Heterotopic Ossification
[…] the joint capsule, in planes not connected to periosteum. It is also known as myositis ossificans.1 Etiology HO occurs following spinal cord injury (SCI), traumatic brain injury (TBI), and less commonly after other neurological disorders such as stroke or anoxic encephalopathy. It also occurs after severe burns, fractures (particularly acetabular and elbow fracture), or joint arthroplasty (particularly of the hip).2 Epidemiology including risk factors and primary prevention Risk factors for HO include long bone fracture, immobility, coma >2 weeks, edema, trauma and pressure ulceration. Common locations of HO after injury: SCI patients: Hips and knees commonly affected […]
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, […]
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 […]
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 […]
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 […]
Neurogenic Bowel
[…] (fecal constipation, fecal impaction) or failure to contain stool (fecal incontinence). Etiology NB can be seen in multiple conditions, including spinal cord injury (SCI), brain injury, stroke, spina bifida, Parkinson’s disease (PD), amyotrophic lateral sclerosis, multiple sclerosis (MS), peripheral nerve injuries and […]