Pain Pathways and Nervous System

Intended Learning Outcomes

• Students should understand the pain pathway and related nervous system parts
• Students must know the definition of pain
• It is key to understand methods of controlling pain
• Students must describe neuroanatomy
• Describe neurophysiology
• Describe nerve anatomy

Definition of Pain

• Pain is an unpleasant sensation from a harmful stimulus
• This sensation travels as an impulse along a specific nerve pathway to the CNS, where it's interpreted
• Harmful stimuli can be thermal, electrical, chemical, or mechanical

Fundamentals of Impulse Propagation

• The neuron, or nerve cell, is the nervous system's structural unit
• Neurons transmit messages between the CNS and all body parts
• Sensory (afferent) and motor (efferent) neurons are the two neuron types
• Sensory neurons send impulses from sensory receptors to the CNS
• Motor neurons conduct impulses from the CNS peripherally
• Nerves are either myelinated or non-myelinated
• Myelinated nerves have a lipid-rich myelin layer for faster impulse conduction
• Constrictions at regular intervals on myelinated nerves are called nodes of Ranvier

Classification of Peripheral Nerve Fibers

• Type A Fibers are myelinated
  • A-alpha fibers control motor function
  • A-beta fibers govern touch and pressure
  • A-gamma fibers handle touch and motor functions
  • A-delta fibers control pain and temperature
• Type B Fibers comprise myelinated autonomic nerves
• Type C Fibers are non-myelinated nerves, responsible for pain and temperature

Electrophysiology of Nerve Conduction

• Step 1: A nerve has a resting potential of -70mV, with the interior negative relative to the exterior
• Step 2: A stimulus excites the nerve, leading to a firing potential of -55mV, followed by depolarization to +40mV; the interior becomes positive
• Step 3: Repolarization occurs via the sodium-potassium pump
  • The interior gradually becomes more negative until the original resting potential is restored

Dual Aspect of Pain

• Pain Perception refers to the reception of pain by pain receptors
  • Subsequent transmission occurs via neural structures to the CNS
  • In healthy individuals, this phase is consistent
  • Diseases can affect this phase
  • An intact neural mechanism is necessary
• Pain Reaction
  • It's the patient's manifestation of their pain perception
  • Pain reaction varies among individuals and at different times for the same person
  • Pain threshold is inversely proportional to pain reaction
  • Higher pain thresholds result in a lesser pain reaction
  • Manifestation includes facial expressions, crying, and tapping
  • Pain reaction relies on the functioning of the thalamus and cortex
  • Depressed thalamic action reduces pain reaction
  • Slight cortical depression increases pain threshold
  • Increased cortical depression eliminates pain reaction

Factors Affecting Pain Threshold

• Emotional Status: Emotionally unstable patients have a low pain threshold and greater pain reaction
• Fatigue: Fatigued patients have a low pain threshold and greater pain reaction
• Age: Young patients display a low pain threshold and greater pain reaction, while adults have a high pain threshold and less pain reaction
• Sex: Male patients usually possess a high pain threshold and less pain reaction
• Fear and Apprehension: Fearful patients lower their pain threshold

Factors Summary

• Pain threshold is lower in females, children, fatigued people, those with unstable emotions, and fearful individuals

Trigeminal Nerve Nuclei

• Sensory trigeminal nerve nuclei extend through the midbrain, pons, and medulla
• The nucleus is divided into 3 parts:
• Mesencephalic Nucleus: Lies in the midbrain and deals with proprioception
• Main Sensory Nucleus: Found in the pons, associated with touch and pressure
• Accessory Sensory Nucleus: Located in the medulla, it is responsible for pain and temperature

Trigeminal Motor Nucleus

• A distinct trigeminal motor nucleus lies medial to the main sensory nucleus in the pons

Sensory Pain Pathway of the Teeth

• Separate pathways exist for touch, pain, and temperature sensation
• Each pathway begins at a sensory receptor (for example, a tooth) and ends at the cerebral cortex, where sensory sensation is interpreted
• Each pathway consists of 3 connected neurons
• 1st Neuron (From sensory receptors to sensory nucleus)
  • The sensory stimulus is first received by mechano-heat nociceptors in the pulp
  • It’s carried by myelinated A delta fibers (acute pain) and unmyelinated C fibers (chronic pain) of the trigeminal nerve
  • The impulse travels along elongated dendrites to the trigeminal ganglion (gasserian or semilunar ganglion)
  • Then, the impulse is mediated by the sensory root of the trigeminal nerve into the pons
  • In the pons, the sensory root ends directly in the main sensory nucleus (touch), or travels via spinal tract fibers (pain/temperature) to the accessory sensory nucleus in the medulla
• 2nd Neuron (From sensory nucleus to posterioventral nucleus of the thalamus)
  • Axons of the 2nd neuron emerge from the accessory sensory nucleus
  • They cross the midline and ascend to join fibers of the mesencephalic nucleus
  • It forms the spinothalamic tract to the contralateral thalamus
  • From the main sensory nucleus, axons cross the midline and ascend via the trigeminal leminiscus to the contralateral thalamus
  • The 2nd neurons terminate in the posterioventral nucleus (PVN) of the thalamus
• 3rd Neuron (From posterioventral nucleus of the thalamus to cerebral cortex)
  • Pain impulses are conveyed to the third neuron
  • Projects from the PVN to the posterior central area of the posterior cortex for pain sensation

Methods of Pain Control

• Removing the cause of pain prevents the initiation of painful impulses
• Blocking the pathway of the impulse
  • Injecting a drug with local analgesic properties prevents nerve depolarization, stopping impulse conduction
• Raising the pain threshold
  • Using analgesic drugs raises the pain threshold
  • Risk of undesirable side effects
• Preventing pain reaction via cortical depression
  • General anesthetics depress the CNS, preventing conscious reaction
• Using psychosomatic methods
  • Effectiveness relies on the patient's state of mind

Management of Acute Postoperative Pain

• Non-opioid mediated analgesia (peripheral or central)
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
    • Inhibit cyclooxygenase enzymes (COX) to prevent prostaglandin release and inflammation
    • Has a peripheral mode of action
  • Acetaminophen (Tylenol or Paracetamol)
    • Analgesic effect but limited anti-inflammatory action
    • Acts mainly centrally but possesses limited peripheral anti-inflammatory activity
• Opioid mediated analgesia is potent; used for severe pain unrelieved by NSAIDs/acetaminophen, many disadvantages include mental issues, tolerance, dependence, and respiratory depression
• Preoperative administration of NSAIDs: Reduces the severity of postoperative pain and extends analgesic effect
• Long-acting local anesthesia: Nerve blockade provides surgical anesthesia and postoperative analgesia
  • Agents like Bupivicaine can last 5-9 hours
  • Etidocaine has an analgesic effect up to 20 hours
  • Prevents pain during hypersensitivity or hyperalgesia after surgery
• Combined strategy: Preoperative NSAIDs and long-acting local anesthesia are combined