Neuropati

Pengertian
Neuropati adalah penyakit atau trauma dari
saraf perifer ( sensorik, motorik, autonom)
dgn berbagai penyebab
 Pembagian saraf perifer

Saraf Motorik
Saraf Sensorik
Saraf Otonomik
 Saraf sensorik

Sensory fibres are divided into at least three groups

anatomically, physiologically, and functionally:
A (or A )large diameter, myelinated, fast
conducting;
mediating vibration, position, and touch sensations
A small diameter, myelinated, slow conducting;
mediating cold sensation
C fibresvery small diameter, unmyelinated, very
slow
conducting; mediating hot and pain sensations.
 Pembagian neuropati
Those which are bilaterally symmetrical
polyneuropathies
(for example, most neurotoxins, diabetes
mellitus)
Those which are focal mononeuropathies (nerve
entrapment, exp CTS)
Multiple mononeuropathies (vasculitidies, leprosy,
multifocal
motor).
Other subdivisions are based on the predominant
site of dysfunction:
Axonsaxonopathies (diabetes,
organophosphates)
Nerve cell bodiesneuronopathies (poliomyelitis,
 Keluhan
Keluhan awal neuropati perifer
Tingling (rasa geli/gatal)
Burning (rasa terbakar)
Pricking (tusuk jarum), stabbing (ditikam), or
shock-like pain
Muscle cramping
Numbness (mati rasa)
Sensitivity to touch
Bila kerusakan saraf berlanjut
mengakibatkan simptom memburuk
Kelumpuhan
Pengecilan otot (atropi)
Gangguan pencernaan
Disfungsi ereksi pada laki-laki
Dizziness
Masalah keseimbangan dan berjalan
Risiko ulkus dan infeksi meningkat pada kaki.
 Klasifikasi Seddon utk kerusakan saraf
tepi.

Neurapraxia (Class I)

Main article: Neurapraxia

It is a temporary interruption of conduction without loss of axonal
continuity.
In neurapraxia, there is a physiologic block of nerve conduction in
the affected axons.
Other characteristics:
It is the mildest type of peripheral nerve injury.
There are sensory-motor problems distal to the site of injury.
The endoneurium, perineurium, and the epineurium are intact.
There is no wallerian degeneration.
Conduction is intact in the distal segment and proximal segment,
but no conduction occurs across the area of injury.
Recovery of nerve conduction deficit is full,and requires days to
weeks.
EMG shows lack of fibrillation potentials (FP) and positive sharp
Axonotmesis (Class II)

Main article: Axonotmesis

It involves loss of the relative continuity of the axon and its
covering of myelin, but preservation of the connective tissue
framework of the nerve ( the encapsulating tissue, the
epineurium and perineurium, are preserved ).
Other characteristics:
Wallerian degeneration occurs distal to the site of injury.
There are sensory and motor deficits distal to the site of lesion.
There is no nerve conduction distal to the site of injury (3 to 4
days after injury).
EMG shows fibrillation potentials (FP),and positive sharp waves
(2 to 3 weeks postinjury).
Axonal regeneration occurs and recovery is possible without
surgical treatment.Sometimes surgical intervention because of
scar tissue formation is required.
Neurotmesis (Class III)

Main article: Neurotmesis

It is a total severance or disruption of the entire nerve fiber. A
peripheral nerve fiber contains an axon (Or long dendrite), myelin
sheath (if existence), their schwann cells, and the endoneurium.
Neurotmesis may be partial or complete.
Other characteristics:
Wallerian degeneration occurs distal to the site of injury.
There is connective tissue lesion that may be partial or complete.
Sensory-motor problems and autonomic function defect are
severe.
There is no nerve conduction distal to the site of injury (3 to 4
days after lesion).
EMG and NCV findings are as axonotmesis.
Because of lack of nerve repair, surgical intervention is necessary.
 Sunderland's classification
In 1951, Sunderland expanded Seddon's classification to five degrees of
peripheral nerve injury:

First-degree (Class I)
Seddon's neurapraxia and first-degree are the same.
Second-degree (Class II)
Seddon's axonotmesis and second-degree are the same.
Third-degree (Class II)
Sunderland's third-degree is a nerve fiber interruption. In third-degree
injury, there is a lesion of the endoneurium, but the epineurium and
perineurium remain intact. Recovery from a third-degree injury is
possible, but surgical intervention may be required.
Fourth-degree (Class II)
In fourth-degree injury, only the epineurium remain intact. In this case,
surgical
repair is required.
Fifth-degree (Class III)
Fifth-degree lesion is a complete transection of the nerve. Recovery is not
possible without an appropriate surgical treatment.
Seddon Sunderland Injury

Neurapraxia Grade I Focal segmental demyelination

Axonotmesis Grade II Axon damaged with intact

endoneurium
Axonotmesis Grade III Axon and endoneurium damaged
with intact perineurium
Axonotmesis Grade IV Axon, endoneurium, and
perineurium damaged with intact
epineurium
Neurotmesis Grade V Complete nerve transection.

Grade VI Mixed levels of injury along the

(MacKinnon & nerve
Dellon)
Seddon Classification Type of nerve injury
Jenis trauma saraf
 Penyebab polyneuropati
Category Spesific process
Infectious diseases Leprosy
HIV infection
Borreliosis (Lyme disease)
Inflammatory diseases Acute inflammatory demyelinating polyneropathy
(SGB)
Chronic inflammatory demyelinating
polyneuropathy
Multifocal motor neuropathy
Collagen vasculer disease ( RA, sarcoidosis
Vasculitis
Other systemic DM, Chronic renal failure, Thyroid disfunction,
diseases Parathtyroid disfunction,paraproteinemia,
Amyloidosis, def Vit B12 Critical illness neuropathy,
Acute intermitten porphyria
Genetic disorders Hereditary motor sensory neuropathy (Charcot-
Marie-Tooth family of disease)
Hereditary sensory and autonomic neuropathis
Toxins Therapeutic drug ( Chemoterapy agents, antiviral,
statins)
Obat-obatan simtomatik
 CTS
(Carpal Tunnel Syndrome)
 Pengertian

CTS adalah timbulnya perasaan

paresthesia, tingling, numbness, dan/atau
nyeri sesuai dgn distribusi n. medianus ke
jari 1-3 dan separoh jari 4 akibat dari
penekanan pada nervus medianus
dipergelangan tangan (terowongan carpal)
Gambar anatomi n. medianus
 Etiologi
1. Hereditary : chronic interstitial hypertrophic neuropathy
2. Traumatic ; dislocation, fracture, hematom formation at
the wrist, occupational complication of repetitive
percussion to the wrist or repetitive flexion and extension
of the wrist
3. Infection : tenosynovitis, tuberculosis, sarcoidosis
4. Metabolic : amyloidosis, gout
5. Endocrine : acromegaly, diabetes melitus, pregnancy,
hypotyroidisme
6. Neoplasma: lipoma, metastatic infiltration, myeloma
7. Vascular : scleroderma, SLE
8. Degenerative : RA, osteoartritis
9. Iatrogenic : radial artery puncture, hematom, complication
anticoagulant therapy
 Keluhan CTS
Tanda dan gejala berkaitan dgn penekanan
n. medianus di dalam carpal tunel berupa:
paresthesia, tingling, numbness, dan/atau
nyeri sesuai dgn distribusi n. medianus ke
jari 1-3 dan separoh jari 4.
Keluhan sering muncul malam hari, shg
sering mengganggu tidur.
Nyeri berkurang bila tangan di ayunkan.
Pemeriksaan fisik

Tinel test

Revers
e
Phalen
s
Diagnosis
1. Klinis dgn keluhan
2. Pem neurologis
Tinel test dan Phalens test (+)
3. EMG
4. USG pergelangan tangan
 Penanganan
1. Konservatif
Medikamentosa
NSAID
Steroid injeksi lokal
Rehabilitasi medik
2. Operasi
Ada atropi otot thenar/hipothenar
Konservatif tdk berhasil
 TTS
(Tarsal Tunnel Syndrome)
 Pengertian
Tarsal Tunnel Syndrome (TTS) adalah rasa terbakar
pada tumit, dan lekukan medial telapak kaki akibat
adanya entrapment/ compression dari saraf tibialis
posterior atau salah satu cabangnya di dalam
terowongan tarsal yg berjalan sepanjang bgn dalam
pergelangan kaki.
Bila penekanan saraf berlangsung lama akan
menyebabkan kelumpuhan
Anatomi
 Etiologi

Aktivitas berulang dorsofleksi dan plantarfleksi

selama beraktifitas seperti pelari cepat dan
melompat menyebabkan peningkatan tekanan pada
terowongan tarsal dgn akibatnya iritasi pada saraf.
Selain itu ada juga faktor lain seperti
Faktor Intrinsik : tendo-nopathies, osteophytes,
anatomical
anomalies and space
occupying lesions such
as accessory muscles, ganglia
or lipomas
Faktor Extrinsik : trauma, foot malformations,
constrictive
footwear, edema and iatrogenic
TTS
 Gejala

Rasa terbakar pada tumit, dan lekukan medial

telapak kaki
Nyeri tekan disekitar malleolus dari bgn belakang
ke tengah.
Nyeri tambah hebat ketika berjalan
Toe Flexion Weakness
Keluhan makin jelas malam hari
Tingling and Numbness.
 Pemeriksaan fisik

1. Palpasi daerah fleksor retinakulum

2. Tinel test

3. Dorsofleksi eversion

4. Plantarflexion + Inversion nyeri berkurang

Diagnosis
1. Klinis dgn keluhan
2. Pem neurologis
Tinel test dan Dorsofleksi eversion (+)
3. EMG
4. MRI pergelangan kaki
 Penanganan

1. Konservatif
Medikamentosa
NSAID
Steroid injeksi lokal
Rehabilitasi medik
2. Operasi
Ada atropi otot yg dipersarafi oleh n.
tibilialis posterior
Konservatif tdk berhasil
Course of Wallerian axon degeneration.As early as 530 min after nerve injury, the axonal segments proximal (left) and
distal (right) to the injury site exhibit short-distance acute axon degeneration (AAD), an event that is principally mediated by
extracellular Ca2+influx and activation of the intracellular Ca2+-dependent protease calpain. This event is followed by a slower
axonal retraction and formation of axonal bulbs at the injury sites (arrowheads). For the next 24 to 48 h after injury there is a
period of relative latency in which the distal axon remains morphologically stable and electrically excitable. Although beading
occurs along the distal axon at irregular intervals, there are few signs of physical fragmentation. At more than 72 h after injury,
rapid fragmentation and cytoskeletal breakdown occur along the full length of the distal axon, followed by increased glial
(consisting primarily of astrocytes, macrophages and, in the PNS, Schwann cells) influx to clear axonal remnants (blue circles)
and to possibly promote regenerative attempts by the proximal axon.