Neuro physiology local anesthesia

Oral Surgery

Local Anesthesia

Neurophysiology

The neuron or the nerve cell is the structural unit of the nervous system it is able to transmit messages between the central nervous and all part of the body . There are two types of neuron : the sensory neuron and motor neuron .





Sensory neuron that are capable of transmitting the sensation of pain. consist of three major part which are cell body , the axon , and dendrites . The dendrites which ends in the free nerve endings and is the most distal segment of sensory neuron which respond to stimulation produced in tissue in which they lies provoking an impulse that is transmitted centrally along the axon . The axon is a thin cable – like structure that may be quite long ( the giant axon has been measured as 100-200 cm ) it is composed from neural cytoplasm and covered by thin sheath which is the nerve membrane, in some nerves a lipid rich layer of myelin covers this membrane and the membrane is known as myelinated nerve fiber , current theories stated that nerve excitability and conduction are both attributed to the changes developing within the nerve membrane .



The nerve membrane consist of two layers of lipid molecules ( phospholipids ) and associated proteins , lipid and carbohydrates . since the nerve membrane has selective permeability , therefore significant differences exist for ions between the intracellular and the extracellular concentrations .








The cell body in the sensory neuron located at a distance from the axon , or the main pathway of impulse transmission in the nerve, or their cell bodies are interposed between axon and dendrites . The cell body is therefore , not involved in the process of impulse transmission . The primary function of the cell body is to provide metabolic support to the entire neuron .




The function of a nerve is to carry messages from one part of the body to another , these messages in the form of electrical action potentials are called impulses , action potentials are transient depolarization of the membrane that result from a brief increase in the permeability of the membrane to sodium , and usually from a delayed increase in the permeability to potassium . Impulses are initiated by chemical , thermal, mechanical , or electrical stimuli .

Electrophysiology of the nerve conduction

Resting state (phase 1 ):
The unstimulated nerves or nerves at rest , are said to possess an electrical potential across the nerve membrane and is known as a resting potential which is a negative electrical potential of -70 to – 90 mV it indicates that the inside of the nerve membrane becomes 70 to 90 mv more negative than the outside , this electrical potential that exists across the nerve membrane produced by differing in the concentrations of ions on either side of the membrane .

Depolarization (phase 2):

When a stimulus of significant intensity is applied to the nerve it will excites the nerve and the following events occur in sequence :
1. Slow depolarization : this is the initial phase where in the electrical potential inside the nerve become slightly less negative .
2. Rapid depolarization : the electrical potential which is becoming less negative , reaches a critical level , it results in an extremely rapid phase of depolarization.
3. Reversal of electrical potential : with the phase of rapid depolarization there is reversal of electrical potential across the nerve membrane , the interior of the nerve is now electrically positive and the exterior is negative .





The depolarization occur due to an increase in permeability of the membrane to Na ions . the rapid influx of Na ions to the anterior of the nerve will cause depolarization of the nerve membrane form the resting level to its firing threshold of approximately (-50) to (-60) mv , the firing threshold is actually the magnitude of the decrease in the negative membrane potential that is required to initiate an action potential (impulse) , when firing threshold is reached permeability of the membrane to Na increases and at the end of depolarization the electrical potential of the nerve is reversed an electrical potential of (+40) mv exists , this process takes 0.3 millisecond .

Re _ polarization (phase 3)

It occurs at the end of the various phases of depolarization , the electrical potential gradually becomes more negative inside the nerve relative to the outside until the original resting potential of -70 mv is restored , this is achieved by increasing permeability to k ions , and thus k ions move to outside leading to membrane re – polarization and return to its resting potential (-70mv) , this process take 0.7 millisecond .


The movement of Na icon to the inside of the nerve during depolarization and the movement of K ions out of the nerve during re – polarization are process ( not require energy ) since each ions moves along its concentration . When the nerve return to its resting a slight excess of Na ions exist within the nerve cell and slight excess of K ions exist extra – cellularity , according a period of metabolic activity being called sodium pump leading to the movement of Na to the outside as well as movement of k to inside this pumping mechanism require energy that is coming from oxidative metabolism of adenosine triphosphate (ATP)

Accordingly the action potential could be defined as a transient membrane depolarization that result from a brief increase in the permeability of the membrane to sodium and also from delayed increase in the permeability to potassium .
Once an impulse has been initiated it moves along the surface of the axon to the CNS .

Mechanism of action of local anesthesia :

The concept behind the action of L.A is that it prevents both the generation and the conduction of an never impulse thereby they act like a roadblock between the source of impulse ( as surgical incision in soft tissue ) and the brain
Many theories have been suggested to explain the mechanism of action of L.A , in general the nerve membrane is the site at which local anesthetic agents exert their pharmacological actions , the most popular theories are :

1. Membrane expansion theory : this theory states that anesthetic molecules diffuse through the nerve membrane producing a general disturbance of the bulk membrane structure and expanding some critical region in the nerve membrane and thus preventing an increase in the permeability to sodium ions thus inhibiting both conduction and nerve excitation .



2. Specific receptor theory : this is most favored theory today , it proposes that local anesthetics act by specific receptors in the sodium channel (protein channel along the membrane) in the nerve membrane , once the local anesthetics has gained access to these receptors permeability to Na ions is decreased or eliminated and nerve conduction is interrupted.





Factor affecting local anesthetic action
1- PH value
It is well known that the PH of local anesthetic solution and the PH of the tissue into which it is injected greatly influences its nerve blocking action Acidification of the tissue decreases local anesthetic effectiveness , inadequate anesthetic results when local anesthetic injected into inflamed or infected areas since the inflammatory process produces acidic products .
2- Lipid solubility
Increased lipid solubility of local anesthetic permit the anesthetic to penetrate the nerve membrane more effective conduction blockage at lower concentration than less lipid soluble solutions .

3- Protein binding

The degree of protein binding of the anesthetic molecule is responsible for the duration of local anesthetic activity . local anesthetic possessing a great degree of the protein binding appear to attach more securely to the protein sites and to possess a longer duration of clinical activity
4- Vasodilator activity
Local anesthetic solution with greater Vasodilator activity will increase blood flow to the area , this will lead to rapid removal of anesthetic molecules from the injection site , decreasing anesthetic potency and duration .

Duration of local anesthesia

As the local anesthesia is removed from the nerve , the function of the nerve returns , rapidly at first but gradually slowing .
There are certain factors affecting the duration of local anesthesia such as :
1- protein binding : the rate at which an anesthetic is removed from nerve has an effect on the duration of nerve block , longer acting local anesthetic are more firmly bound to the nerve than shorter acting drug and are therefore released from the receptor sited in the sodium channel more slowly .
2- vascularity of the injection site : the duration is increased in areas of decreased vascularity .
3- presence or absence of vasoactive substance : the addition of a vasopressor into local anesthetic solution decrease the tissue perfusion thus increasing the duration of action .





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