Post on 25-Dec-2015
Definitions & classifications of pain
Akhavn akbari, MD
Clinical Assistant Professor
Department of Anesthesiology
Fatemi Hospital
pain
An unpleasant sensation The reason for initial contact with any physician Descartes :physiological pain classification in
the 17th century History of pain condition classification=history of
pain in humankind Only Recently: Focus on pain mechanism(the
foundation for understanding pain conditions)
The main reason to classify clinical presentations of symptoms:to facilitate communication between patient & doctors for better pain care outcomes
Pain theory & thought
Described in: Temporal terms:chr.,subacute,acute Characterizations: intermittent ,intractable ,
lancinating ,referred, burning ,dull Med. Diag.: phantom pain ,cancer,
vascular ,arthritic ,nerve pain ,muscle , fibromyalgia , myofacial , sympathetically maintained ,CRPS
Mechanistic/etiologic:neuropathic & nociceptive Anatomic perceptional:headache,back pain,neck
pain Source:central(spinal cord or brain),peripheral Psychiatric/psychogenic:psychosomatic
Theory Caudill(1995): biologically—as a signal (harm) psychologically—emotional suffering behavioral—alter(moves &acts) cognitively spiritually—reminder of morality
classification
Simplest :acute(stimulation of pain detection system) chronic(3-6 months) Dr lippe(1998):eudynia(good pain=acute) maldynia(bad pain=chronic) Biopsychosocial(little relationship to
mechanism):acute;recurrent acute;cancer related;chr.nonmalignant;
Pathogenetic:primary;secondary;Tx effect(chemo,tissue trauma, edema)
IASP(detailed,failed to approach the cause):region;system;chronology ;intensity;etiology
The Most advanced conceptsby Craig(2002):
Pain is just one manifestation of the mind-body homeostasis system
Pain is a microscopic event
Nociceptive pain: is not a psychological event is microscopic;physical;chemichal or
thermal event Acute, noxious stimulation of nociceptive(also
precede neuropathic pain) at microscopic pain n. ending
NT &neurotoxic substances are micro. Peripheral& central n. are mic. Neuropathic pain=pathology of n. are micr. SO: neuropathic pain is a micro. event
Macroscopic pathology is not necessory for pain to occur
85% of LBP is nonspecific µscopic Pain is measurable;
(perception=physiological brain phenomena): Functional MRI or PET scan show characteristic areas of activation in painful stimuli
(Suffering manifested ±coincidence of pain:Lepers =pain without suffering)
Pain mechanisms
Pain signal transmission by: Somatic Aб :cold quickly –thermal _mechanical Sympathetic C fibers :slowly thermal _ mechanicalPresent pain classifications: helpful but 1-complex 2-not organized
for effective Tx.
Mech.
Pain Tx.should focus on reversing the pathologic mechanism the cause the pain
Microscopic mech. Of pain: “sensor” stimulation neural”wire” misfiring CNS/”perception “dysfunction
Neuroanatomy &Neurophysiology WHAT?: Neurons ;long tubes of protoplasm –motor
neurons( efferent=brain to muscles) _sensory n.
( afferent=periphery to brain) Nerves interactions: electrical (gap junction) chemical 3 types : --“zing” Aб(somatic;sharp, lancinating ,easily localized)
Aβ (deep-lancinating & vibratory signals
-- “fogged glass” C (generalized,burning/aching pain)
Neuro
HOW?: Neural signals:↓↑Na &K ions voltage gated channels voltage gated channels: concentrated in Ranvier nodes of
somatic n.(A fiber) distributed in primitive UnM. N.(C
fiber) Ns. have:switching stations free n. endings(distal) perceptor area of the brain (proximal) WHERE?: n. fibers cover & line most of the tissue plane surfaces
throughout the body
Pain measurement
Pain & suffering Aб & C fibers tested -------
electrically(CPT=current perception threshold)) -------thermally(BASIC
PHYS.EXAM=cold & warm sensation) Pain n. pathway functions (machines) Imaging of pain perception: PET SPECT(single
photon emission cumputed tomo.) NIRS(near infrared
spectroscopy) fMRI
Proposed physiological pain model
Focuses on underlying causative mechanism nociceptive pain :NL.functioning of sensor/wire/perception system neuropathic & central pain:true dysfunction =disease Bundle of axons: Neuropraxia,axonotmesis.neurotmesis Individual axon: —NL function __hyper function (irritation or sensitization
hyperesthesia, hyperalgesia , hyperpathia ,allodynia
__ hypo function ( hypoesthesia,hypoalgesia,conduction block
__ Free n. ending sensitization or irritation==neuropathic category __
Proposed 2
All pain are problems of stimulation of sensors/conduction along n./perception in the spinal cord & brain
Perception __ involve feedback: positive or negative(endorphins= painkiller)
If negative:dysfunction stand alone Neural net: --pain sensors (free n. endings)=simple --wires (peripheral n.)=are simpler --CNS=is incredibly complex,spinal cord have
comlex interactions(not just a transmission device) Stimulation of sensors is nociceptive or eudynia Malfunction of the wires & perception is neuropathic
Essentially no pain condition is unifactorial
… Stimulation of pain sensors
(nociception):mechano-ceptor;chemo-ceptor,thermo-ceptors=eudynia(the gift nobody wants)
Misfireing of wires (neuropathic): during NL transmission of neural signals to CNS,any neural pathway damage manifest=static radio transmission→alter the n. signal------as pain perception
Mechanisms of hypersensitive or pain neuropathology:Rapid Repriming of Na channels(specific to the spinal sensory n.),
Dysfunction of perception (central pain ): CNS,perception can occur in the dorsl horn Dysfunction of this complex system
(PERCEPTRON):central neurogenic pain
Antinociceptive dysfunction : - occurs in perceptron(brain and/or
spinal cord ) - worsen both nociceptive &
neuropathic pains - is a dysfunction of the natural pain
modulation system Externally delivered painkillers=antinociceptive
Referred pain
Pain perceived in body areas that are not tender on palpation
Mechanisms:KOSEK : is a concequence of
misinterpretation of the origin of input from the stimulate Ombregt(2003):principles;1-radicular pain directly related
to spinal segment 2-percieved pain site&
causative pathology are on same side of midline 3-main pain felt deeply 4-referred distally within a
dermatom 5-may be contagiuous with or
seperated from pathology
Underlying mechanisms
Convergence-projection:one neuron receiving impulses from 2 sources
Peripheral branching of primary afferent nociceptors:single Ns.(long) various branches come from different peripheral sources
Convergence –facilitation:impulses from different body areas( Ns.in close proximity)
Symp. Nervous system activity:restricted blood flow to an area---( same as hyperesthesia,allodynia)
Convergence or image projection at the supra spinal level(ephaptic transmission in central location)
Radicular pain Origin: nerve root,cervical,thoracic,lumbar,sacral along a dermatom This type is neuropathic(even if momentary) Minor patho.→ ---local pain More compression→ ___fool the brain –pain toward the
limb pathologies: 1-n. root compression(herniated disc) 2-foraminal stenosis(bone spur )or arthrities irritating the
n.root 3-chemical changes at n. roots(DM) 4-n. root lesion pressure from mass lesion 5-scarring from previous spinal surgery
Referred muscular pain
In voluntary muscles Accompanied by secondary
hyperalgesia &hypotrophic changes Myotomal pain :problems with the fascial
tissue planes that surround muscle groups
(hypertonic saline injection—referred pain
sclerotomes
Ref. from tendinous and/or ligamentous interfaces with bone surfaces has no specific name
Sclertomes :pain referral patterns from sites of enthesopathy,pathology of the collagenous attachments
(tendons,ligaments,cartilage,…)→to bones(generated by inflammation)
Dural pain patterns
Spinal dura is innervated(symp. C fiber) Pain perception pattern: - do not resemble
dermatomal distributions Example:dural stimulation by scar in lumbar
region→pain throughout the legs Kernigs & Brudzenski’s sign:meningeal
irritation,dural irritation(where Aб & C fiber n. ending occur)=anteriorly & laterally)
Thermatomes
Thermal pattern of pain related to symp. C fiber
Like collateral ciculation(reestabilish transmission pathways in compensation
Facial referral patterns
Guyton shows : Nasal sinus & eye aches→around the
eyes(from below the nose& up to mid-fore
Cerebral vault aches→ F. to P. at the ear
Brainstem& cerebellar vault aches→from the ear through the entire occiput
Phantom pain
The ultimate referred pain Brain perceive the existence of a body part, From which no nerve impulses could possibly
be emnanting Perceived pain location is not where the pain is
originating(no peripheral pain n. stimulation) Stump & neuroma pains are not referred pain And are not phantom pain
Referred pain due to healing pain nerves By these: 1-Inflammation (part of healing process);natural chemicals Tx. Dilemma: If you stop the pain with anti inflammatory→stop the healing??! 2-Consequent muscle spasms occur; Muscle spasm→ischemia→pain(causatic microenviornment
around n. endings Spasm/cramping muscles→pressure on Aб & c fibers 3-Improper healing contort the tissue→pain &
#dysfunction(nociceptive pain by pressure/causatic chemicals; #Neuropathic pain come from ghange
neuroanatomy_neurophys._chemical microenviornment
How pain classification help?
For nociceptive pain :primary goal: cure or remove the stimulant ,pathology For neuropathic pain: stop the irritation; promote rebuilding
damaged n .or normalizing their function For central pain :techniques to change CNS neural
environment For antinociceptive pain: normalize pain perception&
reestablish natural painkiller production & function Suffering is the most difficult part to quantify & treat But as we improve our abilities to treat pain ,suffering will
improve