Head Pain Flashcards
Old arts
Onset Location Duration Characterization Aggravating factors Relieving factors Radiation Timing Severity
Physical exam
HEENT
Neuro examstructural exam
Psychological disposition
Special tests as indicated
Structural exam
TART, lymphatics Cranial Cervical Upper thoracic Upper ribs Upper extremities Sacrum Posture/leg length
Head pain anterior 2/3
Trigeminal nerve
Head pain posterior 1/3
Lesser occipital (C1-3), recurrent branches of IX and X
Head pain sympathetic
T1-4
Onset tension headache
25-30
Peak prevalence tension head ache
30-39
Female to male ratio tension headache
5:4
Mean lifetime prevelance of tension headache worldwide
30-78%
Risk factors head ache
Stress
Mental tension
Emotional disturbance
Possible risk factors headache
Poor self-related health
Inability to relax after work
Sleeping few hours per night
Associated conditions head pain
Anxiety and depression often associated with chronic tension type headache
Migraine, including migraine without aura
Medication overuse headache
Causes tension headache
Uncertain
Twin studies-genetic studies
Active myofascial trigger points where for tension HA
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
Episodic tension type HA
Peripheral pain mechanisms are more likely important
Chronic tension type Ha
Central pain mechanisms are more likely involved
Clinical features tension HA
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
Episodic tension hA
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
Chronic tension HA
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
Tension headache what is the most common HEENT finding
Pericardial msucle tenderness
- mostly the scalp
- absence of tenderness does not r/o diagnosis
What other muscles may contribute totension HA
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
Neck finding tension HA
Muscle tenderness may be present
Tension HA neurologic findings
Normal exam
Neurological signs, if presnt, warrant additional investigation
5 model
Behavioral
Neurologic
Biomechanical
Metabolic
Respiratory-circulatory
Behavioral tension HA
- identify and address possible triggers
- encourage following prescription recommendations
- biofeedback
- cognitive behavioral therapy and relaxation training
- counseling
Neurologic tension HA
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)
Biochemical
Physical therapy and acupuncture, level 2
OMTmanual therapy, level 2
Intra-oral appliance (possible placebo)
Metabolic tension HA
Sleep hygeine
Hormonal influences-menstrual
Hydration
Respiratoy circulatory
Hydration
Which model is OMT
Biomechanical
What does biomechanical address
Myofascial somatic dysfunctions
Address joint somatic dysfunction with cranial, mET, stills, HVLA or FPR
Respiratory/circulatory
Address lymphatics first o reduce irritants from inflammatory milieu
Neurologic
Address Counterstrain points anteriorly and posteriorly in the cervical , upper thoracics, upper ribs, and upper extremities
Use cranial to address other contributing SD
Metabolic
Improvement is due to other approaches
Behavioral
Exercise to support treatment of SD contributing to symptoms
Effectiveness of direct vs indirect technique myofascial release in the management of tension type HA
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
MFR tension HA study control vs treat
Control-slow soft stroking with finger pdas all over the head
Treatment-MFR
Outsome MFr tension HA
- 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
Study conclusion
This study provides evidence that myofascial release is more effective than the control intervention for tension HA
Myofascial trigger point pain referral patterns
Levator scapulae
Trapezius
Scm (sternal division, clavicular division)
Suboccipitals
Longus colli
Temporalis
Masseter
Splenic capitals
Splenic cervicis
Occipitalis-frontalis
Medial pterygoid
Lateral pterygoids
Chronic migraine
> _ 3 months, including .0 8 days/month
Menstrual migraine
Typically without urea and more severe than on menstrual migraine
Migraine with aura
Typical aura with HA
Typical aura w/o HA
Hemiplegic migraine (aura and weak)
Migraine with brainstem aura
Retinal migraine
What percent of adults get HA
15% of all adults
21% of US females
10% of US males
Female to male ration migraine
2:1
What races get severe head aches and migraine more
American Indian or Alaska native
White
Black
Hispanic
Native Hawaiian
Asian
Likely migraine risk factors
Analgesic overuse
MS
Oral contraceptives (possible)
Not associated (BP)
Analgesic overuse migraine
Use of analgesics daily or weekly at baseline
Defined as daily or almost daily for ._ 1 month
MS migraine
With and without aura
Episodic syndromes
Recurrent GI disturbances (cyclic vomiting, abdominal migraine)
Vestibular migraine
Benign paroxysmal torticollis
Migraine during pregnancy
Preeclampsia,vascular diagnoses (stroke, MI, PE, HTN, DM, smoking)
Migraine associated conditions
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
Migraine diagnosis POUND
Pulsating Duration 4-72 hours Unilateral Nausea or vomiting Disabling
How may pound criteria née for definite or possible migraine
4/5
How many POUND criteria for likelihood ratio 3.5 for definite or possible migraine
3/5
0-2 pound met
Criteria meta has negative likelihood ratio .41 for definite or possible migraine
Precipitating factors
Menses, perimenstrual
Diet
Fasting Stree, stress alleviation Exertion Altered sleep Visual stimuli Odors Smoking Alcohol Caffeine withdrawal Oral contraceptives Vasodilator Change in weather
Differential diagnosis
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
Cluster headache
More common in men, strictly unilateral, periorbital in 80% of patients, and lasts <1 hour in 54%
Cavernous sinus thrombosis
Associated with fever and periorbital edema
Migrain pathogenesis with aura
Spreading olive is (reduced blood volume) in brain is pathognominic for migraine with aura
Pathogenesis migraine without aura
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
Intracranial pain sensitive structures
Meninges at base of brain
Intracranial blood vessels
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
Dorsal pontine activation demonstrated using positron emission tomographic PET scan in 5 patients with episodic migraine
Cervicogenic HA
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.
Cervical nerves C_-C_ innervate the posterior 1/3 of the head
1-3
Facet pain from C2-3 to c4-5 may refer where
Head
Involvement of C2-3 facet is the most frequent source of
Cervicogenetic HA, accounting for up to 70% of cases
Involvement of AA
Probably the second most common source of cervicogenetic HA, but the true frequency is unknown
Facet pain c50c6 and c60c7
May contribute to a somato-somatic reflex resulting in TrP pain referral to the head
Diagnosis of cervicogenis HA
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
Mgiraine diagnosis
POUND
Tension HA
Bilateral, mild to moderate intensity, pressing or tightening quality, not aggravated by routine physical activity, absence of nausea and vomiting
C2 neuralgia
Paroxysmal sharp or shock like pain centered in the occipital region
Ipsilateral eye lacrimation and conjunctival injection are commonly associated
Neck tongue syndrome
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
