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Headaches Lecture Flashcards

1
Q

Primary vs. Secondary headache disorders

A

Primary — have a pathomechanical process not caused by other diseases or disorders

Secondary — headaches caused by other disorders (something else referring pain to the head)

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2
Q

What examples of the primary vs. Secondary headaches

A

Primary — migraine and tension type headaches

Secondary — cervicogenic, TMD, occipital neuralgia, post-traumatic headaches

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3
Q

What is SNOOP4

A

S: systemic symptoms
N: neurological
O: onset sudden — peaks within 1 minute onset.
O: onset after the age of 50 years
P: Pattern change
4: progressive HA/increasing frequency, precipitation by valsalva/sex, postural aggravation, papilledema

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4
Q

Red flag items from the history

A
  1. History of mechanical trauma
  2. Recent respiratory or GI infection
  3. Neurological or ischemic syndrome
  4. Referral patterns from vertebral artery or internal carotid artery
  5. Neuro or ischemic signs and symptoms including balance deficits
  6. Jolt accentuation of HA is a new/less well-recognized physical exam which assesses meníngeas irritation
  7. Lhermitte’s sign
  8. Vertebral artery test
  9. Horner’s syndrome
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5
Q

Referral patterns for internal carotid and vertebral artery

A

Internal carotid artery — sudden intense temporal headache and neck pain

Vertebral artery — unilateral neck/upper trap type pain

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6
Q

Key features of Horner’s syndrome

A
  • Decreased pupil size
  • Ptosis
  • Decreased sweating on the affected side of the face
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7
Q

Most common encountered primary headache

A

Tension type

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8
Q

Description of tension type HA

A
  • Peripheral sensitization of nociceptors in myofascial tissue
  • Increased muscle tenderness (contributory but not causative)
  • Chronic TTH = occurs >/= 15 days per month for >3 months, altered pain sensitivity and central pain modulation
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9
Q

Diagnostic criteria for TTH

A
  1. > 10 episodes fulfilling B-D
  2. HA lasting 30 minutes to 7 days
  3. At least 2 of following
    — bilateral location
    — pressing or tightening (not pulsating quality)
    — mild-mod intensity
    — not aggravated by routine physical activity
  4. Def both of following
    — no N+V
    — no >1 of photophobia or phenophobia
  5. Not better accounted fro by another ICHD-3 dx
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10
Q

What is frequency criteria for chronic TTH

A

> 15 days / month for > 3 months

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11
Q

Medical management for TTH

A
  • Acute management - analgesic meds, or analgesic plus caffeine, muscle relaxers
  • Preventative - tricyclic antidepressants, beta-blockers, and divalproex sodium
  • TrP injections — usually in SCM, UT, temporalis, typically using lidocaine and bupivacine
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12
Q

Manual therapy for TTH

A
  • Thrust and non-thrust spinal mobs/manips
  • mobilization with movement
  • STM/IASTM
  • dry needling — really really strong evidence
  • everything you would treat myofascial dysfunction
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13
Q

Exercise and education for TTH

A
  • Posture and ergonomic adjustment
  • Stretching
  • Postural strengthening
  • Neural mobilization exercises
  • if patients have chronic TTH they need education and PNE
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14
Q

Description of migraine headache

A
  • Stimulation of peripheral afferents int he trigeminocervical complex (all branches of TN, posterior dura, and C1/2 dermatomes)
  • Up to 70% report neck pain
  • Pathophysiology is complex and unclear but may have genetic abnormalities that increase CNA excitability
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15
Q

Prevalence for migraine headaches

A

Peak prevalence woman is 20-60 yo

Peak prevalence men is 30-40 yo

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16
Q

What are 4 phases of migraine

A
  1. Prodrome — days or hours heading up to headache.
  2. Aura — know its coming any minute. Changes in vision, numbness/tingling, difficulty speaking or understanding others.
  3. Headache — actual headache and key for diagnostic criteria
  4. Postdrome — when it goes away but you still feel crappy, fatigue/lightheadedness/decreased energy
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17
Q

Potential mechanism for prodrome

A

Thought to be due to hypothalamic activation

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18
Q

Potential mechanism for aura

A

Thought to be due to cortical spreading depolarization which often begins in the visual cortex

19
Q

Potential mechanism for HA pain

A

Vasodilation and/or sural swelling thought to be due to release of neurotransmitters such as Substance P, neurokinin A, CGRP

20
Q

Potential mechanism for postdrome

A

Mechanism less well understood

21
Q

What is CGRP

A

Calcitonin gene-related peptide
- Neuropeptide found in CNS and PNS that has pain-signaling and vasodilator functions
- In MH it is thought to contribute to dural meníngeas inflammation

22
Q

Diagnostic criteria for migraine without Aura

A
  1. > 5 attacks fulfilling B-D
  2. HA lasting 4-72 hours (untreated or unsuccessfully treated)
  3. At least 2 of following
    — unilateral location
    — pulsating quality
    — moderate-severe intensity
    — aggravated by (or causes avoidance of) routine physical activity
  4. During attack at least 1 of following
    — N and/or V
    — photophobia and phonophobia
  5. Not better accounted for by another ICHD-3 dx
23
Q

How are migraines different from other headaches

A
  1. Lasting 4-72 hours
  2. Unilateral location
  3. Pulsating quality
  4. Moderate to severe intensity
  5. Aggravated by physical activity
  6. Association with nausea, vomiting, phonophobia, or photophobia
24
Q

Acute medical management for migraine headaches

A
  1. Ergot alkaloids — similar MOA but not as selective as Triptans. Higher incidence of AEs
  2. Triptans — selective serotonin receptor agonists (high affinity for the 5-HR1B/D receptors.
    — vasoconstriction of distended intracranial extra cerebral vessels
    - inhibits vasoactive neuropeptides and nociceptive neurotransmitters
25
What are abortive migraine meds
- Abortive treatments work to stop a migraine attack as its happening, while preventive treatments aim to prevent additional migraine attacks - Patients should take absorptive meds ASAP hopefully within 30 minutes of headache onset, and may need to bring their meds to PT in case a headache is triggered - Triptans are first-line absorptive treatments for moderate-severe migraine bu less effective in patietns with prolonged and severe migraines.
26
Signs of medication overuse for HAs
Almost 1/2 of patients with chronic HA have med overuse history - Triptans should not be used >10 days/month !!!!!
27
Advances in MH medical management
- Recent pharma advances in CGRP receptor antagonists - game changer for migraine sufferers. Brings the frequency of migraines down in the month
28
Chronic MH medical management
Botox A has been shown to reduce the number of HA days/months by 8-9 days - Helps bring sensitivity down. Once sensitivity is down then PT is a must after that
29
What are HA management strategies
1. Management of HA triggers 2. Medical management often multidisciplinary 3. Management of associated symptoms 4. Management of MSK impairments 5. Exercise considerations — need to reintroduce SLOWLY
30
What are HA triggers
- dietary triggers = dehydration, fasting, alcohol, cured meats, aged cheese, citrus, chocolate, caffeine, wine, high sodium, MSG - poor sleep hygiene and quality - stress
31
Examples of management of associated symptoms
1. Reduced Lightning or dark room 2. Altered lighting source 3. Blue light screen or glasses 4. Dry eye control 5. Noise cancelling headphones or earplugs
32
Manual therapy for MH
1. Thrust and non thrust spinal mobs/manips 2. Mobilization with movement 3. STM/IASTM 4. Dry needling
33
Exercise for MH patients
- Altered cervical muscle motor control - Stretching - Aerobic exercise
34
Typical exercise prescription
40-60 mintues of exercise 2-3 times/week with 15-30 minutes of aerobic exercise RPE 14-16/20 or 70% HRmax but not > 150 bpm BUT HAVE TO BUILD TO THIS
35
What are some dietary supplements for migraine prevention
Magnesium (400-800 mg) Riboflavin (400 mg) Coenzyme Q10 (300 mg)
36
Description of cervicogenic headaches
- Convergence of cervical (C1-3) and trigeminal afferents in the brainstem and spinal cord (C1-4) - High incidence post WAD *brain doesn’t know where the signal is coming from whether its upper spinal nerves or trigeminal nerves but most of the time with CGH its from upper cervical nerves*
37
Referral patterns for C0-C3
Look at slides
38
Diagnostic criteria for CGH
1. Any HA fulfilling C 2. Clinical and/or imaging evidence of Cx spine disorder or soft tissues of the neck known to cause HA 3. Evidence of cessation by at least 2 of following — HA developed in tempral relation to onset of Cx disorder — HA significantly improved or resolved in parallel with improvement in Cx disorder — Reduced Cx ROM and HA worsened with provocative maneuvers — HA abolished with diagnostic block 4. Not better accounted fro by another ICHD-3 dx
39
Major criteria for CGH
1. S/S of Cx involvement 2. Precipitation of HA by: neck movement and/or sustained awkward positioning, and/or external pressure ipsilateral upper Cx spine or occipital regions 3. Restriction of Cx ROM 4. Ipsilateral neck, shoulder, or arm pain OTHER CHARACTERISTICS — moderate/severe, non-throbbing, non-lancinating pain typically starting in the neck, of varied duration — marginal effects of income that in, ergo to mines, or triptans — can have photophobia, phonophobia, or nausea, but not as marked as MH
40
Medical management of CGH
1. PT - GOLD STANDARD 2. Analgesics 3. Peripheral nerve blocks of greater and lesser occipital nerves 4. TrP injections typically using lidocaine and bupivacaine
41
Manual therapy for CGH
1. Thrust and non-thrust spinal mobs/manips 2. Mobilization wiht movement 3. STM/IASTM 4. Dry needling
42
Exercise and education for CGH
1. Posture and ergonomic adjustment 2. Craniocervical flexion endurance 3. Stretching 4. Postural strengthening 5. Neural mobilization exercises
43
Gold standard special test for CGH
Cervical flexion rotation test
44
Overall what are the most common headaches seen by PT
1. Migraine headaches 2. Tension type 3. Cervicogenic

Advanced MSK (7 decks)

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