CASE REPORT FOOT DROP

CHAPTER I

Background

Foot drop is a deceptively simple name for a potentially complex problem. It can be

defined as a significant weakness of ankle and toe dorsiflexion. The foot and ankle

dorsiflexors include the tibialis anterior, the extensor hallucis longus, and the extensor

digitorum longus. These muscles help the body clear the foot during swing phase and

control plantar flexion of the foot on heel strike. Weakness in this group of muscles

results in an equinovarus deformity. This is sometimes referred to as steppage gait,

because the patient tends to walk with an exaggerated flexion of the hip and knee to

prevent the toes from catching on the ground during swing phase. During gait, the force

of heel strike exceeds body weight, and the direction of the ground reaction vector passes

behind the ankle and knee center. This causes the foot to plantar-flex and, if uncontrolled,

to slap the ground. Ordinarily, eccentric lengthening of the tibialis anterior, which

controls plantar flexion, absorbs the shock of heel strike. Foot drop can result if there is

injury to the dorsiflexors or to any point along the neural pathways that supply them

The diagnostic process includes a comprehensive assessment of the patient's

symptoms, past and current medical histories, physical and neurological examinations,

imaging studies such as MRI (magnetic resonance imaging), and EMG

(electromyogram). The spine specialist must determine the cause of drop foot before

formulating a treatment plan.

The type of treatment is dependent on the underlying cause of drop foot. Some

patients may be fitted with an Ankle Foot Orthosis (AFO), brace, or splint that fits into

the shoe to stabilize the ankle/foot. Gait training may be incorporated into the patient's

physical therapy treatment plan. Surgery may be an option to correct or alleviate the

underlying problem causing drop foot. For example, if drop foot is caused by nerve

compression from a lumbar herniated disc, then a spinal surgical procedure called

discectomy (disc removal) may be required to relieve or 'decompress' the nerve.

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http://www.spineuniverse.com/treatments/surgery/foraminotomy-taking-pressure-spinal-nerves

http://www.spineuniverse.com/treatments/surgery/foraminotomy-taking-pressure-spinal-nerves

CHAPTER II

1. Defenition

Manifestation of peripheral neuropathy, characterized by an inability to actively

dorsiflex and evert the foot at the ankle. The foot drops when the lifts the foot off the

ground in the swing phase of ambulation–thus requiring a high stepping gait. It is

associated with paresthesiae of feet, loss of vibratory and position sense, spasticity,

exaggerated tendon reflexes in legs.

2. Epidemiology

Peroneal neuropathy caused by compression at the fibular head is the most common

compressive neuropathy in the lower extremity. Foot drop is its most notable symptom.

All age groups are affected equally, but the condition is more common in males (male-to-

female ratio, 2.8:1). About 90% of peroneal lesions are unilateral, and they can affect the

right or the left side with equal frequency. A foot drop of particular concern to orthopedic

surgeons is the peroneal nerve palsy seen after total knee arthroplasty (TKA; 0.3-4% of

cases) or proximal tibial osteotomy (3-13% of cases). Ischemia, mechanical irritation,

traction, crush injury, and laceration can cause intraoperative injury to the peroneal nerve.

It has also been suggested that correction of a severe valgus or flexion deformity can

stretch the peroneal nerve and lead to palsy. Postoperative causes of peroneal nerve palsy

include hematomas and constrictive dressings. A series of patients who developed foot

drop after primary hip arthroplasty were carefully examined and found to have spinal

stenosis. As many as 70% of patients undergoing hip arthroplasty have electromyographic

(EMG) evidence of nerve injury, but they rarely have clinical symptoms. Patients with

preexisting spinal stenosis are believed to be at increased risk for foot drop after hip

arthroplasty because of this proximal compromise; this is the double-crush phenomenon

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Anatomy

Fibers from the dorsal branches of the ventral rami of L4-S1 are found in the

peroneal nerve, which is paired with the tibial nerve to constitute the sciatic nerve. The

sciatic nerve leaves the pelvic cavity at the greater sciatic foramen, just inferior to the

piriformis. It bifurcates to form the peroneal and tibial nerves either in the distal third of

the thigh or at the midthigh level.

The peroneal nerve crosses laterally to curve over the posterior rim of the

fibular neck to the anterior compartment of the lower leg, dividing into superficial and

deep branches. The superficial branch travels between the two heads of the peronei and

continues down the lower leg to lie between the peroneal tendon and the lateral edge of

the gastrocnemius. It then branches to the ankle anterolaterally to supply sensation to the

dorsum of the foot. The deep branch divides just after rounding the fibular neck. Its initial

branch supplies the tibialis anterior, and the remaining branches supply the extensor

digitorum longus, the extensor hallucis longus, and a small sensory patch at the first

dorsal web space.

3

The peroneal nerve is susceptible to injury all along its course. As part of the

sciatic nerve, its funiculi are relatively isolated from those of the tibial nerve. Therefore,

trauma to the sciatic nerve may affect only one of its divisions. The funiculi of the

peroneal nerve also are larger and have less protective connective tissue than those of the

tibial nerve, making the peroneal nerve more susceptible to trauma. The peroneal nerve

runs a more superficial course than the tibial nerve does, especially at the fibular neck,

and this relatively exposed position makes it vulnerable to direct insult. Its close

adherence to the periosteum of the proximal fibula renders it susceptible to injury during

surgical procedures in this area.

4

3. Etiology

Hip arthroplasty, pelvic or femoral fractures, or posterior dislocation of the hip.

Result from traumatic mechanisms including misplaced injections into the

inferior medial quadrant of the buttock.

5

Mass lesions including nerve sheath tumors and external compression from

hematoma, aneurysm, endometriosis, and other mechanisms have been

described. Sciatic neuropathies may occur in patients with systemic vasculitis.

Axons originating from the L4, L5, S1 and S2 roots, primarily L5 nerve root

fibers, come together to form the common peroneal nerve. It is one of the two

major divisions of the sciatic nerve and separates from it as a distinct nerve in

the mid-to distal thigh. It travels through the popliteal fossa and gives off the

lateral sural cutaneous nerve, which unites with the medial sural cutaneous

nerve (a branch of the tibial nerve) to form the sural nerve. The lateral

cutaneous nerve of the calf also branches off in the popliteal fossa. It provides

sensation to the skin of the lateral leg just below the knee. On its course around

the fibular head, the common peroneal nerve is very superficial and covered

only by skin and subcutaneous tissue. It then pierces through a fibrous,

sometimes tight opening in the peroneus longus muscle (fibular tunnel) and

divides into superficial and deep branches.

Common peroneal neuropathy is the most frequent lower extremity

mononeuropathy. The common peroneal nerve is most susceptible to external

compression at the fibular head, where it is very superficial. Predisposing

causes include recent substantial weight loss, habitual leg crossing, or

prolonged squatting. External devices such as casts, braces, and tight bandages

can also cause peroneal neuropathy.

Diabetes mellitus, vasculitis, and rarely hereditary tendency to pressure palsy

(HNPP) are other etiologic conditions.

An acute anterior or lateral compartment syndrome below the knee can also

lead to acute common, deep, or superficial peroneal neuropathies.

Autoimmune process, perhaps with a vasculitic component. Vasculitis, such as

polyarteritis nodosa, may manifest as mononeuritis multiplex, with acute

involvement of the femoral nerve.

Femoral neuropathies occasionally follow prolonged surgeries or childbirth in

the lithotomy position, presumably from anatomic predisposition to kinking

6

beneath the inguinal ligament. Iliacus hematoma or abscess, misplaced

attempts at femoral artery or vein puncture, or iatrogenic injury after

nephrectomy or hip arthroplasty are other recognized causes.

4. Pathophysiologi

The pathophysiology of nerve damage that commonly causes foot drop is as

follows. The functional integrity of an axon and its target depends on the continued

supply of trophic substances synthesized in the neuronal perikaryon and transported

down the axon (axoplasmic flow). A laceration interrupts axoplasmic flow; a crush injury

may compromise it as well. A double-crush phenomenon occurs when a proximal insult

in a nerve root diminishes axoplasmic flow, making it more susceptible to injury.

A distal lesion further compromises axoplasmic flow, and clinical palsy results. This is

the phenomenon thought to be responsible for the increased risk of foot drop after hip

replacement in a patient with preexisting spinal stenosis. The spinal stenosis causes the

proximal compromise, and intraoperative stretch of the sciatic nerve provides the distal

insult

5. Sign and Symptom

Distal leg weakness, pain, and sensory loss.

Foot pain is a frequent complaint. Because of predominant affliction of the

peroneal division, the weakness often manifests itself as foot drop and needs

to be differentiated from a common peroneal neuropathy at the fibular head.

Weakness of the more proximal muscles (hamstrings) and of foot plantar

flexion and inversion (gastrocnemius, tibialis posterior) helps differentiate

between the two entities. The ankle jerk and internal hamstring reflex are

usually depressed or absent.

Sensory loss and dysesthesia of the sole and dorsum of the foot and

posterolateral lower leg are common

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6. Risk Factor

The peroneal nerve controls the muscles that lift your foot. This nerve runs near

the surface of your skin on the side of your knee closest to your hand. Activities that

compress this nerve can increase your risk of foot drop. Examples include:

Crossing your legs. People who habitually cross their legs can compress the

peroneal nerve on their uppermost leg.

Prolonged kneeling. Occupations that involve prolonged squatting or

kneeling — such as picking strawberries or laying floor tile — can result in

foot drop.

Wearing a leg cast. Plaster casts that enclose the ankle and end just below

the knee can exert pressure on the peroneal nerve

7. Test and Diagnosis

Foot drop is usually diagnosed during a physical exam. Your doctor will want to

watch you walk and may check a number of your leg muscles for weakness. He or she

may also check for numbness on your shin and on the top of your foot and toes. In some

cases, additional testing is recommended.

Imaging tests

Foot drop is sometimes caused by an overgrowth of bone in the spinal canal or

by a tumor or cyst pressing on the nerve in the knee or spine. Imaging tests can

help pinpoint these types of problems.

X-rays. Plain X-rays use a low level of radiation to visualize a soft tissue

mass or a bone lesion that may be causing your symptoms.

Ultrasound. This technology uses sound waves to create images of internal

structures. It may be used to check for cysts or tumors that may be

pressing on the nerve.

Computerized tomography (CT) scan. Computerized tomography

combines X-ray images taken from many different angles to form cross-

sectional views of structures within the body.

8

Magnetic resonance imaging (MRI). This test uses radio waves and a

strong magnetic field to create detailed images. MRI is particularly useful

in visualizing soft tissue lesions that may be compressing a nerve.

Nerve tests

Electromyography (EMG) and nerve conduction studies measure electrical

activity in the muscles and nerves. These tests can be uncomfortable, but they're

very useful in determining the location of the damage along the affected nerve.

8. Treatment and Drug

Treatment for foot drop depends on the underlying cause. If the underlying

cause is successfully treated, foot drop may improve or even disappear. If the underlying

cause can't be treated, foot drop may be permanent. Specific treatment for foot drop may

include:

Braces or splints. A brace on your ankle and foot or splint that fits into your

shoe can help hold your foot in a normal position.

Physical therapy. Exercises that strengthen your leg muscles and help you

maintain the range of motion in your knee and ankle may improve gait

problems associated with foot drop. Stretching exercises are particularly

important to prevent the development of stiffness in the heel.

Nerve stimulation. Sometimes stimulating the nerve that lifts the foot improves

foot drop.

Surgery. Depending upon the cause, and if your foot drop is relatively new,

nerve surgery may be helpful. If foot drop is long-standing, your doctor may

suggest surgery that fuses ankle or foot bones or a procedure that transfers a

functioning tendon to a different position.

9

Mononeuropathies of the Lower Extremities Sciatic Neuropathies

The sciatic nerve is the body’s largest nerve, receiving contributions primarily

from the L5, S1, and S2 nerve roots, but also carrying L4 and S3 fibers. It has two

primary divisions: the laterally situated more superficial peroneal nerve and the more

medially placed tibial nerve . These separate into two distinct nerves in the mid-to distal

thigh. The sciatic nerve and its branches innervate the hamstrings (biceps femoris,

semimembranosus, and semitendinosus muscles), distal adductor magnus, anterior and

posterior lower leg compartments, and intrinsic foot musculature. Through sensory

branches of the tibial nerve (sural, medial and lateral plantar, and calcaneal) and the

superficial peroneal nerve, the sciatic nerve also supplies sensation to the skin of the

entire foot and the lateral and posterior lower leg.

ETIOLOGY

Sciatic neuropathies can be due to hip arthroplasty, pelvic or femoral fractures,

or posterior dislocation of the hip. Like femoral neuropathies, they are sometimes caused

by a prolonged lithotomy position, presumably from stretching of the nerve in individuals

who are anatomically predisposed. Occasionally, sciatic neuropathies develop from

external pressure in patients who are comatose or immobilized for protracted periods

such as with drug overdose. They may result from traumatic mechanisms including

misplaced injections into the inferior medial quadrant of the buttock. Mass lesions

including nerve sheath tumors and external compression from hematoma, aneurysm,

endometriosis, and other mechanisms have been described. Sciatic neuropathies may

occur in patients with systemic vasculitis.

CLINICAL PRESENTATION

Acute sciatic neuropathies typically present with distal leg weakness, pain, and

sensory loss. Foot pain is a frequent complaint. Because of predominant affliction of the

peroneal division, the weakness often manifests itself as foot drop and needs to be

10

differentiated from a common peroneal neuropathy at the fibular head. Weakness of the

more proximal muscles (hamstrings) and of foot plantar flexion and inversion

(gastrocnemius, tibialis posterior) helps differentiate between the two entities. The ankle

jerk and internal hamstring reflex are usually depressed or absent. Sensory loss and

dysesthesia of the sole and dorsum of the foot and posterolateral lower leg are common.

DIFFERENTIAL DIAGNOSIS

A lumbosacral plexus lesion is the primary consideration in most patients with

sciatic neuropathies, when findings clearly encompass a territory outside the peroneal

nerve. Diminished sensation on the posterior thigh points to a concomitant neuropathy of

the posterior femoral cutaneous nerve, which exits the greater sciatic foramen in

proximity to the sciatic nerve. Hip extension and abduction should be preserved in sciatic

neuropathies. When clinical or EMG evidence suggests gluteal muscle involvement,

primary lesions within the pelvis, such as benign tumors, for example, schwannoma, or

malignant processes, particularly, lymphoma are considerations. Piriformis syndrome is a

poorly understood disorder that is phenomenologically similar to the thoracic outlet and

tarsal tunnel syndromes. The piriformis muscle lies deep to the gluteal muscles; it

originates from the sacral spine and attaches to the greater trochanter of the femur. The

sciatic nerve passes posterior to the piriformis muscle. It is postulated that acute or

chronic injury of the muscle may cause irritation of the sciatic nerve, resulting in

posterior thigh and gluteal pain. Patients with an aberrant course of the nerve through the

muscle are particularly predisposed to this condition. Objective clinical or electro-

diagnostic evidence of sciatic neuropathy is not seen in most patients in whom piriformis

syndrome is suspected.

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Peroneal Neuropathies

Axons originating from the L4, L5, S1 and S2 roots, primarily L5 nerve root

fibers, come together to form the common peroneal nerve. It is one of the two major

divisions of the sciatic nerve and separates from it as a distinct nerve in the mid-to distal

thigh. It travels through the popliteal fossa and gives off the lateral sural cutaneous nerve,

which unites with the medial sural cutaneous nerve (a branch of the tibial nerve) to form

the sural nerve. The lateral cutaneous nerve of the calf also branches off in the popliteal

fossa. It provides sensation to the skin of the lateral leg just below the knee. On its course

around the fibular head, the common peroneal nerve is very superficial and covered only

by skin and subcutaneous tissue. It then pierces through a fibrous, sometimes tight

opening in the peroneus longus muscle (fibular tunnel) and divides into superficial and

deep branches

ETIOLOGY

Common peroneal neuropathy is the most frequent lower extremity mononeuropathy.

The common peroneal nerve is most susceptible to external compression at the fibular

head, where it is very superficial. Predisposing causes include recent substantial weight

loss, habitual leg crossing, or prolonged squatting. External devices such as casts, braces,

and tight bandages can also cause peroneal neuropathy. Diabetes mellitus, vasculitis, and

rarely hereditary tendency to pressure palsy (HNPP) are other etiologic conditions. An

acute anterior or lateral compartment syndrome below the knee can also lead to acute

common, deep, or superficial peroneal neuropathies. Patients with insidious onset and

progressive course require evaluation for mass lesions, including a Baker cyst or

ganglion, osteoma, or schwannoma.

12


Most peroneal neuropathies involve the common peroneal nerve at the fibular head

causing weakness of foot dorsiflexion and eversion. Ambulation reveals a “steppage gait”

with compensatory hip and knee flexion in order to lift the foot off the floor. Sensory

symptoms are limited to the web space between the first and second toes with deep

peroneal neuropathies. Superficial peroneal neuropathies can diminish sensation on the

dorsum of the foot and lateral distal half of the leg. Common peroneal sensory symptoms

occur on the dorsal foot surface extending up the lateral half of the leg. EMG

involvement of the short head of the biceps femoris is the major distinguishing feature

with proximal peroneal division sciatic neuropathies. Biceps femoris function cannot be

isolated clinically; therefore, EMG is crucial to diagnosis.


Differential diagnoses of peroneal neuropathies include anterior horn cell disease, L5

radiculopathy, lumbosacral trunk or plexus lesions, sciatic neuropathy, or rarely

neuromuscular junction disorders. Sciatic neuropathies are sometimes mistakenly diag-

nosed as peroneal neuropathies. The peroneal division of the sciatic nerve is more

superficial than its tibial division and therefore external compressive proximal lesions of

the sciatic nerve involve the common peroneal nerve more than the tibial nerve. Most

sciatic neuropathies also affect some tibial nerve functions with weakness of knee

flexion, foot plantar flexion, and foot inversion. The ankle jerk is characteristically

depressed or absent if there is involvement of the tibial component of the sciatic nerve,

whereas it is typically unaffected in primary peroneal neuropathies. Sensory loss involves

the common peroneal territory described above and the plantar and lateral foot surface.

L5 radiculopathy remains a consideration in any patient with a foot drop. Back pain is

common with nerve root lesions and is uncommon in peroneal neuropathies; the pain is

typically radicular, with buttock, thigh, and leg components sometimes aggravated by

positional change. The distribution of weakness is very important; involvement of

muscles outside the peroneal nerve territory, such as the tibialis posterior or gluteus

13

medius innervated by the L5 root is critical. Isolated weakness of great toe extension

occurs with mild L5 radiculopathy but is uncommon in peroneal neuropathy. In

moderate–severe L5 radiculopathies, foot inversion will be weak because of involvement

of the tibial nerve innervated posterior tibial muscle. Uncommonly, hip abduction

weakness due to involvement of gluteus medius, an L5 muscle supplied by the superior

gluteal nerve, is noticeable. Careful evaluation of patients with an L5 root lesion should

demonstrate these deficits in addition to weakness of the peroneal innervated muscles.

The distribution of sensory symptoms in L5 radiculopathies overlaps significantly with

peroneal neuropathies, although L5 nerve root sensory loss may extend more proximally

onto the lateral leg. Lumbosacral plexus lesions rarely enter the differential diagnosis of

peroneal neuropathies but are a consideration in patients who have a foot drop, proximal

lower extremity pain, and motor and sensory findings extending beyond a single

peripheral nerve or root distribution. Involvement of hip abduction and extension,

clinically and/or by EMG, suggests plexus localization. Polyneuropathy is easily

distinguished from peroneal neuropathy, the clinical examination and EMG usually

reveal bilateral widespread motor and sensory abnormalities, not confined to a particular

nerve or root distribution, muscle tendon reflexes are depressed or absent. The possibility

of motor neuron disease exists with insidious onset of a foot drop without pain or sensory

findings. Motor neuron disease or amyotrophic lateral sclerosis is a slowly progressive

disorder and may be associated with evidence of upper motor neuron dysfunction. In

patients with myasthenia, a disorder of neuromuscular transmission, unilateral foot drop

is not seen. Distal myopathies may produce foot drop but usually do so bilaterally, and

there is often evidence of weakness elsewhere. Unilateral foot drop with or without

sensory symptoms can occur with disorders of the spinal cord or parasagittal frontal lobe;

these conditions are usually associated with hyperreflexia; magnetic resonance imaging

(MRI) is useful to diagnose these conditions.

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Tibial Neuropathies

Tibial nerve fibers arise primarily from L5, S1 and S2 nerve roots with some

contributions from L4 and S3. The tibial nerve leaves the sciatic nerve in the mid-to distal

thigh (see Fig. 66-1). The medial sural cutaneous nerve comes off in the popliteal fossa

and joins the lateral sural cutaneous nerve (a branch of the common peroneal nerve) in

the distal calf to form the sural nerve, which supplies the skin of the lateral aspect of the

foot and the posterior lower leg to a variable degree. After innervating the gastrocnemius

and soleus muscles, the nerve travels distally between the tibialis posterior and

gastrocnemius muscles. It sends branches to the tibialis posterior, flexor digitorum

longus, and flexor hallucis longus before entering the tarsal tunnel under the flexor

retinaculum. Here, the tibial nerve typically divides into the medial plantar, lateral

plantar, and medial calcaneal nerves. Although the medial calcaneal nerve is a purely

sensory branch to the medial heel, the medial and lateral plantar nerves are mixed nerves

innervating the intrinsic foot muscles as well as the skin of the sole

Proximal Lesion

Proximal tibial neuropathies may result from Baker’s cysts, ganglia, tumors, or rarely

indirectly from severe ankle strains, the latter presumably resulting from traction injury.

They rarely occur in isolation. They are characterized by weakness of foot plantar flexion

and inversion; although flexion, abduction, and adduction of the toes may be affected,

these latter functions are difficult to evaluate clinically. The ankle jerk is absent if the

neuropathy occurs proximal to the branch points of the gastrocnemius-soleus complex.

Sensory loss occurs on the heel and plantar foot surface.

Tarsal Tunel Syndrom

Tarsal tunnel syndrome (TTS), a distal tibial neuropathy, presents primarily with sensory

symptoms. It is classified as an entrapment neuropathy of the posterior tibial nerve and of

its primary branches, the medial and lateral plantar nerves, at the ankle. Although well

described, there is controversy regarding its prevalence as electrophysiological documen-

tation is infrequent. Whether this reflects its uncommon occurrence or the inadequate

15

sensitivity of diagnostic procedures is unclear. Fractures, ankle sprain, foot deformities

due to rheumatoid arthritis or other conditions, varicose veins, tenosynovitis and fluid

retention have been implicated as possible etiologies. Patients typically present with

burning pain and numbness on the sole of one or both feet. Symptoms may occur while

weight bearing and are often exacerbated at night. In well-established instances,

examination may disclose intrinsic plantar surface muscle atrophy. However, weakness

of these muscles is difficult to appreciate because the more proximal long toe flexors in

the leg mask weakness from the involved short toe flexors within the foot. Toe abduction

weakness occurs early but is difficult to assess even in healthy individuals. Sensory loss

is confined to the sole of the foot; there is sparing of the lateral foot (sural distribution),

the dorsum of the foot (peroneal territory), and the instep (saphenous nerve). Muscle

stretch reflexes are unaffected. A Tinel sign elicited from the tibial nerve at the ankle is

supportive, although not confirmatory. Initial treatment of TTS is nonoperative,

consisting of footwear modification, particularly avoidance of high-heeled and poorly

fitting footwear. Anti-inflammatory medications may help. Steroid injections, augmented

with lidocaine, can be helpful if flexor tenosynovitis is suspected. Care is taken to avoid

an intraneural injection with the unlikely possibility of causing local nerve sclerosis. Hind

foot valgus deformities may benefit from orthoses. When nonoperative measures fail in

TTS, surgical intervention may be considered. The results of surgical decompression are

not always rewarding. Release of the flexor retinaculum and fibrous origin of the

abductor hallucis muscle is required. Local flexor tenosynovitis is resected with radical

tenosynovectomy. Enlarged and varicose veins are ligated and resected. Postoperatively,

an open shoe is used with partial weight bearing for 2 weeks

Femoral Neuropathies

The femoral nerve comes off the lumbar plexus and is formed by the posterior

divisions of the L2–L4 roots (Fig. 66-5). It travels between two important hip flexors, the

iliopsoas and iliacus muscles, which it innervates. Approximately 4 cm proximal to the

inguinal ligament, the femoral nerve is covered by a tight fascia at the iliopsoas groove. It

exits the pelvis by passing beneath the medial inguinal ligament to enter the femoral tri-

16

angle just lateral to the femoral artery and vein. Here, the nerve separates into the anterior

and posterior divisions. The anterior division innervates the sartorius muscle and the

anteromedial skin of the thigh via the medial cutaneous nerve of the thigh. The posterior

division gives off muscular branches to the pectineus and quadriceps femoris muscles as

well as the saphenous nerve, a cutaneous branch to the skin of the inner calf. The nerve

can be compressed anywhere along its course, but it is particularly susceptible within the

body of the psoas muscle, at the iliopsoas groove, and at the inguinal ligament.

ETIOLOGY

Femoral mononeuropathies are infrequent. Historically, diabetic femoral neuropathies

were considered common, although most of these were actually diabetic

radiculoplexopathies in which the femoral component dominated. They may represent an

autoimmune process, perhaps with a vasculitic component. Vasculitis, such as

polyarteritis nodosa, may manifest as mononeuritis multiplex, with acute involvement of

the femoral nerve. Femoral neuropathies occasionally follow prolonged surgeries or

childbirth in the lithotomy position, presumably from anatomic predisposition to kinking

beneath the inguinal ligament. Iliacus hematoma or abscess, misplaced attempts at

femoral artery or vein puncture, or iatrogenic injury after nephrectomy or hip arthroplasty

are other recognized causes. Tumors, benign and malignant, may rarely cause femoral

neuropathy. Isolated saphenous nerve injuries may result from knee arthroscopy,

femoral–popliteal artery bypass surgery, and in the course of coronary artery bypass graft

surgery.


When the more proximal femoral nerve is involved, weakness of the iliopsoas manifests

as limited hip flexion. Mild hip flexion weakness may also occur with more distal

femoral nerve involvement from poor function of the rectus femoris, the only head of the

quadriceps muscle originating within the pelvis and contributing to hip flexion. Patients

with severe quadriceps weakness are unable to extend the leg or lock the knee; when

severe, this often interferes with or precludes walking. Initially, mild thigh, and medial

17

lower leg. A pure motor syndrome with quadriceps weakness and atrophy can result from

lesions distal to the branching of the saphenous nerve in the thigh.


A nerve root lesion at L3–L4 is the most common consideration. Unlike L5–S1

radiculopathies, a herniated nucleus pulposus infrequently involves the level L3–L4.

Lumbosacral plexus lesions primarily affecting the lumbar nerves may also mimic

femoral neuropathies.

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STATUS NEUROLOGI

1. Identitas

Nama : Tn. U

Jenis Kelamin : Pria

Usia : 59 tahun

Pekerjaan : Wiraswasta

Agama : Islam

Tgl. Masuk : 11-05-2015

2. Anamnesis

Autoanamnesis Tgl : 11 Mei 2015

Keluhan utama : Kaki kanan terasa lemas

Keluhan Tambahan : Telapak kaki kesemutan dan baal.

Riwayat Perjalanan Penyakit

± 3 hari yang lalu Pasien mengeluh kaki kanan lemas, tidak dapat digerakkan.

Sehingga pasien sulit untuk berjalan dan menapak, sehingga ketika berdiri pasien

bertumpu menggunakan kaki kanan. Keluhan ini sudah pasien rasakan sejak ± 13

tahun yang lalu tapi pasien tidak ingat bagaimana sampai kaki pasien tidak dapat

digerakkan lagi, karena pasien tidak pernah mengalami kecelakaan ataupun jatuh

sebelumnya. Untuk membantu menggerakan kaki kanan pasien menggunakan tali

yang di ikat . Selain itu pasien sering merasakan ksemutan dan baal di telapak kaki.

Riwayat Penyakit Terdahulu

Riwayat Darah tinggi terkontrol ( amlodipin 1x10mg)

Riwayat Diabetes Melitus disangkal

Riwayat Kecelakaan, jatuh, jatuh terduduk disangkal

19

Riwayat Kebiasaan Pasien:

- Perokok (satu hari 1 bungkus)

- (dulu) mengangkat barang berat

- Banyak duduk

Pemeriksaan Fisik

Status Generalis:

Keadaan umum : Tampak Sakit Ringan

Kesadaran : Composmentis (E4M6V5)

Tekanan Darah : 140/80 mmHg

Nadi : 80 x/menit

Pernafasan : 20 x/menit

Suhu : 36,2° C

Status Regional

Kepala : Normocephali

Wajah : Simetris

Mata : Konjungtiva anemis (-/-), Sklera ikterik (-/-)

Hidung : Bentuk biasa, Lapang +/+, Sekret -/-

Mulut : Mukosa bibir lembab

Telinga : Liang lapang +/+, membran timpani intake/intake, Serumen -/-

Leher : KGB tidak teraba membesar

Toraks : Pergerakan dinding dada simetris kanan = kiri

Paru-paru : Bunyi nafas dasar vesikuler, Ronkhi -/-, Wheezing -/-

Abdomen : Tampak datar, BU (+), Timpani, Nyeri ketok (-)

Hepar : Tidak teraba

Lien : Tidak teraba

Genitalia externa : Tidak dilakukan

Extremitas : Akral hangat, Edema - - / - -

20

Status Neurologi

1. Rangsang meningeal

Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-

Laseque : >70º / >70º

2. Syaraf Kranial

N.I: Cavum nasi : tidak lapang/lapang

Tes penghidu : ± / + N.II: Visus kasar :

Lihat warna :

Lapang pandang : Luas

Funduscopy : tidak dilakukan

N.III, IV, VI :

Sikap bola mata : Simetris

Ptosis : -/ -

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-

Deviasi konjugee : -/-

Pergerakan bola mata : Dapat kesegala arah

Pupil : Bulat, isokor 3mm/3mm, letak di tengah, tepi rata

Refleks cahaya langsung : +/+

Refleks cahaya tidak langsung : +/+

Refleks akomodasi : +

21

N.V

Motorik :

Buka tutup mulut : +

Gerakan rahang : +

Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : tidak dilakukan

Refleks : Refleks kornea : +/+

Refleks maseter : +

N.VII

Sikap wajah : Simetris

Mimik : Biasa

Angkat alis : +/+

Kerut dahi : +/+

Kembung pipi : +

Lagoftalmus : -/-

Menyeringai : Sulcus Naso

Labialis tidak ada yang mendatar

Chovstek : -/-

N. VIII

Nistagmus : -/-

Vertigo : -

Suara berbisik : +/+

Gesekan jari : +/+

Tes rinne : +/+

Tes weber : tidak ada lateralisasi

Tes swabach : tidak di lakukan

N. IX, X

Arkus faring : simetris

Palatum molle : intake

Uvula : ditengah

Disartria : -

Disfagia : -

Disfonia : -

Refleks okulokardiak : +/+

Refleks sinus caroticus: +/+

Refleks faring : +

22

N. XI

Angkat bahu : +

Menoleh : +

N. XII

Sikap lidah : ditengah

Atrofi : -

Fasikulasi : -

Tremor : -

Julur lidah : -

Tenaga otot lidah : +

3. Motorik

Derajat kekuatan otot :

Tonus Otot : hipotonus / normotonus

Trofi otot : atrofi / eutrofi

Gerakan spontan abnormal : -

4. Refleks

Fisiologis : Biceps ++/++

Triceps ++/++

KPR +/++

APR --/++

Patologis :

Babinski -/-

Chaddock -/-

Gordon -/-

Oppenheim -/-

Schaefer -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

23

5. Koordinasi :

Statis

Duduk : Baik

Berdiri : sempoyongan

Berjalan : bertumpu pada kaki kiri

Telunjuk telunjuk : Baik

Telunjuk hidung : baik

Tumit lutut : tidak dilakukan

Test Romberg : +

6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +

Rasa Suhu : tidak dilakukan

Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : - / +

Rasa Sikap : - / +

7. Vegetatif :

Miksi : terasa sedikit sakit

Defekasi : 3hari 1kali

8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Resume :

Laki-laki 59tahun datang dengan keluhan kaki kanan lemas, kaki kanan lemas sampai

tidak bisa digerakkan dan untuk berjalan sejak 3 hari terakhir ini. Sebelumnya sudah 13

tahun OS sulit berjalan karena tidak dapat melakukan dorso flexi, plantar flexi, disertai

dengan sensibilitas mulai dari bawah lutut sampai ke kaki. Kaki kanan lemas seringkali

juga terasa baal dan kesemutan. Tanpa disertai gangguan miksi dan defekasi. Pada

pemeriksaan didapat :

24

Status Generalis : Baik

Keadaan umum : Tampak Sakit Ringan

Kesadaran : Composmentis (E4M6V5)

Tekanan Darah : 140/80 mmHg

Nadi : 80 x/menit

Pernafasan : 20 x/menit

Suhu : 36,2° C

Status Regional : Tidak ada Kelainan

Status Neurologis : Dorsoflexi kaki Kanan, Tenaga 0, Plantar Flexi- tenaga 0

Atrofi Gastrocnemius dextra +

Hipotonus gastrocnemius dextra +

Miksi dan Defekasi tidak ada kelainan

Sensibilitas berkurang pada tungkai kanan 4jari dibawah

lutut sampai telapak kaki.

Refleks KPR +/++ APR --/++

Diagnosa

Klinis : Drop Foot Dextra

Topis : Nervus Tibialis Dextra

Etiologis : neuropati

Diagnosa Banding : Poliomyelitis, Entrapment Neuropaty

Pemeriksaan Penunjang :

1. EMG

2. Rotgen Foto

3. Lumbal Pungsi

4. Laboratorium

25

Terapi

Diet : Diet Rendah Garam

IVFD : I RL / 24 jam

MM/ : - Amlodipin 1 x 10

- Neurobion inj 1x1

Pemeriksaan dalam ruangan : Foto Lumbosakral

Pemeriksaan laboratorium :

Prognosis

Ad Vitam : Dubia

Ad Sanationum : Dubia ad malam

Ad Fungsionum : Dubia ad malam

26

Jenis Pemeriksaan Nilai normalHb 12.6 gr/dL 14-16 gr/dLLeukosit 6.1 ribu/uL 5-10 ribu/uLHt 40.7 % 40-48 %Trombosit 316 ribu/uL 150-400 ribu/uLUreum darah 30 mg/dL 15-45 mg/dLCreatinin darah 1.21 mg/dL 0.70 – 1.10Gula Darah Sewaktu 102 mg/dL <200

Follow UpTanggal 12 Mei 2015 (PH : 1)

S : Kaki kanan terasa lemas, tidak bisa digerakkam

O :

Status generalis

Keadaan umum : Tampak sakit sedang

Kesadaran : Compos mentis

Tekanan darah : 140/80 mmHg

Nadi : 82x/menit

Suhu : 36.6ºC

RR : 20x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


2. Syaraf Kranial


Tes penghidu : ± / +

N.II: Visus kasar : 1/60 / 1/60

Lihat warna : Tidak Buta Warna



27

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-


Pergerakan bola mata : kesegala arah

Pupil : Bulat, isokor 3mm/3mm, letak

di tengah, tepi rata Refleks

cahaya langsung +/+

Refleks cahaya tidak langsung +/+

Refleks akomodasi tidak dilakukan: +

N.V

Motorik :

Buka tutup mulut : Baik

Gerakan rahang : Baik

Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :

Refleks kornea : +/+

Refleks maseter : Baik

N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +

Kembung pipi : + / +

Lagoftalmus : -/-

Menyeringai : Sulcus Naso Labialis

tidak mendatar

Chovstek : -/-

N. VIII

Nistagmus : -/- Vertigo : -

28

Suara berbisik : + / +

Gesekan jari : + / +

Tes rinne : + / +



N. IX, X

Arkus faring : Simetris

Palatum molle : Intake

Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI

Angkat bahu : Baik Menoleh : Baik

N. XII

Sikap lidah : Ditengah

Atrofi : -

Fasikulasi : -

Tremor : -

Julur lidah : ditengah

Tenaga otot lidah : Baik

3. Motorik

Derajat kekuatan otot : 5555, 5555

5550, 5555


Trofi otot : atrofi / Eutrofi


4. Refleks


Triceps ++/++

KPR +/++

APR --/++

29

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik

Berdiri : bertumpu pada kaki kiri

Berjalan : sempoyongan

Dinamis:

Telunjuk telunjuk: baik

Telunjuk hidung: baik


Test Romberg : tidak dapat dilakukan

6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

7. Vegetatif :

Miksi : Tidak ada kelainan


8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

30

Visuospasial : Baik

Diagnosa

Klinis : Drop Foot Dexra

Topis : Nerve Tibilalis Dextra

Etiologis : Neuropati

Diagnosa Banding : Entrapment Neuropathy, poliomyelitis

Pemeriksaan Penunjang : Foto lumbosakral

PEMERIKSAAN LAB :


Terapi

Diet : Makanan Biasa, Rendah Garam

IVFD : I RL + I amp Neurobion / 24 jam

MM/ : Amlodipin 1 x 10

Neurobion inj 1 x 1

31



O :

Status generalis




Nadi : 82x/menit

Suhu : 36.6ºC

RR : 20x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


4. Syaraf Kranial


Tes penghidu : ±/ +





32

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-





cahaya langsung +/+



N.V

Motorik :



Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :



N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +


Lagoftalmus : -/-


tidak mendatar

Chovstek : -/-

N. VIII


33



Tes rinne : + / +



N. IX, X



Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI


N. XII


Atrofi : -

Fasikulasi : -

Tremor : -



3. Motorik


5550, 5555




4. Refleks


Triceps ++/++

KPR +/++

APR --/++

34

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik



Dinamis:





6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

35

7. Vegetatif :



8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Diagnosa




Diagnosa Banding : Entraptment Neuropathy, poliomyelitis


PEMERIKSAAN LAB :


Terapi




Neurobion 1 x 1 IV

36



O :

Status generalis




Nadi : 92x/menit

Suhu : 36ºC

RR : 20x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


2. Syaraf Kranial

N.I: Cavum nasi : lapang/lapang

Tes penghidu : ↓ / +





37

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-





cahaya langsung +/+



N.V

Motorik :



Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :



N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +


Lagoftalmus : -/-


tidak mendatar

Chovstek : -/-

N. VIII


38



Tes rinne : + / +



N. IX, X



Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI


N. XII


Atrofi : -

Fasikulasi : -

Tremor : -



3. Motorik


5550, 5555




4. Refleks


Triceps ++/++

KPR +/++

APR --/++

39

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik



Dinamis:





6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

40

7. Vegetatif :



8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Diagnosa




Diagnosa Banding : Entraptment Neuropathy, poliomyelitis


PEMERIKSAAN LAB :


Terapi




Neurobion 1 x 1 IV

41



O :

Status generalis




Nadi : 86x/menit

Suhu : 36ºC

RR : 18x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


2. Syaraf Kranial







42

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-





cahaya langsung +/+



N.V

Motorik :



Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :



N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +


Lagoftalmus : -/-


tidak mendatar

Chovstek : -/-

N. VIII


43



Tes rinne : + / +



N. IX, X



Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI


N. XII


Atrofi : -

Fasikulasi : -

Tremor : -



3. Motorik


5550, 5555




4. Refleks


Triceps ++/++

KPR +/++

APR --/++

44

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik



Dinamis:





6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

45

7. Vegetatif :



8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Diagnosa






PEMERIKSAAN LAB :


Terapi




Neurobion inj 1 x 1

46



O :

Status generalis

Keadaan umum : Tampak sakit ringan



Nadi : 82x/menit

Suhu : 36.6ºC

RR : 20x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


2. Syaraf Kranial







47

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-





cahaya langsung +/+



N.V

Motorik :



Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :



N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +


Lagoftalmus : -/-


tidak mendatar

Chovstek : -/-

N. VIII


48



Tes rinne : + / +



N. IX, X



Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI


N. XII


Atrofi : -

Fasikulasi : -

Tremor : -



3. Motorik


5550, 5555




4. Refleks


Triceps ++/++

KPR +/++

APR --/++

49

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik



Dinamis:





6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

50

7. Vegetatif :



8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Diagnosa






PEMERIKSAAN LAB :


Terapi




Neurobion inj 1 x 1

51



O :

Status generalis




Nadi : 82x/menit

Suhu : 36.6ºC

RR : 20x/menit

GCS :E4M6V5

Status Neurologi


Kaku kuduk : -

Brudzinski I : -/-

Brudzinski II : -/-

Kerniq : -/-


2. Syaraf Kranial







52

N.III, IV, VI :


Ptosis : -/-

Strabismus : -/-

Enoptalmus : -/-

Eksoptalmus : -/-

Diplopia : -/-





cahaya langsung +/+



N.V

Motorik :



Sensorik :

Rasa nyeri : + / +

Rasa raba : + / +

Rasa suhu : + / +

Refleks :



N.VII


Mimik : Biasa

Angkat alis : + / +

Kerut dahi : + / +


Lagoftalmus : -/-


tidak mendatar

Chovstek : -/-

N. VIII


53



Tes rinne : + / +



N. IX, X



Uvula : Ditengah

Disartria : -

Disfagia : -

Disfonia : -



Refleks faring : +

N. XI


N. XII


Atrofi : -

Fasikulasi : -

Tremor : -



3. Motorik


5550, 5555




4. Refleks


Triceps ++/++

KPR +/++

APR --/++

54

Patologis :

Babinski : -/-

Chaddock : -/-

Gordon : -/-

Oppenheim : -/-

Schaefer : -/-

Rossolimo -/-

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

5. Koordinasi :

Statis

Duduk : Baik



Dinamis:





6. Sensibilitas :

Eksteroseptif :

Rasa Raba : ± / +

Rasa Nyeri : ± / +


Propioseptif :

Rasa Getar : ± / +

Rasa Gerak : ± / +

Rasa Sikap : ± / +

55

7. Vegetatif :



8. Fungsi Luhur :

Memori : Baik

Bahasa : Baik

Kognitif : Baik

Emosi : Baik

Visuospasial : Baik

Diagnosa






PEMERIKSAAN LAB :

Terapi




Neurobion inj 1 x 1

56


Documents

CASE REPORT FOOT DROP