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.
1
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 ambulationthus 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-tofemale 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
2
(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
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.
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.
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.

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.
6
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
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
7
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
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.
8
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 crosssectional views of structures within the body.
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
9
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.
10
Mononeuropathies of the Lower

Extremities
Sciatic Neuropathies
The sciatic nerve is the bodys 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
11
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 electrodiagnostic evidence of sciatic neuropathy is not seen in most patients in whom piriformis
syndrome is suspected.
12
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.
13
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 diagnosed 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
14
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
moderatesevere 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.
15
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 Bakers 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 documentation is infrequent. Whether this reflects its uncommon occurrence or the inadequate
sensitivity of diagnostic procedures is unclear. Fractures, ankle sprain, foot deformities
16
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 L2L4 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 triangle 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
17
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,
femoralpopliteal 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
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.
18
A nerve root lesion at L3L4 is the most common consideration. Unlike L5S1
radiculopathies, a herniated nucleus pulposus infrequently involves the level L3L4.
Lumbosacral plexus lesions primarily affecting the lumbar nerves may also mimic
femoral neuropathies.
19
STATUS NEUROLOGI
1. Identitas
Nama
Jenis Kelamin
Usia
Pekerjaan
Agama
Tgl. Masuk
: Tn. U
: Pria
: 59 tahun
: Wiraswasta
: Islam
: 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
Riwayat Kebiasaan Pasien:
- Perokok (satu hari 1 bungkus)
- (dulu) mengangkat barang berat
- Banyak duduk
20
Pemeriksaan Fisik
Status Generalis:
Keadaan umum
Kesadaran
Tekanan Darah
Nadi
Pernafasan
Suhu
: Tampak Sakit Ringan

: Composmentis (E4M6V5)
: 140/80 mmHg
: 80 x/menit
: 20 x/menit
: 36,2 C
Status Regional
Kepala
Wajah
Mata
Hidung
Mulut
Telinga
Leher
Toraks
Paru-paru
Abdomen
Hepar
Lien
Genitalia externa
Extremitas
: Normocephali
: Simetris
: Konjungtiva anemis (-/-), Sklera ikterik (-/-)
: Bentuk biasa, Lapang +/+, Sekret -/: Mukosa bibir lembab
: Liang lapang +/+, membran timpani intake/intake, Serumen -/: KGB tidak teraba membesar
: Pergerakan dinding dada simetris kanan = kiri
: Bunyi nafas dasar vesikuler, Ronkhi -/-, Wheezing -/: Tampak datar, BU (+), Timpani, Nyeri ketok (-)
: Tidak teraba
: Tidak teraba
: Tidak dilakukan
: Akral hangat, Edema - - / - -
Status Neurologi
1. Rangsang meningeal
Kaku kuduk : Brudzinski I : -/Brudzinski II : -/Kerniq
: -/Laseque
: >70 / >70
2. Syaraf Kranial
N.I: Cavum nasi : tidak lapang/lapang
Tes penghidu : / +
N.II: Visus kasar
:
Lihat warna
:
Lapang pandang
: Luas
Funduscopy
: tidak dilakukan
21
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 : +
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
Lagoftalmus : -/-
Mimik
: Biasa
Menyeringai : Sulcus Naso
Angkat alis
: +/+
Labialis tidak ada yang mendatar
Kerut dahi
: +/+
Chovstek
Kembung pipi
:+
: -/-
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
: +/+
Gesekan jari
: +/+
22
Tes rinne
: +/+
Tes swabach
Tes weber
: tidak ada lateralisasi
: tidak di lakukan
N. IX, X
Arkus faring
: simetris
Disfagia
:-
Palatum molle
: intake
Disfonia
:-
Uvula
: ditengah
Refleks okulokardiak : +/+
Disartria
:-
Refleks sinus caroticus: +/+

Refleks faring
:+
N. XI
Angkat bahu
:+
Menoleh
:+
N. XII
Sikap lidah
: ditengah
Tremor
:-
Atrofi
:-
Julur lidah
:-
Fasikulasi
:-
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 -/23
Oppenheim -/-
Rossolimo -/-
Schaefer -/-
Mendel bechtrew -/-
Hoffman trommer -/Klonus lutut -/Klonus kaki -/-
5. Koordinasi :
Statis
Telunjuk telunjuk : Baik
Duduk
: Baik
Telunjuk hidung : baik
Berdiri
: sempoyongan
Tumit lutut
: tidak dilakukan
Berjalan
: bertumpu pada kaki kiri
Test Romberg
:+
6. Sensibilitas :
Eksteroseptif :
Rasa Raba
:/+
Propioseptif
Rasa Nyeri
:/+
Rasa Getar
:/+
Rasa Suhu
: tidak dilakukan
Rasa Gerak
:-/+
Rasa Sikap
:-/+
24
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 :
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
25
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.
2.
3.
4.
EMG
Rotgen Foto
Lumbal Pungsi
Laboratorium
Terapi
Diet
IVFD
MM/
: Diet Rendah Garam

: I RL / 24 jam
: - Amlodipin 1 x 10
- Neurobion inj 1x1
Pemeriksaan dalam ruangan : Foto Lumbosakral

Pemeriksaan laboratorium :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
26
Prognosis
Ad Vitam
: Dubia
Ad Sanationum
: Dubia ad malam
Ad Fungsionum
: Dubia ad malam
27
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
: 36.6C
RR
: 20x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
2. Syaraf Kranial
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-
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: +
28
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Menyeringai : Sulcus Naso Labialis
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
29
N. XI
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Berjalan
Duduk
: Baik
Berdiri
: sempoyongan
30
Telunjuk hidung: baik

Dinamis:
Tumit lutut
: tidak dilakukan
Telunjuk telunjuk: baik
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
7. Vegetatif :
Miksi
: Tidak ada kelainan
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
: Nerve Tibilalis Dextra
Etiologis
: Neuropati
Diagnosa Banding : Entrapment Neuropathy, poliomyelitis

Pemeriksaan Penunjang : Foto lumbosakral
PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
12.6 gr/dL
6.1 ribu/uL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
31
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
: Makanan Biasa, Rendah Garam
IVFD
: I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion inj 1 x 1
32

O:
Status generalis
Keadaan umum
Kesadaran
: Compos mentis
Tekanan darah
: 140/80 mmHg
Nadi
: 82x/menit
Suhu
: 36.6C
RR
: 20x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
4. Syaraf Kranial
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-

cahaya langsung +/+
33
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
34
N. XI
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Berjalan
Duduk
: Baik
Berdiri
: sempoyongan
Dinamis:
35
Tumit lutut
: tidak dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
36
7. Vegetatif :
Miksi
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
Etiologis
: Neuropati
Diagnosa Banding : Entraptment Neuropathy, poliomyelitis

PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
IVFD
Neurobion 1 x 1 IV
37

O:
Status generalis
Keadaan umum
Kesadaran
: Compos mentis
Tekanan darah
: 140/70 mmHg
Nadi
: 92x/menit
Suhu
: 36C
RR
: 20x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
2. Syaraf Kranial
N.I: Cavum nasi : lapang/lapang
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-

cahaya langsung +/+
38
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
N. XI
39
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Duduk
: Baik
Berdiri
Berjalan
: sempoyongan
Dinamis:
40
Tumit lutut
: tidak dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
41
7. Vegetatif :
Miksi
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
Etiologis
: Neuropati
Diagnosa Banding : Entraptment Neuropathy, poliomyelitis

PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
IVFD
Neurobion 1 x 1 IV
42

O:
Status generalis
Keadaan umum
Kesadaran
: Compos mentis
Tekanan darah
: 140/80 mmHg
Nadi
: 86x/menit
Suhu
: 36C
RR
: 18x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
2. Syaraf Kranial
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-

cahaya langsung +/+
43
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
N. XI
44
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Duduk
: Baik
Berdiri
Berjalan
: sempoyongan
Dinamis:
45
Tumit lutut
: tidak dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
46
7. Vegetatif :
Miksi
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
Etiologis
: Neuropati

PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
IVFD
Neurobion inj 1 x 1
47

O:
Status generalis
Keadaan umum
: Tampak sakit ringan
Kesadaran
: Compos mentis
Tekanan darah
: 140/80 mmHg
Nadi
: 82x/menit
Suhu
: 36.6C
RR
: 20x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
2. Syaraf Kranial
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-

cahaya langsung +/+
48
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
N. XI
49
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Duduk
: Baik
Berdiri
Berjalan
: sempoyongan
Dinamis:
50
Tumit lutut
: tidak dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
51
7. Vegetatif :
Miksi
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
Etiologis
: Neuropati

PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
IVFD
Neurobion inj 1 x 1
52

O:
Status generalis
Keadaan umum
Kesadaran
: Compos mentis
Tekanan darah
: 140/80 mmHg
Nadi
: 82x/menit
Suhu
: 36.6C
RR
: 20x/menit
GCS
:E4M6V5
Status Neurologi
: -/Laseque
: >70 / >70
2. Syaraf Kranial
Tes penghidu : / +
N.II:
Visus kasar
Lihat warna
Lapang pandang
Funduscopy
: 1/60 / 1/60
: Tidak Buta Warna
: Luas
: tidak dilakukan
N.III, IV, VI :
Sikap bola mata
Ptosis
Strabismus
Enoptalmus
Eksoptalmus
Diplopia
Deviasi konjugee
: Simetris
: -/: -/: -/: -/: -/: -/-

cahaya langsung +/+
53
N.V
Motorik
Buka tutup mulut

Gerakan rahang
Sensorik
Rasa nyeri
Rasa raba
Rasa suhu
Refleks
: Baik
: Baik
:
:+/+
:+/+
:+/+
:
Refleks kornea
Refleks maseter
: +/+
: Baik
N.VII
Sikap wajah
: Simetris
Lagoftalmus : -/-
Mimik
: Biasa
Angkat alis
:+/+
Kerut dahi
:+/+
Kembung pipi
:+/+
tidak mendatar
Chovstek
: -/-
Tes rinne
:+/+
Tes weber
N. VIII
Nistagmus
Vertigo
: -/:-
Suara berbisik
:+/+
Gesekan jari
:+/+
Tes swabach
: tidak di lakukan
N. IX, X
Arkus faring
: Simetris
Disfagia
:-
Palatum molle
: Intake
Disfonia
:-
Uvula
: Ditengah
Disartria
:-
Refleks faring
:+
N. XI
54
Angkat bahu
: Baik
Menoleh
: Baik
N. XII
Sikap lidah
: Ditengah
Tremor
:-
Atrofi
:-
Julur lidah
: ditengah
Fasikulasi
:-
Tenaga otot lidah
: Baik
3. Motorik
: 5555, 5555
5550, 5555
Tonus Otot
Trofi otot
: atrofi / Eutrofi
:-
4. Refleks
Fisiologis
: Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
Patologis
Babinski : -/-
Rossolimo -/-
Chaddock : -/-
Mendel bechtrew -/-
Gordon : -/-
Hoffman trommer -/-
Oppenheim : -/-
Klonus lutut -/-
Schaefer : -/-
Klonus kaki -/-
5. Koordinasi :
Statis
Duduk
: Baik
Berdiri
Berjalan
: sempoyongan
Dinamis:
55
Tumit lutut
: tidak dilakukan
6. Sensibilitas :
Eksteroseptif :
Propioseptif
Rasa Raba
:/+
Rasa Getar
:/+
Rasa Nyeri
:/+
Rasa Gerak
:/+
Rasa Suhu
: tidak dilakukan
Rasa Sikap
:/+
56
7. Vegetatif :
Miksi
Defekasi
: 3hari 1kali
8. Fungsi Luhur
Memori
: Baik
Bahasa
: Baik
Kognitif
: Baik
Emosi
: Baik
Visuospasial
: Baik
Diagnosa
Klinis
: Drop Foot Dexra
Topis
Etiologis
: Neuropati

PEMERIKSAAN LAB :
Jenis Pemeriksaan
Hb
Leukosit
Ht
Trombosit
Ureum darah
Creatinin darah
Gula Darah Sewaktu
12.6 gr/dL
6.1 ribu/uL
40.7 %
316 ribu/uL
30 mg/dL
1.21 mg/dL
102 mg/dL
Nilai normal
14-16 gr/dL
5-10 ribu/uL
40-48 %
150-400 ribu/uL
15-45 mg/dL
0.70 1.10
<200
Terapi
Diet
IVFD
Neurobion inj 1 x 1
57

Case Report Foot Drop

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Case Report Foot Drop

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CHAPTER I

inferior medial quadrant of the buttock.

divides into superficial and deep branches.

can also cause peroneal neuropathy.

(HNPP) are other etiologic conditions.

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

involvement of the femoral nerve.

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

5. Sign and Symptom

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

usually depressed or absent.

Prolonged kneeling. Occupations that involve prolonged squatting or

7. Test and Diagnosis

8. Treatment and Drug

shoe can help hold your foot in a normal position.

important to prevent the development of stiffness in the heel.

Mononeuropathies of the Lower

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

: Kaki kanan terasa lemas

: Telapak kaki kesemutan dan baal.

Riwayat Perjalanan Penyakit

: Tampak Sakit Ringan

Buka tutup mulut

Refleks : Refleks kornea

Menyeringai : Sulcus Naso

Labialis tidak ada yang mendatar

: tidak ada lateralisasi

Refleks okulokardiak : +/+

Refleks sinus caroticus: +/+

Tenaga otot lidah

Gerakan spontan abnormal

Mendel bechtrew -/-

Hoffman trommer -/Klonus lutut -/Klonus kaki -/-

Telunjuk telunjuk : Baik

Telunjuk hidung : baik

: bertumpu pada kaki kiri

: terasa sedikit sakit

: Tampak Sakit Ringan

: Tidak ada Kelainan

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

Sensibilitas berkurang pada tungkai kanan 4jari dibawah

: Drop Foot Dextra

: Nervus Tibialis Dextra

: Poliomyelitis, Entrapment Neuropaty

: Diet Rendah Garam

Pemeriksaan dalam ruangan : Foto Lumbosakral

Follow UpTanggal 12 Mei 2015 (PH : 1)

: Tampak sakit sedang

Pergerakan bola mata : kesegala arah

Buka tutup mulut

Menyeringai : Sulcus Naso Labialis

: tidak ada lateralisasi

Refleks okulokardiak : +/+

Refleks sinus caroticus: +/+

Tenaga otot lidah

Gerakan spontan abnormal

Mendel bechtrew -/-

Hoffman trommer -/-

Klonus lutut -/-

Klonus kaki -/-

: bertumpu pada kaki kiri

Telunjuk hidung: baik

Telunjuk telunjuk: baik