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#9860Topic: ACDF Surgery for 82 Year Old in forum NECK PAIN |
My father was diagnosed with compression in his spinal cord (C6-7, T1) and the doctors have recommended an ACDF procedure to mitigate it. He is 82 years old and is in very good health. His symptoms are weakness/numbness/jelly-like feeling in his left leg, numbness in his right foot, and a tingling sensation in his right tricep. Because of that he now uses a cane. We have been told that surgery is his the only option, and if he doesn’t do it, he will ultimately lose use of his legs. Are there any other treatments besides surgery, and is this a procedure that is recommended for an 82 year old?
Below are report summaries of the MRI’s he’s done:
MRI C-Spine Report of May 13 2013.
REPORT
Serial Sagittal T1 as well as axial T1, T2 images of the cervical spine show discs dehydration at all levels.
Images show evidence of subluxation at C7/TH1. The change is seen with a slip of about 6mm. The change is seen with an underlying disc herniation observed to cause focal canal stenosis and cord compression. Images also show subtle disc prolapses at C4/C5, C5/C6, and C6/C7. These changes are also seen to cause relative canal narrowing with cord compressions. Cuts are seen to show nerve roots compressions that show prominence on the right at C4/C5 and C5/C6, but of about equal magnitude at C6/C7. The change at C7/TH1 is also seen to show prominence on the right that observes to involve both sides. Images also show fatty degeneration of bony marrow at C5, C6 and C7. There is no appreciable bony change.
IMP
Degenerative disc disease with multiple discs prolapses seen to cause nerve roots and cord compressions with a severer herniation seen at C7/TH1 following subluxation which is seen to cause severer cord compression with severe bilateral nerve roots compressions and evidence of an underlying or attendant myelopathy.MRI L-Spine of April 26 2013
REPORT
Serial axial T1 and T2 weighted MRI images of the lumbar spine show generalized disc dehydration and posterior herniation of the L4/L5 as well as the L5/S1 discs with resultant spinal canal stenosis. Bilateral L4 and L5 neural foramina stenosis with likely compression of the in dwelling nerve root is also noted. Normal vertebral body heights, posterior vertebral elements and paravertebral soft tissues. The spinal cord ends at the level of the L2 vertebral is normal in appearance.
IMP
1. Spinal canal stenosis due to disc prolapse as described
2. Likely bilateral L4 and L5 nerve root compression as describedMRI T-Spine of April 26 2013
REPORT
Serial axial and sagittal T1 and T2 weighted MRI images of the thoracic spine show mild osteophytosis and generalized dehydration of the intervertebral disc. No significant posterior disc herniation or spinal canal stenosis is however noted and there is no evidence of cord compression. No significant neural foramina narrowing is noted. The spinal cord is normal in signal and appearance.
IMP
Mild spondylosis of the thoracic spine. No evidence of coed compression noted.#9837 In reply to: direct cord contact relevant within cervical spine |That is my confusion then…Central stenosis VS cervical stenosis, since both can cause myelopathy.
When there is no CSF in the C5- C6 anterior aspect of the spinal CANAL because a disc has herniated and compresses the spinal cord ( creating an indention in the spinal cord itself …..in conjunction with 2 areas of buckling or hypertrophy of the ligamentum flavum ( posterior to the C5-C6 disc herniation ) can that cause myelopathy, with flexion or extension given the there is no telling how much dinging is going on ( walking, bending, driving, laying, turning over in bed and lying on side in bed )
A still image ( ie ) MRI of cervical spine laying down shows the anterior aspect of spinal CORD is indented at the C5-6 region with NO CSF obviously since the disc is pushed into the spinal cord, and in addition at same region, but posterior to the C5-6 which further narrows the spinal canal ( cervical stenosis) is the buckling or hypertrophy of the ligamentum flavum, and there is CSF present in the posterior section as described, just not the anterior portion, which again is because the disc has pressed into the spinal cord….
I hope I am explaining this right…..there is no increased signal in the spinal cord ( which represents permanent damage to the spinal cord )
But my concern, and because of my symptoms that do indicate myelopthy, IF there is too much pressure on the cord, whether medical science feels the cord has to be squashed significantly before there can possibly be myelopathy……….due to my hands upper wrist, feet, chins…. disequilibrium, severe ear ringing and such….
of which are really bothersome for me, in addition the spine clinic evaluation that noted hyerflexia in all extermities, but then subsequent to the spine clinic reflex test, the neurology Doctor repeated test and said my reflexes in legs were 1+ otherwise absent, he also later did the EMG which was abnormal and said mild to moderate periphreal neuropathy as well as some portion of the EMG was indicative of L5- S1 ( but have had NO MRI of lumbar spine )
I am 5’3 1/2 109 lbs on a good day……I am not diabetic……so I am so confused :(
I just want to find a root cause and treat if I could get better :(
Is cervicogenic neural coupling “real”? In other words, can “cervicogenic” headaches, facial numbness, etc. really be explained by cervical spinal neurological issues (nerve entrapment for example).
Facial numbness cannot be explained by cervical spine problems. The facial nerve exits through the skull directly into the face and bypasses the spine. Occipital headaches however can be generated by the neck. The greater and lesser occipital nerves originate from the neck and travel over the head to the top of the eyes and ears.
There are a handful of patients I have who think that facial numbness originate from the neck as they have neck pain associated with facial symptoms but I have not been able to make a neurological connection between these two structures. There is some evidence that there are cranial nerve nuclei (the origin of these nerves) that may descend into the upper cord at C1 or C2. Even if this is true, there is no evidence of cord compression that will affect these nuclei in patients who connect facial numbness to cervical spine issues.
Can cervical spinal problems (stenosis, foraminal narrowing leading to root compression/entrapment, etc.) also account for lower limb symptoms (i.e. tingling and numbness in the toes, loss of cutaneous sensation)? Again, both neurologists contend that this is not “anatomically” possible!
These neurologists may not understand the question as I see this pattern every week. This symptom pattern is produced from myelopathy (see website) and these symptoms are common. When the cord is compressed and malfunctioning, legs can become weak with strange symptoms such as paresthesias (pins and needles), weird cutaneous symptoms (cold water trickling down the leg or bugs crawling on the skin) and numbness.
Parkinson’s disease is a disorder of the substancia nigra within the brain and can cause many weird symptoms. I am by no means an expert on Parkinson’s disease but I do have patients with this disorder. The stiffness and change in gait associated with Parkinson’s disease can abnormally load the spine and magnify any spinal disorder that is not previously symptomatic.
Your MRI report of “Moderate C5-6 and C6-7 and mild C4-5 central canal stenosis, based on disc/osteophyte complexes, with slight indentation of the anterior aspect of the spinal cord at the C5-6 and C6-7 levels. No evidence of myelopathy.
c) Mild to moderate left and moderate to severe right C5-6 and severe right and
moderate left C6-7 neural foraminal narrowing” could be an indication of the beginnings of myelopathy but the radiologist is not too concerned about this compression.What are the findings of your physical examination? Do you have long tract signs (hyperreflexia, clonus, Hoffman’s sign, imbalance, incoordination)? Do you have the typical symptoms of myelopathy (see website)?
Dr. Corenman
PLEASE REMEMBER, THIS FORUM IS MEANT TO PROVIDE GENERAL INFORMATION ON SPINE ANATOMY, CONDITIONS AND TREATMENTS. TO GET AN ACCURATE DIAGNOSIS, YOU MUST VISIT A QUALIFIED PROFESSIONAL IN PERSON.
Donald Corenman, MD, DC is a highly-regarded spine surgeon, considered an expert in the area of neck and back pain. Trained as both a Medical Doctor and Doctor of Chiropractic, Dr. Corenman earned academic appointments as Clinical Assistant Professor and Assistant Professor of Orthopaedic Surgery at the University of Colorado Health Sciences Center, and his research on spine surgery and rehabilitation has resulted in the publication of multiple peer-reviewed articles and two books.#9734Topic: Cervicogenic numbness, cervical => lower limb, Parkinson's Disease in forum NECK PAIN |I’ll post my questions up front so that readers can decide whether or not to wade through the full details:
Questions:
1) Is cervicogenic neural coupling “real”? In other words, can “cervicogenic” headaches, facial numbness, etc. really be explained by cervical spinal neurological issues (nerve entrapment for example).2) Has anyone else experienced facial cutaneous lack of or change in sensation (numbness or tingling) that is correlated with cervical spinal issues?
3) Is there really a known nociceptive feedback pathway between the trigeminal nerve (facial innervation) and the cervical spinal nerves? If so, how far down does this coupling extend (C2-C3 or as low as C5-C6). I’ve read the med. literature and this seems to be in dispute. My neurologists (two now) both refuse to believe that cervical spinal neurological issues can cause facial numbness, despite my presenting them peer reviewed articles from multiple medical journals.
4) Can cervical spinal problems (stenosis, foraminal narrowing leading to root compression/entrapment, etc.) also account for lower limb symptoms (i.e. tingling and numbness in the toes, loss of cutaneous sensation)? Again, both neurologists contend that this is not “anatomically” possible!
5) Do any forum members also have Parkinson’s Disease? Has it (in your opinion) in any way contributed to your spinal issues?
Background:
I have early-onset Parkinson’s Disease (I’m 52, male). I don’t believe that is directly related to my spinal issues, but the muscular hypertonicity associated with PD may be a contributing factor. I have been active in several different sports (cycling, mt. biking, go-kart racing, windsurfing, snow-boarding, etc.) most of my life.
I have symptoms that are similar to those described by multiple participants on your forum.Symptoms:
1) Neck spasms (predominantly trapezius and sternocleidomastoid), which lead to progressive, bilateral numbness and “tingling” sensation, starting with my toes, spreading to my fingers, and eventually resulting in the loss of all cutaneous sensation on the right side of my face. This is often accompanied by a “burning” sensation in my forearms and calves (predominantly right side, sometimes bilaterally).2) During these acute spasm episodes, which are typically induced by turning my head to the ROM limit on either side (with right ROM much more limited), a “feedback” effect seems to occur. By this I mean that the neck muscles begin to (involuntarily) tighten, leading to increasing numbness with the following progression: right toes, left toes, right finger tips, left finger tips, right cheek, right earlobe). This is coincident with a noticeable displacement of my neck (without head rotation) to the right, predominantly along the axial plane.
3) During onset of one episode (fearing myelopathy or other irreversible neurological damage) I went to the local E.R. There I was given an intra-muscular injection of Diazapam. Within 15 minutes, the muscle hypertonicity began to subside, as did the other symptoms (tingling and numbness).
4) An oral dosage (5mg) of Diazapam also produces the same mitigation of symptoms, but with some delay (typically being effective within 30-45 minutes). I have been prescribed Metaxalone and Cyclobenzaprine (standard adult dosages), but neither is effective when an acute “spasm” occurs. Either may be effective if taken prior to acute onset as a prophylactic. I don’t have enough experience with these drugs (yet) to determine this.
5) I was also prescribed 10mg/350mg of hydrocodone/acetaminophen, but do not have much (if any) pain associated with these symptoms.
I have had the following tests performed:
1) Cervical, Thoracic, and Lumbar spinal MRI imaging without contrast, all in the standard prone position. I have the radiologist’s reports and raw DICOM images for all three. The Thoracic and Lumbar MRI were unremarkable, with no indication of stenosis, myelopathy, or central canal narrowing. The relevant “impression” portion of the Cervical imaging study is:a) Degenerative disc disease, hypertrophic spondylitic, and mild to moderate
disc bulges changes of the posterior elements scattered throughout the cervical
spine.
b) Moderate C5-6 and C6-7 and mild C4-5 central canal stenosis, based on
disc/osteophyte complexes, with slight indentation of the anterior aspect of the
spinal cord at the C5-6 and C6-7 levels. No evidence of myelopathy.
c) Mild to moderate left and moderate to severe right C5-6 and severe right and
moderate left C6-7 neural foraminal narrowing.
2) MRI of the brain, taken in 2010 to rule out other causes of my tremor (attributed to PD). There were no unusual findings here, per the radiologist’s report.3) Upper and lower limb EMG/NCV tests. I do not yet have the final report for this, but was told during the testing that some of the latencies were abnormally long. The EMG action potentials and velocities were normal (good CAP and >50 m/s velocities). The abnormal latencies are unilateral (right side only), but present in both upper and lower limbs. Upper limb abnormal onset delays are only evident in the ulnar nerve. In the lower limb only the peroneal nerve appears to be affected.
I have been to two neurologists and a physical medicine M.D. (who performed the EMG/NCV) and have an appointment in 2 weeks with a neurosurgeon. Both neurologists claim to have no explanation for my symptoms. Both claim that neither the cervical stenosis nor spurring is severe enough to account for my symptoms. The T2 cervical MRI images show none of the “telltale” signs of myelopathy (no white spots in the cord itself). Both claim it is simply not anatomically possible for cervical spinal entrapment (or foraminal root compression) to cause the numbness in my toes (which is now chronic)!
The facial numbness perplexes them completely. Based on my own research (I’m not an M.D., but have a Ph.D. in bio-medical engineering), I have found several references in the med. literature documenting cervocogenic headache, and (less commonly) facial numbness resulting from C2-C3 spinal abnormalities. This is based upon a postulated (and disputed) nociceptive neural feedback pathway between the Trigeminal nerve and the cervical nerves, possibly extending as low as C5-C6.
I suspect cervical spinal instability can explain some of these symptoms. During an acute event, the displacement of my neck is quite visible (confirmed by my wife).
Per my physical medicine specialist’s recommendation, I am scheduled for a cervical epidural steroid injection. Clearly there is some (albeit small) level of risk associated with this procedure.
Any comments/suggestions would be greatly appreciated, especially opinions as to whether or not the steroid injection is advisable (i.e. benefits outweigh the risks).
Dr Corenman, I hope this finds you well and your spine well aligned. I have continued to struggle with the same infraspine/scapular pain since c5/c6 acdf. As stated in previous posts, most problems started post wreck, of which the kinetics aren’t your typical rearend/frontend collision. Their were rotational forces along with being broadsided on the passenger side mid rotation, throwing me backwards and sideways where my upper back took some heavy blunt trauma from the drivers seat as I struck the side of the seat. Speeds from my vehicle and other vehicle were in the 50-60 mph range. The first mri I was given was a thoracic approx 1 month 1 week post wreck. The findings were incidental, being mild degenerative changes at t8-9, and t9-10. At this point the thoracic issue was laid aside and never readdressed.It occurred to me recently that the same radiologist that missed key points including a focal herniation with cord impingement at c5-c6, was the same radiologist that read my thoracic and I decided to put my own eyes on it. Frankly, I was dumbfounded by what I saw. The localizer view showed what appears to be a large area of edema in the vicinity of where my back took the blow. The anterior longitudinal ligament appears to be avulsed from t5-t10, with a large pocket of fluid(edema) between it and my vertebrae, coinciding with the localizer view. Their appears to be a couple of places where their are fractures at the rib joints, 1 at t3. Also, what appears to be a compression/wedge fracture at t4-t5, starting a cascade of vertebral problems including other fractures down to around t10, with vertebra touching vertebrae in numerous places. The other concerning aspect of the imaging is the axial view shows what appears to be almost every posterior part of the vertebrae on the image whether I’m looking at the lamina or spinous process shoved forward from the blunt trauma as the vertebal column was compressed, breaking the posterior parts of the vertbrae that hug my cord off, or splintering them…in some places broken off and touching the cord, or damaging the white material as they were shoved forward, taking gouges out of it before being stopped by compression or going back into place by the recoil. Is this a naturally built in mechanism to prevent the bones from cutting my cord? It appears that it missed my cord in places by mm. Their also appear to be numerous facet joints that are missing or broken? Not to be redundant, but I’m not a radiologist and that’s just some of the stuff that sticks out to me. I know for sure that parts of my posterior vertebrae are touching the white matter of my cord, within mm of the cord itself. What’s perplexing is why none of this is noted? The only thing I can surmise is that when the images come up the default image from the saggital view looks fairly good. I can see why mild degenerative changes are noted. Its not until you rotate to the other side that the damage becomes apparent. Could the radiologist have biased himself from even looking through all the images if 1 side looks good? Especially it being the thoracic which is so muscled and reinforced? Seeing so many precautionary mri’s that don’t show problems, could mine just have received a cursory glance? My myelopathic symptoms persist post acdf, including constant urinary frequency and urgency, tinnitus, dropping things, weird musical hallucinations if I “unfocus my eyes” while looking at something, e.d. dysfunction at times. My left arm still hurts post acdf with persisting and digressing bicep weakness and pain, cold hypersensitivity, tingling in all fingers at different times with the worst now being pinkie and ring. Odd twitches in all parts of my body. The list goes on and on, with the focal spot of pain and burning(neuropathy) being left interspine, medial/lower scapula area. Their appears to be a direct correlation between length of time on my feet daily and the intensity of pain in my upper back,along with bending, twisting, sitting in the “thinking position”(possibly from facet damage). As stated, I am pain free for the most part if I lay down. Is it possible that my thoracic spine took that kind of beating and having that degree of spinal stenosis, while still being able to walk around and function(although albeit a struggle). Why can’t I get anybody to seriously re-evaluate my thoracic? I think my neurosurgeon thinks either I’m crying wolf due to either a) expecting results of acdf to resolve scapular pain quicker than usual, b) more pain medication(which I can’t get by without right now),c)because he doesn’t make mistakes and I’m just a regular person who knows nothing about neuroogy,d)liability(which I have chalked acdf to being necessary due to associated myelopathy whether it was really the pain generator or not, or e) all of the above. I know the reference lines on mri show 33 reference lines , including numerous that stop mid vertebrae, 2 of which have very odd angles <. It appears on multiple images that I'm looking through endplate disc, endplate. Or disc, end of posterior endplate from adjacent plane. I'm to the point that I'm about to walk into the e.r. and tell them I have upper thoracic pain and let them take it from there. Any insight would be appreciated?
#9607Topic: Pars defect after L4-L5 laminectomy, discectomy in forum BACK PAIN |Hi Dr. Corenman,.
I am wondering whether to contact my orthopedic surgeon regarding my recent MRI results. Here’s my spine history in a nutshell. I had a successful cervical laminoplasty with plate fixation C4,5,6 in 2009 for congenital cervical stenosis and spondylosis with myelopathy C3-4, C4-5, C5-6, C6-7. The doc told me I would always be hyper reflexive, have a positive babinski and clonus. I found that really interesting as I’m an R.N. After six weeks I was back to everything, no restrictions. :-)
I have lived with low back pain/spasm for about twenty years…rarely was it incapacitating. Usually, I just had a moderate burning sensation and used ice, heat Motrin to treat. Last September, I developed sciatica down the back of my leg and eventually a horrendous back pain that limited my walking for two days. I ended up getting an MRI via my internist which showed:
1. A posterior central to left paramedian disc herniation measuring 5 mm in AP and 9mm in transverse dimension at L4-L5 causing, ventral thecal impingement and also probable impingement on the intrathecal portion of left L5 nerve root accompanied by a severe central spinal stenosis due to combination of this and hypertrophy of the facets and ligamenta flava.
2. Mild central stenosis at L3-L4 and diffuse bulging of discs associated with degenerative disc disease without spinal stenosis or focal disc herniation at L2-L3 and L5-S1.
I had a lumbar decompression with partial discectomy last November. Follow up x-rays showed stable spine. I was released without restriction. :-)On a side note, I was diagnosed with osteoporosis in June and had a Reclast infusion due to hx gastric ulcers.
I was peachy for a bit, but began to have intermittent mild pain on lateral side of left thigh from low back to hip and down. It continued off and on. Within about a month I had two consecutive nights where I could not lay on my left side due to severe pain. I was fine during the day….lateral leg pain continued and mildly worse. I saw my surgeon; X-rays of lumbar spine were fine. My leg strength good. I think he said it could be ligaments and if worse I could get a steroid injection. Ok…
I kept on chugging along. I walk (aiming for 10,000+ steps daily) or use ARC trainer and/or elyptical at the Y for an hour. I do weight training 2x/wk….I limit training with any back strain. The pain continued from back to lateral thigh with intermittent tingling in toes. I saw my internist when the toes started. He x-rayed left hip and put me on Medrol dose pack. I was to call him if pain returned a week after I finished dose pack. I had no discomfort on the pack, but it did return along with toe tingling. just had an MRI with/without contrast. It showed:
1. Laminectomy decompressing thecal sac L3 and L5 vertebral body levels with enhancement of postoperative bed and epidural enhancement extending to a portion of the right lateral recess and to a lesser extent left lateral recess L4/5 with component fibrosis. This is nonspecific, but may contribute to patient’s symptoms. No abnormal nerve root enhancement.
2. Interval development of left L4 pars defect.Can you please interpret my most recent MRI. I have never been told of a pars defect and don’t know if I should let my surgeon know. My internist said he can send me to pain clinic but I’m just going to wait and see how I do. I am 55, 5’1″ and weigh 135. I do not smoke. I feel like I’m becoming a whiner and don’t want that. At the same time, given my 4 year history I want to be proactive. Thank you so very much!!!
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