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Adult Clinical Medicine > Headache > Flashcards

Headache Flashcards

1
Q

Migraine or headache pain are almost as common as back pain and the burden of headache is highest for females ages ___

A

18 to 44

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2
Q

In new onset and severe headache, the probability of finding a potentially serious cause is Considerably___ than in recurrent headache.

A

greater

*Patients with recent onset of pain require prompt evaluation and appropriate treatment

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3
Q

Serious causes of severe acute onset of HA to be considered include

A
  1. meningitis,
  2. subarachnoid hemorrhage,
  3. epidural hematoma or
  4. subdural hematoma,
    5, glaucoma,
    6, tumor, and
  5. purulent sinusitis
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4
Q

Among secondary causes of headache, ___ is by far the most prevalent, Followed by ___, Both of which are readily ruled out by a Good review of systems and physical exam.

A

Systemic infection

head injury

*Vascular disorders and brain tumor, common concerns for patients, Are relatively Low In prevalence among the causes of secondary headache.

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5
Q

Among primary causes of headaches, ___ is by far the most prevalent

A

tension headache

*Almost 4 times as prevalent as migraine

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6
Q

Migraines still make up __% of primary headaches, __ times more common than the rare cluster headache

A

16

160

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7
Q

Most common types of primary HAs

A
  1. Tension
  2. Migraine
  3. Idiopathic stabbing
  4. Exertional
  5. Cluster
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8
Q

Most common types of Secondary HAs

A
  1. Systemic infection
  2. Head injury
  3. Vascular disorder
  4. Subarachnoid hemorrhage
  5. Brain tumor
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9
Q

Secondary HA red flag symptoms

A
  1. Systemic symptoms (fever, weight loss, vomiting preceding HA)
  2. Secondary risk factors: underlying disease (HIV, cancer)
  3. Neurologic symptoms (confusion, impaired alertness)
  4. Onset: sudden, abrupt or split-second (first severe HA, worst ever)
  5. Older: new onset and progressive HA over days/weeks, esp age > 55 or under age 5
  6. Previous HA history or HA progression: pattern change, first HA, or different (change in quality, frequency or severity)
  7. Pain induced by bending lifting or cough
  8. Wakens from sleep or presents immediately upon awakening
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10
Q

___ is an essential first step in the evaluation of headache.

A

A complete neurologic exam

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11
Q

In one study, __, __ and __ predicted serious intracranial pathology in adults presenting to an ED with nontraumatic HA. The presence of any one of these three features detected serious intracranial pathology with 98.6% sensitivity

A

age older than 50 years, sudden onset, and abnormal neurological exam

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12
Q

In most Cases, patients with __ or ___ should be evaluated by a CT or MRI study.

A

an abnormal neurologic examination or a history of recent new onset headache

  • That concludes neuroImaging is usually not warranted for patients with migraine or a normal neurologic examination.
  • An imaging study is not necessary in the vast majority of patients presenting with headache.
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13
Q

When is a LP indicated?

A
  1. clinical suspicion of subarachnoid hemorrhage in the setting of a negative or normal head CT scan
  2. Clinical suspicion of an infectious or inflammatory etiology of HA
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14
Q

An abnormal neurological exam may suggest:

A

Focal logic signs suggests an

  1. intracranial mass lesion,
  2. Arteriovenous malformation, Or
  3. collagen vascular disease.
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15
Q

Neck Stiffness and especially meningismus (Resistance to passive neck flexion) Is strongly suggestive of __

A

meningitis.

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16
Q

Papilledema suggests the presence of:

A
  1. an intracranial mass lesion,
  2. benign intracranial hypertension (Pseudotumor cerebri),
  3. Encephalitis, Or
  4. meningitis
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17
Q

Temporal artery palpation should be performed to rule out ___

A

temporal arteritis

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18
Q

Once we’ve ruled out serious underlying Pathology and secondary causes of headache, We may determine the type of primary headache using ___ as the primary diagnostic tool.

A

the patient history

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19
Q

Common primary causes of headache can be identified via

A
  1. location,
  2. characteristics,
  3. activity,
  4. duration, and
  5. associated symptoms
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20
Q

The term ___ is commonly used to describe a chronic head pain syndrome characterized by Bilateral tight, band like discomfort.

A

tension type headache

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21
Q

What is the main way to differentiate migraine from tension HA

A

tension type headache is that it is completely without accompanying features such as

  1. nausea,
  2. Vomiting,
  3. Photophobia,
  4. Phonophobia,
  5. Throbbing, or
  6. aggravation with movement
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22
Q

A core feature of cluster headache is ___

A

periodicity

*At least one of the daily attacks of pain recurs at about the same hour each day.

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23
Q

Describe the pattern of onset of cluster HAs

A
  1. The typical cluster headache patient has daily bouts of one or two attacks of relatively short duration and unilateral pain for 8 to 10 weeks a year;
  2. This is usually followed by pain free interval that averages a little less than a year.
    * Patients are generally perfectly well between episodes
  3. Onset is nocturnal in about 50% of patients
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24
Q

Describe whether men or women are more effected by migraines and cluster HA

A

Migraines: F>M

Cluster: M>F, 3x more

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25
Q

Cluster headache is associated with ipsilateral symptoms of:

A
  1. cranial parasympathetic autonomic activation:
  2. Conjunctival injection or
  3. Conjunctival lacrimation,
  4. Rhinorrhea or
  5. nasal congestion, Or
  6. cranial sympathetic dysfunction such as ptosis.
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26
Q

Compare the location of migraine, tension and cluster HAs

A

Migraine: 60-70% unilateral

Tension: bilateral

Cluster: unilateral, usually begins around eye or temple (retro orbital)

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27
Q

Describe the characteristics and associated sx of migraine HAs

A
  1. Gradual onset
  2. Pulsating
  3. Moderate-severe pain
  4. Worse w/ activity
  5. N/V
  6. photo/ phonophobia
  7. aura
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28
Q

Describe the characteristics and associated sx of tenison HAs

A
  1. tight band-like
  2. fluctuating pain/ waxes and wanes
  3. pressure or tightness
  4. No associated N/V, aura, photo/phonophobia
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29
Q

Describe the characteristics and associated sx of Cluster HAs

A
  1. Explosive in quality
  2. Non-fluctuating, continuous
  3. Peaking w/in minutes
  4. Deep, and excruciating pain
  5. Ipsilateral eye drop,
  6. tearing
  7. and redness
  8. Runny nose
  9. Sweating
30
Q

Describe the activity and duration of migraine HAs

A
  1. Prefers to rest in a dark quiet room

2. 4-72 hrs

31
Q

Describe the activity and duration of tension HAs

A
  1. may remain active

2. persists days, but is variable

32
Q

Describe the activity and duration of cluster HAs

A
  1. Remains active

2. lasts 30min- 3 hrs

33
Q 
Describe the pattern of:
Cluster HA:
Tension type:
Migraine:
Sinusitis:
A
  1. Cluster HA: around 1 eye/half of face
  2. Tension type: band-like w/ wt on top of head
  3. Migraine: unilateral band
  4. Sinusitis: around facial sinuses
34
Q

What are some things that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. Diet
  2. Hormones
  3. Sensory stimuli
  4. Stress
  5. Changes in the environment or habits
35
Q

What are dietary factors that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. Alcohol
  2. Chocolate
  3. Aged cheese
  4. Monosodium glutamate
  5. Aspartame
  6. caffeine
  7. nuts
  8. nitrates, nitrites
36
Q

What are hormonal factors that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. menses
  2. ovulation
  3. Hormone replacement (progesterone)
37
Q

What are sensory stimulis that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. Strong light
  2. Flickering lights
  3. Odors
  4. Sounds, noise
38
Q

What are stress factors that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. let down periods
  2. times of intense activity
  3. loss or change (death, separation, divorce, job change)
  4. Moving
  5. Crisis
39
Q

What are changes of environment or habits that can trigger or worsen HAs (migraines or pre-existing tension HAs)

A
  1. Weather
  2. travel (crossing time zones)
  3. altitude
  4. schedule changes
  5. sleeping patterns
  6. dieting
  7. skipping meals
  8. irregular physical activities
40
Q

When patients get frequent HAs, they should keep a HA diary to help ID:

A
  1. triggers: diet, sleep, event prior
  2. warning signs
  3. effective Tx

*can also help you to decide whether acute or prophylactic treatment is needed.

41
Q

Tx of Tension HAs

A
  1. Avoid triggers
  2. OTC simple analgesics (acetaminophen, ASA, NSAIDs)
  3. Behavioral changes like relaxation techniques
42
Q

___ is a commonly encountered type of secondary headache that should be suspected in patients you have frequent or daily headaches despite, or because of, the regular use of headache medications.

A

Medication overuse headache (MOH)

43
Q

How do you dx MOH (medication overuse HA)

A
  1. The diagnosis is based upon clinical impression
  2. The course of the headache disorder and the history of the drug intake and intake frequency are the only available methods for diagnosis
  3. other disorders causing secondary headache must be excluded
44
Q

A history of Analgesic use averaging more than ___ in association with chronic daily headache supports the diagnosis of MOH

A

2 to 3 days per week

*All acute symptomatic medications used to treat headaches have the potential for causing an MOH.

45
Q

All acute symptomatic medications used to treat headaches have the potential for causing an MOH. But the risk appears to be highest with:

A
  1. opioids
  2. Butalbital containing combination analgesics
  3. ASA/acetaminophen/caffeine combos
46
Q

The suggested outpatient approach for withdrawal of overuse medications other than barbiturates, Opioids, Or benzodiazepines is straightforward:

A
  1. Stop all the overused medication abruptly
  2. Use bridge therapy with a long acting NSAID (Naproxen 550mg BID) or prednisone
  3. Start a preventative medication And
  4. revisit possible triggers (preventative medications will be discussed later)

*Withdrawl from barbiturates, opioids or benzodiazepines is more complicated and won’t be covered here. These medications are best avoided for treatment of HA for this exact reason.

47
Q

Tx of cluster HAs

A
  1. 100% O2 at 10-12 L/min for 15-20 minutes (1st line)
  2. Sumatriptan and zolmitriptan nasal sprays
  3. Or sumatriptan subcutaneous are both effective at acute cluster headaches, Offering useful options for patients For home use.
48
Q

Description of auras

A
  1. Scotoma (blind spots)
  2. Teichopsia (bright, wavy lines)
  3. Fortification (zigzag patterns)
  4. Photopsia (flashing lights)
  5. Visual and auditory hallucinations
  6. Paresthesias
  7. Metamorphopsia (distorted size of objects)
49
Q

Migraine attacks typically unfold through a sequence of events that occur over several hours to days, and usually go through 4 phases:

A
  1. Prodrome
  2. Aura
  3. HA
  4. Postdrome
50
Q

Describe the Prodrome phase

A
  1. occurs in up to 60% of patients
  2. symptoms include euphoria, depression, irritability, food cravings, constipation, neck stiffness and increased yawning
  3. symptoms begin 1-2 days before aura and/or HA onset
51
Q

Describe the Aura phase

A
  1. occurs in ~25% of pts having migraines
  2. usually visual, but can be sensory, verbal or motor disturbance
  3. typically precedes the HA, but can occur during an attack; may last 15-30 min before HA onset
  4. can also include language problems or motor weakness in limbs or face.
52
Q

-visual aura classically begins as

A

a small area of visual loss that expands to form different shapes

53
Q

-sensory aura can follow visual aura and typically begins as

A

tingling in a limb or side of the face

54
Q

Describe the Postdrome phase

A
  1. as the throbbing headache resolves, patients typically feel drained or exhausted
  2. sudden head movement may cause transient pain
55
Q

Describe the HA phase of migraines

A
  1. associated with certain features such as Sensitivity to light, Sound, Or movement; Nausea and vomiting often accompanied a headache
  2. Migraine patients are particularly sensitive to environmental and sensory stimuli- This sensitivity is amplified in females during the menstrual cycle.
56
Q

Migraines were previously thought to be caused by ____ while the aura phase was caused by ___

A

dilation of cerebral blood vessels,

vasoconstriction.
* Vasodilation is now widely considered to be a secondary phenomenon, and is not the initial cause.

57
Q

Describe the neurovascular migraine hypothesis of migraines

A

Current consensus is that migraines are caused by a primary neuronal dysfunction that results in a sequence of changes that account for the different phases of headache. Cortical spreading depression is a central mechanism in the initiation of migraine. This is a self-propagating wave of neuronal and glial (astrocyte) depolarization that spreads across the cortex

58
Q

Cortical spreading depression is believed to:

A
  1. cause the migraine aura
  2. activate trigeminal nerve afferents, which cause inflammation of pain sensitive meninges and dilation of affected cranial blood vessels, which generates the headache
  3. alter blood/brain barrier permeability by activating and upregulating proteases
59
Q

Tx of acute migraine HA

A
  • depends on severity of attack
    1. Trial combination of acetaminophen, ASA, And caffeine is by the FDA for the treatment of mild-mod. migraine
    2. NSAIDs (best if taken early in attack ie. prodrome sx)
    3. Failed NSAIDs/analgesic: Ergotamines and Triptans
60
Q

What are the 3 major drug categories that are effective for migraines

A
  1. Anti-Inflammatory agents,
  2. 5–HT receptor agonists (Also called triptans or ergotamines), and
  3. Dopamine receptor antagonist’s.
61
Q

Stimulation of the __ can stop an acute migraine attack.

Examples of selective and nonselective agonists

A

5-HT receptors

  • nonselective receptor agonists- Ergotamine And dihydroergotamine
  • selective 5-HT-1 receptor agonists- triptans
62
Q

How do triptans work to stop migraines

A

5-HT-1 receptor types are found in meningeal arteries, the trigeminal nerve, and vascular smooth muscle.
-There is an increase in the rate of brain serotonin (5HT) synthesis during migraine attacks, and triptans exert a negative feedback action as well as having an effect on pain pathways.

63
Q

When are 5HT agonists CI

A
  1. CV hx
  2. Cerebrovascular dz hz
  3. Do not combine w/ SSRIs as this can lead to serotonin syndrome
64
Q

Who are good candidates for migraine prophylaxis?

A
  1. those w/ increasing frequency
  2. attacks that are unresponsive, poorly responsive, or CI to abortive tx
  3. 5 or more attacks per month
  4. occurring 2 days/weeks
  5. HA that severely limits quality of life despite abortive therapy.
  6. Presence of uncommon migraine conditions including hemiplegic or basilar migraine, or migraine with prolonged aura
65
Q

What meds are used for migraine prophylaxis

A

FDA approved:

  1. Propranolol/Timolol
  2. Valproate
  3. Topririmates (anticonvulsant)

Not FDA approved

  1. TCAD- Amitriptyline and Nortriptyline
  2. Gabapentin

*The probability of success with any one of the antimigraine drugs is 50 to 75%.

66
Q

Describe how migraine prophylaxis meds work

A
  1. take daily and start w/ LD and gradually increase
  2. period of 2-12 weeks before effect is seen
  3. Once effective stabilization is achieved the drug is continued for approximately 6 months
  4. then slowly tapered to assess the continued need.
67
Q

What are SE of BB used for migraine prophylaxis

A
  1. Reduce energy/tired
  2. Postural sx
  3. CI in asthma
68
Q

What are SE of TCAD used for migraine prophylaxis

A

Drowsiness

69
Q

What are SE of Topirimate used for migraine prophylaxis

A
  1. Paresthesias,
  2. Cognitive symptoms,
  3. Weight loss,
  4. Glaucoma,
  5. Caution with nephrolithiasis
70
Q

What are SE of Valproate used for migraine prophylaxis

A
  1. Drowsiness,
  2. Weight gain,
  3. Tremor,
  4. Hair loss,
  5. Fetal abnormalities,
  6. Hematologic abnormalities and or
  7. liver abnormalities
71
Q

What are SE of Gabapentin used for migraine prophylaxis

A
  1. Dizzy

2. Sedation

Adult Clinical Medicine (26 decks)

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