Lumbosacral Plexopathy and Sciatic Neuropathy: Differential Diagnosis and Treatment
Disease/ Disorder Definitions Lumbosacral plexus: network of nerves formed by the ventral rami of the lumbar and sacral spinal cord. Lumbosacral plexopathy (LSP): an injury to the nerves in the lumbar or sacral plexus. Lumbosacral-radiculoplexus neuropathy (LRPN): injury involving the […]
Metabolic / Nutritional / Toxic / Radiation Myelopathies
[…] used, including the Functional Independence Measure, the WeeFIM for children, the Spinal Cord Independence Measure, and/or the Walking Index for Spinal Cord Injury. Cognition can be screened using the Mini-Mental Status Examination. Laboratory studies Tests may include the following: Vitamin B12 deficiency: […]
Impaired Thermoregulation
[…] temperature less than 35°C/95°F) or hyperthermia (core temperature > 37.8°C /100°F). Etiology Impaired thermoregulation is a known complication seen in persons with spinal cord injury (SCI), particularly those with level of injury above T6, traumatic brain injury (TBI), stroke, and other conditions that cause […]
Transverse Myelitis
[…] and 21 days after onset of symptoms (part of diagnostic criteria).2 Clinically, it can present as a complete or partial spinal cord injury syndrome. Complete ATM characteristically results in paresis of lower and/or upper extremities and a sensory level, whereas a partial ATM would present with asymmetric neurological impairments.8 The course is typically monophasic but relapsing idiopathic TM may occur.2 Most recovery occurs in the first 3 months after injury, but improvement may occur up to a year or longer.2 Specific secondary or associated conditions and complications TM is a form of nontraumatic spinal cord injury (NTSCI), and thus has medical complications of NTSCI depending on the severity of injury to the cord. As with spinal cord injury (SCI), medical complications involving every organ system are common after TM. Medical management and complications are similar to SCI and should be managed in the same manner.9 It is crucial to determine the etiology, whether disease-associated or idiopathic, as this helps identify recurrence risk, appropriate treatment and surveillance that may be required to improve outcomes.10 Specifically, secondary complications such as impaired mobility, and sensation, pressure ulcers, bowel and bladder dysfunction, sexual dysfunction, spasticity, movement disorders, autonomic dysregulation, and pain, should also be addressed. Essentials of Assessment History Signs of myelopathy, such as motor weakness, sensory abnormalities, pain, bowel or bladder dysfunction, as well as recent infections, vaccinations, travel, medical history, review of systems, social history, family medical history, and surgical history, should be considered in order to direct the investigation for a specific etiology. In the pediatric population 50-100% of the cases are preceded by a mild febrile illness 3 weeks prior to onset of symptoms.10 Physical examination The physical exam will likely change as the neurologic deficits progress or improve depending on the patient’s individual course. Serial exams will help identify the nadir of clinical findings. Initial physical exams should evaluate the following: Muscle strength, tone, and muscle stretch reflexes. Sensory reflexes, including abdominal and bulbocavernosus reflexes. Rectal exam Detailed sensory exam of dermatomes. Sensory loss is often described in a band-like or transverse level, with decreased sensation distally. 10 Autonomic instability or dysfunction. Consider using the American Spinal Injury Association (ASIA) exam to classify completeness of the SCI. Skin evaluation for pressure ulcers, especially over insensate areas and bony prominences such as the occiput, sacrum, ischia, and heels. Functional assessment The Functional Independence Measure (FIM) and WeeFIM (for children) are commonly used tools to measure motor and cognitive functional status.11 Spinal Cord Independence Measure (SCIM) are an alternative to the FIM to assess 16 categories of functional independence. Walking Index for Spinal Cord Injury (WISCI) assesses the amount of physical assistance and devices needed for ambulation. The SCIM and WISCI can be used for traumatic and nontraumatic and acute and chronic SCI for ages 13 to >65 years. Laboratory studies Lab studies focus on determining the etiology of the TM syndrome. This includes serology, cerebrospinal fluid, […]
Paroxysmal Sympathetic Hyperactivity
[…] a lesion in the inhibitory centers in the brainstems and diencephalon reduces tonic descending inhibition to afferent sensory information from spinal cord circuits. This amplifies normally non-nociceptive afferent input from the periphery and leads to over-excitation of the sympathetic response.3,17 […]
Cervical Whiplash
[…] be identified with ultrasound. 13 More advanced imaging modalities (MRI, CT) are used for suspected cases of nerve root or spinal cord injury; MRI or CT is also commonly used prior to performing a spine procedure to treat pain. MRI can detect ligament disruption and subtle or stress vertebral or posterior element fracture. Although alar ligament damage has been previously demonstrated in chronic WAD, recent literature showed that MRI can also reveal deep muscle fat infiltration in those at risk of developing chronic WAD.14 Supplemental assessment tools Upper limb radicular symptoms and/or paresthesias are often noted following cervical whiplash injury. The onset of these symptoms may be immediate or delayed and caused by acute compression in the neural foramina at the time of the collision or from a traumatically induced cervical disc herniation. After three weeks have elapsed, if radicular symptoms persist, then electrodiagnostic studies can help to identify and quantify injuries to the cervical nerve roots, brachial plexus, and/or peripheral nerves. Early predictions of outcomes Delayed recovery is associated with female gender, older age, high initial intensity of neck pain, neurologic deficit, and preexisting neck pain. Recovery is improved by early resumption of pre-injury activities, exercise, manual therapy, and positive attitude. Delayed recovery or chronicity is observed with use of cervical collars, rest, and negative attitudes.15 Not only did nonrigid cervical collars provide no obvious benefit for recovery but use of these collars was associated with increased time off work.16 The majority of patients will recover quickly, but a subset of at-risk patients will develop chronic WAD. Environmental Environmental factors including home environment, work status, work-life modifications, community involvement, and current mode of transportation should be considered when creating a treatment plan. If necessary, modifications to motor vehicle should include seatbelts and headrests with adequate height. Energy absorbing seats and active head restraints significantly reduced WAD claims or subjective complaints of neck pain up to 75%.17 Social role and social support system Generally speaking, mood affects the perception of symptoms and the appraisal of one’s health.18 Often when a person suffers a disabling injury and has chronic pain, the entire family is affected by the injury. Family members can lend encouragement to the injured individual to seek treatment and participate in rehabilitation to restore their function and place within the family dynamic. Coping style involving the patient actively seeking social support may be associated with shorter duration of whiplash symptoms. Passive coping including internalizing symptoms may be associated with subsequent development of chronic WAD.19 Professional Issues Patients who suffer a cervical whiplash injury as the result of a motor vehicle accident will often obtain legal representation in order to acquire more comprehensive medical treatment as well as seek monetary retribution for their injury. Sometimes there is concern from independent treating physicians that a patient with whiplash will have either conscious or unconscious barriers to recovery because the patient may feel he or she must remain “injured” to collect such a settlement. The difference between nations in annual whiplash incidence is significant. Chronic WAD development has been found to be inversely associated with the absence of compensation.20 The elimination of insurance payments for WAD was associated with decreased injury claims. 21 The subjective nature of WAD make insurance settlements and litigation challenging, but medial branch blocks have been cited as an underutilized but objective assessment.22 Although compensation has been associated with incidence and prognosis, recent literature shows that litigation does not correlate with persistence of pain. 23-25 Medical legal literature outlines the following risk factors for poor recovery following whiplash injury: less than post-secondary education, failure to wear a seatbelt, post injury pain >6/10, number and severity of injury related symptoms, presence of radicular symptoms, post injury headache, post injury low back pain, neuropathic pain, Neck Disability Index score >40%, post traumatic stress symptoms, catastrophizing, reduced pressure pain threshold at shin, and cervical spine cold hyperalgesia.26 Rehabilitation Management and […]
Neurogenic Bladder
[…] causes include stroke, traumatic brain injury, multiple sclerosis (MS), multiple systems atrophy, Alzheimer’s disease, and hydrocephalus. Spinal (infrapontine-suprasacral) causes include spinal cord injury/disease of various etiologies. Traumatic SCI is the most common spinal lesion affecting voiding. Other spinal etiologies include demyelination (multiple sclerosis, transverse myelitis), vascular (arteriovenous malformations, spinal cord infarct), neoplasm, hereditary (hereditary spastic paraplegia), infectious (tropical spastic paraplegia), or degenerative causes (cervical spondylosis). Infrasacral (spinal root and peripheral) causes include spinal dysraphism, arachnoiditis, intervertebral disk prolapse, cauda equina lesions, diabetes mellitus, hereditary (hereditary motor sensory neuropathy), and iatrogenic (pelvic or retroperitoneal surgery). Epidemiology including risk factors and primary prevention The prevalence of neurogenic bladder varies based on the underlying neurological condition, the duration of disease, and the severity of underlying neurological diagnoses. For instance, more than half of stroke patients report urinary incontinence during the acute phase of stroke. The prevalence of neurogenic bladder in Parkinson’s disease ranges between 38 and 71%. Lower urinary tract symptoms are reported in 32 to 96% of patients with multiple sclerosis (MS). SCI leads to neurogenic bladder in about 70–84% of patients.4 Lower urinary tract dysfunction is common in spina bifida, reported in more than 90% of children.5 Patho-anatomy/physiology Control of micturition is coordinated between 3 main centers6 Sacral micturition center (S2-4 reflex center) – Afferent impulses from the bladder enter the S2-S4 sacral segments and trigger efferent parasympathetic impulses to the bladder causing bladder contraction. This reflex is usually triggered by bladder distention. Pontine micturition center ‑ Coordinates relaxation of the urinary sphincter when the bladder contracts. Cerebral cortex ‑ Inhibitory control of to the sacral micturition center. It allows for voluntary control of micturition Voiding dysfunction can be classified according to the level of the lesion2,6 Suprapontine lesions (e.g., cerebrovascular accident CVA): Patients present predominantly with storage symptoms. Spontaneous involuntary detrusor contractions occur due to removal of the tonic inhibition of the PMC. Urodynamic studies (UDS) show detrusor overactivity without detrusor sphincter dyssynergia. Suprasacral lesions (e.g., spinal cord lesions and disorders): Patients may present with both storage and voiding symptoms. Loss of coordinated activity results in detrusor-sphincter dyssynergia (DSD), which is the simultaneous contraction of the detrusor and external urinary sphincter. This leads to incomplete bladder emptying and abnormally high bladder pressures. UDS may show detrusor overactivity and DSD. Sacral/Infrasacral lesions (e.g. injuries to the conus, sacral nerve roots): This results in predominantly voiding symptoms. Patients may present with a highly compliant and acontractile bladder with high bladder volumes. Postvoid residuals (PVR) are more than 100 mL. UDS may show hypocontractile or acontractile detrusor. Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) New onset/acute Many central neurologic disorders temporarily result in an areflexic bladder. Suprapontine lesions: Detrusor areflexia often develops immediately post-stroke. Urinary incontinence is common. Uninhibited detrusor overactivity and urge incontinence may develop.7 Suprasacral lesions: During the spinal shock period (6- to 12-weeks post injury), patients with SCI have a competent bladder neck, but there is detrusor acontractility/underactivity. Urinary retention is common, and incontinence occurs when there is overflow. The return of the bulbocavernosus reflex marks the recovery from spinal shock, at which time detrusor activity gradually returns.6 Infrasacral lesions: In cauda equina syndrome (CES), early symptoms of bladder dysfunction can be subtle, such as difficulty in initiating the urinary stream.8 Early stage bladder dysfunction in diabetes may present with bladder hypertrophy, remodeling and increased contractility.9 Subacute and chronic Suprapontine lesions: Post-stroke incontinence is multifactorial. Detrusor overactivity is the most common UDS finding in stroke patients. Urinary incontinence is more prevalent in post-stroke patients with impaired awareness and cognition, poor lower limb motor function and depression. Many patients show improvement in voiding dysfunction by one year post-stroke. Persistence of urinary incontinence at 1 year is a poor prognostic factor for mortality, functional recovery and institutionalization.7 Suprasacral lesions: Once there is recovery from spinal shock, patients with SCI develop incontinence because of involuntary detrusor contractions. Suprasacral lesions can present with high bladder pressures and PVR because of the coexistence of detrusor overactivity with dyssynergia.10 Infrasacral lesions: Most patients with CES develop an areflexic or acontractile detrusor and present with urinary retention and/or overflow incontinence. Detrusor overactivity has been reported in 15-31% of patients with CES.11 In late stage diabetes, decreased peak voiding pressures are seen, and patients may present with atonic bladder, decreased sensation and poor emptying.9 Specific secondary or associated conditions and complications Both supraspinal and suprapontine injuries result in detrusor overactivity and incontinence. In spinal cord pathologies the simultaneous presence of reduced bladder wall compliance and DSD cause increased bladder pressure, which leads to structural bladder wall changes such as trabeculations and diverticuli.12 Vesicoureteral reflux (VUR) and hydronephrosis may develop with increased bladder pressures (> 40 cm H2O).1 This can lead to renal impairment and even end stage renal disease.12,13 Patients with SCI are prone to upper […]
Aging with a Neurological Disability
[…] had an average life expectancy of an added 19.6 years (20.8 years for women and 18.2 years for men). Spinal Cord Injury5 54 per 1 million (17,500 cases per year) 250,000-368,000 Age 20, paraplegia: 44.7 years Age 60, ventilator dependent: 3.6 years Stroke6,7 Decreased by 32% from 1987 to 2017 in adults ≥ 65 years of age 7.6 million 60 to 69 years of age: 6.8 for men and 7.4 for women. 70 to 79 years of age: 5.4 for men and 6.4 for women. ≥80 years of age: 1.8 for men and 3.1 for women. TBI8-10 87 million TBI-related ED visits 5.3 million require long-term assistance with activities of daily living Mild TBI: No change in life expectancy Moderate TBI: reduced by 4.11years Severe TBI: reduced by 13.77 years PD11-13 5-35 per 100,000 930,000 14.6 years after diagnosis ALS14-16 1.5-1.7 per 100,000 5 per 100,000 2-4 years after symptom onset MS17-19 3 per 100,000 900,000 Reduced by 6-10 years Key epidemiological data regarding some of the major causes of neurological disabilities are summarized in Table 1. Additional details about the epidemiology of these and other neurological disorders can be found under topics related to those individual conditions. Pathoanatomy/pathophysiology Consequences of the normal aging process are amplified by concomitant neurological injury. Disease progression: natural history, disease phase or stage, and disease trajectory (clinical features and presentation over time) Care must be tailored to the individual, the neurological disease, and additional comorbidities. For instance, modifying cardiovascular risk factors after stroke can reduce future events. In addition, dementia becomes more prevalent with age, and in the general population, affects 3% of people aged 65-74 years, 17% of people 75-84 years, and 32% of people age 85 and older.20 PD, ALS, and MS are all associated with cognitive impairment and dementia. Neuropsychological evaluation can identify specific deficits and determine compensatory strategies. Specific secondary or associated conditions and complications Secondary conditions associated with aging and neurological disability are noted in all organ systems. For example, cardiovascular disease can reduce the efficiency of mobility, visual decline can further impair balance and diabetes mellitus adversely affects many organ systems that are already compromised by the neurological disease. Essentials of Assessment History When collecting a history from an aging individual with a neurological disability, it is critical to capture medical details and information on premorbid function, higher level physical function (balance, coordination), psychosocial factors, support systems, spirituality, home safety, and economic stability. Physical examination A thorough physical exam should include cognition, strength, sensation, balance, vision, hearing, and nutritional assessment. Functional assessment A clinical assessment should include an evaluation of mobility and self-care ability (including activities of daily living), as well as cognition and safety (including instrumental activities of daily living). Laboratory studies Routine laboratory studies should be consistent with general health maintenance guidelines and relevant to the specific neurological condition. In the elderly, it is important to note that abnormalities such as electrolyte imbalance, can accentuate cognitive and functional impairment related to underlying baseline neurological disorders. Imaging Appropriate imaging should be performed in individuals with abnormal neurological findings or progressive neurological decline, such as recent loss of motor control or decline in cognitive function. Environmental With aging, balance, gait, strength, power, and endurance typically decline. A home safety evaluation can identify risk factors for injury and enhance independence in activities of daily living. Comprehensive home assessment interventions have been shown to significantly reduce the risk of falls among the elderly by 21%.21 This may include securing cords out of walkways and installing grab in the bathroom and railings next to stairs. If mobility deteriorates, assistive devices such as walkers, wheelchairs, power mobility, transfer boards, lifts, hospital beds, and bathing equipment may be considered. In addition, visual and auditory acuity can decline with age. Vision loss affects 12.2% of Americans 65 to 74 years of age and 15.2% of Americans 75 years of age and over.22 Assistive technology such as auditory amplification devices, low vision adaptations, and augmentative communication devices can facilitate communication and safety. Social role and social support system An assessment of support systems for supervision and other required assistance should be completed. Professional issues Not all patients may be competent to make decisions about health care matters. Patients may become temporarily incompetent during acute illness or become permanently incompetent, such as in the later stages of advanced neurological diseases. Health care and other decisions must still be made, even when patients cannot make these decisions themselves. If cognition and judgment are impaired, the individual’s capacity for decision-making and the level of supervision needed should be considered. In some cases, a guardian may need to be appointed. Treatment and Rehabilitation Management Available or current treatment guidelines Musculoskeletal and neurological Musculoskeletal problems are a major cause of pain and physical disability in older adults and represent a significant contribution to the global burden of disease.23 Overuse injuries, rotator cuff pathology, compression mononeuropathies, and musculoskeletal pain are more common in aging patients with in neurological disabilities, especially in those who utilize their upper limbs for mobility. Osteoarthritis alone affects 10.4% of adults in the United States with a steep increase in prevalence with increasing age.17 The most significant functional deficiencies contributing to impaired balance include marked loss of muscle strength, reduced range of movement of the spine and peripheral joints, and loss of joint proprioception. Physical and occupational therapists can assess joint mechanics, joint protection, mobility efficiency, and provide energy conservation techniques. Cardiovascular An estimated 6 million Americans had cardiac failure from 2015 to 2018, and both the prevalence and incidence of cardiac failure increase with age.6 Heart failure remains a severely debilitating condition for many older adults and can accelerate functional decline in patients with neurological disorders. Resting metabolic rate declines with increasing age and often decreases after an injury to the central nervous system. This predisposes the individual to weight gain, which can worsen functional status and lead to complications in other organ systems (musculoskeletal, skin, endocrine, etc.). If cardiovascular risk factors such as hypertension, diabetes, and hyperlipidemia are well controlled at younger ages, additional comorbidities can be minimized later in life. Respiratory Changes in the alveolar membrane, including loss of the alveolar–capillary interface and an increase in alveolar size due to the destruction of individual alveolar walls, are the major form of damage found in the aging lung.24 In normal aging, vital capacity (VC) declines by 40-50%. This anticipated decline can become clinically significant for individuals with neurological disorders. In SCI, individuals with higher levels of injury typically have reduced VC, though often can breathe without ventilators. However, with accompanying age-related loss of VC, a patient may require a ventilator. In ALS, the criteria for initiating non-invasive ventilation include having a VC less than half of the predicted value. Disorders such as nocturnal hypoventilation and sleep-disordered breathing are seen more often in SCI (15-69%) and stroke (>50%), potentially resulting in daytime sleepiness, cognitive dysfunction, and medical morbidity.25,26 This should be evaluated when clinically indicated. Gastrointestinal Gastrointestinal […]
Vascular Malformations of the Brain and Spine in Children
[…] to accommodate for resultant persistent functional impairments. Social Acute neurologic sequala with resultant functional impairment from an acquired brain or spinal cord injury requires good family and social support. As the child transitions back into the home, school and community, proper accommodations and assistance may be required for mobility and activities of daily living. Support, counseling, education, and developmental guidance is needed for family and other caregivers. Resources for opportunities to be creative and social for children of all ages, including infants and teens, is beneficial. Professional There is often a delay in diagnosis due to the low overall incidence, thus heightened clinical suspicion is necessary for prompt diagnosis. In the initial phase, when emergent symptoms are being controlled and addressed, there may be a delay in definitive treatment of the AVM. This may pose as a stressful time for patients and families with concerns about the risk of recurrence of emergent symptoms. Rehabilitation Management and Treatments Current treatment guidelines Treatment may be conservative or interventional depending on lesion features, clinical presentation and patient specific factors.25 Treatment options include endovascular embolization via catheter delivery of liquid embolics or coils, microsurgical resection, and stereotactic radiosurgery (e.g., Gamma knife). Embolization alone rarely represents a curative treatment. However, a reduction in the size of the nidus or AVM flow may enable the performance of stereotactic radiosurgery or facilitate surgical removal. The risk of all treatment modalities should be weighed against the natural history risks of AVMs. The Spetzler-Martin (SM) grading scale is utilized as a decision tool to estimate the risk of surgical resection by evaluating the AVM size, pattern of venous drainage and eloquence of brain location, with higher grades of 4 and 5 being associated with greater surgical morbidity and mortality.1,16,26 Generally, AVMs with high grades are managed with conservative management due to rupture risk and worse prognosis with operative treatment including partial resection.15,25,27 Further, there is evidence that medical management alone of unruptured AVMs of the brain is superior to interventional therapy or medical plus interventional therapy at 5 year follow up.27 At different disease stages Acute: Observation, medical management and emergent surgical intervention may be warranted based on AVM characteristics and clinical presentation. With acute hemorrhagic presentation, prompt life saving measures to prevent further neurologic compromise are essential. Definitive treatment may be delayed to allow for characterization, healing, or adjuvant therapy as part of a staged treatment plan due to the size, location and complexity of the lesion.16 However, despite variances in clinical courses, treatment outcomes, and complications, pediatric patients with AVMs who underwent acute inpatient rehabilitation saw improvement in their WeeFIM scores upon discharge.28 Subacute: Depending on the location and type of vascular malformation, subsequent monitoring of the lesion with symptom presentation and imaging studies is done. This will guide further need for surgical intervention with a goal of lesion obliteration and prevention of re-bleeding and further neurologic sequela. In some asymptomatic AVMs that are incidentally found, clinical observation with monitoring is appropriate.16 Chronic/stable: Long term follow-up is necessary due to risk of recurrence and re-rupture. There are currently no established guidelines for length of monitoring. New or evolving symptoms warrant additional imaging/workup to ensure stability of the vascular lesion. Neurologic deficits may improve or persist indefinitely.16 Rehabilitation strategies apply as with any other cause of acquired brain or spinal cord injury. (Please see rehabilitation care for pediatric stroke and spinal cord injury). Coordination of care To date, no definitive guidelines exist for the management of brain and spinal AVMs. Multispecialty interdisciplinary care is vital given the complex nature and course of AVMs with the risks of intervention balanced against the natural course of each individualized treatment strategy.29 This pertains to both medical/surgical management of the vascular lesion as well as in the rehabilitation management of acquired brain and spinal cord injury. Patient and family education Patient and family education as to the diagnosis and possible treatment options, with a good understanding of its risk and benefits, as well as the need for subsequent follow-up and rehabilitation cannot be over-emphasized. With the high rate of persistent neurological deficits, it is important to be able to counsel families on the likelihood of long-term deficits following AVM surgeries. These neurological deficits can be predicted using preoperative deficits, lesions of the eloquent cortex, and AVMs > 3 cm.30 Measurement of treatment outcomes Treatment must prevent recurrence that can worsen clinical status. Outcome measures are mainly based […]
Post-Laminectomy Pain
[…] the implementation of International Classification of Disease (ICD-11) on January 1st, 2022, this diagnosis was changed to “chronic pain after spinal surgery (CPSS)”. However, the ICD-11 has yet to be widely adopted. The terms “post-laminectomy pain” and “FBSS” will be used throughout this document for continuity and to improve search engine optimization for this topic, but readers should be aware of the new terminology for future reference. The term “persistent spinal pain syndrome (PSPS)” with two subtypes (T1 – no spine surgery performed and T2 – post-spine surgery) has also been proposed to address some ambiguity with CPSS but has not yet been added to the ICD-11.1,2 Post-laminectomy pain is defined by the IASP as “lumbar spinal pain of unknown origin either persisting despite surgical intervention or appearing after surgical intervention for spinal pain originally in the same topographical location”.3 There may be many causes for this chronic pain creating a complex pathophysiology. Predictive risk factors include preoperative (patient) factors, intraoperative factors, and postoperative factors.4,5,6,7,8 Preoperative: this can be divided into patient-specific and surgery-specific factors. Depression, anxiety, hypochondriasis, obesity, smoking, worker’s compensation or ongoing litigation, and radiographic findings such as disc herniation, stenosis, and fibrosis increase the risk of FBSS.9,10 Psychosocial factors are strongly linked to developing disability from low back pain (LBP).11 However, this does not exclude an organic problem, and these factors should be optimized before the surgery.12 Earlier surgery in patients with poor psychometrics and lumbar disc disease may actually improve pain outcome, as prolonged pain and distress can reduce the efficacy of the surgery.13 Selecting an inappropriate patient for surgical treatment (e.g., isolated axial back pain for microdiscectomy or multiple revision surgeries) or an inappropriate surgical approach (e.g., inadequate decompression) can increase the risk of developing FBSS.6 Patients with previous back surgeries have a lower chance of pain relief following surgery and a higher chance of developing FBSS.8 Surgical: operating at the wrong vertebral level or operating at a single vertebral level when the pain generators are multiple levels can lead to poor pain relief.6,8 Lumbarization of the sacral vertebra or sacralization of the lumbar vertebra can lead to operating at the incorrect level. Poor surgical technique is also significant factor in the development of FBSS, especially if there is inadequate decompression at the lateral recess or neural foramina.14,15 Conversely, spine instability may occur if > 33% of the bilateral articular or 100% unilateral articular surfaces are removed.14 Minimally invasive techniques with limited exposure can increase […]