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Pain & Headache

Terms in this set (57)

what is pain
perception of nocicpetive stimulation
pain: sensory & emotional expereinces affected by
beliefs, fears, anxiety
pain: characteristics-phsyical
Pallor, sweating, tachycardia, tachypnea, high blood pressure, nausea, vomiting, fainting, dizziness
pain: characteristics-emotional & behavioral
Anxiety, fear, clenched fist, rigid face, restless, constant motion vs. immobilization, body posture
pain descriptions often related to tissue injury
pp 5
red flags assocaited w pain
• Pain that wakens patient at night
• Deep-aching or throbbing pain
• Bowel or bladder changes with pain
• Migratory arthralgia
• Skin rash
• Fatigue
• Weight loss
• Low grade fever
• Recent infection
• Bilateral symptoms of any kind
acute pain
pp 7
ss acute pain
- increase BP/resp/HR

-cool/pale/moist skin

-increase skeletal muscle tension
Brain interprets info from:
Nociceptors are distributed through the body:

--skin, viscera, muscles, joints, meninges

• Are AFFERENT nerves
Nociceptors respond to
• Thermal = extremes of heat & cold

• Mechanical= pressure & other physical stress

• Chemical = histamine, prostaglandin, serotonin, bradykinin

--- Released from damaged tissues
---reduce activation threshold of nociceptors
Pain Pathway: From Nociceptor to Spinal Cord
Stimulus--> nociceptors --> sc --> thalamus -->

MANY parts of brain on 2 types of primary afferent pain fibers
a delta fibers
• info travels rapidly

• Respond to thermal and mechanical stim

• Acute, sharp, well-localized pain
c fibers
• info travels slowly

• Carries mechanical, thermal, and chemical info

• Chronic pain, dull, burning, aching, poorly localized
excitatory NT
-glutamate

-substance P
Brain Modulation: THREAT
tissue= contain nocicpetors (NOT PAIN)

---brain decides if input is threat and will produce an output of pain
categorizing pain
1. nociceptive (tissue)

2. peripheral neurogenic

3. central (brain issue)

**pp 13
Neuropathic Pain
injury to nervous tissue itself

---central (PCA stroke) or peripheral
CRPS:
-occur following a lesion or after a series of trauma

-affecting 1 limb
CRPS: results in
-abnormal sensory changes

- altered blood flow or excessive sweating due to ANS involvement

-motor system disorders & major functional limitations
Phantom Pain
-adults following amputation

-pain, itch, tingle in lost limb

-temp or persistent

*PAIN IS IN BRAIN*
peripheral neuropathy
pp 18
reffered pain
perceived at site distanct from source
reffered pain: due to
multiple sensory fibers from different sources converging at the same level in the spinal cord makes it hard for brain to identify original source
visceral pain: ss
-diffuse
-poorly localized
-deep/dull
chronic pain: aka
nociplastic pain or central pain
chronic pain occurs
after all tissue has healed!

--initiates pain cycle
-depression/fatigue/ sleep

*pain is real to pt*
Tissues heal, why does pain persist?
Central sensitization:

1. Too much c fiber firing to dorsal horn
---Lowered threshold for movement

2. Damage to interneurons that filter info to brain
---Inappropriate synapse, info from above/below/ contralateral

3. Damage to nerve changes the ion channels
---Stress, temperature, illness, movement
Normal Tissue Changes: pain or no pain
-ab image w no pain

-experience pain...PERCEPTION to enviroment & sensitive nervous system
Neuroplastic Changes
- not 1 pain center in brain

-mult areas impact (pp 26)

----> can lead to map changes to homolocus (smear, change in size, confusion)
changes to mapping
brain confused --> ramp up SNS (threat increases):

• Looks bigger/smaller

• L vs. R discrimination impaired

• Impaired 2-pt discrimination and localization
Nociplastic Pain: more likely to occur in people
were injured in a stressful situation
as brain continues to perceive a threat=
increase adrenaline, cortisol sensitivity --> increase inflammation
--> increase nerve inflammation
The longer pain persists, the greater the probability that pt. will become
-depressed

-fearful

-irritable

-erratic in search of relief
Important Issue in Chronic Pain Management- Behavioral Goals
-malingering

-ss magnify


pp34
pain assessment tools
body diagrams tells us alot if central
Sudden onset of HA may indicate
-intracranial disorder

----like hemorrhage, tumor, meningitis
headache (cephalgia): usually a ss of another disease process like
sinusitis, HTN, meningitis, anemia, constipation, PMS, tumors
etiology HA
•tension of facial, neck & scalp mm

• Vascular changes - vasodilation or constriction in the head

• May be produced by stress, noise, toxic fumes, lack of sleep, alcohol or drug consumption
HA: brain tissue
has NO sensory nerves so pain does not come from brain itself...

---from receptors in meninges, facial tissue & scalp
Tension HA: caused by
stress, strain or pressure on facial, neck & scalp mm
tension HA: pain in the
temples or occipital areas w associated tightness & tenderness in cervical & suboccipital musculature
tension HA: pain last
30 min to several days
tension HA: may also have
Poor concentration, visual disturbances, tinnitus, dizziness, clumsiness, sleep disorders
cluster HA:
• Rare but most painful

• Severe throbbing pain behind nose or one eye usually due to vasodilation; unilateral
cluster HA: occus most often
just prior to waking or at night during sleep

• More common in young males,> 30 years old, related to alcohol use
cluster HA: ss
• Eye may water, skin may become red; some correlation to Horner's syndrome

• Autonomic nervous system component
Migraine HA: prevalence
25% female, 8% male
migraine HA: ss
photophobia, noise sensitivity, N & V, visual disturbances (aura), throbbing pain
migraine HA: etiology
unknown:

-herreditary (60%)

-triggered by foods: (milk, eggs, corn, wheat, chocolate, wine, cheese, caffeine)
migraine HA: prodromal ss
signal a migraine is coming; may have excessive yawning, euphoria, cravings
migraine HA: auras
25%

may be visual: sensory paresthesias of hand & face with tingling & numbness, some motor weakness may occur
Status migrainosus
HA that lasts more than 72 hours often results in prolonged vomiting with dehydration
Cervicogenic Headaches:
• Originate in neck and spine; spreads to oculofrontal & temporal areas of head

• Tend to be unilateral
Cervicogenic Headaches: contribute factors
-fatigue

-poor posture

-stress
Cervicogenic Headaches: triggered
certain neck mvt or positoons

*PT greatest impact on this type*
HA dx & tx
pp 46
HA red flags
•sudden & severe

• w/ a fever, stiff neck, rash, confusion, seizure, double vision, weakness, numbness or difficulty speaking

• Follows a head injury

•worse despite rest & meds

• Is a new type in someone over 50

• Wakes you from sleep
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