptoms
A person experiencing a visual aura…
near the center of vision, the patient has a ____ _____ that prohibits reading
in the periphery, the person experiences ____ and pulsating ____ of light across the visual field
near the center of vision, the patient has a BLIND SPOT that prohibits reading
in the periphery, the person experiences FLASHING and pulsating BANDS of light across the visual field
Phase 3:
Three main locations where it can occur:
Onset timing:
Duration:
Associations (5 main categories)
Phase 3: Pain
Locations: Head (most common), abdomen (abdominal migraine) or chest (precordial migraine)
Onset: gradual, minutes –> hours
Duration: hours to days
Associations: Phobia to light, sound, odor, temp, N/V
Photophobia, phonophobia
Nausea/vomiting
Osmophobia, Termophobia
Spreading Cortical Depression:
A genetically susceptible patient has a multifactoria defect in brain metabolism leading to a ______ in _______ receptor function.
This receptor is ________ (inhibitor/excitatory)
Activation of the receptor leads to a burst of focal _____ activity causing local _______ (INC/DEC of blood) and ______ (+/-) symptoms
It is usually in the ______ lobe of the brain
Burst is then followed by a ______ (gain/loss) of neuronal activity = ___ ___
Moves at _____ mm/min and advances until there is a ______ in ____ _____.
Spreading Cortical Depression:
A genetically susceptible patient has a multifactorial defect in brain metabolism leading to GAIN in NMDA receptor function.
This receptor is EXCITATORY (inhibitor/excitatory)
Activation of the receptor leads to a burst of focal cerebral activity causing local HYPEREMIA (INC/DEC of blood) and POSITIVE (+/-) symptoms (probably why you see lights, etc) = WAVE FRONT
It is usually in the OCCIPITAL lobe of the brain
Burst is then followed by a LOSS (gain/loss) of neuronal activity = CEREBRAL DEPRESSION
Moves at 3 mm/min and advances until there is a CHANGE in CORTICAL ARCHITECTURE
*What are ways to optimize the treatment of acute attacks of migraines (5):
treat EARLY in the attack when the pain is still mild
NSAIDS are first line, followed by triptans
Use effective DOSES
AVOID butalbital-containing medications
RX associated symptoms
*What is the first line medication effective for migraine HA?
OTC NSAIDS
*What if the patient does not respond to analgesics, pain is too much, what are second line medications?
TRIPTAN
agonist of 5HT (1b/d) R
may lead to vasoconstriction
(7 different types with a range of half lives 3-26 hours, and routes of delivery; inadequacy to one doesn’t mean ineffective response to all)
Who would NOT be a good candidate for triptan therapy (7)?
*AVOID in thsoe with vascular risk factors*
NO: has/at risk for ischemic heart disease
NO: uncontrolled HTN, renal disease
NO: pregnancy
NO: basilar migraine, hemiplegic migraine
AVOID within 24 hours with ergotamine
NO: if pt is on MAO inhibitor
What are the TRIPTAN SENSATIONS (aka - side effects) (6)?
pressure, pain, tightness, warmth, heaviness and tingling
notify the patient of the potential side effects they could experience; should be okay since they should be screened for vascular disease prior to be prescribed this medication
(ppttw)
*What are two other alternative migraine therapies that could be used after Triptan?
Ergot Alkaloids: Ergotamine and DHE
more powerful, yet more side effects
Ergotamine: Seratonin syndrome; “triptan on steroids” lots more contraindications and precautin with its use especially on people potentially with ischemic disease.
*When should preventative therapy be considered (4)?
- Incidence of attacks > 2-3 times per month
- Attacks are severe and impair normal activity
- Patient is psychologically unable to cope with the attacks
- Optimal abortive therapies have failed or produced serious side effects
What are alternative therapies/aside from medication, that could be considered (5):
- Avoid triggers
- relaxation, biofeedback, acupuncture
- physical therapy
- dietary/vitamin supplementation
- Botulinum Toxin (only for chronic migraines after many failed attempts)
*Cluster Headaches:
Criteria (3)
Risk Factors
Associated Syndromes (2)
Treatment (6)
“one of the most severe headaches”
Criteria: 1-4 attacks/day, >30 minutes
rapid onset (15-30 minutes)
clusters lasting 6-12 weeks
INC Risk Factors: M>F, 40s, smokers, drinkers, spring/autumn, nights, unilateral during attack
Associated Syndromes: Horner’s, unilateral rhinorrhea
RX: Inhaled O2 (100% by rebreather at 10-15 L/min)
Injectable sumatriptan
Nasal spray triptans
intranasal lidocaine
intranasal DHE
- Prednisone (not first line)*
- [oral medication NOT useful]*
*Tension-type Headache:
Clinical Features (6)
Treatment
Clinical Features:
Bilateral, >30 minutes, lasting usually 4-6 hours
Band-like head pain with pressing or tightening quality
Mild - moderate intensity
NOT aggravated by routine activity
NO N/V
Phonophobia OR photophobia (either NOT BOTH)
Treatment:
Screen for depression and sleep disorders
TCA may be helpful (amitriptyline)
Physiotherapy, biofeedback
Trigeminal Neuralgia
Clinical Featuers:
(most affected area is the _____; with ___ and ___ divisions the TN)
Treatment:
Paraoxysmal attacks of pain lasting from a fraction of a second to two minutes, affecting one or more divisions of the trigeminal nerve (V1/V2 usually; affecting the _jaw_ mostly)
Clinical features:
Peak incidence 60-70, worse with talking or eating, often after dentist visit
MS is the most common associated disease
Treatment: Carbamazepine (first line)
[Others: oxcarbazepine, baclofen, Iamotrigine]
*Pseudotumor Cerebri:
Clinical Features
Treatment
*MEDICAL EMERGENCY*
Clinical Features:
ICP >250 mm H20 (spinal tap)
HA is the presenting feature in >75% of pt
No localizing features, no mass lesion or enhancement, normal CSF content, no CVT
Fundascope: papilledema (signifying increased pressure)
Treatment: spinal tap to reduce pressure +
actezolamine, topiramate, surgical intervention
Primary Exertional Heachache:
Clinical Features
Treatment
Clinical Features:
Pulsating HA from 5 minutes to 48 hours
occuring only during or after physical activity
Younger patients, M>F
Treatment:
Beta-blockers, Indomethacin
(prophylaxis before exertion, screen for aneurysms, treat for 3-6 months)