Cervicogenic Headaches Flashcards
Convergence theory?
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.
Upper cervical spine and trial treatment?
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)
IHS diagnostic criteria for CGH (1988, 2004)?
- Aggravated by neck movement or sustained postures but patients often have difficulty recognizing aggravating and easing factors (Jull 1997)
- Reproduced by pressure over upper cx spine
- Ipsilateral neck, shoulder, or arm pain (hard to explain neuroanatomically)
- Unilateral pain without side-shift during an episode, as may occur with migraine (CGH can change between episodes)
- Start in suboccipital region and spread into occiput, there are some without neck pain though
- Head pain characteristics of little value with differential diagnosis
- Diagnostic block confirms
Outcome measures with CGH?
- NDI
- Frequency, intensity, and duration
- 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
- CCFT with PBU (20-30 mmHg): valid and reliable, 26, 28 mmHg with 10 x 10 sec holds is normal
- Neck flexor endurance test (reliability established, but not validity): 30 sec hold
Cervicogenic HA’s?
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.
What percent of HA’s are cervicogenic?
CGH’s account for 15-20% of all chronic and recurrent headaches (Nilsson 1995; Pfaffenrath & Kaube 1990)
TTH?
- Most common primary headache (Schwarts 1998)
- Lifetime prevalence 69% men, 88% women (Rasmussen 1991)
- 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
- Diagnosis based on history taking alone
- Systematic review by Lenssnick (2004) concluded there is insufficient evidence to support or refute PT and SMT for TTH.
Primary sources of pain in CGH?
Bogduk (2005): C0-C3 joints, discs, ligaments, muscles, and dura, as well as local arteries
Short definition of CGH?
Jull (1997) says CGH’s are those which arise from musculoskeletal impairments in the neck
Most likely source of CGH pain?
- Bogduk (2005) says C2/C3 facet through diagnostic injections
- 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
Zito
(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%
Impairments seen with CGH?
Jull (1997): The following should be present and their absence would indicate that HA likely not CGH
- Pain (familiar) on upper cervical palpation
- C0-C3 dysfunction on PPIVM/PAIVM
- Decreased DNF endurance or synergy
- Decreased lower trap and serratus control
- Decreased cervical JPS
Trigeminal Nerve?
Crossman and Neary (2000):
- CN V
- Main sensory nerve of scalp, face, cornea, oral/nasal cavities, and cranial dura mater
- Proprioceptive pathway for muscles of mastication and TMJ (auriculotemporal branch from mandibular branch of trigeminal nerve supplies TMJ)
- Motor supply to muscles of mastication by mandibular branch (masseter, temporalis, pterygoids)
Neurodynamic Headache?
- Von Piekartz (2006) found 36 degrees neck flexion during long sitting slump for CGH patients 6-12 y.o.
- Shacklock (2005) and Jull (2002) would argue approximately 10% of CGH’s have neurodynamic component.
- Do symptoms change with distal tension or shoulder abduction and then flexion upper cervical spine
Other afferents with TCN?
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.
