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Clinical Reasoning Typical cases are discussed there. The cases are brought by practioners.

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Old 22-02-2012, 05:35 PM   #1
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Default An interesting neurological case

Last week I had a patient visit me. It was one of the stranger cases I have seen. Here are the details.

MOI/Hx:

End of January he stated that he lost consciousness laughing at joke (this has happened 4-5x before in his life). Losing consciousness he fell face forward, scrapped up his face and emergency personal responded. He was unsure of the amount of time he was unconscious. He did have a few drinks at the time and his had a BAC of 0.0107.

Subjective:

At the first visit pt. had pain in the right side anterior, posterior aspect of the forearm, some pain in the wrist, and non specific pain of the shoulder. Most of his symptoms are worse with rest i.e. sleeping at night (however this was improving at the time of the first visit) and better with work related activity--he is on light duty office work from forklift operating.

Obejective:
Neurological- no sensory abnormalities to light touch or sharp dull, absent biceps and triceps reflexes bilaterally, grip test was 60 lbs R and 100lbs L (he is R hand dominant),
Myotomes were grossly WNL, however the R side was possibly just a shade weaker than his left side, hoffman's sign -, babanski -, clounus 2-3 beats

Shoulder ROM grossly WNL, Pain with PROM for horizontal abduction with the palm facing the ceiling, less pain with forward flexion (tested in supine), ULNTT +median nerve and radial nerve right side, slightly positive on the left side.

Posture: Pt. sits with a habitual very slumped posture.

Assessment: Well given his protective responses and his increased pain with PROM and nerve tension testing I surmised that it was possible that he had some sort of peripheral nerve injury. It was unclear in my initial assessment if it more proximate or distal.

Initial tx: Basic pain education, graded motor exercise of AROM of horizontal abduction, scapular mobility, and quadruped shoulder blade retraction. All motions were pain free (when performed in the tolerable ROM) and led to increased ROM post tx.

Follow up eval (yesterday): Movements went well at home, pt. noted increased mobility i.e. greater tolerable ROM without increased pain in the forearm and wrist. However, after going skiing-against medical advice, he now has bilateral inability to flex the DIP joint of the first and second phalanges.

Re-eval: No other changes in his objective measures from the initial assessment other than increased tolerance to PROM of the UE to horizontal abduction and medial radial nerve tension testing (but these were still positive). He did have 1/5 strength in his 1st and 2nd DIP bilaterally.

He did have a workup by his MD today and he is scheduled to get a cervical/thoracic MRI.

No tx was given on his second apt because he arrived 45 min late.

My thoughts: I am suspecting either a lower brachial plexus injury C7, C8, T1 or a mild central SC lesion at the same levels. That being said I have never seen this sort of presentation of progressing isolated loss of nerve function that initially started with unilateral pain symptoms to bilateral loss of isolated neuromuscular function especially in such a narrow distribution.

I have seen plenty of cervical radiculopathies and peripheral nerve sensitivities of the UE but this presentation is markedly different. Also, he does not seem to have any work related motivational issues because he said he wanted to return to work even though he could not use the distal aspects of his index finger and thumb.

My plan was to continue with pain education, evaluate skin sensitivity to stretch over the regions of pain distribution, and continue with graded motor exercise.

I am interested to know what the group thinks and any other ideas you may have regarding the case.

I follow up with the patient tomorrow.

Thanks,
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Old 22-02-2012, 05:55 PM   #2
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I would also be suspicious of brainstem (incl. VA) - upper c-spine issues. LOC during laughter (possibly "throwing head back"), from uni- to bilateral peripheral symptoms/signs - I'd be interested in an MRI of the whole neck and brainstem. Very curious case indeed - thanks for sharing!
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Old 22-02-2012, 05:59 PM   #3
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I would want to rule out a cervical myelopathy. What is his gait like? Does he appear to have a wider base of support or clumsy? HAve you checked Romberg test? How about Lhermitte's sign?
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Old 22-02-2012, 06:52 PM   #4
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Per his report, he also feels like he has coordination issues of his R UE, this was mostly noted during our first visit. I did not do any cerebellar coordination specific tests like finger to nose, or RAMS. However, he did appear to have greater deviations throughout the pain free ROM when performing AROM horizontal abduction and adduction in supine. This was very slight and I would not suspect many people would pick this up, and so slight I may have been suffering from confirmation bias; I am not sure.

I did not detect any large coordination issues during gait. He also did some skiing which was fairly high level and did not note any impairment to his coordination or balance.

These are all issues I could take a closer look at though. Thanks for the help.

Eric
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Old 22-02-2012, 08:24 PM   #5
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The LOC raises a yellow flag; I would follow up with soft ULNTT1,2 and 3 movements under close observation, working distal to proximal.
I suspect something pathological is going on.

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Old 22-02-2012, 11:45 PM   #6
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The patient did self diagnosis himself as having laugh syncope (I believe through the internet).

This is some of what I have found in case studies over at the sound of silence.

Eric
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Old 23-02-2012, 01:10 AM   #7
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I wonder if I can ask a question regarding central and/or peripheral nerve lesions.
Here is a definition of nerve lesion as I found it on wisegeek.com
Quote:
A nerve lesion is an injury which affects one of the nerves in the body. Nerve lesions can be caused by a wide variety of situations and medical conditions, and they can cause an assortment of symptoms. Treatment for nerve lesions depends on locating the lesion and determining its cause, and it may not always be possible for a doctor to deliver a good prognosis for a patient with a nerve lesions.

In a complete nerve lesion, the nerve is so damaged that signals cannot pass across it. This damage may be permanent in nature. Partial nerve lesions involve partial damage to the nerve which causes an interruption in the nerve's function. Partial lesions are more likely to have a positive outcome, because it is possible for the body to adapt to the physical change.

Some causes of nerve lesions include: degenerative diseases of the nervous system, tumors, burns, cuts, and abrasive injuries such as those caused by bones which grate against nerves. In all cases, part of the nerve is damaged, and the myelin, the thick sheath which covers the nerve, may be partially removed. Demyelinated nerves are usually more difficult to treat, especially when the layer is stripped away by a disease, as is the case with multiple sclerosis.


To my question: For the same reason that we cannot blame mesoderm for causing pain (pain is in the brain), how can we blame nerve lesions for pain? I realize that nerves are the actual conduits that transmit information to and from the brain and that damage to them will interrupt/modify how information is transmitted. But how is any form of therapy going to change a nerve lesion (the suggested cause of problem)? Is that the point of the therapy you're applying to the patient that is being described? Are you trying to reroute the brain's map of the area to circumvent the nerve lesion?
I am struggling with this for the same reason I struggled to understand what Diane said in the Placebo for the Layman thread; that it isn't the muscle/tendon/ligament's fault the pain/movement dysfunction is present, it's the misperception by the brain due to excessive signaling. So now it is the nerve's fault? How are mesoderm and nerves different such that a nerve lesion CAN be the cause and how is it that therapy can fix this?

Thank you for your thoughts,
Nathan
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Old 23-02-2012, 01:32 AM   #8
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Nathan, nerves ARE ectoderm.
Most ectoderm signals electrically. The brain thinks nerves are part of itself. It knows mesoderm is not. That's the difference.
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Old 23-02-2012, 05:15 AM   #9
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Ok. So how can therapy repair a lesion? If I understand your reply, a lesion is a big deal and the cause of aberrant output.
Same question for mesoderm. Are there situations where a tendon/ligament/muscle/artery is injured to the point of being the source of sufficient nociception to cause the brain to signal pain? If so, how can a therapist differentiate between a brain misunderstanding that is triggering pain and an sufficiently threatening mesodermal tissue that is perpetuating pain?
Always grateful for your wisdom.
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Old 23-02-2012, 05:22 AM   #10
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Quote:
Originally Posted by zendogg View Post
Ok. So how can therapy repair a lesion? If I understand your reply, a lesion is a big deal and the cause of aberrant output.
Same question for mesoderm. Are there situations where a tendon/ligament/muscle/artery is injured to the point of being the source of sufficient nociception to cause the brain to signal pain? If so, how can a therapist differentiate between a brain misunderstanding that is triggering pain and an sufficiently threatening mesodermal tissue that is perpetuating pain?
Always grateful for your wisdom.
Nathan
It can't. That's the point.

Therefore... ?
If therapy "helps" (i.e., pain is reduced, function improves) there was not a problem to start with. It was just a nervous system glitch that created a mesodermal "damage" mirage, or a movement defense, which everyone tries to turn into defect.
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Old 23-02-2012, 06:27 AM   #11
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If I may add one thing, maybe this is a banal statement, but the pain experience does serve as a very useful perception in our nervous system. Even in occasions where there is mesodermal damage or even just the threat of it, it is still very useful information. I think there is a misconception that we should eliminate all pain without insight. At least this is what probably our modern medical establishment strives for--we know how good it is at treating pain.

Pain gives us much insight into our brains and bodies and we must understand it within the context of ourselves and our surroundings. Many people are so disassociated from this sort of understanding of themselves that they need guidance. Thus patients seek out MDs, chiros, and PTs for validation and understanding. Just like when a young child takes a fall, he looks to those around him to make sense of his internal sensations. We are the stewards of information regarding the body just as parents were stewards during our first steps.

Unfortunately our medical system is much better at labeling than creating a context for healing to occur. Most patients who enter our health care system are met with gimmicks and insufficient explanatory models--when they work they serve to reinforce the confirmation bias of the advocate--when they don't the medical system has just another difficult patient.

Going back to a nerve injury in question. Given a proper explanatory model, physical therapy does not actually "fix the nerve", it convinces the patient they are in an environment where their own natural mechanisms of restoration of health can occur. Much of this is the nervous system accommodating to the changes that have occurred and to maximize the function it has remaining. Proper PT helps the patient make sense of their internal sensations and facilitates appropriate action.

IMO, given the proper context the balance of movement and recovery is the key to this re-appropriation of internal sensations. Once the context is created, the therapist is free to use any strategy of sensory inputs to help facilitate this balance (manual, visual, verbal etc.).
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Last edited by Milehigh; 23-02-2012 at 06:36 AM.
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Old 23-02-2012, 06:31 AM   #12
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EGGGGGGGGGGzactly.
Thank you Milehigh.
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Old 23-02-2012, 12:28 PM   #13
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TIME, POSITION, METABOLIC ECONOMY - these are the three things necessary for healing when tissues have lost their continuity. Until they are achieved to a sufficient degree pain will usually ensue if one or another is insufficient.

Too often pain persists because the second of these was never fully achieved through corrective movement and that's why a little ideomotion can make a big difference rapidly.
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Old 24-02-2012, 01:01 AM   #14
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Thanks again everybody. And I hope I haven't hijacked the thread. Milehigh, really loved your last post.
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Old 25-02-2012, 11:01 PM   #15
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So I saw the patient in question again for a third visit.

Essentially there have been no changes in his motor output to the 1st and 2nd DIP. He is having worse shoulder pain, with new reported pains in his scapular region on the R side (the more affected side). He tried to return to full work duty and could only make it 2 hours before he quit due to both increased shoulder pain an inability to work the fork lift controls properly without use of his DIP of the index and thumbs.

The patient generally has a distant and mild apathetic affect given his current situation. It is almost like he is on about a 10-20 second delay in interpreting his own bodies internal sensations. As an example I was passively flexing and extending his elbow while he was relaxed in supine. I could feel catching and increased resistance to passive mobility especially as we approached the end ROM of extension. Suggesting to me that he was having a protective response. I could visually see increased fasciculations in the biceps and the forearm during these passive motions also suggesting a nonconcious protection. I asked him to tell me what he was feeling during this and if he was in pain. He was vague but after some time and further questioning I did get the sense that he was experiencing pain--again his responses were delayed aprox 10-15 sec. This was only on his R side.

Neural mobility testing, the median, radial and musculocutaneous seemed to be most affected across the elbow.

My treatment included gentle skin stretches, glides of the above nerves and graded motor movements in the pain free ROM. The patient had extreme difficulty recognizing pain barriers--when performing graded motor movements he would often blow past the barrier to where I could see facial grimacing and withdrawal of his R (affected UE).

Also during movement testing he needed extensive cueing for protraction and retraction ( UE at 90 deg flex in hooklying position) on his R (affected) shoulder. His L shoulder was just fine.

An additional note the patient works nights and he visits me at aprox 3 or 4 pm--at the end of his night shift. Therefore, I believe some of his apparent kinesthetic disassociation may be due to his tiredness at the time he is visiting me.

It is becoming more apparent, that he is suffering from some periperhial never irritation. It is a combination of his poor kinesthetic ability and lack of interest of internalizing his condition that he does not recognize appropriate pain barriers unless he is involved with a vigorous activity i.e. skiing or fork lift operating. His poor awareness of these barriers is causing him to further exacerbate his peripheral symptoms as he is not allowing for recovery and graded motor activity for re-appropriation of the balance between incoming nociception and descending voluntary commands.

I also did have a brief look at his MRI without a radiology report--nothing obvious and glaring but I would liked to have examined it a bit closer--we'll see what the radiologist has to say.

I still an unable to completely resolve his delayed and spontaneous bilateral DIP 1st and 2nd weakness. One hypothesis I have is that if he has a very poor nociceptive warning system/proprioceptive representations in his motor cortex, but is getting a lot of nociceptive input of his lower spinal segments (secondary to peripheral nerve irritation). While this noicioceptive input is not being adequately represented in his own interoceptive conscious representations, it is creating an inhibitory block of descending voluntary motor commands for this musculature bilaterally. This is just a very hypothetical and evolving hypothesis and is with the assumption that other work-ups (CT, MRI, nerve EMG study) remain inconclusive.

My interpretation at this point in assessing and progression of this patient is limited by his ability to delve into his own senses and sort out what is going on. I am unclear of his own motivating factors preventing this. More to follow.
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Old 29-08-2012, 05:18 AM   #16
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I certainly hope I am not out of line, but it strikes me that someone may want to look for the possibility of an Arnold Chiari malformation.

I am new to the forum and didn't see a follow up post regarding the radiology reading.

I did some research on this many years ago, so I don't know if any information has changed, but I did pull this link http://www.ncbi.nlm.nih.gov/pmc/articles/PMC491597/ which may be of use.

And in another quick search I pulled this, for you to have something to chase. From: http://www.pspinformation.com/diseas...ormation.shtml
"What is the Chiari (Kee-AR-ee) Malformation?<scroll down>

Syncope (sin-co-pe)


Episodes of passing out or loss of consciousness are reported in the literature, however, this is a less common complaint. The episodes are unpredictable and brief, lasting from 30 seconds to 2 minutes, associated with loss of consciousness, and prompt, complete recovery. Drop attacks have been also been reported in the literature, however, less commonly in the adult population. There are generally no symptoms of seizure and no state of confusion after the event. Persons may also complain of occasional vertigo, without loss of consciousness."



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Old 29-08-2012, 05:48 AM   #17
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Certainly a condition to be considered, CO.

Eric, I know you looked at the MRI, but it might be a possibility something was missed? Just a thought.

The ACM patients I often saw in the Acute Neuroscience ward did have pain, but it was not the most troublesome feature - LOC and weakness were primary concerns. If they were not type111, they did well with neurosurgery.

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Old 29-08-2012, 02:41 PM   #18
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Have just seen a patient with right medulla oblongata stroke - a very small one - who was in an MRI 6 hours after symtoms occurred which showed the location.
Repeat MRI a week later showed compoletely normal.
He has residual weakness in arm and hand - very mild.

Just wondering if this applies to your case in addition to all the other issues he has.
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