Nerve Conduction Studies
[…] tibial nerve behind the knee. The H-reflex is orthodromic – starting with sensory fibers that travel proximally, synapsing in the spinal cord, reflexively triggering an AP in motor neurons that travel distally, where the recording electrode obtains the waveform. The H-reflex is typically used to test proximal S1 segments, but also has utility in the assessment of C6 or C7 radiculopathy by evaluating the C7 spinal reflex arc at the flexor carpi radialis. In contrast, an F-wave is a pure motor study and generated from a supramaximal stimulation of distal motor neurons. The AP is transmitted proximally in an antidromic direction through a motor neuron to the spinal cord. In the spinal cord, the motor neuron synapses with an interneuron, which then sends the signal orthodromically back down the same motor nerve where the stimulus originated. The arrival of the signal at the distal muscle is seen at the recording electrode. F-waves are commonly obtained from ulnar, median, fibular (peroneal), and tibial nerves, but can be obtained from any peripheral nerve in the body that can be stimulated by the nerve stimulator. They have variable latencies, amplitudes and morphologies and may not appear with each stimulus but will generally fall within a set timeframe in healthy patients. Common errors affecting accuracy Above all else, technical errors can impact the accuracy of NCS findings. Examples include incorrect electrode placement, measurement errors, poor instrument maintenance, or the incorrect use of filters on the recording equipment. Operator error should be an electrodiagnostician’s first thought when unusual findings are recorded. Decreased temperature leads to delayed Na+ channel inactivation and prolonged depolarization, which results in a larger voltage change and an increase in CMAP and SNAP signal amplitudes. The delay in Na+ channel inactivation will delay AP propagation and saltatory conduction, thus delaying onset response latencies and conduction velocities.1 These effects tend to be more prominent in SNAPs than in CMAPs. A lack of supramaximal stimulation can lead to artificially low signal amplitudes.5 Too intense of a stimulus can lead to co-stimulation of adjacent nerves through volume conduction of the electrical signal in tissues, which may lead to artificially high signal amplitude or faster conduction velocities. A common indicator of volume conduction is a sudden change in waveform morphology from its traditional pattern after the stimulus intensity has been increased. One typically sees this change after reaching maximum amplitude and increasing the intensity beyond supramaximal stimulation. However, in smaller or leaner patients, volume conduction can also occur at low stimulus intensities. In addition, too intense of a stimulus can enlarge the area of depolarization, leading to nerve activation further distal to the cathode at the time of stimulation, resulting in a decreased distal/onset latency.5 Improper electrode placement can lead to error for several reasons. If the G1 is not placed over the motor point, the amplitude will be artificially lowered, which could be misconstrued as an axonal problem. One may also see an initial positive deflection or variation from the typical waveform as evidence of an improperly placed G1 electrode. Additionally, in sensory studies, if G1 and G2 are too close or too far away, the resulting waveform can be affected. Stimulating with the cathode distal to the anode can also produce error. This mistake, termed polarity reversal or anodal block, can artificially prolong latency and decrease conduction velocity measurements.6 Failure to account for patient height, weight, age and gender can also result in false positive or false negative results error. Longer nerves, in general, have slower conduction velocities due to the smaller diameter of the nerve as they taper distally. Taller individuals may have slowed conduction velocities due to more tapering of the nerve and the tendency of recording NCS distally in the limbs. Furthermore, longer limbs tend to be cooler than shorter ones due to the physical limitations of euthermia resulting from arterial and venous flow.1 Obesity can also cause technical challenges. NCSs are more difficult to obtain in obese individuals, due to signal attenuation between the nerve and the skin’s surface where the stimulus originates. Conduction velocities tend to slow with age. If using reference values for younger individuals, these velocities could be artificially construed as prolonged. The NDTF data takes into account all these factors.4 Anomalous innervations can also contribute to errors. Without prompt recognition, the presence of an accessory peroneal nerve, Martin-Gruber anastomosis (a median to ulnar anastomosis in the forearm) or other anatomic variation can lead to the false interpretation of normal findings as pathologic.1,5 Neuropathology – NCS correlation Nerve conduction studies are commonly used to evaluate for specific nerve injuries or entrapments, but can also help with the diagnosis of polyneuropathies, myopathy or NMJ disorders. Lesions of the motor or sensory axon typically result in loss of CMAP and SNAP amplitudes. Decreased distal latency and conduction velocity is only seen when there is severe large fiber loss. While postsynaptic NMJ disorders tend to have normal latencies, amplitudes and conduction velocities, presynaptic NMJ disorders have variable CMAP amplitudes. Lesions affecting myelin result in slowed conduction and can present with prolonged distal latencies for distal entrapments. Another feature of diseases or injuries to myelin is conduction block, which is defined as a drop in the amplitude during stimulation proximal to the lesion, but a normal amplitude on distal stimulation.7 This finding indicates that some of the individual axon’s impulses fail to traverse the area of injury, although that nerve is still alive, viable and able to be stimulated distal to the site of entrapment. Temporal dispersion may also occur with demyelinating lesions. When some axons have slowed APs through a region and others conduct normally, the resultant waveform is one that is wider due to a larger difference between the conduction of the fastest and slowest fibers. Moreover, the spreading of AP velocities results in a lower amplitude, as the APs through the various nerves in the axon arrive at G1 at variable times and do not summate as they would if arriving at a more uniform time.1,5 Relevance to Clinical Practice There is a wide variety of potential nerve conduction studies available for each patient. A history and physical examination prior to performing the study will lead to a differential diagnosis. The differential diagnosis will guide selection of appropriate sensory and motor nerve conduction studies as well as possible evaluation of proximal responses. Performing a routine nerve conduction “screen” is inappropriate as selection of specific studies should be tailored to each individual patient.8,9 Electrodiagnosticians should never lose sight of the fact that the NCS and EMG are an extension of their physical exams. NCSs are not diagnostic in isolation and should be accompanied by needle EMG.9 Using NCSs to make a diagnosis requires a detailed understanding of the history, physical exam, and interpretation of NCS and EMG findings.10 Nerve conduction studies are useful in evaluating for generalized neuropathies. In axonal neuropathies, the primary abnormality will be the loss of SNAP and CMAP amplitudes with proximal or distal testing. Prolongation of distal latency or decrease in conduction velocity will only occur after extensive large fiber loss and is only a secondary feature. In acquired demyelinating neuropathies, salient nerve conduction findings include prolonged distal latencies, decreased conduction velocities, and the presence of conduction block with proximal stimulation. Loss or prolongation of F-wave latencies and H-reflexes, as well as temporal dispersion, may also be seen. In congenital demyelinating neuropathies, similar findings are seen but without the features of conduction block or temporal dispersion. The most common generalized neuropathy is diabetic peripheral neuropathy. While the entirety of the disease is beyond the scope of this review, there have been advances in the literature as it relates to NCS usage. First, an A1c >9% and the presence of neuropathic pain show a strong correlation with NCS pathology.11 Second, the development of pathology in […]
Infectious Encephalopathies and Leukoencephalopathies
[…] involvement is widely variable, including meningitis, encephalitis affecting variable areas of the brain–mostly subcortical white matter and deep gray matter, spinal cord involvement with transverse mellitus, or it may present as Guillain-Barre syndrome (GBS).15 In St. Louis encephalitis, the vast majority of the infected elderly develop actual encephalitis, while infection in those younger than 20 years old have presentations equally distributed between meningitis and encephalitis.16 John Cunningham virus (JCV) is a polyoma virus that infects the oligodendrocytes causing sub-acute demyelinating disease.17It rarely affects neurons and spares astrocytes. WNV fever can cause meningitis and encephalitis and may also affect the anterior horn cells, leading to flaccid paralysis, sometimes involving the diaphragm. It presents with a picture of axonal loss with no evidence of demyelination similar to polio.18,19 Other presentations can include spastic cervical myeloradiculopathy with severe clonus, pain, brainstem signs, and loss of VIII cranial nerve function.20 Natalizumab for the treatment of multiple sclerosis (MS) was associated with more than 30 cases of progressive multifocal leukoencephalopathy (PML) and was almost pulled from the market by the FDA.20In one study there were 100 reported cases of non-Hodgkin’s lymphoma treated with rituximab that also developed PML.21 More recently measles has reemerged as a cause of encephalitis due to declining vaccination rates.22 With Dengue, rash can present with a low platelet count and low white blood cell count (WBC).10 HHV-6 has a predilection for the medial temporal lobe and the limbic system of the brain leading to the clinical picture of short-term memory loss, seizures and sleep disturbance.8 CMV infection has been reported to lead to a reversible encephalopathy and poly-radiculopathy.1-4 Only one out of 300 exposed to Japanese encephalitis or St. Louis encephalitis virus infections end up developing clinical manifestations.18 California encephalitis primarily affects children but results in a very low mortality and morbidity rates.1,10 Prion encephalitis, when detected, is almost invariably fatal.3,4 There have been three proposed hypotheses for the pathophysiology of how encephalitis can be caused by COVID-19, including direct invasion of the virus into the brain parenchyma; systemic inflammation due to activation of the innate immune system and release of large amounts of inflammatory cytokines; and cross-reactivity of host antibodies and lymphocytes via molecular mimicry.7 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Disease Progression/Phases/Trajectory The natural course of the disease is often very variable depending on the infecting agent, age, and immune status of the patient. A 2-week viral prodrome/incubation state is common in many etiologies due to infections. The diagnosis of the cause of the encephalitis is important as it impacts the prognosis, progression and rehabilitation potential as well as the long term course of recovery. Important acute treatment principles for patients without a definitive diagnosis include the following: In herpetic encephalitis the mortality without IV acyclovir treatment can be nearly 70%. Early treatment with IV acyclovir level (A-I) is the only parameter known to lower morbidity and mortality in herpetic encephalitis.23Hence, treatment of all patients suspected of having encephalitis should be first started on acyclovir until the workup has progressed further. Post-infectious autoimmune encephalitis can cause significant damage beyond the infection itself. Aggressive management of this condition is needed once the infection is controlled. These treatments include:24 Steroids (usually intravenous methylprednisolone) are often the first-line therapy. Intravenous immunoglobulin (IVIG) is used but can cause aseptic meningitis as well. Plasma exchange has been useful in some case series. Rituximab and cyclophosphamide are also utilized in some cases. Both require long term surveillance over time for malignancy.24 Specific secondary or associated conditions and complications encephalitis Different infectious etiologies lead to different secondary conditions. Seizure Disorder: Viruses that have predilection for cerebral cortex, especially those involving the frontal-temporal and parietal lobes like HSV and HHV-6, are more likely to cause seizures. Infections that involve white matter or deep brain structures such as WNV or PML are much less likely to cause seizures.23 Movement Disorders: Parkinsonism, choreoathetosis, myoclonic jerks and dystonia are seen in infections of the basal ganglia and deep grey matter associated with St. Louis encephalitis and Japanese encephalitis.25 Cranial nerve involvement with facial weakness, paranesthesia, and/or ptosis is very common with WNV18and Japanese encephalitis. Flaccid paralysis is usually due to axonal injury and anterior horn cell involvement in WNV12 GBS has been reported in some cases of EBV and also with HIV encephalitis in cases that are predominately demyelinating.15,18,21 Visual disturbance, such as alien hand phenomenon, has been noted in some cases of non-HIV PML which involves the subcortical occipital area of the brain.26 Communicating hydrocephalus, as noted by cognitive changes, ataxia and incontinence, can be a late occurrence in all causes of encephalitis.1 Many of these patients will have problems with cognitive, behavioral, and motor disorders, similar to patients with traumatic brain injury (TBI). Similar management is recommended for these problems. Depression and anxiety are very common in HHV-6 infection due to involvement of the limbic system.27 Acute Zika virus infection presents with pruritic rash, retro-orbital pain, diarrhea, nausea, malaise, joint problems, and headaches.11 More recently there have been increased reports of patients presenting with GBS, acute myelitis, viral meningoencephalitis and sensory neuropathy.11,28 Congenital anomalies, especially microcephaly, have been frequently reported due to acute Zika virus infection of pregnant mothers.28 Complications due to encephalitis secondary to COVID-19 that have been reported in the literature include seizures, sleep disturbances, hallucinations, language and cognitive deficits, and stroke.29 Essentials of Assessment History A comprehensive history of patients with suspected encephalitis should include assessment of the premorbid functional, vocational, medical and social status, along with a detailed history of focal and generalized neurologic impairments, including seizures. Specific details pertaining to diagnosing potential treatable causes of infectious encephalitis include1: Exposure to mosquito or tick bites as seasonal risk factors. Impaired immune status of the affected individual such as HIV infection with documented CD4 count trends. Duration of time between symptom onset and treatment. Presence of documented increased intracranial pressure, seizures or hydrocephalus during the acute hospital stay.1,23 Any recent travel history to high risk areas for some types of infectious agents. Physical examination The clinical presentation ranges from obtunded encephalopathy to more specific focal neurological deficits. A detailed neurological examination should include assessment of mental status and overall orientation. In severely obtunded patients, one should rule out subclinical seizures with the use of EEG.1 Cranial nerve exam should be performed, including ophthalmologic exam evaluating for any signs of raised intracranial pressure. Manual muscle testing may reveal findings consistent with polyradiculopathy, axonal loss, or demyelinating lesions. Skin rash can raise suspicion for a bacterial cause of encephalitis/meningitis (Neisseria meningitis), which is important to diagnose early since it is acutely life-threatening requiring contact isolation and usually responds very well to intravenous (IV) third-generation cephalosporin.1 Functional assessment Assessment should include a detailed motor and sensory examination as well as a cognitive examination. Cognitively, at a minimum, a mini-mental status examination is required. If this is abnormal, a more detailed cognitive battery utilizing the measures commonly employed after brain injury medicine is useful.30-32The supplemental assessment tools often mentioned in the literature for patients with impaired consciousness from encephalitis included the orientation log (which carries same clinical value as the Galveston Orientation and Amnesia Test),30the cognition-log,31as well as the Coma Recovery Scale-Revised.32,33 The Functional independence measure (FIM), including all 18 components assessing cognitive and physical function, is often administered during inpatient rehabilitation for these patients. Laboratory studies All patients should to be tested for syphilis and HIV as these are very treatable causes of encephalitis. Specific assessment tools for infectious encephalitis can include CSF and serum viral load in cases like HSV, and VZV, and following the CD4 counts in HIV patients.1 CSF analysis should be obtained in all patients with suspected encephalitis. A pleocytosis (10-2,000 cells/μL) with lymphocytic predominance, an elevated protein and normal to mildly low glucose level associated with a negative Gram stain and bacterial cultures suggests a viral encephalitis. Any time infectious encephalitis is suspected, polymerase chained reaction (PCR) studies of the CSF should include viral DNA studies for HSV, WNV, VZV, EBV, CMV, HIV, and SARS-CoV-2. These tests are highly specific when positive, but they are not very sensitive. Virus-specific CSF to serum IgG ratios should be obtained as a high ratio indicates an infection of CSF. For herpes viruses one should test for CSF immunoglobulin M (IgM) as IgM does not pass through the blood-brain barrier. Serums studies should include serology for WNV, EBV, mycoplasma, borrelia, rickettsia, coccidiosis and histoplasma infections.1 The common EEG picture with encephalitis is not very different from that of encephalopathy with generalized slowing, but in cases of HSV encephalitis focal abnormalities involving the temporal lobes are commonly found. EEG is valuable in evaluating an obtunded patient with encephalitis to rule out subclinical status epilepticus.1,23,24 Imaging Acute assessment should include a head computerized tomography (CT) to rule out any space-occupying lesions and contraindications to lumbar puncture with elevated intracranial pressure. Magnetic resonance imaging (MRI) is the diagnostic tool of choice in patients with encephalitis,1 with variable T2 lesions corresponding to different etiologies. For example, HSV commonly involves the frontal-temporal lobes and it’s almost never seen outside the frontal-temporal areas alone. WNV fever does not usually have any prominent MRI findings. Varicella zoster (VZV) vasculitis presents with multiple areas of hemorrhagic infarction while progressive multiple leukoencephalopathy (PML) causes primarily demyelinating lesions.26 Early predictions of outcomes The most significant early predictor of better outcome is the early administration of IV acyclovir in the case of HSV encephalitis and for this reason all patients with suspected encephalitis should be started on acyclovir pending further studies.1,23The type of infectious agent can predict long-term complications and outcome. For example, clinically symptomatic encephalitis due to Japanese or St. Louis encephalitis have a low incidence of permanent neurologic deficit, they do have a higher prevalence of long-term neurological dysfunction than that seen with California encephalitis.1,10 Cognitive impairment in patients with PML and low CD4 counts associated with HIV infection is usually progressive, irreversible, and ends with dementia.26,34 Worse outcomes are expected with secondary complications such as intraparenchymal hemorrhage in cases of VSZ CNS vasculitis and in cases of severe intracranial edema with Herpes encephalitis.1,27 Zika is associated with congenital anomalies with an increased risk for microcephaly due to infection of the mother affecting the fetus. Other possible fetal problems from Zika infection can include cardiac disorders, hearing loss, blindness, spinal cord lesions, and birth defects, with infection in the first trimester conferring the highest risk.28 Environmental As with any patient with neurological impairment, accommodations have to be provided for patients, ranging from supervision to home care for those with cognitive impairments. The utilization of assistive devices and orthotics and physical assistance for those with primarily motor weakness should be obtained early on. For caretakers of these patients it should be stressed that the viral etiologies of encephalitis are not routinely contagious, so patients need not be under contact isolation. Caretakers need not worry about close physical contact with their dependent patients. Social role and social support system Etiologies like Japanese and California encephalitis mostly affect children, resulting in need for special accommodations at home/school and playground. Some of the tick-mediated infections can affect otherwise healthy functioning and employed adults causing issues pertaining to long-term loss of productivity and work. Patients and their families require education regarding how long it may take for recovery, if ever. Similar to patients with TBI, prognosis may be difficult to make in the first 6 months. Rehabilitation medicine treatment issues on initial evaluation Given the high rate of misdiagnosis in the acute setting, which can be up to 2/3 of the initial cases, rehabilitation physicians need to be versed in evaluating the diagnosis. A delayed diagnosis carries significant implications related to the potential therapeutic windows of antivirals. The earlier treatments such as acyclovir in the case of HSV and VZV,1,34,35 or ganciclovir with foscarnet in CMV encephalitis1,27are initiated the better the potential outcome. A proper diagnosis is also necessary for planning rehabilitation goals, family education and training as well as for discharge planning. In addition, risk stratification for patients with MS encephalitis, should be screened for PML particularly for anyone to be treated with natalizumab.15 Rehabilitation Management and Treatments Available or current rehabilitation treatment guidelines Given the relatively low incidence of encephalitis, rehabilitation studies are sparse, consisting mainly of case reports. Some medications used for other neurologic disorders have been tried for encephalitis. As an example, the utilization of dopamine agonists such as amantadine may improve alertness and arousal.34,36 There are reports of utilizing dopamine agonists to improve cognitive function in encephalitis when deep grey matter structures are involved, as in the case of St. Louis and Japanese encephalitis.37 The utilization of donepezil may be helpful for short-term memory loss and aphasia commonly seen in WNL, PML and HHV-6 similar to brain injury.36 Sertraline for prevention of depression and potential improvement of motor recovery may be helpful, especially in those illnesses that involve the limbic system and deep white matter like HHV-6, PML and WNL.38 There is some evidence for benefits of cognitive rehabilitation for short-term memory and amnesia in post-viral encephalitis.39More recently there have been reports of SSRI medications such as fluoxetine linked to improved motor recovery in brain injuries associated with stroke.40 Coordination of care Close coordination of care with the infectious disease specialist, primary care physician, local infection control agencies (as some cases have to be reported to the CDC), and neurologist, along with the rest of the rehabilitation team, is of great importance. Coordination with community integration (schools, vocational, geriatric) resources and support groups should be maximized. Patient & family education Patient and family should be educated about the prognosis and potential long-term complications and need for long-term assistance for the affected individual. The potential progressive nature of some diseases such as PML26or prion disease17 should be well discussed with families and care-givers. Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills Risk stratification for patients with MS, including serologic testing for JC virus17 has been implemented for anyone to be treated with natalizumab, due to documented cases of PML (see pathophysiology section above). Those with positive JC serology are not good candidates for natalizumab.17 Cutting Edge/ Emerging and Unique Concepts and Practice Nakayama vaccine was developed for Japanese encephalitis (the world’s most common infectious encephalitis, affecting 50,000 annually) with > 95% immunity rate, despite Japanese encephalitis virus being very hybrid and with different lineages.41Work is ongoing for vaccines in susceptible […]
Ulnar Nerve Mononeuropathy at the Elbow
[…] is a nerve branch of the brachial plexus. It originates primarily from the anterior rami of the C8 and T1 spinal nerves (with some contribution from C7); these fibers travel through the lower trunk then medial cord of the brachial […]
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 […]
Shoulder Instability, Dysfunction and Scapular Dyskinesis
[…] intervention may be considered for the bone and joint factors prior to beginning rehabilitation treatment.10 Nerve damage: long thoracic or spinal accessory nerve palsy Inflexibility factors: glenohumeral internal rotation deficit (GIRD), total range of motion deficit or tightness of pectoralis […]
Rehabilitation Management of Prostate Cancer
[…] low threshold to obtain spinal MRI (or CT if MRI is contraindicated) in cases of vertebral metastasis and concern for spinal cord injury. Additionally, plain films in areas of known appendicular skeletal metastasis (most often hips and shoulders) can help to guide activity restrictions and need for orthopedic referral. Supplemental assessment tools In patients with spinal metastasis, the Spine Instability Neoplastic Score (SINS) can be utilized to determine stability of spinal metastases.13 For long bone metastases, Mirels’ Criteria can be used to determine stability and need for prophylactic fixation.14 SINS Component Score Location Junctional Occiput-C2, C7-T2, T11-L1, L5-S1 3 Mobile spine (C3-C6, L2-L4) 2 Semirigid (T3-T10) 1 1 Rigid (S2-S5) 0 Pain Yes 3 Occasional pain but not mechanical 1 Pain-free lesion 0 Bone Lesion Lytic 2 Mixed (lytic/blastic) 1 Blastic 0 Radiographic Spinal alignment Subluxation/translation present 4 De novo deformity (kyphosis/scoliosis) 2 Normal alignment 0 Vertebral body collapse > 50% collapse 3 < 50% collapse 2 No collapse with > 50% body involved 1 None of the above 0 […]
Lumbar Disc Disorders
[…] on events that ultimately lead to the development of spondylosis and stenosis. The theory highlights the interaction between the posterior spinal elements (facet joints) and the anterior spinal element (intervertebral disk) in establishing a 3-joint complex that undergoes 3 phases in a parallel fashion with a gradual change in the anterior spine bearing 80% to 90% in a healthy spine to equal weightbearing as degeneration reaches end stage.1 Phase 1, the dysfunctional phase, involves development of annular fissures and tears secondary to repetitive microtrauma which leads to blood vessel damage and subsequent inability to supply cells with nutrients and remove cytotoxic waste. These factors predispose the disk to herniation and impacts its ability to retain water, leading to a loss of disk height. Phase 2, the instability phase, involves disk resorption, internal disk disruption, and additional tears, causing loss of mechanical integrity at the 3-joint complex. Phase 3, the stabilization phase, involves further diskspace narrowing, fibrosis, and osteophyte formation.1,5 Epidemiology including risk factors and primary prevention The lifetime prevalence of low back pain is 80%, with disk disorders being the most common cause of adult low back pain.6 The most consistent risk factor for degeneration is increasing age. No difference related to gender has been determined. Correlations have been found with Body mass index, mechanical loading, and genetic predisposition.5 Genes coding for collagen, aggrecan, vitamin D receptors, matrix metalloproteinase, cartilage intermediate layer protein, and interleukins.7 Smoking and increased rates of disk degeneration, with animal models showing increased proinflammatory markers, alterations to annular structure, vasoconstriction, and altered nutrient distribution to the disk.8 Patho-anatomy/physiology Lumbar disks are generally 4-cm wide, 7 to 10 mm in height, and are involved with transmitting loads and providing flexibility to facilitate movement. There is an outer ring (annulus fibrosis) and an inner core (nucleus pulposus), both made up of differently organized collagen and elastin fibers with a highly hydrated aggrecan-containing gel found in the nucleus,9 which are surrounded by cartilage endplates superiorly and inferiorly. The nerves that supply innervation to the disk are located in the outer 1/3 of the annulus fibrosis Pathophysiology: disk degeneration develops as previously described. Herniations are seen with progressive loss of hydration, which leads to a loss of disk height and inappropriate transfer of load to the annulus and endplates. About 95% of herniations take place at the L4-5 and L5-S1 levels. Next most common are L3-4 and L2-3. Despite knowing the anatomic changes that take place, there is no clear relations between those changes and generation of pain. Inflammatory cascades, mechanical compression, instability, muscular imbalances, and psychosocial factors also contribute to perception of pain.2 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Lumbar disc degeneration is common, often found incidentally in otherwise asymptomatic patients. It is usually benign, having little correlation with function or pain.10 When symptomatic, the most common complaint is pain. About 85% of patients seen for low back pain do not receive a specific diagnosis.11 Of those patients with back pain, it is estimated that 39% are related to diskogenic pain. 12Given the limited ability to isolate the pain generators, establishing the diagnosis of and defining the course of symptomatic lumbar disk disorders can be challenging. It is generally reported that 90% of patients with low back pain will have their symptoms subside within 6 weeks,5 without medical intervention. Of those with herniations, it is thought that spontaneous regression of the disk contributes to improvement of symptoms. The exact mechanism of regression is unclear; hypotheses include dehydration leading to shrinking of disks, retraction of disks, and recognition of disks as a foreign body, resulting in macrophage phagocytosis of the disk.13 It has been shown that regression is far more likely in disc extrusion and sequestration compared to bulging and protruding disc.14 Specific secondary or associated conditions and complications Complications include myelopathy or cauda equina syndrome, which can result in neurogenic bowel, neurogenic bladder, motor weakness, sensory loss or impairment, impaired mobility, and long-term disability. Essentials of Assessment History Onset: after inciting event, which required flexion and rotation, some may not have an identifiable event. Character: aching, sore, and stabbing. Location: most likely midline lower back pain,15 but can refer to groin, genitals, abdomen, buttocks, and extremities. Worse with flexion, sitting, twisting, lifting, vibration, coughing, and sneezing. Better with frequent position change or extension.1,6 Medical history: prior spine surgeries (lumbar arthrodesis, diskectomy, or laminectomy make remaining disks susceptible),1 history of cancer, steroid/drug use, and recent systemic or local infections. Because psychosocial factors also play a role in pain, review psychiatric and social history. Red flags: bowel or bladder issues (retention/incontinence), saddle anesthesia, and motor weakness are concerning for myelopathy or cauda equina syndrome. Fevers/chills should raise suspicion for infectious etiology. Night sweats, constant pain that is worse at night, unintentional weight loss, and pain not improved with conservative therapy should raise suspicion for malignancy. Low back pain in older adults or the immunosuppressed merit workup for fracture. Physical examination Vitals: fever, tachycardia, or blood pressure abnormalities may indicate systemic pathology. Inspection: need for repositioning, preferred position (standing or sitting in extension decreases disk load), body habitus (excess weight may add load to disks), surgical scars, mood, and reaction to exam maneuvers. Range of motion: Lumbar range of motion may be limited, particularly in flexion. Palpation: paraspinals may be tender or tight and spinous tenderness or step deformity may indicate spondylolisthesis. Neurologic exam: sensation, strength, reflexes, and gait may be full and symmetric. Impaired sensation, focal weakness, or hyperreflexia may localize associated radiculopathy. Provocative maneuvers: seated and supine straight leg raise and femoral nerve stretch test.1,2 Functional assessment Cognition usually within normative limits, unless a preexisting condition exists. Behavior: pain out of proportion to exam may indicate nonorganic pathology. Mobility/gait: evaluate tandem, heel, and toe walking, which may assist in identifying associated radiculopathy or myelopathy. Laboratory studies There is no indicated laboratory study or marker for lumbar disk disorders. Specific laboratory studies may be indicated to evaluate for systemic inflammatory or neoplastic diseases when appropriate, but are rarely necessary.1,16 Imaging Lumbar radiograph: initial imaging, obtain anteroposterior and lateral view; signs of pathology include loss of disk height and end plate sclerosing.1 Magnetic resonance imaging (MRI): current standard, may see desiccation, herniations, Modic endplate changes, and high intensity zones, indicating annular tears.1,17 While considered the gold standard, MRI is overused, despite evidence-based guidelines and recommendations to avoid obtaining an MRI within the first six weeks of pain without red flags, or before conservative treatments have been attempted given the sensitivity rate as low as 0.52 and a sensitivity of 0.82. Based on these results, MRI findings need to be correlated to symptoms and physical examination findings.18,19 Computed tomography: an alternative when MRI is contraindicated (pacemakers, non-clinical tattoos, aneurysm clips).2 Can see calcified disk herniations, which might predict that surgery could be indicated. Bone scan: sensitive in identifying occult fractures, bone metastasis, and infections.2 Of note, diagnostic studies are not recommended in otherwise healthy patients with no red-flag symptoms as above where pain has been present for less than 6 weeks without the completion of physical therapy with the exception of pain causing complete immobilization or hospital admission.16 Supplemental assessment tools Provocative diskography is a controversial diagnostic test for diskogenic pain. Contrast material is injected into the suspected disk and adjacent disks. Exact reproduction of the patient’s pain at low pressures with painless adjacent disks indicates a positive test.9,20 Despite its questionable safety and diagnostic utility given the poor correlation with outcomes after spinal surgery, diskogram is still being widely performed although rates are trending downward.20 Postdiskography diskitis is considered one of the more severe possible complications. Other complications include triggering degeneration of a previously healthy disk, vasovagal reactions, paravertebral muscle pain and penetration of the disk’s ventral ramus. Retrospective studies have shown a significant increase in lumbar surgeries, prolonged back pain episodes, and work loss in diskography patients compared to controls over the long term (10 years), showing that some of the negative outcomes from this procedure may take up to a decade or more to become apparent.21 Early predictions of outcomes Research involving prognostic factors has focused on outcomes after surgical intervention for disk herniation. In that setting, lack of back pain, absence of a work-related injury, radicular symptoms, or leg pain on straight leg raise were predictive of satisfactory outcomes.22 Poor prognostic factors for development of chronic low back pain and disability include smoking, lower level of education, being out of work while receiving worker’s compensation, and depression.1,2,23 Rehabilitation Management and Treatments Available or current treatment guidelines Guidelines published in 1994 by the Agency for Health Care Policy and Research.24 and more recent guidelines from American College of Physicians (ACP) published in 2017 emphasize conservative, non-pharmacological, medical treatment and reduction of diagnostic testing, except in cases where red flags were apparent.25 Prevention: use of back belt in populations at higher risk particularly those with repetitive tasks involving lifting and carrying heavy objects Conservative: having excluded red flags, initial treatment includes superficial heat, myofascial release, massage and nonsteroidal anti-inflammatory drugs if needed and for more chronic issues, exercise, multi-modal rehabilitation, stress reduction and even behavioral therapy are recommended before stronger pharmacologic options. Epidural steroid injections may be considered for radicular leg symptoms, if greater than axial pain. Surgical: for diskogenic low back pain, the current options are fusion or disk arthroplasty. However, in the setting of predominantly axial pain (without cauda equina syndrome or progressive neurological deficit, which are surgical indications), role of surgery has been questioned given the unclear benefit of surgery long term despite statistical improvement with surgery at the 4- and 8-year marks given the numerous cofounders.26 Despite this, surgical rates for lumbar degenerative disk disease have increased 2.4-fold over the last decade.27 At different disease stages Emergency: if progressive neurologic deficits or cauda equina syndrome is present, surgical intervention is indicated.28 Acute: evaluate for red flags, conservative management, and relative rest with avoidance of painful movements. Epidural injections are also an option, which provide pain relief and functional improvement for at least 6 weeks, particularly in patients with radicular pain because of disk herniation. Of those patients, the use of a transforaminal approach also enabled reduction in the need for surgery following treatment.29 Chronic (pain >3 mo): assess psychosocial factors/comorbidities (depression) and encourage regular exercise focusing on muscle strengthening and endurance to return to prior […]
Endocrine Abnormalities Affecting the Musculoskeletal System
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[…] N Am. 2013 Nov; 24(4):673-86. Goessaert AS, Everaert KC. Onabotulinum toxin A for the treatment of neurogenic detrusor overactivity due to spinal cord injury or multiple sclerosis. Expert Rev Neurother. 2012 Jul; 12 (7):763-75. Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi […]
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