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#41 rentalguy1


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Posted 11 April 2008 - 08:21 PM

Just found this: VA Training Letter on SCI. Originally posted by allan on 3/5/07

July 10, 2003

Director 211A
All VBA Regional Offices and Centers Training Letter 03-04

SUBJECT: Training letter on spinal cord injuries and potential complications

1. This training material was written in cooperation with Dr. Barry Goldstein, Assistant Chief Consultant, Spinal Cord Injury and Disorders Strategic Healthcare Group, Seattle, Washington. It includes primarily medical information on spinal cord injuries and complications from spinal cord injuries. The intent of this letter is to increase rater sensitivity to the catastrophic nature of these types of injuries. This letter is not intended to make policy.

2. If you have any questions or comments about the content of this letter, or note any errors, please check the appropriate calendar pages at:


Ronald J. Henke
Director, Compensation and Pension Service


An injury or disease that affects the spinal cord may profoundly change one’s life and how one lives it. To insure each veteran with a spinal cord injury receives a fair and accurate rating, it is helpful to have an understanding of complications that can result from this particular type of injury.

Medical information from this training letter is in large part from the Veterans Health Initiative publication titled “Spinal Cord Injury.” For a more detailed discussion regarding spinal cord injuries, please refer to this publication on the Internet at: http://www.va.gov/vhi/.

Most veterans with spinal cord injuries are entitled to special monthly compensation (38 CFR 3.310). Before rating a veteran for a spinal cord injury, it is essential to understand how and when to apply 38 CFR 3.350. The four part video broadcast on special monthly compensation which aired in October of 2000 is available in a condensed format on CD. You can obtain a copy of these CDs through your training co-ordinator. The supplementary training material for this course is available on the intranet at:

This training letter parenthetically references particular AMIE Worksheets, sections of the Rating Schedule and Diagnostic Codes that you may find useful. Because there are changes from time to time in these, this parenthetical information may have changed.

Terminology and Causes

Traumatic spinal cord injuries (spinal cord injury) and disease processes (spinal cord disorder) may result in spinal cord dysfunction. There are several major causes of traumatic spinal cord injuries (SCI). These include: spinal cord injury caused by a fracture of the vertebral body with the bony fragments impinging on the cord; encroachment on the spinal cord by dislocation of the vertebral bodies; transient narrowing of the spinal canal in the absence of bony fracture and traction on the cord causing damage to the cord. There are other traumatic causes such as gunshot and knife wounds.

Some nontraumatic spinal cord disorders (SCD) include multiple sclerosis, narrowing of the spinal canal with subsequent compression of the spinal cord (spinal stenosis), spinal cord tumor, HIV-related myelopathy, amyotrophic lateral sclerosis (ALS), post polio syndrome, and spinal cord infarction. In some situations, there is shared symptomatology and similarly associated complications between SCIs and SCDs.

Neurologic Classification

The spinal cord is the body’s primary pathway for transmitting information between the brain and the peripheral nervous system. An intact spinal cord is necessary for voluntary movement and to sense the environment. An intact spinal cord is also necessary for proper functioning of internal organs and blood pressure. SCIs and disorders (SCI&D) disrupt the ability to move, and the ability to sense pain, temperature, vibration and position. SCI&D can also disrupt functions of internal organs such as the bladder, bowel, and blood pressure regulation.

By convention, the “neurologic level” refers to the first level with normal function. To determine the neurologic level, the examiner tests functions at each neurologic level by testing the function of the corresponding segment of spinal cord and “nerve root”. For motor function, the examiner tests voluntary movement; for sensory function, the examiner tests the ability to sense light touch and pinprick. With reference to the spinal cord, the first neurologic level is designated as cervical 1 (C1), the next level down is cervical 2 (C2), and so on. Cervical levels include C2-C8 and supply the neck and upper limb. This is followed by thoracic levels (T1-T12) which supply the chest and abdominal wall, lumbar levels (L1-L5) which supply parts of the abdominal wall and lower limb, and sacral levels (S1-S5) which supply parts of the lower limb, genitalia, and organs (bladder and bowel).

The level is often different for motor and sensory functions as well as right and left sides due to anatomical differences and asymmetric injuries. Therefore, the examiner will often determine separate motor and sensory functions, as well as for the right and the left sides. The neurologic level for sensation is the level closest to the head with intact light touch and sharp/dull discrimination. For motor function, the neurologic level is the level closest to the head where the examiner indicates the person can move through a full range of motion against gravity.

Pathophysiology of Spinal Cord Injuries

After the initial injury, swelling, bleeding, ischemia and inflammatory reactions can cause additional damage to the spinal cord. It is rare for the cord to be actually severed (“transected”). Worsening of neurologic function may occur months or years after the initial injury by scar formation, traction on the spinal cord, or cavitation within the spinal cord (post-traumatic syringomyelia).

The International Standards for Neurological Classification of Spinal Cord Injury defines “complete” and “incomplete” injury. A complete spinal cord injury is when there is complete absence of sensory function and complete loss of motor function in the lowest sacral segment. An incomplete injury is when there is at least some preserved function in either the motor component or in the sensory component of the lowest sacral segment and some preserved sensory function or some preserved motor function below the neurologic level.

Complications and Consequences of SCIs may include impairment or disability to many body systems including:

5. Gastrointestinal (THE DIGESTIVE SYSTEM)
7. Dermatologic (THE SKIN)
8. Psychologic (MENTAL DISORDERS)

(38 CFR 4.124 a Schedule of ratings – neurological conditions and convulsive disorders)

Autonomic Dysreflexia (AD) is potentially a life threatening condition manifested by a sudden and extreme increase in blood pressure. It occurs when an internal or superficial noxious (i.e., painful) stimulus causes a sudden imbalance in the autonomic nervous system. Up to 85% of those with a spinal cord injury at or above the sixth thoracic neurologic level (T6) experience at least one episode of AD. Signs and symptoms of AD include hypertension or hypertensive crisis, headache, visual changes and flushing. In those with long-standing spinal cord injury, AD may cause only minimal symptoms and the only complaint may be that “something is not right.” The stimulus that causes AD may not be sensed as pain; in fact, the stimulus may not be sensed at all. Two common causes of AD are distention of the bladder and distention of the bowel. Some other causes of AD include pressure ulcers, tight clothing, genital stimulation or intercourse, uterine contraction associated with menstruation, and ingrown toenails. AD is treated by searching for the inciting cause and removing it. When simply removing the inciting cause does not eliminate the elevated blood pressure, pharmacologic intervention with blood pressure monitoring is necessary. Proper bladder management, and regular bowel care helps prevent AD. In some individuals, chronic prophylactic medication is necessary.

Chronic pain after a spinal cord injury is common. “Central neuropathic” pain is pain that is caused by injury to or irritation of the nerves. It is characterized as burning, tingling, stabbing and shooting pain. There is no known cure. Several medications are used in the treatment of neuropathic pain. Medications include antidepressants, anticonvulsants, local anesthetics, and narcotics. Of people with SCIs, 10-20% report that narcotics help central pain. Complications of narcotic use may include addiction and constipation.

Spasticity and spasms occur in about 35% of people with SCIs. In some people, spasticity may interfere with transfers, walking, and activities of daily living. Severe spasticity may cause pressure ulcers and other secondary problems. There are several medications available that diminish spasticity. Medications used to treat spasms are often associated with side effects. Common side effects of these medications may include sedation, withdrawal hallucinations and seizures (baclofen), sedation and hypotension (clonidine), and depression and addiction (diazepam).

Invasive treatments for spasticity include neurolytic blocks with ethyl alcohol, phenol, or botulinum toxin, intrathecal baclofen infusion, myelotomy (incising the lumbar cord) or dorsal rhizotomy (cutting the dorsal roots).

Posttraumatic syringomyelia (syrinx) occurs in 3-4% of people with SCI. Syringomyelia is a slowly progressive syndrome where a slowly enlarging fluid filled cavity forms in the central segments of the spinal cord. The syrinx can expand either up or down or radially (outwards) and may compress the spinal cord. This may cause progressive neurologic defects generally consisting of segmental muscular weakness and atrophy along with loss of pain and temperature sensation while sense of touch is preserved. Symptoms and signs depend upon the location of the syrinx and area of spinal cord affected. Post traumatic syringomyelia is treated by percutaneous CT-guided drainage and surgical shunting.

(38 CFR 4.71a Schedule of ratings – musculoskeletal system.)

Musculoskeletal complications from SCIs often lead to additional functional problems. One factor that is essential in maintaining normal bone mass and strength is weight bearing. Bone loss below the level of the neurologic impairment starts soon after a spinal cord injury and may rapidly progress to osteoporosis. As osteoporosis progresses, minor forces (e.g., slip from a wheelchair or range of motion) can result in a fracture. Falls cause most fractures because people with SCIs have both weak bones and an increased incidence of falls. Complications from fractures include autonomic dysreflexia (AD), skin breakdown, and blood clots. In most people, fractures are treated with a splint and immobilization. Occasionally, surgery is performed. Immobilization, the risk of skin breakdown from a splint, rehabilitation, mobility, and surgery are more involved in people with SCIs.

Neck and back pain are common in people with SCIs. Causes for back pain include mechanical problems following fractures, dislocations, fusion and instrumentation of the vertebral column. After the initial SCI, surgery is sometimes performed to stabilize the back. Hardware may be used during this surgery. Spine pain can occur when this hardware loosens, brakes or gets infected.

Myositis ossificans (DC 5023), at times also referred to as heterotropic ossification, affects approximately 20-30% of people with SCIs. This is the development of ectopic bone within the soft tissues surrounding peripheral joints. Almost half of the time myositis ossificans is identified it is clinically insignificant. When it is clinically significant, signs and symptoms may include decreased range of motion, localized swelling, redness, and/or fever. If pain sensation is intact in the affected area, the person may experience pain. Treatment for HO may include etridronate disodium and / or nonsteroidal anti-inflammatories. Surgery is often performed if the HO causes functional problems. Surgery is associated with significant risks of bleeding, infection, and recurrence. Low dose radiation is also used but the use of low dose radiation in this setting remains controversial.

Repetitive motion disorders of the soft tissues and joints of the upper extremity are common in people with SCI. People with SCI&D, often use their upper limbs for weight-bearing and mobility thus increasing biomechanical stresses on the shoulders, arms, wrists, and hands.

Approximately one-third to one-half of people with SCI have significant chronic shoulder pain that interferes with daily activities and sleep. Frequently there is no preceding trauma. Propelling a wheelchair, transfers, or using crutches may be associated with repetitive motion disorders of the shoulder, wrist, and hand. These injuries include rotator cuff tears, bursitis, tendonitis, carpal tunnel syndrome, and osteoarthritis. Physical therapy intervention is often necessary to change posture, seating, equipment, and home and work environments.

(38 CFR 4.97 Schedule of ratings – respiratory system.)

Nerves from the upper portion of the spinal cord (C3 to C5) allow a person to breath. C3, C4, and C5 innervate the diaphragm. The ability to cough and to fully expand the lungs comes from abdominal muscles, and intercostals muscles that are innervated by thoracic nerves (T1 – T12).

People with damage to the spinal cord at the C1 to C3 affecting their breathing, require mechanical ventilation. Unilateral or bilateral paralysis of the diaphragm will predispose a person to atelectasis and pneumonia. Cervical and upper thoracic SCI will also predispose a person to respiratory complications like pneumonia due to restrictive pulmonary function and an impaired ability to cough. Ineffective cough leads to retained secretions, mucous plugging, and infections. Restrictive changes with a low forced vital capacity (FVC) may be seen on pulmonary function tests.

(38 CFR 4.104 Schedule of ratings - cardiovascular system.)

The spinal cord is vital to proper regulation of heart rate and blood pressure. In response to exercise, and to sustain this physical exertion, the spinal cord and brain work to increase the heart rate and blood pressure. People with SCI&D generally have a reduced exercise capacity. They may experience fatigue and exhaustion after minimal exertion.

People with SCI&D may be at increased risk for coronary artery disease. (DC 7005). Risk factors after SCI&D include physical inactivity, increased low-density lipoprotein levels (LDL), low high-density lipoprotein levels (HDL), obesity, and an increased incidence of glucose intolerance.

Chest and jaw pain are sometimes symptoms of cardiac ischemia. People with SCIs above T5 may not experience these symptoms. Since exercise testing is often not possible after a SCI, a pharmacologic stress test (e.g., adenosine thallium stress test) is used to evaluate cardiac disease.

Edema of the lower extremities (commonly referred to as “peripheral edema” or more simply, “edema”) is common in people with SCIs. Edema is swelling caused by fluid within tissues. Normally the muscles of the lower extremities act to pump fluid out of the legs. In people with SCIs the leg muscles do not work properly. This causes lack of normal pump action and this leads to edema. Edema can lead to skin breakdown. (DC 7899 – 7120). Leg elevation and compression stockings can minimize edema. Diuretics can get rid of excess fluid. However, diuretics lower blood pressure. People with a spinal cord injury generally have a low baseline blood pressure and cannot tolerate any further drop in blood pressure. Therefore, diuretics are not used to treat edema in someone who has a spinal cord injury. Edema may predispose a person to deep venous thrombosis (DVT). DVT can lead to life threatening pulmonary embolism. Though DVT occurs more frequently within the first three months following the acute spinal cord injury, thereafter its incidence still remains increased when compared to the general population. DVT can lead to chronic problems including post phlebitic syndrome. (DC 7121).

5. Gastrointestinal (THE DIGESTIVE SYSTEM)
(38 CFR 4.114 Schedule of ratings – digestive system.)

SCIs can affect the nerve supply to the gastrointestinal tract. This can lead to slow gastric emptying, increased acid secretion, ulcers, ileus, and changes in colonic motility. Gastrointestinal complications can be a source of inconvenience, frustration and expense. To avoid constipation and incontinence, most people with an SCI will need a “bowel program”. These programs vary depending on whether the person has an “upper motor neuron bowel” or a “lower motor neuron bowel”. An "upper motor neuron bowel" results from an injury above the S2 level whereas a "lower motor neuron bowel" results from an injury at the S2-S4 levels. Whether upper or lower motor neuron bowel, both result in loss of voluntary anal sphincter control. (DC 7332; See also 38 CFR 3.350 (e) (iv) (2) regarding SMC).

Bowel programs help establish routine bowel movements. These programs often require special equipment (accessible toilet, foam rubber commode cushions to prevent pressure damage to the buttocks) supplies (plastic gloves, lubricant), medications (e.g. suppositories, fiber tablets), and special dietary measures. Bowel care often requires insertion of a well lubricated suppository high up against the mucosa of the rectal wall to start peristalsis. Then 15 minutes later the person should be on the toilet with his or her feet up on a foot stool. This body position helps bowel evacuation. The person with the SCI or the attendant may need to use “digital stimulation”. Digital stimulation involves inserting a gloved, lubricated finger into the rectum. Gentle rotation of the finger in a circular motion pressing all sides results in subsequent bowel evacuation.

People with SCIs have an increased incidence of esophagitis, and intermittent abdominal distention. They also have an increased incidence of hemorrhoids. (DC 7336).

(38 CFR 4.115a Ratings of the genitourinary system-dysfunctions.)

Genitourinary complications after SCI&D are common. Some of these complications include recurrent infections, stones, incontinence, and high pressure voiding.
Within the first year after the injury, most will have had at least one urinary tract infection.

A spinal cord injury as low as S4 can result in loss of volitional voiding (voiding under voluntary control). Several techniques may be used to avoid incontinence and minimize infections. A person may use intermittent catheterization, indwelling or suprapubic catheters or, (if male) condom catheters. Other voiding techniques include anal sphincter stretch to promote relaxation of the external urethral sphincter and detrusor compression via Crede maneuver (pressure applied over the lower abdominal area over the bladder). (Voiding dysfunction; DC 7542; See also 38 CFR 3.350 (e) (iv) (2) regarding SMC).

Two classes of medications are sometimes used to help manage voiding problems associated with SCIs. Depending on the level of the injury, a person may use either anticholinergic medications (including oxybutynin, propantheline and imipramine) or alpha-adrenergic antagonists (including prazosin, terazosin and doxazosin). Sometimes antihistamines and other medications used for general medical conditions can further compromise voiding in a person with a spinal cord injury.

Kidney stones are more common in people with SCIs. The incidence is approximately 8% by 10 years after injury. (DC 7508).

In men with SCIs, the degree of erectile dysfunction depends on the completeness and level of the injury. Men with incomplete lesions or injuries to the upper part of the spinal cord are more likely to retain reflex erectile capabilities than those with complete lesions or injuries to the lower cord. Though 75% of men with SCIs have some erectile capability, only 25% have erections sufficient for penetration.

Surgical treatment is sometimes used for genitourinary complications. These include denervation procedures, insertion of an artificial urinary sphincter, Teflon periurethral injections, sphincterotomy, and electrical stimulation.

7. Dermatologic (THE SKIN)
Dermatologic Skin breakdown / Pressure Ulcers
(38 CFR 4.118 Schedule of ratings – skin)

Skin breakdown and pressure ulcers are common in people with SCI. (DC 7899-7803). If sensation is impaired, normal messages to shift weight while sitting are not transmitted. Throughout the day and night people with SCIs must remember to reposition themselves, or must be repositioned by someone else. More than half of those with SCIs experience skin breakdown or pressure ulcers at some point. Sepsis, cellulitis and osteomyelitis are potential complications of skin breakdown and pressure ulcers.

Without intervention, skin breakdown progresses through a series of four stages.

Stage I A Stage I pressure ulcer is an observable pressure related alteration of intact skin whose indicators as compared to the adjacent or opposite area on the body may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel) and/or sensation (pain, itching).The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or purple hues.
Stage II is where there is partial-thickness skin loss. At this stage the ulcer can look like an abrasion, a blister or a shallow crater.
Stage III is when the ulcer includes either damage to or “necrosis” (tissue death) of the adipose tissue just beneath the skin.
Stage IV is where there is full-thickness skin loss with extensive destruction, and tissue necrosis. A Stage IV pressure ulcer can be associated with muscle or bone destruction.

Treatment may include nutritional supplements, debridement, dressing changes and educational programs with an eye towards implementing measures to decrease the chance for a recurrence. Proper cushions, mattresses, positioning and equipment are critical. Avoiding excess moisture including sweating and incontinence is important to prevent further skin breakdown. Meticulous skin care using proper skin hygiene with daily bathing using nonirritating nonalkaline soap helps. People with SCIs may need assistance to implement these measures.

8. Psychologic
(38 CFR 4.130 Schedule of ratings – mental disorders)

In people with SCIs, estimates of the incidence of depression range up to 25% for men and up to 47% for women. (DC 9434). They may use alcohol and substances to self-medicate for symptoms of depression. Paradoxically, prolonged alcohol and substance use can cause depression. In addition to depression, veterans may have PTSD as a result of the circumstances surrounding their injury. (DC 9411). Other frequent psychological problems after SCI include grief, denial, and anger. Many of these problems will dissipate on their own, particularly as people become more autonomous and informed.

Are You Ready To Rate?
While medical records may provide a complete picture of a veteran’s disability from a spinal cord injury, there may be times when you want to order a medical exam. You may want to verify that the exam you are requesting will give you the information you need by checking the exam worksheet at this intranet site:
Feel free to use the General Remarks field “to ask” the examiner to answer specific questions regarding the veteran’s claim. Many conditions may be service connected on a secondary basis (38 CFR 3.310). The proper question to ask in these situations is: “Is it at least as likely as not that veteran’s (claimed or inferred) condition is a consequence of the spinal cord injury?”
The Brain and Spinal Cord worksheet is a good exam to order to start with evaluating disability from a spinal cord injury.
Language in the general remarks section could read as follows:
Please evaluate veteran for residuals of spinal cord injury. Please refer to additional AMIE worksheets as necessary to capture a complete picture of veteran’s disability (ies) from this condition. Please pay particular attention to Section C7 of Brain worksheet regarding bladder and bowel function.

Spinal Cord Injury; Veterans Health Initiative, 2001
Depression Following Spinal Cord Injury: A Clinical Practice Guideline for Primary Care Physicians, Consortium for Spinal Cord Medicine; August 1998.
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#42 rentalguy1


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Posted 13 April 2008 - 11:33 AM

Not exactly for VBA claims, but could prove beneficial information for someone. Could be used in a claim for A&A:

Department of Veterans Affairs VHA HANDBOOK 1176.02

Veterans Health Administration Transmittal Sheet

Washington, DC 20420 June 13, 2007


1. REASON FOR ISSUE. This Veterans Health Administration (VHA) Handbook defines the procedures for providing extended care services to eligible veterans with Spinal Cord Injury and Disorders (SCI&D).

2. SUMMARY OF CONTENTS/MAJOR CHANGES. This new Handbook describes the
range of the Department of Veterans Affairs (VA) Extended Care (EC) Services available to veterans with SCI&D and the referral guidelines necessary to link them to VA’s SCI&D Center (Hub and Spoke) system of care.

3. RELATED ISSUES. VHA Directive 1176 and VHA Handbook 1176.1.

4. RESPONSIBLE OFFICE. The Chief Consultant, SCI&D Service (11S) in the Office of
Patient Care Services is responsible for the contents of this VHA Handbook. Questions may be referred to the Chief Consultant, SCI&D at 206-768-5401. Facsimile transmissions may be sent to 206-768-5258.


6. RECERTIFICATION. This VHA Handbook is scheduled for recertification on or before
the last working day of June 2012.

Michael J. Kussman, MD, MS, MACP
Under Secretary for Health

DISTRIBUTION: CO: E-mailed 6/15/07
FLD: VISN, MA, DO, OC, OCRO, and 200 – E-mailed 6/15/07
(June 13, 2007 VHA HANDBOOK 1176.02)




1. Purpose ...... 1

2. Background and Authority .. 1

3. Definitions.....2

4. Scope ......... 5

5. Goals ......... 6

6. Delivery of Services ......7

7. Responsibilities of the Facility Director .. 8

8. Construction Issues.........9

(June 13, 2007 VHA HANDBOOK 1176.02)


This Veterans Health Administration (VHA) Handbook describes the range of the
Department of Veterans Affairs (VA) Extended Care (EC) services available to veterans with SCI&D and the referral guidelines necessary to link them to VA’s SCI&D Center (Hub and Spoke) system of care.


a. Background

(1) Public Law (Pub. L.) 106-117, the “Veterans Millennium Health Care and Benefits
Act” (Mill Bill).

(a) Prior to enactment of Pub. L. 106-117, the “Veterans Millennium Health Care and
Benefits Act” (Mill Bill), VA nursing home care and other VA long-term care services were provided based on the availability of resources.

(:) Pub. L. 106-117, the “Veterans Millennium Health Care and Benefits Act” (Mill Bill),
was enacted on November 30, 1999. The Mill Bill provided a requirement for the Department of Veterans Affairs to operate and maintain a program of extended care for veterans.

(2) Title 38, United States Code (U.S.C.), Section 1710A – Required Nursing Home
Care. This section mandates the Secretary of VA to provide nursing home care which the Secretary determines is needed to:

(a) Any veteran for a service-connected disability, and

(B) Any veteran who has a service-connected disability rated at 70 percent or more. Other veterans may receive nursing home care as resources are available.

(3) Title 38, U.S.C. ,Section 1710B - Extended Care Services. This section requires the Secretary of VA to operate and maintain a program to provide EC services to eligible veterans (see par. 3). Such services must include the following:

(a) Geriatric evaluation.

(B) Nursing home care in facilities operated by the Secretary and in community-based
facilities through contracts under 38 U.S.C.1720.

© Domiciliary services under 38 U.S.C. 1710(B).

(d) Adult day health care under 38 U.S.C. 1720(f). (VHA HANDBOOK 1176.02 June 13, 2007)

(e) Such other non-institutional alternatives to nursing home care as the Secretary may furnish as medical services under 38 U.S.C. 1701(10).

(f) Respite care under 38 U.S.C. 1720B.

(4) Veterans with SCI&D are residents in a variety of VA extended care settings. These veterans live in the following VA SCI&D long-term care (LTC) Centers: VA nursing home care units, VA contract community nursing homes, State Veterans’ Homes, and in private homes supported by VA non-institutional LTC services. The serious nature of their disabilities makes coordination of their acute, sustaining, and LTC a necessity in order to maximize the individual’s functional ability and to prevent, to the greatest extent possible, the secondary medical conditions associated with their spinal cord injury or disease. NOTE: Compliance with the referral guidelines established in VHA Handbook 1176.1 ensures that coordination of care within VA’s SCI&D Hub and Spoke system is fully achieved.

b. Authorities

(1) Title 38 U.S.C. 1717, Home health services; invalid lifts and other devices.

(2) Title 38 U.S.C. 1720C, Transfers for nursing home care; adult day health care.

(3) Title 38 Code of Federal Regulations (CFR) 17.38, Medical benefits package. The
medical benefits package is available to all enrolled veterans.

(4) Title 38 U.S.C .1710, Eligibility for hospital, nursing home and domiciliary care.

(5) Pub. L. 106-117, requires VA to operate and maintain a program of Extended Care

(6) Pub. L. 104-262, the Veterans’ Health Care Eligibility Reform Act, (Eligibility Reform) enacted on October 9, 1996. Eligibility Reform required VA to maintain its capacity at 1996 levels to provide for the specialized treatment and rehabilitative needs of disabled veterans within distinct programs or facilities; subsequent Pub. L. 107-135, the Department of Veterans Affairs Health Care Programs Enhancement Act of 2001, (VA Enhancement Act of 2001) enacted on January 23, 2002, specified how VA should measure capacity within the distinct programs or facilities.

(7) VHA Handbook 1176.1.


a. SCI&D Center Services. The SCI&D Centers system of care includes components of
EC services. NOTE : A list of the SCI&D centers is available by calling (206) 768-5401, in VHA Handbook 1176.1, or on the VA internet at www.va.gov Public Affairs, Fact Sheets. (June 13, 2007 VHA HANDBOOK 1176.02)

(1) SCI&D Long-Term Care (LTC) Centers. SCI&D LTC Centers provide: LTC, long-stay services beyond 90 days, chronic ventilator care, skilled nursing or rehabilitation care for specific conditions or interventions, respite care, hospice care, palliative care (comfort care, death not a predicted outcome); restorative time limited care; rehabilitation therapies; psychological assessment and treatment; social work services; and age appropriate programs for transportation, therapeutic recreation (including outings), and peer support.

(2) SCI&D Home Care (HC). SCI&D-HC is provided through the SCI&D Center to
veterans, identified by the SCI&D interdisciplinary team, in need of this care and living within a 100 mile radius of the SCI&D Center. Goals of care include maintaining health and fostering independent living.

(3) SCI&D Respite Care. SCI&D respite care is recognized as an important consideration for families and caregivers of physically-dependent veterans. Each veteran using attendant care is offered respite care on the SCI&D unit in a VA medical center having an SCI&D center, unless a veteran requests its provision in another setting. The duration of any respite care admission, absent complicating medical factors, is not to exceed 14 days. However, the total of all respite care for a veteran in a year, absent complicating factors, generally does not exceed 30 days.

(4) SCI&D Referral Guidelines. SCI&D referral guidelines recommend the conditions for
treatment by each element of the SCI&D Hub and Spoke system. It is important that all clinicians be aware of the specific conditions that may confront individuals with SCI&D to ensure that those individuals get the right care, at the right time, in the right place. What may be a relatively minor symptom, or problem in the person without SCI&D, may indicate a grave and even life-threatening problem for the individual with SCI&D. Greater awareness of the
specialized health care issues facing persons with SCI&D and guidance about the most appropriate sites of care for various health issues is needed to ensure therapeutically appropriate clinical processes. NOTE: For a list of SCI&D presenting problems with recommendations for appropriate treatment referrals refer to VHA Handbook 1176.1.

b. VA Extended Care Services. VA extended care services are listed in VHA Handbooks 1140.1, 1140.2, 1140.3, 1140.5, 1143.1, and 1143.2 and include, but are not limited to:

(1) VA Nursing Home Care Unit (NHCU). VA NHCUs provide care for veterans who
have a primary diagnosis of SCI&D when eligible for care or are difficult to place in the community. Primary resources for care include skilled nursing, physical therapy, occupational therapy, recreational therapy, as well as lifetime care for veterans that are unable to be managed at home.

(2) Contract Nursing Home Care. VA may provide institutional LTC to mandatory
veterans (see 38 U.S.C. Pt. II, Ch. 17, Subch. 11, par. 1710A) through contracts with community nursing homes. Contract nursing home care is provided on a limited basis to all other enrolled veterans with SCI&D in need of nursing home care while pay arrangements are pursued through Federal, state, community, or personal payer methods. (VHA HANDBOOK 1176.02 June 13, 2007)

(3) State Veterans Homes. The State Veterans Home Program is a grant program between VA and the state where VA contributes to the costs of construction and a portion of the per diem. A state veterans home is a nursing home or domiciliary for veterans owned and operated by the state in which it provides service. The admission requirements of State Veterans Homes vary from state to state. VA social workers at the VA medical center where the veteran is being treated can provide information about State Veterans Homes.

(4) Domiciliary. Domiciliaries are VA facilities that provide care on an ambulatory self-care basis for veterans disabled by age or disease who are not in need of acute hospitalization and who do not need the skilled nursing services provided in a nursing home.

(5) Community Residential Care (CRC) Homes. The CRC Program is operated under the
authority of 38 U.S.C. 1730 and 38 CFR 17.61-17.72. Any veteran placed in a VA-approved residence in the community is under the oversight of the CRC Program. VA can assist with the placement of eligible veterans in CRC programs.

(a) These programs provide health care supervision to veterans not in need of hospital or nursing home care, but who, because of medical or psychosocial health conditions as determined through a statement of needed care, are not able to live independently and have no suitable family or significant others to provide the needed supervision and supportive care. The veteran must be capable of self-preservation with minimal assistance.

(B) Examples of CRC’s enriched housing may include, but are not limited to: Medical Foster Homes, Assisted Living Homes, Group Living Homes, Family Care Homes, and Psychiatric CRC Homes.

© Care must consist of room, board, assistance with activities of daily living and
supervision as determined on an individual basis.

(d) The cost of residential care is financed by the veteran's own resources.

(e) Placement is made in residential settings inspected and approved by the appropriate VA facility, but chosen by the veteran.

(6) Skilled Home Care. Skilled home care is provided by VA or through contract agencies to veterans who are home bound with chronic conditions, such as SCI&D.

(a) Home Care Services. Home care services such as colostomy bag changes, dressing changes, medication administration, prosthetic devices assistance, turning in bed, and transfers are defined as medical services for persons with SCI&D and may be authorized as fee-basis home health services when lack of support within the home requires institutional care and/or these services facilitate discharge from VA to community living.

(B) Fee Basis Bowel and Bladder Care(B&B). B&B care is considered a supportive medical service when provided to quadriplegic and paraplegic veterans who are unable to manage these functions independently. B&B care is regarded as skilled home care that is provided by VA, or (June 13, 2007 VHA HANDBOOK 1176.02) through contract agencies, to veterans that are home bound with chronic conditions such as SCI&D.

1. This program is essential to allowing these veterans to reside in a non-institutional
setting, improving quality of life and optimizing the health of this population.

2. The VA standard for B&B care requires that it is provided by a licensed or registered health care provider or a trained paraprofessional working under the direction and supervision of a licensed health care provider.

a. A family member or other care giver may receive reimbursement for provision of B&B care when they have been trained and certified by SCI&D trained personnel as being competent to provide this care.

b. Aside from family members, veterans may also recruit individuals who are willing to
receive training from VA to provide these health services at a low cost. This situation is considered better for family psychosocial relationships, and also diminishes the care burden for family caregivers.

(7) Homemaker and/or Home Health Aide (H/HHA). The H/HHA Program provides
services as an “alternative” to nursing home care. The facility H/HHA Coordinator along with the interdisciplinary team makes a clinical judgment that the veteran would, in the absence of H/HHA services, require nursing home equivalent care.

(8) Respite Services. Respite care services provide caregivers a planned period of relief from the physical and emotional demands associated with providing care. These services may be provided by VA SCI&D Centers, VA NHCUs, purchased by VA through contract services or arranged through a community service.

(9) Home-based Primary Care (HBPC). HBPC is available in many VA facilities and the
HBPC Director is responsible for planning and coordinating admission to HBPC. The SCI&D Primary Care Teams at non-SCI&D Center facilities are to be consulted to assist in planning the care and treatment of the veteran with SCI&D.


a. A broad scope is to be used in determining the needs for placement in a SCI&D LTC Center, NHCU, or an EC service, as age, level of function, level of support, co-morbidities, etc., are highly variable in placement decisions. The objective is to assist the veteran with SCI&D who can no longer live safely and independently within the community due to loss of functional ability and/or caregiver support, or who has co-morbid medical complications requiring ongoing skilled nursing care.

b. The SCI&D system of care includes a component of care that addresses SCI&D LTC. This care is unique as it is provided within SCI&D Services specialty care and is designed specifically for the needs of this population, allowing for more complex medical problems (VHA HANDBOOK 1176.02 June 13, 2007) associated with SCI&D requiring hospital based care, SCI&D home care and SCI&D specialty experience and services. NOTE: The facility SCI&D Service is responsible for this program.

c. In addition to LTC within the SCI&D Program, the SCI&D Program formally links to
Geriatrics and Extended Care and Fee-Basis Services including, but not limited to: VA NHCUs, Contract Nursing Homes, CRC Homes, HBPC, Skilled Home Care, H/HHA, geriatric evaluation and management, and inpatient or outpatient respite services. Such services fall within the domain of the facility Geriatrics and Extended Care Office.

d. Veterans meeting the clinical criteria for SCI&D specialty care (described in VHA
Handbook 1176.1) and identified by SCI&D staff as appropriate for LTC or EC services, must be considered for placement in any available SCI&D Center designated LTC bed, appropriate VA NHCU bed, or for EC services.

e. SCI&D and EC service decisions must consider the least restrictive level of care and attempt to incorporate the veteran’s and families’ personal choices.


a. It is the goal of VA’s health care professionals to ensure that veterans with SCI&D are appropriately placed within VA’s continuum of EC services in the least restrictive setting. Appropriate VA EC program placement facilitates access to necessary health and social services while maximizing the SCI&D veteran’s independence.

(1) A comprehensive combination of services fosters optimal participation in meaningful personal and societal roles, while minimizing activity limitations and secondary complications. For example, EC services may range from alternate emergency personal care attendant plans to prevent unnecessary health care admissions disruptive to social support and community participation, to access to knowledgeable neighborhood-oriented skilled nursing home care that fosters continued community participation, wellness, and satisfaction with life.

(2) Such services need to occur in close proximity to the veteran’s residence and active social support systems. The overriding principle associated with such an approach is that availability and access to a unique comprehensive combination of EC resources need to follow, or address, the needs of veterans with SCI&D to assist in accomplishing their participatory goals.

NOTE: This approach has been supported and strengthened by the Olmstead Supreme Court decision [OLMSTEAD v. L. C. (98-536) 527 U.S. 581 (1999) 138 F.3d 893], the American Disabilities Act of 1990 (Pub. L. 101-336), and the President’s New Freedom Initiative (Executive Order 13217).

b. SCI&D veterans are placed in a VA nursing home only when their general health status and social circumstances necessitate such placement. Every effort is made to meet the individual SCI&D veteran’s EC needs while facilitating the veteran's engagement in all types of community based social and economic activities.

c. Planning for the optimal comprehensive range of VA EC services is to be done at the onset of SCI&D and periodically throughout the lifespan of the individual veteran. Initial (June 13, 2007 VHA HANDBOOK 1176.02) extended care evaluation and planning should be done during the initial rehabilitation phase of new injury and/or disease treatment and is to be reviewed at each SCI&D veteran’s annual evaluation.


a. Early, comprehensive planning for the optimal combination of EC services to foster
participation in meaningful personal and societal roles while minimizing activity limitations and secondary complications can often minimize the need for institutional EC services. Life care plans are developed by the patient with guidance and information provided by the SCI&D Center social worker and/or SCI&D Coordinator.

b. Decisions for admission to a SCI&D LTC Center or VA NHCU are to be made by a
designated SCI&D or NHCU admission coordinator and/or the SCI&D or NHCU
interdisciplinary screening or admissions committee.

c. Veterans with SCI&D cared for in an extended care setting will continue to have access to acute and sustaining SCI&D specialty care on a regular and recurring basis as determined by the veteran’s needs. The SCI&D Center staff and SCI&D primary care teams (at non-SCI&D Center facilities) provide consultative care to veterans in EC settings, and facilitate referrals for annual evaluation.

d. SCI&D specialty care needs (e.g., surgical or diagnostic procedures, acute rehabilitation, urological complications, seating evaluations, annual evaluation, skin repair, etc.) are referred to the SCI&D Center, SCI&D Support Clinic and/or SCI&D primary care team for review, regardless of the veteran’s primary placement.

(1) When SCI&D specialty care needs are identified, the patient is referred to the closest SCI&D Center for care in accordance with referral guidelines in VHA Handbook 1176.1.

(2) Annual evaluation is an important component of maintaining health for people of all ages and durations of SCI&D.

(a) Particularly as one ages, the annual evaluation needs to focus on musculoskeletal issues associated with aging, additional loss of function, potential ventilator use, modified equipment needs, evaluation of mental status and end-of-life care.

(B) A life care plan is a critical component of annual evaluations and needs to address present and future needs to maximize and encourage an independent life style.

(3) SCI&D Primary Care Team member(s) will consult with NHCU staff and residents with SCI&D on a regular and recurring basis, as determined by the resident's needs.
NOTE: National education tools are available to LTC staff in focused areas of SCI&D
management.(VHA HANDBOOK 1176.02 June 13, 2007)

The facility Director is responsible for ensuring that:

a. The Resident Assessment Instrument Minimum (RAI)-Data Set (MDS) is used for SCI&D LTC Centers and VA NHCUs that are accredited under The Joint Commission (TJC) LTC standards to assess resident level of function and the development of a treatment plan.

NOTE: Quality of care is monitored per TJC and Office of Quality and Performance processes.

b. Staffing within VA Nursing Home Care Units meets nursing home care requirements and is consistent with MDS generated case mix.

c. SCI&D Center staff and SCI&D Primary Care teams serve as a resource for training
NHCU staff.

d. Staffing requirements of VA SCI&D LTC Centers would include: 1.42 nursing Full-time Equivalent (FTE) employee per required staffed bed; one physician for every 25 required staffed beds (plus .5 for administrative responsibilities of the full-time SCI&D Chief); one social worker for every 40 available beds, one psychologist for every 40 available beds and one therapist for every 14 available beds. The need for other personnel such as physician assistants, nurse practitioners, administrative support staff, speech pathologists, vocational rehabilitation specialists, respiratory therapists, dietitians, etc., is critical to SCI&D programs.

NOTE: SCI Centers must provide evidence of clinical considerations and/or unique factors when making adjustments to the preceding required staffing.

e. Veterans admitted for EC in VA NHCUs and SCI&D LTC Centers are medically stable.

f. The SCI&D population is tracked.

(1) The SCI&D population in VA NHCUs is tracked through use of SCI&D-related
diagnostic codes and appropriate NHCU treating specialty codes.

(2) The SCI&D population in VA SCI&D LTC Centers is tracked through use of SCI&D-related diagnostic codes and use of SCI&D Bed section treating specialty code 22.

(3) The SCI&D Coordinator tracks patients in the community to ensure that SCI&D
specialty care needs, such as the annual evaluation, are appropriately referred to the SCI&D Support Clinic or SCI&D Center.

(4) The SCD Registry is used by the SCI&D Coordinator and SCI&D Center to track care of the population and offer needed services.

g. SCI&D Home Care programs provide outreach to veterans in community nursing home care.

h. All equipment needs are met for eligible SCI&D veterans that include:(June 13, 2007 VHA HANDBOOK 1176.02)

(1) Items normally required by contract are those which are for general use, e.g., hospital beds, mattresses, trapeze assemblies, side rails, over-bed tables, bedside tables, etc. If contract community nursing homes or state homes are required by contract or regulation to provide specified appliances, equipment, or supplies, the VA needs to ensure that the appropriate items are furnished as it is delineated in the care plan and contract.

(2) Items which are not furnished by a community nursing home by contract and which are intended for the personal use of the veteran, e.g., artificial limbs, braces, hearing aids, eyeglasses, walkers, canes, crutches, wheelchairs, cushions, etc.

i. The SCI&D veteran is assessed annually, or as needed, for modifications or additions of equipment needs.

Structure and function of the NHCU care environment of care are as important as the
relationships between nursing home residents and care providers. Design elements for SCI&D
LTC may be found in the current SCI&D Design Guide at:
http://vaww.va.gov/f...d/dg_clinic.asp . Functionality and environmental
consideration are important to creating an environment supportive of quality of life.

#43 dansdad


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Posted 13 April 2008 - 12:58 PM

this is a great IDEA!!!!!!!!!!! sure will save all the extra research,for us lazy guys.well what would you expect from a old,old man. :) B) thanks rentalguy......

#44 dansdad


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Posted 13 April 2008 - 01:01 PM

btw im in the process of puting together a back claim after the last MRI with ivds written all over it! ill talk more later

#45 rentalguy1


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Posted 13 April 2008 - 03:21 PM

this is a great IDEA!!!!!!!!!!! sure will save all the extra research,for us lazy guys.well what would you expect from a old,old man. :) B) thanks rentalguy......

LOL...I put it together out of my own laziness...I got tired of searching for my old posts.

#46 rentalguy1


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Posted 13 April 2008 - 03:29 PM

Here's a scholarly article that I included in my claim:

Author: Michael B Furman, MD, MS, Fellowship Director, Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, Orthopedic and Spine Specialists

Michael B Furman is a member of the following medical societies: Alberta Medical Association, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, International Spine Intervention Society, North American Spine Society, Pennsylvania Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Coauthor(s): Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute; Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd; Jeremy Simon, MD, Interventional Spine Fellow, Department of Physical Medicine and Rehabilitation, Orthopaedics and Spine Specialists, Ltd

Editors: J Michael Wieting, DO, MEd, Professor, Department of Physical Medicine and Rehabilitation, Director, Physical Medicine and Rehabilitation Residency Training, Michigan State University College of Osteopathic Medicine, Medical Director, Rehabilitation Center, Ingham Regional Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, UMDNJ-New Jersey Medical School; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center

Author and Editor Disclosure

Synonyms and related keywords: central stenosis, central canal stenosis, foraminal stenosis, intervertebral foramen stenosis, lateral gutter stenosis, lateral recess stenosis, stenosis, subarticular stenosis, subpedicular stenosis, spinal stenosis, neurogenic claudication, NC, lumbar spinal stenosis, LSS, neural compression, spinal canal narrowing, ligamentum flavum hypertrophy, facet hypertrophy of cephalad vertebra, vertebral body osteophytosis, herniated nucleus pulposus, HNP, foraminal canal stenosis, incomplete vertebral arch closure, spinal dysraphism, segmentation failure, achondroplasia, osteopetrosis, early vertebral arch ossification, osseous exostosis, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking, Morquio syndrome, posterior disc protrusion, zygapophyseal joint hypertrophy
, spondylolisthesis, laminectomy, discectomy, Paget disease, fluorosis, acromegaly, ankylosing spondylitis, disc desiccation, degenerative disc disease, DDD, failed back surgery syndrome, bilateral neurogenic claudication, cauda equinamicrovascular ischemia, intraneuralfibrosis, radiculopathy

Lumbar spinal stenosis (LSS) implies spinal canal narrowing with possible subsequent neural compression. LSS is classified by anatomy or etiology. Anatomic subclassifications include central canal and lateral recess stenosis. The classification of lumbar stenosis is important because of the implications of the underlying etiology and because it affects the therapeutic strategy, specifically the surgical approach.

  • Central canal stenosis, commonly occurring at an intervertebral disk level, defines midline sagittal spinal canal diameter narrowing that may elicit neurogenic claudication (NC) or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum flavum hypertrophy, inferior articulating process (IAP), facet hypertrophy of the cephalad vertebra, vertebral body osteophytosis, vertebral body compression fractures and herniated nucleus pulposus (HNP). Abnormalities of the disk usually do not cause symptoms of central stenosis in a normal-sized canal. In developmentally small canals, however, a prominent bulge or small herniation can cause symptomatic central stenosis. Large disk herniations can compress the dural sac and compromise its nerves, particularly at the more cephalad lumbar levels where the dural sac contains more nerves.
  • Lateral recess stenosis (ie, lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal stenosis, intervertebral foramen stenosis) is defined as narrowing (less than 3-4 mm) between the facet superior articulating process (SAP) and posterior vertebral margin. Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region is compartmentalized into entrance zone, mid zone, exit zone, and far-out stenosis.
  • The entrance zone lies medial to the pedicle and SAP, and, consequently, arises from facet joint SAP hypertrophy. Other causes include developmentally short pedicle and facet joint morphology, as well as osteophytosis and HNP anterior to the nerve root. The lumbar nerve root compressed below SAP retains the same segmental number as the involved vertebral level (eg, L5 nerve root is impinged by L5 SAP).
  • The mid zone extends from the medial to the lateral pedicle edge. Mid-zone stenosis arises from osteophytosis under the pars interarticularis and bursal or fibrocartilaginous hypertrophy at a spondylolytic defect.
  • Exit-zone stenosis involves an area surrounding the foramen and arises from facet joint hypertrophy and subluxation, as well as superior disk margin osteophytosis. Such stenosis may impinge the exiting spinal nerve.
  • Far-out (extracanalicular) stenosis entails compression lateral to the exit zone. Such compression occurs with far lateral vertebral body endplate osteophytosis and when the sacral ala and L5 transverse process impinge on the L5 spinal nerve.

Amundsen and colleagues found concomitant lateral recess stenosis in all cases of central canal stenosis; consequently, in his study, pure central stenosis without lateral stenosis failed to exist.

Parenthetically, Keim and colleagues mention the following simplistic LSS anatomical classification scheme:

  • Lateral, secondary to SAP hypertrophy
  • Medial, secondary to IAP hypertrophy
  • Central, due to hypertrophic spurring, bony projection, or ligamentum flavum/laminar thickening
  • Fleur de lis (clover leaf), from laminar thickening with subsequent posterolateral bulging

LSS arises from the following primary and secondary etiologies:

  • Primary stenosis encompasses congenital malformations and developmental flaws. Congenital malformations include incomplete vertebral arch closure (spinal dysraphism), segmentation failure, achondroplasia, and osteopetrosis. Developmental flaws include early vertebral arch ossification, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking (Morquio syndrome), and osseous exostosis. Primary stenosis is uncommon, occurring in only 9% of cases.
  • Secondary (acquired) stenosis arises from degenerative changes, iatrogenic causes, systemic processes, and trauma. Degenerative changes include central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, and spondylolisthesis. Iatrogenic changes result following surgical procedures such as laminectomy, fusion, and diskectomy. Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis.

Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results from HNP, ligamentum flavum hypertrophy, and disk space narrowing.

Alternatively, the caudal vertebral body SAP contributes to lateral recess and foraminal stenosis. Indeed, facet hypertrophy between L4 and L5 vertebrae may impinge the L4 nerve root in the foramen and the L5 proximal nerve root sheath in the lateral recess.

Jenis and An eloquently describe foraminal stenosis pathoanatomy, characterized by disk desiccation and DDD, which narrows disk height, permitting the caudad SAP to sublux anterosuperiorly. Such subluxation decreases foraminal space. Continued subluxation with resulting biomechanical disruption provokes osteophytosis and ligamentum flavum hypertrophy, further compromising foraminal volume. Anteroposterior (transverse) stenosis ultimately results from narrow disk height and hypertrophy anterior to the facet; specifically, the SAP and posterior vertebral body transversely trap the nerve root. Furthermore, in vertical (craniocaudal) stenosis, posterolateral vertebral endplate osteophytes and a lateral HNP may impinge the spinal nerve against the superior pedicle.

The 2 lower motion segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis. These segments are in a transition zone from the rigid sacrum to the mobile lumbar spine. Also, the posterior joints in this area have less of a sagittal orientation, which affords more rotation, and are therefore more vulnerable to rotatory strains.

Dynamic foraminal stenosis implies intermittent lumbar extension-provoked nerve root impingement from HNP, osteophytosis, and vertebral body slippage. Such dynamic stenosis with associated intermittent position-dependent symptoms may not manifest on imaging studies, thereby confounding diagnosis. Other factors promoting development of LSS include shortened gestational age, and synovial facet joint cysts with resulting radicular compression. Adult degenerative scoliosis, secondary to DDD-induced instability with subsequent vertebral rotation and asymmetric disk space narrowing, promotes facet hypertrophy and subluxation in the curve concavity. Degenerative spondylolisthesis, when combined with facet hypertrophy, causes both central canal and lateral recess stenosis.


United States
LSS remains the leading preoperative diagnosis for adults older than 65 years who undergo spine surgery. The cost of more than 30,000 LSS surgeries performed in 1994 exceeds 1 billion dollars.

The incidence of lateral nerve entrapment is reportedly 8-11%. Some studies implicate lateral recess stenosis as the pain generator for 60% of patients with symptomatology of failed back surgery syndrome.

Incidence of foraminal stenosis increases in lower lumbar levels because of increased dorsal root ganglion (DRG) diameter with resulting decreased foramen (ie, nerve root area ratio). Jenis and An cite commonly involved roots as L5 (75%), L4 (15%), L3 (5.3%), and L2 (4%). The lower lumbar levels maintain greater obliquity of nerve root passage, as well as higher incidence of spondylosis and DDD, further predisposing patients to L4 and L5 nerve root impingement.

In their review of LSS, Fritz and colleagues cite several studies suggesting that many patients show symptomatic and functional improvement or remain unchanged over time. For example, they mention Porter and colleagues' study in which 90% of 169 untreated patients with suspected lateral recess stenosis improved symptomatically after 2 years. Additionally, they report Johnsson and colleagues' 4-year study of 32 patients treated conservatively for moderate stenosis, of whom only 16% worsened clinically and 30% reported diminished walking tolerance.

No known correlation exists between incidence of LSS and race.

Patients typically are male.

Patients with LSS due to degenerative causes generally are aged at least 50 years; however, LSS may be present at earlier ages in cases of congenital malformations.

LSS classically presents as bilateral NC. Unilateral radicular symptoms may result from severe foraminal or lateral recess stenosis. Patients, typically aged more than 50 years, report insidious-onset NC manifesting as intermittent, crampy, diffuse radiating thigh or leg pain with associated paresthesias. Indeed, leg pain affects 90% of patients with LSS.

In a retrospective review of 75 patients with radiographically confirmed LSS, reports of weakness, numbness or tingling, radicular pain, and NC were in almost equal proportions. The most common symptom was numbness or tingling of the legs.

NC pain is exacerbated by standing erect and downhill ambulation and is alleviated with lying supine more than prone, sitting, squatting, and lumbar flexion. Getty and colleagues documented 80% pain diminution with sitting and 75% with forward bending. Lumbar spinal canal and lateral recess cross-sectional area increases with spinal flexion and decreases with extension. Furthermore, cross-sectional area is reduced 9% with extension in the normal spine and 67% with severe stenosis. The Penning rule of progressive narrowing implies that the more narrowed the canal by stenosis, the more it narrows with spinal extension. Schonstrom and colleagues have shown that spinal compressive loading from weight bearing reduces spinal canal dimensions.

NC, unlike vascular claudication, is not exacerbated with biking, uphill ambulation, and lumbar flexion and is not alleviated with standing. LSS patients compensate for symptoms by flexing forward, slowing their gait, leaning onto objects (eg, over a shopping cart) and limiting distance of ambulation. Unfortunately, such compensatory measures, particularly in elderly osteoporotic females, promote disease progression and vertebral fracture. Pain radiates downward in NC and, in contrast, upward in vascular claudication. Hall and colleagues note the presence of radiculopathy in 6% and NC in 94% of LSS patients.

Distinguishing between neurogenic and vascular claudication is important because the treatments, as well as the implications, are quite different. Vascular claudication is a manifestation of peripheral vascular disease and arteriosclerosis. Other vessels, including the coronary, vertebral, and carotid, are also often affected. Further complicating diagnosis and treatment in some patients, both neurogenic vascular and claudication may occur together. This is because both conditions frequently occur in the elderly population.

Proposed mechanisms for development of NC include cauda equina microvascular ischemia, venous congestion, axonal injury, and intraneural fibrosis. Ooi and colleagues myeloscopically observed ambulation-provoked cauda equina blood vessel dilation with subsequent circulatory stagnation in LSS patients with NC. They propose that ambulation dilates the epidural venous plexus, which, amidst narrow spinal canal diameter, increases epidural and intrathecal pressure. Such elevation of pressure ultimately compresses the cauda equina, compromises its microcirculation, and causes pain.

Another pain generator may be the DRG, which contains pain-mediating neuropeptides, such as substance P, that possibly increase with mechanical compression. The DRG varies spatially within the lumbosacral spine, with L4 and L5 DRG in an intraforaminal position and S1 DRG located intraspinally. Such foraminal placement may predispose to stenotic compression with subsequent radicular symptomology.

Lastly, severe radiologic stenosis in otherwise asymptomatic individuals suggests inflammation, not just mechanical nerve root compression. Specific inflammation generators may include HNP, ligamentum flavum, and facet joint capsule.

Katz and colleagues report that the historical findings most strongly associated with LSS include advanced age, severe lower extremity pain, and absence of pain when the patient is in a flexed position. Fritz and colleagues contend that the most important elements involve the postural nature of the patient's pain, stating that absence of pain or improvement of symptoms when seated assists in ruling in LSS. Conversely, LSS cannot be ruled out when sitting is the most comfortable position for the patient and standing/walking is the least comfortable.

Physical examination findings frequently are normal in patients with LSS. Nevertheless, review of the literature suggests diminished lumbar extension appears most consistently, varies less, and constitutes the most significant finding in LSS. Other positive findings include loss of lumbar lordosis and forward-flexed gait. Charcot joints may be present in long-standing disease. Radiculopathy may be noted with motor, sensory, and/or reflex abnormalities. Asymmetric muscle stretch reflexes and focal myotomal weakness with atrophy occur more with lateral recess than central canal stenosis. Some report objective neurologic deficits in approximately 50% of LSS cases. Provocative maneuvers include pain reproduction with ambulation and prone lumbar hyperextension. Pain alleviation occurs with stationary biking and lumbar flexion.

Patients may also have a positive result from the stoop test, which was described by Dyck in 1979. This is performed by having the patient walk with an exaggerated lumbar lordosis until NC symptoms appear or are worsened. The patient is then told to lean forward. Reduction of NC symptoms is a positive result and is suggestive of NC.

Negative findings in the physical examination include skin color, turgor, and temperature; normal distal lower extremity pulses; and an absence of arterial bruits. Importantly, remember the 5 Ps of vascular claudication in the assessment of these patients: pulselessness, paralysis, paraesthesia, pallor, and pain. The absence of these problems, excluding pain and paraesthesias, which are common to both neurogenic and vascular claudication, should give the clinician confidence in the diagnosis of NC. Please refer to the excellent eMedicine article
Peripheral Vascular Disease for more information on peripheral vascular disease and vascular claudication.

Dural tension signs should be unremarkable. Lumbar segment mobilization often fails to reproduce pain, and palpation locates no trigger points.

Katz and colleagues report physical examination findings most strongly associated with LSS include wide-based gait, abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular abnormalities; however, Fritz and colleagues state physical examination findings do not seem helpful in determining the presence or absence of LSS.

Johnsson and colleagues' single study of the natural course of LSS reports unchanged symptoms in 70% of patients, improvement in 15%, and worsening in 15% after a 49-month observation period. Walking capacity improved in 37% of patients, remained unchanged in 33%, and worsened in 30%.

See sections on Background and Pathophysiology.

[Lumbar Degenerative Disc Disease]
Achilles Tendon Injuries and Tendonitis
Cancer and Rehabilitation
Chronic Pain Syndrome
Diabetic Lumbosacral Plexopathy
Diabetic Neuropathy
Lumbar Compression Fracture
Lumbar Facet Arthropathy
Lumbar Spondylolysis and Spondylolisthesis
Mechanical Low Back Pain
Myofascial Pain
Neoplastic Lumbosacral Plexopathy
Osteoporosis (Primary)
Osteoporosis (Secondary)
Piriformis Syndrome
Radiation-Induced Lumbosacral Plexopathy
Scheuermann Disease
Trochanteric Bursitis

Other Problems to be Considered


Ankylosing spondylitis/spondyloarthropathy
Diffuse idiopathic skeletal hyperostosis (DISH)


Epidural, subdural, intradural abscess
Pott's Disease


Parathyroid disease
Vitamin B-12 or folic acid deficiency


Lumbar strain




Peripheral vascular disease (with vascular claudication)
Abdominal aortic dissection

Psychogenic Conversion disorder

Lab Studies

  • Lab studies are not necessary to support the diagnosis of LSS.

Imaging Studies

  • Plain radiograph (x-ray)
    • Nonspecific plain radiographic findings possibly implicating LSS include the following:
      • Disk space narrowing
      • Facet hypertrophy and arthrosis
      • Spondylosis
      • Degenerative scoliosis and spondylolisthesis
      • Osteochondrosis
      • Transitional segmentation
      • Spinous process settling
      • Shortened interpedicular distance
    • Interpedicular distance, considered subnormal if less than 18 mm, commonly increases from upper to lower lumbar segments.
    • Some sources define pure absolute central canal stenosis as a mid-sagittal canal diameter of less than or equal to 10 mm, pure relative at 10-12 mm, and mixed as a combination thereof. Mid-sagittal canal diameter less than 15 mm and transverse diameter less than 20 mm usually are considered abnormal.
    • Posterior disk height of 4 mm or less and foraminal height of 15 mm or less may suggest foraminal stenosis; nevertheless, clinical correlation is required. No convincing correlation has been found between clinical symptoms and radiologic findings in a study of 100 symptomatic patients with LSS. Similarly, no correlation has been shown between physical function and radiologic findings.
  • CT scan
    • CT scan provides excellent central canal, lateral recess, and neuroforaminal visualization. Additionally, CT scan offers contrasts between intervertebral disk, ligamentum flavum, and thecal sac. Unfortunately, CT scan, like MRI, yields a high false-positive rate (35.4% when correlated with surgically proven LSS).
    • Parasagittal reconstructed CT scan findings suggesting stenosis include posterolateral vertebral body or facet osteophytosis extending into the foramen.
  • MRI
    • MRI remains the imaging modality of choice for LSS. Fritz and colleagues maintain that MRI effectively rules LSS in or out anatomically.
    • Advantages include nonionizing radiation and superior multiplanar soft tissue visualization without osseous artifact. A trefoil-shaped central spinal canal may provoke more symptoms than a round or oval canal by depressing the lateral recess.
    • Sagittal T1-imaged adipose tissue outlines neuroforaminal nerve root segments and dorsal root ganglia. Therefore, parasagittal MRI findings suggesting foraminal stenosis include paucity of T1-weighted perineural adipose tissue surrounding the nerve root and diminished foraminal size. Unfortunately, MRI abnormalities have been documented in 20% of asymptomatic subjects.
  • Myelography
    • This test effectively documents central canal stenosis and remains superior in evaluating lumbar disk herniation. Predictive value of myelography versus CT scan has been reported as 83% versus 72%, respectively, for lumbar disk herniation, and 93% versus 89% for LSS. Furthermore, myelography images the entire lumbar spinal canal, and enhances stenotic segments due to hyperextension during imaging; however, it may miss lateral stenosis and HNP because the dural sac terminates at the lateral mid zone, preventing contrast spread to the distal nerve root sheath.
    • Myelography is less sensitive and specific than CT scan or MRI.
    • Procedural complications include spinal headache, seizure, allergic reaction, and nausea.
  • If vascular claudication is suspected, referral to an internist for a workup is indicated. This includes a serum cholesterol level, arterial Doppler studies, ankle-brachial index values, and, in some cases, arteriography.

Other Tests

  • Electrodiagnosis (EDX), including needle electromyography (EMG), nerve conduction studies (NCS), and somatosensory evoked potentials (SSEP), evaluates nerve root and peripheral nerve function.
    • Needle EMG diagnoses lumbosacral radiculopathy by detecting increased insertional activity, spontaneous potentials (eg, positive waves, fibrillations, fasciculations, chronic repetitive discharges), and decreased motor unit recruitment in paraspinal and lower extremity muscles innervated by the same nerve root. The presence of polyphasic motor unit potentials helps establish long-standing disease.
    • Limitations include inability to evaluate sensory and upper motor neurons.
    • Multisegmental muscle innervation may cause false negative results by preserving motor unit function despite nerve root compromise. Such innervation may elicit multilevel abnormalities in severe LSS.
    • Johnsson and colleagues have correlated myelographic LSS severity with multisegmental EMG abnormality.
  • NCS differentiates LSS from other confounding neuropathic conditions such as lumbosacral plexopathy, generalized peripheral neuropathy, and mononeuropathy (eg, peroneal neuropathy at the fibular head, tarsal tunnel syndrome).
    • Canal stenosis may compress the cauda equina with resulting polyradicular insults. Such multiple lumbosacral radiculopathies involve lower lumbosacral (especially S1) nerve roots, are often bilateral and asymmetric, and frequently may manifest NCS abnormalities. Such abnormalities include decreased or unelicitable posterior tibial and peroneal compound motor action potentials (CMAPs) reflecting axon loss, and unobtainable H reflexes signifying bilateral S1 compression. Sensory nerve action potentials (SNAPs) remain unaffected (unless impingement occurs distal to the dorsal root ganglion), but may not be detectable in older persons. F waves may also be absent or prolonged in persons with LSS
    • Wilbourn and Aminoff advocate measuring peroneal CMAP amplitude from tibialis anterior and M-wave amplitude during H-reflex testing to gauge the extent of L5 and S1 acute denervation, respectively.
    • Overall, Wilbourn and Aminoff report variable EDX findings, including multiple, bilateral lumbosacral radiculopathies in 50% of LSS patients, with prominent chronic motor unit action potential (MUAP) changes, and fibrillations solely in distal musculature. The remaining 50% of patients demonstrate varied abnormalities, with some manifesting 2 radiculopathies commonly as a single radicular insult in each lower extremity, either symmetrically (eg, bilateral L5) or asymmetrically (eg, left S1 and right L5). Other patients display isolated L5 or S1 radiculopathy. Limited nondiagnostic findings may be elicited, including bilaterally absent H reflexes with normal lower extremity needle EMG and sural SNAPs, as well as fibrillations in a single S1-innervated limb muscle. Lastly, many patients demonstrate normal EDX tests.
    • Diagnostically, EMG complements MRI in assessing radiculopathy. Specifically, EMG rarely presents false-positive results and carries high specificity (85%). Conversely, MRI carries high sensitivity and poor specificity (50%) and, consequently, demonstrates many false-positive asymptomatic abnormalities. Some advocate using highly specific EMG to determine whether structural abnormalities imaged on MRI carry functional and pathologic significance. Indeed, Robinson proposes that such use of needle EMG ultimately might prove helpful in avoiding costly and high-risk invasive interventions.
  • Somatosensory evoked potentials (SSEPs) are dispatched through large dorsal column myelinated fibers that are affected earlier than smaller fibers. Peripheral nerve lesions prolong SSEP latency and duration, while nerve root and spinal cord pathology induce further morphologic alterations.
    • Keim and colleagues have documented posterior tibial abnormalities in 95%, peroneal abnormalities in 90%, and sural abnormalities in 60% of LSS patients studied. A high incidence of L4, L5, and S1 nerve root involvement existed, amidst a paucity of upper lumbar segment abnormality (measured by the saphenous nerve). Bilateral lower limb changes were documented in 7 of 20 patients, suggesting that bilateral lower limb SSEPs can uncover previously unsuspected lesions. SSEPs are useful intraoperatively during decompressive surgery to assist the physician in diagnosis of LSS amidst equivocal clinical and imaging studies. SSEPs also appear to be more sensitive than other EDX approaches in evaluating LSS-provoked nerve root compression.
    • Kraft contends the best EDX technique for assessing LSS is dermatomal somatosensory evoked potentials (DSEPs). Insidious low-grade compression from LSS causes impaired nerve conduction, which is best appreciated by DSEPs (similar to nerve conduction study [NCS] slowing in carpal tunnel syndrome). Such pathology contrasts sharply with dramatic acute-onset HNP root compression, inducing axon loss with subsequent denervation best detected by needle EMG.
    • Using CT scan and MRI comparison standards, Kraft and colleagues demonstrated 78% sensitivity and 93% predictive value with DSEPs for an anatomical study positive for LSS when using multiple root disease (MRD) criteria. When criteria of multiple root disease and single root disease (SRD) were added, the sensitivity rose to 93%, with a positive predictive value of 94%. Kraft emphasized that the DSEP electrophysiologic signature of LSS is MRD, but SRD can suggest LSS, especially amidst applicable clinical history, physical examination, and positive EMG findings. Conversely, Dumitru found DSEPs to be of low sensitivity when compared to needle EMG-proven radiculopathies.
Rehabilitation Program

Physical Therapy
Patients with LSS often benefit from conservative treatment and participation in a physical therapy (PT) program. Lumbar extension exercises should be avoided in this population, as spinal extension and increased lumbar lordosis are known to worsen LSS. Flexion exercises for the lumbar spine should be emphasized, as they reduce lumbar lordosis and decrease stress on the spine. Spinal flexion exercises increase the spinal canal dimension, thus reducing NC. Williams' flexion-biased exercises target increased lumbar lordosis, paraspinal and hamstring inflexibility, and abdominal muscle weakness. These exercises incorporate knee-to-chest maneuvers, pelvic tilts, wall-standing lumbar flexion, and avoidance of lumbar extension.

Two-stage treadmill testing has demonstrated longer walking times on an inclined treadmill, presumably due to promotion of spinal flexion. Conversely, level treadmill testing is thought to promote more spinal extension-induced NC and elicit earlier symptom onset and longer recovery time. Ancillary exercises to target weak gluteals, as well as shortened hip flexors and hamstrings, are indicated. Physical examination should be performed to assess for concurrent degenerative hip disease, which may mimic LSS. Traction harness-supported treadmill and aquatic ambulation to reduce compressive spine loading has been shown to improve lumbar range of motion (ROM), straight leg raising, gluteal and quadriceps femoris muscle force production, and maximal (up to 15 min) walking time.

Others advocate stationary cycling and abdominal muscle strengthening. Passive modalities such as heat, cold, transcutaneous electrical nerve stimulation (TENS), and ultrasound may provide transient analgesia and increased soft tissue flexibility in LSS patients.

The addition of a rolling walker is often necessary in many cases. The rolling walker provides some stability and promotes a flexed posture, which allows the afflicted patient to ambulate greater distances.

Medical Issues/Complications
In rare cases, central canal stenosis may provoke cauda equina syndrome with associated saddle anesthesia, bladder and/or bowel dysfunction and altered muscle reflexes. Additionally, patients with lateral recess stenosis-induced radiculopathy may manifest significant lower limb weakness or numbness. Lastly, intractable axial, radicular, or NC pain may result.

Surgical Intervention
LSS remains one of the most common conditions leading to lumbar spine surgery in adults aged 65 years and older. Increasing rates of LSS surgery among the Medicare population has been shown to be due possibly to imaging techniques that enable physicians to diagnose LSS more frequently. Other contributing factors may include improved surgical techniques that might allow patients previously managed conservatively to undergo surgery, as well as a philosophy that LSS surgery prevents future morbidity.

  • Widely agreed upon indications for LSS surgery do not exist. Typically, patients undergo elective surgery to improve walking tolerance and disabling leg and back pain. Preoperatively, such disability infrequently is measured in objective quantitative terms. Some suggest preoperative treadmill testing to facilitate objective selection of potential surgical candidates. Surgical emergencies (eg, cauda equina syndrome, rapid neurologic deterioration) rarely arise.
    • Surgical techniques include standard wide laminectomy and decompression, which first removes lamina and ligamentum flavum from the lateral borders of one lateral recess to the other and then decompresses entrapped nerve roots.
    • Foraminal enlargement surgery is used to address refractory foraminal stenosis-induced radicular pain. Other surgical decompressions include the following:
      • Laminotomy
      • Medial facetectomy
      • Medial or lateral foraminotomy.
    • Midline interlaminar approaches are used to address concurrent central and foraminal stenosis.
    • The Wiltse approach with foraminotomy is used for isolated foraminal stenosis by providing the following:
      • Widening the longissimus-multifidus muscle interval
      • Removing the lateral pars interarticularis and facet joint
      • Exposing the nerve root with subsequent decompression
    • In addition to decompression and foraminal enlargement, some patients with segmental instability from facet joint removal and pain secondary to DDD may require fusion.
      • Fusion stabilizes the intervertebral segment while maintaining lordosis and foraminal size.
      • Additional options include arthrodesis and instrumentation.
  • Surgical outcomes for patients with LSS vary.
    • Surgical outcome literature is difficult to assess due to observer bias, inadequate outcome data categorization, vaguely defined outcome measures, and study design.
    • Reports show widely varied outcomes (26-100% success and 31% dissatisfaction at 4.6 years), due to disparate research methodologies.
  • Conservative versus surgical treatment for LSS remains controversial due to wide variations in outcome study type and quality.
    • Johnsson and colleagues document improvement in 60% of surgically treated patients with 25% worsened, compared with improvement in 30% of conservatively treated patients and no change in 60%.
    • Atlas and colleagues tracked 67 conservatively treated and 81 surgically treated patients over 12 months; surgically treated patients reported greater improvement in pain relief than those treated conservatively.
    <LI class=plain>
    • Treatment outcome predictors do not exist; specifically, severe spinal degenerative changes do not necessarily correlate with an unfavorable prognosis or mandate surgery.
  • Simotas and colleagues cite that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection, reported sustained improvement. Conservative and surgical treatments have not been subjected to rigorous well-designed study.


  • Consultation with an internal medicine specialist or subspecialty may be indicated when low back pain (LBP) suggests an underlying systemic illness such as malignancy, infection, or metabolic bone disease. Also, if the diagnosis of vascular claudication is in question, referral to an internist is indicated.
  • Consultation with a rheumatologist may be considered when back pain suggests a rheumatologic condition such as ankylosing spondylitis, rheumatoid arthritis, osteoporosis, or fibromyalgia.
  • Consultation with a surgeon is warranted for deteriorating neurologic status (eg, cauda equina syndrome), segmental instability, and/or intractable radicular or NC pain.

Other Treatment
Epidural steroid injection (ESI) provides aggressive-conservative treatment for LSS patients who demonstrate limited response to oral medication, physical therapy, and other noninvasive measures. Corticosteroids may inhibit edema formation from microvascular injury sustained by mechanically compressed nerve roots. Furthermore, corticosteroids inhibit inflammation by impairing leukocyte function, stabilizing lysosomal membranes, and reducing phospholipase A2 activity. Lastly, corticosteroids may block nociceptive transmission in C fibers. When using oral steroids (in rapid tapering fashion), remember that possible side effects may include fluid retention, skin flushing, and shakiness. Local anesthetic may be combined with corticosteroids to provide immediate pain relief and diagnostic feedback on the proximity of the injectate to the putative pain generator.

  • Caudal ESI
    • Caudal ESI entails needle placement through the sacral hiatus into the sacral epidural space.
    • Advantages include ease of performance and low risk of dural puncture.
    • Disadvantages include large injectate volumes (6-10 mL) necessary to ensure adequate medication spread to more cephalad pathology (ie, above L4-L5). Furthermore, such large volumes potentially may dilute the effect of the corticosteroid.
  • Interlaminar ESI
    • Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the epidural space. Consequently, delivery of medication occurs closer to the affected spinal segmental level than in caudal ESI.
    • Disadvantages include greater potential for dural puncture, and, like caudal ESI, limited spread of medication to the target site if a midline raphe or epidural scarring exists. Furthermore, interlaminar injection delivers medication to the posterior epidural space with possible limited ventral diffusion to nerve root impingement sites.
  • Transforaminal ESI
    • Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment, and, consequently, might prove more efficacious in reducing pain.
    • Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis.
    • Bilateral transforaminal ESI also may be used to treat bilateral central stenosis-induced NC pain when imaging studies demonstrate limited posterior epidural space, thereby precluding safe interlaminar ESI. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.
  • Absolute contraindications to ESI include bleeding diathesis and anticoagulation therapy because of the increased risk of epidural hematoma. While the actual incidence of this complication is unknown, estimates in the literature suggest is occurs less than 1 in 150,000 outpatient epidural injections. Anticoagulation therapy (eg, warfarin, heparin) should be stopped a few days prior to injection. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking coumadin, PT/INR should be drawn the day of the procedure. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued before the procedure in accordance with their half-life and hematologic profile.
  • Other absolute contraindications include systemic infection, injectate allergy, and pregnancy (because of the teratogenicity of fluoroscopy). Relative contraindications include diabetes mellitus (DM) and congestive heart failure, given the hyperglycemic and fluid retention properties of corticosteroids, respectively. Other relative contraindications include adrenal dysfunction and hypothalamic-pituitary axis suppression.
  • Serious complications, although rare, include infection (eg, epidural or subdural abscess) and epidural hematoma. Epidural hematoma has been associated with traumatic needle insertions, but this is neither sensitive nor specific for predicting development. Vandermeulen et al reported 61 case reports in the literature between 1904 and 1994 after central nervous blocks. Dural puncture (in 5% of lumbar interlaminar ESIs and 0.6% of caudal injections) with possible subsequent subarachnoid anesthetic/corticosteroid deposition may provoke neurotoxicity, sympathetic blockade with hypotension, and/or spinal headache; however, contrast-enhanced fluoroscopic guidance minimizes the possibility of dural puncture and intravascular injection.
  • Therapeutic epidural steroid injection (ESI) techniques are performed ideally using fluoroscopic guidance and radiologic contrast dye enhancement to ensure delivery of injectate to the target site. Studies document misplacement of 40% of caudal and 30% of interlaminar injections performed without fluoroscopy, even by experienced injectionists.
  • Transient corticosteroid dose-related side effects include facial flushing, low-grade fever, insomnia, anxiety, agitation, hyperglycemia, and fluid retention. Steroids may suppress the hypothalamic-pituitary axis for 3 months following the injection. Lastly, vasovagal reaction, nerve root injury, injectate allergy, and temporary pain exacerbation can occur as well.
  • Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for HNP-induced radicular pain, appear promising, suggesting that a significant inflammatory component amenable to corticosteroid treatment may accompany HNP-nerve root pathology.
  • Studies of ESI for LSS treatment demonstrate mixed results due to varying injection and guidance techniques, patient populations, follow-up periods and protocols, ancillary treatments (eg, physical therapy, oral medication), and outcome measures. This lack of consistency limits the ability to assess ESI efficacy for LSS.
  • Some studies, nevertheless, suggest that, unlike HNP-provoked radicular pain, NC may be more mechanical or ischemic than inflammatory in nature. Consequently, corticosteroid anti-inflammatory properties may fail to provide designed long-term symptom relief. Studies report that 50% of patients with LSS or HNP-provoked radicular pain received temporary relief and that such results were close to those associated with the placebo effect.
  • Because of concomitant lateral recess stenosis from facet hypertrophy or lateral HNP, patients may fail transforaminal ESI therapy for HNP-induced radicular pain. ESI may do little to relieve chronic lateral recess stenosis-related radicular pain. Additionally, studies show patients with a preinjection duration of symptoms greater than 24 weeks may respond to ESI as favorably as those with symptoms of less than 24 weeks' duration. This finding, may suggest that chronic nerve compression could induce irreversible neurophysiologic change that ultimately renders the nerve root refractory to ESI.
  • Future studies require controlled design, contrast-enhanced fluoroscopic guidance, and objective validated outcome measures before definitive conclusions can be drawn regarding efficacy of ESI treatment of LSS.
First-line pharmacotherapy for LSS includes NSAIDs, which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when used in combination with other medications.

Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, cotreatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. Patients may be asked to sign a medication contract restricting them to one practitioner, one pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.

Drug Category: Anticonvulsants

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain. These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Drug Category: Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

Drug Category: Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission. They block the active reupdate of norepinephrine and serotonin.

<H3>Further Inpatient Care</H3>

  • Inpatient care is necessary for patients with LSS who elect to undergo surgery. The length of stay in the hospital is dependent on the type of procedure performed, but, on average, the patient is released 2-5 days following surgery. Following the operation, it is important that these patients resume basic mobility, activities of daily living (ADL), and ambulation as soon as possible and become educated on proper body mechanics and back safety techniques prior to their dismissal. A short course of active physical therapy may be recommended after surgery for these patients to strengthen the lower back and abdominal muscles to speed recovery time. Ideally, an appropriate exercise program can be initiated before surgery and continued thereafter.

<H3>Further Outpatient Care</H3>

  • Many patients with LSS choose to receive conservative treatment for back and leg pain. An active physical therapy program often is beneficial for these patients to improve flexibility and strength to maintain or improve their current activity levels. Other forms of treatment (eg, ESI) may be administered on an outpatient basis and used in conjunction with other medications and physical therapy. Please see the Physical Therapy and Other Treatment sections for further discussion of these treatments.


  • No prevention exists for LSS.


  • Complications that may develop in patients with LSS include the following:
  • Cauda equina syndrome (in rare cases)
  • Lower extremity weakness and numbness
  • Intractable axial, radicular, or NC pain
  • Disability and loss of productivity
Complications that may develop in patients after surgery include the following:
  • Sustained axial and radicular pain
  • Progressive spinal deformity
  • Cerebrospinal fluid leak
  • Epidural hematoma
  • Pulmonary embolism (PE)
<li>Some authors report spondylolisthesis as a complication of lumbar decompression without arthrodesis, especially after total facetectomy. Preoperative risk factors for postoperative development or progression of L4 or L5 spondylolisthesis include the following:
  • Absence of degenerative osteophytosis
  • Small and sagittally oriented facets
  • Well-maintained disk height
<li>Ciol and colleagues report a substantial reoperation rate following LSS surgery in the Medicare population, for reasons that remain unclear.
  • Possible explanations may include the following:
  • Failure of implanted devices
  • Changed patient expectations
  • Aggressive surgical philosophy
<H3>[b]Patient Education

[*]Patients should be educated to avoid aggravating factors, such as excessive lumbar extension and downhill ambulation. Additionally, patients should be instructed on correct posture and a home exercise program (eg, flexion-biased lumbar stabilization, flexibility training, gluteal strengthening, aerobic conditioning).
[*]For excellent patient education resources, visit eMedicine's <A href="http://www.emedicine...ons/CO1546.asp" target=_blank>Back, Ribs, Neck, and Head Center and Muscle Disorders Center. Also, see eMedicine's patient education articles, [color="#333399"]Back Pain<

#47 rentalguy1


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Posted 13 April 2008 - 03:43 PM

Here's a link to another one I used. It covers Degenerative Disc Disease. Pay particular attention to the "cascade of degenerative changes" that are discussed.

For some reason, I can't post the body of this article here?

#48 Tbird


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Posted 15 April 2008 - 03:47 AM

Please Do NOT post any personal identifying information on the forum. This is for your protection, make sure if you post anything or attach a file that none of your personal information is visible. The internet is a wide open place and we don't want anyone to use your information in a nefarious way.


#49 Armand


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Posted 19 April 2008 - 01:51 PM

I am currently writing a research paper on PTSD. Your experience concerning vision loss occurred as far back as the civil war and in the wars that followed. Vision loss was directly associated with experiencing a traumatic event, this resulting in PTSD.

#50 a173


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Posted 26 May 2008 - 05:15 PM

hey the list is nice to find. thanks...

#51 a173


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Posted 26 May 2008 - 08:22 PM

Please Do NOT post any personal identifying information on the forum. This is for your protection, make sure if you post anything or attach a file that none of your personal information is visible. The internet is a wide open place and we don't want anyone to use your information in a nefarious way.


#52 a173


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Posted 26 May 2008 - 08:43 PM

Please Do NOT post any personal identifying information on the forum. This is for your protection, make sure if you post anything or attach a file that none of your personal information is visible. The internet is a wide open place and we don't want anyone to use your information in a nefarious way.


hey wow what a site. i'm new here.. and yep........... i gave my my docket# out of my claim on the forum... the dva has buried it so long - i want folks to read claim.... not the first mistake i've made... given out the number.......... got any idea of possible probes i may get, or areas of harm i've exposed myself to....... please email if think of major concern .. i'd be most thankful. know you got ta be busy... thanks......... and those words of being "adrift" lost on some bizzarre sea.... scuse' me. sort of hangin' on the side catchin' my breath here......... i'll try my best not to flip anything over. very nice, poetic words you've spoken............ with respect to you, and the whole raft i'll try my best to keep my bearings. and my hat is off to any and all that have made this site what it is.... thanks. got plenty bear, lion wildlife up here in the northern rockies. not much information or brotherhood...

#53 carlie


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Posted 26 May 2008 - 11:22 PM

Welcome. Docket numbers are just fine to post -- BVA posts them all, so they are public information anyway. Just so you know, BVA doesn't post the personal info. like name,
SSA number, address etc.... so you'r cool on that issue.

#54 Tbird


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Posted 27 May 2008 - 05:18 AM

welcome aboard, glad you found us. hang in, you are not alone here.

hey wow what a site. i'm new here.. and yep........... i gave my my docket# out of my claim on the forum... the dva has buried it so long - i want folks to read claim.... not the first mistake i've made... given out the number.......... got any idea of possible probes i may get, or areas of harm i've exposed myself to....... please email if think of major concern .. i'd be most thankful. know you got ta be busy... thanks......... and those words of being "adrift" lost on some bizzarre sea.... scuse' me. sort of hangin' on the side catchin' my breath here......... i'll try my best not to flip anything over. very nice, poetic words you've spoken............ with respect to you, and the whole raft i'll try my best to keep my bearings. and my hat is off to any and all that have made this site what it is.... thanks. got plenty bear, lion wildlife up here in the northern rockies. not much information or brotherhood...

#55 Chick


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Posted 27 May 2008 - 12:21 PM

I am 100% service connected. It is broken down like this: 70% P & T, 30% unemployable. If I have other injuries that are service connected can I get them added to my disability so as to get rid of the 30% unemployable?

#56 yelloownumber5


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Posted 06 June 2008 - 02:57 PM

Yes that identity theift is not a good thing...........

Humana/Tricare Regional person sent us someone elses EOB with some of our Eob's.......name, address, ssn, phone, - toyota. Because Tricare wanted to be a butts and act like they cannot add numbers we are looking who to send this HIPPA violation to. Tricare/Humana is all up the DME's tails do they get kick backs if they keep customers and do not let complaints through.?

Has anyone dealt with Mr. Brembry or Walker?

#57 yelloownumber5


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Posted 06 June 2008 - 03:04 PM


Edited by yelloownumber5, 06 June 2008 - 03:07 PM.

#58 halos2


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Posted 22 June 2008 - 06:25 PM

Thanks for this informative site. B)

#59 firedawgs


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Posted 24 June 2008 - 04:04 PM

Wow, this is really great information. I have a 10% for DDD; which I thought was low? I factured my back while on active duty and now have two bulged disc. Back pain will be with me for ever I guess.

#60 mobie16r


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Posted 12 July 2008 - 04:22 PM

Chick,you are not 30% unemployable.This is the way it go,for you to be able to get TDIU,you have to be 70% service connected.You are only 70% service connected,but you are ungainful employable because of your 70% service connected disabitlities,and for thst reason,you are being paying at the 100% rate,But you are still 70% and IU. I hope this helps

#61 Tbird


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Posted 13 July 2008 - 05:23 AM

link broke thanks for the heads up i fixed the link and here it is http://www.hadit.com...help_guide.html


Where is the self-help guide? I am no longer able to access it from the link at the bottom of this post. I read it before and would like to read it again but I can't find it on the site (and I used the Google search hadit.com tool as well as trying to get to it from your posted link).


#62 jbasser


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Posted 27 July 2008 - 09:43 PM

Good job Shane. I am rated for Cervicel Spine C3 thru C7, Diaphragm paralysis, with Pulmonary HTN to boot.
The VA will rate the nerves separately but with the Pulmonary HTN it is a separate 100 percent rating.

(38 CFR 4.97 Schedule of ratings – respiratory system.)

Nerves from the upper portion of the spinal cord (C3 to C5) allow a person to breath. C3, C4, and C5 innervate the diaphragm. The ability to cough and to fully expand the lungs comes from abdominal muscles, and intercostals muscles that are innervated by thoracic nerves (T1 – T12).

People with damage to the spinal cord at the C1 to C3 affecting their breathing, require mechanical ventilation. Unilateral or bilateral paralysis of the diaphragm will predispose a person to atelectasis and pneumonia. Cervical and upper thoracic SCI will also predispose a person to respiratory complications like pneumonia due to restrictive pulmonary function and an impaired ability to cough. Ineffective cough leads to retained secretions, mucous plugging, and infections. Restrictive changes with a low forced vital capacity (FVC) may be seen on pulmonary function tests.

#63 fanaticbooks


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Posted 14 August 2008 - 08:51 AM

link broke thanks for the heads up i fixed the link and here it is http://www.hadit.com...help_guide.html

This is a wonderful site about the inner workings of the VA. I think it helps to know.

On the opposite side, the veterans side, I would like to mention my website. It is a site designed to help veterans, veterans' dependents and those helping veterans to research, organize and assemble their va claims. It is free with absolutely no hidden agenda. If a claim/appeal is organized with as much mentioned for proofs it has to help everyone, va or vet rep or vet. It describes in step-by-step detail how to actually create a written attachment as well as getting info that might help the claim/appeal. It is addressed from a secretary's organizational viewpoint.

The site is www.howtoassemblevaclaims.com

Good luck and God Bless. Thank you for protecting me and mine.
Thank you TBIRD for giving me permission to post info about my site here. B)

#64 Tinman


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Posted 18 August 2008 - 07:40 PM

this poll was requested by rsg and he was kind enough to provide the following links for further information







#65 Tinman


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Posted 18 August 2008 - 07:46 PM

Hello, I was stationed at T.Island in the early 70's. I read the reports. Are they <VA> testing us for problems due to exposer. Should I be calling a Dept. to report mt T.I. duty?
THANKS for the info
  • SDVIKING likes this

#66 Chuck75


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Posted 23 August 2008 - 09:02 AM

There is no specific test done by the VA concerning A.O. or other HAZMAT exposure.
The "A.O. exam" is really nothing more than a general medical examination with lab tests. It might or might not show the effects of HAZMAT exposure, depending upon what chemicals and substances were involved.

In general, a large number of Vietnam era sailors were likely exposed to some form of HAZMAT, with unknown and largely unprovable exposure. Many were sent to the far east via the T.I. Navy base, as I was in 1967. The fire fighting training was likely the largest source of HAZMAT exposure, and "working parties" sent to Hunter's point were another. Old WWII barracks were full of asbestos, and the area was contaminated by decades of use as a Navy base.

Hello, I was stationed at T.Island in the early 70's. I read the reports. Are they <VA> testing us for problems due to exposer. Should I be calling a Dept. to report mt T.I. duty?
THANKS for the info

Edited by Chuck75, 23 August 2008 - 09:05 AM.

#67 sayad111


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Posted 24 August 2008 - 12:29 PM

Laws and regulations on the use and handling of hazardous materials may differ depending on the activity and status of the material. For example one set of requirements may apply to their use in the workplace while a different requirements may apply to spill response, sale for consumer use, or transportation. Most countries regulate some aspect of hazardous materials.

#68 sayad111


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Posted 24 August 2008 - 12:38 PM

hey , it liek how many % is the minimum to get the veterians claims approved ?
Has any one got any idea , it is liek i have been visiting many of thee threads , but none of them had teh topic , i just found alittle touch over here.
Can any one help ?

#69 Pete53


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Posted 24 August 2008 - 01:40 PM

Laws and regulations on the use and handling of hazardous materials may differ depending on the activity and status of the material. For example one set of requirements may apply to their use in the workplace while a different requirements may apply to spill response, sale for consumer use, or transportation. Most countries regulate some aspect of hazardous materials.

Please do not use a url for an advertisement in your signature.I removed the ad if you do not agree please feel free to contact me or any Moderator here.

#70 allan


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Posted 24 August 2008 - 07:10 PM

the question here is about exposure to hazardous materials on the base, in the soil, buildings etc. One building used for training personel was a neuclear desaster site in the 50's. I suppose radiation disapates quickly so theres nothing to wory about?
Damage control training area and that old traing ship they had was full of radioactive material, plutonium discs. Much of the base had agent orange used on it.
If you did any fishing off the docks or the ship, you may have ingested contaminates.

They didn't write any laws or regulations on the plutonium discs that were hiddin on the base, nor were we trained for it. They didn't want anyone to know it was there.

#71 WhoopAssSmitty


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Posted 05 October 2008 - 12:41 PM

hey , it liek how many % is the minimum to get the veterians claims approved ?
Has any one got any idea , it is liek i have been visiting many of thee threads , but none of them had teh topic , i just found alittle touch over here.
Can any one help ?


If I'm understanding you correctly, you want to know what the minimum percentage is, that a vet could get and be considered as Service connected.

The answer to that is 0% is the minimum, that means the issue is service connected and can be treated at a VA Medical Center-VAMC.
For this rating, the vet will normally have a copay, of if memory serves me correctly of about $8.00 for the doctor and meds.

With a 0% rating, the vet will not get any monthly compensation, meaning he/she will not get paid for that 0% rating.

Hope this is what you were looking for.


#72 rentalguy1


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Posted 19 October 2008 - 10:17 AM

Lumbar (Intervertebral) Disk Disorders

Thanks for posting this link Allan

#73 rentalguy1


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Posted 13 November 2008 - 07:41 PM

Interesting find...VA algorithm (flowchart) for non-specific back pain.
Table of Contents

#74 rentalguy1


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Posted 13 November 2008 - 07:48 PM

More VHA stuff: LBP Interventions

#75 hurryupnwait


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Posted 13 November 2008 - 07:49 PM

Interesting find...VA algorithm (flowchart) for non-specific back pain.
Table of Contents

That's a cool find! Is this a VA flow chart? Interesting loop on page B One just keeps getting cycled thru.

#76 rentalguy1


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Posted 13 November 2008 - 07:50 PM

VHA LBP Glossary

#77 rentalguy1


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Posted 13 November 2008 - 07:52 PM

Found on the VA web site. Could prove useful in claims.

Diagnosis and Treatment of Low Back Pain: A Joint Clinical PracticeGuideline from the American College of Physicians and the AmericanPain Society

#78 rentalguy1


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Posted 13 November 2008 - 08:30 PM


#79 rentalguy1


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Posted 02 December 2008 - 08:32 PM

From Stretch:





#80 hollywoodnc


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Posted 07 December 2008 - 08:29 AM

Geez Rentalguy, and I thought that I knew about spinal conditions!

I am impressed with all of your links and info regarding spinal disorders.

Thanks for the info!!!

I do have several questions though...

First, HISTORY: (So what I ask can be better understood, or in the least, tied in)

1975: Suffered a Left hip compression Fx, while training, and it was found that a Knowles Pin was penetrating the joint space.
4/1976: Medically Discharged
5/1976: Diagnosed w/Osteoarthritis, and a 'Slipped Prosthesis', and lt. leg atrophy, and a 1/2" left leg length differential.
6/1976: Involved in a MVA, and compressed L/2-3.(NON S/C disability)
6/1976: Awarded 10% S/C.

It is a FACT that I've tried to connect Antalgic Gait due to the painful left hip and leg length differential, to the improper healing of L/2., based on a pelvic tilt, with each step taken, since 1977 on...but to NO avail. The DVA has denied this connection, and will not approve the spinal condition as 'Secondary to'. I remained at 10% till 1980. Severe DJD, only warranted a 20% rating from 1980 till a THR was finally installed in 1989 which warranted a 30% rating.
I suspect that this denial is due to the DVA not making the connection, due to the opening up of Pandoras Box. As your research clearly shows, once the spine is rated, and/or found to be "Secondary To", this rating would force the DVA to treat ailments involving any future conditions which may arise.
IF it's DIRECTLY S/C, than the VA has no alternatives, but to classify it as such...but secondary to, they won't touch with a ten foot pole!

#1) In 2004-05, I submitted 200+ pages of documentation from websites such as The University of Maryland, e-medicine, Mayo clinic, etc., I guess to 'Educate' the reader, and to tie in my conditions involving gait to a non service connected disability, and it was viewed as "Lay Evidence". In this package, I clearly showed what VA doctors have said, -vs- what the respectable medical facilities were saying...in short, contradicting the (supposed) doctors opinion(s).
Now mine wasn't as "Detailed" as yours, however it was to the point.

The question here is... Did the DVA view your submitting of such information as "Lay Evidence"?
If so, how did you convince them otherwise?

No matter what I say, these brain dead imbeciles cannot comprehend the logical connection, that Antalgic Gait could have an adverse effect on spinal geometry (in particular-Lumbar). Any painful hip, including a hip which has a pin protruding into the acetabular, will create Gait. Gait, effects pelvic geometry/tilt with each step. Each unnatural movement by the pelvis + time will effect the lumbar region. In THIS case, I have a fresh injury to the L/2. What will the overall effect be to this effected joint?

#2) In what little that you know about my case, is this case conceivably winnable in Federal Court, if you use a biomechanical POV to show causation?
#3) Am I just blowing Smoke up a Judges' skirt?

#4) Even though I possess crucial evidence, I do not possess a writeup by any doctor that can "Tie In" antalgic Gait effecting spinal conditions. Mine are vague, but it isn't concrete. I DO have a Neurologists' writeup that goes along the line of: "It is more likely than not..."...however it would not compete against: "I seriously doubt that..." (submitted by a VA quack).
Question is...Do you have a Bona Fied statement or link which directly ties in Gait contributing to spinal deformities or in the least has stronger wording then what I possess?

#5) With your knowledge of Title 38, is there a regulation that also shows that a hip disability could lead to spinal conditions?
#6) (supra @#5) but instead using "Case Law", if applicable?

Thank You so much, for your diligence, in educating us in these ailments, and how to apply appropriate law.

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