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EVELYN PATRICIA
405110196
PEMICU 8 BLOK SISTEM SARAF DAN
KEJIWAAN

ANATOMI

Divisi Sensorik

SST

Divisi Motorik

DIVISI AFFERENT
Menghantarkan impuls dari reseptor ke SSP
Menginformasikan kepada SSP tentang keadaan di
dalam dan di luar tubuh
Serabut saraf sensorik bisa bersifat somatik (dari
kulit, otot skelet, atau sendi) maupun viseral
(organ-organ dalam tubuh)
DIVISI EFFERENT
Menghantarkan impuls dari SSP ke organ efektor
(otot, kelenjar)
Serabut saraf motorik

Sistem Saraf
Somatik
Sistem Saraf Simpatis
Sistem Saraf
Otonom
Sistem Saraf Parasimpatis

Anatomi Sistem Saraf


Tepi

Spinal Cord
Fungsi : mengirimkan pesan

ke dan dari otak (substansia


alba) dan berperan sebagai
pusat refleks (substansia
grisea)

31 pasang nervus spinalis

melekat pada corda melalui


sepasang radix dan keluar dari
canalis vertebralis melalui
foramen intervertebralis

Mirip kupu-kupu
Kedua substansia grisea dihubungkan oleh gray commissure
Proyeksi posterior cornu dorsalis (posterior)
Proyeksi anterior cornu ventralis (anterior)
Pada corda bagian thoracic dan lumbar, terdapat pula cornu

lateralis

Radix ventralis
Berisi serabut saraf eferen

membawa rangsang motorik


dan keluar dari medulla
spinalis dalam alur dis
sulcus venro lateralis.
Terbentuk dari axon sel2
cornu anterior yg terletak di
substantia grisea MS
Keluar dari durameter
serabut ini bergabung
dengan radix dorsalis dan
membentuk serabut
campuran-sensorik dan
motorik

Medulla spinalis

Skematik penampang lintang medulla spinalis

Nervus Spinalis
31 saraf

menghubungkan
corda spinalis
dengan berbagai
bagian tubuh.

GANGLIA
Ganglia adalah kumpulan neuron yang letaknya diluar

SSP.
Ada 2 macam ganglia yaitu:
1. Ganglia Kranio-spinal (sensorik) yang terdiri atas saraf
kranial dan saraf spinal.
2. Ganglia Autonom yang berfungsi motorik dan
berhubungan dengan sistim saraf otonom.

Saraf Otonom
Dibagi menjadi dua:

Sistem saraf simpatis


2. Sistem saraf parasimpatis
1.

Pusat SSO

Fungsi

Medulla spinalis

miksi,defekasi,ereksi

Medulla oblongata

Kv,respirasi,pencernaan

Hipotalamus

Somatik dan endokrin yg menyertai


emosi(saat emosi
TD,denyut,pernafasan meningkat)

Korteks frontalis

Ekspresi emosi

Somatik Vs Otonom
SOMATIK
Volunter
Otot skelet
1 neuron efferent
Axon terminal
melepaskan acetylcholine
Selalu tereksitasi
Dikontrol oleh cerebrum

OTONOM
Involunter
Otot polos, otot jantung,
kelenjar
Multipel neuron efferent
Axon terminal melepaskan
norepinephrine
Dapat dieksitasi maupun
diinhibisi
Dikontrol oleh pusat
homeostatik di otak (pons,
hypothalamus, medulla
oblongata)

Basic pathologic processes of peripheral nerves


disease

Clinical patterns of peripheral


neuropathy
Polyneuropathy

Generalized process affecting peripheral nerves symmetrical


& bilateral

Radiculopathy / polyradiculopathy

Polyradiculopathy multiple spinal roots disease that are


asymmetrical

Neuronopathy (motor / sensory)

Sensory ganglion cells are predominantly affected


Motor disorder of anterior horn cells

Mononeuropathy

Most circumscribed weakness, sensory loss in territory of a


single peripheral nerve

Multiple mononeuropathies
Plexopathy

Most confusing pattern of motor & sensory involvement


One limb affected, but the motor, sensory & reflex loss doesnt
conform to a pattern of several adjacent nerve roots / nerves

MYASTHENIA GRAVIS

Preface
fluctuating weakness of certain voluntary muscles,

particularly those innervated by motor nuclei of the


brainstem, i.e., ocular, masticatory, facial,
deglutitional, and lingual
Manifest weakening during continued activity, quick
restoration of power with rest, and dramatic
improvement in strength following the
administration of anticholinesterase drugs such as
neostigmine

Incidence
43 to 84 per million persons and the annual

incidence rate is approximately 1 per 300,000


20 and 30 years in women and between 50 and 60
years in men

Under the age of 40, females are affected two to three times as
often as males whereas in later life

males is higher (3:2)


patients with thymomas, the majority is older (50 to

60 years) and males predominate

Etiology
Associated disorders

Disorders of the thymus: thymoma, hyperplasia


Other autoimmune disorders: Hashimoto's thyroiditis, Graves'
disease, rheumatoid arthritis, lupus erythematosus, skin
disorders, family history of autoimmune disorder
Disorders or circumstances that may exacerbate myasthenia
gravis: hyperthyroidism or hypothyroidism, occult infection,
medical treatment for other conditions
Disorders that may interfere with therapy: tuberculosis,
diabetes, peptic ulcer, gastrointestinal bleeding, renal disease,
hypertension, asthma, osteoporosis, obesity

Recommended laboratory tests or procedures

associated with associated disorders

CT or MRI of mediastinum
Tests for lupus erythematosus, antinuclear antibody,
rheumatoid factor, antithyroid antibodies
Thyroid-function tests
PPD skin test
Chest radiography
Fasting blood glucose measurement, hemoglobin A1c
Pulmonary-function tests
Bone densitometry in older patients

Pathophysiology

Findings in MG reduced number of AChRs (stippling); flattened, simplified


postsynaptic folds; widened synaptic space

myasthenic weakness and fatigue are a result of the

failure of effective neuromuscular transmission on the


postsynaptic side

reduced number of receptors


competitive activity of anti-AChR antibodies
produce postsynaptic potentials of insufficient amplitude to
discharge some muscle fibers

How antibodies disturb the neuromuscular transmission

block the binding of ACh to the AChR


serum IgG from myasthenic patients has been shown to induce an
increase in the degradation rate of AChR
complement-mediated destruction of the postsynaptic folds

Clinical manifestations
Repeated or persistent activity of a muscle group

exhausts its contractile power, leading to a


progressive paresis, and rest restores strength
1st muscles affected eyelids and the muscles of the
eyes, jaws, throat, and neck

weakness of the levator palpebrae or extraocular muscles


(initial manifestation)
Ocular palsies and ptosis
Diplopia

Thymic abnormalities
Other ocular signs

Sustained upgaze for 30 or more seconds exaggerate


ptosis
twitching of the upper eyelid that appears a moment after
the patient moves the eyes from a downward to the primary
position (lid-twitch sign)
Unilateral painless ptosis without ophthalmoplegia or
pupillary abnormality
Bright sunlight is said to aggravate the ocular signs and cold
to improve them

Muscles of facial expression, mastication,

swallowing, and speech are affected (80%)

natural smile becomes transformed into a snarl


jaw may sag, so that it must be propped up by the patient's
hand
chewing tough food may be difficult

early involvement of the flexors and extensors of

the neck, muscles of the shoulder girdle, and


flexors of the hips (less often)

Women may complain of inability to fix their hair or makeup


because of fatigue of the shoulders
Weakness of the neck muscles causes fatigue in holding up
the head

Of the trunk muscles, the erector spinae are the most

frequently affected
Weakened muscles in myasthenia gravis undergo
atrophy to only a minimal degree or not at all
Tendon reflexes are seldom altered

Clinical grading
Myasthenia Gravis foundation

I: Any ocular muscle weakness

weakness of eye closure


All other muscle strength is normal

II: Mild weakness affecting other than ocular

muscles; ocular muscle weakness of any severity

IIA: Predominantly affecting limb, axial muscles, or both;


lesser involvement of oropharyngeal muscles
IIB: Predominantly affecting oropharyngeal, respiratory
muscles, or both; lesser or equal involvement of limb, axial
muscles, or both

III: Moderate weakness affecting other than ocular

muscles; ocular muscle weakness of any severity

IIIA: Predominantly affecting limb, axial muscles, or both; lesser


involvement of oropharyngeal muscles
IIIB: Predominantly affecting oropharyngeal, respiratory muscles,
or both; lesser or equal involvement of limb, axial muscles, or both

IV: Severe weakness affecting other than ocular muscles;

ocular muscle weakness of any severity

IVA: Predominantly affecting limb, axial muscles, or both; lesser


involvement of oropharyngeal muscles
IVB: Predominantly affecting oropharyngeal, respiratory muscles,
or both; lesser or equal involvement of limb, axial muscles, or both;
need NGT

V: Intubation, with or without mechanical

ventilation, except when employed during routine


postoperative management

Diagnosis
Clinical manifestations

changeable diplopia or ptosis and the typical myasthenic


facies

unequally drooping eyelids,


relatively immobile mouth turned down at the corners,
a smile that looks more like a snarl,
a hanging jaw supported by the hand

Electrophysiologic testing

rapid reduction in the amplitude of compound muscle action


potentials during a series of repetitive stimulations of a
peripheral nerve at a rate of 3 per second

Edrophonium (Tensilon) and Neostigmine Tests

1 mg (0.1 mL) of edrophonium is given intravenously 45s no


definite strength 4 to 9 mg is injected
Neostigmine methylsulfate is injected intramuscularly in a
dose of 1.5 mg / atropine sulfate (0.8 mg) objective
improvement occurs within 10 to 15 min, reaches its peak at 20
min, and lasts up to 1 h

Measurement of receptor antibodies in blood

Persistently negative AChR antibody tests are more frequently


found in patients with ocular myasthenia
Patients with a thymoma and severe generalized myasthenia
are practically always seropositive
presence of antibodies directed against striated muscle in
almost half of myasthenic patients

Other procedures

some myasthenic patients that their weakness improves in the


cold, a test has been devised in which an ice pack is placed over
a ptotic eyelid for 2 min or to the limit of the patient's tolerance
CT of the chest (for the detection of thymic enlargement or
thymoma),
tests of thyroid function for reasons
magnetic resonance imaging of the cranium and orbits to
exclude compressive and inflammatory lesions of the cranial
nerves and ocular muscles

Treatment
Anticholinesterase Drugs

Corticosteroids

who is responding inadequately to anticholinesterase drugs


prednisone 15 to 25 mg daily

beginning with 15 to 20 mg/d and increasing the dose gradually


until a satisfactory clinical response is obtained or until a daily dose
of 50 to 60 mg is reached

Azathioprine & other immunosuppressive drugs

Azathioprine begins with 50 mg (1 tablet) bid for a few days; if


this is tolerated, the dosage is raised to 2 to 3 mg/kg/d
Cyclosporine 2 divided doses daily, to a total of 6 mg/kg

SE hypertension, nephrotoxicity (serious)

Mycophenolate
IV Cyclophosphamide 50 mg/kg/d for 4 consecutive days
followed by granulocyte-stimulating factor to "reboot" the
immune system in refractory cases

Plasma exchange & IVIg

several exchanges of 2 to 3.5 L each (totaling approximately


125 mL/kg) performed over a week usually suffice

In a crisis requiring plasma exchanges and mechanical ventilation,


it has been our practice to discontinue or curtail the use of
anticholinesterase drugs and resume them as the patient is being
weaned from the ventilator

IVIg 2 g/kg given in divided doses over 3 to 5 days

Thymectomy

Guillain-Barr Syndrome

Preface
most common cause of acute or subacute generalized

paralysis in practice
mild respiratory or gastrointestinal infection or
immunization precedes the neuropathic symptoms
by 1 to 3 weeks (60%)
Etiology

Campylobacter jejuni is the most frequent


viruses of the herpes family (cytomegalovirus [CMV], EpsteinBarr virus [EBV], HIV)
Mycoplasma pneumoniae, Lyme disease
antirabies vaccines & influenza vaccines

Incidences
varied between 0.4 and 1.7 cases per 100,000

persons per year


nonseasonal and nonepidemic,

isolated outbreaks have been recorded in rural China following


exposure of children to C. jejuni through chicken feces
deposited in rice paddies

Females appear to be slightly more susceptible


50 to 74 years of age

Pathogenesis

Antigens targetted antibodies

Sign & symptoms


Paresthesias and slight numbness in the toes and

fingers (earliest)
Major clinical symptoms

weakness that evolves more or less symmetrically over a period


of several days to a week or two

usually the lower extremities before the upper (thus

the older term Landry ascending paralysis)


ocular motor nerves are paralyzed and even the
pupils may be unreactive (severe cases)

burning in the fingers and toes if early

persistent problem
End of the week vibration and joint position
sense in the toes and fingers are usually reduced
deep sensibility (touch-pressure-vibration) tends to
be more affected
Facial diplegia; other cranial nerves (later)
Reduced and then absent tendon reflexes
Disturbances of autonomic function

sinus tachycardia and, less often, bradycardia, facial


flushing, fluctuating hypertension and hypotension, loss of
sweating

Variants of Guillain-Barr Syndrome


Regional

Fisher syndrome of ophthalmoplegia, ataxia, and areflexia


Cervico-brachial-pharyngeal, often with ptosis
Oculopharyngeal weakness
Predominant paraparesis
Bilateral facial or abducens weakness with distal paresthesias
Ophthalmoplegia with GQ1b autoantibodies

Functional

Generalized ataxia without dysarthria or nystagmus


Pure sensory
Pure motor
Pandysautonomia
Axonal (AMAN)

Acute axonal form of Guillain-Barr


Syndrome
similar to typical GBS but characterized

pathologically by widespread and severe axonal


degeneration
muscle atrophy became apparent relatively early in
the axonal form (within weeks)
most cases of abrupt and severe denervating
paralysis, particularly if postinfectious, are caused by
the axonal form of GBS

Postmortem examination

severe axonal degeneration in nerves and roots with minimal


inflammatory changes and little demyelination, even early in
the disease

appear to be triggered largely by C. jejuni infections


But can also induce demyelinating type

Laboratory findings
CSF examination

under normal pressure and is acellular or contains only a few


lymphocytes
persistent pleocytosis additional process producing aseptic
meningitis such as neoplastic infiltration, HIV, or Lyme
infection
Protein contents usually normal rise reach the peak in 4-6
weeks

EMG examination

reduction in the amplitude of muscle action potentials, slowed


conduction velocity, and conduction block in motor nerves
singly or in combination
Normal in the early phase

gadolinium enhancement of the cauda equina roots

on magnetic resonance imaging


Abnormalities of liver function CMV or EBV
infections
Hyponatremia syndrome of inappropriate
antidiuretic hormone secretion (SIADH)

Pathologic findings
endoneural perivascular (mainly perivenous)

lymphocytic infiltrates segmental demyelination


and a variable degree of wallerian degeneration
cellular infiltrates are scattered throughout all
peripheral nerves & cranial nerves swelling of
nerve roots

Treatment
General medical care

Respiratory assistance

Measurement of maximal inspiratory force and expiratory vital


capacity

required mechanical ventilation (1/3 patients)

vital capacity diminishes to below about 10 mL/kg endotracheal


intubation and mechanical ventilation

Incipient respiratory failure may be evident by tachypnea and a


decrease in arterial oxygen tension (PO2 less than 85 mm Hg)
atelectasis
Oropharyngeal weakness earlier intubation

Hypotension from dysautonomia intravenous infusions of


saline and by the use of vasopressor agents for brief periods
Extremes of hypertension short-acting and titratable
antihypertensive medications (IV labetalol)
Bedbound patient prevention of electrolyte imbalances,
gastrointestinal hemorrhage, and particularly pulmonary
embolism (heparin)
Caution of adynamic ileus (abdominal pain + NGT feeding +
bloating) perforation

Plasma exchange & immunoglobulin

If patient unable to walk/shows reduction in vital


capacity/oropharyngeal weaknes plasma exchanges OR
IVIg (not both)
advised regimen of plasma exchange removes a total of 200 to
250 mL/kg of plasma in 4 to 6 treatments on alternate days

Measurement of fibrinogen

IVIg (0.4 g/kg per day for 5 consecutive days

NEUROPATI

Polineuropati

NEUROPATI

Radikulopa
ti

Mononeuropati

g3 bersifat simetris kedau sisi


tungkai lebih dulu dibanding lengan
Gejala sensorik: parestesia,
disestesia, baal ujung kaki menyebar
ke proksimal
Kadang parestesai berupa: rasa tidak
menyenangkan, rasa seperti terbakar.
atrofi otot,hipotoni, refleks tendon
turun.
Saraf otonom terkena: g3an trofik
kulit, hilangnya keringat, g3an
vaskuler nyebabkan hipotensi
lesi utama di radiks proksimal
sebelum masuk foramen
intravertebral
Lesi di sekitar ruangan subaraknoid
reaksi CSS disosiasi sito-albumin
Otot lemah, reflek turun
Lesi perifer lokal karea infeksi,
kompresi, iskemk 1 saraf

NEUROPATHY
Definisi : Gambaran kerusakan saraf yang berada di
luar otak dan sumsum tulang belakang (saraf perifer).
Etiologi :
Cedera fisik
Penyakit sistemik
Infeksi dan gangguan autoimun
Genetik

TANDA dan GEJALA


Perubahan pada sensasi
Sensitivitas meningkat
Mati rasa
Kelemahan otot
Gangguan keseimbangan
Pusing

POLINEUROPATI
DEFINISI :
kelainan fungsi yang berkesinambungan pada
beberapa saraf perifer di seluruh tubuh.

Macam-Macam Polyneuropathy
Polyneuropathy metabolic:
Diabetes melitus
Uremic acid di hepar
Hipotiroid
Polineuropati malabsorpsi

- atau paraproteinemia
Polyneuropathy karena
infeksi:

Tifus dan paratifoid tifus


HIV
Difteri
Botulisme

Polyneuropathy karena vaskular:


> Polyarteritis nodosa
> Other collagenoses
> Atherosclerosis
Polyneuropathy karena penyebab
lain
Serogenic
Malignant neoplasia
Sarcoidosis

KLASIFIKASI
Berdasarkan onset : akut, subakut, kronik
Berdasarkan gejala : sensorik, motorik, otonom,

campuran
Berdasarkan penyebaran : distal atau proksimal, simetis
atau asimetris, multifokal
Berdasarkan EMG : aksonal, demyelinating

GEJALA
Kesemutan, mati rasa, nyeri terbakar.
Nyeri

memburuk di malam hari, bisa timbul jika


menyentuh daerah yang peka atau karena perubahan suhu.
Tidak bisa merasakan suhu dan nyeri, terjadi ulkus akibat
tekanan.
neuropati perifer mengenai saraf otonom, terjadi:
diare atau sembelit
ketidakmampuan
untuk
mengendalikan
saluran
pencernaan atau kandung kemih
impotensi
tekanan darah tinggi atau rendah
keringat berlebihan

DIAGNOSA
Diagnosis ditegakkan berdasarkan gejala-gejala dan hasil

pemeriksaan fisik.
Elektromiografi dan uji kecepatan penghantaran saraf
dilakukan untuk memperkuat diagnosis.
Pemeriksaan darah dilakukan jika diduga penyebabnya
adalah kelainan metabolik (anemia pernisiosa karena
kekurangan vitamin B12), diabetes (kadar gula darah
meningkat) dan gagal ginjal (kadar kreatinin meningkat).
Pemeriksaan air kemih bisa menunjukkan adanya
keracunan logam berat atau mieloma multipel.

PEMERIKSAAN PENUNJANG
Anti-GM1 antibody (acute motor axonal neuropathy)
Anti-GQ1b (Miller Fisher variant of Guillain Barre

syndrome)
Anti-Hu antibody (carcinomatous sensory neuropathy)
Anti-myelin-associated glycoprotein antibody (multiple
myeloma)
Anti-sulfatide antibody (symmetric polyneuropathy with
prominent distal sensory loss)
Pungsi lumbal (AIDP, CIDP, infectious and neoplastic
diseases)
EMG
Biopsi (vasculitis, amyloidosis, sarcoidosis, giant axonal
neuropathy, leprosy)

Mononeuropathy
Kerusakan saraf perifer tunggal
Etiologi : cedera atau trauma fisik seperti dari kecelakaan
tekanan pada saraf yg berkepanjangan seperti di
kursi roda atau tempat tidur,atau gerakan tekanan
berulang
Contoh :Carpal tunnel syndrome Orang-orang
yang bekerja memerlukan gerakan pergelangan tangan
berulang (buruh fisik, menggunakan keyboard komputer
untuk waktu lama)
Palsy N. ulnaris terjadi ketika saraf yang lewat dekat
permukaan kulit pada siku rusak.
Palsy N .Radial disebabkan oleh cedera pada saraf yang
berjalan sepanjang lengan bawah.

Multipleks Mononeuritis
sindrome berat yang diakibatkan oleh autoimun pada
pembuluh darah yg memperdarahi saraf tepi ,yg
disebabkan oleh inflamasi,sumbatan,dan iskemia
Diagnosa banding : stroke multipel,regional peripheral

nerve sindromes,polineuropaty atipik,dan multiple


compressive mononeuropathies
Penatalaksanaan
Dekompensasi akut : imunosupresif yg kuat (IV
cyclophosphamid,dosis tinggi kortikosteroid,atau
keduanya)
Gejala respirasi: ventilasi mekanik

Neuritis
Peradangan dari sistem saraf perifer.
Gejala tergantung pada saraf yang terlibat, rasa sakit ,

paresthesia , paresis , hypoesthesia (baal), anestesi ,


kelumpuhan , dan hilangnya refleks
Jenis-jenis neuritis meliputi:
Polyneuritis atau Multiple neuritis
Brachial neuritis
Optic neuritis
Neuritis vestibular
Kranial neuritis , diwakili Bell's Palsy
Arsenik neuritis

ETIOLOGI

Infeksi :

Herpes simplex
Shingles
Kusta
Guillain-Barre syndrome
cedera kimia
Cedera fisik
Radiasi
kondisi menyebabkan neuritis lokal (yang
mempengaruhi saraf tunggal):
Difteri
cedera lokal
Diabetes

Pengobatan neuropati
Koreksi
Nutrisi
suplementasi vitamin
Pengobatan DM
Hilangkan kompresi
Jika neuropati diperkirakan karena reaksi

imun steroid
Tirah baring
Bagian paralisis disanggah (splint)
Analgesik untuk nyeri

CARPAL TUNNEL SYNDROME


Sindrom ini terjadi akibat kompresi nervus

medianus pada pergelangan tangan saat saraf ini


melalui terowongan karpal.
Jenis Kelamin P:L = 3:1

ETIOLOGI
Herediter
Trauma langsung pada pergelangan tangan
Infeksi
Metabolik
Endokrin
Neoplasma
Penyakit kolagen vaskular
Degeneratif
Iatrogenik

Patofisiologi

Peningkatan tekanan di
dalam Carpal Tunnel

Iskemi N. Medianus

Gangguan konduksi
saraf
Nyeri
Paresthesia

FAKTOR RISIKO
Kehamilan
Diabetes melitus
Deformitas lokal, misalnya akibat osteoartritis,

fraktur
Arthritis reumatoid
Miksedema
Akromegali
Amiloidosis
Genetik

GAMBARAN KLINIS
Nyeri pada tangan atau lengan, terutama pada

malam hari, atau saat bekerja


Pengecilan dan kelemahan otot2 eminensia tenar
Hilangnya sensasi pada tangan, pada distribusi n.
medianus
Parastesia seperti kesemutan pada distribusi nervus
medianus saat dilakukan perkusi pada telapak
tangan daerah terowongan (tanda Tinel)
Kondisi ini sering bilateral.

PEMERIKSAAN PENUNJANG
Electromyogram
Wrist x-rays
Nerve Conduction Velocity

TERAPI
Balut tangan terutama pada malam hari, pada

posisi ekstensi parsial pergelangan tangan


Pemberian diuretik
Injeksi lokal kortikosteroid pada terowongan
karpal
Dekompresi nervus medianus pada pergelangan
tangan dengan pembedahan, pada divisi fleksor
retinakulum

Tarsal tunnel syndrome


(posterior tibial neuralgia)

Tarsal tunnel celah sempit berisi arteri, vena,

tendon, and nervus di bawah flexor retinaculum


Definisi : adanya tekanan pada bagian posterior
nervus tibia atau yg berhubungan dgn cabang dari
nervus yang melewati bagian bawah flexor
retinaculum

Etiologi : disebabkan oleh hal2 yg memberikan

kompresi nervus tibia posterior :

Org dengan telapak kaki yang datar because the outward


tilting of the heel that occurs with fallen arches can
produce strain
Pembesaran abnormal dari struktur berada di dalam tunel.
(co: varicose vein, ganglion cyst, swollen tendon)
Trauma (co: ankle spraininflamasi pembengkakan
kompresi pada nervus)
Penyakit sistemik (co: diabetes atau arthritis
pembengkakan)

Gejala

Tingling, burning, or a sensation similar to


an electrical shock
Numbness
Pain, including shooting pain Pain is
more intense at night
Gejala dirasakan pada bagian dalam ankle
maupun bagian bawah kaki. Bisa menlebar
ke heel, arch, toes, and even the calf.
Muncul pada penggunaan kaki saat
aktivitas yg lama ( berdiri, berjalan,
olahraga)

Diagnosa
Dengan menepuk atau mempalpasi
nervus tibia posterior pada bagian yg
terkompresi atau terluka. distal
tingling (Tinels sign)
Electrodiagnostic
Penatalaksanaan

Jika belum terdapat fibro-osseous


compression local infiltration of
insoluble corticosteroid with lidocaine
membungkus kaki dan meletakkan alat
orthotic yang dirancang khusus di dalam
sepatu untuk mengurangi tekanan pada
syaraf
The surgery involves the release of the
retinaculum.

POLIOMIELITIS

Definisi
Suatu penyakit sistemik akut yang disebabkan oleh
infeksi virus polio dan mengakibatkan kerusakan
pada sel motorik di kornu anterior medula spinalis,
dapat pula mengenai batang otak (mesensefalon,
serebelum, ganglia basal ) dan area motorik kortex
cerebri.

Etiologi

Virus classification
Group:

Group IV ((+)ssRNA)

Family:

Picornaviridae

Genus:

Enterovirus

Species:

Poliovirus

Tiga strain yaitu:


1.
brunhilde
2.
Lanzig
3.
Leon

virus polio tahan terhadap alkohol dan lisol namun peka


terhadap formaldehide.
Ketahanan virus di tanah dan air tergantung pada kelembaban
dan suhu, dalam tinja tahan sampai berbulan-bulan.

GAMBARAN KLINIS
Masa inkubasi 7-14 hari.
Jenis-jenis gejala klinik:
1. Jenis asimptomatik
2. Jenis abortive
hanya gejala-gejala
prodormal, spt:
Anoreksia, mual,
konstipasi, nyeri
abdomen, nyeri
tenggorokan, demam
ringan dan sakit kepala

3.

Jenis non paralitk


Terdapat tanda
rangsangan meningeal
tanpa adanya
kelumpuhan.
Suhu 38-39oC disertai
sakit kepala dan nyeri
otot
Kesadaran baik
kaku kuduk dan
punggung +
tanda kernig,
Brudzinsky dan
laseque +
head drops
kekakuan otot spinal
(tripod sign)

4. Jenis paralitik
kelumpuhan timbul 3 hari setelah stadium
preparalitik. Mula-mula otot yang terkena terasa
nyeri dan spastik, kemudian paralitik.
Berdasarkan lesi pada susunan syaraf yang

terkena:
a.

Bentuk spinal

Mengenai

sel motorik kornu anterior medula spinalis


terjadi kelumpuhan otot leher, tubuh, diafragma,
thorak, dan ekstremitas bawah, terutama m.
Quadrisep femoris.
Paralisis tidak simetris dan tidak didapati gangguan
sensorik, reflek tendon menurun atau menghilang.

b. Bentuk bulber
Mengenai inti motorik dibatang otak, dengan atau
tanpa gangguan sistem vital
c. Bentuk bulbospinal
campuran bentuk bulber dan spinal.
d. Bentuk polio encephalitik
Mengenai cerebrum, ditandai penurunan kesadaran
sampai delirium, tremor, dan kadang-kadang kejang.
e. Bentuk cereberal
Ditandai adanya ataksia dengan atau tanpa
kelumpuhan.
Otot-otot yang lumpuh tidak dapat sembuh lagi.
Ketidakseimbangan otot-otot antagonis
menyebabkan deformitas.

LABORATORIUM
Oral swab (minggu pertama)

Pemeriksaan urin : bervariasi,

Pemeriksaan tinja (sampai

kadang albuminuria ringan


Pemeriksaan likuor
serebrospinalis : pleiositosis <
500/mm3
Awalnya PMN > limfosit.
Kemudian menjadi limfosit
yang lebih dominan (kembali
normal setelah 10-14hari).
Pada stadium awal kadar
protein normal, minggu ke2
dapat naik sampai 100mg%,
dan kembali normal dalam
4-6 minggu.

beberapa minggu).
Pemeriksaan serologi:
tes neutralisasi dengan
memakai serum pada fase akut
dan
konvalesen(penyembuhan).
positif : kenaikkan titer 4x atau
lebih.
sangat spesifik dan bermanfaat
untuk menegakkan diagnosa
poliomielitis.
Pemeriksaan CF (Complement
Fixation), tetapi ditemukan
reaksi silang diantara ketiga
tipe virus ini.

DIFFERENSIAL DIAGNOSA
Meningitis TBC (gejalanya mirip poliomielitis

nonparalitik)
Sindroma Guillain-Barre
Mielitis tranversa
Encephalitis
Meningitis purulenta
Lymphocytic choriomeningitis
Neurosyphilis

Penatalaksanaan
Tirah baring total pada semua Poliomielitis
Poliomielitis paralitik bentuk spinal:
tirah baring total dan pengobatan simptomatis
Lengan dan tangan di beri splint sedang untuk
menghindari drop foot dan papan penyangga pada
telapak kaki agar selalu dalam posisi dorsoflexi.
Fisioterapi sebaiknya dilakukan setelah 2 hari demam
hilang.
Bila terjadi kegagalan pernafasan diperlukan
respiratoar
Paralisis bulbaris:
kebutuhan cairan diperhatikan
Sekresi faring dapat menyebabkan aspirasi
bila ada disfagia diberikan sonde lambung

2 macam vaksin polio :


IPV (Inaktivated Polio Vaccine, vaksin salk)

mengandung virus polio yang sudah dimatikan dan diberikan


melalui suntikan.

OPV (Oral Polio Vaccine, Vaksin Sabin)


mengandung vaksin hidup yang telah dilemahkan dan diberikan
dalam bentuk pil atau cairan.
Bentuk trivalen (TOPV) efektif melawan semua bentuk polio, dan
bentuk monovalen (MOPV) efektif melawan 1 jenis polio.
Imunisasi dasar polio diberikan 4 kali dengan interval 4-6 minggu.
Kekebalan aktif didapatkan sesudah infeksi asimptomatis atau

pemberian vaksin polio.


Kekebalan pasif diperoleh dari ibu secara transplasenta atau
pemberian gamma globulin.

Komplikasi
Aspirasi & pneumonia sekunder
Ulcera decubitas
Hypertensi arterial pada status akut tetapi

bisa berlanjutan (serta hyperkalsemia)


sampai konvulsi
Kelumpuhan, kelemasan & atrofi pada otot
yang diserang
Kontraktur yang mengakibatkan terjadi
talipes quino varus atau skoliosis
Subluxatio

Pencegahan
Vaksin harus melawan 3 serotipe (trivalent)
Vaksin diberi 4 kali pada umur:

2 bulan,
4 bulan,
6 - 18 bulan,
4 s/d 6 tahun (booster)

OPV (oral) & eIPV (intramuscular)

RADIKULOPATI

DEFINISI :
kondisi yang disebabkan oleh saraf yang
terjepit (tertekan) pada spine yang dapat
meyebabkan nyeri, mati rasa,
kesemutan, atau kelemahan sepanjang
jalur saraf.

Radikulopati Servikalis
Radikulopati servikal adalah rasa nyeri pada leher

dan bahu ke lenganperubahan posisi leher,


terbatasnya gerakan leher, rasa sakit pada
penekanan tulang, & parestesi pada lengan .
Namun seringkali pula gejala nyeri radikuler
tersebut tidak terlokalisasi baik sesuai dermatomal
tumpang tindih daerah persarafan .

Radikulopati Servikalis
Etiologi

Gejala

Tumor medula spinalis


Ruptur/herniasi diskus thorakalis
Arakhnoiditis
Trauma

1.

Spondilitis
Radiokulopati diabetika thorakis
Herpes zoster

2.

3.

Nyeri servikal tanpa adanya nyeri


radikuler dan defisit neurologis
Nyeri servikal yang diikuti dengan
nyeri radikuler dan defisit
neurologis.
Gangguan motorik (cram, atropi
twiching dan refleks fisiologi yang
menurun)

Pemeriksaan Fisik
Observasi :
posisi kepala dan leher menekukkan kepala menjauhi sisi
yang cedera dan leher terlihat kaku.
Gerak leher terbatas
Palpasi :
kekakuan dan nyeri pada sisi otot maupun radiks saraf yang
terkena, dapat pula disertai hipertonus maupun spasme pada
sisi otot yang nyeri.

Pemeriksaan Neurologi
Motorik :
Pemeriksaan motorik menentukan tingkat radiks
servikal yang terkena sesuai dengan distribusi
myotomal. Cth:

Kelemahan pada abduksi pundak radikulopati C 5.


Kelemahan pada fleksi siku dan ekstensi pergelangan tangan
radikulopati C 6.
Kelemahan pada ekstensi siku dan fleksi pergelangan tangan
radikulopati C 7
Kelemahan pada ekstensi ibu jari dan deviasi ulnar dari
pergelangan tangan radikulopati C 8

Pemeriksaan refleks tendon menentukan tingkat


radiks yang terkena

Seperti : Refleks biseps mewakili tingkat radiks C5-6, Refleks


triseps mewakili tingkat radiks C7-8.

Pemeriksaan Neurologi
Sensorik :
seringkali gangguan sensorik tidak jelas daerah
persarafan yang bertumpang tindih satu sama lain .
Test Provokasi :

Tes Spurling atau tes kompresi foraminal : posisi leher ekstensi


dan rotasi kepala ke salah satu sisi kemudian berikan tekanan ke
bawah pada puncak kepala.

Tes dikatakan positif nyeri radikuler ke arah ekstresimitas ipsilateral


sesuai arah rotasi kepala.

Pada pasien yang datang masih dalam keadaan nyeri, dapat


dilakukan distraksi servikal secara manual : pasien dalam posisi
supinasi, kemudian dilakukan distraksi leher secara perlahan.

Tes dikatakan positif bila nyeri servikal berkurang.

Pemeriksaan Penunjang
Pemeriksaan foto polos servikal diagnostik mendeteksi adanya

fraktur dan subluksasi pada pasien dengan trauma leher.


CT Scan :

memberikan visualisasi komponen tulang servikal dan sangat membantu bila


ada fraktur akut.
mendeteksi adanya herniasi diskus.
Akurasi dapat mencapai 96 % bila mengkombinasikan CT dengan myelografi.

MRI :
metode imajing pilihan untuk daerah servikal .
MRI dapat mendeteksi kelainan ligamen maupun diskus. Seluruh daerah
medula spinalis , radiks saraf dan tulang vertebra dapat divisualisasikan.
Elektromiografi ( EMG) :

membantu mengetahui apakah suatu gangguan bersifat neurogenik atau tidak.


Selain itu juga untuk menentukan level dari iritasi/kompresi radiks ,
membedakan lesi radiks dan lesi saraf perifer, membedakan adanya iritasi
atau kompresi

kerusakan
C3
C4

menyebabkan
nyeri di leher dan bahu
jarang mengalami kelumpuhan
sebagian

C5

nyeri dengan atau tanpa hypalgesia


kelemahan deltoideus dan bisep

C6

nyeri dengan atau tanpa hypalgesia


kelemahan brakioradialis
berkurang refleks bisep

C7

nyeri dengan atau tanpa paresthesia


atau hypalgesia kelemahan otot
pronator teres dan trisep
berkurang refleks triceps

C8

nyeri dengan atau tanpa paresthesia


atau hypalgesia di dermatom C8
kelemahan dan mungkin atrofi otot
hipotenar, triceps
penurunan refleks Trmner

Radikulopati Thorakalis
Manifestasi klinis:

paresthesia dan
rasa raba yang berkurang,
gangguan motorik (cram, atropi twiching dan refleks fisiologi
yang menurun)
serta nyeri pada vertebra

DIAGNOSA BANDING
CERVICAL
RADICULOPATHY
Cervicalgia
Shoulder pathology
Elbow disorders
Brachial plexus
disorders
Thoracic outlet synd.
Peripheral nerve
entrapment

LUMBOSACRAL
RADICULOPATHY
Low back strain
Hip and knee disorders
Lumbosacral pleus
disorders
Peripheral nerve
entrapment

TREATMENT
Pharmacotherapy:

NSAID
Short course Corticosteroid for acuteherniated disk, but
still contoversial
Narcotics reserved for control of severe pain
Gabapentin, lidocaine patch 5%, tramadol, tricyclic
antidepressants- neuropathic pain
NONpharmaco : Heat,ice, massage, limit activity,
postural modification
Epidural corticosteroid injection for pain caused by
herniated disks
Surgery for lumbosacral disk herniation : laminectomy
and disk excision

PROGNOSIS
Baik
Tidakan operatif biasanya berdampak baik

PERONEAL PALSY

PERONEAL PALSY
Common peroneal nerve dysfunction is damage to

the peroneal nerve leading to loss of movement or


sensation in the foot and leg
Can affect people at any age
Mononeuropathy

ETIOLOGY
Trauma or injury to the knee
Fracture of the fibula (a bone of the lower leg)
Use of a tight plaster cast (or other long-term

constriction) of the lower leg


Crossing the legs regularly
Regularly wearing high boots
Pressure to the knee from positions during deep sleep
or coma
Injury during knee surgery or from being placed in an
awkward position during anesthesia

RISK FACTORS
Very thin people, anorexia nervosa
Diabetic polyneuropathy
Polyarteritis Nodosa
Toxin exposed
Charcot-Marie-Tooth syndrome

SIGNS & SYMPTOMS


SIGNS

SYMPTOMS

Loss of muscle control in the legs (usually the

lower legs) and feet


Atrophy of the foot or leg muscles
Difficulty lifting up the foot and toes and
making toe-out movements

Decreased sensation, numbness, or

tingling in the top of the foot or the outer


part of the upper or lower leg
Foot that drops (unable to hold the foot
straight across)
"Slapping" gait (walking pattern in
which each step makes a slapping noise)
Toes drag while walking
Walking problems
Weakness of the ankles or feet

DIAGNOSIS
Tests :

EMG
Nerve Conduction Test
MRI
Muscle and Nerve Biopsy

TREATMENT
Corticosteroid injection

Pain : analgesics

to reduce swelling and


pressure
Surgery indication

Physical Therapy

The disorder does not go


away
problems with movement
There is evidence that the
nerve axon is damaged

Occupational Therapy
Orthopedic devices

COMPLICATION

PROGNOSIS

Decreased ability to

walk
Permanent decrease
in sensation in the legs
or feet
Permanent weakness
or paralysis in the legs
or feet
Side effects of
medication

Not life threatening


In severe cases permanent damage
Treated need months of recovery