toxins

Communication Ankle and Foot Spasticity Patterns in Chronic Stroke Survivors with Abnormal Gait

Sheng Li 1,2,*

1 Department of Physical Medicine and Rehabilitation, McGovern Medical School, University of Texas Health Science Center, Houston, TX 77030, USA 2 TIRR Memorial Hermann Research Center, TIRR Memorial Hermann Hospital, Houston, TX 77030, USA



Received: 9 September 2020; Accepted: 2 October 2020; Published: 7 October 2020


Abstract: Chronic stroke survivors with spastic hemiplegia have various clinical presentations of ankle and foot muscle spasticity patterns. They are mechanical consequences of interactions between spasticity and weakness of surrounding muscles during walking. Four common ankle and foot spasticity patterns are described and discussed through sample cases. The patterns discussed are equinus, varus, equinovarus, and striatal toe deformities. Spasticity of the primary muscle(s) for each deformity is identified. However, it is emphasized that clinical presentation depends on the severity of spasticity and weakness of these muscles and their interactions. Careful and thorough clinical assessment of the ankle and foot deformities is needed to determine the primary cause of each deformity. An understanding of common ankle and foot spasticity patterns can help guide clinical assessment and selection of target spastic muscles for botulinum toxin injection or nerve block.

Keywords: spasticity; gait; stroke; botulinum toxin; nerve block

Key Contribution: The article describes and discusses four common ankle and foot deformities after stroke. Understanding these common presentations can help guide clinical assessment and selection of target spastic muscles for botulinum toxin injection or nerve block.

1. Introduction About 80% of chronic stroke survivors have varying degrees of abnormal gait and impaired locomotion capability [1]. Spasticity in the ankle and foot muscles is very common, and often results in various ankle and foot deformities, including equinus, varus, equinovarus, and striatal toe deformities. The spastic equinovarus deformity is the most common deformity seen [2–4]. An ankle and foot joint abnormality could have subsequent effects on the knee, hip, and trunk position and control in post-stroke hemiplegic gait through a kinetic chain effect. For example, an equinovarus deformity shifts the ground reaction force anterior to the knee joint, and thus facilitates knee (hyper)extension during the stance phase. Stroke survivors are often forced to increase hip extension to compensate for knee (hyper)extension to keep the center of gravity within the forefoot. During the swing phase, increased knee and hip flexion is required to clear the equinovarus foot from the floor. However, they are often unable to do so due to weak hip and knee flexors, and, instead, present with hip hiking and leg circumduction. Additionally, stroke survivors have a smaller base of support due to the equinovarus deformity. The stance phase is shortened to minimize the risk of fall. Therefore, the ankle and foot deformity is often associated with kinetic and kinematic gait abnormalities, such as gait asymmetry, slow speed, genu recurvatum, etc [3,5]. Joint abnormalities in the hip, knee, ankle, and foot joints observed in post-stroke hemiplegic gait are mechanical consequences of the interactions among muscle spasticity, weakness, and disordered motor control during locomotion [6]. Depending on the severity of spasticity and weakness of muscles

Toxins 2020, 12, 646; doi:10.3390/toxins12100646 www.mdpi.com/journal/toxins Toxins 2020, 12, x FOR PEER REVIEW 2 of 9 Toxins 2020, 12, 646 2 of 9 disordered motor control during locomotion [6]. Depending on the severity of spasticity and weakness of muscles surrounding a joint, various joint abnormalities can develop. The complex ankle surroundingand foot anatomy a joint, contribute various jointdirectly abnormalities to observed can deformities develop.. TheAs shown complex in ankleFigure and 1, four foot groups anatomy of contributemuscles (invertors, directly to evertors, observed dorsiflexors deformities., and As shownplantarflexors) in Figure act1, four on the groups ankle of– musclesfoot complex. (invertors, Any evertors,isolated ankle dorsiflexors, movement and is plantarflexors) a net result of act the on combined the ankle–foot activation complex. of a Anygroup isolated of target ankle muscles, movement e.g., isinversion a net result occurs of the when combined dorsiflexors activation (primarily of a group the oftibialis target anterior muscles, muscle) e.g., inversion and plantarflexors occurs when dorsiflexors(primarily the (primarily tibialis posterior the tibialis muscle) anterior co muscle)-activate. and In plantarflexors the presence (primarilyof spasticity, the stroke tibialis survivors posterior muscle)have less co-activate. control and Inisolated the presence activation; of spasticity,activation strokeis more survivors diffuse and have divergent less control [7,8]. andTherefore, isolated a activation;variety of activationankle–foot is deformities more diffuse could and divergentbe observed, [7,8]. depending Therefore, aon variety the severity of ankle–foot of spasticity deformities and couldweakness be observed, of individual depending muscles. on the severity of spasticity and weakness of individual muscles.

Figure 1. The muscles involved in ankle movement. EHL: extensor hallucis longus; EDL: extensor Figure 1. The muscles involved in ankle movement. EHL: extensor hallucis longus; EDL: extensor digitorum longus; FHL: flexor hallucis longus; FDL: flexor digitorum longus; Gastroc: gastrocnemius. digitorum longus; FHL: flexor hallucis longus; FDL: flexor digitorum longus; Gastroc: gastrocnemius. Note: Tendons of the soleus and gastrocnemius merge and form the Achilles tendon. The soleus tendon Note: Tendons of the soleus and gastrocnemius merge and form the Achilles tendon. The soleus is located in the medial portion of the Achilles tendon, thus contributing more to inversion, while the tendon is located in the medial portion of the Achilles tendon, thus contributing more to inversion, gastrocnemius tendon forms the lateral portion and contributes more to eversion. They plantarflex the while the gastrocnemius tendon forms the lateral portion and contributes more to eversion. They ankle joint when acting together [9,10]. plantarflex the ankle joint when acting together. [9,10]. Among the spectrum of treatment options for ankle and foot deformities and gait disorders, interventionsAmong the such spectrum as botulinum of treatment toxin (BoNT) options injection for ankle and and phenol foot neurolysis deformities are and commonly gait disorders, used to manageinterventions spasticity suchof as the botulinum ankle and toxin foot (BoNT) muscles injection [2,4,11,12 and]. Tophenol achieve neurolysis the best are clinical commonly outcomes, used it to is importantmanage spasticity to identify of thethe primaryankle and causes foot ofmuscles the deformity. [2,4,11,1 Based2]. To onachieve the assessment the best clinical from instrumented outcomes, it gaitis important analysis, BoNTto identify treatment the forprimary spasticity causes of target of the muscles deformity. has shown Based to on improve the assessment gait pattern from and walkinginstrumented speed gait [13 –analysis,15]. However, BoNT antreatment instrumented for spasticity gait analysis of target lab muscles is not available has shown inmost to improve clinics andgait itpattern is not and practical walking to perform speed [1 a3 computer–15]. However, assisted an gaitinstrumented analysis for gait every analysis patient. lab Understandingis not available commonin most clinics ankle andand footit is spasticitynot practical patterns to perform is helpful a computer to guide our assisted clinical gait assessment analysis for and every development patient. ofUnderstanding a treatmentplan. common These ankle common and foot ankle spasticity and foot patterns spasticity is helpful patterns to guide are presented our clinical here assessment through sampleand development cases. In all ofcases, a treatment no significant plan. These component common of ankle contracture and foot was spasticity detected. patterns The common are presented ankle andhere footthrough spasticity sample patterns cases. include:In all cases, equinus, no significant varus, equinovarus, component and of contracture striatal toe. was detected. The common ankle and foot spasticity patterns include: equinus, varus, equinovarus, and striatal toe. 2. Common Deformities 2. Common Deformities 2.1. Equinus (Plantar Flexion) 2.1. Equinus (Plantar Flexion) An equinus ankle and foot deformity in stroke survivors with spasticity is a condition where the ankleAn and equinus foot isheld ankle in and the plantarflexedfoot deformity position, in stroke and survivors there is diwithfficultly spasticity with voluntaryis a condition dorsiflexion where the of theankle ankle. and foot This is is held primarily in the causedplantarflexed by spasticity position, of theand ankle there plantarflexors is difficultly with (gastrocnemius voluntary dorsiflexion and soleus muscles)of the ankle. with This or without is primarily toe flexor caused spasticity. by spasticity Figure2 ofshows the ankle a 65-year-old plantarflexors female stroke(gastrocnemius survivor with and asoleus spastic muscles) equinus with ankle or and without foot deformity toe flexoron spasticity the right. Figure side, due 2 shows to a left a basal65-year ganglia-old female hemorrhage stroke fromsurvivor hypertension with a spastic three equinus years prior. ankle She and presented foot deformity with righton the spastic right side hemiplegia, due to anda left abnormal basal ganglia gait. Herhemorrhage main complaint from hypertension was right foot three drop years with prior. diffi cultShe footpresented clearance with during right spastic walking. hemiplegia This equinus and

Toxins 2020, 12, 646 3 of 9 Toxins 2020, 12, x FOR PEER REVIEW 3 of 9 deformityabnormal isgait. evident Her main by comparing complaint was the ankleright foot and drop foot positionswith difficult between foot clearance the left and during right walking. sides in FigureThis equinus2A,B. During deformity the midstanceis evident phaseby comparing of the una theff ankleected and left legfoot (Figure positions2A), between the left footthe left has and full contactright sides with in the Figure floor, 2A while and thereB. During is foot the drop midstance on the aphaseffected of right the unaffected side. The toesleft leg are (Fig almosture touching2A), the left foot has full contact with the floor, while there is foot drop on the affected right side. The toes are the floor. In contrast, during the midstance phase of the affected right leg (Figure2B), the right heel is almost touching the floor. In contrast, during the midstance phase of the affected right leg (Figure off the floor, while the left ankle is kept in the neutral position for foot clearance. On inspection, a callus 2B), the right heel is off the floor, while the left ankle is kept in the neutral position for foot clearance. was noted on her right forefoot, mainly located over the first metatarsophalangeal area. The modified On inspection, a callus was noted on her right forefoot, mainly located over the first Ashworth scale (MAS) of the ankle plantarflexor spasticity was assessed with the knee joint in both the metatarsophalangeal area. The modified Ashworth scale (MAS) of the ankle plantarflexor spasticity flexed and extended positions. With the knee joint flexed to 90 degrees (Figure2C), the ankle joint was was assessed with the knee joint in both the flexed and extended positions. With the knee joint flexed resting at 107 degrees. MAS for the ankle plantarflexors was a 1+. With the knee joint in the extended to 90 degrees (Figure 2C), the ankle joint was resting at 107 degrees. MAS for the ankle plantarflexors position (Figure2D), the ankle joint was resting at 130 degrees. MAS of plantarflexors was a 3. In both was a 1+. With the knee joint in the extended position (Figure 2D), the ankle joint was resting at 130 configurations, no clonus was detected, and full passive range of motion was achieved, as compared to degrees. MAS of plantarflexors was a 3. In both configurations, no clonus was detected, and full the contralateral side. However, no active dorsiflexion was observed on the right side. No spasticity passive range of motion was achieved, as compared to the contralateral side. However, no active was detected for the toe flexors (flexor hallucis longus and flexo digitorum longus) or invertors (tibialis dorsiflexion was observed on the right side. No spasticity was detected for the toe flexors (flexor anterior or posterior muscles). hallucis longus and flexo digitorum longus) or invertors (tibialis anterior or posterior muscles).

Figure 2. (A) Stroke survivor with an equinus ankle and foot deformity on the right side. (A): Left leg inFigure the midstance 2. (A) Stroke phase, survivor (B): right with leg an in equinus the midstance ankle and phase, foot deformity (C): the resting on the ankle right joint side. with (A): L theeft knee leg jointin the flexed, midstance and ( Dphase,): the ( restingB): right ankle leg in joint the midstance with the knee phase, joint (C fully): the extended.resting ankle joint with the knee joint flexed, and (D): the resting ankle joint with the knee joint fully extended. The difference in the resting ankle joint angle and MAS scores for the ankle plantarflexors with the kneeThe joint difference flexed in and the extended resting ankle revealed joint thatangle the and spasticity MAS scores of the for gastrocnemius the ankle plantarflexors muscle was with the primarythe knee cause joint flexed of the equinusand extended deformity. revealed The that gastrocnemius the spasticity muscle of the spansgastrocnemius across both muscle the kneewas the and ankleprimary joint, cause while ofthe the soleus equinus muscle deformity. crosses The the gastrocnemius ankle joint only. muscle Therefore, spans knee across joint both position the knee does and not aankleffect soleus joint, while muscle the spasticity. soleus muscle However, crosses the the contribution ankle joint of only the. spasticity Therefore, of knee the soleusjoint position muscle todoes the equinusnot affect deformity soleus muscle cannot spasticity. be definitively However, ruled the out. contribution Intramuscular of the needle spasticity electromyography of the soleus muscle (EMG) wasto the utilized equinus to furtherdeformity evaluate cannot muscle be definitively spasticity. ruled Spontaneous out. Intramuscular motor unit needle firing haselectromyography been commonly observed(EMG) was in spastic utilized muscles to further [16– 18evaluate]. This strokemuscle survivor’s spasticity. muscles Spontaneous were tested motor while unit lyingfiring on has an been exam bedcommonly with the observed right leg in relaxed spastic comfortably. muscles [16 Interestingly,–18]. This stroke mild survivor’s spontaneous muscles firing were was presenttested while in the lying on an exam bed with the right leg relaxed comfortably. Interestingly, mild spontaneous firing tibialis posterior, flexor hallucis longus, flexor digitorum longus, and tibialis anterior muscles, but not was present in the tibialis posterior, flexor hallucis longus, flexor digitorum longus, and tibialis in the gastrocnemius and soleus muscles. This finding supports diffuse and divergent involvement in anterior muscles, but not in the gastrocnemius and soleus muscles. This finding supports diffuse and post-stroke spasticity [7,8]. However, when taking all of the information (history, observational gait divergent involvement in post-stroke spasticity [7,8]. However, when taking all of the information analysis, physical exam, and EMG assessment) into consideration, the decision was made to inject (history, observational gait analysis, physical exam, and EMG assessment) into consideration, the botulinum toxin to the ankle plantarflexors only (150 units of incobotulinum toxin to the gastrocnemius decision was made to inject botulinum toxin to the ankle plantarflexors only (150 units of muscle and 50 units to the soleus muscle) to correct the equinus deformity. At the six week follow-up incobotulinum toxin to the gastrocnemius muscle and 50 units to the soleus muscle) to correct the visit, the patient reported that she walked much smoother at a faster pace than before the injection. equinus deformity. At the six week follow-up visit, the patient reported that she walked much It was observed that her right foot had full contact to the floor during the midstance phase, and she smoother at a faster pace than before the injection. It was observed that her right foot had full contact was able to dorsiflex her right ankle for foot clearance during the midswing phase. to the floor during the midstance phase, and she was able to dorsiflex her right ankle for foot clearance during the midswing phase.

2.2. Varus (Inversion)

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A varus ankle ankle and and foot foot deformity deformity is is a acondition condition where where the the ankle ankle and and foot foot complex complex is held is held in the in thevarus varus position, position, i.e., i.e., inversion. inversion. This This abnormal abnormal joint joint position position is is primarily primarily caused caused by by coexistence coexistence of spasticity in both the tibialis anterior muscle and the tibialis posterior muscle in spastic hemiplegia. As shown in Figure1 1,, thethe tibialis tibialis anterior anterior musclemuscle causescauses thethe ankleankle dorsiflexiondorsiflexion andand inversion,inversion, whilewhile the tibialis posterior muscle causes ankle plantarflexionplantarflexion and inversion. The net effect effect of concomitant activation ofof these these two two muscles muscles results results in anklein ankle inversion, inversion with, thewith ankle the jointankle in joint a near in neutral a nearposition, neutral i.e.,position, varus i.e., deformity. varus deformity. The varus The deformity varus deformity is shown inis Figureshown3 .in This Figure patient 3. This was patient a 65-year-old was a 65 female-year- whoold female sustained who a sustained left intracranial a left intracranial hemorrhage hemorrhage two years agotwoat years an outside ago at an hospital. outside She hospital. presented She withpresented right with spastic right hemiplegia, spastic hemiplegia, abnormal abnormal gait, and gait, a varus and deformity. a varus deformity. She ambulated She ambulated with apoint with canea point in cane her left in her hand. left Her hand. right Her ankle right was ankle fixed was in fixed the varus in the position varus position during during both stance both stance and swing and phases.swing phases. As such, As such, she bore she herbore weight her weight on the on anteriorthe anterior lateral lateral foot foot during during the the stance stance phase phase (Figure (Figure3, pre-injection).3, pre-injection). A callusA callus directly directly reflected reflected the the focal focal pressure pressure of weight of weight bearing bearing on thaton that area area of the offoot the (Figurefoot (Fig4A).ure On4A). physical On physical exam, exam, full passive full passive range range of motion of motion into ankleinto ankle dorsiflexion dorsiflexion andeversion and eversion was unablewas unable to be to achieved. be achieved. Examination Examination revealed revealed an MAS an of MAS 3 for of the 3 tibialisfor the anterior tibialis andanterior tibialis and posterior tibialis muscles,posterior 2muscles, for the plantarflexors, 2 for the plantarflexors, 1 for the flexor 1 for digitorum the flexor longus, digitorum and 0 longus for the, flexor and 0 hallucis for the longus. flexor Nohallucis ankle longus. clonus wasNo elicited.ankle clonus No active was ankle elicited. movement No active was observedankle movement in all directions. was observed Taking history in all anddirections. physical Taking exam findingshistory and into physical consideration, exam andfindings to correct into consideration, the varus deformity and to for correct better anklethe varus and footdeformity positioning for better for weightankle and bearing, foot positioning the decision for was weight made bearing, to perform the decision phenol (6%, was aqueous made to solution)perform neurolysis.phenol (6%, Under aqueous ultrasound solution) and neurolysis. electrical stimulationUnder ultrasound guidance, and motor electrical branches stimulation of the tibial guidance, nerve tomotor the tibialisbranches posterior of the tibial muscle nerve (1.0 to mL), the tibialis medial posterior (2.0 mL) andmuscle lateral (1.0 (2.0mL) mL), medial gastrocnemius (2.0 mL) and muscles, lateral and(2.0 motormL) gastrocnemius branches of the muscles, peroneal and nerve motor to the branches tibialis anterior of the peroneal muscle (2.0 nerve mL) to were the blocked. tibialis anterior As seen inmuscle Figure (2.30, hermL) ankle were andblocked. foot positionAs seen in immediately Figure 3, her improved ankle and after foot phenol position blocks. immediately improved after phenol blocks.

Figure 3. Figure 3.A A stroke stroke survivor survivor with with a varus a varus deformity. deformity. Her foot Her and anklefoot and position ankle improved position immediately improved after phenol blocks. immediately after phenol blocks.

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FigureFigure 4. 4.The Thecallus callus formationformation on the anterior anterior lateral lateral board board of of the the foot foot with with a varus a varus deformity. deformity. Figure 4. The callus formation on the anterior lateral board of the foot with a varus deformity. 2.3. Equinovarus 2.3.2.3. Equinovarus Equinovarus An equinovarus deformity is the most common deformity of the ankle and foot complex in spastic AnAn equinovarusequinovarus deformitydeformity isis thethe mostmost commoncommon deformitydeformity ofof thethe ankleankle andand footfoot complexcomplex inin hemiplegia. It is part of the “typical” hemiplegic gait pattern in stroke survivors [3,4]. This deformity spasticspastic hemiplegia.hemiplegia. ItIt isis partpart ofof thethe “typical”“typical” hemiplegichemiplegic gaitgait patternpattern inin strokestroke survivorssurvivors [3,4[3,4]]. . ThisThis is characterized by ankle plantarflexion and inversion. It is primarily caused by spasticity of the ankle deformitydeformity is is characterizedcharacterized byby ankleankle plantarflexionplantarflexion andand inversion.inversion. ItIt is is primarilyprimarily causedcaused byby spasticityspasticity plantarflexorsofof thethe ankleankle plantarflexors andplantarflexors invertors, andand with invertors,invertors, minimal withwith to no minimalminimal contributions toto nono contributionscontributions from the dorsiflexors. fromfrom thethe dorsiflexors.dorsiflexors. In contrast to InIn the varuscontrastcontrast deformity, to to the the varus varus spasticity deformity, deformity, of the spasticity spasticity tibialis anterior of of the the tibialis tibialis muscle anterior anterior plays amuscle muscle minimal plays plays role, a a minimal minimal if at all present,role,role, if if at at inall allthe equinovaruspresent,present, inin thethe deformity. equinovarusequinovarus Thus, deformity.deformity. the tibialis Thus,Thus, anterior thethe tibialistibialis muscle anterioranterior should musclemuscle not be shouldshould the target notnot bebe for thethe interventions targettarget forfor (botulinuminterventionsinterventions toxin (botulinum (botulinum or phenol). toxin toxin However, or or phenol). phenol). ankle However, However, plantarflexor ankle ankle plantarflexor plantarflexor spasticity may spasticity spasticity be present may may be be in present present the equinus in in deformity.thethe equinus equinus If present,deformity. deformity. itshould If If present, present, be addressedit it should should be be as addressed addressed demonstrated as as demonstrated demonstrated in Figure2. in in Figure Figure 2. 2. FigureFigureFigure5 shows 55 showsshows a stroke aa strokestroke survivor survivorsurvivor with with anwith equinovarus anan equinovarusequinovarus deformity deformitydeformity before beforebefore and after andand phenol afterafter phenolphenol injection. Thisinjection.injection. 34-year-old ThisThis patient3434--yearyear-- hadoldold patient anpatient intracranial hadhad anan hemorrhagicintracranialintracranial hemorrhagichemorrhagic stroke four yearsstrokestroke ago. fourfour He yearsyears presented ago.ago. HeHe with presented with right spastic hemiplegia, abnormal gait, and an equinovarus deformity. He rightpresented spastic hemiplegia,with right spastic abnormal hemiplegia, gait, and anabnormal equinovarus gait, and deformity. an equinovarus He ambulated deformity. with a quadHe ambulated with a quad cane. During the stance phase of the affected right leg, his right heel was off cane.ambulated During with the stancea quad phase cane. During of the a theffected stance right pha leg,se of his the right affected heel right was leg, off thehis floorright heel and was the ankleoff the floor and the ankle was inverted (Figure 5A). He bore his weight on the right lateral forefoot, as wasthe inverted floor and (Figure the ankle5A). was He boreinverted his weight(Figureon 5A). the He right bore lateral his weight forefoot, on the as manifestedright lateral byforefoot, a callus as in manifested by a callus in that area (Figure 5C). He had full passive range of motion of his right ankle. thatmanifested area (Figure by 5aC). callus He in had that full area passive (Figure range 5C). of He motion had full of passive his right range ankle. of motion MAS was of his a 3 right for the ankle. ankle MAS was a 3 for the ankle plantarflexors, 2 for the invertors (the tibialis posterior muscle), 0 for the plantarflexors,MAS was a 3 2for for the the ankle invertors plantarflexors, (the tibialis 2 for posterior the invertors muscle), (the 0tibialis for the posterior flexor hallucis muscle), longus 0 for the and flexorflexor hallucis hallucis longus longus and and flexor flexor digitorum digitorum longus, longus, and and 00 for for the the tibialis tibialis anterior anterior muscles. muscles. No No clonus clonus flexorwas digitorumelicited. He longus, had weak and voluntary 0 for the tibialisankle plantarflexion, anterior muscles. but no No active clonus dorsiflexion was elicited. was He detected. had weak voluntarywas elicited. ankle He plantarflexion, had weak voluntary but no active ankle dorsiflexion plantarflexion, was but detected. no active Under dorsiflexion ultrasound was and detected. electrical UnderUnder ultrasoundultrasound andand electricalelectrical stimulationstimulation guidance,guidance, motormotor branchesbranches toto thethe medialmedial (1.5(1.5 mLmL)) andand stimulation guidance, motor branches to the medial (1.5 mL) and lateral (1.5 mL) gastrocnemius, soleus laterallateral (1.5(1.5 mLmL)) gastrocnemius,gastrocnemius, soleussoleus (1.0(1.0 mmLL)), , andand tibialistibialis posteriorposterior (0.(0.55 mLmL)) musclesmuscles werewere blockedblocked (1.0 mL), and tibialis posterior (0.5 mL) muscles were blocked with 6% phenol (aqueous solution). withwith 6%6% phenolphenol (aqueous(aqueous solution)solution). . HisHis ankleankle andand footfoot positionposition immediatelyimmediately improvedimproved afterafter thethe His ankle and foot position immediately improved after the injection (Figure5B, post-injection). injectioninjection (Figure (Figure 5B, 5B, p postost--injection).injection).

Figure 5. A stroke patient with right spastic hemiplegia and equinovarus deformity during the mid-stance phase before (A) and after (B) phenol injection. Note, the callus formation is in the lateral

forefoot (C) in the equinovarus deformity. Toxins 2020, 12, x FOR PEER REVIEW 6 of 9

Figure 5. A stroke patient with right spastic hemiplegia and equinovarus deformity during the mid- Toxins 2020stance, 12 ,phase 646 before (A) and after (B) phenol injection. Note, the callus formation is in the lateral 6 of 9 forefoot (C) in the equinovarus deformity.

2.4. Striatal Toe 2.4. Striatal Toe The striatal toe deformity describes a condition of hyperextension of the great toe (Figure6). The striatal toe deformity describes a condition of hyperextension of the great toe (Figure 6). It It is seen in patients with dystonia, Parkinson’s disease, and spastic hemiplegia after stroke [19,20]. is seen in patients with dystonia, Parkinson’s disease, and spastic hemiplegia after stroke [19,20]. The The striatal toe deformity is primarily caused by spasticity of the extensor hallucis longus (EHL) in striatal toe deformity is primarily caused by spasticity of the extensor hallucis longus (EHL) in stroke stroke survivors. Botulinum toxin (BoNT) treatment has been effective, but the dose and accompanied survivors. Botulinum toxin (BoNT) treatment has been effective, but the dose and accompanied involvement of other muscles are variable [19,20]. Though it is easy to recognize this deformity and to involvement of other muscles are variable [19,20]. Though it is easy to recognize this deformity and treat it with BoNT, the clinical outcome depends on the dose and treatment of accompanied spastic to treat it with BoNT, the clinical outcome depends on the dose and treatment of accompanied spastic muscles. The case in Figure6 is a good example. muscles. The case in Figure 6 is a good example.

FigureFigure 6.6. TheThe striatalstriatal toetoe beforebefore andand twotwo monthsmonths afterafter botulinumbotulinum toxintoxin injection.injection. This was a 64-year-old female with a medical history of a patent foramen ovale and right middle This was a 64-year-old female with a medical history of a patent foramen ovale and right middle cerebral artery stroke 15 months prior, with residual left hemiplegia and abnormal gait. She presented cerebral artery stroke 15 months prior, with residual left hemiplegia and abnormal gait. She presented with a one-year complaint of hyperextension of her left great toe with associated pain. She regained with a one-year complaint of hyperextension of her left great toe with associated pain. She regained the ability to walk several weeks following her stroke with subsequent development of great toe the ability to walk several weeks following her stroke with subsequent development of great toe hyperextension. She had two previous injections to her left extensor hallucis longus (EHL) (50 hyperextension. She had two previous injections to her left extensor hallucis longus (EHL) (50 and and 100 units of Onabotulinum toxin A, respectively) at an outside facility without improvement. 100 units of Onabotulinum toxin A, respectively) at an outside facility without improvement. The The patient was referred to our clinic for possible phenol neurolysis for EHL spasticity. patient was referred to our clinic for possible phenol neurolysis for EHL spasticity. On exam, the patient had hyperextension of her left great toe of ~60 degrees in a resting supine position (Figure6, pre-injection). Walking with a cane, she initially had full foot contact on the left affected side during the mid-stance phase, but the left ankle then became plantarflexed (~30 degrees) and the great toe hyperextended after a few steps. Needle electromyography showed spontaneous firing greatest in the left gastrocnemius and EHL muscles, with moderate activity of the soleus muscle and faint activity of the tibialis anterior muscle. A diagnostic lidocaine block of her tibial nerve motor branches to the gastrocnemius and soleus muscles was performed, resulting in full foot contact with the floor and greatly reduced great toe hyperextension during the stance phase. The patient was then scheduled for incobotulinum toxin injections to the left gastrocnemius (75 units), soleus (50 units), and EHL (25 units). Two months after injections, she exhibited full foot contact with the floor without great toe extension during the mid-stance phase, with concomitant reduction of pain and improved walking speed (Figure7).

3. Discussion Figure 7. A stroke survivor with a left striatal toe has ankle plantarflexion during the mid-stance phase Theto compensate above ankle for great and toe foot hyperextension deformitiesare (left commonly). After a successful seen in lidocaine clinical block practice. of the These tibial nerve common spasticitymotor patterns branches usually (middle present), she received with diff botulinumerent levels toxin of severity. (BoNT) to Proximal the gastrocnemius, knee and hip soleus muscles, and also haveextensor different hallucis degrees longus of weakness (EHL) with and a successful spasticity outcome that may (right alter). the ankle and foot deformities over time. In addition, other rare presentations may be seen, for example, focal spasticity of the extensor digitorumOn exam, longus the or patient toe curling had hyperextension from intrinsic foot of her muscle left great spasticity toe of [ 21~60]. degrees Therefore, in a various resting clinical supine presentationsposition (Figure of ankle6, pre and-injection). foot spasticity Walking are with observed a cane, inshe the initially presence had of full a spastic foot contact hemiplegic on the gait. left Despite a general presentation of extensor spasticity in the lower extremity, there is no typical ankle and foot deformity in post-stroke hemiplegia. Similar to various spastic hemiplegic gait patterns, Toxins 2020, 12, x FOR PEER REVIEW 6 of 9

Figure 5. A stroke patient with right spastic hemiplegia and equinovarus deformity during the mid- stance phase before (A) and after (B) phenol injection. Note, the callus formation is in the lateral forefoot (C) in the equinovarus deformity.

2.4. Striatal Toe The striatal toe deformity describes a condition of hyperextension of the great toe (Figure 6). It is seen in patients with dystonia, Parkinson’s disease, and spastic hemiplegia after stroke [19,20]. The striatal toe deformity is primarily caused by spasticity of the extensor hallucis longus (EHL) in stroke survivors. Botulinum toxin (BoNT) treatment has been effective, but the dose and accompanied involvement of other muscles are variable [19,20]. Though it is easy to recognize this deformity and to treat it with BoNT, the clinical outcome depends on the dose and treatment of accompanied spastic muscles.Toxins 2020 The, 12, 646case in Figure 6 is a good example. 7 of 9 this versatility of ankle and foot spasticity involvement reflects that ankle and foot deformity is a mechanical consequence between muscle spasticity, weakness, and its interactions with the ground reaction forces [6]. The standard algorithm to treat ankle and foot deformities and gait disorders can be found elsewhere [2,11]. Understanding common ankle and foot spasticity patterns is helpful to guide clinical assessment and selection of target spastic muscles for botulinum toxin injection or nerve block. However, contracture should be identified first, since, if present, different treatment plans are necessary [2,11]. Comprehensive and careful assessment is needed to determine the primary cause of each deformity. In addition to routine history and physical exam including observational gait analysis, EMG and diagnostic lidocaine blocks may be required to make an accurate diagnosis. It is Figure 6. The striatal toe before and two months after botulinum toxin injection. ideal to have instrumented gait analysis, but this is not practical for most clinics. EMG findings of spontaneousThis was a motor 64-year unit-old firing female should with a be medical used with history caution. of a patent These foramen findings ovale suggest and right the presence middle cerebralof spasticity artery in stroke a muscle. 15 months However, prior, EMG with residual findings left do hemiplegia not explain and how abnormal or whether gait. spastic She presented muscles withcontribute a one-year to abnormal complaint ankle of hyperextension and foot position of her or left gait great patterns. toe with In theassociated equinus pain. deformity She regained seen in theFigure ability2, spontaneous to walk several motor weeks unit firing following was di herffusely stroke present, with subsequent which is not development uncommon[ 8of]. great However, toe hyperextension.history and physical She had exam two suggested previous the injections gastrocnemius to her andleft soleusextensor muscle hallucis spasticity longus was (EHL) the (50 primary and 100contributor units of toOnabotulinum the gait disorder. toxin Lidocaine A, respectively) blocks should at an beoutside diagnostic facility and without confirmatory improvement. of the clinical The patientobservations was referred (Figure to7). our clinic for possible phenol neurolysis for EHL spasticity.

FigureFigure 7. 7. A Astroke stroke survivor survivor with with a left a leftstriatal striatal toe has toe ankle has ankle plantarflexion plantarflexion during during the mid the-stan mid-stancece phase tophase compensate to compensate for great for toe great hyperextension toe hyperextension (left). After (left). a Aftersuccessful a successful lidocaine lidocaine block of block the tibial of the nerve tibial motornerve branches motor branches (middle (middle), she received), she received botulinum botulinum toxin (BoNT) toxin (BoNT) to the togastrocnemius, the gastrocnemius, soleus soleus,, and extensorand extensor hallucis hallucis longus longus (EHL) (EHL) with witha successful a successful outcome outcome (right (right). ).

OnUnderstanding exam, the patient the di ffhaderent hyperextension ankle and foot of spasticity her left patternsgreat toe and of ~60 their degrees underlying in a resting primary supine causes positionis helpful (Figure to guide 6, thepre- interventioninjection). Walking plan. Tibialis with a anterior cane, she muscle initially spasticity had full is afoot primary contact contributor on the left of the varus deformity, while its role is negligible in the equinovarus deformity. However, management of tibialis anterior muscle spasticity has been controversial. Targeting this muscle is included in the treatment decision-making algorithm by one group of clinicians [2], but it is not considered by other groups [11,22]. As demonstrated in Figure3, successful suppression of tibialis anterior muscle spasticity contributes to correction of the varus deformity. However, successful correction of the equinovarus deformity does not need to address spasticity of the tibialis anterior muscle. These two contrasting examples reveal that whether the tibialis anterior muscle spasticity needs to be managed depends on the severity of spasticity and its mechanical consequences. If spasticity is severe, sustained involuntary activation of this muscle causes ankle dorsiflexion and inversion. The net result is a varus deformity in the presence of tibialis posterior muscle spasticity. Apparently, tibialis anterior muscle spasticity is not severe enough to counterbalance the plantarflexion activity from the tibialis posterior muscle spasticity in the equinovarus deformity. If uncertain, lidocaine diagnostic block is helpful. Toxins 2020, 12, 646 8 of 9

It is important to understand the mechanical consequences of spastic muscles during functional tasks, i.e., gait. The striatal toe deformity (Figure7) is another prime example. Great toe hyperextension is caused by spasticity of the extensor hallucis longus (EHL). Only treating the EHL spasticity was not adequate to solve the problem. The fact that the patient’s heel was elevated off the floor after a few steps suggests that EHL spasticity may develop gradually to improve ankle and foot stability during the stance phase in order to compensate for plantarflexor spasticity and its mechanical consequence of an equinus deformity. It is evident by the fact that a lower dose of BoNT was sufficient to suppress the EHL spasticity, with concomitant treatment of plantarflexor spasticity (Figure7). It has been reported that co-treatment of the plantarflexors and EHL are needed in some striatal toe cases [19,20].

4. Conclusions Clinical presentations of ankle and foot spasticity are various. There are mechanical consequences of interactions between spasticity and weakness of surrounding muscles during walking. Careful and thorough clinical assessment of the ankle and foot deformities is needed to determine the primary causes of each deformity. Understanding common ankle and foot spasticity patterns is helpful to guide clinical assessment and selection of target spastic muscles for botulinum toxin injection or nerve block.

Funding: This research received no external funding. Acknowledgments: I thank Jaskiran Ghuman DO for her editorial assistance and Bei Zhang MD, MS for her assistance in drawing Figure1. Conflicts of Interest: The authors declare no conflict of interest.

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