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Evidence Based Vet Forum • View topic - no functional recovery difference for dog back surgery

no functional recovery difference for dog back surgery

Issues involving ear crops, declaws and knee and back surgery. Questions, answers, theories, and evidence. Why are these surgeries more common in the United States than Europe?

no functional recovery difference for dog back surgery

Postby malernee » Mon Oct 27, 2003 10:47 am


General Information
The spine is made up of bony segments called vertebrae, which are joined by ligaments, muscles, and fibrous structures called intervertebral disks. The intervertebral disks act as shock absorbers between vertebrae.
A disk consists of a fibrous outer ring and an inner section that is soft and jelly-like. The fibrous outer ring is thinner at the top portion than it is at the bottom. When a disk becomes diseased, either through gradual degeneration or injury, the thinner top portion of the outer ring gives way, and the disk bulges into the spinal canal located directly above the disk. If the disk ruptures completely, the outer ring collapses and the inner jelly-like portion is forced into the spinal canal.
The spinal cord is located in the spinal canal. A bulging or ruptured disk causes pressure or damage to the spinal cord, resulting in pain, weakness, incoordination, or paralysis.
Intervertebral disk disease is diagnosed by physical signs, neurologic tests, and radiographs (x-rays). In some cases, a dye must be injected into the spinal canal so that areas of damage can be observed on the radiographs (x-rays). This procedure is called myelography.

Important Points in Treatment
1. Both medical and surgical treatments are used for intervertebral disk disease. Such factors as the pet's age, severity and duration of signs, neurologic findings, and physical status help determine whether surgery should be performed. In many cases, hospitalization is necessary for effective medical treatment.
2. Activity: Exercise should be severely restricted . Do not let your pet jump up on or down from furniture, engage in rough play, or chase balls.
3. Medication: All medication must be given as directed. Please call the doctor if you cannot complete any treatments.
4. Diet: If your pet is overweight, weight reduction is desirable because excess weight puts additional strain on the back. In all cases, less food is necessary during the treatment period because of the exercise restriction.
Feed as follows:

Notify the Doctor if Any of the Following Occur
o Your pet seems increasingly uncomfortable.
o Your pet loses control of its bowel movements or is constipated.
o Your pet has difficulty urinating.
o Your pet has breathing problems, rigid front legs, or seizures.

Functional Outcome in Dogs After Surgical Treatment of Caudal Lumbar Intervertebral Disk Herniation
Sarit Dhupa, BVSc, Nita W. Glickman, MPH, MS and
David J. Waters, DVM, PhD, Diplolmate ACVS
From the Department of Veterinary Clinical Sciences (Dhupa, Waters), 1296 Lynn Hall, and the Center for the Human-Animal Bond (Glickman), Purdue University, West Lafayette, Indiana 47907-1248. Address all correspondence to Dr. Waters.
Caudal lumbar disk herniations (i.e., third lumbar [L3] to seventh lumbar [L7] intervertebral spaces) represent approximately 15% of surgically treated thoracolumbar disk herniations in dogs. A retrospective case-control study was conducted to determine the postoperative outcome of this subset of dogs in the authors' neurosurgical practice. Medical records (1985 through 1996) were reviewed for dogs with caudal lumbar disk herniation confirmed at surgery. Thirty-six cases were identified. For each case, two dogs that underwent surgical treatment for upper motor neuron thoracolumbar disk herniation (tenth thoracic [T10] to L3 intervertebral spaces) were selected as controls. Probabilities of functional recovery for cases and controls were 81% and 85%, respectively (p value of 0.49). In dogs with caudal lumbar disk herniation, complete sensorimotor loss was the only significant predictor of functional recovery (p value of 0.005). Disk herniations that occur at the thoracolumbar junction and those that occur in the caudal lumbar region should not be considered to be different in terms of surgical treatment and postoperative outcome. The lower motor neuron signs that often accompany caudal lumbar disk herniation reflect the site of spinal cord injury and do not necessarily predict a poor prognosis. J Am Anim Hosp Assoc 1999;35:323-31.

Introduction [Top]

Thoracolumbar intervertebral disk disease is a major cause of myelopathy in dogs. The clinical syndrome, including signalment predisposition and response to decompressive surgery, is well characterized.1-5 Prognostic factors which predict likelihood of postoperative functional recovery in dogs with thoracolumbar disk disease include rapidity of neurological decline, severity of preoperative neurological deficits, and duration of complete sensorimotor loss.3,4,6-8 Approximately 85% of thoracolumbar disk herniations occur within two to three disk spaces of the thoracolumbar junction (tenth thoracic [T10] to third lumbar [L3] intervertebral disk spaces), often resulting in upper motor neuron (UMN) signs to the pelvic limbs.1,3,7,9-11 In contrast, caudal lumbar disk herniations (L3 to seventh lumbar [L7] intervertebral disk spaces) represent a relatively small subset of cases. Disk herniation at this level causes ischemia and compression of the lumbosacral intumescence and frequently is associated with lower motor neuron (LMN) signs. It has been suggested that dogs with caudal lumbar disk herniation and LMN signs may have a poorer prognosis than dogs with UMN lesions.12 However, a review of the veterinary neurosurgical literature3-10,12-22 revealed data on the likelihood of functional outcome in only four surgically treated dogs with caudal lumbar disk herniation.

The purpose of this study was to determine if dogs with caudal lumbar (L3 to L7) disk herniation have a poorer prognosis after surgical treatment than dogs with thoracolumbar junction (T10 to L3) disk herniation. In this report, the clinical features and postoperative outcome of 36 dogs with caudal lumbar disk herniation that underwent decompressive surgery are described.

Materials and Methods [Top]

Selection of Cases

Medical records of the Purdue University Veterinary Teaching Hospital (PUVTH) from January 1985 through December 1996 were reviewed for dogs with herniation of a caudal lumbar disk (L3 to L7 intervertebral spaces) confirmed at the time of decompressive surgery. Dogs with LMN signs attributable to L7 to first sacral (S1) disk herniation were excluded, because lumbosacral disease (i.e., cauda equina syndrome) represents a heterogeneous clinical entity.23 Dogs with T10 to L3 disk herniations that had LMN signs attributable to ascending-descending myelomalacia24 also were excluded. Cases were included if information on preoperative and postoperative neurological status, intraoperative findings, and follow-up of at least four weeks were available. The following data was tabulated from the medical records of 36 dogs that satisfied the inclusion criteria: signalment; duration and severity of neurological deficits; perioperative corticosteroid therapy; information from the operative report including date of surgery, site of disk herniation, surgical technique employed (e.g., dorsal laminectomy, hemilaminectomy, durotomy), and training level of surgeon (e.g., faculty, surgical resident); as well as postoperative neurological status at either the time of discharge from the PUVTH or at the time of euthanasia. Follow-up data was obtained by reevaluation at the PUVTH or by telephone contact with pet owners. Time interval from surgery until walking and the completeness of neurological recovery were also recorded.

Selection of Controls

In order to determine if dogs with caudal lumbar disk herniation had a poorer prognosis than dogs with a thoracolumbar disk herniation, a comparison group of 72 dogs was selected. For each case of caudal lumbar disk herniation, two dogs were selected that had surgical confirmation of a thoracolumbar disk herniation cranial to L3 (i.e., T10 to L3 intervertebral spaces) and UMN signs to the pelvic limbs. Controls were matched to cases on the basis of body weights and severity of preoperative neurological deficits. For selection of controls, dogs (cases and controls) were subdivided by body weight into two categories (i.e., less than 20 kg; 20 kg or greater) and into three categories based upon severity of preoperative pelvic limb neurological deficits: 1) intact voluntary motor function; 2) absent voluntary motor function with intact deep pain; and 3) absent voluntary motor function with absent deep pain. Voluntary motor function was defined as purposeful movement of the pelvic limbs. Deep pain perception was considered intact if the dog actively acknowledged (by vocalization or biting) the clamping of its pelvic limb toes with hemostatic forceps.

Comparison of Postoperative Functional Outcome in Cases and Controls

Cases (n=36) and controls (n=72) were compared to determine if there were differences in postoperative outcomes. Three measures of functional outcome were analyzed: 1) probability of regaining voluntary motor function at the time of discharge; 2) time to walking; and 3) likelihood of functional recovery. For the purpose of this study, functional recovery was defined as regaining the ability to walk, with fecal and urinary continence, without persistent back pain. Because 15 dogs with L3 to L4 herniation had UMN signs, a separate analysis was performed comparing the subset of cases with LMN signs (n=21) to their controls (n=42).

Analysis of Potential Prognostic Factors in Surgically Treated Dogs With Caudal Lumbar Disk Herniation

Cases were analyzed to determine if the following potential prognostic factors were predictive of functional recovery: age (less than seven years versus seven years or older) at surgery; body weight (less than 20 kg versus 20 kg or greater); severity of preoperative neurological deficits (three categories); type of decompressive surgical procedure (dorsal laminectomy versus hemilaminectomy); and level of surgical training (faculty versus surgical resident). In order to determine if LMN signs conferred a poorer prognosis, the likelihood of functional recovery in 15 dogs with L3 to L4 lesions and UMN signs was compared to functional recovery in eight dogs with L3 to L4 lesions and LMN signs.

Data Analysis

Data was analyzed using the SAS System for Windows.a Conditional logistic regression was used to compare cases and controls for differences in age at surgery, likelihood of functional recovery, likelihood of return to voluntary motor function at discharge, and time to return to walking. Chi-square and Fisher's exact tests were used to determine if age, body weight, surgical procedure, level of surgeon training, site of disk herniation, or severity of preoperative neurological deficits were predictive of functional recovery in the 36 cases. Differences were considered statistically significant if the p value was less than 0.05.

Results [Top]

Prevalence and Clinical Features of Caudal Lumbar Disk Herniation

Forty-three (14.5%) of 296 dogs that underwent decompressive surgery for thoracolumbar disk herniation had caudal lumbar (L3 to L7) disk herniation. The clinical features of 36 dogs with caudal lumbar disk herniation that satisfied the inclusion criteria are summarized in Table 1. Median age at surgery was five years (range, two to 12 yrs). Dachshunds represented 15 (42%) of 36 cases. Median body weight of dogs with caudal lumbar disk herniation was 8 kg (range, 3 to 34 kg). Thirty-one dogs weighed less than 20 kg; only five dogs weighed 20 kg or more. The most common site of disk herniation was L3 to fourth lumbar (L4) intervertebral spaces, which accounted for 23 (64%) of 36 cases; L4 to fifth lumbar (L5) intervertebral spaces (n=10) and L5 to sixth lumbar (L6) (n=3) disks were affected less frequently. No dogs had L6 to L7 herniation.

Most cases had severe, preoperative pelvic limb neurological deficits. Voluntary motor function was intact in only eight (22%) of 36 dogs. Deep pain was absent in three (8%) of 36 dogs with caudal lumbar disk herniation. Twenty-one cases had LMN signs (i.e., depressed patellar reflexes, cranial tibial reflexes, or both, and hypotonicity of the pelvic limbs). Fifteen dogs with L3 to L4 herniation had UMN signs. All dogs underwent decompressive spinal surgery consisting of dorsal laminectomy (n=12) or hemilaminectomy (n=24). Durotomy was performed in 12 cases, and prophylactic fenestration of adjacent disks was performed in three cases. All cases received perioperative corticosteroids, which usually consisted of either dexamethasone (1 mg/kg body weight, intravenously [IV]) or methylprednisolone sodium succinate (30 mg/kg body weight, IV).

Functional Recovery in Dogs With Caudal Lumbar Disk Herniation

Twenty-nine (81%) of 36 surgically treated dogs with caudal lumbar disk herniation had functional recovery. Seven dogs failed to achieve functional recovery. Three dogs that never regained ambulatory status or fecal/urinary continence were euthanized one month postoperatively. One dog was euthanized 60 months after surgery due to urinary incontinence. Three dogs were alive at 11, 84, and 108 months after surgery; two of these dogs had regained the ability to walk, but all three had fecal incontinence.

Comparison of Functional Outcome in Cases (L3 to L7 Disk Herniation) and Controls (T10 to L3 Disk Herniation)

Median time interval from surgery to follow-up was 42 months (range, one to 108 mos) for cases, compared to 48 months (range, one to 144 mos) for controls. Three parameters were analyzed to assess postoperative functional outcome [Table 2]. Likelihood of return of voluntary motor function at discharge was not significantly different between the two groups. Fifty percent of cases and 41% of controls that had no voluntary motor function prior to surgery regained motor function by the time of discharge (p value of 1.0). The time interval for return to walking was not significantly different between the two groups (p value of 1.0). There was no difference between cases and controls in the percentage of dogs that achieved functional recovery. Probability of functional recovery for cases and controls were 81% and 85%, respectively (p value of 0.49). Similarly, when 15 cases with L3 to L4 disk herniation and UMN signs were excluded from analysis, functional recovery was achieved in 86% of LMN cases compared to 93% of controls (p value of 0.36) [Table 3]. Table 2

Comparison of Postoperative Outcome in 36 Cases With Caudal Lumbar (L3 to L7 Intervertebral Spaces) Disk Heriation to a Control Group of 72 Dogs
Wth T10 to L3 Thoracolumbar Disk Herniation*

Caudal Lumbar Disk Herniation Cases Control Group**
p Value

Percentage of dogs that regained voluntary motor function at discharge*** 50%

Median (range) time interval from surgery to walking 13 days
(1-365 days)
7 days
(1-42 days)

Likelihood of functional recovery+ 81%

* T10=tenth thoracic vertebra; L3=third lumbar vertebra; L7=seventh lumbar vertebra
** Dogs in the control group underwent decompressive surgery for T10 to L3 upper motor neuron thoracolumbar disk herniation and were matched with cases on the basis of body weight (less than 20 kg versus 20 kg or greater) and severity of preoperative pelvic limb neurological deficits (intact voluntary motor versus absent voluntary motor function, intact deep pain versus absent deep pain).
*** Analysis performed on the 28 cases (and 56 controls) that had absent voluntary motor function prior to thoracolumbar disk surgery. Median interval from surgery to discharge from the veterinary teaching hospital was five days for both groups.
+ Functional recovery defined as regaining the ability to walk, with fecal and urinary continence, without persistent back pain.
Table 3

Comparison of Postoperative Outcome in 21 Cases With Caudal Lumbar (L3 to L7 Intervertebral Spaces) Disk Herniation and Lower Motor Neuron Signs to a Control Group of 42 Dogs With T10 to L3 Thoracolumbar Disk Herniation*

Control Group**
p Value

Percentage of dogs that regained voluntary motor function at discharge*** 52%
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the advisability of surgery for prolapsed disc

Postby guest » Mon Oct 27, 2003 12:07 pm

BMJ 2003;327:985-986 (25 October)

"Failed back surgery syndrome"
Lina Talbot, general medicine registrar, retired1
1 Torquay, Devon TQ1 3TB llinatalbot@aol.com

An inappropriate diagnostic label may exacerbate the discomfort of patients who develop persistent and disabling symptoms after back surgery

Every general practitioner has one—a patient who has had back surgery but hasn't improved. Around 2000 cases of failed back surgery syndrome are produced each year in the United Kingdom.1-3 This is an uncomfortable statistic, and it is an uncomfortable condition to manage. Patients are often young and were previously active but now face chronic pain for years. They come from the surgeons but are no longer surgical candidates. They have been through the gamut of orthopaedic, neurological, and radiological opinions followed by physiotherapy, occupational therapy, and possibly clinical psychology, funnelling them inexorably towards the pain clinic. Unfortunately, they fare badly there too, with just over one in three patients achieving more than 30% pain relief.

I know about this dreary path at first hand. Nowadays, we may increasingly be questioning the advisability of surgery for prolapsed disc, but not operating can also produce long term disability. Comparison of the UK rate of spinal surgery with that in other countries shows that UK surgeons are not sharpening their scalpels to the ringing of cash tills. Yet 5-10% of patients who have back surgery return home without relief of their radicular pain.2 3 Worse still, after about six months, the pain may be showing an unpleasant whiff of neuropathy.

False colour nuclear magnetic resonance image of prolapsed disc

Personal view

I practised general medicine in both England and Germany. When the radicular pain returned after my microdiscectomy, I battled for months to cope with ward work while seeking out an unoccupied bed in a quiet corner for periodic breaks. The availability of beds, in Germany at least, makes medicine seem the perfect occupation for someone with failed back surgery. I returned to the neurosurgeon, who did computed tomography, pronounced that the prolapse had not recurred, and told me it would take more time. Despite twice weekly physiotherapy and utmost care with all physical activities, I gradually worsened and developed bladder problems.

Only after many consultations and investigations did I pick up a book and read about Postdiskotomie-Syndrom. I then began to understand that, although the nerve roots were not damaged directly by the surgery, they were now encased in a web of scar tissue causing pain and spasm every time this was tweaked enough by movements of the spine and legs.


But I am also caught in a web myself, resulting from the lack of awareness of what is actually not such a rare condition. Having had access to the German diagnosis, I may have had a head start on my fellow sufferers in the United Kingdom. Here, a major difficulty is the uncritical use of the label "low back pain" to cover all patients with and without radicular pain, irrespective of possible aetiology. This confuses patients, therapists, and doctors alike. The impression is of a lack of precision in both diagnosis and treatment. But failed back surgery syndrome is also an unfortunate term, implying failure of the surgeon or possibly of the patient. In most cases, neither is true.

Despite the plethora of investigations that can be used for such a condition, the diagnosis remains essentially clinical. Magnetic resonance imaging and computed tomography are necessary to rule out lesions amenable to surgical intervention, but they cannot determine whether the intraspinal scarring is causing the symptoms. Neuropathic pain may not always have a burning quality, but other recognisable features are often present—for example, delayed summation of pain after provocation, the extension of pain perception beyond dermatomal boundaries, and allodynia (pain resulting from touch alone).

Support for patients

In many ways failed back surgery syndrome resembles multiple sclerosis: the conditions have the same range of symptoms of pain and numbness, weakness and spasm in the limbs, and bladder and bowel difficulties. But whereas some neurological units offer specialist expertise in treatment and lifestyle support for people with multiple sclerosis, patients with failed back surgery syndrome are left outside the door. In terms of numbers, there is roughly one person with failed back surgery syndrome for every two with multiple sclerosis.

After four years I still haven't found appropriate rehabilitative support in the United Kingdom. Pain management programmes, where well-intentioned encouragement of generic measures is the rule, generally fail to take into account the real danger of further nerve damage and a permanent increase in symptoms. I have learnt to be wary of enthusiastic physiotherapists. Even in Germany, where I participated in a rehabilitation programme, this was very much batch processing, with little attention to variations between patients.

Summary points
Surgery for prolapsed disc fails to relieve pain in 5-10% of patients

Patients with failed back surgery syndrome face increasing disability as well as chronic pain

The condition has fallen into a no-man's land between surgery and medicine

Rehabilitative medicine is poorly developed, focusing mainly on pain relief

Patients with failed back surgery syndrome live with the constant anxiety of relapse and steady deterioration of a range of neurological symptoms, yet current medical management focuses narrowly on relieving pain. This is another strand in the web in which patients are caught: good pain relief brings the illusion of improved physical ability. However, for many patients, after a brief honeymoon period pain, spasm and weakness appear at a lower activity level, and the web tightens to immobilise the ensnared nerve roots (and patients) even more.

Competing interests: None declared.

Porter RW. Spinal surgery and alleged medical negligence. J R Coll Surg Edinb 1997;42: 376-80.[ISI][Medline]
Resnick D. Failed back surgery syndrome. In: Medcyclopaedia. www.amershamhealth.com/medcyclopaedia.com (accessed 17 Sep 2003).
Helthoff KB, Burton CV. CT evaluation of the failed back surgery syndrome. Orthop Clin North Am 1985;16: 417-44.[ISI][Medline]
(Accepted September 23, 2002)

Rapid Responses:
Read all Rapid Responses

BMJ 2003 327: 986-987. [Full text]

© 2003 BMJ Publishing Group Ltd

herniated lumbar discs never require surgery

Postby guest » Wed Dec 10, 2003 6:42 pm

EBM Reviews - ACP Journal Club

Accession Number

Surgery for Herniated Lumbar Disc: A Review.

ACP Journal Club. v120:p.15, Jan-Feb, 1994.

Reviewed Source
Abstract and Commentary for: Hoffman RM, Wheeler KJ, Deyo RA. Surgery for herniated lumbar discs: a literature synthesis. J Gen Intern Med. 1993 Sep;8:487-96.

Commentary Author
Nortin M. Hadler, MD

Commentary Author's Institution
University of North Carolina, Chapel Hill, North Carolina

Backache; Chemonucleolysis; Discolysis; Exercise; Intervertebral chemonucleolysis; MEDLINE; Neuralgia-neuritis of sciatic nerve; Physical activity; Physical activity endurance; Physical exercise; Sciatica; Thromboembolic events; Vertebrogenic pain syndrome


To evaluate the risks and benefits of surgery for herniated lumbar discs.

Data Sources:

English-language studies were identified using MEDLINE (1966 through 1991) with the following MeSH headings and key words: lumbar, backache, herniated disc, intervertebral disc displacement, sciatica, laminectomy, disc surgery, discectomy, microdiscectomy, and percutaneous discectomy. Reference lists of retrieved articles, book bibliographies, and experts' files were reviewed for additional studies.

Study Selection:

Studies were selected if the sample size was >= 30, if the mean age of patients was >= 30 years, if baseline and follow-up data were available for >= 75% of all patients receiving surgery, and if the minimum follow-up was >= 1 year or if the mean follow-up was >= 24 months. Review articles, studies with >= 10% of patients with a primary diagnosis other than herniated disc, and studies of anterior discectomy or spinal fusion were excluded.

Data Extraction:

Data pertaining to study design, patient demographics, clinical description, diagnostic testing, surgical techniques, operative findings, clinical outcomes, reoperations, and operative complications were extracted. A successful outcome was defined as the sciatica being completely absent or occasionally mild with minimal or no restriction of physical activity and a return to previous employment. Point estimates and 95% confidence intervals of the proportion of successful outcomes, complications, and reoperations were obtained by fitting a random-effects logistic regression model.

Main Results:

81 studies met the inclusion criteria. Most studies had substantial design flaws; only 4 were prospective comparison studies. The 2 randomized controlled trials of standard discectomy showed better 1-year patient- or physician-rated outcomes after surgery (65% to 85%) compared with either conservative treatment (36%) or chymopapain (63%), but longer-term outcomes did not differ. Data from randomized trials were not available for microdiscectomy or percutaneous discectomy. Approximately 10% of patients who received discectomy had further back surgery, and this rate increased over time. Reoperations occurred most frequently after percutaneous discectomy. Serious complications after discectomy were rare. The mortality rate was < 0.1%, the rates of deep wound infection and permanent nerve root damage were < 1%, and the rates of thromboembolic events, wound infections, and discitis were < 2%.


Standard discectomy appeared to provide better short-term outcomes than conservative treatment, but long-term outcomes were similar. Discectomies were safe, but reoperations were common and increased over time.

The review by Hoffman and colleagues is another assault on the literature of backache. Again, we learn that the literature is voluminous but is mostly inadequate for quantitative review. The authors have therefore drawn their inferences from a small subset of studies. The results reiterate the precedent literature. In their dispassionate service to objectivity, the authors fail to stress the salient messages of their exercise. Here is what is left unsaid.

First, herniated lumbar discs never require surgery. A small percentage of patients with regional radicular pain benefit from surgery, often done to alter discal structure. Herniated lumbar discs are common and usually asymptomatic.

Second, there is no compelling evidence that surgery for a regional backache benefits any patients. There is the suggestion of benefit for subacute sciatica but not for pain in the low back.

Third, there is compelling evidence that whatever the indication (generally sciatica), patients are less well served by chemonucleolysis than traditional laminectomy. Similarly, they are less well served by percutaneous microdiscectomy than by chemonucleolysis. Each year tens of thousands of persons with backache are misled into considering these procedures as 'advances.'

Finally, the benefit afforded the patient with subacute sciatica is not uniform across series. It varies in both relative and absolute magnitude of likelihood. In the absence of progressive neurologic compromise, laminectomy is an elective procedure even for subacute sciatica.

This literature synthesis spans the 3 decades during which the Federal Drug Administration (FDA) was empowered by the Kefauver-Harris amendments to demand a clearly favorable benefit-to-risk ratio before any pharmaceutical could be purveyed. If those amendments had added surgery for regional back-pain syndromes to the purview of the FDA, many American backs would have been spared the scar that denotes an unproved remedy. Judging from the incontrovertible message of the literature, this empowerment is long overdue.

Publication Type

Document Type

operative treatment gave no better prognosis

Postby guest » Wed Dec 10, 2003 6:46 pm

EBM Reviews - Cochrane Central Register of Controlled Trials

Accession Number

Weber H

The effect of delayed disc surgery on muscular paresis

ACTA ORTHOPSCAND 46(4):631-642, 1975.

A prospective study was carried out in 280 patients suffering from sciatica caused by myelographically verified disc prolapse. The patients were divided into three groups according to the following criteria: The doubtful group, selected at random. Patients with doubtful indications for surgery. Treated operatively or not, by drawing lots. Non operated group. Patients with moderate symptoms and/or continued improvement. Operated group. Patients with imperative indications for surgery. The muscle strength of the lower limbs was measured during maximal isometric voluntary contractions in all the patients 2 wk after admission. Approximately 50% had paresis. Control examinations of these patients 1 yr later showed that operative treatment gave no better prognosis than conservative treatment with regard to the motor function, neither in the group chosen at random nor in the selected groups. The causative factors are discussed.

EMBASE keywords: Muscle Paresis (0124902)/ Ischialgia (0024762)/ Myelography (0031944)/ Leg Muscle (0027995)/ Muscle Strength (0031743)

External Accession Number
Embase 1976158267

Cochrane Group Name
Cochrane Back Review Group For Spinal Disorders

Serials Code

Study Design
Randomized Control Trial

pred not helpful for lumbar disc surgery

Postby guest » Wed Dec 10, 2003 6:49 pm

EBM Reviews - Cochrane Central Register of Controlled Trials

Accession Number

Manniche C, Lauritsen B, Vinterberg H

Dept. of Rheumatology, Hillerod Hospital, Denmark.

Peroperative prednisolone fails to improve the clinical outcome following surgery for prolapsed lumbar intervertebral disc. A randomized controlled trial.

Scandinavian Journal of Rheumatology. 23(1):30-5, 1994.

Ninety three patients undergoing their first conventional hemilaminectomy for lumbar disc protusion were randomized to a double blind clinical trial. Half of the patients were treated immediately following surgery with prednisolone; 50 mg per day for fourteen days and then 25 mg per day for another 14 days. The other patients were treated for the same time period with placebo tablets. Assessments using subjective and objective outcome criteria at 26 weeks, 52 weeks and 156 weeks of follow-up, demonstrated no statistically significant differences between the randomized groups. It is concluded that systemic prednisolone administration in the pre- and postoperative period does not in this study improve the clinical outcome after first time lumbar discectomy.

Publication Type
Clinical Trial. Journal Article. Randomized Controlled Trial

back surgery outcome not associated with presurg MRI results

Postby quest » Fri Feb 06, 2004 7:38 pm

June 1, 2000 (Volume 216, No. 11)
Association between postoperative outcome and results of magnetic resonance imaging and computed tomography in working dogs with degenerative lumbosacral stenosis
Jeryl C. Jones, DVM, PhD, DACVR; Catherine M. Banfield, DVM, MS, DACVR; Daniel L. Ward, MS *
Objective—To determine whether results of magnetic resonance imaging (MRI) and computed tomography (CT) are associated with postoperative outcome in working dogs with degenerative lumbosacral stenosis.

Design—Prospective cohort study.

Animals—12 dogs treated surgically for degenerative lumbosacral stenosis.

Procedure—The lumbosacral vertebral column was examined before surgery by use of MRI and CT and after surgery by use of CT. Outcome, based on performance in standardized training exercises, was assessed 6 months after decompressive surgery. Associations between imaging results and postoperative outcome were determined by use of a Fisher exact test and logistic regression.

Results—None of the dogs were able to perform their duties before surgery. By 6 months after surgery, 8 of 12 dogs had been returned to full active duty. Nerve tissue compression was effectively localized by use of CT and MRI. Significant associations between results of imaging studies and postoperative outcome were not identified.

Conclusions and Clinical Relevance—Surgical intervention is justified in high-performance working dogs with degenerative lumbosacral stenosis. However, results of imaging studies may be less important than clinical or surgical factors for predicting outcome in affected dogs. (J Am Vet Med Assoc 2000;216:1769–1774)

Lumbosacral stenosis is defined as an abnormal narrowing of the L5-S3 vertebral canal or intervertebral foramina, with compression of the cauda equina nerve roots or their blood supply.1-4 This abnormal narrowing can be caused by idiopathic or acquired disorders. The most common acquired cause of lumbosacral stenosis in dogs is degenerative disease.5-15 Other acquired causes of lumbosacral stenosis include diskospondylitis, neoplasia, and trauma.5,6,11,13 Degenerative lumbosacral stenosis is primarily characterized by intervertebral disk degeneration, intervertebral disk protrusion, bone proliferation on the vertebral endplates and articular processes, vertebral subluxation, and hypertrophy of the joint capsules and interarcuate ligament (ligamentum flavum).6-12

Large, working-breed dogs are particularly at risk for development of degenerative lumbosacral stenosis.7-10 Male dogs are affected more commonly than female dogs. Early clinical signs may include signs of pain in the lumbosacral area, self-mutilation, reluctance to sit, reluctance to jump up into a car or truck, refusal to climb walls or other obstacles, and hind limb lameness that is most severe following work.11 Dogs with more severe disease may develop hind limb paresis, muscle atrophy, tail paresis, or urinary or fecal incontinence. Surgery and excision of compressive tissues are indicated when clinical signs fail to respond to appropriate conservative treatment.7,8,10,12-15 Fixation and fusion may also be warranted when there is concurrent lumbosacral instability.8,16

A noninvasive technique for predicting postoperative outcome would be of benefit for owners and trainers of working dogs with lumbosacral stenosis. Computed tomography (CT) and magnetic resonance imaging (MRI) are sensitive, noninvasive imaging techniques for evaluating the lumbosacral vertebral column in dogs.17-23 Both modalities provide excellent discrimination of compressive tissues in the vertebral canal and intervertebral foramina, primarily by eliminating superimposition of overlying structures. The choice of MRI versus CT is often made on the basis of cost, availability, surgeon's preference, and radiologist's experience.24-26

Diagnostic sensitivities of CT and MRI are similar for identifying lumbar disk herniation.27,28 Relative advantages of CT versus MRI include lower cost and better discrimination of bone spurs, articular process joint disease, soft-tissue calcification, and soft-tissue gas opacities.25,29-31 Relative advantages of MRI versus CT include better soft-tissue contrast resolution, earlier detection of disk degeneration, ability to acquire images in multiple planes, and ability to evaluate the entire lumbar vertebral column in a single examination.25,32-34 The objective of the study reported here was to determine whether results of MRI or CT were associated with postoperative outcome in a group of high-performance working dogs with degenerative lumbosacral stenosis.

Materials and Methods

Dogs—The study population consisted of 11 military working dogs and 1 US Customs dog with degenerative lumbosacral stenosis. Diagnostic work-ups, surgical treatments, and postoperative evaluations for all dogs were performed at the same military referral center from March 1995 to July 1997.a The diagnosis of degenerative lumbosacral stenosis was made on the basis of history and results of physical and neurologic examinations, radiography, CT, and MRI. Before the onset of clinical signs, 10 of the military working dogs performed both patrol and drug detection work (ie, they were dual-trained). One military working dog performed patrol work, and the US Customs dog performed drug detection work (ie, they were single-trained). After the onset of clinical signs, all dogs were unable to perform at mission standards despite appropriate conservative treatment. Initial complaints included reluctance to jump up or search high, hind limb lameness, abnormal gait, hind limb ataxia or weakness, and self-mutilation. Candidates for surgery were defined using the following criteria: signs of pain during palpation of the lumbosacral area or elevation of the tail, no or mild hind limb motor deficits, no or mild hind limb muscle atrophy, age < 10 years, and imaging findings consistent with degenerative lumbosacral stenosis.5,15,19,22 Dogs with degenerative myelopathy, diskospondylitis, vertebral neoplasia, or severe concurrent orthopedic diseases were excluded.

Imaging and surgical techniques—All dogs were evaluated before surgery by use of MRI and CT and after surgery by use of CT. For MRI and CT, dogs were anesthetized and positioned in dorsal recumbency with the hind limbs flexed.35 Magnetic resonance imaging of the vertebral column from L1 to S3 was performed, using a 1.5 Tesla scannerb (technique settings: 90 degree flip angle, 12 to 28 × 12 to 28 fields of view, 256 × 256 matrix, 3 to 5-mm slice thickness, and 1-mm slice gap). Images were acquired in sagittal and transverse planes. Imaging sequences included T1-weighted (15 to 17 milliseconds TE and 450 to 600 milliseconds TR), T2-weighted (102 to 108 milliseconds TE and 3,000 to 3,600 milliseconds TR), and fat-suppressed, contrast-enhanced T1-weighted (17 to 23 milliseconds TE and 566 to 700 milliseconds TR). Contrast-enhanced images were obtained immediately following IV administration of gadopentetate dimeglumine (0.2 ml/kg [0.09 ml/lb] of body weight; 469.1 mg of gadopentetate dimeglumine/ml). Stenotic areas were identified on the basis of attenuation of epidural fat in the vertebral canal, lateral recesses, or intervertebral foramina.19 Computed tomography of stenotic vertebral segments was performed, using a helical CT scannerc (technique settings: 10-cm field of view, detail algorithm, 120 kilovolt (peak), 270 to 280 mA, 0 degree tilt, 512 × 512 matrix, 3-mm slice thickness, 3-mm slice interval). Transverse slices were retrospectively reconstructed from the helical scan to be 1-mm thick with 1-mm intervals. Transverse and reformatted sagittal/dorsal planar images were viewed, using window settings for bone (4,000 window and 400 level) and soft tissue (400 window and 35 level).

Surgery was performed at the vertebral level(s) where imaging abnormalities best correlated with history, clinical signs, and results of neurologic examination.22 Following dorsal laminectomy, tissues encroaching on cauda equina nerve roots or their blood supply were excised.8,12,15 Foramenotomy and facetectomy were also performed as needed for stenosis involving the lateral recesses or intervertebral foramina. Postoperative CT of the surgically-decompressed vertebral segments was performed at least 1 month prior to outcome assessment.

Outcome assessment—After surgery, dogs were confined to cage rest for 8 to 10 weeks and then allowed to gradually resume regular exercise sessions with their handlers. Six months after surgery, dogs were assigned to 1 of 2 outcome groups on the basis of their performance in standardized obstacle course and training exercises. Dogs assigned to outcome group 1 were fit for full duty, defined as able to deploy and meet performance standards with no limitations. Dogs assigned to outcome group 2 were not fit for full duty, defined as unable to deploy because of limitations in performance. All outcome group assignments were made by an experienced performance evaluator (CMB), without reference to surgical, MRI, or CT findings.

Data recorded—Magnetic resonance images and tomograms were independently reviewed by a separate observer (JCJ) without reference to surgical findings or outcome assessment. Data recorded from magnetic resonance images included number of lumbar disk levels with stenosis, locations of compressive tissues (central spinal canal, lateral recess, intervertebral foramina), presence of soft-tissue contrast enhancement, presence of vertebral subluxation, severity of degenerative disk disease, and severity of disk margin bulging (Figure 1). Degenerative disk disease was graded on the basis of a relative decrease in T2 signal intensity. Data recorded from tomograms included presence of vertebral malformation, presence of vertebral subluxation, locations of bone spurs and compressive soft tissues, and severity of disk margin bulging (Figure 2 and Figure 3). For MRI and CT, severity of disk margin bulging was graded on the basis of maximum percentage of vertebral canal attenuation seen in sagittal and transverse planar images (0 = none, 1 = mild [< 25%], 2 = moderate [25 to 50%], and 3 = severe [> 50%]). After imaging data collection was completed, patient records were reviewed, and surgical estimates of disk bulge severity were determined from descriptions in the surgery reports.

Data analyses—The association between outcome and each dichotomous (present or absent) imaging result was evaluated by use of the Fisher exact test.d Associations between the imaging estimates of disk bulge severity and surgical estimates of disk bulge severity were also tested by use of the Fisher exact test. Logistic regression was used to test for the effect of disk bulge severity or disk degeneration severity on outcome.e Significance was set at P < 0.05.


Three breeds were represented in the study population: Belgian Malinois (n = 8), German Shepherd Dog (3), and Labrador Retriever (1). Dogs ranged from 4 to 9 years old (mean, 6.7 years) and weighed between 25 and 40 kg ([55 and 88 lb]; mean, 31 kg [68.2 lb]). All were males (9 sexually intact and 3 castrated). Duration of clinical signs prior to surgery ranged from 2 to 17 months (mean, 5.5 months). Eight dogs were able to return to full active duty after surgery (outcome group 1). Four dogs were unable to return to full active duty because of persistent performance limitations (outcome group 2). We did not detect significant associations between imaging results and postoperative outcome (Table 1). Results of MRI for all dogs in group 2 and 7 dogs in group 1 revealed contrast enhancement of compressive soft tissues. On preoperative and postoperative tomograms, all dogs in group 2 had evidence of central vertebral canal stenosis. However, this was also evident in 6 of the group-1 dogs. Postoperative CT revealed bilateral foraminal stenosis in all group-2 dogs and 6 of 8 group-1 dogs. Vertebral subluxation was evident on postoperative tomograms of 3 group-2 dogs and 3 group-1 dogs.

We did not detect a significant effect of severity of disk degeneration or disk bulging on postsurgical outcome (Table 2). Severe disk degeneration was evident in 5 group-1 dogs and 3 group-2 dogs. Severe disk bulging was seen on magnetic resonance images of 1 of the group-2 dogs and none of the group-1 dogs. On tomograms, severe disk bulging was seen in 3 of the group-2 dogs and 3 of the group-1 dogs. Surgical estimates of disk bulging were available for 11 dogs. No significant associations were found between surgical estimates of disk bulge severity and estimates of disk bulge severity from either MRI or CT. Fisher exact P values within mild, moderate, and severe disk bulge categories, as determined by use of MRI, were 0.364, 1.00, and 1.00, respectively. Fisher exact P values within mild, moderate, and severe disk bulge categories, as determined by use of CT, were 1.00, 0.182, and 1.00, respectively.


Postoperative outcome for dogs with lumbosacral stenosis is likely influenced by multiple factors. We attempted to minimize variability attributable to breed, temperament, activity, pain threshold, concurrent disease processes, and outcome expectations by choosing as homogenous a study population as possible. Because of preprocurement selection procedures, military dogs have similar temperaments and a low incidence of other musculoskeletal problems (eg, hip dysplasia, elbow dysplasia, osteochondrosis). Most are either German Shepherd Dogs or Belgian Malinois. All are maintained at similar levels of athletic fitness through regularly scheduled training exercises, have standardized criteria for performance, and are monitored closely by handlers familiar with each dog's capabilities. Outcome prediction is of particular importance in this population, because each dog represents a considerable financial investment. This is especially true for dual-trained dogs. Dual-trained dogs are highly valued, because they can be used worldwide for sentry duty and detection of explosives or contraband. Given the strenuous physical activities required (eg, climbing airplane stairs, jumping onto high shelves, leaping over fences, biting and holding on while a trainer violently shakes the dog), it is remarkable that 8 of our dogs were able to return to full active duty after lumbosacral surgery. Three of the 4 dogs that were unable to return to full active duty were still able to perform at a reduced duty status.

We also attempted to minimize imaging result variability by using similar positioning and imaging protocols for all dogs. All imaging results were recorded by the same person, without reference to clinical and surgical data. Both CT and MRI were used, because we wanted to determine whether one of these modalities would prove more valuable than the other for predicting outcome. This increased the cost of data collection for our study and necessitated a small sample size. Both modalities were effective in identifying sites of nerve tissue compression, but neither was predictive of outcome. Surgical decisions were made, using a combination of history, clinical signs, neurologic examination findings, and imaging results. Other methods, such as paraspinal electromyography, may also be of benefit for cases warranting more diagnostic certainty.36

Some population bias was imposed by the stringent criteria for surgical candidacy at this referral center. Dogs were not considered to be good surgical candidates if they were > 10 years old, had severe concurrent orthopedic disease, and severe motor deficits or muscle atrophy. These criteria were selected on the basis of prior clinical observations by one of the authors (CMB). Dogs with severe motor deficits were assumed to have irreversible nerve degeneration. This assumption was recently supported by results of a Swedish study evaluating postoperative outcome in 131 dogs with lumbosacral stenosis.15 In that study, 76 dogs were considered to be active working dogs. Of the 2 dogs with severe preoperative clinical signs, only 1 was able to return to a high degree of postoperative activity. In contrast, 18 of 23 (78.3%) working dogs with mild preoperative clinical signs and 40 of 51 (78.4%) with moderate preoperative clinical signs returned to a high degree of activity.

The small sample size used in the present study may have limited our ability to detect significant associations between imaging results and postoperative outcome (power of the tests of association, ≤ 0.22). However, in 2 recently published studies that evaluated humans with lumbar spinal stenosis, study populations were larger, and results also indicated no significant associations between imaging findings and postoperative outcome.37,38 In 1 of these studies, postoperative MRI findings were compared with clinical observations in 56 patients 10 years after laminectomy for lumbar spinal stenosis. Significant differences in clinical outcome scores were not detected between groups with and without evidence of persistent stenosis on postoperative magnetic resonance images.37 In the other study, preoperative and postoperative CT findings were compared with clinical outcome in 92 patients with lumbar spinal stenosis. Significant differences in outcome scores were not found among groups without evidence of stenosis on postoperative tomograms and those with evidence of adjacent stenosis, residual stenosis, or spinal instability.38

The reasons for observed discrepancies between estimates of disk bulge severity determined by use of MRI and CT in some of our dogs are not known. These discrepancies may have been attributable to differences in contrast and spatial resolution of the 2 techniques. Soft-tissue contrast resolution for MRI is superior to that of CT; therefore, MRI estimates of disk bulge severity may have been more accurate.28,34,39 Alternatively, CT estimates of disk bulge severity may have been more accurate because of the superior spatial contrast resolution. Slices used for magnetic resonance images in our dogs were thicker than those used for tomograms (5 mm vs 1 mm). Thinner collimation reduces errors caused by the partial volume averaging and, therefore, increases spatial resolution.18,28,35 Slight differences in patient positioning may also have accounted for the discrepancies between results of the 2 techniques. Vertebral canal height can be miscalculated if the spine is positioned obliquely relative to the slice plane.40,41 Differences in positioning may also explain the discrepancies between surgical and imaging estimates of disk bulge severity. Dogs were positioned in dorsal recumbency with the hind limbs flexed for imaging and in ventral recumbency with the hind limbs partially extended for surgery. Because of concurrent ligamentous instability and hypertrophy, the dimensions of the vertebral canal in the lumbosacral area can be considerably altered by flexion versus extension of the vertebral column.42,43

Our findings indicate that surgery is justified for high-performance working dogs with degenerative lumbosacral stenosis. Both MRI and CT are effective techniques for identifying the locations of nerve tissue compression. However, imaging results may be less important than clinical or surgical factors for predicting postoperative outcome.

aDepartment of Defense Military Working Dog Veterinary Services, Lackland Air Force Base, Lackland, Tex.
bGE Signa Modular MRI Unit, System No. MR010C0, General Electric Medical Systems, Milwaukee, Wis.
cGE HiSpeed Advanced System No. HSA2, Helical CT Scanner, General Electric Medical Systems, Milwaukee, Wis.
dFREQ procedure, SAS version 6.12, SAS Institute Inc, Cary, NC.
eLOGISTIC procedure, SAS version 6.12, SAS Institute Inc, Cary, NC.



1. Indrieri RJ. Lumbosacral stenosis and injury of the cauda equina. Vet Clin North Am Small Anim Pract 1988;18:697–710.

2. Jones JC, Wright J, Bartels J. Computed tomographic morphometry of the lumbosacral spine of dogs. Am J Vet Res 1995;56:1125–1131.

3. Arnoldi CC, Brodsky AE, Cauchoix J, et al. Lumbar spinal stenosis and nerve root entrapment syndromes. Definition and classification. Clin Orthop 1976;115:4–5.

4. Schatzker J, Pennal G. Spinal stenosis, a cause of cauda equina compression. J Bone Joint Surg Br 1968;50:606–618.

5. Braund KG. Neurological diseases. In: Braund KG, ed. Clinical syndromes in veterinary neurology. 2nd ed. St Louis: Mosby Year Book Inc, 1994;171–172.

6. Palmer RH, Chambers JN. Canine lumbosacral diseases. Part I. Anatomy, pathophysiology, and clinical presentation. Compend Contin Educ Pract Vet 1991;13:61–69.

7. Leighton RL. Surgical treatment of canine lumbosacral spondylopathy. Vet Med 1983;78:1853–1856.

8. Watt PR. Degenerative lumbosacral stenosis in 18 dogs. J Small Anim Pract 1991;32:125–134.

9. Chambers JN. Degenerative lumbosacral stenosis in dogs. Vet Med Rep 1989;1:166–180.

10. Oliver JE, Selcer RR, Simpson S. Cauda equina compression from lumbosacral malarticulation and malformation in the dog. J Am Vet Med Assoc 1978;173:207–214.

11. Wheeler SJ. Lumbosacral disease. Vet Clin North Am Small Anim Pract 1992;22:937–950.

12. Chambers JN, Selcer BA, Oliver JE. Results of treatment of degenerative lumbosacral stenosis in dogs by exploration and excision. Vet Comp Orthop Traumatol 1988;3:130–133.

13. LeCouteur RA, Child G. Diseases of the spinal cord. In: Ettinger SJ, ed. Textbook of veterinary internal medicine. 3rd ed. Philadelphia: WB Saunders Co, 1989;672–675.

14. Prata RG. Cauda equina syndrome. In: Slatter D, ed. Textbook of small animal surgery. 2nd ed. Philadelphia: WB Saunders Co, 1993;1101–1105.

15. Danielsson F, Sjostrom L. Surgical treatment of degenerative lumbosacral stenosis in dogs. Vet Surg 1999;28:91–98.

16. Slocum B, Devine T. L7-S1 fixation-fusion for treatment of cauda equina compression in the dog. J Am Vet Med Assoc 1986;188:31–35.

17. deHaan JJ, Shelton SB, Ackerman N. Magnetic resonance imaging in the diagnosis of degenerative lumbosacral stenosis in four dogs. Vet Surg 1993;22:1–4.

18. Karkkainen M, Punto LU, Tulamo R. Magnetic resonance imaging of canine degenerative lumbar spine diseases. Vet Radiol Ultrasound 1993;34:399–404.

19. Adams WH, Daniel GB, Pardso AD, et al. Magnetic resonance imaging of the caudal lumbar and lumbosacral spine in 13 dogs. Vet Radiol Ultrasound 1995;36:3–13.

20. Jones JC, Cartee RE, Bartels JE. Computed tomographic anatomy of the canine lumbosacral spine. Vet Radiol Ultrasound 1995;36:91–99.

21. Feeney DA. Computed tomography of the normal canine lumbosacral spine: a morphological perspective. Vet Radiol Ultrasound 1996;37:399–411.

22. Jones JC, Sorjonen DC, Simpson ST, et al. Comparison between computed tomographic and surgical findings in nine large-breed dogs with lumbosacral stenosis. Vet Radiol Ultrasound 1996;37:247–256.

23. Jones JC, Shires PK, Inzana KD, et al. Evaluation of canine lumbosacral stenosis using intravenous contrast-enhanced computed tomography. Vet Radiol Ultrasound 1999;40:108–114.

24. Lange M, Hamburger C, Waidhauser E, et al. Surgical treatment and results in patients suffering from lumbar spinal stenosis. Neurosurg Rev 1993;16:27–33.

25. Spivak JM. Current concepts review: degenerative lumbar spinal stenosis. J Bone Joint Surg Am 1998;80:1053–1066.

26. Grumme T, Bittl M. Imaging and therapy of degenerative spine diseases—a neurosurgeon's view. Eur J Radiol 1998;27:235–240.

27. Thornbury JR, Fryback DG, Turski PA, et al. Disk-caused nerve compression in patients with acute low-back pain: diagnosis with MR, CT myelography, and plain CT [published erratum appears in Radiology 1993;187:880]. Radiology 1993;186:731–738.

28. Deyo R. Reproducibility and accuracy of lumbar spine imaging studies. In: Wiesel SW, Weibstein JN, Herkowitz H, et al, eds. The lumbar spine. Philadelphia: WB Saunders Co, 1996;434–446.

29. Heithoff KB. Myelography and computed tomography of the lumbar spine. In: Wiesel SW, Weibstein JN, Herkowitz H, et al, eds. The lumbar spine. Philadelphia: WB Saunders Co, 1996;376–434.

30. Donmez T, Caner H, Cila A, et al. Diagnostic value of computed tomography in spinal and lateral recess stenosis, pre-operatively and for long-term follow-up: a prospective study in 50 cases. Radiat Med 1990;8:111–115.

31. Hathcock J. Vacuum phenomenon of the canine spine: CT findings in 3 patients. Vet Radiol Ultrasound 1994;35:285–289.

32. Loke TK, Ma HT, Ward SC, et al. MRI of intraspinal nerve sheath tumours presenting with sciatica. Australas Radiol 1995;39:228–232.

33. Murata M, Morio Y, Kuranobu K. Lumbar disc degeneration and segmental instability: a comparison of magnetic resonance images and plain radiographs of patients with low back pain. Arch Orthop Trauma Surg 1994;113:297–301.

34. Patel PR, Lauerman WC. The use of magnetic resonance imaging in the diagnosis of lumbar disc disease. Orthop Nurs 1997;16:59–65.

35. Jones JC, Wilson ME, Bartels JE. A review of high resolution computed tomography and a proposed imaging protocol for regional examination of the canine lumbosacral spine. Vet Radiol Ultrasound 1994;35:339–346.

36. Haig AJ, Talley C, Grobler LJ, et al. Paraspinal mapping: quantified needle electromyography in lumbar radiculopathy. Muscle Nerve 1993;16:477–484.

37. Herno A, Partanen K, Talaslahti T, et al. Long-term clinical and magnetic resonance imaging follow-up assessment of patients with lumbar spinal stenosis after laminectomy. Spine 1999;24:1533–1537.

38. Herno A, Saari T, Suomalainen O, et al. The degree of decompressive relief and its relation to clinical outcome in patients undergoing surgery for lumbar spinal stenosis. Spine 1999;24:1010–1014.

39. Sprung C, Fabian A. Pitfalls in computed tomography of the cervical and lumbar spine. Neurosurg Rev 1994;17:19–28.

40. Paushter DM, Modic MT, Masaryk TJ. Magnetic resonance imaging of the spine: Applications and limitations. Radiol Clin North Am 1985;23:551–562.

41. Roub L, Drayer B. Spinal computed tomography: limitations and applications. AJR Am J Roentgenol 1979;133:267–273.

42. Lang J. Flexion-extension myelography of the canine cauda equina syndrome. Vet Radiol 1988;29:242–257.

43. Schonstrom N, Lindahl S, Willen J, et al. Dynamic changes in the dimensions of the lumbar spinal canal: an experimental study in vivo. J Orthop Res 1989;7:115–121.

non surgical option study in paralyzed dogs

Postby guest » Sat Feb 07, 2004 1:55 pm

July 1, 2000 (Volume 217, No. 1) 

Use of physiatry as the sole treatment for three paretic or paralyzed dogs with chronic compressive conditions of the caudal portion of the cervical spinal cord

John Speciale, DVM, DABVP, DACVIM, and James M. Fingeroth, DVM, DACVS *

  Anatomic lesions of the CNS may be best detected with advanced imaging techniques (computed tomography or magnetic-resonance imaging [MRI]). Although one would assume that the use of these techniques should lead to an accurate prognosis and determination of appropriate treatment, this assumption is not necessarily true. Severe lesions confirmed by use of MRI frequently are observed in asymptomatic humans. Furthermore, the clinical outcome of human patients with MRI-confirmed disc herniation appeared to be independent of surgical intervention.13 Observations for the dogs reported here as well as observations reported for animals with experimentally induced spinal cord injury are compatible with clinical observations for human patients. Therefore, it appears that clinicians cannot justify their ability to predict outcome in dogs and cats with spinal cord injuries solely on the anatomic appearance of lesions and the animal's immediate neurologic deficits.
Physical medicine (physiatry) as a primary means of treatment for paralyzed animals is a reasonable and affordable intervention. Although of unproven benefit in veterinary medicine, use of physical medicine in humans is cost effective and of great clinical value.16 Physiatry emphasizes function (a modality that owners can readily observe and evaluate) over pathologic characteristics or biomechanics.
16.   Brandstater ME, Brown SE. Physical medicine and rehabilitation. JAMA 1996;275:1843–1844.

Are Americans are being subjected to excessive surgery

Postby guest » Sat Feb 07, 2004 8:16 pm

1: Spine. 1994 Jun 1;19(11):1201-6. Related Articles, Links

An international comparison of back surgery rates.

Cherkin DC, Deyo RA, Loeser JD, Bush T, Waddell G.

Department of Health Services, University of Washington, Seattle.

SUMMARY OF BACKGROUND DATA. Although high geographic variation in back surgery rates within the United States have been documented, international comparisons have not been published. METHODS. The authors compared rates of back surgery in eleven developed countries to determine if back surgery rates are higher: 1) in the United States than in other developed countries, 2) in countries with more neurologic and orthopaedic surgeons per capita, and 3) in countries with higher rates of other surgical procedures. Data on back surgery rates and physician supply were obtained from health agencies within these eleven countries. Country-specific rates of other surgical procedures were available from published sources. RESULTS. The rate of back surgery in the United States was at least 40% higher than in any other country and was more than five times those in England and Scotland. Back surgery rates increased almost linearly with the per capita supply of orthopaedic and neurosurgeons in the country. Countries with high back surgery rates also had high rates of other discretionary procedures such as tonsillectomy and hysterectomy. CONCLUSIONS. These findings illustrate the potentially large impact of health system differences on rates of back surgery. Better outcome studies, however, are needed to determine whether Americans are being subjected to excessive surgery or if those in other developed countries are suffering because back surgery is underutilized.

medicine professor says no evidence back surgery works

Postby guest » Sat Feb 07, 2004 8:45 pm

MRIs Don't Improve Back Pain Care
They're costlier than X-rays, and lead to unnecessary surgery
By Adam Marcus
HealthScoutNews Reporter

TUESDAY, June 3 (HealthScoutNews) -- Patients and doctors may prefer high-tech spine scans over X-rays, but offering a sharper picture doesn't necessarily lead to better outcomes for people with lower back pain.

That's the conclusion of a new study, which acknowledges that rapid magnetic resonance imaging (MRI) tests may provide physicians a clearer view of the anatomy than an X-ray, and quickly. However, their use doesn't help resolve back problems. In fact, the researchers say the costly MRIs are much more likely than X-rays to lead to disc surgery, a procedure with limited value to all but a few people with low back pain.

"MRI scanning clearly is an important imaging method for the spine and it gives us some of the best pictures we have of the anatomy. But unfortunately the anatomy doesn't always match very closely with peoples' symptoms," says study co-author Dr. Richard Deyo, a professor of medicine at the University of Washington in Seattle. "It really is a much better picture, but sometimes a picture is more than you want to know."

Deyo's group reports its finding in the June 4 issue of the Journal of the American Medical Association . The study looked at a relatively new form of MRI called rapid MRI, which is similar to the conventional imaging test but takes only a fraction of the time to conduct. In the process, it provides detailed pictures of the anatomy that X-rays can't touch.

The study followed 380 men and women with low back pain who were being seen at Seattle-area clinics. Half underwent rapid MRI as a first resort, while the rest had more conservative spinal X-rays to detect the cause of their discomfort.

After a year, most patients had improved significantly. Yet the two groups were equally likely to report continued back disability, back pain and other measures of distress. That suggests the group that got rapid MRI wasn't receiving more finely tuned treatment, Deyo says.

However, those who had the MRI test were 2.5 times as likely to have undergone spinal surgery to correct a problem than those in the X-ray group -- 10 people versus four.

Dr. Jeffrey Jarvik, a neurosurgeon at the University of Washington and lead author of the study, says he was somewhat surprised by the results: "I really thought the rapid [MRI] might in fact improve patient outcomes, or at least there might not be the suggestion that it was a more expensive alternative."

By doing an early scan, Jarvik says, the hope was to rule out serious problems and avoid more expensive tests later on. That happened to a degree, he adds, but it was more than outweighed by the additional back surgeries.

Dr. Nortin Hadler says back surgery should be consigned to the waste bin of medical procedures. "There's absolutely no evidence that it works," says Hadler, a professor of medicine at the University of North Carolina and author of an editorial accompanying the journal article. "It ought to be a vanishingly rare procedure."

what, if anything, is doing any good

Postby guest » Mon Feb 09, 2004 11:15 am

New York Times

Healing a Bad Back Is Often an Effort in Painful Futility

February 9, 2004

Treating back pain costs Americans $26 billion a year, or
2.5 percent of the total health care bill, according to a
new study from Duke University, and far more if disability
payments, workers' compensation and lost wages are taken
into account. The costs are rising, researchers say, as
patients get ever more aggressive forms of treatment.

Back problems are the leading reason for visits to
neurologists and orthopedists and the eighth leading reason
for visits to doctors over all - ahead of fever, knee pain,
rashes, headaches and checkups for healthy babies. More
than 70 percent of adults suffer back pain at some time in
their lives, studies show. A third have had it in the past
30 days.

Yet for all the costs, for all the hours spent in doctors'
offices and operating suites, for all the massage therapy
and acupuncture and spinal manipulations, study after study
is leading medical experts to ask what, if anything, is
doing any good.

A variety of studies have suggested that in 85 percent of
cases it is impossible to say why a person's back hurts,
said Dr. Richard Deyo, a professor of medicine and health
services at the University of Washington. And most of the
time, the pain goes away with or without medical treatment.

"Nearly everyone gets better, nearly everyone improves,"
said Dr. Deyo, citing evidence from large epidemiological
studies. But he cautioned, "Getting better doesn't
necessarily mean pain-free."

"For a small number of patients," he added, "surgery can
offer quick relief, although even then it is common to have
mild symptoms and recurrences."

The Duke researchers, led by Dr. Xeumei Luo, used national
data from 1998. Back pain expenses, they say, included
$11.1 billion for office visits; $4.5 billion for
hospitalization; $3.9 billion for prescription drugs; $4.7
billion for outpatient services; and $1.1 billion for
emergency room care, with the rest made up of such things
as medical devices. The total, $26 billion, was a 30
percent increase from 1977 after adjusting for inflation.

"It's not like there's an explosion of new back pain," said
Dr. Steven Atlas, an assistant professor of medicine at
Harvard Medical School, who investigates back treatments.
"The number of cases isn't increasing; the cost per case is
increasing. There is a lot more that is being done, but the
issue is, Is it helping or not?"

Back pain has always been around, like headaches, or the
common cold. What has changed, doctors say, are people's

"People say, `I'm not going to put up with it,' " Dr. Deyo
said. "And we in the medical profession have turned to ever
more aggressive medication, narcotic medication, surgery,
more invasive surgery."

But studies find little evidence that patients are better
off for all the treatment.

Researchers asked, for example, what is the meaning of disk
abnormalities, so often seen when a back patient undergoes
an magnetic resonance imaging, or M.R.I.? So they examined
people with no back pain. One study, of 98 people, found
that two-thirds had problems like bulging or protruding
disks, herniated disks and degenerated disks. A third had
more than one abnormal disk.

Sometimes a problem like a herniated, or ruptured, disk
causes the pain, and surgery can relieve it, said the
study's author, Dr. Michael N. Brant-Zawadzki, a
radiologist at Hoag Hospital in Newport Beach, Calif. But
usually, he added, it may be more coincidence than cause
and effect when an M.R.I. finds an abnormal disk in someone
with back pain. And even when a herniated disk causes the
pain, the problem often goes away by itself.

It is easy to see the appeal of an M.R.I., said Dr. Stanley
J. Bigos, an emeritus professor of orthopedic surgery and
environmental health at the University of Washington. "The
reality is, patients want an answer, the doctor wants to
get the patient out of the room, and the hypotheses start
to flow."

Other studies have indicated that the development of
abnormal disks is usually inherited. But there were no
links to occupation, sports injuries or weak muscles, said
Dr. Nortin Hadler, a professor of medicine at the
University of North Carolina.

Researchers then asked whether patients who have M.R.I.'s
do any better.

In a study published last year in The Journal of the
American Medical Association, Dr. Deyo and his colleagues
randomly assigned 380 patients with back pain to X-rays or
M.R.I.'s. X-rays can reveal tumors or fractures but not
abnormal disks.

Half the M.R.I. patients had disk abnormalities, and the
imaging patients, as a group, ended up with more intensive
treatment - more doctor visits, physical therapy,
acupuncture and chiropractic manipulations as well as more
surgery. And while they were happier with their care, they
fared no better than the X-ray patients. Within a few
months, most patients in each group were feeling better and
were back at work.

Many in each group continued to feel some pain but were
living with it. "Many continue to have grumbling symptoms
and occasional flare-ups," Dr. Deyo said. "Their pain was
better but certainly not gone."

Since no one knows the cause of most back pain, Dr. Hadler
said, imaging is not much help. Nor are most treatments.
"Maybe you're better off not going to a doctor," he said.

Dr. Deyo concurs that while a small proportion of patients
may be helped by surgery, medical care may not be necessary
for most.

Surgery, too, is under new scrutiny, with a national study
getting started at 11 medical centers. About 1,000 patients
with the problems that most often lead to surgery will be
randomly assigned to have surgery or not. The problems
under study are herniated disks, spinal stenosis, which is
a narrowing of the spinal canal that usually occurs with
arthritis and aging, and degenerative spondylolithesis, a
slipped vertebra.

One of the investigators in the study is Dr. James N.
Weinstein, a Dartmouth professor of orthopedics and
community and family medicine and the editor in chief of
Spine, the professional journal that published the Duke
report in its January issue.

"I've met with two groups who said they fear the results
will take away their practice," Dr. Weinstein said. "I
don't know how to deal with that. I don't know what the
results will be."

Back experts say it is clear that surgery can make some
patients feel better immediately.

"Let's say you have a herniated disk and let's say you have
leg pain and let's say you are as miserable as hell and you
convince somebody to operate on you," said Dr. Michael
Modic, chairman of the radiology department at the
Cleveland Clinic. "You have a 95 percent chance of waking
up with no pain."

Most people will get better anyway, Dr. Modic said, but
surgery can "reduce the symptomatic time period."

Dr. Thomas Errico, president of the North American Spine
Society, says surgery is a last resort. His patients have
X-rays or M.R.I.'s. They try over-the-counter
anti-inflammatory drugs. They are given an exercise
program, or get muscle relaxants or painkilling injections.
They are told to stretch and to get their weight under
control. They might get a steroid injected into the spine
to reduce inflammation.

"That's what the vast majority of the 3,700 members of the
North American Spine Society do," Dr. Errico said. "The
vast majority discourage surgery or don't offer surgery as
the first recourse."

Whether patients benefit from treatment or whether their
pain eases on its own, back experts agree that 10 percent
of cases are intractable. Dr. Rowland Hazard, a professor
of orthopedics and medicine at Dartmouth, estimates that 80
percent to 90 percent of spending on back pain "is devoted
to this 10 percent who don't get well."

Their prognosis is disheartening. Those with disabling pain
for three or four months have just a 10 percent to 20
percent chance of getting better in the next year.

For this group, some doctors are now advocating a different
approach altogether: teaching people to live with pain, to
put aside the understandable fear that any motion will
aggravate their injury. They have to learn, Dr. Weinstein
said, that "hurt doesn't mean harm."

In programs often known as functional restoration, that is
the goal. Patients are trained in strength, flexibility and
endurance. They are counseled about their fears of
re-injury and about anxiety and depression.

It can be difficult to get them back to work, noted Dr.
Bigos, of the University of Washington, because many left
their jobs on disability and had bitter disputes with their
former employers or with insurance companies. "Usually,
lines have been drawn in the sand by one or both sides," he

But success is possible, said Dr. Thomas Mayer, director of
a clinic called Pride, for Productive Rehabilitation
Institute of Dallas for Ergonomics. Among the 3,500 back
patients who entered his one- to two-month program and
completed it, almost all returned to work and nearly half
went back to their original employer, Dr. Mayer said.

"We deal with it face on," Dr. Mayer said. "What are you
going to do for the rest of your life? What are you getting
from being disabled? What would you get if you were not

The lesson, Dr. Weinstein says, is that "you can have pain
and still function." And while there may appear to be more
treatments that ever, he adds, "more isn't necessarily

suicide in the spinal cord an active form of cell death

Postby malernee » Fri Mar 26, 2004 12:51 pm


Peter K Shires BVSc, MS, Diplomate ACVS, VA-MD Regional College of Veterinary Medicine, Blacksburg, Virginia
ACVS Symposium Equine and Small Animal Proceedings
October 9, 2003

The full text of the article is below.

Peter K Shires BVSc, MS, Diplomate ACVS

VA-MD Regional College of Veterinary Medicine, Blacksburg, Virginia

Small Animal Proceedings

Neurosurgery Track

Keywords: canine, feline, disk,herniation, intervertebral,

When surgically decompressing an intervertebral disk (IVDD) lesion, the primary justification for giving pharmaceuticals in the perioperative period is that it may ameliorate some of the acute effects of the acute phase of spinal cord injury, and perhaps prevent some of the secondary events from developing. This review will briefly outline current thinking about the pathophysiology associated with acute spinal injuries, and then report the findings of several studies about interventions that may target some of the described mechanisms.

In people, nearly all spinal-cord injuries damage both upper and lower motor neurons. If segmental lower motor neurons are incapacitated or destroyed in the central grey matter, it results in flaccid paralysis at the injury level (no deep pain and no motor function). Variable injury to the surrounding white matter affects the long tracts, producing signs of upper motor-neuron damage distal to the level of the injury. In acute trauma cases it is usual (in people) for a lesion to be confined to the central grey matter––which contains nerve-cell bodies––and to spare the surrounding white matter. This confines motor and sensory disturbances to areas innervated at that level (a C6 lesion affects the hands) without affecting functions much below that level. By contrast, white-matter destruction at the same segment, even if grey matter is spared, renders a person tetraplegic and incontinent [1].

In dogs with IVDD lesions, the clinical signs usually reflect white matter damage from acute or chronic injuries. What degree of grey matter damage occurs is less clinically evident unless the injury is at the cervical or lumbar intumescence. The events described below by McDonald1 are typical in any external spinal trauma (vehicular accident) which may include disk herniation. The assumption being made in this paper is that it is valid to apply the same description to dogs with acute disk herniation but without external trauma.

Acute Compression

The vascular supply is damaged, axons are injured and neural cell membranes are disrupted. Microhemorrhages develop in the central grey matter immediately and spread out radially and axially over the next few hours. Within minutes, the spinal cord swells to fill the spinal canal at the site of injury. Secondary ischemia occurs when cord swelling exceeds venous blood pressure. Auto-regulation of blood flow ceases, and spinal neurogenic shock leads to systemic hypotension, thus exacerbating the ischemia. Ischemia, release of toxic chemicals from disrupted neural membranes, and electrolyte shifts trigger a secondary injury cascade that substantially compounds initial mechanical damage by harming or killing neighboring cells.

Secondary Events

After injury, the hypoperfusion that develops in grey matter2 extends to surrounding white matter. This hypoperfusion slows or completely blocks propagation of action potentials along axons, contributing to spinal shock. Although the term has been in use for over 150 years, the pathophysiology of spinal shock remains poorly defined3.

Damaged cells, axons and blood vessels release toxic chemicals that attack intact neighboring cells. One chemical, glutamate, plays a key part in a highly disruptive process known as excitotoxicity. In the healthy spinal cord, the end tips of many axons secrete minute amounts of glutamate, which binds to receptors on target neurons, stimulating those cells to fire impulses. By contrast, glutamate floods out of injured spinal neurons, axons and astrocytes overexciting neighboring neurons. The overexcited cells let in waves of calcium ions that trigger a series of destructive events, including production of free radicals. These highly reactive molecules can attack membranes and other cell components, killing healthy neurons.

Excitotoxicity was thought to affect only neurons, but results of studies suggest it also kills oligodendrocytes, the nervous system's myelin-producing cells.4 Glutamate receptors called AMPA (amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors play a key part in oligodendrocyte injury. This function could explain why intact axons become demyelinated and therefore unable to conduct impulses after spinal-cord trauma.

In the past few years, neurobiologists have also documented a more active form of cell death, somewhat akin to suicide, in the cord. Days or weeks after initial trauma, a wave of cell suicide, or apoptosis, might sweep through oligodendrocytes, affecting as many as four segments from the trauma site.5

Assessment and Prognosis

American Spinal Injury Association simple five-level (A–E) assessment:6

Motor: function in ten muscle groups (arms, C5–T1; legs, L2–S1)

Sensation: (light touch and pinprick) in 28 dermatomes (C2–S4/5) both sides of the body

A report of expectations for neurologic improvement in people with various degrees of spinal injury7 indicates significant difference between those with injuries resulting in no pain sensation versus those who retain some sensation after injury. About 10–15 % of Level A patients (no motor, no deep pain = no sacral sensation to pinprick) convert to level B–D, but only 3% regain functional strength below the lesion level. About 54% with deep pain (with or without motor) regain functional strength below the lesion. About 86% of patients with good pain sensation and some motor function will regain useful motor function.

Reports of recovery in dogs with disk disease are confusing because of a variation in expectations by the authors. The definition of functional return is not standardized in veterinary medicine and may include animals showing what Sherrington describes as more than simple reflexive “spinal walking.”8 After observing that paraplegic animals can regain complex, reciprocal alternating patterns of hindlimb movements, he suggests that the spinal cord has some built-in, “smart” properties. The centers responsible for coordination of complex gait activities, called central pattern generators (CPGs), are more complex than simple spinal reflexes. Repetition of task-specific movements, including part- weight-supported walking9, can reactivate these CPGs. Thus, part-weight-supported walking training can improve speed of ambulation, improve endurance, and achieve as normal a gait as possible in paraplegic human patients.10,11 Rehabilitation efforts in recovering veterinary patients along these lines have not been assessed. This may account for the lack of consensus that we currently have regarding the prognosis for animals with no deep pain.

In trying to identify factors that influenced neurologic recovery, a study of 412 human patients with incomplete tetraplegia, showed that gender, race, type of fracture, or mechanism of injury were not significant. High-dose methylprednisolone administration, early definitive surgery, early anterior decompression for burst fractures or disc herniations, or decompression of stenotic canals without fracture were also not significant factors in recovery. The most important prognostic variable relating to neurologic recovery is the completeness of the lesion.12

In animals, early decompression (up to 6–8 h) is reported to enhance recovery7,13 — rat studies, subacute surgical interventions in people (24–72 h) have yielded unsatisfactory results because most tissue damage is irreversible by that time.14-18 In one study of 36 beagles (eighteen in each group), methyl prednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. The authors concluded that the Methyl prednisolone did not provide a large or significant lasting benefit with regard to neurological preservation or restoration.19

Future Directions

A theoretical model for management of spinal injuries has been postulated by McDonald:1

Prevent progression of secondary injury; necrotic and apoptotic cell death are prevented by anti-excitotoxic drugs (glutamate-receptor blockers) and anti-apoptotic treatments (growth factors such as NT-3, BDNF, and ICE-protease inhibitors).
Compensate for demyelination; use chemicals (which?) that prevent action potentials from dissipating at demyelinated areas (prevent conduction block), and agents that encourage surviving oligodendrocytes to remyelinate axons. Lost oligodendrocytes would be replenished (how?).
Remove inhibition; use agents (which?) that block the actions of natural inhibitors of regeneration (the inhibitor neutralizing antibody IN-1 masks an inhibitory protein), or drugs that downregulate expression of inhibitory proteins.
Promote axonal regeneration; provide growth factors that promote regeneration (sprouting) of new axons — NT-3, BDNF.
Direct axons to proper targets; provide guidance molecules (which & how?) or increase their expression in host cells.
Create bridges; bridges are implanted into the syrinx, which provides directional scaffolding that encourages axon growth –– transplants of peripheral nerves or cells, such as ensheathing glia, that support axonal growth.
Replacement of lost cells; implant cells capable of generation of all cell types (stem cells or embryonic stem cells). Provide substances that induce undifferentiated cells to replace dead cells. Use transplanted cells to deliver regenerative molecules on command –– vectors producing NT-3, bFGF or PDGF.

Blight reports that, in the cat, fewer than 10% of functional long-tract connections are needed to enable locomotion.20 Greater than 20% level of connectivity often remains in the preserved doughnut-like outer rim of white matter after trauma, but axons in this rim might be non-functional because of faulty myelination.21 Therefore, remyelination of intact connections is one reasonable approach to improvement of function.

It is apparent that the quest for rational and documented successful medical intervention in spinal trauma is underway. It is also apparent that well-defined protocols have not yet been tested. What is clear, is that the current recommendation for Methyl prednisolone is unsubstantiated in the criterion-based literature.22-28

1. McDonald JW, Sadowsky C. Spinal-cord injury. The Lancet 359(9304):417-425, 2002

2. Tator CH, Koyanagi I: Vascular mechanism in pathophysiology of human spinal cord injury. J Neurosurg 86:483-492, 1997

3. Atkinson PP, Atkinson JL: Spinal shock. Mayo Clin Proc 71 (1996), pp 384–389

4. McDonald JW, Althomsons SP, Hyrc KL, Choi SW, Goldberg MP: Oligodendrocytes are highly vulnerable to AMPA/kainate receptor-mediated excitotoxicity. Nat Med 4:291-297, 1998

5. Beattie MS, Farooqui AA, Bresnahan JC: Review of current evidence for apoptosis after spinal cord injury. J Neurotrauma 17:915-926, 2000

6. Maynard, Jr FM, Bracken MB, Creasey G, et al.: International standards for neurological and functional classification of spinal cord injury: American Spinal Injury Association. Spinal Cord 35:266-274, 1997

7. Delamarter RB, Sherman J. Carr JB: Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am 77A:1042-1049, 1995

8. Sherrington CS: Flexion-reflex of the limb, crossed extension-reflex and reflex stepping and standing. J Physiol 40:28–121, 1910

9. Barbeau H, McCrea DA, O'Donovan MA, Rossignol S, Grill WM, Lemay MA: Tapping into spinal circuits to restore motor function. Brain Res Rev 30:27-51, 1999

10. Wernig A, Muller S: Laufband locomotion with body weight support improved walking in persons with severe spinal cord injuries. Paraplegia 30:229–238, 1992

11. Barbeau H, Ladouceur M, Norman KE, Pepin A, Leroux A: Walking after spinal cord injury: evaluation, treatment, and functional recovery. Arch Phys Med Rehabil 80:225-35, 1999

12. Pollard ME, Apple DF: Factors associated with improved neurologic outcomes in patients with incomplete tetraplegia. Spine 28(1):33-39, 2003

13. Dimar JR, Glassman SD, Raque GH, Zhang YP, Shields CB: The influence of spinal canal narrowing and timing of decompression on neurologic recovery after spinal cord contusion in a rat model. Spine 24:1623-1633, 1999

14. Heiden JS, Weiss MH, Rosenberg AW, Apuzzo ML, Kurze T: Management of cervical spinal cord trauma in southern California. J Neurosurg 43:732-736., 1975

15. Marshall LF, Knowlton S, Garfin SR, et al.: Deterioration following spinal cord injury: a multicenter study. J Neurosurg 66:400-404, 1987

16. Vaccaro AR, Daugherty, Reza BA, et al.: Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine 22:2609-2613, 1997

17. Chen TY, Dickman C, Eleraky M, Sonntag-Volker KH: The role of decompression for acute incomplete cervical spinal cord injury in cervical spondylosis. Spine 23:2398-2403, 1998

18. Mirza SK, Krengel III WF, Chapman JR, et al:, Early versus delayed surgery for acute cervical spinal cord injury. Clin Orthop 359:104-114, 1999

19. Carlson GD, Gorden CD, Nakazawa S, Wada E, Smith JS, LaManna JC: .:Sustained spinal cord compression part II: effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials. J Bone Joint Surg Am 85-A(1):95-101, 2003

20. Blight AR: Cellular morphology of chronic spinal cord injury in the cat: analysis of myelinated axons by line-sampling. Neuroscience 10:521-543, 1983

21. Bunge RP, Puckett WR, Becerra JL, Marcillo A, Quencer RM: Observations on the pathology of human spinal cord injury: a review and classification of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination. Adv Neurol 59:75-89, 1993

22. Bracken MB, Shepard MJ, Collins WF, et al.: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury: results of the second national acute spinal cord injury study. N Engl J Med 322:1405–1411, 1990

23. Bracken MB, Shepard MJ, Holford TR, et al.: Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury: results of the third national acute spinal cord injury randomized controlled trial. JAMA 277:1597-1604, 1997

24. Ducker TB, Zeidman SM: Spinal cord injury: role of steroid therapy. Spine 19:2281-87, 1994.

25. Hurlbert RJ: Methylprednisolone for acute spinal cord injury: an inappropriate standard of care. J Neurosurg 93:1-7, 2000

26. Qian T, Campagnolo D, Kirshblum S: High-dose methylprednisolone may do more harm for spinal cord injury. Med Hypotheses 55:452-453, 2000

27. Short DJ, El Masry WS, Jones PW: High dose methylprednisolone in the management of acute spinal cord injury: a systematic review from a clinical perspective. Spinal Cord 38:273-286, 2000

28. Geilser FH: Clinical trials of pharmacotherapy for spinal cord injury. Ann NY Acad Sci 19:374-381, 1998
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medscape back surgery treatments

Postby malernee » Wed May 26, 2004 6:30 pm

This was in Medscape. I thought some of you might find it interesting.

May 20, 2004 - A mini-intervention is beneficial for the treatment and
management of patients with subacute low back pain (LBP), according to the
results of a randomized trial published in the May 15 issue of Spine.

"A mini-intervention was earlier proved to be an effective treatment for
subacute LBP," write Kaija Karjalainen, MD, from the Finnish Institute of
Occupational Health in Helsinki, and colleagues. "Whether the beneficial
effect is sustained is not known. Furthermore, modifiers of a treatment
effect are largely unknown."

Of 164 patients with subacute LBP, 56 patients were randomized to a
mini-intervention, 51 patients to a mini-intervention plus a worksite visit,
and 57 patients to usual care. The mini-intervention consisted of a detailed
evaluation by a physician and a physiotherapist of the patient's history,
beliefs, and physical findings, followed by recommendations and advice.

During a 24-month follow-up, there were no differences between the three
treatment arms regarding intensity of pain, perceived disability, or
health-related quality of life. However, compared with usual care,
mini-intervention decreased occurrence of daily (P = .01) and bothersome (P
< .05) pain, increased treatment satisfaction, and reduced costs resulting
from LBP (4,670 Euros vs. 9,510 Euros; P = .04). Costs were not reduced
further by adding a worksite visit to the mini-intervention (5,990 Euros;
N.S. vs. mini-intervention alone).

The average number of days on sick leave was 30 in the mini-intervention
group, 45 days in the mini-intervention plus worksite visit group, and 62
days in the usual care group (P = .03 for mini-intervention vs. usual care).

Of 13 candidate modifiers tested for each outcome, the perceived risk of not
recovering was the strongest modifier of treatment effect. The
mini-intervention was most effective in reducing pain in the patients with a
high perceived risk of not recovering.

"Mini-intervention is an effective treatment for subacute LBP," the authors
write. "Despite lack of a significant effect on intensity of low back pain
and perceived disability, mini-intervention, including proper
recommendations and advice, according to the 'active approach,' is able to
reduce LBP-related costs."

The Social Insurance Institution of Finland funded this study. The authors
report no financial conflicts of interest.

Spine. 2004;29:1069-1076

a.. Patients recruited into the study were between the ages of 25 and 60
years and reported LBP that had interfered with work for 4 to 12 weeks.
Patients with back pain due to other pathologic conditions, a history of
substance abuse, or more than 3 months of sick leave due to back pain during
the previous year were excluded from participation.
b.. Participants were randomized to 1 of 3 intervention groups. Patients
in the physiatrist-advice group were referred to a senior physiatrist and
physiotherapist, who reviewed the case with the patients and made treatment
recommendations, including home exercises and workplace modifications. These
sessions lasted approximately 2.5 hours. Participants in the worksite-visit
group received this same intervention plus a 75-minute visit by the
physiotherapist to the subjects' worksite. Participants in the usual care
group served as a control and received a leaflet from their primary care
physician on back pain.
c.. Study subjects were followed for up to 24 months for the intensity and
frequency of back pain, along with perceived disability and health-related
quality of life. Healthcare costs and sick leave were also evaluated in the
study cohort.
d.. 164 patients were randomized into the study. The average age was
slightly older than 43 years, and 20% to 25% of the subjects were employed
in blue collar jobs.
e.. 93% to 96% of participants completed 24 months of follow-up. Other
healthcare visits, such as for alternative treatments, were similar between
the 3 groups.
f.. Neither the physiatrist-advice group nor the worksite-visit group
experienced a significant difference in pain intensity at any follow-up
point compared with the usual care group, but the frequency of pain was
improved in the 2 active intervention groups.
g.. Perceived disability from pain and health-related quality of life were
similar between the 3 treatment groups.
h.. Those in the 2 intervention groups were more satisfied with their
healthcare compared with the usual care group.
i.. Healthcare consumption and direct healthcare costs were similar
between the 3 groups. Both of the active intervention groups had reduced
number of sick days and total healthcare costs compared with usual care
group, but only the physiatrist-advice group achieved statistical
j.. Previous sick leave, intensity of pain, degree of disability, and
perceived risk of recovery were baseline values demonstrated to alter the
intensity of pain during the 2-year follow-up. The perceived risk of
recovery was the most significant of these factors in affecting treatment,
with those in the intervention groups displaying an optimistic attitude
toward recovery with a higher perception of pain than those in the control
group. In that same paradoxical vein, intervention subjects who did not
believe they would recover experienced less pain intensity than those in the
usual care group.
k.. Neither active intervention group was superior to the other in any of
the study outcomes.
l.. The efficacy of the interventions was concentrated in those subjects
without blue collar jobs.
Pearls for Practice
a.. Many treatments for subacute LBP are poorly proven.
b.. A brief evaluation by a physiotherapist can reduce the frequency of
subacute LBP as well as time missed from work.
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risk of developing cauda equina syndrome from back surgery

Postby malernee » Fri Oct 22, 2004 6:50 am

BMJ 2004;329:938 (23 October), doi:10.1136/bmj.329.7472.938-a

Surgeon found liable for not warning of partial paralysis risk
BMJ Clare Dyer legal correspondent

Britain’s highest court, the House of Lords, made new law last week when it took the rare step of departing from long established legal principles to hold a consultant neurosurgeon liable for a patient’s paralysis even though on normal principles his negligent failure to warn her of the risk had not caused her injury.

English law has long required anyone suing for compensation for personal injury to prove not only that the person sued was negligent but that the negligence caused the damage.

But by a 3 to 2 majority the law lords ruled that surgeon Fari Afshar must compensate a travel journalist, Carole Chester, for negligently failing to warn her of a 1-2% unavoidable risk of partial paralysis, even though she would not have declined surgery had she known of the risk.

The judge who originally heard the case in the High Court accepted Ms Chester’s claim that, had she been warned, she would have gone away and sought a second or even third opinion and would not have had the operation on that occasion.

Had she decided to have it later, the risk of developing cauda equina syndrome, as she did, would have been just as small and therefore it was unlikely it would have happened, the judge said. The surgeon’s failure to warn therefore caused her injury.

Mr Afshar performed the operation in 1994, three days after he was consulted by Ms Chester, who had experienced years of back pain.

The judge who originally heard the case in the High Court ruled that the operation had not been performed negligently but that the surgeon was liable for a negligent failure to warn. The ruling was upheld by the Court of Appeal.

Last week the House of Lords rejected the doctor’s appeal; Lords Bingham and Hoffmann dissented.

Lord Bingham, the senior law lord, said in his view the law should not seek to reinforce the patient’s right to know "by providing for the payment of potentially very large damages by a defendant whose violation of that right is not shown to have worsened the physical condition of the claimant."

He added that the timing of the operation was irrelevant as "the injury would have been as liable to occur whenever the surgery was performed and whoever performed it."

Lord Hoffmann said: "In my opinion this argument is about as logical as saying that if one had been told, on entering a casino, that the odds on number 7 coming up at roulette were only 1 in 37, one would have gone away and come back next week or gone to a different casino."

In 2002 in a case involving a worker exposed to asbestos by two employers, where it could not be proved which one had caused his illness, the law lords departed for the first time from the normal principle that a claimant must prove that the person sued caused the injury. They allowed him to claim damages from both employers.

Lord Steyn said that case had shown that "where justice and policy demand it, a modification of causation principles is not beyond the wit of a modern court."

He said a ruling in favour of Ms Chester was "in accord with one of the most basic aspirations of the law, namely to right wrongs." Moreover, the ruling reflected "the reasonable expectations of the public in contemporary society" and was a "narrow and modest departure from traditional causation principles."

Lord Hope said: "On policy grounds I would hold that the test of causation is satisfied in this case." Lord Walker agreed.

Ms Chester is claiming £500 000 ($0.9m; €0.7m) damages, although the rulings so far have focused only on liability, and the amount of her compensation still has to be determined.
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each opacified disk increased risk by 1.4 times

Postby guest » Fri Dec 24, 2004 8:16 am

Risk Factors for Recurrence of Clinical Signs Associated with Thoracolumbar Intervertebral Disk Herniation in Dogs: 229 Cases (1994-2000)
J Am Vet Med Assoc 225[8]:1231-1236 Oct 15'04 Retrospective Study 22 Refs

* Philipp D. Mayhew BVM&S; Robert C. McLear VMD, DACVR; Lisa S. Ziemer VMD, DACVR; William T. N. Culp VMD; Kelli N. Russell VMD; Frances S. Shofer PhD; Amy S. Kapatkin DVM, DACVS; Gail K. Smith VMD, PhD
Department of Clinical Studies, College of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6010 [* address correspondence]
OBJECTIVE: To assess risk factors for recurrence of clinical signs associated with thoracolumbar intervertebral disk disease (IVDD) in dogs that had decompressive laminectomy without attempted prophylactic treatment of other disk spaces.

DESIGN: Retrospective study.

ANIMALS: 229 dogs.

PROCEDURE: Medical records of dogs that had decompressive laminectomy without prophylactic fenestration for a first episode of IVDD and were available for follow-up were reviewed. Information on 7 clinical and 8 radiographic potential risk factors were recorded.

RESULTS: Clinical signs associated with recurrence of IVDD developed in 44 (19.2%) dogs. Ninety-six percent of recurrences developed within 3 years after surgery. Recurrence developed in 25% of Dachshunds and 15% of dogs of other breeds combined. Number of opacified disks was a significant risk factor for recurrence. Risk increased with number of opacified disks in an almost linear manner; each opacified disk increased risk by 1.4 times. Dogs with 5 or 6 opacified disks at the time of first surgery had a recurrence rate of 50%.

CONCLUSIONS & CLINICAL RELEVANCE: When all likely episodes of recurrence are considered and a long follow-up period is achieved, true rate of recurrence of IVDD appears to be higher than in many previous reports. Dogs with multiple opacified disks at the time of first surgery should be considered a high-risk subpopulation.

Re: the advisability of surgery for prolapsed disc

Postby Guest » Tue Jan 24, 2006 9:54 pm



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