Disorders of Consciousness
[…] projections to the cortex may enhance cognitive and physical function. Other potentially efficacious, although unproven, treatments include median nerve stimulation, spinal cord stimulation, intrathecal baclofen and extradural cortical stimulation. Gaps in the Evidence- Based Knowledge Treatment effectiveness of many modalities […]
Lumbar Spondylosis Without Myelopathy/Radiculopathy
[…] zygapophysial joints (z-joints) of the lumbar spine. Degenerative lumbar spondylosis is a term used to describe a “mixed group of spinal bone diseases related to degeneration of the lumbar motion segment and associated pathologies.”30 The term spondylosis is not used as a clinical diagnosis but rather as a term to illustrate spinal pathology. Spondylosis may be associated with low back pain (LBP) and is associated with numerous spinal pathologies including spinal stenosis (narrowing of the spinal canal), vertebral instability, degenerative spondylolisthesis, osteoarthritis and malalignment.29 Etiology Though the etiology of lumbar spondylosis remains unclear, many have characterized it as osteoarthritis of the spine. It is thought to result from cumulative stresses combined with repetitive microtrauma, leading to an imbalance between the synthesis and degeneration of cartilage. When combined with increased stresses placed on the vertebrae and ligaments, osteophytes and calcifications occur, respectively.1,3 Bone spurs, also known as osteophytes, most commonly occur along the anterolateral aspect of the lumbar vertebral body. Posterior vertebral osteophytes are rare but can cause impingement on the nerve roots or spinal cord. Lumbar spondylosis can also occur due to new bone formation in areas where the annular ligament is stressed over time.29 Epidemiology including risk factors and primary prevention The prevalence of radiographic spondylosis increases with age.4,5 It is present only in a small percentage of the population in the first few decades of life but is relatively common by the age of 65. In those with LBP, the prevalence ranges from 7% to 75%, depending on the diagnostic criteria.6 Despite its frequency in patients with LBP, there is no validated correlation between the radiographic findings of lumbar spondylosis and presence of LBP. In the United States, approximately 80% of individuals older than 40 years old were found to have lumbar spondylosis, contrasted to3% of individuals aged 20-29 years.5 Recent studies have shown a positive correlation with the CC genotype of the transforming factor B1 gene and postmenopausal women.31 Risk factors Age is the greatest risk factor for lumbar spondylosis, but other risk factors including disc desiccation, previous injury, joint overload from malalignment and/or abnormal z-joint orientation, as well as genetic predisposition have been identified.2 Studies evaluating the role of body mass index, level of activity and gender on the incidence and severity of lumbar spondylosis do not show a clear correlation.5,7 Patho-anatomy/physiology Some investigators believe that lumbar spondylosis is due to a “degenerative cascade” that is initiated by intervertebral disc desiccation.8 The degenerative changes which characterize lumbar spondylosis are thought to be due to cumulative stresses on the annular ligaments which then form (i.e., marginal osteophytes).29 Failure of annulus and nucleus collagen cross-linking and the discs’ inability to retain water results in stiffening of the cartilaginous and capsular structures, further restricting z-joint mobility causing earlier and more advanced degenerative changes. This is particularly true at the L4/L5 and L5/S1 levels likely because of their proximity to the fused sacral segments.1,3 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Although variable, most patients experience a benign clinical course. Studies have shown the following: radiologic spondylosis directly increases with age, irrespective of pain.9 spondylosis was shown to be equally present in those with and without LBP.2 no correlation between the magnitude of z-joint arthropathy and the severity of pain.6 Thus, progression is variable and unpredictable, and therefore difficult to study, but seems to be most closely linked to aging. Specific secondary or associated conditions and complications Z-joint hypertrophy in combination with ligamentous redundancy from disc desiccation may contribute to central canal, lateral recess and neuroforaminal stenosis. The increase in translational forces from disc desiccation, combined with the z-joints’ decreased ability to resist these factors, may also result in spondylolisthesis. Clinically, these changes can cause lumbosacral radiculopathy and neurogenic claudication. Disuse atrophy of the erector spinae and multifidi muscles secondary to pain-limited spine motion can also occur. Essentials of Assessment History As mentioned previously, lumbar spondylosis refers to certain radiographic findings that do not rely on clinical symptoms for diagnosis. However, in some patients with acute, subacute or chronic LBP, the radiological changes which make up lumbar spondylosis can be potential pain generators. Patients with lumbar spondylosis often complain of axial lumbosacral back pain with potential nociceptive input from the sacroiliac joints, overlying myofascial structures, intervertebral discs, nerve roots, and facet joints.30 Pain may refer unilaterally, bilaterally, or to the contralateral buttock, hip, groin and thigh regions; although, typically, it does not extend past the knee.6,10 The pain tends to worsen with extension, rotation and standing and is better with lying down and lumbar flexion.10 By definition, the term lumbar spondylosis is not associated with a neurologic deficit. However, spinal stenosis, spondylolisthesis, lumbar disc herniation and radiculopathy are known to be associated with neurological deficits. This is why it is imperative for the clinician to ask about weakness, gait and balance and bowel/bladder function when assessing patients with lumbar spondylosis. There are several validated outcome measures for grading functional limitations including the McGill Low Back Pain Scale, Oswestry Disability Index and the Medical Outcomes Study 36-Item Short-Form Health Survey.11 These should typically be administered at every office visit for following the patient’s progression. Physical examination A systematic review revealed that most physical exam maneuvers have limited or no diagnostic validity for spondylosis.6 Paraspinal tenderness is the only physical exam maneuver that seems to correlate with z-joint arthropathy, but not with high diagnostic confidence. Although classically felt to diagnose z-joint pain, joint loading with pain on extension and ipsilateral rotation has not been shown to consistently correlate with spondylosis.12,13 The pain distribution of lumbar spondylosis may overlap with other clinical entities. A comprehensive physical exam that includes evaluation for radiculopathy, including dural tension signs, as well as hip and sacroiliac joint provocative maneuvers can help guide clinical decision making. Neurologic deficits seen with lumbar nerve root compression should be evaluated through muscle, sensation, reflexes, gait, and balance testing. Discogenic pain is exacerbated when the patient is asked to repeatedly bend forward or when the patient is sitting up and one leg is placed in a flexed position by the examiner. Laboratory studies Although laboratory studies are not routinely indicated, C-reactive protein, sedimentation rate, and a complete blood count, may be ordered if there is clinical suspicion for conditions such as malignancy, infection or rheumatologic disease. Imaging Lumbar spondylosis is visible on multiple imaging modalities, including plain radiographs, magnetic resonance imaging (MRI) and computed tomography (CT) studies. However, as spondylosis on imaging does not constitute a cause for LBP, imaging is typically ordered to rule out other disorders.13,14,15 Plain radiographs are not sensitive for detecting early z-joint arthropathy or spondylosis but are often obtained. Lateral views are important for sagittal alignment and to assess for spondylolisthesis. If present, patients should undergo flexion and extension radiographs to rule out segmental instability which may necessitate earlier surgical consultation. MRI is generally not needed but is useful for evaluating the soft tissues and neural elements within the spine, especially to rule out neuroforaminal stenosis in patients with concomitant leg pain. The presence of small amounts of fluid or synovial cysts within the z-joints may be physiologic or may represent instability and/or infection within the lumbar spine, and therefore would warrant further work up and/or treatment. However, this is beyond the scope of this article. CT is typically utilized when an MRI is unobtainable, if fracture is suspected or for the assessment of pseudoarthrosis. It can also be helpful in identifying synovial cyst borders with implications for surgical vs percutaneous treatment.34 Supplemental assessment tools Diagnostic Injections Given the low correlation of radiographic spondylosis with axial low back pain, the only means for an accurate diagnosis of symptomatic lumbar spondylosis secondary to facet arthropathy are controlled diagnostic blocks of the medial branch nerves that innervate the z-joints.16 This assumes that the patient’s pain generator(s) are the z-joints and not the intervertebral discs. Each z-joint has dual innervation from the medial branch of the dorsal ramus of the spinal nerve at the corresponding level and the level above. To treat the pain associated with a specific z-joint, both nerves must be targeted. Several key principles exist for diagnostic medial branch blocks: Because of the inaccuracy of landmark guidance, all blocks should be performed utilizing image guidance. Both fluoroscopic and ultrasound guidance have been described in literature.34 False positive blocks occur at a high rate of 17% to 41% in the lumbar spine, thus necessitating a second control block for confirmation of the diagnosis. Ideally, the two injections should be performed with anesthetics of differing duration. Concordant pain relief (>1h with lidocaine and >3h with bupivacaine hydrochloride), greatly enhances the sensitivity and specificity of the injections.13 The greater the percentage of pain relief […]
The Philosophical Foundations of Physical Medicine and Rehabilitation
[…] neck pain, brain injury including concussion, chronic pain, complex wounds, congenital disorders, industrial and work injuries, muscle and nerve disorders, spinal cord injury, sports injury, and stroke.1 Board-certified physiatrists have many opportunities for primary and subspecialty certification. The ABPM&R’s seven subspecialty certification […]
Steroids and Corticosteroids
[…] adverse events when used for axial spine injections, including blood vessel injury or spasm, or even embolization through vessels causing spinal cord infarction. Methylprednisolone has significantly higher percentage of large particles and may occlude vessels. Light microscopy studies have demonstrated that the particles in these steroid preparations are either larger than red blood cells or form aggregates larger than red blood cells9. Triamcinolone preparations have an intermediate particle size and betamethasone has the smallest particle size of the particulate steroids9,10. Chart 1: Potency, Solubility and Preparations* Steroids-and-Corticosteroids-Chart-1Download Indications Steroids are frequently used both for diagnostic and therapeutic purposes and to control inflammation when more conservative measures (i.e. NSAIDs, rest, ice, compression, elevation, physical therapy) have been exhausted6. Typically, steroids can provide short-term pain relief (from weeks to months); few injections are associated with long-term relief of symptoms. Studies support the use of corticosteroid injections for carpal tunnel syndrome, trigger finger, de Quervain’s tenosynovitis, and bursitis and tenosynovitis associated with rheumatic diseases. The role of corticosteroid injectables for rotator cuff disease is unclear12. The use of injectable corticosteroids has shown to provide short term pain relief for subacromial impingement syndrome, adhesive capsulitis, medial and lateral epicondylitis, and hip or knee osteoarthritis13. Although spinal steroid injections are commonly used for treatment of axial pain due to traumatic or degenerative conditions, the US Food and Drug Administration (FDA) has not approved any drug for spinal injection to treat neck and back pain. FDA requires the addition of a Warning to the drug labels of injectable corticosteroids to describe the risks of rare but serious adverse events, including loss of vision, stroke, paralysis, and death14. Contraindications A steroid injection is contraindicated in the setting of overlying soft tissue infections, sepsis, bacteremia, anatomic inaccessibility, an uncooperative patient, articular instability, septic arthritis, avascular necrosis, osteonecrosis, periarticular fracture and Charcot joints. A joint with a surgical implant would be a relative contraindication6. Precautions should be taken with patients with diabetes mellitus, as part of their picture of overall comorbidities. The American Academy of Orthopedic Surgeons15, American College of Sports Medicine16, American Diabetes Association17, and American Medical Society for Sports Medicine18 do not have established recommendations with regards to steroid injections in patients with diabetes mellitus. However, precautions should be taken after an injection is performed. Transient increases in post-injection blood glucose levels (BGL) were noted in ten studies. Mean blood sugar elevations have ranged from 125 to 320 mg/dL with peak post-injection BGL occurring within 1 to 5 days. BGL returned to baseline within 10 days and usually in less than 24 hours. Patients with Type1 DM or insulin-dependent diabetes mellitus (IDDM) had higher post-injection BGL than those with Type 2 DM not requiring insulin in two studies. Patients with HgA1C >7.0% had BGLs that were higher and lasted longer than those with lower HgA1C levels. Although none of the studies […]
Environmental Assessment
[…] 2004; 31(4): 946-960. Tamayo, N., Zuziak, N., Conetsco, S., Zillich, N., Lash, A., Kuemmel, A. A Checklist for Travel for Spinal Cord Injury Patients: A Pilot Project. American Spinal Cord Injury Association Annual Meeting. September 2018; New Orleans, LA. Zuziak, N., Oboudiyat, […]
Anticonvulsants
[…] pain Side Effects: Dizziness, sedation Major Clinical Pearls: Decrease dosing in patients with renal insufficiency Indications: Post-herpetic neuralgia, diabetic neuropathy, spinal cord injury associated pain10-12 Zonisamide: Mechanism of Action: Blocks T-type calcium channels and sodium channels, which increases the release of GABA […]
Contractures
[…] injury developed contractures between 16% and 81%.6 60% of stroke, 36% of cerebral palsy, and about 11 to 48% of spinal cord injury patients develop some form of joint contracture.7 Children who have an obstetric brachial plexus injury were found to have […]
Geriatric Gait and Balance Disorders
[…] or atrophy Osteoarthritis Podiatric conditions Spasticity or contractures Central Neurologic disorders Cerebellar dysfunction or degeneration Cerebral palsy Cervical spondylosis Cervical spinal stenosis Delirium Dementia Huntington’s disease Lumbar spinal stenosis Microvascular white matter disease Multiple sclerosis Muscular dystrophy Myelopathy Normal-pressure hydrocephalus […]
Injectable Agents
[…] femoral nerve.4 Intrathecal systems are used for long-term symptomatic management of malignancy-related chronic pain or in spastic hypertonia caused by cerebral palsy, spinal cord injury, or brain injuries.5 Table 1. Locations and Types of Commonly Used for Injectable Agents Intrathecal Intramuscular Intravenous Perineural Intraarticular […]
Influence of Psychosocial Factors on Illness Behaviors
[…] and act on their symptoms.1 Illness behavior has been studied in many health conditions,2–5 including: musculoskeletal injuries, traumatic brain injury, spinal cord injury, heart disease, immune disorders, and cancer. Psychosocial factors affect both psychological as well as physical functioning over time5 which can lead to either adaptive or maladaptive illness behaviors. Classes of adaptive illness behaviors include: Active coping (in contrast to passivity, avoidance, or prolonged emotions) Social support Patient optimism and use of humor Positive cognitive appraisal and acceptance (versus negative appraisal such as catastrophizing). The issue is complex, however, because coping behaviors vary among health conditions. Maladaptive coping for some conditions may be adaptive in other diseases.5 For example, denial, stoicism, emotional coping (e.g., emotional release, problem-solving emotional reactions), or cognitive avoidance6 may be adaptive in spinal cord injury and cancer but in other conditions might be counter-productive. Therefore, one large clinical challenge is to identify the specific coping behaviors that could be productive for any given patient. There is mounting evidence that chronic low grade inflammation triggers changes that contribute to the mental and physical ill health of patients with major depression.7 Relevance to Clinical Practice Understanding that there are psychological associations between certain ailments, such as musculoskeletal disorders and anxiety and depression,8,9 may help to guide the clinician in their approach. Studies have shown that clinicians need to be more sensitive towards patients’ psychological concerns.8 In addition, “psychological assessment and assistance from a mental health professional should be considered during the hospital stay and rehabilitation period.”8 Patients with traumatic brain injury (TBI) are shown to have higher rates of psychiatric illness and poor psychological health, especially during the first 3 years post-injury.10 Decreased independence with activities of daily living (ADLs) is associated with poor psychological health.10 Areas most effected are “vitality, role limitations at work, school or home due to emotional problems and social functioning.”10 Few TBI patients receive any mental health treatment post-injury,10 further emphasizing the need to address these psychosocial issues in patients undergoing rehabilitation. The coping patient General coping behaviors, which are typically considered beneficial to many patients, and in various diseases, include:3,11 Optimal use of medications and health resources Exercise Optimal sleep hygiene Anxiety/arousal reduction (e.g., by breathing control, biofeedback) Activity pacing Body mechanics Control over interpersonal behavior (e.g., irritability) Return to roles (e.g., work, avocations, parenting, spouse), and Actions by “significant others” that enable or prompt those behaviors and others (e.g., weight reduction, social outings, distraction, diet). Resilience: Resilience, in the context of a disease process with chronic effects and associated long-term disability, is conceptualized as the person’s ability to cope with and effectively adapt to changed circumstances and continue to engage in meaningful activities and maintain quality of life. In the RISE Model of Resilience, factors including intrapersonal factors (e.g., coping, personality), interpersonal characteristics (e.g., relationship quality and social support) that influence the development and expression of resilience, and socio-ecological influences (e.g., accessibility, cultural attitudes) play a part in coping and provides an important framework to guide intervention development and research as well as clinical practice.12 Cognitive-behavioral approaches involve combining: patient training in these coping behaviors conceptual training on the interactive nature of symptoms, feelings, behaviors, and thoughts, to help shift attention to behavior and thinking, and training in general problem solving principles to help with stress management.13 For example, patients may be encouraged to use a step-by-step approach to social problems, to address one aspect of illness at a time, and to break down overwhelming problems into manageable parts.14–16 A major objective of cognitive-behavioral approaches is health self-management. The Common-Sense Model of Self-Regulation (the “Common-Sense Model”, CSM) is a widely used theoretical framework that explicates the processes by which patients become aware of a health threat, navigate affective responses to the threat, formulate perceptions of the threat and potential treatment actions, create action plans for addressing the threat, and integrate continuous feedback on action plan efficacy and threat-progression.17 What is “abnormal” illness behavior? Pilowsky18 described “abnormal” illness behavior to involve “an inappropriate or maladaptive mode of experiencing, perceiving, evaluating or responding to one’s own state of health which persists despite the fact that a doctor (or other appropriate social agent) has offered an accurate and reasonably lucid explanation of the nature of the person’s health status and the appropriate course of management (if any), with provision of adequate opportunity for discussion, clarification and negotiation based on a thorough examination of all parameters of functioning …”2 By this definition, illness behavior is only abnormal if the physician has a sufficient understanding of the presence or absence of potentially relevant pathology and its implications for symptom generation, disability, and methods of recovery. Illness behavior is not abnormal if the patient is not given sufficient chance to understand what is present and absent with regard to pathology and how it could cause their symptoms and functional limitations. It is not abnormal until the specific illness behaviors that they can adopt to “normalize”19 (meaning sufficiently improve), their coping have been described or demonstrated. Steps to address illness behavior Assess the patient’s understanding of the pathology, nature and prognosis of disease By providing a thorough medical work-up, the patient, clinical team, and system decision makers (e.g., insurer, employer) can be provided with the most meaningful medical determination of medical causes that might contribute to the patient’s distress. Assess the patient’s perception of their disease When patients chronically perceive their diagnosis as worse than is actually is, it is known as catastrophization, a maladaptive social coping mechanism,5,20 and can enhance impairments related to the diagnosis. It is important to note that “catastrophizing has been shown to be the strongest and most consistent psychosocial factor associated with pain and dysfunction” in patients with chronic pain.5 In a number of studies, pain catastrophizing was identified as a significant predictor of chronic pain persisting >3 months following orthopedic surgery. In a systemic review of literature, there was moderate-level evidence for pain catastrophizing as an […]