PT 22 Pain, Headache, and Thermal Sensation

Pain

Present when there is tissue damage

Causes individual to remove painful stimulus; protective mechanism

If impaired (such as in SCI), can result to skin or tissue breakdown resulting to pressure ulcers

Removal of somatosensory areas of the cortex does not destroy the ability to perceive pain

Pain impulses to lower areas can cause conscious perception of pain

Cortex

determines quality of pain

Reticular areas and intralaminar nuclei of thalamus

causes widespread arousal of the nervous system

Fast-sharp pain

felt within 0.1 seconds of the stimulus and sharp, pricking, acute, & electric in character; not felt in most deep tissues of the body

Transmitted by A-delta fibers

Transmitted in the neospinothalamic tract

Via mechanical or thermal pain stimuli

HIGHLY LOCALIZED

slow chronic pain

begins after a second or more and is throbbing, aching, nauseous, unbearable, and chronic in nature; can occur in skin & any deep tissue/organ

Transmitted by type C fibers

Transmitted in the paleospinothalamic tract

Mostly via chemical type of stimuli

MORE DIFFUSED

Related to tissue destruction

Neospinothalamic tract

Terminate mainly in lamina I (neurons in dorsal horn)

2nd order neuron decussates immediately and passes to the brain in the anterolateral columns

Some neurons terminate in the reticular substance but must go all the way to the ventrobasal complex of the thalamus

3rd order neurons from the thalamus go to the cortex

Can be localized well; must be stimulated with other tactile receptors (such DCML)

Paleospinothalamic tract

Terminate in laminae II and III (substantia gelatinosa)

2nd order neurons decussate immediately and pass to brain in anterolateral column

Only 10-25% terminate in the thalamus; most go to the:

Reticular nuclei of medulla, pons, & mesencephalon

Tectal area of midbrain

Periaqueductal grey region surrounding Aqueduct of Sylvius

Poor localization (often to just affected part)

Substance P

Glutamate

Substance P

slow-chronic neurotransmitter of type C nerve endings; released more slowly and causes lagging sensation

Glutamate

gives a faster pain sensation; acts instantaneously but only lasts for a few seconds

All pain receptors are?

free nerve endings

Hyperalgesia

increase in sensitivity of pain receptors

Pain occurs when skin is heated?

above 45 Celsius

Bradykinin

causes the MOST pain & may be the single agent mostly responsible for pain after tissue damage

Mediates inflammation

Causes pain by directly stimulating primary sensory neurons and provoking release of substance P, neurokinin, and calcitonin gene-related peptide

Tissue ischemia

blood flow to tissue is blocked; greater rate of tissue metabolism leads to faster appearance of pain

Mechanical pain from tight BP cuff

Accumulation of lactic acid

Muscle Spasm

direct stimulation of mechanosensitive receptors; overstretch or repeated stretch

Spasms cause compression of blood vessels leading to ischemia

Pain Suppression

Activation of analgesia system via nervous signals entering the periventricular areas and periaqueductal gray

Inactivation of the pain pathways by morphine-like substances (natural opiates)

Lateral inhibition

Analgesia system

pain control system of the brain that grants its capability to suppress input of pain signals to the nervous system

Major components of analgesia system

Periaqueductal gray area

Raphe nuclei

Paragigantocellularis

Brian's Opiates: Descending Inhibition

Periventricular nucleus nerve fibers

Raphe magnus nerve fibers

Serotonin at aqueduct of Sylvius

Enkephalin

Periventricular nucleus

secrete enkephalin at nerve endings

Raphe magnus nerve fibers

secrete serotonin at nerve endings

Serotonin at aqueduct of sylvius

causes local neurons to secrete enkephalin

Enkephalin

believed to cause both pre- and postsynaptic inhibition of type A-delta & C fibers

Endogenous opiate systems

Morphine-like agents (mainly opiates) act on many points in the analgesia systems, including the dorsal horns of the spinal cord

All opiate-like substances found in the nervous system were breakdown products of large protein molecules (pro-opiomelanocortin, proenkephalin, and prodynorphin)

Met enkephalins and leu enkephalins

brainstem and SC

Beta endorphins

hypothalamus & pituitary gland

Dynorphin

same area as enkephalins but in lower quantities

Opiate system

functions as pain suppression during times of stress

Reduction of responsiveness to pain is important during emergency situations

Effective in defense, predation, dominance and adaptation to environmental challenge

Gate control hypothesis

stimulation of large type A-beta sensory fibers (mechanoreceptor) from peripheral tactile receptors may depress transmission of pain signals

Referred pain

Pain from internal organs are often "referred" to a distant area of skin

Referred to the dermatome of embryological origin

Visceral Pain

have few sensory fibers except for pain fibers; highly-localized damage results in little pain but widespread damage results in severe pain

Difficult to localize; pain generalized by the brain if coming internally

DIFFUSE

Sensations from thoracic and viscera transmitted via 2 pathways (visceral and parietal)

True visceral Pain

via sensory fibers within ANS and sensations referred to surface of the body, FAR from the painful organ

Parietal sensations

conducted directly into local spinal nerves from parietal peritoneum, pleura or pericardium; DIRECTLY OVER the painful area

All visceral pain that originates in the?

thoracic and abdominal cavities is transmitted through small type C pain fibers and, therefore, can transmit only the chronic, aching, suffering type of pain

Ischemia

Formation of acidic metabolic end products or tissue degenerative products such as bradykinin, proteolytic enzymes or others stimulate pain nerve endings

Chemical stimuli

Damaging substances may leak from the GI tract into the peritoneal cavity through a ruptured ulcer

May cause digestion of visceral peritoneum causing excruciating pain

Spasm of hollow viscus

Spasm of the gut, gallbladder, bile duct, ureter can cause pain, via mechanical stimuli

May also be caused by decreased blood flow to the muscle and increased metabolic need for nutrients

Pain from spastic viscus often occurs in the form of cramps

Overdistention of hollow viscus

Overfilling of viscera can cause pain due to overstretching

Can cause collapse of the blood vessels causing ischemic pain

Sensitive viscera

Some viscera are insensitive to pain on any type

Liver capsule - extremely sensitive to direct trauma & stretch

Bile ducts, bronchi, & parietal pleura are sensitive to pain

Parietal pain caused by visceral disease

disease in viscus often spreads to parietal peritoneum, pleura, or pericardium

Headache of intracranial origin

Not likely caused by damage within the brain itself

Can be a result of:

Tugging on venous sinuses

Damage to the tentorium or stretching of dura

Stretching crushing, traumatizing stimuli to the blood vessels of the meninges

Stimulation of pain receptors in the cerebral vault above tentorium initiates pain impulses from the 5th nerve causes referred headache to the front half of the head

Subtentorial pain stimuli causes occipital headache, referred to the posterior part of the head

Types of Intracranial Headache

Meningitis

CSF pressure

Migraine

Alcoholic

Types of Extracranial headache

Muscle Spasm

Irritation of nasal and accessory structures

Eye disorders

Meningitis

One of the most severe

Pain referred over entire head

CSF pressure

Intense intracranial headache

Can be caused by a decrease of as little as 20 ml of fluid from the spinal canal

Increased intracranial pressure

Weight of the brain stretches & distorts dura

Migraine

Specific cause unknown

Often begin with various prodromal sensations (nausea, loss of vision in part of the field of vision, visual aura, and other types of sensory hallucinations)

Prodromal symptoms begin 30-60 minutes before actual headache

Possibly caused by prolonged emotion or tension, which leads to vasospasm of arteries in the head

Other causes may be spreading of cortical depression, psychological abnormalities, vasospasm as a result of

increased potassium in the cerebral fluid, genetics (65-90% has positive family history)

Alcoholic

Following excessive alcoholic consumption; alcohol directly irritates meninges (toxic to tissues)

"Hangover" as a result of dehydration, causing headache

Muscle Spasm (extracranial)

from emotional tension

Causes muscles of the head (especially scalp) and neck muscles (occiput) to become spastic & tight

Irritation of nasal and accessory structures

Mucous membranes of nose & nasal sinuses are sensitive to pain but not intensely

Infection or irritation in widespread areas of nasal structures summate & cause headache

Referred behind the eyes or in frontal surfaces of forehead & scalp (front sinusitis)

Pain from lower sinuses can be felt in the face

Eye disorders

Difficulty to focus clearly causes excessive contraction of the ciliary muscles to gain clear vision; results to retro-orbital headache

Excessive attempts to focus eyes result in reflex spasms of facial & extraocular muscles

Headache can also occurs when eyes are exposed to excessive irradiation by light rays, especially UV (looking at sun causes headache for 24-48 hours)

Irritation of conjuctivae results in referred retro-orbital pain

Focusing on intense light may burn retina & cause headache

Warm receptors

free nerve endings, mainly type C fibers

Cold receptors

small A-delta myelinated fibers and some are type C, suggesting that some free nerve endings might function as cold receptors

Cold receptors respond?

from 7 to 44°C with the peak response at 24°C;

Cold pain occurs at?

15°C

Warm receptors respond?

from 30 to 49°C with the peak response at 44°C

Heat pain occurs at

45°C

At 45°C, heat pain fibers begin to be stimulated by heat and some cold fibers get stimulated again because of damage to the cold endings caused by excessive heat

Thermal receptors adapt but?

NOT FULLY

Thermal senses respond greatly to?

changes in temperature in addition to responding to steady states of temperature

Mechanism of stimulation

Stimulated by changes in metabolic rates

Temperature alters rate of intracellular chemical reactions more than twofold for each 10°C change

Thermal detection does not come from physical effects but from?

chemical stimulation to the nerve endings

Temperature Pathway

In general, thermal signals are transmitted in pathways parallel to those for pain signals

Travels up or down in Lissauer tract