Cervicogenic Headaches Flashcards Preview

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Flashcards in Cervicogenic Headaches Deck (31)
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1
Q

Convergence theory?

A

Convergence of CN V with upper cervical nociception (C0-C3) is possible but has never been empirically demonstrated in humans, only animals (Jull and Niere 2004). Still the favored explanation by most experts.

2
Q

Upper cervical spine and trial treatment?

A

Manual exam of upper c-spine can distinguish CGH from migrain (Zito 1995), but often it is only possible to predict who will respond by trial treatment, but look for early change (should see change in 1-3 sessions)

3
Q

IHS diagnostic criteria for CGH (1988, 2004)?

A
  1. Aggravated by neck movement or sustained postures but patients often have difficulty recognizing aggravating and easing factors (Jull 1997)
  2. Reproduced by pressure over upper cx spine
  3. Ipsilateral neck, shoulder, or arm pain (hard to explain neuroanatomically)
  4. Unilateral pain without side-shift during an episode, as may occur with migraine (CGH can change between episodes)
  5. Start in suboccipital region and spread into occiput, there are some without neck pain though
  6. Head pain characteristics of little value with differential diagnosis
  7. Diagnostic block confirms
4
Q

Outcome measures with CGH?

A
  1. NDI
  2. Frequency, intensity, and duration
  3. FRT (Ogince 2007 = valid): 20 degrees mean FRT for those with CGH, 32 degrees is cutoff. Has 91% sensitivity and 90 percent specificity for identifying CGH from migrain or controls
  4. CCFT with PBU (20-30 mmHg): valid and reliable, 26, 28 mmHg with 10 x 10 sec holds is normal
  5. Neck flexor endurance test (reliability established, but not validity): 30 sec hold
5
Q

Cervicogenic HA’s?

A

Convergence of spinal nucleus of trigeminal nerve and dorsal horns of 1st 3 spinal segments in brainstem is basis of referred head pain. Because much of the head is innervated by trigeminal nerve, it is argued that head pain must involve trigeminocervical nucleus. C1-C3 spinal nerves integrate with TCN and body unable to distinguish origin of this afferent info. Brain interprets activity in TCN evoked by upper cervical stimulation as frontal, periorbital, facial, occipital, or temporal region pain/headache. Afferents from maxillary and mandibular branches have only weak projections to C1-C3, versus dense projections from opthalmic branch, so referral is more common here.

6
Q

What percent of HA’s are cervicogenic?

A

CGH’s account for 15-20% of all chronic and recurrent headaches (Nilsson 1995; Pfaffenrath & Kaube 1990)

7
Q

TTH?

A
  1. Most common primary headache (Schwarts 1998)
  2. Lifetime prevalence 69% men, 88% women (Rasmussen 1991)
  3. IHS (1988,2004): Can last 30 minutes to several days, pain is pressing or tightening, bilateral in location, does not worsen with routine physical activity
  4. Diagnosis based on history taking alone
  5. Systematic review by Lenssnick (2004) concluded there is insufficient evidence to support or refute PT and SMT for TTH.
8
Q

Primary sources of pain in CGH?

A

Bogduk (2005): C0-C3 joints, discs, ligaments, muscles, and dura, as well as local arteries

9
Q

Short definition of CGH?

A

Jull (1997) says CGH’s are those which arise from musculoskeletal impairments in the neck

10
Q

Most likely source of CGH pain?

A
  1. Bogduk (2005) says C2/C3 facet through diagnostic injections
  2. Manual exam suggests C1/C2
    a. Hall and Robinson (2004) had 24/28 subjects with C1/C2 restriction unilaterally
    b. Jull (1997) had 19/20 painful
11
Q

Zito

A

(2006) : Examined 3 groups (CGH, migraine with aura, and controls
1. No difference between head/neck postural angles, PPT, or JPS
2. CGH had significantly less cervical AROM in flex/ext than other groups
3. Pain and hypomobility of C0-C3 was provoked more frequently and to greater extent in CGH group vs. others. All hypomobile joints were not necessarily painful but all painful upper cervical joints were hypomobile (is it really about hypermobility)
4. Significantly more muscle tightness with CGH group
5. CGH group demonstrated poorer performance on CCFT at 26, 28, and 30 mmHg
6. Upper cervical joint dysfunction principally at C1/C2 segment on PPIVM testing was able to discriminate CGH from migrain/control with sensitivity of 80%

12
Q

Impairments seen with CGH?

A

Jull (1997): The following should be present and their absence would indicate that HA likely not CGH

  1. Pain (familiar) on upper cervical palpation
  2. C0-C3 dysfunction on PPIVM/PAIVM
  3. Decreased DNF endurance or synergy
  4. Decreased lower trap and serratus control
  5. Decreased cervical JPS
13
Q

Trigeminal Nerve?

A

Crossman and Neary (2000):

  1. CN V
  2. Main sensory nerve of scalp, face, cornea, oral/nasal cavities, and cranial dura mater
  3. Proprioceptive pathway for muscles of mastication and TMJ (auriculotemporal branch from mandibular branch of trigeminal nerve supplies TMJ)
  4. Motor supply to muscles of mastication by mandibular branch (masseter, temporalis, pterygoids)
14
Q

Neurodynamic Headache?

A
  1. Von Piekartz (2006) found 36 degrees neck flexion during long sitting slump for CGH patients 6-12 y.o.
  2. Shacklock (2005) and Jull (2002) would argue approximately 10% of CGH’s have neurodynamic component.
  3. Do symptoms change with distal tension or shoulder abduction and then flexion upper cervical spine
15
Q

Other afferents with TCN?

A

Trigeminal nerve also innervates nasal/oral cavities, teeth, paranasal sinuses, and dura mater of anterior and posterior cranial fossa. CN VII, IX, and X also innervate the ear, pharynx, and larynx. Therefore, any of the structures innervated by these CN’s or C1-C3 spinal nerves can become a source of headache.

16
Q

Niere and Robinson

A

(1997): Significant reduction in HA frequency, duration, and intensity. 62 out of 91 subjects indicated HA’s improved more than 50% because of SMT. HA frequency may be most valuable as indicator of treatment effect rather than intensity or duration.

17
Q

Haas (2004)

A

Patients allocated to 1, 3, or 4 visits for 3 weeks receiving HVLAT, STM, TrP therapy, and heat for CGH. 9-12 treatments better than 3 total, was also better than 1 visit per week. Larger doses better for CGH.

18
Q

Peri-orbital trochlea?

A

Fernandez-de-las-penas (2005) found TrP’s in superior oblique muscle that would evoke pain patterns in patients with TTH. Pain could be:

  1. Deep within eye
  2. Retro-orbital
  3. Supraorbital
  4. Homo-lateral forehead
19
Q

When was CGH 1st introduced?

A

Introduced as a term by Sjaastad in 1983.

20
Q

Other characteristics of CHG?

A
  1. Female 4:1
  2. Unlike migraines, no familial tendency
  3. History of head or neck trauma or increase in sedentary nature
  4. May present with nausea, phonophobia, photophobia, dizziness, blurred vision, swallowing difficulties, or periocular edema (Jull and Niere 2004) but they are not dominate features as in migraine or cluster HA’s
21
Q

Evidence for SMT in CGH?

A

Cochrane review (Bronfort 2005) showed SMT and low intensity endurance training effective for CGH. For migraine it has similar effect as amytryptyline but less effective than amytryptyline for TTH’s.

22
Q

Which CGH patients will respond?

A
  1. Jull (2002): 24% of those diagnosed with CGH didn’t respond to SMT and/or exercise
  2. Jull and Stanton (2005): found age, high intensity, and chronicity not suggestive of poor outcome
  3. Niere (1998): found low frequency suggestive of poor outcome, high frequency suggestive of good outcome
  4. Don’t treat dogmatically just based on IHS criteria
23
Q

Differential diagnosis of CGH?

A
  1. Success of treatment depends on patient having condition for which treatment is being administered
  2. Xiaobin (2005)
    a. Occipital/cervical/facial pain and tension of neck and shoulders also commonly occur in TTH and migrain, they aren’t specific to CGH
    b. No specific test for migraine, rather, its diagnosis is largely based on clinical observation, namely patient’s history and physical exam
  3. Mixed headache presentations are common (migraine and CGH coexisting) and symptoms for CGH, TTH, and migraine often overlap. Therefore, if meds for migrain only offer partial relief, check upper cervical spine.
24
Q

Jull

A

(2002): 200 subjects with CGH got meds only, MT alone (manip and/or mob), exercise (CCFT and SA/LT exercises), or combination of MT + Exercise for 8-12 sessions over 6 weeks. All significantly reduced HA frequency, intensity, and Northwick scores compared to controls at 6 weeks, 3,6, and 12 months. No evidence that combined treatment better than either alone for HA frequency or intensity. Median medication intake at 12 months decreased 93-100% for all 3 interventions but increased 33% in controls. Treatment that included exercise performed better on CCFT at 6 weeks and 12 month follow up. Also, Hides (1996) showed MT failed to improve performance on DNF test, despite pain relief.

25
Q

Value of C1/C2 flexion-rotation test?

A

Hall and Robinson (2004): Compared 28 CGH patients with 28 asymptomatic. 24/28 CGH patients had positive FRT (32 degree cutoff) and C1/C2 as dominant symptomatic motion segments. Other 4/28 CGH found to have C2/C3 as dominant symptomatic motion segment and had negative FRT. All 28 asymptomatics had negative FRT. AROM in cardinal planes no different among groups (adjacent levels compensate). Average FRT was 44 degrees to each side for controls and 28 degrees towards headache side in CGH group. Pearson’s correlation indicated the greater the restriction with FRT, the more severe the headache. C1/C2 by far most frequent symptomatic segment (Agrees with Jull 1997, contrasts Bogduk 2005 = C2/C3)

26
Q

Trigeminocervical Nucleus?

A

Crossman and Neary (2000): located in the midbrain with 3 sub-nuclei with segregated distribution of afferent fiber termination
1. Principle sensory nucleus (touch/pressure)
2. Mesencephalic nucleus (proprioception)
3. Spinal nucleus (pain/temperature) - this descends from the pons through the medulla, to the upper cervical spine
Bogduk (2005): The entire column of grey matter that receives trigeminal and cervical afferents is the trigeminocervical nucleus. The spinal nucleus of the trigeminal nerve and the dorsal horms of 1st 3 cervical spine segments converge in the brainstem. Fibers of the trigeminal nerve descend through the brainstem, forming the spinal tract of the trigeminal nerve and terminate in the grey matter of the upper 3 cervical segments. Trigeminocervical nucleus also receives afferents from CN VII, IX, and X.

27
Q

Additional sources of CGH pain?

A
  1. T1-T4 supplies sympathetic efferent outflow for head, face, and neck
  2. Myofascial TrP’s (UT, SCM, splenius cap/cerv, occipitofrontalis, temporalis, semispin. cap, OCS
  3. GB-20 (major headache acupoint - semispinalis capitis)
  4. Superior oblique muscle
28
Q

Systematic reviews for CGH

A
  1. Astin and Ernst (2002) and Vernon (1999) looked at RCT’s for SMT of multiple HA types. Astin and Ernst only used 1 RCT for SMT for CGH (Nilsson 1997) and Vernon used 2 studies by Nilsson (95 and 97) where subjects and data overlapped, so they both really only used 1 RCT.
29
Q

RCT’s on CGH

A
  1. Nilsson (95 and 97)
  2. Jull (2002)
  3. Haas (2009, 2010, 2010)
30
Q

Nilsson (95 and 97)

A

(1995) : 39 patients with CGH. 1/2 got cervical HVLAT and other 1/2 low level laser and deep friction massage. 2x/week for 3 weeks. From week 2 to 6 there was decrease in analgesic use/day, HA intensity, and number of HA hours/day in SMT group but group difference was not statistically significant
(1997) : Same premise as 1995 study but now with 53 subjects. Outcomes at 1 week after showed statistically significant decrease in all of those 3 previous outcomes.

31
Q

Haas (2010)

A

RCT looking at efficacy of SMT of CGH. Looked at 8 vs. 16 sessions of HVLAT to both cervical and thoracic spine over 8 weeks. Found no difference in HA pain and disability between 8 and 16 treatments sessions. Found clinically and statistically significant differences between HVLAT and light massage/hot pack groups. All subjects in 2 HVLAT groups also got hot packs and massage.