Cervicogenic headaches and cervical stability retraining

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Information about Cervicogenic headaches and cervical stability retraining

Published on November 6, 2012

Author: seandadswell

Source: slideshare.net

Cervicogenic Headaches and Cervical Stability IST By Sean Dadswell October 2008

AimIncrease knowledge of physiology, diagnosis and treatment of cervicogenic headaches with specific attention to cervical stability.

Content• Overview of • Diagnosis headaches • Treatment• Types and • Specifically Cervical Classification spine stability training• Prevalence (theory and practical)• Aetiology• Cervicogenic headache mechanism• Clinical features

Headaches• Effect about 90% population at some time• Arise from nocioceptive input from head and structures that refer to the head• CNS dysfunction (processing and perception)• Many different types with a lot of overlap particularly cervicogenic, migraine and tension type

Classification• 1988 Headache Classification Committee of the International Headache Society (IHS) produce Classification and Diagnostic Criteria for Headache Disorders, Cranial Neuralgias and Facial Pain• 13 Categories including headaches and facial pain associated with neck pain• 2004 Cervicogenic headache (CGH) published in revised international classification as discrete headache type by IHS• Progressively increasing body of evidence relating to CGH particularly with manual and physical therapies

Definition• “Headache that can be characterised symptomatically as a unilateral or unilateral dominant headache, without side shift, associated with ipsilateral neck, shoulder or arm pain. Pain begins in the neck and headache is aggravated by neck movements or postures.” (Sjaastad et al1998)• Controversial as IHS contend these are not unique to CGH• Symptom overlap major problem in differential diagnosis

CGH Classification• Sjaastrad et al 1998 developed specific CGH diagnostic criteria1. S&S of Neck involvement – Pain precipitation with: • Csp movement or sustained posture • External pressure over upper Csp or occipital region – Restricted Csp ROM – Ipsilateral Csp, shoulder or arm pain1. Confirmatory evidence by diagnostic block2. Unilaterality of head pain, without side shift3. Head pain Characteristics • Mod/severe, non throbbing and non lancinating pain • Episodes of varying lengths • Fluctuating continuous pain

CGH classification cont.1. - Marginal effects or lack of effect of idomethician, ergotamine or sumatriptan - Female sex - H/O Csp or head trauma (of medium severity)1. Various attack related S&S - Nausea, photo/phonophobia, dizziness, ipsilateral blurred vision, dysphagia, ipsilateral oedema This is a reliable classification but user should be aware that there may be difficulty with differential diagnosis of CGH and tension headache (Jull & Niere, 2004)

Prevalence and Effect• Often related to head/neck injury• Estimated 0.4-2.5% Population• 13.8-20% patients with chronic headaches• Mean age 42.9 (no age limit)• Female/male ratio 4:1• Reduced quality of life• Greater loss of function than other headache disorders(Biondi 2005; Jull et al 2004)

AetiologyPossible theory:• Any MSK structure innervated by upper 3 cervical nerve roots• Afferent input from these interact with the Trigeminal nucleus caudalis (region of the upper cervical spinal cord)• Functional convergence of upper csp and trigeminal sensory pathways allows bidirectional referral of pain sensations between the neck and trigeminal sensory receptive fields of the face and head.• This area is called the trigeminocervical nucleus• Different levels of excitation lead to different levels of pain• Excitation regulated by areas such as the hypothalamus using serotonin and noradrenaline

1. Falx cerebri2. Capsula interna3. Tentorium cerebelli4. Corpus callosum5. Sinus frontalis6. M. orbicularis oculi7. M. nasalis8. Ductus parotideus9. Nervus facialis/ Rami buccales10. N. alveolaris inferior11. N. lingualis12. A. facialis13. Glandula submandibularis14. Ansa cervicalis profunda15. N. vagus16. A. occipitalis17. N. occipitalis major18. M. digastricus/ Venter posterior19. Porus acusticus externus20. M. stylohyoideus

1. M. rectus capitis posteriorminor2. M. semispinalis cervicis3. M. longissimus cervicis4. M. rectus capitis posteriormajor5. M. obliquus capitis superior6. A. occipitalis7. N. occipitalis minor8. Ramus dorsalis C III9. M. obliquus capitis inferior10. A. vertebralis

(Aetiology cont.) “ Vicious Circle” Peripheral Peripheral sensitisation and nocioception dysfunction Central sensitivity

Why does this effect Diagnosis?• Other headache types cause sensitisation of Trigeminocervical Nucleus (migraine and Tension type)• Leading to MSK dysfunction as secondary effect of headache (into vicious circle)• Consider biopsychosocial approach to treatment

Dermatome Distribution of the Trigeminal NerveThe trigeminal nerve is the largest of the cranial nerves. Its name derives from thefact that it has three major branches: the ophthalmic nerve (V1), themaxillary nerve (V2) and the mandibular nerve (V3). The ophthalmic and maxillarynerves are purely sensory. The mandibular nerve has both sensory and motor functions.(http://en.wikipedia.org/wiki/Trigeminal_nerve, 2006)

Clinical Features(Additional to those in the classification)• Unilateral, but can be bilateral with one side dominant• Not band like or whole head• Side consistent• Associated with csp or occipital pain (good indicator if csp pain prior to headache)• Little relationship of area of pain and segmental dysfunction• Variable intensity even within headache phase• Other symptoms can be nausea, lightheadedness or dizziness but are more common and frequent in migraine and cluster

Features cont.• Onset and duration can help differentiate.• CGH usually related to sustained or awkward csp postures• Other headaches can have typical pattern• Stress related• Difficulty with aggs and eases• Trauma(Jull 1997)

Diagnosis• Clear History to exclude serious pathology• Red Flags: Severe sudden onset with photophobia, csp stiffness, nausea and vomiting => ? Subarachnoid Haemorrhage Aneurysm can leak for hours/days/weeks and be related to exertion or injury• Tumour: changing symptoms, progressively worsening, abnormal neuro• Infection ie. Meningitis: Worst headache of life, associated with fever• CVA/subarachnoid: Changing neuro• Giant cell arteritis: tenderness templesIf in doubt of pathology get it checked especially if not progressing

Diagnosis cont. (Biondi 2005, Jull 1997, Jull & Niere 2004)• 3 System: Articular, Muscular/neuromotor and nervous systems• Tests appropriate to 3: – Posture – Active movements considering range, pattern, control and pain – Pay attention to any movement that provokes headache( likely ext or ext with rotation)• Articular system – Best assessed manually (multiple studies) • Aiming for provocation of pain and muscular reaction – Active ROM can be unreliable• Muscular system – Trigger points – Neck and scapular musculature important – Stability (particularly important in upright position)

Diagnosis cont.• Nervous system – Pain sources when irritated mechanically or inflammed – C2 or C3 compression linked to CGH – Dura mater of upper csp and post crainial fossa supplied by ventral rami of upper 3 csp nerves therefore => CGH – Digital pressure to greater occuipital nerve – Closely linked to muscular activity• Presence of articular and/or muscular impairment for CGH is mandatory not neck pain alone

Diagnosis contMedical Diagnosis:• Imaging: can not confirm CGH but can support diagnosis or offer differential diagnosis ie MRI shows equal amounts of pathology in symptomatic and controls van der Velde et al 2008)• Bloods: for systemic diseases that may contribute (RA, Lupus etc)• Blocks: Zygapophyseal joint, cervicle nerve or medial branch blockade (can predict treatment modalities)• Be aware all jts between C0/1, C1/2 and C2/3 can refer to head.• C2/3 very susceptible to “whiplash”• Occuipital neuralgia false localisation with nerve block• Trigger point anaesthetic injestions (can assist in diagnosis and theraputic management

Treatment Increasing evidence base all treatments recommended by Cochranes Systematic Review,2006• Multifaceted• Pharmacological• Manual/Physiotherapy• Anaesthetic• Surgical• Psychosocial

Pharmacological Treatment• No standard protocol or guidelines• Does not provide good relief when used independantly• Aim to increase participation in rehab• Requires regular re evaluation• Antidepressants: increase serotonin etc inhibition• Antiepileptics: Modulate peripheral and central pain transmission• Analgesics: NSAIDs or simple analgesics can be used as scheduled meds (COX-2 can be used to reduce effects of long term NSAID use)

Pharamacology treatment cont• Narcotics: rarely used except to increase compliance with manual treatment• Muscle relaxants: especially with central activity i.e. baclofen. Botox into cervical and peri cranial musculature

Manual/Physiotherapytreatment• Combination has optimum outcome but both superior long term outcome than control• Exercise programmes need to be ongoing• Csp manipulation• Trigger points• Csp stability exercises• Joint mobilisations• METs• Some evidence forcsp manual traction

Anaesthetic and surgical treatment• Cervical epidural steroid injection (multi level degeneration)• Occipital nerve blocks (indicator for surgical liberation or transection)• Cervical nerve, medial branch or Zygapophyseal jt blockade (indication for neurolysis)• Triggerpoint injections

Biopsychosocial treatment• Relaxation• CBT• Psychotherapy if chronic pain has prominent behavioural component

Cervical Stability: Introduction• Csp function: – 3D movements – Load distribution (head and upper limbs) – Mechanical stability in any orientation – Linked with vestibular and proprioceptive systems• Structure: – 20% stability osseoligamentous (end range) – 80% Muscular (dynamic through range) – When pathology effects ligs and jts muscular control even more important

Cervical stability cont• Superficial muscles (SCM, scalenes) => movement but have buckling effect on csp• Deep neck flexors (deep longus colli, longus capitus) supply segmental stability (along with deep extensors)• Chronic csp pain => reduced strength and endurance of all csp muscles (Silverman et al 1991, Vernon 1992, Watson & Trott 1993 ref in Jull 1997)• Occurs early in painful neck regardless of onset• Does not recover with resolution of pain• Neck extensors also important (as work in co contraction with flexors) but min research as yet• Scapular stability important for posture and load transfer (Serratus ant, traps and levator scap)

Clinical Examination(Examination & treatment programme supported by Jull et al 2002)• Muscle control in posture – Pattern of postural correction to upright “neutral” posture – Orientation of scapulae in upright posture• Analysis of movement patterns – Pattern of cervical extension and return to upright – Pattern of scapular muscle activity and control with arm movements• Specific muscle tests – Craniocervical flexion test – Scapular retraction/depression test• Muscle length testing – Axio-scapular-girdle muscles

Clinical examination cont.• Range of movement – All usual ROM – Cervical Flexion Rotation test – Identifies upper csp dysfunction (specificity and sensitivity above 90%) (Ogince et al 2007)

Pattern of postural correction to “neutral” andscapular orientationPatient asked to sit upright from relaxed positionWhat to look for:• Should start by gaining pelvic neutral not thoracolumbar ext• T and C sp posture should follow good pelvic neutralScapular positioningWhat to look for:• Neutral posture if not neutral therapist should position pt then ask them to maintain this (pay attention to muscle activity)• Pt should then be asked to regain this position

Analysis of movement patternsActive Csp ext and return to upright (tests deep flexor eccentric then concentric control) What to look for: (neutral to ext) – Pt not willing to move head posteriorly=> upper csp ext only – Pts head moves backwards but reduced flexor activity => drop or backwards translation loading osseoligamentous structures (ext to neutral) – Should be craniocervical flexion initiated not lower csp with use of SCM and ant scalenes

• Scapular activity – Observe levator scap, upper traps, serratus ant SCM and scalene activity during: – Low load activity without significant shoulder flex – Through repeated elevation of shoulder

Treatment• Aim to reduce any Csp dysfunction• Restore ROM!!!!• C1-2 SNAGs – Performed 2 x day (3 sets 6 reps) (Hall et al, 2008)

Craniocervical flexion (CCF) test• 2 Stages – Stage 1: CCF done to 5 increments – Stage 2: CCF Test of holding capacity• Both performed in crook lying – Forehead and chin level horizontally – Horizontal line from tragus should bisect csp – Pressure biofeedback put in and inflated to 20mmHg – Correct movement taught (gentle nod of head)• Stage 1: pt to increase pressuse in 2mmHG increments upto 30mmHg• Stage 2: pt to hold each increment for 10 seconds 3 repsALWAYS WATCH SCM/SCALENE ACTIVITY IS NOT DOMINANT

Testing and rehab• CCF rehab should be done twice a day at level where pt can maintain good pattern• Should do 10 reps 10 sec hold then progress to next increment• Should be achieved over 4-6 weeks possibly up to 12 for difficult pathology• Once improvement made progress to ext in sitting/standing (done in pain free range)• Progressed by increasing range then adding isometric holds through range

Rehab cont• Craniocervical extensors rehab. – Eccentric flexion followed by concentric ext – Sitting followed by four point kneeling (can incorporate scapular positioning – Progression isometric rotation to encourage co- contraction – Final progression lifting head off bed (beware of upper csp ext secondary to SCM dominance)• Scapular repositioning and retraining – In sitting coracoid away from hand over pecs – Done with small to large sh flex increasing weight and reps – Serratus training (on elbows or against wall)• Postural training

Scapular retraction and depression• In prone, arms by side, pt asked to maintain position of scap neural set by physio• Watch for inappropriate movement or loss of position• Common dysfunctions: – Elevation (levator scap) – Downward rotation (rhomboids) – Arm add and ext (lat dorsi) – Winging (serratus) – Unable to gain passive position (tight pecs)• Muscle lengths should also be tested and treated where appropriate.

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