S.

IRWANSYAH
DEFINISI
GANGGUAN FUNGSIONAL ATAU ORGANIK
DARI SARAF PERIFER

GANGGUAN INI DAPAT MENGENAI :

SARAF SENSORIK
SARAF MOTORIK
SARAF OTONOM
KOMBINASI
KLASIFIKASI

BANYAK KLASIFIKASI DARI NEUROPATI.

1.MENURUT ONSET SERANGAN:
NEUROPATI AKUT
MIS : POLINEUROPATI IDIOPATIK AKUT
NEUROPATI KRONIK
MIS : BERI BERI
DIABETES MELLITUS
LEPRA
2.MENURUT DERAJATNYA

1. NEUROPATI RINGAN :
SENSORIK SAJA
2. NEUROPATI SEDANG :
SENSORIK, MOTORIK,
REFLEKS 
3. NEUROPATI BERAT :
SENSORIK, MOTORIK,
REFLEKS , ATROFI OTOT
3. MENURUT JUMLAH SARAF YANG
TERLIBAT

1. MONONEUROPATI SIMPLEKS:
GANGGUAN PADA SATU SARAF PERIFER SAJA.

2. MONONEUROPATI MULTIPLEKS:
MENGENAI BEBERAPA SARAF TEPI, BIASANYA
TIDAK BERDEKATAN DAN TIDAK SIMETRIS.

3. POLINEUROPATI:
BBRP SARAF TEPI, SIMETRIS DAN SERENTAK,
BIASANYA PREDOMINAN DI DAERAH DISTAL.
4. MENURUT LETAK LESI

1 AKSONOPATI DISTAL:
GANGGUAN PADA AKSON.
2. MIELINOPATI :
GANGGUAN PADA SELUBUNG MIELIN.
3. NEURONOPATI :
GANGGUAN PADA BADAN SEL SARAF DI
CORNU ANTERIOR, MEDULLA SPINALIS
ATAU PADA DORSAL ROOT GANGLION.
ETIOLOGI

1. IDIOPATHIC INFLAMMATORY NEUROPATHIES

- POLINEUROPATI IDIOPATIK AKUT
(GUILLAIN BARRE SYNDROME)
- CHRONIC INFLAMMATORY DEMYELINATING
POLYNEUROPATHY

2. METABOLIC AND NUTRITIONAL NEUROPATHIES

- DIABETES, HIPOTIROIDI, ACROMEGALI
- UREMIA
- LIVER DISEASES
- VIT B1, OR VIT B12 DEFICIENCY
ETIOLOGI (lanjutan)

3. INFECTIVE AND GRANULOMATOUS

NEUROPATHIES:
AIDS, LEPROSY. DIFTERI, SARCOIDOSIS

4. VASCULITIS NEUROPATHIES:
- POLYARTERITIS NODOSA
- RHEUMATOID ARTHRITIS
- SYSTEMIC LUPUS ERYTHEMATOSUS
ETIOLOGI (lanjutan)

5. NEOPLASTIC AND PARAPROTEINEMIC

NEUROPATHIES:
- COMPRESSION AND IRITATION BY TUMOR
- PARANEOPLASTIC SYNDROME
- PARAPROTEINEMIAS
- AMYLOIDOSIS
ETIOLOGI (lanjutan)

6. DRUGS INDUCED AND TOXIC NEUROPATHIES

- DAPSON, ISONIAZIDE, PHENYTOIN, PIRIDOKSIN
VINCRISTIN, HIDRALAZINE.
- ALKOHOL
- TOKSIN: ORGANOPHOSPHAT
ARSENIC
LEAD
THALIUM
GOLD
ETIOLOGI (lanjutan)

7. HEREDITARY NEUROPATHIES
- IDIOPATHIC
HEREDITARY MOTOR AND SENSORY NEUROPATHIES
HEREDITARY SENSORY NEUROPATHIES
FAMILIAL AMYLOIDOSIS
- METABOLIC
PORPHYRIA
METACHROMATIC LEUCODYSTROPHY
ABETALIPOPROTEINEMIA
ETIOLOGI

8. ENTRAPMENT NEUROPATHIES
- UPPER LIMBS
MEDIAN NERVE (CARPAL TUNNEL SYNDROME)
ULNAR NERVE
RADIAL NERVE
- LOWER LIMBS
PERONEAL NERVE
FEMORAL NERVE
OBTURATOR NERVE
MOST COMMON DISEASES AFFECTING
THE PERIPHERAL NERVE

“DANG THE RAPIST”

Diabetes Trauma Rheumatic (collagen

vascular)
Alcohol Hereditary Amyloid
Nutritional Environmental Paraneoplastic
Guillain Barre toxin and drugs Infections
Systemic diseases
Tumors
PATOFISIOLOGI

ADA BEBERAPA PROSES PATOLOGI YANG

MENGENAI SERABUT SARAF a.l.:

1. DEGENERASI WALLERIAN
TERJADI DEGENERASI AKSON DAN
SELUBUNG MIELIN KEARAH DISTAL DARI
LESI.
DEGENERASI BISA JUGA KE PROKSIMAL
SATU ATAU DUA SEGMEN.
PATOFISIOLOGI

2. DEMIELINISASI SEGMENTAL
TIMBUL BILA TERJADI LESI PADA SEL
SCHWANN
PROSES DIMULAI DI DAERAH NODUS
RANVIER DAN MELUAS TAK TERATUR
MENGENAI SEGMEN-SEGMEN INTERNODUS
LAIN.
AKSON DAPAT MENGALAMI DEGENERASI
ATAU TIDAK TERGANGGU SAMA SEKALI.
PATOFISIOLOGI

3. DEGENERASI AKSON PRIMER

DISEBUT JUGA DENGAN AKSONOPATI.

DEGENERASI AKSON INI BIASANYA DI IKUTI
OLEH DEMIELINISASI SEGMENTAL YANG
SEKUNDER.
SERING PADA UREMIA, KERACUNAN
ALKOHOL, LEPRA, KARSINOMA.
PATOFISIOLOGI

KERUSAKAN SARAF DIBAGI 3 TINGKAT 

PENTING UNTUK MENENTUKAN
PROGNOSE.
1. NEUROPRAKSIA:
- KERUSAKAN PALING RINGAN
- HANYA TERJADI GANGGUAN HANTARAN
- TANPA GANGGUAN KONTINUITAS
- PEMULIHAN TERJADI DALAM BEBERAPA MENIT
SAMPAI BEBERAPA MINGGU
PATOFISIOLOGI

2. AKSONOTMESIS:
- KERUSAKAN PADA AKSON DISERTAI
DEGENERASI
- TANPA KERUSAKAN ENDONEURAL
- REGENERASI KEMUNGKINAN DAPAT
TERJADI DENGAN HASIL YANG BAIK
PATOFISIOLOGI

3. NEUROTMESIS:

- SARAF TERPUTUS TOTAL ATAU

SEBAGIAN
- PENGOBATAN DGN PENYAMBUNGAN
- KEMUNGKINAN PERBAIKAN 50%
GEJALA KLINIK

1. GANGGUAN SENSORIK:
Involvement of sensory axons produces
impairment of sensation with dysesthesias or
paresthesias.
- RASA KAKU, DINGIN, PEDAS
- GATAL DAN KEBAS-KEBAS
- NYERI SEPERTI DITUSUK JARUM
- RASA TERBAKAR
- RASA BERJALAN DI ATAS KAPAS
- RASA TERSANDUNG WAKTU BERJALAN
- RASA TIDAK STABIL
GEJALA KLINIK

2. GANGGUAN MOTORIK:
Involvement of motor axons produces muscle
wasting and weakness followed by atrophy and
fasciculations
- KELEMAHAN BERSIFAT LMN
- SULIT MEMUTAR KUNCI PINTU
- SULIT MEMBUKA KANCING BAJU
- SULIT MEMUTAR TUTUP BOTOL
- FOOT DROP
- WRIST DROP
- GANGGUAN GERAKAN TANGKAS
GEJALA KLINIK

3. GANGUAN REFLEKS TENDON:

The tendon reflexes supplied by the affected nerve
are depressed or absent.
Contoh :
- REFLEKS TENDON BISEPS
- REFLEKS TENDON TRISEPS
- KPR
- APR
GEJALA KLINIK

4. GANGUAN OTONOMIK:
Involvement of axons supplying autonomic
function produces loss of sweating, alteration
in bladder fuction, constipation, and impotence
in male
Contoh : - GANGGUAN GASTROINTESTINAL:
DIARE, KONSTIPASI, DILATASI
LAMBUNG, MUAL DAN MUNTAH.
GEJALA KLINIK

GANGGUAN OTONOMIK (lanjutan) :

- GANGGUAN KANDUNG KEMIH :
ATONI KANDUNG KEMIH, RESIDU URINE
- IMPOTENSI
- GANGGUAN KARDIOVASKULER:
HIPOTENSI ORTOSTATIK, SINKOP
- GANGGUAN BERKERINGAT
- CARDIO RESPIRATORY ARREST
PREDOMINANTLY MOTOR
NEUROPATHIES

Guillain-Barre Syndrome
Diphtheric neuropathy
Dapsone-induced neuropathy
Porphyria and multifocal motor
neuropathy
PREDOMINANTLY SENSORY
NEUROPATHIES

Drug toxicity : pyridoxine, doxorubicine

Autoimmune : paraneoplastic, Sjogren
syndrome, etc.
Infectious : diphtheria, HIV
Deficiency : vit. E
Inherited : abetalipoproteninemia.
DIAGNOSA

1. GEJALA KLINIK
2. LABORATORIUM
3. FOTO THORAKS
4. PUNKSI LUMBAL
5. EKG
6. BIOPSI : paling sering n. suralis atau n. cutaneus
radialis
7. ELEKTROFISIOLOGI: EMG
NCV
ELEKTRO MIOGRAFI

ELEKTRODA DITUSUKKAN KEDALAM SUATU OTOT SKELET

UNTUK MEMPELAJARI PERUBAHAN POTENSIAL
LISTRIKNYA.
INDIKASI:
GANGGUAN LOWER MOTOR NEURON, YANG LESINYA DI:
1. KORNU ANTERIOR
2. RADIKS
3. PLEKSUS
4. SARAF PERIFER
5. NEUROMUSCULAR JUNCTION
6. OTOT
MANFAAT EMG

 MEMBANTU DIAGNOSA SECARA DINI

 MENENTUKAN LETAK LESI
 MEMBEDAKAN LESI MIOGEN ATAU NEUROGEN
 MENENTUKAN LESI PARSIAL ATAU TOTAL
 MEMBEDAKAN SENSORIK ATAU MOTORIK
 EVALUASI PENGOBATAN
 MEMBANTU MENENTUKAN PROGNOSE
NERVE CONDUCTION VELOCITY( NCV)

NCV ATAU KHS

NILAI NORMAL :
N. ULNARIS = 47 - 72 m / s
N. MEDIANUS = 46 - 72 m / s
N. PERONEUS = 42 - 63 m / s
N. TIBIALIS = 40 - 67 m / s
DISTAL LATENCY ( DL )
NILAI NORMAL N. MEDIANUS
2,7 + 0,3 m/s
MANFAAT PENGUKURAN KHS

MENGIKUTI PERJALANAN PENYAKIT

MENGEVALUASI EFEK PENGOBATAN
MENENTUKAN PROGNOSE, APAKAH
MASIH MUNGKIN DIPEROLEH
PERBAIKAN LAGI.
EMG DAN KHS PADA NEUROPATI

DIJUMPAI PENURUNAN KHS.

PEMANJANGAN DISTAL LATENCY
PENURUNAN AMPLITUDO GELOMBANG M
DURASI YANG MEMANJANG
POTENSIAL POLIFASIK
FIBRILASI
NEUROPATI DIABETIK

PREVALENSI : 10 - 20 % (SIMTOMATIK)
KHS 80 % ABNORMAL
KLINIS DAPAT MENGENAI:
SENSORIK
MOTORIK
OTONOMIK
KOMBINASI
PATOGENESE NEUROPATI DIABETIK

The etiology is uncertain.

4 hypothesis (not necessarily exclusive) :

1. Hyperglycemia-polyol-myoinositol hypothesis.
2. Microvascular hypothesis
3. Structural changes at the node of Ranvier.
4. Vasculitic neuropathy.
1. Hyperglycemia-polyol-myoinositol
hypothesis

Normal : glucose  hexokinase  glucose-

6-phosphate  Krebs cycle.

Hyperglycemia  saturates hexokinase activity

 glucose shunted to polyol pathway 
production of sorbitol assoc w/ a decrease in
intracelluler myoinositol  defective Na/K
ATPase activity  defect axon transport 
slowing NCV
2. Microvascular hypothesis

DM : ** thickening of capillary basement

membrane
** increase in the size and number
of capillary endothelial cells

Microangiopathy  increase number of closed

capillaries in peripheral nerves  progressive
hypoxia  secondary changes in axons and
Schwann cells
3. Structural changes at the node of
Ranvier

Na/K ATPase defiency  increase intra-axonal

Na and nodal axonal swelling  detachment of
myelin  myelin retraction from the nodal area
 slowing of axonal conduction.
Exposure of paranodal K channels  leakage of
K  impairment of axonal conduction.
Impairment of axonal transport  gradual dying
back of axons starting at the distal axons and
progressing proximally.
4. Vasculitic neuropathy

Some cases of NIDDM and proximal

diabetic have a inflammatory
vasculopathy with perivascular collections
of lymphocytes and axonal neuropathy
PAINFUL DIABETIC NEUROPATHY

 cranial nerve neuropathy

Acute thoracoabdominal neuropathy
Acute distal sensory neuropathy
Acute lumbar radiculoplexopathy
Chronic distal small-fiber neuropathy
Terapi

Intensive diabetic therapy

Maintain ideal body weight
Adjuvant analgetics :
TCA antidepressants
carbamazepine
gabapentin
intravenous lidocaine, etc
CARPAL TUNNEL SYNDROME

 CHARACTERIZED BY :
FLUCTUATING NUMBNESS, PARESTHESIA AND
PAIN IN THE HAND DUE TO COMPRESSION OF THE
MEDIAN NERVE AT THE WRIST.
 80% in WOMEN, A COMMON TEMPORARY
PHENOMENON DURING PREGNANCY
 PRESSURE TO THE NERVE WHEN PASSING
BENEATH THE FLEXOR RETINACULUM 
OBSTRUCTION OF VENOUS CIRCULATION AND
EDEMA  ISCHEMIA  INCREASING PRESSURE
ON THE NERVE  ISCHEMIC ATROPHY OF NERVE
FIBERS
Etiologi

1. Hereditary : HMSN type III

2. Traumatic : dislocation, fracture, hematoma, wrist sprain
3. Infection : tenosynovitis, tbc, sarcoidosis
4. Metabolic : amyloidosis, gout
5. Endocrine : acromegaly, DM, hypothyroidism, pregnancy
6. Neoplastic : ganglion cysts, lipoma , myeloma
7. Collagen vascular diseases : RA, polymyalgia rheumatica,
SLE
8. Degenerative disease : OA
9. Iatrogenic : radial artery puncture, shunt for dialysis,
anticoagulant therapy
Gejala Klinis

The earliest symptoms : numbness and

paresthesias in the sensory distribution of the
median nerve in the hand (thumb, index, middle
and lateral half of the ring finger)
Later on : pain, worst at night
Late : inability to screw bottle caps or grip
properly
Terapi

Identified causes should be treated

Corticosteroid injection around the median
nerve in the carpal tunnel.
Surgical division of the transverse ligament
(flexor retinaculum)
Endoscopic carpal tunnel release
GUILLAIN - BARRE SYNDROME
(GBS)

ACUTE INFLAMMATORY POST INFECTIOUS

POLYNEUROPATHY
- INSIDEN: 2 PER 100.000 POPULASI
PERTAHUN
- 1-3 MINGGU SETELAH INFEKSI :
VIRUS
BAKTERI
IMUNISASI
G B S (lanjutan)

- INFLAMASI TERHADAP SERABUT SARAF

MERUPAKAN RESPON AUTOIMMUN BAIK
MELALUI REAKSI ANTIBODI MAUPUN CELL
MEDIATED RESPONSE
- TERJADI DEMIELINASI SEGMENTAL DISERTAI
DENGAN KERUSAKAN AKSON BILA PROSESNYA
BERAT
- DIJUMPAI INFILTRASI LIMFOSIT PERIVASKULER
PADA SARAF PERIFER DAN NERVE ROOTS
- LIMFOSIT DAN MAKROFAG MENGHASILKAN
SITOTOKSIN YANG MERUSAK MIELIN
G B S (lanjutan)

- KELUMPUHAN KEEMPAT ANGGOTA GERAK

- UMUMNYA DIMULAI DARI TUNGKAI, MELUAS
KEATAS, LENGAN, OTOT LEHER DAN WAJAH
KADANG-KADANG OTOT MENELAN
- SEBAGIAN BESAR KASUS MENGELUH PARASTESI
PADA EKSTREMITAS INFERIOR
- GANGGUAN OTONOMIK DIJUMPAI PADA
25% KASUS
- PADA LP DIJUMPAI DISOSIASI SITOALBUMIN
G B S (lanjutan)

KRITERIA DIAGNOSTIK
DIJUMPAINYA 5 DARI 6 KRITERIA INI :
1. DIFFUSE FLACCID PARALYSIS
2. GANGGUAN SENSORIK < GANGGUAN MOTORIK
3. REMISI SEMPURNA DALAM 6 BULAN
4. PENINGKATAN PROTEIN PADA CSF DLM 2 MGG
5. DEMAM (-) ATAU SUHU SEDIKIT MENINGGI
6. LEUKOSIT NORMAL HANYA KEMUNGKINAN LED
SEDIKIT MENINGGI
PREDICTORS OF SEVERE DISEASE
AND POORER OUTCOME

Old age
Rapid onset of severe tetraparesis
Need for early artificial ventilation
Severely decreased compound muscle
action potential (<20% normal)
Acute motor-sensory axonal form of the
disease
TERAPI

1. PLASMAPHARESIS
2. IMMUNOGLOBULIN IV 0,4 gr/kg BB
SELAMA 5 HARI
3. PERAWATAN UMUM
4. FISIOTERAPI
5. PERAWATAN DI ICU BILA TERJADI
GAGAL NAFAS