NEUROPATHY
SURYADI
HORNER’S SYNDROME
Penyebab :
- Lesions sympathetic fibers
( hypothalamus to cervical cord, C8 – T2 roots to superior
cervical ganglion, cavernous sinus)
Gejala :
- Miosis
- Ptosis
- Anhidrosis hemifasialis ipsilateral
- Hiperemia hemifasialis ipsilateral
- Best seen in dark
- Pupillary asymmetry
CARPAL TUNNEL SYNDROME
• Penyebabnya bermacam-macam
• Terapinya beraneka-ragam
Progressive degeneration of
• anterior horn cells
• corticospinal fibers, and
• motor nuclei in the medulla
REVERSIBLE
1. Brief
2. Moderate HEALING
IIREVERSIBLE
TISSUE LOSS
3. Severe
4. Chronic
Inflammation
NERVE
5. Neuropathy
PERSISTENT DAMAGE
OR
6. Axotomy REGENERATION
INFLAMASI
MI SENSITISASI
Si-Na+ Pg
SSA B NOS
5HT
Adenosin AKTIFASI
R-NE
ECT. DISC.
KORNU DORSALIS
Pengalaman
Kognitif Inhibisi OTAK
Behaviour desenden
Psikologik
PAIN – NO PAIN
Axonal polyneuropathy Demyelinating Neuropathy Neuronopathy (Ganglionopathy)
Polyneuropathy is caused by the degeneration of axon terminals and results in symmetric distal
sensory loss with shading to normal sensation. A compression neuropathy often results in
demyelination with the axon left relatively intact. Sensory loss follows a radicular pattern. When
the neuronal cell body dies the condition is called "neuronopathy." If the cell body is in the sensory
ganglion the condition is often referred to as "ganglionopathy." The pattern is usually random
PENGERTIAN MODEL NYERI
PERILAKU NYERI
(PAIN BEHAVIOUR)
PENDERITAAN
(SUFFERING)
NYERI
(PAIN)
NOSISEPSI
(NOCICEPTION)
BIOMEDIKAL BIOPSIKOSOSIAL
(BIOMEDICAL) (BIOPSYCHOSOCIAL)
Fear
Depression
PSYCHOLOGICAL
A
B
Noxious Stimuli
NOCICEPTIVE
EPIDEMIOLOGI
• Nyeri Neuropati : 20 % di klinik nyeri
• Nyeri Neuropati : 2 – 40 % dari nyeri
kronik
• Nyeri Neuropati :
- Neuropati Diabetes 60,4 %
- Polineuropati distal 47,3 %
- Herpes Zoster 4,8 promil
KESULITAN MENENTUKAN PREVALENSI
Neuron
Motorik
Radik
ventralis
saraf
spinal
Saraf
Spinal
Kelumpuhan LMN
• Akibat langsung hilangnya fungsi kerusak-
an sel kornu anterior atau akson dari radik
anterior dan saraf tanda dan gejala
sesuai lokasi lesi.
K
e
l
u
m
p
u
h
a
n
Normal AChR
3
Auto antibodies bind to the acetylcholine receptor and cause
increased receptor degradation.
The combination of the binding and the turnover effects results
loss of receptor so that an action potential in the motor neuron
does not always result in an action potential in the muscle fiber
• Neonatal myasthenia
Transient illness, lasting less than 1 month, 1 in 8 babies of myasthenic mothers
• Juvenile myasthenia
Myasthenia in the younger age group, generally similar to those of myasthenia in young adults
• Penicillamine-induced myasthenia
Usually resolves over several month after drug withdrawal
• Congenital myasthenia
• Familial myasthenia
SYMPTOMS AND SIGNS
weakness of skeletal muscle is
characteristically increased by exercise,
but is not associated with muscle pain
(in contrast to ‘physiological” fatigue)
• Ocular muscles
• Limb weakness
• Bulbar muscle weakness
• Respiratory muscle involvement
CLINICAL CLASSIFICATION
• Anti-ACHR antibody
• Antistriated muacle antibody
• Electromyographic techniques
• Thymoma
MODES OF THERAPY
• Anticholinesterase therapy:
– Pyridostigmine, 30-120 mg orally
– Neostigmine bromide, 15-30 mg orally every 3 hours except at
night
Higher dose than those given above are seldom indicated and
greatly increase the risk of choinergic crisis.
Side-effects are caused by para sympatithetic stimulation and
include: - pupillary constriction
- colic
- diarrhoea
- Increased salivation
- Increased sweating
- Increased lacrimation
- Increased bronchial secretions
MODES OF THERAPY
• Corticosteroids:
Prednisolone - suitable
- once daily on alternate days to avoid
side-effects
- initial dose 10 mg, increased slowly
out patients: 5-10mg / week
in patients: 5-10 mg / dose
to avoid the exacerbation of
symptoms that can occur when the drug is started at
a high dose
- Maximal dose: 1-1.5 mg / kg body weight
- (or symptoms are controlled)
Thymectomy
Intravenous immunoglobuln
Plasma exchange
• The lag between the initial attack and development of so-called post-
polio syndrome often is measured in decades
SELESAI