Lumbar Pathology Flashcards
what hydrophilic properties of the disc change with degeneration
decrease in proteoglycans and increase in collagen in NP and AF
with degeneration, the disc becomes more __ and less ____
more fibrous
less flexible
how is the disc’s ability to transmit forces affected with degeneration
less able to transmit vertical load and shear forces
what type of fissuring occurs with degeneration
circumferential
with degeneration, what happens to the disc height?
relative increase due to structures around it becoming weaker
what happens to the disc height with degradation
decreases - loss of height
describe the order of susceptibility to compression overload
- end plate (weakest)
- VB
- disc
describe the pathology of disc degradation, starting with excessive compression
compression -> end plate fx -> NP exposed to blood -> inflammatory process ->NP loses water and height -> decreased ability to resist loads -> more load to AF -> radial fissure of AF -> herniation
what are the 4 stages of disc herniation (in order)
protrusion
prolapse
extrusion
sequestration
what happens with protrusion
disc bulge without rupture of AF
what happens with prolapse
only outer layers of AF contain nucleus (still intact)
what happens with extrusion
AF is perforated and discal materials move to epidural space
what happens with sequestration
discal fragments from AF and NP are disconnected
which stages of HNP are you likely to see symptoms of radiculopathy
extrusion and sequestration
describe the clinical presentation of someone with an end plate fx
- some MOI/incident
- acute pain/spasm lasting few days to 3 wks
- negative SLR
describe the clinical presentation of protrusion and prolapse
- LBP and/or hip/upper leg referred pain
- pain with increase in intradiscal pressure (cough, sneeze, sitting, bending, etc.)
- negative SLR
describe the clinical presentation of extruded and sequestrated disc
- LBP
- pain with increase in intradiscal pressure
- true sciatica (radicular pain)
- (+ )SLR
- severe pain (prob did not move for a week or so)
describe the referral pattern for disc
- extensive referral
back -> thigh -> leg
what causes radiculopathy
compression or block of n root
describe the symptoms of radiculopathy
- paresthesia (dermatome)
- myotomal weakness
- hypo-reflexia
- may or may not have radicular pain
Lateral HNP is more likely to cause ______ while central HNP is more likely to cause _____
lateral = radiculopathy
central = myelopathy
NOT only causes and NOT every case
what is radicular pain
lancinating pain, traveling along the length of LE (2-3 inches wide)
what is the most common cause of radicular pain
HNP -> inflammation of n (dorsal root or ganglion)
radicular pain only occurs in what types of nerves?
unhealthy
what does somatic referred pain feel like?
dull, aching, gnawing, or expanding pressure
a disc pathology located at L4-5 will affect what nerve roots
L5 NOT L4 - will affect the one below
CT and MRI are abt equally accurate for dx ______
HNP and stenosis
when is imaging recommended?
in the absence of systemic diseases/red flags, not until after 6 wks of failed conservative therapy
narrowing of the spinal canal or IV foramen causing a nerve pinching
spinal stenosis
describe the clinical presentation of a pt with spinal stenosis
- persistent pain (mild to mod) in butt
- limping
- lack of feeling in LE (claudication)
- decreased walking/standing ability (feel better w/ flexion)
describe the ROM findings for spinal stenosis
usually WNL but stiff in all directions
for pts with spinal stenosis, is there a MOI?
no, usually a gradual/insidious onset
a thickened ligamentum flavum or osteophytes in spinal canal can cause what type of stenosis
central stenosis
describe the different presentation of central and lateral stenosis
central - bilat, neurogenic claudication or pain in butt, thigh, leg
lateral - unilat, may have radiculopathy and radicular pain
what are 2 degenerative causes of stenosis
osteophytes
thickened ligamentu flavum
other than degenerative causes, what things can cause stenosis
- HNP + another congenital or acquired
- spondylolisthesis
- post-trauma
- post-op
what are the 2 most common causes of n root entrapment
HNP and lateral recess stenosis
s/s of radiculopathy
- paresthesia (dermatome)
- fatigable weakness (myotome pattern)
- hyporeflexia
- may or may not have radicular pain
- sensory loss (dermatome)
what dx imaging tool is best for N root entrapment
MRI
what are the 2 types of instability
end zone and neutral zone
how does end zone instability occur
loss of PASSIVE restraints to motions with loss of active NM control - disc, capsule, ligament injury
how does end zone instability present?
abnormal center of motion with enlarged neutral zone
- emphasis on abnormal motion rather than hypermobility
describe neutral zone instability
during motion that occurs during normal posture, minimal resistance is offered by passive restraints - joints move too rapidly or too early from neutral zone even though strength of end restraints or range is normal
defect in pars interarticularis connecting superior and inferior facets
spondylolysis
what will you see in an exam that indicated spondylolisthesis
step deformity at segment above affected
when does spondylolisthesis occur
when the VB of affected segment translates anteriorly
describe the grading system for spondylolisthesis (grade 1-5)
Grade 1: 25% translation over segment below
Grade 2: 26-50%
3: 51-75%
4: 76-100%
5: > 100%
which grades for spondylolisthesis require surgery for sure
3-5
what radiograph view is needed to grade the slippage associated with spondylolisthesis
lateral view
describe the clinical presentation of severe (grade 3-4) spondylolisthesis
- SEVERE pain and leg pain (radicular or not)
- often have neuro deficit
- kyphotic L4-5 and L5-S1
- pain increases with walking
what radiographic view is required to see a pars interarticularis deficit
oblique view - neck of Scottie dog
A unilateral pars interarticularis deficit is most commonly seen at which segment
L5
when is surgery recommended for unilateral pars interarticularis
- symptoms > 6 mo
- non healing on CT
- no disc degeneration on MRI
what are some examples of causes of unilateral pars interarticularis deficit
people that do lots of twisting/rotation - especially in one direction
- golf, baseball
describe the process of a unilateral pars interarticularis injury due to torsion forces starting with an excessive rotary force
excess rotary force ->
compression fx of subchondral bone on facet ->
neural arch is shorter after healing ->
increased rotation stress on disc ->
fx pars interarticularis (unilat) ->
facet joint capsule tears ->
AF circumferential tear
what is acute locked back
segmental facet dysfunction
describe the initial presentation of segmental facet dysfunction
sudden onset of pain on attempt extension from bent position
what is the most likely underlying pathology of segmental facet dysfunction
instability associated with recurrent episodes
describe the incident that a pt may describe for segmental facet dysfunction
usually an incident with excessive force (rotation)
- twist and fall, swing bat, MVA
can also be as simple as bend over to pick up a pencil
describe the meniscal entrapment theory
the meniscoid covers the surface of the facet when the facet is gapped or exposed - when the pt tries to return to neutral position (ex: extend from a flexed position) the meniscoid gets stuck
describe the 3 s/s of pt with segmental facet dysfunction
- LBP with occasional radiating/referral pain to butt and posterior thigh
- pain with hyperextension
- paraspinal tenderness
does a pt with segmental facet dysfunction have neurological signs
not usually
where is the referral pattern for pts with segmental facet dysfunction
butt and maybe posterior thigh
DOES NOT usually refer below knee
what should you do/look for after you get a pt with segmental facet dysfunction unstuck?
look for underlying instability
what quadrant motions will you see in a pt with segmental facet dysfunction
restriction in 1 quad loss
chronic inflammatory disease of unknow origin, first affecting spine and progressing to fusion of involved joints
AS
who is AS most common in
males, < 30 yrs age
most pts with AS have what ____
human leukocyte antigen B27 (HLA-B27) gene
ASAS classification criteria for axial spondyloarthritis is used in what pts?
> 3 mo of back pain and age onset < 45
what are the classification criteria for ASAS
- sacroiliitis on imaging + >/= 1 SpA feature
OR
- HLA-B27 + >/= 2 SpA features
spinal fusion that occurs in AS is secondary to _____
syndesmophytes
what 2 things will you see on a radiograph to indicate bamboo spine?
- ossificaiton of AF
- squaring of VB
repetitive and abnormal afferent input from a pathological segment of spinal or visceral sources would converge on the same segment of spine
facilitated segment
in the facilitated segment theory, the repeated input would decrease ______, making transmission impulse to the efferent segment ____
synaptic resistance
easier
what is the outcome of facilitated segment
a lesser degree of afferent input would be able to have a greater efferent output
facilitated segment - the affected nerve tends to _____ and fire ________
over-react
excessively
6 s/s of facilitated segment
- tender to palpation in referred area
- brisk reflex
- non-fatigable weakness
- hypertonicity
- hyper aesthesia
- orange peel appearance (vasoconstriction)
why does a facilitated segment have non-fatigable weakness
due to inhibition of n root
enhancement in function of neurons and circuit in nociceptive pathway caused by increase in membrane excitability and synaptic efficacy in response to activity, inflammation and neural injury
central facilitation/sensitization
central facilitation/sensitization - pain is no longer _____
protective
what are 4 clinical manifestations of sensitization
- allodynia
- hyperalgesia
- after sensation
enhanced temporal summation
pain can be elicited by normally innocuous stimuli
allodynia
pain is exaggerated and prolonged in response to noxious stimuli
hyperalgesia
what is after sensation?
after the stimuli is removed, pt still has pain
what is enhanced temporal summation in relation to pain
after repeated stimuli, pain gets worse
