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NEUROPATHIC PAIN

Susi Aulina
Makassar September 16th, 2006

Sub Division of Pain


Dept. of Neurology Faculty of Medicine
Hasanuddin University

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

contd

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

contd

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

contd

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-evoked pain

Stimulus-independent pain

Continous

non-noxious
stimulus

Paroxysmal

Mechanical
Allodinia
Dynamic

Static

Therma
Allodinia

Noxious
stimulus

Mechanical
Hyperalgesia

Dynamic

Thermal
Hyperalgesia

Static

Hyperalgesia >< Allodynia


Non noxious
stimulus

Noxious stimulus

Hyperalgesia
Respons

Allodinia
Stimulus Intensity
Martin, 1998.

Normal

Alodinia
Nerve injury triggers central reorganization on dorsal horn
of spinal cord

normal

A
C

Ganglion radiks dorsalis


deep

after injury

Woolf, 1994.

Midline

Superficial

Hyperalgesia
Mechanism : peripheral sensitization
Vasodilatasi

Hiperalgesia

6
5

Edema

4
3
2
1

Hyperalgesia

Continuous
noxious stimuli

Fields, 1987; Willis, 1992.

CLINICAL FEATURE

contd

THE RANGE OF SEVERITY OF PAIN IS WIDE IT


MAY BE SO EXTREME AS TO TOTALLY CONSUME a
PATIENTS LIFE
NeP must be differentiated from NOCICEPTIVE PAIN
(NoP)
DD is IMPORTANT because NoP and NeP respond to
different treatment modalities

CLINICAL FEATURE

contd

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
is :
NeP
PAIN
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

> metabolic derangement


> injury
> 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 patients life

Hence, the management of Ne P :


Involves a multidisciplinary approach

TREATMENT of Ne P

contd

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

contd

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

contd

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
desenden

Lesi

Otak
TCA

Th/

NE/5HT
Reseptor
opioid

Medulla
Spinalis
Sensitisasi perifer/ ion Na

Th/

GABAPENTIN
Karbamazepin
Okskarbazepin
FENITOIN
Meksiletin
Lidokain, dll

Beydoun, 2002; modifikasi penulis

Tramadol
Opioid
dll

Sensitisasi
sentral
(NMDA,
Calcium)

Th/

GABAPENTIN
Okskarbazepin
Lamotrigin
Ketamin
Dextromethorphan

Mechanism of action of Tricyclic anti depressant


NO
BRAIN
PAIN
PAIN
PAIN
Inhibisi
Descenden
Th/

NE/SHT
Reseptor
Opoid

Sensitisasi perifer ion Na

TCA
Tramadol
Opioid
DLL

Medula
Spinalis

Beydoun, 2002
Modifikasi Meliala, 2003

Mechanism of action of anti convulsant (1)


NO
NO
BRAIN
PAIN
PAIN
PAIN
PAIN
Inhibisi
Descenden
NE/SHT
Reseptor
Opoid

Sensitisasi perifer ion Na

Medula
Spinalis

GABAPENTIN
KARBAMAZEPIN
OKSKARBAZEPIN

Th/

FENITOIN
MEKSILETIN
LIDOKAIN
DLL

Beydoun, 2002
Modifikasi Meliala, 2003

Mechanism of action of anti convulsant (2)


NO
BRAIN
PAIN
PAIN
Inhibisi
descenden
NE/SHT
Reseptor
Opoid

Medula
Spinalis
Sensitisasi perifer
ion Na

Beydoun, 2002
Modifikasi Meliala, 2003

Sensitisasi
Sentral
(NMDA,
Calcium)

Th/

GABAPENTIN
Okskarbazepin
Lamotrigin
Ketamin
Dextrometorphan
Metorphan
DLL

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)


contd :

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
contd

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
Most invasive

Less invasive

Psychologic/physical therapy
Topical therapy
Oral therapy
Injection therapy
Interventional therapy

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