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 &microscopic 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