Pain Pathway And Pain Control Theories PDF

Pain pathway and pain control theories By Dr. Maram Breshah Lecturer of Oral & Maxillofacial Surgery Faculty of Dentistry, Tanta University  Topic Outline  pain and pain pathway.  Nerve Conduction and action potential.  Mechanisms of Action of Lo...

Pain pathway and pain control theories By Dr. Maram Breshah Lecturer of Oral & Maxillofacial Surgery Faculty of Dentistry, Tanta University  Topic Outline  pain and pain pathway.  Nerve Conduction and action potential.  Mechanisms of Action of Local Anesthetics.  Definition of local anesthesia.  Ideal properties of local anesthesia.  Recovery of Local Anesthetics.  Pain pain defined as an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the CNS.  Pain perception  Physio anatomical process by which pain is received and transmitted by neural structures from end organs through perceptive and conductive mechanisms.  The same in all healthy persons but can be affected by disease and toxic state  Pain nerve fibers  These are very thin unmyelinated nerves.  A-delta and C fibers within the nerve.  More easily blocked by L.A.  The thicker and myelinated fibers, such asA-alpha, beta, gamma and B fibers, transmit other sensation such as touch and pressure with the motor fibers.  Nociceptors Are special receptors that respond only to noxious stimuli and generate nerve impulses which the brain interprets as (pain)  Proprioceptive receptors  These are nerve endings  Respond only to pressure  Sensation from the teeth: Pain sensation from pulp Propriception from investing structures  Pain reaction  Patient manifestation of his perception of an unpleasant experience  Differ from person to person  Determined by patient’s pain threshold  Pain threshold Is the minimum stimulus that elicits pain. Differ between individuals. Vary in the same individual on different occasions Pain threshold is affected by:  Emotional status  Fatigue  Age  Sex  Fear and apprehension  Pain control By 1. Removal of the cause 2. Blocking pathway of painful impulses (LA) 3. Raising pain reaction threshold (Analgesic) 4. Preventing pain reaction by cortical depression (GA) Pain pathway  Impulse generation & transmission The concept behind the action of L.A. is prevention of both the generation & conduction of a nerve impulse.  Nerve cell (Neuron)  Structural unit of the nervous system. It is able to transmit messages between the (CNS) and all parts of the body.  Two types of neuron sensory (afferent) and motor (efferent).  PARTS OF NEURON 1.Dendritic zone: It respond to stimulation produced in the tissues in which they lie provoking an impulse that is transmitted centrally along the axon. 2.Axon: It is a thin cable like structure transmits impulses. 3.Cell Body: Provides the vital metabolic support for the entire neuron. Neuron  Neuron Sensory (afferent) neuron Transmit nerve impulses from sensory receptors to the CNS. These neurons are specialized to detect changes in their environment (Stimuli). Stimuli can be in the form of touch, pressure, heat, light, or chemicals. Motor (efferent) neuron Transmit nerve impulses from the CNS to muscles or glands, called motor neurons because most of them extend to muscle cells, and the nerve impulses they transmit cause these cells to contract. The muscle and gland cells that receive nerve impulses from motor neurons are called effectors , because their stimulation produces a response or effect. Unmyelinated C nerve fiber Slow forward creeping process Conduction rate is 1.2 m/sec Myelinated A alph & A delta nerve fiber Saltatory process ( current leap from one node to other) Conduction rate is 14.8 to 120 m/sec PHYSIOLOGY OF THE PERIPHERAL NERVES The function of a nerve is to carry messages (impulses) initiated by chemical, thermal ,mechanical and electrical in the form of electrical action potential from one part of the body to another. PHYSIOLOGY OF THE PERIPHERAL NERVES Action potentials: Are Transient depolarization of the nerve membrane that result from a brief increase in the permeability to sodium ions & usually also from delaying permeability to potassium ions. Electrophysiology OF Nerve Conduction Resting Potential(Step 1): Nerve membrane is  Slightly permeable to (Na+)  Freely permeable to (K+)  Freely permeable to (Cl−) Electrophysiology OF Nerve Conduction Step 2- A stimulus excites the nerve leading to the following sequence of events: A. Initial phase of slow depolarization. Excitation of a nerve segment leads to an increase in permeability of the cell membrane to (Na+) B.Firing threshold When the falling electrical potential reaches a critical level. Electrophysiology OF Nerve Conduction C- Rapid depolarization  caused by dramatic increased permeability to Na+& permeability to K+ also increases  The interior of the nerve is now electrically positive in relation to the exterior. Electrophysiology OF Nerve Conduction D- Repolarization  The action potential is terminated when the membrane repolarizes. This is caused by the extinction.  (inactivation) of increased permeability to sodium. In many cells, permeability to potassium also increases, resulting in the efflux of K+, Electrophysiology OF Nerve Conduction Step 3-After these steps of repolarization occurs resulting in the efflux of K+, and leading to more rapid membrane repolarization and return to its resting potential. The electrical potential gradually becomes more negative inside the nerve cell relatively to outside until the resting potential of -70mV is again achieved.  Local anesthesia interfere reversibly with the generation of the action potential and with cellular impulse conduction by blockading the sodium channels in the nerve cell. This results in a local insensibility to pain stimuli.  Definition of local anesthesia  Transient loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves without inducing loss of consciousness.  It prevent both the generation and the conduction of a nerve impulse.  local anesthetics set up a chemical roadblock between the source of the impulse and the brain  Desirable Properties of Local Anesthetics  It should not be irritating to the tissue  It should not cause any permanent alteration of nerve structure.  Its systemic toxicity should be low.  It must be effective.  The time of onset of anesthesia should be as short as possible.  The duration of action must be long enough but not so long.  Desirable Properties of Local Anesthetics  It should have potency sufficient to give complete anesthesia without the use of harmful concentrated solutions.  It should be relatively free from producing allergic reactions.  It should be stable in solution and should readily undergo biotransformation in the body.  It should be sterile or capable of being sterilized by heat without deterioration MODE AND SITE OF ACTION OF L.A  Altering the basic resting potential of the nerve membrane  Altering the threshold potential (firing level)  Decreasing the rate of depolarization  Prolonging the rate of repolarization  THEORIES OF ACTION OF L.A  Acetylcholine theory  Calcium displacement theory  Surface charge (repulsion) theory  Membrane expansion theory  Specific receptor theory  Acetylcholine theory Stated that acetylcholine was in nerve conduction in addition to its role as a neurotransmitter at nerve synapses. LA interfere with acetylcholine (neurotransmitter) at synaptic junction So prevent nerve conduction  Calcium displacement theory Displacement of calcium ions from the sodium channel receptor site, which permits binding of the local anesthetic molecule to this receptor site, and decrease permeability to sodium ions which depress the rate of electrical depolarization ……… producesfailure to achieve the threshold potential level & propagated action potential ……..Conduction blockade Surface charge theory ( Electrical potential theory)  Membrane expansion theory  LA diffuse to hydrophobic region (projecting to the middle of excitable membrane ) Produce general disturbance of bulk membrane structure  Expanding some critical regions Preventing an increase in permeability to sodium ions….inhibit sodium conduction and neural excitation  Specific receptor theory  The most favored today.  LA act by binding to specific receptors on the sodium channel so eliminates permeability to sodium ions so no impulse conduction  Action of drug is direct and is not mediated by change in cell membrane Active form of local anesthetic molecule R=N HCL ⇌ R=NH+ + CI- Hydrochlorid salt Cation Anion  DISSOCIATION OF LOCAL ANESTHETICS LA salt dissolved in sterile water or saline RNH ⇌ RN + H+ RN (uncharged, lipiophilic , free base)…….. Responsible for diffusion through nerve sheath RNH (positive charge…cations)………. Responsible for binding receptor and conduction blockade The proportion of each form in the solution varies with: I. PH of solution or surrounding tissue  Higher PH (alkaline medium) …………….. RNH+ < RN + H+  lower PH (acidic medium) ……………… RNH+ > RN + H+ SO:  if solution is alkaline a precipitation of active base radicle (RN) would occur ---------- solution would lose its active component before its uses.  Too acidic solution ------------- inhibit ionization which liberate analgesic base The proportion of each form in the solution varies with: Pka or dissociation constant of the agent is a measure of the affinity of a molecule for hydrogen ions (H+) i.e ability to form cations RNH+ LA have Pka value > 7.4 If Pka > PH → RNH+ > RN + If Pka < PH → RN > RNH  The free base of these salts (RN) is the effective agent on nerve tissues  Base is liberated from it is salt by interaction with slightly alkaline body fluid in the tissues  Determine onset of LA action------ Drugs with a lower pKa possess a more rapid onset of action than those with a higher pKa.  Induction of Local Anesthesia Diffusion Blocking Process Induction Time:  is defined as the period from deposition of the anesthetic solution to complete conduction blockade.  Several factors control the induction time: Concentration of the drug PH of the local anesthetic solution Diffusion constant of the anesthetic drug Anatomic diffusion barriers of the nerve.  Diffusion of LA  Rate of diffusion related to concentration gradient Greater initial concentration → faster diffusion → Rapid onset Mantle fibers ( surface fasciculi) LA conc is high Innervate proximal regions (molars) ē IANB Core fibers (center fasciculi) LA conc is less high Innervate distal regions (centrals & lateral incisors) ē IANB Clinically Inadequate pulpal anesthesia developing in presence of subjective symptoms of adequate soft tissue anesthesia Factors Affecting Local Anesthetic Action  pKa: Low----------rapid onset  Lipid solubility: Increased--------- Increased potency-  Protein binding: Increased----------Increased duration  Non nervous tissue diffusibility: Increased----decreased onset  Vasodilator activity: Increased-----Decreased potency &duration RECOVERY FROM LOCAL ANESTHETIC BLOCK The extra-neural conc is continually depleted by Diffusion dispersion uptake of the drug The intra-neural conc of local anesthetic remains relatively stable until… conc gradient is reversed then the intra-neural conc exceeds the extra-neural conc, and anesthetic molecules begin to diffuse out of the nerve. Mantle fiber lose LA much earlier than Core fiber SO Recovery from 3rd molar before central incisors  Readministration of Local Anesthetic  Usually this repeat injection immediately results in a return of profound anesthesia.  On some occasions, however, the clinician may encounter greater difficulty in reestablishing adequate pain control with subsequent injections.  Tachyphylaxis Increasing tolerance to a drug that is administered repeatedly, likely to develop if nerve function is allowed to return before reinjection. (i.e if patient complains of pain) ……….↓ LA duration,intensity,spread It may be due to following factors: 1. Edema 2. Localized hemorrhage 3. Clot formation 4. Transudation (isolate nerve from contact ē LA ) 5. Hypernatremia (raise sodium ion gradient counteract the decrease in sodium ion conduction by LA) 6. Decreased pH of tissues (fewer LA molecules transformed to free base RN)