pain physiology and management

PAIN PHYSIOLOGY AND MANAGEMENT

Presented by

Manasa.A

CONTENTS

Pain – introduction and definition Organization of nervous system The receptors of sensory nerves Synapse and neurotransmitters Pathophysiology of pain: pain theories Dual nature of pain Pain pathway Oro facial pain Measurement of pain and management Management of pain in periodontitis Diagnosis and management of some orofacial pain disorders

PAIN – INTRODUCTION AND DEFINITION

Pain:Pain is a feeling triggered in the nervous system and it

is the presenting symptom of a broad spectrum of diseases

Etymology:

Latin ‘poina’- punishment Greek ‘a paine’- penalty (An etymology dictionary of

English language, by Walter W Skeat, 1893)

History-

14-15 century-Leonardo Da Vinci- ‘brain’ central organ- spinal cord tranmits sensations

17-18 centuries Rene Descartes- a french philosopher- described ‘pain pathway’ – illustrated how particles of fire,in contact with foot, travel to brain- compared pain with ringing bell

19 century- discovery of opium, morphine, codeine, cocaine, asprin and anesthesia

Definitions:

“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (IASP)

“The psychical (=pertaining to mind) adjunct (=joined to) of an imperative (=urgent) protective reflex”, i.e. pain is a sensation that draws attention of the individual as a whole (Sherrington)

Pain is an unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such (Monheim’s local anesthesia and pain control )

Pain is a protective mechanism: pain occurs

whenever any tissues are being damaged, and it causes the individual to react to remove the pain stimulus ( Guyton and Hall )

NERVOUS SYSTEM

Central nervous system: Brain and spinal cordPeripheral nervous system: Somatic nervous system

Autonomic nervous system

Nerve: a cord like structure that has the ability to convey electrical and chemical impulse

Nerve cell (neuron): structural and functional unit.

Contains, a nerve cell body (soma or perikaryon) and processes dendrites and axon

Nerve cell body (soma) contains following structures: Nucleus, Nissls bodies (organelles containing ribosomes), Mitochondria, Golgi apparatus, Neurofibrils

Nerve cell body or SOMA: Contains

Nissl granules, basophilic granules composed of thin parallely arranged, membrane bound cavities covered by minute particles consisting of RNA with proteins.

Neuro fibrillae, fine threads 6-10 nm in diameter of varying length forming a loose framework in cytoplasm

DENDRITES

Greek word – means tree.

Branched arborizing process, 5-7 in number

Conducts impulses towards cell body

Also contain Nissl granules, mitochondria and neuro fibrillae.

They are receptive processes of neurons.

AXON (Nerve fiber) Arises from axon hillock, no Nissl granules,

containing axoplasm in the centre and enveloped by axolemma.

Length varies few µ to 90 cm Conduct impulses away from the cell body Myelinated and nonmyelinated Myelin sheath propagation of action potential is

faster It is a protein-lipid complex Responsible for white color of the nerve

GLIAL CELLSTYPES MICROGLIA: Phagocytic role in CNS

MACROGLIA: Astrocytes Ependymal and Choroidal cells Oligodendrocytes Satellite cells Bergmann Glia Of Cerebellum Schwann cellsPituicytes of Neurohypophysis

CLASSIFICATION OF NEURON:

BASED ON MORPHOLOGY -Unipolar -Bipolar -Multipolar

BASED ON FUNCTION - MOTOR NEURONS (EFFERENT)SENSORY NEURONS (AFFERENT)

BASED ON THE LENGTH OF THE AXONGOLGI TYPE IGOLGI TYPE II

Classification of nerve fibers:ERLANGER AND GASSER

CLASSIFICATION:

RECEPTORS OF SENSORY NERVES:

A receptor is defined as a specific structure meant for perceiving specific sensation. Acts as a transducer and converts different forms of stimuli into electrical impulse.

Extero receptora. Merkel’s Corpuscles b. Meissner’s Corpuscles c. Ruffini’s Corpuscled. Pacinian Corpuscle e.Free nerve endingsf. Krauses end organ

Proprioceptors

Muscle spindlesGolgi tendon organsPacinian corpuslesPeriodontal mechanoreceptorsFree nerve endings

Interoceptors

Pacinian CorpusclesFree nerve endings

Synapse:

It is a physiological junction without anatomical union between two neurons or between a neuron and an effector such as muscle or gland

Based on mode of action:

RAPID ACTING NEUROTRANSMITTERS:

Acetylcholine Norepinephrine Glutamate Aspartate Serotonin GABA Glycine Dopamine Histamine

SLOW ACTING NEUROTRANSMITTERS:

Substance P

Endorphin

Bradykinin

REFLEXES Reflex is an involuntary (automatic) response to the

stimulus which depends on integrity (completeness) of reflex pathway i.e. the reflex arc (review of medical physiology William F Ganong 22ed edition)

A reflex is a mechanism by which ‘a sensory impulse is automatically converted into a motor effect through the involvement of the central nervous system’ (concise medical physiology chaudhuri 6th edition)

A group of nerve fibers travelling in the CNS is called tract or pathway

Ascending (sensory) tractsDescending (motor) tracts

Sensation General

special

General classified into somatic and visceral Somatic – touch, pressure, warm, cold, pain Visceral- pain

Special- Vision Touch Smell Taste

Classification of pain

Fast pain and slow pain

somatic and visceral

Somatic - superficial (from skin and subcutaneous tissue). E.g: superficial cuts and burns

Deep (from muscles, bones, joints, fascia, periosteum) E.g: fractures, arthritis

Visceral- e.g. angina pectoris, peptic ulcer, renal colic etc.

Nerve conduction

It is the self-propagated passage of an electric current

Brought about by the flow of current across the membrane

Transition of the nerve from resting to active state

Normally , electrolytic solutions containing equal concentration (approximately 155 mEq) of anions and cations are present on both sides of cell membrane

Resting state:

Potassium ions are concentrated inside

Sodium and chloride ions are outside the cell membrane

The difference respective ion concentrations-potential electrical difference.

The electrochemical gradient across the membrane is -70 to -90 mv said to be resting potential.

Maintained by an active mechanism-sodium pump, which moves the sodium from the lesser concentration (10 mEq) inside to greater concentration (142 mEq) outside

Depolarization:

The membrane is activated by alteration in its permeability permitting sodium to diffuse into the cell

Occurs as a result of displacement of calcium ions from a phospholipid binding site.

This alteration in permeability is a result of release of ach (neurotransmitter) at the site of stimulation .

Repolarization:

The permeability of nerve membrane to sodium decreases

High permeability to potassium is restored, moves freely out of the cell

Restores the resting potential

The return of resting potential occurs in 3 to 4 msec

During which nerve cannot be stimulated called absolute refractory period.

the normal ionic distribution begins to return the nerve can be stimulated, only by a greater than usual stimulus.

It is said to be in relative refractory period.

ALL OR NONE LAW

Once the impulse has been initiated in a particular nerve fiber, the amplitude of electricity as well as the speed of conduction remains constant regardless the quality and intensity of stimulus applied, which explains all or none law of nerve action

PATHOPHYSIOLOGY OF PAIN: PAIN THEORIES

Specificity theory: Descartes 1644, pain – ‘ a straight through

channel from the skin to brain’. 19th century Muller – ‘information transmission

only by way of the sensory nerves’ Late nineteenth century, Von Frey – specific

cutaneous receptors for the mediation of touch, heat, cold, pain. Free nerve endings – pain receptors. A pain ‘center’ was thought to exist in the brain, which was responsible for overt manifestations of unpleasant experience

Pattern theory: Goldscheider 1894,

Stimulus intensity and central summation are the critical determinants of pain.

Particular patterns of nerve impulses that evoke pain are produced by the summation of sensory input within the dorsal horn of the spinal column.

Pain results when the total output of the cells exceeds a critical level

e.g. touch + pressure + heat results in a manner that pain were the modality experienced.

Gate control theory: Melzack and Wall 1965

Postulates - information about the injury is transmitted to CNS by small peripheral nerves

Cells in spinal cord or nucleus of V, excited by these injury signals are facilitated or inhibited by other large peripheral nerves that carry information about innocuous events e.g. temperature and pressure

Descending control systems in the brain modulate the excitability of cells that transmit information about injury

Peripheral nerves- Aᵟ - 3-20µ - diameter – 100m/sec (fast or first pain)

C- .05-1µ- diameter – 0.5- 2 m/sec (slow or second pain)

Substantia gelatinosa- facilitation and inhibition occur within the dorsal horn of spinal cord and V nucleus. The dorsal horn can be divided into 6 laminae of which II and III constitute substantia gelatinosa

This modulation (either facilitation or inhibition) that occurs in SG influences the T cell, T cell stimulation further activates the action system

Action system:

Cortical and subcortical areas

Limbic system

Thalamus and Hypothalamus

Reticular activating system

Sensory discriminative system:

Under ordinary conditions, a noxious stimulus can quickly be localized in time and place.

Somato sensory pathways ascending in dorsal and dorsolateral columns of spinal cord transmit this information rapidly.

Dorsal column nucleus cells are clustered together and are physically adjacent to the neurons that receive input from contiguous areas of the body

Thus help in identification of pain duration and its exact location.

Motivational affective system:

Paleospinothalamic system consists of fibers of ventrolateral system that synapse in the reticular formation of brain stem

Brain stem acts as relay station for nociceptive impulses

This reticular formation regulates vasomotor and autonomous functions.

This system provide neural pathways for aversive motivational component of pain i.e. the suffering aspects associated with painful experiences

Activation of Motor Mechanism Startle response

Flexion reflex

Postural readjustment

Vocalization

Orientation of head and eyes towards damaged area etc.,

Descending Control:

This is an active inhibitory system

Present within the pons and medulla projects into dorsal horn

There is another system descends directly from periaqueductal grey matter of mid brain to the SG

Stimulation of this area produces profound analgesia

Gate control system

Central control processes

Motivational affective system

(central intensity monitor)

Sensory discriminative system

(spatio-temporal analysis)

Motor mechanism

DUAL NATURE OF PAIN

Pain perception: physioanatomical process, impulse is generated, following application of an adequate stimulus, and is transmitted to CNS

This aspect is remarkably similar in all healthy individuals and varies little from day to day

Pain reaction: psychophysiological process that represents incividual’s overt manifestation of the unpleasant perceptual process that just occurred

This aspect of pain combines extremely complex neuroanatomical and psychological factors involving cortex, limbic system, hypothalamus and thalamus

Unlike the pain perception pain reaction varies markedly from one individual to another and from day to day in the same individual

The pain reaction treshold is commonly interpreted as inversely proportional to pain reaction

Basics Of Pain Transmission

Nociceptors

Brain stem Spinal cord

Cranial nerve

Spinal nerve

AA

Thalamus

Cortex

B B

C

A - 1st order neuronB - 2nd orderC - 3rd order.

PAIN PATHWAY

Dual pathways for transmission of pain signals into the CNS:

The two pathways mainly corresponds to the two types of pain

Fast-sharp pain pathway Slow-chronic pain pathway

In the cord and brain stem On entering the spinal cord, the pain signals take two

pathways to the brain1. Neospinothalamic tract2. Paleospinothalamic tract

Neopspinothalamic pathway

Transmits acute pain 1st order neurons - A δ fibers terminate in Lamina

marginalis 2nd order neurons arise, these cross immediately to the

opposite side of the cord through the anterior commissure then pass upwards in the antero-lateral columns to the brain stem.

Localization of pain is seen. Neurotransmitter substance involved is Glutamate. Few fibers terminate in the reticular areas Most terminate in the ventrobasal complex in thalamus.  From these areas impulses are transmitted to

Somatosensory cortex in the form of 3rd order neurons.

Paleospinothalamic Pathway

Transmits the Slow, chronic pain (via C fibers).

1st order neurons terminate in the Substantia Gelatinosa Rolando (SGR).

Neurotransmitter substance is Substance P.

For ex. After pin prick, immediate pain is due to glutamate & continuing pain is due to substance P.

Fibers terminate in the Reticular nuclei of medulla, and few in intralaminar & ventrolaminar nuclei of thalamus.

Pain suppression(analgesia) System in Brain and Spinal cord

Analgesia system three main components: The periaqueductal grey and periventricular areas of

mesencephalon and upper pons Aqueduct of sylvius and portions of III and IV

ventricles Raphe magnus, a midline nucleus in lower pons and

upper medulla, Nucleus reticularis paragigantocellularis, located

laterally in medulla

Pain inhibitory complex located in the dorsal horns of spinal cord

At this point, the analgesia signals can block the pain before it is relayed to the brain

Transmitters involved in analgesia system: enkephalin and serotonin

REFERRED PAIN

Referred pain is a spontaneous heterotropic pain that is felt in an area innervated by a different nerve from the one that mediates the primary pain.

DERMATOMAL RULE When pain is referred it is usually to a structure that developed from the same embryonic segment or dermatome as the structure in which the pain originates.

ROLE OF CONVERGENCE

There is presumably a considerable degree of convergence of peripheral sensory fibers on the spinothalamic neurons. Somatic and visceral afferents converge in the same spinothalamic neuron.

ORO FACIAL PAINAnatomic considerations: Nociceptive transmission associated with

trigeminal nerve:

Pain transmission is carried in 3 divisions of trigeminal nerve to the trigeminal sensory ganglion

Central processes of these neurons enter the pons, where they descend in the brain stem as the spinal trigeminal tract (STT)

Fibers from the STT synapse in the adjacent trigeminal nucleus

Spinal nucleus of CN V extends from chief sensory nucleus of V to spinal cord

It is divided into 3 nuclei, the most caudal, nucleus caudalis is considered as principal site in the brain stem for nociceptive information

Axons from the spinal nucleus of CN V cross to opposite side and ascend to the ventral posteromedial nucleus of thalamus

From the thalamus, neurons course and end at the somatosensory cortex.

TRIGEMINAL PATHWAY

Types of orofacial pain:

Acute pain

Chronic pain

Acute pain: Provoked by specific disease or injury Serves a useful biologic purpose Associated with skeletal muscle spasm and

sympathetic nervous system activation Self-limited Therapy is aimed at treating the underlying cause

Chronic pain:

It may be considered as diseased state

Pain that outlasts the normal time of healing, if associated with a disease or injury

May arise from psychological stress, serves no biological purpose and has no recognizable end-point

Must rely on a multidisciplinary approach

Inflammatory Pain:

Tissue injury initiates an inflammatory reaction that characteristically induces pain

Cheifly due to action of prostaglandin and bradykinin Increases local vasodilation and capillary permeability

of the receptors in the area Prostaglandin like substances released in the CNS that

sensitized nociceptive interneurons May involve different kinds of tissue with different

reactive responses

Non Inflammatory Pain:

Originate from somatic or neurogenous structures

TYPES OF PAIN

Somatic Pain

Superficial somatic painCutaneous painMucogingival pain.

Deep somatic painMusculoskeletal pain

Muscle pain Protective co contraction. Delayed onset muscle soreness Myofascial pain Myospasm Myositis

TMJ pain Ligamentous pain Retrodiscal pain. Capsular pain. Arthritic pain

Neuropathic Pain Trigeminal neuralgia Glossopharyngeal neuralgia Geniculate neuralgia Superior laryngeal neuralgia Nervus intermeduis Occipital neuralgias

Classification by American board of orofacial pain:

Masticatory musculoskeletal pain Cervical musculoskeletal pain Neurovascular pain Neuropathic pain Sleep disorders related to orofacial pain Orofacial Dystonias Intraoral, intracranial, extracranial, and systemic

disorders that cause orofacial pain  

MEASUREMENT OF PAIN AND DISABILITY Visual analog scale (VAS) Numerical scales Descriptive rating scales McGill pain questionnaire(MPQ) Turk and Rudy- multi axial assessment of pain (MAP) Dworkin, LeResche, and colleagues –

The grade chronic pain severity scaleSCL- 90-R(symptom checklist 90 revised) depression scalesJaw disability check list

MANAGEMENT OF PAIN

Examination and assessment

History

Physical examination

Behavior assessment

Behavioral assessment

Questionnaires: e.g. Minnesota multiphasic personality invertory (MMPI) Beck depression inventory Zung self-rating depression scale Personality diagnostic questionnaire General health questionnaire

Instruments: The TMJ scale IMPATH: it is an microcomputer assessment RDC (research diagnostic criteria)

Diagnostic imaging

Diagnostic nerve blocks

Laboratory tests

Orofacial pain disorders that may beconfused with toothache:

Trigeminal neuralgia

Trigeminal neuropathy (due to trauma or tumor invasion)

Atypical facial pain and atypical odontalgia

Cluster head ache

Acute and chronic maxillary sinusitis

Myofacial pain of masticatory muscles

Systemic diseases associated with headache and orofacial pain

Paget’s disease

Metastatic disease

Hyperthyroidism and hyperparathyroidism

Multiple myeloma

Vitamin B deficiencies

Systemic Lupus Erythematosis

Vincristine therapy for cancer

Folic acid and iron deficiency anemia

TREATMENTMethods of pain control:

Removing the cause

Blocking of pathway of pain impulses

Raising the pain threshold

Preventing pain reaction by cortical depression

Psychosomatic methods

Treatment of chronic pain:

Cognitive therapy

Relaxation therapy

Drug therapy

Physical Therapy

Drug therapyNon opioid analgesics: NSAIDS and acetaminophenNon selective cox inhibitors

Preferential cox2 inhibitors:

Nimisulide

Meloxicam

Selective cox2 inhibitors:

Celecoxib

Etoricoxib

Rofecoxib

Opioids:

Naturally occurring- codeine, morphine

Semi synthetic: heroin, di hydro codeine

Synthetic: pethidine, methadone, pentazocaine, fentanyl

Adjuvant drugs:

Anticonvulsants like carbamazepine Antidepressants like amitriptyline Antihistaminics Caffeine Topical medications like capsaicin Antianxiety drugs like diazepam Muscle relaxants for myogenous pain Α adrenergic blockers like ergotamine for

neurovascular pain like migraine

Physical Therapy:

Sensory stimulation i) Cutaneous

ii) Transcutaneous

iii)Percutaneous

Ultrasound

Electro-galvanic stimulation

Deep heat

Trans cutaneous nerve stimulation

Ultra sound therapy

Management of pain in periodontitis:

Periodontitis is a chronic inflammatory disease causing attachment loss and periodontal pocket formation, in general progression rate is slow, unless an acute event such as a periodontal abscess occurs.

Often occurs in case of untreated periodontitis and also may be found during maintenance after scaling and root planing of deep pockets

Chronic abscess may be of no pain or dull pain

Acute abscess is of mild to severe discomfort and tenderness to percussion or biting

(TFO also causes severe tenderness to percussion)

Treatment

It is through drainage of abscess with sufficient topical and local anesthetic to ensure comfort

Appropriate antibiotics

Analgesic

For chronic abscess, scaling and root planing or surgical therapy

Management of postoperative pain

Only minor pain and discomfort, overextended packs should be avoided

For healthy persons, postoperative dose ibuprofen 600-800 mg every 8 hours for 1-2 days

Ibuprofen can also be used in cases of acute gingival infections like acute herpetic gingiva stomatitis, necrotizing ulcerative gingivitis and periodontitis, acute pericoronitis

DIAGNOSIS AND MANAGEMENT OF

SOME SPECIFIC OROFACIAL PAIN DISORDERS:

Trigeminal neuralgia

Clinical features : intense shooting stabbing pain that last for a few seconds and then completely disappears

Unilateral

Middle age

Maxillary branch is most commonly affected

Trigger zone - nasolabial fold, corner of the lip

Treatment

Medical management Carbamazepine 100 mg BD, increase dose of 100

mg every 48 hrs. Slowly withdraw at a rate of 100 mg every 48 hrs. Baclofen and clonazepam can also be used

Surgery Micro vascular decompression surgery Percutaneous Rhizotomy Peripheral trigeminal nerve blocks

Glossopharyngeal Neuralgia: Neuralgia of ninth cranial nerve Is rare Average age is 50 yrs. Pain may be felt in the ear ,infra-auricular

area ,tonsil ,base of the tongue, posterior mandible or lateral wall of the pharynx

Talking ,chewing ,swallowing ,yawning or touching a blunt instrument to the tonsil

Treatment: Topical anesthetic agent Rest end nutrition Carbamazepine ,Oxcarbazepine ,Beclofen Resection of the Glossopharyngeal nerve

Nervous Intermedius (Geniculate) Neuralgia:

Uncommon neuralgia of VII cranial nerve.

Pain in ear & less frequently in the anterior tongue & soft palate.

Trigger zone within ipsilateral distribution of nerve.

Pain not as sharp & intense as TN.

Some degree of facial paralysis.

Ramsay Hunt Syndrome.

Short course of high dose steroid therapy, acyclovir & carbamazepine for treatment.Non-responsive cases : surgery

Post herpetic Neuralgia:

Usually pain of HZ resolve within a month, if it persists longer then is classified as Post Herpetic Neuralgia (PHN).

Some authors classify after 3-6 months of persistent pain.

Diagnostic Criterion:History of HZ infection

Topical therapy: Local anesthetic such as Lidocaine. Capsaicin.

Systemic therapy: Antidepressants such as Amitriptyline, Nortriptylin,

Doxepin & Dexiprimine. Anticonvulsant viz. Phenytoin & Carbamazepine. Gabapentin {fewer side effects}. If medical therapy ineffective then then nerve blocks or

surgery at the level of peripheral nerve or dorsal root

Vascular head ache (migraine) Triggered by foods:

Nuts, chocolate, red wine, stress, sleeps deprivation, hunger

Most common in women

Several major types: Classic Common Basilar Facial ( Carotidynia )

Treatment: Avoid food triggers

Relaxation techniques for stress

Drug therapy:

Ergotamine and sumatriptin

Propranolol, verapamil, Tri cyclic anti depressents (TCA)

Methysergide and phenelzine for difficult cases

CONCLUSION

PAIN IS A COMPLEX PHENOMENON IN WHICH DIAGNOSIS NOT ONLY BASED ON ITS ETHIO-PATHOLOGY BUT ALSO ON THE COGNITIVE

EVALUATION OF THE PATIENT AND ALWAYS A MULTI DISCIPLINARY APPROACH IS NEEDED FOR ITS

MANAGEMENT

REFERENCES: Text book of medical physiology : Guyton and Hall Review of medical physiology: William F Ganong Concise medical physiology: Sujit K Chaudhuri Monheim’s local anesthesia and pain control in

dental practice Burket’s oral medicine diagnosis and treatment Bell’s Orofacial Pain. Jeffery P Okeson Carranza’s clinical periodontology Human physiology : A K Jain Essentials of medical pharmacology: K D Tripathi

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