Lumbar decompression surgery for spinal canal stenosis outcome

Lumbar decompression surgery for spinal canal stenosis outcome

Lumbar laminectomy, represents the standard operative treatment for lumbar spinal stenosis, but this procedure is often combined with fusion surgery. It is still discussed whether minimal-invasive decompression procedures are sufficient and if they compromise spinal stability as well.

Decompression of lumbar spinal stenosis without fusion led to a significant and similar reduction of back pain and leg pain in a short-term and a long-term follow-up group. Patients without previous surgery benefited significantly better, whereas patients with previous decompression benefited regarding back pain, especially for long-term follow-up with a clear trend in favor of leg pain 1).

Currently, there is interest in minimally invasive surgery and various technical modifications of decompressive lumbar laminectomy without fusion.

Particularly, depression has been shown to be associated with less improvement following lumbar fusion surgery 2) 3) 4) 5) 6) 7) 8).

Karp et al. 9) reviewed 158 patients who underwent epidural spinal injections for low-back pain with or without radiculopathy. These investigators found that depression and sleep disturbance were prognostic of worse Patient-Reported Outcome Measurement Information System (PROMIS) outcomes following epidural spinal injections.

Hägg et al. 10) performed a randomized controlled trial of 264 patients with severe chronic low-back pain who underwent either surgical or nonsurgical treatment, and assessed the impact of underlying affective disorders. They found that baseline depression correlated with worse outcomes following both operative and nonoperative treatment.

Interestingly, they also observed that depressed patients tended to have better outcomes with nonoperativecare, whereas nondepressed patients tended to have better outcomes with fusion.

In the study of Lubelski et al. 11) found that worsening depression (as measured by the PHQ-9) independently significantly predicted worse EQ-5D index outcomes following conservative treatment for LSS (p = 0.0002). This effect was most evident when comparing patients with severe depression, who improve 0.14 points less than those with no depression. This difference exceeds the MCID and confirms that depression is a poor prognostic factor for QOL improvement following nonoperative treatment for LSS. Further investigation is needed to determine whether treatment of depression prior to conservative or surgical management of LSS will improve posttreatment QOL outcomes. There are several limitations that should be considered when interpreting the results. Multiple treating physicians were included, and factors such as participation in physical therapy, treatment with NSAIDs, opioid medications and other nonsurgical treatments varied by practitioner and patient; this increases the variability, but also improves the generalizability.

They adjusted for the increased variability by using the random effect in the regression models. Many patients were also lost to follow-up at the 4-month evaluation.

The cohorts were similar for most characteristics; however, there were statistically significant, albeit small differences for estimated percent below poverty threshold and median income by zip code. The analysis is only valid for patients who did follow-up assessments at these time points. Additionally, this was a retrospective study with a relatively short follow-up period.

Prospectively designed studies with longer follow-up are needed to further validate the findings. Nonetheless, this is the largest study investigating the correlation between depression and QOL outcomes following conservative management of LSS.

Lubelski et al. have used the validated PHQ-9 measure of depression and have found a statistically and clinically significant impact on EQ-5D index outcomes.

The results of this study suggest that depressed patients with LSS have significantly less improvement following conservative management compared with nondepressed patients. Both physicians and surgeons who treat patients with LSS should consider using validated questionnaires such as the PHQ-9 for pretreatment evaluation of depression, to better assess the likelihood of success following treatment. Further investigation is needed to evaluate the effect of depression treatment prior to management of the spinal disorder. Future prospective studies with longer follow-up intervals may be useful in further evaluating the QOL outcomes in this patient population 12).


In cases of lumbar spinal stenosis (LSS) treated with surgical decompression, a postoperative magnetic resonance imaging (MRI) is sometimes required. In the experience of a study, the obtained decompression observed on early postoperative MRI tends to be disappointing compared to the decompression achieved intraoperatively. This raises the question of whether the early postoperative MRI, performed after lumbar decompression, is a fair representation of the ‘real’ decompression. A study investigated the correlation between intraoperative and postoperative measurements of the lumbar spinal canal.

Surgical decompression of the spinal canal effectively decreases the compression of the dural sac. However, early postoperative MRI after lumbar decompression does not adequately represent the decompression achieved intraoperatively 13).

Back pain improvement

Through the 1st postoperative year, patients with lumbar stenosis-without spondylolisthesis, scoliosis, or sagittal malalignment-and clinically significant back pain improved after decompression-only surgery 14).


The most common surgical method currently used is lumbar laminectomy, with complete decompression; this technique has a 5-year follow-up effective rate of 81.6% 15).

Apart from acute complications such as hematoma and infections, same-level recurrent lumbar stenosis and adjacent-segment disease (ASD) are factors that can occur after index lumbar spine surgery.

While looking for predictors of revision surgery due to re-stenosis, instability or same/adjacent segment disease none of these were found. Within our cohort no significant differences concerning demographic, peri-operative and radiographic data of patients with or without revision wer noted. Patients, who needed revision surgery were older but slightly healthier while more likely to be male and smoking. Surprisingly, significant differences were noted regarding the distribution of intraoperative and early postoperative complications among the 6 main surgeons while these weren’t obious within the intial index group of late revisions 16).


A systematic review was conducted using MEDLINE for literature published through December 2014. The first question focused on the effectiveness of lumbar spine surgery for symptomatic lumbar spinal stenosis in elderly patients. The second question focused on safety of surgical intervention on this elderly population with emphasis on perioperative complication rates.

Review of 11 studies reveals that the majority of elderly patients exhibit significant symptomatic improvement, with overall benefits observed for pain (change visual analog scale4.4 points) and disability (change Oswestry Disability Index 23 points). Review of 11 studies reveals that perioperative complications were infrequent and acceptable with pooled estimates of mortality (0.5%), inadvertent durotomy (5%), and wound infection (2%). Outcomes seem less favorable with greater complication rates among patients with diabetesor obesity.

Based on largely low-quality, retrospective evidence, Shamji et al. recommend that elderly patients should not be excluded from surgical intervention for symptomatic lumbar spinal stenosis 17).

Fusion Is Not a Safeguard to Prevent Revision Surgery in Lumbar Spinal Stenosis 18).

A cohort study showed no significant association between the type of index operation for Degenerative Lumbar Spinal Stenosis-decompression alone or fusion-and the need for revision surgery or the outcomes of pain, disability, and quality of life among patients after 3 years. Number of revision operations was associated with more pain and worse quality of life 19).


1)

Geiger MF, Bongartz N, Blume C, Clusmann H, Müller CA. Improvement of Back and Leg Pain after Lumbar Spinal Decompression without Fusion. J Neurol Surg A Cent Eur Neurosurg. 2018 Dec 5. doi: 10.1055/s-0038-1669473. [Epub ahead of print] PubMed PMID: 30517963.
2)

Aalto TJ, Malmivaara A, Kovacs F, Herno A, Alen M, Salmi L, et al: Preoperative predictors for postoperative clinical outcome in lumbar spinal stenosis: systematic review. Spine (Phila Pa 1976) 31:E648–E663, 2006
3)

Adogwa O, Parker SL, Shau DN, Mendenhall SK, Aaronson OS, Cheng JS, et al: Preoperative Zung Depression Scale predicts outcome after revision lumbar surgery for adjacent segment disease, recurrent stenosis, and pseudarthrosis. Spine J 12:179–185, 2012
4)

Adogwa O, Parker SL, Shau DN, Mendenhall SK, Bydon A, Cheng JS, et al: Preoperative Zung depression scale predicts patient satisfaction independent of the extent of improvement after revision lumbar surgery. Spine J 13:501–506, 2013
5)

Arpino L, Iavarone A, Parlato C, Moraci A: Prognostic role of depression after lumbar disc surgery. Neurol Sci 25:145– 147, 2004
6)

Chaichana KL, Mukherjee D, Adogwa O, Cheng JS, McGirt MJ: Correlation of preoperative depression and somatic perception scales with postoperative disability and quality of life after lumbar discectomy. J Neurosurg Spine 14:261– 267, 2011
7)

Sinikallio S, Aalto T, Airaksinen O, Herno A, Kröger H, Viinamäki H: Depressive burden in the preoperative and early recovery phase predicts poorer surgery outcome among lumbar spinal stenosis patients: a one-year prospective follow-up study. Spine (Phila Pa 1976) 34:2573–2578, 2009
8)

Trief PM, Grant W, Fredrickson B: A prospective study of psychological predictors of lumbar surgery outcome. Spine (Phila Pa 1976) 25:2616–2621, 2000
9)

Karp JF, Yu L, Friedly J, Amtmann D, Pilkonis PA: Negative affect and sleep disturbance may be associated with response to epidural steroid injections for spine-related pain. Arch Phys Med Rehabil 95:309–315, 2014
10)

Hägg O, Fritzell P, Ekselius L, Nordwall A: Predictors of outcome in fusion surgery for chronic low back pain. A report from the Swedish Lumbar Spine Study. Eur Spine J 12:22–33, 2003
11) , 12)

Lubelski D, Thompson NR, Bansal S, Mroz TE, Mazanec DJ, Benzel EC, Khalaf T. Depression as a predictor of worse quality of life outcomes following nonoperative treatment for lumbar stenosis. J Neurosurg Spine. 2015 Mar;22(3):267-72. doi: 10.3171/2014.10.SPINE14220. Epub 2014 Dec 19. PubMed PMID: 25525957.
13)

Schenck C, van Susante J, van Gorp M, Belder R, Vleggeert-Lankamp C. Lumbar spinal canal dimensions measured intraoperatively after decompression are not properly rendered on early postoperative MRI. Acta Neurochir (Wien). 2016 May;158(5):981-8. doi: 10.1007/s00701-016-2777-5. Epub 2016 Mar 23. PubMed PMID: 27005673; PubMed Central PMCID: PMC4826663.
14)

Crawford CH 3rd, Glassman SD, Mummaneni PV, Knightly JJ, Asher AL. Back pain improvement after decompression without fusion or stabilization in patients with lumbar spinal stenosis and clinically significant preoperative back pain. J Neurosurg Spine. 2016 Nov;25(5):596-601. PubMed PMID: 27285666.
15)

Bouras T, Stranjalis G, Loufardaki M, Sourtzis I, Stavrinou LC, Sakas DE. Predictors of long-term outcome in an elderly group after laminectomy for lumbar stenosis. J Neurosurg Spine. 2010;59:329–34.
16)

Melcher C, Paulus AC, Roßbach BP, Gülecyüz MF, Birkenmaier C, Schulze-Pellengahr CV, Teske W, Wegener B. Lumbar spinal stenosis – surgical outcome and the odds of revision-surgery: Is it all due to the surgeon? Technol Health Care. 2022 Jun 10. doi: 10.3233/THC-223389. Epub ahead of print. PMID: 35754243.
17)

Shamji MF, Mroz T, Hsu W, Chutkan N. Management of Degenerative Lumbar Spinal Stenosis in the Elderly. Neurosurgery. 2015 Oct;77 Suppl 4:S68-74. doi: 10.1227/NEU.0000000000000943. PubMed PMID: 26378360.
18)

Austevoll IM, Ebbs E. Fusion Is Not a Safeguard to Prevent Revision Surgery in Lumbar Spinal Stenosis. JAMA Netw Open. 2022 Jul 1;5(7):e2223812. doi: 10.1001/jamanetworkopen.2022.23812. PMID: 35881401.
19)

Ulrich NH, Burgstaller JM, Valeri F, Pichierri G, Betz M, Fekete TF, Wertli MM, Porchet F, Steurer J, Farshad M; Lumbar Stenosis Outcome Study Group. Incidence of Revision Surgery After Decompression With vs Without Fusion Among Patients With Degenerative Lumbar Spinal Stenosis. JAMA Netw Open. 2022 Jul 1;5(7):e2223803. doi: 10.1001/jamanetworkopen.2022.23803. PMID: 35881393.

Spinal epidural abscess

Spinal epidural abscess

Spinal infection in the epidural space.

Spinal epidural abscess epidemiology.

Spinal Epidural Abscess Classification.

Spinal epidural abscess etiology.

Spinal epidural abscess pathophysiology.

Spinal epidural abscess clinical features.

Spinal epidural abscess diagnosis.

Spinal epidural abscess differential diagnosis.

Spinal epidural abscess treatment.

Spinal epidural abscess outcome.

Spinal epidural abscess case series.

Spinal epidural abscess case reports.

Incomplete spinal cord injury

Incomplete spinal cord injury

Any residual motor or sensory function is more than 3 segments below the level of the injury.

Look for signs of preserved long-tract function.

Signs of incomplete lesion:

  1. sensation (including position sense) or voluntary movement in the LEs in the presence of a cervical or thoracic spinal cord injury

  2. “sacral sparing”: preserved sensation around the anus, voluntary rectal sphincter contraction, or voluntary toe flexion

  3. an injury does not qualify as incomplete with preserved sacral reflexes alone (e.g. bulbocavernosus)


An incomplete spinal cord injury is the term used to describe damage to the spinal cord that is not absolute. The incomplete injury will vary enormously from person to person and will be entirely dependant on the way the spinal cord has been compromised.

An “incomplete” spinal cord injury involves preservation of motor or sensory function below the level of injury in the spinal cord.

If the patient has the ability to contract the anal sphincter voluntarily or to feel a pinprick or touch around the anus, the injury is considered to be incomplete. The nerves in this area are connected to the very lowest region of the spine, the sacral region, and retaining sensation and function in these parts of the body indicates that the spinal cord is only partially damaged. This includes a phenomenon known as sacral sparing.


The true extent of many incomplete injuries isn’t fully known until 6-8 weeks post injury. The spinal cord normally goes into what is called spinal shock after it has been damaged. The swelling and fluid masses showing on any resultant X-ray, MRI or CT scans, may well mask the true nature of the underlying injury. It is not uncommon for someone who is completely paralysed at the time of injury to get a partial or very near full recovery from their injuries after spinal shock has subsided.

Central cord syndrome.

Anterior cord syndrome.

Brown-Séquard syndrome.

Posterior cord syndrome: rare

The results of kinesiotherapy treatment in patients after incomplete spinal cord injury (iSCI) are inconclusive, mostly due to different, subjective evaluation methods. A study aimed to evaluate the range of functional regeneration in long-term 13 months follow-up using comparative neurophysiological tests after uniform kinesiotherapy in patients with thoracic iSCI.

Material and methods: Comparative tests were performed of sensory perception in dermatomes Th1-S1, electromyography (at rest-rEMG and during maximal contraction-mcEMG) in the muscles of the trunk and lower extremities, electroneurography (ENG) of the motor fibers of the lower extremities, and motor-evoked potential induced transcranially (MEP) before and after treatment in 25 iSCI patients. All subjects were treated with the same kinesiotherapeutic procedures.

A moderate increase was found in amplitudes in rEMG and mcEMG recordings from the rectus abdominis and rectus femoris muscles, MEPs amplitudes, and amplitudes after peroneal nerve stimulations in ENG studies. There was no improvement in sensory perception.

Following the proposed kinesiotherapy algorithm, patients after thoracic iSCI presented a moderate more motor than sensory functions improvement. Applied neurorehabilitation evoked normalization of muscle tension, moderate improvement of rectus abdominis and rectus femoris muscles motor units activity, and motor central and peripheral neural impulses transmission. The comparative neurophysiological assessment provides more precise and objective insight into the functional status of afferent and efferent systems than the classical clinical approach in iSCI patients 1).

Following incomplete spinal cord injuries, neonatal mammals display a remarkable degree of behavioral recovery.

Previously, it has been demonstrated in neonatal mice a wholesale re-establishment and reorganization of synaptic connections from some descending axon tracts (Boulland et al., 2013).

To assess the potential cellular mechanisms contributing to this recovery, Chawla et al., have characterized a variety of cellular sequelae following thoracic compression injuries, focusing particularly on cell loss and proliferation, inflammation and reactive gliosis, and the dynamics of specific types of synaptic terminals. Early during the period of recovery, regressive events dominated. Tissue loss near the injury was severe, with about 80% loss of neurons and a similar loss of axons that later make up the white matter. There was no sign of neurogenesis, no substantial astroglial or microglial proliferation, no change in the ratio of M1 and M2 microglia and no appreciable generation of the terminal complement peptide C5a. One day after injury the number of synaptic terminals on lumbar motoneurons had dropped by a factor of 2, but normalized by 6 days. The ratio of VGLUT1/2+ to VGAT+ terminals remained similar in injured and uninjured spinal cords during this period. By 24 days after injury, when functional recovery is nearly complete, the density of 5HT+ fibers below the injury site had increased by a factor of 2.5. Altogether this study shows that cellular reactions are diverse and dynamic. Pronounced recovery of both excitatory and inhibitory terminals and an increase in serotonergic innervation below the injury, coupled with a general lack of inflammation and reactive gliosis, are likely to contribute to the recovery 2).


1)

Wincek A, Huber J, Leszczyńska K, Fortuna W, Okurowski S, Tabakow P. Results of a long-term uniform system of neurorehabilitation in patients with incomplete thoracic spinal cord injury. Ann Agric Environ Med. 2022 Mar 21;29(1):94-102. doi: 10.26444/aaem/135554. Epub 2021 Apr 15. PMID: 35352911.
2)

Chawla RS, Züchner M, Mastrangelopoulou M, Lambert FM, Glover JC, Boulland JL. Cellular reactions and compensatory tissue re-organization during spontaneous recovery after spinal cord injury in neonatal mice. Dev Neurobiol. 2016 Dec 29. doi: 10.1002/dneu.22479. [Epub ahead of print] PubMed PMID: 28033684.
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