Physio Charlie

http://www.vision6.com.au/download/files/15928/879371/Sim...

STORIES FROM AROUND THE GLOBE ON SIMPLE NEURAL MOBILISATION from the NOI website: http://noigroup.com/home.php

SIMPLE RESPONSE TO A LONG TERM PROBLEM

Patient: 10 year old girl with a history of 2-3 years of left ankle pain. She complained of it

continuously "turning" and swelling with pain. Her response was to protect it and rest it

for a few days. A pattern was thus established of her behaviour around pain. She is a

very active young lady and loves all sports plus ballet.

She did not complain of any other painful joints. She had become increasingly frustrated

about her problem and the ankle pain had begun to effect her level of activity. The

mother had not been given any appropriate advice on management apart from RICE.

She was now turning her foot several times a day.

EXAMINATION

She had marked hypermobility in both ankles on plantar flexion and inversion. Eversion

was within normal limits, active dorsiflexion was reduced. Muscle power of all muscle

groups around the lower leg - Grade V. Some loss of muscle bulk of gastrocnemius.

SLR bilateral limited to 45 degrees with restriction of dorsiflexion increased passively.

In long sit she was unable to establish a lumbar lordosis and maintained her pelvis in

posterior rotation.

TREATMENT PLAN

Explain effect of chronicity on the ability of the brain to manage the repeated "trauma"

Stop playing the pain tune

Change neural dynamics

Change fear avoidance behaviour

Strengthen all muscles around ankle

Stimulate the proprioception in lower leg & foot

Manual therapy mobilisation to thoracic spine T 3- 8

WHAT DID I DO?

As we had just purchased a mirror box, I explained how she could "trick the brain" to

stop playing the “pain tune". This was an experiment on my behalf. Place painful foot in

box - requested that she did all normal physiological movements of ankle with nonpainful

foot. I requested very slow repetitions (5 x each movement). She observed all

movements in the mirror. I then asked her to relax for a few moments and then repeated

the exercise (X 5). I then requested that she moved the painful foot with the non painful

foot with the same repetitions at the same speed.

Manual therapy to thoracic spine as per plan. SLR immediately improved to 90 degrees.

Move foot on a "Disco sit" for stimulating proprioceptors.

HOME WORK

Continue with home made mirror box - using technique explained.

Maintain SLR to 90 degrees.

Use hot water bottle to stimulate proprioceptors when sitting doing home work or

watching TV.

Encourage thoracic extension in prone lying.

Avoid ballet for the time being but continue all other activities.

HOMEWORK AFTER 2 WEEKS

Strengthening of evertors of foot using theraband

Discontinue mirror box

Use stretching & wriggling more frequently during the day.

Challenge the ankle with increasing loading of activity.

Feel good factor about tricking the brain to stop believing "I've hurt my self again”.

Distraction techniques such as breathing or wriggling another part to stop the pain

behaviour learnt before treatment.

RESULT

I saw the patient a week later. She had been pain free since the day we started the

treatment and was overjoyed. I told her to wriggle and move the foot frequently to

persuade the brain that the problem could be resolved. She had taken on board very

quickly that she did not need to be fearful of re-injury.

I continued to see the young girl on weekly sessions for 8 sessions.

I progressed her to more & more challenging movements (walking on uneven surfaces)

and we worked on her posture & neural dynamics. I continued to work closely with the

mother on beliefs around pain.

CONCLUSION

This case demonstrates well the powerful effect of changing the brain's perception and

consequent behaviour around painful stimuli. The young girl has been able to use simple

techniques to overcome what was increasingly becoming a disabling condition. She was

able to return to ballet.

Penny, United Kingdom

THE PROBLEM SHOULDER

Shoulder pain (often diagnosed as tendonosis or impingement) is a common condition

seen in clinics. The precise history may vary between patients, with some indicating the

pain resulted from trauma while others associate symptoms with overuse. Sometimes

there is no identifiable trigger for the symptoms leading patients to be quite fearful that

something spontaneously went wrong in their shoulder. While the numerous subsystems

of the shoulder can be quite overwhelming at times from an orthopedic

standpoint, a broader perspective grounded in neuroscience can often provide a much

more straightforward solution to the patient’s pain.

CLINICAL FINDINGS

The shoulder is notoriously poor at localizing symptoms. Rarely do people come in

saying “my supraspinatus hurts”. Symptoms may be localized to the peril-acromial area,

but more commonly are diffusely spread throughout the proximal (and sometimes even

distal) arm. There is often a painful limitation in range of motion particularly as the arm is

actively elevated, passively rotated laterally, or both. A traditional ULTT1 is often difficult

to perform in this population due to the apprehension and pain that results as the arm is

taken into provocative positions. Fortunately we have the ULTT2: With the wrist in a

neutral position and elbow supinator / extended, the shoulder is gently abducted in the

frontal plane. Symptoms may be aggravated with wrist extension, but it is important to

perform the test gently and compare it to the contralateral shoulder. The noninvolved

shoulder will often present with greater shoulder abduction and/or considerably less

pain!

HOW TO FIX - FIVE KEY POINTS

Shoulder pain can be amazingly straightforward with a neuron-orthopedic approach:

1. Educate the patient about what is going on with the shoulder. The condition often

begins as an injury to the muscles that help stabilize the shoulder. Shoulder pain is a

normal response to injury as the nervous system attempts to organize the healing

process. The nervous system communicates with the shoulder through a network of

nerves that run through the shoulder area and down through the arm. If the pain alarm

goes unheeded, the nervous system may turn the volume up by sensitizing nearby

nerves, amplifying signals in the spinal cord! The entire process is just the brain’s way of

saying “Look! I need you to pay attention to this problem and do something about it!”

After the clinical exam, educate the patient that the actual damage to the shoulder is

often quite small, but so is a paper cut to the finger. Once the volume of pain is turned

down, movement becomes much easier and even effortless!

2. If the shoulder is in considerable pain, consider performing distal sliders to the

terminal branches of the upper extremity nerves first. Move the wrist and elbow into a

variety of positions provided they do not trigger the patient’s symptoms. Additionally you

may have the patient perform gentle lower cervical movements such as side-bending

and rotation to generate proximal sliding as well. After only a few sessions, the sliders

can begin to incorporate movements of the shoulder to include greater amounts of

abduction or external rotation. During this early period, teach the patient it is ok to move

by having them perform the gentler self neurodynamic movements as outlined in the

Neurodynamics DVD. These movements can be performed 3-5 times daily provided the

patient can prevent setting of the alarm.

3. Traditional ROM and strengthening exercises can be initiated at the therapist’s

discretion, but my observation is that, in the presence of moderate to significant pain, the

level of contraction achieved by the patient is insufficient to generate a strengthening

response. Instead of “strength” as the outcome of early exercises, use traditional

movements as tools to enhance attention and awareness of the area. Improvements in

motor skill after an episode of shoulder pain may require a motor relearning process that

first starts with attention to the shoulder during simple movement. After the patient can

perform attended movements without setting off the pain alarm, add a challenge by

performing another attention demanding task. Dividing attention during a shoulder

movement can be as simple as asking the patient to say the alphabet backwards during

the task, or having them perform the activity standing on an unstable surface.

4. Traditional movements and progressive strengthening can begin as the pain resolves.

This is a good opportunity to help the patient develop further awareness between the

transient ischemic discomforts of a workout with the pathological pain state they were

previously enduring. The end result is a healthier shoulder and an empowered patient

who understands how to keep it that way!

5. Although this encapsulated process sounds easy enough, most episodes of chronic

shoulder pain encounter periods of flare-ups. This can occur if the patient over works the

shoulder, but sometimes can occur for no good reason at all! It is important for the

therapist to be attentive to the patient during their time of need, but to also remind them

that the “flare-up” is a common occurrence as this quirky body part is moved. Our aim is

to keep these flare-ups to mere hiccups as the nervous system readjusts and lowers its

hyper vigilance in monitoring the shoulder.

Roderick, United States

I had a patient, female, 50ish, complaining of persistent shoulder pain, deltoid region and

down to elbow. Occasional neck discomfort, but this was normal for the patient. Been

seen in orthopaedics after previous physiotherapy had failed, and was in line for subacromial

decompression. This lady was getting increasingly limited by the pain and was

sure she would need the operation. She was referred for pain relief, some R.C

strengthening and posture work.

On assessment she did have strong shoulder signs but also had very positive median

nerve and upper limb neurodynamic signs. She had previously had lots of strengthening

done so I treated her neurodynamic issues. Her neck was slightly restricted and slightly

tender but not reproducing the pain.

Treatment consisted of neurodynamic mobilisation techniques, reassurance regarding

her pain and postural advice. Within 1 treatment she was 90% better and had been

returning to some of her hobbies, 3 treatments later she was pain free and no longer

needed surgery.

This lady had been initially quite pessimistic regarding physiotherapy and how effective it

could be. Simple neural mobilisation and off loading techniques had helped immensely

and she was able to return to normal life with very few problems.

Paul, UK

He was late. A biology professor limped into the clinic. He’d sprained his ankle while

collecting specimen samples on the rocky coastline four months earlier. He’d had a lot of

swelling and bruising at the time which had settled, but the movement was still pretty

stiff, and the dorsum of his foot swelled whenever he tried to walk on uneven ground.

He was angry. He’d had sprains before and they’d always resolved. He was sure that

this was an indication that he was now too old, and his body was no longer healing like it

used to.

He was depressed. Walking was his primary source of serotonin. He was unable to carry

out his field work without walking. Worse still, it meant that he was unable to keep up

with his students on field trips.

He was sceptical. He was convinced that I would recommend putting him out to pasture,

much as his GP had. He was unconvinced when I told him his superficial peroneal nerve

had been gummed up by the initial swelling and bruising. Fortunately he couldn’t argue

with my biology – plantar flexion/inversion was immediately painful, worse the moment I

initiated a straight leg raise, better when his knee was flexed, and the SPN was tender

from the lateral malleolus down.

He was absent. I’d given him a few sliders and advised him to give his nerve a bit of

love. He didn’t turn up to his next appointment. It turned out that he was out on the

coastline, catching up on what he missed over the last few months.

Ben, NZ

A patient, male, 40 years old, works with computer science (lots of data entry), with

complaints of pain and paresthesia on the surface corresponding to the extensors

tendons of the first finger of the right hand (dominant), painful palpation over this area

and positive test ULNT2 (radial nerve). The physician diagnosis was De Quervain´s

tenosynovitis.

The complaints are common when he types for more than 1 hour and the pain is relieved

when he doesn’t work. After evaluation we decide to treat with nerve mobilisation of the

radial, using first passive techniques in the position of the ULNT2 - seated variation and

beginning the order of movement from the wrist to the shoulder. The patient was

instructed to begin self management with the exercises of "pouring water" and "look at

your hand behind your elbow", in intervals of 10 minutes every hour. The symptoms

lasted for 2 weeks and after that we started a program of strengthening. The patient was

educated about the pathology, ergonomics and about the physiology of his treatment

and pain conditions. The total period of rehab was 4 weeks.

Luciano, Brazil

I had an interesting patient a couple of years ago. He had persistent lateral ankle and

foot pain after an ankle sprain. I’m not sure how he got to me but he had seen another

therapist previously who had shown him stretches and elastic band strengthening which

seemed to flare his symptoms.

His sural nerve test appeared to be the most sensitive. The peroneal nerve test was also

slightly cranky. His main therapy involved self neural mobilizations, as well as manual

therapy to address some movement restrictions with the talocrural joint, cuboid and

super tibiofibular joint. I also threw in some acupuncture. It was amazing to see how

quickly the neural mobilizations improved his problem. Since then, I have become

increasingly more interested in neurodynamics and the science of pain.

Aaron, Canada

A couple of years ago, Larissa came in to see me on crutches following an alarming

injury to her foot involving a PTO drive at the back of a tractor. This PTO drive,

unguarded, which is illegal as well as being extremely dangerous, had caught her

trouser leg and dragged her foot into it. She had the presence of mind to react fast and

"reefed her foot out with a lot of force. Fortunately she was wearing elastic sided boots,

so her foot came out from her boot and the PTO thing, which consumed her boot, it was

shredded. Her foot was seemingly, when she had the courage to look, unscathed, but

she couldn't weight bear at all.

When I saw her, she was on her way on holidays, so after a quick look over, some

advice and so on, she went on her crutches. A month or so later, she returned, still on

crutches, her foot looking like it was developing a sympathetic dystrophy. She was

terrified of doing anything with it and couldn't even touch it. However, it wasn't yet red

and shiny, so I thought we stood a good chance of nipping it in the bud before things got

worse. Now I see that a good part of the treatment was neural mobilisation as well as

desensitising.

Larissa still talks of the immense force she used while pulling her foot free of the PTO.

The structural damage was probably nerve traction as well as bruising to the whole foot.

An MRI showed nothing. Anyway, she made a full recovery, although it took a good 6

months.

Kathryn, Australia

Here is a case of a simple neural mobilisation that had fantastic results. It is slightly

further upstream than the problem ankle, but just as exciting...

I recently saw a patient with a 2 month history of left sided low back pain that “wrapped

around” into the front of her hip and thigh. The pain had come on after doing a lot of

cycling preparing for a 50km Mountain Bike race and the patient was referred to me for

clinical pilates after physiotherapy treatment of her low back had failed to reduce her

symptoms.

The patient complained of pain with flexing and externally rotating hip (ie: getting into the

glut stretch position prescribed by her previous physiotherapist), getting up after

sustained sitting and driving, walking long distances and at the time she was unable to

ride her bike.

After taking her history, and checking her lumbar spine, I quickly tested Slump test,

expecting to clear this and move on to working on her stability – after all that was the

reason for her referral! To my surprise slump testing on right side reproduced her left

sided symptoms... exactly and reliably each time we tested it! I was puzzled but keen to

get to the bottom of things. A colleague of mine had just ordered NOI’s “Neurodynamic

Techniques” and I promptly devoured the entire thing before the patient’s next

appointment!

At our second appointment I prescribed a Femoral Nerve Slider (in elbow prop did PKB

with CSP extension). When I reviewed her two days later, her slump test was negative

and her symptoms much better.

The patient continued to use her slider exercise at home and we progressed her

treatment by incorporating neurodynamic techniques into her pilates exercises – for

example: doing lumbar spine extension on the Trapeze table with the knee in flexion and

then moving onto exercises that mimicked being on the bike

I am happy to report that within 2 weeks her pain had resolved and she was back in the

saddle happy as Larry!

Louise, New Zealand

I have a great ankle injury neurodynamics story. Last year I sprained my ankle (Grade 2)

and fractured my 5th metatarsal and had a delayed union last year (4 mo NWB and 1 ½

mo more in a boot before the Jones fracture was healed). I started doing proximal neural

tensioners including thoracic SB and rotation for sympathetic tensioners within the first

week or so since my foot would immediately turn dark red and swell as soon as it was

dependent, even though I worked w/ my foot 90 degrees horizontal on a stool. A couple

weeks after the fracture, I noted that my sensation wasn’t normal in my entire foot (felt

pins and needles with palpation), I started doing a lot of sensory stim to my toes instead

of movement since I couldn’t move without a lot of pain at the unhealed fracture site- the

only time I had any pain in the foot.

So I was trying to do all the right stuff including hip strengthening to prevent problems

once I was allowed to walk on my foot. Based on the prior neurodynamics class I took

about 15 years ago with Elvey, I had been adding on the affected segment (ie ankle

DF/EV and DF/IN) last once the fracture healed. Nine months after the injury, I still had

decreased DF with the knee extended, pretty good w/ knee flexed. Although my gait was

pretty normal at a regular length step, rapid walking and especially walking uphill with

their increased angle of DF made it swell up and mildly ache, very consistently. MRI

showed a bone bruise on the talus and bony changes consistent w/ RSD, but I had no

pain otherwise, just the vascular and temperature changes.

At this point, I went to ‘Mobilisation of the Nervous System’. Since the conference room

was at the top of a steep hill from the parking lot, my foot was pretty swollen by the time I

got to class. I was horribly positive for tibial and sural, and less so for peroneal,

especially with distal motions first. My lab partner was leaving big dents in my swollen

foot just holding it to do the tests. This also was the same side that previously had a bad

bout of sciatica after my car was totaled, but no symptoms for 10 years and almost equal

slump/Lesegues before this injury.

Steve Schmidt, the course instructor, told us about doing manual mobilization of the

nerves at site of entrapment (why didn’t I think of that!!), and adding the most affected

component on 1st, changing the sequencing of the tensioners and sliders. So while in

the shower before day 2 of the course, I did a bunch of mobs to sural and tibial nerves in

the foot, calf and ankle, and while sitting on the shower chair, did a bunch of tensioners

adding DF 1st, then inversion or eversion, and finally knee extension.

For the first time, I didn’t have any anterior ankle pain walking up the hill to class and my

foot was not swollen! I picked up about 10 degrees of DF in about 20 minutes, and

suddenly a lot more range with the neurodynamic tests. Doing inversion or eversion then

dorsiflexion first instead of the reverse also dramatically changed the tension in the

ankle, and the ROM afterward

Now I have no problems with swelling in my foot- it has not returned at all after that first

session. Still slightly stiff for the first few steps in the morning, but no problems including

with hiking, jumping, jogging. The only sympathetic symptom I get now is an occasional

prolonged ‘hot flash’ in my entire foot when I get really stressed (a few extra

adrenoreceptors and a teenage son).

So not only have my patients made some pretty dramatic changes (like severely

pronated feet no longer being pronated after manual neural mobilization at

foot/ankle/knee and tensioners/sliders), just having my foot back in working order so

rapidly definitely made me look at the effects of the nervous system on ALL my pts even

more. I can’t wait until the next course in Northern California (hint, hint).

Kathy, United States

I have a new website!!

 

http://physiocharlie.vpweb.co.uk

 

 

 

 

http://en.wikipedia.org/wiki/Conversion_disorder

Conversion disorder is a condition where patients present with neurological symptoms such as numbness, paralysis, or fits, but where no neurological explanation can be found. It is thought that these problems arise in response to difficulties in the patient's life, and conversion is considered a psychiatric disorder in the International Statistical Classification of Diseases and Related Health Problems (ICD-10)

Conversion disorder: the modern hysteria, Owens and Dein Advances in Psychiatric Treatment 12 (2): 152. (2006)

http://apt.rcpsych.org/cgi/reprint/12/2/152

See presentation on the iCSP:

http://www.interactivecsp.org.uk/network/viewArticle.cfm?...

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=250...

http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmce...

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

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 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_...

Dermatome map:

http://www.google.co.uk/imgres?imgurl=http://www.aaofl.co...

 

Nerve root	Dermatome	Myotome	Reflex
C1	Top of head	(Contributes to cervical flexion)	None
C2	Temporal, occipital regions of the head	Cervical flexion (longus colli, sternocleidomastoid, rectus capitus)	None
C3	Posterior cheek, neck	Lateral neck flexion (trapezius, splenus capitis)	None
C4	Superior shoulder, clavicle area	Shoulder shrug (trapezius, levator scapulae)	None
C5	Deltoid patch, lateral upper arm	Shoulder abduction (deltoid), elbow flexion (biceps)	Biceps (brachioradialis)
C6	Lateral forearm, radial side of hand, thumb and index finger	Elbow flexion (biceps, supinator), wrist extension	Brachioradialis (biceps)
C7	Posterior lateral arm and forearm, middle finger	Elbow extension (triceps), wrist flexion	Triceps
C8	Medial forearm, ulnar border of hand, ring and little finger	Ulnar deviation, thumb extension, finger flexion and abduction	None

Nerve Root Dermatome Myotome Reflex L1   upper anterior thigh   hip flexion   NONE   L2   middle anterior thigh (hip flexors)   hip flexion   NONE   L3   lower anterior thigh (hip adductors)   knee extension   NONE   L4   medial lower leg   ankle INV/DF (tibialis anterior)   patellar tendon   L5   lateral lower leg, dorsum of foot   great toe extension (interossei)   NONE   S1   lower leg (around lateral malleolus) and 5th MET   ankle EV/PF (peroneals)   Achilles tendon   S2   middle posterior thigh (popliteal fossa)   ABD/ADD of toes (intrinsics)   NONE