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Transcript
Pain Theories
• Specificity
– Separate sensory modality
• Pattern
– Different patterns of activity in neural networks
• Gate-control
Gate Theory of Pain
• Segmental level gating mechanism
• Internuncial neurons may modify activity of
pain circuits
• Activated by large diameter (tactile) axons
Three Factors Involved in Opening
and Closing the Gate
• The amount of activity in the pain fibers.
• The amount of activity in other peripheral
fibers
• Messages that descend from the brain.
Conditions that Open the Gate
• Physical conditions
– Extent of injury
– Inappropriate activity level
• Emotional conditions
– Anxiety or worry
– Tension
– Depression
• Mental Conditions
– Focusing on pain
– Boredom
Conditions That Close the Gate
• Physical conditions
– Medications
– Counter stimulation (e.g., heat, massage)
• Emotional conditions
– Positive emotions
– Relaxation, Rest
• Mental conditions
– Intense concentration or distraction
– Involvement and interest in life activities
Pain Perception
• Provides information
on the location,
amount and duration
of tissue injury
• Reactions to pain,
include; emotion,
autonomic, and
behavioural responses
Pain Perception
• Autonomic sympathetic response
• Emotional response- fear, anger, anxiety,
panic, depression
• Behavioural response- spinal cord reflexes
to pull tissue away, immobilising wound,
coping
• Pain informs of danger- attempt to remove
stimulus, seek help
Pain Mechanisms and Pathways
•
•
•
•
Receptors
Transmission
Pathways
Endogenous analgesia
Receptors
• Nociceptors
nocioceptors
Touch receptors
Enclosed in end organ
Transmission
• A-delta neurons
• C-fiber neurons
A fibres
• myelinated-conduct AP’s fast
• found in skin, mucous membranes
• fire immediately on stimulation, stop when
stimulus removed
• produce sharp pain (eg. getting injection),
well localised
C fibres
• unmyelinated-slower
• found in same areas as type A, and in
organs, skeletal muscle, tendon
• Tend to be stimulated by substances
(bradykinin, serotonin, histamine,
potassium) released from damaged tissues
C fibres
• Discharge is slow to develop, but lasts long
after the original stimulus is removed
• Produce dull, aching pain
• Poorly localised
Pathways
• Pain fibers synapse in the dorsal horn.
• Neurons may carry impulse to ventral
root to initiate spinal reflexes
• And/or, impulses proceed up the
spinothalamic tract to the medulla and
thalamus
Pain and the CNS
• fibres synapse in SC; travel up
spinothalamic tracts and activate the
following regions of brain:
–
–
–
–
Sensory cortex
Reticular activating system
Hypothalamus
Limbic system
Sensory association cortex
(perception and meaning)
Primary sensory cortex
(discrimination: location and intensity)
Thalamus (sensation)
Limbic cortex*
(emotional experience)
A-delta
(fast)
C-fiber
(slow)
Paleospinothalamic tract
(dull, aching pain)
Nociceptive
Stimuli
Neospinothalamic tract
(sharp, bright pain)
Sensory nuclei
Periaqueductal gray (PAG)*
(endogenous analgesic centre)
Pontine
noradrenergic neurons
Medullary raphe nucleus
Spinal cord and dorsal horn*
Pain modulating circuits
Primary touch fibers
Types of Pain
• Source
–
–
–
–
cutaneous
deep somatic
visceral
functional or psychogenic
• Fast Pain
• Slow Pain
• Referred Pain
Types of Pain
• Acute Pain
• Chronic Pain
Acute Pain
• Mild to severe
• Caused by noxious or tissue damaging
stimuli
• Protective or warning system
Chronic Pain
•
•
•
•
Mild to severe
Lasts longer than 6 months
Usually serves no useful purpose
Pain is a major focus of care
Special Types of Pain
•
•
•
•
Neuropathic Pain
Causalgia
Neuralgia
Phantom Limb Pain
Neuropathic Pain
• Pathologic change or dysfunction of
peripheral nerve
• Tumour infiltration, compression,
constriction, damage, side effect of medical
treatment or other peripheral nerve disease
Causalgia
• Extremely painful
• Follows sudden and violent deformation of
peripheral nerves of limbs
• Nerve typically damaged, but not severed
• Pain characteristically burning, easily
excitable and excruciating
Neuralgia
• Severe, brief, often repetitive attacks of
lightening-like or throbbing pain
• Occurs along distribution of a spinal or
cranial nerve
• Usually precipitated by stimulation of
cutaneous region supplied by nerve
• Trigeminal neuralgia one of most common
and severe
Phantom Limb Pain
• Up to 70% of amputees
• Often begins as sensations of tingling, heat
and cold, or heaviness, followed by burning,
cramping, or shooting pain
• May experience painful sensations that were
present before amputation
Headache
•
•
•
•
•
Migraine
Cluster
Tension
Chronic Daily Headache
Temporomandibular Joint Pain
Migraine
• Females = 2 x males
• With aura (15%) or without
• Without aura is an idiopathic, recurring
disorder that lasts 1 – 3 days
• Unilateral, pulsating, moderate to severe
aggravated by normal physical activity
• Associated with nausea, photophobia and
phonophobia
Cluster
• Affect ore males than females
• Tend to occur nightly over weeks or months
with long remission period
• Typically severe, unrelenting, unilateral
pain
• Most commonly around the eye
• Pain radiates to ipsilateral trigeminal nerve
Tension
• Most common, slightly more common in
women
• Dull aching diffuse, nondescript headaches
not associated with vomiting nor worsened
by activity
• May be associated with disorders of the
pericranial or scalp muscles
Chronic Daily headache
• 40% of patients in headache clinics
• Cause unknown
Temporomandibular Joint Pain
• Common
• Usually due to imbalance in joint movement
because of bruxism or joint problems
• Almost always referred and commonly
presents as facial muscle pain, headache,
neckache or earache
• Aggravated by jaw action
Narcotics and Pain Inhibition
• Endorphins
• Morphine
• Endorphins bind to receptors in brain stemactivate AP’s down the spinal cord. Here
they limit A and C fibres by releasing
enkephalins
Analgesics and Pain Management
• Types:
–
–
–
–
Peripheral
Central
Local
Indirect
Peripheral Analgesics
• Act by blocking the production of
substances produced in the inflammatory
response (eg prostaglandins or bradykinins)
which stimulate pain receptors
• eg Aspirin; NSAID’s, Tylenol
Central Analgesics
• Narcotics - already mentioned
• There are different types of endorphin
receptors in CNS, each narcotic analgesic
acts on a different type of receptor
• eg. codeine, morphine, methadone,
oxycodone
• May produce respiratory depression
Local Analgesics
• Local Analgesics can be injected into site of
injury or applied topically (eg. Novocaine)
Indirectly Acting Drugs
• Affect non-pain conditions such as
emotions that can exacerbate pain
experience