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Head and Face Pain > Head and Face Pain Secondary Headaches > Flashcards

Head and Face Pain Secondary Headaches Flashcards

1
Q

What are secondary HA disorders defined as?

A

HA associated with:

  1. Head Trauma
  2. Vascular d/o
  3. Nonvascular Intracranial d/o
  4. Substance and Withdrawl
  5. Non cephalic Infection
  6. Metabolic d/o
  7. d/o of face and cranial structures
  8. Cranial Neuralgias and Nerve Trunk Pain
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2
Q

What are the RED FLAGS for secondary HA?

A
  1. New Onset HA
  2. Significant change in ongoing HA
  3. “Thunderclap”
  4. HA Triggers like sitting up, coughing, straining, sex, exertion activity
  5. HA with fever
  6. HA with underlying disease
  7. Abnormal neurological exam like papilledema, weakness, or mental status
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3
Q

What is the most important component in the evaluation of secondary HA?

A

Physical Examination, because these d/o are due to another physiological or pathological process

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4
Q

Which advanced diagnostic studies may be helpful in Dx 2’ HA?

A 
MRI
MRA
MRV
CT
Cerebral Angiography
Lumbar Puncture
Blood Laboratories
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5
Q

What are the 6 types of Head Trauma HAs?

A
  1. Acute post traumatic
  2. Chronic post traumatic
  3. Acute d/t whiplash
  4. Chronic d/t whiplash
  5. Traumatic d/t intracranial hematoma
  6. HA d/t other head or neck trauma
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6
Q

What are the first and second most common Sx’s following head trauma?

A
  1. HA

2. Dizziness

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7
Q

(T/F) Whiplash is a type of closed brain injury.

A

True

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8
Q

What are Post Traumatic HAs most frequently caused by?

A
  1. MVAs
  2. Athletic
  3. Neck Injuries
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9
Q

How does Post Traumatic HA present?

A

Chronic Intermittent
or
Daily HA

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10
Q

What is the clinical presentation of Post Traumatic HA?

A 
Dizziness
Difficulty Sleeping
Decreased Energy and Appetite
Blurred Vision
Cognitive Difficulties
Psychological Disorders
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11
Q

Head trauma may result in:

A

Intracranial Hemorrhage
Edema
Dural Tears leading to Low Pressure HA

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12
Q

What is common in PTH suffers?

A

Overuse of medication

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13
Q

What is the main pathophysiology paradigm of PTH?

A

Activation of Trigeminal Sensory r/c and continues nociceptive input resulting in maintained pain

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14
Q

In PTH, what are the sites of nociceptive input?

A 
Meninges
Blood Vessels
Skin and Subcutaneous Tissue
Periosteum
Neck mm. Vertebral joints and ll.
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15
Q

What is the pathophysiology of chronic PTH?

A

Central sensitization and biological changes secondary to the trauma

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16
Q

What is the relationship observed about PTH incidence?

A

Incidence of PTH is inversely proportional to the severity of head trauma

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17
Q

In PTH, what does imaging show?

A

Multifocal damage to the axons, d/t shearing and impaired axonal transport

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18
Q

In PTH, how long does the cascade d/t damage last?

A

Several Days

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19
Q

In PTH, where does the damage to the axons occur?

A

Near the junction of gray and white matter

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20
Q

What is almost implicated in the chronicity of PTH?

A

Downstream Deafferentation

Diaschisis

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21
Q

What is proportional to the clinical outcome of PTH?

A

Excess release of glutamate resulting in excitotoxicity

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22
Q

(T/F) PTH related glutamate excitotoxicity only occurs in moderate to severe head trauma?

A

False

This occurs in even mild cases of head trauma

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23
Q

In PTH, what changes with blood flow?

A

Decreased regional blood flow and inter hemispheric perfusion

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24
Q

In PTH, which regions are most affected by decrease blood flow and perfusion?

A

Basal Ganglia

Frontal Lobes

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25
Q

In PTH, which Cx structures are involved?

A

AA-AO Joints
ZP Joints and Vert Discs
mm. and ll. of the Cx spine

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26
Q

Why doesn’t head and neck pain follow dermatomal patterns?

A

D/t the convergence of first order trigeminal neurons and Cx afferents onto the second order neuron

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27
Q

What are the Tx therapies for PTH?

A 
Patient Education
Medication
Psychotherapy
PT
CMT
Occipital Nerve Block
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28
Q

What are the HA from vascular d/o’s?

A
  1. Giant Cell Arteritis (GCA)
  2. Cranial Arteritis
  3. Large Vessel Arteritis
  4. System Inflammatory Syndrome
  5. Arterial Dissection
  6. Ischemic Stroke
  7. TIA
  8. Hemorrhage
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29
Q

What is GCA?

A

an immune mediated inflammatory condition affecting medium and large sized arteries

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30
Q

What is the first stage of GCA?

A
  1. Activated T-cells and macrophages cause granulomatous changes in the artery walls
  2. Release PDGF, metalloproteinases, and ROS that injure vessel wall
  3. Vessel develops intimal hyperplasia leading to lumen occlusion
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31
Q

What is the second stage of GCA?

A
  1. Macrophages release IL-1 and IL-6 promoting inflammatory cascade
  2. Acute phase response seen in Liver, CNS, vascular tissue, bone marrow, and immune system resulting in distinct clinical syndromes
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32
Q

What clinical syndromes are associated with GCA?

A

Cranial Arteritis
Large Vessel Arteritis
System Inflammatory Syndrome with Arteritis

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33
Q

What is Cranial Arteritis?

A

Acute phase response involving branches of the carotid artery

34
Q

What branches of the carotid artery are implicated in Cranial Arteritis?

A 
Superficial Temporal
Ophthalmic
Occipital
Posterior Ciliary
Vertebral Arteries
35
Q

What is the clinical presentation in GCA?

A

Scalp tenderness
Temporal arteries tender and thickened
unilateral or bilateral
Jaw claudication with decreased flow to the masseter, temporals, and the tongue

36
Q

What is AION?

A

Anterior Ischemic Optic Neuropathy

37
Q

What is AION present with?

A

Posterior ciliary artery involvement

38
Q

What is the presentation of AION?

A

Painless vision loss, sudden and often unilateral blindness

39
Q

What is AION treated with?

A

Corticosteroids

40
Q

What is Benign Cerebral Fluid Pressure HA due to?

A
  1. High and low production of CSF
  2. Reduced or increased absorption of CSF
  3. Obstruction of CSH pathways
41
Q

What is idiopathic intracranial hypertension also known as?

A

Pseudotumor Cerebri

42
Q

Are there structural problems associated with Pseudotumor Cerebrr?

A

No

43
Q

What are examples of High CSF pressure HAs?

A
  1. Pseudotumor Cerebri
  2. Intracranial Hypertension
  3. Hydrocephalus
44
Q

What causes Intracranial Hypertension?

A

Metabolic, toxic, or hormonal causes

45
Q

What are examples of Low CSF pressure HAs?

A
  1. Postdural Puncture
  2. CSF Fistula
  3. Idiopathic
46
Q

How does a post dural puncture present?

A

Develops within 5 days
Worse with sitting/standing
Associated w/ tinnitus, neck stiffness, Nausea and photophobia

47
Q

How does a CSF Fistula present?

A

D/t leaking
Develops within 5 days
Worse with sitting/standing
Associated w/ tinnitus, neck stiffness, Nausea and photophobia

48
Q

What is idiopathic low CSF pressure linked to?

A

Leaks of CSF

49
Q

What is the current model of HA and Sleep d/o?

A

HA or Sleep Disturbance is Sx of 1’ sleep disorder

HA and Sleep Disturbance is 2’ to unrelated d/o, or common pathogenesis

50
Q

What areas are involved with HA and Sleep d/o?

A

Hypothalamus
5HT
Melatonin

51
Q

What is wakefulness dependent on?

A

The reticular activating system (RAS) in brainstem and influenced by NE, DA, and ACh

52
Q

What initiates REM sleep?

A

Release of ACh stim pontine neurons in the Dorsal Raphe Nuc (5HT)

53
Q

What is the MOA of HA and Sleep d/o?

A

Wakefulness and REM sleep

54
Q

How does REM sleep connect with central modulation of pain?

A

The dorsal raphe nucleus is part of both systems

55
Q

What is the MOA in sleep d/o HAs that are Migrainous?

A

The Spinal Trigeminal Nuc activates the vasculature during migraine attacks

56
Q

How is the hypothalamus implicated in HA and sleep d/o?

A

Involved with yawning, hunger, cravings, mood changes, sensory and visual distortions.

57
Q

What structures does the hypothalamus have a connection to in HA and Sleep d/o?

A 
Limbic System
Pineal Gland
NTS
Locus Ceruleus
PAG
58
Q

What role does the Pineal Gland play in HA and Sleep d/o?

A

Melatonin

59
Q

What role does the Locus Ceruleus play in HA and Sleep d/o?

A

Sleep Stage and Motor Control

60
Q

What role does the PAG play in HA and Sleep d/o?

A

Pain

61
Q

How do you evaluate HA and Sleep d/o?

A

Polysomnography
Actigraphy
Questionnaires
Sleep Diary

62
Q

What is an Medication Overuse HA (MOH)?

A
  1. HA > 15 days/mo
    Med overuse 2. > 3 mo of 1+ drug used to treat HA Sx
  2. HA worse with meds
  3. HA improves w/in 2 mo of discounting meds
63
Q

Which medication are found in overuse HA?

A

Ergotamine
Triptans
Opiates
Compound Analgesics

64
Q

Which meds are used for TTH?

A

Analgesics and Ergotamine preps

65
Q

Which meds are used for daily Migraine?

A

Triptans

66
Q

How can opiod use result in pain?

A

Down regulation of opiate r/c and inc production of adenylyl cyclase (AC), which is inhibited by opioids.
.: rebound pain sensitivity with cessation of chronic opioid use

67
Q

What do opiates activate?

A

descending pain facilitation pathways in the RVM (5HT) which results in higher tonic firing of the “on” cells

68
Q

What do the activation of the “on” cells cause?

A

Release of GLU and CGRP, through inc dynorphin concentrations, causing increased excitation in the dorsal horn and trigeminal caudal nun, increasing pain signaling

69
Q

What can result from impaired GLU uptake?

A

Excitotoxicity leading to apoptosis of the pain inhibitory cells, which may lead to permanent pain sensitization

70
Q

How can excessive NSAID use cause pain?

A

Localized inflammation prevention activate the PAG descending opiod pathways, triggering anti-opioid proprioception leading to hyperalgesia

71
Q

How can acetaminophen use result in pain?

A

It inc 5HT and NE in the hypothalamus and brainstem. Compensatory neuroplasticity contributes to HA

72
Q

How can triptans and ergotamins use result in pain?

A

vasodilation

73
Q

How can caffeine use result in pain?

A

Upregulates pain inhibition centrally and locally in muscle tissue.

74
Q

How can chronic caffeine use result in pain?

A

Use then withdrawal results in HA due to alteration of pain inhibition pathways

75
Q

Tx for HA and substance abuse

A

Education
Detoxification
Preventative Medication

76
Q

What is a chronic daily HA?

A 
Occur 15+ days/mo
4+ hrs/day
3+ mo duration
High level of disability and impairment
Most are 1' but some are intracranial and systemic abnormalities
77
Q

What are the RED FLAGS for chronic daily HA?

A
  1. Focal Neurological S/Sx
  2. Alteration of Mental Status
  3. Systemic Sx
  4. Cancer
  5. Sudden Onset
  6. New HA over age of 50
  7. “Thunderclap”
  8. Explosive HA with orgasm
  9. Valsalva induced HA
  10. Exertional, 1st/Worst, Change in HA
78
Q

What is Occipital Neuralgia also known as?

A

C2 Neuralgia

Arnold’s Neuralgia

79
Q

What is Occipital Neuralgia?

A

Chronic pain in the upper neck, back of the head, and behind the eyes.

80
Q

What does the location of pain in Occipital Neuralgia correspond to?

A

The locations of the lesser and greater occipital nerves

81
Q

What S/Sx may be seen in Occipital Neuralgia?

A

Photophobia
Aching, Burning, and Throbbing pain at the base of the head
Tender scalp
Pain with neck movement

Head and Face Pain (8 decks)

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