Physio Charlie - cx

New website!!

noreply@blogspirit.com (PhysioCharlie) — Mon, 09 Mar 2009 19:22:00 +0100

I have a new website!!

http://physiocharlie.vpweb.co.uk

Junior Supervision

noreply@blogspirit.com (PhysioCharlie) — Fri, 21 Nov 2008 10:51:00 +0100

Yesterday I took supervision with my junior on Cx clinical reasoning.

We looked at two sets of notes then did some practical:

Notes 1. 26 yr old female, RTA 3/12 ago when she fell of her motorbike. Injury to L sh and bilat wrists.

Sx: RTA details need to expand ie. speed? any LOC? to A+E in ambulance? wearing helmet? X-rays of wrists, sh, Cx? where was RTA in UK or Poland?

Body Chart: Need Constant or I/M defining ie. 0-8/10 or 8-10/10. 24 hr; which pain has a pattern? 5 D's, 3 N's

Ox: AROM Sh: Flx FROM Pa @ EOR or T/O ROM. PROM L rot if decreased = capsular pattern, Sp tests: VBI/ Alar/ Transverse Lig// NAD. Palpn: Trp's in upper traps, get position correct for Cx palpn. Passive sh girdle elevation with and without Cx L or RSF = ? upper traps or Cx origin of pain

C-spine fractures following falls in older patients

noreply@blogspirit.com (PhysioCharlie) — Fri, 14 Nov 2008 13:46:44 +0100

http://www.trauma.org/index.php/main/case/705/

Cx instability

noreply@blogspirit.com (PhysioCharlie) — Tue, 04 Nov 2008 15:20:00 +0100

Cervical instability by S Easton

ANATOMY AND BIOMECHANICS

¢The dens, anterior arch of atlas and the transverse ligament are the primary anteroposterior stabilizers of the atlantoaxial segment with the alar ligaments acting as secondary restraints.

¢The principle role of the ligament is to prevent the atlas from translating anteriorly on the axis during flexion.

¢ The structures that may be compromised include the upper spinal cord, the medulla, the vertebral arteries, the superior sympathetic ganglia positioned over the anterolateral aspects of the axis.

ATLAS and AXIS

¢Commonly known as C1 and C2.

¢Atlas AKA “the cradle”

¢Articulates with the occipital condyles

ATLANTO-OCCIPITAL JOINTS

Flexion and extension primarily occurs here 15-20 deg

Upper cervical instability

¢Most commonly affects atlanto-axial joint

¢Instability may compromise vascular and neurological structures

¢Instability is detected through pathology, i.e symptoms

¢Transverse and alar ligaments involved

ALAR Ligament

¢Alar ligament injury is a relatively common occurrence in post-whiplash victims with frequently both ligaments being injured. The numbers of the grade 1 injury might be exaggerated by non-whiplash causes but the grade 2 and 3 injuries seem to be the result of whiplash.

¢Insufficiency of the alar ligament will produce and increase the average contralateral rotation at the atlantoaxial joint by up to 30% or almost 11 degrees. Mechanical dysfunction of this region, either due to alar ligament, odontoid process or transverse ligament insufficiency, has been shown to be a factor in the production of vertigo and associated symptoms possibly by occlusion of the vertebral artery.

¢Partial or complete tears of the alar ligament, generally, are not an immediate serious danger to the patient’s Life.

CARDINAL SIGNS

¢Overt loss of balance with relation to head movements

¢Facial lip paraesthesia reproduced by active or passive neck movements

¢Bilateral or qudrilateral limb paraesthesia either constant or reproduced by neck movements

¢Nystagmus produced by active or passive neck movements

PHYSICAL TESTS

¢The Sharp-Purser Test

¢The patient is asked to flex the head and relate to the examiner any signs or symptoms that this might evoke.

¢ Local symptoms such as soreness etc. are ignored for the purposes of evaluating the test.

¢ If no cardinal symptoms are provoked, the test is discontinued.

¢However, if cardinal symptoms are provoked a provisional assumption is made that they are caused by excessive translation of the atlas compromising one or more of the sensitive structures listed above.

¢ The assumption is tested when the examiner employs one of two methods of reducing the potential anterior translation.

¢ With the flexed position maintained, either the forehead can be stabilized and the axis manually translated anteriorly, or the axis can be stabilized and the head translated posteriorly with pressure against the forehead. In either case, the segmental effect is the same. The dens is either relatively or actually moved anteriorly out of the spinal canal.

¢ If the anterior excessive translation is in fact the cause of the cardinal signs or symptoms and if the Sharp-Purser manoeuvre has managed to reduce the translation, the signs and symptoms will disappear thereby proving that the sagittal instability of the atlanto-axial complex is the cause

¢Lateral flexion stress test

¢ The test can be carried out in sitting or lying,

¢ The therapist palpates the spinous process of C2 and then side flexes the head around an axis roughly through the nose. There is movement of the spinous process to the side opposite the side flexion. This movement is the result of rotation of the axis putatively due to the tension generated in the contra lateral alar ligament.

¢ A positive test is one where there is a delay in the onset of movement.

¢The test has pros and cons like most tests. The main pro is that it can be carried out in the acute patient without stress the region. The con is that it is not a stress test and it is unlikely to reproduce symptoms.

VBI

¢ “A transient or permanent reduction or cessation of blood supply to the hind brain through the left and right vertabral arteries and the basilar artery”

Cardinal signs

¢5 D’s

¢3 N’s- nausea

nystagmus

numbness

¢Ataxia

¢Two types:- Ischaemic/ non Ischaemic

Ischaemic signs and symptoms

¢Loss of short term memory

¢Vagueness

¢Limb weakness

¢ Anhidrosis (lack of facial sweating)

¢Hearing disturbances

¢Photophobia

¢Clumsiness and agitation

TIA

¢Iscaemic stroke

¢Retinal ascaemia

¢Amaurosis fugax- Curtain affect on field of vision

Non-Ischaemic signs and symptoms

¢Ipsilateral posterior neck pain/occipital headache (sudden and intense)

¢Horner’s syndrome ( damage to the Sympathetic nervous system)

¢Pulsatile tinnitus

¢Cranial nerve palsies

Major risk factors to consider

¢Hypertension (bp 140/90 above)

¢ Cholesterol

¢DM

¢FH of MI/angina/CVA/TIA

¢Smoker

¢BMI 30

¢Upper Csp instability

Minor risk factors

¢Oestrogen based contraceptive

¢HRT

¢Infections

¢Poor diet

¢RA

¢Blood clotting disorders

¢Hypermobility

¢BMI 25-29

Cervical spine Mx

noreply@blogspirit.com (PhysioCharlie) — Fri, 31 Oct 2008 11:25:00 +0100

We had an IST yesterday lead by my colleague which was very interesting:

Management of acute neck pain in general practice

(Vos et al 2007)

High incidence of neck pain - 66% of people will experience neck pain at some point.

Prevalence rises with age.

Gender differences: women 2x more common than in men.

10% of neck pains become chronic.

Study looked at what did the GP do with new neck pain presentations:

No advice given 2%
Wait and see 23%
Improve posture 22%
Rest 18%
Specific home exs 9%
Sick leave 3%
"Other" 3%
Medication 42%

74% of those referred for physio reported recovery in a year.

79% of those not referred for physio reported recovery in a year.

2 main pathways

"Wait and see" and NSAIDs/analgesics.

Physio plus more restricted analgesia.

"Expectations of GP's role in acute neck pain seem to differ substantially between patient and GP"

Problems with that research:

No results re which method worked best.
No idea of whether the physio group were worse off at the start of treatment or not.
No discussion re whether the baseline was the same.
Non-representative group.

Vos et al, “Management of acute neck pain in general practice”, BJGP;57:23-28

So what's physios role in management of neck pain?

Moffet and McLean (2005) wrote a paper about this very thing!

First contact: usually GPs but now us as well - hence we need to know red flags.
History taking (subjective exam)
Physical (objective) exam
Explanation / education.
Encouragement / motivation

Evidence for “brief intervention”

Less useful with neck pain than with back pain.
More recent research showed good exercises with info as useful as “physiotherapy”.

Neck schools:

Potentially cost effective.
No evidence cited re neck schools.
No evidence to support effectiveness of back schools.

Psychosocial factors:

“psychosocial factors are very important and must be considered for each patient, especially those with chronic pain”.
Hurt ≠ harm.
CBT.
Consistency of message.

Specific exercises

Euro guidelines do not recommend the use of any specific programmes.
Exercise choice comes down to experience and how you were trained.
Stabilization exercises have been shown to be helpful.

General exercises

Multimodal treatment appears to be more effective than single treatment regimes. IE mobes + HEP better than either mobes or HEP on their own.

Manips and mobes:

Manips + “best GP care” is better than just “best GP care”.
Mobes “can be useful”.

Massage:

Usually not recommended in clinical guidelines.
“However, as a preliminary to more active forms of treatment, on pragmatic grounds its use should not be totally discounted”.

Other physical modalities:

TENS/heat/cold/traction/US/laser/IF/collars.
No good evidence.
Might have large placebo effect.
Could encourage dependency/passivity.

Persistent problems

Needs MDT approach.
Pain management.
EPP.

Moffet J and McLean S, “The role of physiotherapy in the management of non-specific back pain and neck pain”, Rheumatology 2006;45:371-378

Assessment part 1 - Subjective

Mechanism of injury
Acute/Sub-acute/chronic
Progression of problem
Pre-existing condition
Investigations
Red flags
- Age <20 or >55
- Trauma
- Constant unremitting pain not related to movement/activity
- T.spine pain
- Hx of Ca
- Steroid use
- Drug abuse or immunosuppression
- systemically unwell
- weight loss
- structural deformity
- fever
D’s
- Dizziness
- Diplopia
- Dysarthria
- Dysphagia
- Drops
N’s
- Nausea
- Nystagmus
- Numbness
Yellow flags
- Belief that pain is harmful and/or disabling.
- Fear/pain avoidance behaviour.
- Reduced activity level.
- Low mood / withdrawal from social interaction.
- Belief that passive treatment will help.
Pattern of pain – where is it?
Aggs and ease factors.

Predictors of persistent neck pain after whiplash

(Atherton et al 2006)

Study to look at

Relative contribution of pre-accident health and psychosocial factors, collision factors, and psych response to the collision.
To identify those at high risk by using info on the factors in A.

Over 25% of WAD patients report persistent pain 1 year after the accident.

Can we predict which 25%?

Results:

Associated with increased risk:

- Age. Increased age = increased risk
- “widespread body pain prior to collision”.
- Self-rated collsion severity “medium or high” increased risk.
- Being in a vehicle that wasn’t a car.
- Psych distress.

Not associated:

- Self-reported general health prior to collision.
- History of neck pain prior to collision.
- Speed.
- Direction of impact.
- Anticipation of impact.
- Position in car.
- Lack of head rest.
- Air bag or not.

Issues:

50% questionnaire return. Would those not suffering bother to fill them in?
Didn’t look at predictors of severity of pain in short term.
Didn’t look at compensation claims, although it is noted that those with significant psych distress were more likely to claim compensation. Another point is that they’re looking at initial presentation (IE directly after the accident in A+E) so the patient may not have known re compensation.
The WAD classification system was not used – “[it’s] only moderately predictive of persistent pain”.
No of participants who were in “other vehicles” was a very small subset so stats may not be reliable.

Atherton et al, “Predictors of persistent neck pain after whiplash injury”, Emergency Medicine 2006;23:195-201

Assessment part 2 - Objective

Posture
Basic ROM ± over-pressure
Neuro
- Reflexes
- Myotomes
- Dermotomes
- Neurodynamics
Signs of instability (thanks Sheena for these)
- Loss of balance with relation to head movements.
- Face/lip parasthesia, reproduced by active or passive c.spine movements.
- Bilateral or quadrilateral limb parasthesia, constant or reproduced by c.spine movement.
- Nystagmus produced by neck movements.
Special tests
- Spurling’s – should recreate radicular pain.
  - Found to be “not sensitive” but “highly specific”.
  - In other words, loads of false negatives but when positive it’s strongly indicative of radicular problem.
- Sharp-Purser – instability.
- Alar and transverse ligament tests.
- VBI
  - When NOT to test?
    - Hypertension (140/90 or higher)
    - Increased cholesterol.
    - DM
    - Family history of cardiac or vascular disease.
    - Smoking.
    - BMI >30
    - C.spine instability signs.
  - Minor risk factors
    - Oestrogen contraceptive.
    - HRT.
    - Infections.
    - Poor diet.
    - Diseases which may have upper c.spine instability involved eg RA, Down’s syndrome.
    - Clotting disorders.
    - Hypermobility.
    - BMI 25-29
Palpation
Assess shoulders?
- Where do other joints refer to on the neck?
  - ACJ
  - SCJ
  - 1st rib
Trigger points?

So how good can we be at C.spine assessment?

We know that certain histories produce likely outcomes. Eg RTA is likely to lead to WAD.

But we need to know what else may happen.

So we have our red flags and yellow flags. Patients are normally pre-screened by GPs as well but this can’t be taken for granted.

Pool et al (2004) studied how much the interrater reliability was for physical examination of c.spine.

Their starting point was “Several studies have drawn different conclusions with regard to the reproducibility of manual assessment techniques.”

They used a standard protocol to assess “general mobility” and “intersegmental mobility”.

All their subjects had neck pain.

2 Physios, experienced and specifically trained in how to use the standard protocol assessed these patients separately.

They tested

General mobility
- Full flexion and extension.
- High cervical flexion (nodding) and extension C0-1.
- Left and right rotation.
- Side flexion.
- Combined rotation, side flexion and extension.
- Combined side flexion with “heterolateral” rotation.
All tested with overpressure.
Segmental mobility
- Passively done in supine (PPIVMs).

Result

“Despite considerable training and the use of a standardized protocol, the results of this study showed that the reproducibility of cervical mobility and pain provoked during mobility assessments was highly variable and unacceptable.”

“[…] it is difficult to achieve reasonable agreement and reliability between 2 examiners.”

Problems/issues with the study

Limited number of patients (32).
No PPAIVMs.

Pool et al, “The interexaminer reproducibility of physical examination of the cervical spine.” J Manipulative Physiol Ther 2004;27:84-90

Out if interest there is a published case of a man “referred for physical therapy for the treatment of neck pain following trauma” (Ross and Cheeks 2008).

It’s a case study of a man post-RTA.

Subjective:

62 years old.
“He drove off a 10m cliff in reverse”.
Head and neck pain immediately.
Xray c.spine = NAD. CT head = NAD. (NB PT had no access to the reports re these)
Prescribed analgesia at A&E and sent home.
Pt returned to A&E 3 days later with no improvement to symptoms to be given reassurance and no further investigation.
GP supplied further analgesia and referred for physio.
Saw physio 8 weeks post accident.

Pain:

Constant dull ache throughout c.spine.
Intermittent sharp pain upper c.spine with rotation.
Unable to turn neck.
Aggravated by rotation mainly.
Eased by heat.
Best 1st thing am, worse through the day.
Slight improvement in pain intensity since accident.
No prior Hx of c.spine pain.
No d’s, no n’s.
Only PMH was hypertension which is controlled.
Borg scale: 1-2/10 at rest, 4-5/10 at worst.

Obj:

All c.spine movements reduced, limited by pain.
Neuro: NAD.
PAs revealed “significant pain C2-3 with muscle guarding.
Shoulders NAD.

Physio went for manual therapy and HEP. But she also referred for xrays again before trying any manual therapy.

Xray showed major “Hangman’s fracture”.

Referred to neurosurgeon.

Final outcome was no pain, improved ROM and function. He had no surgery and no further physio beyond the initial assessment and HEP/advice.

Ross M and Cheeks J, “Undetected Hangman’s fracture in a patient referred for physical therapy for the treatment of neck pain following trauma”, Physical Therapy, 2008;88:98-104

Cx injuries

noreply@blogspirit.com (PhysioCharlie) — Wed, 29 Oct 2008 15:38:00 +0100

http://users.rowan.edu/~sterner/pathologyandevalII/CervicalSpineInjuries.ppt#21

Anterior Cervical Fusion

noreply@blogspirit.com (PhysioCharlie) — Mon, 08 Sep 2008 17:32:10 +0200

http://www.youtube.com/watch?v=3uQbhSQBJk4

http://www.youtube.com/watch?v=7S3NBG97gsc&NR=1

Accessory nerve injury

noreply@blogspirit.com (PhysioCharlie) — Wed, 27 Aug 2008 12:05:00 +0200

Iatrogenic accessory nerve injury. London et al, Ann R Coll Surg Engl. 1996 Mar;78(2):146-50

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2502542&blobtype=pdf

http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2148098&blobtype=pdf

http://en.wikipedia.org/wiki/Image:Gray1210.png

"Accessory nerve injury produces considerable disability. The nerve is most frequently damaged as a complication of radical neck dissection, cervical lymph node biopsy and other surgical procedures. The problem is frequently compounded by a failure to recognise the error immediately after surgery when surgical repair has the greatest chance of success.

Clinical features of accessory nerve injury

A clinical picture associated with SAN (Spinal Accessory Nerve) injury has been described, however, in practice, the patient may present with a variety of symptoms and signs. Clinical features, due primarily to the paralysis of the trapezius muscle may be divided into immediate and late. Immediate symptoms, recognised by the patient, include pain over the affected muscle, limitation of movement (in particular, loss of abduction), and a feeling of heaviness in the arm. Late sequelae of the injury are as follows:

1 Drooping of the shoulder secondary to trapezius paralysis

2 Atrophy of the trapezius with appreciable asymmetry

3 Weakness or loss of shoulder abduction (usually less than 90);

4 Pain which is usually mild-a persistent ache in the region of the affected muscle-but may be severe and involving not only the shoulder but also the arm, forearm, hand, scalp, and face of the affected side. Contralateral pain has also been recorded. The aetiology of this pain is not completely understood, but theories include traction on the cervical sensory nerves or traction on the brachial plexus as a result of postural changes, direct damage to sensory fibres in the SAN derived from the cervical plexus and entrapment syndromes (10);

5 Subjective sensory disturbance including paraesthesia in the forearm and fingers secondary to traction on the brachial plexus and impingement on the first rib.

"In patients with an intact but damaged nerve, the only reliable method of predicting spontaneous recovery is by serial nerve conduction studies; however, such studies delay treatment until the results of operative intervention are likely to be poor. In one large series, surgical treatment was proposed unless there were historical, clinical or electromyographical evidence of axonal re-innervation of muscle by the time of initial referral. Operative intervention is most effective within 3 months of injury".

Wikipedia:

In anatomy, the accessory nerve is a nerve that controls specific muscles of the neck. As a part of it was formerly believed to originate in the brain, it is considered a cranial nerve. Based on its location relative to other such nerves, it is designated the eleventh of twelve cranial nerves, and is thus abbreviated CN XI. Although anatomists typically refer to the accessory nerve in singular, there are in reality two accessory nerves, one on each side of the body.

Traditional descriptions of the accessory nerve divide it into two parts: a spinal part and a cranial part.^[1] But because the cranial component rapidly joins the vagus nerve and serves the same function as other vagal nerve fibers, modern descriptions often consider the cranial component part of the vagus nerve and not part of the accessory nerve proper.^[2] Thus in contemporary discussions of the accessory nerve, the common practice is to dismiss the cranial part altogether, referring to the accessory nerve specifically as the spinal accessory nerve.

The spinal accessory nerve provides motor innervation from the central nervous system to two muscles of the neck: the sternocleidomastoid muscle and the trapezius muscle. The sternocleidomastoid muscle tilts and rotates the head, while the trapezius muscle has several actions on the scapula, including shoulder elevation and adduction of the scapula.

Range of motion and strength testing of the neck and shoulders can be measured during a neurological examination to assess function of the spinal accessory nerve. Limited range of motion or poor muscle strength are suggestive of damage to the spinal accessory nerve, which can result from a variety of causes. Injury to the spinal accessory nerve is most commonly caused by medical procedures that involve the head and neck

Hoffmann's sign

noreply@blogspirit.com (PhysioCharlie) — Wed, 27 Aug 2008 11:26:25 +0200

http://en.wikipedia.org/wiki/Hoffmann's_sign

"Hoffmann's sign is often considered the upper limb equivalent of the Babinski's sign because it, like the Babinski sign, indicates upper motor neuron dysfunction. Mechanistically, it differs considerably from the Babinski which is also known as the plantar reflex; Hoffmann's sign involves a monosynaptic reflex pathway in Rexed lamina IX of the spinal cord, normally fully inhibited by descending input. The pathways involved in the plantar reflex are more complicated, and different sorts of lesions may interrupt them. This fact has led some neurologists to reject strongly any analogies between the finger flexor reflex and the plantar response".

Nerve Root Block

noreply@blogspirit.com (PhysioCharlie) — Wed, 27 Aug 2008 11:14:28 +0200

Nerve root blocks are injections of local anaesthetic, with or without the addition of steroid (cortisone) around the spinal nerves at the point at which they leave the spine (their roots). The object of the block is to numb the root with local anaesthetic for immediate relief and counteract the inflammation and swelling with the anti-inflammatory action of the steroid for longer relief. A positive response to a root block means that the pain is arising at this point on the nerve and confirms the diagnosis as well as being therapeutic.

Bupa has a good page on this:

http://hcd2.bupa.co.uk/fact_sheets/html/nerve_root_block_injection.html