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J Head Trauma RehabilVol. 19, No. 2, pp. 89100

c 2004 Lippincott Williams & Wilkins, Inc.

Acute Care Management

of Post-TBI SpasticityRoss Zafonte, DO; Elie P. Elovic, MD; Lisa Lombard, MD

The management of persons with traumatic brain injury (TBI) who have acute spasticity remainsa challenge. A correct stratification is essential to clinical care and determination of efficacy fromproposed interventions. The secondary severe sequlae of spasticity after TBI can result in pro-found functional impairment. These concerns are often best addressed early in the patientscourse.Limited research in the area of the acute care treatment of severe spasticity is available. The au-thors employ a review of the available data as well as recount their own clinical experience inthe acute care management of severe spasticity to assist in developing an order for the plethoraof potential treatments available to clinicians and researchers. We propose to use a case exam-

ple to emphasize key clinic points in the management of spasticity in the acute care setting.Key words: acute care, intensive care, spasticity, TBI

M ANAGEMENT of the person with trau-matic brain injury (TBI) who has con-siderable spasticity must begin in the acutecare setting. Throughout the rehabilitationprocess it is important to treat someone whohas sustained a TBI with the expectation that

he/she will have significant recovery. Perhapsthe most important yet difficult goal for spas-ticity management in the acute care settingis maintaining range of motion, but despiteaggressive approaches, this may not alwaysbe possible. Confounding acute medical is-sues may limit treatment options and makespasticity management even more challeng-ing. However the authors have seen individu-als who have emerged from low-level states,only to have their functioning greatly lim-ited by loss of range of motion as a resultof ineffective spasticity intervention. There-

From the Department of Physical Medicine andRehabilitation, University of Pittsburgh, Pittsburgh,Pa (Drs Zafonte and Lombard); the Kessler MedicalRehabilitation Research and Education Corporation,West Orange, NJ, and the University of Medicine and

Dentistry, NJ (Dr Elovic).

Corresponding author: Ross Zafonte, DO, Departmentof Physical Medicine and Rehabilitation, University of

Pittsburgh, 3471 fifth ave suite 201, Kaufman Bldg,Pittsburgh, PA 15213 (e-mail: [email protected]).

fore, an ordered approach to both physicaland pharmacological interventions is essentialto possibly prevent the secondary sequelae ofspasticity. Since the literature regarding spas-ticity therapy is sparse, this review will em-ploy a case example to emphasize key points

in the decision-making paradigms for suchpersons.

CASE DISCUSSION

A 24-year-old male was admitted to the inten-sive care unit (ICU) after a motor vehicle crash.He required a prolonged extrication time and wasnoted to be mildly hypotensive at the seen of theaccident. He was transported to a trauma cen-ter where his post resuscitation Glasgow ComaScale was 3T. Computed axial tomographic (CAT)scan imaging noted multiple petechial hemor-rhages and a markedly depressed skull fracture

in the left parietal region, as well as a large sub-dural hematoma and a midline shift of 5 mmwas appreciated. He underwent evacuation ofthe hematoma and repair of the depressed skullfracture. A 24-hour period of elevated intracranialpressure was responsive to intermittent manni-tol therapy. His course was complicated by respi-

ratory insufficiency and pneumonia. It is now 1-week post injury and we are invited into the ICUto evaluate the patients severe tone. Our case

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90 JOURNAL OF HEAD TRAUMA REHABILITATION/MARCHAPRIL 2004

discussion will focus only on the acute treatmentof spasticity.

EVALUATION

Evaluation in the acute care setting

Review

There is literature that has demonstratedthe importance and efficacy of a rehabilita-tion evaluation in the acute care setting. Wag-ner and colleagues have reported that earlyacute care rehabilitation consultation resultsin improved outcome at acute care discharge,in addition to shorter acute care length ofstay.1 The rehabilitation teams role in themanagement of spasticity especially amongthose with more severe injuries may be mostcritical.

Hinderer has proposed that the clinicalevaluation of such patients be divided into5 components: clinical history, stretch re-flex examination, passive motion examina-tion, active motion examination, and func-tional examination.2While all of the above are

important, it may be challenging to evaluatefunctional status in the acute care setting andmaintaining range of motion is often the pri-mary focus in this setting. A careful evalua-tion of the history and care record will help

Figure 1. Evaluation of the acute TBI patient with spasticity.

to delineate risk factors and issues that mayinterfere with therapy. Care should be takento discuss prior functional history and deter-mine prior neurological or gait dysfunction.

Risk factors for early spasticity include im-mobilization, motor dysfunction (hemiplegiaor tetraplegia), associated hypoxic ischemicinjury, spinal cord injury, and age.2,3 While re-specting range of motion precautions as wellas spinal stability a comprehensive evaluationof both the active and passive range of mo-tion of each available extremity should be per-formed. At this time it is helpful to also notethe perceived tone and range of motion ateach major joint. The positioning of a venti-lator may make shoulder evaluation difficultat times. Serial assessments of tone are oftenof value since severity may vary with stimuli(ie, prior medications, procedures that day).Tone is an important issue for the rehabilita-tion team to address as the acute care teamrarely attends to this issue and it may play arole in ultimate outcome and disposition. Itis recommended that some objective measureof tone such as the Ashworth Scale be used to

quantify tone at each joint.The evaluation of patients with spasticity

requires clinicians to adopt an organized sys-tematic approach to the problem (see Fig 1).After documenting tone and range of motion


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Acute Care Management of Post-TBI Spasticity 91

the next step is to evaluate for any second-ary factors, such as occult injury (fracture,neurodysfunction [hydrocephalus or occultcerebral lesion], infection, heterotopic ossi-

fication, and pain that may be exacerbatingthe motor dysfunction.4 Several medicationscan impact the evaluation of spasticity in theperson with TBI. In the intensive care set-ting the use of neuroparalytic agents, opioids,benzodiazepines, and propofol may mask theseverity of the spasticity that exists at base-line. Neuroparalytics remove almost all tone,while opioids and benzodiazepines appear todecrease tone. Propofol is a unique lipid solu-ble agent that produces a sedative effect, yetcan be quickly stopped to allow for motor andcognitive evaluation.5

Chronology of spasticity

One does not have a thorough understand-ing of how to evaluate spasticity, unless oneunderstands the importance of chronologyof spasticity and severity of the motor dys-function. The development of early spasticitycarries with it a more challenging prognosis.

Those with more severe brain injuries, as wellas those with associated spinal cord injury, hy-poxic ischemic injury, and/or associated au-tonomic dysfunction, tend to develop earliermore aggressive forms of the dysfunction. Wepropose the term malignant spasticity to fur-ther define those persons in the acute care pe-riod whose spasticity is so severe that withoutaggressive early intervention care cannot beprovided and loss of functional range of mo-tion is almost certain.

Case discussion

A systematic evaluation of the patients situ-ation yields some concerning clinical data. The

patients spasticity developed very early in hisclinical course and over a 2-day period of timehis tone progressed rapidly. The patient showsevidence of flexor tone in the upper extremitiesand extensor tone in the lower extremities. Serialevaluation of tone in the right upper and lower ex-tremities noted Ashworth 2 tone and Ashworth 3

tone respectively. The patient had dysautonomicepisodes and severe posturing. Adductor tonewas already profound. Our team noted early de-

crease in range of motion at the right ankle andelbow. His symptoms had been relieved only withsedatory therapy.

TREATMENTS

Physical modalities

Physical modalities offer treatment withoutthe risk of systemic side effects that can occurwith systemic medications. Passive stretchingremains a core therapy in the management ofspasticity as well as in the prevention of con-tracture formation. This technique has beenshown to decrease spasticity in persons withstroke6 and cerebral palsy.6 Standing has alsobeen used as a form of prolonged stretch toreduce spasticity in those with spinal cordinjuries.7 An examination in a population ofbrain injured patients indicated that a seriesof passive flexion and extension movementsof the elbow result in a short-term reductionof tone.8 Clinically, the stretching program istypically performed 1 to 2 times a day. This isa relatively easy modality that can be taught

to family members and selected patients toaid in spasticity management. One of themost accessible adjunctive therapies to pas-sive stretch is cryotherapy, the application ofcold acts to reduce stretch reflex activity9,10

and induce analgesia. Treatment should be re-stricted to a maximum of 20 minutes at atime to reduce the risk of skin injury.11 Un-fortunately, the reduction of spasticity withcold application alone is limited to a half anhour.

Splinting and serial casting, while morecommonly used in both inpatient and outpa-tient rehabilitation, can also be a valuable toolin the acute care setting. Casting in the up-per extremity has been shown to decrease the vibratory inhibitory index of the H-reflex.12

After 5 weeks of casting, Singer et al founddecreased torque and reflexive stretch re-sponses in adults with spastic equinovarusdeformities due to brain injury.13 In addition

to the physiological evidence of the benefitsof casting, studies have demonstrated an im-provement in function after the application


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of casts to spastic limbs.14,15 Casting does re-quire a significant length of time before im-provements are seen15,16; however, constant vigilance on the part of physicians, nurses,

and therapists is required to mitigate pres-sure sore formation. Complication rates canbe decreased with a reduction of the cast-ing interval from 57 days to 14 days withno detriment to the improvement in range ofmotion.16 While treatment of patients withspasticity with casts in a population of pa-tients with a recent TBI (


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of the agents when they are used in the TBIpatient.

Dantrolene sodium: (Dantrium)

Dantrolene is used in patients with mus-cle spasticity and is the only known effec-tive treatment for malignant hyperthermia.However, its effects on muscle relaxationand energetics are unknown and mayhave important consequences in diaphrag-matic function.26 Dantrolene sodium, 1([5-(nitrophenyl)furfurylidend]amino) hydan-toin sodium hydrate, is indicated for use inchronic disorders characterized by skeletalmuscle spasticity, such as spinal cord injury,stroke, cerebral palsy, and multiple sclerosis.Dantrolene is believed to act directly on thecontractile mechanism of skeletal muscle todecrease the force of contraction in the ab-sence of any demonstrated effects on neuralpathways, on the neuromuscular junction,or on the excitable properties of the musclefiber membranes.27 Dantrolene acts at thescaroplasmic reticulum by inhibiting calciumactivity. It has been evaluated in the treat-

ment of those with cerebral palsy, multiplesclerosis, and spinal cord injury. Its role inthe treatment of severe spasticity in theacute care setting has not been adequatelyexplored.

Laboratory evaluation of the potential roleof dantrolene in the management of acutecare spasticity raises some compelling issues.Cho et al evaluated the hemodynamiceffects of dantrolene in dogs that whereinstrumented to further define cardiac

parameters.28 They noted that dantrolenereverses the hypotensive action produced bypropofol and causes an increase in coronaryblood flow with a decrease in coronary vascular resistance, but does not signifi-cantly change the negative inotropic effectsof propofol. In a laboratory investigation,Nakayama et al noted that intracerebroven-tricular dantrolene prevents delayed neuronalloss in the rat hippocampal CA1 region

subjected to transient ischemia.29

Popescuhas demonstrated that dantrolene sodiummay protect against kanic acid induced

apoptosis.30 This agent does appear to crossthe blood brain barrier but only in modestfashion. While the evidence is relatively weakthere may be some theoretical advantages of

dantrolene sodium in the acute care setting.Little literature exists to refine the clin-

ical use of dantrolene among those withbrain injury. Seinberg et al studied the ef-fects of dantrolene sodium in 23 patients withhemiplegic spasticity of various etiologies.31

The drug was most effective in reducing orabolishing clonus and somewhat less effica-cious in decreasing the resistance to stretchand the tendon reflexes. These authors re-ported that gait was improved and the pa-tients found it easier to take care of theirpersonal needs and in general, motor perfor-mance was improved.31 Of interest is a studyof enteral administration by Meyler, in which25 patients with spasticity underwent evalu-ation of the pharmacokinetics and effects ofdantrolene sodium after prolonged adminis-tration. The results were better on 100 mgdaily than on a higher daily dose and an in-crease of the daily dose from 200 to 400 mg

was not associated with higher blood levels.32

Weis has evaluated the differences in pharma-cokinetics between enteral and intravenousadministration of dantrolene.33 Thus changesin dosages are appropriate when intravenousroute administration is considered and theauthors administer it based on the patientsweight.

In the acute care setting, enteral treatmentoften begins with low-dose therapy via na-sogastic tube or percutaneous gastrostomy.

Doses begin at 25 to 50 mg and increase by25 to 50 mg every 4 to 5 days. Dantrolenecarries the advantage of minimal cognitiveside effects and only modest pharmacologicinteractions. The authors have occasionallyemployed the use of intravenous dantrolenetherapy for severe spasticity in persons withTBI; however, this should be done with greatcaution. Dantrolene therapy has been asso-ciated with hepatic toxicity.34 This is espe-

cially true, when other agents that may facili-tate hepatotoxicity and careful monitoring ofliver function profiles are warranted. Durham


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has reported that the hepatotoxicity is notrelated to biotransformation issues,34 whileChan has discussed that those at highest riskare females older than 40 years and receiv-

ing more than 300 mg of dantrolene.35

Severaldrugs may impact the effects of dantroleneGilman has reported that metochlorpromideincreases the bioavailability of dantrolene,36

while Chou has discussed that dantrolene in-hibits platelet activation mainly due to sup-pression of phosphoinositide breakdown.37

This could be a concern in the post multi-trauma patient where bleeding is an issue.

Despite its limitationsside effectstheauthors consider dantrolene to be the first-line pharmacologic agent for the treatmentof severe spasticity resulting from TBI. Inthe acute care setting dantrolene is likely ap-propriate in those with severe or malignantspasticty.

Baclofen (Lioresal)

Baclofen is active at the GABA b receptorboth presynaptically and postsynaptically. Ithas been employed for the treatment of spas-

ticity in persons with spinal cord injury (SCI),cerebral palsy, multiple sclerosis, stroke, andbrain injury. Its utility in the treatment of spas-ticity in the acute care setting has not beenwell evaluated.

Baclofen has been noted to produce seda-tion, especially among those with cerebral dis-orders. Concerns including asthenia, depres-sion, as well as altered attention and memoryadditional concerns have been raised in ani-mal models and observed with humans. GABA

a facilitatory agents may impair recovery.38

Wallace et al have reported that agents thatact postsynaptically at the GABA receptor canbe associated with impaired functional recov-ery in an animal model.39 The phenomenonhas not been evaluated in a model utilizing in-trathecal delivery systems. Memory dysfunc-tion has also been associated with baclofentherapy in both animals and humans.40,41

Additional concerns with baclofen include

lowered seizure threshold and withdrawalsyndrome.42 Of particular concern in theacute care setting is the fact that baclofen

can increase bronchoconstriction and inhibitthe cough reflex. Such responses may makeventilatory weaning more challenging, espe-cially in those with a history of respiratory

compromise.The majority of studies demonstrating the

efficacy of baclofen have been conducted inpersons with SCI and multiple sclerosis.43 Ba-clofen appears effective at improving flexorspasms among those with spinal cord dysfunc-tion, yet little data exist to show improved ac-tivities of daily living or ambulatory capacity.Among those with spasticity of cerebral originlittle efficacy has been demonstrated. How-ever, enteral baclofen therapy may be war-ranted for those with severe spasticity whocannot tolerate dantrolene sodium and facethe risk of severe contracture or loss of rangeof motion.

Early intrathecal baclofen (ITB) therapy hasnot been evaluated. ITB therapy has beengenerally considered only after 6 months ofinjury.44 Several studies have demonstratedthe efficacy of ITB in cerebral spasticity.4547

This treatment has also been noted to

have beneficial effects on sphincter function,sleep, and voluntary movement. In those withsevere spasticity who are not responding toother treatments, perhaps earlier intervention with ITB therapy is warranted. While issuesregarding the role of baclofen, GABA, andneurorecovery must be weighed, ITB treat-ment may be preferable to long-term contrac-tures and its associated complications. Theseissues are often made more difficult becausemany such patients have concomitant infec-

tion making surgical implantation a difficultchoice. In such cases our own experience hasconsidered the role of intermittent bolus ther-apy or delivery via lumbar catheter to helpmaintain range of motion.

Diazepam (Valium)

Diazepam is a benzodiazepine and its ac-tion is mediated via the GABA a receptorand appears to increase presynaptic inhibi-

tion of polysynaptic and monosynaptic re-flexes. These agents may be administered en-terally or via intravenous administration. Since


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the action of this medication is also mediatedthrough the GABA system in a similar fashionto baclofen, concerns are raised regarding po-tential negative impact on neurorecovery.48

This agent can produce sedation and impairedcognitive processing; intoxication with thisagent can produce somnolence and evencoma.

The majority of data in support of this agentexists among those with spasticity of spinalorigin.49 In a study of persons with cerebralspasticity ambulation speed and grip strengthdeteriorated. In the acute care setting thisagent may have value as a temporizing agentamong those with severe spasticity and devel-oping contracture.

Medications in the intensive care setting

Propofol is an intravenous anesthetic agenthaving anticonvulsant property. It has uniquelipophilic properties and is ultra rapidlycleared after discontinuation. This agent pro-vides sedation that can be ultra rapidly clearedfrom the system. It has been used to treatmyoclonus that appears after therapeutic hy-

pothermia treatment in acute TBI and canbe employed to temporarily treat severe spas-ticity while additional agents are employed.However, Cremer et al have noted that 5 pa-tients with TBI who had received propofolhad experienced cardiac arrest and may haveexperienced propofol infusion syndrome.50

That work has suggested that propofol infu-sion at rates higher than 5 mg/kg per hourshould be discouraged for long-term sedationin the ICU. In the most severe cases neuropar-

alytic agents can be considered. Midazolamis a unique water-soluble benzodiazepine thathas action at the GABA and opioid receptors.Dahm et al have reported the use of intrathe-cal midazolam for spasticity.51 Of note, mida-zolam therapy if given as a continuous intra-venous infusion may carry a specific benefitfor those with pain as an exacerbating fac-tor to their severe spasticity.51 Neurorecoveryand cognitive related issues remain with the

use of midazolam.Rossier et al have reported on the role of

magnesium in the treatment of severe spas-

ticity in a woman with paraplegia.52 Magne-sium may also have anticonvulsant effects andhas a potential role in ameliorating a portionof the acute excitotoxic process after TBI via

its action as an N-methyl-D-aspartate (NMDA)antagonist. Morphine is a water-soluble opi-oid characterized by its slow absorption. Ithas substantial tone relieving properties andhas been used via intrathecal route for spastic-ity. Morphine can however produce respira-tory depression and hypotension.53 Many pa-tients with the most severe forms of acutespasticty following TBI also have marked auto-nomic dysfunction. When medically feasibleour own experience has noted that the treat-ment of such patients with lipophilic betablockers often results in a substantial declinein Ashworth score and improvement in dysau-tonomic symptoms.

Imidazolines

Both clonidine (Catapress) and tizanidine(Zanaflex ) act as agonists at the alpha-2adrenergic receptor, which inhibits excitatoryamino acid release. They also facilitate the ac-

tion of glycine, an inhibitor neurotransmitter.While clonidine is the older of the two agents,its clinical efficacy has been studied primar-ily in the spinal cord injury population.5456

However, in a case series, Dall and colleaguesreported good results in the control of cere-bral spasticity with clonidine.57 Peak plasmalevels of clonidine occur at 3 to 5 hours af-ter oral administration, and its half-life is 5 to19 hours. The starting dose can be 0.1 mga day. Clonidines transdermal form provides

an additional effective option for medica-tion delivery.58,59 Studies comparing tizani-dine with baclofen suggest equal or better ef-ficacy in control of spasticity in persons withmultiple sclerosis and strokes.60,61 A doubleblind, placebo-controlled trial in brain injuredpatients demonstrated tizanidines success intreating spasticity in this population.62 Thestarting dose is 2 to 4 mg at bedtime, increas-ing to a maximum of 36 mg per day. Tizani-

dines peak effect is in 1 to 2 hours, and itshalf-life is 2.5 hours. Both clonidine and tizani-dine carry significant side effects of dizziness,


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drowsiness, and hypotension. Some careshould be given in the consideration of us-ing these medications; animal research63 andstudies in human stroke survivors64 suggest

alpha-2 agonists may slow recovery from braininsult. Thus in the authors opinion the roleof these agents in the acute care setting islimited.

Gabapentin (Neurontin)

While its mechanism of action is unclear,the anticonvulsant gabapentin has been sug-gested for use as an antispastic agent. In stud-ies of persons with multiple sclerosis6567 andspinal cord injury,68,69 gabapentin was effec-tive in reducing spasticity with minimal ef-fects on cognition. This agents pain control-ling effects may play a role in its ability toimprove spasticity. It has also been used forthe treatment of dementia-related agitation70

and the mentally ill71; however, Childers andHolland72 reported 2 cases of increased agi-tation during its use in TBI patients. The ef-fective dose for the treatment of spasticity is400 mg 3 times a day or higher, to a maxi-

mum of 3600 mg a day total. Since this agentis mostly metabolized via the renal system itmay be helpful in those with hepatic dysfunc-tion or those where multiple drug interactionsare a concern. Gabapentin is limited by thefact that no intravenous preparation exists;however, it may also be a useful choice inthose with seizures who need anticonvulsanttherapy.

Neurolytic therapy

Cognitive side effects or tolerance issueslimit many systemic therapies. Thus in thosewith severe spasticity a reasonable portfolioof therapy might turn to interventional proce-dures, especially when it is focal. Phenol canbe delivered via indirect mixed nerve block-ade or via motor point block.73 Phenol via per-ineural injection causes a denaturation of pro-tein. The cost of this agent is minimal. It hasimmediate anesthetic effects and it impacts all

neural fibers. Concerns include sensory loss,dysestheias, and vascular complications.74,75

In the acute care setting perineural injection

in the treatment of lower extremity adductorand elbow flexor tone may offer the advan-tage of easy access, reasonable positioning,and immediate onset. If the patient can toler-

ate prolonged side lying then the tibial nervecan also be accessed. In experienced handsphenol can be an extremely effective treat-ment for focal spasticity and helps to maintainfunctional range in the acute care setting.75

Phenol chemoneurolysis can also be used tofacilitate the application of a serial casting pro-gram. The duration of action varies with prox-imity of delivery and concentration of phenol.In some cases duration of action of greaterthan 1 year is not desired and may cause con-cern. Alcohol at low concentrations acts as alocal anesthetic and at higher concentrationsit appears to cause degeneration of neuronsand fibrosis.75 Pain, vascular complications,and skin discomfort have also been reportedwith the use of alcohol.

Chemoneurolysis with Botulinum toxintherapy is now available as 2 differentserotypes: Botulinum toxin A and B.76 Theseagents have been approved for the treatment

of dystonia but have been employed success-fully for the treatment of focal spasticity asan off-label use.7682 Development of futureserotypes may allow for varying duration ofaction that may show benefit for the intensivecare setting. Toxins are reasonable to delivereven in the acute care setting and have theadvantage of a relatively short duration of ac-tion. Of concern is the potential interaction with neuroparalytic agents and aminioglyco-side antibiotics. While cost has been cited as

a reason not to utilize these agents during anacute inpatient stay, further evaluation mayprove that they are cost-efficacious in prevent-ing secondary complications. Phenol and al-cohol have a very quick, almost immediate,onset of action, which is not the case withthe toxins where weeks may pass prior tofull treatment effect.83 Another serious prob-lem is the ceiling effect of safe administra-tion of this agent. This is a specific concern

when there is widespread tone. Botulinumtoxin can only be one of the tools used in themanagement of spasticity and will need to be


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supplemented with phenol chemoneurolysisand/or systemic medications.

Case discussion

Our patients tone continued to worsen despiteaggressive range of motion and splinting ther-apy. Propofol therapy was weaned to allow for in-creased arousal and respiratory independence. Atrial of dantrolene therapy was begun and carefulmonitoring of hepatic enzymes were undertaken.Given the extent of the patients brain injury it waschosen to avoid baclofen as well as immediate im-idazoline therapy. The team also chose to closelymonitor the patients magnesium and keep the pa-tient at the higher end of normal magnesium level.He was placed on beta blocker therapy to ame-liorate severe dysautnomia, resulting in an as-sociated amelioration of the posturing episodes.Tone appeared to improve to Ashworth 2 in theright lower extremity, but adductor tone remained

severe bilaterally as did right elbow flexor tone.During the course of treatment the patient hadrecently received aminoglycoside antibiotic ther-apy secondary to sepsis. Thus, we chose to per-form phenol neurolytic blockade of the obturatornerves and resulted in marked decline in adduc-tor tone. A phenol motor point block of the right

biceps was undertaken and produced a reductionin right elbow flexor tone. This therapy was com-plemented by the addition of a right elbow serialcast.

Fortunately over the next year the patient pro-gressed to recover cognitively and regained sig-nificant motor function in his right side. While no

one can be sure, we believe that early aggressiveintervention was helpful in preventing secondarycomplications.

CONCLUSION AND FUTURE DIRECTION

The management of spasticity in the acutecare unit remains problematic. There is only very limited research to guide clinicians intheir decision process. Thus each case is anindividual decision making process. We haveknowledge concerning potential limitationsconcerning our early intervention efforts, butonly limited knowledge of what is efficacious.Much work still needs to be done to develop

interventions with proven efficacy and ac-ceptable risk/benefit ratios. Progressive lossof range of motion and the development ofcontractures may impel the clinician to utilizemedications that could have potentially nega-tive consequences on recovery. ITB adminis-tration performed early on may prevent con-tractures and viscoelastic changes with onlylimited risks to motor recovery because ofthe low cerebral concentrations. Finally, re-

search addressing the potential to increase theefficacy of botulinum toxin injections withincreased dilution or endplate localization,which may increase the amount of spasticitythat can be treated, as well as lowering costmay increase its utility as a spasticity interven-tion in the acute care environment.

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