pain sensation

- protective mechanism

- Occurs whenever tissues are being damaged causing person

to react thereby removing the pain stimulus

- E.g sitting for a long period of time

- Lost pain sensation --- total breakdown and desquamation of

skin on pressure areas

2 types: FAST PAIN and SLOW PAIN

PAIN

protective mechanism

PAIN

Occurs whenever tissues are being damaged causing person to react thereby removing the pain stimulus

PAIN

• Felt within about 0.1 sec after pain stimulus applied

• Sharp pain, pricking pain, acute pain, electric pain

• Not felt in most deeper tissues of the body

• Elicited by either mechanical or thermal stimuli

• Conveyed from small type Aδ fibers

• Velocity between 6 and 30m/sec

• Eg. Needle stuck into the skin, cut skin, acute burn, electric

shock

Fast Pain

Felt within about 0.1 sec after pain stimulus applied

Fast Pain

Sharp pain, pricking pain, acute pain, electric pain

Fast Pain

Not felt in most deeper tissues of the body

Fast Pain

Elicited by either mechanical or thermal stimuli

Fast Pain

Conveyed from small type Aδ fibers

Fast Pain

Velocity between 6 and 30m/sec

Fast Pain

Begins after 1 sec or more then increases slowly over many seconds or minutes

Slow Pain

Slow burning pain, throbbing pain, nauseous pain, chronic pain

Slow Pain

Usually associated with tissue destruction and lead to prolonged, unbearable suffering

Slow Pain

Occurs in skin and any deep tissue or organ

Slow Pain

Elicited mostly by chemical type of pain stimuli or persisting mechanical or thermal stimuli

Slow Pain

Conveyed from Type C fibers

Slow Pain

Velocities between 0.5 and 2m/sec

Slow Pain

• Represented by free nerve endings

• Widespread in superficial layers of the skin

• Internal tissues ( periosteum, arterial walls, joint surfaces, falx

and tentorium cerebri)

• Adapt very little or not at all

• Excitation of pain fibers become progressively greater

• HYPERALGESIA – increase in sensitivity of the pain receptors

Pain Receptors

• Represented by free nerve endings

Pain Receptors

• Widespread in superficial layers of the skin

Pain Receptors

• Internal tissues ( periosteum, arterial walls, joint surfaces, falx

and tentorium cerebri)

Pain Receptors

• Adapt very little or not at all

Pain Receptors

• Excitation of pain fibers become progressively greater

Pain Receptors

• – increase in sensitivity of the pain receptors

HYPERALGESIA

3 types of stimuli

mechanical

thermal

chemical

Chemical

o Bradykinin, serotonin, histamine, K ions, acetylcholine

These are slow or fast pain?

slow pain

these enhance the sensitivity of pain endings

prostaglandinds and substance P

what are the causes of pain?

chemical pain stimuli

tissue ischemia

muscle spasm

• Bradykinin more painful than other chemical

• Most responsible for causing pain following tissue damage

• Intensity of pain felt correlates with the local increase in ion concentration or Increase in proteolytic enzymes directly attacking the nerve endings and excites pain

  • Making nerve membranes permeable to ions

Chemical pain stimuli

Bradykinin more painful than other chemical

Chemical pain stimuli

Most responsible for causing pain following tissue damage

Chemical pain stimuli

• Intensity of pain felt correlates with the local increase in ion concentration or Increase in proteolytic enzymes directly attacking the nerve endings and excites pain

  • Making nerve membranes permeable to ions

Chemical pain stimuli

• Blood flow of tissue is blocked

• Accumulation of large amounts of lactic acid in the tissues as a result of anaerobic metabolism

• Greater the rate of metabolism of the tissue, the more rapidly the pain appears

• Bradykinin and proteolytic enzymes may have also formed because of cell damage

Tissue Ischemia

Blood flow of tissue is blocked

Tissue Ischemia

Accumulation of large amounts of lactic acid in the tissues as a result of anaerobic metabolism

Tissue Ischemia

Greater the rate of metabolism of the tissue, the more rapidly the pain appears

Tissue Ischemia

Bradykinin and proteolytic enzymes may have also formed because of cell damage

Tissue Ischemia

• Common cause of pain

• Basis of many clinical pain syndromes

• Results from mechanosensitive pain receptors

• Indirect effect to compress blood vessels causing ischemia

• Increases rate of metabolism in muscle in muscle tissue making ischemia greater

Muscle Spasm

Common cause of pain

Muscle Spasm

Basis of many clinical pain syndromes

Muscle Spasm

Results from mechanosensitive pain receptors

Muscle Spasm

Increases rate of metabolism in muscle in muscle tissue making ischemia greater

Muscle Spasm

Indirect effect to compress blood vessels causing ischemia

Muscle Spasm

what are the dual pain pathways?

NEOSPINOTHALMIC TRACT

PALEOSPINOTHALMIC TRACT

• Fast type A-delta pain fibers (mechanical and thermal)

• Terminate mainly in the Lamina I (lamina marginalis) → excite 2nd order neurons of the tract → giving rise to long fibers crossing immediately to opposite side of cord → terminates in the reticular areas of the brainstem

NEOSPINOTHALAMIC TRACT

• Transmits pain mainly from type C pain fibers

• Peripheral fibers terminate in the SC almost entirely on Lamina II and III (substantia gelatinosa) à passes thru the anterior commissure to the opposite side of the cord.

PALEOSPINOTHALAMIC TRACT

Fast type A-delta pain fibers (mechanical and thermal)

NEOSPINOTHALAMIC TRACT

Terminate mainly in the Lamina I (lamina marginalis) → excite 2nd order neurons of the tract → giving rise to long fibers crossing immediately to opposite side of cord → terminates in the reticular areas of the brainstem

NEOSPINOTHALAMIC TRACT

Transmits pain mainly from type C pain fibers

PALEOSPINOTHALAMIC TRACT

Peripheral fibers terminate in the SC almost entirely on Lamina II and III (substantia gelatinosa) à passes thru the anterior commissure to the opposite side of the cord.

PALEOSPINOTHALAMIC TRACT

Spinal Cord gray matter: Rexed’s Laminae

Layer I

Layer II

Layer III & IV

Layer V

Layer VI

Layer VII

Layer VIII

Layer IX

Layer X

Layer I – Lamina Marginalis

Layer II – Substantia Gelatinosa

Layer III & IV – Nucleus Proprius

Layer V

Layer VI

Layer VII – Nucleus Dorsalis/ Clarke’s Column

– Intermediolateral horn (IML)

Lamina VIII

Lamina IX – Anterior Horn Cell

Lamina X – Central Gray Commissure

• Pain control system

• Capability of the brain to suppress input of pain signals to the nervous system

• 3 major components:

  1. Periaqueductal gray and periventricular areas of mesencephalon and upper pons

  2. Raphe magnus nucleus located in lower pons and upper medulla

  3. Pain inhibitory complex in the dorsal horns of the spinal cord

Analgesia

Pain control system

Analgesia

Capability of the brain to suppress input of pain signals to the nervous system

Analgesia

These areas should be electrically stimulated so we can suppress strong pain signals

periaqueductal gray area

raphe magnus nuclei

These are believed to cause both presynaptic and postsynaptic inhibition of type C and Type A-delta pain fibers

enkephalin and serotonin