Effect of Electrical Stimulation and Splint in Foot Drop Introduction Foot drop is a simple term for a potentially complex problem. It is usually a symptom of a greater problem. It is characerized by the inability or difficulty in moving the ankle and toesupward (dorsiflexion). In walking, while stepping forward, the front of the foot must be lifted upward to prevent the foot from dragging along the ground. Foot drop can be caused by just nerve damage. It is also caused by muscle damage, or abnormal anatomy, neurological damage, tumors, or diseases, neuro-spinal injury or diseases or associated problems, diabetes, neuropothies, stroke, dorsiflexor injuries, drug toxicities, multiple sclerosis, amyotrophic lateral sclerosis (ALS), Parkinson's disease, Lou Gehrig’s disease, and muscular dystrophy. It may be caused by incorrect posture, sitting with the foot unrested on the floor or other surface, for extended periods of time, such as whilst using a PC. Foot drop is caused by problems and diseases, such as those listed above, that damage the long nerves or communication between them, or more directly, damage the brain/spinal cord. The deep fibular/peroneal nerve innervates the front (anterior) compartment of the leg. Damage to this nerve will lead to the inability for the leg to dorsiflex the foot, therefore causing foot drop. The result is an abnormal gait. Features Foot drop is characterized by steppage gait. When the person with foot drop walks, the foot slaps down onto the floor. To accommodate the toe drop, the patient may use a characteristic tiptoe walk on the opposite leg, raising the thigh excessively, as if walking upstairs, while letting the toe drop. This serves to raise the foot high enough to prevent the toe from dragging and prevents the slapping. Other gaits such as a wide outward leg swing (to avoid lifting the thigh excessively or to turn corners in the opposite direction of the affected limb) may also indicate foot drop. Patients with painful disorders of sensation (dysesthesia) of the soles of the feet may have a similar gait but do not have foot drop. Because of the extreme pain evoked by even the slightest pressure on the feet, the patient walks as if walking barefoot on hot sand. links ANATOMY There are 26 bones in the foot 7 tarsals , 5 metatarsals, 14 phalanges The tarsals are :
Calcaneum ,talus,cuboid ,naviculum and the three cuniforms (medial, intermediate,lateral)
The ankle joint is a synovial hinge joint . Articulation : The lateral malleolus of the fibula and the medial malleolus of the tibia along with the inferior surface of the distal tibia articulate with three facets of the talus. These surfaces are covered by cartilage. Bone Anatomy Ankle Mortise Talus Trochlea Anterior surface vs Posterior surface Leg
Tibia Fibula Remember Foot and Ankle are Interrelated Biomechanics of Foot, Ankle and Leg
Articulations and Ligament Support Talocrural Joint Comprised of: Talus acts as a wedge Ligaments of the Lateral Talocrural Joint Anterior Talofibular
Talocrural Joint Comprised of: Talus acts as a wedge Ligaments of the Lateral Talocrural Joint Anterior Talofibular Sinus Tarsi Calcaneofibular Posterior Talofibular Talocrural Joint Ligaments of the medial Talocrural Joint Deltoid Anterior Tibiotalor Tibiocalcaneal Posterior Tibiotalor Tibionavicular
Talocrural Joint Ligaments of the medial Talocrural Joint
Deltoid Anterior Tibiotalor Tibiocalcaneal Posterior Tibiotalor Tibionavicular Tibia-Fibula Fixation Interosseous Membrane Distal Tibiofibular Ligament Anterior Posterior 3 structures stabilize syndesmosis joint Biomechanics of Syndesmosis Joint Muscles of the Leg and Ankle Anterior Compartment Borders Lateral Shaft of Tibia Medial Shaft of Fibula Interosseous membrane Anterior Compartment Structures Tibialis Anterior Extensor Hallucis Longus Extensor Digitorum Longus Peroneus Tertius Deep Peroneal Nerve Anterior Tibial Artery Anterior Tibial Vein Anterior Compartment Structures Tibialis Anterior Extensor Hallucis Longus
Extensor Digitorum Longus Peroneus Tertius Deep Peroneal Nerve Anterior Tibial Artery Anterior Tibial Vein
Lateral Compartment Borders Lateral Fibula Intermuscular fascia between anterior compartment and posterior compartment Lateral Compartment Structures Peroneus Longus Peroneus Brevis Superficial Peroneal Nerve Peroneal Artery Superior and Inferior Peroneal Retinaculum Lateral Compartment
Structures Peroneus Longus Peroneus Brevis Superficial Peroneal Nerve Peroneal Artery Superior and Inferior Peroneal Retinaculum
Lateral Compartment Structures Peroneus Longus Peroneus Brevis Superficial Peroneal Nerve Peroneal Artery Superior and Inferior Peroneal Retinaculum
Superficial Posterior Compartment Borders Deep posterior compartment Fascia Superficial Posterior Compartment Structures Soleus Gastrocnemius Plantaris Tibial Nerve Posterior Tibial Artery Superficial Posterior Compartment Structures Soleus Gastrocnemius Tibial Nerve Posterior Tibial Artery
Borders Interosseus Membrane Posterior Tibia Posterolateral Fibula Superficial Posterior Compartment Structures Tom, Dick and Harry Tibialis Posterior Flexor Digitorum Longus Flexor Hallucis Longus Tibial Nerve Posterior Tibial Artery
Ankle Bursa Retrocalcaneal Bursa Subcutaneous Calcaneal Bursa NEUROVASCULAR SUPPLY OF FOOT OBJECTIVES By the end of this lecture students should be able to: • Describe vascular and nervous supply of sole and dorsum of foot • Tell their course through foot • Explain relationships ARTERIES OF THE SOLE OF THE FOOT
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Medial plantar arteries Lateral plantar arteries Both are terminal branches of the posterior tibial artery.
MEDIAL PLANTAR ARTERY • • •
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Smaller than the lateral Arises: beneath flexor retinaculum Course: – Runs along the medial side of the foot – First: above the abductor hallucis – Then: b/w abductor hallucis and flexor digitorum brevis Anastomose: with the first dorsal metatarsal artery Supplies: Abductor hallucis, Flexor digitorum brevis, medial side of big toe
LATERAL PLANTAR ARTERY • • •
Larger than the medial Arises: beneath flexor retinaculum Course: – Runs Laterally and forward – First : between the calcaneus and abductor hallucis – Then : between the flexor digitorum brevis and quadratus plantæ – Turns Medially and extends from the base of the fifth metatarsal bone to the proximal part of the first interosseous space, and forms the plantar arch – Unites with the deep plantar branch of the dorsalis pedis artery
PLANTAR ARCH •
Perforating branches : – Three in number – Anastomose with the dorsal metatarsal arteries
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Plantar metatarsal arteries: – Divides into a pair of plantar digital arteries
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To adjacent side of lateral four toes and lateral side of little toe
NERVE SUPPLY OF FOOT •
Terminal branches of the tibial nerve: – Medial planter nerves – Lateral plantar nerves
MEDIAL NERVE
PLANTAR
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Arises: beneath flexor retinaculum Course: – Runs forward deep to abductor hallucis with medial planter artery – Lies in interval between abductor hallucis and flexor digitorum brevis
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Branches: Muscular: – abductor hallucis muscle – flexor digitorum brevis – flexor hallucis brevis (in the third layer) – 1st lumbrical
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Cutaneous: – Plantar digital nerve - Skin of medial three and half toes – On dorsum, nail bed and tips of toes
LATERAL PLANTAR NERVE •
Arises: beneath flexor retinaculum
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Course: – Runs forward deep to abductor hallucis and flexor digitorum brevis with lateral planter artery – On reaching base of 5th metatarsal bone, divides into superficial and deep branch
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Branches:
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Main trunk: – abductor digiti minimi – accessory flexor (quadratus plantae) – Cutaneous: Skin of lateral part of sole
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Superficial terminal: – flexor digiti minimi brevis – interossei (4th intermetatarsal space) – Planter digital branch – lateral one and half toes – On dorsum – nail beds and tips of toes
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Deep terminal: – lumbricals 3, 4, 5 – adductor hallucis – Interossei (except 4th intermetatarsal space)
VEINS OF SOLE OF FOOT • • • •
Medial plantar vein Lateral plantar vein Accompany corresponding arteries Unite behind medial malleolus to form posterior tibial venae comitantes
ARTERIES OF DORSUM OF FOOT DORSALIS PEDIS ARTERY • • • •
Continuation of the anterior tibial From the ankle joint along the tibial side of the dorsum of the foot to the proximal part of the first intermetatarsal space Pass down b/w 2 heads of 1st dorsal interossei muscle Joins lateral plantar artery
BRANCHES OF THE DORSALIS PEDIS ARTERY •
Lateral tarsal artery : – Crosses navicular àsupply extensor digitorum brevis
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Medial tarsal arteries : – Ramify on the medial border of the foot and join the medial malleolar network
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Arcuate artery : – Passes lateralward, over the bases of the metatarsal bones – Gives off the second, third, and fourth dorsal metatarsal arteries
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First dorsal metatarsal artery : – Supply the adjoining sides of the great and second toes.
SUPERFICIAL PERONEAL NERVE • • •
Emerges from between peroneus brevis and extensor digitorum longus Branches: – medial and lateral cutaneous Supply: – Skin on dorsum of foot – Medial side of big toe – Adjacent dies of 2nd, 3rd, 4th and 5th toes
DEEP PERONEAL NERVE • • • • •
It enters the dorsum of the foot by passing deep to extensor retinacula on lateral side of dorsalis pedis artery in front of the ankle joint Divides into a lateral and a medial terminal branch Lateral terminal branch: supplies the extensor digitorum brevis Medial terminal branch: At the first interosseous space, divides into two dorsal digital nerves, supply the adjacent sides of the great and second toes Both give articular branches to joints of foot
SAPHENOUS NERVE • •
Passes onto dorsum of foot in front of medial malleolus Supply: Skin along medial side of foot as far forward as 1st metatarsal bone
SURAL NERVE • •
Enters foot behind lateral malleolus Supply: – –
Skin along lateral margin of foot Lateral side of little toe
head of
DORSAL VENOUS ARCH • Lies in subcutaneous tissue over heads of metatarsal bones • Drains: – on medial side into great saphenous vein – on lateral side into small saphenous vein • Greater part of blood from whole foot drains into arch via digital veins and communicating veins from sole, which pass through interosseous spaces Other joints in the foot : 1- the sub-talar joint. 2- This joint lies between the calcaneum and the talus . 3-the mid-tarsal joint. This joint is really two joints - the joint between the talus and the navicular bone as well as the joint between the calcaneum and the cuboid bone. There is only one muscle on the dorsum of the foot ( digitorum brevis). The muscles on the planter aspect of the foot are divided into four layers: first layer:abductor hallucis,flexor digitorum brevis,abductor digiti minimi. second layer:quadratus plantae,lumbricalis,flexor digitorum longus tendon,flexor hallucis longus tendon. third layer: flexor hallucis brevis,adductor hallucis,flexor digiti minimi brevis. Forth layer: interossei , peroneus longus tendon,tibialis posterior tendon
The planter fascia is a very important structure that takes its origin from the heel (calcaneum) and inserts into the bases of the proximal phalanges of the toes.
 Blood supply of the foot is from : 1-anterior tibial artery which gives dorsalis pedis artery. 2-posterior tibial which gives the medial and lateral plantar arteries. 3- peroneal arteries.
Blood supply  Nerve supply of the foot is from: *****(saphenous, sural, superficial & deep peroneal)*****
Nerve supply Movements at the ankle joint : are mainly dorsiflexion and plantarflexion. The anterior talus is wider than the posterior talus. When the foot is dorsiflexed, the wider part of the superior talus moves into the articulating surfaces of the tibia and fibula, creating a more stable joint than when the foot is plantar flexed.  The foot externaly rotates with dorsiflexion and internally rotates with plantarflexion
BIOMECHANICS "Bio" means life or living organism. "Mechanics" is the original discipline of physics as it applies to forces on matter. For our purposes, biomechanics is defined as the mechanics of the human body, especially the forces of the muscles and gravity on the skeletal structure of the lower extremity. Biomechanics is the term used to describe movement of the body. This section is a review of basic foot and ankle biomechanics. In order to understand the biomechanics of the foot and ankle it is important to understand their anatomy. Please read the sections on basic foot anatomy and basic ankle anatomy before reading this section.
The ankle is a modified hinge joint. It plays a key role in transferring the forces from the foot to the leg. The ankle joint is made up of three bones, which are connected by ligaments, muscles and tendons. A strong ligament joins the ends of the tibia and fibula to form the ankle "mortis". The "dome" of the talus (the highest bone of the foot) fits inside the ankle mortis to form the ankle joint. The ankle allows movement in only one plane. It allows the foot to move upwards (dorsiflexion) and downwards (plantar flexion). The foot is made up of 26 bones. There are numerous joints between these bones that allow the foot to be both a rigid lever and a shock absorber. The largest joint in the foot is the subtalar joint. Inward movement of the foot (inversion), and outward movement of the foot (eversion) occur primarily at the subtalar joint. The normal end ranges of motion for the foot and ankle vary between individuals and between children and adults. The following are approximate end ranges of motion for adults: • Dorsiflexion - 20 degrees
• Plantar flexion - 60 degrees
• Eversion - 15 degrees
• Inversion - 35 degrees Foot Terminology: Anatomic terms for location of body parts and motions are necessary for a variety of reasons. We can not simply say "outside of the toe" because not everyone will agree on which part of the toe is the "outside." Although it may seem simple to refer to the "top of the foot", as soon as the foot moves or is rotated or has a deformity, the top of the foot is no longer on top. Medical professionals need a uniform way to describe both locations and movements.
Locations
Medial means towards the center line of the body. Lateral means away from the center line of the body. Distal means further from the body. Proximal means closer to the body. Anterior means the front of the body Posterior means the back of the body Dorsal means the top of the foot Plantar means the bottom of the foot foot orientation image Looking at the foot diagram above, the big toe is medial and the little toe is lateral. The toes are distal to the midfoot and the midfoot is distal to the heel bone. The heel bone is proximal to the toes. The toes are also considered anterior to the midfoot and the heel sits posterior to the midfoot. Definitions: Motions of the foot and ankle
Dorsiflexion: movement of the foot up.
Plantarflexion: movement of the foot down.
Abduction: movement of the foot away from the center line of the body.
Adduction: movement of the foot towards the center line of the body.
Inversion: twisting movement of the foot inward
Eversion: twisting movement of the foot outward. Supination and Pronation Supination and pronation are a combination of the above motions. It is common to use supination and inversion interchangeably and pronation and eversion interchangeably. But, supination is actually a combination of inversion, plantarflexion and adduction. Pronation is a combination of eversion, dorsiflexion and abduction.
Supination: is a triplanar motion involving the foot moving down and towards the center of the body.
Pronation: is a triplanar motion of the subtalar joint involving the foot moving up and away from the center of the body. To better understand supination, look at the right foot in the image below. The heel rotates towards the center of the body, the big toe moves towards the center of the body, the foot flexes down and the ankle rolls out.
To better understand pronation, look at the right foot in the image below. The heel rotates away the center of the body, the little toe moves away from the center of the body, the foot flexes up slightly and the ankle rolls in.
To understand these motions while standing, try this with your own feet. Stand with your feet parallel and facing foward. Rotate your body and look over your left shoulder, without moving your feet. Your left leg has rotated out (external leg rotation) and your weight will be on the outside of your left foot. Your left foot is supinated. Your right leg has rotated in (internal leg rotation) and your weight is on the inside of your right foot. Your right foot is pronated.
Gait Cycle
Contact/ Heel Strike: The beginning of the gait cycle is marked by the heel contacting the ground. This is called heel strike. Forefoot contact: The forefoot contacts the ground, stabilizing the foot and the body. Midstance: When the weight of the body is directly over the foot. The opposite foot is swinging from the rear of the body towards the front of the body. Heel Off: When the heel starts to lift from the ground, the weight shifts to the front of the foot. The opposite foot has made contact with the ground. Propulsion/ Push off: Also called toe off, this phase is the terminal stance phase of the gait cycle, which means that the foot is pushing off the ground and will be entering the swing phase (swinging from the rear of the body to the front of the body).
During the normal gait cycle (normal walking) the feet supinate and pronate. It's important to understand that pronation is a normal motion when walking. When the feet pronate too much, this is when people experience problems like plantar fasciitis, tendonitis and painful arches. An abnormal amount of supination can cause also cause problems. When the foot supinates too much people may develop tendonitis and joint problems at the forefoot and big toe joint.
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Foot drop is an inability or difficulty in moving the ankle and toes upward (dorsiflexion). In walking, the leg must be lifted higher than usual to prevent the foot from dragging along the ground. ... a deficit in turning the ankle and toes upward. Conditions leading to foot drop may be neurologic, muscular or anatomic in origin, often with significant overlap. Foot drop is characterized by steppage gait. When the person with foot drop walks, the foot slaps down onto the floor. ... This describes the condition when a person cannot flex their ankle upwards towards the knee (opposite of pointing your toe). It may develop suddenly or slowly and may or may not be painful depending on the underlying condition. Foot drop is not a disease, and depending on the cause, it may be either temporary or permanent. Foot drop is the symptom of an underlying problem, which is usually a neuromuscular disorder. According to spineuniverse.com, foot drop is most often caused by injury to the peroneal nerve. There are many different types of injuries that can occur to the peroneal nerve--the most common are: a disc herniation that causes nerve compression, a stroke, a tumor near the nerve or any type of crushing injury.
Foot Drop Causes, Symptoms F oot drop, or drop foot as it may also be called, refers to a weakening of the muscles that allow one to flex the ankle and toes, causing the individual to drag the front of the foot while walking and to compensate for this scuffle by bending the knee to lift the foot higher than usual. A quick way to test for foot drop is to try to walk on the heels. If this proves difficult, drop foot may be present. In This Article: • Foot Drop Causes, Symptoms • Foot Drop Symptoms, Steppage Gait & Other Warning Signs • Foot Drop Causes • Foot Drop Diagnosis • Foot Drop Treatments While foot drop is a neuromuscular disorder that affects the nerves and muscles, it is not actually a disease in itself but rather a symptom of some other medical problem, possibly by a condition in the low back. The possibility that foot drop may be caused by a condition in the low back may be overlooked, but it is important to evaluate in order to pursue appropriate foot drop treatment. Article continues below Drop Foot Complications Regardless of the foot drop cause for the specific patient, the fact remains that a dropped foot can produce many difficulties, including the inability to:
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Point the toes upward at the body (this movement is known as dorsiflexion) Walk normally in the heel-to-toe fashion.
Foot Dropped Considerations Patients with dropped foot should be aware of the following: Foot drop may be experienced in one oFoot Drop Symptoms, Steppage Gait & Other Warning Signs Foot drop typically affects the muscles responsible for moving the ankle and foot upward, specifically the anterior tibialis, extensor hallucis longus and extensor digitorum longus. With drop foot, these muscles are inhibited from performing several functions during a normal walking stride, including swinging the toes up from the ground at the start of a stride and controlling the foot after the heel is planted near the end of a stride. Consequently, the most recognized foot drop symptom occurs: high steppage gait. In This Article: • Foot Drop Causes, Symptoms • Foot Drop Symptoms, Steppage Gait & Other Warning Signs • Foot Drop Causes • Foot Drop Diagnosis • Foot Drop Treatments High Steppage Gait from Drop Foot The most common symptom of drop foot, a high steppage gait is often characterized by raising the thigh up in an exaggerated fashion while walking, as if climbing the stairs. Article continues below High steppage gait is associated with one of the following: • • •
Dragging of the foot and toes Scraping of the toes across the ground Uncontrolled slapping of the toes against the ground.
The affected muscles are usually used to keep the foot off the ground during the swingthrough portion of walking. When these are weak, they cannot keep the foot up and the foot will scrape across the ground if the foot is not picked up high. Other Foot Drop Symptoms Some other foot drop symptoms may include: •
An exaggerated, swinging hip motion. With foot drop, the hip may swing out in an effort to counteract the toes from catching the ground.
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Limp foot. Specifically, a foot that flops away from the body is another common drop foot symptom. Tingling, numbness & slight pain in the foot. Ranging from a slight tingling sensation to a complete lack of feeling in the foot, these foot drop symptoms may make everyday activities like walking and driving a car very difficult. Such foot pain may specifically be linked to the lower back, specifically to a series of symptoms known as sciatica. Difficulty with certain activities requiring the use of the front of the foot. As just one example, foot drop may make an activity like climbing the stairs especially difficult. Muscle atrophy in the leg. Muscle atrophy refers to a muscle decreasing in mass and weakening. As the anterior tibialis, extensor hallucis longus and the extensor digitorum longus muscles are most affected by foot drop, atrophy may occur and make it much harder to exert force with the leg and the foot.
As there are various symptoms of foot drop, there are many different drop foot causes that merit understanding and evaluation when seeking treatment.
Foot drop can be diagnosed by a many types of physicians. If the lower back is suspected as a cause, a complete workup by a spine specialist, such as a physiatrist, orthopedic spine surgeon or neurosurgeon, may be advisable. Once a cause is determined, various foot drop treatments may be implemented depending on the specific patient’s condition. Articles Related to
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"Foot Drop Diagnosis" Causes of Leg Pain and Foot Pain Leg Pain and Numbness: What Might These Symptoms Mean? Lumbar and Cervical Radiculopathy
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Foot Drop Causes When learning about drop foot, it should be reiterated that it is a symptom of an underlying condition. Generally speaking, foot drop causes may include: 1. Muscle damage 2. Skeletal or anatomical abnormalities affecting the foot 3. Nerve damage. Common Drop Foot Causes Specific causes of foot drop that should be considered may include: • • • • • • • •
A lower back condition (see below for more detail) A stroke or tumor Parkinson’s disease Diabetes Motor Neuron disease Multiple sclerosis Adverse reactions to drugs or alcohol An injury to the foot or lower leg.
This article focuses on the first cause, the specific lower back conditions that can cause foot drop. Article continues below How the Lower Back Causes Drop Foot There are a number of conditions in the lower back that put pressure on the nerve that leads to the peroneal nerve in the lower leg, which innervates the muscles that allow the foot to flex up. When compromised, peroneal nerve damage may occur and prompt foot drop as a result of the following lower back problems: •
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Lumbar herniated disc. While there are many causes of foot drop, one of the most common cause tends to be a herniated disc in the lower back (lumbar spine) that is putting pressure on the nerve that runs down the leg and into the foot. Putting pressure on the weakest spot of the disc (located right under the nerve root), a herniated disc may prompt pain to nerves beyond the sciatic nerve (including the peroneal nerve) that is referred to the leg and foot. More specifically, this pain will usually run below the knee and to the foot, with the foot pain accompanied with numbness. Spinal stenosis. Occurring gradually over time and usually in elderly patients, spinal stenosis occurs when the spinal nerve roots are compressed and choked as a result of a number of potential factors, most commonly enlarged facet joints (e.g. from osteoarthritis). With lumbar spinal stenosis, nerve compression can produce symptoms of pain, especially with activities involving standing and walking, and possibly foot drop.
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Spondylolisthesis. Prompting an unstable and compromised spine segment as a result of a vertebra slipping forward over a lower vertebra, spondylolisthesis may result in a pinched nerve in the lower back. Bone fractures or lacerations. A fracture to a vertebra in the lower back, such as from osteoporosis, can cause stress and irritation to related nerves, leading to referred pain in the foot and possibly foot drop. For anyone with who is diagnosed with or at risk for osteoporosis, a vertebral fracture should be considered as a possible cause of foot drop.
It should be known that while some foot drop treatments may be directed at symptoms, determining the underlying cause of a dropped foot is often necessary in order to effectively treat it. Articles Related to "Foot Drop Causes "
Peroneal Nerve Symptoms The peroneal nerve, which runs along the outside part of the lower knee, has an important when it comes to a person's mobility. This nerve transmits impulses to and from three areas: the leg, the foot and the toes. If this nerve becomes damaged, the muscles in the lower leg and foot become weak. This causes a person to be unable to raise the foot upwards, a condition commonly known as foot drop. 1.
Symptoms The most common symptom of foot drop is the inability to raise the foot at the ankle. More specifically, a person with foot drop may be unable to point her toes toward her body, or in some more severe cases, she may not be able to move her foot at the ankle inward or outward. When this loss of function occurs, many times pain, weakness and numbness, as well as a tingling or prickling sensation, are noticed.
Since there is nerve damage, when a person with foot drop tries to walk, she may drag the affected foot or toes. 2.
Causes While damage to the peroneal nerve is the most common cause for foot drop, there are other causes as well. It can also be caused by injury to the sciatic nerve, which is the largest nerve in the body, originating in the network of nerves found in the lower back. Foot drop is most commonly the symptom of a nerve problem; however, muscle damage, nerve and muscle disorders, some central nervous system disorders, and even a reaction to different drugs, such as chemotherapy drugs and certain drugs used to treat multiple sclerosis, may also be the cause, as they can have a severely toxic effect on the body, according to mayoclinic.com
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If a person finds he cannot lift his foot or if he drags his foot when walking, it is time to seek medical advice. A doctor will give a complete physical exam as well as go over medical history thoroughly; she will also want to observe foot and leg movement to better determine the diagnosis. In some cases, a person who is thought to have foot drop may be referred to a neurologist for further testing. Treatment depends on how the injury was sustained as well as the severity of the injury. Some people with foot drop are fitted with a splint, an ankle foot orthotic or simply a brace that fits in the shoe and helps to stabilize the foot and ankle. Often physical therapy is also recommended. In some cases, surgery is an option to correct the underlying problem, such as repairing a nerve that has been damaged, if possible; or if the cause is a herniated disc, the disc may be removed . Drop foot is a complex problem because there are so many variables as to cause. Therefore, the best first step in handling the condition is to speak to a medical
The common fibular nerve (common peroneal nerve; external popliteal nerve; peroneal nerve; lateral popliteal nerve), about one-half the size of the tibial nerve, is derived from the dorsal branches of the fourth and fifth lumbar and the first and second sacral nerves. It descends obliquely along the lateral side of the popliteal fossa to the head of the fibula, close to the medial margin of the biceps femoris muscle. Where the common peroneal nerve winds round the head of the fibular, it is palpable[1]. It lies between the tendon of the biceps femoris and lateral head of the gastrocnemius muscle, winds around the neck of the fibula, between the peronæus longus and the bone, and divides beneath the muscle into the superficial fibular nerve (superficial peroneal nerve) and deep fibular nerve (deep peroneal nerve). It innervates the Peroneus longus and Peroneus brevis muscles. [ Previous to its division it gives off articular and lateral sural cutaneous nerves. The articular branches (rami articulares) are three in number:
Two of these accompany the superior and inferior lateral genicular arteries to the knee; the upper one occasionally arises from the trunk of the sciatic nerve. The third (recurrent) articular nerve is given off at the point of division of the common fibular nerve; it ascends with the anterior recurrent tibial artery through the tibialis anterior to the front of the knee.
The lateral sural cutaneous nerve (n. cutaneus suræ lateralis; lateral cutaneous branch) supplies the skin on the posterior and lateral surfaces of the leg. The motor branches: As the common fibular nerve exits the popliteal fossa, it courses around the lateral aspect of the leg just below the head of the fibula. Here it is apposed with fibula and gives off two branches, the superficial fibular (peroneal) branch and deep fibular (peroneal) branch. The superficial peroneal nerve supplies the muscles of the lateral compartment of the leg namely: peroneus longus and peroneus brevis. These two muscle help in eversion and plantar flexion of the foot. The deep peroneal nerve innervates the muscles of the anterior compartment of the leg which are: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and the fibularis (peroneus) tertius. Together these muscles are responsible for dorsiflexion of the foot and extension of the toes.
Clinical significance Chronic peroneal neuropathy can result from, among other conditions, bed rest of long duration, hyperflexion of the knee, peripheral neuropathy, pressure in obstetric stirrups, and conditioning in ballet dancers. The most common cause is habitual leg crossing that compresses the common fibular nerve as it crosses around the head of fibula. [2] Transient trauma to the nerve can result from peroneal strike. Damage to this nerve typically results in foot drop, where dorsiflexion of the foot is compromised and the foot drags (the toe points) during walking; and in sensory loss to the dorsal surface of the foot and portions of the anterior, lower-lateral leg.
Surgical procedures Peroneal nerve decompression:
In the surgical treatment of fibular nerve compression, an incision is made over the neck of the fibula. Fascia surrounding the nerves to the lateral side of the leg is released.[3] Deep peroneal nerve decompression: In the surgical treatment of deep fibular nerve entrapment in the foot, a ligament from the extensor digitorum brevis muscle that crosses over the deep peroneal nerve, putting pressure on it and causing pain, is released.
Nervous system Sacral plexus
Medical Therapy Foot drop is very distressing, and attention to the patient's psychological needs is very important. If painful paresthesias develop, they can sometimes be effectively managed with sympathetic blocks or laparoscopic synovectomy. Alternative treatments are amitriptyline, nortriptyline, pregabalin, and gabapentin. Local treatment with transdermal capsaicin or diclofenac can also reduce symptoms. Even if there is significant pain, narcotic medications should be kept to a minimum. Optimizing glucose control in diabetic patients and managing vitamin deficiencies with supplements of B-1, B-6, or B-12 can also be useful. Erythropoietin is a naturally occurring hormone that is approved by the Food and Drug Administration for the treatment of anemia but also has neuroprotective and possibly neurotrophic properties. The proposed mechanism of action is anti-apoptotic and antiinflammatory, promoting cell survival. Erythropoietin is given in 3 doses of 5000 U/kg over a week following nerve injury. It has a minimal side-effect profile. An animal study showed that erythropoietin treatment accelerated functional recovery after peripheral nerve injury. Treatment of foot drop is directed to its etiology. If foot drop is not amenable to surgery, an ankle-foot orthosis (AFO) often is used. An AFO also is used during surgical or neurologic recovery. The specific purpose of an AFO is to provide toe dorsiflexion during the swing
phase, medial and/or lateral stability at the ankle during stance, and, if necessary, push-off stimulation during the late stance phase. An AFO is helpful only if the foot can achieve plantigrade position when standing. Any equinus contracture prohibits its successful use. The most commonly used AFO in foot drop is constructed of polypropylene and inserts into a shoe. If it is trimmed to fit anterior to the malleoli, it provides rigid immobilization. This is used when ankle instability or spasticity is problematic, such as in patients with upper motor neuron diseases or stroke. If the AFO fits posterior to the malleoli (posterior leaf spring type), plantar flexion at heel strike is allowed, and push-off returns the foot to neutral for the swing phase. This provides dorsiflexion assistance in instances of flaccid or mild spastic equinovarus deformity. A shoe-clasp orthosis that attaches directly to the heel counter of the shoe also may be used. In patients in whom foot drop is due to hemiplegia, peroneal nerve stimulation can be considered. This type of stimulation was first applied in 1961. Nerve stimulation has advantages to the AFO, as it provides active gait correction and can be tailored to individual patients. In this system, a short burst of electrical stimulation is applied to the common peroneal nerve between the popliteal fossa and fibular head. A switch in the heel of the affected limb controls this burst. The stimulator is activated when the foot is lifted, and it is then stopped when the foot contacts the ground. This achieves dorsiflexion and eversion during the swing phase of gait. In a study by Ring et al, the effects of a radiofrequency-controlled neuroprosthesis were compared with those of a standard ankle-foot orthosis (AFO) in 15 patients with foot drop caused by stroke or traumatic brain injury. The authors found that compared with AFO, the studied neuroprosthesis enhanced balance control during walking and, thus, more effectively managed foot drop. Surgical Therapy Foot drop due to direct trauma to the dorsiflexors generally requires surgical repair. When nerve insult is the cause of foot drop, treatment is directed at restoring nerve continuity, either by direct repair or by removal of the insult. If foot drop is secondary to lumbar disc herniation (a finding in 1.2-4% of patients with this condition), consider discectomy. In the early phase of this condition, decreased blood flow due to compression is thought to lead to nerve root ischemia. The nerve root is more susceptible to compression injury than is the peripheral nerve because the vascular network of the nerve root is less developed, with no regional arteriolar blood supply. Foot drop due to nerve root injury may depend on the magnitude and duration of nerve root compression. Early decompression is recommended in cases accompanied by severe motor disturbance, especially in older patients. A Japanese study of 46 patients with degenerative lumbar disease who presented with drop foot noted that palsy duration and preoperative strength were the factors that most affected recovery after surgical intervention. Foot drop following hip replacement can also be treated with sciatic nerve decompression, particularly if there is any concern about bleeding at the operative site. Shortening of the hip prosthesis may be helpful if the limb was lengthened during surgery.
A review of surgical management of peroneal nerve lesions demonstrated that neural repair is the first priority in selected patients with peroneal nerve palsy. This may be accomplished with nerve decompression (either central or peripheral) or nerve grafting or repair. For foot drop from deep peroneal nerve injuries of less than 1-year duration, one study has reported success with transfer of functional fascicles to deep peroneal-innervated muscle groups, using either the superficial peroneal or tibial nerve as a donor. Failing sufficient recovery with those measures, tendon transfer procedures may be considered. It has been suggested that a tendon transfer may be considered if there is no significant neural recovery at 1 year. If a foot drop is chronic and accompanied by contracture, Achilles tendon lengthening may be necessary to achieve adequate dorsiflexion. In patients in whom foot drop is due to neurologic and anatomic factors (eg, polio, Charcot joint), arthrodesis may be the preferred option. The goal is to achieve a stable, well-aligned foot and ankle. This may be accomplished via ankle arthrodesis, Lisfranc arthrodesis, and triple or pantalar arthrodesis with or without Achilles tendon lengthening. Functional electrical stimulation Functional electrical stimulation (FES) is a technique that uses electrical currents to activate nerves innervating extremities affected by paralysis resulting from spinal cord injury (SCI), head injury, stroke and other neurological disorders. FES is primarily used to restore function in people with disabilities. It is sometimes referred to as Neuromuscular electrical stimulation (NMES) FES was initially referred to as Functional Electrotherapy by Libersonand it wasn't until 1967 that the term Functional Electrical Stimulation was coined by Moe and Post and used in a patent entitled, "Electrical stimulation of muscle deprived of nervous control with a view of providing muscular contraction and producing a functionally useful moment" Offner's patent described a system used to treat foot drop. The first commercially available FES devices treated foot drop by stimulating the peroneal nerve during gait. In this case, a switch, located in the heel end of a user's shoe, would activate a stimulator worn by the user. Common Applications Spinal Cord Injury Injuries to the spinal cord interfere with electrical signals between the brain and the muscles, resulting in paralysis below the level of injury. Restoration of limb function as well as regulation of organ function are the main application of FES, although FES is also used for treatment of pain, pressure, sore prevention, etc. Some examples of FES applications involve the use of Neuroprostheses that allow people with paraplegia to walk, stand, restore hand grasp function in people with quadriplegia, or restore bowel and bladder function.
Stroke FES is commonly used in foot drop neuroprosthetic devices. Other Electrical stimulation for the purpose of helping persons with paralysis of the arms or legs mainly focuses on the neuromuscular transmission peripherally. E-stim can also be used for central nervous system stimulation to hasten awakening from coma or the vegetative state. There is a long history of neurosurgeons who have implanted electrodes into the brain and spinal cord, especially in Japan, for increasing cerebral blood flow and certain neurotransmitters in persons in long term coma states. Beginning in 1991 in Greenville, North Carolina (East Carolina University) and shortly after that in Charlottesville,Virginia (University of Virginia), the right median nerve has been used as a portal to help awaken injured human brains. Trains of differentiated square electrical pulses at 40 Hz (a frequency for upregulation of the thalamus), 20 seconds on and 40 seconds off, have been applied to the palmar side of the right wrist for transdermal stimulation of the right median nerve at low amplitudes, enough to produce contraction of the thumb. Battery powered FDA approved electrical neuromuscular stimulators have been used in these research projects connected by wires to the pair of right wrist electrodes embedded in a custom made plastic orthosis to localize the stimulation target. The right median nerve was selected as the electrical portal as there is large cortical representation of that nerve in the dominant left cerebral hemisphere. By subcortical connections, the transmitted signals go to Broca's motor/speech planning area (whether the person is right or left-handed, the majority are left hemisphere dominant). Awakening from deep coma from motor vehicle crashes with closed head injury in the Glasgow Coma Scale range of 4-6 can be expected to respond in half of the treated cases after two to four weeks of 8 hours/day electrical treatment,if started within one to two weeks of the severe brain trauma. The advantage of the shorter than expected period of unconsciousness is a quicker start into a neurorehabilitation program to encourage ambulation and talking. Over the last decade, this RMNS project has spread from the USA East Coast to Central Japan, parts of Europe, and most recently in 2005 to Shanghai, China. Functional electrical stimulation (FES) of paraplegics allows paraplegics with complete paralysis due to spinal cord injury at the thoracic level of their spinal cord to walk distances that average 450 meters per walk under some training procedures and 110 meters per walk when undergoing less demanding training, when using the noninvasive Parastep FES system that received the USA FDA approval in 1994. Certain such patients can walk one mile (1.6 km) using that same system. FES for ambulation also shows improvements in blood flow to lower extremities and in other medical and psychological parameters including bone density.
The use of electrical stimulation for correction of dropped foot in subjects with upper motor neuron lesions. Paul Taylor
The concept of Functional Electrical Stimulation (FES) was put forward by Liberson in 1960 when he and his team produced the first electrical stimulation device for the correction of dropped foot due to an upper motor neurone lesion. His concept was that by applying electrical stimulation to paralysed muscles, functional movement could be produced, providing the user with a useful orthotic device. Liberson’s device was a portable neuromuscular stimulator which produced pulses of between 20 and 250Οs at a frequency of 30-100Hz and current amplitudes of up to 90mA. Stimulation was timed using a switch placed under the heel of the affected side. When weight was taken from the switch, stimulation was delivered to carbon rubber electrodes placed over the common peroneal nerve as it passes over the head of fibula, causing dorsiflexion. Liberson reported that the gait of hemiplegics was significantly improved by use of the device and that on several occasions users acquired the ability of voluntary dorsiflexion for short periods after its use. Since that time several groups have developed similar systems and the devices have received some clinical use, most notably in the former Yugoslavia. However, until recently, the technique has not been widely used in the UK and there has been a shortage of evidence to support its use. There has not been much reported in the literature on the use of dropped foot stimulators with PWMS. The first report is by Carnstam et al. who reported increased active dorsiflexion strength and reduced calf tone after peroneal stimulation observed in one PWMS. Karsnia et
al. reported a retrospective study of 99 stimulator users, 43 of whom had MS. Twenty-five, mainly those with MS had stopped using the device because of a decline in their condition while 16, mainly CVA, had stopped due to improved mobility. Overall the device was well accepted. Crone et al. demonstrated disynaptic reciprocal inhibition in 74 neurologicaly intact subjects by showing the H reflexes induced in the soleus muscle were inhibited by stimulation of the common peroneal nerve. The effect was greatly reduced in 39 patients who had spasticity except for 4 PWMS who were regular dropped foot stimulator users. This suggests that regular stimulation of the common peroneal nerve may help to preserve this reflex. The Odstock Dropped Foot Stimulator (ODFS) is a single channel, foot switch triggered stimulator designed to elicit dorsiflexion and eversion of the foot by stimulation of the common peroneal nerve, (max. amplitude 100mA, 350Îźs pulse, 40 Hz). It is a development of the device first described by Liberson. Skin-surface electrodes are placed, typically, over the common peroneal nerve as it passes over the head of the fibula and the motor point of tibialis anterior. If greater knee flexion is required, the indifferent electrode can be placed over the common peroneal nerve as it passes through the popliteal fossa, eliciting a withdrawal reflex. The rise and fall of the stimulation envelope can be adjusted to prevent a sudden contraction, which might induce a stretch reflex in the calf muscles. There is also a facility to add an extension to the stimulation envelope after heel strike which mimics the natural activity of the anterior tibialis muscle which contracts eccentrically lowering the foot to the ground. The Odstock 2 Channel Stimulator (O2CHS) is a version of the ODFS allowing the correction of bilateral dropped foot controlled by a single foot switch and the stimulation of other combinations of muscles. By provision of dorsiflexion and eversion, the foot clears the ground in the swing phase more easily. This reduces the effort of gait, reducing compensatory activities such as hip hitching and circumduction. Reduction in effort will lead to a reduction of associated reactions and result in a general lowering of tone. Contraction of the tibialis anterior muscle and the hamstrings via the withdraw reflex may, by reciprocal inhibition, reduce antagonist activity leading to a more normal modulation of tone in gait. Repeated use of the stimulator may then lead to a pattern of "normal" walking being relearned centrally and long term potentiation of the required pattern of synapses may lead to a reinforcement of this pattern of walking. However, a more immediate benefit from the orthotic use of the device is that walking is easier and safer and therefore confidence will improve leading to an extension of mobility range and an overall improvement in quality of life. The ODFS was the subject of a randomised controlled trial in which 32 stroke patients who had had a stroke for in excess of 6 months were allocated to a treatment group or a control group. The treatment group used the device and also received 12 sessions of physiotherapy in the first month, while the control group who received the same contact time only received physiotherapy. After three months of use the treatment group showed a statistically significant increase in walking speed of 16% and a reduction in the Physiological Cost Index (PCI) of 29% when the stimulator was used while no changes were seen in the control group. No significant 'carryover' effect was seen although a trend was present. Users of the ODFS showed a continuing reduction in quadriceps spasticity measured using the Wartenberg Pendulum Drop Test, which was only seen in the control group while physiotherapy continued. The treatment group also showed a reduction in the Hospital Anxiety and Depression index suggesting an improvement in quality of life. Cost benefit analysis showed that use of the device gave a QALY (quality adjusted life years) gain over the control group
of 0.042, indicating that the use of the device met the requirements for a treatment within the NHS. The trial results together with case series data from subjects who had multiple sclerosis were presented to the South and West Regional Health Authority Development and Evaluation Committee9. After examining this and evidence from other groups, the committee recommended the ODFS for use in the UK's National Health Service for patients with upper motor neurone lesions. Following the trial and some publicity in a national newspaper, there was some considerable demand for treatment and it was therefore decided to set up a clinical service. As previously mentioned the idea of FES is not new and it was our opinion that the reason for its poor take up into clinical practice was for several reasons. Firstly, initial devices had been unreliable with poor technical back up. Secondly, the clinical techniques for its successful application have been poorly documented and practitioners received no training in its use. Thirdly, it was plain from our clinical experience that regular follow up was required to ensure continued effective use of the device. The first problem we hoped we had solved by using new technology and careful design based on considerable clinical experience. The second problem was tackled by writing a detailed clinical manual and by running a regular two day training courses for clinicians that wished to use the device. To satisfy the need for follow up the following clinical model has been adopted. Patients are first seen at an assessment clinic. Subjects are suitable for treatment if they have a dropped foot due to an upper motor neurone lesion and are able to walk at least a few metres with appropriate aids or assistance. The following are contraindications; fixed contractures of the ankle, poorly controlled epilepsy (there is some anecdotal evidence of symptoms being exacerbated by electrical stimulation) and poor skin condition in the area of the electrodes. The effect of the stimulation is not known in pregnancy and pacemaker users are assessed by a cardiologist to ensure the ODFS doses not interfere with the pacemaker. The stimulator is tried and if gait can be improved, the patient is recommended for treatment. The ODFS is fitted over two clinic sessions on consecutive days. On the first day the user is taught how to apply the device while on the second day their ability to do so is assessed and further training given if necessary. If appropriate, carers are also instructed in its use. If the patient has severe calf spasticity it has been found useful to use an exercise stimulator for a period of about an hour a day for one month. By using a stimulator with a slow rising edge ramp, calf spasticity can be reduced and range of motion increased. A recent pilot study has shown that botulinum toxin may also be beneficial in such casesUse of the stimulator is increased gradually over 2 to 3 weeks until it can be used all day. Follow up is made at 6 weeks, 18 weeks, 45 weeks and 72 weeks from first use and then yearly for as long as the device is used. If users experience problems they are encouraged to contact the clinic so advice can be given, equipment repaired or extra clinic sessions arranged if necessary. Following the establishment of a clinical service, it was decided to continue recording the main outcome measures of walking speed and PCI that had been recorded in the RCT. While increased walking speed was not highlighted as a significant reason for continued use of the ODFS, it has been shown by Wade et al. to be representative of overall gait function. An audit of these parameters over the first 18 weeks of use confirmed the results of the original RCT and also showed a significant carryover effect, i.e. an improvement in walking ability when not using the stimulator, in a group of 111 stroke subjects. Overall, users walked 27% faster when they used the device
with a carryover effect of 14%. In a subgroup of 27 ODFS users walking speed both with and without the device was observed to improve over the first 18 weeks and thereafter remain unchanged. As the ODFS users were an average of 5.4(sd Âą10.7) years post stroke this supports the hypothesis that the carryover observed was due to use of the stimulator rather than natural recovery following the stroke. In a group of 78 MS subjects, users walked 20% faster when using the device Although no overall carryover effect was observed, one third showed an improvement in unaided walking speed of more then 10%. In a subgroup of 20 MS users, this improved walking speed with the device was shown to also peaks at 18 weeks with no significant change from initial values after that time. 18 MS users of the bilateral dropped foot stimulator showed a 48% increase in walking speed at 18 weeks but again no significant carryover effect although a strong trend was observed.
A questionnaire survey indicated that the most common reasons for using the ODFS were that it reduced the effort of walking, reduced tripping and improved confidence 14. Overall, compliance was 92% at 18 weeks and 86% at 1 year. However, if MS users are looked at separately, out of 134 who started using FES between January 1999 and December 2001, 9 stopped its use within 1 year, a compliance of 93%. In the year 2000 the device was recommended by the Royal College of Physicians in their publication "National clinical guidelines on stroke"15. Future developments While the ODFS has been shown to improve gait by correction of dropped foot, problems often remain with movement of other joints, in particular the knee and hip. The O2CHS can be used to add a second channel of stimulation. Hip extension in the stance phase can be improved by stimulation of the gluteus maximus while hip abduction can be improved by
stimulation of the gluteus medius. Knee flexion can be improved by stimulation of the hamstrings at terminal stance and initial swing while the same muscle can be used to control knee hyperextension at initial floor contact. The calf muscles can be stimulated to improve push off and triceps can be stimulated to improve arm swing and therefore balance while walking in patients with significant associated reaction in the upper limb16. Preliminary investigations suggest that the ODFS may be applied in cases of Parkinson’s Syndrome to help initiate gait and prevent freezing17. WOUND & SKIN CARE ELECTRICAL STIMULATION can help speed wound healing by increasing capillary density and perfusion, improving wound oxygenation, and encouraging granulation and fibroblast activity. Several manufacturers make the high-voltage pulsed current simulator used for this therapy. Electrical stimulation can be applied in one of two ways. For the first method, one electrode (positive or negative polarity) is applied to sterile, conductive material, such as salinemoistened gauze, placed in the wound. The conductive surface of the other electrode is applied nearby on intact dry skin. The second method involves positioning the conductive surfaces of two electrodes with the same polarity on intact dry skin on opposite borders of the wound, straddling the wound. A third electrode with the opposite polarity is placed nearby on intact dry skin. In both methods, the pulse frequency is set to 100 pulses/second and the voltage is set to deliver a current that produces a moderately strong but comfortable tingling sensation (in sensate skin) or a just-- visible muscle contraction (in insensate skin, as in patients with spinal cord injuries). The voltage required is typically between 50 and 150 volts. Polarity of the electrode or electrodes placed on or straddling the wound depends on the wound's clinical needs. To promote autolysis, use positive polarity to attract negatively charged neutrophils and macrophages. To encourage granulation tissue development, use negative polarity to attract positively charged fibroblasts. To stimulate wound resurfacing, use positive polarity to attract negatively charged epidermal cells. Treatments are typically given for 1 hour a day, 5 to 7 days a week, as long as documented assessment indicates that the wound is healing. Electrical stimulation can be used on chronic wounds, including pressure ulcers, diabetic ulcers, venous ulcers, and arterial ulcers. The treatment is contraindicated in patients who have basal or squamous cell carcinoma in the wound or peri-- wound skin, and in wounds with osteomyelitis that aren't responding to systemic antibiotic therapy. Also avoid this therapy if the wound contains ion residues of iodine or silver, if the patient has a pacing device, or if the wound is over the heart. In general, electrical stimulation therapy is applied in the same way regardless of wound type. However, you may need to change electrode polarity and the dosage of current as the wound heals. For example, if you were treating a quadriplegic patient with a Stage IV pressure ulcer that hadn't responded to 4 weeks of standard wound care, you'd first apply negative polarity
to increase granulation and fibroblast activity. After granulation tissue has filled the wound cavity, however, you'd switch to positive polarity to promote epidermal cell migration. Similarly, if you were treating a full-thickness venous ulcer on the ankle that hadn't responded to standard therapy, you'd first apply negative polarity to increase fibroblast activity and capillary density, then positive polarity to enhance epidermal resurfacing. Patients receiving electrical stimulation therapy should be under the supervision of a physical therapist or licensed health care provider who's trained in using this therapy. A wound care specialist can determine when standard interventions have failed. A physical therapist then would determine the appropriate polarity to use in electrical stimulation therapy and when the polarity should be changed. Electrical stimulation of foot drop
ASSESSMENT
The Bioness NESS L300 features a gait sensor that is worn in the shoe to detect different walking surfaces and speeds, and adjust stimulation accordingly.
I would first start off by doing a comprehensive muscle test that assesses the distal and proximal muscle groups in Shirley's leg. When assessing the foot I test both intrinsic and extrinsic muscles. Following the muscle test, I assess Shirley's range of motion (ROM), spasticity, and posture. With the postural assessment I look at trunk strength and look for any asymmetry in the posture while standing still and during walking. I also utilize a number of standardized balance tests such as the Berg Balance Scale and the Tinetti Assessment Tool. It is very common for a patient with MS to have weak intrinsic muscles in their foot and have some type of asymmetry in their posture. As a result, balance problems are typically seen. Assessing patients on a treadmill is very helpful as it shows me how the patient's gait pattern changes as I increase the treadmill's speed or increase its incline. Assessing patients on a treadmill also gives me a measurable time of how long it takes a patient to fatigue. Fatigue is important as foot drop becomes more pronounced. Then assessing patients with and without their shoes helps me see what exactly is going on with their foot when walking: Is it pronating, supinating, plantarflexed, swollen? Are the toes curling, and if so, when is that curling occurring during the gait cycle? more efficient in their walking than the custom AFO with a joint. ELECTRICAL STIMULATION
The WalkAide from Innovative Neurotronics utilizes a tibial tilt accelerometer to determine the proper stimulation timing during a gait cycle. Research has shown that NMES and FES are effective in treating foot drop. 1 By incorporating electrical stimulation, we are retraining the muscles as the device dorsiflexes
the ankle during foot clearance. The biofeedback assists a patient to actively try to move their ankle, instead of passively keeping the ankle in one position. Research has also shown that electrical stimulation can decrease spasticity and swelling.2 The Empi 300PV NMES device (which can be ordered as a home unit or be used solely in the clinic by the PT during treatment) has an external trigger that the PT can use during the patient's gait training session to help facilitate foot clearance. PTs can create a home exercise program by setting exercise parameters on the patient's home unit. The NESS L300 from Bioness Inc, Valencia, Calif, and the WalkAide速 System from Innovative Neurotronics, Austin, Tex, are two FES devices/neuro-prostheses currently on the market. Both are designed solely for treatment of foot drop and are easy for the PT and the patient to operate. FES has the same concept as NMES in that it stimulates the dorsiflexor muscles to help with clearing the foot during gait and reeducate the muscles so that the muscle can become stronger. However, these two devices that utilize the FES function are cordless/wireless and allow the patient to use it during ambulation at home or in the community. Both the NESS L300 and the WalkAide have cuffs that are placed under the knee to hold the electrodes in place, and are easy to put on and take off by patients using one or two hands. Both require an experienced PT or orthotist to program the patient's parameters, and can be used during therapy or as a home unit. The WalkAide uses a tibial tilt accelerometer to determine the proper stimulation timing during a gait cycle. The device's electrical stimulation is triggered every time the tibia advances forward. The WalkAide is a single-unit system that has two components: the cuff, which comes in large, medium, or small; and the control unit (attached on the cuff) that is used to adjust the level of stimulation, turn the device on/off, and change modes. The NESS L300 uses a heel sensor mechanism. The device's electrical stimulation is triggered every time the heel leaves the ground. The NESS L300 has three components: a gait sensor placed inside the shoe at the heel; the cuff, which comes in large, medium, or small; and a wireless portable control unit that allows patients or clinicians to adjust the level of stimulation, turn the device on/off, and change parameters to gait mode, exercise mode, or clinician mode. This portable control unit device is not attached to the cuff and is small enough that the patient can put it in their pocket. The gait sensor requires the patient to wear shoes because it automatically detects different surfaces and speeds, sending a signal to the leg cuff to help adjust stimulation to fit the terrain and speed. Treating Dropfoot with Ankle-Foot Orthoses
Buy Dropfoot Braces Here A tutorial on braces for patients with dropfoot Drop foot (also known as dropfoot, footdrop and foot drop) is a term that describes a disorder
where a patient has a limited ability or inability to raise the foot at the ankle joint. This makes walking difficult as the toes tend to drag on the ground which leads to tripping and instability. Patients adapt to this by using their hip muscles to exaggerate lifting the foot above the ground (known as a “steppage gait”) or by swinging their leg outward so that the foot can clear the ground (known as “circumduction”). More information on the cause of foot drop is available at the end of this page. To understand how AFOs work, you must first understand two standard motions that occur at the ankle joint – “dorsiflexion” and “plantarflexion”. Plantarflexion is the motion the ankle joint makes when the toes point downward. Dorsiflexion is the motion the ankle joint makes when the foot points upward. This motion needs to occur when the foot comes off the ground so that the patient does not drag their toes. Patients with dropfoot usually have a partial or complete weakness of
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Foot Drop Splint with External Fixator A foot drop splint allows your ankle to be positioned normally at rest. You may exercise by pushing against the splint. Exercise will keep your muscles toned. • The foot drop splint is made up of the post-op shoe and the theraband. • The post-op shoe fits on your foot like a shoe. • The theraband is spread over the ball of the foot on the outside of the post -op shoe. • The theraband is attached directly onto the external fixator. Wearing Schedule Wear the foot drop splint 24 hours a day. Take the splint off 2 to 3 times a day for 10 to 15 minutes and move your foot up and down. Have someone check the skin on the bottom of your foot to make sure there are no areas of skin irritation. Also, wash your foot during this time when the splint is off your foot. Reattach the splint by putting the post-op shoe on your foot then adding the theraband. Spread the theraband over the ball of the shoe and then attach it to the fixator. External Fixator A foot drop splint allows your ankle to be positioned normally at rest. You may exercise by pushing against the splint. Exercise will keep your muscles toned. • The foot drop splint is made up of the post-op shoe and the
theraband. • The post-op shoe fits on your foot like a shoe. • The theraband is spread over the ball of the foot on the outside of the post -op shoe. • The theraband is attached directly onto the external fixator. Wearing Schedule Wear the foot drop splint 24 hours a day. Take the splint off 2 to 3 times a day for 10 to 15 minutes and move your foot up and down. Have someone check the skin on the bottom of your foot to make sure there are no areas of skin irritation. Also, wash your foot during this time when the splint is off your foot. Reattach the splint by putting the post-op shoe on your foot then adding the theraband. Spread the theraband over the ball of the shoe and then attach it to the fixator. Tightening the Theraband As you are feeling better, each day tighten the theraband to pull your foot up. The goal is to keep your foot at a 90 degree angle to your leg. Talk to your doctor or others on your health care team if you have questions. Foot Drop Splint with External Fixator A foot drop splint allows your ankle to be positioned normally at rest. You may exercise by pushing against the splint. Exercise will keep your muscles toned. • The foot drop splint is made up of the post-op shoe and the theraband. • The post-op shoe fits on your foot like a shoe. • The theraband is spread over the ball of the foot on the outside of the post -op shoe. • The theraband is attached directly onto the external fixator. Wearing Schedule Wear the foot drop splint 24 hours a day. Take the splint off 2 to 3 times a day for 10 to 15 minutes and move your foot up and down. Have someone check the skin on the bottom of your foot to make sure there are no areas of skin irritation. Also, wash your foot during this time when the splint is off your foot. Reattach the splint by putting the post-op shoe on your foot then adding the theraband. Spread the theraband over the ball of the shoe and then attach it to the fixator. Page 2 Tightening the Theraband
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Posey Foot-Drop Splint Dimensions Replacement foam liner Top of Form
CONCLUSIONS The large increases in MVC and MEP suggest that regular use of a foot-drop stimulatorwith splin strengthens activation of motor cortical areas and their residual descending connections, which may explain the therapeutic effect on walking speed. It has been demonstrated by RCT that the who have a dropped foot following. A clinical service has ODFS can improve the mobility of people been successfully set up and these techniques successfully transferred to other centres. Audit of these services has confirmed the RCT results and further indicated that mobility can be improved in people with A RCT with this group is now underway. Use of the bilateral system in MS can delay final dependence on a wheel chair, providing a means of access where a chair can not be used. Compliance of both devices is high suggesting that they are well accepted and provide a useful benefit to their users. REFERENCES [1] W. T. Liberson, H. J. Holmquest, D. Scott, and M. Dow, "Functional electrotherapy, stimulation of the peroneal nerve synchronized with the swing phase of the gait of hemiplegic patients," Arch Phys Med, vol. 42, pp. 101-105, 1961. [2] R. L. Waters, D. McNeal, and J. Perry, "Experimental correction of foot drop by electrical stimulation of the peroneal nerve," J. Bone Joint Surg, vol. 57A, pp. 1047-1054, 1975. [3] J. A. Hoffer, "Initial results with fully implanted Neurostep FES system for foot drop," presented at 10th Annual IFESS Meeting, Montreal, 2005. [4] A. I. R. Kottink, H. P. J. Buschman, L. P. J. Kenney, P. H. Veltink, P. Slycke, G. Bulstra, and H. J. Hermens, "The sensitivity and selectivity of an implantable two-channel peroneal nerve stimulator system for restoration of dropped foot," Neuromodulation, , [5] J. H. Burridge, M. Haugland, B. Larsen, R. M. Pickering, N. Svaneborg, H. K. Iversen, P. B. Christensen, J. Haase, J. Brennum, and T. Sinkjaer, "Phase II trial to evaluate the ActiGait implanted drop-foot stimulator in established hemiplegia," J Rehabil Med, vol. 39, pp. 212-8, 2007. [6] A. Kralj, R. Acimovic, and U. Stanic, "Enhancement of hemiplegic patient rehabilitation by means of functional electrical stimulation," Prosthet Orthot Int, vol. 17, pp. 107-114, 1993. [7] J. Burridge, P. Taylor, S. Hagan, and I. Swain, "Experience of clinical use of the Odstock dropped foot stimulator," Artif Org, vol. 21, pp. 254-60., 1997. [8] R. B. Stein, "Assembly for functional electrical stimulation during
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