Disc bulges impinging on nerve root. Pins needles... - LUPUS UK
Sorry to hear you're in pain, sounds like sciatica alright. Do you get shooting pains down the back of the leg, and strange sensations on the sole of your foot? I find difene helps a lot, and every few years get an epidural injection. You should get an MRI, if you haven't already.
Good question! Been asking my clinicians about this for years...am 67 & been managing chronic cervical + lumbo/sacral spine conditions pretty much all my life
Most recently have been officially diagnosed clinically + via MRI with scoliosis, vertebral fractures AND nerve root entrapment/impingement @ both L4/5 & L5/S1 (foraminal stenosis due to vertebral bodies entrapping/impinging on nerve root). Both times, I asked my clinicians the diff between this sorta thing & sciatica. Both times the answer was:
- sciatica is non-persistent impingement, ie episodic + can be managed via conscientious first line self-help techniques + OTC analgesics into clearing up for significant periods of time between flares
- sciatica is not the right term for lumbar or sacral nerve root impingement when symptoms are severe + persistent & don’t settle down in response to conscientious first line self-help techniques + OTC analgesics etc
- sciatica is also not the right term for lumbar or sacral nerve root &/or spinal cord impingement when bowel &/or urinary tract function is affected
After a lifetime managing chronic spine pain inc lumbo/sacral symptoms that responded relatively 😉 pos to first line & OTC stuff, my version of this segued into persistent horror...and finally In 2019 I gave in: went through the diagnostic mill & ended up having surgery (instrumented fusion) for the L4/5 stenosis/entrapment/impingement...but due to my scoliosis + vertebral fractures + extremely hypermobile spine (hEDS) that surgery has set me up for persistent horror @ L5/S1, so am now on the waiting list for surgery down there 🙄
Hope something in there is useful 🍀❤️ Coco
Cheers mate. I have had the problem for 15 years. Had epidural injections, which was useless. Decided to put up with it until 8 months ago when climbing the stairs, put left foot down and weight on it to lift right leg up onto next step and I went over. No pain apart from pins and needles. Just like I didn't have a left leg. Had another MRI just waiting them get back in touch. It's happened further 6 times since then.
Yep: sounds more or less like my version of this. Am betting on the MRI confirming some sort of stenosis/impingement/entrapment down there. Hope you’ll let us know how you get on 🤞🍀
This is really useful thanks! I have Scoliosis and degenerative disc disease confirmed by xray and MRIs. The cervical DDD is severe but not yet causing significant nerve inpingement. The neurologist told me what symptoms to be alert for when I was scheduled for an occipital nerve block recently for related migraine.
Then I started having an intermittent collapsing left leg with intense electric shock pain down the outer side after a few weeks of left buttock and lower back pain. I phoned the GP last week to clarify if this was sciatica as I presumed but I’ve never had this collapsing knee before. He said yes spot on - but looked at my notes and confirmed herniated L5/S1 identified by emergency MRI three years ago.
I asked at what point I should push for another MRI of my lower spine (had head and neck looked at last year).
He said the general advice is if sciatic pain continues intermittently for longer than 8 weeks then I should come back. 8 weeks is the guideline time frame for sciatic flares apparently.
Obviously loss of sensation with bladder or bowel function should be a big alert and warrant urgent medical attention as it could be Cauda Equina. However I have other conditions causing similar issues in bowel and bladder already and advanced small fibre neuropathy - so it was good to know about the collapsing knee and sciatica time frame as well. X
Sounds like radiculopathy secondary to nerve impingement as BarnClown has also explained. Sometimes when our vertebrae have no cushion (aka disc is gone), the bodies rub and get inflamed. The outsides start to callous in a way that builds up bone outside the vertebral body which narrows the holes through which nerves pass. They pass through front and back. Front ones control motor and back ones control sensory, pain and proprioception. The back ones typically get hit first so that’s probably why you feel pins and needles. Your vertebrae can also slip forward, hit a nerve and that’s called spondylolysis.
Sciatica is typically from compression of a large nerve that runs from the lower part of your butt into the calf. Men get it a lot from sitting in their wallets. The nerve is huge and runs through a small, stiff hole so it’s easy irritate. Many describe it as a shock from the butt into the leg. It isn’t typically exacerbated by leg raises or back movement.
I also have horrid lumbrosacral problems and severe DDD. I am only 37. No children. Never been overweight. I see physical medicine and rehab next week. PM&R can help assess your functionality but sounds like you might want a good neuro evaluation. If you lose too much sensory or motor then surgery is sometimes discussed. It doesn’t help too much with pain but will help with loss of function/sensory. A short course of steroids will also dampen nerve inflammation until you get appropriate evaluation and treatment.
Sorry you’re in pain. Sending hugs. ❤️xx
Hi, thanks for message. I am in no pain... Ache lower back... Bad pins needles, but can't say I'm in pain. Would put up with that but not with loosing use of left leg x
My lower lumbar issues started suddenly in my 30s when my kids were young. I assumed it was caused by childbirth (large babies with difficult deliveries) but now I wonder.
I had a lumbar puncture 6 years ago and the neuro surgeon really struggled to insert the needle and told me after she finally drew enough that I must surely get an MRI to see that was causing this obstruction. It never happened though - everyone too busy telling me what I didn’t have (MS) to look at what I did clearly have (a systemic autoimmune disease overlap and severe DDD).
I only learnt last year from an incidental finding that I have thoracic scoliosis. Even as a child my joints would slip and I was terribly uncoordinated. Now in my late 50s I’m looking back and realising I have probably always had hEDS - but once we hit fifth decade with other connective tissue diseases confirmed - it’s impossible to get this recognised.
I often wonder whether hyper-mobility would explain things for a lot of younger people diagnosed with wear and tear arthritis eg my late mum and both my sisters.
Absolutely. I saw a geneticist for hEDS but I’m not hyper mobile. I exhibit a lot of features from type 4 vascular EDS. I bruise easily, my skin has been described as paper thin among a family history of aortic aneurysms. I have a small cerebral one as well.
Since my joints weren’t super mobile/double jointed, they wouldn’t test me for EDS. But I agree with your suspicions as well. Short of paying out of pocket for a mail in genetic test, I’ll never know.
Same here - although I was hypermobile when younger and still just meet the Beighton hypermobility score I think. But I’m 58 and the only reason I’d bother getting tested now is because I suspect it makes Scleroderma present unusually for me.
I also have some scleroderma features. I looked quite CRESTy in the beginning. But once the aPL came back positive and I started having NPSLE symptoms, all was chalked up to lupus. But like you said, I feel like any connective tissue disease would cause pseudo EDS problems since cartilage and supporting tissues degrade in both. I honestly was very surprised to hear that I had severe DDD. I’ve always been super active and still make myself exercise every day. I know that nothing will make it better so I just keep on keeping on until I start getting radiculopathy and/or weakness. It’s bound to happen at some point.
My joints sometimes lock like they wiggle out the socket and my skin has always been stretchy. But I couldn’t touch my toes bent over if you paid me a million dollars. I sometimes also feel Marfan-like at times. But I’m not that tall. I think the likeness of autoimmune CTDs to genetic mutation causing CTDs is interesting. I’m sure there is a ton of overlap.
Oh yes I think we are both on track here re CTD related over-stretchiness combined with excessive stiffness and premature wear and tear. They weren’t previously known as collagen vascular diseases for nothing?!
I just don’t know with antibodies anymore. People who don’t have any specific antibodies tend to focus a lot on antibodies being unnecessary tools for diagnosis. I know this because it was me until a few years ago. Ten years ago I was diagnosed with seronegative (RF was positive and no one tested by ANA) RA. Then this changed up lip biopsy positive Sjögren’s.
Only my ANA was positive (nucleolar pattern) and then only strongly positive when I was on too low a dose of thyroxine 5 years ago. But I always have raised immunoglobulins which I’m told is specific to Sjögren’s - usually seropositve.
Since then ANA has dropped incrementally to a consistent weak 1:80 and was more or less discounted by the vascular/ Scleroderma dr I used to be under.
Then a very specific limited/ cresty antibody showed up as weakly positive 3 years ago - but again this was discounted as belonging to my nucleolar ANA panel and viewed as a false positive.
Now, under a new rheumatologist who specialises in Lupus, I have a strongly positive Scleroderma antibody (U3 RNP - very rare) which showed up the same high titre 3 times in 12 months. Its arrival corresponded with strange skin changes and marked deterioration in circulation and my GI issues
A Lupus friend from here has just described this as “probably rogue” - but no it’s not. She just doesn’t know anything much about how heterogeneous Scleroderma is and how significant its various antibodies are.
Similarly to gene mutations - I now find I’m a great believer in the significance of antibodies - and the likelihood that many are under tested or haven’t yet been found.
With scleroderma, antibodies are particularly relevant/useful guides to overall prognosis because systemic scleroderma generally has a poorer prognosis overall than the other rheumatic autoimmune diseases.
And although mine is apparently too rare to be diagnostically enough in itself - prognostically it points to a high risk of pulmonary arterial hypertension. And whether of not I’m Cresty or Sjögren’sy - or even Lupusy - I’m definitely corresponding prognostically with my rare antibody - which often shows much later skin involvement but more early stage organ and MSK involvement - particularly for severe GI issues.
So I do feel lucky to have an antibody now in many ways - and am newly fascinated by the significance of autoantibodies in general x
What a great little blurb. I had no clue they were once called collagen vascular diseases. I’ve always and only known them as connective tissue diseases. You learn something new everyday!
My rheum tested me for the whole spectrum of antibodies when all of this started. This included U3 RNP. She tested me for Sjogrens, scleroderma, dermatomyositis, polymyositis, drug induced lupus. I’ve only been ANA positive once. As a matter of fact, my labs scream more of a lymphoma picture. Never have had a positive dsDNA but my rheum is beyond convinced at this point that I have SLE even with no antibodies except LAC, so I get a dsDNA checked every 6 mos. Although, of all the aPL antibodies, LAC alone has the highest correlation with clotting and lupus so I have to agree with my diagnosis. I do have all of the classic lupus diagnostic criteria. Once my renal function started to decline, rheum felt more confident about my diagnosis. I was UCTD for a while because I didn’t have antibodies. Saw 2 prominent lupus specialists who said I screamed of lupus.
I know what you mean about antibodies and they are particularly important for prognostication especially in scleroderma. You are spot on the money there. I hope you do not develop pulmonary hypertension or muscle problems. I know RNA polymerase III is the scariest because these people tank quickly once their kidneys get hit. I’ve had the unfortunate, fortunate experience of caring for a gentleman when I was medical school student who had a scleroderma renal crisis, went on dialysis and died within a month.
Sometimes, I’m a little lackadaisical about getting more tests at this point because I’m prodded out. Just trying to coast until the next major event which always helps clarify the picture for me. There are tons of antibodies that have yet to be found I am sure of.
I’ve actually been talking with a few people in the US who are teeing up testing for personalized, targeted care in lupus. One company is looking a gene expression and tailoring immunosuppressive therapy to the expression of diff inflammatory markers. Some want to just test the presence of certain proteins and cytokines to help tailor treatment. I’m hoping we can help decipher the heterogeneity of these diseases soon enough.
Great chatting about this stuff. I’m on a lot of meds to prevent sudden renal crisis of Sclero and also hopefully to prevent PAH.
However, following what you’ve just written, I do hope that it’s not just “personalised, targeted care” for Lupus patients. I feel strongly that the relative commonality of Lupus and RA are part of the problem where it comes to researching and raising awareness for all the others, particularly overlaps. The more rare, the more underdiagnosed, underesearched and the more underestimated the others will remain.
I just don’t think it works out too well when we assume that research into either RA or Lupus will also help those with scleroderma, Vasculitis, Myositis or Sjögren’s, Stills etc - or overlap syndromes. This certainly hasn’t been my experience to date anyway - having gone from diagnosis to diagnosis over the past ten years.
For instance why do patients with the various types of Myositis often qualify for IViG where those with neurological manifestations of Sjögren’s don’t? I have two friends who died as a consequence of neuro Sjögren’s so I’m bewildered by this kind of coding.
I feel it’s high time for the international medical community stopped getting hung up on titles and perhaps revert to the heading “collagen vascular diseases” or just CTDs - and see this as one overarching heading - one huge spectrum with very many subtypes, some unique, all potentially life threatening and all with degrees of severity which can all impact greatly on our quality of life?
This way plasma therapies, dmards, biologics etc could start being personalised and targeted at all of us rather than only at Myositis over Sjögren’s or RA over Lupus - or whatever.
I’m so glad that I have doctors who are being led by my antibody now rather than by a disease label. To me this seems the way forwards for all of us under rheumatology and immunology. Amd this chat with you has helped clarify what has been bothering me for years - and why. X
CTDs definitely overlap. It’s a spectrum for sure. I think anything used for lupus can be applied to other CTDs. However, there really aren’t as many FDA approved treatments for lupus like some other autoimmmune disorders esp MS and IBD. They are stocked and loaded with choices. Albeit, they aren’t smoking guns but choice for SLE treatment are quite limited. Scleroderma is actually approved for bone marrow transplant in the states.
When it comes to funding and applications, goals must be specific. To get a grant for research, you can’t be vague and have to pick a target CTD to study because funding is syphoned from different departments and groups that may fund only one specific CTD. Once discovered and patented, it can be utilized to help diagnose and treat other autoimmune disorders. Long term, I don’t think the technique will specifically apply to lupus. I just think lupus research rakes in more funding. Got to start somewhere.
I think RA is actually the only rheumatic autoimmune diseases that is very well served from both research and pharma disease modifying treatments perspectives.
And somehow it doesn’t seem obvious at all to me that the rest of us have benefited greatly from the research and awareness of RA as a common systemic autoimmune disease - as people with RA assume we will. Same goes for greater awareness and more treatment options for lupus helping those with Sjögren’s. Using one disease as umbrella for all doesn’t work well as far as I can see.
Whereas viewing all these diseases as part of a spectrum with personalised targeting of treatment protocols might work much better I feel. Maybe this is where autoantibodies and genetic markers need to play more of a role?
In fact I think a lot of the international Covid risk research has focussed on inflammatory arthritis sufferers and their medications and their inherent vulnerabilities at the expense of those with rare rheumatic autoimmune diseases. Rare so often gets lost by the wayside - and in the scheme of all things rheumatic, Lupus isn’t that rare. Nor is Sjögren’s but it’s definitely the poorer relation.
But also - having followed a couple of scleroderma communities - one in the US and one a local group - I would say that stem cell transplants for some young people with Scleroderma are not treatments that can be compared with ours - they are literally about life saving due to acute renal crisis or lung fibrosis or total GI failure.
This is very different to having treatments which prevent things getting that bad. 4/6 of those I’ve met in person with systemic sclerosis have died due to this disease, one overnight when I was on a hospital ward with her. There’s an 18 year old lass across the way from me who has already lost one lung due to fibrotic disease of SSc and urgently needs a stem cell transplant in order to hopefully survive. Another young woman in the US - of around the same age - has just died in the early hours due to the same form of systemic sclerosis.
Whereas people with Sjögren’s and Lupus are probably pretty quits on the mortality stakes - some with more severe disease coping with progressive heart, lung, kidney and lymphoma related issues. I know that these patient communities I’m on are much larger than the scleroderma ones. So relative to patient populations the risk of death from scleroderma has to be considerably higher than it is for those with Lupus or Sjögren’s or overlaps.
I hear you. The diagram I attached addresses your exact point of overlap. Unfortunately, it is hard to ask for funding that would address all CTDs at once as a spectrum. Funding just doesn’t work like that. We depend very much on lab criteria and antibodies when studying different autoimmune disorders. It’s the only way we can separate them.
Much of what gets studied depends on who is affected by certain disorders. Because many CTDs are more prevalent in women, minorities and are a source of shame (at least in the US), they don’t get much attention. I hate to say it (sorry Paul) but R+D in the CTD field or any field is still white male led. Much of the problem I see is that the people doing the research are not focusing on what would improve our quality of life. It’s all about predicting how to save money and keep people out of the hospital. I have emailed multiple researchers offering to help brainstorm and develop clinical trials on a VOLUNTEER basis. I NEVER hear back from them.
I understand your frustration but from a realistic point of view as someone who has worked in both research and clinical trials, it’s not easy getting grants for these things. And when asking for money, you have to be specific and it has to be on something that affects a lot of people like millions for someone to even pay attention. Some CTDs are just hard to study because the numbers aren’t there to actually run a strong powered study with meaningful data. It can take decades to gather enough patients for trials because these illnesses aren’t that common.
I think most CTDs get the shaft when it comes to treatments but I also think rheumatology here in the US doesn’t attract the strongest physician candidates. It’s not a competitive specialty here while the best and brightest go into hematology and oncology. There’s a lot that must be changed to put CTD research at the forefront but I don’t think it’s for lack of understanding that it’s a spectrum. It’s about finding the right people with enough money to do the work.
I think Sjogren’s has been sorely neglected in terms of research. I am not sure why. In the US you can only qualify for IVIG if there is evidence of effectiveness. Sjogren’s neuropathy and gastroparesis do qualify, I believe.
You are definitely right that they can’t make any assumptions about treatment from other connective tissue diseases. We need more and better research.
According to that Mayo neurologist it’s very hard to get insurance to pay for IViG for Sjögren’s autonomic neuropathy in US too.
In UK I can’t get it - my rheumy has checked. If I had Myositis which wasn’t responding to Mycophenolate then I’d qualify. This inequality is why I wish that all CTDs were afforded the same status where choice of treatments are concerned - because I know that they are all part of one huge systemic spectrum - each with degrees of severity. We all need personalised medicine.
And to get back to the post - no one should have to get to the stage of incontinence and cauda equina in order to qualify for neuro surgery X
PS I too exhibit loads of signs of vEDS. I guess this goes hand in hand with connective tissue tissue diseases for both. X
Doesn’t VEDS usually have at least one major medical emergency before we are thirty? I believe most V EDS patients’ life expectancy (51) is still not very high even with the heart and vascular protocols in place.
Yes. My uncle died at age 41 of a ruptured aortic aneurysm. It’s the one thing that has always sat in the back of my mind. A lot of my family are heavy smokers on that side so sometimes I wonder if smoking hardened their vessels so they aren’t as stretchy.
I’ll never know and just figured even if I did, would I want to know? Kind of would rather be ignorant because once I knew, I’d be more fearful and careful. Not like they can do anything for it once diagnosed. Just puts you in the don’t do caths on this person, which no one with lupus really needs.
TJB1 This is the story of my life since 2009 ,surgeon is useless ,tells me until I loose bowel or bladder control who will not even think about doing an operation, whilst he's not doing an operation I can walk probably two to three steps and then my back goes into full spasm and I can't actually move so I have no idea when when or what is going to happen I just sit at home vegetating,getting more and more depressed, it's a bloody nightmare 55 years old and I could sit here all day crying because of the pain ,I've got more oral morphine in my house than they have at the chemist down the road????.
So sorry, hope yer situation improves
Thanks i do as well but it's not looking very lightly at the moment ,it is what it is unless I get bowel or bladder control problems noting is going to happen ,if something doesn't happen soon I'll be in a wheelchair the way things are going ,you wouldn't have thought that breathing could cause pain in you back would you but that's what's happening but the moment !
Not to scare you or make you more furious but this is exactly what happened to my pal. She had years of pain blamed on sciatica and then suddenly one day she lost complete control of her bladder and bowels.
She lived on an island and her GP sent her by air ambulence to the mainland hospital where a junior dr tried to dismiss as sciatica and would have sent her home.
But thankfully there were no flights so he sent her for an mri and put her on the orthopaedic ward overnight. However in the early hours she was told that a neurosurgeon had looked at mri and said this woman is half an hour of being paralysed from waist down by complete cauda equina. She was operated on immediately and is broadly okay now.
So maybe just do whatever it takes to get taken seriously ie pee or poo yourself. It’s disgraceful that we have to wait until potential paralysis to get the surgery we need.
I've tried but it just can't do it for some reason,I know what your saying and I have thought about it ,but I just can't, I've got an actual hospital appointment next month in the pain clinic so I will wait and see if they are going to do something ,because something has to happen and soon.
Aww I totally understand. I recall a friend’s brother in law who’s a consultant rheumatologist advising me once at a picnic to paint a lupus rash on my face or slam my knuckles in a door just before my next rheumy appointment, in order to get onto biologic drugs.
And he added that I should not get landed with Sjögren’s as a diagnosis as it doesn’t tick the necessary boxes to get these drugs that RA and Lupus would qualify me for.
Despite being desperate to get back onto a better treatment at the time because I felt constantly awful - there was no way I could ever fake any symptom. I can’t tell lies for toffee - not even if my life or mobility depended on it. But if I do get worse incontinence I’m taking my lead from my pal’s experience and phoning 999. Hope it never comes to this for you but if it is just pull out all the stops. X
I can pee for England and am on nedatol to stop me. Doctor hasn't picked up if its connected to my back problem. Just ct scan to check my bladder level b4 and after peeing.
I hope they have made the mri tube a bit bigger because if they haven't i will probably have to use some sort of greasing agent to get in the bloody thing to be honest ,I used to work all over the country doing new prison blocks ,up and down site all day out on the night few ,well I say a few by few I'm talking at least 10 pints minimum,eat what I wanted and when I wanted it was well built let's say not fat just a bit stocky ,10 years sat on my bottom i think there's an least two of me now ,no exercise at all ,not because I'm idle I just can't do it to much pain ?