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Head Pain Flashcards

1
Q

Old arts

A 
Onset
Location
Duration
Characterization
Aggravating factors
Relieving factors
Radiation
Timing
Severity
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2
Q

Physical exam

A

HEENT
Neuro examstructural exam
Psychological disposition
Special tests as indicated

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3
Q

Structural exam

A 
TART, lymphatics
Cranial
Cervical
Upper thoracic
Upper ribs
Upper extremities
Sacrum
Posture/leg length
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4
Q

Head pain anterior 2/3

A

Trigeminal nerve

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5
Q

Head pain posterior 1/3

A

Lesser occipital (C1-3), recurrent branches of IX and X

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6
Q

Head pain sympathetic

A

T1-4

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7
Q

Onset tension headache

A

25-30

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8
Q

Peak prevalence tension head ache

A

30-39

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9
Q

Female to male ratio tension headache

A

5:4

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10
Q

Mean lifetime prevelance of tension headache worldwide

A

30-78%

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11
Q

Risk factors head ache

A

Stress
Mental tension
Emotional disturbance

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12
Q

Possible risk factors headache

A

Poor self-related health

Inability to relax after work

Sleeping few hours per night

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13
Q

Associated conditions head pain

A

Anxiety and depression often associated with chronic tension type headache

Migraine, including migraine without aura

Medication overuse headache

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14
Q

Causes tension headache

A

Uncertain

Twin studies-genetic studies

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15
Q

Active myofascial trigger points where for tension HA

A

Head, neck, shoulder muscles might cause myotonic referred pain

-sensitization of active myofascial trigger points could cause long term sensitization or potentiation of second order nociceptive neurons int he spinal trigeminal nucleus which could gradually lead to chronic tension type headache

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16
Q

Episodic tension type HA

A

Peripheral pain mechanisms are more likely important

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17
Q

Chronic tension type Ha

A

Central pain mechanisms are more likely involved

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18
Q

Clinical features tension HA

A

Bilateral HA
Mild to moderate intensity
Pressing or tightening quality(nonpulsating)
Not aggravated by routine physical activity
Absence of nausea and vomiting
May have photophobia or phonophobia, but not both
May increase in frequency or duration over time

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19
Q

Episodic tension hA

A

Last 30 minutes to 7 days

Infrequent>10 episodes occurring on <1 day per month (<12 days per year)
Frequent > 10 episodes on 1-14 days per month for >_3 months (>-12 days and <180 days per year)

Develops into chronic tension type headache usually

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20
Q

Chronic tension HA

A

Episodes on >_ 15 days per month on average for >_3 months (>_180 days per year)

Headache may be continuous and unremitting

Patients with chronic type more likely to seek care, may have history of episodic type

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21
Q

Tension headache what is the most common HEENT finding

A

Pericardial msucle tenderness

  • mostly the scalp
  • absence of tenderness does not r/o diagnosis
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22
Q

What other muscles may contribute totension HA

A

Frontal, temporal, masseter, pterygoid, SCM, selenium and trapezius muscles may al refer/contribution to tension HA
-muscle TrP tenderness is more common with episodic variant and less so with chronic tension HA

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23
Q

Neck finding tension HA

A

Muscle tenderness may be present

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24
Q

Tension HA neurologic findings

A

Normal exam

Neurological signs, if presnt, warrant additional investigation

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25
Q

5 model

A

Behavioral

Neurologic

Biomechanical

Metabolic

Respiratory-circulatory

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26
Q

Behavioral tension HA

A
  • identify and address possible triggers
  • encourage following prescription recommendations
  • biofeedback
  • cognitive behavioral therapy and relaxation training
  • counseling
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27
Q

Neurologic tension HA

A

Analgesics and NSIDS 1st line

Combination analgesics with caffeine, 2nd line

Opoids and muscle relaxants are generally not used for tension HA

Metaclopramide (stimulant of upper GI motility and potent dopamine receptor antagonist)

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28
Q

Biochemical

A

Physical therapy and acupuncture, level 2

OMTmanual therapy, level 2

Intra-oral appliance (possible placebo)

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29
Q

Metabolic tension HA

A

Sleep hygeine

Hormonal influences-menstrual
Hydration

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30
Q

Respiratoy circulatory

A

Hydration

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31
Q

Which model is OMT

A

Biomechanical

32
Q

What does biomechanical address

A

Myofascial somatic dysfunctions

Address joint somatic dysfunction with cranial, mET, stills, HVLA or FPR

33
Q

Respiratory/circulatory

A

Address lymphatics first o reduce irritants from inflammatory milieu

34
Q

Neurologic

A

Address Counterstrain points anteriorly and posteriorly in the cervical , upper thoracics, upper ribs, and upper extremities

Use cranial to address other contributing SD

35
Q

Metabolic

A

Improvement is due to other approaches

36
Q

Behavioral

A

Exercise to support treatment of SD contributing to symptoms

37
Q

Effectiveness of direct vs indirect technique myofascial release in the management of tension type HA

A

Design: randomized, controlled, single blinded triad

63 patients with episodic or chronic tension type HA

Interventions: DT-MFR, IDT-MFR or control treated 24 sessions 12 weeks

38
Q

MFR tension HA study control vs treat

A

Control-slow soft stroking with finger pdas all over the head
Treatment-MFR

39
Q

Outsome MFr tension HA

A
  • difference in numbers of days with HA between weeks 1-4 (4 weeks prior to intervention) and weeks 17-20 (after 12 weeks of intervention) as eroded in headache diaries
  • number of days with HA per 4 weeks decreased by 7 days in he DT-MFR group compared with 6.7 days in the IDT-MFR group and 1.6 days int he control group

Patients in the DT-MFR group, IDT-MFR group and control group reported a 60%, 54% and 13% reduction in their HA frequency in weeks 17-30 compared o that in weeks 1-4

40
Q

Study conclusion

A

This study provides evidence that myofascial release is more effective than the control intervention for tension HA

41
Q

Myofascial trigger point pain referral patterns

A

Levator scapulae

Trapezius

Scm (sternal division, clavicular division)

Suboccipitals

Longus colli

Temporalis

Masseter

Splenic capitals

Splenic cervicis

Occipitalis-frontalis

Medial pterygoid

Lateral pterygoids

42
Q

Chronic migraine

A

> _ 3 months, including .0 8 days/month

43
Q

Menstrual migraine

A

Typically without urea and more severe than on menstrual migraine

44
Q

Migraine with aura

A

Typical aura with HA

Typical aura w/o HA

Hemiplegic migraine (aura and weak)

Migraine with brainstem aura

Retinal migraine

45
Q

What percent of adults get HA

A

15% of all adults

21% of US females

10% of US males

46
Q

Female to male ration migraine

A

2:1

47
Q

What races get severe head aches and migraine more

A

American Indian or Alaska native

White

Black

Hispanic

Native Hawaiian

Asian

48
Q

Likely migraine risk factors

A

Analgesic overuse

MS

Oral contraceptives (possible)

Not associated (BP)

49
Q

Analgesic overuse migraine

A

Use of analgesics daily or weekly at baseline

Defined as daily or almost daily for ._ 1 month

50
Q

MS migraine

A

With and without aura

51
Q

Episodic syndromes

A

Recurrent GI disturbances (cyclic vomiting, abdominal migraine)

Vestibular migraine

Benign paroxysmal torticollis

52
Q

Migraine during pregnancy

A

Preeclampsia,vascular diagnoses (stroke, MI, PE, HTN, DM, smoking)

53
Q

Migraine associated conditions

A

Tension HA, episodic syndromes, migraine during pregnancy, endometriosis, obesity, depression and other psychiatric disorders, other pain conditions and physical diagnosis, syncope and Ménière’s disease

54
Q

Migraine diagnosis POUND

A 
Pulsating
Duration 4-72 hours
Unilateral
Nausea or vomiting 
Disabling
55
Q

How may pound criteria née for definite or possible migraine

A

4/5

56
Q

How many POUND criteria for likelihood ratio 3.5 for definite or possible migraine

A

3/5

57
Q

0-2 pound met

A

Criteria meta has negative likelihood ratio .41 for definite or possible migraine

58
Q

Precipitating factors

A

Menses, perimenstrual

Diet

Fasting
Stree, stress alleviation
Exertion
Altered sleep
Visual stimuli
Odors
Smoking 
Alcohol
Caffeine withdrawal
Oral contraceptives
Vasodilator
Change in weather
59
Q

Differential diagnosis

A 
Tension HA
Cervical spine disease
Acute cervical strain
Intracranial mass
Meningitis
Subarachnoid hemorrhage
Transient ischemic attack 
Cluster hA
Cavernous sinus thrombosis
Optic neuritis
Acute glaucoma
Pseudotumor cerebri
Systemic lupus erythematosus
Cervical artery dissection 
TMD
Epilepsy 
Sinusitis
60
Q

Cluster headache

A

More common in men, strictly unilateral, periorbital in 80% of patients, and lasts <1 hour in 54%

61
Q

Cavernous sinus thrombosis

A

Associated with fever and periorbital edema

62
Q

Migrain pathogenesis with aura

A

Spreading olive is (reduced blood volume) in brain is pathognominic for migraine with aura

63
Q

Pathogenesis migraine without aura

A

Uncertain

  • previous theories of vascular based phenomena not well supported
  • cortical spreadingdepression not seen on regional cerebral blood flow imaging during attacks, but some studies disagree
  • messenger molecules involved appear to include NO, 5HT, and CGRP

No longer considered vascular based phenomena

64
Q

Intracranial pain sensitive structures

A

Meninges at base of brain

Intracranial blood vessels

65
Q

Visually triggered migraine and visual change in patients with migraine associated with spreading suppression of initial neuronal activation and increased occipital cortex oxygenation
-based on magnetic resonance imaging blood oxygenation level dependent contrast in 12 migraine and 6 healthy subjects

A

Dorsal pontine activation demonstrated using positron emission tomographic PET scan in 5 patients with episodic migraine

66
Q

Cervicogenic HA

A

Caused by disorder of the cervical spine and its component bony, joint and/or soft tissue elements, usually but not invariably accompanied by neck pain.

67
Q

Cervical nerves C_-C_ innervate the posterior 1/3 of the head

A

1-3

68
Q

Facet pain from C2-3 to c4-5 may refer where

A

Head

69
Q

Involvement of C2-3 facet is the most frequent source of

A

Cervicogenetic HA, accounting for up to 70% of cases

70
Q

Involvement of AA

A

Probably the second most common source of cervicogenetic HA, but the true frequency is unknown

71
Q

Facet pain c50c6 and c60c7

A

May contribute to a somato-somatic reflex resulting in TrP pain referral to the head

72
Q

Diagnosis of cervicogenis HA

A

A. Any headache fulfilling criterion C
B. Clinical and/or imaging evidence of a disorder or lesion within the cervical spine of soft tissues of the neck, known to be able to cause HA
C. Evidence of causation demonstrated by at least two of the following
1. Developed in temporal relation to the onset of the cervical disorder/lesion
2. Significantly improved or resolved with improvemen tin or resolution of the cervical disorder/lesion
3. Cervical range of motion is reduced and HA is made significantly worse by provocative maneuvers
4. Abolished following diagnostic blockade of a cervical structure or its nerve supple

D. Not better accounted for by another ICHD-3 diagnosis
-myofascial pain, IHS prefer classification at tension HA

73
Q

Mgiraine diagnosis

A

POUND

74
Q

Tension HA

A

Bilateral, mild to moderate intensity, pressing or tightening quality, not aggravated by routine physical activity, absence of nausea and vomiting

75
Q

C2 neuralgia

A

Paroxysmal sharp or shock like pain centered in the occipital region
Ipsilateral eye lacrimation and conjunctival injection are commonly associated

76
Q

Neck tongue syndrome

A

Rapid head turning causes subluxation of the posterior AA joint and C2 spinal root compression. Symptoms include neck pain, occipital pain, may be associated with ipsilateral tongue sensory symptoms. Onset is typically during childhood or adolescence

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