Lecture 41: Pain Flashcards
Pain is?
an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
4 components of pain?
Sensory - where the pain is actually felt and how it’s felt
Affective - mood and emotion
Autonomic - inc. HR, RR, BP sweat
Motor - withdrawal, immobilisation, vocalisation
Physiological response to pain?
- Increased HR, BP and RR
- increased blood sugar
- Decreased gastric mobility and BF to vsicera, kidney and skin
- pallor
- nausea
- Dilated pupils
- Diaphoresis (excessive sweating)
Pain thershold?
The point at which a stimulus is percieved as pain
affected by: personality, stress, anxiety, culture, exercise, previous experience, behavior, culture, mood, emotion etc.
Pain Tolerance?
Duration or intensity of pain that an individual will tolerate before initiation of overt pain response
Increased tolerance: Alcohol, medication, hypnosis, warmth, distractions, strong beliefs or faith
Decreased tolerance: Repeated exposure to pain, fatigue, anger, boredom, apprehnesion, sleep deprivation
Age variability with perception of pain?
Newborns: less sensitive to pain (or they lack the ability to verbalise it)
Children: lower pain thershld than adults
Adults: Pain threshold tends to increase with age (probably from peripheral neuropathies and increased thickness of the skin)
Analgesia, anaesthesia, hyperalgesia, allodynia paresthesia, causalgia, central pain?
Analgesia : Absence of pain in tresponse to normal painful stimulus
Anaesthesia: absence of ALL sensory modalities
Hyperalgesia: increased respose to a stimulus normally painful
Allodynia: pain due to stimulus normally NOT painful
Parasthesia: abnormal sensation of burning, numbness, tingling, itching
Causalgia: A syndrome of sustained burning pain and allodynia (after a traumatic nerve lesion)
Central pain: pain associated with a lesion of the CNS
Nociception, nociceptors and noxious stimulus?
Nociception:
- the sensory process of detecting tissue damage
Nociceptors:
- Free nerve endings
- Distributed throughout the body
- stimulated by noxious mechanical, thermal or chemical stimuli
Nocious Stimulus:
- one that is due to an event potentially or actually damaging to body tissue
Two types of primary afferents?
C Fibres:
- most nemerous (4:1)
- smaller diameter
- unmyelinated - slow conduction (0.5-2 m/s)
A-delta Fibres:
- medium diameter
- myelinated - fast conduction (4-30 m/s)
Primary Receptors and pain quality?
C fibres:
- Polymodal - respond to more than one type of noxious stimulus (mechanical, thermal and chemical)
- diffuse, dull, burning, ‘slow’ or secondary pain
A-delta fibres:
- Respond to noxious mechano-thermal stimuli over a certain intensity
- Well-localised, sharp, stinging, ‘fast’ or first pain
Transduction?
Sensory cells convert external painful stimuli >>> electrical signals (AP)
2nd Order neurons in DH?
- Nocioceptive specific (NS) - (rexed lamina I and II)
- activated ONLY by noxious stimuli
- A delta and C fibres
- Wide dynamic range (WDR)- (rexed lamina V)
- Activated by both noxious and innocuous
- cutaneous and/or visceral stimuli
- A delta, C and A beta fibres)
Where does perception of pain occur?
- The reticular system- Autonomic and motor response to pain
- The limbic system- Emotional and behavioral response
- Somatosensory cortex- Perception and interpretation of sensations
Pain dampening?
Down regulation of pain by:
- Segmental inhibition
- Descending inhibitory nerve system
Gate control theory? Three input variables?
Is based on the premise that a gate, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses
Implies that a non-painful stimulus can block the transmission of a noxious stimulus.
- A delta and C fibres open the gate
- A beta fibres carrying messages of light touch- close the gate
- Messages from the brain - open or close the gate
Mechanism of segmental inhibition?
There are special inhibitory inter-neurons in the spinal cord (that keep the gate closed) These neurons make a pain blocking endogenous opioid called Enkephalin
This blocks neurotransmitter release from the C and A delta fibres keeping the gate closed
Mechanism of Descending Modulatory Pain pathways
- Stimulation of the periaqueductal gray area (PAG) in the midbrain by ascending pathways activates neurons that project to the Locus ceru leus (in pons) and Nucleus Raphe magnus (in medulla)
- These areas release noradrenaline and 5-HT respectively, stimulating the inhibitory inter-neurons in the DH that release enkephalin
Pain amplification (up-regulation) of pain. Machanism?
A term used to describe the process of:
Increased action potential output from the dorsal horn cells (2nd order)
In response to sustained low frequency input from nocioceptive afferents via C fibres. ( ie. snesation of pain is heightened) - hyperalgesia/allondyia
- Extended continuous stimulation leads to increased calcium influx
- Pathophysiological changes take place in DH neurons
- Lower threshold and more responsive
- = Central sensitisation
Nociceptive pain?
Pathway?
Due to stimuli from somatic and vsiceral structures after tissue damage
- chemical (dec. in pH)
- Intense heat (above 42˚)
- mechanical (forces)
Usually opioid sensitive
- Nocioceptive receptors stimulated by ‘mediators’ released from tissue damage (algesic substances)
- signal travels to the spinal cord and then the brain
Neuropathic Pain?
Damage to neuronal structures themselves
(often co-exists with nociceptive pain)
Usually opioid resistant but sensitive to:
- Membrane stabilizers (gabapentin, carbamazapine)
- Tricyclics (amitriptyline)
- Spinal cord stimulators (electrical pulses)
- Peripheral (outside the CNS)
- Diabetic neuropathy, trigeminal neuralgia
- Bruning, tingling, shooting, stinging
- Central
- The Thalamic Pain Syndrome
- Damage to the spinal cord
Complex regional pain syndrome?
cause, symptoms, signs, management?
aka: reflex sympathetic dystrophy, causalgia, sympathetically maintained pain
Caused by: major injury or relatively minor trauma
Symptoms: severe debilitating pain
Signs in affected limb: abnormal circulation, temp, sweating, loss of function, atrophy of muscles, changes in hair and skin
Managment: physical therapy, SNS blocks
Inflammation is divided into?
- Non-neurogenic inflammation
- involves release of inflammatory substances (eg. histamines, PG, cytokiines, leukotrines, bradykinin) from BV and CT
- done in response to tissue damage
-
Neurogenic inflammation
* Includes the release of neuropeptides (eg. substance P, noradrenaline etc) from C-fibres terminals
BOTH PROCESSES LEAD TO LOWERING THE THRESHOLD OF THE RECEPTORS LEADING TO HYPERALGESIA
Primary and secondary hyperalgesia?
Primary hyperalgesia occurs in the area where tissue damage has occured due to the inflammation process.
Secondary hyperalgesia occurs when the pain is not treated and happes in the directly surrounding areas because the touch sensation is being sensed by the 2nd order neuron as pain as the pain threshold is heavily reduced.
Referred Pain?
There is sypmathetic supply to internal organs as well as skin that have the same destination so pain coming from the internal organs etc can be felt as if they are coming from the skin area.
Chronic pain mechanism?
Neuroplasticity: Changes to the neuronal anatomy and physiology in DR
Glial cells in the dorsal horn are affected by the continuous neurotransmitter release. They then begin to produce cytokines that cause increased neurotransmitter release. Even now if the source of pain is treated there is still pain beeing percieved.
