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Head and Face Pain > Head and Face Pain Primary Headaches > Flashcards

Head and Face Pain Primary Headaches Flashcards

1
Q

What is the “World’s Leading Membership Org for those Committed to Treating Those who suffer from Headaches?”

A

The International Headache Society (IHS)

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2
Q

What has the IHS developed?

A

The most comprehensive classification of pain disorders of the head, face, and neck.

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3
Q

What does ICHD stand for?

A

The International Classification of Headache Disorders

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4
Q

What year was the current, more comprehensive version of the ICHD developed?

A

ICHD-II was developed in 2004.

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5
Q

What are the three primary classifications of ICHD-II?

A

Part 1 - Primary HA
Part 2 - Secondary HA
Part 3 - Cranial neuralgias, central and primary facial pain, other HA

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6
Q

What are the 4 types of primary headaches?

A
  1. Migraine
  2. Tension-Type HA
  3. Cluster Type and its relatives
  4. Other Primary HA
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7
Q

What are the 8 types of secondary headaches?

A
  1. Post-Traumatic
  2. Vascular Disease
  3. Other Intercranial Pathology
  4. Substances
  5. CNS Infection
  6. Homeostatic Disorders
  7. Cervicogenic, Eyes, Ears
  8. Psychiatric
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8
Q

What are the types of headaches in Part 3?

A
  1. Cranial Neuralgias and Neuropathies
  2. Central and Primary Face Pain
  3. Other HA
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9
Q

What are the types of Migraine?

A
  1. Migraine w/o Aura
  2. Migraine w/ Aura
  3. Childhood periodic syndromes that are common precursors to Migraine
  4. Retinal Migraine
  5. Complications of Migraine
  6. Probable Migraine
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10
Q

When and where was the first medical description of headaches?

A

1550 B.C.E. in Ancient Egypt

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11
Q

Hemicranial (Migraine) was first coined in what year by who?

A

130-200 C.E. by Galenus

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12
Q

Define Migraine

A

Recurrent, chronic, headaches of moderate to severe intensity

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13
Q

What percentage does Migraine occur in each gender?

A

6% in Men

18% in Women

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14
Q

What is the most important clinical presentation?

A

Aura

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15
Q

(T/F)

Attacks occur with and without Aura

A

True

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16
Q

(T/F)

Aura occurs up to 1/2 of cases.

A

False

Aura occurs up to 1/3 of cases

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17
Q

(T/F) Aura is only visual

A

False

Aura is generally visual but can be somatosensory, aphasic, and/or motor

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18
Q

What symptoms can be associated with Migraine?

A
  1. Anorexia
  2. Nausea
  3. Photophobia
  4. Photophobia
  5. Osmophobia
  6. Blurred Vision
  7. Vomiting
  8. Diarrhea
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19
Q

Which factors contribute to Migraine generation?

A

Genetic and Environmental

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20
Q

What are the primary contributors to the manifestations of migraine?

A

CNS
Endocrine System
Autonomic System

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21
Q

What percent of Migraineurs have a family history with Migraine?

A

60-70% have 1st degree relatives with migraine

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22
Q

What is the risk of developing migraine?

A

45% when 1 parent is affected

70% when both parents are affected

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23
Q

Do genetics play a larger role in Migraine with or with aura?

A

Migraine with Aura

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24
Q

What is the Migraine Susceptibility Theory?

A

Migraine is a paroxysmal disorder in which a threshold builds between attacks

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25
Q

What is the Migraine Threshold characterized by?

A

Transient or persistent hyper excitation in the cerebral cortex, with the occipital cortex most affected

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26
Q

How can the trigeminovascular system play a role in Migraine?

A
  1. Extracranial Neurogenic Inflammation
  2. Extracranial Arterial Vasodilation
  3. Decreased Central Pain Inhibition
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27
Q

Which artery is usually associated with extra cranial artery vasodilation?

A

The frontal branch of the superficial temporal artery

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28
Q

In extra cranial artery vasodilation, pain occurs on the ipsilateral or contralateral side of vasodilation?

A

Ipsilateral

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29
Q

What is Extracranial Neurogenic Inflammation

A

Increased levels of calcitonin gene related peptide (CGRP) in the external jugular vein resulting in decreased threshold at the site of pain

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30
Q

What does central sentiziation in the trigeminal system result in?

A

Decreased pain threshold at the site of Migraine

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31
Q

In Migraine, where is Allodynia found?

A

In the head, upper trunk, and limbs

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32
Q

What indicates central sensitization in Migraine?

A

The late phase, which is dull and constant

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33
Q

What is found in the CSF during Migraines?

A

Decreased levels of Enkephalin

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34
Q

What is Enkephalin?

A

An endogenous opiod

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35
Q

(T/F) Aura can occur without HA

A

True

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36
Q

How long is the recovery usually for Migraine Aura?

A

20-60 minutes

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37
Q

What is Migraine Aura characterized by?

A

Focal Neurological Symptoms

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38
Q

What is Migraine Aura currently attributed to?

A

Cortical Spreading Depression

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39
Q

What is Cortical Spreading Depression (CSD)?

A

A slow spreading, short duration, of increased neuronal activity followed by inhibition of activity implicated in aura

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40
Q

At what rate does Cortical Spreading Depression recover?

A

At the same rate as the onset

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41
Q

What are visual auras characterized by?

A

Sparkly, scintillating, crenellated shapes in one field

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42
Q

What phase is represented by the visual auras?

A

The excitation phase

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43
Q

What phase is represented by the scotoma?

A

The inhibition phase

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44
Q

Define Scotoma

A

A partial loss of vision or a blind spot in an otherwise normal visual field

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45
Q

What does current clinical research draw as the Aura-HA connection?

A

Aura is not connected to HA, but may be a completely separate event

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46
Q

What is the HA of Migraine theorized to be?

A

An interplay between vasodilation of extracranial arteries, as a result of hemispheric vasoconstriction, and resultant neurogenic inflammation

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47
Q

How does blood vessel diameter play into onset of HA?

A

Vasoconstriction restiling in Vasodilation occurs after the onset of HA

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48
Q

What does the timing of changes in vessel diameter show about the Aura-HA connection?

A

Aura is not associated with the pain generator of Migraine, and is confirmed to be CSD

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49
Q

How can an Aura cause HA?

A

The CSD activates the TVS resulting in vasodilation and neurogenic inflammation.

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50
Q

How can an Aura occur w/o HA?

A

If the CSD fails to activate the TVS an isolated Migraine Aura occurs w/o HA

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51
Q

What is the Central Migraine Generator?

A

An alternative to the CSD/TVS connection; a Brainstem Mechanism (Trigeminal Caudal Nucleus)

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52
Q

What is the Brainstem Mechanism in the Central Migraine Generator?

A

CSD, the aura generator, occurs without any connection to the HA generator

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53
Q

What is the Brainstem Mechanism of Migraine Generation based on?

A

The variability of occurrence between Aura and HA

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54
Q

What is the Criteria for Migraine w/o Aura?

A
  1. At/L 5 attacks
  2. HA lasting 4-72 hrs
  3. HA with two of the following (Unilateral, pulsating, moderate-severe, aggravation by or avoidance of routine physical activity
  4. During HA: N/V, Photo/Phonophobia
  5. Not attributed to another disorder
55
Q

What is the Criteria for Migraine w/ Aura

A
  1. At/L 2 attacks
  2. Aura fulfilling 1 or 2 subforms
    - One of the following fully reversible Sx w/o motor weakness
    - - Visual Sx
    - - Sensory Sx
    - - Dysphagic Speech
  3. At/L 2 of the following
    - Homonymous visual Sx and/or unilateral sensory Sx
    - At/L 1 Aura gradually over > 5 min and/or different aura Sx occur in succession over > 5 min
56
Q

Describe the facial pain distribution pattern of a sinus headache.

A

Pain is usually behind the forehead and/or cheekbones

57
Q

Describe the facial pain distribution pattern of a Cluster HA

A

Pain is in and around one eye

58
Q

Describe the facial pain distribution pattern of a Tension HA

A

Pain is like a band squeezing the head

59
Q

Describe the facial pain distribution pattern of a Migraine HA

A

Pain, nausea, and visual changes are typical of classic form (unilateral)

60
Q

What do childhood periodic HA syndromes include?

A

Cyclic Vomiting
Abdominal Migraines
BPPV of Childhood

61
Q

What are childhood periodic syndromes shown to be precursors of?

A

Migraines

62
Q

What are the 4 types of Tension-Type HA?

A
  1. Infrequent, episodic
  2. Frequent, episodic
  3. Chronic
  4. Probable
63
Q

What is the most common type of HA?

A

Tension-Type HA

64
Q

What is the subjective and objective diagnostic criteria?

A

Clinical presentation is the sole criteria, no reliable objective testing has emerged

65
Q

What did Tension-Type HA used to be called?

A

Muscle Contraction HA

66
Q

What is the most consistent clinical finding?

A

Significantly increased tenderness to palpation of the pericranial mm, proportional to the intensity and freq of HAs

67
Q

What else may cause Tension-Type HA?

A

Muscle tension in the face, neck, and shoulders

68
Q

What are the Tension-Type Headache Subgroups?

A
  1. Myofascial
  2. Psychosocial
  3. Mild Migraine
69
Q

What is the myofascial subgroup of TTH?

A

Characterized by MFTPs and pain referral patterns (WDRN)

70
Q

Describe the quality of pain in the myofascial subgroup

A

Similar to myofascial pain in other areas in the body

71
Q

What is the myofascial TTH pathogenesis thought to be?

A

Unabated myofascial pain lead to central sensitization resulting in inc peripheral tenderness of the mm. of mastication and Cx spine

72
Q

What is the basis for Cervicogenic TTH?

A

Trigeminal pain afferents and spinal afferents to the level of C4 share the same neuronal pathways.

73
Q

What can biomechanics stress create?

A

MFTPs

74
Q

What are MFTPs?

A

A hyper irritable spot in muscle

75
Q

What do MFTPs represent?

A

Dysfunctional motor endplates leading to spontaneous electrical activity

76
Q

What is the Psychosocial TTH pathogenesis thought to be?

A

Corticolimbic disinhibition, similia to limbic pain augmentation, leading to generalized muscle tissue sensitivity

77
Q

Is pain in the Psychosocial TTH attributed to nociception?

A

No

78
Q

What happens in Chronic Psychosocial TTH?

A

They may plasticize the corticolimbic state making them resistant to somatic based treatments

79
Q

What is the Mild Migraine TTH subgroup distinguished by?

A

Clinical Presentation

80
Q

How does Mild Migraine TTH differ from Migraine?

A

An individual w/ a Migraine genotype may experience milder HA that are phenotypically TTH

81
Q

How does the pain modulating systems work in Mild Migraine TTH?

A

They have well functioning pain modulating systems allowing them to dampen the severity of a migraine to a less severe TTH

82
Q

Which muscles are prone to MFTP in TTH?

A 
Temporalis
Masseter
Trapezius
Splenius Capitis
SCM
83
Q

What are examples of Tx for TTH?

A
  1. MFTP Acupuncture
  2. MFTP Injection
  3. PT
  4. Muscle Relaxers
  5. Botulinum Toxin
  6. Corticolimbic Subgroup
84
Q

What are examples of Tx for TTH in the corticolimbic subgroup?

A
  1. CBT
  2. Biofeedback
  3. Antidepressants
  4. SSRI/SSNRI
85
Q

What are Trigemincal Autonomic Cephalgias? (TAC)

A

Primary HA pain with lacrimation, ptosis, rhinorrhea, and Horner’s Syndrome

86
Q

How long do TAC’s typically last?

A

Short duration with severe intensity

87
Q

What conditions are associated with TACs?

A
  1. Cluster HA
  2. Paroxysmal Hemicrania
  3. SUNCT
  4. Hemicrania Continua
88
Q

What does SUNCT stand for?

A

Short Lasting Unilateral Neuralgiform HA w/ Conjunctival Injection and Tearing

89
Q

How do TACs present?

A

With Trigeminal based pain and Sx of Parasympathetic activation. Sympathetic activation is less common

90
Q

What is the hypothesized Trigeminal-Parasympathetic connection?

A

A brainstem connection links the Trigeminal system to the Parasympathetic system at the level of the CN VII and the Sup Salivatory Nuc, containing Preganglionic Parasympathetic Neurons

91
Q

What is the evidence for the Trigeminal-Parasympathetic connection?

A

Elevation of CGRP and Vasoactive Intestinal Peptide (VIP) in the jugular vein during attacks of cluster HA and Paroxysmal HC

92
Q

Which is a Trigeminal marker?

A

CGRP

93
Q

Which is a Parasympathetic Marker?

A

VIP

94
Q

How is it hypothesized that the sympathetic system is involved?

A

Pain is excitatory to the IML, which stim adrenal release of plasma NE/E, also ICA dilation from Para activation stim the sympathetic plexus on the ICA

95
Q

What is the primary generator of TACs?

A

Hypothalamus and the HPA Axis

96
Q

What is the regulating system for the body?

A

The HPA Axis, along with the sympathetic system

97
Q

Which are the most severe of all the HA syndromes?

A

Cluster HA

98
Q

How long does it take a sufferer to be Dx with a Cluster HA correctly and why?

A

6.6 years due to misdiagnosis as a Migraine or Sinus HA

99
Q

Describe a Cluster HA

A
  1. Episodic and Frequent
  2. Short Duration
  3. Severe
  4. Unilateral
  5. Autonomic Symptoms
100
Q

What are Cluster periods?

A

The cycle in which they have daily attacks

101
Q

How often and how long do cluster periods last?

A

2-12 weeks

2x a year

102
Q

What is Cluster HA remission?

A

6 months

2 years

103
Q

What is the intensity of Cluster HA

A

Always Severe

104
Q

What is the pain distribution in cluster HA?

A

Always Unilateral

Same side for entire life

105
Q

How often and how long do Cluster HAs last?

A

Duration - 15-180min
Freq - 1-3/Day
Peak - 1-2AM, 1-3PM, After 9PM

106
Q

When do Cluster HAs occur in sleep?

A

In the first REM phase, typically 60-90min into sleep

107
Q

What are the associated Autonomic Symptoms of Cluster HA?

A
  1. Most often unilateral
  2. Lacrimation
  3. Conjunctival Injection
  4. Nasal Congestion
  5. Nasal Rhinorrhea
  6. Horner’s Syndrome
108
Q

Which Sx are comorbid between Cluster and Migraine?

A
  1. Nausea
  2. Vomiting
  3. Photophobia
  4. Phonophobia
109
Q

What are the risk factors for Cluster HA?

A 
Gastric Ulcers
GERD
Head Trauma
Cigarette Smoking
Alcohol
110
Q

What are the abortive therapy Tx’s for Cluster HA?

A

Sumatriptan
Oxygen
Zolmitriptan

111
Q

What are the short term preventative therapy Tx’s for Cluster HA?

A

Corticosteroids
Dyhydroergotamine
Occipital Nerve Block

112
Q

What are the preventative therapy Tx’s for during the Cluster HA cycle?

A 
Verapamil
Lithium Carbonate
Valproic Acid
Topiramate
Melatonin
113
Q

What other Tx are used for Cluster HA?

A

Surgery to the Cranial Parasympathetic System
Surgery to the Sensory CN V
Radio frequency Coagulation
Hypothalamic stimulation

114
Q

How does Chronic Paroxysmal Hemicranial present?

A 
Rare
Short duration
High freq
Severe rad to neck and shoulder
Autonomic Sx
Does not occur during sleep
Unilateral - orbital, temple, auricular
Mild pain common between attacks
115
Q

What do PET studies indicate about Chronic Paroxysmal HC?

A

Activation of the contralateral posterior hypothalamus and contralateral ventral midbrain

116
Q

How does SUNCT present?

A 
Unilateral
Brief
Moderate-Severe
Orbital with rad to temple, nose, cheek, palate
Conjunctival Injection
Tearing
Rhinorrhea
Nasal Obstruction
117
Q

What is the age of onset for SUNCT?

A

40-70 years old

118
Q

How often daily can SUNCT occur?

A

1-80 episodes a day

119
Q

What does functional imaging indicate about SUNCT?

A

Hypothalamic Activation

120
Q

What is Hemicrania Continua?

A

Very rare condition of unilateral severe HA with autonomic and migrainous Sx

121
Q

What are the two most prevalent primary HA in women?

A

Migraine

Tension-Type HA

122
Q

Which HA occurs more in men?

A

Cluster HA

123
Q

What is the gender discrepancy in primary headaches attributed to?

A

Influence of ovarian steroid cycles on phenotypic expression of HA

124
Q

In which primary HA do ovarian steroids play to most prominent role?

A

Migrainous HA

125
Q

What are female specific triggers for a Migraine HA?

A

Falling Estrogen during late luteal phase

Estrogen withdrawal in postmenopausal women

126
Q

How do you monitor autonomics?

A
  1. General Appearance
  2. Skin Inspection
  3. Capillary Refill
  4. Radial Pulse
  5. Eyes
  6. Respiration & Lung Expansion
  7. Pulse Ox, BP, Auscultation
127
Q

How do you monitor autonomics through skin inspection?

A

Appearance
Temperature
Moisture
Varicosities

128
Q

Where do you monitor autonomics through capillary refill?

A

Hands and Feet

129
Q

How do you monitor autonomics through radial pulse?

A

Look for changes in pulse with head neutral, head left, and head right

130
Q

How do you monitor autonomics through the eyes?

A 
Pupil dilation
Pupil Reflexes
Ptosis
Lid Lag
Palpebral Fissure
131
Q

In TTH, what is Exteroceptive Suppression (ES)?

A

The inhibition of voluntary EMG activity by the temporalis m. induced by CN V stimulation

132
Q

In TTH, what is ES2?

A

ES2 is a multi synaptic reflex subject to limbic and other modulation, is absent in 40% of pts with CTTH, and reduced in duration 87%

ES2 may be absent in more HA prone patients

133
Q

In TTH, what is ES1?

A

ES1 is a normal oligosynaptic reflex

134
Q

In Cluster HA, what are the 8 clinical features to memorize?

A
  1. Conjunctival Injection
  2. Lacrimation
  3. Congestion
  4. Rhinorrhea
  5. Swelling
  6. Miosis
  7. Ptosis
  8. Eyelid Edema

Head and Face Pain (8 decks)

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