Facultad Ciencias de la Salud

Terapia Ocupacional
Orttica y Adaptaciones I
Docente: Daniela Larran D.

Palancas, principios biomecnicos y mecnicos, rtesis estticas y

Mano Gravemente Lesionada

Tipos de Palancas:
ANTES DEBEMOS SABER QUE:
APOYO: Punto de apoyo.
POTENCIA: Fuerza que hay que generar para vencer o equilibrar la resistencia.
RESISTENCIA: Carga a vencer o equilibrar.

Primer orden: El punto de apoyo est

entre la potencia y la
INTERAPOYO resistencia.
(Equilibrio) El brazo de potencia a
de ser mayor que el
brazo de resistencia.

Segundo orden: La resistencia se

encuentra entre la
INTERRESISTENC potencia y el fulcro
IA (apoyo). La potencia
siempre es menor que
(Fuerza) la resistencia;
disminuye la velocidad
transmitida.

Tercer orden: La potencia se

encuentra entre la
INTERPOTENCIA resistencia y el fulcro
(apoyo). La fuerza que
(Velocidad) se aplica es mayor que
la resultante y se utiliza
para ampliar la
velocidad a transmitir.
Sistema Nervioso Perifrico:
Constituido por neuronas y prolongaciones neuronales que se
disponen fuera del encfalo y la medula espinal; su funcin
principal hacer la conexin de los estmulos que recibe el
cuerpo (ya sean internos, externos o propioceptivo) con el
sistema nervioso central.
Desde un punto de vista funcional, este puede dividirse en
una parte somtica (relacionada con el movimiento voluntario
musculo esqueltico) y otra vegetativa (relacionada al
movimiento involuntario de rganos o viceras).

Nervios:
Haces de axones, los cuales estn envueltos
por clulas de Schwann y tejido conectivo (a
esto se le denomina Fibras Nerviosas).
Los nervios pueden ser craneales (salen del
encfalo) o raqudeos (salen de la medula
espinal); aquellos que llevan informacin
desde el SNC al organismo se llaman
EFERENTES (motores), mientras que aquellos
que traen informacin desde la perisferia
hacia el SNC se llaman AFERENTES
(sensitivos).
El ser humano posee 31 pares de Nv.
Raqudeos
8 cervicales
12 torcicos
5 lumbares
5 sacros
Un par en la zona coxal
Cada nervio est formado por una raz posterior (sensitiva ! fibras Aferentes) y otra
Anterior (motora! Eferente), la excepcin la posee el primer cervical que posee solo
raz motora.
Anatoma del Nervio:
Las clulas de Schwann rodean varios axones, a esta
fibra se le denomina amielinica. Sin embargo, en la
gran parte de los casos, la clula de Schwann rodea
mltiples capas de su membrana a un nico axn,
formando fibras nerviosas mielinicas; cada una de
estas fibra ya sea amielinica o mielinica, son rodeadas
por una pequea capa de tejido conjuntivo llamado
ENDONEURO; grupos de fibras se agrupan en pequeos
fascculos y se rodean de un tejido conectivo llamado
PERINEURO , y finalmente una tercera capa de tejido
conectivo denso, el EPINEURO, une y rodea los
fascculos para finalmente formar el NERVIO.

Plexo Braquial:
El plexo braquial est formado por las ramos anteriores de los nervios espinales de C5, C6, C7, C8
y parte de T1. En su trayecto se distinguen dos porciones: supraclavicular e infraclavicular.

SUPRACLAVICULAR:Las fibras nerviosas se distribuyen formando tres troncos primarios

1) Tronco superior: Proviene de las ramas anteriores de los nervios C5 y C6. En l se origina el
nervio supraescapular, que va a inervar los msculos supra e infraespinoso, y el nervio subclavio
que va a inervar el msculo con el mismo nombre.
2) Tronco medio: Proviene de la rama anterior del nervio C7.
3) Tronco inferior: Proviene de las ramas anteriores de los nervios C8 y T1.

INFRACLAVICULAR: cada tronco se divide en una divisin anterior y otra posterior, que se van a
reorganizar para formar lostroncos secundarios, fascculos o cuerdas.
Las divisiones anteriores del tronco superior y medio van a unirse formando elFascculo o Cuerda
lateral. Sus nervios terminales sern:
Nv. Torcico medial
Nv. Cutneo medial del brazo y del antebrazo
Nv. Musculocutneo
La rama lateral del N. Mediano.

La divisin anterior del tronco inferior formar el Fascculo o Cuerda medial. Sus nervios
terminales sern:
Nv. Cubital
La rama medial del Nv. Mediano.

Las tres divisiones posteriores formarn elFascculo o Cuerda posterior. Son ramas terminales el:
Nv. subescapular
 Nv. toracodorsal
Nv. axilar
Nv. radial

Recorrido y topografa del la inervacin nerviosa del miembro

superior:
Nervio Radial:
!Origen: C5 T1

!Inervacin Motora:
(ExtensoSupinadores)
-Trceps Braquial
-Anconeo
-Supinador
-Ext. Radial Corto
-Ext. Radial largo
-Ext. Ulnar del carpo
-Ext. Comn de los dedos
-Ext. Largo del pulgar
-Ext. Corto del pulgar
-Ext. Propio del ndice
-Ext. Propio del meique
-Abductor largo del pulgar

!Inervacin de la mano: Desde el pulgar al dorso del dedo anular por dorsal,
desde la mueca hasta la IF del pulgar y la IFD de los dedos largos.
Parte de la eminencia tenar por palmar.

!Manifestacin: Mano en gota

Deformidad de la mano que puede ir de leve

a severa.
Prdida parcial o total de la sensibilidad en
la mano.
Prdida parcial o total de los movimientos en
extensin de la mueca y la mano.

Nervio Mediano:
!Origen: C6 T1

!Inervacin Motora:
(FlexoPronadores)
-Pronador redondo

-Palmar mayor
-Flex. Radial
-Flex. Largo del pulgar
-Flex. Superficial de los dedos
-Flex. Profundo de los dedos 2 y 3
-Abductor corto del pulgar
-Oponente del pulgar
-1er y 2do lumbrical

!Tipo: Motor

!Inervacin de la mano: Por palmar, desde el

pulgar al dorso del dedo anular, desde falange distal
hasta la mueca.
Por dorsal, dedo pulgar, ndice, medio y dorso del
anular hasta interfalangica distal.
Perdida de sensibilidad de a porcin lateral de la
palma.

!Manifestacin Clnica: Mano de Simio.

Prdida parcial o total del movimiento de la

mano.
Prdida parcial o total de la sensibilidad en
los dedos.
Atrofia Tenar

Nervio Ulnar/Cubital:

!Origen: C8 T1

!Inervacin Motora:
-Flex. Ulnar del carpo
-Flex. Profundo 4to y 5to dedo
-Interseos
- 3er y 4to lumbrical
-Abductor del pulgar
-Abductor del meique
-Oponente del meique
-Flex. Corto del pulgar

!Tipo: Motor

!Inervacin de la mano: Del dedo meique al dorso

del dedo anular por palmar y dorsal.
Desde mueca a falange distal de ambos dedos.
!Manifestacin Clnica: Garra Cubital

Alteracin en la sensibilidad en mitad cubital de 4to y 5to dedo por palmar.

Dolor
Debilidad de musculatura cubital de la mano.
Signo de Froment +

Lesin de Nv. Perifricos:

Clasificacin segn SEDDON:

NEUROPRAXIA Compresin leve sin degeneracin.

Recuperacin espontanea entre la 3ra y 6ta semana.
AXONOTMESIS Interrupcin del axn, causando degeneracin.
Conservacin del epineuro, perineuro y endoneuro.
Posee buen pronstico.
Recuperacin hacia el 6to mes.
NEUROTMESIS Interrupcin de seccin completa.
Requiere tratamiento quirrgico.

Clasificacin segn SUNDERLAND:

1 Edema del Nervio, causa parlisis motora y leve compromiso de la

sensibilidad y del Sistema autnomo.
Compromiso transitorio.
2 Disfuncin motora de la sensibilidad y del sistema nervioso autnomo.
Los tubos neuronales se encuentran intactos y es de buen pronstico.
3 Axones con cicatrices irreversibles.
Clnicamente se compara con Axonotmesis.
4 Lesin sin cruce de axones y desorden fasicular.
5 Discontinuidad nerviosa (Neurotmesis).
Msculo:
Es un rgano compuesto por clulas alargadas llamadas fibras colocadas en forma de
haces, que se encuentran envueltas por vainas conjuntivas se al prolongarse forman el
tendn.
Las propiedades musculares son:
Pueden deformarse
Pueden contraerse
Son blandos
Su funcionamiento esencial es el contraerse y estirarse para permitir el movimiento de
segmentos del cuerpo.
Poseemos tres tipos de tejido muscular
!Estriado: Poseen contraccin rpida y voluntaria; se insertan en procesos seos, a
travs de un tendn.
!Liso: Recubren conductos anatmicos, poseen contraccin lenta e involuntaria.
!Cardiaco: Es un caso especial ya que trata de una variante del musculo estriado,
pero que posee contraccin involuntaria.

Fascia y sus Extensiones:

La Fascia est compuesta por tejido
conectivo resistente. Su funcin es de
envolver y conectar todas las estructuras
corporales; esta entrega soporte,
proteccin y forma.
La Fascia est encargada tambin des
desplazamiento y deslizamiento que
realizan los segmentos.
Las extensiones de la Fascia profunda son:
Epimisio: Recubre al msculo.
Perimisio: Recubre a los fascculos.
Endomisio: Recubre a las miofibrillas
Lesiones musculares:

Lesiones musculares directas Lesiones musculares indirectas

*Contusin: Compresin muscular por
traumatismo directo.
*Laceracin Muscular: Lesin
penetrante (politraumatizado).
Lesin por elongacin
Son resultado de una fuerza intrnseca y
generada por el musculo.
Se clasifican en:
*Distencin Muscular (Grado I): Dolor
difuso.
*Desgarro Parcial (Grado II): Dolor focal
mas equimosis.
*Desgarro Completo (Grado III): Vientre
muscular mas hematoma.

Lesiones Tendneas:

Zonas de la Mano:
Nuestras manos poseen una topografa y distribucin nica, la cual nos permite casi con plena
exactitud la identificacin y distribucin de las estructuras anatmicas que se encuentran en
cada segmento topogrfico de la mano.
Zonas de la mano Flexora

Zona uno:
Desde la insercin del tendn superficial hasta la
falange distal.
Posee un solo tendn en su topografa.
Posee un grado de deslizamiento mnimo por lo
cual en pacientes de edad avanzada con dao en
esta zona, la lesin se mantiene.
En pacientes jvenes se realiza el procedimiento
de tenorrafia el cual permite buenos resultados.

Zona Dos:
Conocida como la zona de nadie (Bunnell).
En esta zona existen dos tendones el superficial y el profundo.
El tendn pasa a travs del canal digital intrasinovial.

Una vez intervenido debe realizarse el protocolo de activacin temprana, ya que esta
zona posee muchas adherencias.
Los resultados son regulares dependiendo de la intervencin realizada y en el tiempo
realizado.

Zona Tres:
Desde la polea A1 hasta el borde distal del tnel del carpo.
Ubicada en la palma de la mano.
Zona extrasinovial (Los msculos lumbricales van en pro al proceso de recuperacin).
Posee un buen pronostico post intervencin y rehabilitacin.

Zona Cuatro:
Zona del tnel del carpo.
Es rara la lesin de esta zona ya que est protegida por el ligamento anterior del carpo.
 Si existe lesin, se asocia con el nervio mediano y lesin de arcos palmares.
Por existencia de varios tendones, en caso de lesin, deben realizarse varias tenorrafias
con el fin de obtener el resultado esperado.

Zona Cinco:
Zona del paquete vascular.
Es una zona con abundante irrigacin.
Con frecuencia asociada a :

-Lesin de flexores de la mueca

-NV. Mediano y Cubital

-Arteria Radial y Cubital

Las intervenciones poseen buen pronstico.
Estas lesiones se ven frecuentemente en intentos de suicidio (heridas corto punzantes).

Ortesis Flexora de IF (circuito, dos puntos)

Velcro solidario (flexin de dedo adyacente por funcin de dedo indemne)

Puede ser rgida o de neopreno.
Zonas de la mano Extensora

Zona Uno:
A la altura de la insercin del tendn extensor.
Articulacin interfalangica distal.
Se ven las lesiones conocidas como:

-Mallet finger
-Mallet Fracture
Su lesin ve afectada extensin del segmento.

Zona Dos:
Falange media.
Las lesiones por aplastamiento o heridas cortantes
son comunes en esta zona.

Zona Tres:
Articulacin interfalagica proximal.
Lo ms visto: Dedo en Boutonniere.

Zona Cuatro:
Falange proximal
Zona de mucha adherencia tensinosa.

Zona Cinco:
Articulacin Metacarpofalangica
 Lesin comn: lesin de la banda sagital radial del 3er dedo.
Zona Seis:
Metacarpiano
Es una zona que tiende a la adherencia tendinosa ya que posee poco tejido celular
subcutneo.

Zona Siete:
Retinaculo extensor.

Zona Ocho:
Antebrazo

Sistema extensor

Estructura y funcin del Tendn:

El tendn es una estructura alargada, que posee gran resistencia tensil, el cual est constituido
por haces fibrosos (colgeno tipo I) envueltos por un tejido conjuntivo laxo. La continuidad del
tendn con el musculo se consigue por prolongacin del endomisio, perimisio y epimisio; la
insercin en el hueso es causada por la penetracin de las fibras tendinosas que conectan con las
fibras de colgeno seo a travs de las fibras de Sharpey.
La funcin del tendn es de transmitir las fuerzas tensiles
originados por el musculo y los movimientos de los huesos.
Los tendones no se contraen ni se relajan.

Todo tendn tiene un capacidad de elongacin en respuesta

a una fuerza tensil y toda fuerza tensil es originada por una
carga; por lo tanto existe una relacin carga, fuerza tensil y
elongacin.

Cuando el tendn es sometido a una fuerza tensil por

encima del 3% en forma continua, este se comienza a
deformar en forma permanente.

El tendn se ve tambin sometido a fuerzas de compresin,

estas fuerzas no se originan de tensiones externas sino de la
carga que recibe al dar vuelta una curva anatmica o
insertarse en una articulacin desviada. Al mover el
miembro, el tendn es sometido a fuerza de friccin conocida como fuerza de roce. Esta
fuerza de roce aumenta la carga que el tendn recibe y tiene consecuencias prcticas a la hora
de ubicar las articulaciones en el espacio de una forma determinada.

Los tendones Extensores poseen inervacin del Nervio Radial, en cambio los tendones Flexores
reciben inervacin nerviosa por parte del Nervio Mediano.

Vainas Sinoviales:
Es un saco membranoso el cual recubre los tendones
que recorren un tnel seo o fibroso; su funcin es
facilitar el deslizamiento del tendn evitando el
roce de este sobre otras estructuras. La gran parte
de los tendones de la mano y del pie poseen su
vaina sinovial.

Todas las vainas sinoviales tienen una capa

superficial fibrosa y una interior serosa, la cual
segrega sinovia, reduciendo al mnimo el roce del
tendn.

Cuando existe una lesin, las vainas sinoviales son

las de mayor riesgo de adherencia.
En la palma de la mano, los tendones se deslizan por tres vainas carpianas las cuales son:

1) Vaina Radiopalmar.
2) Vaina Media.
3) Vaina cubitopalmar.

Poleas:
Los tendones Flexores quedan sujetos al segmento seo por tres poleas fibrosas en cada dedo;

! La polea A1 se encuentre ligeramente por encima de la cabeza metacarpiana

!La polea A3 en la cara anterior de la primera falange

!La polea A5 en la cara anterior de la segunda falange

Entre las poleas de fibras transversales, la continuidad
de la vaina fibrosa queda garantizada por poleas
constituidas por un sistema de fibras tanto oblicuas
como cruzadas que pasan en banderola por delante de
la articulacin, menos gruesas para adaptarse a los
movimientos de flexin de las falanges. Se trata de la
polea A2, en la cara palmar de la articulacin
metacarpofalangica y de la polea A4, delante de la
articulacin interfalangica proximal. De este modo, con
la cara anterior ligeramente cncava de las falanges, las
poleas constituyen autenticas correderas osteofibrosas.

Poleas Anulares:

Son 5 y estn distribuidas de forma

transversal en los tendones flexores; son
ms gruesas y estn bien definidas.

Poleas Cruciformes:
Son 4 y estn distribuidas sobre las articulaciones en forma de cruz.

Fase de Inflamatoria
Fase Fibroblastica
Fase de remodelacin
Lesiones del Ligamento:
Funcin ! Unin y estabilizacin de estructuras anatmicas, como articulaciones
interconectadas entre s.
Ambas poleas estn encargadas de la disociacin de un
movimiento y otro, a nivel de cada articulacin que compone a
los dedos; estas estn dividas en tres zonas de distal a proximal
en zona 1, zona 2 y zona 3.
Fases de la cicatrizacin del tendn
Migracin celular del tejido sinovial y del propio tendn.
Los primeros 7 das (1ra semana).
Das crticos con posibilidad de mayor generacin de
adherencias, por lo cual se recomienda movilizacin del
segmento antes del noveno da.
Ocurre la proliferacin de fibroblastos.
Sntesis de colgeno
Aumento en la fuerza tensil del tendn (al noveno da) por lo
cual favorece la cicatrizacin y la calidad de este; lo cual
depende netamente de la calidad de sutura y procedimiento
realizado.
Puede perder su capacidad de deslizamiento por falta de
movilidad.
Reorganizacin a lo largo del eje del tendn.
Comienza en la tercera semana.
 Mecanismo de lesin !habitualmente por traccin torsin articulares que sobrepasan
su resistencia. ! ESGUINCE

ESGUINCES
GRADO I
Distencin con dao microscpico.
Con poco o sin dolor.
Mantiene estabilidad articular.
Mnima interferencia con actividad
fsica.
GRADO II
Dao parcial de la estructura.
Lesin visible con edema y equimosis.
Inestabilidad articular leve.
Suspensin de actividad fsica
Inmovilizacin
 GRADO III
Lesin severa.
A l t o c o m p r o m i s o a r t i c u l a r,
inestabilidad mecnica.
Edema y dolor
Postura antialgica.
Reparacin quirrgica.
Suspensin de actividad.

Fracturas:
Solucin de continuidad de un segmento
seo.
Clasificacin:
Habitual
Patolgica
Fatiga o stress

Mecanismos de produccin:
Directo !lugar de impacto de
fuerza.
Indirecto!
1) Compresin
2) Flexin
3) Cizallamiento
4) Torsin
5) Traccin
- Fracturas Abiertas
- Fracturas Cerradas
-Fracturas Estables
- Fracturas Inestables
- Fracturas Completas
(Simples/Desplazadas/Conminuta)
- Fracturas Incompletas

Consolidacin sea:
1) Hematoma fracturara
2) Callo blando o fibroso (hasta la 3 semana).
3) Callo seo (hasta 6 o 12 semanas).
4) Remodelacin sea (hasta 2 aos).

Edema:
Inflamacin significativa causada por la acumulacin de
lquido proveniente de tejidos de cuerpo. Este se
produce por un desequilibrio entre las fuerzas que
regulan el paso del lquido de un compartimiento a otro;
si el paso del agua es abundante del compartimiento
intravascular al intersticial, se dar origen al edema.

Osteofitos:
Son el crecimiento excesivo de tejido seo; son
pequeas protuberancias redondas de hueso extra
que crecen alrededor y dentro de las articulaciones.
Estos son un intento del cuerpo, de compensar el
deterioro de la articulacin debido a la edad,
degeneraciones articulares o alguna lesin, sin
embargo no es una buena forma del cuerpo de auto
ayudarse ya que causan dolor y destruccin de
segmentos adyacentes (ligamentos, tendones,
articulaciones, etc.).

PATOLOGIAS

Artrosis:
Enfermedad articular crnica cuya lesin bsica se encuentra en las alteraciones
degenerativas del cartlago articular.
Presencia de fenmenos degenerativos especialmente a nivel osteoarticular (osteofitos)
y fenmenos inflamatorios sinoviales (sinovitis).
Caractersticas:
- Destruccin del cartlago articular
- Causa impacto en el hueso subcondral
(erosiones).
- Presencia de osteofitos
- Disminucin del espacio articular
- No es infecciosa
- Evolutiva
- Compromete secundariamente el resto
de tejidos que componen la
articulacin
- No tiene cure (solo se puede estancar
el progreso de la enfermedad).
Sntomas:
- Dolor durante la actividad
- Dolor en reposo
 - Rigidez
- Diminucin de ROM
- Limitacin funcional
- Aumento de volumen
- Crepitaciones
- Movimientos dolorosos
- Cambios de eje

Rizartrosis:
Artrosis de la articulacin trapecio metacarpiana, corresponde a la
abrasin o dao progresivo de la superficie articular, la cual est
asociada a la formacin de osteolitos.
En la clnica:
- Rigidez
- Limitacin del ROM
- Dolor
- Prdida progresiva de la F.
- Puede derivar en deformidad
- Subluxaciones (en grados variables).
- Disminucin del espacio articular

Enfermedad de Dupuytren:
Enfermedad que presenta cambios fibroblasticos prolifrativos
del tejido celular (los fibroblastos generan ms colgeno por lo
cual hay mayor consistencia) que involucra a la aponeurosis
palmar. Aparicin de ndulos y cordones fibrosos que se
entrelazan a la aponeurosis palmar, haciendo que la movilidad
de las articulaciones se vea limitada y finalmente termine en
una mano rgida y retrada.
De origen desconocido.
Clnica:
- Presencia de ndulos o quistes.
- Deformidad en los dedos involucrados.
- Perdida de movilidad
- Perdida de ROM

Dedo en gatillo:
Es un Tenosinovitis estenosante de la vaina del
tendn flexor del dedo.
Ocurre un engrosamiento fusiforme inflamatorio.
Zona involucrada! zona II flexora
Clnica:
- Secundaria o microtraumas
- Dolor a la palpacin de la polea A1

Artritis Reumatoide:
Inflamacin crnica de etiologa desconocida mediada por el sistema inmune, que hace
proliferar la sinovial en forma pseudotumoral, llevando a la destruccin de los tejidos
circundantes y produciendo manifestaciones sistmicas.
Clnica:
- Inicio insidioso
- Enfermedad progresiva
- Involucra la inmunidad
- Manifestaciones sistmicas
- Formacin de pannus (tejido de granulacin
compuesta por clulas sinoviales
proliferativas).
- Anquilosis (rigidez en articulaciones)
- Dolor
- Subluxaciones
- Bursitis
- Debilidad
- Perdida de arcos longuitudinales y
transversos
- Deformidad

Rfaga Cubital:

Desviacin cubital de la base de la falange proximal, afectando la

articulacin metacarpofalngica (hiperextensin) e interfalngica
(flexin).
Se ve en enfermedades reumticas.

Dedo en Butonniere:
El tendn extensor se desgarra o separa de los dems tendones;
esto provoca un desgarre que se asemeja a un ojal (de ah su
nombre); la articulacin se ve forzada a bajar y el extremo distal del
dedo se dobla hacia atrs.
Clnica:
- Se ve afectada la articulacin metacarpolangica en adelante
- Afeccin de la zona 3 y 4 de la mano Extensora.
- Dolor e inflamacin
- Deformidad
- ROM interferido
- Sensibilidad en el dedo

Mallet finger o dedo en martillo:

Alteracin causada por la ruptura del tendn extensor a nivel de la falange distal. Se
caracteriza con la cada en flexin de la falange distal. Tambin puede presentarse en
fractura.
Alteracin en la zona I y II de los extensores.
Mallet fractura! Es la fractura de este segmento.

Cuello de Cisne:
Es la hiperextensin de la articulacin interfalngica proximal y flexin de la
articulacin interfalngica distal. La falange proximal se flexiona y por tenodesis se
flexiona la distal.
Es limitante y progresiva.
Afecta la zona extensora de los dedos.
Sndrome del tnel del Carpo:
Es el aumento de presin o compresin del nervio mediano; al
elevarse el ligamento transverso facilita esta compresin
generando mayor punto de dolor.
Clnica:
- Dolor
- Parestesia en territorio inervado por el nervio mediano
- Prdida de fuerza en pinzas
- Atrofia tenar

Sndrome del tnel cubital:

Es el atrapamiento del nervio cubital en el segmento del codo, entre los dos fascculos
del cubital anterior.
Clnica:
- Dolor punzante
- Parestesia en dedo anular y meique
- Hiperflexion del codo genera la sintomatologa
- Debilidad en prensin
- Aplanamiento y atrofia en zona hipotenar
- Debilidad muscular
Canal de Guyn:
Sndrome neurolgico producido por le atrapamiento o
compresin del nervio cubital en el canal de guyn (canal
anatmico de procesos seos localizado entre el gancho del
ganchoso, el pisiforme y el ligamento anular anterior del
carpo).
Clnica:
- Atrofia hipotenar
- Hipoestesia cubital de 4to y 5to dedo
- Dolor
- impotencia funcional

Epicondilitis / Codo de tenista:

Inflamacin de la musculatura a nivel de la zona lateral
del Codo. Origen de los msculos extensor radial del
carpo y del extensor comn de los dedos.
Mecanismo ! movimientos de flexo extensin en
combinacin de pronosupinacin de antebrazo,
extensin de mueca y flexin de los dedos.
Clnica:
- Dolor
- Impotencia funcional

Epitrocleitis / Codo de golfista:

Es la inflamacin de la epitrclea (prominencia sea en
la parte interna del humero) y de los tendones que se
insertan en el.
Mecanismo!sobre uso y estrs repetitivo, traumatismos,
soporte de altas cargas de peso con el brazo y el codo,
realizacin de movimientos que involucren la flexin del
codo con la flexin de mueca.
Clnica:
- Dolor local
- Dolor a la palpacin
- Dolor y molestia al extender o flexionar la
mueca.
- Parestesia

Tendosinovitis de Quervain:
Es la inflamacin que afecta a los tendones del primer comportamiento extensor de la
mueca (abductor largo y extensor corto del pulgar).
Mecanismos!movimientos repetitivos con pinzas forzadas, extensin forzada o contra
resistencia del pulgar, procesos infecciosos o inflamatorios, tambin asociada a artritis
reumatoide y actividades laborales.
Clnica:
- Dolor
- Inflamacin
- Prdida de fuerza en prensin

Consecuencias de una mala intervencin Ortsica

Ulceras:
Son reas localizadas de necrosis celular cuyo origen se debe a la presencia de
presiones elevadas, localizadas en zonas blandas, durante largos periodos de
tiempo, normalmente debido al mantenimiento de una posicin fija.
Sus causantes son la insuficiente vascularizacin de los tejidos celulares por
altas presiones (principalmente en las prominencias seas, como las
tuberosidades, trocantes procesos).

Deformidad:
El mal moldeo por mal posicionamiento del segmento, es la causa comn de la
deformidad en procesos rtesicos; el terapeuta al no cumplir los
posicionamientos bsicos para el moldeo o al no necesitar el paciente la rtesis
en el proceso patolgico causante, se genera las deformaciones.
Tambin la poca expertis del TO o el mal manejo de la tcnica.

Rigidez:
Es la prdida o limitacin de la posibilidad de efectuar
un movimiento, aun pasivo, entre dos segmentos
anatmicos.
Causas! manejo inadecuado y mala entrega de
informacin sobre el uso vs tiempo de utilizacin de la
rtesis.
rtesis Esttica:
Aparato rtesico que no posee ningn componente mvil o articulado.

Ejemplo:

Dorsaleta
Cock up
Palmeta

Principios:
1. PROTEGER
2. CORREGIR
3. ASISTIR

1. PROTEGER:
- Prevenir el dolor y los edemas
-Disminuir tono
-Mantener ROM (ganado en las terapias)
-Evitar acortamiento y elongacin de tejidos blandos
-Prevenir movimientos no deseados
-Proteger estructuras

2. CORREGIR:
-Aumentar ROM de forma progresiva
-Mantener alineamiento seo

3. ASISTIR:
-Dar Soporte a una articulacin dolorosa
-Base de dispositivo de ayuda (ejemplo: lesiones de nervio radial por limitacin
funcional).

Clasificacin rtesica:
No articular: Sin influencia directa en la articulacin.
Ejemplo: Brace de hmero
 Esttica, no bloqueo de movimiento: Permite ROM completo activo en una
direccin y movimiento activo y restringido en direccin opuesta.

Esttica: inmoviliza completamente la articulacin.

Seriada: segn tolerancia se aumenta rango.

Ejemplo: En mano espstica puedo ir remoldeando la rtesis para aumentar el
grado de apertura de la mano.

Principios Biomecnicos:

Biomecnica articular y tensin de los tejidos

Por funcin
Por patologa

Principios mecnicos aplicados a las rtesis

!Alineacin
rtesis, alinea el segmento de acuerdo a los principios bsicos de fuerzas que ejerce
sobre la articulacin.

!Superficie de contacto
Es como el material adquiere la forma del segmento y si cumple los principios.
!Solucin de continuidad
Referente al moldeo que ejerce.
Ejemplo: ptos de presin, mala solucin de continuidad.

!Brazo de Palanca
Es el suficiente largo para realizar la conversin que se requiere realizar.

!Fijacin
Las sujeciones dependen del tipo de rtesis.

!Fuerzas especfica sobre los tejidos

Ejemplo: las correas.

!Concavidad
Curvatura del segmento

Otros: Contencin; tipo de palanca o circuito, ventaja mecnica, tipos de fuerzas que se
ejercen, etc.

rtesis: Palmeta
 Posicin de Seguridad Posicin Funcional

Grados de moldeo: Grados de moldeo:

Mueca: 30 extensin. Mueca: 20 - 35 extensin.
MTCF: 45 flexin.
MTCF: 70- 90 de flexin. IFP: 30 flexin.
IFP / IFD: extensin. IFD: 20 flexin.
Pulgar: abducido/ eminencia tenar Pulgar: abducido/ eminencia tenar
libre. libre.
Patologas: Patologas:
Mano gravemente lesionada. Espasticidad.
Manos con mucho edema Hipotona.
Artritis
Molde:

Puntos de referencia:
- Pliegue distal de la mano
- Pliegue proximal de la mano
- Pliegue de la mueca
- Tercer dedo
- 1er espacio interdigital
- 2/3 antebrazo
- Ancho longitudinal del antebrazo
 rtesis: Cock Up

Cock Up
Grados: Grados:
En tnel del carpo: Otras Patologas o Casos:
Mueca: 0 - 5 de extensin. Mueca: 30 de extensin.
Patologas:
Sndrome del tnel del carpo.
Tendinitis de extensores de mueca.
Post quirrgica.
Quemaduras.
Artritis reumatoide.
ACV.
Lesiones medulares y nervios perifricos (mano en gota).

Molde:
Puntos de referencia:
- Pliegue distal de la mano
- Pliegue proximal de la mano
- Pliegue de la mueca
- Tercer dedo
- 1er espacio interdigital
- Eminencia tenar
- 2/3 antebrazo
- Ancho longitudinal del antebrazo

Tiempo de uso:
Va a depender de
 Patologa
Caractersticas individuales del paciente
Ritmos fisiolgicos
Edad
Piel (calidad de esta)
Educacin

Educacin:
Patologa
Objetivo del uso de la frula en el tratamiento
Resultados esperados
Plan de ejercicios
Mal uso de la rtesis y precauciones
Aseo y cuidado de la rtesis.

Mano Gravemente Lesionada:

Lesin devastadora que afecta a muchas estructuras de la mano y que produce una
incapacidad funcional significativa directa o por impacto psicosocial.

Lesin de tres sistemas importantes

de la mano:
1. Compromiso de partes blandas
2. Compromiso de aparato flexor-extensor (en diversos grados).
3. Compromiso seo
Estructuras Comprometidas:
Tendones extensores y flexores
Nervios
Sistema vascular
Articulaciones y seo
Qu es?:
Patologa grave
Gran posibilidad de secuelas
 Equipo multidisciplinario para intervencin y
rehabilitacin
Complicaciones:
Rigidez
Dolor crnico
Infecciones post ciruga y reconstruccin
Mala consolidacin de fracturas o la no unin de estas.
Rehabilitacin:
Protocolo de duran
Protocolo de kleinert
Palmeta o dorsaleta

Objetivos:
Recuperar ROM
Recuperar fuerza
Recuperar Pinzas
Manejo de cicatriz
Manejo de sensibilidad
LOGRAR LA MEJOR FUNCIONALIDAD POSIBLE
 Lesiones de tendones
Tenorrafa Intervencin en la cual se suturan los dos extremos
seccionados del tendn.

Tenolisis Intervencin la cual tiene como finalidad liberar un tendn

englobado por presencia de adherencias.

Tenodesis Operacin que consiste en la fijacin del extremo del tendn

de un musculo a un hueso.
 Tenotoma Intervencin que consiste en la intervencin quirrgica de un
tendn.

Extracto traducido de Pgina oficial de la Orfit

Ortesis estticas

Hablar sobre qu termoplstico se va a utilizar y cual es ms adecuado para ciertos

diseos especficos nos entrega una gua bsica para el uso de rtesis estticas en
traumatologa. Podemos tambin especificar algunos principios bsicos que pueden ser
considerados cuando usamos distintos tipos de termoplsticos segn el propsitos de la
rtesis.

Elegir el material adecuado

Hay muchas opciones en diseo cuando consideramos la fabricacin de una rtesis

esttica. Puede ser un diseo volar, palmar, dorsopalmar (en ojal ) o circunferencial.

La rigidez del termoplstico no depende solo de la dureza del material. puede tambin
depender de la forma. entre ms circunferencial sea el diseo, ms rgida es la rtesis.

Hay una variedad de termoplsticos para seleccionar dependiendo del diseo:

Para las rtesis palmares o dorsopalmares, el termoplstico altamente recomendado por

su mnima capacidad de estiramiento y su resistencia al estrs hace una rtesis
completamente rgida. El orfibrace, Eco orfit, Eco orfit negro NS y orfit classic (versin de
Stiff) con un grosor de 3.2 es una excelente eleccin para este tipo de rtesis.

Para las rtesis por dorsal elija un material con cubierta para proveer un excelente
contorno a la anatoma y deje que lo asista la gravedad (por ejemplo: la rtesis para
protocolo de rehabilitacin de tendones flexores). Los materiales como el orfit flex,
orfitlight, orfitlight black NS, orfitlight atomic blue NS y orfit Ease en 3.2, trabajan
extremadamente bien.

Las rtesis circunferenciales se fabrican mejor con un producto con antiadherente (NS).
Este material puede ser adherido sobre si mismo o traslapado durante la fabricacin, y
luego ser separado cuando se corta en fro. Orfit NS, Aquavit NS, Orfit color NS y Orfilight
Black/ atomice blue NS son excelentes elecciones de uso de material. El grosor puede
variar entre 1.6 y 2.5.

El orficast es una buena solucin para dedos y manos pequeos dependiendo de la

rtesis.

Para cada una de las discusiones sobre los diseos siempre es importante seguir los
principios bsicos para la fabricacin de las rtesis:

1.- La posicin de reparacin ms comn es el intrinsic plus.

2.- La posicin de apertura de la rtesis es opuesta a la posicin del dao.
3. Cuando se inmoviliza un dedo largo o se inmovilizan todos o solo se inmoviliza el dedo
daado con el correcto soporte para el dedo adyacente.
4. Para inmovilizar una articulacin hay que incluir las estructuras proximales y dislates
para limitar el movimiento. Sin embargo cuando hay una fractura muy prxima a la
articulacin MTCF (por ejemplo el 5to metatarsiano), no es necesario inmovilizar la
articulacin proximal (la mueca en este caso).
5. Para inmovilizar el segmento hueso se debe incluir la articulacin prxima y distal para
prevenir el movimiento.

Los tiempos de uso y productos recomendados

Injuria muscular: 4 semanas

Dao de estructuras colgenas: 6 semanas.
Fractura de huesos:
Diafisis: 12
Epifisis: 6 semanas
La fractura de escafoide requiere sobre 12 semanas.

What is the Crucial Time for Initiation of

Intervention (splinting)?
Muscle contractures are likely to develop both immediately (acute phase) and through
several weeks, months poststroke (chronic phase). Acute phase contracture development
cascade is triggered by immobilization of the muscle in the shortened position primarily
due to paralysis and malpositioning. Reduction in protein systhesis, sarcomere
disorganization, shortening of muscle fiber length and increase in connective tissue
perimysium are changes that happen within hours to days.2 Therefore, delaying onset of
intervention up to an average of 4 weeks and a maximum of 8 weeks may be a late start.

Previous SectionNext Section

How Many Intervention Sessions Are Ideal
to Expect/Perceive Visible Macroscopic
Changes (extensibility)?
The contracture cascade initiated in the acute phase continues to evolve into the chronic
phase of spastic paresis, with the emergence of additional muscle overactivity, caused by
both the lesion and the paresis related disuse, leading to further contractures.3 This
observation continues to unfold over weeks, months and even after years. Because there is
paucity of studies that explain the time course of muscle contracture evolution and
deterioration in stroke survivors, it is difficult for the clinician to decisively earmark the
time to initiate intervention and sustain intervention, for a sufficiently optimal duration, to
cause significant changes in muscle extensibility. Therefore, a 4-week/28-session
intervention period, with a short duration 2-week follow-up, may or may not be sufficient
to study muscle extensibility in totality.

Previous SectionNext Section

Is There Consensus/Understanding on the

Optimal Duration of Splint-Wear During
Each Session?
There is lack of unison in the understanding among experts on the optimal splint-wear
(positioning) duration. It is evident from the current effort that immobilizing for 10 to 12
hours has no positive effect in contrast to the finding of Ada et als, two 30-minute sessions
per day of positioning for the shoulder.4 The possibility of multiple short sessions of wrist
positioning with splint, yielding positive results have not been ruled out entirely. Therefore,
introspection and emphasis in future efforts on the importance attached to the time duration
of splint wear per session before drawing premature conclusions is vital.

Other aspects of the study which need careful and close reflection are: lateral photographs:
in the absence of proven validity and reliability, the use of lateral photographs in estimating
the wrist angle, the primary outcome measure, cautions the reader on potential
methodological errors or biases1; secondary outcome measures: the chosen secondary
outcome measures are applaudable. However, acknowledging these subtle but definite
changes between groups, at baseline, 4-weeks and 2-weeks of follow-up, as indirect
reflectors of improved muscle extensibility would have appeared as a more balanced
presentation to the reader (vide Table- II).1 The Tardieu spasticity angle has decreased in the
extended splint group versus other groups, from 6.3 to 4.7, indicating a reduction in
spasticity or an improvement in the mechanical restraint of the soft tissue.1 Pain, an
established indicator of soft tissue tightness and spasticity has decreased again in the
extended splint group against other groups, from

58.3 to 53.3. The DASH score too has marginally improved in both the splint groups
compared with the control signifying reduction in disability.
In conclusion, we suggest developing a rehabilitation protocol that titrates between
activity and immobility, as opposed to simply discontinuing splinting completely as the
authors very strongly assert. Intervention dosimetry pertaining to the time of initiation,
number of interventional sessions and duration of each session, are to be meticulously
considered within that proposed protocol.NeuroRehabilitation 28 (2011) 2128 21 DOI
10.3233/NRE-2011-0628
IOS Press

Neurorehabilitation splinting:
Theory and principles of clinical
use
Natasha A. Lannina, and Louise Adab
aRehabilitation Studies Unit, Sydney Medical School, The University of Sydney, NSW,
Australia bDisciplineof Physiotherapy, The University of Sydney, NSW, Australia

Abstract. The use of splints in neurorehabilitation is common, with splints being used to meet
varied clinical aims. This paper explores the use of splints after stroke and examines the rationale
underpinning current use. It covers the use of splints to reduce spasticity, prevent contracture and
improve activity. As well as presenting the theoretical rationale underpinning splinting as an
intervention, it examines the current evidence from randomised trials testing the theories. In
summary, there is strong evidence that wearing a splint all night has no additional effect in reducing
spasticity over usual therapy or in preventing contracture, whether the wrist is splinted in neutral or
in maximum extension. It is not surprising that splinting has not shown an effect on activity, given
that there was little effect on the impairments that it was directed towards. In conclusion, it is now
time to re-focus on improving muscle performance in order to enable activity rather than preparing
the patient for function by affecting abnormal reflex activity.

1. Introduction

The aim of this paper is to trace the use of splints in neurorehabilitation and to examine the
rationale under- pinning current use. With the terms splint, brace, and orthosis being used
interchangeably, we have chosen to use the term splint since it is widely accepted. We will
cover the use of splints to reduce spasticity, prevent contracture and improve activity after
stroke. The em- phasis will be on the theoretical rationale underpinning splinting as an
intervention and the current evidence from systematic reviews and randomised trials.

1.1. History of use of splints

Using splints in neurorehabilitation is not a new con- cept, and yet clinicians are often not
aware of the his- tory and theories beyond their own experiences. Un- derstanding the
premise on which our clinical decision
Corresponding author: Natasha A. Lannin, PhD, Rehabilitation Studies Unit, Sydney Medical School, The University of

Sydney, 59 Charles Street, Ryde, NSW 2112, Australia. E-mail: Natasha.Lannin @sydney.edu.au.

making is based strengthens the foundation of our clin- ical practice.

The definition of terms provides a foundation from which to work. A splint is defined as
being a remov- able device designed for the support of weak or inef- fective joints or
muscles [1]. Text books cite that the purpose of splints are variously to increase function,
prevent deformity, correct deformity, substitute for lost motion, protect healing structures,
maintain range of motion, stabilise joints, restrict motion, allow tissue re- modelling,
improve muscle balance, control inflamma- tion, protect normal structures, decrease pain,
strength- en weak muscles, reduce spasticity, and increase patient independence.

The earliest application of splints in neurorehabili- tation can be traced back to the late
1500s when metal splints were used to manage contracted joints. Splint- ing today has
become an accepted and integral part of neurorehabilitation, from the time of admission to
long after formal rehabilitation has ended. However, there is much inconsistency in the way
splints are used.

1.2. Current use of splints

A splint offers a therapeutic means of maintaining specific positions of a limb. Splints may
be static; not

ISSN 1053-8135/11/$27.50 2011 IOS Press and the authors. All rights reserved

22 N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use

allowing motion, or dynamic. Static splints are able to immobilize a joint in any position
that the therapist chooses, thus providing a means of either rigidly sup- porting body
structures or applying a prolonged stretch to muscles or skin [16]. The American Society
of Hand Therapists [7] classify splints as: mobilization, immobilisation and restrictive. This
classification is based on the key functions of the splint. Mobilisation splints are designed
to mobilize joints, muscles and/or skin, while immobilisation splints aim to immobilise.
Restrictive splints limit a specific aspect of movement for a specific purpose, as in the case
of tenodesis splints.

The use of splints in neurorehabilitation has histori- cally developed from the clinical
experiences of thera- pists [8]. In general, however, therapists apply a splint to achieve one
or more of the following aims:

To decrease spasticity [4,6,810].

To prevent or reduce contractures. The wrist and

fingers assume a relaxed position of flexion fol- lowing acquired brain impairment,
which con- tributes to the formation of a contracture. The splint is thought to act as
 an opposing force against the flexion contracture by providing a sustained stretch
[2,4,11,12]

To improve activity at a joint. For example, posi- tioning a flexed wrist in more
extension may place the fingers at a better position for active move- ment [4,6,13].
Static splinting in a functional posi- tion is usually considered to maintain correct
joint alignment and increase the patients ability to use their hand while more
controlled movement is be- ing regained [2,4,12].

To protect joint integrity by immobilising the joint which is believed to decrease

mechanical irritation caused by overstretching of a joint. Overstretch- ing is thought
to occur due to decreased proprio- ception within the joint following acquired brain
impairment [4,9].

To reduce pain [6,9,10].

There has been much debate about the mechanism by which splinting appears to be
effective [14,15]. Orig- inally, development and subsequent research regard- ing
splinting was driven primarily by the theory that splints inhibit reflexive contraction
of muscles (the neu- rophysiological rationale). With increased knowledge about
both the neurological and musculoskeletal sys- tems, clinicians continued to use
splints but theorized that splints position the limb into a biomechanically ad-
vantageous position. While both the neurophysiologi- cal and biomechanical
approaches have their advocates

and opponents, there is a lack of consensus about the design, wearing duration and wearing
compliance of splints. In short, the use of splints for people during neurorehabilitation
remains controversial.

It is likely that much of the controversy surrounding splinting in neurorehabilitation may be

eliminated if therapists had a good working knowledge of the capa- bilities and limitations
of each type of splint, as well as a theoretical understanding of the scientific evidence
underpinning these clinical opinions. This paper will cover the use of splints to reduce
spasticity, prevent contracture and improve activity. For each topic, the clinical construct
for the use of splinting will be cov- ered, followed by the theoretical rationale for splinting,
and finally the practical evidence will be put forward. Splints that are static and removable
will be investigat- ed, ie, casting will not be included because casts are not removable on a
daily basis. Clinical applications for adults after stroke will be highlighted because these in-
dividuals are the largest group with brain damage seen by therapists.

2. Splinting to decrease spasticity

2.1. Clinical construct

Many commonly used splints in neurorehabilitation are applied with the aim that they will
inhibit spas- ticity with an end result of improving activity. This of course depends on the
premise that (a) a splint is able to inhibit spasticity, and (b) that inhibiting spas- ticity leads
to greater activity. The points of contact of a splint are thought by some clinicians to impact
on whether or not a splint inhibits or elicits spasticity. Such thoughts have stemmed from
early publications (Rood [16]) where spasticity was thought to increase as a result of
sensory stimulation of the palmar surface of the hand, which would then result in unwanted
mus- cle contractions. Based on these assumptions, many therapists recommend splinting
on the dorsal surface of the hand only. In addition to concerns that splinting the flexor
surface of the hand will trigger spasticity, there is also a belief by some clinicians that
certain po- sitions break patterns of spasticity. Stemming from a single case study
conducted in 1962 [17], some ther- apists believe that to inhibit spasticity the hand must be
positioned with the wrist in neutral, and the fingers abducted and extended.

N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use 23

2.2. Theoretical rationale

In neurologically-normal people, passive stretch of relaxed muscles does not result in reflex
muscle activ- ity and the limb feels normal, ie, neither stiff nor ex- ceptionally loose. The
presence of exaggerated stretch reflexes in spastic patients means that passive stretch of
relaxed muscles elicits reflex activity which results in increased resistance, ie, hypertonia.
Hypertonia needs to be clearly distinguished from reflex hyperexcitabil- ity in patients with
spasticity. The most widely ac- cepted definition of spasticity is that of Lance [18] who
described it as a motor disorder characterized by a velocity-dependent increase in tonic
stretch reflexes (muscle tone) with exaggerated tendon jerks, result- ing from
hyperexcitability of the stretch reflex, as one component of the upper motor neuron
syndrome. Fur- thermore, the specificity of this definition was reiterat- ed [19] with the
added rider that spasticity does not include impaired voluntary movement and an abnormal
posture. Therefore, the primary feature of spasticity is the exaggeration of stretch reflexes.
Some of the con- fusion about clinically identifying spasticity has likely arisen because the
clinical measurement of spasticity involves gauging the resistance of the limbs to passive
movement (ie hypertonia) [20]. This procedure does not allow different causes of an
increase in resistance to be identified.

It is now well recognised that factors other than reflex hyperexcitability may produce an
increase in resistance to passive movement [2123], the most common be- ing muscle
contracture. As a consequence of this, un- less stretch-evoked muscle activity can be
demonstrat- ed via EMG, an increased resistance to passive move- ment cannot
automatically be attributed to reflex hy- perexcitability. ODwyer et al. [20] found that 13
out of 24 (54%) people less than one year after stroke ex- hibited an increase in resistance
to stretch, ie, hyperto- nia, but only 5 out of 24 (21%) exhibited stretch-related muscle
activity, ie, spasticity. Perry [21] reported no stretch-related muscle activity in 10% of
people who were labelled as spastic after stroke and Lin et al. [24] suggested that up to 30%
of hypertonia after stroke may not be due to spasticity.
This places importance on the measurement tool used to quantify spasticity. It is now well
recognized that the most commonly used tool the Ashworth Scale is deficient in
quantifying spasticity because it cannot differentiate spasticity from contracture [25 28].
This is because it is mostly a scale assessing hy- pertonia. A study of the validity of the
Ashworth Scales

versus the Tardieu Scale found that the Ashworth Scale overestimated the incidence of
spasticity in stroke 15% of the time [29]. In all of these cases, participants had a
contracture, suggesting that the Ashworth Scale is con- founded by contracture. The
Tardieu Scale is a more valid measure of spasticity, probably because it takes into account
the main factor to which the stretch reflex is known to be sensitive the velocity of stretch.
This velocity-dependence of the stretch reflex has been well established (eg, Thilmann et al.
[30]).

Although splinting will reduce stimulation of hyper- reflexia by immobilising the joint, this
does not mean that it will reduce spasticity in the long term when the splint comes off.
Importantly, the incidence of spastic- ity after stroke is quite low with ODwyer et al. [20]
reporting it at 21%, Watkins et al. [31] reporting it at 27%, Sommerfeld et al. [32] and
Welmer et al. [33] at 19%, Lundstrom et al. [34] at 17% and Wissel et al. [35] at 22%. It is
interesting to note that most of these studies used the Modified Ashworth Scale to quanti- fy
spasticity which overestimates spasticity. Further- more, studies investigating the link
between spasticity and activity have found that the two are not correlated after stroke
[20,36] and that when spasticity has been reduced it does not necessarily lead to better
activi- ty [37]. These findings suggest that routine interven- tion for reducing spasticity
during rehabilitation after stroke, in particular splinting, is inappropriate.

In terms of tactile stimulation exacerbating spastic- ity, the primitive reflexes sometimes
seen after brain injury (such as the palmer grasp reflex) are cutaneous reflexes whereas
spasticity is a disorder of the propri- oceptive reflexes. Furthermore, it is more common to
observe grasp reflexes after traumatic brain injury rather than after stroke. Therefore, it is
not likely that tactile stimulation from a volar hand splint will trigger spasticity.

2.3. Practical evidence

Is there evidence that spasticity can be reduced by splinting after stroke? There have been
four random- ized trials carried out examining the benefits of splint- ing to reduce spasticity
after stroke.

Two randomized trials examined whether spasticity was reduced as a result of splinting.
One high qual- ity trial (PEDro score 8/10) compared splinting with the wrist in neutral
overnight versus splinting with the wrist extended overnight versus a no splint intervention
for 4 weeks in 63 stroke patients [38]. There was no difference in the Tardieu spasticity
angle between the

24 N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use
wrist extended splint and no splint (mean difference 1 deg, 95% CI 2 to 5). One low
quality trial (PEDro score 1/10) compared wearing a finger-spreader splint for 6 hours
versus 12 hours versus 22 hours/day over 2 weeks in 9 stroke patients [39]. There was no
difference in wrist stiffness (hypertonicity) between the different lengths of time wearing
the splints (mean difference 0.00 Nm.rads, 95% CI 0.42 to 0.44).

Two randomized trials examined whether dorsal splinting reduced spasticity more than
volar splinting. One moderate quality trial (PEDro score 4/10) com- pared splinting the
hand in the functional position in either volar or dorsal splints for 2 hours in 10 stroke
patients [40]. Both volar and dorsal splints resulted in an immediate statistically significant
decrease in hyper- tonus. One low quality trial (PEDro score 2/10) com- pared splinting the
hand in dorsal versus volar splints for 2 hours/day in 30 stroke patients [12]. There was no
significant difference between the splints in decreasing hypertonus (mean difference 0.1 lb,
95% CI 1.4 to 1.5).

In summary, there is strong evidence that wearing a splint all night has no additional effect
in reducing spasticity over usual therapy. Furthermore, even wear- ing the splint up to 22
hours per day did not affect spas- ticity. Results from studies also suggest that there is no
difference between using a dorsal splint to a volar splint this is not surprising since people
after stroke rarely exhibit exaggerated cutaneous reflexes.

3. Splinting to decrease contracture

3.1. Clinical construct

Neurological conditions are often accompanied by physiologic joint restriction and

contractures [3]. Splints are used by clinicians with the aim of maintain- ing or lengthening
soft tissues and maintaining joint integrity [41].

Submaximal range splinting is still used in neurore- habilitation, despite a lack of evidence
underpinning its efficacy. The design is based on the reasoning that mus- cles splinted on
full stretch or maximal range will in- crease hypertonicity. Although rarely seen any longer
that a clinician would splint a (for example) wrist in flexion to address a flexion contracture,
it does remain common practice to splint to decrease contracture at less than full available
range. For instance, text books cite a position commonly referred to as functional as
being the optimal position for handsplinting, that is, 20

to 30 degrees of wrist extension [4]. The use of the functional position has not been
supported scientif- ically and appears to contradict the beneficial effects of full stretch in
animal studies. An unwillingness to provide full stretch when splinting has meant that a po-
tentially effective treatment has not been offered to a patient by therapists. This rejection
may deprive peo- ple following acquired brain impairment of an oppor- tunity to apply
stretch at its optimal muscle lengthen- ing efficacy if, in fact, stretch to end of joint range is
effective [42,43].

3.2. Theoretical rationale

Contracture is the loss of joint range of motion. This is partially the result of a shortening of
muscle length due to a decrease in the number of sarcomeres in series along the myofibrils
[44]. It is accompanied by an in- crease in the resistance to passive stretch which is prob-
ably attributable to remodelling of muscle connective tissue [44]. The range of joint motion
is reduced both by the shortening of the muscle fibres and by the loss of muscle
compliance.

Contracture can be easily produced in experimen- tal animals via immobilisation of

muscles in shortened positions. Similar prolonged muscle shortening may arise in humans
through immobilisation or muscle im- balance. Furthermore, in stroke patients with reduced
range of elbow extension, ODwyer et al. [20] mea- sured increased passive resistance
during elbow exten- sion that was independent of muscle activity. Contrac- ture is therefore
an important contributor to hypertonia and the potential to confuse this with spasticity is
clear.

Recognition of the role of increased passive tissue stiffness is crucial in the measurement of
muscle con- tracture. When assessing range of joint motion, it is im- portant that the force
applied is standardized and does not exceed the magnitude of force that is normally suf-
ficient to stretch the muscles through the joint range. Even if a muscle has some
contracture, it may still be possible to achieve a full range of joint motion if suf- ficient
force is applied [45] and the increased stiffness wrongly be attributed to spasticity.

Animal studies have shown that positioning at-risk muscles in the lengthened position for
prolonged pe- riods of time, whether by casting or suspension, has resulted in the
prevention of loss of sarcomeres in se- ries [46]. This maintenance of sarcomeres was pre-
sumed to be accompanied by prevention of loss of mus- cle length and joint range of
motion. Therefore, based on these principles, splinting at-risk muscles in a maxi-

N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use 25

mally lengthened position for considerable proportions of the day should have an effect on
maintaining the length of muscles after stroke.

3.3. Practical evidence

Is there evidence that contracture can be prevented by splinting after stroke? There have
been five ran- domized trials examining the benefits of splinting to prevent contracture after
stroke.

Three randomized trials examined whether contrac- ture was prevented/reduced as a result
of splinting. One high quality trial (PEDro score 8/10) compared splint- ing with the wrist
in neutral overnight versus splinting with the wrist extended overnight versus a no splint in-
tervention for 4 weeks in 63 stroke patients [38]. There was no difference in range of
motion of wrist and fin- ger flexors between the wrist extended splint and no splint (mean
difference 1 deg, 95% CI 4 to 2). An- other high quality trial (PEDro score 8/10)
compared hand splinting in the neutral position overnight with no splint for 4 weeks in 28
stroke patients who were also having daily upper limb stretches [47]. There was no
difference in range of motion of wrist and finger flexors between the splint and the no splint
group (mean differ- ence 1 deg, 95% CI 4 to 6). A third high quality tri- al (PEDro score
8/10) compared wearing a splint with the wrist in neutral and no finger support 6 hours/day
versus no splint for 13 weeks in 30 stroke patients [48]. There was no difference in the
proportion of partici- pants having a contracture (defined as <2/24 on Fugl Meyer
Assessment joint range of motion subtest) be- tween the splint and no splint groups (risk
difference 27%, 95% CI 8 to 54).

One randomised trial examined splinting in the low- er limb versus another intervention for
prevention of contracture. This high quality trial (PEDro score 8/10) compared wearing a
splint with the affected ankle at plantargrade 7 nights (12 hr) per week with standing on a
tilt table for 30 min with the ankle at maximum dorsiflexion 5 times per week in 30 stroke
patients over 4 weeks [49]. They found no difference in range of ankle dorsiflexion (mean
difference 1 deg, 95% CI 5 to 7). Both groups did not develop a contracture; how- ever,
since there was no control group, the prevention of contracture may have been due to other
factors.

A last randomized trial examined the immeditate ef- fect of two different splints. This
moderate quality ran- domized trial (PEDro score 4/10) compared splinting the hand in the
functional position in either volar or dor- sal splints for 2 hours in 10 stroke patients [40].
They

found that either volar or dorsal splints resulted in an immediate statistically significant
increase in passive range of wrist extension; however, point measures and measures of
variability were not reported.

In summary, there is strong evidence that wearing hand splints all day or night additional to
usual therapy after stroke has no effect in preventing contracture, whether the wrist is
splinted in neutral or in maximum extension. Furthermore, it appears that there is no
difference between using a splint to other means of contracture prevention.

4. Splinting to improve activity

4.1. Clinical construct

Splints are also used in neurorehabilitation to im- prove activity, be that by holding a joint
in a position that assists in an activity, such as in the case of ther- moplastic molded ankle-
foot splint, or a thumb abduc- tion splint which positions the thumb in an enhanced
prehension position for grasp/release; or by compen- sating for weakness by providing
external support or movement, such as in the case of a posterior leaf spring, ankle-foot
splint, or newer technology advances such as electronic stimulation splints (BioNESS) or
dynamic handsplints such as Saebo splint. Many neurorehabili- tation protocols,
particularly in the management of the upper limb after stroke, call for long-term splinting.

4.2. Theoretical rationale

Given that wearing a splint, particularly early in a re- habilitation training program, sends a
message that an external positioning device is responsible for aligning a joint, it is likely
that the patient may fail to integrate movement training from therapy into everyday move-
ment training. Thus, the concern that early and/or con- tinual splinting predisposes a patient
to learned non- use.

One of the disadvantages of using splinting is that it effectively immobilises the joint(s) and
therefore dis- courages or even disallows muscle activity and there- fore movement. For
example, when wearing an ankle- foot splint, the ankle is immobilised at plantargrade and
this results in a decrease in muscle activity in the dorsiflexors [50]. For this reason, it would
seem inap- propriate to prescribe splints during the early stages of rehabilitation, when the
emphasis is on using the neural plasticity of the system to harness the potential for re-

26 N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use

covery of muscle strength. On the other hand, using an ankle-foot splint often increases
confidence and results in faster walking with more symmetry [51,52], making it more
appropriate for ongoing use once recovery has effectively reached a plateau. In this
situation, there is not necessarily an expectation that activity will im- prove as a result of
wearing the splint. For example, wearing an ankle-foot splint for 6 months resulted in
deterioration when walking without the splint in stroke survivors.

4.3. Practical evidence

Is there evidence that activity can be improved as a result of short-term splinting after
stroke? There have been four randomized trials examining the effect of splinting on activity
after stroke.

Few of these randomised trials investigated splinting where the main aim is to improve
motor activity. One moderate quality trial (PEDro score 5/10) compared wearing an
inflatable pressure splint with the shoulder in 90 degrees of flexion and maximum external
rotation and the elbow fully extended versus a no splint inter- vention for 30 minutes/day
over 3 weeks in 18 stroke patients [54]. In terms of activity, it found no differ- ence in Fugl-
Meyer Assessment scores (mean differ- ence 0/57, 95% CI 10 to 10) between the splint
and the no splint group.

Most randomized trials have investigated splinting where the main aim is to reduce
impairments such as spasticity or contracture and the carry over to motor ac- tivity has been
measured as a secondary outcome. One high quality trial (PEDro score 8/10) compared
splint- ing with the wrist in neutral overnight versus splinting with the wrist extended
overnight versus a no splint intervention for 4 weeks in 63 stroke patients [38] in order to
prevent contracture. In terms of activity, it found no difference in Motor Assessment Scale
scores for the upper limb between the wrist extended splint and no splint (mean difference
0.0/18 points, 95% CI 0.4 to 0.4). Another high quality trial (PEDro score 8/10) compared
hand splinting in the neutral position overnight with no splint for 4 weeks in 28 stroke pa-
tients who were also having daily upper limb stretch- es [47] in order to prevent
contracture. In terms of ac- tivity, it also found no difference in Motor Assessment Scale
scores for the upper limb (mean difference 0.1/18 points, 95% CI 2.3 to 2.7) between the
splint and the no splint group. A third high quality trial (PEDro score 8/10) compared
wearing a splint with the affect- ed ankle at plantargrade 7 nights (12 hours) per week

with standing on a tilt table for 30 min with the an- kle at maximum dorsiflexion 5 times
per week in 30 stroke patients over 4 weeks [49] in order to prevent contracture. In terms of
activity, it found no difference in Motor Assessment Scale scores for standing up from a
chair (mean difference 0.5/6 points, 95% CI 0.4 to 1.4).

In summary, its not surprising that splinting had little effect on activity, given that there was
little effect on the impairment (such as contracture or spasticity) that it was directed
towards. A major obstacle to functional use of the hand is the inability to open the hand
sponta- neously, and the potential benefit of dynamic and newer technology splints on hand
opening, activity and func- tional use has yet to be adequately studied in clinical trials.

5. Summary

As the rehabilitation of adults following stroke con- sumes substantial health resources, it is
crucial that an evidence-based approach be adopted in response to controversies and
clinical uncertainties, such as those abundant in the debate about splinting. Despite the
widespread use of splints for adult stroke patients, sur- prisingly few randomized trials (n =
5), have examined the effect of splinting in this population. However, sev- eral of these are
of high quality and can be used to guide clinical practice. Unfortunately, the evidence
suggests that splinting as currently provided in neurorehabilita- tion is not effective in
decreasing spasticity, preventing contracture or improving activity. The time may have
come to reconsider our clinical practices and beliefs.

It is unsurprising that static splinting has little effect on activity, given that these splints are
provided primar- ily to influence contracture development or decrease spasticity with an
anticipated improvement in activi- ty that should occur with less contracture and/or less
spasticity. Static splinting has not been able to demon- strably reduce either spasticity or
contracture and since it was shown to do neither, a subsequent effect on ac- tivity was also
not detected. Studies to date have fo- cused their attention on investigating the benefits of
static splints and thus the potential benefit of dynamic and newer technology splints such as
those that deliv- er electrical stimulation or EMG-triggered stimulation have yet to be
adequately studied. While further re- search is needed on the many possible interventions
for increasing activity, including splint use and how they contribute to maximizing
functional use, future stud-

N.A. Lannin and L. Ada / Neurorehabilitation splinting: Theory and principles of clinical use 27

ies should use large sample sizes and simple, accurate, and reliable measures of relevance
to the primary clin- ical reasons for applying splints which will ensure the clinical utility of
study findings.

[17] J.M. Zislis, Splinting of hand in a spastic hemiplegic patient, Arch Phys Med Rehabil 45 (1964), 4143.
[18] J.W. Lance, Symposium synopsis, in: Spasticity: Disordered Motor Control, R.G. Feldman, R.R. Young and W.P.
Koella, eds, Chicago: Year Book Medical Publishers, 1980, pp. 485

Examination of current evidence for splints to re- 494.

duce spasticity and prevent contracture shows that clin- ical theories held by
neurorehabilitation professionals require reconsideration. Clinicians are encouraged to re-
focus on improving muscle performance in order to enable hand activity, rather than
preparing the patient for function by affecting abnormal reflex activity.

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