1
Q
percentages of adults with HA disorder
A
- 46% in general
- 11% Migraine
- 42% Tension
- 3% chronic daily HA
- To 10 most disabling conditions for both genders worldwide (2007)
- 16% of adults report migraine or other severe HA in last 3 months
- 5th leading cause of ED visits and 1.2% of all office visits (2013)
- Cluster HA more common in males but tension are more common in women
- 5:9 M:F
- 90% primary
- Australian study showed 15% of population used headache meds
2
Q
primary headache types
A
- tension
- migraine
- cluster
3
Q
tension headache
A
- Most common primary HA
- Constant, daily HA
- Worst late in day – usually pts don’t wake up with the headache, they get it throughout the day and get worse
- Bilateral – usually back of the head, back of the neck
- Vise-like, “band”
- Emanates from neck and shoulders
- “Featureless” HA – they don’t have very specific qualities to them
- Constant, daily HA
4
Q
primary headache
A
- HA and associated features are the disorder
- Tension 69%
- Migraine 16%
- Cluster 0.1%
5
Q
secondary headache
A
- HA caused by other disorder
- Infection 63% - sinus infection (hurts on front of face, purulent discharge, leaning forward hurts) (Meningitis – you feel like crap, nuchal rigidity, Dental abscess)
- Trauma 4%
- Vascular Disorder 1%
- SAH <1%
- Tumor 0.1%
6
Q
mechanism of tension HA
A
- No significant increase in muscle tone in HA sufferers – probably more about inflammatory pathways getting triggered – neuronal inflammation
- Research now focused on changes in brain chemistry that activate pain pathways and inhibit suppression of pain
7
Q
S.C.A.L.P
A
- Skin
- Connective Tissue
- Aponeurosis
- Loose connective tissue
- Pericranium
- You can have inflammatory markers that affect any of these layers
8
Q
Tension HA triggers
A
- Stress – common
- Depression/Anxiety – common, particularly in those that have daily headaches (They will often times wake up in the morning with the headache, Will still get worse throughout the day like a tension headache)
- Posture – clenching shoulders, etc. (Focus on fixing ergonomic body posture at work)
- Jaw clenching
- Female
- Middle age
9
Q
acute management of tension HA
A
- Simple analgesia (Add caffeine) - When people get a tension headache, they vasodilate so caffeine will help by vasoconstricting
- Avoid opiates
- Avoid rebound
- Avoid triggers
10
Q
Preventative managment
A
- TCA (amitriptyline) – this has been the most studied and effective for headaches
- EMG biofeedback with relaxation therapy – triggering the muscles at the back of the neck with electrical stimulation (Massage therapy can be helpful for acute headaches, not really chronic, TENS can be used for tension headache as well – it is electrical stimulation of the muscles)
- Acupuncture
11
Q
migraine
A
- “We can describe the thoughts of Hamlet, but we cannot describe a Migraine.”
- 2nd MCC HA
- 17% females and 6% of males in US
- Females are triggered around puberty and males tend to start earlier
- Higher in boys prepubertally, then flips – this is because boys start earlier but there are more women in general that start once puberty hits
- Incidence peaks in teen years
- FH in 70% of patients
12
Q
migraine pathophysiology
A
- Wolff et al (1940s) theorized vasoconstriction responsible for aura, followed by dilation (pain)
- Probably neurovascular (Neuronal hyperexcitability demonstrated in migraneurs without HA, Aura explained by theory of cortical spreading depression of Leao (1944) – wave of excitation followed by depression)
- Related to vasodilation (CN V) – stimulated by ions from cortical activity (Cortical spreading depression is a widespread wave that triggers inflammatory mediators to be released and vasodilation in trigeminal system - Depolarizes cortex that cause vasodilation and inflammation)
- Parasympathetic nerve fibers
- MRI studies show modified activity in brainstem regions relating to sensory processing – even after pain aborted with meds (Weiler)
- Regional cerebral blood flow diminished followed by hyperemia
13
Q
migraine triggers
A
- FH in 70%
- Stress 80%
- Lack/excess of sleep >50%
- Missed meals 57%
- Foods (chocolate, EtOH) 27-38%
- Light/noise 38%
- Odors 44%
- Menstruation (catamennial) 65%
- Weather changes 53%
14
Q
migraine clinical findings
A
- Unilateral
- Throbbing
- Episodic with early onset – usually start in childhood (New diagnoses later in life is not as common)
- Anorexia
- N/V
- Photophobia/phonophobia/osmophobia
- Cognitive impairment – problem with word finding or confusion
- Blurred vision
- Build gradually, last hours to days
- Focal neurological deficits, or sensations may precede onset – i.e. tingling in the 3rd and 4th finger or blurring of one eye
- NOT EVERYONE GETS AURA!!
15
Q
chronic migraine
A
- Frequent or long lasting migraines
- Migraines causing significant disability or decreased QOL
- Consider prophylactic therapy: Improve QOL, decrease disability, Decrease risk of neurologic damage in uncommon migraine types, Patients who have failed, have contraindications to, or serious adverse effects with acute therapies, Menstrual migraine
16
Q
acute management of migraine
A
- NSAID
- Triptan – injection can cause nausea
- Sumatriptan + naproxen – has been shown to be very effective
- Antiemetic – if you have a pt with a migraine, there have been studies that show that giving just an antiemetic will help with the migraine, but that’s not what is recommended
17
Q
preventative management of migraine
A
- Lifestyle modifications
- Beta blockers (Metoprolol, timolol, propranolol - There isn’t a certain med that works better than the other, but it’s the class that works)
- Antidepressants (Amitriptyline*, venlafaxine - Amitriptyline is very effective at low doses)
- Anticonvulsants (Topiramate*, valproate - Topiramate at very low dose is extremely effective) - She has seen this be the most effective of all the other meds – also comes with appetite suppression and weight loss
- CCB (less effective) (Verapamil)
- Ones with stars are recommended by UpToDate
18
Q
treatment for adults with mild to moderate migraine attacks not associated with vomiting or severe nausea
A
-we suggest initial treatment with simple analgesics, including NSAIDs or acetaminophen, rather than other migraine-specific agents
19
Q
treatment for adult outpatients with moderate to severe migraine attacks
A
-we suggest treatment with a triptan or the combination of sumatriptan-naproxen, rather than other migraine-specific agents
20
Q
efficacy of abortive migraine treatments
A
Abortive treatments for migraine are usually more effective if they are given early in the course of the headache; a large single dose tends to work better than repetitive small doses
21
Q
therapeutic lifestyle modifications for migraines
A
-include sleep hygiene, regular meals, regular exercise, avoidance of triggers, biofeedback, relaxation therapy, acupuncture, transcutaneous electrical nerve stimulation (TENS).
22
Q
cluster HA
A
- Disease of middle-aged men, 2:1 (down from 6:1 in 60’s) (Uptodate has it at 4:1)
- Prevalence up to 1%
- Usually no FH
23
Q
pathophysiology of cluster HA
A
- Unknown
- Theories: Hemodynamic (dilation possible but studies inconsistent), Trigeminal Nerve (substance P fibers carry sympathetic information in CNVI&II, Somatostatin inhibits and reduces intensity/duration of HA), Ipsilateral hypothalamus implicated – circadian connection (HA recur same time every day)
- Triggers trigeminal vascular fibers
24
Q
possible triggers of cluster HA
A
- EtOH
- Stress
- Glare
- Specific foods
- The people that she has seen are men in their 40s that have gone on a bender
25
presentation of cluster HA
- Diagnosis made on 5 episodes from 1 qod to 8/d without other cause
- Severe, deep, unilateral, periorbital pain
- Pain is “explosive” in nature – deep, unilateral, periorbital pain (Feel like eye is going to explode)
- Episodic, episodes last weeks
- Pts appear restless and agitated
- Often awaken pt
- Associated with (ipsilateral parasympathetic activation): Nasal congestion, rhinorrhea, Lacrimation and redness of eye, Horner syndrome (sympathetic deficit associated with parasympathetic activation with injury to ascending fibers surrounding dilated carotid artery)
26
cluster HA treatment
- Acute Management (Oxygen – 1st line therapy, Triptan – work but they take a bit longer)
- Preventive Management (<2 months - Prednisone (high dose taper); >2 months - Verapamil (240-320 mg daily dosed TID up to 960 mg) (CCB) – for several months )
- Acute alternative therapies include intranasal lidocaine, oral ergotamine, IV dihydroergotamine
27
less common causes of HA
- Trauma
- Mass
- Giant Cell (Temporal) Arteritis
- Analgesia rebound
- Subarachnoid hemorrhage (SAH) – thunderclap or “worst HA of my life”
- “sunken brain” – post lumbar puncture HA
- Older person (over 65), youre not thinking migraine
28
Symptoms suggesting serious cause
SNOOP:
- Systemic symptoms, illness or infection
- Neurologic symptoms or abnormal signs
- Onset is new (>50 yo) or sudden
- Other associated conditions or features
- Previous HA history with change or progression of HA features
29
HA red flags
- “worst HA of life” – especially if they get HAs frequently (If they say this is different or way worse)
- First severe HA – especially if they are 30-40-50
- Subacute worsening over days
- Abnormal neurological examination – if theres a focal neurological deficit, this is not just a regular HA
- Systemic signs
- Vomiting preceding HA – this is concerning for increased intracranial pressure – need to ask when the vomiting start
- Pain with pressure change (cough) – can indicate increased intracranial pressure
- Wakes from sleep – can happen with cluster HA, but everything else is ABNORMAL!!! Need to really look deeper into this
- Onset >55 – worrisome for intracranial pathology
- Symptoms suggesting serious cause
Medicine 2
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