Details of pain sensation

Pain sensation

Pain receptors are also called as nociceptors They are located at the ends of small 'C unmyelinated or myelinated A delta fibers

 a) Definition

Pain sensation is unpleasant but protective sensation aroused by noxious stimuli that damage or can damage body tissues

b) Physiology (properties & reaction)

Purpose or importance: Protective

 Stimulus: noxious (chemicals like- Ach, bradykinin, serotonin, hydrogen ions, potassium ions, prostaglandins or mechanical or thermal)

 Receptors: free nerve endings (polymodal receptors)

 Adaptation: non or slow adapting receptors

Nerve fibers: fast pain is carried by A-delta nerve fibers while slow pain by 'C' type.

Neurotransmitters: glutamic acid (at spinal cord) for fast pain, substance P (at spinal cord) for slow pain and Lewis P factor for muscle pain,

 Pathway: lateral spinothalamic (specific neo spinothalamic for fast pain and diffuse and non specific paleo spinothalamic for slow pain)

 Reaction: pain is associated with muscle spasm, withdrawal reflex (due to spread in spinal cord, specially with fast pain), arousal (due to collaterals to reticular formation), unpleasant emotions (due to collaterals to limbic system, specially with slow pain) and autonomic changes- nausea, vomiting, pulse and BP changes (hypothalamus, specially with slow pain)

 Localization: Usually pain is poorly localized. Superficial pain is comparatively better localized than deep pain. 

Intensity discrimination: is also comparatively better for Superficial pain than deep pain

c) Types of pain

Visceral Pain

Causes:

1. Over distension of hollow viscera (commonest)

 2. Ischemia

3. Obstruction

4. Spasm of hollow viscera

Pain is caused due to mechanical stimulation of pain endings and ischemia.

 Pathway: From free nerve endings via type C autonomic nerves to lateral STT,

 Properties: Causes referred and radiating pain (like viscera to peritoneum). It is more commonly associated with muscle guarding, unpleasant emotions and autonomic changes (nausea, vomiting, low pulse and low BP).

 Visceras insensitive to pain: Parenchyma of liver and alveoli of lungs are insensitive to pain But liver capsule, bronchi, parietal pleura are very sensitive to pain

 

Ischemic muscle pain_(SN)

During muscle activity Lewis P factor (adenine, K+ & lactic acid) pass from muscle to tissue space & get cleared by blood

But if level of Lewis P factor becomes high (e.g during exercise), pain starts till it is cleared,

 - Clinical

 i)intermittent claudication (leg pain on walking when arteries are blocked),

 ii) angina pectoris (chest pain on exercise when coronary arteries are blocked )

 

Referred Pain_(SN).

Referred Pain is the pain that is felt away from the damaged tissue,

 Dermatome rule-

Visceral pain is often referred to embryonic corresponding dermatome. The dermatome and the viscera are innervated by the nerves arising from the same spinal segment.

 Example-

- Cardiac pain is referred to inside of the left arm.

 - Pain of Appendix & ovary is referred to umbilicus,

 - Diaphragm to right shoulder

Theories of Referred Pain

1) convergence theory

Sensory nerve carrying pain sensation from the viscera and the sensory nerves carrying pain sensation the dermatome converge on to same second order neuron.

 

2) Facilitation theory-

Sensory nerve carrying pain sensation from the viscera via branches (collaterals) stimulates sensory nerve carrying pain sensation from the dermatome. (produce subliminal fringe effect)

d)Pain Pathway

Pain sensation has a dual pathway, one for the fast pain and other for the slow pain. Fast pain is carried by A delta nerve fibers while slow pain by type C fibers.,

 Nerves carrying pain sensation-

1) From face- by trigeminal nerve (5 cranial nerve)

 2) From esophagus, trachea & pharynx- 9 & 10 CN (parasympathetic nerves)

 3) From thoracic & abdominal viscera- sympathetic nerves

 4) From pelvic region- parasympathetic nerves 5) From skin of rest of the body- by free nerve endings in lateral spinothalamic tract

 

Origin, course & crossing of pain pathway

1 order neurons

Arise from receptors (free nerve endings) to dorsal horn of spinal cord, Marginal nucleus (MN) for fast pain & Substantia gelatinosa (SG) for slow pain

2 order neurons

Arise from Marginal nucleus and Substantia gelatinosa, cross to opposite side thro, anterior commissure and finally ascend in lateral column of spinal cord as neo spinothalamic tract (fast pain) and paleo spinothalamic tract (slow pain) and relay at vantrobasal complex of thalamus & nearby structure.

 

3 order neurons

arise from VBC of thalamus (mainly fast & few slow pain fibers) and terminate at primary sensory cortex (area 3,1,2)

 Termination

All fast pain fibers and few (20%) slow pain fibers terminate at primary sensory cortex while majority of slow pain fibers, subcortically at diffuse nuclei of thalamus, tectal nucleus and reticular formation.

 

Center

Is primary sensory cortex but is perceived at the level of thalamus and reticular formation,

 Collaterals

Collaterals

To reticular formation (aurosal), limbic system (emotion) and hypothalamus (autonomic changes)

e) Analgesic or pain control system of brain & spinal cord

 ⁃ Analgesic or pain control system of brain and spinal cord Or Mesenchephalic descending pain suppressing pathway

 1. Periaqueductal grey area These fibers cause release of encephalin & stimulate neurons in raphe nucleus

 2. The raphe magnus nucleus These fibers cause release of serotonin & stimulate neurons in spinal cord.

 3. Local neurons present in dorsal horns of spinal cord These fibers cause release of encephalin. Encephalin causes presynaptic inhibition of pain fibers entering into dorsal horn of spinal cord.

Stimulants of Analgesic System

⁃ Fibers from limbic system, hypothalamus

⁃ Stress, psychological stimuli

⁃ Collaterals from pain pathway

⁃ Brain opiates system (endorphins and encephalin)

 ⁃ Gait control theory of pain (dorsal horn of spinal cord)

 In the dorsal horn A beta, fine touch fibers, cause pre-synaptic inhibition of pain fibers & closes the gate for pain sensation

Role of brain in gate control

Terminals of pain fibers at dorsal horn have opiate receptors, here descending cortical fibers can also inhibit pain fibers & close the gate by secreting opiates

 

f) Clinical

Hyperalgesia- increase sensitivity to pain is known as hyperalgesia. It may be due to:

 1) primary hyperalgesia- increase sensitivity of receptors

 2) secondary hyperalgesia increase sensitivity of pathway. (thalamic overreacton)

 Hypoalgesia- is decrease sensitivity to pain while

 Paralgesia is abnormal pain sensation Acute pain (good pain) & chronic pain (bad pain)