#bilateral foraminal stenosis

[the--social--anarchist]

Bone Spurs and Spinal Stenosis

My cervical MRI result came in tonight. Obviously, I have yet to speak with a doctor about them but I can see the report via the MyChart app my hospital uses. Everything is “unremarkable” EXCEPT the C5/6 area. It reads as follows. “Left paracentral soft tissue protrusion and disc spur complex. Mild/moderate canal stenosis. Mild bilateral proximal foraminal stenosis.”

To the best of my knowledge (with the help of Dr. Google,) I has bone spurs that are causing soft tissue protrusion, as well as foraminal spinal stenosis; aka narrowing or tightening of the openings between the bones in your spine, specifically the foramen area where my nerves pass from the spinal cord to the rest of my body.

The symptoms/signs are spot on and I am feeling all the emotions right now. For one, I am elated that they actually found physical proof and an explanation for my pain. For two, I am absolutely devastated that my symptoms and pain started at age 11 and I am now 25. For those of you that are new around here, my mother is a narcissist who denied me medical care and treatment for most of my physical ailments. Namely the pain I have been experiencing. My therapist believes that she suffers from Munchausen Syndrome by Proxy, and that keeping me sick under the guise of “metal illness” was her poison. That being said, I told her my results and her only response was “Oh! I have that too! In TWO places!” and she bounced away. I’m not sure what sort of response I was expecting but it definitely was not that. 

At least I have the answer to one piece of this puzzle that is my failing body. At least now I have half a response when people ask “whats wrong with you?” At least now I can possible receive appropriate treatment, and seek advice from the appropriate doctors. At least now I have definitive proof that it’s not all in my head.

The original doctor I saw at the pain management clinic moved practices. I have to decide whether or not I want to follow him considering he was absolutely amazing, or if I want to see a different doctor at my existing office. 

Any advice or commentary is welcome. Let me know who treats your conditions. Neurology? Rheumatology? Let me know.

[thetigerlady]

MRI results...

TECHNIQUE: Multiplanar, multisequence MR imaging obtained through the

lumbar spine without contrast.

COMPARISON: None.

INDICATION: Low back pain for 3 years, radiation to left leg.

FINDINGS:

Osseous structures: Normal marrow signal. No fracture or vertebral body

height loss. No aggressive osseous lesions. No pars defects. Extensive

endplate degenerative signal changes at L3-4.

Conus medullaris/cauda equina: Tip of the conus terminates at L1-2.

Unremarkable cauda equina.

Paraspinous soft tissues: Unremarkable.

Lower thoracic spine: Unremarkable.

Alignment: 2 mm anterolisthesis of L3 5 on S1.

Levels:

Background relative congenital canal narrowing mid and lower lumbar

spine due to short pedicles.

T12-L1: No significant stenosis.

L1-L2: Small broad-based posterior disc bulge with mild canal stenosis.

The foramina are patent.

L2-L3: Congenitally short pedicles. Trace posterior disc bulge. Mild

facet arthrosis and thickening the ligamentum flavum. Mild stenosis of

the central canal and right foramen.

L3-L4: Congenitally short pedicles. Diffuse loss of disc space height

with broad-based posterior disc osteophyte bulge, facet arthrosis and

thickening the ligamentum flavum. There is severe stenosis of the

central canal and moderate bilateral foraminal stenosis.

L4-L5: Congenitally short pedicles. Small broad-based posterior disc

bulge with bilateral facet arthrosis and thickening of ligamentum

flavum. Moderate canal stenosis. Moderate foraminal stenosis, left

greater than right.

L5-S1: Congenitally short pedicles. 2 mm anterolisthesis with

uncovering and mild bulge of the disc posteriorly. Bilateral facet

arthrosis. Mild/moderate stenosis of the bilateral subarticular

recesses. The foramina are patent.

IMPRESSION:

1. Background relative congenital canal narrowing due to short

pedicles. Superimposed disc degenerative change and facet arthrosis at

multiple levels as detailed.

2. At L3-4 there is multifactorial severe central canal stenosis and

moderate bilateral foraminal stenosis.

3. At L4-5 there is moderate stenosis of the central canal and left

greater than right foramen.

4. Minimal anterolisthesis and mild/moderate subarticular recess

stenosis bilaterally at L5-S1.

Electronically Signed by Bradley S Van Dyke, MD; 5/5/2019 12:44 PM

[lostinafairytaleofchaos]

Throughout the last several months I have written about chronic pain and autoimmune illnesses, etc.

I sit still and think back about the days where I would promise myself I would always be healthy. I ate healthily, I exercised, I had a positive mindset, I did everything I thought was going to keep me in good health. On my mother’s side, between her health and all of her sisters, mother, aunt, even grandmother, their health was horrible. I did  NOT want to live that way. Yet here we are today. The mysterious pains and symptoms have been adamantly clear since at least since 1993ish. As time went onI focused more on my family and career. Once 2013 hit, it was all health issues down the hill from there.

Don’t get me wrong, I am still hopeful, I believe God heals and I can receive a healing miracle. Honestly every time I think I know my body, I am correct, Then comes another diagnosis, round of doctors, tests, treatments. I just hide behind a smile.

Let’s now move on to the latest discoveries, how exciting (do you hear and feel the sarcasm?)

A couple of months ago, my headaches and migraines began to intensify. Since 2012, I’ve received Botox injections for these migraines and for TMJ. It has always worked, like clockwork, every 91 days I go for treatment. I then take Topamax daily to control breakthrough headaches as well as a mood stabilizer.

Once the headaches began to migrate from the back of my neck into the back of my head, radiate down my shoulders, arms, into my hands and even my lower back, I knew this was different. I sought help from my rheumatologist. My rheumatologist diagnosed me with Impingement syndrome of the right and left shoulder, Occipital neuritis, and Sacroiliac dysfunction. During that visit, I was treated with lidocaine/ steroid shots in my neck, shoulders, the back of my head and lower back. I received minimal relief at all. My rheumatologist then ordered x-rays.

These x-rays showed:

Degenerative change at C5-C9 and C6-C7 with uncinate spurs

Lower lumbar facet joint space narrowing of the L5-S1 disc

Lucency proximal medial aspect fourth finger proximal phalanx, erosion

My rheumatologist suggested that I go to physical therapy. I thought about it, I decided against it. A friend of ours referred us to a great pain management doctor at UVA in Charlottesville, VA. I went to his office a couple of weeks ago. He thoroughly listened to my concerns and my pain. He scheduled me for a series of MRIs before proceeding any further. In the meantime, my rheumatologist called in two more muscle relaxers, which again did not alleviate the pain.

Last Wednesday, my new pain management doctor contacted me with the MRI results and explained that there were major findings as he suspected.

Findings:

C3-4: Bilateral uncovertebral hypertrophy

C4-5: Diffuse disc bulge and left greater than right uncovertebral joint hypertrophy.

Left foraminal stenosis

 C5-6: Diffuse disc bulge and uncovertebral hypertrophy. Bilateral lateral recess stenosis. Mild right and moderate left foraminal stenosis.

C6-7: Diffuse disc bulge and uncovertebral hypertrophy. Bilateral foraminal stenosis.

As you can see, this is a big deal, at least to me, not to include RA attacking two of the joints in my neck.

This is not my actual x-ray, it is just an example x-ray to show spurs

Foraminal stenosis is the narrowing or tightening of the openings between the bones in your spine. These small openings are called the foramen. Foraminal stenosis is a specific type of spinal stenosis. Nerves pass through the foramen from your spinal cord out to the rest of your body.

My pain management doctor was confident that he could help me, He explained there was a procedure called “the epidural steroid injection”.

I researched the procedure, watched videos to prepare myself (I always do this). Upon arrival at the pain management office, Dr. Messinger informed me of the procedure and the medications being injected was FDA approved, the procedure was updated, he explained that there is a space in the neck actually called the epidural area, that it was not the same as an epidural being placed at the time of labor. This was a relief because I had both children naturally, my last pregnancy, I attempted an epidural, however, it would not go through and caused an air bubble in my spine (that’s another story).

We discussed the risks overall. He did explain that I would not be sedated in any way, he allowed me to take my anxiety medication before the procedure. He explained the time it would take and that he would walk me through every step.

He did just that! It was almost painless. I lay face down on the table, with my face through a round cushion, the neck area is cleaned, the proper coverings are applied, there is an x-ray machine under and above. A local anesthetic is injected, this I was barely felt, he warned that I would feel pressure as he inserted the needle into the epidural area, this was minimal pressure. He let me know exactly what to expect as he pushed through the medication. There again, minimal pressure. A band-aid was placed over the site and I was told not to immerse myself in water for at least 48-72 hours. He placed me on Zanaflex, this is a different type of muscle relaxer. Dr. Messinger explained it could take 2 weeks for the full effect and relief could last 6 months or longer. He warned about the flushing of the face for 24-48 hours, my glucose levels could rise (I am also a controlled type 2 diabetic). Then I was off. The procedure took less than 10 minutes.

Throughout the day, there was minimal discomfort. The main discomfort was I had felt for months was being alleviated. During the night, I did feel a little achy and I took the muscle relaxers as prescribed. This morning I woke up with an elevated glucose reading.

All in all, so far, I am very delighted with the results and the decision that was made.

I will continue to drive over the hour it takes to see Dr. Messinger. I am pleased with his bedside manner, his professionalism, and his overall care for patients.

If I may offer any advice at all, please do yourself a favor, know your pain. If you have a doctor dismissing you, find another. If you have medications not working, speak up, they obviously are not treating your condition. If it doesn’t feel right, it most likely is not. Be your own advocate. You DO NOT have to settle.

Additional information below

What Are The Causes of Uncovertebral Hypertrophy?

 (https://bestdoctor.com/blog/uncovertebral-hypertrophy-causes-symptoms-and-treatment/)

Uncovertebral hypertrophy can be caused by many factors. Rheumatoid arthritis can cause the lining of joints to be swollen and inflamed. Or, the joints cartilage can wear away, which is mentioned as facet joint osteoarthritis. Once the cartilage disappears, the body recompenses by extra bone growth on the joints defined as bone spurs. These bone spurs can make it appear as if the joints are larger and thicker in a few areas. Therefore, either by extra bone growth or inflammation, facet joint “enlargement,” or “hypertrophy,” can happen.

What Are The Symptoms Of Uncovertebral Hypertrophy?

The pain of facet joint hypertrophy does not appear from the inflammation itself, nonetheless slightly from the inflammation effect has on surrounding spinal nerves. The vertebrae are enclosed by openings defined as foramina, via that our spinal nerves pass on their way to and from the sensory organs and muscles.

The swelling of uncovertebral hypertrophy can press on these nerve passageways, compelling the nerves to become restricted. This is why symptoms can frequently be “mentioned,” which defines they seem in places that are far from the damage site. For example, even though you may have uncovertebral hypertrophy in your lower back, the pain and numbness can spread all the way via the leg and buttocks.

What Is Right Uncovertebral Hypertrophy?

Right uncovertebral hypertrophy is a kind of a spinal disorder. Like sclerosis, it comprises the narrowing of spine parts. This can cause meddling with the spinal cord, leading to pain. You should see a physician/chiropractor immediately if you experience it.

What Is The Treatment Of Uncovertebral Hypertrophy?

Traditional treatments, such as physical therapy and pain medication, can achieve many cases of compression of nerve compression because of bone spurs. You can consult the best doctor to find the best kind of nonsurgical treatment for uncovertebral hypertrophy depending on your medical history and condition. If chronic pain continues after several months of traditional treatment, a doctor may recommend surgery as an option.

Cervical Facet Hypertrophy

(https://www.panoramaortho.com/wp-content/uploads/2015/03/Dr._Knight-Cervical_Facet_Hypertrophy.pdf)

 Degeneration and enlargement of facet joint.

 Each vertebra has two facet joints, one on each side. They are like the “knuckles” of the spine. They are small joints that have cartilage lining like other joints in your body. These wear down over time, with obesity, and with trauma (ex: MVA).

Sometimes you have facet disease without any other cause just due to your genetics.

Facet joints glide and allow movement to provide flexibility, stability, and support to the spine.

Enlargement of facet joints can cause pressure on the surrounding spinal nerves and can cause radiating nerve type pains.

Symptoms of Facet Disease

Stiffness, discomfort when tilting neck backward, joint swelling, decreased mobility, tenderness near inflamed facet joints, muscle spasms and/or weakness. May cause neck pain that wraps around the neck and/or radiates to the top of shoulders.

Symptoms usually present themselves more with reading, sitting at the computer, driving, and/or jobs where you have to look up or down for prolonged periods.

 Usually, Facet Disease of the cervical spine will present with neck pain only.

However, if the facets are enlarged enough, they can compress the surrounding nerve roots and cause radiating nerve pain.

 Therefore, figuring out facet disease can involve a process of elimination. An injection can help to do this. If your pain goes away with a facet injection, then we know this is where your pain is coming from. Sometimes you can have both facet disease and nerve compression. So, sometimes you need an injection to the facets as well as to the nerves.

    I plan to keep everyone updated on my journey, stay tuned.

As always thank you for reading, following, and please comment or ask questions. You can comment on this blog directly or via colorfulchaosthejourney.com

Share and have your friends subscribe to receive every post as they update!

A Pain In The Neck Leads to More Throughout the last several months I have written about chronic pain and autoimmune illnesses, etc. I sit still and think back about the days where I would promise myself I would always be healthy.

[lupine-publishers-sjfn]

Lupine Publishers | Central Nervous System Manifestation of Multiple Myeloma: A Case Report

Lupine Publishers | Open Access Journal of Oncology and Medicine

Abstract

Multiple myeloma accounts for <1% of all malignancies and Central nervous system (CNS) manifestation of multiple myeloma (MM) is rare. Multiple myelomais characterized by malignant transformation of plasma cells that produces immunoglobulin chains. The accumulation of plasma cells in bone marrow results in clinical features like anaemia, osteolytic lesions, hypocalcaemia, renal failure and immunodeficiency [1,2]. The involvement of central nervous system is very uncommon in multiple myeloma and it may present early or late during the course of disease. The neurological symptoms can be diffuse headache, persistent vomiting, vertigo, weakness in limbs, urinary incontinence etc. Symptoms can be attributed to spinal cord or nerve root compression, peripheral neuropathies, and uremia [3,4]. Likely risk factors of CNS manifestation are unfavourable cytogenetics, high tumour load, low marrow involvement. In this report we describe a patient with CNS involvement after receiving systemic chemotherapy and symptomatic treatment.

Keywords: Central nervous system, Multiple myeloma

Case Report

A 52 years pleasant lady presented with complaint of pain in left leg with lower backache and tingling sensations for 10 days. Subsequently she developed pain in right leg followed by urine incontinence. MRI Lumbosacral Spine was done which reported ill defined lesions at L3-L4 vertebra (with associated periosseous fluid collections) and multiple focal lesions in the L4 vertebra, bilateral sacral ala and both iliac bones along with indentations upon the thecal sac by spondyliticridges, secondary spinal canal stenosis and neural foraminal narrowing at multiple levels and left exiting nerve root compression at L3-L4, L5-S1 levels (Table 1). She underwent L1-L5 stabilization, L3 decompression with laminectomy, biopsy, posterolateral fusion with local autograft. Histopathology reported plasma cell dyscrasia at L3-L4 level. Immunohistochemistry reported tumor cells are focally positive for CD-138 and kappa light chain and negative for lambda light chain. On further evaluation bone marrow biopsy reported plasma cells approximately 50% of total nucleated cells suggestive of plasma cell myeloma. Bone marrow aspiration shows plasmacytosis approximately 24% of total nucleated cells which confirmed the diagnosis. She received 15 cycles of Bortezomib and Thalidomide.

In view of persistent pain in legs MRI dorsal spine was done which reported well defined altered intensity expansile lesion in L3 vertebra extending into epidural space. She received palliative external beam radiotherapy to L3 vertebra 30Gy/10 fractions. She remained asymptomatic for a month. Then she presented with complaint of lower limbs weakness and nausea, loss of appetite, constipation, weight loss (Table 2). USG whole abdomen was done which reported multiple hypoechoic masses in epigastric region. Whole body PET CT reported metabolically active soft mass lesion in gastro hepatic region measuring 9.7x5.5 cm SUV max 20.3, recto uterine pouch measuring 9.2 x 7.8cm SUV 20.9, left iliac fossa measuring 7.2x4.0cm- ?mitotic, metabolically active mesenteric nodes measuring upto 2.2cm-? mitotic and metabolically active lytic lesion involving L3 vertebra with paravertebral soft tissue component infiltrating left psoas muscles.

To confirm the diagnosis CT guided core needle biopsy from supraumbilical mass was done which was compatible with multiple myeloma. She then received 1st cycle of Bortezomib, cyclophosphamide and dexamethasone. After few days, she developed headache, giddiness and syncopal attacks. On evaluation CEMRI brain reported diffuse leptomeningeal enhancement involving both cerebral as well as cerebellar hemispheres. Mild enhancement of basal cistern with associated marginal dilation of ventricular system (Figure 1). In view of above mentioned complaints, cerebrospinal fluid study was done (Table 3) (Figure 2). CEMRI spine was done which reported no abnormal enhancement in vertebra, cord or thecal sac (Figures 3 & 4). She received 7 fractions (14 Gy) out of 12 planned fractions (24Gy) of whole brain radiotherapy and two intra thecal injection of methotrexate. MRI upper abdomen with MRCP reported large mass replacing entire head and body region of pancreas. Mass encases and compresses CBD with mild bilobar intra hepatic biliary radical dilation. There is also encasement of second part of duodenum with possible infiltrartion of adjacent hepatic parenchyma as well. Features are suggestive of aggressive pancreatic malignanacy, possibility of pancreatic lymphoma. Thickening and edema of gall bladder wall was seen which was suggestive of concomitant cholecystitis. She was advised for ERCP with SEMS placement which was refused by attendants (Figure 5). In view of her deranged liver function test, both radiotherapy and methotrexate were discontinued and she was maintained on supportive care (Table 4).

Discussion

Central nervous system is a rare location of involvement in MM, however it should be considered if a patient with MM presents with neurologic symptoms. Patients with MM often have neurological complications, either due to metabolic disorders such as hypocalcaemia, uraemia and hyper viscosity or due to peripheral neuropathy, spinal cord compression and cranial nerve infiltration [1,2]. The most common cause is spinal cord compression and cranial nerve infiltration [3,4]. The patient may present as a known case of MM with CNS features or as a new case with CNS symptoms. The clinical presentation depends on degree and site of infiltration. The symptoms and signs are headache, memory loss, behavioural changes, convulsions, nausea, vomiting, vertigo, urinary incontinence, backache, and limb weakness [3,4]. These symptoms can be attributed to spinal cord or nerve root compression, raised intracranial tension, meningeal inflammation [5]. In our case she presented with the complaint of headache, giddiness and syncopal attacks. This can be explained by CEMRI brain imaging which reported diffuse leptomeningeal enhancement involving both cerebral as well as cerebellar hemispheres. CSF study was done to reported to be negative. She received 7 fractions out of 12 fractions planned for whole brain radiotherapy and two injections of intrathecal Methotrexate injections [6]. In view of deranged LFT, radiotherapy and IT chemotherapy was stopped and was managed conservatively. She passed away after 2 weeks due to sepsis with LRTI with MM as underlying cause.

Conclusion

In conclusion this patient had an aggressive disease in view of abdominal deposits and unresponsiveness to multiple lines of systemic disease. CNS involvement in cases of MM portends extremely poor prognosis and median overall survival of <6 months. While in this case there was CSF infiltration which would portend even poorer prognosis but she succumbed to sepsis due to Lower respiratory tract infection. CNS disease in MM can be effectively palliated especially because of relative radio sensitivity of MM due to which early responses are seen at lesser doses and an early diagnosis can improve quality of life effectively.

[niklioni]

The World ENDED: December 15th, 2012

Yes. My world ended. Lett me explain to you why.

I am forty years old. I have worked in construction until my back gave out. I have flipped burgers, watched my demon child grow up, and been a complete MMORPG addict. I enjoyed television shows, read scifi/fantasy books, and dabbled in computers. While my kiddo made and still does make me happy to be alive, there was always something missing. A drive... a calling to do.. SOMETHING...

I found that during NaNoWrimo... Writing. I had a dream when I was only a kid to write. To make a living writing. NaNo rekindled that dream and it was burning bright. I wrote 133333 words during the NaNoWriMo competition, whose goal was to get you to write 50k words in a month. I didn't write a single word the last five days of the competition. I think I won.

I started on another story set some ten to fifteen years ahead of the story I wrote in November. In a week I filled up one and put down fifteen pages of another 70 page notebook with this story. And then I woke up on Saturday, December 15th with a crik in my neck. I worked it out and it went away. But I had this numbness in my right hand. I chuckled and thought little of it.

Sunday rolled around and the numbness had evolved to include electrical tingling. My ring and pinky ringers on my right hand were decidedly weaker, and that incessant electrical activity.. It felt like I had hit my funny bone, and some perverse god had frozen the most painful sensation and made it permanent in my arm. I was concerned, but not overly so.

Monday and Tuesday rolled through, and my hand, while annoying was not really that bad. The pain had stretched up my arm and back shoulder blade, but I could still handle it. I was concerned, and started getting myself prepared to go get it looked at. My daughter was doing finals that week, so I felt I had to be there for her if she needed me -at least for moral support if nothing else-.

Wednesday was a shocker. I woke up with absolutely no strength in my thumb, forefinger and middle finger. I went to pull up my pants like I normally do with both hands, and they bound up at my knees as I was only lifting with my left hand. My right hand couldn't even grasp the fabric.

I pushed the sense of panic into the back of my mind, I had no time for that kind of childish bullshit. I'm a damned adult. I needed to act like one. My elbow felt like someone was inserting long needles between the joints, but that was nothing to the lack of feeling in my pinky and ring finger. My hand felt dead. Half of it could feel just fine, but had no strength. The other half had only half its normal strength, but dexterity but reduced to an infant's. Still I waited.

Last day of school! I get my kiddo home from school, and immediately prepare to go to the ER. Yeah, I was scared, but the sensations in my arm and hand had not gotten any worse. I couldn't hold a fork to eat. I couldn't use a knife to cut my food. Couldn't zip up my pants with my right hand.

I couldn't write.

I CAN'T FUCKING WRITE!!

Even now, I'm stomping the keyboard with one finger on that hand. It's painful. My elbow is aching. My shoulder hurts. But I MUST WRITE. I Love writing.

But I feel no joy right now. I can't get lost in the story. All I feel is pain rather than the emotions of my characters. I can't develop a proper scene if all I'm thinking about is where I should throw my ONE FINGER to get the right letters on the screen.

My dream is being tested.

[ourhaileydavies]

Posterolateral Percutaneous Endoscopic Discectomy with Partial Pediculotomy for the L1-L2 High-Grade Downward Migrated Disc Herniation-Juniper publishers

Abstract

Background: Percutaneous endoscopic discectomy (PED) is one of the most useful minimally invasive surgical techniques for lumbar disc herniation (LDH). However, high-grade migrated disc is difficult to treat with only the standard posterolateral approach (posterolateral PED, PLPED).

Purpose: To overcome this difficulty, we combined the pediculotomy with PLPED for the treatment of high-grade migrated LDH. The pediculotomy is the recent technic for PED that has been explored with development of high-speed drill.

Case report: A 72-year-old man had a 6-month history of left L2 radiculopathy. His general state was too poor to perform general anesthesia and invasive surgery. The left L1-L2 downward migrated fragment compressed his L2 nerve root axial portion on magnetic resonance imaging. PLPED with partial pediculotomy was used for complete total removal, which cured his symptoms without any complications. Thirty minutes after fragmentectomy, we needed to control 100-ml bleeding from the anterior epidural venous plexus (AEVP).

Discussion: Upper-level migrated large lumbar disc fragments often require facetectomy with some fusion in conventional microscopic surgery. This case was too complicated for indicating the conventional technique. Only the flexible bipolar device helps control hemostasis in the PED system, but some bleeding cannot be controlled easily.

Conclusion: PLPED with partial pediculotomy was useful for a migrated fragment in patients with poor general conditions. Although the PED system requires a new device to control the bleeding from the AEVP.

Keywords: Lumbar disc herniation; Posterolateral percutaneous endoscopic discectomy

Introduction

Percutaneous endoscopic discectomy (PED) is one of the most useful minimally invasive surgery for lumbar disc herniation (LDH) (1,2). Especially, high-grade migrated fragments are difficult to treat with the standard posterolateral PED (PLPED) technique (3,4). PED with a high-speed drill is a minimally invasive method of approaching the deep narrow lumbar space (5-8). This paper presents a successful case of PLPED with partial pediculotomy for a high-grade downward migrated fragment and discusses a hemostatic technique for severe bleeding.

Case Report

A 72-year-old man had severe untreatable lumbago and left femoral radicular pain for 6 months. His health condition was poor with chronic renal failure requiring dialysis 3 times per week, hypertrophic cardiomyopathy, and obstructive ventilation impairment .The initial physician referred the patient to us to undergo a minimally invasive spine surgery.

During his first visit, the patient's numeric rating scale (NRS) scores were 8/10 for low back pain and 8/10 for left front femoral pain. His leg pain increased after 10 minutes of slow walking, so he needed a wheelchair. Neurological examination revealed normal deep tendon reflexes. His thigh circumference was asymmetrical (right, 35.5cm; left, 35.0cm). Owing to his pain, he could not get into a prone position for examination with the femoral nerve stretch test. The straight leg raising test result was negative bilaterally.

On sagittal T2-weighted magnetic resonance imaging (MRI),a high-grade downward migrated disc was observed at the L1-L2 level on the left side (Figure 1a). The axial view at the L2 pedicle midline level showed a large fragment impinging the L2 nerve root (Figure 1b).

PLPED with partial pediculotomy under local anesthesia was planned to decompress the left L2 nerve root. Our anesthesiologist performed deep sedation of the patient. The patient was placed in a prone position, and the puncture point under fluoroscopy was simulated prior to the calculation of data (9). An 8mm skin incision was made 5 cm to the left of the midline. The standard PLPED procedure was started after local anesthesia. Owing to the L1-L2 foraminal severe stenosis, we selected the outside- in technique. The adverse walking technique could be used to approach the crossing point of the superior facet and transverse process (Figure 2a). Partial pediculotomy was started from this point, and a quarter of the craniomedial portion was drilled (Figure 2b) for the total fragmentectomy (Figure 2c) (10). We could decompress the L2 nerve root from the L1 endoplate level to under the midline of the L2 pedicle (Figure 2d).

The operative time was 2 hours; 100ml of bleeding from the L1 AEVP due to injury by the tip of the Beak-type cannula took 30min to control. We first attempted the standard hemostatic techniques of increasing the irrigation pressure (100 to 110cm H2O for 3min) several times and compression the bleeding point with rigid dissector but did not succeed the hemostasis. We then attempted the techniques for such a vigorous bleeding situation include slow cannula rolling and bleeding point compression by a flexible bipolar device with hemostatic cotton materials. We finally achieved the hemostasis and placed a drainage tube. Little outflow stayed only in the tube, which was withdrawn the next morning without hematoma formation.

The patient did not have any dysesthesia and paresis. The time to ambulation was 2 hours, and his hospital stay was 7 days. The NRS score of his affected leg improved from 8 to 1 after 2 months. In the next morning, his wound pain NRS score was 1. The axial view of the MRI scan (Figure 1c) showed that the migrated fragment was completely removed.

Discussion

The standard treatment for higher-level lumbar disc herniation is conventional discectomy with some fusion after facetstomy (11). Nowadays, many types of minimally invasive percutaneous pedicle screw systems are available (12). Owing to the poor general condition of our patient, we selected the operative procedures suitable for local anesthesia were limited. Interlaminar PED (ILPED) with partial laminectomy (7,8) and PLPED with partial pediculotomy are the best minimally techniques for patients with poor general conditions.

The major difference between ILPED and PLPED with partial pediculotomy is the direction of the operative approaches. ILPED accesses from dorsal side of vertebral laminae, thereby even combined with laminectomy the migrated fragment is still covered with neural structures. On the other hand, PLPED with partial pediculotomy can directly expose the migrated fragment covering neural structures. In other words, as the migrated fragment protects underneath neural structures, we can safely drill the inner cortical bone layer of the pedicle. Additionally, the width of spinal canal at high vertebral level (ex. L1-L2) is narrower than that at low vertebral level (ex. L5-S1) (13). Consequently ILPED at high vertebral level requires more skillful technic. Our case was affected at L1-L2 vertebral level and the migrated fragment extended lateral part of the spinal canal (Figure 1b), we therefore planned to perform the PLPED with partial pediculotomy.

The disadvantages of PLPED under the situation of severe foraminal stenosis include the possibility of complicating the exiting nerve injury and bleeding from the AEVP. As the beak- type cannula has a wider view than the square-type cannula, we changed the square-type cannula with the beak-type cannula to complete the decompression of the L2 nerve root. When the joystick maneuver was used to observe the narrow disc space, the tip of the beak-type cannula injured the L1 AEVP The flexible bipolar unit is the only instrument for hemostasis with the PED system. We needed 30min to control 100ml of bleeding from the AEVP The robotic general surgery system already has many useful instruments developed for dissection and coagulation (14). One of the urgent needs of PED surgeons is the development of a bipolar dissector for fine manipulation like under microscopic surgery

On the basis of this case of higher-level migrated lumbar disc herniation, PLPED with partial pediculotomy is a useful procedure for patients with poor general conditions. For the appropriate development of this procedure, the PED system requires new devices to control the bleeding from the AEVP.

Acknowledgment

All the authors made a significant contribution to this case report.

To know more about Open Access Journal of Head Neck & Spine Surgery please click on:

https://juniperpublishers.com/jhnss/index.php

To know more about Open access Journals Publishers please click on : Juniper Publishers