CM: Headache, Back Pain, & Management Flashcards

1
Q

What is nociceptive vs.neuropathic pain?

A
nociception = transmission of nerve impulses along certain pathways in response to application of potentially tissue-damaging stimuli
neuropathic = sharp, burning, gnawing, aching, shooting, lancinating, often persists w/o application of stimulus, poorly responsive to Rx
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2
Q

What does the term “pain” encompass that nociception does not?

A

emotional responses to having pain

serves a protective role

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3
Q

What is peripheral sensitization?

A

inflammatory soup accompanies painful stimulus and lowers threshold for pain generation from peripheral nociceptors
can lead to central sensitization

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4
Q

What is hyperalgesia and allodynia?

A

allodynia: normally innocuous stimuli produce sensation of pain when applied to peripherally sensitized tissues
hyperalgesia: normally painful stimuli provoke exaggerated responses

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5
Q

What is the physiological basis for central sensitization?

A

wind-up: progressive build up of amp of response of dorsal horn neurons during repetitive stimuli to C fibers = C fiber dependent
peripheral sensitization and structural changes (increase in nerve fiber density)
decreased inhibition

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6
Q

What are the three types of axons for peripheral nociception?

A

alpha-delta: finely myelinated, slow conducting, small diameter - pricking, sharpness, achy feelings, do what C fibers do with more gusto
C: unmyelinated, very slow, very small, employ substance P - burning sensation

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7
Q

What is substance P?

A

peripherally: dilates cutaneous vessels, releases histamine from mast cells, chemoattractant for leukocytes - result in increased hypersensitive area
centrally: nociceptive transmitter in dorsal horn - excites relay neurons involved in pain transmission

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8
Q

When is substance P released?

A

when normally propagating AP rebounds antidromically through other axonal branches, which activates other C fibers to release it

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9
Q

What are the pathophysiological correlates to neuropathic pain?

A

damage to larger, more myelinated fibers –> loss of vibration and proprioception = weakness, not as painful
damage to small, myelinated fibers –> loss of pain, light touch, and temp = pinprick, more painful

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10
Q

What different fiber types are involved in polyneuropathies?

A

small fiber = painful, no EMG findings necessarily

large fiber = can be painful, sensory ataxia, should have EMG findings

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11
Q

What is a brief ddx of polyneuropathies?

A

DIABETES!

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12
Q

What are different ways that neuropathies are classified?

A

fiber type
etiology
pathophysiology (axonal, demyelinating, mixed) - demyelinating has weakness earlier and more severe than axonal

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13
Q

How can polyneuropathies be evaluated?

A

labs, CXR, EMG, hemoccult stools x3, skeletal survey, repeat labs 6-12 mos, ANS testing, Ab testing

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14
Q

What are characteristics of referred pain?

A

deep, achy, intensity similar to that of local
upper lumbar –> flank, hip, groin, ant thigh
lower lumbar –> buttock, sciatica

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15
Q

What are characteristics of radicular pain?

A

similar to referred but more severe, radiates distally, in a nerve root distribution
increases with valvalva maneuvers, straight leg raising
sharp, intense superimposed on dull, achy referred
often has numbing and tingling

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16
Q

What are characteristics of pain from muscle spasm?

A

local, dull, crampy
can see or feel muscle
stiffness, limited movement, numbness/tingling, weakness, bowel/bladder incontinence
characteristic postural adjustments: knees and hips flexed, fetal position
prolonged sitting and standing from sitting is painful

17
Q

What is cauda equina syndrome?

A

LMN findings only, intense low back pain, bilateral sciatic distribution, decreased perianal sensation = saddle anesthesia, loss of both ankle jerks, asymmetric LE weakness, radicular symptoms, may have urinary retention or impotence

18
Q

What is conus medullaris syndrome?

A

mixed UMN and LMN findings, bowel bladder and sexual dysfunction early, poor rectal tone, perianal sensory chages = saddle anesthesia, sometimes lower extremity weakness, less severe radicular pain

19
Q

What are alarm signs suggestive of a secondary cause of acute headache?

A

worse headache ever
first headache >50
change in headache pattern (esp accelerating)
apocalyptic onset (rapid progression to max intensity)
onset w exertion (cough, sneeze, sex)
subacute that worsens
headache w systemic illness
associated w abnormal neurological symptoms or physical findings

20
Q

What are alarm signs suggestive of a secondary cause of chronic headache?

A
increasing frequency
dyscoordination
hx of localized signs
awakened BY (not with) headache
occipitonuchal location
21
Q

How can a tension type headache be recognized?

A

can cause chronic daily headache
dull ache, located posteriorly/occiptionuchally
“band around head”, tightness, pressure
no nausea/vomiting, not increased by physical activity, no sonophobia/light sensitivity*
tight stiff neck, neck movement causes radiation
chronic - lightheadedness, dizziness, fatigue
not everyone has evidence of muscle overactivity

22
Q

How can a rebound headache be recognized?

A

= medication overuse

only in migraine pts, hard to treat

23
Q

What are sinus headaches?

A

usually not - mostly migraines (including TTH)

lack any other sinus symptoms

24
Q

How can migraine with aura be recognized?

A

unilateral, pulsing/throbbing, usually in frontal, temporal, orbital or overlapping
worsened by physical exertion
lasts 4-72 hrs
uncontrolled bouts of dysautonomia

25
Q

What are the four phases to a migraine attack?

A

prodrome (hrs-days before)
aura (immediately proceeding): mostly visual, can be sensory or motor, see bright moving lights, can have tingling/numbness/weakness, don’t return to normal before headache
headache pain (<72 hrs)
postdrome (hrs-days after): poor concentration, tired, refreshed or euphoric, anorexic or food cravings

26
Q

How can cluster headaches be recognized?

A

adult men
severe unilateral orbitotemporal/retroorbital headache with no crescendo for pain <1 hr
associated w Horners
2 aspects: headache is time-locked in circadian pattern, occurs for weeks to months then remits then recurs often with spring and fall
*purse physical activity, unlike migraines (pacing, rocking, hitting head)
alcohol can provoke