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Pain Pathways Perhaps the capacity of the human brain falls short of the ability to understand its own complexity INTRODUCTION •

Pain is an unpleasant experience that perhaps motivates the individual far greater than any other life experience.

It seriously impairs the lives of millions of people around the world.

In 1984, Bonica reported that nearly 1/3rd of the population in industrialized nations suffer to some extent from chronic pain.

This results in loss of billions annually in health care services, loss of work, decreased productivity and disability compensation

The clinical management of pain is the primary concern of health professionals around the world

Clinical pain differs from surgical pain. The cause of surgical pain is obvious, and its management consists of either suppressing the passage of nociceptive impulses or making the patient insensible to them. The solution lies in the grasp of the clinician Clinical pain is not so easily identified; sometimes the initiating cause may no longer be present. These mechanism involved is not well understood which are different from those of surgical pain. As a clinical symptom, pain is an experience that cannot be shared. It is wholly personal, belonging to the sufferer alone. The ability to diagnose the disease and treat a person afflicted with pain rests largely on the knowledge of the mechanisms and behavioral characteristics of pain in its various manifestations.


Homer à pain was due to arrows shot by the gods

Aristotle à a “passion of the soul” that somehow resulted from intensification of other sensory experience

Platoà pain and pleasure arose from within the body i.e. pain is an emotional experience more than a localized body disturbance

Bibleà anguish of the soul

Freudà symptoms such as pain could develop as a solution to emotional conflicts


By the subcommittee on taxonomy of the international association for the study of pain “An unpleasant sensory or emotional experience associated with actual or potential tissue damage, described in terms of such damage” Or

Pain can also be defined as 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 DIMENSIONS OF PAIN •

Sensory nature à quality, intensity, location & duration

Cognitiveà subject’s ability to comprehend and evaluate the significance of the experience

Emotional à feelings that are generated

Motivationalà drive to terminate it

EMERGENCY NATURE OF THE PAIN Relates to the significance the patient attaches to it. If the cause is obvious, such as a cut finger, little or no alarm ensues because the subject is able to recognize the cause of his suffering and evaluate it realistically. If, however, the pain is located in an area of greater

significance or if discomfort arises from deeper structures where its cause is less obvious and its seriousness less certain, the pt becomes more concerned. the emergency. The emergency nature of pain relates more to the fear it generates than to the actual intensity of the discomfort LEVEL OF PAIN PROCESSING Nociception refers to the noxious stimulus originating from the sensory preceptor. This info is carried into the CNS by the primary afferent neuron Pain is an unpleasant sensation perceived in the cortex usually as a result of incoming nociceptive input Suffering refers to how the human reacts to the perception of pain Pain behavior refers to the individual’s audible and visible actions that communicate his or her suffering to others PHYLOGENIC CONSIDERATIONS Human brain can be functionally divided into three components. 1) Basic reptilian brain, i. spinal cord and medulla ii. functions on a primitive level iii. protective







environment 2) Mammalian brain i. limbic structures wrapped around medulla and spinal cord ii. provides individual with instinctive drives and emotions iii. they represent the basic needs of the individual : hunger, thirst, sleep, sexual activity iv. pain and pleasure center v. when pain is felt individual will instinctively direct behavior towards activities that will reduce pain and when possible stimulate the pleasure side of this center

3) Complex portion i. consists of cortex ii. provides human with the ability to think and reason iii. at this level when subject experiences pain begins to apply meaning and consequence to the sensation It is important for the clinician to recognize that the info related to the therapist is not nociception nor pain nor suffering. The pt relates only his or her pain behavior


The human being is a phenomenal organism with the complexity far beyond the imagination of the best scientific minds

Because of its complexity, a master control system known as the nervous system …coordinate all the activities.

In order to manage the patients pain problem understanding the normal function of the nervous system is necessary

COMPONENTS OF THE NERVOUS SYSTEM NEURAL PATHWAYS OF PAIN Fields has described that the subjective experience of pain arises by four distinct processes 1. Transduction 2. Transmission 3. Modulation 4. Perception Transduction: is the process by which the noxious stimuli lead to electrical activity in appropriate sensory nerve endings Transmission: refers to the neural events that carry the nociceptive input into the CNS for proper processing Components:

1. primary afferent neuron carries nociceptive input from sensory organ into the spinal cord 2. second order neuron which carries the input to higher centers 3. interaction of neurons between thalamus, cortex and limbic system as the nociceptive input reaches those higher centers Modulation: refers to the ability of the CNS to control pain transmitting neurons Perception: occurs if nociceptive input reaches the cortex. It initiates a complex interaction of neurons between the higher centers of the brain, it is at this point that suffering and pain behavior begins

THE NEURAL ANATOMY OF PAIN A nerve is a cord like structure that has the ability to convey electrical and chemical impulses. Consists of CT sheath à epineurium Each bundle à by perineurium Each nerve fiber in the bundle is separated à endoneurium Fibers with myelin sheath form the white nerve and those without form gray nerves. Myelination increases the conduction of the nerve fiber. STRUCTURAL UNIT OF NERVOUS SYSTEM NEURON: Composed of a mass of protoplasm called nerve cell body (perikaryon), which gives off a number of processes called dendrites and axons. Contains a spherical nucleus. Cell bodies outside the CNS are grouped together in ganglia Nucleus is a gross structure of the CNS used to designate a group of nerve cells that bear direct relationship to the fibers of a particular nerve Depending on the no of axons present the neuron may be unipolar, bipolar, multipolar Peripheral neurons are unipolar.

Depending on their functions and location They can be classified as: i. Afferent neuron: conducts nerve impulse towards the CNS ii. Efferent neuron: conducts nerve impulse peripherally iii. Internucial or Interneurons lie wholly within the CNS Types of sensory neurons i. First order ii. Second order iii. Third order Preganglionic neuron: is an autonomic efferent neuron whose cell body is located in the CNS and terminates in an autonomic ganglion Post ganglionic neuron: has its nerve cell body in the autonomic ganglion and terminates peripherally RECEPTORS Sensory receptors àhighly specialized àrespond to environmental changes àaction potentials for transmission to the CNS. Transduction Specific receptors àspecific stimuli. Pain receptors respond specifically to pain. The term ‘nociceptor’ is used to describe a nerve ending that responds to stimuli that actually or potentially produce tissue damage TYPES A) Exteroceptors B) Proprioceptors C) Interoceptors EXTEROCEPTORS: are sensory receptors that are stimulated by the immediate external environment

1. Merkel’s receptor: tactile receptors in the submucosa of the tongue and oral mucosa 2. Meissner’s corpuscles: tactile receptors in skin 3. Ruffini’s corpuscles: pressure and warmth receptors 4. Krause’s corpuscles or end-bulbs: cold receptors 5. Free Nerve Endings: perceive superficial pain and touch PROPRIOCEPTORS: •

provide info from the musculoskeletal structures

The presence, position, and movement of the body. Responsible for automatic functioning below the level of consciousness.

Types: 1. Muscles spindlesà mechanoreceptors àrespond to passive stretchà myotactic reflex 2. Golgi tendon organs à mechanoreceptors àsignal muscle tension in both contraction and stretching à inverse stretch reflex. 3. Pacinian corpuscles : perception of pressure 4. Periodontal mechanoreceptors : biochemical stimuli 5. Free nerve endings: perceive deep somatic pain and other sensations INTEROCEPTORS: Located in and transmit impulses from the viscera of the body 1. Pacinian corpuscles: perception of pressure 2. Free nerve endings: perceive visceral pain and other sensations IMPULSE INITIATION IN SENSORY RECEPTORS Impulse Initiation The voltage across the membrane is approximately -70mV (-40 to -90mV)

The negative sign indicates that the inside of the membrane is –vely charged w.r.t to the outer. This is called resting membrane potential and the membrane is said to be polarized. The cell cytoplasm contains less concentration of Na and a higher concentration of K in the ECF. The membrane at rest is slightly permeable to Na but 75% more permeable to K. hence the K ions can easily diffuse out of the cell across the concentration gradient. The net result is that a slightly greater no of + ions diffuse out than in, leaving the cell interior with a slight excess negative charge. Action potentials The principal way the neurons communicate is by generation and propagating action potentials. An action potential is a brief reversal of membrane potential with total amplitude of about 100mV (from -70 to +30mV). The whole event just takes a few milliseconds. When a neuron is adequately stimulated a nerves impulse is transmitted. This results in opening of voltage gated channels which leads to changes in permeability of neurons membrane. 1. Resting state: all the channels are closed 2. Depolarizing phase: increase in Na permeability and reversal of membrane potential. When depolarization of the membrane reaches a certain critical level called “threshold� (-55 to -50mV), depolarization becomes self generating. At this point the Na permeability is about 1000 times greater than it is in the resting neuron. The cell membrane becomes more and more +ly charged and overshoots about +30mV, this rapid depolarization and polarity reversal produces a sharp upward rising spike of the action potential. 3. Depolarizing phase: decrease in Na permeability. The +ve intra cellular charge resists further Na entry, in addition inactivation of the Na channels influx of Na declines and finally stops. 4. Repolarizing phase: increase in K permeability. As Na entry declines voltage gated K channels open and K rushes out of the cell. Then the membrane potential moves towards the resting potential

5. Undershoot: K permeability continues. The K gates are sluggish and slow to respond to depolarization, the period of increased K permeability lasts longer than necessary to restore the polarized state. As a result of excessive K efflux, an after hyperpolarization called undershoot may be seen Although repolarization restores the resting electrical conditions, it does not restore the original ionic distribution of the resting state. This is accomplished by revving up the NA-K pump. PROPAGATION OF ACTION POTENTIAL After depolarization of a patch of cell membrane, the + ions in the axoplasm move laterally from the area of polarity reversal to the area where it is still negative, and those in the ECF migrate back to the area of greatest –ve charge to complete the circuit. This establishes local current flows that depolarize adjacent membrane areas in the forward direction, which opens voltage gated channels and triggers an action potential there. Because the area in the opposite direction has just generated an action potential, the Na gates are closed and no new action potential is generated there. In a myelinated nerve the action potential is propagated by a process called saltatory conduction All or none phenomenon The action potential either happens completely or it doesn’t happen at all. Coding for stimulus intensity Once generated all action potentials are independent of the stimulus strength, and all action potentials are alike. How does the CNS determine which stimulus is intense or weak? Strong stimuli cause nerve impulses to be generated more often in a given interval of time than do weak stimuli. Thus stimulus intensity is coded for by the no of impulses generated per sec- i.e. by frequency of impulse transmission

Absolute or Relative refractory period When a patch of neuron membrane is generating an action potential and it’s Na voltage gates are open, the neuron is incapable of responding to another stimulus no matter how strong it may be à Absolute refractory period Relative refractory period àis the interval following the absolute refractory period when the Na gates are closed, and the K gates are open, and repolarization is occurring. During this time the axons threshold for impulse generation is substantially elevated. A threshold stimulus is unable to trigger an action potential, but an exceptionally strong stimulus can reopen the Na gates and allow another impulse to be generated. SYNAPSE OR SYNAPTIC JUNCTION •

It is a unique junction that mediates the transfer of info from one neuron to the next, or neuron to an effector cell

Types 1. Electrical 2. Chemical

Electrical synapses 1. Contain protein channels that interconnect the cytoplasm of adjacent neurons, and allow the current carrying ions to flow directly from one neuron to the next. 2. Neurons joined in this way are said to be electrically coupled. 3. Transmission across these synapses is very rapid. 4. Communication may be unidirectional or bidirectional 5. In adults it is found in area where stereotyped movements such as jerky movements of the eye 6. More abundant in embryonic tissue. Chemical synapses 1. Because the synaptic cleft is filled with fluid and current from the presynaptic cleft dissipates in this fluid, chemical synapses effectively prevent a nerve impulse from being directly transmitted from one neuron to another.

2. Chemical synapses convert electrical impulses into chemical signal where they travel across the synapse to the post synaptic cells and are reconverted back into electrical signals. 3. Only unidirectional communication is possible. Procedure 1. Ca gates open in the presynaptic axonal terminal when a nerve impulse reaches them 2. Neurotransmitter is released by Exocytosis: Ca acts as an intracellular messenger, directing the release of the neurotransmitter substance. The Ca is then removed by the mitochondria or ejected to the outside by CA membrane pumps 3. neurotransmitter binds reversibly to the post synaptic receptors 4. ion channels open in the post synaptic membrane when the receptor proteins bind with the neurotransmitter. The resulting current flow produces changes in the membrane potential. NEUROTRANSMITTERS The neurochemicals that transmit impulses across the synaptic cleft are called neurotransmitters. Types 1. rapid acting (small molecule) neurotransmitters 2. cause the most acute responses of the nervous system 3. transmit sensory signals to and inside the brain and motor signals back to the muscles 4. slow acting (large molecule) neurotransmitter 5. they are neuropeptides 6. are manufactured not in the presynaptic vesicle but by the ribosomes of the neuronal body 7. longer acting

RAPID ACTING TRANSMITTERS Acetylcholine 1. most common neurotransmitter 2. secreted by neurons in the brain, those innervating the skeletal muscle, preganglionic neurons of ANS , pre and postganglionic neuros of parasymapathetic and sympathetic nervous system 3. has an excitatory effect on post synaptic neuron Norepinephrine 1. secreted by neurons whose cell bodies are located in the brain stem and hypothalamus 2. excitatory neurotransmitter Serotonin 1. secreted by nuclei located in the median raphe of the brain stem 2. peripherally àalgonenic agent related to vascular pain syndromes 3. in CNS àinvolved in endogenous nociceptive mechanisms thought to potentiate endogenous endorphin analgesia Others Glutamate and Aspartate àexcitation Gamma amino butyric acid, glycine , dopamine àinhibitory SLOW ACTING NEUROTRANSMITTERS Substance P 1. polypeptide composed of 11 amino acids 2. released at the central terminals of primary nociceptive neurons and act as transport substances 3. Act as a transport system 4. Centrally it act as an excitatory neurotransmitter for nociceptive impulse 5. Its modulating action on pain is both rapid and short-lived 6.

Its concentration is highest in the most

severely inflamed joints.

Endorphins a. Are polypeptides, behave like morphine b. They are displaced from their receptors by morphine antagonist Naloxone. c. Bind to morphine receptors to obtund pain. d. Important contributors to pain threshold & pain tolerance. Bradykinin 1. is an endogenous poly peptide that consists of a chain of 9 amino acids 2. released as a part of inflammatory reaction 3. powerful vasodilator 4. it requires the presence of prostaglandins to act 5. released during ischemic episodes ELIMINATION OF NEUROTRANSMITTER FROM THE SYNAPSE Once the neurotransmitter has been released there has must be a mechanism to remove it. It this does not occur the transmitter effect on the postsynaptic neuron is prolonged Elimination occurs by three ways 1. Diffusion à the released neurotransmitter will merely diffuse out of the synaptic cleft 2. Enzymatic destruction à some neurotransmitters are immediately destroyed by enzymes present in the synaptic cleft 3. Neurotransmitter reuptake à some neurotransmitters are actively transported back into the presynaptic terminal itself for reuse. NEUROCHEMISTRY OF NOCICEPTION The peripheral nociceptor can be activated by thermal, mechanical and chemical stimulation Once the thermal or mechanical stimulation has terminated, the reason for continued nociceptive input is likely to be chemical. There are three sources for maintaining nociceptive input

a. damaged cells à release of K, histamine, serotonin, ATP, acetylcholine etcà activate or sensitize nociceptors b. secondary to plasma extravasation and lymphocytic migration c. nociceptor itselfà release of substance P NEURONAL SENSITIZATION When the excitatory neurotransmitters are released in the synaptic cleft, the post synaptic neuron is excited and an impulse is started and carried down the axon. If the excitatory neurochemicals remain in the region of the synapse, the neuron can be depolarized quicker with the next release of neurotransmitter. This process is called sensitization. This could be the cause for hyperalgesic state in inflammatory tissues. AXON TRANSPORT SYSTEM The axon transport system can move neurotransmitters in the primary efferent neurons both centrally (orthodromically) as well as peripherally (antidromically)àrelease of neurotransmittersàsensitization of other neurons in the adjacent area à neurogenic inflammation FIRST ORDER NEURON Each sensory receptor is attached to a first order or primary afferent neuron that carries the impulses to the CNS i.e. dorsal horn of the spinal cord or to the relay nuclei of the medulla Type A fibers 1. Alpha fibers: size 13-20μm in diameter; velocity, 70 -120 m/s 2. Beta fibers: size 6-13μm in diameter; velocity, 40 -70 m/s 3. Gamma fibers: size 3-8μm in diameter; velocity, 15 -40 m/s 4. Delta fibers: size 1-5μm in diameter; velocity, 5 -15 m/s Type C fibers: size 0.5-1μm in diameter; velocity, 0.5-2 m/s


It has both gray and white matter.

The gray matter is located in the center and looks like the letter ‘H’. Projections of the gray matter are –

Dorsal horns àhouse the cell bodies somatic sensory neurons

Ventral hornsà house the cell bodies somatic motor neurons

Lateral horns àhouse autonomic motor neurons that serve the visceral organs

the white matter consists of nerve tracts –

Ascending à sensory

Descending à motor

Transverse à commissural run from one side of the cord to the other

SECOND ORDER NEURON The second order (transmission) neurons carry impulses from the dorsal horn of the spinal cord or in the relay nuclei of the medulla into the higher centers and synapses with the third order neurons in the Thalamus. Types 1. Low threshold mechanosensitive neurons: transfer light touch, proprioception and pressure 2. Nociceptive specific neurons: carry impulses related to noxious stimulation 3. Wide dynamic range neuron: responds to a wide range of stimulus intensities from non-noxious to noxious THIRD ORDER NEURON Have their cell bodies in the sensory relay nuclei of the Thalamus and carry impulses to the primary somatosensory cortex HIGHER CENTERS Impulses are carried to the higher centers for interpretation and evaluation.

Subdivided into four regions 1. Brain stem a. Medulla oblongata b. Pons c. Midbrain (mesencephalon) 2. Cerebellum 3. Diencephalons a. Thalamus b. Hypothalamus 4. Cerebrum a. Cerebral cortex b. Basal ganglia c. Limbic system BRAIN STEM MEDULLA OBLONGATA Larger extension of the spinal cord located just above the foramen magnum. It is composed of white matter It also have regions of gray and white matter called the reticular formation. It plays an important role in monitoring the impulses that enter the brain stem. It enhances or inhibits the impulses to the brain. Within this are concentrations of cells or nuclei that represent various centers for various functions. PONS Is located just above the medulla and is composed of both gray and white matter and reticular formation It ahs centers for reflexes mediated by the 5th, 6th, 7th & 8th cranial nerves

MIDBRAIN It consists of several tracts that relay impulses to the cerebrum. Two important structures Red nucleus Substantia nigra CEREBELLUM The outer portion of the cerebellum is made up of gray matter while the inner portion is predominantly white matter. Controls the skeletal muscles in three ways 1. acts with the cerebral cortex to produce skilled movements by coordinating the activities of groups of muscles 2. controls skeletal muscles to maintain equilibrium and posture 3. functions below the level of consciousness to make movements smooth instead of jerky, steady instead of trembling, and coordinated instead of inefficient awkward and uncoordinated DIENCEPHALON Referred to as the “between brain� since it links the brain stem with the cerebrum. Important structures are thalamus and hypothalamus THALAMUS Is located in the very center of the brain with the cerebrum surrounding it from the top and sides and the mid brain below. It is made up of a number of nuclei that function to interrupt impulses. 1. It acts as a relay station for most of the communications between the brainstem, cerebellum and cerebrum. 2. As impulses arrive at the thalamus it makes assessments and directs the impulses to appropriate regions in the higher centers for interpretation and response. 3. It enables cortex to communicate with other regions and hence with out it cortex is useless.

Hypothalamus Is a small structure in the middle of the base of the brain. It is the major center of the brain for controlling the internal functions body functions. The important nuclei present are 1. preoptic nucleusà body temperature control 2. Supra optic nucleusà secretion of antidiuretic hormone. 3. medial nucleià sense of satisfaction associated with food 4. lateral regionàcauses a person to become very hungry 5. anterolateral regionsà causes a person to become very thirsty 6. posterior hypothalamusà excites the sympathetic nervous system throughout the body CEREBRUM Is the largest and upper most division of the brain Consists of two halves. Its functional units are cerebral cortex, basal ganglia and limbic system Cerebral cortex Represents the outer region of the cerebrum and is predominantly made up of gray matter. It is associated with the thinking process. It is where all our memories are stored Responsible for our ability to acquire our many muscle skills Fissures on the cerebral cortex divide the cerebral hemisphere into 1. Frontal lobe 2. Parietal lobe 3. Temporal lobe 4. Occipital lobe 5. Insula (island of Reil)

Wernicke’s area is a region of the cortex that is important for sensory integration where meaning of sensory input is interpreted. Deep to the gray matter of the cerebral cortex lie tracts made up of white matter Types 1. Projection tractsà extensions of ascending or sensory spinothalamic tracts 2. Association tractsà most numerous & extend from one convolution to another in the same hemisphere 3. Commissural tractsàcomprise the corpus callosum which extend form one convolution to corresponding convolution in the other hemisphere Basal ganglia Central to cerebral cortex is a portion of gray matter called the basal ganglia It is important in coordinating cerebral activities with other brain stem functions Nuclei are caudate, putamen and globus pallidus It is important in controlling background gross body movements Limbic structures It comprises of the border structures of the cerebrum and the diencephalon. It controls emotional and behavioral activities There appears to be a pain and pleasure center that on instinctive level drives the individual towards behaviors that stimulate the pleasure side of the center. These drives are generally not perceived at a conscious level but more as a basic instinct. The functional structures are 1. amygdale controls appropriate behavior of the person for each type of social function 2. hippocampus it determines if the experience is important enough, then the experience will be stored as a memory in the cerebral cortex 3. Mammillary bodies controls the persons degree of wakefulness and his feeling of wellbeing 4. septum pellucidum stimulation causes anger and rage

5. Cingulate gyrus, Cingulum Insula, Parahippocampal gyrus interactions coordinates the conscious cerebral functions with the subconscious behavioral functions of the deeper limbic system OTHER IMPORTANT STRUCTURES Periaqueductal gray Capable of producing powerful neurotransmitters that can greatly modulate nociceptive impulses Raphe Magnus Nucleus Functions to modulate nociceptive input ascending to the thalamus SOMATOSENSORY PATHWAYS •

From the trunk and extremities course is in the spinal cord

Those transmitting impulses from the face, form the trigeminal system

Can be subdivided into three groups –

Direct or discriminative or lemniscal pathway

Indirect pathways

Spinocerebellar tracts


Are contralateral

Somatotopically organized pathways

Synapse in veteroposterior complex of thalamus

Are involved in sensory discrimination

Clinically useful for localizing lesions 1. Pathways for tactile discrimination and conscious proprioception i. Dorsal column – lemniscal pathway ii. Parallel pathways 2. Pathways for discriminative aspects of pain and temperature sensation i. Direct or neospinothalamic tract


Have poor somatotopy

Ascend bilaterally

Have multiple connections with reticular formation

Not help for localization of lesion

Important for transmission of affective- arousal components of pain and visceral sensation

Imp for initiation of reflex somatic, autonomic, and hormonal responses to external stimuli 1. Paleospinothalamic tract 2. Spinoreticular 3. Spinomesencephalic 4. Propriospinal multi synaptic pathway

SPINOCEREBELLAR TRACTS 1. Dorsal Spinocerebellar tracts 2. Ventral Spinocerebellar tracts Transmit unconscious proprioceptive information to the ipsilateral cerebellum PATHWAYS FOR PAIN AND TEMPERATURE •

The sensation of pain has two components:

A sensory-discriminative component that informs about quality, intensity, and the location of the stimulus.

The arousal-affective component is involved in the emotional, behavioral, and autonomic responses to pain.

These two components are carried in direct and indirect pathways respectively. These are intermingled and ascend mainly in the spinothalamic tract.


Are free nerve endings.

high threshold mechanoreceptive units

innervated by small myelinated axons

respond to pressure and transmit the first pain

polymodal nociceptive units à innervated by unmyelinated axons –

respond to noxious mechanical, thermal, and chemical stimuli

mediate second or slow pain

Primary afferents •

The first order neurons enter the spinal cord via the ventral roots to reach the dorsal horn

Second order neurons •

Cross to the opposite side to continue rostrally in the anterolateral quadrant of the spinal cord primarily in the spinothalamic pathway

SPINOTHALAMIC TRACT Components of this tract includes 1. Direct pathway, neospinothalamic pathway à mediates discriminative aspects of pain and temperature and is imp for localization 2. Indirect pathways 1. paleospinothalamic 2. Spinoreticular 3. Spinomesencephalic tracts for affective arousal components of pain. 4. Multisynaptic ascending Propriospinal system NEOSPINOTHALAMIC PATHWAY (Transmission of fast pain) The fast type a-delta pain fibres transmit mainly mechanical and acute thermal pain. They terminate mainly in lamia I (lamina marginalis of the dorsal horns)

PALEOSPINOTHALAMIC PATHWAY (Transmission of slow chronic pain) The paleospinothalamic system transmits pain mainly carried in the peripheral slowchronic type-C pain fibres, although it does transmit some signals from type A-delta fibres



The peripheral fibres terminate almost entirely in laminas II and III of the dorsal horns, which together are called as substantia gelatinosa.

Most of the signals then pass through one or more additional short fibres within the dorsal horn themselves before entering lamias V through VI Here the last neuron in the series give rise to long axons that mostly join the fibres from the pathway passing through the anterior commisure to the opposite side of the cord and then upward to the brain in the same anterolateral pathway.

Projection of paleospinothalmic tract The slow chronic paleospinothalmic pathway terminates widely in the brain stem. of Only 1/10th of the fibres pass all the way to the thalamus. Instead they terminate principally in one of the three areas. 1. The reticular nuclei of the medulla, pons and mesencephalon. 2. The tectal area of the mesencephalon deep to the superior and inferior colliculi 3. The periaqieductal gray region of surrounding the aqueduct sylivius From the brain stem pain area, multiple short fibres neurons relay the pain signal upward into the intralaminar and central lateral nuclei of the thalamus and into certain portions of the hypothalamus and other adjacent regions of the basal brain TRIGEMINAL SYSTEM •

Impulses carried by the nerve enter directly to the brain stem in the region of the Pons to synapse in the trigeminal spinal nucleus.

It consists of two parts 1. main sensory trigeminal nucleus à periodontal and pulpal afferent 2. spinal tract 1. subnucleus oralis 2. subnucleus interpolaris 3. subnucleus caudalis



Involved at the peripheral level à loss of pain or pain and temperature sensation in the distribution of the affected nerve.

Of the CNS à no pain, unless pain sensitive structures are involved or central pain controlling pathways are interrupted.

If a central lesion interrupts the tract à inability to perceive painful stimuli and to discriminate between hot and cold in the areas below the level of the lesion

A lesion at the spinal level involving the tract à contralateral loss of pain and temperature sensation

Lesion at the post fossa à contralateral loss of pain and temperature in trunk and extremities

If the same lesion involves the pain fibers in the descending tract of the trigeminal nerve, à ipsilateral loss of pain and temperature sensation of the face

Lesions at the level of medulla à crossed anesthesia

Rostral to the medulla à complete contralateral hemianesthesia

Suprathalamic lesions àcrude pain perception is intact, but precise localization of painful stimuli is impaired


CENTRAL PAIN: Pain that emanates from the structures of the CNS felt peripherally as pain  Projected pain  Mainly neurogenous pains and follow the dermatome distribution faithfully  Ex. Peripheral neuritis, Herpes zoster


REFERRED PAINS -Spontaneous heterotrophic pain felt in the area innervated by a different nerve from the one that mediates the primary pain. 

Occurs without any provocation

Wholly dependent of the original source of pain.

In mammilian embryo body is divided into metamere

A typical metamere consist of 1. Skin and subcutaneous tissue. 2. Skeletal muscles 3. Viscera Vicerotome, Myotome and dermatome of each metamere are supplied by the corresponding spinal cord segment. In post natal life D, V, M of a given segment of the cord occupy geographically different area of the body (NEURAL CONNECTIONS ARE RETAINED) E.G Dermatome of the T1 segment is inner side of the forearm and the corresponding vicerotome is part of the heart.

Mechanism of referred pain Following mechanism are responsible for the phenomenon of referral pain. 1. Convergence 2. Subliminal fringe effect


Sympathetic afferent fibres carrying pain sensation from the viscus ends at the posterior horn of the spinal cord. Afferent somatic nerve, emerging from the pain receptor, of the corresponding dermatome of this viscus, enters the same segment and terminate on the same cell where the sympathetic nerve is terminating. ( i.e Two different neurons converge on the same next order neuron)

Subliminal fringe effect

The afferent sympathetic nerve bringing pain sensation from the viscus terminates on the second order neuron, It also gives a collateral which stimulate another second order neuron This second order neuron synapse with the somatic neuron of the corresponding dermatome. Therefore, when pain is felt by the patient he feel as if the pain is coming from the corresponding dermatome


Theories of Pain Specificity theory (Von Frey (1890))


He proposed that free nerve endings gave rise to pain sensation in brain.


This theory is concerned primarily with the sensory discrimination aspects of pain, its quality, location on skin, intensity and duration.


Specificity theory cannot explain a) Any pathologic pain produced by mild noxious stimuli. b) Referred pain that can be triggered by mil innocuous stimulation of normal skin. c) Do not explain the paroxysmal episodes of pain produced by mild stimulation of trigger zone in trigeminal neuralgia.

Intensives or Summation theory (Gold Sheider) He proposed that pain results from over stimulation of other primary sensations. ď Ź

He proposed that pain resulted when activity exceeded a critical level due to excessive activation of receptors resulting in convergence and summation of activity.

Noordenbos sensory interaction theory

He proposed that rapidly conducting large fiber pathway inhibit or suppresses activity in slowly conducting small fiber pathway that conveys noxious information.

A decrease in the ratio of large to small fiber activity results in central summation and an increase in pain and vise versa.

It explains different pathologic pain status. ☛

Hyperalgesia following peripheral nerve injury.

Gate Control theory – Melzack and Wall (1965)

The term gate refers to relative amount of inhibition or facilitation.

The gating mechanism is modulated presumably S.G. layer of spinal cord.

The gating mechanism is influenced by the relative activity in large diameter (Aβ)fibers activated by low threshold non noxious stimuli.

Small diameter (A-delta + C) fibers activated by intense noxious stimuli

Activity in large fibers tends to close the gate.

Small fiber activity tends to facilitate transmission.

Large fibers in particular, are postulated to activate, central control mechanism related to cognitive processing, which intern modulate gating mechanism.

When the output of the transmission cell exceeds a critical layer activates the two major systems.

Sensory discriminative system, involving neospinothalamic fibers projecting into the ventroposterior thalamus and the somatosensory cortex.

The descending control exerted by neocortical activity is thought to modulate activity is sensory discriminative and motivational affective systems.

All this systems ultimately influence the motor mechanisms responsible for behaviour elicited by noxious stimuli.

Reflex arc Definition : Sensory impulse is automatically converted into motor effect through the involvement of central nervous system.

THE PSYCHOLOGY OF PAIN Once the nociceptive impulses reach the higher centers, the patient makes judgment on the pain experience according to four factors or conditions 1. The level of arousal of the brain stem 2. Prior experiences 3. Emotional state 4. Certain behavioral traits

The level of arousal of the brain stem The dorsal root ganglia continuously generate an ongoing barrage of sensory impulses that are poured into the CNS. This constant flow of sensory input can be enhanced by the reticular formation and countered by the descending inhibitory system. This means there is already a source of potentially painful neural impulses at all times just waiting for a decrease in the level of systemic inhibitory influence. When inadequately inhibited these neural impulses are felt as pain even when there is no local cause. If a nociceptive impulse enters a normally calm, well-functioning brain stem, the impulse may never reach the higher centers and if it did not likely initiate a significant response. If however the same impulse enters a brain stem with an upregulated reticular formation and little descending inhibition, the impulse could greatly affect higher center response. Prior experiences Once the nociceptive impulses pass through the brain stem, they move to the thalamus where it recognizes as important and directs them to the sensory cortex and limbic structures for interpretation. Cortex is responsible for storing all memories of experiences. Humans are subject to autoconditioning, which can greatly affect their response to pain. The repetition of similar circumstances can generate clinical pain like that associated with a former traumatic experience even though no noxious stimulation occurs. Emotional State In the limbic system the pain experience is evaluated on a different level; emotional level. •

Early on these emotions may be fear or rage, which represent protective actions in an attempt to move the individual away from the source of nociception

If the pain experience is prolonged, the emotion may change to a sense of helplessness, sadness, or depression.

If the patient is calm, comfortable and has a sense of well being. The pain experience is minimized

If the patient is excited, agitated or angry, the pain experience is enhanced.

The sympathetic nervous system is responsible for the fight or flight response which helps to rapidly respond to a threat.

Behavioral traits Once the limbic has emotionally labeled the pain and the cortex has given the pain meaning and consequence according to past experience, the individual reacts with certain behavior. Some individuals may place significant meaning and emotion on the pain and suffer greatly. Others experiencing the same level of pain may place little meaning and emotion and do not suffer a lot. MECHANISTIC MODEL VERSES THE BIOPSYCHOSOCIAL MODEL •

For a clinician to better understand the patient’s pain disorder one must first begin with the understanding of the disease model on which he or she is basing therapy.

There are basically two models 1. Mechanistic Model 2. Biopsychosocial model

Mechanistic model Of disease implies that when present there is always something wrong with a part of the body. According to this all the physician has to do is to find the offending part and repair it. Although this must be appropriate for some somatic pains, it certainly does not represent all pains. Biophysical model This model suggests that the person is a complex unit and that one cannot separate the mind from the body especially when nociception is being experienced In other words it doesn’t matter if the individual actually has cancer, if the individual believes him has cancer, the suffering begins. “Psychology is really neurology not understood”.

MECHANISMS OF PAIN AND ANALGESIA Organic pain can be divided into 1. Nociceptive pain 2. Neurogenic pain Nociceptive pain: •

Is related to activation of normal pain mechanisms in response to tissue injury or inflammation.

Neurogenic pain: •

Is due to CNS or PNS lesions that affect processing of info in the pain transmission pathways.

Transmission of pain is modulated by 1. Segmental 2. Descending suprasegmental mechanisms -which include primary afferents, descending pathways, interneurons Segmental mechanisms 1. Gate control mechanism 2. Wind up phenomenon: 3. Central pain controlling network (endogenous analgesia system) 4. Pain Modulation In The Reticular Formation 5. Pain modulated by psychologic factors Gate control theory Proposed by Melzack and Wall 1. The transmission of nerve impulses from afferent fibers to the spinal cord transmission cells (T) is modulated by a spinal gating mechanism (SG) in the dorsal horns 2. the spinal gating mechanism I s influenced by the relative amount of activity in large diameter (L) and small diameter (S) fibers: activity in large fibers tends to inhibit transmission (close the gate),whereas activity in small fibers tend to facilitate transmission (open the gate)

3. the spinal gating mechanism is also influenced by the nerve impulses that descend from the brain 4. when the output of the spinal transmission cell exceeds a critical level, it activated the action system—those neural areas that underlie the complex, sequential patterns of behavior and experience that are characteristic of pain Wind up phenomenon: •

Involves exaggeration of pain transmission after repetitive activation of small nociceptive fibers. This explains the pain present in nerve injury and during nerve regeneration.

Central pain controlling network (endogenous analgesia system): The important components of this system are i. Periaqueductal gray matter of the midbrain ii. Raphe nucleus of the medulla which produces serotonin iii. Locus ceruleus which produces nor adrenaline These structures have several properties in common 1. contain endogenous opioid neurons and receptors 2. They are stimulated by opioids and mediate the analgesic effects of morphine-like drugs. 3. receive input from indirect ascending nociceptive pathways and thus provide feedback inhibition of pain transmission 4. When stimulated they produce analgesia. They do not effect the transmission of non nociceptive info in the dorsal horn. Mechanism: The opioids excite antinociceptive neurons in the Periaqueductal gray. This stimulated the serotoninergic neurons in the Raphe nuclei and Norepinephrine-synthesizing cell groups of the reticular formation of ventral medulla. Descending serotoninergic and Norepinephrine pathways inhibit pain transmission in the dorsal horn.

Pain Modulation in the Reticular Formation The reticular formation is the portion of the brain stem that contains a number of nuclei that can either excite or inhibit the incoming impulses. This region contains a group of neurons that secrete Ach, an excitatory neurotransmitter. Fibers passing through region terminate in the nuclei of thalamus. Pain signals increase the activity in this area and strongly excite the brain to attention.

PAIN MODULATION BY PSYCHOLOGIC FACTORS Excitatory modulating factors 1. Egocentric psychological conditions that center the subject’s attention towards himself have an excitatory effect on pain 2. It is also related to the degree of attention directed towards the injury at that time. The more one is absorbed with his suffering, the more intense it becomes. 3. Expectancy, whatever one expects (whether due to memory, anticipation, prior conditioning), in terms of pain is likely to be what one experiences. 4. Anxiety and fear are potent excitatory modulators. Inhibitory modulating factors 1. outgoing psychological conditions that direct one’s attention to energies away from self have a favorable modulating effect on pain 2. a feeling of serenity born of confidence and assurance have marked inhibitory effect 3. Distraction by hypnosis, mental absorption and physical activities have an inhibitory effect. GENERAL CLASSIFICATION OF PAIN ACUTE PAINS 1. Are of short duration

CHRONIC PAIN 1. Of long duration. 2. Any pain lasting longer than 6 months regardless of the origin 3. Pains that last longer than the healing time. 4. psychological intensification PRIMARY AND SECONDARY PAIN •

If the pain emanates from the structures that hurt, it constitutes a primary nociceptive input

If the true source of pain located elsewhere the area of discomfort represents the secondary pain è heterotrophic pain

STIMULUS INVOKED AND SPONTANEOUS PAIN Most primary somatic pains result from stimulation of neural structures that innervate the site. •

Some pains occur spontaneously and do not require a stimulating force. Ex. Neuropathic and heterotrophic pains. SLOW PAIN Difficult to locate Felt as deep, dull, aching sensation Responsible for suffering Primarily carried by C fibers

FAST PAIN Easily localized to the exact location Perceived a sharp pain

Primarily carried by A-delta fibers

Substance P is the major neurotransmitter TYPES OF HETEROTROPHIC PAINS Central pain: •

Pain that emanates from the structures of the CNS felt peripherally as pain

Projected pain

Is felt in the peripheral distribution of the same nerve that mediates the primary nociceptive input,

Mainly neurogenous pains and follow the dermatome distribution faithfully

Ex. peripheral neuritis, herpes zoster

REFERRED PAINS 1. Spontaneous heterotrophic pain felt in the area innervated by a different nerve from the one that mediates the primary pain. 2. Occurs without any provocation 3. Wholly dependent of the original source of pain. CLASSIFICATION OF OROFACIAL PAIN SOMATIC PAIN Pain resulting from noxious stimulation of somatic structures & the nociceptive impulses are being received and transmitted by normal components of the sensory system SUPERFICIAL SOMATIC PAIN •

Pains which can be located precisely and relate faithfully to provocation in timing location and intensity


Pains which are more diffusely felt and are less faithful to provocation and frequently initiate secondary effects such as referred pain and muscle spasm

Deep Somatic Musculoskeletal Pain

Pains which yield a graduated response to stimuli and bear a close relationship to the demands of biochemical function are called musculoskeletal pains •

Deep Somatic Visceral Pain

Pains which do not yield a graduated response to noxious stimulation and are less responsive to biomechanical function are called visceral pains

NEUROPATHIC PAIN Pain may emanate from an area not due to an abnormality in the structures of the area but because of abnormality in the neural components that innervate the area EPISODIC NEUROPATHIC PAINS 1. characterized by periods of very intense pains followed by total remission 2. can last from seconds to hours 3. patient is able to localize the pain 4. response to provocation at the site of pain is unfaithful 5. characterized by a bright, stimulating, burning quality that simulates superficial somatic pain CONTINUOUS NEUROPATHIC PAINS 1. result from interference in the normal transmission of afferent impulses by the primary neurons 2. felt as persistent, ongoing, unremitting burning sensation 3. there is fluctuation of intensity but no periods of total remission 4. cause is trauma or damage to the neuron 5. enlargement of the receptive field and diminished central inhibitory activity TYPES 1. Neuritis 2. deafferentation pains 3. sympathetically mediated pains NEURITIS 1. Occurs as a result of alteration in the afferent fibers in a nerve trunk.. Inflammatory in nature 2. Accurately related in location to the site of inflammation 3. Inaccurately related to the intensity of stimulus

Diagnosis The most important aid to the diagnosis of pain is the 1) History, followed by clinical examination & appropriate 2) Investigation which includes radiographs, a computerized or magnetic resonance scan. The history should include 1) Its character, eg. Sharp, dull, throbbing, burning or stabbing. 2) The site or sites from which it arises, and to which it travels. 3) Its timing, when did the first attack occur its frequency & duration. 4) The provoking factors. 5) The relieving factors. 6) Associated phenomena eg., swelling, discharge, bruxism, trismus. 7) Does the patient suffer from anxiety or depression? 8) The current and previous general medical history and drug therapy. P =the pattern of the pain 

how it started

how the pain affects your life, work and leisure time

what activities make the pain better and what make it worse

what medications relieve the pain, or don't work

whether the pain is constant or comes and goes

how long the pain lasts

A = the area affected by the pain 

location of the pain and/or if it moves or "radiates" (spreads out from a core spot) or stays in the same place

I = the intensity of the pain N = the nature of the pain HOW TO MEASURE PAIN 

Pain measurement is a complex and controversial psycho physiologic subject

There is no simple method of measuring pain.

Pain can be measured by Self-report (what children say), Biological markers (how their bodies react), Behavior (what children do). Because pain is a subjective event, self-report is best if it is available. Unfortunately, in many infants, young children, or children with cognitive or physical impairments, selfreport is not available and behavioral or biological measures must be used. VISUAL ANALOG SCALE (VAS).

(Top) Faces scale from Kuttner and LePage (1989); (Bottom) faces scale from Bieri, Reeve, Champion, and Addicoat (1990). A VAS consists of a 10cm line on which (Word graphic rating scale from Tesler, Savedra, Holzemer and Wilkie 1991)

Biological markers 

Heart rate is an easy and generally valid measure of short, sharp pain. Unfortunately, there appear to be no biological measures suitable for use as a clinical pain measure for longer-term pain.

 

Oxygen saturation decreases during painful procedures steroids

Behavior (what children do) 

The seven-item Toddler-Preschool Postoperative Pain Scale14 includes items on vocal expression, facial expression, and bodily expression.

The new method, called Apocis 

record seven types of behaviour which are related to pain. Staff observe the child unobtrusively, noting a score for

whether it is crying, how it breathes (panting, holding its breath or breathing regularly),

the way it moves its arms and fingers (in the case of pain, cramped, clenched fists, wild movements),

how it moves its legs (kicking, legs drawn up), the posture of the back and body (cramped, twisted, trembling) and

the facial expression (grimace, wrinkled up nose, frown).

the total scale gives a measure of the pain: no pain (0), mild pain (1-2), pain (3-4) or severe pain (5-7).

MC GILL PAIN QUESTIONNAIRE Measures the Motivational-affective and Cognitive-evaluative Equalities of Pain in addition to the sensory experience. 

The questionnaire enables patient to choose from 78 adjectives that describe pain.

Meant to assess sensory groups (group1-10), affective groups (group11-15) and evaluative group (group 16) dimensions of pain and produce a pain rating index.


Turk and Rudy

consists of a 61 item questionnaire, West Haven-Yale Multidimensional Pain Inventory.

The following distinct three profiles emerged 


Interpersonally distressed.

Adaptive copers

Various means in diagnosing pain. 

Blood tests or X-rays

CT or CAT scan





Bone scans

Ultrasound imaging

MODALITIES FOR MANAGING OROFACIAL PAIN DISORDERS 1. Pharmacological Therapy a. analgesic agents i. non-narcotic agents ii. narcotic agents iii. adjuvant analgesics b. anesthetic agents i. topical anesthetic ii. injectable local anesthetic c. anti-inflammatory agents d. muscle relaxants

e. antidepressants f. antianxiety g. vasoactive drugs h. Norepinephrine blockers i. antimicrobial agents j. antiviral agents k. antihistamine agents l. anticonvulsive agents m. neurolytic agents n. uricosuric agents o. dietary considerations 2. Physical therapy a. modalities i. sensory stimulation ii. ultrasound iii. electrogalvanic stimulation iv. deep heat b. manual techniques i. massage ii. spray and stretch technique iii. exercise iv. physical activity c. psychological therapy i. counseling and behavioral modification training 1. stress reduction training 2. relaxation training

PHARMACOLOGIC THERAPY Antidepressant agents Some patients with neurovascular pain and patients with chronic pain who verbalize with active depression may respond to judicious use of these agents Tricyclic antidepressants increase the availability of serotonin and nor epinephrine in the CSF. Vasoactive agents Neurovascular pain disorders may be favorably influenced by alpha adrenergic blocking action of Ergotamine tartrate, which causes a stimulating effect on the smooth muscle of peripheral and cranial blood vessels. Norepinephrine blockers In lieu of analgesic blocking of the stellate ganglion for the control of sympathetically maintained pains the Norepinephrine blocking agent Guanethidine has been used. It blocks the uptake of NE by sensitized deafferented axons. Anti convulsive agents Phenytoin (Dilantin) Is an anticonvulsant and cardiac depressant and cardiac depressant that also has the capability of suppressing the pain paroxysmal neuralgia. Neurolytic agents The common neurolytic agent used to destroy peripheral nerves is 95% ethyl alcohol, and phenol. It provides only temporary relief as the nerve regenerates. Injection of glycerol (0.30mL) into the retrogasserian space for the treatment of trigeminal neuralgia is more affective. 90% of the patients remain symptom free after one or two injections. Uricosuric agents Hyperuricemia involving the TMJ is treated by Colchicine which suppresses the acute attacks of gout and relives pain that the attack generates For chronic gouty arthritis Probenicid is used

Dietary considerations The chief relationship between diet and pain appears to be with L-Tryptophan, which converts into serotonin. Increased activity of serotonin interneurons is associated with analgesia and enhanced drug potency. 1. Adequate dosage: 4g/day 2. Low protein, low fat, high carbohydrate diet 3. Adequate Vit B6 intake: 10-15 mg/day 4. Four weeks or more of continuous therapy PHYSICAL THERAPY Modalities: refer to those treatments that utilize an instrument, device or agent to accomplish the desired effect Sensory stimulation 1. Cutaneous stimulation The effect occurs through the stimulation of thick myelinated cutaneous afferents, Abeta neurons 1. superficial massage 2. counterirritant application 3. Vapocoolant therapy: in Myofacial trigger point pain. 4. infra red heat 5. mechanical vibration 6. hydrotherapy: agitated circulating water bath is used 2

Transcutaneous stimulation a. Transelectric nerve stimulation (TENS): the units employ a low intensity current at high frequency (50-100 Hz) applied to the skin through electrodes attached by conducting paste. Stimulate A-beta afferents that activate the descending inhibitory pathways. b. Electro acupuncture: utilizes low frequency (2Hz) but high intensity electric current. It is applied to specific cutaneous sites, acupoints. Antinociception of

teeth and mouth occur segmentally by applying EA at the infraorbital acupoint; more general effects from Ho Ku acupoints located between thumb and index finger. 3

Percutaneous Stimulation: is done by electrodes that penetrate the skin. a. SC electric nerve stimulation produces prolonged analgesia that is not reversible by Naloxone. b. Ultrasound: i. produces an increase in the temperature at the interface of the tissues and therefore affects the deeper tissues than does the surface heat ii. it increase the blood flow in the deeper tissues iii. separates the collagen fibers all these improve the flexibility and extensibility of the connective tissues iv. it is also used to administer drugs through the skin – phonopheresis c. Electrogalvanic nerve stimulation: utilizes the principle that electrical stimulation of a muscle causes it to contract. A rhythmic electrical impulse is applied to the muscle, creating repeated involuntary contractions and relaxations. This will help break Myofacial spasms as well as increase blood flow to the muscles. Both effects lead to a reduction of pain in compromised muscle tissues. d. Deep heat therapy: physical therapy in the form of penetrating heat has value in treating patients with pain. Diathermy and ultrasound are used for this purpose. The judicious use of deep heat is beneficial in treating inflammatory pain.

MANUAL TECHNIQUES 1. Massage Gentle massage of the tissues can reduce pain perception Deep massage is often helpful in reducing pain and reestablishing normal muscle function than gentle massage. It should be provided by a Physical therapist.

It can assist in mobilizing tissues, increasing blood flow to the area and eliminating trigger points. 2. Spray and stretch technique: primary physical therapeutic technique for treatment of myofascial trigger points. A mixture of fluorocarbons is used as the vapocoolant. .when the muscle is stretched just short of pain, the vapocoolant is applied by using parallel sweeps in one direction, traveling towards the reference area. It is held 15-18 inches away from the tissues and the steam is directed at an angle of 30 degrees, the sweeps are made at the rate of 4 in/s. after two or three sweeps the muscle should be rewarmed. At the end of the treatment, moist heat should be applied and the range of motion exercises should be instituted. 3. Exercise: are used to elevate pain threshold. Forceful contraction of antagonist muscles causes reflex relaxation of the agonist muscle. 4. Physical activity: during periods when the pain is increased, extending exercises to the limit of patients tolerance is significantly beneficial; the more exercises performed, the fewer the pain behaviors displayed. It kept the body in a better condition and reduced the time in bed 5. Psychological Therapy: are oriented towards minimizing axis II factors that either influence or create the pain disorder. COUNSELING The following 5 factors should be discussed with the patient when discussing the pain condition. 1. Provide a definitive diagnosis 2. Provide assurance 3. Explain the problem in appropriate terms 4. Do not deny the patients pain 5. Provide realistic explanations BEHAVIORAL MODIFICATION TECHNIQUE 1. Stress reduction technique 2. Relaxation training: it aids in reducing the level of ANS activity

Modification of Jacobson’s technique (1968) is used in dentistry. The patient tenses his muscles and then relaxes them until a relaxed state can be felt and maintained. The patient is instructed to concentrate on relaxing the peripheral areas and to move progressively centrally. Another method is the reverse of the Jacobson’s technique. This is more suitable for patients with pain.

BIBLIOGRAPHY 1. Bell’s Orofacial Pains – Jeffrey P. Okeson, 5th edition 2. Medical Neurosciences an Approach to Anatomy, Pathology, and Physiology by systems and levels - Eduardo E, Benarroch et al 4th edition 3. Oral Bioscience - Ferguson 4. Essentials of Oral Physiology - Robert Bradbury 5. Human Anatomy and Physiology – Elaine N. Marieb, 4th edition 6. British Dental Journal vol 196 no 8 April 24 2004. The Enigma of Pain.

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