Transcript Central pain

Chronic Pain
Dr. Muhannad Y. Al-Muhanna
What is Chronic Pain?
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Chronic pain is persistent or recurrent pain,
lasting beyond the usual course of acute
illness or injury, or more than 3 - 6 months,
and adversely affecting the patient’s wellbeing.
Pain that continues when it should not.
Acute vs Chronic Pain
Characteristic
Acute Pain
Chronic Pain
Cause
Generally known
Often unknown
Duration of pain
Short,
well-characterized
Persists after healing,
3 months
Treatment
approach
Resolution of underlying
cause, usually selflimited
Often not cure by treating the
underlying cause
Classification of chronic pain
chronic pain
Neuropathic pain
peripheral
central
Nociceptive pain
superficial
deep
somatic
Visceral
Nociceptive vs Neuropathic Pain
Nociceptive
Pain
Neuropathic
Pain
Caused by activity in
neural pathways in
response to potentially
tissue-damaging stimuli
Postoperative
pain
Initiated or caused by
primary lesion or
dysfunction in the
nervous system e.g.
Arthritis
Mechanical
low back pain
Sickle cell
crisis
Sports/exercise
injuries
*Complex regional pain syndrome
Postherpetic
neuralgia
Trigeminal
neuralgia
Neuropathic
low back pain
Distal
polyneuropathy
(eg, diabetic, HIV)
Pathophysiology of chronic pain
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Persistent activation of nociceptive transmission to
the dorsal horn may induce a pain wind-up
phenomenon.
(Pain wind-up: is a frequency-dependent increase
in the excitability (hyperexcitability) of spinal cord
neurons, evoked by electrical stimulation of afferent
C-fibers. It occurs due to sustained and repeated
state of excitation of the projection neurons. Causing
the dorsal horn neuron to transmit progressively
increasing numbers of pain impulses.
Pathophysiology of chronic pain
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This induces pathological changes that lower
the threshold for pain signals to be
transmitted.
It may generate non-nociceptive nerve fibers
to respond to pain signals.
In chronic pain this process is difficult to
reverse or eradicate once established.
Central pain
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Central pain state: a neurological condition
caused by damage or malfunction in the
NS which causes a sensitization of the pain
system. It is almost always generated by
wind-up of the projection neurons of the
spinothalamic and spinoreticular
pathways. The extent of pain and the areas
affected are related to the cause of the
injury .
Central (thalamic) pain syndrome
Dejerine–Roussy syndrome
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is a condition developed after a thalamic stroke, a
stroke causing damage to the thalamus.
An initial lack of sensation and tingling in the
opposite side of the body.
Weeks to months later, numbness can develop
into severe and chronic pain that is not
proportional to an environmental stimulus,
called dysaesthesia or allodynia.
Chronic Pain Syndrome
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Chronic Pain Syndrome (CPS) is a common
problem that is complex in nature of poor etiology
and poor response to therapy.
Most consider ongoing pain of 3~6 months are
diagnostic.
Two or more co-existing pain conditions or
widespread generalized pain.
Although CPS has been known to resolve
completely with (and very rarely without) treatment, it
is uncommon for full relief to be achieved
Management of pain
Opioids act on GPCRs: act by closing
calcium channels or opening potassium
channels. Opioids receptors are present
centrally and peripherally.
 WHO Analgesic ladder:
1- start with non-opioid analgesics.
2- weak opioids.
3- strong opioids.
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Basic nerve conduction study
MOTOR CONDUCTION STUDIES
The compound muscle action potential (CMAP) is
a biphasic potential with an initial negativity, or
upward deflection from the baseline.
For each stimulation site: the latency, amplitude,
duration, and area of the CMAP are measured .
A motor conduction velocity can be calculated
after two sites of stimulation, one distal and one
proximal.
It’s called M response
CMAP
The active recording electrode is
placed on the center of the muscle
belly (over the motor endplate), and
the reference electrode is placed
distally about 3:4 cm
The stimulator then is placed over
the nerve that supplies the muscle,
with the cathode placed closest to
the recording electrode.
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current is slowly increased from a baseline:
more of the underlying nerve fibers are brought to
action potential, and subsequently more muscle
fiber action potentials are generated.
The recorded potential, known as the compound
muscle action potential (CMAP), represents the
summation of all underlying individual muscle
fiber action potentials.
When the current is increased to the point that the
CMAP no longer increases in size the
supramaximal stimulation has been achieved.
Latency
Latency measurements usually are made in
milliseconds (ms).
The latency is the time from the stimulus to
the initial negative deflection from baseline.
The only major difference between CMAPs
produced by proximal and distal stimulations
is the latency.
Conduction Velocity
It’s measurement of the speed of the fastest
conducting nerve axons.
It is calculated by dividing the change in
distance (between proximal stimulation site
& distal stimulation site in mm) by the
latency (time) difference (in ms)
Conduction Velocity
Amplitude
it
is most commonly measured from
baseline to the negative peak (baseline-topeak) and less commonly peak-to-peak.
CMAP amplitude reflects the number of
muscle fibers that depolarize.
low CMAP amplitudes most often result
from loss of axons (as in a typical axonal
neuropathy)