NEUROPATHIC PAIN

Susi Aulina

Sub Division of Pain

Dept. of Neurology Faculty of Medicine
Hasanuddin University
• General Objective Instructional :
To know about Neuropthic Pain

• Spesific Objective Instructional :

1. To know Neuropathic Pain Mechanisms
2. To Know Neuropathic Pain Characteristic
3. Neuropathic Pain in Clinical Practice
Further books to read :
1. Dasar-dasar I.P.Saraf (Prof. Ngoerah) hal. 348-349
2. Konsensus Nasional Penanganan Nyeri Neuropatik.
(Pokdi Nyeri - PERDOSSI)
3. Nyeri akut : Mekanisme & prinsip pengelolaannya
(Prof. A.H.Tanra)
4. Penatalaksanaan Nyeri (dr. Samuel Lazuardi)
Majalah NEURONA vol.17 oktober 1999
5. Nyeri neuropatik dan pengobatannya
dr. Troeboes Poerwadi
6. Buku : Penyakit Neuromuskuler & Muskuloskeletal
Badan Penerbit UNDIP - Semarang 1993
7. Terapi rasional nyeri (tinjauan khusus Nyeri Neuropatik)
karangan KRT Lucas Meliala
INTRODUCTION

NEUROPATHIC PAIN (Ne P) can be defined as :

PAIN ASSOCIATED WITH A FUNCTIONAL
ABNORMALITY OF THE NERVOUS
SYSTEM (Field 1907)
ANY PART OF THE NERVOUS SYSTEM
(peripheral, central or autonomic) MAYBE
DISRUPTED
 INTRODUCTION
cont’d

CHARACTERISTICALLY : The pain persists

for months or years
THE ETIOLOGY OF NeP IS DIVERSE but the
pathophysiological mechanisms are thought to
be similar whatever the etiology (Teng and
Mekhail, 2003)
CLINICAL FEATURE (FIELDS 1987)

ABSENCE OF ONGOING NOR

NEUROLOGICAL TISSUE DAMAGED
ABNORMAL UNPLEASANT SENSATION
(DYSESTHESIA)
BURNING OR ELECTRICAL QUALITY IN
OCCASION : PAROXYSMAL, BRIEF,
SHOOTING or STABBING QUALITY
 CLINICAL FEATURE
cont’d

THERE IS NO ABSOLUTE TEMPORAL

RELATIONSHIP TO THE ORIGINATING
NEURAL TRAUMA : days, weeks, months or
even years later.
PAIN MAYBE FELT IN A REGION OF
SENSORY DEFICIT
NON-NOXIOUS STIMULI MAY BE PAINFUL
(allodinia)
 CLINICAL FEATURE
cont’d

NOXIOUS STIMULI MAY PRODUCE GREATER

THAN NORMAL RESPONSE (hyperalgesia)
AN INCREASE IN THE INTENSITY OF PAIN
WITH REPEATED STIMULI
THE PAIN MAY PERSIST AFTER THE
REMOVAL OF STIMULI
 CLINICAL FEATURE

Neuropathic Pain

Stimulus-independent pain Stimulus-evoked pain

non-noxious Noxious
Continous
stimulus stimulus
Paroxysmal

Mechanical Therma Mechanical Thermal

Allodinia Allodinia Hyperalgesia Hyperalgesia

Dynamic Static Dynamic Static

 Hyperalgesia >< Allodynia
Non noxious
stimulus Noxious stimulus

Hyperalgesia Normal
Respons

Allodinia

Stimulus Intensity

Martin, 1998.
 Alodinia
Nerve injury triggers central reorganization on dorsal horn
of spinal cord

normal Ab
Superficial

Midline
C
Ganglion radiks dorsalis

deep

after injury

Woolf, 1994.
 Hyperalgesia
Mechanism : peripheral sensitization

Vasodilatasi

Hiperalgesia
6
5
4 Hyperalgesia
Edema 3
2
1

Continuous
noxious stimuli

Fields, 1987; Willis, 1992.

 CLINICAL FEATURE
cont’d

THE RANGE OF SEVERITY OF PAIN IS WIDE  IT

MAY BE SO EXTREME AS TO TOTALLY CONSUME a
PATIENT’S LIFE

NeP must be differentiated from NOCICEPTIVE PAIN

(NoP)

DD is IMPORTANT because NoP and NeP respond to

different treatment modalities
 CLINICAL FEATURE
cont’d

NoP :
 is mediated by activation of pain receptors
 by algogenic substances (histamine, bradykinin,
substance P, etc)
 can be further classified as :
Somatic (localized aching or throbbing)
Or visceral (colicky) pain
Examples of NoP : post operative pain, arthritis
Gabapentin
 ETIOLOGY OF NEUROPATHIC
PAIN
• NeP is :
– initiated or caused by :
 a primary lesion or dysfunction
 in the nervous system
• Any condition that damages neural tissue
or impairs its function
can be a source of NeP

• > injury > metabolic derangement

> inflammation > toxins
> ischemia > tumor
> primary neurologic disease, etc.
MECHANISMS of NEUROPATHIC
PAIN (Woolf and Mannion, 1999)

The pathophysiology of Ne P is COMPLEX

Involving both peripheral and central
mechanisms
DIFFERENT MECHANISMS MAY COEXIST
IN A SINGLE PATIENT and PERHAPS
CHANGE OVER TIME.
 PERIPHERAL MECHANISMS

Sensitization of primary afferent

nociceptor terminals :
Ectopic activity
Alteration of neurotransmitter
Coupling between the sympathetic and
sensory nervous system
 CENTRAL MECHANISMS

Anatomical reorganization
Ectopic activity
Loss of segmental inhibition
Sensitization of spinal neurons
 TREATMENT of NEUROPATHIC
PAIN
Regardless of the cause, Ne P :
Affects multiple aspects of patient’s life

Hence, the management of Ne P :

 Involves a multidisciplinary approach
 TREATMENT of Ne P
cont’d

The “ideal” team should comprise :

Neurologists
An experienced phycisian in the evaluation
diagnosis and treatment of pain.
A psychiatrist or psychologist experienced in
cognitive and behavioural therapy
A team of therapists
Neurosurgeons
Pain anesthetist
 TREATMENT of Ne P
cont’d

The tools that a pain team implements include use

of both :
– Non-interventional therapies
(pharmacological, psychological and physical
therapy)
– Interventional therapies.
The overall objectives are : (Teng and Mekhail, 2003)
– to minimize pain
– to restore normal functional capacity and
quality of life
 PHARMACOLOGICAL TREATMENT

Woolf and Mannion (1999) have suggested :

• targeting treatment based on the mechanism
(s) involved
• at present : treatment mainly depends on
empirical symptomatic treatment with a
multitude of medications that affect neuronal
function
 PHARMACOLOGICAL TREATMENT
cont’d

There are several categories of

medications that can be used in Ne P :
– Antidepressants
– Anticonvulsant
– Local anesthetics
– Sympatholytics
– Opioids
Guidelines for drug treatment of neuropathic pain
 Adjuvan Therapy for Neuropathic Pain
 based on mechanisms

Inhibisi Otak
desenden
TCA
NE/5HT Tramadol
Lesi Th/ Opioid
Reseptor dll
opioid GABAPENTIN
Okskarbazepin
Sensitisasi
Medulla Lamotrigin
sentral Th/ Ketamin
Spinalis (NMDA, Dextrome-
Sensitisasi perifer/ ion Na Calcium) thorphan
GABAPENTIN
Karbamazepin
Th/ Okskarbazepin
FENITOIN
Meksiletin
Lidokain, dll
Beydoun, 2002; modifikasi penulis
 Mechanism of action of Tricyclic anti depressant

NO
BRAIN
PAIN
PAIN
PAIN
Inhibisi
Descenden

NE/SHT Th/ TCA

Tramadol
Reseptor Opioid
Opoid DLL

Medula
Spinalis
Sensitisasi perifer ion Na

Beydoun, 2002
Modifikasi Meliala, 2003
 Mechanism of action of anti convulsant (1)
NO
NO PAIN
BRAIN
PAIN
PAIN
PAIN
Inhibisi
Descenden

NE/SHT

Reseptor
Opoid

Medula
Spinalis
Sensitisasi perifer ion Na
GABAPENTIN
KARBAMAZEPIN
OKSKARBAZEPIN
Th/ FENITOIN
MEKSILETIN
LIDOKAIN Beydoun, 2002
DLL Modifikasi Meliala, 2003
 Mechanism of action of anti convulsant (2)
NO
BRAIN
PAIN
PAIN
Inhibisi
descenden

NE/SHT

Reseptor
Opoid

GABAPENTIN
Okskarbazepin
Medula Sensitisasi Th/
Lamotrigin
Ketamin
Spinalis Sentral Dextrometorphan
Sensitisasi perifer Metorphan
ion Na DLL
(NMDA,
Calcium)

Beydoun, 2002
Modifikasi Meliala, 2003
Severe side effect of carbamazepine

Steven Johnson Syndrome

© 2001-04, Johns Hopkins University School of Medicine

 PAIN ASSESSMENT
Visual Analog Scale (VAS)

Numeric Pain Rating Scale (NPRS)

Faces Pain Rating Scale (for children)

 Teng and Mekhail (2003)
cont’d :

3. Combination therapy is frequently necessary to

to achieve adequate pain relief.
Choose combination of medications with
different mechanisms of action but not the
some adverse effects
PSYCHOLOGICAL TREATMENT

The goal : to modulate pain at spinal and

supraspinal level
The first step is to decrease or to
eliminate depression
The methods for example : cognitive
behavioural therapy (CBT) and hypnosis
 PSYCHOLOGICAL TREATMENT
cont’d

CBT :
 are multimodal treatment packages
 combine education about pain and training
in a variety of cognitive and behavioural
coping skills
 PHYSICAL TREATMENT

• Pain modulation : thermal modalities,

Trans cutaneous
Electrical Nerve
stimulation
(TENS), acupuncture
• Muscle exercises
• Vocational rehabilitation
INTERVENTIONAL TREATMENTS

These procedures include :

• nerve blocks (somatic/sympathetic blocks)
• a tunneled epidural catheter for long term
temporary treatment
• neurostimulation (typically with an implantable
spinal cord stimulator)
• an intrathecal pump.
 SUMMARY :
STRATEGIES FOR Ne P MANAGEMENT
Less invasive Most invasive

Psychologic/physical therapy

Topical therapy

Oral therapy

Injection therapy

Interventional therapy