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PC 705 Module 1 Pain

Terms in this set (39)

Stages of the Pain Response

Stage 1
Transduction:

Stimulation of nociceptors / nerve endings begins the pain process.
Stages of the Pain Response

Stage 2
Transmission:

Pain impulses move via sensory fibers.

Large / "fast" is transmitted via A delta fibers (myelinated) - skin, muscles; this type of pain is sharp, stingy, highly localized pain.

small / "slow" is transmitted via C fibers (un-myelinated) - internal organs; this type of pain is dull, achy, poorly localized pain.

The slower fibers cause more anxiety / stress.
Stages of the Pain Response

Stage 3
Perception:

Awareness and interpretation of meaning of pain and is the result of neural processing of the pain sensation in the brain.

This perception is influenced by attention, distraction, anxiety fear, fatigue, previous experience and expectations about pain.
Stages of the Pain Response

Stage 4
Modulation:

Occurs at the spinal cord and peripheral noise receptor endings and within the brain; it attempts to decrease perception of pain.

This will begin spontaneously because modulation i.e. rub it / press it / itch it.
Pain Nerve Impulses ...
Pain nerve impulses move to the spinal cord via the sensory afferent fibers to the posterior nerve roots and dorsal root ganglion to enter the dorsal horn and up and down the spinal cord stimulating the injured body part to move away from the pain stimulus.
Dermatones
The brain is able to localize pain sensation because noise receptor transmission pathways are in anatomic order in the spinal cord and the somatosensory cortex.

Each spinal nerve has noise receptor fibers for a particular area of the body surface; these are called sensory dermatones.
Dermatomal Distribution.
Pain that has a dermatomal distribution is due to spinal nerve compression or trama; this is called radiculopathy.

Herpes Zooster occurs in a specific nerve root.

Periperal Neuropathy does not follow a dermatomal pattern
Pain Threshold
The pain threshold is the level of pain needed to be perceived; close to the same in most people
Pain Tolerance
The pain tolerance is the amount of pain one is willing to bear; this varies widely among individuals.

Pain tolerance is influence by age, culture, upbringing, gender, and previous pain and environmental experiences i.e. noise / bright light / lack of sleep.
Pain Expression
Pain expression is the way we express our pain experience to others.

Varied among individuals and is what makes pain difficult to assess because we all express pain differently.
Gate Control Theory
Developed in 1965, the gate control theory proposes that a neural mechanism in the dorsal horns of the spinal cord acts like a gate that can increase or decrease nerve impulses from the peripheral nerves to the central nervous system.

This increase or decrease is determined by the activity of the large / small diameter fibers in brain.

To close gate we need to stimulate the large neural fibers to block the small fibers; for example TENS unit / sterile water injection.
Neuromatrix Pain Theory
This is an expansion of the gate control theory and emphasizes that pain is multi-dimensional; whole body-mind experience.

Massage / heat used etc.
Endogenous Opiate Peptides
Endorphins / Enkephalins decrease the perception of pain.

Produced in the CNS and secreted from anterior pituitary during times of stress, pain, emotion - "stress induced analgesia". Also released when eat chocolate, by laughter, and by massage or acupuncture.

Reduce pain and produce sedation and euphoria.
Types of Pain
Pain is a symptom - the character, location and duration helps in diagnosing the problem.

Pain is subjective and learned via Hx.
Physiologic pain
Physiologic pain is due to tissue injury.

It occurs / aids in prevention of further injury.

Example: touching a hot stove.
Pathologic pain
Pathologic pain occurs after tissue injury with long term changes that enhance pain sensation.

Example: Neuropathic pain / fibromyalgia.
Acute pain
Acute pain is the result from tissue injury and will resolve when healed; < 3 months / may be recurrent.

Accompanied by sympathetic response (stress response i.e. alarm phase) including responses of increased V/S, sweating, nausea, pallor.
Headache
Most common cause of acute pain

Types include tension, migraine and sinus
Migraine
Migraine - very common, often misdiagnosed and affects adults and children

Current theory of migraines including stimulation of the Trigeminal nerve (CN V) along with changes in neurotransmitter levels in the CNS and alterations in blood vessel tone

Related causes - dysfunction of brainstem areas that control craniovascular afferent nerves
Release of inflammatory chemicals - calcitonin gene-related peptide >> vasodilation
Migraine - Triggers
Certain "triggers" may activate changes that lead to headache:

-Wine
-Cheese
-Skipped meals, artificial sweeteners
-Change in sleep patterns, etc
-Genetic predisposition to triggers that begin the migraine
Migraine - Clinical Manifestations
Severe unilateral pounding or throbbing pain that is increased by activity.

Nausea, vomiting, photophobia, phonophobia, lacrimation, nasal congestion, neck muscle stiffness or pain, dizziness, changes in bowel patterns
Classic Migraine vs Common Migraine
Classic migraine is preceded by aura i.e. odor / visual manifestation.

Common has no aura.
Chronic Pain
Lasts more than several months (>6).
Causes:
malignancy - easy to diagnose reason.

Peripheral sensitization >> decreased pain threshold and increased response of nociceptors; increases peripheral transduction.

Central sensitization >>changes in CNS neurons - abnormal state of increased responsiveness of nociceptors
Chronic Pain has ...
Chronic pain has no sympathetic signs or symptoms.

But it is often associated with psychological symptoms - lack of sleep, fatigue, irritability, psychosocial difficulties.

Depression - very common
Fibromyalgia
Chronic pain syndrome; affects women more than men.

Risk factors: medical history of excessive stress, trauma, sexual abuse, viral illness, endocrine disorder.

Etiology unknown - theory is that it is a disordered central pain processing problem.
Fibromyalgia Diagnostic Criteria
Diagnostic Criteria for Fibromyalgia include:

Chronic widespread pain for >3 months without explanation on all quadrants of the axial skeleton.

There has to be presence of 11 of 18 tender points with both :
Hyperalgesia ( increased sensitivity to pain)
Allodynia (pain from a stimulus that other would not consider painful).
Fibromyalgia - Clinical Manifestations
-Pain in several areas of the body that comes and goes and does not follow a dermatomal distribution
-Pain worsens with exertion
- There are noted sleep disturbances with sequential fatigue.
-Depression and anxiety
-Decreased attention and short-term memory
Cancer Related Pain
Growing cancer within an organ or compression of structures by growing tumor.

Can be caused by radiation therapy or chemotherapy tissue destruction.
Neuropathic Pain
Complex - nerves are damaged or dysfunctional.

It is due to altered central processing of nociceptive input.

There is nerve injury that leads to excitotoxic and apoptopic(planned) cell death of neurons.

There is depleted GABAergic interneurons which leads to hyperalgesia and allodynia.
Trigeminal Neuralgia
Very painful; more prevalent in women; seen in middle aged and older adults.

Etiology - chronic compression of the trigeminal nerve (CN 5) by a vessel that causes demylination of the 5th CN and alteration in nerve signaling.
Trigeminal Neuralgia Clinical Manifestations
Sudden, sharp, shooting pain along the second and third segments of 5th CN.

Like an electrical shock during attack, then dull ache between attacks.

Anxiety related to waiting for the next attack.
Diabetic Neuropathy
Affects 60-70% of persons with DM; lower extremities.

Etiology - damage to peripheral nerves due to occult inflammation and demylination of larger peripheral nerves; causes small bombardment of smaller fibers..

Loss of mechanism to inhibit sensory input; ischemia also contributes.
Diabetic Neuropathy Clinical Manifestations
Varies patient to patient but pain is worse at night.

Loss of fine touch and vibratory sense; numbness / tingling.

Loss of proprioception ("one's own", "individual" and perception).
Postherpetic Neuralgia
Disabling complication of Shingles.

Persistent pain that lasts >8 weeks after onset of lesions - burning pain over the affected dermatome.

Risk factors - advanced age; immune compromise.
Ischemic Pain
Pain that results from decrease or loss of blood flow to tissue.

Tissue hypoxia causes release of inflammatory and pain producing chemicals.

Pain described as aching, pressing, heavy, prickling
Ischemic Pain Examples
Classic example - Myocardial infarction.

Arterial occlusion - sudden onset.

Peripheral artery disease (PAD) - due to atherosclerosis - LE pain on exercise.

Venous occlusions - pain has more gradual onset; causes deep ache and swelling of LE.
Referred pain
Pain felt in an area other than the site of injury.

Areas of the body share sensory dermatomes.

It is part of the embryonic development; shared nerve endings continue throughout life.

Patterns are predictive - help in diagnosis; i.e. appendicitis LRQ pain
Physiologic Response to Pain
Autonomic Nervous System:

Sympathetic Nervous System - Increase heart rate, respiration, and B/P. Dilated pupils, diaphoresis, pallor (due to vasoconstriction to divert blood to vital organs), bronchodilation, and increased blood glucose.

Release of stress hormones - cortisol, aldosterone, antidiuretic hormone
Pain in Young and Elderly
Infants, even very young premature, have pain perception.

Elderly - experience pain and it can have a very negative effect on quality of life.
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