Gary M. Abrams, MD, FAAN; Karunesh Ganguly, MD, PhD
ABSTRACTPurpose of Review: Both acute and chronic spinal cord disorders presentmultisystem management problems to the clinician. This article highlights keyissues associated with chronic spinal cord dysfunction.Recent Findings: Advances in symptomatic management for chronic spinal corddysfunction include use of botulinum toxin to manage detrusor hyperreflexia,pregabalin for management of neuropathic pain, and intensive locomotor trainingfor improved walking ability in incomplete spinal cord injuries.Summary: The care of spinal cord dysfunction has advanced significantly over thepast 2 decades. Management and treatment of neurologic and non-neurologiccomplications of chronic myelopathies ensure that each patient will be able tomaximize their functional independence and quality of life.
Continuum (Minneap Minn) 2015;21(1):188–200.
INTRODUCTIONNeurologists are frequently challengedwith managing chronic medical andfunctional deficits associated with mye-lopathies (Case 11-1). While acute trau-matic spinal cord injury is a relativelyrare disorder in the United States (esti-mated 300,000 survivors in 2013),1 ac-quired myelopathies secondary todiseases are three to four times moreprevalent.2 The few existing systematicstudies comparing nontraumatic mye-lopathies with acute traumatic spinalcord injuries have consistently notedthat outcomes are more related to leveland completeness of lesion and age,rather than etiology.3Y6 Most clinicalobservations presented in this sectionare derived from investigations in in-dividuals with traumatic spinal cordinjuries. However, the various medicaland rehabilitative concepts are reason-ably generalizable to patients with alltypes of chronic spinal cord dysfunction.The interested reader should consult themany helpful clinical practice guidelines
for management of spinal cord injuriesdeveloped by The Consortium for SpinalCord Medicine (www.pva.org).
CARDIOPULMONARY ANDAUTONOMIC COMPLICATIONSProphylactic anticoagulation for deepvenous thrombosis with low molecularweight heparin should start as soon aspossible following traumatic spinal cordinjury. Although the duration of prophy-lactic anticoagulation remains controversial,a minimum of 3 months is recommen-ded for paralyzed patients. While oneseries that studied rehabilitation patientsand compared traumatic spinal cordinjuries with nontraumatic myelopathiesfound a threefold increased incidence ofdeep venous thrombosis in the traumaticinjuries,7 it is generally accepted that theincidence of deep venous thrombosisis not increased over the generalpopulation after 3 months.
Cardiovascular issues such as arrhyth-mias or fluctuating blood pressures arecommon after acute spinal cord injury,
Address correspondence toDr Gary M. Abrams, Universityof California, San FranciscoMedical Center, 400 ParnassusAvenue, ACC 887/Box 0348,San Francisco, CA 94145,[email protected].
Relationship Disclosure:
Dr Abrams has received personalcompensation as a consultantfor Boston Scientific; theCalifornia Health BenefitsReview Program; ClarityNeurorehab, LLC; DartNeuroscience, LLC; HaloNeuroscience; and the LosAngeles Biomedical ResearchInstitute at Harbor-UCLAMedical Center. Dr Abrams hasalso received personalcompensation as a lecturerfrom Contemporary Forumsand the Hawaii NeurologicalSociety; has received royaltiesfrom UpToDate, Inc; and hasreceived honoraria for grandrounds from New YorkUniversity, Stanford University,and the University of CaliforniaHarbor-UCLA Medical Center.Dr. Abrams has received grantsfrom Innovative Neurotronicsand the NIH. Dr Gangulyreports no disclosures.
Unlabeled Use ofProducts/InvestigationalUse Disclosure:Drs Abrams and Gangulydiscuss the unlabeledinvestigational use of prazosinand terazosin for theprevention of autonomicdysreflexia, indomethacin andbisphosphonates forthe treatment of heterotopicossification, and clonidineand gabapentin for thetreatment of spasticity.
and orthostatic hypotension and re-duced cardiac reflexes occur in chronicspinal cord injury. Autonomic dys-function also disrupts normal temper-ature regulation, particularly with highcervical and high thoracic injuries,due to loss of sympathetic control oftemperature and sweat regulation be-low the level of injury. Hyperthermia,hypothermia, or poikilothermia maybe observed.8
Autonomic dysreflexia may compli-cate acute and, less commonly, chronicspinal cord injuries at or above thelevel of T6.9 Autonomic dysreflexia isusually associated with complete trau-matic spinal cord injury, but has beenreported in inflammatory disorders,10,11
spinal cord tumors,12 or neurosurgical
interventions.13 Neurologists shouldbe aware that noxious stimuli belowthe level of injury can trigger an exag-gerated sympathetic response. Systolicblood pressures of 250 to 300 mg Hgand diastolic blood pressures of greaterthan 200 mm Hg have been reported,leading to hypertensive crisis compli-cated by intracranial hemorrhage andseizures. It is important to recognizethat patients with chronic spinal cordinjury frequently have low baselineblood pressures. Thus, normotensiveblood pressure readings may indicatehypertension. The source of stimula-tion is usually bladder distention orbowel impaction, but bladder calculi,pressure sores, occult bone fractures,visceral disturbances, or sexual activity
KEY POINTS
h Outcomes innontraumaticmyelopathies and acutetraumatic spinal cordinjuries are more relatedto level and completenessof lesion and age, ratherthan etiology.
h Autonomic dysreflexiaoccurs with spinal cordinjury above T6.Bladder and boweldistention or bowelimpaction are themost common stimulithat can trigger anunmodulated sympatheticresponse, leading todangerous hypertension.
Case 11-1A 45-year-old man sustained a C7 American Spinal Injury Association (ASIA)complete spinal injury (ASIA A) while snowboarding. He was stabilized ata trauma center and subsequently transferred to a rehabilitation unit.Anticoagulation was started for deep venous thrombosis prophylaxisand was discontinued at 3 months. At the conclusion of inpatientrehabilitation, his neurologic examination was notable for a spasticquadriplegia with absent sensation below C7. Functionally, he wasindependent in level-surface transfers, manual wheelchair mobility, andbasic activities of daily living. He was placed on baclofen 20 orally mg3 times a day with modest control of symptomatic spasticity. Four monthspostinjury, he developed a pulmonary embolus secondary to a venousthrombosis in his leg. He was treated with warfarin for 6 months.Five months postinjury he began to note deep, nonlocalized pain below thelevel of injury. Spinal cord MRI showed no evidence of cystic transformationat the site of injury. He was treated unsuccessfully with gabapentin and wassubsequently switched to pregabalin with 30% pain relief. Videourodynamic study revealed detrusor hyperactivity withhigh-pressure contractions; renal ultrasound was normal. His wife wasassisting him with his bladder management, which was clean intermittentcatheterization every 5 to 6 hours and long-acting oxybutynin to preventoccasional bladder leakage. He was interested in fertility. He had usedvibratory stimulation unsuccessfully for ejaculation and had a semenanalysis by electroejaculation with consideration of semen cryopreservation.
Comment. This case is representative of cervical traumatic spinal cordinjury and demonstrates the need for multidisciplinary medical andrehabilitation interventions. The course reflects pitfalls (pulmonaryembolus), challenges (below-level of neurologic injury neuropathic pain),and successes (effective bladder continence) that characterize managementof spinal cord injury.
can also be triggers. Autonomicdysreflexia may complicate medical pro-cedures such as cystoscopy or labor anddelivery. The sympathetic activation ischaracterized by abnormal vasomotorregulation. Dangerous hypertension isassociated with spinal cord injury at T6or above, which blocks compensatoryparasympathetic vasodilatation.9 Para-sympathetic activation above the levelof injury may also produce bradycardia,sweating, nasal congestion, and flushing.
Management of acute attacks in-cludes immediately sitting the patientupright to orthostatically lower bloodpressure and loosening tight-fittingclothing. Identification and removal ortreatment of the inciting stimulus gen-erally resolves the situation. The bladdershould be investigated for an obstructedcatheter or urinary tract infection. Espe-cially given that myelopathies are asso-ciated with chronic constipation, fecalimpaction should be assessed for onrectal examination. If antihypertensiveagents are needed (systolic blood pres-sure greater than 150 mm Hg), short-acting agents such as topical or sublin-gual nitrates should be considered.Check that the patient has not takena phosphodiesterase 5 inhibitor (eg,sildenafil) within 24 to 48 hours inorder to avoid excessive hypotension.Other options include sublingual nifed-ipine or captopril, but there are limiteddata supporting the efficacy or safety ofany specific treatment. In more severecases, IV hydralazine or labetalol may benecessary. Prevention of autonomicdysreflexia rests on patient educationand careful management of urinary tractissues associated with the neurogenicbladder. Adrenoceptor blockers such asprazosin or terazosin may be tried forprophylactic management.9
Coronary artery disease risk factorsare elevated in patients with spinal cordinjury. Depending on severity and neu-rologic level, these individuals experi-
ence the consequences of immobilityand inactivity. Risk factors for coronaryartery disease are similar to able-bodiedindividuals, and problems such as ab-normal glucose metabolism and lipidprofiles are more prevalent in thespinal cord injury population.14 Notsurprisingly, an increased incidence ofstroke has been reported in spinal cordinjury.15 Development of an appropriatenutritional and exercise program is im-portant.14 Exercise options such as swim-ming, hand-crank ergometry, or body-weightYsupported treadmill walking16
can be considered. Depending on theseverity and level of the injury, physio-logic responses will be altered, thus,exercise programs should be supervisedand monitored.
Disorders involving the cervical andthoracic spinal cord may affect respira-tory muscles. Impaired cough andreduced ability to mobilize secretionsincrease the risk of pneumonia.17 Long-term compromise of pulmonary reserveplaces patients with chronic spinal cordinjuries at greater risk for obstructivesleep apnea, ventilatory failure, andreduced exercise tolerance.17
Genitourinary DisordersMyelopathies often produce bladderdysfunction (neurogenic bladder). Uro-logic evaluation is recommended for allpatients with traumatic spinal cordinjuries and should be seriously consid-ered for patients with any myelopathyand a neurogenic bladder. Bladdercontrol is complex, requiring the coor-dinated function of the cerebral cortex,pontine and sacral micturition centers,and the peripheral nervous system.17
Patients with complete spinal cordinjuries rarely regain volitional bladdercontrol, however, recovery or mainte-nance of bladder sensory function is agood prognostic sign for voluntaryvoiding, particularly in younger pa-tients.18 Similarly, in many nontraumatic
KEY POINT
h Abnormal glucosemetabolism and lipidprofiles are moreprevalent in the spinalcord injury population.Development of anappropriate nutritionaland exercise programis important. Exerciseoptions includeswimming, hand-crankergometry, orbody-weightYsupportedtreadmill walking.
myelopathies, retained bladder sensoryfunction is a favorable prognostic sign.Older patients with vascular diseases ofthe spinal cord are more likely toexperience significant bladder dysfunc-tion than patients with myelopathyassociated with degenerative spine dis-ease.19 In general, neurologic control ofbladder function depends on the loca-tion and completeness of the lesion,rather than the underlying pathology.
The two major functions of thebladder are storage and emptying ofurine, and the principal goal of bladdermanagement is to maintain detrusorpressure within limits that preserveupper urinary tract (kidneys) integrity,avoid infections, and maintain conti-nence. The most effective methods forassessing lower urinary tract (bladderand urethra) function in myelopathiesare a clinical history, a voiding diarydocumenting symptoms (eg, urgency,frequency/volume of urination, and in-continence), and a urodynamic study.Although bladder dysfunction dependson the neurologic level of injury,detrusor hyperreflexia (spastic bladder)with or without sphincter dyssynergia islikely the most common problem en-countered by neurologists who treatmyelopathies. Typical symptoms areurgency and frequency that may beaccompanied by episodic incontinence.Cauda equina injuries or injuries to theconus medullaris may result in chronicurinary retention due to atonic bladderand, in more severe cases, overflowincontinence or leakage due to urinarysphincter incompetence.
The cornerstone of treatment isclean intermittent catheterization, whichis less likely to lead to infections com-pared with chronic indwelling cathe-ters.20 Bladder volumes should be keptat less than 500 mL of urine. In selectedpatients, clean intermittent catheteriza-tion and adjustment of fluid intake cansupplement voluntary voiding. In addi-
tion to posing an increased risk ofinfection, indwelling catheters increasethe risk of epididymitis, prostatitis,urethral stricture, and possibly bladdercancer.21 Asymptomatic bacteriuriawith or without pyuria should not betreated. Antimicrobial prophylaxis andcranberry juice are not effective.22 Sym-ptomatic urinary tract infections shouldbe treated promptly. A recent review ofurologic follow-up after spinal cordinjury suggested no specific monitor-ing for infections other than annualurinalysis, which is recommended forneurogenic bladders associated withmyelopathy of any etiology. An annualrenal ultrasound to detect upper tractproblems and urinary tract lithiasis isalso recommended.23
Pharmacologic interventions can beguided by urodynamic assessment ofbladder and sphincter physiology. Inpatients with detrusor hyperreflexia orinstability, anticholinergic medications,24
or tricyclic antidepressants can decreasebladder tone, inhibit involuntary bladdercontractions, and reduce urinary fre-quency. Botulinum toxin injected intobladder musculature for treatment ofneurogenic detrusor overactivity de-creases urinary incontinence and im-proves quality of life in patients withmultiple sclerosis (MS) and other causesof spinal cord dysfunction.25 In caudaequina lesions with reduced bladder orsphincter tone, cholinergic medicationsmay facilitate bladder emptying, while!1-adrenergic agents such as ephedrinepromote bladder storage. Older menwith myelopathies may have urinarytract outflow obstruction due to prostatichypertrophy. "1-Adrenergic receptorblockers reduce sphincter tone and pro-mote bladder emptying. In detrusorsphincter dyssynergia, which is moretypically seen in complete traumatic spinalcord injury rather than incomplete myelo-pathies, the bladder contracts against aclosed sphincter, which may produce
KEY POINT
h Clean intermittentcatheterization is thecornerstone of treatmentfor a neurogenic bladderand is less likely toproduce a urinary tractinfection than anindwelling catheter. Onlysymptomatic infectionsshould be treated.Prophylactic antibioticsare discouraged.
elevated intravesicular pressure withvesicoureteral reflux that can threatenupper urinary tract integrity (Figure 11-126).For patients with neurogenic bladdersin whom satisfactory management can-not be achieved through medicationsor catheters, urologic surgical proce-dures or neural stimulation devices maybe options.
Sexual dysfunction with spinal cordinjury is an important factor affectingquality of life. An open and frank dis-cussion regarding sexual issues is re-commended.27 In men, libido, potency,and fertility are reduced, and a varietyof treatment options are available in-cluding medications (eg, phosphodies-terase 5 inhibitors) and mechanical
devices to achieve erections and ejac-ulation. In women with spinal corddysfunction, libido and sexual responsemay be altered, but ovarian functionand fertility are usually retained.28 Theeffects of skin and bowel/bladder careand medical comorbidities on sexualactivity should be considered.
GASTROINTESTINALCOMPLICATIONSWhile bowel dysfunction is commonwith myelopathies, the optimal manage-ment is uncertain. The majority ofmyelopathies in neurologic practice areincomplete injuries occurring above thelevel of the conus medullaris. Suchlesions produce an upper motor neuron
FIGURE 11-1 Detrusor pressure with simultaneous EMG of sphincter during slow infusion offluid into bladder. In the healthy adult patient (upper graph), note the changein sphincter tone with starting and stopping of normal voluntary voiding. In the
paraplegic patient (lower graph), there is abnormal increase in sphincter pressure with reflexvoiding resulting in elevated detrusor pressures.
Modified from Fowler CJ, et al, Nat Rev Neurosci.26 B 2008 The Authors. www.nature.com/nrn/journal/v9/n6/abs/nrn2401.html.
bowel syndrome characterized by in-creased colonic wall and anal sphinctertone, with a tendency toward constipa-tion and fecal retention. Fortunately,most of these patients retain the abilityto maintain continence and bowel evac-uation. Conus medullaris or caudaequina lesions will also be marked byconstipation, but sphincter tone maybe compromised and bowel inconti-nence may be problematic. In eithersituation, the basic approach shouldbe to promote regular and predict-able bowel evacuation. For individualswho cannot be satisfactorily managedwith diet alone, oral medicationsshould be used judiciously. A bowelroutine should be established witha convenient time for evacuationusing a stimulant rectal suppositoryor digital stimulation. Optimal manage-ment for spinal cord injuryYrelatedconstipation and fecal incontinenceremains undetermined.29
Musculoskeletal DisordersMyelopathies are usually characterizedby impaired mobility. Muscle and con-nective tissue maintained in a short-ened position for as little as 1 week willcontract and stiffen. After several weeks,loose periarticular tissue enveloping ajoint will reorganize, leading to reducedmotion and function. The essentialinterventions to prevent developmentof contractures are unknown. A combi-nation of positioning, range-of-motionexercises, and splinting has beenrecommended; however, stretchingand ranging of joints for periods ofup to 7 months have not demonstratedclinically meaningful short-term or long-term effects.30 Resting night splints orremovable casting are frequently usedto prevent upper extremity and ankleplantar flexion contractures, but theirefficacy is also not well documented.While certain contractures may facilitatefunction, others will interfere with
maintenance of hygiene or wheelchairseating and positioning. Surgical inter-vention may be required.
Osteoporosis due to immobility af-fects bones below the level of injury.Sclerostin, produced by osteocytes,appears to be a key mediator ofbone loss immediately after paralysisand is a biomarker of osteoporosis inchronic spinal cord injury.31 Cortico-steroids, which are used to treat somemyelopathies, can contribute to osteo-porosis. Patients receiving glucocorti-coids should receive calcium (800 to1200 mg/d) and vitamin D supple-mentation (more than 800 IU/d).32
Osteoporosis medications, such asbisphosphonates, slow bone loss, butdo not seem to stimulate new boneformation. Effective treatments for in-creasing bone density include weightbearing, functional electrical stimula-tion, and vibration therapy.31
Heterotopic ossification refers todeposition of bone within soft tissuearound peripheral joints. Large jointsbelow the level of injury such as the hipare affected. Heterotopic ossificationoccurs in up to 50% of patients withtraumatic spinal cord injury,33 but ismuch less common in nontraumaticmyelopathies.34 Pain and decreasedrange of motion often precede theappearance of calcification. Triple-phasebone scan is the best diagnostic test.Early administration of indomethacincan prevent heterotopic ossification,and bisphosphonates may stop progres-sion.33 Surgery may restore functionalrange of movement, but ossification islikely to recur.
Repetitive overuse of the arms forcrutches or wheelchairs may lead tovarious injuries. Rotator cuff and othertendon injuries, compression neuro-pathies, bursitis, and osteoarthritis arecommonly seen in late spinal cordinjuries. Proper techniques for wheel-chair transfers and specific exercise
KEY POINTS
h Upper motor neuronbowel syndrome ischaracterized byconstipation and fecalretention. With conusmedullaris or caudaequina lesions, bowelincontinence may beproblematic. Diet shouldbe modified and oralmedications usedjudiciously. Regular andpredictable bowelevacuation needs tobe promoted byestablishing a convenienttime for evacuationusing a stimulant rectalsuppository ordigital stimulation.
h Interventions to preventdevelopment ofcontractures areunknown. Positioning,range-of-motionexercises, and splintinghas been recommended,but ranging of joints forup to 7 months has notdemonstrated clinicallymeaningful short-term orlong-term effects.
programs to minimize injuries andpreserve joint function can be helpful.The prescription of power or power-assisted wheelchairs may postpone orprevent overuse injuries.35
PRESSURE ULCERSPressure sores occur when externalpressure on skin and subcutaneoustissue is combined with distortion orshear. Patients with myelopathiesand preserved sensation are lesslikely to develop pressure sores. Pres-sure on skin while in bed may reduceregional blood circulation. Relievingskin pressure over a bony promi-nence for 5 minutes every 2 hourswill allow for adequate perfusion andprevent tissue breakdown. The besttreatment for pressure ulcers is preven-tion. Patients at risk for ulcers need tolearn techniques for pressure relief andmaintenance of bowel and bladderhygiene. Transfers from bed to chairshould be done with minimal shear, andpressure-relieving wheelchair cushionsshould be prescribed. Good perineal re-gion hygiene is essential. Adequate nutri-tion must also be maintained.36
PAINPain is common with both traumatic andnontraumatic spinal cord injury.37,38 Re-cent classifications have specifically di-vided spinal cord injury pain intonociceptive (pain arising from non-neural tissue injury or irritation) andneuropathic types of pain. Neuropathicpain is divided into at-level of neurologicinjury pain and below-level of neuro-logic injury pain.38 In nontraumaticmyelopathies, pain seems to be particu-larly common with malignant spinal corddisease. In one series of nontraumaticmyelopathies, approximately 70% ofpatients with disorders such as vasculardisease, spinal stenosis, malignant orbenign tumors, and infections reportedthat pain was a problem in daily life.37
At-level neuropathic pain may arise ina segmental pattern from the spinalcord or roots and is typically describedas burning, tingling, or pricking. Sensorydeficits and allodynia or hyperalgesiaoccur within the pain distribution.Below-level neuropathic pain (at leastthree levels below normal sensation)is typically diffuse, nondermatomal,with variable intensity. In cases ofincomplete injuries, allodynia andhyperalgesia may occur within the paindistribution. In traumatic spinal cordinjury, late onset at-level neuropathicpain may be indicative of syrinx for-mation within an area of myelomalacia.In contrast, nociceptive pain (eg,musculoskeletal pain) is dull, aching,and well localized. Although neuro-pathic pain appears to be associatedwith neuronal hyperexcitability,mechanisms are poorly understood.Suggested etiologies include neuro-plastic changes in the cord (eg, sprout-ing of primary afferents); increasedlevels of inflammatory mediators;changes in receptors or ion channels;and loss of inhibitory neurons withinpain pathways.39
Treatments for spinal cord injuryneuropathic pain are generally unsatis-factory.39 Tricyclic antidepressants,gabapentin, or mixed serotonin nor-adrenaline reuptake inhibitors are oftenrecommended as first-line treatments.Opiates (including tramadol) mayalso provide relief. A recent large,multicentered randomized trial ofpregabalin in patients with chronicbelow-level neuropathic spinal cordinjury pain due to trauma reportedimprovements in duration-adjustedaverage change in pain, although alarge proportion of patients did notachieve pain reduction of at least30%.40 Intrathecal therapies and variousneurostimulation techniques andneuroablation procedures have beentried without substantial benefit.
KEY POINTS
h Pressure sores occurwhen externalpressure on skin andsubcutaneous tissue iscombined withdistortion or shear.Relieving skin pressureover a bonyprominence for5 minutes every 2 hourswill allow for adequateperfusion and preventtissue breakdown.
h Pain is common inboth traumatic andnontraumaticmyelopathies. A recentstudy provided class 1evidence for pregabalin150 to 600 mg/d intreatment of paindue to spinal cord injury.
SPASTICITYApproximately 65% to 78% of traumaticspinal cord injuries are associated withsymptoms of spasticity.41 The relation-ship between spasticity and function maybe complex. For example, while severechronic spasticity can result in pain anddystonic posturing of paretic limbs, lesssevere spasticity may aid transfers orweight bearing. However, potential ad-vantages may be offset by spasms thatinterfere with activities of daily living (eg,perineal hygiene or sleep).
Functional goals are essential forguiding treatment. Current evidencedoes not support routine treatment ofspasticity,42 and management decisionsshould be individualized. Exclusion ofpossible exacerbating factors is an impor-tant first step in the evaluation. It is wellknown that common comorbidities withspinal cord injuries increase spasticity,such as infections, pressure ulcers, orother sources of noxious stimuli. Just assyrinx formation may be a source of late-onset pain after traumatic spinal cordinjury, it may also cause unexplained
increasing spasticity, thus, imaging of theaffected area should be considered.
A variety of measures can reducespasticity.42,43 Although its overall effi-cacy can be limited at a populationlevel, physiotherapeutic approachessuch as stretching and weight bearingcan be beneficial in individuals.43 Oralmedications are frequently used, de-spite limited evidence for their efficacy(Table 11-144). In addition, while stud-ies have demonstrated reduction ofclinical spasticity, less evidence existsfor functional improvements,42 thus,therapeutic approaches should be cho-sen with careful consideration of ad-verse effects. Baclofen, a +-aminobutyricacid (GABA) B receptor agonist, is themost commonly used oral medication.Tizanidine, a centrally acting "2-adrenergicagonist, is another possibility. Both canhave side effects such as drowsiness,cognitive slowing, and worsening weak-ness. Benzodiazepines, allosteric modu-lators of GABA A receptors, are anadditional treatment choice. In certainpatients, nocturnal use of medication
KEY POINT
h Spasticity treatmentshould be guided byfunctional goals.Currently available oralmedications may not bevery effective and havelimiting side effects.Local treatment withchemodenervation orintrathecal baclofenmay be options.
TABLE 11-1 Oral Medications Commonly Used for Spasticitya
Medication Starting Oral Dose Maximum Oral Dose Adverse Effects
Gabapentin 100 mg 3 times/d 3600 mg/d in divided doses Sedation, dizzinessa Reprinted from Abrams G, Wakasa M, UpToDate.44 B 2014 UpToDate, Inc. www.uptodate.com/contents/chronic-complications-of-spinal-cord-injury-and-disease.
can reduce spasms that interfere withsleep.Dantrolene sodium reduces calciumrelease from the sarcoplasmic reticulumand diffusely reducesmuscle strength and,therefore, is generally reserved for individ-uals with more severe disability.
Chemodenervation with injections ofbotulinum toxin and intrathecal deliveryof baclofen via an implantable pump aretwo additional treatment modalities.42
Botulinum toxin is currently US Foodand Drug Administration (FDA) ap-proved as a treatment for spastic flexormuscles at the elbow, wrists, andfingers, and is likely also beneficial forspasms of the hip adductor muscles.The FDA has warned about the possi-bility of systemic effects from localinjections, possibly related to inadver-tent overdosing. Patients with refractoryspasticity involving the trunk and lowerextremities may be candidates for treat-ment with intrathecal baclofen. Intra-thecal baclofen allows delivery oftherapeutic, targeted doses of baclofenthrough a programmable pump. Such amethod of delivery can increase overallefficacy while reducing side effectsassociated with oral administration. Al-though no randomized controlled trialsexist, a meta-analysis of multiple caseseries supported intrathecal baclofentreatment.45 In nontraumatic myelopa-thies, a combined approach of botuli-num toxin, intrathecal baclofen, andgeneral rehabilitative measures mayhelp to improve overall function.
PSYCHOSOCIAL ISSUESAcute spinal cord injury is associatedwith increased psychological morbidity,substance abuse, and risk of suicide.Individuals with chronic spinal cordinjury have an increased prevalence ofdepression, anxiety, and posttraumaticstress disorder, and their average lifesatisfaction is below that of the generalpopulation.46 However, subjective well-being after spinal cord injury is fre-
quently better than might be expectedafter such a serious injury. Factorsconsistently associated with subjectivewell-being include perceived control oflife, purpose in life, feelings of self-efficacy, and self-esteem. Various typesof supportive psychotherapy have beentried with mixed results.46
NEUROLOGIC REHABILITATIONRehabilitation goals, functional needs,and expectations are determined by thelevel and completeness of the injury(Table 11-247). While customized reha-bilitation programs can be developedin a similar manner for both traumaticand nontraumatic spinal cord injury,the etiology of the injury can also be afactor. For example, a recent reviewsuggested that infectious myelopathies(eg, epidural abscess) are associatedwith worse outcomes.48 In general,higher levels of injury require in-creased levels of assistance and achievereduced functional independence. In-juries at the level of C5 to C8 areassociated with increasingly greaterlevels of self-care and mobility. Injuriesat or below T1 are typically associatedwith the ability to independently per-form activities of daily living and mo-bility using wheelchairs. Injuries at orbelow L2 also have the potential forindependent ambulation.
A growing body of literature supportsintensive locomotor training as a meansof improving lower extremity functionin incomplete spinal cord injury,49,50
which represents a marked departurefrom historical efforts that focused uponcompensation using assistive devices.Animal studies over the past severaldecades have provided support forfunctional recovery after training. Morerecent studies in human subjects havealso provided support for this ap-proach.49,50 It is unclear, however, if par-ticular training approaches are superior.For example, one popular method uses
KEY POINTS
h With chronic spinalcord injury there is anincreased prevalenceof depression, anxiety,and posttraumaticstress disorder. Averagelife satisfaction isbelow that of thegeneral population.However, subjectivewell-being after spinalcord injury is frequentlybetter than mightbe expected.
h Level and completenessof neurologic injurydetermine functionalabilities. Patients withcomplete injuries at aC7 level have potentialfor independence inactivities of daily livingand wheelchair mobility;patients with injuriesat L2 or below mayambulate independently.
body-weightYsupported treadmill trainingto facilitate task-specific rehabilitation.Recent work suggests that body-weightYsupported treadmill training may not bemore effective than traditional over-ground training.49 Thus, while strongevidence supports task-specific gait train-ing after partial spinal cord injury, thespecific approach can depend on pro-vider and patient preferences.
FUTURE DIRECTIONSSeveral promising therapeutic andrehabilitative methods exist for spinalcord injury patients. Perhaps the mostpromising is neuromodulation usingelectrical stimulation. For example, arecent report described motor im-provements in patients with completespinal cord injury after electrical stim-ulation coupled with rehabilitation.51
Spinal Level Activities of Daily Living Mobility and Locomotion
C1 to C4 Feeding possible with balancedforearm orthoses
Operate power chair with tongue, chin, orbreath controller
Computer access by tongue, breath,voice controls
Weight shifts with power tilt andrecline chair
Mouth stick use
C5 Drink from cup, feed with staticsplints and setup
Propel chair with hand-rim projections shortdistances on smooth surfaces
Power chair with hand controller
C6 Feed, dress upper body with setup Bed mobility with equipment
Dressing lower body possible Level-surface transfers with assistance
Forward weight shifts Propel indoors with coated hand rims
C7 Independent feeding, dressing,bathing with adaptive equipmentand built-up utensils
Independent bed mobility and level-surfacetransfers
Wheelchair use outdoors (power chair forschool or work)
C8 Independent feeding, dressing,bathing
Propel chair, including curbs and wheelies (ie,lifting front wheels of chair for curbs, turns,pressure relief)
Bowel and bladder care with setup Wheelchair-to-car transfers
T1 Independent in all self-care Transfer from floor to wheelchair
T2 to L1 Independent in all self-care Stand with braces for exercise
L2 Independent in all self-care Potential for swing-to gait with long leg bracesindoors
L3 Independent in all self-care Potential for community ambulation
Potential for ambulation with short leg braces
L4 to S1 Independent in all self-care Potential for ambulation without assistive devicesa Reprinted with permission from Frost FS, Saunders.47 B 2000 Elsevier, Inc.
Stem cells also represent a promisingtreatment for spinal cord injury. Alarge body of preclinical literaturesuggests that stem cellYbased thera-pies may improve recovery in animalmodels of spinal cord injury througha variety of mechanisms.52 Even whilepilot translational trials using stemcells occur, a great deal of researchhas to be performed in order tobroadly translate this to patients.Finally, brain-machine interfaces mayallow the patients with the most severespinal cord injury to control externaldevices using their ‘‘thoughts.’’53 How-ever, numerous challenges still existthat limit broader use of these ap-proaches at present.
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