7/22/12

Pain physiology and management

Click to edit Master subtitle style Presented by Manasa.A

7/22/12

contents
Pain

introduction and definition Organization of nervous system The receptors of sensory nerves

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)

7/22/12

7/22/12

History14-15 century-Leonardo Da Vinci- brain central organspinal cord tranmits sensations 17-18 centuries Rene Descartes- a french philosopherdescribed 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

7/22/12

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)

7/22/12

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 (Monheims 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 )

7/22/12

nervous system Central nervous system: Brain and spinal cord Peripheral nervous system: Somatic nervous system Autonomic nervous system

7/22/12

7/22/12

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

7/22/12

Nerve cell (neuron): structural and functional unit.

7/22/12

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

7/22/12

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

7/22/12

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.

AXON (Nerve fiber)

7/22/12

Arises from axon hillock, no Nissl granules, containing axoplasm in the centre and enveloped by axolemma. Length varies few 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 CELLS TYPES

7/22/12

MICROGLIA:

Phagocytic role in CNS

MACROGLIA:

Astrocytes Ependymal and Choroidal cells Oligodendrocytes Satellite cells Bergmann Glia Of Cerebellum Schwann cells

CLASSIFICATION OF NEURON:

7/22/12

BASED ON MORPHOLOGY -Unipolar -Bipolar -Multipolar

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

Classification of nerve fibers: ERLANGER AND GASSER CLASSIFICATION:

7/22/12

RECEPTORS OF SENSORY NERVES:

7/22/12

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 receptor

a. Merkels Corpuscles b. Meissners Corpuscles c. Ruffinis Corpuscle d. Pacinian Corpuscle e.Free nerve endings

7/22/12

Proprioceptors

Muscle spindles Golgi tendon organs Pacinian corpusles Periodontal mechanoreceptors Free nerve endings

Interoceptors

Pacinian Corpuscles Free nerve endings

Synapse:

7/22/12

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

7/22/12

Based on mode of action: RAPID ACTING NEUROTRANSMITTERS: Acetylcholine Norepinephrine Glutamate Aspartate Serotonin GABA Glycine Dopamine

7/22/12

SLOW ACTING NEUROTRANSMITTERS:

Substance P Endorphin Bradykinin

REFLEXES

7/22/12

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)

7/22/12

A group of nerve fibers travelling in the CNS is called tract or pathway Ascending (sensory) tracts Descending (motor) tracts

Sensation

7/22/12

General special

General classified into somatic and visceral

Somatic touch, pressure, warm, cold, pain Visceral- pain

Special- Vision Touch Smell

7/22/12

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

7/22/12

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

7/22/12

Resting state:

Potassium ions are concentrated inside Sodium and chloride ions are outside the cell membrane The difference respective ion concentrationspotential electrical difference. The electrochemical gradient across the membrane is -70 to -90 mv said to be resting potential.

Depolarization:

7/22/12

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 .

7/22/12

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

7/22/12

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.

7/22/12

7/22/12

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

7/22/12

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,

7/22/12

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.

7/22/12

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

7/22/12

Peripheral nerves- A - 3-20 - diameter 100m/sec (fast or first pain) C- .05-1- 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

7/22/12

7/22/12

Action system:

Cortical and subcortical areas Limbic system Thalamus and Hypothalamus Reticular activating system

7/22/12

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

7/22/12

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

7/22/12

Activation of Motor Mechanism

Startle response Flexion reflex Postural readjustment Vocalization Orientation of head and eyes towards damaged area etc.,

7/22/12

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

7/22/12

Central control processes

Gate control system

Motivational affective system (central intensity monitor) Sensory discriminative system (spatio-temporal analysis)

Motor mechani sm

7/22/12

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

7/22/12

Pain reaction: psychophysiological process that represents incividuals 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

7/22/12

Basics Of Pain Transmission Nocicepto rs A Brain stem B Thalamus C Cortex

Cranial nerve

Spinal nerve A B Spinal cord

A - 1st order neuron B - 2nd order C - 3rd order.

7/22/12

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 brain Neospinothalamic tract

1.

7/22/12

Neopspinothalamic pathway

Transmits acute pain 1st order neurons - A 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.

7/22/12

7/22/12

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,

7/22/12

7/22/12

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

7/22/12

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

7/22/12

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.

7/22/12

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 pain

Anatomic considerations:

7/22/12

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

7/22/12

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

7/22/12

Trigeminal pathway

7/22/12

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

7/22/12

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

7/22/12

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

7/22/12

Types of pain
Somatic Pain

Superficial somatic pain

Cutaneous pain Mucogingival pain.

Deep

somatic pain

Musculoskeletal pain

7/22/12

Muscle pain

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

TMJ pain

Ligamentous pain Retrodiscal pain. Capsular pain. Arthritic pain

7/22/12

Neuropathic Pain

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

7/22/12

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 scale (VAS) Visual analog

7/22/12

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 scale

SCL- 90-R(symptom checklist 90 revised) depression scales Jaw disability check list

7/22/12

Management of pain
Examination and assessment

7/22/12

History

Physical examination

Behavior assessment

7/22/12

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

7/22/12

Diagnostic imaging

Diagnostic nerve blocks

Laboratory tests

7/22/12

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

Systemic diseases associated with headache and orofacial pain

7/22/12

Pagets disease Metastatic disease Hyperthyroidism and hyperparathyroidism Multiple myeloma Vitamin B deficiencies

7/22/12

treatment
Methods of pain control:

Removing the cause Blocking of pathway of pain impulses Raising the pain threshold Preventing pain reaction by cortical depression

7/22/12

Treatment of chronic pain:

Cognitive therapy Relaxation therapy Drug therapy Physical Therapy

7/22/12

Drug therapy
Non opioid analgesics: NSAIDS and acetaminophen Non selective cox inhibitors

7/22/12

Preferential cox2 inhibitors:

Nimisulide Meloxicam

Selective cox2 inhibitors:

Celecoxib Etoricoxib

7/22/12

Opioids:

Naturally occurring- codeine, morphine Semi synthetic: heroin, di hydro codeine Synthetic: pethidine, methadone, pentazocaine, fentanyl

7/22/12

Adjuvant drugs:

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

7/22/12

Physical Therapy:

Sensory stimulation i) Cutaneous ii) Transcutaneous iii)Percutaneous

Ultrasound Electro-galvanic stimulation

7/22/12

Trans cutaneous nerve stimulation

Ultra sound therapy

7/22/12

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

7/22/12

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

7/22/12

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

7/22/12

DIAGNOSIS AND MANAGEMENT OF SOME SPECIFIC OROFACIAL PAIN DISORDERS:

7/22/12

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

7/22/12

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

7/22/12

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 Topical anesthetic agent Rest end nutrition

Treatment:

7/22/12

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.

7/22/12

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

7/22/12

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}.

7/22/12

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

7/22/12

Treatment:

Avoid food triggers Relaxation techniques for stress

Drug therapy:

Ergotamine and sumatriptin Propranolol, verapamil, Tri cyclic anti depressents (TCA)

7/22/12

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

7/22/12

REFERENCES:
q

Text book of medical physiology : Guyton and Hall Review of medical physiology: William F Ganong Concise medical physiology: Sujit K Chaudhuri Monheims local anesthesia and pain control in dental practice Burkets oral medicine diagnosis and treatment Bells Orofacial Pain. Jeffery P Okeson Carranzas clinical periodontology Human physiology : A K Jain Essentials of medical pharmacology: K D Tripathi

q q q

q q q q q

7/22/12

THANK YOU