Transcript Pain

‫بسم هللا الرحمن الرحيم‬
‫﴿و ما أوتيتم من العلم إال قليال﴾‬
‫صدق هللا العظيم‬
‫االسراء اية ‪58‬‬
By
Dr. Abdel Aziz M. Hussein
Assist Prof. of Medical
Physiology
Def :
•Pain is an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage
Significance:
1. Pain is a warning signal for tissue damage. It is the
prominent symptom of tissue damage
2. Pain has a protective function. It initiates protective
reflexes that;
•Get rid of the painful stimulus.
•Minimize tissue injury or damage.
A) According to its duration:
•Pain is classified into 2 types;
1. Acute
Fast or epicritc
Occurs at the time of
injury
2. Chronic
Slow or
protopathic
After injury
B) According to site of origin: 3 types;
Cutaneous
pain
• From skin and subcutaneous
tissues
• Usually pricking or burning pain
Deep pain
• From structures deep to the
skin e.g. skeletal ms, joints, and
tendons
• Usually dull aching or throbbing
Visceral pain
• From internal viscera e.g.
stomach
• Usually colicky or dull aching
C) According to its mechanism or cause:
•Pain is classified into 2 main types;
1. Physiological
Pain
Also called
Nociceptive pain
Caused by stimulation of
pain receptors by
tissues damage e.g. in
inflammation
2. Pathological
Pain
Also called
neuropathic
pain
Caused by damage
of nerve pathway
e.g. sciatica
Pain sensation
Painful
stimulus
10
•Pain Rs are morphologically similar but functionally
they are specific
1) Morphology: are specific free nerve endings
2) Highly specific i.e. respond to tissue damage only
• Classified according to their adequate stimulus into:a) Mechanical Pain Rs:
• Respond to strong mechanical trauma e.g. cutting
b) Thermosensitive pain Rs:
• Respond to excessive changes in temp (above 45°C and
below 10°C).
c) Chemical Pain Rs: respond to noxious chemical stimuli.
d) Polymodal Pain Rs: respond to a combination of
mechanical, thermal, and chemical noxious stimuli
3) Distribution:
a) Abundant in the skin and some internal tissue such as
the periosteum, arterial wall, joint surfaces, and the dura
of the tentorium cerebelli.
b) Few in deep tissues and all viscera. So, for pain to
occur, painful stimulus must by intense and widespread.
The deep & visceral pain is poorly localized.
c) Brain itself and the parenchymal tissues of the
liver, kidneys, and lungs have no pain receptors “pain
insensitive structures”
4) Threshold :
•It is the lowest intensity of injurious agent needed
to stimulate the pain receptors to cause pain
sensation
•Pain receptors are of high threshold: the pain
receptors needs sufficient degree of tissue damage to be
stimulated.
•Measured by;
1. By pricking the skin with a pin at measured levels.
2. By compressing the skin against hard objects.
3. Thermal method (more accurate) (45 C)
5) Adaptation:
•Slowly adapting receptors even non adapting
receptors
•This is very important because it directs the subject to
get rid of the injurious agent
6) Mechanism of stimulation:
Chemical stimuli
Mechanical stimuli
Thermal stimuli
Strong acids or Alkalies
Cutting or pricking
temp. > 45 C and < 10 C
Tissue damage
1st class
K ions, Histamine,
Serotonin, and Bradykinin
Directly stimulate
Pain Receptors
Release of Pain
Producing
Compounds (PPS)
2nd class
PGE2, leukotriens and
Substance P
Sensitize the pain Rs
by lowering its
threshold to stimuli
Pathway: Neospinothalamic tract
A) 1st order neuron :
• A delta afferent fibers
• End in lamina I of dorsal horn of spinal cord
B) 2nd order neuron :
• Axons of neurons lamina I of dorsal horn of spinal cord cross
the opposite side in front of central canal and ascend as
neospinothalamic in spinal cord and as spinal leminiscus
in brain stem
• End in posteroventral nucleus of thalamus (PVNT)
Pathway:
C) 3rd order neuron :
• Axons of neurons of PVNT ascend in sensory radiations
• End in primary somatic sensory area (area 3,1,2)
Note:
• The chemical transmitter released at the central end of A
delta fibers that carry fast pain is glutamate
PVNT
Sensory Radiations
Spinal Leminiscus
Lamina I
A delta
Receptors
Free nerve endings
Lateral spinothalamic tract
Pathway: Paleospinothalamic tract
A) 1st order neuron :
• C afferent fibers
• End in lamina II and III (called substantia Gelatinosa of
Rolandi SGR) of dorsal horn of spinal cord
B) 2nd order neuron :
• Axons of neurons SGR of dorsal horn of spinal cord cross
the opposite side in front of central canal and ascend in
spinal cord and as;
1. Spinoreticular tract end in RF of MO and Pons
2. Spinotectal tract end in PAG areas of midbrain
3. Paleospinothalamic tract end in non specific thalamic
nuclei (intralaminar and midline)
Pathway:
C) 3rd order neuron :
• Axons of neurons from RF and NSTN of thalamus
ascend in sensory radiations
• Terminate diffusely in all areas of the cerebral cortex
Note:
• The chemical transmitter released at the central end
of c fibers that carry fast pain is substance P
All cortical areas
Non-specific nuclei
of thalamus
Periaqueductal gray
area (PAG) in
midbrain
Reticular formation
In MO and Pons
SGR
Laminae II, III
Receptors
Free nerve endings
Afferent
C fibers
Paleospinothalamic tracts
Significance of Pain Pathways
Neospinothalamic
Paleospinothalamic
a) Rapidly inform the
C.N.S about the injurious
agent → initiate rapid
protective reflexes as
flexion withdrawal reflex.
a) Continuously inform
the C.N.S about the
presence of tissue damage
→ direct the person to
remove the injurious agents.
b) Determines accurately b) Strong arousal state
the site “locality” of the due to potent activation of
painful stimuli.
RAS
c)
Initiation
of
the
emotional & autonomic
reactions, through RF
Comparisons Between Slow and Fast
Pain
Acute (Fast)
Chronic (Slow)
Source
Skin only
Quality
Onset
Pricking
Within 0.1 sec after
stimulation
Short (one second)
Well –localized
A-delta
Neospinothalamic
tract
Cerebral cortex
Glutamate
Skin, deep tissues, and
viscera
Burning
One or more seconds
after stimulation
Long (few minutes)
Diffuse
C
Paleospinothalamic
tract
Thalamus
Substance P
Duration
Localization
Afferent
Tract
Centre
Chemical
trans.
Def:
• Referred pain is pain felt away from the
site of its origin
• Radiating pain is pain appear to migrate
away from the its original site e.g. sciatic
pain
• Referred pain is a part of radiating pain
N.B.
• Visceral pain usually referred, deep pain
may be referred but cutaneous pain never
referred
Site of referral is determined by dermatomal
rule:
•The pain from a viscera is referred to a somatic
structure (skin or deep structure) which were
developed in the same embryonic segment
and supplied by the same dorsal root ganglia.
•Abnormal sites are due to migration of
viscera.
Pain
Injury
Mechanism :
Convergence Projection Theory:
• Afferents pain fibers from skin area and diseased
viscera converge on the same neuron of SGR and
finally stimulate the same cortical neuron
• The cortex project (feel) pain as it is coming from the
skin because the sensory cortex is accustomed to
receive pain from the skin
• Convergence may occurs also at the level of thalamus
or sensory cortex
Def. :
• Is a chronic type of pain caused by damage to or
pathological changes in the nerve fibers either in
the peripheral or central nervous system.
Examples:
a. Central → Central pain e.g. thalamic infarct
b. Peripheral → e.g. nerve compression e.g. Sciatica
(Lesley Smith), neuralgias and neuropathy
c. Mixed → e.g. post herpetic neuralgia.
Nociceptive pain
Neuropathic Pain
Characters:
1. Described as tingling, numbness, , burning or
shooting pain.
2. It occurs in bouts or paroxysms.
3. Usually accompanied by hyperalgasia and
allodynia.
4. Hardly to be treated.
5. Partially responsive to opioid therapy
6. May respond to tricyclic antidepressant
1) Def,
• System which control pain transmission in CNS or
inhibit pain transmission i.e. endogenous
analgesia system
N.B
• The activity of this system differs from one person to
another and from time to time in the same person.
2) Components :
1. Periventricular
hypothalamic area
2. Periaqueductal
area (PAG)
3. Nucleus raphe
magnus (NRM)
3. Nucleus reticularis
paragigantocellularis
(NRPG) and locus
cerulus
4. Pain Inhibitory
Complex (PIC)
3) Neurochemistry:
• This system act through the release of endogenous opioid
peptides which act on opiate receptors.
Opioid peptides:
• They include 3 groups; enkephalins, endorphins and dynorphins.
Opiate Receptors:
• 3 types of opiate receptors : delta (δ), kappa (κ), and mu (μ).
 Enkephalins bind with the delta (δ) receptors
 Endorphins bind with the mu (μ) receptors
 Dynorphins bind with the kappa (κ) receptors.
•These receptors can be blocked by naloxone, which is a
morphine antagonist
Activation of the Pain Control System
Clinical (Experimental)
1- Electrical stimulation of
certain regions of pain
control system
2- Local application of opiates
(such as morphine) at particular
regions in the nervous system.
(pharmacological analgesia)
Natural (physiological)
Exposure to severe stress,
particularly when associated
with strong emotional
excitement.
Stress induced analgesia
Ascending
pathway
Glutamate
Substance P
Posterior horn of spinal cord
1st order
neuron of pain
Limbic system
RF
Hypothalamus
Cerebral cortex
PAG
NRM
Serotonin
++
Ascending
pathway
Encephalin
++
•Severe stress
•Strong emotions
LC
Noradrenaline
++
Encephalins
Glutamate -Substance P
Posterior horn of spinal cord
1st order
neuron of pain
• Was proposed by Melzack and Wall in 1965.
• States that, the sites of synapses along the pain pathway
are considered as gates through which pain transmission can
be;
 Facilitated (if the gate is open) or
 Blocked (if the gate is closed).
Sites:
 The main pain gates are:
1- Spinal gate: at the SGR.
2- Brain stem gate: at the nuclei of reticular formation.
3- Thalamic gate: At neurons of PVLNT & intalaminar thalamic
nuclei.
3
2
1
At spinal gate pain transmission is blocked by;
1. Descending inhibitory impulses through the pain control
system activating enkephalin-secreting interneuron
2. Stimulation of the large diameter nerve fibers (A delta
and A beta) terminating peripherally in mechanoreceptors,
such as tactile receptors or proprioceptors (A beta), and
pricking pain fibers (A delta).
• This may explain why simple maneuvers such as
rubbing the skin (thus exciting tactile and pressure
receptors), near a painful area is often effective in
relieving certain types of pain → A beta
• Also block of pain by acupuncture (A delta fibers)
Interneuron
Rubbing of the skin
A beta fibers
Pain C fiber
Painful stimuli
Interneuron
Acupuncture
A delta fibers
Pain C fiber
Painful stimuli
• This theory provides basis for various methods of pain
relief
1. Massaging a painful area
2. Applying irritable substances to a painful area
(counter-irritation)
3. Transcutaneous Electrical Nerve Stimulation
(TENS)
4. Acupuncture
•Acupuncture has been practiced in China for more than
4000 years as a method for pain relief.
Mechanism:
1- Needles in appropriate body regions are thought to
excite certain sensory neural pathways which feed into the
brain stem centers (such as the PAG) involved in the pain
control system, with release of endogenous opioid peptides.
2- Simultaneous suppression of pain transmission at the
spinal pain-gate by acupuncture
Def.,
•TENS is any stimulating device which delivers electrical
currents across the intact surface of the skin
Mechanism:
•TENS causes relieve of pain by activate large diameter
‘touch’ fibres (Aβ) without activating smaller diameter
nociceptive fibres (Aδ and C) this causes;
1- Excitation of certain sensory neural pathways which activate
PAG area involved in the pain control system, with release of
endogenous opioid peptides.
2- Simultaneous suppression of pain transmission at the spinal
pain-gate by acupuncture
TENS
Physical
conditions
Conditions that
open the Gate
Conditions that
closes the Gate
Extent of injury
Extra activity
medications
Counter stimulation, e.g.
massage, heat
Emotional Depression, tension
conditions
Anxiety, worry
Mental
conditions
Focusing on pain
Relaxation
Positive emotion
Distraction
Involvement in life
activity
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