Pain Perception Control
Pain is a complex, multidimensional phenomenon mediated by physicochemical processes in the peripheral and central nervous system (CNS). Perception of pain can be significantly modified by any of a host of mechanisms, including drugs, environmental stimuli, cognitive and emotional processes, and social and cultural conditions. In terms of a conceptual context, pain may be thought of as a continuum whose boundaries are limited yet variable for each individual. On the lower end of the continuum is the pain perception threshold. The pain perception threshold can be defined as the least amount of stimulation applied to tissue that an individual can barely detect as being unpleasant. The pain tolerance threshold is a notable point of intensely noxious stimulation on the pain continuum above which the individual cannot reasonably endure and will seek definitive measures to relieve the pain. Determination of the pain perception threshold usually is associated with experimental conditions; however, more intense stimulation approaching or exceeding the pain tolerance threshold is more characteristic of clinical conditions.
The overwhelming majority of pharmacologic agents used in dentistry are administered to control anxiety and pain. Generally the elimination of pain sensation in the dental setting requires blocking of pain perception either peripherally using local anesthesia or centrally with general anesthesia. Anxiety is controlled, in part or completely, by using sedation that may involve pharmacologic or nonpharmacologic techniques or both. Anxiety and pain control in actual clinical practice overlap to a significant degree.
There is no best technique for control of anxiety and pain. A practitioner may have a favorite technique, but one technique is not useful for all dental patients in all situations. The prudent and wise dentist has a working knowledge of several techniques and selects, on an individual basis, the one that appears to be the most appropriate for a particular patient. In some cases, this may necessitate referral.
General anesthesia renders the patient unconscious through depression of the CNS, thus eliminating patient cooperation as a factor. There are categories of patients in whom the only reasonable anesthetic alternative for safe treatment is general anesthesia. Examples may include very young, precooperative children, and children with intellectual or developmental disabilities who are unable to cooperate during complicated or extensive dental procedures.
General anesthesia should be administered under the direction or supervision of an individual who has completed a Commission on Dental Accreditation (CODA) or Accreditation Council on Graduate Medical Education (ACGME) accredited training program, or its equivalent, which provides comprehensive and appropriate training necessary to manage general anesthesia cases. Dentists with such training must be licensed by the state to administer general anesthesia.
Pain perception may be altered at the peripheral level by blocking propagation of nerve impulses using local anesthesia. The initial process of pain perception involves production of nerve impulses by a noxious stimulus that activates specialized nerve fibers, termed nociceptors and classified as A-delta and C fibers, that transmit pain information to the CNS. The nerve impulses travel along the nerve fibers via a physiochemical process involving ion transport across the neuronal membrane. The primary effect of local anesthetic agents is to penetrate the nerve cell membrane and block receptor sites that control the influx of sodium ions associated with membrane depolarization.4 Current thinking holds that the sequence of events involved in a local anesthetic block consists of (1) intraneuronal penetration of the local anesthetic and subsequent binding to a receptor site that exists on the inside of the cell membrane, (2) blockade of the sodium channels through which the sodium ions would normally enter during depolarization, (3) decrease in sodium conductance, (4) depression of the rate of electrical depolarization, (5) failure to achieve threshold potential, and (6) lack of development of a propagated action potential and thus blockade of conduction of the nerve impulse.2 In general, small nerve fibers are more susceptible to the onset of action of local anesthetics than large fibers. Accordingly, the sensation of pain is one of the first modalities blocked, followed by cold, warmth, touch, and at times, pressure.
Local anesthetic agents are weak chemical bases and are supplied generally as salts, such as lidocaine hydrochloride. The salts may exist in one of two forms: either the uncharged free base or a cation whose charge is determined by its dissociation constant (pKa). The free-base form, which is lipid soluble, is capable of penetrating the nerve cell membrane. Penetration of the tissue and cell membrane is necessary for the local anesthetic to have an effect because the receptor sites are located on the inside of the cell membrane. This explains in part why local anesthetic agents are not as effective when injected in areas of an acute infection where the local tissues are acidic. Once the free base has penetrated the cell, it reequilibrates, and the cation is thought to be the form that then interacts with the receptors to prevent sodium conductance.
Discovered in 1860, cocaine was the first local anesthetic. Because of the number of adverse side effects associated with cocaine, attempts were made to develop alternatives that retained the local anesthetic properties of cocaine while eliminating the side effects. Several other benzoic acid ester derivatives were developed, including benzocaine, procaine (Novocain), tetracaine (Pontocaine), and chloroprocaine (Nesacaine). The major problem with the ester class of local anesthetics is their propensity to produce allergic reactions.
The amides were introduced with the synthesis of lidocaine in 1943. These compounds are amide derivatives of diethylaminoacetic acid. They are relatively free from sensitizing reactions. Since lidocaine was synthesized, several other local anesthetics have been introduced for dental use. All are amides and include mepivacaine (Carbocaine, Polocaine), prilocaine (Citanest), bupivacaine (Marcaine), etidocaine (Duranest), and articaine (Septocaine).
Individual local anesthetic agents differ from each other in their pharmacologic profiles (Table 7-1). They vary in their potency, toxicity, onset time, and duration. All these characteristics may be clinically important, and all vary as a function of the intrinsic properties of the anesthetic agent itself and the regional anesthetic procedure employed. Furthermore, these characteristics may be modified by the addition of vasoconstrictors.