Introduction

The physiology of the peripheral nerve

The function of the nerve to carry massages from one parts of the body to another as electrical action potential called impulse, which initiated by a chemical, thermal, mechanical or thermal stimulus.

The amplitude and shape of impulse remain constant regardless of changes in the quality or strength of the stimulus and the distance traveling through the neurons.

They are actually complex electro-chemical structures. The electrical events that occur within a nerve during conduction as impulse through these steps:-

Step 1

A nerve possesses a resting potential, which is a negative electrical potential of -70 mv that exists across the nerve membrane, produced by differing concentrationsof ions on either side, produced by differing concentration of ions on either side of the membrane. The interior of the nerve is negative in relation to the exterior.

Ion / Intracellular
(mEg/L) / Extracellualr
(mEg/L) / Ratio
(approximate)
Potassium / 110 to 170 / 3 to 52 / 7:1
Sodium / 5 to 10 / 140 / 1:14
Chloride / 5 to 10 / 110 / 1:11

In the resting state the nerve membrane is:-

  1. Slightly permeable to Na+
  2. Freely permeable to K+
  3. Freely permeable to Cl-

Step 2

A stimulus excites the nerve, leading to the following sequence of events:

  1. An initial phase of slow depolarization, the electrical potential within the nerve becomes slightly less negative.
  2. Threshold potential or firing threshold when the falling electrical potential reaches a critical level, an extremely rapid phase of depolarization results.
  3. The rapid depolarization results in a reversal of electrical potential across the nerve membrane, the interior is now electrically positive in relation to the exterior which about +40 mV.

Step 3

Following the depolarization repolarization occurs. The electrical potential gradually becomes more negative inside the nerve cell relative to outside until the original resting potential of -70 mV is again achieved.

The entire process for step 2 requires 0.3 msec. and for step 3 0.7 msec. and for both 1msec.

The preceding sequence of events depends on two important factors:-

  • The concentration of electrolytes.
  • The permeability of the nerve membrane to sodium and potassium ions.

Depolarization: Excitation of a nerve segment leads to an increase in permeability of the cell membrane to sodium ions. The rapid influx of sodium ions to the interior of the nerve cell causes a depolarization of the nerve membrane from its resting level to its firing threshold of approximately -50 to -60 mV. The firing threshold is actually the magnitude of the decrease in negative transmembrane potential that is required to initiate an action potential as impulse.

Repolarization: The action potential is terminated when the membrane repolarizes. This is caused by the inactivation of increased permeability to sodium. In many cells permeability to potassium also increases resulting in the efflux of K+ leading to a more rapid membrane repolarization and return to its resting potential.

How nerves conduct an impulse

The connective tissue that is associated with each neuron is composed of a special material called myelin which is itself made up of the cell bodies of specialized cells called Schwann cells.

The myelin sheath is almost continuous along the entire axon. There are, however tiny breaks in the continuity of the myelin sheath between each succeeding Schwann cell. These breaks are called "nodes of Ranvier". These nodes are quite important in the conduction of an impulse along a nerve axon on its way to the cell body in the ganglion, mostly because their presence along the way speeds the impulse quite a bit.

How a nerve fiber transmits an impulse

When a nerve is stimulated, this sets up a chain reaction in which sodium ions begin to penetrate through the nerve cell membrane and flow into the axon, while potassium ions begin to flow out. This activity happens at the nodes of Ranvier. The imbalance in the chemical makeup of the extracellular fluid then causes an imbalance in the concentration of sodium ions at the adjacent node which stimulates an identical depolarization at this node as well. This process proceeds from node to node until the impulse reaches the cell body of another nerve in the ganglion where it stimulates a similar cascade in a network of other neurons which make contact with it.

All the potassium and sodium ions have exchanged places, the nerve would no longer be able to conduct impulses. The nerve, however, is a living entity and can regenerate the original concentrations of ions using energy from the food you eat. It does this using proteins embedded in the cell membrane which act as "ion pumps".

The anatomy

Impulses originating in the nerve ending of the dental pulp and the supporting structures of the teeth are conveyed to the central nerves system by the maxillary and mandibular division of the trigeminal nerve. From the cell bodies in the Gasserian ganglion which is located in meckel’s cavity on the anterior surface of the petrous of the temporal bone, these neural pathways pass to the sensory nucleus of the trigeminal nerve which is situated in the medulla oblongata and extends to the level of the 2nd cervical segment of the spinal cord. They then pass via the trigeminal lemniscus to the postero-ventral nucleus of the thalamus and then via connecting neurones to the postero-central convolutions on the contra-lateral side of the cortex of the brain.

There are some important landmarks are:

  1. The anterior surface of the maxilla shows canine eminence as prominent tuberosity over the root of the upper canine, distal to the eminence the canine fossa present and superior to the fossa the infra-orbital foramen located though which blood vessels and nerve emerge. The hard palate consists from two parts the anterior two third from the palatine process of maxilla, anteriorly behind the upper central incisor at midline there is incisive foramen through which the incisive blood vessels and nerve emerge. The posterior one third formed from the horizontal plate of palatine bone, At the lateral angle of the horizontal process inferiorly are the openings of the greater and lesser palatine foramen through which the corresponding blood vessels and nerve emerge, from the greater palatine foramen the greater palatine groove passes anteriorly and end between the 1st and 2nd upper premolar. The bone of maxillae is consisted form the concellous spongy bone.
  1. The mandible consists of a horseshoe-shaped body and a pair of rami. On the outer aspect of the body, midway between the superior and inferior borders opposite the 2nd premolar tooth, is the mental foramen for the mental nerve and vessels. Its opining is directed backwards. At about the middle of the inner surface of the ramus, about the level of the crown of the last molar tooth, a foramen leads into the mandibular canal for the inferior alveolar nerve and blood vessels. The sharp and prominent anterior margin of the foramen is called the lingula. Leading downwards on the medial surface of the ramus from the mandibular foramen called the mylohyoid groove in which lies the mylohyoid nerve. The lingual nerve lies on the bone just above the posterior end of the mylohyoid ridge. The body of the mandible is consisted from loss cancellous bone when directed posteriorly specially over the molars teeth.

Pain

Pain is a distressing sensation as of soreness, or as a disturbed sensation causing suffering or distress. Pain can be divided into two components, perception of pain and reaction to pain.

Pain perception: The skin and mucous membranes are provided with numerous nerve end organs for the perception of touch, temperature, and pain stimuli. The end organs which subserve pain are free non-medullated fibers and the application of an electrical, thermal, chemical, and mechanical stimulus may produce an impulse, or wave of excitation in the nerve fibers which is self-propagating and of uniform intensity because each fiber obeys the all or none law, so if a stimulus is sufficient to produce an impulse at all, the resulting impulse is of a uniform pattern and cannot be magnified by increasing the amount of exciting stimulus. The severity of the pain depends on the number of nerve fibers that are activated and not by the alteration in the size of the impulses conveyed by the individual nerve fibers.

The stimulus is conveyed along neural pathways to the thalamus, sharp pain being conducted by peripheral nerve fibers with an axon core of larger diameter than those which convey dull pain.

Pain reaction: is the integration and appreciation of pain within the central nervous system which in the cortex and posterior thalamus. This is a variable factor which accounts for the clinical observation that the intensity of pain and the patient's response to it may very not only between individuals but also from time to time in the same individual.

Pain threshold: is when the variable response to pain. The high pain threshold when the patient exhibits little or no reaction to a painful stimulus, but the low pain threshold is liable to react violently to an identical or even lesser stimulus.

The pain threshold also varies between individuals and in the same individual at different times. The factors which determine the level of tolerance include:-

  1. Psychological make up
  2. Fear and apprehension of dental pain
  3. Fatigue
  4. Age.

The control of pain

Pain may be controlled by interruption the neural pathways at various levels and by different means which can produce either permanent or temporary results.

The methods of pain control is either analgesia or anaesthesia.

Analgesia is loss of pain sensation unaccompanied by loss of other forms of sensibility.

Anaesthesia is loss of all forms of sensation including pain, touch, temperature, and pressure perception and may be accompanied by impairment of motor function.

As a general rule, a large dose of drug is required to obtain anaesthesia than to induce analgesia.

Local analgesia or anaesthesia when part of the body is affected.

General analgesia or anaesthesia when whole body is affected.

The history of local anesthesia started in 1859, was Cocaine which was isolated from coca leaves by Albert Niemann in Germany.

The very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction.

In 1884, the opthalmologist Koller was the first, who used cocaine for topical anesthesia in ophthalmological surgery.

Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia, and in the same year, regional anesthesia in the oral cavity was first performed by the surgeon Halsted, when he removed a wisdom tooth without pain.

However, a number of adverse effects were observed with the clinical use of cocaine. Thus, other local anesthetic agents had to be developed. In 1905, Einhorn reported the synthesis of procaine, which was the first ester-type local anesthetic agent. Procaine was the most commonly used local anesthetic for more than four decades.

In 1943, Löfgren synthesized lidocaine, which was the first “modern” local anesthetic agent, since it is an amide-derivate of diethylamino acetic acid. Lidocaine was marketed in 1948 and is up to now the most commonly used local anesthetic in dentistry worldwide, though other amide local anesthetics were introduced into clinical use: mepivacaine 1957, prilocaine 1960, bupivacaine 1963.

In 1969, articaine was synthesized by the chemist Muschaweck and was approved in 1975 as a local anesthetic in Germany.