CM: Headache, Back Pain, & Management Flashcards
What is nociceptive vs.neuropathic pain?
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
What does the term “pain” encompass that nociception does not?
emotional responses to having pain
serves a protective role
What is peripheral sensitization?
inflammatory soup accompanies painful stimulus and lowers threshold for pain generation from peripheral nociceptors
can lead to central sensitization
What is hyperalgesia and allodynia?
allodynia: normally innocuous stimuli produce sensation of pain when applied to peripherally sensitized tissues
hyperalgesia: normally painful stimuli provoke exaggerated responses
What is the physiological basis for central sensitization?
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
What are the three types of axons for peripheral nociception?
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
What is substance P?
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
When is substance P released?
when normally propagating AP rebounds antidromically through other axonal branches, which activates other C fibers to release it
What are the pathophysiological correlates to neuropathic pain?
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
What different fiber types are involved in polyneuropathies?
small fiber = painful, no EMG findings necessarily
large fiber = can be painful, sensory ataxia, should have EMG findings
What is a brief ddx of polyneuropathies?
DIABETES!
What are different ways that neuropathies are classified?
fiber type
etiology
pathophysiology (axonal, demyelinating, mixed) - demyelinating has weakness earlier and more severe than axonal
How can polyneuropathies be evaluated?
labs, CXR, EMG, hemoccult stools x3, skeletal survey, repeat labs 6-12 mos, ANS testing, Ab testing
What are characteristics of referred pain?
deep, achy, intensity similar to that of local
upper lumbar –> flank, hip, groin, ant thigh
lower lumbar –> buttock, sciatica
What are characteristics of radicular pain?
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
What are characteristics of pain from muscle spasm?
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
What is cauda equina syndrome?
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
What is conus medullaris syndrome?
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
What are alarm signs suggestive of a secondary cause of acute headache?
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
What are alarm signs suggestive of a secondary cause of chronic headache?
increasing frequency dyscoordination hx of localized signs awakened BY (not with) headache occipitonuchal location
How can a tension type headache be recognized?
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
How can a rebound headache be recognized?
= medication overuse
only in migraine pts, hard to treat
What are sinus headaches?
usually not - mostly migraines (including TTH)
lack any other sinus symptoms
How can migraine with aura be recognized?
unilateral, pulsing/throbbing, usually in frontal, temporal, orbital or overlapping
worsened by physical exertion
lasts 4-72 hrs
uncontrolled bouts of dysautonomia
What are the four phases to a migraine attack?
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
How can cluster headaches be recognized?
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
