I'm not Alex, but for starters muscle twitches sound a lot more like a sign than a symptom. Unless it's possible for us to fake an isolated muscle visibly jumping around for a while?
I suppose abnormal neurotransmitter levels could be considered a sign of neurological dysfunction as well, even if the levels do not originate as the result of a neurological problem.
And on a bad day, I develop a severely ataxic gait after doing "too much", which can vary between having walked for half an hour or trying to walk at all. This seems to be related to orthostatic intolerance in my case, since the problem has largely disappeared while taking OI meds.
Oh, and I suppose some forms of OI are themselves signs of neurological dysfunction, easily measurable by such cutting-edge technology as a blood pressure monitor and a heart rate monitor.
There's no single specific neurological sign saying "THIS IS ME/CFS AND ONLY ME/CFS", but there are plenty of signs - unless you're a neurologist that believes ME/CFS is entirely psychological and any neurological signs necessarily mean you have a "real" disease, not ME/CFS.
Replying to Firestormms post 300 on neurological signs.
Anything that can be confirmed by a test is a sign, not a symptom. So gait ataxia is a sign. Slowed cognitive processing is a sign. Poor executive brain function, dysautonomia of various kinds, central sleep apnoea, altered sleep patterns (investigated in a sleep lab), peripheral neuropathy ... all neurological signs. Furthermore many of us, though based on a tiny autopsy sample size so far, probably have lesions in the dorsal root ganglia. These same kinds of lesions developed when monkeys were injected with plasma from ME patients from the 1949 ME atypical polio epidemic. I suspect obstructive sleep apnoea is also neurological, though this is not absolutely clear.
None of these are mandatory for ME. Many of these do however fulfil parts of an ME diagnosis. The problem is, I suspect, many neurologists have bought the idea that CFS and ME cohorts are identical patient cohorts, and CFS in the UK does not require neurological signs.
The other problem is that nearly all of these require expensive and time consuming tests. They cannot be done routinely by a neurologist in a clinic. Dorsal root ganglia lesions are also only visible on autopsy .. not very useful clinically.
Bye, Alex
Hi chaps,
I think you are both wrong about this and here's why. A doctor has to observe a symptom and recognise it as a neurological sign. It has to be obvious and also something that is indicative of a likely problem outside of what might already have been diagnosed.
An example of personal nature. Seizures. I had them. Still get them. These were observed. There were diagnosed as being something outside of my existing diagnosis (ME). I received (what I recall as being) an EEG. As a result I had an epilsepsy diagnosis attached. I receive specific pills for that. It has helped better manage the frequency and extent of these episodes.
My muscle twitching, was not considered something worth further testing. However, it was regarded as a symptom of my ME. I was prescribed Baclofen. It has helped. Not cure. But helped as well as helping relax my muscles generally - aiding what little sleep and relaxation I can achieve.
Here's another. Drunken wobbling about the place. This was observed clearly. At work. Was even accused of being drunk. The bastards. Accompanied by Nausea. Constant. Now this one took some time to get treated but again no specific tests were made. Eventually I saw a specialist in ME and was prescribed Betahistine Dihydrochloride. It not only fixed (largley) the nausea (thank the Gods and praise be!) but it has helped stablise what was previously always considered some labyrinthine dysfunction and indeed still might be.
How about encephalitis? Now I had that diagnosed: 'viral encephalitis'. Way back when I also had a diagnosis (or before I can't remember) of PVFS after a failed recovery from the Parvo-virus that kicked all this off for me). How was that diagnosed? I honestly do not know. There were not obvious or specific symptoms, nor were there SIGNS that I could point to. But two doctors came to the same conclusion. What was the result? Nada. There was no specific treatment recommended.
Now, take the trembling that is associated with Parkinsons. Right? Deemed to be a neurological SIGN. For a doctor who is listening to what the patient is describing (completely i.e. holistically/whatever), and observing, (because it's far more than simply having a trembling arm - e.g. one might enquire of the patient: 'Does the trembling stop when you grip a glass of water?') he might conclude - right this looks like it could be Parkinsons' Better run some further tests and refer to neurologist.
Same, for Multiple Sclerosis. Signs may well be observed represented as symptoms from the patient point of view or anomalies, strange behaviour, inability to control limbs, weakness, whatever. But the doctor has to associate them with what might be a SIGN of something deeper and refer accordingly.
Sometimes it can take a while.... Sometimes you get shit doctors.... Sometimes as a patient you don't do enough of a good job in explaining how changes are affecting you... Lots of reasons SIGNS might be missed or confused with other things, but 'ME' is not recognised as having any CLEAR NEUROLOGICAL SIGNS and more importantly perhaps - a diagnosis of 'ME' is able to be applied without further investigation and/or testing.
Why should e.g. a neurologist become involved and/or carry out further testing to confirm a diagnosis of something that can be diagnosed with the current NICE Guideline?
Because until such time as we are able to research the effectiveness of the NICE Guideline - or even compare the CCC with ICCME on the ground in real life - then what's the point for either the improved patient outcome or in terms of additional cost to the NHS?
What I mean is - anyone wishing to claim that 'ME' is somehow different to 'CFS/Whatever' is going about it the wrong way in my opine.
You need to be able to demonstrate that patients with 'ME' will have an improved outcome if they were so diagnosed and that the extra expense can be justified.
Flinging tests at the establishment who don't recognise them ain't gonna cut the mustard. They will and are able to say - so what? In what way will patients benefit? In what way can we justify the added expense?
Well that's a couple of things that say I think. But mainly you'll need to better fight for on the ground research data reporting back to a central source that undermines the existing patient outcomes from the three therapies generally recommended: activity management (Severe), CBT and GET (Moderate and Mild).
Anecdotal patient reports - the MEA Survey even whilst good - doesn't really bring home any message being shouted from the rooftops by the loudest few I am afraid.
p.s. added edit about encephalitis above