case report foot drop
DESCRIPTION
NeurologyTRANSCRIPT
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 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
2
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
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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.
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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.
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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
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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.
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CLINICAL PRESENTATION
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 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
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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-
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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.
CLINICAL PRESENTATION
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.
DIFFERENTIAL DIAGNOSIS
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
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 : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
27
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
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 : + / +
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
7. Vegetatif :
Miksi : Tidak ada kelainan
Defekasi : 3hari 1kali
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 :
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
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
Follow UpTanggal 13 Mei 2015 (PH : 2)
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
3. Rangsang meningeal
Kaku kuduk : -
Brudzinski I : -/-
Brudzinski II : -/-
Kerniq : -/-
Laseque : >70º / >70º
4. Syaraf Kranial
N.I: Cavum nasi : tidak lapang/lapang
Tes penghidu : ±/ +
N.II: Visus kasar : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
32
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
Mimik : Biasa
Angkat alis : + / +
Kerut dahi : + / +
Kembung pipi : + / +
Lagoftalmus : -/-
Menyeringai : Sulcus Naso Labialis
tidak mendatar
Chovstek : -/-
N. VIII
Nistagmus : -/- Vertigo : -
33
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
34
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
35
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 : Entraptment Neuropathy, poliomyelitis
Pemeriksaan Penunjang : Foto lumbosakral
PEMERIKSAAN LAB :
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
Terapi
Diet : Makanan Biasa, Rendah Garam
IVFD : I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion 1 x 1 IV
36
Follow UpTanggal 14 Mei 2015 (PH : 3)
S : Kaki kanan terasa lemas, tidak bisa digerakkam
O :
Status generalis
Keadaan umum : Tampak sakit sedang
Kesadaran : Compos mentis
Tekanan darah : 140/70 mmHg
Nadi : 92x/menit
Suhu : 36ºC
RR : 20x/menit
GCS :E4M6V5
Status Neurologi
1. Rangsang meningeal
Kaku kuduk : -
Brudzinski I : -/-
Brudzinski II : -/-
Kerniq : -/-
Laseque : >70º / >70º
2. Syaraf Kranial
N.I: Cavum nasi : lapang/lapang
Tes penghidu : ↓ / +
N.II: Visus kasar : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
37
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
Mimik : Biasa
Angkat alis : + / +
Kerut dahi : + / +
Kembung pipi : + / +
Lagoftalmus : -/-
Menyeringai : Sulcus Naso Labialis
tidak mendatar
Chovstek : -/-
N. VIII
Nistagmus : -/- Vertigo : -
38
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
39
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
40
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 : Entraptment Neuropathy, poliomyelitis
Pemeriksaan Penunjang : Foto lumbosakral
PEMERIKSAAN LAB :
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
Terapi
Diet : Makanan Biasa, Rendah Garam
IVFD : I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion 1 x 1 IV
41
Follow UpTanggal 15 Mei 2015 (PH : 4)
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 : 86x/menit
Suhu : 36ºC
RR : 18x/menit
GCS :E4M6V5
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 : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
42
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
Mimik : Biasa
Angkat alis : + / +
Kerut dahi : + / +
Kembung pipi : + / +
Lagoftalmus : -/-
Menyeringai : Sulcus Naso Labialis
tidak mendatar
Chovstek : -/-
N. VIII
Nistagmus : -/- Vertigo : -
43
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
44
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
45
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 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
Terapi
Diet : Makanan Biasa, Rendah Garam
IVFD : I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion inj 1 x 1
46
Follow UpTanggal 16 Mei 2015 (PH : 5)
S : Kaki kanan terasa lemas, tidak bisa digerakkam
O :
Status generalis
Keadaan umum : Tampak sakit ringan
Kesadaran : Compos mentis
Tekanan darah : 140/80 mmHg
Nadi : 82x/menit
Suhu : 36.6ºC
RR : 20x/menit
GCS :E4M6V5
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 : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
47
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
Mimik : Biasa
Angkat alis : + / +
Kerut dahi : + / +
Kembung pipi : + / +
Lagoftalmus : -/-
Menyeringai : Sulcus Naso Labialis
tidak mendatar
Chovstek : -/-
N. VIII
Nistagmus : -/- Vertigo : -
48
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
49
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
50
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 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
Terapi
Diet : Makanan Biasa, Rendah Garam
IVFD : I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion inj 1 x 1
51
Follow UpTanggal 17 Mei 2015 (PH : 6)
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
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 : 1/60 / 1/60
Lihat warna : Tidak Buta Warna
Lapang pandang : Luas
Funduscopy : tidak dilakukan
52
N.III, IV, VI :
Sikap bola mata : Simetris
Ptosis : -/-
Strabismus : -/-
Enoptalmus : -/-
Eksoptalmus : -/-
Diplopia : -/-
Deviasi konjugee : -/-
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
Sikap wajah : Simetris
Mimik : Biasa
Angkat alis : + / +
Kerut dahi : + / +
Kembung pipi : + / +
Lagoftalmus : -/-
Menyeringai : Sulcus Naso Labialis
tidak mendatar
Chovstek : -/-
N. VIII
Nistagmus : -/- Vertigo : -
53
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 : +
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
Tonus Otot : hipotonus / normotonus
Trofi otot : atrofi / Eutrofi
Gerakan spontan abnormal : -
4. Refleks
Fisiologis : Biceps ++/++
Triceps ++/++
KPR +/++
APR --/++
54
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
Tumit lutut : tidak dilakukan
Test Romberg : tidak dapat dilakukan
6. Sensibilitas :
Eksteroseptif :
Rasa Raba : ± / +
Rasa Nyeri : ± / +
Rasa Suhu : tidak dilakukan
Propioseptif :
Rasa Getar : ± / +
Rasa Gerak : ± / +
Rasa Sikap : ± / +
55
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 :
Terapi
Diet : Makanan Biasa, Rendah Garam
IVFD : I RL + I amp Neurobion / 24 jam
MM/ : Amlodipin 1 x 10
Neurobion inj 1 x 1
56
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